Chapter 35 – Care of the Patient with Acute Coronary Syndromes
acute coronary syndrome (ACS) Disorder including unstable angina and myocardial infarction; results
from obstruction of the coronary artery by ruptured atherosclerotic plaque and leads to platelet
aggregation, thrombus formation, and vasoconstriction.
angina pectoris Chest pain caused by a temporary imbalance between the coronary arteries’ ability to
supply oxygen and the cardiac muscle’s demand for oxygen.
atypical angina Angina with vague presentation such as indigestion, pain between the shoulders, an
aching jaw, or choking sensation that occurs with exertion.
cardiac rehabilitation The process of actively assisting the patient with coronary disease to achieve and
maintain a productive life while remaining within the limits of the heart’s ability to respond to increases
in activity and stress.
cardiogenic shock Post–myocardial infarction heart failure in which necrosis of more than 40% of the
left ventricle has occurred; also called Class IV heart failure.
chronic stable angina (CSA) Type of angina characterized by chest discomfort that occurs with
moderate-to-prolonged exertion and in a pattern that is familiar to the patient.
coronary artery bypass graft (CABG) Surgical procedure in which occluded arteries are bypassed with
the patient’s own venous or arterial blood vessels or synthetic grafts.
coronary artery disease (CAD) Disease affecting the arteries that provide blood, oxygen, and nutrients
to the myocardium; also known as coronary heart disease or simply heart disease.
infarction Necrosis, or cell death.
intra-aortic balloon pump (IABP) Specialized catheter and balloon inserted into aorta that inflates and
deflates with the cardiac cycle in order to decrease afterload and increase coronary perfusion.
ischemia Blockage of blood flow through a blood vessel, resulting in a lack of oxygen.
metabolic syndrome Collection of related health problems with insulin resistance as a main feature;
increases the risk for cardiovascular disease.
myocardial infarction (MI) Injury and necrosis of myocardial tissue that occurs when the tissue is
abruptly and severely deprived of oxygen.
new-onset angina Cardiac chest pain that occurs for the first time.
non–ST-elevation myocardial infarction (NSTEMI) Myocardial infarction in which the patient typically
has ST- and T-wave changes on a 12-lead ECG; this indicates myocardial ischemia.
percutaneous coronary intervention (PCI) Nonsurgical method of improving arterial flow by opening
the vessel lumen. A balloon is inserted in the coronary artery and inflated to open blood vessels;
procedure may include insertion of a coronary stent.
pulmonary artery occlusion pressure (PAOP) Measurement of pressure in the left atrium using a
balloon-tipped catheter introduced into the pulmonary artery.
ST-elevation myocardial infarction (STEMI) Myocardial infarction in which the patient typically has ST
elevation in two contiguous leads on a 12-lead ECG; this indicates myocardial infarction (necrosis).
vasospastic angina Angina caused by coronary artery vasospasm that often occurs at rest or during the
early morning hours; also called variant or Prinzmetal angina.
ventricular remodeling After a myocardial infarction, permanent changes in the size and shape of the
left ventricle due to scar tissue; such remodeling can decrease left ventricular function and cause heart
failure.
Coronary Artery Disease (CAD)
- Chronic stable angina, acute coronary syndromes
- Ischemia
- Infarction
Coronary artery disease (CAD) is a broad term that includes chronic stable angina and acute coronary
syndrome (ACS). It affects the arteries that provide blood, oxygen, and nutrients to the myocardium.
When blood flow through the coronary arteries is partially or completely blocked, ischemia and
infarction of the myocardium may result.
Ischemia occurs when insufficient oxygen is supplied to meet the requirements of the myocardium.
Infarction (necrosis, or cell death) occurs when severe ischemia is prolonged and decreased perfusion
causes irreversible damage to tissue.
CAD, also called coronary heart disease (CHD) or simply heart disease, is the single largest killer of
American men and women in all ethnic groups. When the arteries that supply the myocardium are
diseased, the heart cannot pump blood effectively to adequately perfuse vital organs and peripheral
tissues. The organs and tissues need oxygen in arterial blood for survival. When perfusion is impaired,
the patient can have life-threatening signs and symptoms and possibly death.
Chronic Stable Angina (CSA) Pectoris
Angina pectoris is chest pain caused by a temporary imbalance between the coronary arteries’ ability to
supply oxygen and the cardiac muscle’s demand for oxygen. Ischemia (lack of oxygen) that occurs with
angina is limited in duration and does not cause permanent damage of myocardial tissue. Angina may be
of two main types: stable angina and unstable angina.
Chronic stable angina (CSA) is chest discomfort that occurs with moderate-to-prolonged exertion in a
pattern that is familiar to the patient. The frequency, duration, and intensity of symptoms remain the
same over several months. CSA results in only slight limitation of activity and is usually associated with a
fixed atherosclerotic plaque. It is usually relieved by nitroglycerin (NTG) or rest and often is managed
with drug therapy. Rarely does CSA require aggressive treatment.
Perfusion Concept Exemplar: Acute Coronary Syndrome Pathophysiology Review
The term acute coronary syndrome (ACS) is used to describe patients who have either unstable angina
or an acute myocardial infarction (MI). In ACS, it is believed that the atherosclerotic plaque in the
coronary artery ruptures, resulting in platelet aggregation (“clumping”), thrombus (clot) formation, and
vasoconstriction. The amount of disruption of the atherosclerotic plaque determines the degree of
coronary artery obstruction (blockage) and the specific disease process. Once the artery reaches 50%
occlusion, blood flow is impaired, creating myocardial ischemia when myocardial demand is increased.
Unstable angina (UA) is chest pain or discomfort that occurs at rest or with exertion and causes severe
activity limitation. An increase in the number of attacks and in the intensity of the pressure indicates UA.
The pressure may last longer than 15 minutes or may be poorly relieved by rest or nitroglycerin. Patients
with unstable angina may present with ST changes on a 12-lead ECG but do not have changes in
troponin levels. Ischemia is present but is not severe enough to cause detectable myocardial damage or
cell death. As the assays for troponins become more sensitive, the diagnosis of UA is decreasing.
UA includes:
- New-onset angina – when a patient has their first angina symptoms, usually after exertion or
other increased demands on the heart.
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Vasospastic angina (variant or Prinzmetal angina) - chest pain or discomfort resulting from
coronary artery spasm and typically occurs after rest
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Pre-infarction angina - chest pain that occurs in the days or weeks before a myocardial
infarction.
The most serious acute coronary syndrome is myocardial infarction (MI), often referred to as acute MI
or AMI. Undiagnosed or untreated angina can lead to this very serious health problem.
Myocardial infarction (MI) occurs when myocardial tissue is abruptly and severely deprived of oxygen.
When blood flow is quickly reduced by 80% to 90%, ischemia develops. Ischemia can lead to injury and
necrosis of myocardial tissue if blood flow is not restored.
Two types of MI: non–ST-segment elevation myocardial infarction (NSTEMI) and ST-elevation myocardial
infarction (STEMI).
NSTEMI (non–ST-segment elevation myocardial infarction)
- Typically have ST segment and T-wave changes on a 12-lead ECG (ST depression and T-wave3
inversion), this indicates myocardial ischemia
- Troponin may be normal, but it elevates over the next 3 to 12 hours.
o This combo indicates myocardial cell death or necrosis
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Asses clinical presentation and history of patient – patients without typical symptoms
(chest discomfort, shortness of breath, nausea) of ACS may have another condition (ex.
Sepsis)
Causes of NSTEMI
o Coronary vasospasm
o Spontaneous dissection
o Sluggish blood flow due to narrowing of the coronary artery.
STEMI (ST-elevation myocardial infarction)
- ST elevation in two contiguous leads on a 12-lead ECG (Indicates MI/necrosis)
- Attributable to rupture of the fibrous atherosclerotic plaque leading to platelet aggregation and
thrombus formation at the site of rupture
- The thrombus causes an abrupt 100% occlusion to the coronary artery; this is a medical
emergency and requires immediate revascularization of the blocked coronary artery.
Often MIs begin with infarction of the subendocardial (inner ventricular walls) layer of cardiac muscle,
which has the greatest oxygen demand and the poorest oxygen supply.
Zone of necrosis - Initial area of infarction
Zone of injury - tissue that is injured but not necrotic
Zone of ischemia—tissue that is oxygen deprived
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Infarction is a dynamic process that evolves over several hours.
Hypoxemia from ischemia may lead to local vasodilation of blood vessels and acidosis.
Potassium, calcium, and magnesium imbalances, as well as acidosis at the cellular level, may
cause changes in normal conduction and contractile functions.
Catecholamines (epinephrine and norepinephrine) released in response to hypoxia and pain may
increase the heart’s rate, contractility, and afterload.
- These factors increase oxygen requirements in tissue that is already oxygen deprived.
- This may lead to life-threatening ventricular dysrhythmias.
- The area of infarction may extend into the zones of injury and ischemia.
- The zone of infarction depends on three factors
o Collateral circulation
o Anaerobic metabolism
o Workload demands on the myocardium.
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Obvious physical changes occur 6 hours after the infarction - infarcted region appears blue/
swollen – need for intervention within first 4-6 hours of symptom onset
After 48 hours – are turns gray with yellow streaks as neutrophils remove the necrotic cells
8-10 days after, granulation tissue forms at the edges of the necrotic tissue
2-3 months – necrotic area develops into a shrunken, thin, firm scar.
Scar tissue causes ventricular remodeling (permanently changes the size and shape of the left
ventricle)
o May decrease left ventricular function (lead to hear failure, morbidity, and mortality)
o Scar tissue does not contract or conduct electrically – often cause of chronic ventricular
dysrhythmias
The patient’s response to an MI also depends on which coronary artery or arteries were obstructed and
which part of the ventricle wall was damaged: anterior, septal, lateral, inferior, or posterior.
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Obstruction of the left anterior descending (LAD) artery causes anterior or septal MIs because it
perfuses the anterior wall and most of the septum of the left ventricle. Patients with anterior
wall MIs (AWMIs) have the highest mortality rate because they are most likely to have left
ventricular failure and dysrhythmias from damage to the left ventricle.
The circumflex artery supplies the lateral wall of the left ventricle and possibly portions of the
posterior wall or the sinoatrial (SA) and atrioventricular (AV) nodes. Patients with obstruction of
the circumflex artery may experience a posterior wall MI (PWMI) or a lateral wall MI (LWMI) and
sinus dysrhythmias.
In most people, the right coronary artery (RCA) supplies most of the SA and AV nodes, as well as
the right ventricle and inferior or diaphragmatic portion of the left ventricle. Patients with
obstruction of the RCA often have inferior wall MIs (IWMIs). About half of all IWMIs are
associated with an occlusion of the RCA, causing significant damage to the right ventricle. Thus it
is important to obtain a “right-sided” ECG to assess for right ventricular involvement
Etiology and Genetic Risk
Atherosclerosis (A thickening or hardening of the arterial wall, often associated with aging) is the
primary factor in the development of CAD.
Nonmodifiable Risk Factors
- Age
- Gender
- Family History
- Ethnic Background
Modifiable Risk Factors
- Smoking
- Obesity
- Stress
- Elevated Cholesterol
- Hypertension
- Diabetes
Metabolic syndrome (insulin resistance syndrome or syndrome X) is a risk factor for cardiovascular (CV)
disease. Patients who have three of the factors in the below table are diagnosed with metabolic
syndrome.
This health problem increases the risk for developing diabetes and CAD. The presence of central obesity,
high blood pressure, and hyperglycemia when diagnosed with metabolic syndrome presents the highest
risk for development of cardiovascular disease. Females have a higher prevalence of metabolic
syndrome, and overall prevalence increases with age.
Health Promotion and Maintenance
◦ AEDs (automatic external defibrillators) available in public places and in homes
◦ Controlling or altering modifiable risk factors is critical
◦ Action
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Create a patient teaching handout that incorporates a list of modifiable and nonmodifiable
risk factors for coronary artery disease (CAD).
Include pertinent teaching information about how patients could modify behaviors to
address modifiable risk factors.
Assessment: Recognize Cues
History:
If symptoms of CAD are present at the time of the interview, delay collecting data until interventions are
started to relieve symptoms.
Physical Assessment/Signs and Symptoms:
- Rapid assessment is crucial
- Differentiate among the types of chest pain and identify the source
- Assess blood pressure, heart rate, distal peripheral pulses, skin temperature, respiratory rate,
breath sounds, presence of jugular venous distention and peripheral edema
- Auscultate for an S 3 gallop, which often indicates heart failure
Psychosocial Assessment:
- Assess the patient’s current coping mechanisms
- Denial, anger, depression, fear, and anxiety are common
Laboratory Assessment:
- There is no single test to diagnose MI
- Most common laboratory tests include troponins T and I
- Troponin is specific for MI and cardiac necrosis
- Troponins T and I rise quickly
Imaging Assessment:
- A chest x-ray may be performed to help rule out aortic dissection, which may mimic an MI.
- Thallium scans use radioisotope imaging to assess for ischemia or necrotic muscle tissue related
to angina or MI. Areas of decreased or absent perfusion, referred to as cold spots, identify
ischemia or infarction. Thallium may be used with the exercise tolerance test.Dipyridamole
thallium scanning (DTS) may also be used.
- Contrast-enhanced cardiovascular magnetic resonance (CMR) imaging may also be done as a
noninvasive approach to detect CAD
- Echocardiography may be used to visualize the structures of the heart
- Use of 64-slice computed tomography coronary angiography (CTCA) has been found to be
helpful in diagnosing CAD. The high-speed CT scanner is a highly reliable, noninvasive way to
evaluate calcified plaque. This plaque is then quantified into the calcium score. Those with a
calcium score (also called the Agatston score) higher than 400 have a higher risk of developing
myocardial infarction and death within the next 2 to 5 years
Other Diagnostic Assessment:
- Twelve-lead ECGs examine the heart from varying perspectives
- Identifying the lead(s) in which ECG changes are occurring can identify both the occurrence and
the location of ischemia (angina) or necrosis (infarction).
- “Right-sided” or 18-lead ECG can determine whether ischemia or infarction have occurred in the
right ventricle
- The ECG should be obtained within 10 minutes of patient presentation with chest discomfort
- 12-lead ECGs obtained during an angina episode reveal ST depression, T-wave inversion, or
both.
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Vasospastic angina, caused by coronary vasospasm (vessel spasm), usually causes elevation of
the ST segment during angina attacks.
These ST and T-wave changes usually subside when the ischemia is resolved and pain is relieved.
However, the T wave may remain flat or inverted for a period of time.
When infarction occurs, one of two ECG changes is usually observed: ST elevation MI (STEMI), or
non–ST-elevation MI (NSTEMI).
An abnormal Q wave (wider than 0.04 second or more than one-third the height of the QRS
complex) may develop, depending on the amount of myocardium that has necrosed.
After the acute stages of an unstable angina episode, the health care provider often requests an
exercise tolerance test (stress test) on a treadmill to assess for ECG changes consistent with
ischemia, evaluate medical therapy, and identify those who might benefit from invasive therapy.
Pharmacologic stress-testing agents such as dobutamine may be used instead of the treadmill
Cardiac catheterization may be performed to determine the extent and exact location of
coronary artery obstructions. Identifies patients who might benefit from percutaneous coronary
intervention (PCI) or from coronary artery bypass graft (CABG)
Analysis: Analyze Cues and Prioritize Hypotheses:
The priority collaborative problems for most patients with acute coronary syndrome (ACS) include:
1. Acute pain due to an imbalance between myocardial oxygen supply and demand
2. Decreased myocardial tissue perfusion due to interruption of arterial blood flow
3. Potential for dysrhythmias due to ischemia and ventricular irritability
4. Potential for heart failure due to left ventricular dysfunction
Planning and Implementation: Generate Solutions and Take Action
Managing Acute Pain
- Decrease pain, decrease myocardial oxygen demand, and increase perfusion (myocardial oxygen
supply).
- The patient may take nitroglycerin to relieve episodic anginal pain.
- Nitroglycerin is contraindicated with the use of phosphodiesterase inhibitors (used for erectile
dysfunction or pulmonary arterial hypertension) because it can cause profound hypotension
- Nitroglycerin (NTG), a nitrate often referred to as “nitro,” increases collateral blood flow,
redistributes blood flow toward the subendocardium, and dilates the coronary arteries
- During administration of long-term oral and topical nitrates, an 8- to 12-hour nitrate-free period
should be maintained to prevent tolerance
Increasing Myocardial Tissue Perfusion
- The primary outcome is that the patient will have increased myocardial perfusion as evidenced
by adequate cardiac output, normal sinus rhythm, and vital signs within normal limits
- Aspirin inhibits both platelet aggregation and vasoconstriction, thereby decreasing the
likelihood of thrombosis
- P2Y 12 platelet inhibitors such as clopidogrel or ticagrelor, may be given with an initial loading
dose followed by a daily dose for up to 12 months after diagnosis. These oral agents work to
prevent platelets from aggregating (clumping) together to form clots
- Glycoprotein (GP) IIb/IIIa inhibitors such as abciximab, eptifibatide, or tirofiban may be
administered IV to prevent fibrinogen from aaching to activated platelets at the site of a
thrombus. These medications are used in unstable angina and NSTEMI. They are also given
before and during percutaneous coronary intervention (PCI) to maintain patency of an artery
with a large clot and are given with fibrinolytic agents after STEMI
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Another antiplatelet, a protease-activated receptor inhibitor (PAR-1), vorapaxar, is shown to
decrease the risk of recurrent MI when added to the regimen of aspirin and clopidogrel
Anticoagulation therapy may also be used to prevent clot formation
Once-a-day beta-adrenergic blocking agents (e.g., metoprolol XL, carvedilol CR), sometimes just
called beta blockers (BBs), decrease the size of the infarct, the occurrence of ventricular
dysrhythmias, and mortality rates in patients with MI. Beta blockers slow the heart rate and
decrease the force of cardiac contraction. Thus, these agents prolong the period of diastole and
increase myocardial perfusion while reducing the force of myocardial contraction. With beta
blockade, the heart can perform more work without ischemia.
Health care providers frequently prescribe angiotensin-converting enzyme inhibitors (ACEIs) or
angiotensin receptor blockers (ARBs) within 24 hours of ACS to prevent ventricular remodeling
and the development of heart failure
For patients with angina, the health care provider may prescribe calcium channel blockers
(CCBs) to promote vasodilation and myocardial perfusion. These drugs are indicated for patients
with vasospastic angina or for those who are hypertensive and continue to have angina despite
therapy with beta blockers (unstable angina). They are not indicated after an acute MI unless
beta blockade is contraindicated
Calcium channel blockers are also used for chronic stable angina (CSA). When they are not
successful in managing CSA, ranolazine may be added to the drug regimen. This drug has
antiangina and anti-ischemic properties and is often effective in relieving the pain associated
with CSA
Statin therapy reduces the risk of developing recurrent MI, mortality, and stroke
Reperfusion Therapy
- One of two reperfusion strategies are used to open a blocked artery in a patient experiencing
acute MI: thrombolytic therapy or percutaneous coronary intervention (PCI). PCI is the
treatment of choice for most patients with STEMI
- Fibrinolytic therapy (also called thrombolytic therapy) dissolves thrombi in the coronary arteries
and restores myocardial blood flow.
- The goal is to administer fibrinolytic therapy within 30 minutes of arrival to the hospital
- It is not indicated for the NSTEMI patient population
- Monitor the patient for indications that the clot has been lysed (dissolved) and the artery
reperfused. These indications include:
o Abrupt cessation of pain or discomfort
o Sudden onset of ventricular dysrhythmias
o Resolution of ST-segment depression/elevation or T-wave inversion
o A peak at 12 hours of markers of myocardial damage
Percutaneous Coronary Intervention
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An invasive but nonsurgical technique that is the treatment of choice to reopen the clotted
coronary artery and restore perfusion.
The goal is to perform PCI within 90 minutes of an acute STEMI diagnosis
Performed in the cardiac catheterization laboratory and combines clot retrieval, coronary
angioplasty, and stent placement. Under fluoroscopic guidance, the cardiologist performs initial
coronary angiography, inserting an arterial sheath and advancing a catheter in a retrograde
manner through the aorta
In the STEMI patient, if a clot is seen, a clot retrieval device is inserted over the guidewire, and
the clot is removed
Once the clot is removed in the STEMI patient or area of narrowing is identified in the NSTEMI
patient, a balloon-tipped catheter is introduced through a guidewire to the coronary artery
occlusion. The physician activates a compressor that inflates the balloon (angioplasty) to force
the plaque against the vessel wall, thus dilating the wall, and reduces or eliminates the
occluding clot.
Balloon inflation may be repeated until angiography indicates a decrease in the stenosis
(narrowing) to less than 50% of the vessel’s diameter
The balloon catheter is then withdrawn, and a balloon catheter with stent is introduced. Once
the stent and balloon are in position, the stent is deployed by the balloon inflation. The balloon
is deflated and the stent stays in place, acting as scaffolding to hold the diseased artery open.
Stents are expandable metal mesh devices that are used to maintain the patent lumen created
by angioplasty or atherectomy
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PCI initially reopens the vessel in most patients. However, within the first 24 hours, a small
percentage of patients have restenosis. At 6 months, a larger number have one or more
blockages. Without stent placement, the artery often reoccludes because of its normal elasticity
and memory.
Identifying and Managing Dysrhythmias
- Dysrhythmias are the leading cause of prehospital death in most patients with ACS.
- When a dysrhythmia develops:
o Identify the dysrhythmia
o Assess hemodynamic status
o Evaluate for discomfort.
- Dysrhythmias are treated when they cause hemodynamic compromise, increase myocardial
oxygen requirements, or predispose the patient to lethal ventricular dysrhythmias
- Typical dysrhythmias for the patient with an inferior ACS are bradycardias and second-degree
atrioventricular (AV) blocks resulting from ischemia of the AV node.
- If the patient becomes hemodynamically unstable, a temporary pacemaker may be necessary.
- The patient with an anterior ACS is likely to exhibit premature ventricular contractions (PVCs)
caused by ventricular irritability. Third-degree or bundle branch block is a serious complication
in this patient because it indicates that a large portion of the left ventricle is involved. The health
care provider may insert a pacemaker.
Monitoring for and Managing Heart Failure
- Decreased cardiac output due to heart failure is a relatively common complication after an MI
resulting from left ventricular dysfunction, rupture of the intraventricular septum, papillary
muscle rupture with valvular dysfunction, or right ventricular infarction.
- The most severe form of acute heart12 failure, cardiogenic shock, causes most in-hospital
deaths after an ACS
Managing Left Ventricular Failure
- The amount of blood that the heart can eject is reduced
- When volume and pressure are markedly increased in the pulmonary vasculature, pulmonary
complications such as, pulmonary edema, can develop
- Hemodynamic monitoring is a term that refers to a variety of monitoring techniques designed to
provide quantitative information about vascular capacity, blood volume, pump effectiveness,
and tissue perfusion. The type of monitoring can vary from noninvasive to highly invasive. Finger
cuff hemodynamic monitoring systems provide noninvasive continuous monitoring of stroke
volume, cardiac output, and blood pressure.
- Invasive hemodynamic monitoring directly measures pressures in the heart and great vessels.
These procedures are usually performed for more seriously ill patients and can provide more
accurate measurements of blood pressure, heart function, and volume status
- Invasive hemodynamic monitoring does involve significant risks; informed consent is therefore
required. The components of this pressure-monitoring system are a catheter with an infusion
system, a transducer, and a monitor. The catheter receives the pressure waves (mechanical
energy) from the heart or the great vessels. The transducer converts the mechanical energy into
electrical energy, which is displayed as waveforms or numbers on the monitor. Patency of the
catheter is maintained with a slow continuous flush of normal saline, usually infused at 3 to 4
mL/hr under pressure to prevent the backup of blood and occlusion of the catheter.
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Because this system is designed to measure pressure, it is important to account for atmospheric
pressure (calibration) and hydrostatic pressure associated with the level of the transducer. \
Identify the phlebostatic axis, a physical reference point on the chest, and level the transducer
to this point
Right atrial pressure is measured by a pressure sensor on the catheter inside the right atrium
(RA). Normal RA pressure ranges from 0 to 8 mm Hg. Increased RA pressures may occur with
right ventricular failure, whereas low RA pressures usually indicate hypovolemia.
Pulmonary artery pressure (PAP) is also assessed and is constantly visible on most hemodynamic
monitors. Normal PAP ranges from 15 to 30 mm Hg systolic to 3 to 12 mm Hg diastolic. When
the balloon at the catheter tip is inflated, the catheter advances and wedges in a branch of the
pulmonary artery. The tip of the catheter can sense pressures transmitted from the left atrium,
which reflect left ventricular end-diastolic pressure (LVEDP).
The pressure measured during balloon inflation is called the pulmonary artery occlusion
pressure (PAOP), also referred to as a wedge pressure because the balloon is wedged within the
small vessel. Normal PAOP ranges from 5 to 12 mm Hg. Elevated PAOP measurements may
indicate left ventricular failure, hypervolemia, mitral regurgitation, or intracardiac shunting. A
decreased PAOP is seen with hypovolemia or afterload reduction.
Classification of post–myocardial infarction heart failure
- The classic Killip system identifies four classes based on prognosis
o Patients with class I heart failure often respond well to reduction in preload with IV
nitrates and diuretics. Monitor the urine output hourly, check vital signs hourly,
continue to assess for signs of heart failure, and review the serum potassium level.
o Patients with class II and class III heart failure may require diuresis and more aggressive
medical intervention, such as afterload reduction and/or enhancement of contractility.
IV nitroprusside or nitroglycerin may be used to decrease both preload and afterload.
These drugs are given as continuous infusions in specialized units where hemodynamic
monitoring can occur. Intra-arterial BP monitoring is preferred for nitroprusside
administration
o Patients in classes II and III are usually started on once-a-day beta blockers. Dosing is
titrated, depending on goal achievement and drug tolerance. Other drugs, including
ACEIs and ARBs, are commonly prescribed to inhibit ventricular remodeling
o Class IV heart failure is cardiogenic shock. In cardiogenic shock, necrosis of more than
40% of the left ventricle occurs. Most patients have a stuttering pattern of chest pain,
resulting in extension of the ACS.
Other interventions for left-sided heart failure
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When patients do not respond to drug therapy with improved tissue perfusion, decreased
workload of the heart, and increased cardiac contractility, mechanical circulatory support, such
as an intra-aortic balloon pump (IABP) may be inserted.
The IABP is a temporary, invasive, percutaneous intervention that is used to improve myocardial
perfusion during an acute MI, reduce preload and afterload, and facilitate left ventricular
ejection.
Inflation of the IABP during diastole augments the diastolic pressure and improves coronary
perfusion by increasing blood flow to the arteries. Deflation of the balloon just before systole
reduces afterload at the time of systolic contraction. This action facilitates emptying of the left
ventricle and improves cardiac output.
The balloon catheter is attached to a pump console, which is triggered by an ECG tracing and
arterial waveform.
In patients undergoing high-risk percutaneous coronary intervention (PCI) or those at risk for
cardiogenic shock, a percutaneous ventricular assist device may be used.
These devices are used temporarily to decrease the myocardial workload and oxygen
consumption of the heart and increase cardiac output and peripheral perfusion. Immediate
reperfusion is an invasive intervention that shows some promise for managing cardiogenic
shock.
The patient is taken to the cardiac catheterization laboratory, and an emergency left-sided heart
catheterization is performed. If he or she has a treatable occlusion or occlusions, the
interventional cardiologist performs a PCI in the catheterization laboratory, or the patient is
transferred to the operating suite for a coronary artery bypass graft (CABG)
Managing Right Ventricular Failure
- In about a third of patients with inferior MIs, right ventricular infarction and failure develop. In
this instance, the right ventricle fails independently of the left.
- Decreased cardiac output with a paradoxical pulse, clear lungs, and jugular venous distention
occurs when the patient is in semi-Fowler position.
- The desired outcome of management is to improve right ventricular stroke volume by increasing
right ventricular fiber stretch or preload.
- To enhance right ventricular preload, give sufficient fluids to increase right atrial pressure to 20
mm Hg
- If medical therapy is not sufficient to support the right ventricle and reverse the shock state, a
right percutaneous ventricular assist device may be needed. This is a temporary measure to
support the failing heart while treating the cardiogenic shock with medical therapy.
Coronary Artery Bypass Graft Surgery (CABG)
- Improve blood flow to myocardial tissue at risk for ischemia or infarction resulting from
occlusion of the artery, if medical regimen not successful
- It is the most common type of cardiac surgery and the most common procedure for older adults.
Almost half of all CABGs are done for patients older than 65 years.
- The occluded coronary arteries are bypassed with the patient’s own venous or arterial blood
vessels or synthetic grafts. The internal thoracic artery (also referred to as the internal
mammary artery [IMA]) is often the graft of choice because it has an excellent patency rate
many years after the procedure.
- CABG is indicated when patients do not respond to medical management of CAD or when
disease progression is evident
- Candidates for surgery are patients who have:
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Angina with greater than 50% occlusion of the left main coronary artery that cannot be
stented
Unstable angina with severe two-vessel disease, moderate three-vessel disease, or
small-vessel disease in which stents could not be introduced
Ischemia with heart failure
Acute MI with cardiogenic shock
Signs of ischemia or impending MI after angiography or percutaneous coronary
intervention
Valvular disease
Coronary vessels unsuitable for PCI
Preop Care:
Standard preop teaching. Familiarize the client and family with the cardiac critical care unit. Inform the
client to expect a sternal incision, possible arm or leg incision(s), one or two chest tubes, a Foley
catheter, and several IV fluid catheters. ET tube so they will be unable to speak. Will be on ventilator,
will need to breathe with the ventilator and not fight it. Pain meds will be available. Medications may be
discontinued preop (usually, diuretics 2 to 3 days before surgery, digoxin 12 hours before surgery, and
aspirin and anticoagulants 1 week before surgery).
Postop Care:
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Manage F&E balance
Complications—hypotension, hypothermia, hypertension, bleeding, cardiac tamponade,
change in level of consciousness
Administer medications as prescribed, which may include potassium chloride,
antihypertensives, antidysrhythmics, and antibiotics.
The patient should report any pain to the nursing staff
Most of the pain will be in the site where the vessel was harvested. (With the use of
endovascular vessel harvesting [EVH] and one or two small incisions, the pain and
edema are less than for previously performed procedures.)
Analgesics will be given to decrease pain
Coughing and deep breathing are essential to prevent pulmonary complications
Early ambulation is important to decrease the risk for venous thrombosis and possible
embolism
All CABG patients, especially those with IMA grafts, are at high risk for atelectasis, the
number-one complication.
Heart-lung bypass circuitry used during cardiopulmonary bypass
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Cardiopulmonary bypass (CPB) is used to provide oxygenation, circulation, and hypothermia
during induced cardiac arrest.
Blood is diverted from the16 heart to the bypass machine, where it is heparinized, oxygenated,
and returned to the circulation through a cannula placed in the ascending aortic arch or femoral
artery
During bypass, the patient’s core temperature remains between 95°F (35°C) (cold cardioplegia)
and normal temperature (warm cardioplegia). Although cooling decreases the rate of
metabolism and demand for oxygen, keeping the heart “warm” decreases postoperative
complications that were more common when cold cardioplegia was used.
The heart is perfused with a potassium solution, which decreases myocardial oxygen
consumption and causes the heart to stop during diastole. This process ensures a motionless
operative field and prevents myocardial ischemia.
Once the heart is arrested, the grafting procedure can begin. The surgeon uses the internal
mammary artery (IMA), a saphenous vein, and/or a radial artery to bypass blockages in the
coronary arteries. The distal end of the vessel graft is dissected and attached below the clot in
the coronary artery. If the surgeon uses a venous graft or the radial artery, it is anastomosed
(sutured) proximally to the aorta and distally to the coronary artery just beyond the occlusion,
thus improving myocardial perfusion.
After flow rates through the grafts are measured, the heart is rewarmed slowly. The cardioplegic
solution is flushed from the heart. The heart regains its rate and rhythm, or it may be
defibrillated to return it to a normal rhythm.
When the procedure is completed, the patient may be rewarmed (if cold cardioplegia was used)
and weaned from the bypass machine while the grafts are observed for patency and leakage.
The surgeon may place atrial and ventricular pacemaker wires and mediastinal and pleural chest
tubes. Finally the surgeon closes the sternum with wire sutures.
Two methods of coronary artery bypass graft
Minimally invasive direct coronary artery bypass. The minimally invasive direct coronary artery bypass
(MIDCAB) may be indicated for patients with a lesion of the left anterior descending (LAD) artery. In the
most common MIDCAB procedure, a left thoracotomy incision is made, and the rib retraction is
required. Then the left internal mammary artery (IMA) is dissected and attached to the still-beating
heart below the level of the lesion. Cardiopulmonary bypass (CPB) is not required.
Endovascular (endoscopic) vessel harvesting. Regardless of whether the traditional CABG or the
MIDCAB is performed, the donor vessel may be obtained using an endoscope rather than a large surgical
incision. The radial artery or a vein in the leg may be taken with this method. Instead of a large, painful
incision, the patient has one or two very small incisions in the leg or arm. This procedure has decreased
hospital length of stay, postoperative complications, and pain.
Off-pump coronary artery bypass Off-pump coronary artery bypass (OPCAB) is a procedure in which
open-heart surgery is performed without the use of a heart-lung bypass machine. Advantages include
shorter hospital stays and decreased mortality rate, risk for infection, and cost. The disadvantage of
OPCAB is that it requires cardiac surgeons to have increased skill to master the technique.
Robotic-assisted heart surgery Less invasive open-heart surgery. Surgeons operate endoscopically
through very small incisions in the chest wall. Simplifies the surgical process, eliminates tremors that can
exist with human hands, increases the ability to reach otherwise inaccessible sites, and improves depth
perception and visual acuity. Shorter hospital stays (average stay is 2 to 3 days), less pain because of
smaller incisions, no need for heart-lung bypass machine, less anxiety for the patient, and greater
patient acceptance.
Care Coordination and Transition Management
Home Care Management
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Patients who have experienced a myocardial infarction (MI), angina, or coronary artery bypass
graft (CABG) surgery are usually discharged to home or to a transitional care setting with drug
therapy and specific activity prescriptions.
Patients should not be discharged to home alone. Assess whether the patient has family or
friends to provide assistance. In some cases, a home care nurse may be needed
Cardiac rehabilitation is available in most communities for patients after an MI or CABG surgery,
but only a small percentage participate in structured rehabilitation programs
Self-Management Education
- Develop a teaching plan, which usually includes education about the normal anatomy and
physiology of the heart, the pathophysiology of angina and MI, risk factor modification, activity
and exercise protocols, cardiac drugs, and when to seek medical assistance.
Risk Factor Modification
- Modifications may include tobacco cessation, altered dietary patterns, regular exercise, BP
control, and blood glucose control.
- The mainstays of cholesterol control are nutritional therapy and antihyperlipidemic agents
- Maintain adequate dietary potassium, calcium, and magnesium intake.
- Collaborate with the cardiac rehabilitation specialist to establish an activity and exercise
schedule as part of rehabilitation, depending on the cardiac procedure that was performed
- Instruct the patient to remain near home during the first week after discharge and to continue a
walking program. Patients may engage in light housework or any activity done while sitting and
that does not precipitate angina.
- During the second week, they are encouraged to increase social activities and possibly to return
to work part-time. By the third week, they may begin to lift objects as heavy as 15 lb but should
avoid lifting or pulling heavier objects for the first 6 to 8 weeks
- Patients may begin a simple walking program by walking 400 feet twice a day at the rate of 1
mile/hr the first week after discharge and increasing the distance and rate as tolerated, usually
weekly, until they can walk 2 miles at 3 to 4 miles/hr.
- After a limited exercise tolerance test, the cardiac rehabilitation specialist or nurse encourages
the patient to join a formal exercise program, ideally one that helps him or her monitor
cardiovascular progress. The program should include 5- to 7-minute warm-up and cool-down
periods and 30 minutes of aerobic exercise. The patient should engage in aerobic exercise a
minimum of three (and preferably five) times a week.
Complementary and Integrative Health.
- Techniques such as progressive muscle relaxation, guided imagery, music therapy, pet therapy,
and therapeutic touch may decrease anxiety, reduce depression, and increase adherence with
activity and exercise regimens after heart surgery.
- Teach patients that adding omega-3 fay acids from fish and plant sources has been effective for
some patients in reducing lipid levels, stabilizing atherosclerotic plaques, and reducing sudden
death from an MI.
- Patients often take a number of other supplements, such as vitamin E, coenzyme Q10, Pantesin,
and vitamin B complex to decrease the risk for heart disease. However, studies do not show that
these substances are helpful in reducing coronary artery disease.
Sexual Activity.
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Inform the patient and his or her partner that engaging in their usual sexual activity is unlikely
to damage the heart
Patients can resume sexual intercourse on the advice of the health care provider, usually after
an exercise tolerance assessment
In general, those who can walk one block or climb two flights of stairs without symptoms can
usually safely resume sexual activity
Drug Therapy.
- Assess patients with diabetes mellitus for their ability to control hyperglycemia
- Teach patients that some medications, such as beta blockers, may block symptoms of
hypoglycemia.
- Many patients with angina are discharged while taking aspirin, a beta blocker, a calcium channel
blocker, a statin agent, and a nitrate. Those who have experienced an MI may require dual
antiplatelet therapy with aspirin and a P2Y12 inhibitor, a beta blocker, a statin drug, and, if the
ejection fraction is below 40%, an ACEI and/or an ARB.
- It is recommended that all patients with cardiovascular disease receive an annual influenza
vaccine and that patients over age 56 also receive the pneumococcal vaccine
Health Care Resources
- The American Heart Association (AHA) is an excellent source for booklets, films, CDs, DVDs,
cookbooks, and professional service referrals for the patient with coronary artery disease (CAD).
- Many shopping malls open before shopping hours to allow a measured walking program
indoors. This opportunity is particularly popular with older patients because it provides a good
support group and allows for an appropriate place to exercise in inclement weather
- Mended Hearts is a nationwide program with local chapters that provides education and
support to coronary artery bypass graft (CABG) patients and their families.
- Smoking-cessation programs and clinics and weight-reduction programs are located within the
community. Many hospitals and places of worship also sponsor health fairs, BP screening, and
risk-factor modification programs.
Evaluation: Evaluate Outcomes
◦ Expected outcomes are that patient will:
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State that pain is alleviated
Have adequate myocardial perfusion
Be free of complications such as dysrhythmias and heart failure
Chapter 15 – Concepts of Infusion Therapy
Key Terms
adverse drug events (ADEs) An unintended harmful reaction to an administered drug
ambulatory pumps Infusion therapy pump generally used with a home care patient to allow a return to
his or her usual activities while receiving infusion therapy
catheter-related bloodstream infection (CRBSI) Health care−acquired bloodstream infections caused by
the presence of any type of intravenous catheter
catheter-related bloodstream infection (CRBSI) prevention bundle A nationally recognized set of
evidence-based practices to prevent CRBSIs
central line−associated bloodstream infection (CLABSI) Health care−acquired bloodstream infections
caused by the presence of a central intravenous line
compartment syndrome A condition in which increased tissue pressure in a confined anatomic space
causes decreased blood flow to the area, leading to hypoxia and pain
extravasation Escape of fluids or drugs into the subcutaneous tissue; a complication of intravenous
infusion therapy.
implanted port A surgically implanted vascular access device (VAD) where the port is placed in a
subcutaneous pocket; used for long-term or frequent infusion therapy.
infiltration Leakage of IV solution into the tissues around the vein.
infusate Solution that is infused into the body
infusion therapy Delivery of parenteral medications and fluids through a variety of catheter types and
locations using multiple techniques and procedures, such as intravenous therapy to deliver solutions
into the vascular system
midline catheters A VAD that is 3 to 8 inches long and inserted through the veins of the antecubital
fossa.
nontunneled central venous catheter (CVC) A multilumen VAD inserted through the subclavian or
jugular vein using sterile technique
peripheral IV therapy IV therapy in which a vascular access device (VAD) is placed in a peripheral vein,
usually in the arm
peripherally inserted central catheter (PICC) A long VAD inserted through a vein at the antecubital fossa
phlebitis Inflammation of a vein that can predispose patients to thrombosis
short peripheral catheter (SPC) A VAD composed of a plastic cannula, built around a sharp stylet for
venipuncture, which extends slightly beyond the cannula and is advanced into the vein
secondary (piggyback) administration set A short tubing set that is attached to the primary
administration set and used to deliver intermittent medications
smart pumps Infusion pumps with dosage calculation software
syringe pumps Pump for infusion therapy that uses a battery-powered piston to push the plunger
continuously at a selected rate; limited to small-volume or intermittent infusions.
thrombophlebitis Presence of a thrombus associated with inflammation
thrombosis Formation of a blood clot within a blood vessel
tunneled central venous catheter A surgically implanted VAD used for long-term infusion therapy in
which the catheter lies in a subcutaneous tunnel, separating the points where the catheter enters the
vein from where it enters the skin
vascular access device (VAD) An infusion catheter placed in a blood vessel to deliver fluids and
medications
vesicant medications Drugs that cause severe tissue damage if they escape into the subcutaneous
tissue; also referred to as vesicants.
Infusion Therapy
- The delivery of medications in solution or fluids by a parenteral route, which requires piercing of
the skin with a needle or catheter
- Intravenous (IV) therapy is the most common route
- The most common reasons for using infusion therapy are
o Maintain fluid balance or correct fluid imbalance
o Maintain electrolyte or acid-base balance or correct electrolyte or acidbase imbalance
o Administer medications
o Replace blood or blood products
Types of Infusion Therapy Fluids
 Normal serum osmolarity (adults) = 270 to 300 mOsm/L
 IV solutions (including parenteral nutrition)
 Isotonic = 270 to 300 mOsm/L
 Hypertonic = Fluids >300 mOsm/L
 Hypotonic = Fluids <270 mOsm/L
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When an isotonic infusate (solution that is infused into the body) is used, water does not move
into or out of the body’s cells and remains in the extracellular compartments. Therefore
patients, especially older adults, receiving isotonic solutions are at risk for fluid overload
Hypertonic solutions are used to correct altered fluid and electrolyte balance and acid-base
imbalances by moving water out of the body’s cells and into the interstitial spaces and
bloodstream. Electrolytes and other particles also move across cell membranes across a
concentration gradient (from higher concentration to lower concentration). Parenteral nutrition
solutions are hypertonic
Hypotonic infusates move water into cells to expand them
Patients receiving either hypertonic or hypotonic fluids are at risk for phlebitis and infiltration.
o Phlebitis is the inflammation of a vein caused by mechanical, chemical, or bacterial
irritation.
o Infiltration occurs when IV solution leaks into the tissues around the vein.
The pH of IV solutions is a measure of acidity or alkalinity and usually ranges from 3.5 to 6.2.
Extremes of both osmolarity and pH can cause vein damage, leading to phlebitis and thrombosis
(blood clot in the vein). Thus fluids and medications with a pH value less than 5.0 and more than
9.0 and with an osmolarity more than 600 mOsm/L are best infused in the central circulation
where greater blood flow provides adequate hemodilution (ex: TPN)
Drugs with vasoconstrictive action (e.g., dopamine or chemotherapeutic agents) are vesicants
(chemicals that damage body tissue on direct contact) that can cause extravasation
Extravasation results in severe tissue integrity impairment as manifested by blistering, tissue
sloughing, or necrosis from infiltration into the surrounding tissues
Blood and Blood Components
- Blood transfusion is given by using packed red blood cells, created by removing a large part of
the plasma from whole blood.
- Other available blood components include platelets, fresh frozen plasma, albumin, and several
specific clotting factors.
Most organizations use the International Society of Blood Transfusion (ISBT) universal bar-coding system
to ensure the right blood for the right patient. The ISBT system includes four components that must be
present on the blood label both in bar code and in eye-readable format
(1) a unique facility identifier
(2) the lot number relating to the donor
(3) the product code
(4) the ABO group and Rh type of the donor
Drug Therapy
- IV drugs provide a rapid therapeutic effect but can lead to immediate serious reactions, called
adverse drug events (ADEs).
- IV administration also requires knowledge of appropriate dilution, rate of infusion, pH and
osmolarity, compatibility with other IV medications, appropriate infusion site (peripheral versus
central circulation), potential for vesicant/irritant effects, and specific aspects of patient
monitoring because of its immediate effect.
Prescribing Infusion Therapy
A prescription for infusion therapy written by an authorized primary health care provider (physician,
nurse practitioner, or physician assistant) is necessary before IV therapy begins. To be complete, the
prescription for infusion fluids should include:
o Specific type of fluid to be infused
o Rate of administration written in milliliters per hour (mL/hr) or the total amount of fluid
and the total number of hours for infusion (e.g., 125 mL/hr or 1000 mL/8 hr)
o Specific drugs and dose to be added to the solution such as electrolytes or vitamins A
drug prescription should include:
o Drug name, preferably by generic name
o Specific dose and route
o Frequency of administration
o Time(s) of administration
o Length of time for infusion (number of doses/days)
o Purpose (required in some health care agencies, especially nursing homes)
Vascular Access Devices
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An infusion catheter, also known as a vascular access device (VAD), is a plastic tube placed in a
blood vessel to deliver fluids and medications.
The location of the VAD, either a peripheral vein or a large central vein in the chest, is
determined by the specific type and purpose of the therapy.
Types of catheters used for peripheral and central IV therapy
 Short peripheral catheters
 Midline catheters
 Peripherally inserted central catheters (PICC)
 Nontunneled percutaneous central venous catheters (CVC)
 Tunneled catheters
 Implanted ports
 Hemodialysis catheters
Peripheral Intravenous Therapy
Short infusion catheters are the most commonly used vascular access devices (VADs) for peripheral IV
therapy. They are usually placed in the veins of the arm. Another catheter used for peripheral IV therapy
is a midline catheter.
Short Peripheral Catheters
- Short peripheral catheters are composed of a plastic cannula built around a sharp stylet
extending slightly beyond the cannula
- The stylet allows for the venipuncture, and the cannula is advanced into the vein. Once the
cannula is advanced into the vein, the stylet is withdrawn.
- These catheters are designed with a safety mechanism to cover the sharp end of the stylet after
it is removed from the patient to decrease the risk of accidental injury.
- The stylet is a hollow-bore, blood-filled needle that carries a high risk for exposure to
bloodborne pathogens if needlestick injury occurs.
Insertion and Placement Methods
- Short peripheral catheters are most often inserted into superficial veins of the forearm.
- In emergent situations, these catheters can also be used in the external jugular vein of the neck.
- Avoid the use of veins in the lower extremities of adults, if possible, because of an increased risk
for deep vein thrombosis and infiltration.
- Short catheters range in length from ¾ inch to 1¼ inch, with gauge sizes from 26-gauge (the
smallest) to 14-gauge (large bore).
- Choose the smallest gauge catheter capable of delivering the prescribed therapy with
consideration of all the contributing factors, including expected duration, vascular
characteristics, and comorbidities
- When selecting the site for insertion of a peripheral catheter, consider the patient’s age, history,
and diagnosis; the type and duration of the prescribed therapy; and, whenever possible, the
patient’s preference.
- Vascular visualization technology (e.g., near infrared and ultrasound devices) are now available
as tools to assist in IV line placement
- Ultrasound-guided peripheral IV insertion can allow insertion into deeper veins. This technology
has been shown to be valuable in assisting with cannulation of peripheral veins that the nurse
cannot access with sight and touch.
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Arteries and nerves often lie parallel to deep veins, and training is essential to learn to identify
these structures and avoid damaging them. In addition, when deeper veins are used, infiltration
may go undetected until a significant amount of fluid has collected in the tissues.
For patients who need IV access but are at risk for fluid overload or do not need additional IV
fluids, the peripheral vascular access device (VAD) can be converted into an intermittent IV lock,
also called a saline lock. This device allows administration of specific drugs given IV push (e.g.,
furosemide) or on an intermittent basis using a medication administration set. IV antibiotics are
frequently administered using a saline lock.
The intermittent device is flushed with saline before and after drug administration to ensure
patency and prevent occlusion with a blood clot.
These VADs are not recommended for obtaining routine blood samples due to the risk of
hemolysis.
Site Selection and Skin Preparation
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The most appropriate veins for peripheral catheter placement include the dorsal venous
network (i.e., basilic, cephalic, and median veins and their branches)
However, cannulation of veins on the hand is not appropriate for older patients with a loss of
skin turgor and poor vein condition or for active patients receiving infusion therapy in an
ambulatory care clinic or home care. Use of veins on the dorsal surface of the hands should be
reserved as a last resort for short term infusion of nonvesicant and nonirritant solutions in
young patients.
Mastectomy, axillary lymph node dissection, lymphedema, paralysis of the upper extremity, and
the presence of dialysis grafts or fistulas alter the normal pattern of blood flow through the arm.
Using veins in the extremity affected by one of these conditions requires a primary health care
provider’s order
Aseptic skin preparation and technique before IV insertion are crucial
Catheter-related bloodstream infection (CRBSI) can occur from a peripheral IV site. Both the CDC
and the INS have best practice guidelines developed to prevent infection
Midline Catheter
- Anywhere from 3 to 8 inches long, 3 to 5 Fr, and double or single lumen
- They are inserted into a vein of the upper arm
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Midline catheters reduce the number of repeated IV cannulations, which reduces patient
discomfort, increases patient satisfaction, and contributes to organizational efficiency
Indications for midline catheters include fluids for hydration and drug therapy that are given
longer than 6 days and up to 14 days
Midline catheters should not be used for infusion of vesicant medications—drugs that cause
severe tissue damage if they escape into the subcutaneous tissue (extravasation). There is
concern that at a midline tip location, larger amounts of the drug may extravasate before the
problem is detected
Central Intravenous Therapy
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In central IV therapy the vascular access device (VAD) is placed in the central circulation,
specifically within the superior vena cava (SVC) near its junction with the right atrium, also called
the caval-atrial junction (CAJ).
A number of types of central vascular access devices (CVADs) are available, depending on the
purpose, duration, and insertion site availability
Peripherally Inserted Central Catheters (PICC)
- A long catheter inserted through a vein of the antecubital fossa (inner aspect of the bend of the
arm) or the middle of the upper arm.
- In adults the PICC length ranges from 18 to 29 inches (45 to 74 cm), with the tip residing in the
superior vena cava (SVC) ideally at the caval-atrial junction (CAJ
- Before the catheter can be used for infusion, a chest x-ray indicating that the tip resides in the
lower SVC is required when the catheter is not placed under fluoroscopy or with the use of the
electrocardiogram tip-locator technique.
Nontunneled Percutaneous Central Venous Catheters
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Inserted through subclavian vein in upper chest or jugular veins in neck
7 to 10 inches (15 to 25 cm) long; up to 5 lumens
Tip resides in superior vena cava
Short term use
Tunneled Central Venous Catheters
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Tunneled central venous catheters are VADs that have part of the catheter lying in a
subcutaneous tunnel, separating the points where the catheter enters the vein from where it
exits the skin.
The catheter has a cuff made of a rough material that is positioned inside the subcutaneous
tunnel. These cuffs commonly contain antibiotics, which also reduce the risk for infection
Single, dual, and triple lumens are available. These catheters were originally named for the
physicians who designed them, including Broviac, Hickman, and Leonard catheters.
Tunneled catheters are used primarily when the need for infusion therapy is frequent and long
term. Tunneled catheters are chosen when several weeks or months of infusion therapy are
needed and a PICC is not a good choice
Implanted Ports
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This type of device is chosen for patients who are expected to require IV therapy for more than
a year
Implanted ports consist of a portal body, a dense septum over a reservoir, and a catheter
They can be single or double lumen and come in various sizes
A subcutaneous pocket is surgically created to house the port body. The catheter is inserted into
the vein and attached to the portal body. The septum is made of self-sealing silicone and is
located in the center of the port body over the reservoir; the catheter extends from the side of
the port body. The incision is closed, and no part of the catheter is visible externally; therefore
this device has the least impact on body image
Hemodialysis Catheters
- Hemodialysis catheters have very large lumens to accommodate the hemodialysis procedure or
a pheresis procedure that harvests specific blood cells
- They may be tunneled for long-term needs or nontunneled for short-term needs
- CRBSIs and vein thrombosis are common complications; therefore this catheter should not be
used for administration of other fluids or drugs except in an emergency.
- The generalist RN generally does not access hemodialysis catheters. These are maintained by
specially trained hemodialysis nurses.
Infusion Systems
Containers
- Infusion containers are made of glass or plastic
- For plastic containers – concern of exposure to PVC and DEHP
Administration Sets
- The administration set is the connection between the catheter and the fluid container.
- Some sets are generic, meaning that they are appropriate for most infusions.
- Other sets are used for specific types of infusions such as blood transfusion.
- Still others are dedicated, meaning that they must be used with a specific manufacturer’s
infusion controlling device
Secondary Administration Sets
- A primary continuous administration set is used to infuse the primary IV fluid by either a gravity
infusion or an electronic infusion pump. A short secondary administration set, also known as a
piggyback set, is attached to the primary set at a Y–injection site and is used to deliver
intermittent medications
- Primary and secondary continuous infusion administration sets used to infuse fluids other than
parenteral nutrition and lipids can be used for up to 96 hours unless the closed system has been
compromised
Intermittent Administration Sets
- When no primary continuous fluid is being infused, use an intermittent administration set to
infuse multiple doses of medications through a catheter that has been capped with a needleless
connection device.
- Because both ends of the set are being manipulated with each dose, the INS standards of
practice state that this set should be changed every 24 hours
Add-on Devices
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Several other types of add-on devices include short extension sets, injection caps, and filters.
Administration sets have two ways to connect to the catheter hub: a slip lock or a Luer-Lok. The
slip lock is a male end that slips into the female catheter hub. A Luer-Lok connection has the
same male end with a threaded collar that requires twisting onto the corresponding threads of
the catheter hub
Filters may be part of the administration set or separate add-on pieces. Their purpose is to
remove particulate mater, microorganisms, and air from the infusion system. Filters should be
placed as close to the catheter hub as possible
Needleless Connection Devices
- Needlestick Safety and Prevention Act. This regulation requires the use of devices engineered
with safety mechanisms and mandates that staff who perform these tasks be directly involved
with selecting products. It also requires each employer to maintain a sharps injury log with
details of each incident. Many products are designed to minimize health care workers’ exposure
to contaminated needles. Luer-lock–activated devices are the most common design for
needleless systems today
- it is imperative that the connector be disinfected with alcohol or chlorhexidine/alcohol before
and after each use with a vigorous scrub for 5 to 60 seconds
Rate-Controlling Infusion Devices
- The ability to regulate the rate and volume of infusions is critical to the safe and accurate
administration of medications and fluids to patients
- Syringe pumps use an electronic or battery-powered piston to push the plunger of a large
syringe inserted into the pump mechanism continuously at a selected milliliter-per-hour rate.
The use of syringe pumps is limited to smallvolume continuous or intermittent infusions and
depends on the syringe size. Antibiotics and patient-controlled analgesia are frequently
delivered with syringe pumps. Patients requiring fluid restrictions can also benefit from using a
syringe pump because smaller yet accurate volumes can be used to dilute medications
- Ambulatory pumps are generally used for home care patients and allow them to return to their
usual activities while receiving infusion therapy. These pumps have a wide range of sizes, with
some requiring a backpack, but they usually weigh less than 6 lb. They are typically used to
accurately deliver continuous infusions such as parenteral nutrition, pain medication, and many
programmable drug schedules.
- In the past few years, smart pumps (infusion pumps with dosage calculation software) have
been promoted to reduce adverse drug events (ADEs). Multiple libraries of drug information are
stored in the pump manufacturer’s medical management system. This software allows the
facility to preprogram dosing limits, especially for high alert drugs
Nursing Care For Patients Receiving Intravenous Therapy
Educating the Patient
- Before catheter insertion, educate the patient and family about:
o The type of catheter to be used
o Hand hygiene and aseptic technique for care of the catheter
o The therapy required
o Alternatives to the catheter and therapy
o Activity limitations
o Any signs or symptoms of complications that should be reported to a health care
professional
Performing the Nursing Assessment
- All central VADs require documentation of tip location at the caval-atrial junction (CAJ) by
electrocardiogram technology, fluoroscopy, or chest x-ray
- Nursing assessment for all infusion systems should be systematic beginning at the insertion site,
working upward following the tubing to the infusion bag. Know the type of catheter your patient
has in place. Be sure to find out the length of catheter, the insertion site, and tip location to
perform a complete assessment.
- Assess the insertion site by looking for redness, swelling, hardness, or drainage. Also assess the
skin underneath the dressing, especially for signs of medical adhesive–related skin injury
- When a midline catheter or PICC is used, assess the entire extremity and upper chest for signs of
phlebitis and thrombosis
- When a tunneled catheter is used, assess the exit site, the entire length of the tunnel, and the
point where the catheter enters the vein
- For implanted ports, assess the incision and surgically created subcutaneous pocket
- Assess the integrity of the dressing, making sure that it is clean, dry, and adherent to the skin on
all sides
- Check all connections on the administration set and ensure that they are secure. Be sure that
they are not taped.
- Check the rate of infusion for all fluids by either counting drops or checking the infusion pump.
- Check all labels on containers for the patient’s name and fluid or medication. Be sure that the
correct solution is being infused!
Securing and Dressing the Catheter
- Securing the catheter is an important step in the prevention of complications. Tape, sutures, and
specially designed securement devices can be used for this purpose.
- the StatLock IV stabilization device prevent peripheral and central catheters from becoming
dislodged. They prevent complications such as phlebitis and infiltration. To prevent skin tears,
remove the adhesive on a StatLock with 70% alcohol.
- PICCs and nontunneled central catheters may be sutured in place; however, this creates
additional breaks in the skin that could become infected\
- Sterile dressings used over the insertion site protect the skin and puncture site
- Change tape and gauze dressings every 48 hours; change transparent membrane dressings, such
as Tegaderm, every 5 to 7 days
- Never pull it off by pulling away from the insertion site because this could dislodge the catheter!
- After removing the dressing from a midline catheter or any central venous catheter, note the
external catheter length. Compare this length with the original length at insertion.
Changing Administration Sets and Needleless Connectors
- Plan the change of administration sets and fluid containers to occur at the same time, if
possible, to minimize the number of times the system is opened.
- Needleless connector devices can be changed when the administration set is changed. If it is
being used for intermittent infusions, the device should be changed at least once per week
- Precautions to prevent air emboli are required when changing the set or connectors attached to
any catheter; however, central venous catheters require special attention. Most catheters have
a pinch clamp that should be closed during this procedure.
- Techniques used to increase the intrathoracic pressure and prevent air embolism during IV set
change include:
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Placing the patient in a flat or Trendelenburg position to ensure that the catheter exit
site is at or below the level of the heart
Asking the patient to perform a Valsalva maneuver by holding his or her breath and
bearing down
Timing the IV set change to the expiratory cycle when the patient is spontaneously
breathing
Timing the IV set change to the inspiratory cycle when the patient is receiving positivepressure mechanical ventilation
Controlling Infusion Pressure
- In order for fluid to flow through the system, the pressure on the external side must be greater
than the pressure at the catheter tip
- Fluid flow can be slowed or obstructed from the catheter tip impinging on the vein wall, a
thrombus distal to the catheter, or a venous spasm.
- Inside the catheter lumen, resistance is created by the catheter length and diameter or deposits
of fibrin, thrombus, or drug precipitate
Flushing the Catheter
- Catheter flushing prevents contact between incompatible drugs and maintains patency of the
lumens.
- Normal saline alone or normal saline followed by heparinized saline may be used, depending on
the device recommendations.
Obtaining Blood Samples From Central Venous Catheters
- Short peripheral catheters should not be used routinely for obtaining blood samples.
- The risks associated with obtaining blood samples from a central venous catheter are numerous.
This procedure requires additional hub manipulation, which is a major cause of CRBSI
- If blood sampling from a central venous catheter is the best alternative, vigorous cleaning of the
connections with 70% alcohol is necessary.
- Vacuum tubes attached via a “vacutainer” to the catheter hub eliminate the need to transfer the
blood from a syringe into the tubes and therefore do not require exposed needles
- After blood draw from any catheter, a flush of 10 to 20 mL sterile normal saline is necessary to
ensure a patent line. Be sure to clear the line and cap of blood to prevent a breeding ground for
infection.
Removing the Vascular Access Device
- Lift opposite sides of the transparent dressing and pull laterally to remove the dressing from the
site while stabilizing the catheter
- Slowly withdraw the catheter from the skin and immediately cover the puncture site with dry
gauze
- Hold pressure on the site until hemostasis is achieved
- Assess the catheter tip to make sure that it is intact and completely removed
- Document the time of catheter removal and appearance of the IV site.
- If you feel resistance, always stop and never apply force to the catheter. Extreme traction or
force could cause the catheter to break and embolize (travel) to the heart or pulmonary
circulation
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Apply heat; allow time for the vein wall to relax. Keeping the extremity warm and dry and asking
the patient to drink warm liquids could facilitate removal. Use of medications to relax the vein
wall may be required if the catheter cannot be removed after several hours.
Nontunneled percutaneous central catheters are removed by removing the dressing as noted
above, clipping any sutures, and gently withdrawing the catheter in short segments
To prevent venous air embolism when removing any central venous catheter (including PICCs),
position the patient in a flat supine or Trendelenburg position according to agency policy. To
ensure that the intrathoracic pressure is higher than atmospheric pressure, have the patient
hold his or her breath or perform a Valsalva maneuver during removal. If the patient is
mechanically ventilated, time the removal to the delivery of an inhalation breath by the
ventilator. Be sure to keep the catheter clamped during this procedure.
When a central venous catheter is removed, a tract between the skin and vein may create a
conduit that could allow air to be pulled into the vein, causing a venous air embolism.
After removal, measure the catheter length and compare it with the length documented on
insertion. If the entire catheter length was not removed, contact the primary health care
provider immediately as this constitutes a medical emergency!
Documenting Intravenous Therapy
- Be sure to document after insertion of a vascular access device (VAD) and throughout the course
of the therapy.
- When inserting a venous catheter, remember to document the following:
o Date and time of the VAD insertion
o Name of the nurse (you) who inserted the VAD
o Vein/location that was used for insertion
o Type of VAD used including gauge and length of catheter
o Number of insertion attempts and locations of attempts before successful insertion
o Response of the patient to the VAD insertion process
o Type of dressing applied
o Type of securement device, if used
o Special barrier precautions used, if any
o Patient and family education provided related to IV therapy
Complications of Intravenous Therapy
- Complications from IV therapy can be minor and limited or life threatening. Serious life-altering
or life-threatening complications are dramatically increasing in frequency and severity, and
present a tremendous financial burden to the U.S. health care system.
Catheter-Related Bloodstream Infection
- Catheter-related bloodstream infection (CRBSI) is one of the most serious problems, often
resulting in patient death. These infections are more common in patients with central VADs but
can also occur with peripheral catheters.
- CRBSI are one of several preventable hospital-acquired infections (HAIs).
Other Complications of Intravenous Therapy
- Local complications of IV therapy occur at or near the catheter.
- Systemic complications of IV therapy involve the entire vascular system or multiple systems.
- For central venous catheters (CVCs), complications can occur during the insertion procedure or
during the dwell time
Intravenous Therapy and Care of the Older Adult
- The aging process causes numerous changes in all body functions, and yet aging occurs
differently in each person. Nutrition, environment, genetics, social factors, and education are
just a few of the factors that influence the older adult’s needs. Because all body functions are
affected, IV therapy can be affected by these changes.
Skin Care
- Aging skin becomes thinner and loses subcutaneous fat, decreasing the skin’s ability for thermal
regulation.
- Fewer nerve endings may alter the way an individual experiences pain and other sensations.
- Older patients may not perceive acute pain from traumatic venipuncture and may tolerate
probing or multiple attempts. However, this action increases the risk for fluid leakage and
subsequent infiltration or extravasation injury. Inserting and removing a catheter and dressing
could tear the skin layers.
- Skin antisepsis is extremely important because of the decreased immunity seen as part of the
aging process.
- Lipids are normally found in skin as a protective agent, and alcohol easily dissolves lipids.
Although greater numbers of organisms may be killed, the skin can also become excessively dry
and cracked.
- Current recommendations call for using friction when cleaning the skin to penetrate the layers
of the epidermis. However, excessive friction may damage fragile skin and cause impaired tissue
integrity.
- Chlorhexidine is the preferred agent, and the product currently available contains alcohol.
- Check for allergies to iodine before using iodine or iodophors. Iodophors such as povidoneiodine require contact with the skin for a minimum of 2 minutes to be effective.
- All antiseptic solutions must be thoroughly dry before applying the dressing or tape to ensure
adequate adherence to the skin.
- Skin should never be shaved before venipuncture as shaving causes microabrasions that can
lead to infection. Shaving can also more easily nick the thin, delicate skin of an older adult. If
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necessary, excessive amounts of hair should be clipped to ensure the bandage adheres to the
skin.
Skin and tissue integrity can easily be compromised by the application of tape or dressings. The
use of skin protectant solutions puts a protective barrier between the skin and dressing and
improves the adherence of the dressing to the skin.
Removal of tape and dressings may require adhesive remover solutions, or an alcohol pad may
accomplish the same purpose.
Securement devices such as the StatLock require the use of a skin protectant (e.g., Skin- Prep)
before applying the device. The protectant prevents skin tearing when the device is removed.
Vein and Catheter Selection
- Choose insertion sites carefully after considering the patient’s skin integrity, vein condition, and
functional ability.
- The general principle of starting with the most distal sites usually indicates use of hand veins.
However, avoid fragile skin and small, tortuous veins on the back of the hand (dorsum); select
the initial IV site higher on the arm
- Venous distention must be accomplished with a flat tourniquet; however, the veins may require
longer to adequately distend
- Avoid hard, cordlike veins.
- Blood pressure cuffs can also be used for venous distention. Inflate the cuff and release until the
pressure is slightly less than diastolic pressure.
- Other methods to distend veins include:
o Tapping the vein lightly, but avoiding forceful slapping
o Asking the patient to open and close the fist so the muscles can force blood into the
veins, making sure that the hand is relaxed when the venipuncture is attempted
o Placing the extremity lower than the heart
o Applying warm compresses or a heating pad (be careful not to make it too hot) to the
entire extremity for 10 to 20 minutes and removing just before making the venipuncture
- As with all patients, venipuncture technique requires adequate skin and vein stabilization during
the puncture and complete catheter advancement
- Veins of an older adult are more likely to roll away from the needle as veins become firmer and
more difficult to puncture with aging
- Low angles of 10 to 15 degrees between the skin and catheter will improve success with
venipuncture.
- Choosing a midline catheter or PICC may be best in older patients with poor skin turgor; limited
venous sites; or veins that are fragile, tortuous, or hard. These catheters are placed in the upper
extremity where venous distention techniques can be used.
- Inserting nontunneled percutaneous central catheters in older adults can be much more
challenging. Venous distention for insertion requires the Trendelenburg position and a wellhydrated patient to ensure that the veins are adequately distended.
Cardiac and Renal Changes
- Because of changes in cardiac and renal status in older adults, the accuracy of infusion volume
and flow rate measurements is very important in the older adult. Older adults are more prone to
fluid overload with resulting heart failure or dehydration with subsequent poor perfusion
- When fluid restrictions are required, medications could be diluted in small quantities and
delivered using a syringe pump or a manual IV push. Consult with a pharmacist to determine the
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smallest amount of diluent required. This alternative may allow the patient to have more fluid
to drink.
Serum sodium levels should be considered when normal saline is routinely used for dilution in
patients with hypertension or cardiac problems
An increasing number of patients with chronic illness require repeated and frequent IV
therapies. Many of these patients are vein depleted and need vein preservation.
Subcutaneous and intraosseous routes have demonstrated effectiveness in emergency
resuscitation. These procedures may also be beneficial for routine infusion of isotonic,
nonirritant, nonvesicant solutions in patients with chronic illness and vein depletion
Subcutaneous Infusion Therapy
- Subcutaneous infusion therapy has been used for a variety of drug infusions. Most commonly it
is used for administration of pain medications and insulin therapy. It is beneficial for palliative
care patients who cannot tolerate oral medications, when IM injections are too painful, or when
vascular access is not available or is too difficult to obtain.
- Hypodermoclysis or “clysis” involves the slow infusion of isotonic fluids into the patient’s
subcutaneous tissue for the purpose of slow, steady rehydration.
- Hypodermoclysis can be used for short-term fluid volume replacement.
- The patient must have sufficient sites of intact skin without infection, inflammation, bruising,
scarring, or edema. The most common sites are the front and sides of the thighs and hips, the
upper abdomen, and the area under the clavicle. Unlike IV therapy, the upper extremities
should not be used because fluid is absorbed more readily from sites with larger stores of
adipose tissue.
- Hypodermoclysis is not appropriate for emergency resuscitations and should not be used for
high quantity or emergent fluid replacement needs.
- Hyaluronidase, an enzyme that improves the absorption of the infusion, may be prescribed by
the primary health care provider and is mixed with each liter of infusion fluid.
- A small-gauge (25 to 27) winged infusion or “butterfly” needle, a small gauge short peripheral
catheter, or an infusion set specially designed for subcutaneous infusion can be chosen.
- When choosing the infusion site, consider the patient’s level of activity. The area under the
clavicle or the abdomen prevents difficulty with ambulation.
- Clip excess hair in the area and clean the chosen site with the antiseptic solution, preferably 2%
chlorhexidine gluconate in 70% isopropyl alcohol to prevent infection.
- Prime the infusion tubing and the attached subcutaneous infusion set or winged needle.
- Gently pinch an area of about 2 inches (5 cm) and insert the needle using sterile technique.
- After securing the needle, cover the site with a transparent dressing.
- Assess the site every 4 hours while in a hospital setting and at least twice daily while at home.
Redness, warmth, leakage, bruising, swelling, and reports of pain indicate tissue irritation and
possible impaired tissue integrity.
- If these symptoms occur, remove the infusion needle. Rotate the site at least once a week.
- Other complications include pooling of the fluid at the insertion site and an uneven fluid drip
rate. Both of these problems may be resolved by restarting the infusion in another location. An
infusion pump may also be used. Small ambulatory infusion pumps can be used to allow for
greater mobility.
•
•
Usually for pain medication, insulin therapy
Benefits
• Patients undergoing palliative care who cannot tolerate oral medications
•
When IM injections are too painful, or when vascular access is not available or difficult
to obtain
Intraosseous Infusion Therapy
- Intraosseous (IO) therapy allows access to the rich vascular network in the red marrow of bones.
- Victims of trauma, burns, cardiac arrest, diabetic ketoacidosis, and other life-threatening
conditions benefit from this therapy because health care providers often cannot access these
patients’ vascular systems for traditional IV therapy
- The IO route is for short-term therapy and should be used only during the immediate period of
resuscitation and should not be used longer than 24 hours. After establishing access, efforts
should continue to obtain IV access as well.
- There are few contraindications for IO infusion. The only absolute contraindication is fracture in
the bone to be used as a site. Conditions such as severe osteoporosis, osteogenesis imperfecta,
or other conditions that increase the risk for fracture with insertion of the IO needle and skin
infection over the site may also be contraindications for some patients.
- Repeated attempts to access the same site should be avoided.
- Any needle can be used to provide IO therapy and access the medullary space (marrow).
However, 15- or 16-gauge needles specifically designed for IO therapy are preferred.
- New technology using a battery-powered drill has improved the ease of IO insertion.
- A number of sites can be used, including the proximal tibia (tibial tuberosity), distal femur,
medial malleolus (inner ankle), proximal humerus, and iliac crest. The proximal tibia is the most
common site accessed for IO therapy
- During insertion, the leg is restrained, and the site cleaned with an antiseptic agent such as
chlorhexidine.
- After successful insertion the needle must be secured to prevent movement out of the bone.
- The same doses of fluids and medications can be infused by IO therapy as IV, and an infusion
pump should be used for rapid flow rates.
- During the procedure most patients rate the pain as a 2 or 3 on a scale of 0 to 10. Lidocaine 1%
is used to anesthetize the skin, subcutaneous tissue, and periosteum to promote comfort.
- Improper needle placement with infiltration into the surrounding tissue is the most common
complication of IO therapy. Accumulation of fluid under the skin at either the insertion site or on
the other side of the limb indicates that the needle either is not far enough in to penetrate the
bone marrow or is too far into the limb and has protruded through the other side of the shaft.
- Needle obstruction occurs when the puncture has been accomplished but flushing has been
delayed. This delay may cause the needle to become blocked with bone marrow.
- Osteomyelitis is an unusual but serious complication of IO therapy. You can help prevent this
with meticulous aseptic technique, proper hand hygiene, and removal of the catheter as soon as
it is no longer needed.
- Compartment syndrome is a condition in which increased tissue pressure in a confined anatomic
space causes decreased perfusion (peripheral blood flow to the area). The decreased circulation
to the area leads to hypoxia and pain in the area.
- Although the complication is rare in IO therapy, the nurse should monitor the site carefully and
alert the primary health care provider promptly if the patient exhibits any signs of decreased
circulation to the limb such as coolness, swelling, moltting, or discoloration. Without
improvement in perfusion to the limb, the patient could ultimately require amputation of the
limb.
•
Usually for Trauma, burns, cardiac arrest, DKA, life-threatening conditions
•
Benefits
• Allows access to rich vascular network in the red marrow of bones
• Can be used in adults
Intra-Arterial Infusion Therapy
• Used to obtain repeated arterial blood samples, monitor hemodynamic pressures, infuse
chemotherapy or fibrolytics
• Used for 3-7 days
Intraperitoneal Infusion Therapy
• Used to treat ovarian and GI tumors that have moved into the peritoneum
• Can be implanted for long-term treatment or used as external for temporary use
Intraspinal Infusion Therapy
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•
Intrathecal medications infused into subarachnoid space and directly into cerebral spinal fluid
Used primarily for postoperative and persistent pain
Key terms:
epistaxis: Nosebleed.
gas exchange: Oxygen transport to the cells and carbon dioxide transport away from cells through
ventilation and diffusion.
hypopnea: Lower than normal respiratory rate and depth insufficient for gas exchange.
inspissated secretions: Thickly crusted oral and nasopharyngeal secretions that can cause an upper
airway obstruction (also known as mucoid impaction).
laryngectomee: An adult who has had a laryngectomy.
obstructive sleep apnea (OSA): A breathing disruption during sleep that lasts at least 10 seconds and
occurs a minimum of five times in an hour.
polysomnography: A formal and definitive overnight sleep study with direct observation of the patient
while he or she wears a variety of monitoring equipment to evaluate depth of sleep, type of sleep,
respiratory effort, oxygen saturation, carbon dioxide exhalation, and muscle movement. rhinoplasty:
Surgical reconstruction of the nose.
upper airway obstruction: Interruption of airflow through nose, mouth, pharynx, or larynx.
Anatomy of the Nose and Sinuses
Upper Airway Obstruction: Assessment: Recognize Cues
Assessment: Recognize Cues Airway obstruction requires prompt care to prevent a partial obstruction
from progressing to a complete obstruction. Partial obstruction produces general symptoms such as
diaphoresis, tachycardia, anxiety, and elevated blood pressure. Persistent or unexplained symptoms must
be evaluated even though vague. Diagnostic procedures include chest or neck x-rays, laryngoscope
examination, and CT. Observe for hypoxia and hypercarbia, restlessness, increasing anxiety, sternal
retractions, a “seesawing” chest motion, abdominal movements, or a feeling of impending doom from air
hunger. Use pulse oximetry or end tidal carbon dioxide (EtCO 2 or PEtCO 2 ) for ongoing monitoring of
gas exchange . Continually assess for stridor, cyanosis, and changes in level of consciousness.
Interventions
Assess for the cause of the obstruction. When the obstruction is caused by the tongue falling back or
excessive secretions, slightly extend the patient’s head and neck and insert a nasal or an oral airway.
Suction to remove obstructing secretions. If the obstruction is caused by a foreign body that cannot be
removed by clearing the oral cavity manually, perform abdominal thrusts (Fig. 26.1)
Upper airway obstruction may require emergency procedures such as cricothyroidotomy or tracheotomy
to improve gas exchange if the object causing the obstruction cannot be removed quickly. When
obstruction is not caused by a foreign object, endotracheal intubation may be needed. Laryngoscopy may
be performed to determine the cause of obstruction or to remove foreign bodies. Cricothyroidotomy is
an emergency procedure performed by emergency medical personnel as a stab wound through the
cricothyroid membrane between the thyroid cartilage and the cricoid cartilage (see Fig. 24.3). Any hollow
tube—but preferably a tracheostomy tube—can be placed through the opening to hold this airway open
until a tracheotomy can be performed. This procedure is used when it is the only way to secure an
airway. Another emergency procedure to bypass an obstruction is the insertion of a 14-gauge needle or a
very small endotracheal tube directly into the cricoid space to allow airflow into and out from the lungs.
Endotracheal intubation is performed by inserting a tube into the trachea via the nose (nasotracheal) or
mouth (orotracheal) by a physician, anesthesia provider, or other specially trained personnel. When
pharyngeal or laryngeal edema formation is expected or likely, an endotracheal tube is placed before
swelling is severe enough to make insertion impossible. Tracheotomy is a surgical procedure and takes
about 5 to 10 minutes to perform. It is best performed in the operating room (OR) with the patient under
local or general anesthesia but can be performed at the bedside. Local anesthesia is used if there is
concern that the airway will be lost during the induction of anesthesia. A tracheotomy is reserved for the
patient who cannot be easily intubated with an endotracheal tube. An emergency tracheotomy can
establish an airway in less than 2 minutes. See Chapter 25 for a discussion of care of the patient with a
tracheotomy. Patients receiving mechanical ventilation for upper airway obstruction or respiratory failure
may require a tracheostomy after 7 or more days of continuous endotracheal intubation. In such cases, a
tracheotomy is performed to prevent laryngeal injury and loss of tissue integrity by the endotracheal tube.
OSA: Etiology and Genetic Risk. OSA: Assessment: Recognize Cues
History:
Patients are often unaware that they have sleep apnea. The disorder is suspected for any adult
who has persistent daytime sleepiness or reports “waking up tired,” particularly if he or she also snores
heavily. Ask about sensations of daytime sleepiness or falling asleep while performing tasks such as
using the computer, reading, or driving. In extreme cases, patients may fall asleep while eating or any
time they sit down. Ask whether the patient can recall ever being awakened by his or her own snoring and
whether family members have noticed heavy snoring. Ask about the frequency of nightmares, which are
associated with OSA. Also ask whether family members have ever observed the patient to have a
disturbed breathing pattern while sleeping. A common pattern consists of breaths that become further
apart followed by a period of no breathing (apnea), which is then followed by chest and abdominal
movements that lead to gasping and snorting with partial awakening to correct the obstruction
temporarily. Also ask patients who may have OSA whether they have tried to induce a deeper sleep with
over-the-counter sleep aids or increased evening alcohol consumption. Many patients with OSA develop
some degree of gastroesophageal reflux disease (GERD) at night. Possible causes include strong
abdominal and chest movements during an apnea episode, overeating, eating or drinking close to bedtime,
and lying flat while sleeping. Ask the patient whether he or she is awakened often with “heartburn,”
stomach contents in the mouth, or a burning, choking sensation with coughing. Determine the frequency
of such episodes.
Physical Assessment/Signs and Symptoms
Assess the patient’s general appearance including height and weight. Many adults with OSA are
overweight, which can both cause OSA and be caused by this disorder. Examine the jaw, external neck,
and chin. OSA is associated with a retracted lower jaw, smaller chin, and shorter neck. Examine the oral
cavity and throat for size and shape of the pharynx, size and shape of the uvula, and tongue thickness and
position, and determine whether other structures (e.g., tonsils, adenoids, pillars, soft palate) are swollen or
enlarged. Chronic OSA is associated with cardiovascular changes, especially hypertension that may not
respond as expected to prescribed drug therapy. Assess the patient’s blood pressure and heart rate and
rhythm, as well as pulse oximetry. If the patient is being treated for hypertension, ask which drug(s) and
drug dosages are used for its management. If the patient is not being treated for hypertension but blood
pressure is elevated on assessment, retake the blood pressure later during the examination. Document
persistent elevations.
Psychosocial Assessment: Irritability and personality changes are common in adults with persistent
OSA, including depression, as is a general loss of interest in social activities. Family members can be
helpful in determining the presence of these psychosocial changes. Ask the patient about problems with
recall, concentration, perceived energy level, and the ability to stay on task when working or studying.
Some clinicians have suggested that long-term untreated OSA with significant cerebral hypoxia can lead
to memory loss and dementia, although no clinical trials have been performed to explore this possibility.
Analysis: Analyze Cues and Prioritize Hypotheses The primary collaborative problem for the patient
with moderate-to-severe OSA is persistent poor gas exchange and hypoxia due to abnormal sleep pattern.
Planning and Implementation: Generate Solutions and Take Action
Improving the Duration of Restorative Sleep Planning Expected Outcomes The patient is expected to
achieve a sleep pattern consistent with adequate gas exchange and longer-duration restorative sleep.
Interventions Management strategies for OSA vary with the severity of the problem and the patient’s
willingness to participate in the treatment process. Both nonsurgical and surgical management approaches
are available to help correct the problem, depending on the cause and the severity. Far more patients are
helped by nonsurgical procedures; surgical management is reserved for anatomic-related causes and
severe OSA that remains resistant to nonsurgical approaches.
Nonsurgical Management Collaborative management for patients with OSA focuses on reducing the
obstruction and improving both the depth and the duration of restorative sleep paerns. Changes in
sleeping position or weight loss may correct mild sleep apnea and improve gas exchange . More severe
OSA requires additional methods to prevent obstruction. Position-fixing devices may prevent
subluxation of the tongue and reduce obstruction. Use of an oral appliance, called maxillomandibular
advancement, can improve airflow by supporting the lower jaw in a more forward position. These devices
are especially helpful for adults who have a retracted lower jaw. Some devices also help prevent the
tongue from slipping backward during sleep. These devices are bulky and some patients cannot tolerate
their presence in the mouth. They may also increase the risk for loss of tissue integrity of the oral mucosa.
Noninvasive positive-pressure ventilation (NPPV) via continuous positive airway pressure (CPAP) to
hold open the upper airways is the most commonly used form of nonsurgical management for OSA.
CPAP delivers a set positive airway pressure continuously during each cycle of inhalation and exhalation
with the use of a small electric compressor and some type of delivery device such as a nasal-oral
facemask, nasal mask, or nasal pillows (with or without cushioned or gel prongs). Any type of delivery
mask or pillow used requires a proper and relatively tight fit to form a seal over the nose and mouth or
just over the nose for successful therapy. Fig. 25.9 in Chapter 25 shows a properly fied standard nasal
CPAP mask. Older CPAP setups had machines that were noisy, were not always humidified, and used
larger masks, all of which contributed to reduced patient adherence with the therapy. Newer machines are
very quiet and humidify the air. Many patients find the use of small masks (with or without cushioned or
gel prongs) such as that shown in Fig. 26.2, rather than a full or partial mask, less intrusive and more
acceptable. Smaller masks can help maintain tissue integrity . In addition, newer CPAP compressors are
able to monitor many patient parameters (e.g., oxygen saturation, number and duration of apnea episodes,
heart rate, air leaks, duration of correct usage, and other data) that can be sent electronically to the
patient’s smart phone and/or the health care provider’s office as a way to measure therapy effectiveness.
Stress to the patient that adherence with the therapy is critical in reducing all the health problem risks
associated with OSA. The equipment can be expensive and much of the cost is covered by Medicare for
older adults if the patient uses it consistently for at least 6 hours daily. After a p y y period of adjustment
many patients who use CPAP therapy consistently sleep well and feel so much beer that adherence is less
of an issue. Other patients find the equipment and routine too intrusive or unacceptable and may not even
try it. Providing accurate information and patient education is therefore essential for therapy success.
Many sleep apnea clinics and practices provide in-depth educational materials and patient-assistance
resources to help reduce patient anxiety and promote adherence. Drug therapy for OSA has not been
very successful. Sedatives to promote nighttime sleep may make OSA worse. Stimulants to help promote
daytime wakefulness have many side effects and do not contribute to restorative sleep. Neither sedatives
nor stimulants treat the cause of OSA.
Surgical Management Surgical intervention is considered when patients are not able to tolerate CPAP
or when its use does not improve OSA.
Care Coordination and Transition Management
Most patients who are prescribed to use CPAP for treatment of OSA are managed in the community.
Usually follow-up with the primary health care provider or a sleep center is ongoing to determine
treatment effectiveness. For those patients who require surgery for management of OSA, the patient is
usually discharged home within 2 to 3 days. At the time of discharge pain is controlled with oral drugs
and the patient should be able to swallow effectively. Self-Management Education An important issue
with CPAP therapy for OSA management is appropriate maintenance of the compressor and the
mask/tubular system. Keeping the system clean is critical to prevent infection and maintain tissue
integrity. With humidification, fungal infections are possible. Most setups require the use of distilled
water in the humidifier. The mask device or pillows must be cleaned daily using agents recommended by
the specific manufacturer. Instruct the patient to not share the mask, pillows, or tubing with other people
to reduce the risk for infection. Teach patients who had surgical interventions for OSA to assess the
oropharynx for bleeding, swelling, or indications of infection. A small amount of blood mixed with saliva
or mucus, particularly after coughing, is normal. However, new-onset bleeding, large clots, or bright red
blood may indicate serious problems. Instruct the patient to notify the surgeon immediately or go to the
emergency department if this should occur. Teach the patient how to examine his or her throat with a
mirror twice daily and assess its internal size (often by comparing it to coin sizes). A narrowing of the
throat or an inability to swallow (with or without pain), and the presence of drooling are indicators of
swelling that may obstruct the airway. Instruct the patient to go to the emergency room should these
occur. Pain is expected to decrease daily and swallowing should become increasingly more comfortable.
Drinking cool liquids, keeping the environment humidified, gargling frequently with warm salt water, and
eating soft foods can help reduce pain. Instruct the patient to report an increase in pain or increasingly
greater difficulty swallowing to the surgeon. Teach the patient the indications of infection and to notify
the surgeon if they occur. Infection indications include an increase in swelling, the presence of pus in any
area of the oropharynx, a change in color of the mucous membrane to a “beefy red,” an increase in pain,
the presence of fever, taste changes, and the presence of bad breath. Activity restriction varies depending
on the exact nature of the procedure performed. Obtain a list of surgeon-directed activity restrictions and
educate the patient about why each restriction has been prescribed. The most common restrictions include
lifting and performing the Valsalva maneuver (holding the breath and bearing down). Psychosocial
Preparation Some patients using CPAP therapy for management of OSA may have anxiety about correct
use of the equipment and possible disruption of nighime routine. All patients require some period of
adjustment to the therapy. Provide the patient with wrien and digital instructions for the use and care of
CPAP. Also provide telephone resource numbers for health care professionals specializing in the
management of OSA and for supplies needed for long-term use of CPAP. After surgery the patient may
have some anxiety about whether the surgical intervention was successful and about pain and swallowing
issues. Remind him or her that pain and difficulty swallowing are expected but should rapidly improve in
a week. Snoring or sleep apnea may continue for a short time after surgery until all swelling is gone.
Evaluation: Evaluate Outcomes
Evaluate the care of the patient with obstructive sleep apnea (OSA) based on the priority patient problem.
The expected outcomes are that the patient: • Does not remain hypertensive or has hypertension that can
be controlled with appropriate therapy • Is adherent with prescribed nonsurgical interventions • Has fewer
sleep-time apnea periods of 10 seconds or longer • Has improved gas exchange with greater duration of
restorative sleep • Reports less daytime sleepiness and has more energy • Has an uneventful recovery
from surgical intervention
Epistaxis Pathophysiology Review
Epistaxis (nosebleed) is a common problem because of the many capillaries within the nose. Nosebleeds
occur as a result of loss of tissue integrity from trauma to the nasal mucosa, hypertension, blood
dyscrasia (e.g., leukemia), inflammation, tumor, decreased humidity, nose blowing, nose picking,
chronic cocaine use, and procedures such as nasogastric (NG) suctioning. Older adults tend to bleed most
often from the posterior portion of the nose.
The patient often reports that the bleeding started after sneezing or blowing the nose. Document the
amount and color of the blood, and take vital signs. Ask about the number, duration, and causes of
previous bleeding episodes. Review the Best Practice for Patient Safety & Quality Care box for
emergency care of the patient with an anterior nosebleed. An additional intervention for use at home or in
the emergency department is a nasal plug that contains an agent to promote blood clotting and expands on
contact with blood to compress mucosal blood vessels. Medical attention is needed if the nosebleed does
not respond to these interventions. In such cases, the affected capillaries may be cauterized with silver
nitrate or electrocautery, and the nose packed. Anterior packing controls bleeding from the anterior nasal
cavity. Posterior nasal bleeding is an emergency because it cannot be easily reached, and the patient
may lose a lot of blood quickly. Posterior packing, epistaxis catheters (nasal pressure tubes), or gel
tampons are placed through the nose within the posterior nasal region to stop the bleeding. Placement of
these devices is uncomfortable; and the airway may be obstructed with reduced gas exchange if the pack
slips (Schreiber, 2020). Observe the patient for respiratory distress and for tolerance of the devices.
Humidity, oxygen, bedrest, and antibiotics may be prescribed. Opioid drugs may be prescribed for pain.
Assess patients receiving opioids at least hourly for gag and cough reflexes. Use pulse oximetry to
monitor for hypoxemia. The tubes or packing is usually removed after 1 to 3 days. For posterior bleeding
that does not respond to packing or tubes, additional options include cauterizing or ligating the blood
vessels or performing an embolization of the bleeding artery with interventional radiology. Potential
complications of embolization include facial pain, loss of tissue integrity with necrosis of skin or nasal
mucosa, facial nerve paralysis, and blindness. After the tubes or packing has been removed, teach the
patient and family these interventions to use at home for comfort and safety: • Apply petroleum
jelly sparingly to the nares for comfort. • Use saline nasal sprays after healing to add moisture and
prevent rebleeding. • Avoid vigorous nose blowing, the use of aspirin or other NSAIDs, and
strenuous activities such as heavy lifting for at least 1 month.
Fractures of the nose
Injury to the nose may result in loss of tissue integrity with nasal fractures that interfere with gas
exchange. If the bone or cartilage is not displaced and no complications are present, treatment may
not be needed. However, displacement of either the bone or cartilage can cause airway obstruction
or cosmetic deformity and is a potential source of infection.
Document any nasal problem, including deviation, malaligned nasal bridge, a change in nasal breathing,
crackling of the skin (crepitus) on palpation, bruising, and pain. Blood or clear fluid (cerebrospinal fluid
[CSF]) may drain from one or both nares as a result of a simple nasal fracture. This is rare and, if present,
indicates a serious injury (e.g., skull fracture). CSF can be differentiated from normal nasal secretions
because CSF contains glucose that will test positive with a dipstick test for glucose. When CSF dries on a
piece of filter paper, a yellow “halo” appears as a ring at the dried edge of the fluid.
Interventions: closed reduction, rhinoplasty, nasoseptoplasty
Take Action The primary health care provider performs a simple closed reduction (moving the bones by
palpation to realign them) of the nasal fracture using local or general anesthesia within the first 24 hours
after injury. After 24 hours the fracture is more difficult to reduce because of edema and scar formation.
Then reduction may be delayed for several days until edema is gone. Management focuses on pain relief
and cold compresses to decrease swelling.
Rhinoplasty post-op:
Reduction and surgery may be needed for severe fractures or for those that do not heal properly.
Rhinoplasty is a surgical reconstruction of the nose performed to repair a fractured nose and also to
change the shape of the nose for improved function or appearance.
Instruct the patient to stay in a semi-Fowler position and to move slowly. Suggest that he or she rest and
use cool compresses on the nose, eyes, and face to help reduce swelling and bruising. After the gag
reflex has returned, urge the patient to drink at least 2500 mL/day. To prevent bleeding, teach the patient
to avoid forceful coughing or straining during a bowel movement, not to sniff upward or blow the
nose, and not to sneeze with the mouth closed for the first few days after the packing is removed. Instruct
him or her to avoid aspirin and other NSAIDs to prevent bleeding. Antibiotics may be prescribed to
prevent infection. Explain that because of edema the final surgical result may require 6 to 12 months.
Facial Trauma
The priority action when caring for a patient with facial trauma is airway assessment for gas exchange.
Signs of airway obstruction are stridor, shortness of breath, dyspnea, anxiety, restlessness, hypoxia,
decreased oxygen saturation, cyanosis, and loss of consciousness.
Le Fort Fracture:
I—Nasoethmoid complex fracture
II—Maxillary and nasoethmoid complex fracture
III — Combination of I & II plus orbital-zygoma fracture; often called craniofacial disjunction
Le Fort Fracture: Assessment: Recognize Cues
•
•
•
•
•
Airway
Site of trauma
Vision and eye movement
Behind ears
Spinal and skull trauma
Le Fort Fracture: Interventions: Take Action
•
•
Establish and maintain airway
Control hemorrhage
•
•
•
Assess for extent of injury
Stabilize jaw fracture (if present)
Surgery may be needed
Laryngeal Trauma
Laryngeal trauma and damage occur with a crushing or direct-blow injury, fracture, or prolonged
endotracheal intubation with loss of tissue integrity. Symptoms include difficulty breathing, inability to
produce sound (aphonia), hoarseness, and subcutaneous emphysema (air present in the subcutaneous
tissue). Bleeding from the airway (hemoptysis) may occur, depending on the location of the trauma. The
primary health care provider performs a direct visual examination of the larynx by laryngoscopy or
fiberoptic laryngoscopy to determine the extent of the injury. Management of patients with laryngeal
injuries consists of assessing the effectiveness of gas exchange and monitoring vital signs (including
respiratory status and pulse oximetry) every 15 to 30 minutes. Maintaining a patent airway is a
priority. Apply oxygen and humidification as prescribed to maintain adequate oxygen saturation.
Surgical intervention is needed for lacerations of the mucous membranes, cartilage exposure, and cord
paralysis. Laryngeal repair is performed as soon as possible to prevent laryngeal stenosis and to cover any
exposed cartilage. An artificial airway may be needed temporarily.
Head and Neck Cancer
Pathophysiology Review: Head and neck cancers are usually squamous cell carcinomas. These slowgrowing tumors are curable when diagnosed and treated at an early stage. The prognosis for those who
have more advanced disease at diagnosis depends on the extent and location of the tumors. Untreated,
these cancers are often fatal within 2 years of diagnosis (ACS, 2020). The cancer begins as a loss of
cellular regulation when the mucosa is chronically irritated and becomes tougher and thicker.
Eventually genes controlling cell growth are damaged, allowing excessive growth of these abnormal and
malignant cells. Initial lesions first appear as white, patchy lesions (leukoplakia) or red, velvety patches
(erythroplakia). Head and neck cancer first spreads (metastasizes) into local lymph nodes, muscle,
and bone. Later spread is systemic to distant sites, usually to the lungs or liver.
Head and Neck Cancer risk factors:
Tobacco and alcohol use
Voice abuse
Chronic laryngitis
Exposure to chemicals or dust
Poor oral hygiene
Long-term GERD
Oral infection with HPV
Assessment: Recognize Cues
Ask about tobacco and alcohol use, history of acute or chronic laryngitis or pharyngitis, oral
sores, swallowing difficulty, and lumps in the neck. Calculate the patient’s pack-years of
smoking history (see Chapter 24). Ask about alcohol intake (how many drinks per day and for how
many years). Also ask about oral exposure to HPV (Schiech, 2016), which has been recognized as
an increasing cause of head and neck cancer. Table 26.1 lists the warning signs of head and neck
cancer. With laryngeal cancer, painless hoarseness may occur because of tumor size and an inability
of the vocal cords to come together for normal speech. Any adult who has a history of hoarseness,
mouth sores, or a lump in the neck for 3 to 4 weeks should be evaluated for laryngeal cancer.
Imaging assessment
◦ X-rays, CT, MRI, SPECT, PET-CT
Interventions
Radiation therapy
Chemotherapy
Biotherapy
Surgical intervention
Post-op care:
Head and neck surgery often lasts 8 hours or longer, and the patient spends the immediate period after
surgery in an ICU. Monitor airway patency, vital signs, hemodynamic status, and comfort level. Take
vital signs and monitor for hemorrhage and other general complication of anesthesia and surgery hourly
for the first 24 hours and then according to agency policy until the patient is stable. Complications after
surgery include airway obstruction, hemorrhage, wound breakdown, and tumor recurrence. The first
priorities after head and neck surgery are airway maintenance and ensuring gas exchange.
Maintaining the Airway and Gas Exchange Immediately after surgery, the patient may need
mechanical ventilation. During weaning, the patient usually uses a tracheostomy collar (over the artificial
airway or open stoma) with oxygen and humidity to help move mucus secretions. Secretions may remain
blood-tinged for 1 to 2 days. Use Standard Precautions, and report any increase in bleeding to the
surgeon. A laryngectomy tube is used for patients who have undergone a total laryngectomy and need an
appliance to prevent scar tissue shrinkage of the skin-tracheal border. This tube is similar to a
tracheostomy tube but is shorter and wider with a larger lumen. Care is similar to tracheostomy tube care
(see Chapter 25) except that the patient can change the laryngectomy tube daily or as needed. A
laryngectomy buon is similar to a laryngectomy tube but is softer, has a single lumen, and is very short.
Provide alternative communication techniques because the patient cannot speak.
Managing the Wound Stoma care after a total laryngectomy is a combination of wound care and airway
care. Inspect the stoma and clean the suture line with sterile saline (or a prescribed solution) to prevent
secretions from forming crusts and obstructing the airway. Perform suture line care every 1 to 2 hours
during the first few days after surgery and then every 4 hours. The mucosa of the stoma and trachea
should be bright pink and shiny and without crusts, similar to the appearance of the oral mucosa. Tissue
“flaps” may be used to close the wound and improve appearance. Flaps are skin, subcutaneous tissue, and
sometimes muscle, taken from other body areas and used for reconstruction after head and neck resection.
The first 24 hours after surgery are critical. Evaluate all grafts and flaps hourly for the first 72 hours.
Monitor capillary refill, color, drainage, and Doppler activity of the major blood vessel to the area. Report
changes to the surgeon immediately because surgical intervention may be needed. Position the patient so
the surgical flaps are not dependent. Wound breakdown with loss of tissue integrity is a common
complication in patients after head and neck surgery, especially if radiation therapy occurred before
surgery. Manage wound breakdown with packing and local care as prescribed to keep the wound clean
and stimulate the growth of healthy granulation tissue. Wounds may be extensive, and the carotid artery
may be exposed, which increases the risk for rupture and hemorrhage.
Managing Pain
Pain after surgery has many causes and should be managed while still allowing the patient to be able to
participate in care. Morphine often is given IV by a patient-controlled analgesia (PCA) pump for the first
1 to 2 days after surgery. As the patient progresses, liquid opioid analgesics can be given by feeding tube.
Oral drugs for pain and discomfort are started only after the patient can tolerate oral intake.
Maintaining Nutrition
All patients are at risk for malnutrition during treatment for head and neck cancer. A nasogastric (NG),
gastrostomy, or jejunostomy tube is placed during surgery for nutrition support while the head and neck
heal and may remain in place for 7 to 10 days. It is removed when the patient is able to swallow safely.
Aspiration cannot occur after a total laryngectomy because the airway is completely separated from the
esophagus.
Promoting Communication
The patient’s voice quality and speech are altered after surgery. This problem has enormous effects on the
patient’s social interactions, continued employment, and quality of life. In collaboration with an SLP,
work with the patient and family toward developing an acceptable communication method during the
inpatient period. Speech production varies with patient practice, amount of tissue removed, and radiation
effects but can be very understandable. The speech rehabilitation plan for patients who have a total
laryngectomy at first consists of writing, using a picture board, smart phone, or computer. The patient
then uses an artificial larynx and may eventually learn esophageal speech. He or she needs encouragement
and support from the SLP, hospital team, and family while relearning to speak. Having a laryngectomee
(an adult who has had a laryngectomy) from one of the local self-help organizations, such as the ACS
Visitor Program or the International Association of Laryngectomees, visit the patient and family is often
beneficial.
Preventing Aspiration
The surgical changes in the upper respiratory tract and altered swallowing mechanisms increase the
patient’s risk for aspiration. Aspiration can result in pneumonia, weight loss, and prolonged
hospitalization. A nasogastric (NG) feeding tube increases the risk for aspiration because it keeps the
lower esophageal sphincter partially open. Most patients who need enteral feeding supplementation have
a percutaneous endoscopic gastrostomy (PEG) tube placed rather than an NG tube. See Chapter 55 for
care of patients receiving enteral nutrition by NG or PEG tube. Swallowing can be a problem for the
patient who has a tracheostomy tube. It can be normal if the cranial nerves and anatomic structures are
intact. In a normal swallow, the larynx rises and moves forward to protect itself from the passing stream
of food and saliva. The tracheostomy tube may fix the larynx in place
Supporting Self-Esteem
The patient with head and neck cancer usually has a change in selfconcept and self-image resulting from
issues such as the presence of a stoma or artificial airway, speech changes, and a change in the method of
eating. Psychosocial issues may include guilt, regret, and uncertainty. He or she may not be able to speak
at all or may have permanent speech deficits. Help the patient set realistic goals, starting with
involvement in self-care. Reinforce the alternative communication methods suggested by the SLP so the
patient can communicate in the hospital and after discharge. After surgery, the patient may feel socially
isolated because of the change in voice and facial appearance. Loose-fiing, high-collar shirts or sweaters,
scarves, and jewelry can be worn to cover the laryngectomy stoma, tracheostomy tube, and other changes
related to surgery. Cosmetics may aid in covering any facial or neck disfigurement.
Managing Pain
Pain after surgery has many causes and should be managed while still allowing the patient to be able to
participate in care. Morphine often is given IV by a patient-controlled analgesia (PCA) pump for the first
1 to 2 days after surgery. As the patient progresses, liquid opioid analgesics can be given by feeding tube.
Oral drugs for pain and discomfort are started only after the patient can tolerate oral intake.
Maintaining Nutrition
All patients are at risk for malnutrition during treatment for head and neck cancer. A nasogastric (NG),
gastrostomy, or jejunostomy tube is placed during surgery for nutrition support while the head and neck
heal and may remain in place for 7 to 10 days. It is removed when the patient is able to swallow safely.
Aspiration cannot occur after a total laryngectomy because the airway is completely separated from the
esophagus. Promoting Communication The patient’s voice quality and speech are altered after surgery.
This problem has enormous effects on the patient’s social interactions, continued employment, and
quality of life. In collaboration with an SLP, work with the patient and family toward developing an
acceptable communication method during the inpatient period. Speech production varies with patient
practice, amount of tissue removed, and radiation effects but can be very understandable. The speech
rehabilitation plan for patients who have a total laryngectomy at first consists of writing, using a picture
board, smart phone, or computer. The patient then uses an artificial larynx and may eventually learn
esophageal speech. He or she needs encouragement and support from the SLP, hospital team, and family
while relearning to speak. Having a laryngectomee (an adult who has had a laryngectomy) from one of
the local self-help organizations, such as the ACS Visitor Program or the International Association of
Laryngectomees, visit the patient and family is often beneficial.
Preventing Aspiration
The surgical changes in the upper respiratory tract and altered swallowing mechanisms increase the
patient’s risk for aspiration. Aspiration can result in pneumonia, weight loss, and prolonged
hospitalization. A nasogastric (NG) feeding tube increases the risk for aspiration because it keeps the
lower esophageal sphincter partially open. Most patients who need enteral feeding supplementation have
a percutaneous endoscopic gastrostomy (PEG) tube placed rather than an NG tube. See Chapter 55 for
care of patients receiving enteral nutrition by NG or PEG tube. Swallowing can be a problem for the
patient who has a tracheostomy tube. It can be normal if the cranial nerves and anatomic structures are
intact. In a normal swallow, the larynx rises and moves forward to protect itself from the passing stream
of food and saliva. The tracheostomy tube may fix the larynx in place,
Home Care Management
Extensive home care preparation is needed after a laryngectomy for cancer. The convalescence period is
long, and airway management is complicated. For the patient with severe respiratory problems, home
changes to allow for one-floor living may be needed. Increased humidity is needed. A humidifier add-on
to a forced-air furnace can be obtained, or a room humidifier or vaporizer may be used. Be sure to stress
that meticulous cleaning of these items is needed to prevent spread of mold or other sources of infection.
A home care nurse is often an important resource for the patient and family. This nurse assesses the
patient and home situation for problems in self-care, complications, adjustment, and adherence to the
medical regimen. Self-Management Education Teach the patient and family how to care for the stoma or
tracheostomy or laryngectomy tube, depending on the type of surgery performed, using the actions listed
in the Patient and Family Education: Preparing for Self Management: Home Laryngectomy Care box.
Stoma care teaching is focused on protection, which is needed as a result of the anatomic changes
resulting from surgery. Instruct the patient to use a shower shield over the tube or stoma when bathing to
prevent water from entering the airway. Suggest that the patient wear a protective cover or stoma guard to
protect the stoma during the day. Communication involves having the patient continue the selected
communication method that began in the hospital. Instruct him or her to wear a medical alert
(MedicAlert) bracelet and carry a special identification card. For patients with a laryngectomy, this card is
available from the local chapters of the International Association of Laryngectomees. The card instructs
the reader about providing an emergency airway or resuscitating someone who has a stoma
Psychosocial Preparation
The many changes resulting from a laryngectomy influence physical, social, and emotional functioning
for both the patient and his or her significant other (Sterba et al., 2016). The patient with a permanent
stoma, tracheostomy tube, NG or PEG tube, and wounds has an altered body image. Stress the importance
of returning to as normal a lifestyle as possible. Most patients can resume many of their usual activities
within 4 to 6 weeks after surgery. The patient with a total laryngectomy cannot produce sounds during
laughing and crying. Mucus secretions may appear unexpectedly when these emotions arise or when
coughing or sneezing occurs. The mucus can be embarrassing, and the patient needs to be prepared to
cover the stoma with a handkerchief or gauze. The patient who has undergone composite resections has
difficulty with speech and swallowing. He or she may need to deal with tracheostomy and feeding tubes
in public places.
27: Concepts of Care for Patients With Noninfectious Lower Respiratory Problems
KEY TERMS
asthma: A chronic disease in which acute reversible airway obstruction occurs intermiently, reducing
airflow.
chronic bronchitis: An inflammation of the bronchi and bronchioles caused by exposure to irritants,
especially cig smoke.
chronic obstructive pulmonary disease (COPD): A collection of lower airway disorders that interfere
with airflow and gas exchange.
control therapy drugs: Asthma drugs used daily to reduce airway sensitivity (responsiveness) to prevent
asthma attacks from occurring and to maintain gas exchange.
cor pulmonale: Right-sided heart failure caused by pulmonary disease occurring with bronchitis or
emphysema.
cystic fibrosis (CF): An autosomal recessive genetic disease that affects many organs with most
impairment occurring to pancreatic and/or lung function.
dyspnea: Perceived shortness of breath.
emphysema: A destructive problem of lung elastic tissue that reduces its ability to recoil after stretching,
leading to hyperinflation of the lung.
hypercapnia: Higher than normal blood carbon dioxide levels. Also known as hypercarbia. hypoxemia:
Low blood oxygen levels. lobectomy Removal of a lobe of the lung.
orthopnea: Breathlessness that is worse in a supine position.
pneumonectomy Surgical removal of an entire lung.
pulmonary artery hypertension (PAH) A condition in which pulmonary vessels and often other lung
tissues undergo growth changes that greatly increase pressure in the lung circulatory system for unknown
reasons (also known as idiopathic pulmonary artery hypertension).
reliever drugs: Asthma drugs used to stop an asthma attack once it has started. Also known as rescue
drugs.
The lower respiratory tract is the tubular system of the trachea (below the larynx), two mainstem bronchi,
five secondary bronchi, thousands of branching bronchi and bronchioles, and the alveolar ducts, which
connect to the final portions of the tract, the alveoli. Air must flow through the entire tubular system for
needed oxygen to reach the alveolar ducts and alveoli where primary gas exchange occurs. When the
function of any of these structures is reduced, both gas exchange and systemic perfusion are impaired.
Asthma Pathophysiology Review
One of the most common lower respiratory disorders that reduces gas exchange is asthma, which can lead
to severe lower airway obstruction and death. Asthma is a chronic disease in which reversible acute
airway obstruction occurs intermittently, reducing airflow (Fig. 27.1). Airway obstruction occurs by both
inflammation and airway tissue sensitivity (hyperresponsiveness) with bronchoconstriction. Inflammation
obstructs the airway lumens (i.e., the hollow insides) (Fig. 27.2). Airway hyperresponsiveness and
constriction of bronchial smooth muscle narrow the tubular structure of the airways. Airway inflammation
and sensitivity can trigger bronchiolar constriction, and many adults with asthma have both problems
(McCance et al., 2019). More than 3300 deaths from acute asthma occur in the United States each year
(Centers for Disease Control and Prevention [CDC], 2019a).
Etiology and Genetic Risk:
Although asthma may be classified into types based on what triggers the attacks, the effect on gas
exchange is the same. Inflammation of the mucous membranes lining the airways is a key event in
triggering an asthma attack. It occurs in response to the presence of specific allergens; general irritants
such as cold air, dry air, or fine airborne particles; microorganisms; and aspirin and other
NSAIDs.
Incidence:
Asthma can occur at any age. About half of adults with asthma also had the disease in childhood.
Asthma affects over 22 million adults in the United States and Canada (19.9 million in the United States
and 2.6 million in Canada) (CDC, 2018b; Statistics Canada, 2017 ). It is more common in urban settings
than rural settings.
Assessment: Recognize Cues
History
The patient with asthma usually has a pattern of intermittent episodes of dyspnea (perceived shortness of
breath), chest tightness, coughing, wheezing, and increased mucus production. Ask whether the
symptoms occur continuously, seasonally, in association with specific activities or exposures, at work, or
more frequently at night. Some patients have symptoms for 4 to 8 weeks after a cold or other upper
respiratory infection. The patient with atopic (allergic) asthma also may have other allergic problems. Ask
whether any family members have asthma or respiratory problems. Ask about current or previous
smoking habits. If the patient smokes, use this opportunity to teach him or her about smoking cessation
(see Chapter 24). Wheezing in nonsmokers is important in the diagnosis of asthma. Physical
Assessment/Signs and Symptoms The patient with mild to moderate asthma may have no symptoms
between asthma attacks. During an acute episode, common symptoms are an audible wheeze and
increased respiratory rate. At first the wheeze is louder on exhalation. When inflammation occurs with
asthma, coughing may increase. The patient may use accessory muscles to help breathe during an aack.
Observe for muscle retraction at the sternum and the suprasternal notch and between the ribs. The patient
with long-standing, severe asthma may have a “barrel chest,” caused by air trapping (Fig. 27.3). The
anteroposterior (AP) diameter (diameter between the front and the back of the chest) increases with air
trapping, giving the chest a rounded rather than an oval shape. The normal chest is about 1.5 times as
wide as it is deep. In severe, chronic asthma, the AP diameter may equal or exceed the lateral diameter
(Jarvis, 2020). Compare the chest AP diameter with the lateral diameter. Chronic air trapping also flaens
the diaphragm and increases the space between the ribs. Along with an audible wheeze, the breathing
cycle is longer, with prolonged exhalation, and requires more effort. The patient may be unable to speak
more than a few words between breaths. Hypoxia occurs with severe aacks. Pulse oximetry shows
hypoxemia (poor blood oxygen levels). Examine the oral mucosa and nail beds for cyanosis. Other
indicators of hypoxemia include changes in the level of cognition or consciousness and tachycardia
Laboratory Assessment
Laboratory tests can determine asthma type and the degree of breathing impairment. Arterial blood gas
(ABG) levels show the effectiveness of gas exchange (see Chapter 14 for discussion of ABGs). The
arterial oxygen level (PaO 2 ) may decrease during an asthma aack. Early in the aack, the arterial carbon
dioxide level (PaCO 2 ) may be decreased as the patient increases the breathing rate and depth. Later in an
asthma episode, PaCO 2 rises, as does the end-tidal carbon dioxide level, indicating carbon dioxide
retention. Allergic asthma often occurs with elevated serum eosinophil counts and immunoglobulin E
(IgE) levels. The sputum may contain eosinophils and mucus plugs with shed epithelial cells
(Curschmann spirals).
Pulmonary Function Tests
The most accurate tests for measuring airflow in asthma are the pulmonary function tests (PFTs) using
spirometry. Baseline PFTs are obtained for all patients diagnosed with asthma. The most important PFTs
for a patient with asthma are the forced vital capacity (FVC), the forced expiratory volume in the first
second (FEV1 ), and the peak expiratory flow (PEF), sometimes called peak expiratory rate flow (PERF).
Definitions of PFTs are listed in Chapter 24. A decrease in either the FEV1 or the PEF (PERF) of 15% to
20% below the expected value for age, gender, and size is common for the patient with asthma (Durham
et al., 2017). Asthma is diagnosed when these values increase by 12% or more after treatment with
bronchodilators. Airway responsiveness is tested by measuring the PEF and FEV1 before and after the
patient inhales the drug methacholine, which induces bronchospasm in susceptible adults
Interventions:
Take Action The purposes of asthma therapy are to control and prevent episodes, improve airflow and
gas exchange , and relieve symptoms. Asthma is best controlled when the patient is an active partner in
the management plan. Priority nursing actions focus on patient education about using his or her personal
asthma action plan, which includes drug therapy and lifestyle management strategies to help him or her
understand the disease and its management.
Self-Management
Education Asthma often has intermittent overt symptoms. With guided self-care, patients can co-manage
this disease, increasing symptom-free periods and decreasing the number and severity of attacks. Good
management decreases hospital admissions and increases participation in patient chosen work and leisure
activities.
Drug Therapy
Control therapy drugs are used to reduce airway sensitivity (responsiveness) to prevent asthma attacks
from occurring and maintain gas exchange . They are used every day, regardless of symptoms. Reliever
drugs (also called rescue drugs) are used to actually stop an attack once it has started. Some patients may
need drug therapy only during an asthma episode. For others, daily drugs are needed to keep asthma
episodic rather than a more frequent problem. Therapy involves the use of bronchodilators and various
drug types to reduce inflammation. Some drugs reduce the asthma response, and other drugs actually
prevent it. Combination drugs are two or more agents from different classes combined together for beer
response. With step therapy, drug therapy is prescribed at different levels, starting with step 1 and
progressing up (stepping up), until acceptable control is achieved. When the patient achieves control and
maintains it for 3 months, the respiratory health care provider adjusts the drug regimen down a step
(stepping down) at a time to reach and maintain a goal of good control at the lowest possible drug
dosages.
•
•
•
Drug therapy
• Control therapy drugs (used daily)
• Reliever drugs (used to stop an attack)
• Bronchodilators
• Anti-inflammatory agents
Exercise and activity
Oxygen therapy
Status Asthmaticus
Status asthmaticus is a severe, life-threatening acute episode of airway obstruction that
intensifies once it begins and often does not respond to usual therapy. The patient arrives in
the emergency department with extremely labored breathing and wheezing. Use of accessory
muscles for breathing and distention of neck veins are observed. If the condition is not
reversed, the patient may develop pneumothorax and cardiac or respiratory arrest. IV fluids,
potent systemic bronchodilators, steroids, epinephrine, and oxygen are given immediately to
reverse the condition. Magnesium sulfate also may be used, although this practice is
controversial. Prepare for emergency intubation.
Gas Exchange Concept Exemplar: Chronic Obstructive Pulmonary Disease
Pathophysiology Review
Chronic obstructive pulmonary disease (COPD) is a collection of lower airway disorders that interfere
with airflow and gas exchange. These disorders include emphysema and chronic bronchitis.
Etiology and Genetic Risk
Cigarette smoking is the greatest risk factor for COPD. The patient with a 20–pack-year history or
longer often has early-stage COPD with changes in pulmonary function tests (PFTs). The inhaled smoke
triggers the release of excessive proteases in the lungs. These enzymes break down elastin, the major
component of alveoli. By impairing the action of cilia, smoking also inhibits the cilia from clearing the
bronchi of mucus, cellular debris, and fluid. Alpha 1 -antitrypsin deficiency is a less common but
important risk factor for COPD, although it is often underrecognized (Southard et al., 2020).
Complications COPD
affects gas exchange and the oxygenation of all tissues. Complications include hypoxemia, acidosis,
respiratory infection, cardiac failure, dysrhythmias, and respiratory failure. Hypoxemia and acidosis
occur because the patient with COPD has reduced gas exchange, leading to decreased oxygenation
and increased carbon dioxide levels. These problems reduce cellular function. Respiratory infection risk
increases because of the increased mucus and poor gas exchange . Bacterial infections are common and
make COPD symptoms worse by increasing inflammation and mucus production and inducing more
bronchospasm. Airflow becomes even more limited, the work of breathing increases, and dyspnea results.
Cardiac failure, especially cor pulmonale (right-sided heart failure caused by pulmonary disease), occurs
with bronchitis or emphysema. Cardiac dysrhythmias are common in patients with COPD
Health Promotion and Maintenance The incidence and severity of COPD would be greatly reduced by
smoking cessation. Urge all adults who smoke to quit smoking or vaping and to avoid particulate maer
exposure using the I-PREPARE model as described in Chapter 24.
Assessment: Recognize Cues
History: Ask about risk factors such as age, gender, and occupational history. COPD is seen more
often in older men. Some types of emphysema occur in families, especially those with alpha1 -antitrypsin
(AAT) deficiency (Southard et al., 2020). Obtain a thorough smoking history because tobacco use is a
major risk factor. Ask about the length of time the patient has smoked and the number of packs smoked
daily. Use these data to determine the pack-year smoking history. Also ask about the use of electronic
cigarettes or vaping, including the type of product inhaled and the duration of the habit. Ask the patient to
describe the breathing problems and assess whether he or she has any difficulty breathing while talking.
Does he or she speak in complete sentences, or is it necessary to take a breath between every one or two
words? Ask about the presence, duration, or worsening of wheezing, coughing, and shortness of breath.
Determine which activities trigger these problems. Assess any cough, and ask whether sputum is clear or
colored and how much is produced each day. Ask about the time of day when sputum production is
greatest. Smokers often have a productive cough when they get up in the morning; nonsmokers generally
do not. Ask the patient to compare the activity level and shortness of breath now with those of a month
ago and a year ago. Ask about any difficulty with eating and sleeping. Many patients sleep in a semisiing
position because breathlessness is worse when lying down (orthopnea). Ask about any difficulty with
ADLs or sexual activity. Document this assessment to personalize the intervention plan. Weigh the
patient and compare this weight with previous weights. Unplanned weight loss is likely when COPD
severity increases, because the work of breathing increases metabolic needs. Dyspnea and mucus
production often result in poor food intake and inadequate nutrition. Ask the patient to recall a typical
day’s meals and fluid intake. When heart failure is present with COPD, general edema with weight gain
may occur.
Physical Assessment/Signs and Symptoms
General appearance can provide clues about respiratory status and energy level. Observe weight in
proportion to height, posture, mobility, muscle mass, and overall hygiene. The patient with increasingly
severe COPD is thin, with loss of muscle mass in the extremities, although the neck muscles may be
enlarged. He or she tends to be slow moving and slightly stooped. The patient often sits in a forwardbending posture with the arms held forward, a position known as the orthopneic or tripod position (Fig.
27.7). When dyspnea becomes severe, activity intolerance may be so great that bathing and general
grooming are neglected. Respiratory changes that occur as a result of obstruction include changes in chest
size, and fatigue. Inspect the chest and assess the breathing rate and pattern. The patient with respiratory
muscle fatigue breathes with rapid, shallow respirations and may have an abnormal breathing pattern in
which the abdominal wall is sucked in during inspiration or may use accessory muscles in the abdomen or
neck.
Psychosocial Assessment
COPD affects all aspects of a patient’s life. He or she may be isolated because dyspnea causes fatigue or
because of embarrassment from coughing and excessive sputum production. Ask the patient about
interests and hobbies to assess whether socialization has decreased or whether hobbies cause exposure to
irritants. Ask about home conditions for exposure to smoke or crowded living conditions that promote
transmission of respiratory infections. Economic status may be affected by the disease through changes in
income and health insurance coverage. Drugs delivered by inhalers are expensive, and many patients with
limited incomes may use them only during exacerbations and not as prescribed on a scheduled basis.
Anxiety and fear from feelings of breathlessness may reduce the patient’s ability to participate in a full
life. Work, family, social, and sexual roles can be affected. Encourage the patient and family to express
their feelings about disease progression and the limitations on lifestyle. Assess their use of support groups
and community services.
Laboratory Assessment
Arterial blood gas (ABG) values identify abnormal gas exchange , oxygenation, ventilation, and acid-base
status. Compare repeated ABG values to assess changes in respiratory status. Once baseline ABG values
are obtained, pulse oximetry can gauge treatment response. A WBC count helps confirm the presence of
infection.
Imaging Assessment
Chest x-rays are used to rule out other lung diseases and to check the progress of patients with respiratory
infections or chronic disease. With advanced emphysema, chest x-rays show hyperinflation with widely
spaced ribs and a flaened diaphragm. Other Diagnostic Assessments COPD is classified from mild to very
severe on the basis of symptoms and pulmonary function test (PFT) changes (Table 27.2; see Table 24.6).
Airflow rates and lung volume measurements help distinguish airway disease (obstructive diseases) from
interstitial lung disease (restrictive diseases). PFTs determine lung volumes, flow volume curves, and
diffusion capacity.
Analysis: Analyze Cues and Prioritize Hypotheses
The priority collaborative problems for patients with chronic obstructive pulmonary disease (COPD)
include: 1. Decreased gas exchange due to alveolar-capillary membrane changes, reduced airway size,
ventilatory muscle fatigue, excessive mucus production, airway obstruction, diaphragm flattening,
fatigue, and decreased energy 2. Weight loss due to dyspnea, excessive secretions, anorexia, and fatigue
3. Anxiety due to a change in health status and situational crisis 4. Decreased endurance due to fatigue,
dyspnea, and an imbalance between oxygen supply and demand 5. Potential for pneumonia or other
respiratory infections
Planning and Implementation: Generate Solutions and Take Action
Improving Gas Exchange and Reducing Carbon Dioxide Retention Planning: Expected Outcomes
The patient with COPD is expected to attain and maintain gas exchange at his or her usual baseline level.
Interventions Most patients with COPD use nonsurgical management to improve or maintain gas
exchange . Surgical management requires that the patient meet strict criteria. Nursing care is most
successful with helping the patient become a partner in COPD management by participating in all
therapies to improve gas exchange . Thus priority nursing management for patients with COPD focuses
on ensuring consistent use of prescribed drug therapy and on airway maintenance, monitoring, breathing
techniques, positioning, effective coughing, oxygen therapy, exercise conditioning, suctioning, and
hydration. Before any intervention, assess the breathing rate, rhythm, depth, and use of accessory
muscles. The accessory muscles are less efficient than the diaphragm, and the work of breathing
increases. Determine whether any factors are contributing to the increased work of breathing, such as
respiratory infection. Airway maintenance is the most important focus of interventions to improve gas
exchange
Drug Therapy
Drug therapy is recommended at all levels of disease to delay progression and promote continued activity
tolerance (GOLD, 2019; O’Dell et al., 2018). Drugs used to manage COPD are the same drugs as for
asthma and include beta-adrenergic agents, cholinergic antagonists, xanthines, corticosteroids, and
cromones (see the Common Examples of Drug Therapy: Asthma Prevention and Treatment box in the
Asthma section). The focus is on long-term control therapy with longer-acting drugs, such as
arformoterol, indacaterol, tiotropium, aclidinium bromide, olodaterol, and the combination drugs, such as
fluticasone/vilanterol (e.g., BREO ELLIPTA), olodaterol/tiotropium, vilanterol/umeclidinium (e.g.,
ANORO ELLIPTA), and a newer triple combination of fluticasone/umeclidinium/vilanterol (e.g.,
TRELEGY ELLIPTA). Just as for asthma management, a key issue for successful drug therapy for COPD
management is the correct technique for inhaler use. Have the patient demonstrate or fully describe
exactly how he or she uses the inhaler(s) at every new outpatient interaction. Reinforce correct technique
use and apply a variety of interventions that can help the patient acquire the knowledge and skills needed
to use the inhaler correctly (see the Systems Thinking and Quality Improvement: Reducing Critical Errors
in Patient Inhaler Use box). The patient with COPD is more likely to be taking systemic agents in
addition to inhaled drugs. Another drug class for COPD is the mucolytics, which thin the thick secretions,
making them easier to cough up and expel. Nebulizer treatments with normal saline or a mucolytic agent
such as acetylcysteine or dornase alfa and normal saline help thin secretions. Guaifenesin is a systemic
mucolytic that is taken orally. A combination of guaifenesin and dextromethorphan also raises the cough
threshold.
Breathing Techniques
Diaphragmatic or abdominal and pursed-lip breathing may be helpful for managing dyspneic episodes.
Teach the patient to use these techniques, shown in the Patient and Family Education: Preparing for
SelfManagement: Breathing Exercises box, during all activities to reduce the amount of stale air in the
lungs and manage dyspnea. Teach these techniques when the patient has less dyspnea.
Preventing Weight Loss Planning: Expected Outcomes The patient with COPD is expected to achieve
and maintain a body weight within 10% of ideal. Interventions: The patient with COPD often has nausea,
early satiety (feeling too “full” to eat), poor appetite, and meal-related dyspnea. The work of breathing
raises calorie and protein needs, which can lead to protein-calorie malnutrition. Malnourished patients
lose muscle mass and strength, lung elasticity, and alveolar-capillary surface area, all of which reduce gas
exchange. Identify patients at risk for or who have this complication and collaborate with a registered
dietitian nutritionist (RDN) to perform a nutrition assessment. Monitor weight and other indicators of
nutrition, such as serum prealbumin levels. Dyspnea management is needed because shortness of breath
interferes with eating. Teach the patient to plan the biggest meal of the day for the time when he or she is
most hungry and well rested. Four to six small meals a day may be preferred to three larger ones. Remind
patients to use pursed-lip and abdominal breathing and to use the prescribed bronchodilator 30 minutes
before the meal to reduce bronchospasm. Food selection can help prevent weight loss. Abdominal
bloating and a feeling of fullness often prevent the patient from eating a complete meal. Collaborate with
the RDN to teach about foods that are easy to chew and not gas forming. Advise the patient to avoid dry
foods that stimulate coughing and caffeine-containing drinks that increase urine output and may lead to
dehydration. Urge the patient to eat high-calorie, high-protein foods. Some supplements are formulated
for patients with COPD and provide nutrition with reduced carbon dioxide production. If early satiety is a
problem, advise him or her to avoid drinking fluids before and during the meal and to eat smaller, more
frequent meals
Minimizing Anxiety Planning: Expected Outcomes The patient with COPD is expected to have
decreased anxiety. Interventions Patients with COPD become anxious during acute dyspneic episodes,
especially when excessive secretions are present. Anxiety also may cause dyspnea. Help the patient
understand that anxiety can increase dyspnea and have a plan for dealing with anxiety. Together with the
patient, develop a wrien plan that states exactly what he or she should do if symptoms flare. Having a
plan provides confidence and control in knowing what to do, which often helps reduce anxiety. Stress the
use of pursed-lip and diaphragmatic breathing techniques during periods of anxiety or panic. Family,
friends, and support groups can be helpful. Recommend professional counseling, if needed, as a positive
suggestion. Stress that talking with a counselor can help identify techniques to maintain control over
dyspnea and panic. Explore other approaches to help the patient manage dyspneic episodes and panic
aacks, such as progressive relaxation, hypnosis therapy, and biofeedback. For some patients, antianxiety
drug therapy may be needed for severe anxiety.
Improving Endurance Planning: Expected Outcomes The patient with COPD is expected to increase
activity to a level acceptable to him or her. Interventions The patient with COPD often has chronic
fatigue. During acute exacerbations, he or she may need extensive help with the ADLs of eating, bathing,
and grooming. As the acute problem resolves, encourage the patient to pace activities and perform as
much self-care as possible. Teach him or her to not rush through morning activities because rushing
increases dyspnea, fatigue, and hypoxemia. As activity gradually increases, assess the patient’s response
by noting skin color changes, pulse rate and regularity, oxygen saturation, and work of breathing. Suggest
the use of oxygen during periods of high energy use such as bathing or walking. Energy conservation is
the planning and pacing of activities for best tolerance and minimum discomfort. Ask the patient to
describe a typical daily schedule. Help him or her divide each activity into its smaller parts to determine
whether that task can be performed in a different way or at a different time. Teach about planning and
pacing daily activities with rest periods between activities. Help the patient develop a chart outlining the
day’s activities and planned rest periods. Encourage the patient to avoid working with the arms raised.
Activities involving the arms decrease exercise tolerance because the accessory muscles are used to
stabilize the arms and shoulders rather than to assist breathing. Many activities involving the arms can be
done sttiing at a table leaning on the elbows. Teach the patient to adjust work heights to reduce back
strain and fatigue. Remind him or her to keep arm motions smooth and flowing to prevent jerky motions
that waste energy. Work with the occupational therapist to teach about the use of adaptive tools for
housework, such as long-handled dustpans, sponges, and dusters, to reduce bending and reaching.
Suggest organizing work spaces so that items used most often are within easy reach. Measures such as
dividing laundry or groceries into small parcels that can be handled easily, using disposable plates to save
washing time, and leing dishes dry in the rack also conserve energy. Teach the patient to not talk when
engaged in other activities that require energy, such as walking. In addition, teach him or her to avoid
breath holding while performing any activity
Preventing Respiratory Infection Planning: Expected Outcomes The patient with COPD is expected
to avoid serious respiratory infection. Interventions Pneumonia is a common complication ofCOPD,
especially among older adults. Patients who have excessive secretions are at increased risk for respiratory
tract infections. Teach patients to avoid crowds, and stress the importance of receiving a pneumonia
vaccination and a yearly influenza vaccine
Home Care Management Most patients with COPD are managed in the ambulatory care setting and
cared for at home. When pneumonia or a severe exacerbation develops, the patient often returns home
after hospitalization. For those with advanced disease, 24-hour care may be needed for ADLs and
monitoring. If home care is not possible, placement in a long-term care seing may be needed. Patients
with hypoxemia may use oxygen at home either as needed or continually. Continuous, long-term oxygen
therapy can reverse tissue hypoxia and improve cognition and well-being. For more information on home
oxygen therapy, see Chapter 25. Collaborate with the case manager to obtain the equipment needed for
care at home. Patient needs may include oxygen therapy, a hospital-type bed, a nebulizer, a tub transfer
bench or shower chair, and scheduled visits from a home care nurse for monitoring and evaluation. The
patient with COPD faces a lifelong disease with remissions and exacerbations. Explain to the patient and
family that he or she may have periods of anxiety, depression, and ineffective coping.
Self-Management Education
Patients with COPD need to know as much about the disease as possible so that they can beer manage it
and themselves. Patients and families should be able to discuss drug therapy, correct use of inhalers, signs
of infection, avoidance of respiratory irritants, the nutrition therapy regimen, and activity progression.
Instruct them to identify and avoid stressors that can worsen the disease. Reinforce the techniques of
pursed-lip breathing, diaphragmatic breathing, positioning, relaxation therapy, energy conservation, and
coughing and deep breathing. Teaching about all of the needed topics may require coordination with the
home care or clinic staff.
Evaluation: Evaluate Outcomes Evaluate the care of the patient with COPD based on the identified
priority patient problems. The expected outcomes of care are that the patient will: Attain and maintain
gas exchange at a level within his or her chronic baseline values • Cough and clear secretions
effectively • Maintain a respiratory rate and rhythm appropriate to his or her activity level • Achieve an
effective breathing pattern that decreases the work of breathing • Maintain a patent airway •
Achieve and maintain a body weight within 10% of his or her ideal weight • Have decreased anxiety
• Increase activity to a level acceptable to him or her • Perform ADLs with no or minimal assistance •
Avoid serious respiratory infections • Use prevention activities such as pneumonia and influenza
vaccination and crowd avoidance
Cystic Fibrosis Pathophysiology Review
Cystic fibrosis (CF) is an autosomal recessive genetic disease that affects many organs with most
impairment occurring to pancreatic and/or lung function. Although CF is present from birth and usually is
first seen in early childhood, almost half of patients with CF in the United States are adults (Cystic
Fibrosis Foundation [CFF], 2019 ; Lomas & Tran, 2020). The underlying problem of CF is blocked
chloride transport in the cell membranes. Poor chloride transport causes the formation of mucus that
has little water content and is thick. The thick, sticky mucus causes problems in the lungs, pancreas,
liver, salivary glands, and testes. The mucus plugs up the airways in the lungs and the glandular tissues in
nonpulmonary organs, causing atrophy and organ dysfunction. Nonpulmonary problems include
pancreatic insufficiency, malnutrition, intestinal obstruction, poor growth, male sterility, and cirrhosis of
the liver. Additional problems of CF in young adults include osteoporosis and diabetes mellitus.
Respiratory failure is the main cause of death. Improved management has increased life expectancy, even
among those with severe disease, to about 47 years (CFF, 2019; Loas & Tran, 2020). The pulmonary
problems of CF result from the constant presence of thick, sticky mucus and are the most serious
complications of the disease. The mucus narrows airways, reducing airflow and interfering with gas
exchange . The constant presence of mucus results in chronic respiratory tract infections, chronic
bronchitis, and dilation of the bronchioles (bronchiectasis). Lung abscesses are common. Over time the
bronchioles distend, and mucus-producing cells have increased numbers (hyperplasia) and increased size
(hypertrophy). Complications include pneumothorax, arterial erosion and hemorrhage, and respiratory
failure. CF is most common among whites, and about 4% (1 in 29) are carriers (CFF, 2019). It is rarer
among Hispanic Americans (1 in 46 are carriers), African Americans (1 in 65 are carriers), and Asian
American (1 in 90 are carriers). Males and females are affected equally
Interprofessional Collaborative Care Assessment: Recognize Cues
Usually, but not always, CF is diagnosed in childhood. The major diagnostic test is sweat chloride
analysis. Non-pulmonary symptoms include abdominal distention, gastroesophageal reflux, rectal
prolapse, foul-smelling stools, and steatorrhea (excessive fat in stools). The patient is often
malnourished and has many vitamin deficiencies, especially of the fat-soluble vitamins (e.g., vitamins
A, D, E, K). As pancreatic function decreases, diabetes mellitus develops with loss of insulin production.
Diabetes is present in more than 50% of adults with CF (Frost et al., 2018). The adult with severe CF is
usually smaller and thinner than average. Another problem seen in adults with CF is the early onset of
osteoporosis and osteopenia, with a greatly increased risk for bone fracture (CFF, 2019). Pulmonary
symptoms caused by CF are progressive (McCance et al., 2019). Respiratory infections are frequent or
chronic with exacerbations. Patients usually have chest congestion, limited exercise tolerance, cough,
sputum production, use of accessory muscles, and decreased pulmonary function (especially forced vital
capacity [FVC] and forced expiratory volume in the first second of exhalation [ FEV1 ]). Chest x-rays
show infiltrate and an increased anteroposterior (AP) diameter. During an acute exacerbation or when the
disease progresses to end stage, the patient has increased chest congestion, reduced activity tolerance,
increased crackles, increased cough, increased sputum production (often with hemoptysis), and severe
dyspnea with fatigue. Arterial blood gas (ABG) studies show acidosis (low pH), greatly reduced arterial
oxygen (PaO 2 ) levels, increased arterial carbon dioxide (PaCO 2 ) levels, and increased bicarbonate
levels.
Interventions: Take Action
The patient with CF needs daily therapy to slow disease progress and enhance gas exchange . There is no
cure for CF. Nonsurgical Management The management of the patient with CF is complex and lifelong.
Nutrition management focuses on weight maintenance, vitamin supplementation, diabetes management,
and pancreatic enzyme replacement (Razga & Handu, 2019). Pulmonary management focuses on
preventive maintenance and management of exacerbations. Priority nursing interventions focus on
teaching about drug therapy, infection prevention, pulmonary hygiene, nutrition, and vitamin
supplementation. Preventive/maintenance therapy involves the use of positive expiratory pressure,
active cycle of breathing technique, and an individualized exercise program. Daily chest physiotherapy
with postural drainage is beneficial for the patient with CF. This therapy uses chest percussion, chest
vibration, and dependent drainage to loosen secretions and promote drainage. Increasingly, the use of a
chest physiotherapy (CPT) vest is recommended (Fig. 27.9), although no specific evidence supports its
use as superior to any other type of chest physiotherapy (Wilson, 2018). This system uses an inflatable
vest that rapidly fills and deflates, gently compressing and releasing the chest wall up to 25 times per
second, a process called high-frequency chest wall oscillation (HFCWO). The action creates minicoughs
that dislodge mucus from the bronchial walls, increase mobilization, and move it toward central airways,
where it can be removed by coughing or suctioning. HFCWO also thins secretions, making them easier to
clear. Pulmonary function tests are monitored regularly. Daily drugs include bronchodilators, antiinflammatories, mucolytics, and antibiotics. Exacerbation therapy is needed when the patient with CF
has increased chest congestion, reduced activity tolerance, increased or new-onset crackles, and a 10%
decrease in FEV1 . Other symptoms include increased sputum production with bloody or purulent
sputum, increased coughing, decreased appetite, weight loss, fatigue, decreased SpO 2 , and chest muscle
retractions. Often infection is present, with fever, increased lung infiltrate on x-ray, and an elevated white
blood cell count
Gene therapy for CF is available for use in patients with specific gene mutations. The drug ivacaftor,
known as a CFTR modulator or potentiator, has been found to be of value to patients with CF who are
heterozygous for any one of about 35 specific mutations in the CFTR gene alleles. It is of no benefit to
patients who are homozygous for the mutations (Coulthard, 2018). This drug helps improve chloride
transport by increasing the time that the ion channels are open. The combination drug
ivacaftor/lumacaftor is effective as therapy for patients whose CF is caused by the F508del (also known
as the Phe508del) mutation, the most common mutation involved in CF, even in patients who are
homozygous for the mutation with both alleles being affected. This oral drug combination is considered a
“corrector” rather than a modulator, by moving the activated CFTR to the membrane surface for
improved function. Another newly approved corrector oral drug, tezacaftor, when combined with
ivacaftor has some effect for patients with the Phe508del mutation and appears to have fewer adverse
respiratory events than the other combination, although decreases in liver function have been found with
the use of all of these drugs. The successful outcome for these agents is increased movement of chloride
ions across epithelial membranes, resulting in reduced sodium and fluid absorption so that mucus is less
thick and sticky. These drugs have no effect in patients whose CFTR gene does not have the specific
mutations. A significant drawback to these therapies is the cost, which is about $250,000/year of
treatment (Coulthard, 2018).
Surgical Management
Surgical management of the patient with CF is lung transplantation. The patient has greatly reduced
symptoms but is at continuing risk for lethal pulmonary infections, especially with antirejection drug
therapy. Nonpulmonary problems are not helped by this treatment. Transplantation extends life for 1 to
15 years with an average of 7 years, but the transplant rejection rate is high, possibly caused by poor GI
absorption of antirejection drugs (CFF, 2019). Fewer lung transplants are performed compared with
transplantation of other solid organs because of the scarcity of available lungs. In addition, many patients
who could benefit from lung transplantation have serious problems in other organs that make the
procedure even more dangerous. Lung transplant procedures include two lobes or a single lung
transplantation, as well as double-lung transplantation. The type of procedure is determined by the
patient’s overall condition and the life expectancy after transplantation. Usually the patient with CF has a
bilateral lobe transplant from either a cadaver donor or a living-related donor.
Pulmonary Arterial Hypertension (PAH):
•
•
•
•
Pulmonary vessels and often other lung tissues undergo growth changes that greatly
increase pressure in the lung circulatory system for unknown reasons
Dyspnea, fatigue
Drug therapy, oxygen
Surgical management
• Lung transplantation
• Heart-lung transplantation (if cor pulmonale)
Pulmonary Arterial Hypertension Pathophysiology Review
Pulmonary hypertension is the chronic increase in pulmonary vascular pressures above 25 mm Hg,
which makes the right side of the heart work much harder for lung perfusion to support proper gas
exchange . Normally the pulmonary vascular pressures are low, 15 to 18 mm Hg, allowing the pressures
generated by the contraction of the less-muscled right ventricle to easily overcome them and move
blood into the pulmonary artery (McCance et al., 2019). Over time, the higher lung vascular pressures
lead to right-sided heart failure (cor pulmonale) that can be fatal. Many lung problems, such as chronic
obstructive pulmonary disease and pulmonary fibrosis, can secondarily cause increased pulmonary
pressures. For secondary pulmonary hypertension, good control of the condition causing it can delay or
prevent cor pulmonale. Primary pulmonary artery hypertension (PAH), also known as idiopathic
pulmonary artery hypertension, is a condition in which pulmonary vessels and often other lung tissues
undergo growth changes that greatly increase pressure in the lung circulatory system for unknown
reasons. Just as with secondary pulmonary hypertension, PAH progresses and leads to cor pulmonale
with reduced perfusion and gas exchange . The absolute cause of PAH is unknown, and it is diagnosed in
the absence of other lung disorders (McCance et al., 2019). Genetic and environmental factors working
together may increase the risk. For example, although it is a relatively rare problem, exposure to some
drugs, such as fenfluramine/phentermine or dasatinib, increases the risk. The disorder occurs mostly in
women between the ages of 20 and 40 years and occurs more often within some families, suggesting a
possible genetic susceptibility. The familial PAH form appears to be transmied in an autosomal dominant
paern with reduced penetrance (OMIM, 2018). Without treatment, death usually occurs within 2 years
after diagnosis, most often from profound heart failure. The pathologic problem in PAH is blood vessel
constriction with increasing vascular resistance in the lung. The events that lead up to increasing
resistance may include an imbalance between those factors that increase vascular resistance and those that
induce blood vessel relaxation. Intrinsic agents that increases vascular resistance are endothelin-1, a very
powerful vasoconstrictor that works by binding to endothelin receptors on vascular smooth muscle, and
thromboxane, which induces arterial vasoconstriction and enhances cloing by activating platelets.
Intrinsic factors that promote vascular relaxation are nitric oxide (NO) and prostacyclin-1. Many adults
with primary PAH have a deficiency of prostacyclin 1
•
Pathophysiology overview
• Poor long-term survival
• SCLC and NSCLC
• Metastasis
• Paraneoplastic syndromes
• Staging
Lung Cancer Pathophysiology Review Lung cancer is a leading cause of cancer-related deaths
worldwide in affluent and less affluent countries. In North America, more deaths from lung
cancer occur each year than from prostate cancer, breast cancer, and colon cancer combined,
although the incidence has been decreasing somewhat for the past decade. In the United
States, more than 228,000 new cases are diagnosed each year and more than 135,000 deaths
occur from lung cancer annually (American Cancer Society [ACS], 2020). In Canada, more than
29,300 new cases are diagnosed each year and more than 21,000 deaths from lung cancer
occur annually (Canadian Cancer Society, 2019). The overall 5-year survival for all patients with
lung cancer is only about 19%. This poor long-term survival is because most lung cancers are
diagnosed at a late stage, when metastasis is present. Only 15% of patients have small tumors
and localized disease at the time of diagnosis. The 5- year survival rate for this population is
56% (ACS, 2020). The prognosis for advanced lung cancer remains poor. Treatment often
focuses on relieving symptoms or increasing survival time (palliation) rather than cure.
Most primary lung cancers arise as a result of failure of cellular regulation in the bronchial epithelium.
Chapter 19 discusses the general mechanisms and processes of cancer development. Lung cancers are
collectively called bronchogenic carcinomas and are classified as small cell lung cancer (SCLC) and non–
small cell lung cancer (NSCLC). NSCLC has several subtypes that are managed in the same ways,
although causes and locations in the lungs differ. Metastasis (spread) of lung cancer occurs by direct
extension, through the blood, and by invading lymph glands and vessels. Tumors in the lungs can grow
and obstruct the bronchus partially or completely, interfering with gas exchange . Tumors in other areas
of lung tissue can grow so large that they can compress and obstruct the airway. Compression of the
alveoli, nerves, blood vessels, and lymph vessels can occur and also interfere with gas exchange . Lung
cancer can spread to the lung lymph nodes, distant lymph nodes, and other tissues including bone, liver,
brain, and adrenal glands. Additional symptoms, known as paraneoplastic syndromes, complicate certain
lung cancers. The paraneoplastic syndromes are caused by hormones secreted by tumor cells and occur
most commonly with SCLC. Table 27.4 lists the endocrine paraneoplastic syndromes that may occur.
Staging of lung cancer is performed to assess the size and extent of the disease using the standard TNM
system described in Chapter 19. Higher numbers represent later stages and less chance for cure or longterm survival.
Incidence and Prevalence
Lung cancers occur as a result of repeated exposure to inhaled substances that cause chronic tissue
irritation or inflammation interfering with cellular regulation of cell growth. Cigarette smoking is the
major risk factor and is responsible for 81% of all lung cancer deaths (ACS, 2020).
Etiology and Genetic Risk: Nonsmokers exposed to “secondhand” or “thirdhand” smoke also have
a greater risk for lung cancer than do nonsmokers who are minimally exposed to cigarette smoke. See
Chapter 24 for a discussion of passive smoking risks. Other lung cancer risk factors include chronic
exposure to asbestos, beryllium, chromium, coal distillates, cobalt, iron oxide, mustard gas, petroleum
distillates, radiation, tar, nickel, and uranium. Air pollution with benzopyrenes and hydrocarbons also
increases the risk for lung cancer. Lung cancer, especially the adenocarcinoma form of NSCLC, does
occur in adults who are “never smokers” particularly among women. Possible contributing factors for
lung cancer in this population include exposure to environmental carcinogens, second-hand smoke
exposure, genetic differences, familial predisposition, and advancing age.
Interprofessional Collaborative Care Assessment: Recognize Cues
History: Ask the patient about risk factors, including smoking, hazards in the workplace, and warning
signals (Table 27.5). Calculate the pack-year smoking history as described in Chapter 24. Ask about the
presence of lung cancer symptoms, such as hoarseness, cough, sputum production, hemoptysis, shortness
of breath, or change in endurance. Symptoms often have been present for years. Ask the patient to
describe any recent symptom changes or if position affects them. Assess for chest pain or discomfort,
which can occur at any stage of tumor development. Chest pain may be localized or on just one side and
can range from mild to severe. Ask about any sensation of fullness, tightness, or pressure in the chest,
which may suggest obstruction. A piercing chest pain or pleuritic pain may occur on inspiration. Pain
radiating to the arm results from tumor invasion of nerve plexuses in advanced disease.
Physical Assessment/Signs and Symptoms—Pulmonary Symptoms of lung cancer are often
nonspecific and appear late in the disease. Specific symptoms depend on tumor location. Chills, fever,
and cough may be related to pneumonitis or bronchitis that occurs with obstruction. Assess sputum
quantity and character. Blood-tinged sputum may occur with bleeding from a tumor. Hemoptysis is a later
finding in the course of the disease. If infection or necrosis is present, sputum may be purulent and
copious. Breathing may be labored or painful. Obstructive breathing may occur as prolonged exhalation
alternating with periods of shallow breathing. Rapid, shallow breathing occurs with pleuritic chest pain
and an elevated diaphragm. Look for and document abnormal retractions, the use of accessory muscles,
flared nares, stridor, and asymmetric diaphragmatic movement on inspiration. Dyspnea and wheezing
may be present with airway obstruction. Ask about dyspnea severity at rest, with activity, and in the
supine position. Assess how much the dyspnea interferes with the patient’s participation in ADLs, work,
recreational activities, and family responsibilities. Increased vibrations felt on the chest wall when the
patient speaks (fremitus) indicate areas of the lung where air spaces are replaced with tumor or fluid.
Fremitus is decreased or absent when the bronchus is obstructed. The trachea may be displaced from
midline if a mass is present in the area. Breath sounds may change with the presence of a tumor. Wheezes
indicate partial obstruction of airflow in passages narrowed by tumors. Decreased or absent breath sounds
indicate complete obstruction of an airway by a tumor or fluid. A pleural friction rub may be heard when
inflammation is present
Physical Assessment/Signs and Symptoms—Non-pulmonary Many other systems can be affected by
lung cancer and have changes at the time of diagnosis. Heart sounds may be muffled by a tumor or fluid
around the heart (cardiac tamponade). Dysrhythmias may occur as a result of hypoxemia or direct
pressure of the tumor on the heart. Cyanosis of the lips and fingertips or clubbing of the fingers may be
present (see Fig. 27.8). Bones lose density with tumor invasion and break easily with lile pressure and
without trauma. The patient may have bone pain or fragility fractures. Late symptoms of lung cancer
usually include fatigue, weight loss, anorexia, dysphagia, and nausea and vomiting. Superior vena cava
syndrome may result from tumor pressure in or around the vena cava. This syndrome is an emergency
(see Chapter 20 ) and requires immediate intervention. The patient may have confusion or personality
changes from brain metastasis. Psychosocial Assessment The poor prognosis for lung cancer has made it
a much-feared disease. Dyspnea and pain add to the patient’s fear and anxiety. Encourage the patient and
family to express their feelings about the possible diagnosis of lung cancer.
Diagnostic Assessment
Most commonly, lung lesions are first identified on chest x-rays. CT scans are then used to identify the
lesions more clearly and guide biopsy procedures. The definitive diagnosis of lung cancer is made by
examination of cancer cells from biopsy or from pleural effusion fluid (if present). A thoracoscopy to
directly view lung tissue may be performed through a video-assisted thoracoscope entering the chest
cavity via small incisions through the chest wall. Other diagnostic studies may be needed to determine
how widely the cancer has spread. Such tests include MRI and radionuclide scans of the liver, spleen,
brain, and bone help. Positron emission tomography (PET) scanning is a thorough way to locate
metastases. These tests help determine the extent of the cancer and the best methods to treat it.
Non-surgical
Chemotherapy is often the treatment of choice for lung cancers, especially small cell lung cancer
(SCLC). It may be used alone or as adjuvant (addon) therapy in combination with surgery for non–small
cell lung cancer (NSCLC). The combination of drugs used depends on tumor response and the overall
health of the patient; however, most include platinum-based agents. Side effects of cancer chemotherapy
include chemotherapy-induced nausea and vomiting (CINV), alopecia (hair loss), open sores on mucous
membranes (mucositis), immunosuppression with neutropenia, anemia, decreased numbers of platelets,
and peripheral neuropathy. Consult Chapter 20 for discussion of the nursing care needs for patients who
have these side effects. Immunosuppression with neutropenia, which greatly increases the risk for
infection, is the major dose-limiting side effect of chemotherapy for lung cancer. It can be managed by
the use of growth factors to stimulate bone marrow production of immune system cells. Teach the patient
and family about precautions to take to reduce the patient’s risk for infection (see Chapter 20 for
information about chemotherapy and associated nursing care). Targeted therapy is common in the
treatment of non−small cell lung cancer (NSCLC). These agents take advantage of one or more
differences in cancer cell growth or metabolism that is either not present or only slightly present in
normal cells. For lung cancer, usually these differences are identified as variations in two different genes,
EGFR (which codes for epidermal growth factor receptors) and ALK (which codes for ALK receptor
tyrosine kinases). Agents used as targeted therapies work to disrupt cancer cell division in one of several
ways. However, these agents only work when the cancer cell has the particular target or specific genetic
mutation. Therefore testing of the cancer cells is needed before therapy begins, and not all cancers of the
same type express the target. These agents are increasing survival time for patients with NSCLC but do
not lead to a cure. The Common Examples of Drug Therapy: Targeted Therapy and Immunotherapy of
Lung Cancer box lists some targeted agents used in lung cancer therapy.
Immunotherapy for lung cancer is a type of targeted therapy designed to allow the patient’s own
immune system to beer recognize and aack his or her cancer cells. Normally, certain immune system cells
including Tcells, B-cells, monocytes, and natural killer (NK) cells recognize and aack foreign cells and
unhealthy self cells. Radiation therapy can be an effective treatment for locally advanced lung cancers
confined to the chest. Best results are seen when radiation is used in addition to surgery or chemotherapy.
Radiation may be performed before surgery to shrink the tumor and make resection easier.
Photodynamic therapy (PDT) may be used to remove small bronchial tumors when they are accessible
by bronchoscopy. This therapy first involves injecting the patient with an agent that sensitizes cells to
light and remains in cancer cells longer than normal cells. After 48 to 72 hours, most of the drug has
accumulated in the cancer cells. A laser light is focused on the tumor with the patient intubated and under
anesthesia. The light activates a reaction that causes irreversible damage and death to cells retaining the
sensitizing drug.
surgical Management
Surgery is the main treatment for stage I and stage II NSCLC. Total tumor removal may result in a cure.
If complete resection is not possible, the surgeon removes the bulk of the tumor. The specific surgery
depends on the stage of the cancer and the patient’s overall health. Lung cancer surgery may involve
removal of the tumor only, removal of a lung segment, removal of a lobe (lobectomy), or removal of
the entire lung (pneumonectomy). These procedures can be performed by open thoracotomy or by
minimally invasive surgery in select patients. Preoperative care is focused on relieving anxiety and
promoting the patient’s participation (see Chapter 9 for routine preoperative care). Reinforce the
surgeon’s explanation of the procedure, and provide education related to what is expected after surgery.
Teach about the probable placement of the chest tube and drainage system (except after pneumonectomy).
Operative procedures for lung cancer may consist of a lobectomy, pneumonectomy, segmental resection,
or wedge resection. A segmental resection is a lung resection that includes the bronchus, pulmonary
artery and vein, and tissue of the involved lung segment or segments of a lobe. A wedge resection is
removal of the peripheral portion of small, localized areas of disease. A lobe or entire lung can be
removed through video-assisted thoracoscopic surgery (VATS), which is minimally invasive, in select
patients. The procedure involves making small incisions in the chest for placement of the instruments.
The lung, section, or lobe is then isolated from its airway, which is surgically closed. The lobe or lung is
closed off from the rest of the lung and sealed in a bag to prevent leakage of tumor tissue and possible
seeding of the cancer. The bagged lung is then removed whole through one of the small incisions.
Postoperative care for patients who have undergone thoracotomy (except for pneumonectomy) requires
closed-chest drainage to drain air and blood that collect in the pleural space. A chest tube drain placed in
the pleural space allows lung re-expansion and prevents air and fluid from returning to the chest (Fig.
27.10). The drainage system consists of one or more chest tubes or drains, a collection container placed
below the chest level, and a water seal to keep air from entering the chest. The drainage system may be a
stationary, disposable, self-contained system (Fig. 27.11) or a smaller, portable, disposable, self-contained
system that requires no connection to a vacuum source (Fig. 27.12). The nursing care priorities for the
patient with a chest tube are to ensure the integrity of the system, promote comfort, ensure chest tube
patency, and prevent complications (Sasa, 2019). Chest Tube Placement and Care The tip of the tube used
to drain air is placed near the front lung apex (see Fig. 27.10). The tube that drains liquid is placed on the
side near the base of the lung. The wounds are covered with airtight dressings, most commonly silicone
foam dressings (Wood et al., 2019). The chest tube is connected by about 6 feet of tubing to a collection
device placed below the chest, allowing gravity to drain the pleural space while the patient can turn and
move without pulling on the chest tube. When two chest tubes are inserted, they are joined by a Yconnector close to the patient and the 6 feet of tubing is aached to the Y-connector. Stationary chest tube
drainage systems, such as the Pleur-evac system, use a water-seal mechanism that acts as a one-way valve
to prevent air or liquid from moving back into the chest cavity. Disposable system use a one-piece
disposable plastic unit with three chambers. The three chambers are connected to one another. The tube(s)
from the patient is (are) connected to the first chamber in the series of three, which is the drainage
collection container. The second chamber is the water seal to prevent air from moving back up the tubing
system and into the chest. The third chamber, when suction is applied, is the suction regulator. Tubing
from the patient penetrates chamber one shallowly, as does the tube connecting chamber one with
chamber two. The fluid in chamber one collected from the patient is measured hourly during the first 24
hours. This drainage fluid must never fill to the point that it comes into contact with any tubes! If the
tubing from the patient enters the fluid, drainage stops and can lead to a tension pneumothorax. Chamber
two is the water seal that prevents air from re-entering the patient’s pleural space. As the trapped air
leaves the pleural space, it will pass through chamber one (collection chamber) before entering chamber
two (the water-seal chamber), which should always contain at least 2 cm of water to prevent air from
returning to the patient. As trapped air from the patient’s pleural space passes through the water seal,
which serves as a one-way valve, the water will bubble. Once all the air has been evacuated from the
pleural space, bubbling of the water seal stops.
Pain Management
Pain control measures are needed regardless of whether surgery is performed as an open procedure or
with minimally invasive techniques. Give the prescribed drugs for pain and assess the patient’s responses
to them. Teach patients using patient-controlled analgesia (PCA) devices to self-administer the drug
before pain intensity becomes too severe. Monitor vital signs before and after giving opioid analgesics,
especially for the patient who is not being mechanically ventilated.
Respiratory Management
Immediately after surgery the patient is mechanically ventilated. See Chapter 29 for nursing care of the
patient receiving mechanical ventilation. Once the patient is breathing on his or her own, the priorities are
to maintain a patent airway, ensure adequate ventilation, and prevent complications. Assess the patient at
least every 2 hours for adequacy of ventilation and gas exchange . Check the alignment of the trachea.
Assess oxygen saturation and the rate and depth of respiration. Listen to breath sounds on the
nonoperative side, particularly noting the presence of crackles. Perform oral suctioning only as needed.
Usually the patient receives oxygen by mask or nasal cannula for the first 2 days after surgery. Assist the
patient to a semi-Fowler position or up in a chair as soon as possible. Encourage him or her to use the
incentive spirometer every hour while awake. If coughing is permitted, help him or her cough by splinting
any incision and ensuring that the chest tube does not pull with movement. Specially designed walkers
that support the patient and all equipment for early ambulation with chest tubes in place are available
(Grondell et al., 2018).
Interventions for Palliation
Oxygen therapy is prescribed when the patient is hypoxemic and helps relieve dyspnea and anxiety. (See
Chapter 25 for issues related to home oxygen therapy.)
Radiation therapy can help relieve hemoptysis, obstruction of the bronchi and great veins (superior vena
cava syndrome), difficulty swallowing from esophageal compression, and pain from bone metastasis.
Radiation for palliation uses higher doses for shorter periods. Thoracentesis is performed when pleural
effusion is a problem for the patient with lung cancer. The excess fluid increases dyspnea, discomfort, and
the risk for infection. The purpose of treatment is to remove pleural fluid and prevent its formation.
Thoracentesis is a procedure for fluid removal by suction after the placement of a large needle or catheter
into the intrapleural space. Fluid removal temporarily relieves hypoxia; however, the fluid can rapidly reform in the pleural space. When fluid development is continuous and uncomfortable, a tunneled pleural
catheter that continuously drains may be placed into the intrapleural space to collect the fluid (Miller et
al., 2018).
Dyspnea management is needed because the patient with lung cancer tires easily and is often most
comfortable resting in a semi-Fowler position. Dyspnea is reduced with oxygen, use of a continuous
morphine infusion, and positioning for comfort. The severely dyspneic patient may be most comfortable
siTTing and sleeping in a lounge chair or reclining chair.
Pain management is usually to help the patient be as pain free and comfortable as possible.
Pharmacologic management with opioid drugs as oral, parenteral, or transdermal preparations is needed.
Analgesics are most effective when given around the clock with additional PRN analgesics used for
breakthrough pain.
Hospice care can be beneficial for the patient in the terminal phase of lung cancer. Hospice programs
provide support to the terminally ill patient and the family, meet physical and psychosocial needs, adjust
the palliative care regimen as needed, make home visits, and provide volunteers for errands and respite
care. (See Chapter 8 for a more complete discussion of end-of life issues.)
Concepts of Care for Patients With Infectious Respiratory Problems
anergy Failure to have a skin response to TB skin testing because of reduced immunity even when
infection is present.
consolidation: An abnormal solidification with lack of air spaces in a segment of area of the lung.
COVID-19: A new coronavirus mutation (CO= corona; VI = virus; D = disease; 19 = 2019, the year the
new virus was identified) that enabled this animal virus to infect humans and is responsible for the 2020
influenza pandemic.
empyema: A collection of pus in the pleural cavity.
endemic infection: Respiratory infection caused by organisms that are much more common within a
geographic location but the actual incidence of the infection is relatively low.
gas exchange: Oxygen transport to the cells and carbon dioxide transport away from cells through
ventilation and diffusion.
immunity Protection from illness or disease that is maintained by the body’s physiologic defense
mechanisms.
induration Localized swelling with hardness of soft tissue.
infection Invasion of pathogens into the body that multiply and cause disease or illness. inflammation A
syndrome of normal tissue responses to cellular injury, allergy, or the invasion of pathogens.
miliary (hematogenous) TB :Spread of TB throughout the body when a large number of organisms enter
the blood.
pandemic infection: An infection with an organism to which most humans have no immunity and that
has the potential to spread globally.
tuberculosis (TB) A highly communicable disease caused by infection with Mycobacterium tuberculosis
Seasonal Influenza Pathophysiology Review Seasonal influenza,
 or “flu,” is a highly contagious acute viral respiratory infection that can occur at any age
(Cannon et al., 2018). Influenza may be caused by different strains of one of several virus
families, referred to as A, B, and C. Epidemics are common and lead to complications of
pneumonia or death, especially in older adults, those with heart failure or chronic lung disorders,
and immunocompromised patients. Most patients are treated at home, but hospitalization may be
needed when symptoms are severe or the patient develops complications such as pneumonia.
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During the 2017−2018 influenza season, more than 30,000 patients were hospitalized for the
infection with about 60% of these being older than 65 years (Centers for Disease Control and
Prevention [CDC], 2018d). The patient with influenza often has a rapid onset of severe
headache, muscle aches, fever, chills, fatigue, and weakness. Adults are contagious 24 hours
before symptoms occur and up to 5 days after they begin. Sore throat, cough, and watery nasal
discharge can also occur. Infection with influenza strain B can lead to nausea, vomiting, and
diarrhea. Most patients feel fatigued for 1 to 2 weeks after the acute episode has resolved Highly
contagious acute viral respiratory infection
Rapid onset of severe headache, muscle ache, fever, chills, fatigue, weakness, anorexia
Preventable (or severity is reduced) with vaccination
Handwashing is critical
Antiviral agents may be effective if started within 24 to 48 hours of symptoms
Pandemic Influenza
A pandemic respiratory viral infection is one that has the potential to spread globally because
the virus has previously infected only birds or other animals, so no human ancestral immunity is
present. Most bird and animal viruses cannot be transmitted to humans. A few notable
exceptions have occurred when these viruses mutated and became highly infectious to
humans, causing pandemics. Example pandemics include the 1918 “Spanish” influenza and the
2009 H1N1 influenza A.
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Potential to spread globally
Avian flu, MERS, SARS
Early recognition and quarantine
Contact and Airborne Precautions (until specific type of pandemic influenza is identified with
routes of transmission known)
 Antiviral drugs such as oseltamivir are stockpiled in the event of a pandemic influenza. They can
be used for prevention or to shorten the duration of the infection. Distribution for treatment is
made on a case-byc2ase basis, as the drug must be started within 48 hours of symptom onset.
Infected patients in the hospital seing should be placed on Droplet Precautions for 7 days and
placed in a private room.
Etiology:
Infectious pneumonia develops when a patient’s immunity cannot overcome the invading organisms
(Arsbad et al., 2016). Organisms from the environment (especially after natural disasters), invasive
devices, equipment, and supplies or other people can invade the body. Risk factors are listed in Table
28.1. Pneumonia can be caused by any organism such as bacteria, viruses, mycoplasmas, fungi,
rickesiae, protozoa, and helminths (worms). Noninfectious causes of pneumonia include inhalation
of toxic gases, chemical fumes, and smoke; and aspiration of water, food, fluid (including saliva),
and vomitus. Infectious pneumonia can be categorized as community acquired (CAP), hospital
acquired (HAP), health care acquired (HCAP) or ventilator-associated (VAP) (see Table 28.2).
Incidence and Prevalence
In the United States 2 to 5 million cases of pneumonia occur annually. About 1 million people are
hospitalized for treatment, and more than 50,000 deaths result from the disease (CDC, 2018b). In Canada,
influenza and pneumonia incidence and deaths are reported together and both disorders are common,
accounting for about 6000 deaths annually (Statistics Canada, 2018). The rate of pneumonia is higher
among older adults, nursing home residents, hospitalized patients, patients with neurologic
problems or difficulty swallowing, and those being mechanically ventilated (Meehan & McKenna,
2020).
Health Promotion and Maintenance
Vaccination can help prevent pneumonia. Currently, there are two pneumonia vaccines: pneumococcal
polysaccharide vaccine (PPSV23) and pneumococcal conjugate vaccine (PCV13) for prevention of
pneumonia (Phillips & Swanson, 2016). The CDC recommends that adults older than 65 years be
vaccinated with both, first with PCV13 followed by PPSV23 about 12 months later. Adults who have
already received the PPSV23 should have PCV13 about a year or more later. These recommendations
also apply to adults between 19 and 64 years of age who have specific risk factors such as chronic
illnesses (CDC, 2018b). Because pneumonia often follows influenza, especially among older adults, urge
all adults to receive the seasonal vaccination annually. Patient education about vaccination and other
means of pneumonia prevention is important. Teaching points are presented in the Patient and Family
Education: Preparing for Self-Management: Preventing Pneumonia box Other pneumonia prevention
techniques include strict handwashing to avoid spreading organisms and avoiding crowds during
cold and flu season. Teach the patient who has a cold or the flu to see his or her primary health care
provider if fever lasts more than 24 hours, the problem lasts longer than 1 week, or symptoms worsen.
Respiratory therapy equipment must be well maintained and decontaminated or changed as
recommended. Use sterile water rather than tap water in GI tubes and institute Aspiration Precautions as
indicated, including screening patients for aspiration risk (Meehan & McKenna, 2020). VAP is on the
rise, but the risk can be reduced with conscientious assessment and meticulous nursing care. The
preventive care for VAP is discussed in Chapter 29 and is listed in Table 28.2
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Vaccination
Avoid crowded places during flu season
Cough, turn, move, deep breathe
Clean respiratory equipment
Avoid pollutants
Stop smoking
Get rest and sleep
Eat healthy diet
Drink 3L of water daily (unless fluids are restricted)
History
Assess for the risk factors for respiratory infection (see Table 28.1). Document age; living, work,
or school environment; diet, exercise, and sleep routines; swallowing problems; presence of a
nasogastric tube; tobacco and alcohol use; and past and current use of or addiction to “street”
drugs. Remember that often aspiration is “silent” with no signs or symptoms. Ask about past
respiratory illnesses and whether the patient has been exposed to influenza or pneumonia or
has had a recent viral infection. Using the I PREPARE model listed in Chapter 24, assess the
patient for particulate maer exposure (PME). Even noninfectious exposures can result in
respiratory inflammation , which increases the risk for pneumonia development. If the patient
has chronic respiratory problems, ask whether respiratory equipment is used in the home.
Assess whether the patient’s cleaning routine for the equipment is adequate to prevent
infection. Ask when he or she received the last influenza or pneumococcal vaccine. Ask family
members whether they have noticed a change in the patient’s cognition .
Physical Assessment/Signs and Symptoms:
Observe the general appearance. Many patients with pneumonia have flushed cheeks and an anxious
expression. The patient may have chest pain or discomfort, myalgia, headache, chills, fever, cough,
tachycardia, dyspnea, tachypnea, hemoptysis (bloody sputum), and sputum production. Severe chest
muscle weakness may also be present from sustained coughing. Observe the patient’s breathing pattern,
position, and use of accessory muscles. The patient with hypoxia and reduced gas exchange may be
uncomfortable in a lying position and will sit upright, balancing with the hands (“tripod position”). Assess
the cough and the amount, color, consistency, and odor of sputum produced. Crackles are heard on
auscultation when fluid is in interstitial and alveolar areas, and breath sounds may be diminished.
Wheezing may be heard if inflammation or exudate narrows the airways. Bronchial breath sounds are
heard over areas of density or consolidation. Fremitus is increased over areas of pneumonia, and
percussion is dulled. Chest expansion may be diminished or unequal on inspiration. In evaluating vital
signs, compare the results with baseline values. A patient with pneumonia, especially an older adult, is
often hypotensive with orthostatic changes because of vasodilation and dehydration. A rapid, weak pulse
may indicate hypoxemia, dehydration, or impending sepsis and shock. Dysrhythmias may occur from
cardiac tissue hypoxia. Common pneumonia signs and symptoms and their causes are listed in Table 28.3.
The primary health care provider uses one of several evidence-based pneumonia severity scales to
determine whether the patient can be managed in the community or requires hospitalization. When
pneumonia is uncomplicated by other health problems, it is often managed in the community.
Psychosocial Assessment
The patient with pneumonia often has pain, fatigue, and dyspnea, all of which promote anxiety. Assess
anxiety by looking at his or her facial expression and general tenseness of facial and shoulder muscles.
Listen to the patient carefully, and use a calm approach. Because of airway obstruction and muscle
fatigue, the patient with dyspnea speaks in broken sentences. Keep the interview short if severe dyspnea
or breathing discomfort is present.
Laboratory Assessment
Sputum is obtained and examined by Gram stain, culture, and sensitivity testing; however, the
responsible organism is often not identified. A sputum sample is easily obtained from the patient who can
cough into a specimen container. Extremely ill patients may need suctioning to obtain a sputum specimen.
In these situations, a specimen is obtained by sputum trap (Fig. 28.1) during suctioning. A complete
blood count (CBC) is obtained to assess for an elevated WBC count, which is a common finding except
in older adults. Blood cultures may be performed to determine whether the organism has entered the
bloodstream. In severely ill patients, arterial blood gases (ABGs) may be assessed to determine baseline
arterial oxygen and carbon dioxide levels and to help identify a need for supplemental oxygen. Serum
electrolyte, blood urea nitrogen (BUN), and creatinine levels are also assessed. A high BUN level may
occur as a result of dehydration. Hypernatremia (high blood sodium levels) occurs with dehydration. A
lactate level may be performed to help assess for sepsis. Because CAP often follows or is present with
influenza, recommend that adults with CAP also have influenza testing (Esden, 2020).
Imaging Assessment
Chest x-ray is the most common diagnostic test for pneumonia but may not show changes until 2 or more
days after symptoms are present. Pneumonia usually appears on chest x-ray as an area of increased
density. It may involve a lung segment, a lobe, one lung, or both lungs. In the older adult, the chest x-ray
is essential for early diagnosis because other pneumonia symptoms are often vague
Other Diagnostic Assessments
Pulse oximetry is used to assess for hypoxemia. Thoracentesis is used in patients who have an
accompanying pleural effusion.
Analysis: Analyze Cues and Prioritize Hypotheses
The priority interprofessional collaborative problems for patients with pneumonia include: 1. Decreased
gas exchange due to decreased diffusion at the alveolarcapillary membrane 2. Potential for airway
obstruction due to inflammation with excessive pulmonary secretions, fatigue, muscle weakness 3.
Potential for sepsis due to the presence of microorganisms in a very vascular area and reduced immunity
4. Potential for pulmonary empyema due to spread of infectious organisms from the lung into the
pleural space
Care Coordination and Transition Management
The patient needs to continue the anti-infective drugs as prescribed. An important nursing role is to
reinforce, clarify, and provide information to the patient and family as needed. Unfortunately, the readmission rate within 30 days after discharge is relatively high, especially among older adults (Goering,
2018). See the accompanying Systems Thinking and Quality Improvement box focusing on one group’s
successful method of reducing preventable re-admissions.
Home Care Management
No special changes are needed in the home. If the home has a second story, the patient may prefer to stay
on one floor for a few weeks, because stair climbing can be tiring. Toileting needs may be met by using a
bedside commode if a bathroom is not located on the level the patient is using. Home care needs depend
on the patient’s level of fatigue, dyspnea, and family and social support. The long recovery phase,
especially in the older adult, can be frustrating. Fatigue, weakness, and a residual cough can last for
weeks. Some patients fear they will never return to a “normal” level of functioning. Prepare them for the
disease course and offer reassurance that complete recovery will occur. After discharge a home nursing
assessment may be helpful. Specific issues to assess for a patient recovering from pneumonia are
presented in the Focused Assessment box.
Self-Management Education
Review all drugs with the patient and family and emphasize the importance of completing anti-infective
therapy. Instruct the patient to notify the primary health care provider if chills, fever, persistent cough,
dyspnea, wheezing, hemoptysis, increased sputum production, chest discomfort, or increasing fatigue
returns or fails to go away completely. Instruct him or her to get plenty of rest and increase activity
gradually. An important aspect of education for the patient and family is avoiding upper respiratory tract
infection and viruses. Teach him or her to avoid crowds (especially in the fall and winter when viruses are
prevalent), people who have a cold or flu, and exposure to irritants such as smoke. A balanced diet and
adequate fluid intake are essential.
Health Care Resources
Inform patients who smoke or vape that these activities are risk factors for pneumonia. Use the
suggestions and interventions discussed in Chapter 24 to help the patient quit or reduce cigarette
smoking and/or vaping. Teach about pneumonia, and urge the patient who has not already been
vaccinated against influenza or pneumonia to get these vaccinations after the pneumonia has resolved.
Evaluation: Evaluate Outcomes
Evaluate the care of the patient with pneumonia based on the identified priority patient problems. The
expected outcomes are that he or she: • Attains or maintains adequate gas exchange with SaO 2 of at
least 95% or his or her normal level • Maintains patent airways as evidenced by absence of crackles and
wheezes on auscultation • Is free from infection as evidenced by absence of fever and a WBC count
within normal limits • Avoids empyema • Returns to his or her pre-pneumonia health status
Infection Concept Exemplar:
Pulmonary Tuberculosis Pathophysiology Review Tuberculosis (TB) is a highly communicable
disease caused by infection with Mycobacterium tuberculosis. It is one of the most common
bacterial infections worldwide and one of the top 10 causes of death (World Health
Organization [WHO], 2019). The organism is transmitted via aerosolization (i.e., an airborne
route) (Fig. 28.2). When a person with active TB coughs, laughs, sneezes, whistles, or sings,
infected respiratory droplets become airborne and may be inhaled by others. Not all TB
infections actually develop into active TB (American Lung Association [ALA], 2018). This is
because the normal protection of immunity prevents full development of TB in the healthy
person (McCance et al., 2019). ( Immunity is the protection from illness or disease that is
maintained by the body’s physiologic defense mechanisms. Secondary TB – reactivation of the
disease in a previously infected person
Etiology
M. tuberculosis is a slow-growing, acid-fast rod transmitted via the airborne route. Adults most often
infected are those having repeated close contact with an infectious person who has not yet been
diagnosed with TB. The risk for infection transmission is reduced after an adult with active TB has
received proper drug therapy for 2 to 3 weeks, clinical improvement occurs, and acid-fast bacilli (AFB) in
the sputum are reduced.
Health Promotion and Maintenance
Many adults who acquire TB have risk factors such as homelessness, living in very crowded conditions,
or substance use with malnutrition. These risk factors are best managed on a societal level. Communities
need to work toward providing adequate housing, substance-use programs that are accessible, and feeding
centers or food banks for those in need. On a personal level, many health conditions make it more likely
to contract TB if exposed. Adults with these health conditions should avoid people who are ill, stay well
nourished, and practice good handwashing and social distancing. Any adult who works with people at
high risk of having TB should be screened yearly.
History:
Assess the patient’s past exposure to TB. Ask about his or her country of origin and travel to or from
foreign countries where incidence of TB is high (Benkert & Rayford, 2018). It is important to ask about
the results of any previous tests for TB. Also ask whether the patient has had bacille Calmee-Guérin
(BCG) vaccine (often given in childhood overseas), which contains attenuated tubercle bacilli. Anyone
who has received BCG vaccine within the previous 10 years will have a positive skin test that can
complicate interpretation for current TB infection . Usually the size of the skin response decreases each
year after BCG vaccination. These patients should be evaluated for TB with a chest x-ray or an interferongamma release assay (IGRA), such as the QuantiFERON-TB Gold test (CDC, 2018e; WHO, 2019).
Physical Assessment/Signs and Symptoms
The patient with TB has progressive fatigue, lethargy, nausea, anorexia, weight loss, irregular
menses, and a low-grade fever. Symptoms may have been present for weeks or months. Night sweats
may occur with the fever. A cough with mucopurulent sputum, often streaked with blood, is present.
Chest tightness and a dull, aching chest pain occur with the cough. Ask about, assess for, and
document the presence of any of these symptoms to help with diagnosis, establish a baseline, and plan
nursing interventions
Psychosocial Assessment
Tuberculosis is a frightening diagnosis. Explain the disease to the patient and family, including the need
to maintain good hygiene and avoid infecting others. The patient may feel isolated and shunned. Take
time to listen to him or her and help to resolve any concerns. The family and friends of the patient may
have similar concerns as well. Often close contacts will be afraid they have contracted the illness.
Encourage all close contacts to get tested. Help the patient notify his or her employer, if needed, about
required time off. Directly observed therapy may feel threatening. Explain how this helps improve
adherence to the long treatment schedule.
Diagnostic Assessment
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Chest x-ray
Sputum culture
NAAT
TST
IGRA (e.g., QuantiFERON-TB Gold In-Tube test)
TB infection can be tested by methods. In addition to chest x-ray, sputum cultures of blood or
respiratory secretions can be tested. Many fully automated nucleic acid amplification tests
(NAATs) for TB are used on respiratory secretions. Results of these tests are available in less
than 2 hours; however, they have limitations. Tuberculin skin testing (TST), also known as the
Mantoux test, is the most commonly used reliable screening test for TB. A small amount (0.1
mL) of purified protein derivative (PPD) is placed intradermally in the forearm. The test is
“read” in 48 to 72 hours. An area of induration (localized swelling with hardness of soft tissue),
not just redness, measuring 10 mm or greater in diameter, indicates exposure to and possible
infection with TB (Fig. 28.3). In adults with reduced immunity , induration of 5 mm is a positive
result. If possible, the site is re-evaluated after 72 hours because false-negative readings occur
more often after only 48 hours. A positive reaction indicates exposure to TB or the presence of
inactive (dormant) disease, not active disease. A reduced skin reaction or a negative skin test
does not rule out TB disease or infection of the very old or anyone who has severely reduced
immunity . Failure to have a skin response because of reduced immunity when infection is
present is called anergy. Blood analysis can be done with interferon-gamma release assays, or
IGRAs. The first IGRA was the QuantiFERON-TB Gold In-Tube test. IGRAs show how the patient’s
immune system responds to the TB bacterium. A positive result means that the person is
infected with TB but does not indicate whether the infection is latent or active. Another blood
test, the Xpert MTB/RIF Ultra, which can detect drug-resistant strains of TB and is also
recommended for testing people with HIV infection, has been approved by both the CDC and
WHO. Sputum culture confirms the diagnosis and is also used to evaluate treatment
effectiveness. Enhanced TB cultures take up to 4 weeks for a valid result. After drug therapy is
started, sputum samples are obtained at specified intervals. Cultures are usually negative after
3 months of effective treatment. Annual screening is needed for anyone who comes into
contact with people who may be infected with TB, including some health care workers.
Screening is very important for foreign-born adults and migrant workers. Participation in
screening programs is higher when programs are delivered in a culturally sensitive and
nonthreatening manner. Urge anyone who is considered high risk to have an annual TB
screening test
Analysis: Analyze Cues and Prioritize Hypotheses
The priority collaborative problems for patients with TB include: 1. Potential for airway obstruction due
to thick secretions and weak cough effort 2. Potential for development of drug-resistant disease and
spread of infection due to inadequate adherence to therapy regimen 3. Weight loss due to inadequate
intake and nausea from therapy regimen 4. Fatigue due to lengthy illness, poor gas exchange, and
increased energy demands
Planning and Implementation: Generate Solutions and Take Action
Promoting Airway Clearance Planning: Expected Outcomes The patient with TB is expected to
maintain a patent and adequate airway. Interventions Interventions to maintain a patent airway are similar
to those for pneumonia and COPD. Instruct the patient to drink plenty of fluids unless another condition
requires restriction. Teach him or her to take a deep breath before coughing. An incentive spirometer may
facilitate effective coughing. Reducing Drug-Resistance and Infection Spread Planning: Expected
Outcomes The patient with TB is expected to become free of active disease and not spread the disease to
others. Improving nutrition, managing fatigue. Many of the interventions for fatigue will be the same
as those for improving nutrition. Poor nutrition can lead directly to fatigue
Home Care Management
Most patients with TB are managed outside the hospital; however, patients may be diagnosed with TB
while in the hospital for another problem. Discharge may be delayed if the living situation is high risk or
if nonadherence to prescribed drug therapy is likely. Ensure collaboration with other members of the
interprofessional team, including the case manager or social service worker in the hospital or the
community health nursing agency, to ensure that the patient is discharged to the appropriate environment
with continued supervision.
Self-Management Education
Teach the patient to follow the drug regimen exactly as prescribed and always to have a supply on hand.
Teach about side effects and ways of reducing them to promote adherence. Remind him or her that the
disease is usually no longer contagious after drugs have been taken for 2 to 3 consecutive weeks and
clinical improvement is seen; however, he or she must continue with the prescribed drugs for 6 months or
longer as prescribed. Directly observed therapy, in which a health care professional watches the patient
swallow the drugs, may be indicated in some situations. This practice leads to more treatment successes,
fewer relapses, and less drug resistance. More recently, DOT has been successfully performed using a
video format (VDOT) in which patients use a phone or other real-time electronic device to demonstrate
compliance with the drug regimen. This method helps patients “live their lives” without having to
physically come to a place for DOT. Drawbacks to this method include whether the patient is willing and
able to use such a device and how good the connectivity is for both the patient’s device and the nurse’s
access to the video (Ingram, 2018). The patient who has weight loss and severe lethargy should gradually
resume usual activities. Proper nutrition is needed to prevent infection recurrence. Provide the patient
with information about how TB can be spread to others. A key to preventing infection transmission is
identifying those in close contact with the infected person so that they can be tested and treated if needed.
Multidrug therapy may be indicated to prevent TB in heavily exposed adults or for those who have other
health problems that reduce immunity. Health Care Resources
Teach the patient to receive follow-up care by a primary health care provider for at least 1 year after
active treatment. The American Lung Association (ALA) can provide free information to the patient
about the disease and its treatment. In addition, Alcoholics Anonymous (AA) and other health care
resources for patients with alcoholism are available if needed. Inform patients who smoke or vape that
smoking and vaping further reduce breathing effectiveness. Use the suggestions and interventions
discussed in Chapter 24 to help the patient quit or reduce cigaree smoking. Assist the patient who uses
illicit drugs to locate a drug-treatment program.
Evaluation: Evaluate Outcomes
Evaluate the care of the patient with TB based on the identified priority patient problems. The expected
outcomes are that he or she: • Effectively clears his or her airways as evidenced by absence of crackles
and wheezes on auscultation • Is free of active TB and does not spread the infection • Demonstrates
improved nutrition as evidenced by weight maintenance or weight gain • Reports decreased fatigue
and increased energy and is able to participate in activities to the extent he or she desires • Returns to
his or her pretuberculosis health status.
Inhalation Anthrax Pathophysiology Review
Inhalation anthrax (respiratory anthrax) is a bacterial infection caused by the gram-positive organism
Bacillus anthracis. This organism lives as a spore in soil where grass-eating animals live and graze. Most
naturally occurring cases of anthrax are on the skin (cutaneous). Inhalation anthrax accounts for only
about 5% of cases and is not spread by person-to-person contact. When infection occurs through the
lungs, the disease is nearly 100% fatal without treatment (CDC, 2017). Although inhalation anthrax is
an occupational hazard of veterinarians, farmers, and others who frequently contact animal wool, hides,
bone meal, and skin, any occurrence in other adults is considered an intentional act of bioterrorism. This
organism first forms a spore (i.e., an encapsulated organism that is inactive). When many spores are
inhaled deeply into the lungs, they enter white blood cells (WBCs), leave their capsules, and replicate.
The active bacteria produce toxins that are released into the infected tissues and into the blood, making
the infection worse. Massive edema occurs along with hemorrhage and destruction of lung cells. Infected
WBCs spread the organisms rapidly to the lymph nodes and blood, causing bacteremia, sepsis, and
meningitis. Lethal toxins produced by the bacteria are the most common cause of death. Inhalation
anthrax has two stages: prodromal (or incubation period) and fulminant (with active disease). Symptoms
(listed in the Key Features: Inhalation Anthrax box) may take up to 8 weeks to develop after exposure.
The prodromal stage is early and difficult to distinguish from influenza or pneumonia. Symptoms
include low-grade fever, fatigue, mild chest pain, and a dry, harsh cough. A special feature of inhalation
anthrax is that it is not accompanied by upper respiratory symptoms of sore throat or rhinitis. Usually the
patient starts to feel beer and symptoms improve in 2 to 4 days. If the diagnosis is made and the patient
begins appropriate antibiotic therapy at this stage, the likelihood of survival is high. The fulminant stage
begins after the patient feels a lile beer. Usually there is a sudden onset of severe illness, including
respiratory distress, hematemesis (bloody vomit), dyspnea, diaphoresis, stridor, chest pain, and cyanosis.
High fever, hemorrhagic mediastinitis, and pleural effusions develop. As the infection spreads through the
blood, septic shock and hemorrhagic meningitis develop. Death often occurs within 24 to 36 hours even if
antibiotics are started in this stage.
Endemic/Geographic Respiratory Infection
Any organism can cause a pulmonary infection if the exposure is high enough, if the adult has lile or no
acquired immunity to it, or if the adult’s general immune responses are reduced by age, drugs, or other
health problems. A variety of respiratory infections are endemic , meaning that the causative organism is
much more common within a geographic location, but even then the incidence of the infection is
relatively low. Adults living in these areas have often developed some immunity to the organism over
time and usually only develop the infection if they come into contact with large numbers of the organism
or have a severely reduced immune response. Most commonly, the organisms are sporeforming fungi,
although some viral infections also have endemic tendencies. Table 28.4 lists common endemic
respiratory infections in North America. These organisms are part of the environment. Healthy adults in
endemic areas who are most susceptible to infection are those who have intense exposures. For soil-borne
organisms, adults who dig in the soil, farm, or work in construction in which soil is disturbed can be
heavily exposed. Everyone can be exposed when the soil is disturbed by dust storms, tornados, flooding,
and other types of natural disasters. Working and living in buildings in which demolition and/or
reconstruction are occurring can release spores trapped within walls that then become airborne. Working
with or camping in areas with organisms that live in soil or decomposing wood and leaves can result in
significant exposures. All of these respiratory infections resemble influenza or pneumonia with fever,
cough, headache, muscle aches, chest pain, and night sweats and are often misdiagnosed. Also, these
infections are not contagious from person to person. Identification of the specific organism is important
for specific treatment and prevention of complications. Always ask anyone with respiratory infection
symptoms whether they have visited endemic regions to help identify possible sources, expected courses,
and appropriate management strategies. Depending on the health and immunity of the infected person and
the number of spores present in the respiratory tract, the resulting infection can be mild, moderate, severe,
or widely disseminated to other major organs. Special populations, such as older adults, pregnant women,
and others who are immunocompromised are at greater risk for more severe disease. With fungal
infections, a chronic infection state is possible. Fungal infections are difficult to eradicate. With moderate
severity, oral antifungal agents may be prescribed for weeks to months. For more severe disease, IV g y p
antifungal agents, including amphotericin, may be needed initially and followed by long-term oral agents.
Supportive care is similar to that provided for patients with influenza and pneumonia.
Chapter 33: Care of Patients with Vascular Problems
Perfusion Concept Exemplar: Hypertension
Desired blood pressure
For people over 60
Below 150/90
For people younger than 60
According to Joint National
Committee 8 (JNC 8) guidelines,
patients whose blood pressures
are above these goals should be
treated with drug therapy and
lifestyle modifications
Below 140/90
HTN most common health problem in primary care settings & can cause stroke, MI, kidney failure, and
death if not treated effectively.
AHA: bp below 130/80
Table 1: AHA/ACCa Guideline Recommendations by Blood Pressure Category
Mechanisms that Influence Blood Pressure
Consequently, any factor that increases PVR (peripheral vascular resistance), HR, or SV increases the
systemic arterial pressure. Conversely, any factor that decreases PVR, HR, or SV decreases the systemic
arterial pressure and can cause decreased perfusion to body tissues.
control systems that maintain blood pressure

Four control systems play a major role in maintaining blood pressure:

The arterial baroreceptor system: primarily in the carotid sinus, aorta, and wall of the
left ventricle. They monitor the level of arterial pressure and counteract a rise in arterial
pressure through vagally mediated cardiac slowing and vasodilation with decreased
sympathetic tone. Reflex control of circulation therefore elevates the systemic arterial
pressure when it falls and lowers it when it rises. Why baroreceptor control fails in
hypertension is not clear

Regulation of body fluid volume: if there is an excess of sodium and/or water in a
person’s body, the BP rises through complex physiologic mechanisms that change the
venous return to the heart, producing a rise in cardiac output (CO). If the kidneys are
functioning adequately, a rise in systemic arterial pressure produces diuresis (excessive
voiding) and a fall in pressure. Pathologic conditions change the pressure threshold at
which the kidneys excrete sodium and water, thereby altering the systemic arterial
pressure.

The renin-angiotensin-aldosterone system:


kidney produces renin, an enzyme that acts on angiotensinogen to split off
angiotensin I, which is converted by an enzyme in the lung to form angiotensin
II. Angiotensin II has strong vasoconstrictor action on blood vessels and is the
controlling mechanism for aldosterone release. Aldosterone then works on the
collecting tubules in the kidneys to reabsorb sodium. Sodium retention inhibits
fluid loss, thus increasing blood volume and subsequent BP.

Renin acts on angiotensin  angiotensin I  angiotensin II
angiotensin II acts on blood vessels  aldosterone release, aldosterone
reabsorbs sodium = fluid loss prevented, blood volume increased  bp
increased

Inappropriate secretion of renin may cause increased peripheral vascular
resistance (PVR) in patients with hypertension. When the BP is high, renin levels
should decrease because the increased renal arteriolar pressure usually inhibits
renin secretion. However, for most people with essential hypertension, renin
levels remain normal
Vascular autoregulation: the process of vascular autoregulation, which keeps perfusion
of tissues in the body relatively constant, appears to be important in causing
hypertension. However, the exact mechanism of how this system works is poorly
understood.
Essential Hypertension

Most common type of HTN

Results in damage to vital organs

Causes medial hyperplasia (thickening) of arterioles: As the blood vessels thicken and perfusion
decreases, body organs are damaged. These changes can result in myocardial infarctions (MIs),
strokes, peripheral vascular disease (PVD), or kidney failure

Common risk factors:

Obesity

Smoking

Stress

Family history
Secondary Hypertension: Caused by specific disease states or drugs
Hypertensive Crisis (Malignant Hypertension)
Medical
emergency
Symptoms
include morning
headaches,
blurred vision,
dyspnea, uremia
Diastolic may be
> 150 mm Hg
Systolic may be >
200 mm Hg
*uremia (accumulation in the blood of substances ordinarily eliminated in the urine
A person with this health problem usually has symptoms such as morning headaches, blurred vision, and
dyspnea and/or symptoms of uremia (accumulation in the blood of substances ordinarily eliminated in
the urine). Patients are often in their 30s, 40s, or 50s with their systolic BP greater than 200 mm Hg. The
diastolic BP is greater than 150 mm Hg or greater than 130 mm Hg when there are pre-existing
complications. Unless intervention occurs promptly, a patient with hypertensive crisis may experience
kidney failure, left ventricular heart failure, or stroke.
Hypertension:
Etiology and Genetic Risk


Essential:

African American ethnicity

Hyperlipidemia

Smoking

Older than 60 years old

Obesity, physical inactivity
Secondary: kidney disease *most common cause of secondary HTN

Hypertension can develop when there is any sudden damage to the kidneys.
Renovascular hypertension is associated with narrowing of one or more of the main
arteries carrying blood directly to the kidneys, known as renal artery stenosis (RAS).
Many patients have been able to reduce the use of their antihypertensive drugs when
the narrowed arteries are dilated through angioplasty with stent placement.
Hypertension:
Health Promotion and Maintenance

Weight: weight reduction

Dash: Dash diet


diet that is high in fruits, vegetables, and low-fat dairy products; enhance intake of
potassium, calcium, magnesium, and fiber.
Reduce: reduce intake of dietary sodium


Reduce the intake of dietary sodium. The optimal goal is less than 1500 mg of sodium
per day.
Increase: increase physical activity

includes aerobic exercise, resistance training, and static isometric exercise.
Hypertension:
Assessment: Recognize Cues



History:

Risk factors

Kidney or CVD

Drug therapy or illicit drug use

Collect data on the patient’s age; ethnic origin or race; family history of hypertension;
average dietary intake of calories, sodium- and potassium-containing foods and alcohol;
and exercise habits.
Physical assessment/Signs & symptoms

May have no symptoms

Fundoscopic examination: Funduscopic examination of the eyes to observe vascular
changes in the retina is done by a skilled health care practitioner. The appearance of the
retina can be a reliable index of the severity and prognosis of hypertension. Physical
assessment is also helpful in diagnosing several conditions that produce secondary
hypertension.

Abdominal bruits: The presence of abdominal bruits is typical of patients with renal
artery stenosis (RAS). Tachycardia, sweating, and pallor may suggest a
pheochromocytoma (adrenal medulla tumor). Coarctation of the aorta is evidenced by
elevation of blood pressure in the arms, with normal or low blood pressure in the lower
extremities.
Psychosocial assessment
Hypertension:
Assessment: Recognize Cues
Diagnostic
assessment
Urinalysis for
protein, RBC,
BUN, creatinine
Chest x-ray
(cardiomegaly)
ECG shows
degree of cardiac
involvement
Although no laboratory tests are diagnostic of essential hypertension, several laboratory tests can assess
possible causes of secondary hypertension. Kidney disease can be diagnosed by the presence of protein
and red blood cells in the urine, elevated levels of blood urea nitrogen (BUN), and elevated serum
creatinine levels. The creatinine clearance test directly indicates the glomerular filtration ability of the
kidneys. The normal value is 107 to 139 mL/min for men and 87 to 107 mL/min for women (Pagana et
al., 2018). Decreased levels indicate acute or chronic kidney disease. Urinary test results are positive for
the presence of catecholamines in patients with a pheochromocytoma (tumor of the adrenal medulla).
An elevation in levels of serum corticoids and 17-ketosteroids in the urine is diagnostic of Cushing
disease. No specific x-ray studies can diagnose hypertension. Routine chest radiography may help
recognize cardiomegaly (heart enlargement). An electrocardiogram (ECG) determines the degree of
cardiac involvement. Left atrial and ventricular hypertrophy is the first ECG sign of heart disease
resulting from hypertension. Left ventricular remodeling can be detected on the 12-lead ECG
Hypertension:
Analysis: Analyze Cues and Prioritize Hypotheses
The priority collaborative problems for most patients with hypertension are:
Need for health
teaching due to
the plan of care
for hypertension
management
Potential for
decreased
adherence due
to side effects of
drug therapy
and necessary
changes in
lifestyle
Hypertension:
Planning and Implementation: Generate Solutions and Take Action

Health teaching

Lifestyle changes are considered the foundation of hypertension control. If these changes are
unsuccessful, the primary care provider considers the use of antihypertensive drugs. There is no
surgical treatment for essential hypertension. However, surgery may be indicated for certain
causes of secondary hypertension, such as kidney disease, coarctation of the aorta, and
pheochromocytoma.

Lifestyle modifications as in Health promotion

Abstain or decrease alcohol consumption (no more than one drink a day for
women and two drinks a day for men), Stop smoking and tobacco use, Use
relaxation techniques to reduce stress

• Restrict dietary sodium according to ACC/AHA guidelines • Reduce weight, if
overweight or obese • Implement a heart-healthy diet, such as the DASH diet •
Increase physical activity with a structured exercise program • Abstain or
decrease alcohol consumption (no more than one drink a day for women and
two drinks a day for men) • Stop smoking and tobacco use • Use relaxation
techniques to reduce stress


Drug therapy: Beta-adrenergic blockers, Renin inhibitors, Central alpha agonists, Alphaadrenergic agonists, Diuretics, Calcium channel blockers, ACE inhibitors, Angiotensin II
receptor antagonists, Aldosterone receptor antagonists

In the largest hypertensive trial done to date, Antihypertensive and LipidLowering Treatment to Prevent Heart Attack Trial (ALLHAT), the use of diuretics
has been practically unmatched in preventing the cardiovascular complications
of HTN

Current guidelines recommend use of one or more of these four classes of
drugs: thiazide-type diuretics, calcium channel blockers (CCBs),
angiotensinconverting enzyme inhibitors (ACEIs), and angiotensin II receptor
blockers (ARBs). Using an ACEI, ARB, and/or renin inhibitor simultaneously is
potentially harmful and is not recommended in the treatment of hypertension.
Patients who do not respond to these first-line drugs may be placed on other
diuretics, an aldosterone receptor antagonist (blocker), a beta-adrenergic
blocker, or a renin inhibitor.

Diuretics. Diuretics are the first type of drugs for managing hypertension. Three
basic types of diuretics are used to decrease blood volume and lower blood
pressure in the order of how commonly they are typically prescribed:

• Thiazide (low-ceiling) diuretics, such as hydrochlorothiazide, inhibit
sodium, chloride, and water reabsorption in the distal tubules while
promoting potassium, bicarbonate, and magnesium excretion.
However, they decrease calcium excretion, which helps prevent kidney
stones and bone loss. Because of the low cost and high effectiveness of
thiazide-type diuretics, they are usually the drugs of choice for patients
with uncomplicated hypertension. These drugs can be prescribed as a
single agent or in combination with other classes of drugs.

Loop (high-ceiling) diuretics, such as furosemide and torsemide, inhibit
sodium, chloride, and water reabsorption in the ascending loop of Henle
and promote potassium excretion
Complementary and Integrative Health

Garlic, coenzyme Q10, and fish oil: Evidence by consensus and case reports do
support garlic’s cholesterol-lowering ability and its ability to decrease blood
pressure in patients with hypertension (National Center for Complementary and
Integrative Health, 2018). Garlic can increase the risk of bleeding in patients
taking anticoagulants and can interfere with the effectiveness of some drugs.
Teach patients to check with their primary health care provider before starting
any herbal therapy because of possible side effects and interactions with other
herbs, foods, or drugs. Some patients have also had success with biofeedback,
meditation, and acupuncture as part of their overall management plan. These
methods may be most useful as adjuncts for patients who experience
continuous and severe stress.

Promoting adherence to the plan of care

Planning: Expected Outcomes The patient with hypertension is expected to adhere to
the plan of care, including making necessary lifestyle changes. Interventions Patients
who require medications to control essential hypertension usually need to take them for
the rest of their lives. Some patients stop taking them because they have no symptoms
and have troublesome side effects. In the hospital setting, interprofessional
collaboration with the pharmacist to discuss the outcomes of therapy with the patient,
including potential side effects, can help the patient tailor the therapeutic regimen to
his or her lifestyle and daily schedule. Patients who do not adhere to antihypertensive
treatment are at a high risk for target organ damage and hypertensive crisis, a severe
elevation in blood pressure (>180/120) that can cause organ damage in the kidneys or
heart (target organs) (see the Best Practice for Patient Safety & Quality Care: Emergency
Care of Patients With Hypertensive Crisis box). Patients in hypertensive crisis are
admitted to critical care units, where they receive IV antihypertensive therapy such as
nitroprusside, nicardipine, fenoldopam, or labetalol. For adults without a compelling
condition, systolic BP should be reduced by no more than 25% within the first hour;
then, if stable, to 160/100 mm Hg within the next 2 to 6 hours; and then cautiously to
normal during the following 24 to 48 hours (Whelton et al., 2017). A gradual reduction
in blood pressure is preferred because rapid reduction can cause cerebral ischemia, MI,
and renal failure. Provide oxygen to the patient and monitor oxygen saturation levels.
When the patient’s blood pressure stabilizes, oral antihypertensive drugs are given.
Hypertension:
Care Coordination and Transition Management

Home care management: Hypertension is a chronic illness. Allow patients to verbalize feelings
about the disease and its treatment. Emphasize that their involvement in the collaborative plan
of care can lead to control of the disease and can prevent complications. Some patients do not
adhere to their drug therapy regimen at home because they have no symptoms or they simply
forget to take their drugs. Others may think they are not sick enough to need medication. Some
patients may assume that once their blood pressure (BP) returns to normal levels, they no
longer need treatment. They may also stop taking their drugs because of side effects or cost.
Develop a plan with the patient and family and identify ways to encourage adherence to the
plan of care.

Self management education: Health teaching is essential to help patients become successful in
managing their BP. Provide oral and written n information about the indications, dosage, times
of administration, side effects, and drug interactions for antihypertensives. Stress that
medication must be taken as prescribed; when all of it has been consumed, the prescription
must be renewed on a continual basis. Suddenly stopping drugs such as beta blockers can result
in angina (chest pain), myocardial infarction (MI), or rebound hypertension. Urge patients to
report unpleasant side effects such as excessive fatigue, cough, or sexual dysfunction. In many
instances, an alternative drug can be prescribed to minimize certain side effects. Teach the
patient to obtain an ambulatory BP monitoring (ABPM) device for use at home so the pressure
can be checked. Evaluate the patient’s and family’s ability to use this device. If weight reduction
is a desired outcome, suggest having a scale in the home for weight monitoring. For patients
who do not want to self-monitor, are not able to self-monitor, or have “white-coat” syndrome
when they go to their primary health care provider (causing elevated BP), continuous ABPM may
be used. The monitor is worn for 24 hours or longer while patients perform their normal daily
activities. BP is automatically taken every 15 to 30 minutes and recorded for review later. The
advantage of this technique is that the primary health care provider can view the changes in BP
readings throughout the 24-hour period to get a picture of a true BP value. Research strongly
supports 24-hour ambulatory BP monitoring as a first-line procedure to determine the need for
antihypertensive therapy (U.S. Preventive Services Task Force, 2017). Instruct the patient about
sodium restriction, weight maintenance or reduction, alcohol restriction, stress management,
and exercise. If necessary, also explain about the need to stop using tobacco, especially
smoking.

Health care resources

A home care nurse may be needed for follow-up to monitor the BP. Evaluate patient or
family ability to obtain accurate BP measurements and assess adherence with
treatment. The American Heart Association, the Red Cross, or a local pharmacy may be
used for free BP checks if patients cannot buy equipment to monitor their BP. Health
fairs and BP screening programs located in faith-based centers are also available in most
locations.
Hypertension:
Evaluation: Evaluate Outcomes

Verbalize understanding of the plan of care, including drug therapy and any necessary lifestyle
changes

Report adverse drug effects, such as coughing, dizziness, or sexual dysfunction, to the primary
health care provider immediately

Consistently adhere to the plan of care, including regular follow-up with the primary health care
provider
Arteriosclerosis and Atherosclerosis
Pathophysiology Overview


Arteriosclerosis

Thickening or hardening of arterial wall

Often associated with aging
Atherosclerosis

Type of arteriosclerosis involving formation of plaque within arterial wall

Leading risk factor for cardiovascular disease

Arteriosclerosis is a thickening, or hardening, of the arterial wall that is often
associated with aging. Atherosclerosis, a type of arteriosclerosis, involves the
formation of plaque within the arterial wall and is the leading risk factor for
cardiovascular disease (CVD). Usually the disease affects the larger arteries,
such as coronary artery beds; aorta; carotid and vertebral arteries; renal, iliac,
and femoral arteries; or any combination of these. The exact pathophysiology of
atherosclerosis is not known, but the condition is thought to occur from blood
vessel damage that causes inflammation (Fig. 33.2). Inflammation occurs in
response to cellular injury. After the vessel becomes inflamed, a fatty streak
appears on the intimal surface (inner lining) of the artery. Through the process
of cellular proliferation, collagen migrates over the fatty streak, forming a
fibrous plaque. The fibrous plaque is often elevated and protrudes into the
vessel lumen, partially or completely obstructing blood flow through the artery.
Plaques are either stable or unstable. Unstable plaques are prone to rupture
and are often clinically silent until they rupture.

In the final stage, the fibrous plaques become calcified, hemorrhagic, ulcerated,
or thrombosed and affect all layers of the vessel. The rate of progression of the
process may be influenced by genetic factors; certain chronic diseases (e.g.,
diabetes mellitus); and lifestyle habits, including smoking, eating habits, and
level of exercise. When stable plaque ruptures, thrombosis (blood clot) and
constriction obstruct the vessel lumen, causing inadequate perfusion and
oxygenation to distal tissues. Unstable plaque rupture causes more severe
damage. After the rupture occurs, the exposed underlying tissue causes platelet
adhesion and rapid thrombus formation. The thrombus may suddenly block a
blood vessel, resulting in ischemia and infarction (e.g., myocardial infarction
[MI]). Endothelial (intimal) injury of the major arteries of the body can be
caused by many factors. Elevated levels of lipids (fats) such as low-density
lipoprotein cholesterol (LDL-C) and decreased levels of high-density lipoprotein
cholesterol (HDL-C) can cause chemical injuries to the vessel wall. (Chapter 30
discusses lipids in detail.) Chemical injury can also be caused by elevated levels
of toxins in the bloodstream, which may occur with renal failure or by carbon
monoxide circulating in the bloodstream from cigarette smoking. The vessel wall
can be weakened by the natural process of aging or by diseases such as
hypertension. Genetic predisposition and diabetes have a major effect on the
development of atherosclerosis. Some patients have familial hyperlipidemia, an
elevation of serum lipid levels. In these people, the liver makes excessive
cholesterol and other fats. However, some people with hereditary
atherosclerosis have a normal blood cholesterol level. The reason for the
development and progression of plaque in these patients is not understood
(McCance & Huether, 2019). Adult patients of any age with severe diabetes
mellitus frequently have premature and severe atherosclerosis from
microvascular damage. The premature atherosclerosis occurs because diabetes
promotes an increase in LDL-C and triglycerides (TGs) (lipids) in plasma. In
addition, arterial damage may result from the effect of hyperglycemia. Other
factors are indirectly related to atherosclerosis development. A list of risk
factors is found in Table 33.4.

Pathophysiology of Atherosclerosis

Discuss physical manifestations:

Monitor BP

Palpate pulses in all major sites of body

Assess for prolonged capillary refill

Assess for bruit
Atherosclerosis
The image to the left compares a normal artery to an artery with fat buildup (plaque) and an artery blocked
with fat
Arteriosclerosis and Atherosclerosis:
Assessment: Noticing

Assess blood pressure in both arms

Palpate carotid arteries separately

Capillary refill

Bruits

Cholesterol and triglycerides

The assessment of a patient with atherosclerosis includes a complete cardiovascular assessment
because associated heart disease is often present. Because of the high incidence of
hypertension in patients with atherosclerosis, assess the blood pressure in both arms. Palpate
pulses at all the major sites on the body and note any differences. Palpate each carotid artery
separately to prevent blocking blood flow to the brain! Also feel for temperature differences in
the lower extremities and check capillary filling. Prolonged capillary filling (>3 seconds in youngto–middle-age adults; >5 seconds in older adults) generally indicates poor circulation, although
this is not the most reliable indicator of perfusion. With severe atherosclerotic disease, the
extremity may be cool or cold with a diminished or absent pulse. Many patients with vascular
disease have a bruit in the larger arteries, which can be heard with a stethoscope or Doppler
probe. A bruit is a turbulent, swishing sound, which can be soft or loud in pitch. It is heard as a
result of blood trying to pass through a narrowed artery. A bruit is considered abnormal, but it
does not indicate the severity of disease. Bruits often occur in the carotid, aortic, femoral, and
popliteal arteries. Patients with atherosclerosis often have elevated lipids, including cholesterol
and triglycerides (TGs). Elevated cholesterol levels are confirmed by HDL and LDL
measurements. Increased low-density lipoprotein cholesterol (LDL-C) (“bad” cholesterol) levels
and low highdensity lipoprotein cholesterol (HDL-C) (“good” cholesterol) indicate that a person
is at an increased risk for atherosclerosis. The triglyceride level may also be elevated with
atherosclerosis. Elevated TGs are considered a marker for other lipoproteins. They also suggest
metabolic syndrome, which increases the risk for coronary disease (see Chapter 30 for in-depth
serum lipid information).
Arteriosclerosis and Atherosclerosis:
Interventions: Take Action

Low risk people should have total serum cholesterol levels evaluated every 4-6 years

Those with risk factors and older than 40 years old should have evaluation more frequently

Atherosclerosis progresses for years before signs and symptoms occur. Adults who are at risk for
the disease can often be identified through cholesterol screening and history. Because of the
high incidence in the United States, low-risk people 20 years of age and older are advised to
have their total serum cholesterol level evaluated at least once every 4 to 6 years. More
frequent measurements are suggested for people with multiple risk factors and those older than
40 years. People with multiple risk factors are grouped into high-risk patient categories.
Interventions for patients with atherosclerosis or those at high risk for the disease focus on
lifestyle changes. Teach patients about the need to make daily changes by avoiding or
minimizing modifiable risk factors. Modifiable risk factors are those that can be changed or
controlled by the patient, such as smoking, weight management, and exercise. Nutrition is one
of the most important parts of the risk-reduction plan. If lipoprotein levels do not improve after
lifestyle changes, the primary health care provider may prescribe drug therapy to lower
cholesterol and/or TGs.

Modifiable risk factors

Nutrition

Consume a dietary pattern that emphasizes intake of vegetables, fruits, whole
grains

Consumer low-fat diary products, poultry (without the skin), fish, legumes,
nontropical (e.g., canola) vegetable oils, and nuts. • Limit intake of sweets,
sugar-sweetened beverages, and red meats. • Aim for a dietary pattern that
includes 5-6% of calories from saturated fat; limiting trans fat


Activity


These guidelines are similar to the Dietary Approaches to Stop Hypertension
(DASH), which also recommend daily sodium, potassium, and fiber amounts
(National Heart, Lung, and Blood Institute, 2018). Interprofessional
collaboration with the registered dietitian nutritionist to teach the patient about
the types of fat content in food is encouraged. Meats and eggs contain mostly
saturated fats and are high in cholesterol. Instruct patients about increasing
dietary fiber to 30 g each day, which is consistent with DASH guidelines.
aerobic physical activity three or four times a week to reduce LDL-C levels. Each
session should last for 40 minutes on average and involve moderate-tovigorous
physical activity (
Drug therapy

For patients with elevated total and LDL-C levels that do not respond adequately
to dietary intervention, the primary health care provider prescribes a
cholesterol-lowering agent. Drug choice and dosing depend on the serum
cholesterol level, the degree to which the level needs to be decreased, and the
patient’s age (Grundy et al., 2018). Because most of these drugs can produce
side effects, they are generally given only when nonpharmacologic management
has been unsuccessful. A class of drugs known as 3-hydroxy-3-methylglutaryl
coenzyme A (HMGCoA) reductase inhibitors (statins) successfully reduces total
cholesterol in most patients when used for an extended period. Examples
include lovastatin, simvastatin, and pitavastatin, which lower both LDL-C and
triglyceride levels (Table 33.5).
Drug Therapy

HMG-CoA reductase inhibitors (statins)

Ezetimibe: A different type of lipid-lowering agent, ezetimibe, may be used in place of or in
combination with statin-type drugs. This drug inhibits the absorption of cholesterol through the
small intestine, leading to a decrease in the delivery of intestinal cholesterol to the liver, and
increases the clearance of cholesterol from the blood.

Combination drugs (e.g., ezetimibe with simvastatin): Vytorin is a combination drug containing
ezetimibe and simvastatin. This drug works two ways—by reducing the absorption of cholesterol
and by decreasing the amount of cholesterol synthesis in the liver. Amlodipine and atorvastatin
are combined as Caduet to decrease blood pressure while decreasing triglycerides (TGs),
increasing HDL, and lowering LDL. Combining drugs may improve adherence for the patient who
is often taking multiple drugs.

PCSK9 inhibitors: The U.S. Food and Drug Administration (FDA) approved the drug class PCSK9
inhibitors for use in patients with familial hypercholesterolemia or for those in whom existing
therapies are unable to reduce LDLs. These potent drugs inhibit PCSK9, which is a protease
produced primarily in the liver that can cause elevations in LDLs. Alirocumab and evolocumab
are administered by subcutaneous injection on a monthly or bimonthly basis for patients who
are on maximally tolerated doses of statins.
Peripheral Arterial Disease (PAD)

Pathophysiology Overview

Peripheral vascular disease

Systemic atherosclerosis

Alters natural flow of blood through arteries and veins of peripheral circulation

Result of systemic atherosclerosis
Lower Extremity Arterial Disease
The image to the left shows common locations of inflow and outflow lesions.
Peripheral Arterial Disease (PAD): Assessment: Recognize Cues
Stage I:
Asymptomatic
Stage II:
Claudication
Stage III: Rest Pain
Stage IV:
Necrosis/Gangren
e
Peripheral vascular disease (PVD) includes disorders that change the natural flow of blood through the
arteries and veins of the peripheral circulation, causing decreased perfusion to body tissues. It affects
the legs much more frequently than the arms. In general, a diagnosis of PVD implies arterial disease
(peripheral arterial disease [PAD]) rather than venous involvement. Some patients have both arterial
and venous disease. The cost of the disease is very high and is expected to increase as “baby boomers”
age and obesity in the United States continues to be a major health problem. PAD is a result of systemic
atherosclerosis. It is a chronic condition in which partial or total arterial occlusion (blockage) decreases
perfusion to the extremities. The tissues below the narrowed or obstructed arteries cannot live without
an adequate oxygen and nutrient supply. PAD in the legs is sometimes referred to as lower extremity
arterial disease (LEAD). Obstructions are classified as inflow or outflow, according to the arteries
involved and their relationship to the inguinal ligament (Fig. 33.3). Inflow obstructions involve the distal
end of the aorta and the common, internal, and external iliac arteries. They are located above the
inguinal ligament. Outflow obstructions involve the femoral, popliteal, and tibial arteries and are below
the superficial femoral artery (SFA). Gradual inflow occlusions may not cause significant tissue damage.
Gradual outflow occlusions typically do. Atherosclerosis is the most common cause of chronic arterial
obstruction; therefore the risk factors for atherosclerosis apply to PAD as well (see Table 33.4).
Advancing age also increases the risk for disease related to atherosclerosis. Patients with PAD have an
increased risk for developing chronic angina, MI, or stroke. PAD is a marker for systemic atherosclerotic
disease, making people with PAD more likely to have atherosclerosis in other vascular beds such as the
coronary, carotid, and renal arteries and the abdominal aorta (Benjamin et al., 2018). About 8.5 million
people in the United States age 40 and older have PAD. African Americans are affected more often than
any other group, most likely because they have many risk factors such as diabetes and hypertension
(Benjamin et al., 2018
Peripheral Arterial Disease (PAD): Assessment: Recognize Cues

Hair loss & dry, scaly, pale or mottled skin, thickened toenails

Severe arterial disease

Extremity is cold with gray-blue or darkened. Pall may occur with extremity elevation.
Dependent rubor. Muscle atrophy

The clinical course of chronic PAD can be divided into four stages (see the Key Features: Chronic
Peripheral Arterial Disease box). Patients do not experience symptoms in the early stages of
disease. Many patients are not diagnosed until they develop leg pain.

Most patients initially seek medical attention for a classic leg pain known as intermittent
claudication (a term derived from a word meaning “to limp”). Usually they can walk only a
certain distance before discomfort, such as cramping or burning muscular pain, forces them to
stop. The pain stops with rest. When patients resume walking, they can walk the same distance
before it returns. Thus the pain is considered reproducible. As the disease progresses, they can
walk only shorter and shorter distances before pain recurs. Ultimately it may occur even while
at rest.

Rest pain, which may begin while the disease is still in the stage of intermittent claudication, is a
numb or burning sensation, often described as feeling like a toothache that is severe enough to
awaken patients at night. It is usually located in the toes, the foot arches, the forefeet, the heels,
and rarely in the calves or ankles. Patients can sometimes alleviate pain by keeping the limb in a
dependent position (below the heart). Those with rest pain often have advanced disease that
may result in limb loss.

Patients with inflow disease have discomfort in the lower back, buttocks, or thighs. Patients with
mild inflow disease have discomfort after walking about two blocks. This discomfort is not
severe but causes them to stop walking. It is relieved with rest. Patients with moderate inflow
disease experience pain in these areas after walking about one or two blocks. The discomfort is
described as being more like pain, but it eases with rest most of the time. Severe inflow disease
causes severe pain after walking less than one block. These patients usually have rest pain.
Patients with outflow disease describe burning or cramping in the calves, ankles, feet, and toes.
Instep or foot discomfort indicates an obstruction below the popliteal artery. Those with mild
outflow disease experience discomfort after walking about five blocks. Rest relieves this
discomfort. Patients with moderate outflow disease have pain after walking about two blocks.
Intermittent rest pain may be present. Those with severe outflow disease usually cannot walk
more than one-half block. They may hang their feet off the bed at night for comfort & report
more frequent rest pain than patients with inflow disease.

Specific findings for PAD depend on the severity of the disease. Observe for loss of hair on the
lower calf, ankle, and foot; dry, scaly, dusky, pale, or mottled skin; and thickened toenails. With
severe arterial disease, the extremity is cold and gray-blue (cyanotic) or darkened. Pallor may
occur when the extremity is elevated. Dependent rubor (redness) may occur when the extremity
is lowered (Fig. 33.4). Muscle atrophy can result from prolonged chronic arterial disease

Palpate all pulses in both legs. The most sensitive and specific indicator of arterial function is the
quality of the posterior tibial pulse because the pedal pulse is not palpable in a small percentage
of people. The strength of each pulse should be compared bilaterally. Note early signs of ulcer
formation or complete ulcer formation, a complication of PAD. Arterial and venous stasis ulcers
differ from diabetic ulcers (see the Key Features: Chronic Peripheral Arterial Disease box).
Initially, arterial ulcers are painful and develop on the toes (often the great toe), between the
toes, or on the upper aspect of the foot. With prolonged occlusion, the toes can become
gangrenous. Typically, the ulcer is small and round with a hollow appearance and well-defined
borders.
Peripheral Arterial Disease (PAD): Diagnostic Assessment
MRA
Segmental systolic
blood pressure
measurement
Plethysmography
Ankle-brachial
index (ABI)
The ABI is calculated by
dividing the ankle
systolic BPs by the
higher of the left and
right brachial systolic
BP.
Exercise
tolerance
training
A normal ABI is 0.91 to 1.30 and indicates
adequate BP in the extremities. An ABI
between 0.71 and 0.90 indicates mild PAD,
between 0.41 and 0.70 indicates moderate
PAD, and <0.40 indicates severe PAD.
Magnetic resonance angiography (MRA) is commonly used to assess blood flow in the peripheral
arteries. A contrast medium is used to help visualize blood flow through these arteries. This test is often
the only one used to diagnose PAD, although computed tomography angiography (CTA) may also be
performed. Using a Doppler probe, segmental systolic blood pressure measurements of the lower
extremities at the thigh, calf, and ankle are an inexpensive, noninvasive method of assessing PAD.
Normally, blood pressure readings in the thigh and calf are higher than those in the upper extremities.
With the presence of arterial disease, these pressures are lower than the brachial pressure. With inflow
disease, pressures taken at the thigh level indicate the severity of disease. Mild inflow disease may
cause a difference of only 10 to 30 mm Hg in pressure on the affected side compared with the brachial
pressure. Severe inflow disease can cause a pressure difference of more than 40 to 50 mm Hg. The ankle
pressure is normally equal to or more than the brachial pressure. To evaluate outflow disease, compare
ankle pressure with the brachial pressure, which provides a ratio known as the ankle-brachial index
(ABI). The value can be derived by dividing the ankle blood pressure by the brachial blood pressure. An
ABI of less than 0.90 in either leg is diagnostic of PAD. Patients with diabetes are known to have a falsely
elevated ABI.
Peripheral Arterial Disease (PAD) Interventions: Take Action
Collaborative management of PAD may include nonsurgical interventions and/or surgery. The patient
must first be assessed to determine if the altered tissue perfusion is caused by arterial disease, venous
disease, or both. Exercise, positioning, promoting vasodilation, drug therapy, and invasive nonsurgical
procedures are used to increase arterial flow to the affected leg(s).

Exercise & positioning


Promoting vasodilation


Exercise may improve arterial blood flow to the affected leg through buildup of the
collateral circulation. Collateral circulation provides blood to the affected area through
smaller vessels that develop and compensate for the occluded vessels. Exercise is
individualized for each patient, but people with severe rest pain, venous ulcers, or
gangrene should not participate. Others with PAD can benefit from exercise that is
started gradually and slowly increased. Instruct the patient to walk until the point of
claudication, stop and rest, and then walk a little farther. Eventually, he or she can walk
longer distance as collateral circulation develops. Collaborate with the primary health
care provider and physical therapist in determining an appropriate exercise program.
Exercise rehabilitation has been used to relieve symptoms but requires a motivated
patient. The cost of supervised sessions generally is not reimbursed by health care
insurance. Positioning to promote circulation has been somewhat controversial. Some
patients have swelling in their extremities. Teach them to avoid raising their legs above
the heart level because extreme elevation slows arterial blood flow to the feet.
Vasodilation can be achieved by providing warmth to the affected extremity and
preventing long periods of exposure to cold. Encourage the patient to maintain a warm
environment at home and to wear socks or insulated shoes at all times. Caution the
patient to avoid the application of direct heat to the limb with heating pads or
extremely hot water. Sensitivity is decreased in the affected limb. Burns may result.
Encourage patients to prevent exposure of the affected limb to the cold because cold
temperatures cause vasoconstriction (decreasing of the diameter of the blood vessels)
and therefore decrease arterial perfusion. Emotional stress, caffeine, and nicotine also
can cause vasoconstriction. Emphasize that complete abstinence from smoking or
chewing tobacco is essential to prevent vasoconstriction. The vasoconstrictive effects of
each cigarette may last up to 1 hour after the cigarette is smoked.
Drug therapy (anticoagulation or antiplatelet agents)

For patients with chronic PAD, prescribed drugs include hemorheologic and antiplatelet
agents. Pentoxifylline is a hemorheologic agent that increases the flexibility of red blood
cells. It decreases blood viscosity by inhibiting platelet aggregation and decreasing
fibrinogen and thus increases blood flow in the extremities. Many patients report
limited improvement in their daily lives after taking pentoxifylline, and evidence
indicates minimal benefit. However, those with extremely limited endurance for walking
have reported improvement to the point that they can perform some activities (e.g.,
walk to the mailbox or dining room) that were previously impossible. Antiplatelet
agents, such as aspirin and clopidogrel, are commonly used. If there are no
contraindications to antiplatelet therapy, patients with symptomatic PAD should receive
aspirin or clopidogrel to reduce MI, stroke, and vascular death (Gerhard-Herman et al.,
2017). Some patients receive both drugs (dual antiplatelet therapy). Evidence suggests
that dual antiplatelet therapy is reasonable to reduce the risk of limb-related events in
patients with symptomatic PAD after lower extremity revascularization (GerhardHerman et al., 2017). Patients who are taking clopidogrel should not eat grapefruit or
drink grapefruit juice because of risk of kidney failure, GI bleeding, heart failure, or even
death. Patients who experience disabling intermittent claudication may also benefit
from phosphodiesterase inhibitors such as cilostazol because it can help improve
symptoms and increasing walking distance. This drug can also increase HDL-C levels.
Teach patients taking the drug that it may cause headaches and GI disturbances,
especially flatulence (gas) and diarrhea. Controlling hypertension can improve tissue
perfusion by maintaining pressures that are adequate to perfuse the periphery but not
constrict the vessels. Teach about the effect of blood pressure on the circulation and
instruct in methods of control. For example, patients taking beta blockers may have
drug-related claudication or a worsening of symptoms. The primary health care provider
closely monitors those who are receiving beta blockers. If the patient has high serum
lipids, lipid-lowering drugs such as statins are used

Percutaneous vascular intervention

A nonsurgical but invasive approach for improving arterial flow is the use of
percutaneous vascular intervention. This procedure requires an arterial puncture in the
patient’s groin. One or more arteries are dilated with a balloon catheter advanced
through a cannula, which is inserted into or above an occluded or stenosed artery.
When the procedure is successful, it opens the vessel and improves arterial blood flow.
Patients who are candidates for percutaneous procedures must have occlusions or
stenoses that are accessible to the catheter. Reocclusion may occur, and the procedure
may be repeated. Some patients are occlusion free for up to 3 to 5 years, whereas
others may experience reocclusion within a year. During percutaneous vascular
intervention, intravascular stents (wire meshlike devices) are usually inserted to ensure
adequate blood flow in a stenosed vessel. Candidates for stents are patients with
stenosis of the common or external iliac arteries. Stents are also available to effectively
treat superficial femoral artery (SFA) disease. Patients have these procedures in sameday surgery or ambulatory care centers. Another arterial technique to improve blood
flow to ischemic legs in people with PAD is mechanical rotational abrasive atherectomy.
The Rotablator device is designed to scrape plaque from inside the artery while
minimizing damage to the vessel surface and is useful at the popliteal artery and below.

Most patients receive anticoagulant or antiplatelet therapy such as heparin or
clopidogrel, before and/or during the procedure. An antiplatelet drug may also be
prescribed after the procedure to prevent arterial clotting. The most common time
frame for the administration of the antiplatelet is 1 to 3 months following the
procedure. However, this time frame is highly variable

Arterial revascularization

Arterial revascularization is the surgical procedure most commonly used to increase
arterial blood flow in an affected limb. Surgical procedures are classified as inflow or
outflow. Inflow procedures involve bypassing arterial occlusions above the superficial
femoral arteries (SFAs). Outflow procedures involve surgical bypassing of arterial
occlusions at or below the SFAs. For those who have both inflow and outflow problems,
the inflow procedure (for larger arteries) is done before the outflow repair. Inflow
procedures include aortoiliac, aortofemoral, and axillofemoral bypasses. Outflow
procedures include femoropopliteal and femorotibial bypasses. Inflow procedures are
more successful, with less chance of reocclusion or postoperative ischemia. Outflow
procedures are less successful in relieving ischemic pain and are associated with a
higher incidence of reocclusion. Graft materials for bypasses are selected on an
individual basis. For outflow procedures, the preferred graft material is the patient’s
own (autogenous) saphenous vein. However, some patients experience coronary artery
disease and may need this vein for coronary artery bypass. When the saphenous vein is
not usable, the cephalic or basilic arm veins may be used. Grafts made of synthetic
materials have also been used when autogenous veins were not available.
Drug Management of PAD
Medications

Pentoxifylline (Trental) –

for intermittent claudication

↑ Erythrocyte flexibility

↓ Blood viscosity

Cilostazol (Pletal) – vasodilator with some antiplatelet activity

ASA or other antiplatelet (Plavix)

ACE inhibitors

Ramipril (Altace)

↓ Cardiovascular morbidity

↓ Mortality

↑ Peripheral blood flow

↑ ABI

↑ Walking distance
Characteristics of Arterial Ulcers

Located in areas of pressure, tips of toes

Very painful

Deep, may involve joint

Usually circular in appearancedvt

Wound base pale to black

Little, if any, edema
Surgical Management
Patients with severe rest pain or claudication that interferes with the ability to work or threatens loss of
a limb become surgical candidates. Arterial revascularization is the surgical procedure most commonly
used to increase arterial blood flow in an affected limb. Surgical procedures are classified as inflow or
outflow. Inflow procedures involve bypassing arterial occlusions above the superficial femoral arteries
(SFAs). Outflow procedures involve surgical bypassing of arterial occlusions at or below the SFAs. For
those who have both inflow and outflow problems, the inflow procedure (for larger arteries) is done
before the outflow repair. Inflow procedures include aortoiliac, aortofemoral, and axillofemoral
bypasses. Outflow procedures include femoropopliteal and femorotibial bypasses. Inflow procedures
are more successful, with less chance of reocclusion or postoperative ischemia. Outflow procedures are
less successful in relieving ischemic pain and are associated with a higher incidence of reocclusion. Graft
materials for bypasses are selected on an individual basis. For outflow procedures, the preferred graft
material is the patient’s own (autogenous) saphenous vein. However, some patients experience
coronary artery disease and may need this vein for coronary artery bypass. When the saphenous vein is
not usable, the cephalic or basilic arm veins may be used. Grafts made of synthetic materials have also
been used when autogenous veins were not available.
Preoperative
Deep breathing
every 1-2 hr
Intraoperative
Monitor for graft
occlusion
(emergency)
Postoperative
Treatment of
graft occlusion
Monitor for
compartment
syndrome
Assess for
infection
Preoperative Care Preparing the patient for surgery is similar to procedures described for general or
epidural anesthesia (see Chapter 9). Documentation of vital signs and peripheral pulses provides a
baseline of information for comparison during the postoperative phase. Depending on the surgical
procedure, the patient may have one or more IV lines, urinary catheter, central venous catheter, and/or
arterial line. To prevent postoperative infection, antibiotic therapy is typically given before the
procedure.
Operative Procedures The anesthesia provider places the patient under general, epidural, or spinal
anesthesia. Epidural or spinal induction is preferred for older adults to decrease the risk for
cardiopulmonary complications in this age-group. If arterial bypass is to be accomplished by autogenous
grafts, the surgeon removes the veins through an incision. The blocked artery is then exposed through
an incision, and the replacement vein or synthetic graft material is sutured above and below the
occlusion to increase blood flow around the occlusion.
For conventional open aortoiliac and aortofemoral bypass (AFB) surgery, the surgeon makes a midline
incision into the abdominal cavity to expose the abdominal aorta, with additional incisions in each groin
(Fig. 33.5). Graft material is tunneled from the aorta to the groin incisions, where it is sutured in place. In
an open axillofemoral bypass (Fig. 33.6), the surgeon makes an incision beneath the clavicle and tunnels
graft material subcutaneously with a catheter from the chest to the iliac crest, into a groin incision,
where it is sutured in place. Neither the thoracic nor the abdominal cavity is entered. For that reason,
the axillofemoral bypass is used for high-risk patients who cannot tolerate a procedure requiring
abdominal surgery. Minimally invasive surgical techniques are beginning to be performed by vascular
surgeons using robotic-assisted laparoscopic procedures. These newer surgical techniques require
extensive training and further research data to determine their usefulness.
Aortoiliac and Aortofemoral Bypass
The image to the right shows how in aortoiliac and aortofemoral bypass surgery, a midline incision into the
abdominal cavity is required, with an additional incision in each groin.
Patients who have undergone conventional aortoiliac or aortofemoral bypass are NPO status for at least
1 day after surgery to prevent nausea and vomiting, which could increase intra-abdominal pressure.
Those who have undergone bypass surgery of the lower extremities not involving the aorta or
abdominal wall (femoropopliteal or femorotibial bypass) may remain NPO until the first postoperative
day, when they are allowed clear liquids. Warmth, redness, and edema of the affected extremity are
often expected outcomes of surgery as a result of increased arterial perfusion


Post operative:

Deep breathing every 1 to 2 hour

Monitor for graft occlusion (emergency)

Treatment of graft occlusion

Monitor for compartment syndrome

Assess for infection
Postoperative Care Thorough and ongoing nursing assessment for postoperative arterial
revascularization patients is crucial to detect complications. Deep breathing every 1 to 2 hours
and using an incentive spirometer are essential to prevent respiratory complications
Axillofemoral Bypass
To promote graft patency, monitor the patient’s blood pressure and notify the surgeon if the pressure
increases or decreases beyond the patient’s baseline. Hypotension may indicate hypovolemia, which can
increase the risk for clotting. Range of motion of the operative leg is usually limited, with no bending of
the hip and knee. Consult with the surgeon on a case-by-case basis regarding limitations of movement,
including turning. Patients having open procedures may be restricted to bedrest for 24 hours or longer
after surgery to prevent disruption of the suture lines. Patients having minimally invasive surgery (MIS)
may be ambulatory and eat within the day of surgery. Pain and surgical complications tend to occur less
often in patients who have MIS procedures.
Emergency thrombectomy (removal of the clot), which the surgeon may perform at the bedside, is the
most common treatment for acute graft occlusion. Thrombectomy is associated with excellent results in
prosthetic grafts. Results of thrombectomy in autogenous vein grafts are not as successful and often
necessitate graft revision and even replacement. Local intra-arterial thrombolytic (clot-dissolving)
therapy with an agent such as tissue plasminogen activator (t-PA) or an infusion of a platelet inhibitor
such as abciximab may be used for acute graft occlusions. This therapy is provided in select settings in
which health care providers are experts in its use. Other antiplatelet drugs such as the glycoprotein
IIb/IIIa inhibitors tirofiban and eptifibatide may be used as alternatives. The health care provider
considers these therapies when the surgical alternative (e.g., thrombectomy with or without graft
revision or replacement) carries high morbidity or mortality rates or when surgery for this type of
occlusion has traditionally yielded poor results. Closely assess the patient for manifestations of bleeding
if thrombolytics are used. Graft or wound infections can be life threatening. Use sterile technique when
providing incisional care and observe for symptoms of infection. Assess the area for induration,
erythema, tenderness, warmth, edema, or drainage. Also monitor for fever and leukocytosis (increased
serum white blood cell count). Notify the surgeon promptly if any of these symptoms occur. Patients
having conventional open bypass procedures are usually hospitalized for 5 to 7 days. Those having MIS
procedures usually have shorter stays of 2 or 3 days
Peripheral arterial disease (PAD) is a chronic, long-term problem with frequent complications. Patients
may benefit from a case manager who can follow them across the continuum of care. The desired
outcome is that the patient can be maintained in the home. Management at home often requires an
interprofessional team approach, including several home care visits. See the Home Care Considerations:
The Patient With Peripheral Vascular Disease box for home care of patients with peripheral vascular
disease. Instruct patients on methods to promote vasodilation. Teach them to avoid raising their legs
above the level of the heart unless venous stasis is also present. Provide written and oral instructions on
foot care and methods to prevent injury and ulcer development. See the Patient and Family Education:
Preparing for SelfManagement: Foot Care for the Patient With Peripheral Vascular Disease box. Patients
who have had surgery require additional instruction on incision care (see Chapter 9). Encourage all
patients to avoid smoking, limit dietary fat intake, and increase protein intake (Jellinger et al., 2017).
Remind them to drink adequate fluids to prevent dehydration. Patients with chronic arterial obstruction
may fear recurrent occlusion or further narrowing of the artery. They often fear that they might lose a
limb or become debilitated in other ways. Indeed, chronic PAD may worsen, especially in those with
diabetes mellitus. Reassure them that participation in prescribed exercise, nutrition therapy, and drug
therapy, along with cessation of smoking, can limit further formation of atherosclerotic plaques.
Patients with arterial compromise or surgery may need assistance from the family, another caregiver, or
a home care aide with ADLs if activity is limited by pain. They may need to limit or avoid stair climbing,
depending on the severity of disease. Those who have undergone surgery may require a home care
nurse to help with incision care. In collaboration with the case manager, arrange for home care
resources before discharge.
Acute Peripheral Arterial Occlusion

Pathophysiology overview: embolus

May have severe pain below the level of occlusion

Although chronic peripheral arterial disease (PAD) progresses slowly, the onset of acute arterial
occlusion is sudden and dramatic. An embolus (piece of a clot that travels and lodges in a new
area) is the most common cause of peripheral occlusions, although a local thrombus may be the
cause. Occlusion may affect the upper extremities, but it is more common in the lower
extremities. Emboli originating from the heart are the most common cause of acute arterial
occlusions. Most patients with an embolic occlusion have had an acute myocardial infarction
(MI) and/or atrial fibrillation within the previous weeks.
Six Ps of Arterial Insufficiency
Pain
Poikilothermia
(coolness)
Paralysis
Pallor
Paresthesia
Pulselessness
Patients with an acute arterial occlusion describe severe pain below the level of the occlusion that
occurs even at rest. The affected extremity is cool or cold, pulseless, and mottled. Small areas on the
toes may be blackened or gangrenous due to lack of perfusion.
The primary health care provider must initiate treatment promptly to avoid permanent damage or loss
of an extremity. Anticoagulant therapy with unfractionated heparin (UFH) is usually the first
intervention to prevent further clot formation. The patient may undergo angiography. A surgical
thrombectomy or embolectomy with local anesthesia may be performed to remove the occlusion. The
health care provider makes a small incision, which is followed by an arteriotomy (a surgical opening into
an artery). A catheter is inserted into the artery to retrieve the embolus. It may be necessary to close
the artery with a synthetic or autologous (patient’s own blood vessel) patch graft.
Acute Peripheral Arterial Occlusion:
Interventions: Take Action
The primary health care provider must initiate treatment promptly to avoid permanent damage or loss
of an extremity. Anticoagulant therapy with unfractionated heparin (UFH) is usually the first
intervention to prevent further clot formation. The patient may undergo angiography. A surgical
thrombectomy or embolectomy with local anesthesia may be performed to remove the occlusion. The
health care provider makes a small incision, which is followed by an arteriotomy (a surgical opening into
an artery). A catheter is inserted into the artery to retrieve the embolus. It may be necessary to close
the artery with a synthetic or autologous (patient’s own blood vessel) patch graft.
Alterations in comfort should significantly diminish after the surgical procedure, although mild incisional
pain remains. Watch closely for complications caused by reperfusing the artery after thrombectomy or
embolectomy, either of which includes spasms and swelling of the skeletal muscles. Swelling of the
skeletal muscles can result in compartment syndrome. Compartment syndrome occurs when tissue
pressure within a confined body space becomes elevated and restricts blood flow. The resulting
ischemia can lead to tissue damage and eventually tissue death. Assess the motor and sensory function
of the affected extremity. Monitor for increasing pain, swelling, and tenseness. Report any of these
symptoms to the health care provider immediately. Fasciotomy (surgical opening into the tissues) may
be necessary to prevent further injury and save the limb. The use of systemic thrombolytic therapy for
acute arterial occlusions has been disappointing because bleeding complications often outweigh the
benefits obtained. Catheter-directed intra-arterial thrombolytic therapy with fibrinolytics, such as
alteplase or t-PA, has emerged as an alternative to surgical treatment in selected settings. A catheter is
placed percutaneously (through the skin) into the artery with or without ultrasound guidance by the
vascular surgeon or interventional radiologist. The tip of the catheter is embedded in the clot to directly
deliver the thrombolytic infusion until the clot dissolves, which can take 24 to 36 hours. During infusion,
monitor the patient for complications such as bleeding and hemorrhagic stroke. Maintaining a normal
blood pressure is essential in preventing a potential stroke. As the clot dissolves, the patient typically
experiences severe pain due to reperfusion that requires patient-controlled analgesia (PCA)
Aneurysms of Central Arteries

Pathophysiology overview

Aneurysm—permanent localized dilation of artery, enlarging artery to twice its normal
diameter


An aneurysm is a permanent localized dilation of an artery, which enlarges the artery to
at least two times its normal diameter. It may be described as fusiform (a diffuse
dilation affecting the entire circumference of the artery) or saccular (an outpouching
affecting only a distinct portion of the artery). Aneurysms may also be described as true
or false. In true aneurysms, the arterial wall is weakened by congenital or acquired
problems. False aneurysms occur as a result of vessel injury or trauma to all three layers
of the arterial wall. Dissecting aneurysms differ from aneurysms in that they are formed
when blood accumulates in the wall of an artery. Aneurysms tend to occur at specific
anatomic sites (Fig. 33.7), most commonly in the abdominal aorta. They often occur at a
point where the artery is not supported by skeletal muscles or on the lines of curves or
flexion in the arterial tree. This chapter discusses aneurysms of the central arteries.
Brain aneurysms are discussed in Chapter 41. An aneurysm forms when the middle layer
(media) of the artery is weakened, producing a stretching effect in the inner layer
(intima) and outer layers of the artery. As the artery widens, tension in the wall
increases; and further widening occurs, thus enlarging the aneurysm and increasing the
risk for arterial rupture. Elevated blood pressure can also increase the rate of
aneurysmal enlargement and risk for early rupture. When dissecting aneurysms occur,
the aneurysm enlarges, blood is lost, and blood flow to organs is diminished.

Aneurysms can cause symptoms by exerting pressure on surrounding structures or by
rupturing. Rupture is the most frequent complication and is life threatening because
abrupt and massive hemorrhagic shock results. Thrombi within the wall of an aneurysm
can also be the source of emboli in distal arteries below the aneurysm. Atherosclerosis
is the most common cause of aneurysms, with hypertension, hyperlipidemia, and
cigarette smoking being contributing factors. Age, gender, and family history also play a
role
Description

Fusiform

Saccular

True

False

Dissecting
Arterial Aneurysms
*common anatomic sites of arterial aneurysms.
Aneurysms of Central Arteries:
Assessment: Recognize Cues
Sometimes asymptomatic

AAA

Gnawing pain with abdominal, flank, or back pain

Pulsation in upper abdomen

Detectable = at least 5 cm in diameter

Rupture symptoms = severe sudden pain in back, low abdomen; radiates to groin,
buttocks, legs

Critical illness – at risk for hypovolemic shock caused by hemorrhage

Abdominal aortic aneurysms (AAAs) account for most aneurysms, are commonly
asymptomatic, and frequently rupture. Most of these are located between the renal
arteries and the aortic bifurcation (dividing area)

Most patients with abdominal or thoracic aneurysms are asymptomatic when their
aneurysms are first discovered by routine examination or during an imaging study
performed for another reason. However, a few patients do have symptoms that bring
them to their primary health care provider or the emergency department. Assess
patients with a known or suspected abdominal aortic aneurysm (AAA) for abdominal,
flank, or back pain. Pain is usually described as steady with a gnawing quality,
unaffected by movement, and lasting for hours or days. A pulsation in the upper
abdomen slightly to the left of the midline between the xiphoid process and the
umbilicus may be present. A detectable aneurysm is at least 5 cm in diameter.
Auscultate for a bruit over the mass, but avoid palpating the mass because it may be
tender, and there is risk for rupture! If expansion and impending rupture of an AAA are
suspected, assess for severe pain of sudden onset in the back or lower abdomen, which
may radiate to the groin, buttocks or legs. Patients with a rupturing AAA are critically ill
and are at risk for hypovolemic shock caused by hemorrhage. Signs and symptoms
include hypotension, diaphoresis, decreased level of consciousness, oliguria (scant urine
output), loss of pulses distal to the rupture, and dysrhythmias. Retroperitoneal
hemorrhage manifests with hematomas in the flanks (lower back). Rupture into the
abdominal cavity causes abdominal distention.

TAA

Back pain

Shortness of breath

Difficulty swallowing

Not often detected by physical assessment

May have a mass above the suprasternal notch

Thoracic aortic aneurysms (TAAs) are not quite as common and are frequently
misdiagnosed. They are typically discovered when advanced imaging is used to assess
other conditions. TAAs commonly develop between the origin of the left subclavian
artery and the diaphragm. They are located in the descending, ascending, and
transverse sections of the aorta. They can also occur in the aortic arch and are very
difficult to manage surgically.

When a thoracic aortic aneurysm (TAA) is suspected, assess for back pain and
manifestations of compression of the aneurysm on adjacent structures. Signs include
shortness of breath, hoarseness, and difficulty swallowing. TAAs are not often detected
by physical assessment, but occasionally a mass may be visible above the suprasternal
notch. Assess the patient with suspected rupture of a thoracic aneurysm for sudden and
excruciating back or chest pain. Hypovolemic shock also occurs with TAA. Computed
tomography (CT) scanning with contrast is the standard tool for assessing the size and
location of an abdominal or thoracic aneurysm. Ultrasonography is also used.
Diagnostic Assessment
Nonsurgical
management
X-ray “eggshell”
appearance
• Monitor aneurysm growth
• Maintain BP at normal level to
decrease risk of rupture
Ultrasonography
CT
Aortic arteriography
The desired outcome of nonsurgical management is to monitor the growth of the aneurysm and
maintain the blood pressure at a normal level to decrease the risk for rupture. Patients with
hypertension are treated with antihypertensive drugs to decrease the rate of enlargement and the risk
for early rupture. For those with small or asymptomatic aneurysms, frequent ultrasound or CT scans are
necessary to monitor the growth of the aneurysm. Emphasize the importance of following through with
scheduled tests to monitor the growth. Also explain the signs and symptoms of aneurysms that need to
be promptly reported.
Surgical Management
Abdominal aortic
aneurysm
resection
Endovascular
repair
Thoracic aortic
aneurysm repair
Surgical management of an aneurysm may be an elective or an emergency procedure. For patients with
a rupturing abdominal aortic or a thoracic aneurysm, emergency surgery is performed. Patients with
smaller aneurysms that are producing symptoms are advised to have elective surgery. Those with
smaller aneurysms that are not causing symptoms are treated nonsurgically until symptoms occur or the
aneurysm enlarges. The most common surgical procedure for AAA has traditionally been a resection or
repair (aneurysmectomy). However, the mortality rate for elective resection is high and markedly
increases for emergency surgery. Endovascular stent grafts have improved mortality rates and
shortened the hospital stay for select patients who need AAA repair. The repair of AAAs with
endovascular stent grafts is the procedure of choice for almost all patients on an elective or emergent
basis. Stents (wirelike devices) are inserted percutaneously (through the skin), avoiding abdominal
incisions and therefore decreasing the risk for a prolonged postoperative recovery. Postoperative care is
similar to care required after an arteriogram (angiogram). Different designs of endovascular stent grafts
are used, depending on the anatomic involvement of the aneurysm. The stent graft is flexible with either
Dacron or polytetrafluoroethylene (PTFE) material. It is inserted through a skin incision into the femoral
artery by way of a catheter-based system. The catheter is advanced to a level above the aneurysm away
from the renal arteries. The graft is released from the catheter, and the stent graft is placed with a series
of hooks. This procedure is done in collaboration with the vascular surgeon, interventional radiologist,
operating suite team, and at some centers the vascular medicine physician.
Aneurysms of Central Arteries:
Interventions: Take Action

Size and presence of symptoms determines patient management

Nonsurgical management

Surgical management
TAA repair

Postoperative Care

Assess vital signs at least hourly.

Assess the patient hourly for sensation and motion

Patient must follow instructions
Aneurysms of the Peripheral Arteries

Femoral and popliteal aneurysms

Do NOT palpate the mass

Symptoms

Limb ischemia

Diminished or absent pulses

Cool to cold skin

Pain

Treatment: Surgery

Postoperative care: Report sudden development of pain or extremity discoloration

Although femoral and popliteal aneurysms are not common, they may be associated with an
aneurysm in another location of the arterial tree (see Fig. 33.7). To detect a popliteal aneurysm,
assess for a pulsating mass in the popliteal space. To detect a femoral aneurysm, observe a
pulsatile mass over the femoral artery. To prevent its rupture, do not palpate the mass! Evaluate
both extremities because more than one femoral or popliteal aneurysm may be present. The
patient may have symptoms of limb ischemia (decreased perfusion ), including diminished or
absent pulses, cool to cold skin, and pain. Alterations in comfort may be present if an adjacent
nerve is compressed. The recommended treatment for either type of aneurysm, regardless of
size, is surgery because of the risk for thromboembolic complications. To treat a femoral
aneurysm, the surgeon removes the aneurysm and restores circulation using a synthetic or an
autogenous saphenous vein graft-stent repair. Most surgeons prefer to bypass rather than
resect a popliteal aneurysm. After surgery, monitor for lower-limb ischemia. Palpate pulses
below the graft to assess graft patency. Often Doppler ultrasonography is necessary to assess
blood flow when pulses are not palpable. Report sudden development of pain or discoloration
of the extremity immediately to the surgeon because it may indicate graft occlusion.
Aortic Dissection

Pathophysiology Overview

Formerly called “dissecting aneurysm”

Sudden tear in aortic intima; blood enters aortic wall

Highly lethal, emergent situation

Aortic dissection is thought to be caused by a sudden tear in the aortic intima, allowing
blood to enter the aortic wall. Degeneration of the aortic media may be the primary
cause for this condition, with hypertension y p y yp being an important contributing
factor. It is often associated with genetic connective tissue disorders such as Marfan
syndrome. It occurs also in middle-age and older people, peaking in adults in their 50s
and 60s. Men are more commonly affected than women. The circulation of any major
artery arising from the aorta can be impaired in patients with aortic dissection;
therefore this condition is highly lethal and represents an emergency situation. Although
the ascending aorta and descending thoracic aorta are the most common sites,
dissections can also occur in the abdominal aorta and other arteries.
Aortic Dissection :
Interventions: Take Action
Insert two
large-bore
IV
catheters
0.9%
sodium
chloride
and
medication
Indwelling
catheter
Subsequent
treatment
depends on
dissection
location
The expected outcomes for emergency care for a patient with an aortic dissection are increased comfort
and reduction of systolic blood pressure to 100 to 120 mm Hg. Make sure that the patient has two largebore IV catheters to infuse 0.9% sodium chloride and give medication. Insert an indwelling urinary
catheter. The health care provider prescribes IV morphine sulfate to relieve pain and an IV beta blocker,
such as esmolol, p p to lower heart rate and blood pressure (Black & Manning, 2018). If this regimen is
not effective, nitroprusside or nicardipine hydrochloride may be used.
Subsequent treatment depends on the location of the dissection. Patients receive continued medical
treatment for uncomplicated distal dissections and surgical treatment for proximal dissections. For longterm medical treatment, the recommended target for blood pressure is less than 120/80 mm Hg (Black
& Manning, 2018). Beta blockers (e.g., propranolol) and calcium channel antagonists (e.g., amlodipine)
are prescribed to assist with blood pressure maintenance once the patient is stabilized. Patients having
surgical intervention for a proximal dissection typically require cardiopulmonary bypass (CPB) (see
Chapter 35). The surgeon removes the intimal tear and sutures edges of the dissected aorta. Usually a
synthetic graft is used.
Peripheral Venous Disease
Thrombus
formation
Skeletal muscles
that do not
contract to help
pump blood in
the veins
Defective valves
To function properly, veins must be patent (open) with competent valves. Vein function also requires
the assistance of the surrounding muscle beds to help pump blood toward the heart. If one or more
veins are not operating properly, they become distended, and signs and symptoms occur. Three health
problems alter the blood flow in veins:
• Thrombus formation (venous thrombosis) can lead to pulmonary embolism (PE), a life-threatening
complication. Venous thromboembolism (VTE) is the current term that includes both deep vein
thrombosis (DVT) and PE.
• Defective valves lead to venous insufficiency and varicose veins, which are not life threatening but are
problematic.
• Skeletal muscles do not contract to help pump blood in the veins. This problem can occur when weight
bearing is limited or muscle tone decreases.
Venous Thromboembolism

Pathophysiology Overview

Thrombus

Phlebothrombosis

Thrombophlebitis

DVT

Venous thromboembolism (VTE) is one of health care’s greatest challenges and includes
both thrombus and embolus complications. A thrombus (also called a thrombosis) is a
blood clot believed to result from an endothelial injury, venous stasis, or
hypercoagulability. The thrombosis may be specifically attributable to one element, or it
may involve all three elements. It is often associated with an inflammatory process.
When a thrombus develops, immunity is altered, causing inflammation to occur around
the clot, thickening of the vein wall, and possible embolization (the formation of an
embolus). Pulmonary embolism (PE) is the most common type of embolus and is
discussed in detail in Chapter 29. Phlebothrombosis is a thrombus without
inflammation. Thrombophlebitis refers to a thrombus that is associated with
inflammation. Thrombophlebitis can occur in superficial veins. However, it most
frequently occurs in the deep veins of the lower extremities. Deep vein
thrombophlebitis, commonly referred to as deep vein thrombosis (DVT), is the most
common type of thrombophlebitis. It is more serious than superficial thrombophlebitis
because it presents a greater risk for PE. With PE, a dislodged blood clot travels to the
pulmonary artery—a medical emergency! DVT develops most often in the legs but can
also occur in the upper arms as a result of increased use of central venous devices.
Peripheral Venous Disease: Etiology

Virchow’s triad

Blood flow stasis

Endothelial injury

Hypercoagulability

Thrombus formation has been associated with stasis of blood flow, endothelial injury,
and/or hypercoagulability, known as the Virchow triad. The precise cause of these
events remains unknown; however, a few predisposing factors have been identified. The
highest incidence of clot formation occurs in patients who have undergone hip surgery,
total knee replacement, or open prostate surgery. Other conditions that seem to
promote thrombus formation are ulcerative colitis, heart failure, cancer, oral
contraceptives, and immobility. Complications of immobility occur during prolonged
bedrest such as when a patient is confined to bed for an extensive illness. People who
sit for long periods (e.g., on an airplane or at a computer) are also at risk. Phlebitis (vein
inflammation ) associated with invasive procedures such as IV therapy can also
predispose patients to thrombosis.
Peripheral Venous Disease:
Assessment: Recognize Cues
Assess the patient for a history of any type of VTE. In addition, assess him or her for risks that may be
associated with the development of VTE such as prolonged periods of sitting or bedrest, recent surgical
procedures, or any factors that may affect coagulation. The Padua Prediction Score (PPS) has been
suggested as the best available model for the assessment of the risk of VTE in hospitalized medical
patients (Germini et al., 2016). The PPS is meant to assess risk for VTE, not to diagnose VTE. During the
nursing assessment, one point is given for each of the characteristics, which include:
• Active cancer
• Previous VTE (excluding superficial vein thrombosis)
• Reduced mobility
• Known thrombophilic condition
• Recent (≤1 month) trauma and/or surgery
• Older adult (≥70 years)
• Cardiac and/or respiratory failure
• Acute MI and/or ischemic stroke
• Acute infection and/or rheumatologic disorder
• Obesity (body mass index [BMI] ≥30)
• Ongoing hormonal treatment A score of 4 or more indicates that a DVT is likely to occur
Physical Assessment/Signs and Symptoms People with DVT may have symptoms or may be
asymptomatic. The classic signs and symptoms of DVT are calf or groin tenderness and pain and sudden
onset of unilateral swelling of the leg. Pain in the calf on dorsiflexion of the foot (positive Homans sign)
appears in only a small percentage of patients with DVT, and false-positive findings are common.
Therefore checking a Homans sign is not advised because it is an unreliable tool! Examine the area
described as painful, comparing this site with the other limb. Gently palpate the site, observing for
induration (hardening) along the blood vessel and for warmth and edema. Redness may also be present
Peripheral Venous Disease:
Assessment: Recognize Cues

Other Diagnostic Assessments

Venous duplex ultrasonography

Doppler flow studies

Impedance plethysmography

MRI

d-dimer

If a definitive diagnosis is lacking from physical assessment findings alone, diagnostic
tests may be performed. The preferred diagnostic test for DVT is venous duplex
ultrasonography, a noninvasive ultrasound that assesses the flow of blood through the
veins of the arms and legs. Doppler flow studies may also be useful in the diagnosis, but
they are more sensitive in detecting proximal rather than distal DVT. Normal venous
circulation creates audible signals, whereas thrombosed veins produce little or no
sound. The accuracy of the scanning depends on the technical skill of the health care
professional performing the test. If the test is negative but a DVT is still suspected, a
venogram may be needed to make an accurate diagnosis. Impedance plethysmography
assesses venous outflow and can detect most DVTs that are located above the popliteal
vein. It is not helpful in locating clots in the calf and is less sensitive than Doppler
studies. Magnetic resonance direct thrombus imaging, another noninvasive test, is
useful in finding a DVT in the proximal deep veins and is better than traditional
venography in finding DVT in the inferior vena cava or pelvic veins. A D-dimer test is a
global marker of coagulation activation and measures fibrin degradation products
produced from fibrinolysis (clot breakdown). The test is used for the diagnosis of DVT
when the patient has few clinical signs and stratifies patients into a high-risk category
for recurrence. Useful as an adjunct to noninvasive testing, a negative D-dimer test can
exclude a DVT without an ultrasound.
Peripheral Venous Disease: Analysis:
Analyze Cues and Prioritize Hypothesestter
Analysis:
Interpreting
Potential for injury due to
complications of VTE and
anticoagulation therapy
Peripheral Venous Disease: Intervention:
Generate Solutions & Take Action

surgical management

nonsurgical management
The focus of managing thrombophlebitis is to prevent complications such as pulmonary emboli, further
thrombus formation, and an increase in size of the thrombus. Patients with deep vein thrombosis (DVT)
may be hospitalized for treatment, although this practice is changing as a result of the use of newer
drugs. Nonsurgical Management DVT is usually treated medically with a combination of rest and drug
therapy. Prevention of DVT and other types of VTE is crucial for patients at risk. For those at moderateto-high risk, initiate these interventions to prevent VTE:
• Patient education • Leg exercises • Early ambulation • Adequate hydration • Graduated compression
stockings • Intermittent pneumatic compression, such as sequential compression devices (SCDs) •
Venous plexus foot pump • Anticoagulant therapy
Supportive therapy for DVT has typically included bedrest and elevation of the extremity. However,
research shows that ambulation does not increase the risk for pulmonary embolus (Lip & Hull, 2018).
The risk of pulmonary embolism (PE) associated with more aggressive activity is unknown. The accepted
approach is a gradual increase in ambulation as tolerated by the patient. Allowing patients to ambulate
may decrease their fear and anxiety about dislodging the clot and life-threatening complications. Teach
the patient to elevate his or her legs when in the bed and chair. To help prevent chronic venous
insufficiency, instruct patients with active and resolving DVT to wear knee- or thigh-high sequential or
graduated compression stockings for an extended period. Be sure to select the correct stocking size for
the patient according to the sizing chart provided. Some health care providers prescribe intermittent or
continuous warm, moist soaks to the affected area to promote circulation and reduce pain. To prevent
the thrombus from dislodging and becoming an embolus, do not massage the affected extremity.
Monitor all patients for signs and symptoms of PE, which include shortness of breath, chest pain, and
acute confusion (in older adults). Emboli may also travel to the brain or heart, but these complications
are not as common as PE. Chapter 29 describes PE manifestations in detail. Drug therapy.
Anticoagulants are the drugs of choice for actual DVT and for patients at risk for DVT. However, these
drugs are known to cause medical complications and even death. The Joint Commission’s National
Patient Safety Goals (NPSGs) include elements of performance to reduce the likelihood of patient harm
associated with the use of anticoagulant therapy (TJC, 2018).
Medical Management of DVT


Low Molecular Weight Heparin (LMWH)

Enoxaparin (Lovenox)

Dosed based on weight

Dose different for treatment of DVT vs prevention of DVT

Less bleeding issues

More cost effective

Low-molecular-weight heparin. Subcutaneous LMWHs such as enoxaparin or dalteparin
have a consistent action and are preferred for prevention and treatment of DVT.
LMWHs bind less to plasma proteins, blood cells, and vessel walls, resulting in a longer
half-life and more predictable response. These drugs inhibit thrombin formation
because of reduced factor IIa activity and enhanced inhibition of factor Xa and
thrombin. Some patients taking LMWH may be safely managed at home with visits from
a home care nurse. Candidates for home therapy must have stable DVT or PE, low risk
for bleeding, adequate renal function, and normal vital signs. They must be willing to
learn self-injection or have a family member, friend, or home care nurse administer the
subcutaneous injections. Some health care providers place the patient on a regimen of
IV unfractionated heparin (UFH) for several days and then follow up with an LMWH. In
this case, the UFH is discontinued at least 30 minutes before the first LMWH injection.
Assess all stools for occult blood. The aPTTs are not checked on an ongoing basis
because the doses of LMWH are not routinely adjusted. The anti-Xa factor can be
assessed to monitor the effect of the LMWH. Therapeutic range of the anti-Xa factor for
LMWH therapy is 0.5 to 1.2 IU/mL (Pagana & Pagana, 2018)
Un-fractionated Heparin

IV infusion given over 5-7d or until Warfarin brings INR up (2-3)

Warfarin (Coumadin) started at the same time

Usual dose: 80units/kg bolus followed by 18units/kg/hr

Requires monitoring of PTT levels

The conventional treatment has been IV unfractionated heparin (UFH) followed by oral
anticoagulation with warfarin (Coumadin). However, UFH can be problematic because
each patient’s response to the drug is unpredictable and hospital admission is usually
required for laboratory monitoring and dose adjustments. The use of low–molecular-
weight heparin (LMWH) and the development of novel direct oral anticoagulants
(DOACs, also referred to as novel oral anticoagulants [NOACs]) has changed the
management of both DVT and PE. Regardless of the approach to anticoagulation, all
patients should be assessed before and during anticoagulant therapy for bleeding risk.

Unfractionated heparin therapy. Some patients with a confirmed diagnosis of an existing
blood clot are started on a regimen of IV UFH therapy. The health care provider
prescribes UFH to prevent further clotting which often develops in the presence of an
existing clot, and to prevent enlargement of the existing clot. Over a long period of time,
the body slowly absorbs the existing clot. Before UFH administration, a baseline
prothrombin time (PT), activated partial thromboplastin time (APTT or aPTT),
international normalized ratio (INR), complete blood count (CBC) with platelet count,
urinalysis, stool for occult blood, and creatinine level are required. Notify the primary
health care provider if the platelet count is below 100,000 to 120,000/mm3 , depending
on agency protocol. UFH is initially given in a bolus IV dose followed by continuous
infusion via pump (Hull et al., 2018). The infusion is regulated by a reliable electronic
pump that protects against accidental free flow of solution. The health care provider or
clinical pharmacist prescribes concentrations of UFH (in 5% dextrose in water) and the
number of units or milliliters per hour needed to maintain a therapeutic aPTT. aPTT is
measured at least daily, 6 hours after initiation, and 6 hours after any dose change, and
the results are reported to the health care provider as soon as they are available to
allow adjustment of heparin dosage. Therapeutic levels of aPTT are usually 1.5 to 2.5
times normal control levels. While most patients who receive UFH are monitored using
the aPTT value, the heparin anti-factor Xa (anti-Xa) is sometimes used to monitor and
adjust therapy (Zehnder, 2019). The therapeutic range of the anti-Xa factor for UFH is
0.3 to 0.7 IU/mL (Pagana & Pagana, 2018). There is no evidence to suggest that one
value is better for monitoring than another, and the aPTT and anti-factor Xa may be
used together. Refer to specific agency policy for monitoring protocols.

UFH can also decrease platelet counts. Mild reductions are common and are resolved
with continued heparin therapy. Severe platelet reductions, although rare, result from
the development of antiplatelet bodies within 6 to 14 days after the beginning of
treatment. Platelets aggregate into “white clots” that can cause thrombosis, usually in
the form of an acute arterial occlusion. The health care provider discontinues heparin
administration if severe heparin-induced thrombocytopenia (HIT) (platelet count
<150000) or “white clot syndrome,” occurs. Low–molecular-weight heparin (LMWH) is
used more commonly today because of the complications involved with UFH.
Dabigatran is a direct thrombin inhibitor that may be used as an alternative to heparin
or for patients who have had HIT. Like heparin, these drugs increase the risk for
bleeding. Monitor hemoglobin, hematocrit, aPTT, platelet count, urinalysis, fecal occult
blood test, and blood pressure for indications of this complication. An oral anticoagulant
such as warfarin (Coumadin) may also be substituted for heparin if necessary. Ensure
that protamine sulfate, the antidote for heparin, is available if needed for excessive
bleeding. The Best Practice for Patient Safety & Quality Care: The Patient Receiving
Anticoagulant Therapy box highlights information important to nursing care and patient
education associated with anticoagulant therapy.
Medical Management of DVT

Warfarin

Used for long-term therapy

Antidote = vitamin K

Dose individualized

Monitor PT/INR levels closely

Started on day 1 with LMWH or Un-fractionated heparin

Multiple drug and food interactions!

Warfarin therapy .If the patient is receiving continuous UFH, warfarin (Coumadin), an
oral anticoagulant, may be added. This anticoagulant drug overlap is necessary because
heparin and warfarin work differently. Warfarin works in the liver to inhibit synthesis of
the four vitamin K– dependent clotting factors and takes 3 to 4 days before it can exert
therapeutic anticoagulation. The heparin continues to provide therapeutic
anticoagulation until this effect is achieved. IV heparin is then discontinued. Patients
receiving LMWH are placed on the oral drug after the first dose.

According to the National Patient Safety Goals, therapeutic levels of warfarin must be
monitored by measuring the international normalized ratio (INR) at frequent intervals.
Because prothrombin times are often inconsistent and misleading, the INR was
developed. Most laboratories report both results. Most patients receiving warfarin
should have an INR between 1.5 and 2.0 to prevent future DVT and to minimize the risk
for stroke or hemorrhage (Pagana & Pagana, 2018). For patients with additional
cardiovascular problems or pulmonary embolus, the desired INR is higher, up to 3.5 or
4.0. The health care provider specifies the desired INR level to obtain. Be aware of the
critical value for INR according to agency policy (usually greater than 5). Notify the
health care provider immediately if your patient’s INR is at a critical value.

After obtaining the patient’s baseline INR, warfarin therapy should be started with low
doses and gradually titrated up according to the INR. Patients usually receive this drug
for at least 3 months or longer after an episode of DVT if no precipitating factors were
discovered, with recurrence, or if there are continuing risk factors.
Peripheral Venous Disease: Care Coordination
and Transition Management

Home care: Patients recovering from thrombophlebitis or DVT are ambulatory when they are
discharged from the hospital. The primary focus of planning for discharge is to educate the
patient and family about anticoagulation therapy. Patients who have experienced DVT may fear
recurrence of a thrombus. They may also be concerned about treatment with warfarin and the
risk for bleeding. Assure them that the prescribed treatment will help resolve this problem and
that ongoing assessment of prothrombin times and INR values decreases the risks for bleeding.

Self-management education: Teach patients recovering from DVT to stop smoking and avoid the
use of oral contraceptives to decrease the risk for recurrence. Alternative forms of birth control
may be used. Most patients are discharged on a regimen of warfarin (Coumadin) or low–
molecular-weight heparin (LMWH). Patients receiving subcutaneous LMWH injections at home
need instruction on self-injection (see the National Patient Safety Goals: Anticoagulants box).
Teach the appropriate caregiver and family members or friends, if necessary, to administer the
injections. Instruct patients and their families to avoid potentially traumatic situations, such as
participation in contact sports. Provide written and oral information about the signs and
symptoms of bleeding (see the Best Practice for Patient Safety & Quality Care: The Patient
Receiving Anticoagulant Therapy box). Reinforce the need to report any of these manifestations
to the primary health care provider immediately. The anticoagulant effect of warfarin may be
reversed by omitting one or two doses of the drug or by the administration of vitamin K. In case
of injury, teach patients to apply pressure to bleeding wounds and to seek medical assistance
immediately. Encourage them to carry an identification card or wear a medical alert bracelet
that states that they are taking warfarin or any other anticoagulant. Instruct patients to tell their
dentist and other health care providers that they are taking warfarin before receiving treatment
or prescriptions. Prothrombin times are affected by many prescription and over-the-counter
drugs such as NSAIDs. Teach patients to avoid high-fat and vitamin K– rich foods (see the Patient
and Family Education: Preparing for Self- Management: Food and Drugs That Interfere With
Warfarin [Coumadin] box). Remind them to drink adequate fluids to stay well hydrated, avoid
alcohol (which can cause dehydration), and avoid sitting for long periods

Evaluation: reflecting

Evaluate the care of the patient with VTE on the basis of the identified priority problem.
The expected outcome is that he or she:

• Remains free of injury associated with VTE complications such as pulmonary
embolism and bleeding associated with anticoagulation therapy.
Venous Insufficiency
Result of
prolonged venous
hypertension that
stretches veins
and damages
valves
Leg edema, stasis
dermatitis, stasis
ulcers
Nonsurgical
management
unless
complicated by
stasis ulcer
Surgical
management
Venous insufficiency occurs as a result of prolonged venous hypertension that stretches the veins and
damages the valves. Valvular damage can lead to a backup of blood and further venous hypertension,
resulting in edema and decreased tissue perfusion. With time, this stasis (stoppage) results in venous
stasis ulcers, swelling, and cellulitis. The veins cannot function properly when thrombosis occurs or
when valves are not working correctly. Venous hypertension can occur in people who stand or sit in one
position for long periods (e.g., teachers, office personnel). Obesity can also cause chronically distended
veins, which lead to damaged valves. Thrombus formation can contribute to valve destruction. Chronic
venous insufficiency also often occurs in patients who have had thrombophlebitis. In severe cases,
venous ulcers develop. Venous leg ulcers are a major cause of pain, death, and health care costs. Most
venous ulcer care is delivered in the community setting by home care nurses or through selfmanagement
Venous ulcers
Characteristics of Venous Ulcers

Usually located on medial malleolus

Tend to be superficial, infrequently painful

Irregular borders

Wet wounds, wound bed usually granular or yellow fibrous

Venous stasis ulcers are slightly more manageable than ulcers resulting from arterial disease.
They are chronic in nature, with some patients having the same ulcer for years. Ulcers often
heal, only to recur in the same area several years later. Two types of occlusive dressings are
used for venous stasis ulcers: oxygen-permeable dressings and oxygen-impermeable dressings.
Because the role of atmospheric oxygen in wound healing is controversial, opinions vary with
regard to which type of dressing is preferred. An oxygenpermeable polyethylene film and an
oxygen-impermeable hydrocolloid dressing (e.g., DuoDERM) are common. Hydrocolloid
dressings are left in place for a minimum of 3 to 5 days for best effect. Use medical aseptic
technique when changing dressings. If the wound is infected, use Contact Precautions in
addition to Standard Precautions. Artificial skin products can be used for difficult-to-heal venous
leg ulcers. These first-generation products are very expensive but are laying the foundation in
the field, with costs anticipated to come down in the future. Except for cultured epithelial
autografts, artificial skins are only temporary. Artificial skin serves as a biologic cover to secrete
growth factors to promote more growth factor secretion from the patient’s own skin to speed
the wound healing process. If the patient is ambulatory, an Unna boot may be used. An Unna
boot dressing is constructed of gauze that has been moistened with zinc oxide. Apply the boot
to the affected limb, from the toes to the knee, after the ulcer has been cleaned with normal
saline solution. It is then covered with an elastic wrap and hardens like a cast. This promotes
venous return and prevents stasis. The Unna boot also forms a sterile environment for the ulcer.
The health care provider changes the boot about once a week. Instruct the patient to report
increased pain, which indicates that the boot may be too tight. The primary health care provider
may prescribe topical agents, such as Accuzyme, to chemically débride the ulcer, eliminating
necrotic tissue and promoting healing. Remind patients that they may temporarily feel a burning
sensation when the agent is applied. If an infection or cellulitis develops, systemic antibiotics are
necessary. Surgery for chronic venous insufficiency is not usually performed because it is not
successful. Attempts s at transplanting vein valves have had limited success. Surgical
débridement of venous ulcers is similar to that performed for arterial ulcers.

The desired outcome for the patient with chronic venous insufficiency is to be managed in the
home. For patients with frequent acute complications and repeated hospital admissions, case
management can help meet appropriate clinical and cost outcomes. Help patients plan for
opportunities and facilities that allow for elevation of the lower extremities in and outside the
home. In addition, collaborate with the wound specialist to plan care of the ulcers at home. If
the primary health care provider prescribes graduated compression stockings, teach patients to
apply these stockings before they get out of bed in the morning and to remove them just before
going to bed at night. Also advise them that they will probably need to wear these stockings for
the rest of their lives. To improve circulation and aid in weight reduction, collaborate with the
physical therapist to prescribe an exercise program on an individual basis. Encourage all patients
to maintain an optimal weight and consult with the registered dietitian nutritionist to plan a
weight-reduction diet. Patients with venous stasis disease, especially those with venous stasis
ulcers, may require long-term emotional support to help them meet longterm needs. They may
also need help to cope with necessary lifestyle adjustments, such as possible changes in
occupation. Patients with venous stasis ulcers may need the assistance of a home care nurse to
perform dressing changes. Those with Unna boots need weekly transportation to their primary
health care provider for dressing changes. Collaborate with the case manager to arrange for a
sequential compression device (SCD) in the home if the primary health care provider prescribes
one.
Varicose Veins

Distended, protruding veins that appear darkened and tortuous

Treatment includes the three Es
-

Elastic compression hose

Exercise

Elevation
Varicose veins are distended, protruding veins that appear darkened and tortuous. They can
occur in anyone, but they are common in adults older than 30 years whose occupations require
prolonged standing or heavy physical activity. Varicose veins are also frequently seen in patients
with systemic problems (e.g., heart disease), obesity, high estrogen states, and a family history
of varicose veins. As the vein wall weakens and dilates, venous pressure increases, and the
valves become incompetent (defective), causing venous reflux. The incompetent valves enhance
the vessel dilation, and the veins become tortuous and distended. The severity of the disease
depends on the extent of the distention and reflux. Telangiectasias (spider veins) are dilated
intradermal veins less than 1 to 3 mm in diameter that are visible on the skin surface. Most
patients are not bothered by them but may consider them unattractive. Most telangiectasias do
not develop into the more severe varicose vein disease. More advanced disease causes venous
distention (bulging), edema, a feeling of fullness in the legs, and pruritus (itching). As a result,
signs and symptoms of venous insufficiency may occur, including venous stasis ulcers, brown
pigmentation from extravasated red blood cells (also called skin staining), and pain. Varicose
veins and reflux are diagnosed by simple or duplex ultrasonography.
The overall purpose of management for patients with varicose veins is to improve and maintain optimal
venous return to the heart and prevent disease progression. Conservative measures are the treatment
of choice, including the three Es: elastic compression hose, exercise, and elevation. Graduated
compression stockings (GCSs) rely on graduated external pressure to improve venous return by applying
pressure to the muscles. They are available in many grades or strengths, ranging from 8 to 50 mm Hg
pressure. Exercise increases venous return by helping the muscles pump blood back to the heart. Teach
patients to avoid high-impact exercises such as horseback riding and running. Daily walks and ankle
flexion exercises while sitting are common exercises that are helpful in promoting circulation. Elevating
the extremities as much as possible allows gravity to work with the valves in promoting venous return
and preventing reflux. Patients who continue to have pain or unsightly veins despite using the three Es
may opt for more invasive approaches. Surgical ligation and/or removal of veins (“stripping”) were the
procedures of choice for many years. Sclerotherapy to occlude the affected vessel is also an option.
However, newer, less-invasive treatments are more common today. They are less painful and have a
shorter recovery time. A common procedure is an endovenous ablation, which occludes the varicose
vein, most commonly the saphenous vein. Using ultrasound guidance, the clinician advances a catheter
into the vein and injects an anesthetic agent. Then the vessel is ablated (occluded) while the catheter is
slowly removed. After the procedure, teach the patient the importance of using a GCS or other form of
compression (such as elastic compression bandages) for 24 hours a day, except for showers, for at least
the first week. Follow-up ultrasonography ensures that the treated vein is closed. The patient is
monitored carefully for the first 6 to 8 weeks to determine how healing has progressed. Some patients
require continued use of the three Es for many years, depending on the severity of their disease. Assess
the affected limb for vascular status, including any changes in color or temperature of the leg. Monitor
for pain, edema, and paresthesias that could indicate complications such as DVT or nerve damage.
Nerve damage is usually temporary and minimal; it usually resolves within a few months (Wi