Cardiac System Notes
Dysrhythmias
Properties of Cardiac Cells
Term
Definition/Meaning/Significance
Automaticity
Ability to initiate an impulse spontaneously and continuously
Contractility
Ability to respond mechanically to an impulse
Conductivity
Ability to transmit an impulse along a membrane in an orderly manner
Excitability
Ability to be electrically stimulated
Nervous System Control of Heart
Function
Autonomic
 Rate of impulse formation
 Speed of conduction
 Strength of contraction
Parasympathetic
 Decreases rate
 Slows impulse conduction
 Decreases force of contraction
Sympathetic
 Increases rate
 Increases force of contraction
Electrical activity
P wave
PR segment
QRS complex
ST segment
T wave
QT
Isoelectric line
Represents
atrial depolarization
time taken for impulse to spread through atria
ventricular depolarization
end of depolarization and beginning of repolarization of ventricles
ventricular repolarization
time taken for entire electrical depolarization and repolarization of ventricles
baseline
Systematic approach to ECG interpretation
Step
How to
Regularity
• Is the rhythm regular?
• Print strip and measure R - R
• Is the rhythm irregular?
• Are there patterns to the irregularity?
• Any ectopic beats? Early? Late?
Rate
•
Count
•
•
•
•
the number of QRS complexes in 1 minute
the R-R intervals in 6 seconds, and multiply by 10
number of small squares between one R-R interval, and divide this number by 1 500
number of large squares between one R-R interval, and divide this number by 300
Number of R-R
intervals = 8
8 x 10 = 80 bpm
P waves
•
•
•
Are they present?
Upright
One for every QRS
Large squares
between R-R
interval
= ~3
= 300/3 = 100 bpm
Small squares
between R-R interval
= ~17
= 1500/17 = 88 bpm
•
Precedes the QRS
PR interval
•
•
•
Are they constant?
Normal measure 0.12-0.20 seconds
Short? Long?
QRS complex
•
•
•
Normal measure – 0.06-0.10 sec
Are they all the same configuration?
Any ectopic beats?
• Supraventricular – impulse begins above the AV node/ventricles (usually narrow QRS)
• Ventricular – impulse began below the AV node (wide QRS)
• BBB – bundle branch block
Rhythm
Normal Sinus
Rhythm
Rate
60-100 bpm
P Wave
Upright in Lead
II; one per QRS:
Uniform shape
PR Interval
0.12-0.20 sec;
constant
QRS Complex
0.06-0.10 sec
<12
Sinus Bradycardia
<60 bpm
Upright in Lead
II; one per QRS:
Uniform shape
0.12-0.20 sec;
constant
normal shape
and duration
<12
Sinus Tachycardia
101-160 bpm
Upright in Lead
II; one per QRS:
Uniform shape
0.12-0.20 sec;
constant
normal shape
and duration
<12
Premature Atrial
Contraction (PAC)
Can occur at
any rate
unable to be
measured
<12; QRS
absent after
nonconducted
PAC
Paroxysmal
Supraventricular
Tachycardia
161-250 bpm,
once in atrial
tach
Shaped
differently from
sinus Ps; often
hidden in
preceding T
wave
Shaped
differently from
sinus Ps but
same as each
other
unable to be
measured
<12
Atrial Flutter
251-350 bpm
None; flutter
unable to be
waves present
measured
(zigzag or
sawtooth waves)
normal shape
and duration
<12
Example
Atrial Fibrillation
350-700 bpm
None;
fibrillatory
waves present
(waviness of the
baseline)
unable to be
measured
normal shape
and duration
<12
Premature
Ventricular
Complex (PVC)
Can occur at
any rate
Usually none
unable to be
measured
<12; wide and
bizarre in shape
Ventricular
Tachycardia
100-250 bpm
Dissociated if
even present
unable to be
measured
<12; wide and
bizarre in shape
Ventricular
Fibrillation
Cannot be
counted
None
unable to be
measured
None; just a
wav baseline
that looks like
static
Asystole
Zero
None
None
none
Rhythm
Sinus
Bradycardia
Clinical Associations
Clinical Manifestations
• Occurs in response to
• Hypotension
• Carotid sinus
• Pale, cool skin
massage
• Weakness
• Valsalva’s maneuver
• Angina
• Hypothermia
• Dizziness or syncope
• Increased intraocular
• Confusion or
pressure
disorientation
• Increased vagal tone
• Shortness of breath
• Administration of
parasympathomimeti
c drugs
• Occurs in disease states
• Hypothyroidism
• Increased
intracranial pressure
• Obstructive jaundice
• Inferior wall MI
Sinus
Tachycardia
Associated with physiological and
psychological stressors:
• Exercise
• Fever
•
Dizziness, dyspnea, and
hypotension due to
decreased CO
Treatment
• Atropine
• Pacemaker may be required
Determined by underlying cause
• -adrenergic blockers to
reduce HR and myocardial
oxygen consumption
Premature Atrial
Contraction
(PAC)
Paroxysmal
Supraventricular
Tachycardia
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
Pain
Hypotension
Hypovolemia
Anemia
Hypoxia
Hypoglycemia
MI
Heart failure
Hyperthyroidism
Anxiety, fear
Can result from
• Emotional stress
• Physical fatigue
• Use of caffeine,
tobacco, alcohol
• Hypoxia
• Electrolyte
imbalances
• Hyperthyroidism
• COPD
• Heart disease
including CAD and
valvular disease
In a normal heart
• Overexertion, deep
inspiration
• Emotional stress
• Stimulants
Digitalis toxicity
Rheumatic heart disease
CAD
Cor pulmonale
•
Increased myocardial
oxygen consumption may
lead to angina
•
Isolated PACs are not
significant in those with
healthy hearts
In persons with heart
disease, may be warning
of more serious
dysrhythmia
•
•
•
•
•
Prolonged episode and HR
>180 bpm may precipitate
decreased CO
Hypotension
Dyspnea
Angina
•
•
Antipyretics to treat fever
Analgesics to treat pain
Depends on symptoms
• -adrenergic blockers may be
used to decrease PACs
• Reduce or eliminate caffeine
•
•
•
Vagal maneuvers: Valsalva,
coughing
IV adenosine
If vagal maneuvers and/or
drug therapy is ineffective
and/or client becomes
hemodynamically unstable,
DC cardioversion should be
used
Atrial Flutter
Atrial
Fibrillation
•
Usually occurs with
• CAD
• Hypertension
• Mitral valve
disorders
• Pulmonary embolus
• Chronic lung disease
• Cor pulmonale
• Cardiomyopathy
• Hyperthyroidism
• Drugs: digoxin,
quinidine,
epinephrine
•
Usually occurs with
underlying heart disease:
• Rheumatic heart
disease
• CAD
• Cardiomyopathy
• Hypertensive heart
disease
• HF
• Pericarditis
Often acutely caused by:
• Thyrotoxicosis
• Alcohol intoxication
• Caffeine use
• Electrolyte
disturbances
•
•
•
•
•
High ventricular rates
(>100) and loss of the
atrial “kick” can decrease
CO and precipitate HF,
angina
Risk for stroke due to risk
of thrombus formation in
the atria
Can result in decrease in
CO due to ineffective
atrial contractions (loss of
atrial kick) and rapid
ventricular response
Thrombi may form in the
atria as a result of blood
stasis
Embolus may develop and
travel to the brain, causing
a stroke
Primary goal is to slow ventricular
response by increasing AV block
• Drugs to slow HR: calcium
channel blockers, adrenergic blockers
• Electrical cardioversion may
be used to convert the atrial
flutter to sinus rhythm
emergently and electively
• Antidysrhythmic drugs (e.g.,
amiodarone, propafenone) to
convert atrial flutter to sinus
rhythm or to maintain sinus
rhythm
• Radiofrequency catheter
ablation can be curative
therapy for atrial flutter
• Goals:
• Decrease ventricular
rate.
• Prevent cerebral
embolic events
• Drugs for rate control:
calcium channel blockers
(e.g., diltiazem) and βadrenergic blockers (e.g.,
metoprolol)
• Long-term anticoagulation
therapy
• For some clients, conversion
to sinus rhythm may be
considered
•
•
Premature
Ventricular
Complex (PVC)
•
•
•
•
•
•
Stress
Cardiac surgery
Stimulants: caffeine,
alcohol, nicotine,
aminophylline, epinephrine,
isoproterenol and digoxin
Electrolyte imbalances
Hypoxia
Fever
Disease states: MI, mitral
valve prolapse, HF, CAD
•
•
•
Ventricular
Tachycardia
•
•
•
•
•
•
MI
CAD
Electrolyte imbalances
Cardiomyopathy
Mitral valve prolapses
Long QT syndrome
•
•
In normal heart, usually
benign
In heart disease, PVCs
may decrease CO and
precipitate angina and HF
if >10/minute
• Monitor client’s
response to PVCs
• PVCs often do not
generate a
sufficient
ventricular
contraction to
result in a
peripheral pulse
Represents ventricular
irritability
VT can be stable (client
has a pulse) or unstable
(client is pulseless)
Sustained VT: severe
decrease in CO
• Hypotension
•
•
•
Antidysrhythmic drugs
used for conversion:
amiodarone,
propafenone
• The nurse must
determine that the
client has had atrial
fibrillation or atrial
flutter for less than 48
hours
Based on cause of PVCs
• Oxygen therapy for
hypoxia
• Electrolyte
replacement
• Other treatment
according to
symptoms
Precipitating causes must be
identified and treated (e.g.,
electrolyte imbalances,
ischemia)
Monomorphic VT
•
•
•
•
Digitalis toxicity
Central nervous system
disorders
•
•
•
Pulmonary edema
Decreased cerebral
blood flow
• Cardiopulmonary
arrest
Treatment for VT must be
rapid
May recur if prophylactic
treatment is not initiated
Ventricular fibrillation
may develop
•
•
•
•
Hemodynamically
stable (present pulse)
+ preserved LV
function: IV
amiodarone
• Hemodynamically
unstable or poor LV
function: IV
amiodarone followed
by cardioversion
Polymorphic VT with a
normal baseline QT interval:
-adrenergic blockers,
amiodarone, or sotalol
• Cardioversion is used
if drug therapy is
ineffective
Polymorphic VT with a
prolonged baseline QT
interval: IV magnesium and
antitachycardia pacing
• Drugs that prolong the
QT interval should be
discontinued
• If the rhythm is not
converted,
cardioversion may be
needed
VT without a pulse is a lifethreatening situation
• Cardiopulmonary
resuscitation (CPR)
and rapid defibrillation
•
Ventricular
Fibrillation
•
•
•
Asystole
•
•
•
•
•
•
•
•
Pulseless
Electrical
Activity (PEA)
•
•
•
•
•
Acute MI, CAD,
cardiomyopathy
May occur during cardiac
pacing or cardiac
catheterization
May occur with coronary
reperfusion after fibrinolytic
therapy
Accidental electric shock
Hyperkalemia
Hypoxia
Acidosis
Drug toxicity
Advanced cardiac disease
Severe cardiac conduction
system disturbance
End-stage HF
•
Electrical activity can be
observed on the ECG, but
no mechanical activity of
the ventricles is evident, and
the client has no pulse
Prognosis is poor unless the
underlying cause is
identified and quickly
corrected
Hypovolemia
Hypoxia
Metabolic acidosis
•
•
•
•
Unresponsive, pulseless,
and apneic state
If not treated rapidly,
death will result
•
Unresponsive, pulseless,
and apneic state
Prognosis for asystole is
extremely poor
•
Unresponsive, pulseless,
and apneic state
•
•
•
•
Epinephrine if
defibrillation is
unsuccessful
Assessment of circulation,
airway, and breathing (CAB)
Immediate initiation of CPR
and advanced cardiac life
support (ACLS) measures
with the use of defibrillation
and definitive drug therapy
CPR with initiation of ACLS
measures (e.g., intubation,
transcutaneous pacing, IV
therapy with epinephrine and
atropine)
CPR followed by intubation
and IV epinephrine
Epinephrine 1 mg every 3–5
minutes
Treatment is directed toward
correction of the underlying
cause
•
Hyperkalemia or
hypokalemia
Hypothermia
Drug overdose
Cardiac tamponade
MI
Tension pneumothorax
Pulmonary embolus
•
•
•
•
•
•
Heart Failure
Terms
•
Pathophysiology
•
•
•
•
•
•
Cardiac output – measurement of blood pumped by each ventricle in 1 minute
• CO = SV x HR
Stroke volume – amount of blood ejected from the ventricle with the heartbeat
Preload – volume of blood in the ventricles at the end of diastole, before the next contraction
Afterload – peripheral resistance against which the LV must pump
When heart cannot maintain pumping capability
• Cardiac output or stroke volume decreases
• Less blood reaches the various organs
• Decreased cell function
• Fatigue and lethargy
• Mild acidosis develops
• Backup and congestion develop as coronary demands for oxygen and glucose are not met
• Output from ventricle is less than the inflow of blood
• Congestion in venous circulation draining into the affected side of the heart
Heart failure with preserved ejection fraction
• Impaired ability of the ventricles to relax and fill during diastole, resulting in decreased stroke
volume and CO
• Diagnosis based on the presence of heart failure symptoms and normal EF
Mixed heart failure
• Seen in disease states such as dilated cardiomyopathy (DCM)
• Poor EFs (<35%)
• High pulmonary pressures
•
•
•
Biventricular failure
• Both ventricles may be dilated and have poor filling and emptying capacity
Compensatory mechanisms are activated to maintain adequate CO
• Sympathetic nervous system (SNS) activation: first and least effective mechanism
• Release of catecholamines (epinephrine and norepinephrine)
• Increased heart rate (HR)
• Increased myocardial contractility
• Peripheral vasoconstriction
• Initially, increased HR and contractility improve CO
• Over time, these mechanisms are detrimental as they increase the workload of the
failing myocardium and the need for O2
• Neurohormonal responses: Kidneys release renin
• Renin converts angiotensinogen to angiotensin I
• Angiotensin I is converted to angiotensin II by a converting enzyme made in the lungs
• Angiotensin II causes
• Adrenal cortex to release aldosterone (sodium and water retention)
• Increased peripheral vasoconstriction (increases BP)
• Response is known as the renin–angiotensin–aldosterone system (RAAS)
• Neurohormonal responses
• Low CO causes a decrease in cerebral perfusion pressure
• Antidiuretic hormone (ADH) is secreted and causes
• increased water reabsorption in the renal tubules, leading to water retention and
increased blood volume
• Endothelin is stimulated by ADH, catecholamines, and angiotensin II, causing
• arterial vasoconstriction
• increase in cardiac contractility
• Hypertrophy
• Proinflammatory cytokines (e.g., tumour necrosis factor): released by cardiac myocytes
in response to cardiac injury
• Depression of cardiac function by causing cardiac hypertrophy, contractile dysfunction,
and death of myocytes
Consequences of compensatory mechanisms
• Dilation
•
Etiology
Enlargement of the chambers of the heart that occurs when pressure in the left ventricle is
elevated
• Initially an adaptive mechanism
• Eventually this mechanism becomes inadequate, and CO decreases
• Hypertrophy
• Increase in muscle mass and cardiac wall thickness in response to chronic dilation,
resulting in
• Poor contractility
• Higher O2 needs
• Poor coronary artery circulation
• Risk for ventricular dysrhythmias
• Counterregulatory processes
• Natriuretic peptides: atrial natriuretic peptide (ANP), b-type natriuretic peptide (BNP)
• Released in response to increase in atrial volume and ventricular pressure
• Promote venous and arterial vasodilation, reducing preload and afterload
• Chronic HF leads to a depletion of these factors
• Heart failure with reduced ejection fraction (most common)
• Caused by:
• Impaired contractile function (e.g., MI)
• Increased afterload (e.g., hypertension)
• Cardiomyopathy
• Mechanical abnormalities (e.g., valve disease)
• Heart failure with preserved ejection fraction
• Caused by
• Left ventricular hypertrophy from chronic hypertension
• Aortic stenosis
• Hypertrophic cardiomyopathy
Primary Causes
Precipitating Causes
Types of Heart
Failure
Clinical
Manifestations
•
Left-sided HF (most common) from left ventricular dysfunction (e.g., MI hypertension, CAD,
cardiomyopathy)
• Backup of blood into the left atrium and pulmonary veins causes pulmonary congestion
• Dyspnea and orthopnea
• Develops as fluid accumulates in the lungs
• Cough
• Associated with fluid irritating the respiratory passages
• Paroxysmal nocturnal dyspnea
• Indicates the presence of acute pulmonary edema
• Usually develops during sleep
• Excess fluid in lungs frequently leads to infections such as pneumonia
• Right-sided HF from left-sided HF, cor pulmonale, right ventricular MI
• Backup of blood into the right atrium and venous systemic circulation
• Jugular venous distension
• Hepatomegaly, splenomegaly
• Vascular congestion of GI tract
• Peripheral edema
Acute Decompensated Heart Failure (ADHF)
• Pulmonary edema, often life-threatening
• Early
• Increase in the respiratory rate
Diagnostic
Studies
• Decrease in PaO2
• Later
• Tachypnea
• Respiratory acidemia
• Physical findings
• Orthopnea
• Dyspnea, tachypnea
• Use of accessory muscles
• Cyanosis
• Cool and clammy skin
• Cough with frothy, blood-tinged sputum
• Breath sounds: crackles, wheezes, rhonchi
• Tachycardia
• Hypotension or hypertension
Chronic HF
• Fatigue
• Dyspnea, orthopnea, paroxysmal nocturnal dyspnea
• Persistent, dry cough, unrelieved with position change or over-the-counter cough suppressants
• Tachycardia
• Dependent edema
• Edema may be pitting in nature
• Sudden weight gain of >2 kg (4 lb) in 2 days may indicate an exacerbation of HF
• Nocturia
• Skin
• Dusky, cool, damp to touch
• Lower extremities: shiny and swollen, diminished or absent hair growth, pigment changes
• Restlessness, confusion, decreased memory
• Chest pain (angina)
• Weight changes
• Anorexia, nausea
• Fluid retention
• Primary goal: Determine and treat underlying cause
• History and physical examination
Nursing and
Collaborative
Management
•
• Chest x-ray
• ECG
• Lab studies (e.g., cardiac enzymes, BNP)
• Hemodynamic assessment
• Echocardiogram
• Stress testing
• Cardiac catheterization
• Ejection fraction
Overall goals of therapy for ADHF and chronic HF
• Decrease client symptoms
• Improve LV function
• Reverse ventricular remodeling
• Improve quality of life
• Decrease mortality and morbidity
ADHF
• Decrease intravascular volume
• Reduces venous return and preload
• Loop diuretics (e.g., furosemide)
• Ultrafiltration or aquapheresis
• Decrease venous return (preload)
• Reduces the amount of volume returned to the LV during diastole
• High Fowler’s position
• IV nitroglycerin
• Decrease afterload
• Improves CO and decreases pulmonary congestion
• Careful monitoring of vital signs is crucial
• Improve gas exchange and oxygenation
• Supplemental oxygen
• Morphine sulphate
• Noninvasive ventilatory support (BiPAP)
• Improve cardiac function
• For clients who do not respond to conventional pharmacotherapy (e.g., diuretics, vasodilators,
morphine sulphate)
•
Inotropic therapy
• Dobutamine, milrinone
• Hemodynamic monitoring
• Reduce anxiety
• Distraction, imagery
• Sedative medications (e.g., morphine sulphate)
Chronic HF
• Main treatment goals
• Treat the underlying cause and contributing factors
• Maximize CO
• Provide treatment to alleviate symptoms
• Improve ventricular function
• Improve quality of life
• Preserve target organ function
• Improve mortality and morbidity
• Oxygen administration
• Self-management teaching
• Exercise and activity
• Devices
• Cardiac resynchronization therapy (CRT) or biventricular pacing
• Implantable cardioverter defibrillator
• Nonpharmacological therapies
• Mechanical circulatory support
• Intra-aortic balloon pump (IABP)
• Extra-corporeal Membrane Oxygenation (ECMO)
• Ventricular assist device (VAD)
• Therapeutic goals for drug therapy
• Identification of type of HF and causes
• Correction of sodium and water retention and volume overload
• Reduction of cardiac workload
• Improvement of myocardial contractility
• Control of precipitating and complicating factors
• Drug therapy
•
•
•
•
•
Diuretics
• Thiazide
• Loop
• ACE inhibitors
• Neprilysin inhibitors
• -Adrenergic blockers
• Positive inotropic agents
• Dobutamine and milrinone are the two most commonly used agents
Nutritional therapy
• Diet education and weight management: Individualize recommendations and consider cultural
background
• Recommend Dietary Approaches to Stop Hypertension (DASH) diet
• Sodium is usually restricted to 2 g per day
• Fluid restriction not generally required
• Daily weights are important
• Same time, same clothing each day
• Weight gain of 2 kg (4 lb) over 2 days or a 2.5 kg (5-lb) gain over a week should be reported to
health care provider
Assessment
• Subjective data
• Past health history
• Functional health patterns
• Medications
• Objective data
• Physical examination
Nursing diagnoses
• Decreased cardiac output
• Excess fluid volume
• Impaired gas exchange
• Activity intolerance
Planning: Overall goals
• Decrease in symptoms (e.g., shortness of breath, fatigue)
• Decrease in peripheral edema
•
•
•
Complications
•
•
•
•
•
• Increase in exercise tolerance
• Adherence to drug regimen
• No complications related to HF
Implementation: Client education
• Medications (lifelong)
• Taking pulse rate
• Know when drugs (e.g., digitalis, -adrenergic blockers) should be withheld and reported
to health care provider
Implementation: Client and caregiver education
• Home BP monitoring
• Signs of hypokalemia and hyperkalemia if taking diuretics that deplete or spare potassium
• Instruct client in energy-conserving and energy-efficient behaviours
Evaluation
• Respiratory status
• Fluid balance
• Activity tolerance
• Anxiety control
• Knowledge of disease process
Pleural effusion
Dysrhythmias
• Promotes thrombus/embolus formation, increasing risk for stroke
• Treatment can include rate control, cardioversion, antidysrhythmic, and/or systemic
anticoagulation
Left ventricular thrombus
HF can lead to severe hepatomegaly
Renal insufficiency or failure
Obstructive pulmonary disease
Description
Asthma
• Asthma is a chronic inflammatory
lung disorder of the airways that
COPD
• Chronic obstructive pulmonary disease (COPD) is a
preventable and treatable disease state characterized by
airflow limitation that is not fully reversible
•
Etiology
•
results in recurrent episodes of airflow
obstruction, but is usually reversible
Inflammation causes varying degrees
of obstruction in the airways, which
leads to recurrent episodes of:
• Wheezing
• Breathlessness
• Sensation of chest tightness
• Cough, particularly at night
and in the early morning
•
Although the exact mechanisms that
cause airway hyper-responsiveness
and inflammation remain unknown,
multiple triggers are involved:
• Allergens
• Exercise
• Respiratory infections
• Nose and sinus problems
• Drugs and food additives
• Cold, dry air
• Stress
• Hormones, menses
• GERD
• Occupational exposure
•
•
•
The airflow limitation is usually progressive and
associated with an abnormal inflammatory response of
the lungs to noxious particles or gases, primarily caused
by cigarette smoking
Airflow limitation not fully reversible
• Usually progressive
• Abnormal inflammatory response of airway and
lungs to noxious particles or gases
COPD patients display characteristics of
• Chronic bronchitis
• Emphysema
Risk factors
• Cigarette smoking
• Occupational chemicals and dust
• Air pollution
• Infection
• Heredity
• Aging
Cigarette Smoking
• Clinically significant airway obstruction develops in
15% to 20% of smokers.
• 80% to 90% of COPD cases related to tobacco smoking.
• Effects of nicotine
• Stimulates sympathetic nervous system
• Increases HR
• Causes peripheral vasoconstriction
• Increases BP and cardiac workload
• Compounds problems in CAD
• Effects on respiratory tract
• Increased production of mucus
• Hyperplasia of goblet cells
• Lost or decreased ciliary activity
•
Carbon monoxide
• ↓ O2 carrying capacity
• ↑ Heart rate
• Impaired psychomotor performance and
judgement
• Passive smoking (second-hand smoke)
• ↓ Pulmonary function
• ↑ Risk of lung cancer
• ↑ Rates of mortality from ischemic heart disease
Environmental
• COPD can develop with intense or prolonged exposure
to
• Dusts, vapours, irritants, or fumes.
• High levels of air pollution.
Infection
• Recurring infections impair normal defense mechanisms.
• Risk factor for COPD
• Intensify pathological destruction of lung tissue
• HIV infection
• TB is a risk factor
Hereditary
• -Antitrypsin (AAT) deficiency
• Genetic risk factor for COPD
• Severe AAT deficiency occurs in 1 in 5000–1 in
5500 of Canadian and North American
population.
Aging
• Some degree of the same symptoms of emphysema is
common because of physiological changes of aging lung
tissue.
• Aging results in changes in the lung structure and
respiratory muscles that cause a gradual loss of the
•
Pathophysiology
•
•
•
•
•
The hallmarks of asthma are airway
inflammation and airway hyperresponsiveness.
The degree of bronchoconstriction is
related to the degrees of airway
inflammation, airway hyperresponsiveness, and exposure to
endogenous and exogenous triggers
(e.g., infections, allergens, histamine,
and other cell mediators).
Exposure to allergens or irritants
initiates an inflammatory cascade
involving multiple cell types,
mediators, and chemokines.
Typically, there are two possible types
of asthmatic responses to stimuli: an
early-phase response and a late-phase
response.
Early-phase response is characterized
by bronchospasm.
• Increased mucus secretion,
edema formation, and
increased amounts of tenacious
sputum  cause wheeze,
cough, sensation of chest
tightness, shortness of breath
or a combination
• Peaks in 30–60 minutes after
trigger exposure
•
•
•
•
elastic recoil of the lung – as a result, the lungs become
smaller and stiffer
The number of functional alveoli decreases as a result of
the loss of the alveolar supporting structures
Defining features
• Irreversible airflow limitations during forced
exhalation due to loss of elastic recoil
• Airflow obstruction due to mucus hypersecretion,
mucosal edema, and bronchospasm
Primary process is inflammation.
• Inhalation of noxious particles
• Mediators released cause damage to lung tissue
• Airways inflamed
• Parenchyma destroyed
Supporting structures of lungs are destroyed.
• Air goes in easily but remains in the lungs.
• Bronchioles tend to collapse.
• Causes barrel-chest look.
Common characteristics
• Mucous hypersecretion
• Dysfunction of cilia
• Hyperinflation of lungs
• Gas exchange abnormalities
•
•
Clinical
manifestations
•
•
•
Subsides in about 30–90
minutes
Late-phase response can be more
severe than the early-phase response
and is primarily inflammation.
• Peaks in 5–12 hours
• May last several hours to days
• Corticosteroids are effective in
preventing and reversing this
cycle.
• If airway inflammation is not
treated or does not resolve, it
may lead to irreversible lung
damage.
Unpredictable and variable
• Recurrent episodes of
wheezing, breathlessness,
cough, and tight chest
• Particularly at night or early
morning (0200–0500 hours)
• May be abrupt or gradual
• Lasts minutes to hours
Expiration may be prolonged.
• Inspiration-expiration ratio of
1:2 prolonged to 1:3 or 1:4
• Bronchospasm, edema, and
mucus in bronchioles narrow
the airways
• Air takes longer to move out
Wheezing is unreliable to gauge
severity.
•
•
•
•
•
•
•
•
Develops slowly
Diagnosis is considered with
• Cough.
• Sputum production.
• Dyspnea.
• Exposure to risk factors.
Dyspnea usually prompts medical attention.
• Occurs with exertion in early stages
• Present at rest with advanced disease
Causes chest breathing
• Use of accessory and intercostal muscles
• Inefficient
Characteristically underweight with adequate caloric
intake
Anorexia
Chronic fatigue
Physical examination findings
• Prolonged expiratory phase
•
•
•
•
Complications
•
Severe attacks may have no
audible wheezing.
• Usually begins upon
exhalation
• “Silent chest”
Cough variant asthma
• Cough is the only symptom.
• Bronchospasm is not severe
enough to cause airflow
obstruction.
Difficulty with air movement
• Client may feel increasingly
anxious
An acute attack usually reveals signs
of hypoxemia.
• Restlessness
• ↑ anxiety
• Inappropriate behaviour
• ↑ pulse and blood pressure
• Pulsus paradoxus (drop in
systolic BP during inspiratory
cycle >10 mm Hg)
• Respiratory rate > 30
breaths/minute
• Difficulty speaking in full
sentences
• Percussion reveals hyperresonance
Severe acute attack
• Common causes of severe
acute attacks include viral
illnesses, ingestion of Aspirin
•
• Wheezes
• Decreased breath sounds
• ↑ Anterior–posterior diameter
Bluish-red colour of skin
• Polycythemia and cyanosis
Cor pulmonale
• Hypertrophy of right side of heart
• Result of pulmonary hypertension
•
•
•
or other NSAIDs, increases in
environmental pollutants or
other allergen exposure, and
discontinuation of drug
therapy.
Clinical manifestations are
similar to those of non-severe
asthma but are more serious
and prolonged.
Complications may include
pneumothorax,
pneumomediastinum, acute cor
pulmonale with right
ventricular failure, and severe
respiratory muscle fatigue that
leads to respiratory arrest
Respiratory arrest can be fatal.
•
Late manifestation of chronic pulmonary heart
disease
• Eventually causes right-sided heart failure
• Dyspnea
• Distended neck veins
• Hepatomegaly with right upper quadrant tenderness
• Peripheral edema
• Weight gain
• Ascites
• Epigastric distress
Exacerbations of COPD
• Sustained worsening of symptoms
• Signaled by change in usual
• Dyspnea
• Cough
• Sputum
• Associated with poorer outcomes
• Primary causes
• Infection
• Noninfectious causes: Air pollution, allergens,
irritants, cold air
Acute respiratory failure
•
Caused by
• Exacerbations
• Cor pulmonale
• Discontinuing bronchodilator or corticosteroid
medication
• Indiscriminate use of sedatives and opioids
• Surgery or severe, painful illness involving chest
or abdomen
Peptic ulcer disease
Depression/anxiety
•
•
Diagnostic
studies
•
•
•
•
•
•
•
•
•
Detailed history and physical exam
Pulmonary function tests
Peak flow monitoring
Chest x-ray
ABGs
Oximetry
Allergy testing
Blood levels of eosinophils
Sputum culture and sensitivity
•
•
•
•
Collaborative
care
•
•
•
•
•
•
•
Establishment of a confirmed
diagnosis through the use of objective
measures
Development of a partnership between
health care providers and the patients
and families affected by asthma
Limited exposure to triggers
Education of patients
Appropriate pharmacotherapy
Continuous assessment and
monitoring of asthma control and
severity
Implementation of a written action
plan
•
•
•
•
Approximately 40% of COPD clients experience
depression.
If client becomes anxious because of dyspnea, teach
pursed-lip breathing.
Diagnosis confirmed by pulmonary function tests
• Chest x-rays, spirometry, history, and physical
examination are also important in the diagnostic
workup.
Spirometry typical findings
• Reduced FEV1/FVC ratio
• Increased residual volume
ABG typical findings
• Low PaO2
• ↑ PaCO2
• ↓ pH
• ↑ Bicarbonate level found in late stages of COPD
Walk test (6 min.) to determine O2 desaturation in the
blood with exercise
ECG can show signs of right ventricular failure.
Primary goals of care
• Prevent progression.
• Reduce frequency and severity of exacerbations.
• Alleviate breathlessness.
• Improve exercise tolerance and daily activity.
• Treat exacerbations and complications.
• Improve quality of life and reduce mortality risk.
Smoking cessation
• Most effective intervention
• Accelerated decline in pulmonary function slows
and usually improves.
Drug therapy
• Bronchodilators
• Relax smooth muscle in the airway
•
•
•
•
•
•
•
Ensuring regular follow-up.
Medications are divided into two
general classifications:
• Relievers (“rescue”
medications used intermittently
as required to ease asthma
symptoms)
• Controllers (maintenance
therapy used on a daily basis,
typically twice a day).
Teach proper technique
Use metered-dose inhaler (MDI) with
spacer to facilitate uptake of
medication
Acute asthma episode
• Often come to ED
• Respiratory distress
• Treatment depends upon
severity and response to
therapy.
• Severity measured with
flow rates
• Oral corticosteroids
• Therapy may be started and
monitored with pulse oximetry
or ABGs in severe cases
Most therapeutic measures are the
same as for acute episode.
• ↑ in frequency and dose of
bronchodilators
• May require mechanical
ventilation
Severe attack
•
•
•
•
•
•
Reduces airway resistance and dynamic
hyperinflation of the lungs
• Improve ventilation of the lungs
• ↓ Dyspnea and ↑ FEV1
• Inhaled route is preferred.
• Commonly used bronchodilators
• β2-Adrenergic agonists
• Anticholinergics
• Methylxanthines
• Long-acting anticholinergic
• Tiotropium (Spiriva)
• Inhaled corticosteroid therapy
• Used for moderate to severe cases
O2 therapy is used to
• reduce work of breathing.
• maintain PaO2.
• reduce workload on the heart.
Long-term O2 therapy improves
• survival.
• exercise capacity.
• cognitive performance.
• sleep in hypoxemic clients.
O2 delivery systems are high or low flow.
• Low flow is most common.
• Low flow is mixed with room air, and delivery is
less precise than high flow.
Humidification
• Used because O2 has a drying effect on the
mucosa
• Supplied by nebulizers, vapotherm, and bubblethrough humidifiers
Complications of oxygen therapy
• Combustion
•
•
•
•
IV corticosteroids are
administered every 4–6 hours,
then are given orally.
Continuous monitoring of
client is critical
Supplemental O2 is given by
mask or nasal cannula for 90%
O2 saturation.
• Arterial catheter may
be used to facilitate
frequent ABG
monitoring
IV fluids are given because of
insensible loss of fluids.
•
•
•
• CO2 narcosis
• O2 toxicity
• Absorption atelectasis
• Infection
Chronic O2 therapy at home improves
• Prognosis.
• Mental acuity.
• Exercise tolerance
• Hematocrit.
• Pulmonary hypertension.
Surgical therapy
• Lung volume reduction surgery
• Remove diseased lung to enhance
performance of remaining tissue
• Lung transplantation
• Single lung—most common because of
donor shortages
• Prolongs life
• Improves functional capacity
• Enhances quality of life
Breathing exercises
• Decreases dyspnea, improves oxygenation, and
slows respiratory rate
• Pursed-lip breathing
• Prolongs exhalation and prevents
bronchiolar collapse and air
trapping
• Diaphragmatic breathing
• Focuses on using the diaphragm
instead of accessory muscles to
achieve maximum inhalation and
to slow the respiratory rate
•
•
•
Lack of evidence to support or
refute this practice
Effective coughing
• Main goals
• Conserve energy
• Reduce fatigue
• Facilitate removal of secretions
Nutritional therapy
• Weight loss and malnutrition are common among
those with COPD.
• Body mass index (BMI) between 21 and
25 kg/m2
• Rest (30 min.) before eating
• Use a bronchodilator before meals.
• 5–6 small meals a day
• 1.2–1.3 times normal kilocalorie requirements to
maintain weight
• High-calorie, high-protein diet
• 2–3 L fluid intake per day, taken between meals
• Cold foods may cause less fullness than hot
foods.
• Avoid
• Foods that require a great deal of chewing
• Exercises and treatments 1 hour before
and after eating
• Gas-forming foods
Hypertension
Hypertension
•
description
Persistent elevation
of
•
Syst
olic
blo
od
pres
sure
Etiology and pathophysiology
Clinical manifestations
complications
Diagnostic studies
Nursing management
•
•
Isolated systolic hypertension
≥14
0
mm
Hg
or
Dia
stoli
c
blo
od
pres
sure
≥90
mm
Hg
or
Cur
rent
use
of
anti
hyp
erte
nsiv
e
med
icati
on(s
)
•
•
Primary hypertension
•
•
Sustained
elevation of
SBP ≥ 140
mm Hg and
a DBP < 90
mm Hg
Common in
older adults
related to
loss of
elasticity in
large arteries
90% to 95%
of clients
Elevated BP
without an
identified
cause
•
•
T
h
e
r
e
c
o
u
l
d
b
e
s
e
v
e
r
a
l
c
o
n
t
r
Contributing
factors
•
•
•
↑
S
N
S
a
c
t
i
v
i
t
y
↑
S
o
d
i
u
m
r
e
t
a
i
n
i
n
•
•
Hypertension is a
silent disease.
Frequently it is
asymptomatic until
it becomes severe
and target-organ
disease has
occurred.
Secondary
symptoms with
severe hypertension
include fatigue,
reduced activity
tolerance, dizziness,
palpitations, angina,
and dyspnea.
•
Hypertensive
heart disease
•
•
•
•
C
o
r
o
n
a
r
y
a
r
t
e
r
y
d
i
s
e
a
s
e
L
e
f
t
v
e
n
•
•
•
Urinalysis
Blood
chemistry
(potassium
, sodium,
blood
urea, and
creatinine)
Fasting
blood
glucose
Fasting
total
cholesterol
and highdensity
lipoprotein
cholesterol
, lowdensity
lipoprotein
cholesterol
, and
triglycerid
es
Standard
12-lead
electrocar
diography
•
•
•
Risk stratification
Lifestyle modifications
•
Nutritional
therapy
•
Weight
reduction
•
Modification in
alcohol
consumption
•
Physical
activity
•
Avoidance of
tobacco
products
•
Stress
management
Nursing assessment
•
Subjective data
•
I
m
p
o
r
t
a
n
t
h
e
a
i
b
u
t
i
n
g
f
a
c
t
o
r
s
•
Focus on
primary
related to
prevalence in
clinical
practice
•
•
•
g
h
o
r
m
o
n
e
s
a
n
d
v
a
s
o
c
o
n
s
t
r
i
c
t
o
r
s
↑
S
o
d
i
u
m
i
n
t
a
k
e
D
i
a
b
e
t
e
s
m
e
l
l
i
t
u
s
>
I
d
e
a
l
b
o
d
y
w
e
i
g
h
t
•
•
•
•
t
r
i
c
u
l
a
r
h
y
p
e
r
t
r
o
p
h
y
•
H
e
a
r
t
f
a
i
l
u
r
e
Cerebro-vascular
disease
Peripheral
vascular disease
Nephrosclerosis
Retinal damage
•
•
•
•
•
Assess
urinary
albumin
excretion
in clients
with
diabetes
All clients
with
treated
hypertensi
on need to
be
monitored
for the
appearanc
e of
diabetes
Ambulator
y blood
pressure
monitorin
g
Useful in
the
diagnosis
of
uncomplic
ated mildtomoderate
hypertensi
on
Helpful in
clients
with
suspected
white coat
hypertensi
on,
masked
hypertensi
on,
apparent
drug
resistance,
hypotensiv
e
symptoms
with
hypertensi
ve
medicatio
ns,
episodic
hypertensi
on, or
autonomic
nervous
system
dysfunctio
n
.
•
l
t
h
i
n
f
o
r
m
a
t
i
o
n
S
y
m
p
t
o
m
s
:
D
y
s
p
n
e
a
,
f
a
t
i
g
u
e
,
i
n
t
e
r
m
i
t
t
e
n
t
c
l
a
u
d
i
c
a
t
i
o
n
,
n
o
c
t
u
r
i
a
,
•
Risk factors
•
•
•
•
•
•
•
•
•
•
•
•
•
Patho
•
•
•
•
•
•
•
Advancing age
Family history
Heavy alcohol consumption
Obesity
Cigarette smoking
Ethnicity
Diabetes mellitus
Sedentary lifestyle
Elevated serum lipids
Socioeconomic status
High dietary sodium
Psychosocial stress
Gender
Genes
Sodium and water retention
Altered renin–angiotensinaldosterone mechanism
Stress and increased
sympathetic nervous system
activity
Insulin resistance and
hyperinsulinemia
Endothelial cell dysfunction
Obesity
E
x
c
e
s
s
i
v
e
a
l
c
o
h
o
l
i
n
t
a
k
e
d
i
z
z
i
n
e
s
s
,
e
r
e
c
t
i
l
e
d
y
s
f
u
n
c
t
i
o
n
•
Objective data
•
C
a
r
d
i
o
v
a
s
c
u
l
a
r
:
B
P
,
p
u
l
s
e
•
M
u
s
c
u
l
o
s
k
e
l
e
t
a
l
:
T
r
u
•
•
•
•
•
Nursing diagnoses
Planning
Overall goals
•
Achieve and
maintain target
BP.
•
Understand and
implement
therapeutic
plan.
•
Minimal or no
unpleasant
adverse effects
n
c
a
l
o
b
e
s
i
t
y
N
e
u
r
o
l
o
g
i
c
a
l
:
M
e
n
t
a
l
s
t
a
t
u
s
c
h
a
n
g
e
s
P
o
s
s
i
b
l
e
f
i
n
d
i
n
g
s
•
•
Confident of
ability to
manage and
cope with
condition
Nursing implementation
•
Health
promotion
•
•
•
I
n
d
i
v
i
d
u
a
l
c
l
i
e
n
t
e
v
a
l
u
a
t
i
o
n
S
c
r
e
e
n
i
n
g
p
r
o
g
r
a
m
s
C
a
r
d
i
o
v
a
s
c
u
l
a
r
r
i
s
k
f
a
c
t
o
r
m
o
d
i
f
i
c
a
t
i
o
n
•
Ambulatory
and home care
•
P
h
y
s
i
c
a
l
a
c
t
i
v
i
t
y
•
H
o
m
e
b
l
o
o
d
p
r
e
s
s
u
r
e
m
o
n
i
t
o
r
i
n
g
•
C
l
i
e
n
t
a
d
h
e
r
e
n
c
e
•
Secondary hypertension
•
5% to 10%
in adults;
>80% in
children
Many causes; treatment aimed at eliminating
the underlying cause
•
Causes
•
•
•
•
•
•
•
Hypertensive crisis
•
•
•
Severe, abrupt increase in
DBP (defined as >120–130
mm Hg)
Rate of increase in BP is
more important than the
absolute value.
Often occurs in clients with a
history of hypertension who
have failed to comply with
medications or who have
been undermedicated
Evaluation
Coarctation or
congenital
narrowing of
the aorta
Renal disease
such as renal
artery stenosis
and
parenchymal
disease
Endocrine
disorders such
as
pheochromocyt
oma, Cushing’s
syndrome, and
hyperaldosteron
ism
Neurological
disorders such
as brain
tumours,
quadriplegia,
and head injury
Sleep apnea
Medications
Pregnancyinduced
hypertension
•
Hypertensive
emergency =
evidence of acute
target organ damage
•
Hy
pert
ensi
ve
enc
eph
alo
pat
hy,
cere
bral
he
mor
rha
ge
•
Acu
te
ren
al
fail
ure
•
My
oca
rdia
l
infa
rcti
on
•
Acu
te
left
ven
tric
ular
•
•
•
•
•
IV drug
therapy: titrated
to mean arterial
pressure
Monitor cardiac
and renal
function
Neurological
checks
Determine
cause
Education to
avoid future
crises
•
fail
ure
wit
h
pul
mo
nar
y
ede
ma
Dis
sect
ing
aort
ic
ane
ury
sm
Coronary artery disease
Coronary
Artery
Disease
Description
Atherosclerosis: type of blood vessel
disorder
Begins as soft deposits of fat that
harden with age
Referred to as “hardening of arteries”
Can occur in any artery in the body
Atheromas (fatty deposits)
Preference for the coronary arteries
Etiology & Pathophysiology
Atherosclerosis is the major cause of CAD.
Characterized by a focal deposit of lipids, primarily
within the intimal wall of the artery
Endothelial lining altered as a result of inflammation
and injury.
C-reactive protein (CRP)
Nonspecific marker of inflammation
Increased in many clients with CAD
Chronic elevation of CRP is associated with unstable
plaques and oxidation of LDL cholesterol
Developmental stages: fatty streaks
Earliest lesions
Characterized by lipid-filled smooth muscle cells
Potentially reversible
Developmental stages: fibrous plaque
Beginning of progressive changes in the arterial wall
Lipoproteins transport cholesterol and other lipids into
the arterial intima.
Fatty streak is covered by collagen, forming a fibrous
plaque that appears grayish or whitish.
Result = narrowing of vessel lumen
Developmental stages: complicated lesion
Continued inflammation can result in plaque instability,
ulceration, and rupture.
Risk Factors
Nonmodifiable Risk Factors
•
Age
•
Gender
•
Ethnicity
•
Family history
•
Genetic
predisposition
Modifiable risk factors
•
Elevated serum
lipids
•
Hypertension
•
Tobacco use
•
Physical inactivity
•
Obesity
Modifiable Contributing Risk
Factors
•
Diabetes
•
Metabolic
syndrome
•
Psychological states
•
Homocysteine level
•
Substance use
Health Promotion / Healing process
•
Identification of people at high risk
•
Health history, including use of
prescription/nonprescription
medications
•
Presence of cardiovascular
symptoms
•
Environmental patterns: diet,
activity
•
Psychosocial history
•
Values and beliefs about health
and illness
•
Health-promoting behaviours
•
Physical fitness
•
FITT formula: 30
minutes on most days
of the week
•
Regular physical
activity contributes to
•
weight
reduction.
•
reduction of
systolic BP.
•
in some men
more than
women,
increase in
HDL
cholesterol.
•
•
Platelets accumulate and thrombus forms.
Increased narrowing or total occlusion of lumen
Collateral circulation
Normally, some arterial anastomoses
(or connections) exist within the coronary circulation.
Growth and extent of collateral circulation are
attributed to two factors.
•
Inherited predisposition to develop
new vessels (angiogenesis)
•
Presence of chronic ischemia
When occlusion of the coronary arteries occurs slowly
over a long period, the chance that adequate collateral
circulation will develop is greater.
Acute
Coronary
Syndrome
•
•
When ischemia is prolonged
and is not immediately
reversible, acute coronary
syndrome (ACS) develops.
ACS encompasses
•
Unstable angina
(UA)
•
Non–ST-segmentelevation
myocardial
infarction
(NSTEMI)
•
ST-segmentelevation MI
(STEMI)
Deterioration of once-stable plaque -> Rupture ->
Platelet aggregation -> Thrombus
•
•
•
Result
Partial occlusion of coronary artery: UA or NSTEMI
Total occlusion of coronary artery: STEMI
•
•
•
•
•
•
Health education in schools
Nutritional therapy
•
Therapeutic lifestyle
changes
•
Omega-3 fatty acids
Health-promoting behaviours
•
Cholesterol-lowering drug
therapy
•
Drugs that restrict
lipoprotein production:
statins
•
Drugs that increase
lipoprotein removal:
bile acid sequestrants
•
Drugs that decrease
cholesterol absorption:
Ezetimibe (Ezetrol)
•
Antiplatelet therapy
•
ASA
•
Clopidogrel (Plavix)
Within 24 hours, leukocytes infiltrate the
area of cell death.
Enzymes are released from the dead cardiac
cells (important indicators of MI).
Proteolytic enzymes of neutrophils and
macrophages remove all necrotic tissue by
second or third day.
Development of collateral circulation
improves areas of poor perfusion.
Necrotic zone is identifiable by ECG
changes and nuclear scanning.
10–14 days after MI, scar tissue is still
weak and vulnerable to stress.
By 6 weeks after MI, scar tissue has
replaced necrotic tissue.
•
Area is said to be healed, but less
compliant.
Ventricular remodelling
•
Normal myocardium will
hypertrophy and dilate in an
attempt to compensate for the
infarcted muscle.
Sudden
Cardiac
Death
•
•
Unexpected death from
cardiac causes
Rapid CPR, defibrillation
with AED, and early
advanced cardiac life support
increase survival rates.
•
•
•
•
Syncope
•
Brief lapse in consciousness
accompanied by a loss in
postural tone (fainting)
•
•
Abrupt disruption in cardiac function,
resulting in loss of CO and cerebral blood
flow
Death usually within 1 hour of onset of acute
symptoms (e.g., angina, palpitations)
Most SCDs are caused by ventricular
dysrhythmias (e.g., ventricular tachycardia).
SCD occurs less commonly as a result of LV
outflow obstruction (e.g., aortic stenosis).
Primary risk factors
•
Left ventricular
dysfunction
•
Ventricular
dysrhythmias
following MI
•
•
•
•
•
•
•
•
•
Diagnostic workup to rule out or confirm
MI
•
Cardiac markers
•
ECG
Cardiac catheterization
PCI or CABG
24-hour Holter monitoring
Exercise stress testing
Signal-averaged ECG
Electrophysiologic study (EPS)
Implantable cardioverter-defibrillator (ICD)
Psychosocial adaptation
•
“Brush with death”
•
“Time bomb” mentality
•
Possible role changes
•
Driving restrictions
•
Change in occupation
Cardiovascular causes
•
Neurocardiogenic syncope or
“vasovagal” syncope (e.g., carotid
sinus sensitivity)
•
Primary cardiac dysrhythmias (e.g.,
tachycardias, bradycardias)
Noncardiovascular causes
•
Hypoglycemia
•
Hysteria
•
Unwitnessed seizure
•
Vertebrobasilar transient ischemic
attack
Anginas
Chronic Stable
Angina
Etiology & Pathophysiology
Reversible (temporary) myocardial
ischemia = angina (chest pain)
•
O2 demand > O2 supply
•
Primary
reason for
insufficient
blood flow
is narrowing
of coronary
arteries by
atherosclero
sis.
•
Referred
pain in left
Clinical Manifestations
•
Pain usually lasts 3–5
minutes.
•
Subsides
when the
precipitating
factor is
relieved.
•
Pain at rest is
unusual.
•
ECG reveals
ST-segment
depression
and/or T-
Types of Anginas / Complications
Silent ischemia
•
Ischemia that occurs in the
absence of any subjective
symptoms
•
Associated with diabetic
neuropathy
•
Confirmed by ECG
changes
Nocturnal angina
•
Occurs only at night but not
necessarily during sleep
Prinzmetal’s (variant) angina
Occurs at rest usually in response to
spasm of major coronary artery
Diagnostic Studies

Health history/physical examination

Laboratory studies

12-lead ECG

Chest x-ray

Echocardiogram

Exercise stress test

Cardiac catheterization/coronary
angiography
Diagnostic
Coronary revascularization: percutaneous coronary
intervention (PCI)
Balloon angioplasty
Stent
Nursing and Collaborative Management
•
Drug therapy: goal: ↓ O2 demand and/or ↑ O2 supply
•
Short-acting nitrates: sublingual
•
Long-acting nitrates
•
Nitroglycerin (NTG)
ointment
•
Transdermal controlledrelease NTG
•
β-Adrenergic blockers
•
Calcium channel blockers
•
If β-adrenergic blockers
are poorly tolerated,
contraindicated, or do
not control angina
Unstable
Angina
(Myocardial
Infarction)
•
•
•
•
•
shoulder
and arm is
from
transmission
of the pain
message to
the cardiac
nerve roots.
•
Intermittent
chest pain
that occurs
over a long
period with
the same
pattern of
onset,
duration,
and
intensity of
symptoms
Result of sustained
ischemia (>20 minutes),
causing irreversible
myocardial cell death
(necrosis)
Necrosis of entire
thickness of myocardium
takes 5–6 hours
The degree of altered
function depends on the
area of the heart involved
and the size of the infarct.
Contractile function of the
heart is disrupted in areas
of myocardial necrosis.
Most MIs involve the left
ventricle (LV).
•
wave
inversion.
Pain described as
•
Constrictive
•
Squeezing
•
Heavy
•
Choking
•
Suffocating
•
Seen in clients with a history of migraine
headaches and Raynaud’s phenomenon
Spasm may occur in the absence of CAD.
When spasm occurs
•
Used to manage
Prinzmetal’s angina
Angiotensin-converting enzyme
inhibitors
Chest pain
Marked, transient ST-segment elevation
May occur during REM sleep
May be relieved by moderate exercise or
may disappear spontaneously
Microvascular angina
Myocardial ischemia secondary to
microvascular disease affecting the small,
distal branches of the coronary arteries
More common in women
Triggered by ADLs
•
•
Pain
•
•
Total
occlusion →
anaerobic
metabolism
and lactic
acid
accumulation
→ severe,
immobilizing
chest pain
not relieved
by rest,
position
change, or
nitrate
administratio
n
•
Described as
heaviness,
constriction,
tightness,
burning,
pressure, or
crushing
•
Common
locations:
substernal,
retrosternal,
or epigastric
areas; pain
may radiate
to neck, jaw,
arms, back
Stimulation of sympathetic
nervous system results in
•
Release of
glycogen
•
Diaphoresis
•
Vasoconstrict
ion of
•
•
Dysrhythmias
•
Most
common
complication
•
Present in
80% of MI
clients
•
Most
common
cause of
death in the
pre-hospital
period
•
Lifethreatening
dysrhythmias
seen most
often with
anterior MI,
heart failure,
or shock
Heart failure
•
A
complication
that occurs
when the
pumping
power of the
heart has
diminished
Cardiogenic shock
•
Occurs when
inadequate
oxygen and
nutrients are
supplied to
the tissues
because of
severe LV
failure
•
•
•
•
•
•
•
•
Detailed health history and physical
12-lead ECG: changes in QRS complex,
ST segment, and T wave can rule out or
confirm UA or MI.
Serum cardiac markers
Coronary angiography
Others: exercise stress testing,
echocardiogram
Definitive ECG changes occur in
response to ischemia, injury, or
infarction of myocardial cells.
•
Changes seen in the leads
that face the area of
involvement
Ischemia
•
ST segment depression
and/or T wave inversion
•
ST segment depression is
significant if it is at least 1
mm (one small box) below
the isoelectric line.
•
Changes occur in response
to the electrical
disturbance in myocardial
cells due to inadequate
supply of oxygen.
•
Once treated (adequate
blood flow is restored),
ECG changes resolve and
ECG returns to baseline.
Injury
•
ST-segment elevation is
significant if >1 mm above
the isoelectric line.
•
If treatment
is prompt
and
effective,
may avoid
infarction
•
I
f
•
•
•
•
•
Initial Management
•
Ensure patent airway
•
Administer O2 by nasal cannula or
NRB
•
Obtain 12-lead ECG
•
Insert two IV-catheters
•
Assess pain using PQRST
•
Medicate for pain as ordered
•
Initiate continuous ECG monitoring
and determine underlying rhythm
•
Obtain blood test results
•
Obtain CXR
•
Assess for antiplatelet, anticoagulation,
or fibrinolytic therapy or PCI as
appropriate
•
Administer ASA and beta-adrenergic
blockers for cardiac-related CP
•
Administer antidysrhythmic
medications as ordered
Ongoing Management
•
Monitor vital signs, LOC, cardiac
rhythm and O2 saturation
•
Monitor response to medications
•
Provide reassurance and emotional
support to patient/family
•
Explain all interventions and
procedures
•
Anticipate need for intubation if
respiratory distress is evident
•
Prepare for CPR, defibrillation, TCP or
cardioversion
Emergent PCI
•
Treatment of choice for confirmed MI
•
Balloon angioplasty + drug-eluting
stent(s)
Fibrinolytic therapy
•
Indications and contraindications
•
Best marker of reperfusion: return of
ST segment to baseline
•
Rescue PCI if thrombolysis fails.
•
Major complication: bleeding
Drug therapy
•
•
•
peripheral
blood vessels
•
Skin: ashen,
clammy,
and/or cool
to touch
Cardiovascular
•
Initially, ↑
HR and BP,
then ↓ BP
(secondary to
↓ in CO)
•
Crackles
•
Jugular
venous
distension
•
Abnormal
heart sounds
•
S
3
o
r
S
4
•
N
e
w
m
u
r
m
u
r
Nausea and vomiting
•
Can result
from reflex
stimulation
of the
vomiting
centre by
severe pain
Fever
•
Systemic
manifestation
of the
inflammatory
process
caused by
cell death
•
•
•
•
•
Requires
aggressive
management
Papillary muscle
dysfunction
•
Causes mitral
valve
regurgitation
•
Condition
aggravates an
already
compromised
LV
Ventricular aneurysm
•
Results when
the infarcted
myocardial
wall becomes
thinned and
bulges out
during
contraction
Acute pericarditis
•
An
inflammation
of visceral
and/or
parietal
pericardium
•
May result in
cardiac
compression,
↓ LV filling
and
emptying,
heart failure
•
Pericardial
friction rub
may be heard
on
auscultation.
•
Chest pain
different from
MI pain
Dressler syndrome
•
Characterized
by
pericarditis
with effusion
and fever that
develop 4–6
weeks after
MI
•
Pericardial
(chest) pain
•
Pericardial
friction rub
may be heard
on
auscultation.
•
Arthralgia
s
e
r
u
m
c
a
r
d
i
a
c
m
a
r
k
e
r
s
a
r
e
p
r
e
s
e
n
t
,
a
n
S
T
s
e
g
m
e
n
t
–
e
l
e
v
a
t
i
o
n
m
y
o
c
a
r
d
i
a
l
•
•
•
•
•
•
•
•
Intravenous nitroglycerin
Morphine sulphate
Beta-adrenergic blockers
Angiotensin-converting enzyme
inhibitors
•
Antidysrhythmic medications
•
Cholesterol-lowering drugs
•
Stool softeners
•
Anticoagulation
Nutritional therapy
•
Initially NPO
•
Progress to
•
Low salt
•
Low saturated fat
•
Low cholesterol
Coronary surgical revascularization
•
Failed medical management
•
Presence of left main coronary artery
or three-vessel disease
•
Not a candidate for PCI (e.g., lesions
are long or difficult to access)
•
Failed PCI with ongoing chest pain
•
History of diabetes mellitus
Coronary surgical revascularization
•
Coronary artery bypass graft (CABG)
surgery
•
Requires sternotomy and
cardiopulmonary bypass
(CPB)
•
Uses arteries and veins
for grafts
•
Minimally invasive direct coronary
artery bypass (MIDCAB)
•
Alternative to traditional
CABG
Coronary surgical revascularization
•
Off-pump coronary artery bypass
•
Does not require CPB
•
Transmyocardial laser
revascularization
•
For clients with
advanced CAD who are
not surgical candidates
or who have failed
maximum medical
therapy
i
n
f
a
r
c
t
i
o
n
(
S
T
E
M
I
)
h
a
s
o
c
c
u
r
r
e
d
.
•
•
Infarction
•
Physiological Q wave is
the first negative
deflection following the P
wave.
•
Small and
narrow
(<0.04
second in
duration)
•
Pathological Q wave is
deep and >0.03 second in
duration.
•
Pathological Q wave
indicates that at least half
the thickness of the heart
wall is involved.
•
Referred to
as a Q-wave
MI
•
Pathological
Q wave may
be present
indefinitely
•
T-wave inversion related
to infarction occurs within
hours and may persist for
months.
After an MI, certain proteins called
serum cardiac markers are released into
the blood in large quantities from
necrotic heart muscle
•
Troponin
•
•
CK-MB
Myoglobin
Vascular disorders
Arterial Disorders
Peripheral Artery Disease
Description
•
•
•
Acute arterial ischemic Aortic Anyerism
Aortic Disection
disorders
Peripheral arterial
• Acute arterial
• One of the most
 Aortic
disease (PAD) is a
ischemia is a
common problems
dissection
progressive narrowing
sudden
affecting the aorta is
occurs most
and degeneration of the
interruption in
an aneurysm, a
commonly in
arteries of the upper and
the arterial
permanent, localized
the thoracic
lower extremities.
blood supply to
outpouching or
aorta and is
• In most cases, it is
tissue, an
dilation of the vessel
the result of a
a result of
organ, or an
wall (either congenital
tear in the
atherosclerosis.
extremity that,
or acquired).
intimal
Although the exact
if left
• Aortic aneurysms may
(innermost)
cause(s) of
untreated, can
involve the aortic arch,
lining of the
atherosclerosis are
result in tissue
thoracic aorta, and/or
arterial wall
unknown, inflammation
death.
abdominal aorta, but
allowing blood
and endothelial injury
• Common
most are found in the
to “track”
play a major role.
causes include:
abdominal aorta
between the
The most significant risk
• Embolis
below the level of the
intima and
factors for PAD are
m
renal arteries.
media and
tobacco use, diabetes,
• Thromb
• The primary causes of
creates a false
hyperlipidemia, elevated
osis
aortic aneurysms can
lumen of
high-sensitivity C• Trauma.
be classified as
blood flow.
reactive protein, and
degenerative,
• Most experts
uncontrolled
congenital,
attribute
hypertension.
mechanical,
nontraumatic
aortic
•
•
The most common
locations for PAD are the
carotid, common iliac,
superficial femoral,
popliteal, and tibial
arteries.
PAD of the lower
extremities affects the
aortoiliac, femoral,
popliteal, tibial, or
peroneal arteries.
•
•
•
Clinical
Manifestati
ons
•
The classic symptom of
PAD of the lower
extremities is
intermittent
claudication, which is
defined as ischemic
muscle ache or pain that
•
•
Specific
manifestations
depend on the
affected area of
the body.
Signs and
symptoms of an
•
inflammatory, or
infectious
Classified as true or
false
A true aneurysm is
one in which the wall
of the artery forms the
aneurysm, with at
least one vessel layer
still intact
• Further
subdivided into
fusiform and
saccular
dilations
A false aneurysm (or
pseudoaneurysm) is
not an aneurysm but a
disruption of all layers
of the arterial wall,
resulting in bleeding
that is contained by
surrounding structures
Thoracic aortic
aneurysms:
• Often
asymptomatic
• Deep, diffuse
chest pain that
may extend to
•


dissection to
the
degeneration
of the elastic
fibres in the
medial layer.
Chronic
hypertension
accelerates
the
degradation
process.
A sudden,
severe pain in
the anterior
part of the
chest
Intrascapular
pain radiating
•
•
is precipitated by a
consistent level of
exercise, resolves within
10 minutes or less with
rest, and is reproducible.
Paresthesia, manifested
as numbness or tingling
in the toes or feet, may
result from nerve tissue
ischemia. Gradually
diminishing perfusion to
neurons obviates
sensations of both
pressure and deep pain.
Thus, affected patients
may not notice lower
extremity injuries.
Physical findings include
thin, shiny, and taut skin;
loss of hair on the lower
legs; diminished or
absent pedal, popliteal,
or femoral pulses; pallor
or blanching of the foot
in response to leg
elevation (elevation
pallor); and reactive
hyperemia (redness of
the foot) when the limb
is in a dependent
acute arterial
ischemia
usually have an
abrupt onset
and include the
“six Ps:”
• Pain
• Pallor
• Pulseles
sness
• Paresth
esia
• Paralysis
• Poikilot
hermia
(adaptat
ion of
the
ischemic
limb to
its
environ
mental
tempera
ture,
most
often
cool).
•
the
intrascapular
area
• Hoarseness as
a result of
pressure on
the recurrent
laryngeal nerve
• Dysphagia
from pressure
on the
esophagus.
Abdominal aortic
aneurysms (AAAs):
• Often
asymptomatic
• Symptoms may
mimic pain
associated with
abdominal or
back disorders.

down the
spine into the
abdomen or
legs.
The pain is
most
frequently
described as
“sharp” and
“worst ever”
followed by
“tearing” or
“ripping.”
•
Complicatio
ns
•
•
•
Diagnostic
studies
•
position (dependent
rubor).
Rest pain most often
occurs in the forefoot or
toes, is aggravated by
limb elevation, and
occurs when there is
insufficient blood flow to
maintain basic metabolic
requirements of the
tissues and nerves of the
distal extremity.
Complications of PAD
include nonhealing ulcers
over bony prominences
on the toes, feet, and
lower leg, and gangrene.
Amputation may be
required if blood flow is
not restored.
Critical limb ischemia is a
chronic condition
characterized by
ischemic rest pain,
arterial leg ulcers, and/or
gangrene of the leg due
to advanced PAD.
•
The most serious
complication related
to an untreated
aneurysm is rupture
and bleeding.
Tests used to diagnose
PAD include Doppler
•
Chest radiograph
•
Diagno
stic
•
•
•
ultrasound with
segmental blood
pressures at the thigh,
below the knee, and at
ankle level. A drop in
segmental BP of more
than 30 mm Hg indicates
PAD.
Ankle-brachial index
Angiography is used to
delineate the location
and extent of the disease
process.
•
•
•
Electrocardiogram (to
rule out myocardial
infarction)
Echocardiography
CT scan
Magnetic resonance
imaging (MRI) scan
•
•
•
•
•
•
Collaborati
ve Care
•
Collaborative care
• Risk factor
modification
• Drug therapy
• Exercise therapy
• Nutritional
therapy
• Complementary
and alternative
therapies
•
•
•
•
•
Anticoagulation
Thrombolysis
Embolectomy
Surgical
revascularizatio
n
Amputation
•
•
The goal of
management is to
prevent the aneurysm
from rupturing and
extension of
dissection.
Surgical repair of AAA
involves
1. Incising the
diseased
•
•
•
studies
used to
assess
aortic
dissecti
on are
similar
to
those
perfor
med
for
AAA.
Health
history
CXR
CT scan
ECG
MRI
TEE
Conser
vative
therapy
Endova
scular
dissecti
on
repair
Surgical
therapy
•
•
Care of the leg
with critical limb
ischemia
• Interventional
radiology
catheter-based
procedures
• Surgical therapy
Nursing Implementation,
Acute Intervention
• Post operatively:
• Check the
extremity
q15
minutes
for colour,
temperatu
re,
capillary
refill,
presence
of
peripheral
pulses,
and
sensation
and
movemen
t (CSM)
• Notify
physician
•
•
segment of the
aorta
2. Removing
thrombus or
plaque
3. Inserting a
synthetic graft
4. Suturing the
native aortic
wall around
the graft.
Minimally invasive
endovascular
aneurysm repair
(EVAR) is an
alternative to
conventional surgical
repair of AAA and
involves the
placement of a sutureless aortic graft into
the abdominal aorta
inside the aneurysm
via a femoral artery
cutdown.
Nursing
implementation
1. Health
promotion
2. Acute
intervention
•
Preoperatively
• Keep
the
client
in bed
in a
semiFowler’
s
positio
n and
maintai
na
quiet
environ
ment,
to help
keep
the
systolic
BP at
the
lowest
possibl
e level
that
maintai
ns vital
organ
perfusi
on
•
•
if no
pulses
present
Monitor
for
bleeding,
hematom
a,
thrombosi
s,
embolizati
on, and
compartm
ent
syndrome
Dramatic
increase in
pain, loss
of
palpable
pulses,
extremity
pallor or
cyanosis,
numbness
/tingling,
cold
extremity
suggests
occlusion
•
•
•
•
•
•
•
Graft
patency
Cardiov
ascular
status
Infectio
n
Gastroi
ntestina
l status
Neurolo
gical
status
Periphe
ral
perfusi
on
status
Renal
perfusi
on
status
•
(typical
ly
betwee
n 110
and
120
mm
Hg)
• Opioids
and
sedativ
es are
admini
stered
as
ordere
d.
Postoperativel
y
• Client
and
caregiv
er
teachin
g
• Followup with
regularl
y
schedul
ed
•
•
•
of graft or
stent
Do not
flex knee
POD #1 –
out of bed
and in
chair
Monitor
for
infection
•
magnet
ic
resona
nce
imagin
g (MRI)
or
comput
ed
tomogr
aphy
(CT)
All
clients
with a
history
of
aortic
dissecti
on,
regardl
ess of
anatom
ical
locatio
n or
treatm
ent
modalit
y,
require
longterm
medica
l
therapy
to
control
BP.
Venous Disorders
Venous thrombosis
Description
•
•
•
•
Venous thrombo-embolism (VTE),
also known as venous thrombosis, is
the most common disorder of the
veins and involves the formation of a
thrombus (clot) in association with
inflammation of the vein.
Superficial vein thrombosis (SVT) is
the formation of a thrombus in a
superficial vein
Deep vein thrombosis (DVT) involves
a thrombus in a deep vein, most
commonly the iliac and femoral veins,
and can result in embolization of
thrombi to the lungs.
VTE represents the spectrum of
pathology from DVT to pulmonary
embolism.
Varicose Veins
•
•
•
•
Varicose veins, or
varicosities, are dilated,
tortuous subcutaneous
veins most frequently
found in the saphenous
vein system.
Primary varicose veins are
more common in women
and patients with a strong
family history and are
probably caused by
congenital weakness of the
veins.
Secondary varicose veins
typically result from a
previous VTE.
Secondary varicose veins
also may occur in the
Chronic venous
insufficiency and venous
leg ulcers
• Chronic venous
insufficiency (CVI)
is a condition in
which leg veins and
valves fail to keep
blood moving
forward.
• This results in
ambulatory venous
hypertension.
• CVI often occurs as a
result of previous
episodes of VTE and
can lead to venous
leg ulcers.
• It is a common
medical problem in
older adults.
•
•
•
•
Three important factors (called
Virchow’s triad) in the etiology of
venous thrombosis are
• Venous stasis
• Damage of the endothelium
(inner lining of the vein)
• Hypercoagulability of the
blood.
Localized platelet aggregation and
fibrin entrap RBCs, WBCs, and more
platelets to form a thrombus
A frequent site of thrombus formation
is the valve cusps of veins, where
venous stasis occurs
As the thrombus enlarges, increased
numbers of blood cells and fibrin
collect behind it, producing a larger
clot with a “tail” that eventually
occludes the lumen of the vein
•
esophagus, vulva,
spermatic cords, and
anorectal area, and as
abnormal arteriovenous
connections. Reticular
veins are smaller varicose
veins that appear flat, less
tortuous, and blue-green in
colour.
Risk factors include
• Family history of
chronic venous
disease
• Congenital
weakness of the
vein structure
• Female sex
• Use of oral
contraceptives or
hormone therapy
• Latin American
ethnicity
• Increasing age
• Obesity
• Multiparity
• Venous obstruction
resulting from
thrombosis or
extrinsic pressure
by tumours
• Occupations that
require prolonged
standing or sitting.
•
•
•
Causes of CVI
include:
• Vein valve
incompetence
• Deep vein
obstruction
• Congenital
venous
malformation
• Arteriovenous
fistula
The basic problem is
incompetent valves
of the deep veins.
Hydrostatic pressure
in veins increases
and serous fluid +
RBCs leak from
capillaries and
venules into the
tissue  edema
Superficial vein thrombosis
Clinical
• May have a palpable, firm,
Manifestations
subcutaneous cordlike vein
• Area surrounding the vein may be
tender to the touch, reddened, and
warm
• A mild systemic temperature
elevation and leukocytosis may be
present
Venous thrombo-embolism
• The patient with VTE may or may not
have:
• Unilateral leg edema
• Extremity pain
• A sense of fullness in the thigh
or calf
• Paresthesias
• Warm skin
• Erythema
• A systemic temperature
greater than 38oC.
• Positive Homan’s sign (pain
on forced dorsiflexion of the
foot when the leg is raised)
Complications
VTE
•
•
Pulmonary embolism (PE)
Chronic venous insufficiency Chronic venous insufficiency
(CVI) results from valvular
•
•
•
Ache or pain after
prolonged standing
• Relieved by
walking or by
elevating the limb.
Pressure, itchy, burning or
cramp-like sensation
Swelling and/or nocturnal
leg cramps in the calf may
occur.
•
•
•
•
Over time, the skin
and subcutaneous
tissue around the
ankle are replaced by
fibrous tissue,
resulting in thick,
hardened, contracted
skin.
The skin of the lower
leg is leathery, with a
characteristic
brownish or
“brawny” appearance
from the hemosiderin
deposition (break
down of RBCs).
Edema and eczema,
or “stasis dermatitis,”
are often present, and
pruritus (itching) is a
common complaint.
The wound margins
are irregularly
shaped, and the tissue
is typically a ruddy
colour.
•
•
Diagnostic
studies
destruction, allowing
retrograde flow of venous
blood.
Phlegmasia cerulea dolens
(rare complication)
Post-thrombotic syndrome
results from chronic venous
hypertension caused by
valvular destruction, stiffness
and noncompliance
•
VTE
•
•
•
•
•
•
•
Clinical assessment
Blood work
D-dimer testing
Ultrasonography
Computed tomography
venography
Magnetic resonance
venography
Contrast venography
•
•
•
•
•
•
•
Treatment usually is not
indicated if varicose veins
are only a cosmetic
problem
Rest with the affected limb
elevated
Compression stockings
Exercise, such as walking
Sclerotherapy
Laser therapy/highintensity pulsed-light
therapy
Surgical intervention
Prevention is key.
• Client should be
instructed to avoid
sitting or standing
for long periods,
maintain ideal
body weight, take
precautions against
injury to the
•
•
Collaborative
Care
Superficial vein thrombosis
• Immediate removal of the IV catheter
• If edema is present, the extremity
should be elevated to promote
reabsorption of fluid from the
interstitial space into the vasculature
• Application of warm, moist heat may
hep relieve pain and inflammation
• Oral NSAIDs
• Compression
Venous thrombo-embolism
• Prevention and
prophylaxis
• Drug therapy
extremities, avoid
wearing
constrictive
clothing, and walk
daily.
After vein ligation surgery
• Client should be
encouraged to deep
breathe, to promote
venous return.
Long-term management
• Improving
circulation,
relieving comfort,
avoiding
complications
•
Compression
• Elastic wraps,
custom-fitted
compression
stockings,
elastic tubular
support
bandages,
Velcro wrap,
SCDs, paste
bandage with
an elastic
wrap and
multilayer
(three or four)
•
•
•
Vitamin K
antagonsists (ie.
warfarin)
• Thrombin
inhibitors:
indirect
• Thrombin
inhibitors:
direct
• Factor Xa
inhibitors
• Anticoagulation
therapy for
VTE
prophylaxis
• Anticoagulation
therapy for
venous
thromboembolism
treatment
Thrombolytic therapy
for venous thromboembolism
Surgical therapy
•
•
•
•
•
•
•
•
bandage
system
Moist environment
dressings
Routine antibiotic
therapy is not
indicated
Monitor for signs of
infection
Nutritional support
Maintaining normal
blood glucose levels
Long-term
management of
venous leg ulcers
should focus on
teaching the client
about self-care
measures because the
ulcers often recur.
Instruct the client and
caregiver to avoid
trauma to the limbs
and teach them
proper skin care.
Demonstrate the
correct application of
graduated
compression
stockings and stress
the importance of
regular replacement
(every 4–6 months).
Condition
Dysrhythmias
All rhythms
Coronary Artery Disease
Chronic Stable Angina
Unstable Angina
NSTEMI
STEMI
Associated Lab
Values to Consider
Rationale for Considering
Potassium
Potassium impairs repolarization
process
High potassium = peaked T
waves, widened QRS when severe
Low potassium = flattened T
wave, U wave
Troponin
CK-MB
Myoglobin
Heart Failure
BNP
Hypertension
Inflammatory Conditions
Infective Endocarditis
Acute Pericarditis
Rheumatic Fever
Valvular Heart Disease
Cardiomyopathy
Peripheral Arterial Disease
PAD
Blood cultures
Acute Arterial Ischemia
Raynaud’s
Aortic Aneurysm
Venous Disorders
Venous thromboembolism
Varicose Veins
Venous Insufficiency
General Diagnostics
Diagnostic/Lab Test
Central venous pressure
(CVP)
D-Dimer
Normal
2-9 mm Hg
High = right ventricular
failure, volume overload
Low = hypovolemia
Hematocrit
Men 0.42-0.52
Women 0.37-0.47
High = dehydration
Low = anemia
Hemoglobin
WBC count
WBC differential
Platelet count
Activated partial
thromboplastin time (aPTT)
Purpose
Measurement of preload and
can be used to monitor the
pressure in the right atrium
and right ventricle. The CVP
reading is influenced by the
function of the left side of the
heart, pressures in the
pulmonary vessels, venous
return to the heart, and the
position of the patient when
the reading is taken.
Measurement of packed cell
volume of RBCs. Hematocrit
is increased in chronic
hypoxemia. Value is
expressed as a percentage of
the total blood volume.
d-Dimer
International Normalized
Ratio (INR)
Erythrocyte sedimentation
rate (ESR)
Erythropoietin
Chest XRAY
CT Scan
MRI
Positron emission
tomography (PET)
Albumin
Wound cultures
Blood cultures
Cardiac
Diagnostic/Lab Test
MB isoenzyme of creatine
kinase (CK-MB)
Troponin
Myoglobin
C-Reactive protein
B-type natriuretic peptide
(BNP)
Cholesterol
Triglycerides
Lipoproteins (HDL, LDL)
ECG
Holter monitor
Exercise stress test
Echocardiography
Normal
Purpose
Stress echocardiography
Transesophageal
echocardiography (TEE)
Multigated acquisition
(MUGA)
Cardiac catheterization
Coronary angiography
Endocrine
Diagnostic/Lab Test
Thyroid stimulating hormone
(TSH)
Thyroxine (T4) total
Triiodothyronine (T3)
Free T4
Parathyroid hormone
Total serum calcium
Ionized calcium
Serum phosphate
Cortisol (blood + urine)
Aldosterone (blood + urine)
Adrenocorticotrophic
hormone (ACTH)
Normal
Purpose
Fasting blood glucose level
(FBG)
Oral glucose tolerance test
(OGTT)
Capillary glucose monitoring
Glycosylated hemoglobin
(A1C)
Glucose (urine)
Ketones (urine)
Anion gap
8-16 mmol/L
High anion gap = acid gain
Difference between the
measured serum cations and
anions in ECF
Na – (HCO3 + Cl)
Microalbumin
Respiratory
Diagnostic/Lab Test
Arterial blood gas
Venous blood gas
Oximetry
Bronchoscopy
Lung biopsy
Thoracentesis
Pulmonary function test
Ventilation-perfusion (VQ)
scan
Sputum culture and
sensitivity
Sputum gram stain
Acid-fast smear and culture
Cytology study
Normal
Purpose