Med Surg 2 Exam #1 Study Guide
Nursing Assessment: Cardiovascular System
Structures and Functions of Cardiovascular System
 Heart
 Four chambers
o It lies within the thorax in the mediastinal space that separates the right and left pleural cavities.
 Composed of three layers
o Endocardium
o Myocardium
o Epicardium
 Pericardium (fibrous sac)
 Left ventricular wall 2-3 times thicker than right
 APPLICATION: which problem will kill faster? LEFT (pumping blood)
o If in tissue (bruise), CANNOT move so CANNOT get PE
o Stroke has to come from LEFT side
o Immobile –risk for DVT
Blood Flow Through the Heart
 KNOW THIS!!!
 The right atrium receives venous blood from the
inferior and superior venae cavae and the coronary
sinus. The blood then passes through the tricuspid
valve into the right ventricle. With each
contraction, the right ventricle pumps blood
through the pulmonic valve into the pulmonary
artery and to the lungs.
 Blood flows from the lungs to the left atrium by
way of the pulmonary veins. It then passes through
the mitral valve and into the left ventricle. As the
heart contracts, blood is ejected through the aortic
valve into the aorta and thus enters the systemic
circulation.
 STEPS:
o 1. A red blood cell will come from either the
superior vena cava or the inferior vena cava
and enter into the right atrium
2. the blood then flows across the tricuspid valve to the right ventricle
3. the right ventricle then squeezes and ejects that blood cell into a vessel called the “pulmonary
artery”
4. the pulmonary artery splits into two vessels each going to the lungs
5. as the red blood cell makes its way through the lungs, it returns through the pulmonary veins to
the left atrium
6. that blood is now oxygenated
7. its picked up oxygen then goes across the mitral valve into the left ventricle, which does most of
the work in terms of delivery of blood flow to the body
8. that blood cell is now ejected into the aorta to some organ or muscle or skin in the human body
Cardiac Valves
 Valves are structural
 Thickness is mechanical
 Main places get vegetations and
problems are with AV valves
 Aortic (tight noise aortic stenosis) -->
low BP (LOW cardiac output)
o Tx: replace valve (tavern) –
transaortic valvular repair
o This person is in need of
anticoagulation
o Sutured in (going back and forth
between if can have MRI or not)
 The four valves of the heart serve to
keep blood flowing in a forward
direction.
 The cusps of the mitral and tricuspid
valves are attached to thin strands of
fibrous tissue termed chordae
tendineae. Chordae are anchored in the
papillary muscles of the ventricles. This support system prevents eversion of the leaflets into the atria
during ventricular contraction.
 The pulmonic and aortic valves (also known as semilunar valves) prevent blood from regurgitating into
the ventricles at the end of each ventricular contraction.
Coronary Arteries and Veins
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Can’t fix microvascularity
o Most women who have heart attack die within a year (they don’t present with chest pain)
 Stents may not work (only thing we can do is give calcium channel blockers and other
pharmacology)
The myocardium has its own blood supply, the coronary circulation.
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Blood flow into the two major coronary arteries occurs primarily during diastole (relaxation of the
myocardium).
The left coronary artery arises from the aorta and divides into two main branches: the left anterior
descending artery and the left circumflex artery. These arteries supply the left atrium, the left ventricle,
the interventricular septum, and a portion of the right ventricle.
The right coronary artery also arises from the aorta, and its branches supply the right atrium, the right
ventricle, and a portion of the posterior wall of the left ventricle. In 90% of people, the atrioventricular
(AV) node and the bundle of His, part of the cardiac conduction system, receive blood supply from the
right coronary artery. For this reason, obstruction of this artery often causes serious defects in cardiac
conduction.
The divisions of coronary veins parallel those of coronary arteries. Most of the blood from the coronary
system drains into the coronary sinus (a large channel), which empties into the right atrium near the
entrance to the inferior vena cava.
Conduction System
 The conduction system is specialized nerve tissue responsible for creating and transporting the
electrical impulse, or action potential. This impulse starts depolarization and subsequently cardiac
contraction.
 The electrical impulse is normally
started by the sinoatrial (SA) node
(the pacemaker of the heart). Each
impulse coming from the SA node
travels through interatrial pathways to
depolarize the atria, resulting in a
contraction.
 The electrical impulse travels from the
atria to the AV node through
internodal pathways. The excitation
then moves through the bundle of His
and the left and right bundle
branches. The left bundle branch has
two fascicles (divisions): anterior and
posterior.
 The action potential moves through
the walls of both ventricles by means
of Purkinje fibers. The ventricular
conduction system delivers the
impulse within 0.12 second. This triggers a synchronized right and left ventricular contraction.
 The result of the cardiac cycle is the ejection of blood into the pulmonary and systemic circulation. It
ends with repolarization, when the contractile fiber cells and the conduction pathway cells regain their
resting polarized condition.
 Cardiac muscle cells have a compensatory mechanism that makes them unresponsive or refractory to
restimulation during the action potential. During ventricular contraction, an absolute refractory period
occurs, during which cardiac muscle does not respond to any stimuli. After this period, cardiac muscle
gradually recovers its excitability, and a relative refractory period occurs by early diastole.
Electrocardiogram
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ON TEST
The electrical activity of the heart can be detected on the body surface using electrodes and is recorded
on an electrocardiogram (ECG). The letters P, QRS, T, and U are used to identify the separate
waveforms.
The first wave, P, begins with the firing of the SA node and represents depolarization of the atria.
The QRS complex represents depolarization from the AV node throughout the ventricles. Impulse
transmission through the AV node is delayed, which accounts for the time interval between the end of
the P wave and the beginning of the QRS wave.
The T wave represents repolarization of the ventricles.
The U wave, if seen, may represent repolarization of the Purkinje fibers, or it may be associated with
hypokalemia.
Intervals between these waves (PR, QRS, and QT intervals) reflect the length of time it takes for the
impulse to travel from one area of the heart to another. These time intervals can be measured, and
changes from these time references often indicate pathology.
Mechanical System
 Depolarization triggers mechanical activity.
 Systole: Contraction of myocardium
o Systole, contraction of the myocardium, results in ejection of blood from the ventricles.
 Diastole: Relaxation of myocardium
o Relaxation of the myocardium, diastole, allows for filling of the ventricles
 Stroke volume: Amount of blood ejected with each heart beat
o 30-60 ml is normal (healthy)
o Stroke volume is the amount of blood ejected from the ventricle with each heartbeat.
 Cardiac output: Amount of blood pumped by each ventricle in 1 minute
o It is calculated by multiplying the stroke volume (SV) by the heart rate (HR): CO = SV X HR.
o Normal 4-8 L/min
o If too high, heart working WAY too hard (trying to maintain BP)
 Cardiac index: CO divided by body surface area
o Normal 2.8-4.2 L/min/m2
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o More accurate assessment of how heart is doing
If have LVAD (left ventricular assistive device) will not have pulse or hear anything!!! NO HEARTBEAT
o no systolic or diastolic
o Check BP by looking at mean arterial pressure (MAP)
Factors Affecting Cardiac Output
 Preload
o Volume of blood in ventricles at the end of diastole
o Preload determines the amount of stretch placed on myocardial fibers. Preload can be
increased due to a number of causes such as myocardial infarction, aortic stenosis, and
hypervolemia.
 RIGHT
 Ejection fraction (LEFT side)
 Want to be low!!!
 Contractility
o Contractility can be increased by epinephrine and norepinephrine released by the sympathetic
nervous system. Increasing contractility raises the SV by increasing ventricular emptying.
o Dig, Viagra, epinephrine (only drug that hits all four receptors (a1, a2, b1, b2) –increases
contractility
o Beta blockers –decrease
 Afterload
o Peripheral resistance against which the left ventricle must pump
o Afterload is affected by size of the ventricle, wall tension, and arterial blood pressure. If the
arterial blood pressure is elevated, the ventricles will meet increased resistance to ejection of
blood, increasing the work demand. Eventually, this results in ventricular hypertrophy, an
enlargement of cardiac muscle tissue without an increase in CO or the size of the chambers.
 Drug: Nitropreside (Nipride)
Audience Response Question
A patient is receiving a drug that decreases afterload. To evaluate the patient’s response to this drug, what is
most important for the nurse to assess?
a. Heart rate
b. Lung sounds
c. Blood pressure
d. Jugular venous distention
Answer: C
Rationale: Afterload is affected by size of the ventricle, wall tension, and arterial blood pressure.
Structures and Functions of Cardiovascular System
 Vascular system
o Blood vessels
 Arteries, arterioles
 Arteries carry oxygenated blood away from the heart, except for the pulmonary
artery.
 Veins, venules
 Veins carry deoxygenated blood toward the heart, except for the pulmonary
veins.
 Capillaries
o Blood circulates from the heart into arteries, arterioles, capillaries, venules, and veins, and then
back to the heart.
Comparison of Artery, Vein, and Capillary
 The arterial system differs from the venous
system by the amount and type of tissue that
makes up arterial walls.
 Arteries and Arterioles. The large arteries have
thick walls that are composed mainly of elastic
tissue. This elastic property cushions the impact
of the pressure created by ventricular
contraction and provides recoil that propels
blood forward into the circulation. Large
arteries also contain some smooth muscle.
Examples of large arteries are the aorta and the
pulmonary artery.
 The innermost lining of the arteries is the
endothelium. The endothelium serves to
maintain hemostasis, promote blood flow, and,
under normal conditions, inhibit blood
coagulation. When the endothelial surface is
disrupted (e.g., rupture of an atherosclerotic
plaque), the coagulation cascade is initiated
and results in the formation of a fibrin clot.
 Capillaries. The thin capillary wall is made up of endothelial cells, with no elastic or muscle tissue. The
exchange of cellular nutrients and metabolic end products takes place through these thin-walled
vessels. Capillaries connect the arterioles and venules.
 Veins and Venules. Veins are large-diameter, thin-walled vessels that return blood to the right atrium.
The venous system is a low-pressure, high-volume system. The larger veins contain semilunar valves at
intervals to maintain the blood flow toward the heart and to prevent backward flow. The amount of
blood in the venous system is affected by a number of factors, including arterial flow, compression of
veins by skeletal muscles, alterations in thoracic and abdominal pressures, and right atrial pressure. The
largest veins are the superior vena cava, which returns blood to the heart from the head, neck, and
arms, and the inferior vena cava, which returns blood to the heart from the lower part of the body.
Structures and Functions of Cardiovascular System
 Regulation of the cardiovascular system
o Autonomic nervous system
 Epinephrine
 The autonomic nervous system consists of the sympathetic nervous system and the
parasympathetic nervous system.
 Stimulation of the sympathetic nervous system increases the HR, the speed of impulse
conduction through the AV node, and the force of atrial and ventricular contractions.
Additionally, stimulation of α1-adrenergic receptors in vascular smooth muscle results in
vasoconstriction, increasing the blood pressure.
 In contrast, stimulation of the parasympathetic system (mediated by the vagus nerve)
slows HR by decreasing the impulse from the SA node and thus conduction through the
AV node.
o Baroreceptors
Most primal –respond to everything
Ex. When you stand up and are dizzy (decreased in BP leads to increase in HR)
 In aortic arch, don’t respond to beta blockers (ONLY nipride)
 Baroreceptors in the aortic arch and carotid sinus (at the origin of the internal carotid
artery) are sensitive to stretch or pressure within the arterial system. Stimulation of
these receptors (e.g., volume overload) sends information to the vasomotor center in
the brainstem. This results in temporary inhibition of the sympathetic nervous system
and enhancement of the parasympathetic influence, causing a decreased HR and
peripheral vasodilation. Decreased arterial pressure causes the opposite effect.
o Chemoreceptors
 Located in Brain and brainstem
 Sense how high or low pH is
 Tells body to increase or decrease HR
 Chemoreceptors are located in the aortic and carotid bodies and the medulla. They are
capable of causing changes in respiratory rate and BP in response to increased arterial
CO2 pressure (hypercapnia) and, to a lesser degree, decreased plasma pH (acidosis) and
arterial O2 pressure (hypoxia). When the chemoreceptors in the medulla are triggered,
they stimulate the vasomotor center to increase BP.
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Structures and Functions of Cardiovascular System
 Blood pressure
o 120/80 now considered pre-hypertensive
 Systolic blood pressure (SBP)
o < 120 mm Hg
 Diastolic blood pressure (DBP)
o < 80 mm Hg
 BP = CO x SVR
 The arterial blood pressure is a measure of the pressure exerted by blood against the walls of the
arterial system.
o The systolic blood pressure (SBP) is the peak pressure exerted against the arteries when the
heart contracts.
o The diastolic blood pressure (DBP) is the residual pressure in the arterial system during
ventricular relaxation (or filling). BP is usually expressed as the ratio of systolic to diastolic
pressure.
o The two main factors influencing BP are cardiac output (CO) and systemic vascular resistance
(SVR): BP = CO x SVR.
o SVR is the force opposing the movement of blood. This force is created primarily in small
arteries and arterioles.
o Normal blood pressure is SBP less than 120 mm Hg and DBP greater than 80 mm Hg
 Measurement of blood pressure
o Cuff size is important!!!
o BP can be measured by invasive and noninvasive techniques.
o The invasive technique consists of catheter insertion into an artery. The catheter is attached to a
transducer, and the pressure is measured directly.
o Noninvasive, indirect measurement of BP can be done with a sphygmomanometer and a
stethoscope. The sphygmomanometer consists of an inflatable cuff and a pressure gauge.
o The BP is measured by auscultating for sounds of turbulent blood flow through a compressed
artery (termed Korotkoff sounds). The brachial artery is the recommended site for taking a BP.
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After placing the appropriate size cuff on the upper arm, inflate the cuff to a pressure 20 to 30
mm Hg above the SBP. This causes blood flow in the artery to cease. If the SBP is not known,
estimate the pressure by palpating the brachial pulse and inflating the cuff until the pulse
ceases. The pressure noted at this time is the estimated SBP. Inflate the BP cuff 20-30 mm Hg
above this number.
o As the pressure in the cuff is lowered, the artery is auscultated for Korotkoff sounds. There are
five phases of Korotkoff sounds. The first phase is a tapping sound caused by the spurt of blood
into the constricted artery as the pressure in the cuff is gradually deflated. This sound is noted
as the SBP. The fifth phase occurs when the sound disappears and is noted as the DBP.
o BP is recorded as SBP/DBP (e.g., 120/80 mm Hg).
o Proper BP technique (e.g., correct cuff size, positioning arm at heart level) is essential for
accurate readings.
o Another noninvasive way to measure BP indirectly is an automated device that uses
oscillometric measurements to assess BP. Though this method does not involve auscultation,
the same attention to proper technique is essential for accuracy.
o Finally, SBP (and pulse) can be assessed using a Doppler ultrasonic flowmeter. The hand-held
transducer is positioned over the artery (identified by audible, pulsatile sounds). The cuff is
applied above the artery, inflated until the sounds disappear, and then another 20 to 30 mm Hg
beyond that point. The cuff is then slowly deflated until sounds return. This point is the SBP.
o Automated device
 Another noninvasive way to measure BP indirectly is an automated device that uses
oscillometric measurements to assess BP. Though this method does not involve
auscultation, the same attention to proper technique is essential for accuracy.
o Doppler ultrasonic flowmeter
 If feel pulse –central = 60 and peripheral = 80
 Can only get systolic with doppler
 Finally, SBP (and pulse) can be assessed using a Doppler ultrasonic flowmeter. The handheld transducer is positioned over the artery (identified by audible, pulsatile sounds).
The cuff is applied above the artery, inflated until the sounds disappear, and then
another 20 to 30 mm Hg beyond that point. The cuff is then slowly deflated until sounds
return. This point is the SBP.
Pulse pressure
o Different between systolic and diastolic pressures (how much rest heart is getting)
o Narrow = usually means tamponade
o Wide = make burr holes
Mean arterial pressure
o 60 lowest MAP can be to maintain BP to vital organs
Pulse deficit
o Feel 60 beats per min but EKG reads higher (the difference is the pulse deficit)
o Conduction not pushing out
Gerontologic Considerations
 Risk for cardiovascular disease (CVD) increases with age.
 CVD leading cause of death in adults > 85 years of age
 Cardiovascular changes result of aging, disease, environmental factors, and lifetime behaviors
 Age-Related Changes
o Increased collagen, decreased elastin
o Decreased response to stress
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Heart valves become thick and stiff.
Number of pacemaker cells decrease.
Decreased number and function of β-adrenergic receptors
Blood vessels thicken and less elastic
Increase in SBP and decrease or no change in DBP
Incompetent venous valves
Orthostatic hypotension
Postprandial hypotension
Assessment of Cardiovascular System
 Subjective Data (review of systems)
o Health information
 History of present illness
 Past health history
 Past and current medications
 Surgery or other treatments
o Functional health patterns
 Role-relationship pattern
 Has this illness affected any of the roles that you play in your daily life? If yes,
describe.
 How have your significant others been affected by your heart disease?
 Sexuality-reproductive pattern
 Has your heart disease caused a change in your sexual activity? If yes, describe.
 Do you experience any heart-related symptoms during sexual activity? If yes,
describe.
 Do any of your medications affect your ability to participate in sexual activities? If
yes, describe.
 Females: Are you currently taking oral contraceptives, hormonal therapy, or drug
therapy for breast cancer?
 Copingstress tolerance pattern
 Describe your normal coping mechanisms during times of stress or anxiety.
 To whom or where would you turn during a time of stress? Are these people or
services helping you now? If yes, describe.
 Do you practice any stress reduction techniques? If yes, describe.
 Do you have a history of depression? If yes, describe.
 Do you feel capable of handling your present health situation?
 Do you experience any heart symptoms (e.g., chest pain, palpitations) during
times of stress or anger? If yes, describe.
 Values-belief pattern
 What influence have your values or beliefs had during your illness?
 Do you feel any conflicts between your values or beliefs and the plan of care? If
yes, describe.
 Describe any cultural or religious beliefs that may influence the management of
your heart problem.
 Objective Data
o Physical examination
 Vital signs
 Peripheral vascular system
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Inspection
Palpation
Auscultation
Common Sites for Palpating Arteries
 When palpating the arteries identified in this figure, rate the
force of the pulse when it is felt. This done using the following
scale:
o 0 = Absent
o 1+ = Weak
o 2+ = Normal
o 3+ = Increased, full, bounding
 The rigidity (hardness) of the vessel should also be noted. The
normal pulse will feel like a tap, whereas a vessel wall that is
narrowed or bulging will vibrate. The term for a palpable
vibration is thrill.
Assessment of Cardiovascular System Anatomic Landmarks
The raised notch, the angle of Louis, is where the manubrium and the body of the sternum are joined.
It is palpable in the midline of the sternum. The angle of Louis is at the level of the second rib. It is used
to count ICSs and locate specific auscultatory areas.
 The five auscultatory areas include
o the aortic area in the second ICS to the right of the sternum
o the pulmonic area in the second ICS to the left of the sternum
o the tricuspid area in the fifth left ICS close to the sternum
o the mitral area in the left midclavicular line at the fifth ICS
o Erb’s point, located at the third left ICS near the sternum.
 The epigastric area lies on either side of the midline just below the xiphoid process
Assessment of Cardiovascular System
 Physical examination
o Thorax: Inspection & Palpation
 Pulsations
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Thrills (sounds like cat prr)
Heaves (have had HF for long time)
 CPR won’t be very effective (DNR..)
 Point of maximal impulse
 An overall inspection and palpation of the bony structures of the thorax are the initial
steps in the examination.
 Next, inspect and palpate the areas where the cardiac valves project their sounds by
identifying the intercostal spaces (ICSs) and five auscultatory areas. Normally, no
pulsations are felt in these areas unless the patient has a thin chest wall.
 A valvular disorder may be suspected if abnormal pulsations or thrills are felt.
 Next, inspect and palpate the epigastric area. In a thin person, you may see the
pulsation of the abdominal aorta. Normally, you can palpate it here.
 Next, inspect the precordium, which is located over the heart, for heaves. Heaves are
sustained lifts of the chest wall in the precordial area that can be seen or palpated. They
may be caused by left ventricular hypertrophy. Normally no pulsations are seen or felt
here.
 When the patient is supine, palpate the mitral valve area for the point of maximal
impulse (PMI) (also known as the apical pulse). This reflects the pulsation of the apex of
the heart. The PMI lies medial to the midclavicular line in the fourth or fifth ICS. If the
PMI is palpable, record its position in relation to the midclavicular line and ICSs. When
the PMI is below the fifth ICS and left of the midclavicular line, the heart may be
enlarged.
o Thorax: Auscultation
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When auscultating the apical area, you should simultaneously palpate the radial pulse. A
judgment about the rhythm (regular or irregular) is made while listening.
S1 and S2 are heard best with the diaphragm of the stethoscope because they are highpitched.
The first heart sound (S1), which is associated with closure of the tricuspid and mitral
valves, has a soft lub sound.
The second heart sound (S2), which is associated with closure of the aortic and pulmonic
valves, has a sharp dup sound.
S1 signals the beginning of systole and correlates with the QRS complex on the
electrocardiogram.
S2 signals the beginning of diastole and correlates with period immediately following the
T wave on the electrocardiogram.
Normally, no sound is heard between S1 and S2 during the periods of systole and
diastole.
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The S3 heart sound is a low-intensity vibration of the ventricular walls usually associated
with decreased compliance of the ventricles during filling.
The S4 heart sound is a low-frequency vibration caused by atrial contraction. It precedes
S1 of the next cycle and is known as an atrial gallop.
When listening – you are hearing valves slam shut
 Bruit = blockage
 Turbulence =S1 slamming shut
 You are causing turbulence when taking a BP
Diagnostic Studies of Cardiovascular System
 Cardiac Biomarkers
o Troponin
 Troponin T (cTnT)
 Troponin I (cTnI)
 Rises within 4-6 hours, peaks 10-24 hours, detected for up to 10-14 days
 Should NOT have high troponin
 Will be high with a heart attack
 Lab tests show how much damage has been caused
 When cells are injured, they release their contents, including enzymes and other
proteins, into the circulation. These biomarkers are useful in the diagnosis of myocardial
injury and infarction.
 Cardiac-specific troponin is a myocardial muscle protein released into circulation after
injury or infarction. Two subtypes, cardiac-specific troponin T (cTnT) and cardiac-specific
troponin I (cTnI), are specific to myocardial tissue.
 Normally the level in the blood is very low, so a rise in level is diagnostic of myocardial
injury. cTnT and cTnI are detectable within hours (on average of 4 to 6 hours) of
myocardial injury, peak at 10 to 24 hours, and can be detected for up to 10 to 14 days.
 Troponin is the biomarker of choice in the diagnosis of MI.
 Recent development of high-sensitivity troponin (hs-cTnT, hs-cTnI) assays may provide
even earlier detection of a cardiac event.
o Creatine kinase (CK)
 Three isoenzymes
 CK-MB cardiac specific
 Rises in 3-6 hours, peaks in 12-24 hours, returns to baseline within 12-48 hours
 Creatine kinase (CK) enzymes are found in a variety of organs and tissues and occur as
three isozymes.
 These isozymes are specific to skeletal muscle (CK-MM), brain and nervous tissue (CKBB), and the heart (CK-MB).
 CK-MB elevation is specific for myocardial injury or infarction. CK-MB levels begin to rise
3 to 6 hours after symptom onset, peak in 12 to 24 hours, and return to baseline within
12 to 48 hours after myocardial infarction (MI).
 The peak level and return to normal can be delayed in a person who has had a large MI.
 Levels will drop more rapidly in patients who are quickly and successfully treated for an
MI.
o Myoglobin
 Myoglobin is a low-molecular-weight heme protein found in cardiac and skeletal muscle.
Myoglobin elevation is a sensitive indicator of very early myocardial injury but lacks
specificity for MI. Its usefulness in diagnosing MI is limited.
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Correct interpretation of diagnostic tests requires consideration of the time from onset
of symptoms with the time of the expected presence and elevation of the biomarkers.
Additional data (patient symptoms, history, and ECG changes) complete the diagnostic
picture for the patient with suspected myocardial injury or MI.
Additional blood studies
o C-Reactive protein
 Marker for inflammation
 Risk factor for coronary artery disease (CAD)
 C-reactive protein (CRP) is a protein produced by the liver during periods of acute
inflammation.
 CRP can be measured using a high-sensitivity test (hsCRP).
 An increased level of CRP is an independent risk factor for CAD. The level of CRP may
also predict the risk for future cardiac events in patients with unstable angina and MI,
but studies have produced conflicting results.
o Homocysteine
 Elevated levels increased risk for CAD, peripheral vascular disease (PVD), and stroke
 Homocysteine (Hcy) is an amino acid that is produced during protein catabolism.
 Elevated Hcy levels can be either hereditary or acquired from dietary deficiencies of
vitamin B6, vitamin B12, or folate.
 Elevated levels of Hcy have been linked to a higher risk of CAD, peripheral vascular
disease, and stroke.
 It is recommended that Hcy testing be performed in those patients with a familial
predisposition for early CVD or a history of CVD in the absence of other common risk
factors
o Cardiac natriuretic peptide markers
 Three types
 Atrial natriuretic peptide (ANP)
 B-type natriuretic peptide (BNP)
o Check for HF (confirmatory)
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 C-type natriuretic peptide
 Increased levels of BNP levels signify heart failure.
 NT-pro-BNP
Serum Lipids
 Triglycerides
 Triglycerides are the main storage form of lipids and make up about 95% of fatty
tissue.
 Cholesterol
 Cholesterol, a structural component of cell membranes and plasma lipoproteins,
is a precursor of corticosteroids, sex hormones, and bile salts. In addition to
being absorbed from food in the gastrointestinal tract, cholesterol can also be
synthesized in the liver.
 Phospholipids
 Phospholipids contain glycerol, fatty acids, phosphates, and a nitrogenous
compound. Although formed in most cells, phospholipids usually enter the
circulation as lipoproteins synthesized by the liver.
Lipoprotein
 Lipids must bind to protein to circulate in blood.
 Serum lipids circulate in the blood bound to protein. Thus they are often referred to as
lipoproteins.
 Apoproteins are water-soluble proteins that combine with most lipids to form
lipoproteins.
Four classes of lipoprotein
 Chylomicrons
 primarily exogenous triglycerides from dietary fat
 Low-density lipoproteins (LDLs)
 mostly cholesterol with moderate amounts of phospholipids
 High-density lipoproteins (HDLs)
 about one-half protein and one-half phospholipids and cholesterol
 Very-low-density lipoproteins (VLDLs)
 primarily endogenous triglycerides with moderate amounts of phospholipids and
cholesterol
 Increased Triglycerides and LDL risk factor
 Increased HDL decreases risk
 Cholesterol: HDL ratio
 A lipid panel usually measures cholesterol, triglyceride, LDL, and HDL.
 Elevations in triglycerides and LDL are strongly associated with CAD. An increased HDL
level is associated with a decreased risk of CAD.
 High levels of HDLs serve a protective role by mobilizing cholesterol from tissues.
 Although the association between elevated serum cholesterol levels and CAD exists, a
measure of total cholesterol alone is not sufficient for an assessment of CAD. A risk
assessment is calculated by comparing the total cholesterol to HDL ratio over time. An
increase in the ratio indicates increased risk. This provides more information than either
value alone.
Other serum lipoproteins
 Apolipoprotein A-I (Apo A-I)
 Plasma levels of apolipoprotein A-I (apo A-I) (the major HDL protein) and the
ratio of apo A-I to apolipoprotein B (apo B) (the major LDL protein) are stronger
predictors of CAD than the HDL cholesterol level alone. Measurements of these
lipoproteins can be useful in identifying patients at risk for CAD.
 Apolipoprotein B (Apo B)
 Lipoprotein (a) [Lp(a)]
 Lipoprotein (a), or Lp (a), has been studied for its role as a risk factor for CAD.
Increased levels of Lp (a), especially with increased levels of LDH, have been
linked with the progression of atherosclerosis, especially in women.
o Lipoprotein-associated phospholipase A2
 The patient must fast before the blood is drawn for a lipid panel to remove the effects of
a recent meal.
 Lipoprotein-associated phospholipase A2 (Lp-PLA2) is an inflammatory enzyme expressed
in atherosclerotic plaques. Elevated levels of Lp-PLA2 are related to an increased risk of
CAD.
Audience Response Question
A patient arrives at an urgent care center after experiencing unrelenting substernal and epigastric pain and
pressure for about 12 hours. The nurse reviews laboratory results with the understanding that at this point in
time, a myocardial infarction would by indicated by peak levels of
a. Troponin T.
b. Homocysteine.
c. Creatine kinase-MB.
d. Type b natriuretic peptide.
Answer: A
Rationale: Troponin is the biomarker of choice in the diagnosis of myocardial infarction. Troponin is a
myocardial muscle protein released into the circulation after injury. Troponin levels peak at 10 to 24 hours.
Diagnostic Studies of Cardiovascular System Cont.
 A radiographic picture of the chest can show cardiac contours, heart size, and anatomic changes in
individual chambers. The chest x-ray records any displacement or enlargement of the heart, presence
of extra fluid around the heart (pericardial effusion), and pulmonary congestion.

Electrocardiogram
o Resting ECG
o Ambulatory ECG monitoring
o Event monitor or loop recorder
o Exercise or stress testing

o Notes
 The basic P, QRS, and T waveforms are used to assess cardiac activity. Deviations from
the normal sinus rhythm can indicate problems in heart function.
 There are many types of electrocardiographic monitoring, including a resting 12-lead
ECG, ambulatory ECG monitoring, and exercise or stress testing.
 Continuous ambulatory ECG (Holter monitoring) can provide diagnostic information over
a greater period of time than a resting 12-lead ECG.
 An event monitor or loop recorder is used to document less frequent ECG events. An
event monitor is a portable unit that uses electrodes to store ECG data once triggered by
the patient. A disadvantage of this type of monitoring is that if symptoms occur for only
a brief time, they may be over before the patient puts on the device and triggers it to
record. Likewise, if patients are extremely symptomatic (e.g., syncopal), they may not be
physically able to trigger the ECG recording.
 An implantable loop recorder is used for patients who are suspected to have serious yet
rare dysrhythmias. This small recorder is implanted though a small incision into the chest
wall. It is activated to record either by the patient through a remote device or
automatically if the heart rate exceeds or goes below a set rate. External loop recorders
are worn for a month and require electrodes continually placed on the skin. This device
only records when activated by the patient when symptoms occur.
 Cardiac symptoms frequently occur only with activity due to the demand on the
coronary arteries to provide more oxygen. Exercise testing is used to evaluate the heart’s
response to physical stress. This helps to assess CVD and set limits for exercise programs.
Exercise testing is used for individuals who do not have restrictions related to walking or
using a bicycle.
Echocardiogram
o Ultrasound of heart
o With or without contrast
o Provides information regarding structures and motion of heart
o Measures ejection fraction
o Stress echocardiography
o Transesophageal echo (TEE)
o Notes
 The echocardiogram uses ultrasound (US) waves to record the movement of the
structures of the heart. In the normal heart, ultrasonic sound waves directed at the
heart are reflected back in typical configurations.
 A contrast echocardiography involves the addition of an IV contrast agent (e.g., albumin
microbubbles, agitated saline) to assist in defining the images, especially in technically
difficult patients (e.g., obese).
 The echocardiogram provides information about abnormalities of (1) valvular structures
and motion, (2) cardiac chamber size and contents, (3) ventricular and septal motion and
thickness, (4) pericardial sac, and (5) ascending aorta.
 The ejection fraction (EF) or the percentage of end-diastolic blood volume that is ejected
during systole can also be measured. The EF provides information about the function of
the left ventricle during systole.
 Stress echocardiography, a combination of treadmill test and US images, evaluates wall
motion abnormalities. This test provides the information of an exercise stress test with
the information from an echocardiogram. For those individuals unable to exercise, an IV


drug (e.g., dobutamine [Dobutrex], dipyridamole [Persantine]) is used to produce
pharmacologic stress on the heart while the patient is at rest.
 Transesophageal echocardiography (TEE) provides more precise echocardiography of the
heart than surface 2-D echocardiography by removing interference from the chest wall
and lungs. The TEE uses a flexible endoscope probe with an US transducer in the tip for
imaging of the heart and great vessels. The probe is passed into the esophagus to the
level of the heart, and M-mode, 2-D, Doppler, and color-flow imaging can be obtained.
TEE is contraindicated if the patient has a history of esophageal disorders, dysphagia, or
radiation therapy to the chest wall. Patients will require sedation during a TEE.
o Two commonly used types of
echocardiograms are the motionmode (M-mode) echocardiogram and
the two-dimensional (2-D)
echocardiogram. In the M-mode
type, a single US beam is directed
toward the heart, recording the
motion of the intracardiac structures,
as well as detecting wall thickness
and chamber size. The 2-D
echocardiogram sweeps the US beam
through an arc, producing a crosssectional view. This shows correct
spatial relationships among the
structures.
Nuclear cardiology
o MUGA scan
o Stress perfusion imaging
o One of the most common nuclear
imaging tests is the multigated
acquisition (MUGA) or cardiac blood pool scan. This test provides information on wall motion
during systole and diastole, cardiac valves, and EF.
o Perfusion imaging is also used with exercise testing to determine whether the coronary blood
flow changes with increased activity. Stress perfusion imaging may show an abnormality even
when a resting image is normal. This procedure is used to diagnose CAD, make a prognosis in
existing CAD, differentiate viable myocardium from scar tissue, and determine the potential for
success of various interventions (e.g., coronary artery bypass surgery, percutaneous coronary
intervention).
o Exercise stress perfusion imaging is always preferred but, if a patient cannot exercise, IV
dipyridamole or adenosine (Adenocard) can be given to dilate the coronary arteries and
simulate the effect of exercise. After the drug takes effect, the isotope is injected, and the
procedure proceeds.
Cardiovascular magnetic resonance imaging (CMRI)


o Cardiovascular magnetic resonance imaging (CMRI) can detect
and find areas of MI in a 3-D view. It is sensitive enough to find
even small MIs that are not apparent with single-photon emission
computed tomography imaging. CMRI aids in the final diagnosis
of MI and the assessment of EF. It also plays a role in prediction of
recovery from MI and in the diagnosis of congenital heart and
aortic disorders and CAD.
o Examples of coronary calcification of the left anterior descending
coronary artery (large arrow) and the left circumflex artery (small
arrow), as seen on electron beam computed tomography.  
Cardiac computed tomography
o CT angiography (CTA)
o Calcium-scoring screening
o Cardiac computed tomography (CT) is a heart-imaging test that uses CT technology with or
without IV contrast (dye) to see the heart anatomy, coronary circulation, and great blood vessels
(e.g., aorta; pulmonary veins, artery). This technology is often called multidetector CT (MDCT)
scanning. Types of CT scans used to diagnosis heart disease include coronary CT angiography
(CTA) and calcium-score screening heart scan.
o Coronary CTA is a noninvasive test. It can be done faster than a cardiac catheterization with less
risk and discomfort to the patient. Although the use of coronary CTA is increasing, cardiac
catheterization (discussed in the next section) remains the gold standard for finding coronary
artery stenosis. Further, when a cardiac catheterization is done, interventions (e.g., angioplasty,
stent placement) can be performed if coronary blockages are found.
o The calcium-score screening heart scan is used to find calcium deposits in plaque in the
coronary arteries. The most common method used is the electron beam CT (EBCT). It can detect
early coronary calcification before symptoms develop. The amount of coronary calcium is a
predictor of future cardiac events (see next slide).
Cardiac catheterization
o Right-sided to measure pressures
o Left-sided to evaluate coronary arteries
 Gold standard today
o Cardiac catheterization is a common outpatient procedure. It provides information about CAD,
coronary spasm, congenital and valvular heart disease, and ventricular function.
o Cardiac catheterization is also used to measure intracardiac pressures and O2 levels, as well as
CO and EF.
o With injection of contrast media and fluoroscopy, the coronary arteries can be seen, chambers
of the heart can be outlined, and wall motion can be observed.
o Cardiac catheterization is done by inserting a radiopaque catheter into the right and/or left side
of the heart.
o For the right side of the heart, a catheter is inserted through an arm vein (basilic or cephalic) or
a leg vein (femoral). Pressures are recorded as the catheter is moved into the vena cava, the
right atrium, the right ventricle, and the pulmonary artery. The catheter is then moved until it is
wedged or lodged in position. This blocks the blood flow and pressure from the right side of the
heart and looks ahead through the pulmonary capillary bed to the pressure in the left side of
the heart (pulmonary artery occlusive pressure). This pressure assesses the function of the left
side of the heart.





o The left heart catheterization is done by inserting a catheter into a femoral or brachial artery.
The catheter is passed in a retrograde manner up to the aorta, across the aortic valve, and into
the left ventricle.
Coronary angiography
o Uses contrast medium to identify coronary blockages
 Coronary angiography is done with a left-sided heart catheterization.
o The catheter is positioned at the origin of the coronary arteries, and contrast medium is injected
into the arteries. Patients often feel a temporary flushed sensation with dye injection. The
images identify the location and severity of any coronary blockages.
o Complications of cardiac catheterization include bleeding or hematoma at the puncture site,
allergic reactions to the contrast media, looping or kinking of the catheter, infection, thrombus
formation, aortic dissection, dysrhythmias, MI, stroke, and puncture of the ventricles, cardiac
septum, or lung tissue.
Normal Left Coronary Artery Angiogram
o
Intracoronary ultrasound
o Done with coronary angiography
o Intracoronary ultrasound (ICUS), also known as intravascular ultrasound (IVUS), is an invasive
procedure performed in the catheterization laboratory with coronary angiography.
o In this procedure, a miniature transducer attached to a small catheter is moved to the artery to
be studied.
o Once in the artery, US images are obtained. The health of the arterial layers is assessed,
including the composition, location, and thickness of any plaque. ICUS can evaluate vessel
response to treatments such as stent placement and atherectomy, as well as any complications
that may have occurred during the procedure (see Chapter 34). Patients will most often have
ICUS in addition to angiography or a coronary intervention. Thus nursing care is similar to that
following cardiac catheterization.
Fractional flow reserve
o Special wire measures pressure and flow in coronary artery.
o Fractional flow reserve (FFR) is a procedure that is done during a cardiac catheterization. It
involves using a special wire that can measure pressure and flow in the coronary artery. FFR
helps to determine the need to perform angioplasty or stenting on nonsignificant blockages
Electrophysiology study
o Provides information on cardiac conduction
o The electrophysiologic study (EPS) records and manipulates the electrical activity of the heart
using electrodes placed inside the heart chambers.
o It provides information on SA node, AV node, and ventricular conduction. It is particularly
helpful in determining the source and treatment of dysrhythmias. Patients with symptomatic
supraventricular or ventricular tachycardias may be at risk for sudden cardiac death.
Information from an EPS helps to make an accurate diagnosis and guide treatment decisions.
o In EPS, catheters are inserted in a manner similar to a right-sided heart catheterization. These
catheters are placed at specific anatomic sites within the heart to record electrical activity
o Nursing care for patients after EPS is similar to the care of patients after cardiac catheterization.
This includes continuous ECG monitoring and frequent assessment of vital signs and puncture
site.
Audience Response Question
A patient returns to the cardiac observation area following a cardiac catheterization with coronary
angiography. Which of the following assessments would require immediate action by the nurse?
1. Pedal pulses are 2+ bilaterally.
2. Apical pulse is 54 beats/minute.
3. Mean arterial pressure is 72 mm Hg.
4. ST-segment elevation develops on the ECG.
Answer: 4
Rationale: ST elevation on ECG indicates myocardial ischemia or injury with partial or total occlusion of a
coronary artery. This assessment finding requires immediate action. Actions would include assessment for
chest pain, 12-lead ECG, administration of nitroglycerin or morphine, and notification of the health care
provider. Option 1 would need further assessment but is not critical unless the patient is symptomatic (chest
pain, shortness of breath, hypotension, etc.). Options 2 and 3 are normal findings.
Med Surg 2 Exam #1 Study Guide
Chapter 33: Coronary Artery Disease and Acute Coronary Syndrome
Coronary Artery Disease (CAD)
 Atherosclerosis
o Begins as soft deposits of fat that harden with age
o Referred to as “hardening of arteries”
o Atheromas (fatty deposits) prefer coronary arteries
o Also known as ASHD, CVHD, IHD, CHD
 Difference between atherosclerosis and arteriosclerosis
o Atherosclerosis starts at birth
 Care about arteries (coronaries most sensitive where they like to live)
 If you have it in one place, its everywhere! Its not particular (ex. If in carotid in heart too)
 Will be put on statin first (interrupt process of fat build-up)
 Statin blocks cholesterol synthesis
o Arteriosclerosis –tightening of arteries
 Effects the endo (allows for release of hormones that make you more likely to clot)
 Coronary artery disease is a type of blood vessel disorder that is included in the general category of
atherosclerosis.
 The term atherosclerosis comes from two Greek words: athere, meaning “fatty mush,” and skleros,
meaning “hard.” This combination means that atherosclerosis begins as soft deposits of fat that harden
with age.
 Consequently, it is common to refer to atherosclerosis as “hardening of the arteries.”
 Although this disease can occur in any artery in the body, the atheromas (fatty deposits) prefer the
coronary arteries.
 The terms arteriosclerotic heart disease, cardiovascular heart disease, ischemic heart disease, coronary
heart disease, and CAD all describe this disease process.
Coronary Artery Disease: Etiology and Pathophysiology
 Atherosclerosis is major cause of CAD
o Characterized by lipid deposits within intima of artery
o Endothelial injury and inflammation play a major role in development
 NSAIDs –anti-inflammatories
Stages of Atherosclerosis
o A. The endothelium (the inner lining the vessel wall) is normally
nonreactive to platelets and leukocytes, as well as coagulation, fibrinolytic,
and complement factors. However, the endothelial lining can be injured as
a result of tobacco use, hyperlipidemia, hypertension, toxins, diabetes,
hyperhomocysteinemia, and infection causing a local inflammatory
response.
o CAD is a progressive disease that develops over many years. When it
becomes symptomatic, the disease process is usually well advanced.
o The stages of development in atherosclerosis are (1) fatty streak, (2)
fibrous plaque, and (3) complicated lesion.
o B. Fatty Streak
Fatty streaks, the earliest lesions of atherosclerosis, are characterized by lipid-filled
smooth muscle cells. As streaks of fat develop within the smooth muscle cells, a yellow
tinge appears. Fatty streaks can be seen in the coronary arteries by age 15 and involve an
increasing amount of surface area as one ages.
o C. Fibrous Plaque
 The fibrous plaque stage is the beginning of progressive changes in the endothelium of
the arterial wall. These changes can appear in the coronary arteries by age 30 and
increase with age. Once endothelial injury has taken place, lipoproteins (carrier proteins
within the bloodstream) transport cholesterol and other lipids into the arterial intima.
Collagen covers the fatty streak and forms a fibrous plaque with a grayish or whitish
appearance. These plaques can form on one portion of the artery or in a circular fashion
involving the entire lumen. The result is a narrowing of the vessel lumen and a reduction
in blood flow to the distal tissues. (90% occluded)
o D. Complicated Lesion
 The final stage in the development of the atherosclerotic lesion is the most dangerous.
As the fibrous plaque grows, continued inflammation can result in plaque instability,
ulceration, and rupture. Once the integrity of the artery’s inner wall is compromised,
platelets accumulate in large numbers, leading to a thrombus. The thrombus may
adhere to the wall of the artery, leading to further narrowing or total occlusion of the
artery. At this stage, the plaque is referred to as a complicated lesion. (100% occluded,
platelets tried to save the day and forms a clot)
o If dissolve the clot, just goes back to 90% occluded, with stent may get up to 100% blood flow
again.
 Stent stays in!
 Must be careful with stent –PCI (percutaneous coronary intervention)
 Give aspirin OR Plavix, doax and noax (G2B inhibitors) immediately after procedure
 Give 4 tablets baby aspirin (MUST chew)
 4 hour half-life (for temperature, but for platelet inhibition --permanently
damages platelets (changes the membrane) –have to make new platelets (7-10
days)
 Take aspirin only once a day (platelet dangerous when sticks together)
C-reactive protein (CRP)
o Nonspecific marker of inflammation
o Increased in many patients with CAD
o Chronic exposure to CRP linked with unstable plaques and oxidation of LDL cholesterol
o The level of CRP rises when there is systemic inflammation.
Collateral circulation
o Arterial anastomoses (or connections) within coronary circulation
o Increased with chronic ischemia
o May be inadequate with rapid-onset CAD
o Because of collateral circulation will be able to “handle it” (70 yr old)
 Make extra vessels
 By 70 make their own vessels
 Will be too late to put in a stent (100% occluded)
 Will need a bypass instead
o 40 yr old will not have time for building collateral circulation yet
o Normally some arterial anastomoses or connections, called collateral circulation, exist within
the coronary circulation.
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


o Two factors contribute to the growth and extent of collateral circulation: (1) inherited
predisposition to develop new blood vessels (angiogenesis) and (2) presence of chronic
ischemia.
o When plaque blocks the normal flow of blood through a coronary artery and the resulting
ischemia is chronic, increased collateral circulation develops.
o When occlusion of the coronary arteries occurs slowly over a long period, there is a greater
chance of collateral circulation developing, and the heart muscle may still receive an adequate
amount of blood and oxygen.
o However, with rapid-onset CAD (e.g., familial hypercholesterolemia) or coronary spasm, time is
inadequate for collateral development. Consequently, a reduced blood flow results in a more
severe ischemia or infarction.
Vessel Occlusion With Collateral Circulation
Risk Factors for CAD
 MUST BE able to differentiate between modifiable and nonmodifiable
 Nonmodifiable risk factors
o Age
o Gender
 The incidence of CAD is highest among middle-aged men. After age 75, the incidence of
serious heart events in men and women equalizes, although CVD causes more deaths in
women than men.
 On average, women with CAD are older than men who have CAD, and are more likely to
have co-morbidities (e.g., hypertension, diabetes). Most women have atypical symptoms
of angina rather than symptoms of MI when presenting with their initial heart event.
o Ethnicity
 African Americans have an earlier onset and more severe CAD than there CAD
counterparts.
 Additionally, CAD incidence and mortality rates are greater in African American women
than their white counterparts.
o Family history
 Family history is a risk factor for CAD and MI. Often, patients with angina or MI can name
a parent or sibling who has died of CAD.

o Genetic predisposition
 The genetic basis of CAD/MI is complex and poorly understood. It is estimated that the
genetic contribution to CAD/MI is as high as 40% to 60%. This proportion relates mainly
to genes that control known risk factors (e.g., lipid metabolism).
Major modifiable risk factors
o Modifiable risk factors include elevated serum lipids, elevated BP, tobacco use, physical
inactivity, obesity, diabetes, metabolic syndrome, psychologic states, and elevated
homocysteine level.
o Elevated serum lipids
 Cholesterol >200 mg/dL (5.2 mmol/L)
 Triglycerides >150 mg/dL (3.7 mmol/L)
 High-density lipoproteins (HDL)
 Low-density lipoproteins (LDL)
 Treatment according to guidelines based on 10-year and life time risk score
 If comorbidities, may put on statin but if not maybe not
 An elevated serum lipid level is one of the four most firmly established risk factors for
CAD. The risk of CAD is associated with a serum cholesterol level of more than 200
mg/dL (5.2 mmol/L) or a fasting triglyceride level of more than 150 mg/dL (3.7 mmol/L).
 For lipids to be used and transported by the body, they must become soluble in blood by
combining with proteins. Lipids combine with proteins to form lipoproteins. Lipoproteins
are vehicles for fat mobilization and transport, and vary in composition. Three major
lipoproteins are high-density lipoproteins (HDLs), LDLs, and very-low-density lipoproteins
(VLDLs).
 HDLs carry lipids away from arteries and to the liver for metabolism. Therefore, high
serum HDL levels are desirable and lower the risk of CAD.
 In general, HDL levels are higher in women, decrease with age, and are low in persons
with CAD. Physical activity and moderate alcohol intake increase HDL levels.
 LDLs contain more cholesterol than any of the lipoproteins and have an attraction for
arterial walls. Elevated LDL levels correlate most closely with an increased incidence of
atherosclerosis and CAD. Therefore, low serum LDL levels are desirable.
 Guidelines for treating elevated LDL cholesterol are based on a person’s 10-year and life
time risk for having heart disease or stroke. The following data generate a risk score: (1)
age, (2) gender, (3) race, (4) use of tobacco, (5) diabetes, (6) systolic BP (7) diastolic BP,
(8) use of BP drugs, (9) total cholesterol level, and (10) HDL cholesterol level. A 10-year
risk calculator is available at http://www.cvriskcalculator.com/ as well as for
smartphones (e.g., ASCVD Risk Estimator app).
 In general, persons with no or only one risk factor are considered at low risk for the
development of CAD, and their LDL goal is <160 mg/dL (4.14 mmol/L). Those at very high
risk for developing CAD have multiple risk factors. They have an LDL goal of <70 mg/dL
(1.8 mmol/L).
o Hypertension
 >140/90 mm Hg
 Goal for > age 60 is <150/90 mm Hg
 Begin lifestyle changes for prehypertension
 Therapeutic lifestyle changes should begin in people with prehypertension (BP of
120 to 139 mm Hg/80 to 89 mm Hg). Normal BP is <120/80 mm Hg. Stage 1
hypertension is 140 to 159/90 to 99 mm Hg. Stage 2 hypertension is BP >
160/100 mm Hg.
Treat stage 1 or 2 hypertension with drugs
The stress of an elevated BP increases the rate of atherosclerosis. This relates to the
shearing stress that causes endothelial injury.
o Tobacco use
 Risk is proportional to the number of cigarettes smoked.
 Increased catecholamine release (i.e., epinephrine, norepinephrine)
 These neurohormones cause an increased heart rate (HR), peripheral
vasoconstriction, and increased BP. These changes increase the heart’s workload
 ↑ LDL, ↓ HDL, ↑oxygen radicals
 All of these add to vessel inflammation and thrombosis.
 ↑ Carbon monoxide
 Affects the oxygen-carrying capacity of hemoglobin by reducing the sites
available for oxygen transport.
 Thus the effects of an increased cardiac workload, combined with the oxygendepleting effect of carbon monoxide, significantly decrease the oxygen available
to the heart muscle.
 There is also some indication that carbon monoxide is a chemical irritant, and
causes injury to the endothelium.
 Second-hand smoke
 Chronic exposure to environmental tobacco (secondhand) smoke also increases
the risk of CAD. People who live in the same house as the patient should be
encouraged to stop smoking. This reinforces the person’s effort and decreases
the risk of ongoing exposure to environmental smoke. Pipe and cigar smokers,
who often do not inhale, have an increased risk of CAD similar to those exposed
to secondhand smoke.
 The benefits of smoking cessation are dramatic and almost immediate. CAD mortality
rates drop to those of nonsmokers within 12 months. However, nicotine is highly
addictive and often calls for intensive intervention to assist people to quit.
o Physical inactivity
 Physical inactivity is the fourth major modifiable risk factor. Physical inactivity implies a
lack of adequate physical exercise on a regular basis. An example of health-promoting
regular physical activity is brisk walking (3 to 4 miles per hour) for at least 30 minutes 5
or more times a week.
 Physically active people have increased HDL levels. Exercise improves thrombolytic
activity, thus reducing the risk of clot formation. Exercise may also encourage the
development of collateral circulation in the heart.
o Obesity
 The death rate from CAD is higher in obese persons. Obesity is defined as a body mass
index (BMI) of >30 kg/m2 and a waist circumference ≥40 inches for men and ≥35 inches
for women.
 The increased risk for CAD is proportional to the degree of obesity.
 People who tend to store fat in the abdomen (an “apple” figure) rather than in the hips
and buttocks (a “pear” figure) have a higher incidence of CAD.
 Obesity is often linked with hypertension and insulin resistance.
Contributing modifiable risk factors
o Diabetes



The incidence of CAD is 2 to 4 times greater among persons who have diabetes, even
those with well-controlled blood glucose levels, than the general population. The patient
with diabetes manifests CAD not only more often but also at an earlier age.
 The person with diabetes has an increased tendency toward endothelial dysfunction.
This may account for the development of fatty streaks seen in these patients. Patients
with diabetes also have changes in lipid metabolism and tend to have high cholesterol
and triglyceride levels. Management of diabetes should include lifestyle changes and
drug therapy to achieve a hemoglobin A1c (Hb A1c) level <7%.
o Metabolic syndrome
 Metabolic syndrome refers to a cluster of risk factors for CAD whose underlying
pathophysiology may be related to insulin resistance.
 These risk factors include central obesity, hypertension, abnormal serum lipids, and an
elevated fasting blood glucose.
 Notes
 If can control these 2 80% other risk factors will control themselves
 Same patho process (not producing correct amount of insulin)
 No difference between type 1 and 2 for heart disease risk
o Psychologic states
 Certain behaviors and lifestyles may contribute to the development of CAD.
 One type of behavior, referred to as type A, includes perfectionism and a hardworking,
driving personality. The type A person often suppresses anger and hostility, has a sense
of time urgency, is impatient, and often creates stress and tension. This person may be
more prone to MIs than a type B person, who is more easygoing, takes upsets in stride,
knows personal limitations, takes time to relax, and is not an overachiever. However, the
relationship between behaviors and the risk for CAD/MI remains controversial and
complex.
 Psychologic risk factors thought to increase the risk of CAD include depression, acute
and chronic stress (e.g., poverty, serving as a caregiver), anxiety, hostility and anger, and
lack of social support. In particular, depression is a risk factor for both the development
and worsening of CAD. Depressed patients have elevated levels of circulating
catecholamines. This may contribute to endothelial injury and inflammation and platelet
activation.
 Higher levels of depression are also associated with an increased number of adverse
heart events.
 Stressful states can contribute to the development of CAD. Sympathetic nervous system
(SNS) stimulation and its effect on the heart are the physiologic mechanisms by which
stress predisposes a person to the development of CAD. SNS stimulation causes an
increased release of catecholamines (i.e., epinephrine, norepinephrine). This stimulation
increases HR and the force of myocardial contraction. Both results increase myocardial
oxygen demand. Also, stress-induced mechanisms can cause elevated lipid and glucose
levels and changes in blood coagulation, which can lead to increased atherosclerosis.
o Homocysteine level
 Part of inflammatory process
 High blood levels of homocysteine have been linked to an increased risk for CAD and
other CVDs.
 Homocysteine is produced by the breakdown of the essential amino acid methionine,
which is found in dietary protein. High homocysteine levels may contribute to
atherosclerosis by (1) damaging the inner lining of blood vessels, (2) promoting plaque
buildup, and (3) altering the clotting mechanism to make clots more likely to occur.

B-complex vitamins (B6, B12, folic acid) have been shown to lower blood levels of
homocysteine.
 Generally, a screening test for homocysteine is limited to those suspected of having
elevated levels. Theses include older patients with pernicious anemia or people who
develop CAD at an early age.
o Substance abuse
 Cocaine heart will be HUGE (won’t do transplant)
 If hx of substance abuse will want echo
 Need to be alert heart is NOT happy
 Correlation is NOT causation
 The use of illicit drugs, such as cocaine and methamphetamine, can produce coronary
spasm resulting in myocardial ischemia and chest pain.
 Most people who are seen in the emergency department (ED) with drug-induced chest
pain are initially indistinguishable from those with CAD.
 Although MI can occur, these patients often have sinus tachycardia, high BP, angina, and
anxiety.
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Audience Response Questions
Two risk factors for coronary artery disease that increase the workload of the heart and increase myocardial
oxygen demand are
a. Obesity and smokeless tobacco use.
b. Hypertension and cigarette smoking.
c. Elevated serum lipids and diabetes mellitus.
d. Physical inactivity and elevated homocysteine levels.
Answer: B
Rationale: An elevated blood pressure and cigarette smoking (causes vasoconstriction) increase the rate of
atherosclerosis. Atherosclerosis increases the workload of the heart and increases myocardial oxygen demand.
Hypertension BIGGEST risk factor
Which patient is most at risk for developing coronary artery disease?
a. A hypertensive patient who smokes cigarettes
b. An overweight patient who uses smokeless tobacco
c. A patient who has diabetes and uses methamphetamines
d. A sedentary patient who has elevated homocysteine levels
Answer: A
Rationale: The four major modifiable risk factors for coronary artery disease are elevated serum lipids,
hypertension, tobacco use, and physical inactivity. Other risk factors include diabetes mellitus, metabolic
syndrome, psychologic states, high levels of homocysteine, and substance abuse.
Nursing and Interprofessional Care: CAD
 Prevention and early treatment of heart disease must involve a multifaceted approach and needs to be
ongoing throughout the life span.
o Note
 Interprofessionals –anyone else on the healthcare team (NOT patient)
 Don’t use doctor or physician (HCP)
 Health Promotion
o Identification of people at high risk
 Health history, including family history (#1)
 Presence of cardiovascular symptoms (secondary prevention)
Environmental patterns: diet, activity
Psychosocial history: tobacco use, alcohol intake, recent stressful events (e.g., loss of a
spouse), and the presence of any negative psychologic states (e.g., anxiety, depression,
anger) or meds taken (hard on heart)
 Values and beliefs about health and illness
Manage high-risk persons by controlling modifiable risk factors
 People who have modifiable risk factors should be encouraged to make lifestyle changes
to reduce their risk of CAD. You can play a major role in teaching health-promoting
behaviors. For highly motivated persons, knowing how to reduce this risk may be the
information that they need to get started.
 For persons who are less motivated to take charge of their health, the idea of reducing
risk factors may be so remote that they are unable to perceive a threat of CAD. Few
people desire to make lifestyle changes, especially in the absence of symptoms. First
help these patients to clarify their personal values. Then, discuss risk factors and have
them identify their individual risks.
 This can help patients set realistic goals and choose which risk factor(s) to change first.
Encourage lifestyle changes
 Education
 Clarify personal values –pt centered care
 Set realistic goals
Physical fitness
 FITT formula: 30 minutes most days plus weight training 2 days a week
 Frequency (how often)
 Intensity (how hard)
 Type (isotonic)
 Time (how long)
 Regular physical activity contributes to
 Weight reduction (10%)
 Reduction of >10% in systolic BP
 In some men more than women, increase in HDL cholesterol
Nutritional therapy
 ↓ Saturated fats and cholesterol
 ↑ Complex carbohydrates and fiber
 ↓ Red meat, egg yolks, whole milk
 ↑ Omega-3 fatty acids
 Lifestyle changes, including a low-saturated-fat, highfiber diet; avoidance of tobacco; and increase in
physical activity, can promote the reversal of CAD and
reduce coronary events.
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Serum Lipids ***NOT ON TEST
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 Serum lipids and their role in cholesterol metabolism.
 Serum: heavy stuff falls to bottom (electrolytes in serum = serum
study) Ex. Blood sugar
 Chemistries from the serum
Types of Serum Lipids
Types of Dietary Fat
Audience Response Question
The nurse determines that teaching about implementing dietary changes to decrease the risk of CAD has been
effective when the patient says,
a. “I should not eat any red meat such as beef, pork, or lamb.”
b. “I should have some type of fish at least 3 times a week.”
c. “Most of my fat intake should be from olive oil or the oils in nuts.”
d. “If I reduce the fat in my diet to about 5% of my calories, I will be much healthier.”
Answer: C
Rationale: Monounsaturated fats are found in natural foods such as nuts and avocados, and are the main
component of tea seed oil and olive oil (oleic acid). Canola oil is 57% to 60% monounsaturated fat, olive oil is
about 75% monounsaturated fat, and tea seed oil is commonly more than 80% monounsaturated fat. Other
sources include macadamia nut oil, grapeseed oil, groundnut oil (peanut oil), sesame oil, corn oil, popcorn,
whole grain wheat, cereal, oatmeal, safflower oil, sunflower oil, tea-oil Camellia, and avocado oil. Fat intake
should be between 25% and 35% of calories (with most from monounsaturated fats and less from saturated
fats); red meats should be reduced or eliminated from the diet. Only fatty fish (such as tuna and salmon)
should be included in the diet because fatty fish is high in omega-3 fatty acids.
Nursing and Interprofessional Care: CAD Cont.
 An estimated 31.9 million American adults have cholesterol levels greater than or equal to 240 mg/dL
(6.2 mmol/L).
 Guidelines for treatment of high cholesterol focus on LDL cholesterol. A complete lipid profile is
recommended every 5 years beginning at age 20.
 Guidelines recommend the following groups of people receive statin therapy: (1) patients with known
CVD, (2) patients with primary elevations of LDL cholesterol levels greater than or equal to 190 mg/dL
(e.g., familial hypercholesterolemia), (3) patients between 40 and 75 years old with diabetes and LDL
cholesterol levels between 70 and 189 mg/dL, and (4) patients between 40 and 75 years old with LDL
cholesterol levels between 70 and 189 mg/dL and a 10-year risk for CVD of at least 7.5%.
 Treatment also includes weight loss (if overweight), decreased dietary fat and cholesterol intake, and
increased physical activity. Serum lipid levels should be reassessed after 6 weeks of therapy. If they
remain elevated, additional dietary options and drug therapy may be considered.
 Several classifications of drugs are used to decrease serum lipids.
 Lipid-lowering drug therapy
o If diet and exercise ineffective
o Statins
 Most widely used lipid-lowering drugs.
 Inhibit cholesterol synthesis in liver, decrease LDL, increase HDL, lower CRP levels
 Monitor for liver damage and myopathy
 Liver damage is #1 side effect of statins
 Check Liver enzymes (e.g., aspartate aminotransferase, alanine
aminotransferase) and monitor and recheck with any increase in dosage.
 Myopathy that can progress to rhabdomyolysis (breakdown of skeletal muscle).
o Educate pt to call HCP is any signs of rhabdomyolysis
 Take at nigh when liver most active (inhibit at peak effect)
 Tx patient NOT labs! Is your pt yellow?
o Niacin
 Lowers LDL and triglyceride by inhibiting synthesis
 Increases HDL better than many other lipid-lowering drugs.
 Flushing, pruritus, GI side effects, orthostatic hypotension
 OTC (can take an aspirin 15 min prior to reduce itching)
o Fibric acid derivatives (Lopid)
 Decrease triglycerides and increase HDL (most effective)
 No effects on LDLs
 GI side effects (gas, diarrhea)
 Increase lipoprotein removal
o Bile acid sequestrants
o Increase conversion of cholesterol to bile acids
o GI side effects; bind with other drugs
 belching, heartburn, nausea, abdominal pain, and constipation
 bile-acid sequestrants interfere with absorption of many other drugs (e.g., warfarin,
thiazides, thyroid hormones, β-adrenergic blockers)
 Decrease cholesterol absorption
o Ezetimibe (Zetia)
 Decrease absorption of dietary and biliary cholesterol
 It serves as an adjunct to dietary changes, especially in patients with primary
hypercholesterolemia.

o Drug therapy for hyperlipidemia often continues for a lifetime. Concurrent diet modification is
essential to reduce the need for drug therapy. The patient must fully understand the rationale
and goals of treatment, as well as the safety and side effects of lipid-lowering drugs.
Antiplatelet therapy
o ASA (Aspirin)
 Unless contraindicated (e.g., history of GI bleeding), low-dose aspirin (81 mg) is
recommended for most people at risk for CAD. Current recommendations include lowdose aspirin for men over 45 years and high-risk women (i.e., those with a calculated 10year CAD risk of >20%) unless contraindicated.
o Clopidogrel (Plavix)
 Dirt cheap
 Get when have a stent put in
 Sometimes for women who are intolerant to aspirin
o Understand action of antiplatelets and what to do if give too much
 Action: decrease platelet aggregation and inhibit thrombus formation. They are effective
in the arterial circulation, where anticoagulants have little effect.
Gerontologic Considerations: CAD
 Increased incidence and mortality associated with CAD in older adults
 Strategies to reduce risk and treat CAD are effective
 Treat hypertension, ↑ lipids
 Smoking cessation
 Necessary to modify guidelines for physical activity
o Longer warm-up
o Longer periods of low-level activity
o Longer rest periods
o Avoid extremes of temperature
o 30 minutes most days minimum
 Most likely to change when hospitalized or symptomatic
Clinical Manifestations of CAD: Angina
 Chronic and progressive disease
o May be asymptomatic for many years or they may develop chronic stable chest pain
 O2 demand > O2 supply → myocardial ischemia
o When the demand for myocardial oxygen exceeds the ability of the coronary arteries to supply
the heart with oxygen, myocardial ischemia occurs
 Angina = clinical manifestation
o Occurs when arteries are blocked (stenosed) 70% or more
o 50% or more for left main coronary artery
 Needs most blood (less blockage needed)
Clinical Manifestations of CAD: Chronic Stable Angina
 Intermittent chest pain that occurs over a long period with same pattern of onset, duration, and
intensity of symptoms
 Few minutes in duration
o Commonly subsides when the precipitating factor is resolved (resting, calming down, using
sublingual NTG)
 ST segment depression and/or T-wave inversion  ischemia
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Control with drugs
It is often provoked by physical exertion, stress, or emotional upset.
When asked, some patients may deny feeling pain but describe a pressure, heaviness, or discomfort in
the chest. This discomfort is often described as a squeezing, heavy, tight, or suffocating sensation.
It may be associated with other symptoms such as dyspnea or fatigue.
Chronic angina pain usually does not change with position or breathing and is rarely described as sharp
or stabbing.
Locations and Patterns of Angina and MI
 Although most angina pain occurs substernally, it may radiate to other locations, including the jaw,
neck, shoulders, and/or arms.
 Many people with angina complain of indigestion or a burning sensation in the epigastric region.
 The sensation may also be felt between the shoulder blades.
 Often people who complain of pain between the shoulder blades or indigestion type pain dismiss it as
not being heart related.
 Some patients, especially women and older adults, report atypical symptoms of angina including
dyspnea, nausea, and/or fatigue.
 This is referred to as angina equivalent.
Chronic Stable Angina: Types of Angina
 Silent ischemia
o Ischemia that occurs in absence of any subjective symptoms
o Associated with diabetic neuropathy
 Central neuropathy  autonomic nervous system cannot respond normally
 #1 gastroporesis (no gastric emptying)
 Cannot get tachy or brady
 Cannot feel pain (won’t know had MI)
o Confirmed by ECG changes
 Prinzmetal’s (variant) angina
o Rare
o Occurs at rest
o Can be seen in patients with a history of migraine headaches, Raynaud’s phenomenon and
heavy smoking
o Spasm of a major coronary artery
 When spasm occurs, the patient experiences angina and transient ST-segment elevation.
o CAD may or may not be present
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o The pain may occur during rapid-eye-movement (REM) sleep when myocardial oxygen
consumption increases or when exposed to cold temperatures.
o The pain may be relieved by moderate exercise, with SL NTG, or it may disappear
spontaneously.
o Cyclic, short bursts of pain at a usual time each day may also occur with this type of angina.
o Calcium channel blockers and/or nitrates are used to control the pain, as well as stopping any
offending substances.
Microvascular angina
o Syndrome X
 It is more common in postmenopausal women.
o Chest pain occurs in the absence of significant CAD or coronary spasm of a major coronary
artery
o Prevention and treatment follows the same CAD recommendations
o Chest pain is related to myocardial ischemia associated with atherosclerosis or spasm of the
small distal branch vessels of the coronary microcirculation.
o Often the angina is prolonged and brought on by physical exertion.
o These patients usually have positive stress test results and have an inconsistent response to
nitrates.
Chronic Stable Angina: Interprofessional Care
 Goal: ↓ O2 demand and/or ↑ O2 supply
 Short-acting nitrates
o Dilate peripheral and coronary blood vessels (veno and vasodilator)
o Give sublingually or by spray
 The recommended dose of NTG is one tablet taken sublingually (SL) or one metered
spray on the tongue for symptoms of angina.
o If no relief in 5 minutes, call EMS; if some relief, repeat every 5 minutes for maximum 3 doses
o Patient teaching
 At onset of pain take, SIT DOWN, call EMS if no relief after second dose
o Can use prophylactically
 Long-acting nitrates
o To reduce angina incidence
o Main side effects: headache, orthostatic hypotension
o Methods of administration
 Oral
 Nitroglycerin (NTG) ointment
 Transdermal controlled-release NTG
 Take patch off before shocking pt
o Tolerance to long-acting NTG can develop. To limit this, patients are often scheduled a 10-14
hour nitrate-free period every day.
 Angiotensin-converting enzyme inhibitors (ACE) and angiotensin receptor blockers (ARBs)
o Patients with chronic stable angina who have an ejection fraction [EF] of 40% or less, diabetes,
hypertension, or chronic kidney disease should take an ACE inhibitor (e.g., lisinopril [Zestril])
indefinitely, unless contraindicated. Patients with chronic stable angina and a normal EF,
diabetes, and one other CAD risk factor should also take an ACE inhibitor to decrease the risk of
MI, stroke and death.
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o These drugs result in vasodilation and reduced blood volume. Most important, they can prevent
or reverse ventricular remodeling in patients who have had an MI. For patients who are
intolerant of ACE inhibitors (e.g. cough, angioedema), ARBs (e.g., losartan [Cozaar]) are used.
β-Blockers
o β-Blockers are ordered for relief of angina symptoms in patients with chronic stable angina.
Patients who have LV dysfunction, elevated BP, or have had an MI should start and continue βblockers indefinitely, unless contraindicated. These drugs decrease myocardial contractility, HR,
SVR, and BP, all of which reduce the myocardial oxygen demand. β-Blockers that have been
shown to reduce the risk of death in patients with LV dysfunction, heart failure (HF) or MI are
carvedilol (Coreg), metoprolol (Lopressor, Toprol XL), and bisoprolol (Zebeta).
o β-Blockers have many side effects and can be poorly tolerated. Side effects may include
bradycardia, hypotension, wheezing from bronchospasm, and GI complaints. Many patients also
complain of weight gain, depression, fatigue, and sexual dysfunction. Absolute contraindications
to using β-blockers include severe bradycardia and acute HF. Patients with asthma should avoid
β-blockers. They are used cautiously in patients with diabetes, since they mask signs of
hypoglycemia. β-blockers should not be stopped abruptly without medical supervision as this
may result in an increase in the number and intensity of angina attacks.
Calcium channel blockers
o If β-Blockers are contraindicated, are poorly tolerated, or do not control anginal symptoms,
calcium channel blockers are used. The primary effects of calcium channel blockers are (1)
systemic vasodilation with decreased SVR, (2) decreased myocardial contractility, (3) coronary
vasodilation, and (4) decreased HR. There are 2 groups of calcium channel blockers – those
which have more vasodilatory effects and those which have more rate and contractility effects.
Teach patients that they increase serum digoxin levels and therefore levels should be closely
monitored.
Lipid lowering drugs
o Although patients with chronic stable angina are encouraged to follow a diet low in saturated
fat and cholesterol, a moderate or high dose of a lipid lowering drug should be ordered, unless
contraindicated.
o Sodium current inhibitor
 Ranolazine (Ranexa)
 Ranolazine (Ranexa), a sodium current inhibitor, is used to treat chronic angina in
patients who have not had an adequate response with other antianginals.
 It is not a first-line drug for chronic stable angina.
 Because ranolazine prolongs the QT interval, patients with a long QT interval or
who are taking QT-prolonging drugs (e.g., fluoxetine [Prozac]) should not use it.
 Common side effects of ranolazine include dizziness, nausea, constipation, and
headache.
Diagnostic studies
o Chest x-ray
 After a detailed health history and physical examination, a chest x-ray is done to look for
cardiac enlargement, aortic calcifications, and pulmonary congestion.
o 12-lead ECG
 A 12-lead ECG is done and compared with a previous ECG whenever possible to look for
any changes.
o Laboratory studies
 Laboratory tests (e.g., lipid profile, C-reactive protein) are done to identify specific risk
factors for CAD.
o Echocardiogram
 An echocardiogram may be done to look for resting LV wall motion abnormalities, which
may suggest evidence of CAD.
o Exercise stress test
 An exercise stress test with or without echocardiography or nuclear imaging may be
ordered. For patients with physical limitations in walking, a pharmacologic (adenosine
[Adenocard] or dipyridamole [Persantine]) stress test with nuclear imaging, or a
pharmacologic (dobutamine [Dobutrex]) stress echocardiogram may be ordered.
Coronary blockages less than 70% are not usually detected with stress testing.
o EBCT
 The electron beam computed tomography (EBCT) scan locates and measures coronary
calcification. However, additional testing (e.g., stress testing or cardiac catheterization) is
needed to further assess the impact of the lesion on coronary blood flow. Further
studies are needed to determine the accuracy of the EBCT scan to diagnose high-grade
blockages because many atherosclerotic plaques are not calcified.
o CCTA
 Coronary computed tomography angiography (CCTA) may be considered. Using IV
contrast and radiation, CCTA can detect calcified and noncalcified plaques in the artery,
as well as other heart conditions. Limitations of using CCTA include patients with rapid
HRs (greater than 90 beats per minute), extensive coronary artery calcifications, obesity,
and a history of prior coronary artery stent. Patients allergic to IV contrast dye must be
premedicated with corticosteroids. Patients with chronic kidney disease need hydration
pre- and post-procedure. A baseline serum creatinine level should be obtained as the IV
contrast dye can worsen renal function.
Chronic Stable Angina: Nursing/ Interprofessional Care
 Cardiac catheterization/coronary angiography
o Visualize blockages (diagnostic)
o Open blockages (interventional)
 Percutaneous coronary intervention (PCI)
 Balloon angioplasty
 Stent
o For patients with increasing angina a cardiac catheterization is ordered. Cardiac catheterization
and coronary angiography use radiation and IV contrast dye to provide images of the coronary
circulation and identify the location and severity of any blockage.
o If a patient is allergic to IV contrast dye, they must be premedicated with corticosteroids.
Patients with chronic kidney disease need hydration pre- and post-procedure. A baseline serum
creatinine level is obtained because the IV contrast dye can worsen renal function. Monitor
renal function closely after the procedure. This procedure should only be done if the patient is a
candidate for percutaneous or surgical coronary revascularization.
o If a coronary blockage is amenable to treatment, coronary revascularization with an elective
percutaneous coronary intervention (PCI) may be recommended.
o During PCI, a catheter with a deflated balloon tip is inserted into the appropriate coronary
artery. The deflated balloon is positioned in the blockage and inflated. This compresses the
plaque against the artery wall, resulting in vessel dilation and a larger vessel diameter. This
procedure is called balloon angioplasty.
o Intracoronary stents are usually placed along with balloon angioplasty.
Placement of Coronary: Artery Stent
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A stent is an expandable meshlike structure designed to keep the vessel open after balloon angioplasty.
Because stents are thrombogenic, many different types of drugs are used to prevent platelet
aggregation within the stent. Drugs commonly used during PCI are unfractionated heparin (UH) or lowmolecular-weight heparin (LMWH), a direct thrombin inhibitor (e.g., bivalirudin [Angiomax]), and/or a
glycoprotein IIb/IIIa inhibitor (e.g., eptifibatide [Integrilin]). After PCI, the patient is treated with dual
antiplatelet drugs (e.g., aspirin [indefinitely] and clopidogrel) up to 12 months or longer, until the
intimal lining grows over the stent and provides a smooth vascular surface.
There are two types of stents: bare metal stents (BMS) and drug-eluting stents (DES). DESs are coated
with a drug (e.g., paclitaxel, sirolimus) to reduce the risk of overgrowth of the intimal lining (neointimal
hyperplasia) within the stent. This is the primary cause of in-stent restenosis (ISR). Following DES
placement, dual antiplatelet drugs are taken to prevent thrombus formation within the stent (stent
thrombosis) for a minimum of 12 months or longer. The duration of dual antiplatelet drugs for patients
with BMS is a minimum of 1 month but ideally one full year after PCI.
The most serious complications from stent placement are abrupt closure from coronary artery
dissection and vascular injury at the artery access site (femoral or radial), acute MI, stent embolization,
coronary spasm, dye allergy, renal compromise, bleeding (e.g., retroperitoneal), infection, stroke and
emergent coronary artery bypass graft (CABG) surgery. The possibility of dysrhythmias during and after
the procedure is always present.
Chronic Stable Angina: Nursing/ Interprofessional Care Cont.
 Alternative therapies for refractory chronic stable angina
o Enhanced external counterpulsation (EECP)
 Inflatable cuffs are placed around legs
 Increase venous return
 Augment DBP
 For patients with refractory stable angina, enhanced external counterpulsation (EECP)
may be used. EECP consists of placing inflatable BP cuffs around the legs. The cuffs
sequentially inflate during diastole and deflate during systole from the calves to the
thighs.
 This action is thought to increase venous return and augment diastolic BP in order to
increase coronary perfusion, improve LV diastolic filling, and help with collateral
circulation.
 Patients get treatments 5 days a week for a total of 35 treatments.
 EECP is contraindicated in patients with decompensated HF, severe peripheral arterial
disease, and severe aortic insufficiency.
o Spinal cord stimulation
 Spinal cord stimulation may also help relieve symptoms in patients who are refractory to
drugs or revascularization. The stimulation lead is placed in the epidural space between
T1 and T2 and is connected to an implanted subcutaneous pulse generator. The
mechanism by which angina is reduced is not well understood.
Pre-PCI and Post-PCI With Stent Placement
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A, An occluded coronary artery is shown; B, the same artery (now open) after PCI and stent placement.
Acute Coronary Syndrome
 When ischemia is prolonged and not immediately
reversible, acute coronary syndrome (ACS)
develops. ACS includes the spectrum of UA, non–
ST-segment-elevation myocardial infarction
(NSTEMI), and ST-segment-elevation myocardial
infarction (STEMI).
 When patients first present with chest pain, STelevations on the 12-lead ECG are most likely
indicative of a STEMI. The ECG should always be
compared to a previous ECG whenever possible.
 For patients with chest pain who do not show ST-elevation or ST-T wave changes on the ECG, it is
difficult to distinguish between UA and NSTEMI until serum cardiac biomarkers are measured.
 On the cellular level, the heart muscle becomes hypoxic within the first 10 seconds of a total coronary
occlusion. Heart cells are deprived of oxygen and glucose needed for aerobic metabolism and
contractility. Anaerobic metabolism begins and lactic acid accumulates.
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In ischemic conditions, heart cells are viable for approximately 20 minutes. Irreversible heart damage
starts after 20 minutes if there is no collateral circulation.
NSTEMI worse –incomplete MI
o Requires significantly more monitoring because you don’t know what’s happening
STEMI –injury NOT infarction (dead tissue)
o Injury = firemans hat
o Infarction = dead tissue
o Ischemia = sagging at S-T (depression)
EKG is NOT diagnostic of MI
Troponin positive means there is dead tissue
Acute Coronary Syndrome: Etiology and Pathophysiology
 Deterioration of once stable plague  Rupture  Platelet aggregation  Thrombus
 Result
o Partial occlusion of coronary artery: UA or NSTEMI
 Unstable angina =nothing dies
 NSTEMI = probably something died
o Total occlusion of coronary artery: STEMI
 ACS is caused by the decline of a once stable atherosclerotic plaque. The previously stable plaque
ruptures, releasing substances into the vessel. This stimulates platelet aggregation and thrombus
formation.
 This area may be partially occluded by a thrombus (manifesting as UA or NSTEMI) or totally occluded by
a thrombus (manifesting as STEMI).
 What causes a coronary plaque to suddenly become unstable is not well understood, but systemic
inflammation (described earlier) is thought to play a role.
 Patients with suspected ACS require immediate hospitalization.
Clinical Manifestations of ACS: Unstable Angina
 New in onset
 Occurs at rest
 Increase in frequency, duration, or with less effort
 Pain lasting > 10 minutes
o 2 Nitro (if take two and doesn’t help call 911, if not any better after 1 call 911 don’t wait)
 Needs immediate treatment
o Unlike chronic stable angina, UA is unpredictable and must be treated immediately.
 Symptoms in women often under-recognized
o These include fatigue, shortness of breath, indigestion, and anxiety.
o Fatigue is the most prominent symptom.
o However, all these symptoms can relate to many different diseases and syndromes. It is because
of these reasons that women often present with UA before CAD is diagnosed.
Clinical Manifestations of ACS Myocardial Infarction (MI)
 ST-elevation and non-ST-elevation
 Result of abrupt stoppage of blood flow through a coronary artery caused by platelet aggregation,
causing irreversible myocardial cell death (necrosis)
o Preexisting CAD
o STEMI - occlusive thrombus
A STEMI caused by an occlusive thrombus creates ST-elevation in the ECG leads facing
the area of infarction. A STEMI is an emergency situation. In order to limit the infarct
size, the artery must be opened within 90 minutes of presentation. This can be done
either by PCI or thrombolytic (fibrinolytic) therapy. PCI is the preferred treatment if a
hospital is capable of performing PCI.
o NSTEMI - non-occlusive thrombus
 NSTEMI, caused by a non-occlusive thrombus, does not cause ST elevation on the 12lead ECG. Patients may or may not develop ST-T wave changes in the leads affected by
the infarction. NSTEMI patients do not go to the catheterization laboratory emergently
but usually undergo the procedure within 12 to 72 hours if there are no
contraindications. Thrombolytic therapy is not indicated for NSTEMI patients.
 With either a NSTEMI or STEMI, an echocardiogram may show hypokinesis (worsening
myocardial contractility) or akinesis (absent myocardial contractility) in the necrotic
area(s). The degree of LV dysfunction depends on the area of the heart involved and size
of the infarction.
Pain
o Severe chest pain not relieved by rest, position change, or nitrate administration
 Heaviness, pressure, tightness, burning, constriction, crushing
 Substernal or epigastric
 May radiate to neck, lower jaw, arms, back
 Try to ELIMINATE pain in chest pain because means oxygen not getting to heart
 In surgical pain just trying to control (difference)
 Don’t even care about respirations (if in that much pain will be high enough)
 Morphine –vasodilation = decreasing cardiac workload and oxygen needed by
that tissue
o Want pt to be calm
 Nitro and morphine help decrease cardiac workload
o It usually lasts for 20 minutes or longer and is more severe than usual anginal pain.
o Often occurs in early morning
o Atypical in women, elderly
 Although women and men have more similarities than differences in their acute MI
symptoms, some women may experience atypical discomfort, shortness of breath, or
fatigue.
 An older patient may experience a change in mental status (e.g., confusion), shortness of
breath, pulmonary edema, dizziness, or a dysrhythmia.
o No pain if cardiac neuropathy (diabetes)
 Patients with diabetes may experience silent (asymptomatic) MIs because of cardiac
neuropathy or may manifest atypical symptoms (e.g., dyspnea).
 Same as central neuropathy
 First sign is gastroparesis
Catecholamine release and stimulation of SNS (norepinephrine and epinephrine)
o Release of glycogen (liver)
o Diaphoresis (sympathetic nervous system)
o Increased HR and BP
o Vasoconstriction of peripheral blood vessels
o Skin: ashen, clammy, and/or cool to touch
Cardiovascular
o Initially, ↑ HR and BP, then ↓ BP (secondary to ↓ in CO)
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 If severe enough, this may result in decreased renal perfusion and urine output.
o Crackles (acute HF if hear crackles)
o Jugular venous distention, hepatic engorgement, and peripheral edema may indicate right
ventricular dysfunction
o Abnormal heart sounds
 S3 or S4
 New murmur
 This may indicate a ventricular septal defect, papillary muscle rupture, or valve
dysfunction.
Nausea and vomiting
o Reflex stimulation of the vomiting center by severe pain
o Vasovagal reflex
o Look at pt, what is BP?
Fever
o Up to 100.4° F (38° C) in first 24-48 hours
o Systemic inflammatory process caused by heart cell death (normal)
o May last 4-5 days
Myocardial Infarction From Occlusion
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The acute MI process evolves over time.
The earliest tissue to become ischemic is the subendocardium (the innermost layer of tissue in the
heart muscle).
If ischemia persists, it takes approximately 4 to 6 hours for the entire thickness of the heart muscle to
become necrosed.
If the thrombus is not completely blocking the artery, the time to complete necrosis may be as long as
12 hours.
Acute Myocardial Infarction
 Acute myocardial infarction in the posterolateral wall of the left
ventricle. This is demonstrated by the absence of staining in the
areas of necrosis (white arrow). Note the scarring from a previous
anterior wall myocardial infarction (black arrow).
 The majority of MIs affect the LV and are usually described based on
the location of damage (e.g., anterior, inferior, lateral, septal, or
posterior wall infarction). The location of the MI and ECG changes
correlate with the involved coronary artery.
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For example, in most people, the right coronary artery provides blood to the inferior and posterior LV
walls. Blockage of the right coronary artery results in an inferior wall and/or posterior wall MI. Anterior
wall infarctions result from blockages in the left anterior descending artery. Blockages in the left
circumflex artery usually cause lateral LV wall MIs. Damage can occur in more than one location,
especially if more than one coronary artery is involved (e.g., anterolateral MI). Right ventricular MIs are
much less common and treated differently than LV MIs.
Not everyone develops collateral circulation, but if present, the degree of collateral circulation
influences the severity of the MI. An individual with a long history of CAD may develop good collateral
circulation to provide the area surrounding the infarction site with a blood supply. This is one reason
why a younger person may have a more serious first MI than an older person with the same degree of
blockage.
Myocardial Infarction Healing Process
 Within 24 hours, leukocytes infiltrate the area of cell death
 Proteolytic enzymes of neutrophils and macrophages begin to remove necrotic tissue by fourth day →
thin wall
 Necrotic zone identifiable by ECG changes
o The necrotic zone of a STEMI is identified by ECG changes (e.g., lowering of the ST-segments, Twave inversion, pathologic Q wave) within a day or two.
 Collagen matrix laid down
o At this point, the neutrophils and monocytes have cleared the necrotic debris from the injured
area, and the collagen matrix that will eventually form scar tissue is laid down.
 10 to 14 days after MI, scar tissue is still weak
o At risk for rupture (cannot save pt)
 Heart muscle vulnerable to stress
o Want pt to rest
 Monitor patient carefully as activity level increases
 By 6 weeks after MI, scar tissue has replaced necrotic tissue
o Area is said to be healed, but less compliant (doesn’t squeeze well) then surrounding area
 Ventricular remodeling
o Normal myocardium will hypertrophy and dilate in an attempt to compensate for infarcted
muscle
o Remodeling of normal myocardium can lead to the development of late heart failure (HF),
especially in the person with atherosclerosis of other coronary arteries and/or an anterior MI.
o ACE inhibitors and ARBs are given to limit ventricular remodeling.
Complications of Myocardial Infarction
 Dysrhythmias
o Most common complication (put on monitor)
 Any condition that affects the heart cells’ sensitivity to nerve impulses (e.g., ischemia,
electrolyte imbalances, SNS stimulation) can cause dysrhythmias that adversely affect
the damaged heart muscle.
o Present in 80% to 90% of MI patients
o Can be caused by ischemia, electrolyte imbalances, or SNS stimulation
o VT and VF are most common cause of death in prehospitalization period
 If a patient survives a cardiac arrest, initiate a therapeutic hypothermia protocol as soon
as possible.
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o Bradycardias (e.g., complete heart block) develop when key areas of the conduction system are
destroyed.
 VT or VF most often occur within the first 4 hours after the onset of pain.
 Premature ventricular contractions (PVCs) may precede VT and VF.
 Life-threatening ventricular dysrhythmias must be treated immediately.
o With reperfusion, it is not uncommon to see PVCs, asymptomatic nonsustained VT, and
idioventricular rhythms. These rhythms are not associated with an increased risk of sudden
cardiac death (SCD) and are not treated unless the patient is symptomatic.
Heart failure
o Occurs when pumping power of heart has diminished (right or left)
o Left-sided HF
 Mild dyspnea, crackles, restlessness, agitation, slight tachycardia initially
 PRIORITY: sit them up
 Other signs indicating the onset of left–sided HF include pulmonary congestion on chest
x-ray, S3 or S4 heart sounds on auscultation of the heart, crackles on auscultation of the
lungs, paroxysmal nocturnal dyspnea (PND), and orthopnea.
o Right-sided HF
 Jugular venous distention, hepatic congestion (big liver), lower extremity edema
Cardiogenic shock
o Occurs because of
 Severe LV failure, papillary muscle rupture, ventricular septal rupture, LV free wall
rupture, right ventricular infarction (causing inadequate oxygen and nutrients)
 This occurs less often with the early and rapid treatment of STEMI with PCI or
thrombolytic therapy.
 NOW lower head and feet back into bed
o Requires aggressive management
 Associated with a high death rate
 Treatment includes control of dysrhythmias, intraaortic balloon pump (IABP) therapy,
and support of contractility with vasoactive drugs.
 Goals of therapy are to maximize oxygen delivery, reduce oxygen demand, and prevent
complications (e.g., acute kidney injury).
Papillary muscle dysfunction or rupture
o Causes mitral valve regurgitation (rare and life threatening)
o Aggravates an already compromised LV by reducing CO further → rapid clinical deterioration
o Dyspnea, pulmonary edema, and decreased CO result from the backup of blood in the left
atrium.
o Treatment includes afterload reduction with nitroprusside (Nipride) and/or IABP therapy, and
immediate cardiac surgery with mitral valve repair or replacement.
Left ventricular aneurysm
o Myocardial wall becomes thinned and bulges out during contraction
 This can develop within a few days, weeks, or months
 It is more common with anterior MIs.
o Leads to HF, dysrhythmias, and angina
o Besides ventricular rupture, which is usually fatal, ventricular aneurysms can hide thrombi that
can lead to an embolic stroke.
o Anticoagulation therapy is recommended for these patients if not contraindicated.
Ventricular septal wall rupture and left ventricular free wall rupture
o New, loud systolic murmur
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o HF and cardiogenic shock may occur (depending on defect and degree of right LV dysfunction)
o Emergency repair (surgically or percutaneously)
o Rare condition associated with high death rate
 The defect can quickly expand and lead to hemodynamic compromise.
 LV free wall rupture is an emergent clinical situation. Rapid hemodynamic compromise
and death ensues if not treated immediately.
o Free wall rupture is seen more frequently in patients suffering their first MI, patients with
anterior MIs, older adults, and women.
o Supportive care, have has massive MI and not much you can do (deadly)
Acute pericarditis
o Inflammation of visceral and/or parietal pericardium (because of dead tissue)
o May occur 2 to 3 days after an acute MI.
o Mild to sever chest pain
 Increases with inspiration, coughing, movement of upper body
 Relieved by sitting in forward position
 Will hear scratching noise
 TX: ibuprofen (decrease inflammation)
o Pericardial friction rub
 The sound is best heard with the diaphragm of the stethoscope at the mid to lower left
sternal border. It may be persistent or intermittent.
 Fever may also be present.
o ECG changes
 Diagnosis of pericarditis can be made with serial 12-lead ECGs. Typical ECG changes
include diffuse ST-segment elevations. This reflects the inflammation of the pericardium.
o Treatment includes pain relief with high doses of aspirin (e.g., 650 mg every 4-6 hours).
Dressler syndrome
o Pericarditis and fever that develops 1 to 8 weeks after MI
o Chest pain, fever, malaise, pericardial friction rub, arthralgia
o A pericardial effusion may be present.
o Laboratory findings include an elevated white blood cell count and sedimentation rate.
o High dose aspirin is treatment of choice
 Nonsteroidal antiinflammatory drugs (NSAIDs) and corticosteroids are avoided in the
first 4 weeks following MI because they can interfere with myocardial scar formation.
Unstable Angina and MI (AKA acute coronary syndrome): Diagnostic Studies
 Detailed health history
 12-lead ECG
o Compare to previous ECG
o Changes in QRS complex, ST segment, and T wave
 caused by ischemia and infarction can develop slowly or quickly with UA and MI.
o Distinguish between STEMI and NSTEMI
 STEMI patients usually have a complete coronary occlusion. ST elevation is first seen on
the 12-lead ECG. Within a few hours to days, T-wave inversion and pathologic Q waves
develop.
Patients with NSTEMI or UA usually have transient thrombosis or incomplete coronary
occlusion. These patients often develop ST depression or T wave inversion on the initial
ECG. They usually do not develop
pathologic Q waves.
o Serial ECGs reflect evolution of MI
Serum Cardiac Biomarkers After MI
o Serum cardiac biomarkers are proteins
released into the blood from necrotic heart
muscle after an MI.
o These biomarkers are important in the
diagnosis of MI. The onset, peak, and
duration of levels of these biomarkers are
shown in this graph.
o Cardiac-specific troponin has two subtypes:
cardiac-specific troponin T (cTnT) and
cardiac-specific troponin I (cTnI). These biomarkers are highly specific indicators of MI and have
greater sensitivity and specificity for myocardial injury than creatine kinase (CK-MB). Serum
levels of cTnI and cTnT increase 4 to 6 hours after the onset of MI, peak at 10 to 24 hours, and
return to baseline over 10 to 14 days.
o Serial cardiac biomarkers are drawn over 24 hours (e.g., every 8 hours x3). The presence of
biomarkers helps to differentiate between a diagnosis of UA (negative biomarkers) and NSTEMI
(positive biomarkers).
o CK levels begin to rise at about 6 hours after an MI, peak at about 18 hours, and return to
normal within 24 to 36 hours. The CK enzymes are fractionated into bands. The CK-MB band is
specific to heart muscle cells and help to quantify myocardial damage.
o Myoglobin is released into the circulation within 2 hours after an MI and peaks in 3 to 15 hours.
Although it is one of the first serum cardiac biomarkers to appear after an MI, it lacks cardiac
specificity. Its role in diagnosing MI is limited.
Coronary angiography
o For patients with a STEMI
 within 90 minutes of presentation or receive thrombolytic therapy within 30 minutes in
agencies without PCI capability. This will open the totally occluded artery and limit the
infarction size.
o Not for patients with UA or NSTEMI
o Guidelines suggest that it is reasonable to do coronary angiography on stable but high-risk
patients with UA or NSTEMI within 12-72 hours after presentation. If appropriate, a PCI is
performed at this time.
o Some patients may be treated only with conservative medical management.
o Only go to cath lab with NSTEMI if CHANGE IN PAIN
Pharmacologic stress testing
o For patients with abnormal but nondiagnostic ECG and negative biomarkers
 Give dobutamine instead of have pt run (can watch for changes without stressing body)
o When the ECG and serum cardiac biomarkers do not confirm MI, other measures for diagnosing
CAD are considered.
o To assess for ischemia or infarction, pharmacologic stress testing may be done when a patient
has an abnormal but nondiagnostic ECG and negative biomarkers.
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Interprofessional Care: Acute Coronary Syndrome
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Initial interventions
o 12-lead ECG
o Upright position
o Oxygen by nasal cannula – keep O2 sat > 93%
o IV access
o Nitroglycerin (SL) and ASA (chewable)
o Statin (if not already taking)
o Morphine (for pain)
Ongoing monitoring
o Treat dysrhythmias (per agency)
o Some patients are started on glycoprotein IIb/IIIa inhibitors (e.g., eptibibatide) either before
catheterization or at the time of PCI.
o Frequent vital sign monitoring
o Bed rest/limited activity for 12–24 hours
UA or NSTEMI
o Dual antiplatelet therapy (aspirin and clopidogrel) and heparin (prevent any additional clots)
o Cardiac catheterization with PCI once stable
 Can be on heparin because have protamine sulfate
NSTEMI
o Reperfusion therapy
Emergent PCI
o Treatment of choice for confirmed STEMI
o Goal: 90 minutes from door to catheter laboratory
o Balloon angioplasty + stent(s)
o Many advantages over CABG
 The advantages of PCI (compared to thrombolytic therapy) include the following: (1) it
provides an alternative to surgical intervention; (2) it is performed with local anesthesia;
(3) the patient is ambulatory shortly after the procedure; (4) the length of hospital stay is
approximately 3 to 4 days after MI compared with the 4 to 6 days with CABG surgery,
thus reducing hospital costs; and (5) the patient can return to work several weeks
sooner after PCI compared to 6- to 8-week convalescence after CABG.
 Advances in PCI techniques have significantly reduced the need for emergent CABG.
 Currently, there are more PCIs than CABGs performed in the United States.
Thrombolytic (fibrinolytic) therapy
o Only for patients with a STEMI
 Agencies that do not have cardiac catheterization resources
o Given IV within 30 minutes of arrival to the ED
 Gets rid of all clots (Tissue plasminogen activator- TPA)
o Treatment of STEMI with thrombolytic therapy aims to limit the infarction size by dissolving the
thrombus in the coronary artery and reperfusing the heart muscle.
o Patient selection critical
 Because all thrombolytics lyse the pathologic clot, they may also lyse other clots (e.g., a
postoperative site). Therefore patient selection is important because minor or major
bleeding can be a complication of therapy. Inclusion criteria for thrombolytic therapy are
(1) chest pain less than 12 hours with 12-lead ECG findings consistent with acute STEMI
and (2) no absolute contraindications.
 Patients with chest pain lasting 12-24 hours with ECG changes supporting STEMI may be
considered for thrombolytic therapy.
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o Draw blood and start 2–3 IV sites (or 6)
 Baseline data
 IVs in first to prevent hemorrhage
o Complete invasive procedures prior
o Administer according to protocol
o Monitor closely for signs of bleeding
 All other invasive procedures are done before the thrombolytic agent is given to reduce
the possibility of bleeding in the patient.
o Assess for signs of reperfusion
 Return of ST segment to baseline best sign
 Other signs include a resolution of chest pain, and an early, rapid rise of the cardiac
biomarkers within 3 hours of therapy and peaking within 12 hours. These levels increase
as the necrotic heart cells release proteins into the circulation after perfusion is restored
to the area.
o IV heparin to prevent reocclusion (start immediately with heart, NOT brain)
 A major concern with thrombolytic therapy is reocclusion of the artery. The site of the
thrombus is unstable, and another clot may form or spasm of the artery may occur.
Coronary surgical revascularization
o Recommended for
 Failed medical management
 Presence of left main coronary artery or three-vessel disease
 Not a candidate for PCI (e.g., blockages are long or difficult to access)
 Failed PCI with ongoing chest pain
 History of diabetes mellitus, LV dysfunction, chronic kidney disease
 Usually between 2 or 3 stents is all you want to do
Traditional coronary artery bypass graft (CABG) surgery
o CABG surgery consists of the placement of arterial or venous grafts to transport blood between
the aorta, or other major arteries, and the heart muscle distal to the blocked coronary artery (or
arteries)
o Requires sternotomy (opening of chest cavity) and cardiopulmonary bypass (CPB)
 During CPB, blood is diverted from the patient’s heart to a machine. Here it is
oxygenated and returned (via a pump) to the patient.
 Need chest tube when close
o Uses arteries and veins for grafts
 The internal mammary artery (IMA) is most common artery
used for bypass graft
 May also use saphenous vein, radial artery,
gastroepiploic artery, and/or inferior epigastric
artery.
o Cardiopulmonary Bypass (CPD)
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 During CPB, blood is diverted from the patient’s heart to a
machine where it is oxygenated and returned (via a pump)
to the patient.
 This allows the surgeon to operate on a quiet, nonbeating,
bloodless heart while perfusion to vital organs is
maintained.
o Internal Mammary Artery and Saphenous Vein Grafts
The internal mammary artery (IMA) is the most common artery used for bypass graft. It
is left attached to its origin (the subclavian artery) but then dissected from the chest
wall. Next, it is anastomosed (connected with sutures) to the coronary artery distal to
the blockage.
 If artery and gets blocked can
stent (not if 100%)
 Saphenous veins are also used for bypass
grafts. The surgeon endoscopically
removes the saphenous vein from one or
both legs. A section is sutured into the
ascending aorta near the native coronary
artery opening and then sutured to the
coronary artery distal to the blockage.
The use of antiplatelet and statin therapy
after surgery improves vein graft patency.
o Radial Artery Graft
 Radial artery is another potential graft
 Can possibly lose use of hand
 Thick muscular artery that is prone to spasm
 Perioperative calcium channel blockers and long-acting nitrates can control the
spasms
 Patency rates are not as good as IMA but better than saphenous veins
 Other grafts include the gastroepiploic or inferior epigastric artery. Like the radial artery,
these also are prone to spasms.
Minimally invasive direct coronary artery bypass (MIDCAB)
o For patients with disease of left anterior descending or right coronary artery
o Does not involve a sternotomy and CPB
o The technique requires several small incisions between the ribs or a mini thoracotomy.
 A thoracoscope or robotic assistance is used to dissect the IMA from the chest.
 A mechanical stabilizer immobilizes the operative site.
 The IMA is then sutured to the left anterior descending or right coronary artery.
o Some patients undergo hybrid procedures where they have a MIDCAB for the left anterior
descending artery and undergo a PCI of a second or third artery at a later time.
Off-pump coronary artery bypass (OPCAB)
o Sternotomy but no CPB
o OPCAB is associated with less blood loss, less renal dysfunction, less postoperative atrial
fibrillation, and fewer neurologic complications. It is estimated that less than 20% of CABG
procedures are OPCAB procedures. OPCAB is primarily used for patients with multiple
comorbidities who should avoid CPB.
Robotic or totally endoscopic coronary artery bypass (TECAB)
o This technique uses a robot in performing CABG surgery.
o This procedure is done without the use of CPB or with the use of CPB using femoral access.
o TECAB is used for limited bypass grafting.
o The benefits include increased precision, smaller incisions, decreased blood loss, less pain, and
shorter recovery time
Transmyocardial laser revascularization
o Indirect revascularization
o High-energy laser creates channels in heart to allow blood flow to ischemic areas
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o It is used for patients with advanced CAD who are not candidates for traditional CABG surgery
and who have persistent angina despite maximum medical therapy.
o The procedure can be done using a left thoracotomy approach or in combination with CABG
surgery.
o It is as an adjunctive therapy when bypass grafts cannot be placed.
Drug therapy
o IV nitroglycerin (NTG)
 IV NTG (Tridil) is used in the initial treatment of the patient with ACS.
 The goal of therapy is to reduce anginal pain and improve coronary blood flow.
 IV NTG decreases preload and afterload while increasing the myocardial oxygen supply.
 The onset of action is immediate.
 Titrate NTG to control and stop chest pain.
 Hypotension is a common side effect, monitor BP during this time.
 Patients who do become hypotensive are often volume depleted and can benefit
from an IV fluid bolus.
o Morphine
 Morphine is the drug of choice for chest pain that is unrelieved by NTG.
 As a vasodilator, it decreases cardiac workload by lowering myocardial oxygen
consumption, reducing contractility, and decreasing BP and HR.
 In addition, morphine can help reduce anxiety and fear.
 In rare situations, morphine can depress respirations.
 Monitor patients for signs of bradypnea or hypotension, conditions to avoid in
myocardial ischemia and infarction.
o β-adrenergic blockers
 β-Blockers decrease myocardial oxygen demand by reducing HR, BP, and contractility.
 The use of these drugs in patients who are not at risk for complications of MI (e.g.,
cardiogenic shock, bradycardia or hypotension) reduces the risk of reinfarction and the
occurrence of HF.
 β-Blockers are continued indefinitely
o ACE inhibitors
 Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers inhibitors
should be started within the first 24 hours if the BP is stable and there are no
contraindications.
 They are continued indefinitely in patients recovering from STEMI or NSTEMI, with heart
failure, or an EF of 40% or less.
 The use of ACE inhibitors can help prevent ventricular remodeling and prevent or slow
the progression of HF.
 For patients who cannot tolerate ACE inhibitors (e.g., angioedema, cough), ARBs should
be considered.
o Antidysrhythmic drugs
 Dysrhythmias are the most common complications after an MI. In general, they are selflimiting and are not treated aggressively unless they are life threatening (e.g., sustained
ventricular tachycardia).
o Lipid-lowering drugs
 A lipid panel is obtained on all patients with ACS.
 All patients with ACS or diagnosed with CAD should receive lipid-lowering drugs
indefinitely, unless contraindicated.
o Stool softeners
After an MI, the patient may be predisposed to constipation because of bed rest and
opioid administration.
 Stool softeners (e.g., docusate sodium [Colace]) are given to facilitate bowel movements.
 This prevents straining and the resultant vagal stimulation from the Valsalva
maneuver.
o Vagal stimulation produces bradycardia and can provoke dysrhythmias
Nutritional therapy
o Initially NPO until stable
o Progress to
 Low salt
 Low saturated fat
 Low cholesterol
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Audience Response Question
A patient is admitted to the coronary care unit following a cardiac arrest and successful cardiopulmonary
resuscitation. When reviewing the health care provider’s admission orders, which order should the nurse
question?
a. Oxygen at 4 L/min per nasal cannula
b. Morphine sulfate 2 mg IV every 10 minutes until the pain is relieved
c. Tissue plasminogen activator (tPA) 100 mg IV infused over 3 hours
d. IV nitroglycerin at 5 mcg/minute and increase 5 mcg/minute every 3 to 5 minutes
Answer: C
Rationale: Traumatic or prolonged (>10 minutes) cardiopulmonary resuscitation is a relative contraindication
for the administration of fibrinolytic therapy.
Nursing Management: Chronic Stable Angina and ACS
 Nursing Assessment: Subjective Data
o Health history
 CAD/chest pain/angina/ MI
 Valve disease
 Heart failure/cardiomyopathy,
 Hypertension, diabetes, anemia, lung disease, hyperlipidemia
o Drugs
 Use of antiplatelets/anticoagulants, nitrates, angiotensin-converting enzyme inhibitors,
β-adrenergic blockers, calcium channel blockers; antihypertensive drugs; lipid-lowering
drugs; over-the-counter drugs (e.g., vitamin and herbal supplements)
o History of present illness
o Family history
o Indigestion/heartburn; nausea/vomiting
o Urinary urgency or frequency
o Straining at stool
o Palpitations, dyspnea, dizziness, weakness
o Chest pain
 possible radiation to jaw, neck, shoulders, back, or arm
o Stress, depression, anger, anxiety, feelings of impending doom
 Nursing Assessment: Objective Data
o Anxious, fearful, restless, distressed
o Cool, clammy, pale skin
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o Tachycardia or bradycardia
o Pulsus alternans (alternating weak and strong heartbeats)
o Pulse deficit
o Dysrhythmias (especially ventricular)
o S3, S4, ↑ or ↓ BP, murmur
Nursing Diagnoses
o Decreased cardiac output
 related to altered contractility and altered heart rate and rhythm
o Acute pain
 related to an imbalance between myocardial oxygen supply and demand
o Anxiety
 related to perceived or actual threat of death, pain, and/or possible lifestyle changes
o Activity intolerance
 related to general weakness secondary to decreased cardiac output and poor lung and
tissue perfusion
o Ineffective health management
 related to lack of knowledge of disease process, risk factor reduction, rehabilitation,
home activities, and medications
Planning: Overall goals
o Relief of pain
o Preservation of heart muscle
o Immediate and appropriate treatment
o Effective coping with illness-associated anxiety
o Participation in a rehabilitation plan
o Reduction of risk factors
Nursing Management: Chronic Stable Angina
 Acute Intervention
o Upright position
o Supplemental oxygen
o Assess vital signs
o 12-lead ECG
o Administer NTG followed by an opioid analgesic, if needed
o Assess heart and breath sounds
o The BP and HR may be elevated.
o Auscultation of the heart may reveal an atrial (S4) or a ventricular (S3) gallop.
o A new murmur heard during an anginal attack may indicate ischemia of a papillary muscle of
the mitral valve. The murmur is likely to be transient and disappear when symptoms stop.
o Ask the patient to describe the pain and to rate it on a scale of 0 to 10 before and after
treatment to evaluate the effectiveness of the interventions.
o Support and reassure the patient. Use a calm approach to help reduce the patient’s anxiety
during an anginal attack.
 Ambulatory Care
o Provide reassurance
o Patient teaching
Prevention of angina is preferable to its treatment. This is why teaching is important. You
need to give the patient information regarding CAD, angina, precipitating factors for
angina, risk factor reduction, and drugs.
 Give the patient instructions on how to avoid or control precipitating factors. For
example, teach the patient to avoid exposure to extremes of weather and eating large,
heavy meals. If a heavy meal is eaten, tell the patient to rest for 1 to 2 hours after the
meal because blood is shifted to the GI tract to aid digestion and absorption.
 Help the patient to identify personal risk factors for CAD. Once known, discuss the
various ways modifiable risk factors can be reduced.
 Teach the patient and caregiver about diets that are low in salt and saturated fats.
 Maintaining ideal body weight is important in controlling angina because excess weight
increases the heart’s workload.
 It is important that the patient has a regular, individualized program of physical activity
that conditions rather than stresses the heart. For example, tell patients that walking
briskly on a flat surface at least 30 minutes a day, most days of the week is
recommended.
 It is important to teach the patient and caregiver the proper use of NTG. NTG may be
used prophylactically before an emotionally stressful situation, sexual intercourse, or
physical exertion (e.g., climbing a long flight of stairs).
 If needed, arrange for counseling.
CAD and angina
Precipitating factors for angina
Risk factor reduction
Drugs
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Nursing Management: Acute Coronary Syndrome
 Priority interventions are aimed at decreasing the oxygen needs of a compromised heart muscle and
reducing the risk of complications.
 Acute Care
o Pain: nitroglycerin, morphine, oxygen
o Continuous monitoring
 ECG
 Maintain continuous ECG monitoring while in the ED and ICU and after transfer
to a step-down or general unit. Dysrhythmias need to be identified quickly and
treated. During the initial period after MI, ventricular fibrillation is the most
common lethal dysrhythmia. In many patients, premature ventricular
contractions or ventricular tachycardia precedes this dysrhythmia.
 ST segment
 Monitor the patient for the presence of reinfarction or ischemia by monitoring
the ST segment for shifts above or below the baseline of the ECG.
 Silent ischemia can occur without subjective symptoms (e.g., chest pain). It is
noted by ST segment changes only.
 Notify the HCP if you see ST segment changes without any clinical symptoms.
 Heart and breath sounds
 VS, pulse oximetry, I and O
o Rest and comfort
 Balance rest and activity
 Begin cardiac rehabilitation
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o Anxiety reduction
 Identify source and alleviate
 Patient teaching important
 It is important to start teaching at the patient’s level rather than to present a
prepackaged program. For example, patients generally are not ready to learn
about the pathology of CAD. The earliest questions usually relate to how the
disease affects perceived control and independence
o Emotional and behavioral reaction
 Maximize patient’s social support systems
 Consider open visitation
o Phase 1 of cardiac rehab occurs in the hospital. It is important that the patient understands the
reasons why activity is limited but not completely restricted. Gradually increase the patient’s
cardiac workload through more demanding physical tasks so that the patient can achieve a
discharge activity level adequate for home care.
o Phase 2 of rehab begins when the patient is discharged home and continues for 2 to 12 weeks.
o Phase 3 is long-term maintenance for optimal cardiac health.
Coronary revascularization: PCI
o The major nursing responsibilities for the care of the patient following PCI involve:
 Monitor for recurrent angina
 Frequent VS, including cardiac rhythm
 Monitor catheter insertion site for bleeding –LIFT THE SHEETS !!!
 Neurovascular assessment
 Bed rest per institutional policy
Coronary revascularization: CABG
o ICU for first 24–36 hours
o Pulmonary artery catheter
o Intraarterial line
o Pleural/mediastinal chest tubes
o Continuous ECG
o ET tube with mechanical ventilation
o Epicardial pacing wires
o Urinary catheter
o NG tube for decompression
o Most patients will be extubated within 6 hours and transferred to a step-down unit within 24
hours for continued monitoring of cardiac status.
Complications related to CPB
o Bleeding and anemia from damage to RBCs and platelets
o Fluid and electrolyte imbalances
o Hypothermia as blood is cooled as it passes through the bypass machine
o Infections
CABG: postoperative nursing care
o Assess patient for bleeding
o Monitor hemodynamic status
o Assess fluid status
o Replace blood and electrolytes PRN
o Restore temperature
o Monitor for atrial fibrillation (which is common)
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o Β-Blockers should be restarted as soon as possible after surgery (unless contraindicated) to
reduce the incidence of AF.
CABG: postoperative nursing care
o Surgical site care
 Radial artery harvest site
 Leg incisions
 Care of the leg incision is minimal since endoscopy is used to harvest the vein.
 Chest incision
 Chest incisions are usually closed with Dermabond and do not require dressings.
Management of the chest wound, which involves a sternotomy, is similar to that
of other chest surgeries.
o Pain management
o DVT prevention
o Pulmonary hygiene
o Cognitive dysfunction
 This includes impairment of memory, concentration, language comprehension, and
social integration. Patients may inexplicably cry or become teary. Postoperative cognitive
dysfunction (POCD) can manifest days to weeks after surgery and may remain a
permanent disorder.
 Can stroke during bypass and not know it
Ambulatory Care
o Cardiac rehabilitation
 restoration of a person to an optimal state of function in six areas: physiologic,
psychologic, mental, spiritual, economic, and vocational
o Patient and caregiver teaching
 Patient teaching needs to occur at every stage of the patient’s hospitalization and
recovery (e.g., ED, telemetry unit, home care).
 Limit your use of medical terminology.
o Physical activity
 METs scale (1 MET is the amount of oxygen needed by the body at rest)
 Monitor heart rate
 Teach patients to check their HR.
 Low-level stress test before discharge
 Isometric versus isotonic activities
 Isometric activities involve the development of tension during muscular
contraction but produce little or no change in muscle length or joint movement.
 Isotonic activities involve changes in muscle length and joint movement with
rhythmic contractions at relatively low muscular tension. Walking, jogging,
swimming, bicycling, and jumping rope are examples of activities that are mostly
isotonic.
o Isotonic exercise can put a safe, steady load on the heart and lungs and
improve the circulation in many organs.
o Resumption of sexual activity
 Teach when discuss other physical activity
 Erectile dysfunction drugs contraindicated with nitrates
 Prophylactic nitrates before sexual activity
 When to avoid sex
 Typically 7–10 days post MI or when patient can climb two flights of stairs
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Evaluation
o Stable vital signs
 Maintains stable signs of effective cardiac output
o Relief of pain
o Decreased anxiety
o Realistic program of activity
o Effective management of therapeutic regimen
 Describes the disease process, measures to reduce risk factors, and rehabilitation
activities necessary to manage the therapeutic regimen
Sudden Cardiac Death (SCD)
 Unexpected death from cardiac causes – almost 400,000 annually
 Abrupt disruption in cardiac function, resulting in loss of CO and cerebral blood flow
 The affected person may or may not have a known history of heart disease.
o SCD is often the first sign of illness for 25% of those who die of heart disease.
 Most commonly caused by
o Ventricular dysrhythmias (majority)
o Structural heart disease (10%)
o Conduction disturbances (especially < age 45)
 (e.g., prolonged QT syndrome, Wolff-Parkinson-White syndrome).
 Persons who experience SCD because of CAD fall into two groups: (1) those who did not have an acute
MI and (2) those who did have an acute MI.
o No warning signs or symptoms if no MI
o Prodromal symptoms if associated with MI
 Chest pain, palpitations, dyspnea
 Death usually within 1 hour of onset of acute symptoms
Sudden Cardiac Death: Nursing/Interprofessional Care
 Diagnostic workup to rule out or confirm MI
o Cardiac biomarkers
o ECGs
o Treat accordingly
 Cardiac catheterization
o to determine the possible location and extent of coronary artery occlusion
 PCI or CABG may be indicated
 24-hour Holter monitoring (for assessment of dysrhythmias)
 Exercise stress testing (or pharmacological stress testing)
 Signal-averaged ECG
 Electrophysiologic study (EPS)
 Implantable cardioverter-defibrillator (ICD)
o The most common approach to preventing a recurrence is the use of an implantable
cardioverter-defibrillator (ICD).
 Antidysrhythmic drugs
o Drug therapy with amiodarone (Cordarone) may be used in conjunction with an ICD to decrease
episodes of ventricular dysrhythmias.
 LifeVest
o Some patients at risk for SCD may consider using a LifeVest as a bridge to ICD or heart
transplantation.
o A LifeVest is a personal external defibrillator that has two main parts: a garment and monitor.
The garment is worn under clothing and has electrodes that continuously record the patient’s
ECG. The monitor is worn around the waist or from a shoulder strap. If the patient has
ventricular tachycardia or ventricular fibrillation, the device sounds an alarm to confirm that the
patient is unresponsive. If the patient is conscious, the patient can press two buttons to stop the
shock. If the patient does not respond, the device warns bystanders that a shock is about to be
delivered. If the dysrhythmia continues and the patient still does not respond, a treatment
shock is delivered through the electrodes.
Sudden Cardiac Death: Nursing/Interprofessional Management
 Patient teaching
o Teaching people about the symptoms of impending cardiac arrest and the actions to take can
save lives.
o Rapid cardiopulmonary resuscitation (CPR) and defibrillation with an automated external
defibrillator (AED), combined with early advanced cardiac life support, has high long-term
survival rates for a witnessed arrest.
 Psychosocial adaptation
o “Brush with death”
o “Time bomb” mentality (may become anxious, angry, depressed)
o Additional issues
 Driving restrictions
 Role reversal
 Change in occupation
Audience Response Question
The most significant factor in long-term survival of a patient with sudden cardiac death is
a. Absence of underlying heart disease.
b. Rapid institution of emergency services and procedures.
c. Performance of perfect technique in resuscitation procedures.
d. Maintenance of 50% of normal cardiac output during resuscitation efforts.
Answer: B
Rationale: Rapid cardiopulmonary resuscitation and prompt defibrillation (with an automated external
defibrillator) and early advanced cardiac life support can produce high long-term survival rates for a witnessed
arrest.
The nurse is caring for a patient who survived a sudden cardiac death. What should the nurse include in the
discharge instructions?
a. “Because you responded well to CPR, you will not need an implanted defibrillator.”
b. “The most common way to prevent another arrest is to take your prescribed drugs.”
c. “Your family members should learn how to perform CPR and practice these skills regularly.”
d. “Since there was no evidence of a heart attack, you do not need to worry about another episode.”
Answer: C
Rationale: Rapid cardiopulmonary resuscitation, prompt defibrillation (with an automated external
defibrillator), and early advanced cardiac life support can produce high long-term survival rates for a witnessed
arrest.
Med Surg 2 Exam #1 Study Guide
Chapter 35: Dysrhythmias
Properties of Cardiac Cells
 Four properties of heart cells allow the conduction system to start an electrical impulse, send it through
the heart tissue, and stimulate muscle contraction:
o Automaticity is the ability to initiate an impulse spontaneously and continuously.
o Excitability is the ability to be electrically stimulated.
o Conductivity is the ability to transmit an impulse along a membrane in an orderly manner.
o Contractility is the ability to respond mechanically to an impulse.
Conduction System of the Heart (ON TEST!)
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The conduction system of the heart consists of specialized neuromuscular tissue located throughout
the heart.
The above figure depicts the conduction system of the heart.
A normal impulse starts in the sinoatrial (SA) node in the upper right atrium near the entrance of the
vena cava. It spreads over the atrial myocardium via interatrial pathways and internodal pathways,
causing atrial contraction. The impulse then travels to the atrioventricular (AV) node, through the
bundle of His, and down the left and right bundle branches. It ends in the Purkinje fibers, which
transmit the impulse to the ventricles.
Nervous System Control of Heart
 Autonomic nervous system controls
o rate of impulse formation, speed of conduction, and strength of cardiac contraction.
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Parasympathetic nervous system
o Decreases rate of SA node
o Slows impulse conduction of AV node
Sympathetic nervous system
o Increases rate of SA node
o Increases impulse conduction of AV node
o Increases cardiac contractility
If heart transplant it is denervated –biggest problem with this is dysrhythmias
Dysrhythmias
 Disorder of impulse formation, conduction of impulses, or both
 SA node normal pacemaker of heart (60–100 beats/minute)
 Secondary pacemakers
o AV node (40–60 beats/minute)
o His-Purkinje fibers (20–40 beats/minute)
 Only can feel QRS when you feel pulse
Electrocardiogram Monitoring (ON TEST!)
 Graphic tracing of electrical impulses produced by heart
 Waveforms of ECG represent activity of charged ions across membranes of myocardial cells
 The inside of the cell, when at rest, or in the polarized state, is negative compared with the outside.
 When a cell or groups of cells are stimulated, the cell membrane changes its permeability.
o This allows sodium to move rapidly into the cell, making the inside of the cell positive compared
with the outside (depolarization).
o A slower movement of ions across the membrane restores the cell to the polarized state, called
repolarization.
 1) The P wave represents time for the passage of
the electrical impulse through the atrium causing
atrial depolarization (contraction).
 2) The PR interval is measured from the beginning
of the P wave to the beginning of the QRS
complex. It represents the time taken for the
impulse to spread through the atria, AV node, and
bundle of His; the bundle branches; and Purkinje
fibers to a point immediately preceding ventricular
contraction.
 3) The QRS complex consists of three distinct
waves. The Q wave is the first negative (downward) deflection after the P wave, short and narrow, and
not present in several leads. The R wave is the first positive (upward) deflection in the QRS complex,
and the S wave is the first negative (downward) deflection after the R wave. The QRS interval is
measured from the beginning to the end of the QRS complex. It represents the time taken for
depolarization (contraction) of both ventricles (systole).
 4) The ST segment is measured from the S wave of the QRS complex to the beginning of the T wave. It
represents the time between ventricular depolarization and repolarization (diastole). It should be
isoelectric (flat).
 5) The T wave represents the time for ventricular repolarization. It should be upright.
 6) The QT interval is measured from the beginning of the QRS complex to the end of the T wave. It
represents the time taken for entire electrical depolarization and repolarization of the ventricles.
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** EKG: conversion of electrical pathways to something we can see visually
12-Lead ECG
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Typically, an ECG consists of 12 leads (or views) of the heart's activity.
A lead consists of a positive and a negative electrode, with the positive electrode being the "seeing
eye." Activity coming toward the positive electrode produces an upward deflection on the EKG paper,
and one going away from the seeing eye produces a downward deflection (this is the reason for lead
tracings looking different).
Six of the leads measure electrical forces in the frontal plane. These are bipolar (positive and negative)
leads I, II, and III (left column of tracings); and unipolar (positive) leads aVr, aVl, and aVf.
The remaining six unipolar leads (V1 through V6) measure the electrical forces in the horizontal plane
(precordial leads).
The 12-lead ECG may show changes suggesting structural changes, conduction disturbances, damage
(e.g., ischemia, infarction), electrolyte imbalance, or drug toxicity. Obtaining 12 ECG views of the heart
is also helpful in the assessment of dysrhythmias.
Lead Placement (don’t need to know this)
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Accurate interpretation of an ECG depends on the correct placement of the leads on the patient.
A. Limb leads I, II, and III. Leads are located on the extremities. Illustrated are the angles from which
these leads view the heart.
B. Lead placement for limb leads aVR, aVL, and aVF. These unipolar leads use the center of the heart as
their negative electrode.
C. Lead placement for the chest electrodes: V1, fourth intercostal space at the right sternal border; V2,
fourth intercostal space at the left sternal border; V3, halfway between V2 and V4; V4, fifth intercostal
space at the left midclavicular line; V5, fifth intercostal space at the anterior axillary line; V6, fifth
intercostal space at the midaxillary line.
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One or more ECG leads can be used to continuously monitor a
patient’s ECG. The leads most commonly selected are leads II
and V1.
MCL1 is a modified chest lead that is similar to V1 and is used
when only three leads are available for monitoring.
A. Lead placement for MCL, using a three-lead system.
B. Lead placement for V1 or V6, using a five-lead system.
C. Typical electrocardiogram tracing in lead MCL1.
C, Chest; LA, left arm; LL, left leg; MCL1, modified chest lead; RA,
right arm; RL, right leg
ECG Time and Voltage (don’t need to know)
 The monitor oscilloscope continuously displays the heart rhythm. ECG paper attached to the monitor
records the ECG (i.e., rhythm strip). This provides a record of the patient’s rhythm. It also allows for
measurement of complexes and intervals, and assessment of dysrhythmias.
 To correctly interpret an ECG, measure time and
voltage on the ECG paper.
 ECG paper consists of large (heavy lines) and small
(light lines) squares.
 Each large square consists of 25 smaller squares
(five horizontal and five vertical).
 Horizontally, each small square (1 mm) represents
0.04 second. This means that one large square
equals 0.20 second and that 300 large squares
equal 1 minute.
 Vertically, each small square (1 mm) represents 0.1
millivolt (mV). This means that one large square
equals 0.5 mV. Use these squares to calculate the
heart rate (HR) and measure time intervals for the
different ECG complexes.
Calculating HR
 Count
o Number of QRS complexes in 1 minute
 method is time consuming, a simpler process is used
o R-R intervals in 6 seconds, and multiply by 10
o Number of small squares between one R-R interval, and divide this number into 1500
o Number of large squares between one R-R interval, and divide this number into 300
Assessment of Cardiac Rhythm (ON TEST)
 When the rhythm is regular, heart rate
can be determined at a glance. The
estimated heart rate is 70.
Patient Preparation
 ECG leads consist of an electrode pad fixed with electrical conductive gel. Before placing these on the
patient, you must properly prepare the skin.
o Clip excessive hair on chest wall
o Rub skin with dry gauze
o May need to use alcohol for oily skin
o If the patient is diaphoretic, apply a skin protectant before placing the electrode.
 Apply electrode pad
Artifact
 You will see artifact on the monitor
when leads and electrodes are not
secure, or if there is muscle activity
(e.g., shivering) or electrical
interference.
 Artifact is a distortion of the baseline
and waveforms seen on the ECG.
 Accurate interpretation of cardiac
rhythm is difficult when artifact is
present. If artifact occurs, check the
connections in the equipment. You
may need to replace the electrodes if
the conductive gel has dried out.
 Throw away these strips!!!
Telemetry Monitoring
 Observation of HR and rhythm at a distant site
 Two types
o Centralized monitoring system
o Advanced alarm system alerts when it detects dysrhythmias, ischemia, or infarction
 Computerized monitoring systems are not fail-proof. Frequently assess all monitored patients for any
signs of hemodynamic instability.
Assessment of Heart Rhythm
 Interpret the rhythm AND assess the clinical status of the patient
o Do they have a pulse??
 Is the patient hemodynamically stable?
 Determine cause of dysrhythmia
o For example, tachycardias may be the result of fever and may cause a decrease in cardiac
output (CO) and hypotension. Electrolyte disturbances can cause dysrhythmias and, if not
treated, can lead to life-threatening dysrhythmias.
 Assess and treat the patient, not the monitor!
 When assessing a cardiac rhythm, use a consistent and systematic approach. One such approach
includes the following:
o 1. Look for the presence of the P wave. Is it upright or inverted? Is there one for every QRS
complex or more than one? Are there atrial fibrillatory or flutter waves present?
o 2. Evaluate the atrial rhythm. Is it regular or irregular?
o 3. Calculate the atrial rate.
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o 4. Measure the duration of the PR interval. Is it normal duration or prolonged?
o 5. Evaluate the ventricular rhythm. Is it regular or irregular?
o 6. Calculate the ventricular rate.
o 7. Measure the duration of the QRS complex. Is it normal duration or prolonged?
o 8. Assess the ST segment. Is it isoelectric (flat), elevated, or depressed?
o 9. Measure the duration of the QT interval. Is it normal duration or prolonged?
o 10. Note the T wave. Is it upright or inverted?
Additional questions to consider include the following:
o 1. What is the dominant or underlying rhythm and/or dysrhythmia?
o 2. What is the clinical significance of your findings?
o 3. What is the treatment for the particular rhythm?
Normal Sinus Rhythm
 Sinus node fires 60–100 beats/minute
 Follows normal conduction pattern
 Rhythm is regular. The P wave precedes each QRS complex and has a normal shape and duration.
 The PR interval is normal, and the QRS complex has a normal shape and duration.
Sinus Bradycardia
 In sinus bradycardia, the conduction pathway is the same as that in sinus rhythm but the SA node fires
at a rate less than 60 beats/minute.
 The rhythm is regular. The P wave precedes each QRS complex and has a normal shape and duration.
The PR interval is normal, and the QRS complex has a normal shape and duration.
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Normal rhythm in aerobically trained athletes and during sleep
Can occur in response to parasympathetic nerve stimulation and certain drugs
o carotid sinus massage, Valsalva maneuver, hypothermia, increased intraocular pressure, vagal
stimulation, and certain drugs (e.g., β-adrenergic blockers [β-blockers] , calcium channel
blockers).
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Also associated with some disease states
o hypothyroidism, increased intracranial pressure, and inferior myocardial infarction (MI).
Manifestations
o Hypotension
o Pale, cool skin
o Weakness
o Angina
o Dizziness or syncope
o Confusion or disorientation
o Shortness of breath
Treatment
o Atropine
 an anticholinergic drug for the patient with symptoms.
o Pacemaker
o Stop offending drugs
 If bradycardia is due to drugs, these may need to be held, discontinued, or reduced.
Audience Response Question
A patient’s cardiac rhythm is sinus bradycardia with a heart rate of 34 beats/minute. If the bradycardia is
symptomatic, the nurse would expect the patient to exhibit
a. Palpitations.
b. Hypertension.
c. Warm, flushed skin.
d. Shortness of breath.
Answer: D
Rationale: Signs of symptomatic bradycardia include pale, cool skin; hypotension; weakness; angina; dizziness
or syncope; confusion or disorientation; and shortness of breath.
Sinus Tachycardia
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The conduction pathway is the same in sinus tachycardia as that in normal sinus rhythm. The sinus rate
is 101 to 200 beats/minute
The P wave is normal, precedes each QRS complex, and has a normal shape and duration. The PR
interval is normal, and the QRS complex has a normal shape and duration.
Caused by vagal inhibition or sympathetic stimulation
Associated with physiologic and psychologic stressors
Drugs can increase rate
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The discharge rate from the sinus node increases because of vagal inhibition or sympathetic
stimulation.
Sinus tachycardia is associated with physiologic and psychologic stressors such as exercise, fever, pain,
hypotension, hypovolemia, anemia, hypoxia, hypoglycemia, myocardial ischemia, heart failure (HF),
hyperthyroidism, anxiety, and fear.
It can also be an effect of drugs such as epinephrine (EpiPen), norepinephrine (Levophed), atropine
(AtroPen), caffeine, theophylline (Theo-Dur), or hydralazine (Apresoline).
o In addition, many over-the-counter cold remedies have active ingredients (e.g.,
pseudoephedrine [Sudafed]) that can cause tachycardia.
Manifestations
o Dizziness
o Dyspnea
o Hypotension
o Angina in patients with CAD
Treatment
o Guided by cause (e.g., treat pain)
o Vagal maneuver
o β-blockers
Premature Atrial Contraction
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HR varies with the underlying rate and frequency of the PAC. The rhythm is irregular.
The P wave has a different shape from that of the P wave originating from the SA node or it may be
hidden in the preceding T wave.
The PR interval may be shorter or longer than the PR interval coming from the SA node, but it is within
normal limits.
The QRS complex is usually normal. If the QRS interval is greater than or equal to 0.12 second,
abnormal conduction through the ventricles is present.
Contraction originating from ectopic focus in atrium in location other than SA node
Travels across atria by abnormal pathway, creating distorted P wave
May be stopped, delayed, or conducted normally at the AV node
A premature atrial contraction (PAC) is a contraction starting from an ectopic focus in the atrium (i.e., a
location other than the SA node) and coming sooner than the next expected sinus beat.
The ectopic signal starts in the left or right atrium and travels across the atria by an abnormal pathway.
This creates a distorted P wave.
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At the AV node, it may be stopped (nonconducted PAC), delayed (lengthened PR interval), or conducted
normally. If the signal moves through the AV node, in most cases it is conducted normally through the
ventricles.
Causes
o Stress
o Fatigue
o Caffeine
o Tobacco
o Alcohol
o Hypoxia
o Electrolyte imbalance
o Disease states
In persons with healthy hearts, isolated PACs are not significant.
In persons with heart disease, frequent PACs may indicate enhanced automaticity of the atria, or a
reentry mechanism. Such PACs may warn of or start more serious dysrhythmias (e.g., supraventricular
tachycardia)
Manifestations
o Palpitations
o Heart “skips a beat”
Treatment
o Monitor for more serious dysrhythmias
o Withhold sources of stimulation
o β-blockers
Paroxysmal Supraventricular Tachycardia (PSVT)
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Paroxysmal supraventricular tachycardia (PSVT) is a dysrhythmia starting in an ectopic focus anywhere
above the bifurcation of the bundle of His. Identification of the ectopic focus is often difficult even with
a 12-lead ECG as it requires recording the dysrhythmia as it starts.
The HR is 150 to 220 beats/minute, and the rhythm is regular or slightly irregular. The P wave is often
hidden in the preceding T wave. If seen, it may have an abnormal shape. The PR interval may be
shortened or normal, and the QRS complex is usually normal.
Reentrant phenomenon: PAC triggers a run of repeated premature beats
Paroxysmal refers to an abrupt onset and termination
Associated with overexertion, stress, deep inspiration, stimulants, disease, digitalis toxicity
Manifestations
o HR is 150–220 beats/minute (add for clarification)
o HR > 180 leads to decreased cardiac output and stroke volume
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o Hypotension
o Dyspnea
o Angina
Treatment
o Vagal stimulation
o IV adenosine
o IV β-blockers (e.g., sotalol [Betapace])
o Calcium channel blockers (e.g., diltiazem [Cardizem]),
o Amiodarone
o DC cardioversion
Atrial Flutter
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Atrial flutter is an atrial tachydysrhythmia identified by recurring, regular, sawtooth-shaped flutter
waves that originate from a single ectopic focus in the right atrium or, less commonly, the left atrium.
Atrial rate is 200 to 350 beats/minute.
The ventricular rate will vary based on the conduction ratio. In 2:1 conduction, the ventricular rate is
typically found to be approximately 150 beats/minute.
Atrial rhythm is regular, and ventricular rhythm is usually regular.
The PR interval is variable and not measurable.
The QRS complex is usually normal. Because the AV node can delay signals from the atria, there is
usually some AV block in a fixed ratio of flutter waves to QRS complexes.
Typically associated with disease
Symptoms result from high ventricular rate and loss of atrial “kick” → decreased CO → heart failure
Increases risk of stroke
o Risk of thrombus formation in the atria from the stasis of blood.
 Warfarin (Coumadin) is given to prevent stroke in patients who have atrial flutter.
Treatment
o Pharmacologic agent
 Drugs used to control ventricular rate include calcium channel blockers and β-blockers
 Antidysrhythmia drugs are used to convert atrial flutter to sinus rhythm (e.g., ibutilide
[Corvert]) or to maintain sinus rhythm (e.g., amiodarone, flecainide [Tambocor],
dronedarone [Multaq])
o Electrical cardioversion
o Radiofrequency ablation
o Anticoagulation therapy
Atrial Fibrillation
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Atrial fibrillation is characterized by a total disorganization of atrial electrical activity due to multiple
ectopic foci resulting in loss of effective atrial contraction.
During atrial fibrillation, the atrial rate may be as high as 350 to 600 beats/minute.
P waves are replaced by chaotic, fibrillatory waves.
Ventricular rate varies and the rhythm is usually irregular.
When the ventricular rate is between 60 and 100 beats/minute, it is atrial fibrillation with a controlled
ventricular response.
Atrial fibrillation with a ventricular rate greater than 100 beats/minute is atrial fibrillation with a rapid
(or uncontrolled) ventricular response.
The PR interval is not measurable, and the QRS complex usually has a normal shape and duration.
At times, atrial flutter and atrial fibrillation may coexist.
Paroxysmal or persistent
Most common dysrhythmia
Prevalence increases with age
Usually occurs in patients with underlying heart disease
Can also occur with other disease states (thyrotoxicosis, alcohol intoxication, caffeine use, electrolyte
disturbances, stress, and heart surgery)
As with atrial flutter – causes a decrease in CO and an increased risk of stroke
o Atrial fibrillation results in a decrease in CO because of ineffective atrial contractions (loss of
atrial kick) and/or a rapid ventricular response.
o Thrombi (clots) form in the atria because of blood stasis.
o An embolized clot may develop and pass to the brain, causing a stroke.
o Atrial fibrillation accounts for as many as 17% of all strokes.
Treatment
o Drugs to control ventricular rate and/or convert to sinus rhythm (amiodarone and ibutilide most
common)
 Ventricular rate control is a priority for patients with atrial fibrillation. Drugs used for
rate control include calcium channel blockers (e.g., diltiazem), β-blockers (e.g.,
metoprolol), digoxin (Lanoxin), and dronedarone.
o Electrical cardioversion
o Anticoagulation
 If a patient is in atrial fibrillation for longer than 48 hours, anticoagulation therapy with
warfarin is needed for 3 to 4 weeks before the cardioversion and for several weeks after
successful cardioversion.
Anticoagulation therapy is necessary because the procedure can cause the clots to
dislodge. This places the patient at risk for stroke.
o Radiofrequency ablation
o Maze procedure with cryoablation
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Junctional Dysrhythmias
 Dysrhythmias that originate in the AV junction
 SA node has failed to fire, or impulse has been blocked at the AV node
 AV node becomes pacer—retrograde transmission of impulse to atria
 Abnormal P wave; normal QRS
 Associated with disease, certain drugs
o CAD, HF, cardiomyopathy, electrolyte imbalances, inferior MI, and rheumatic heart disease
o Certain drugs (e.g., digoxin, amphetamines, caffeine, nicotine)
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Junctional dysrhythmias include junctional escape rhythm (as shown on this slide), accelerated
junctional rhythm, and junctional tachycardia.
In junctional escape rhythm, the HR is 40 to 60 beats/minute. It is 61 to 100 beats/minute in
accelerated junctional rhythm and 101 to 180 beats/minute in junctional tachycardia.
Rhythm is regular.
The P wave is abnormal in shape and inverted, or it may be hidden in the QRS complex (as shown on
this strip). The PR interval is less than 0.12 second when the P wave precedes the QRS complex.
The QRS complex is usually normal.
Junctional premature beats may occur, and they are treated in a manner similar to that for PACs.
Serves as safety mechanism—do not suppress
If rhythms are rapid, may result in reduction of CO
Treat if patient is symptomatic
o Atropine for escape rhythm
o Correct cause
 In accelerated junctional rhythm and junctional tachycardia caused by drug toxicity, the
drug is stopped.
 In the absence of digitalis toxicity, β-blockers, calcium channel blockers, and amiodarone
are used for rate control
o Drugs to reduce rate if tachycardia
o Cardioversion should not be used
First-Degree AV Block
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First-degree AV block is a type of AV block in which every impulse is conducted to the ventricles but the
time of AV conduction is prolonged. After the impulse moves through the AV node, the ventricles
usually respond normally.
HR is normal and rhythm is regular. The P wave is normal, the PR interval is prolonged (greater than
0.20 second), and the QRS complex usually has a normal shape and duration.
Associated with disease states and certain drugs
o First-degree AV block is associated with MI, CAD, rheumatic fever, hyperthyroidism, electrolyte
imbalances (e.g., hypokalemia), vagal stimulation, and drugs such as digoxin, β-blockers, calcium
channel blockers, and flecainide
Typically not serious
Patients asymptomatic
No treatment
Monitor for changes in heart rhythm
Second-Degree AV Block, Type 1 (Mobitz I, Wenckebach)
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Type I second-degree AV block (Mobitz I or Wenckebach heart block) includes a gradual lengthening of
the PR interval. It occurs because of a prolonged AV conduction time until an atrial impulse is
nonconducted and a QRS complex is blocked (missing).
Atrial rate is regular, but ventricular rate may be slower because of nonconducted or blocked QRS
complexes resulting in bradycardia.
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Once a ventricular beat is blocked, the cycle repeats itself with progressive lengthening of the PR
intervals until another QRS complex is blocked. The rhythm appears on the ECG in a pattern of grouped
beats.
Ventricular rhythm is irregular. The P wave has a normal shape. The QRS complex has a normal shape
and duration
May result from drugs or CAD
Typically associated with ischemia
Usually transient and well tolerated
Treat if symptomatic
o Atropine
o Pacemaker
If asymptomatic, monitor closely
Second-Degree AV Block, Type 2 (Mobitz II)
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In type II second-degree AV block (Mobitz II heart block), a P wave is nonconducted without progressive
PR lengthening. This usually occurs when a block in one of the bundle branches is present.
On conducted beats, the PR interval is constant.
Atrial rate is usually normal. Ventricular rate depends on the degree of AV block.
Atrial rhythm is regular, but ventricular rhythm may be irregular.
The P wave has a normal shape. The PR interval may be normal or prolonged in duration and remains
constant on conducted beats.
The QRS complex is usually greater than 0.12 second because of bundle branch block.
Associated with heart disease and drug toxicity
Often progressive and results in decreased CO
Treat with pacemaker
Third-Degree AV Heart Block (Complete Heart Block)
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Third-degree AV block, or complete heart block, constitutes one form of AV dissociation in which no
impulses from the atria are conducted to the ventricles. The atria are stimulated and contract
independently of the ventricles. The ventricular rhythm is an escape rhythm, and the ectopic
pacemaker may be above or below the bifurcation of the bundle of His.
The atrial rate is usually a sinus rate of 60 to 100 beats/minute.
The ventricular rate depends on the site of the block. If it is in the AV node, the rate is 40 to
60 beats/minute, and if it is in the His-Purkinje system, it is 20 to 40 beats/minute.
Atrial and ventricular rhythms are regular but unrelated to each other.
The P wave has a normal shape.
The PR interval is variable, and there is no relationship between the P wave and the QRS complex.
The QRS complex is normal if an escape rhythm is initiated at the bundle of His or above. It is widened
if an escape rhythm is initiated below
the bundle of His
Associated with severe heart disease,
some systemic diseases, certain drugs
Usually results in decreased CO
Can lead to syncope, HF, shock
Treat with pacemaker
Drugs to increase heart rate if needed
while awaiting pacing
o The use of drugs such as
dopamine (Intropin), and
epinephrine is a temporary
measure to increase HR and
support blood pressure until
temporary pacing is started.
o Patients will need a
permanent pacemaker as soon
as possible.
Premature Ventricular Contractions
 A premature ventricular contraction
(PVC) is a contraction coming from an
ectopic focus in the ventricles. It is the
premature (early) occurrence of a
QRS complex.
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A PVC is wide and distorted in shape compared to a QRS complex coming down the normal conduction
pathway.
PVCs that arise from different foci appear different in shape from each other and are called multifocal
PVCs. PVCs that have the same shape are called unifocal PVCs.
When every other beat is a PVC, the rhythm is called ventricular bigeminy.
When every third beat is a PVC, it is called ventricular trigeminy.
Two consecutive PVCs are called a couplet.
Ventricular tachycardia occurs when there are three or more consecutive PVCs.
R-on-T phenomenon occurs when a PVC falls on the T wave of a preceding beat. This is especially
dangerous because the PVC is firing during the relative refractory phase of ventricular repolarization.
Excitability of the heart cells increases during this time, and the risk for the PVC to start ventricular
tachycardia or ventricular fibrillation is great.
HR varies according to intrinsic rate and number of PVCs. Rhythm is irregular because of premature
beats. The P wave is rarely visible and is usually lost in the QRS complex of the PVC. Retrograde
conduction may occur, and the P wave may be seen following the ectopic beat. The PR interval is not
measurable. The QRS complex is wide and distorted in shape, lasting more than 0.12 second. The T
wave is generally large and opposite in direction to the major direction of the QRS complex.
Associated with stimulants, electrolyte imbalances, hypoxia, heart disease
Not harmful with normal heart but CO reduction, angina, and HF in diseased heart
Assess apical-radial pulse deficit
Treatment
o Correct cause (e.g., oxygen therapy for hypoxia, electrolyte replacement)
o Antidysrhythmics (β-blockers, procainamide (Pronestyl), or amiodarone)
Audience Response Question
A patient has a diagnosis of acute myocardial infarction, and his cardiac rhythm is sinus bradycardia with 6 to 8
premature ventricular contractions (PVCs) per minute. The pattern that the nurse recognizes as the most
characteristic of PVCs is
a. An irregular rhythm.
b. An inverted T wave.
c. A wide, distorted QRS complex.
d. An increasingly long PR interval.
Answer: C
Rationale: Premature ventricular contractions have wide and distorted QRS complexes.
Ventricular Tachycardia
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A run of three or more PVCs defines ventricular tachycardia (VT).
Ventricular rate is 150 to 250 beats/minute.
Rhythm may be regular or irregular.
AV dissociation may be present, with P waves occurring independently of the QRS complex.
The atria may be depolarized by the ventricles in a retrograde fashion.
The P wave is usually buried in the QRS complex, and the PR interval is not measurable.
The QRS complex is distorted in appearance and wide (greater than 0.12 second in duration).
The T wave is in the opposite direction of the QRS complex.
Ectopic foci take over as pacemaker
Monomorphic, polymorphic, sustained, and nonsustained
Considered life-threatening because of decreased CO and the possibility of deterioration to ventricular
fibrillation
Ventricular tachycardia occurs when an ectopic focus or foci fire repeatedly and the ventricle takes
control as the pacemaker.
Different forms of VT exist, depending on QRS configuration.
Monomorphic VT has QRS complexes that are the same in shape, size, and direction.
Polymorphic VT occurs when the QRS complexes gradually change back and forth from one shape, size,
and direction to another over a series of beats.
VT may be sustained (longer than 30 seconds) or nonsustained (less than 30 seconds).
The development of VT is an ominous sign. It is a life-threatening dysrhythmia because of decreased CO
and the possibility of development of ventricular fibrillation, which is a lethal dysrhythmia.
Associated with heart disease, electrolyte imbalances, drugs, CNS disorder
Can be stable (patient has a pulse) or unstable (pulseless)
Sustained VT causes severe decrease in CO
o Hypotension, pulmonary edema, decreased cerebral blood flow, cardiopulmonary arrest
Precipitating causes must be identified and treated (e.g., hypoxia)
VT with pulse (stable) treated with antidysrhythmics or cardioversion
Pulseless VT treated with CPR and rapid defibrillation
Ventricular Tachycardia Torsades de Pointes
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Torsades de pointes (French for “twisting of the points”) is polymorphic VT associated with a prolonged
QT interval of the underlying rhythm.
Accelerated Idioventricular Rhythm (AIVR)
 Develops when the intrinsic pacemaker rate (SA node or AV node) becomes less than that of ventricular
ectopic pacemaker
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Rate is between 40 and 100 beats/minute
Atropine if patient symptomatic
Temporary pacing
Do not suppress rhythm
o (e.g., amiodarone) should not be used as these can terminate the ventricular rhythm and
further reduce the HR
Ventricular Fibrillation
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Ventricular fibrillation (VF) is a severe derangement of the heart rhythm characterized on ECG by
irregular waveforms of varying shapes and amplitude.
This represents the firing of multiple ectopic foci in the ventricle. Mechanically the ventricle is simply
“quivering,” with no effective contraction, and consequently no CO occurs. VF is a lethal dysrhythmia.
HR is not measurable. Rhythm is irregular and chaotic. The P wave is not visible, and the PR interval and
the QRS interval are not measurable.
Associated with MI, ischemia, disease states, procedures
Unresponsive, pulseless, and apneic
If not treated rapidly, death will result
Treat with immediate CPR and ACLS
o Defibrillation
o Drug therapy (epinephrine, vasopressin)
Audience Response Question
A patient in the coronary care unit develops ventricular fibrillation. The first action the nurse should take is to
a. Perform defibrillation.
b. Initiate cardiopulmonary resuscitation.
c. Prepare for synchronized cardioversion.
d. Administer IV antidysrhythmic drugs per protocol
Answer: B
Rationale: Immediate treatment for ventricular fibrillation is the initiation of cardiopulmonary resuscitation,
followed by the use of defibrillation and definitive drug therapy according to advanced cardiac life support
guidelines.
Asystole
 Represents total absence of ventricular electrical activity
 No ventricular contraction
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Patient unresponsive, pulseless, apneic
Must assess in more than one lead
Usually result of advanced cardiac disease, severe conduction disturbance, or end-stage HF
Treat with immediate CPR and ACLS measures
o Epinephrine and/or vasopressin
o Intubation
Poor prognosis
Pulseless Electrical Activity
 Electrical activity can be observed on the ECG, but no mechanical activity of the heart is evident, and
the patient has no pulse
 Prognosis is poor unless underlying cause quickly identified and treated
 Hs and Ts Pneumonic (most common causes)
o H’s
 Hypovolemia
 Hypoxia
 Hydrogen ion (acidosis)
 Hyper-/hypokalemia
 Hypoglycemia
 Hypothermia
o T’s
 Toxins
 Tamponade (cardiac)
 Thrombosis (MI and pulmonary)
 Tension pneumothorax
 Trauma
 Treatment
o CPR followed by intubation and IV epinephrine
o Treatment is directed toward correction of the underlying cause
Sudden Cardiac Death (SCD)
 Death from a cardiac cause
 Majority of SCDs result from ventricular dysrhythmias
o Ventricular tachycardia
o Ventricular fibrillation
Prodysrhythmia
 Life-threatening dysrhythmias caused by antidysrhythmia drugs
 Severe LV dysfunction increases risk
 Digoxin and class IA, IC, and III antidysrhythmia drugs
 Most susceptible first few days of drug therapy
Defibrillation
 Treatment of choice for VF and pulseless VT
 Most effective when completed within 2 minutes of dysrhythmia
onset
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Passage of DC electrical shock through the heart to depolarize myocardial cells
Allows SA node to resume pacemaker role
Monophasic defibrillators deliver energy in one direction
Biphasic defibrillators deliver energy in two directions
o Use lower energies
o Fewer postshock ECG dysrhythmias
Output is measured in joules or watts per second
Recommended energy for initial shocks in defibrillation
o Biphasic: 120 to 200 joules
o Monophasic: 360 joules
Immediate CPR after first shock
The following general steps are taken for defibrillation:
o Start CPR while obtaining and setting up defibrillator
o Turn on and select energy
o Make sure sync button is turned off
o Apply gel pads
o Charge
o Position paddles firmly on chest
o Ensure “All clear”!!!!!
o Deliver charge
Synchronized Cardioversion
 Choice of therapy for ventricular (VT with a pulse) or supraventricular tachydysrhythmias
 Synchronized circuit delivers a countershock on the R wave of the QRS complex of the ECG
 Procedure similar to defibrillation except sync button turned ON
 If patient stable, sedate prior
 Initial energy lower
o 70–75 joules (biphasic)
o 100 joules (monophasic)
 If patient becomes pulseless, turn sync button off and defibrillate
Implantable Cardioverter-Defibrillator (ICD)
 Appropriate for patients who
o Have survived SCD
o Have spontaneous sustained VT
o Have syncope with inducible ventricular
tachycardia/fibrillation during EPS
o Are at high risk for future life-threatening
dysrhythmias
 Decreases mortality
 Consists of a lead system placed via subclavian vein
to the endocardium
 Battery-powered pulse generator is implanted subcutaneously
 Sensing system monitors HR and rhythm – delivering 25 joules or less to heart when detects lethal
dysrhythmia
 Includes antitachycardia and antibradycardia pacemakers
o Overdrive pacing for tachycardias
o Backup pacing for bradycardias
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Preprocedure and postprocedure care same as pacemaker
S-ICD
Variety of emotions are possible
o Fear of body image change
o Fear of recurrent dysrhythmias
o Expectation of pain with ICD discharge
o Anxiety about going home
Participation in an ICD support group should be encouraged
Patient and Caregiver Teaching
o Follow-up appointments
o Incision care
o Arm restrictions
o Sexual activity
o Driving
o Avoid direct blows
o Avoid large magnets, MRI
o Air travel not restricted
o Avoid antitheft devices
o What to do if ICD fires
o Medic Alert ID
o ICD identification card
o Caregivers to learn CPR
Pacemakers
 Used to pace the heart when the normal conduction pathway is damaged
 Pacing circuit consists of
o Programmable pulse generator (power source)
o One or more conducting (pacing) leads to myocardium
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Ventricular capture (depolarization) secondary to signal (pacemaker spike) from pacemaker lead in the
right ventricle.
Pace atrium and/or one or both of ventricles (small, sophisticated, and physiologically precise)
Most pace on demand, firing only when HR drops below preset rate
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o Sensing device inhibits pacemaker when HR
adequate
o Pacing device triggers when no QRS complexes
within set time frame
Antitachycardia pacing: delivery of a stimulus to the
ventricle to terminate tachydysrhythmias
Overdrive pacing: pacing the atrium at rates of 200–500
impulses/minute to terminate atrial tachycardias
Cardiac resynchronization therapy (CRT)
o Resynchronizes the heart cycle by pacing both ventricles
o Biventricular pacing
o Used to treat patients with heart failure
o Can be combined with ICD for maximum therapy
Temporary Pacemakers
 Power source outside the body
o Transvenous
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A transvenous pacemaker consists of a lead or leads that are threaded transvenously to
the right atrium and/or right ventricle and attached to the external power source
 Most temporary transvenous pacemakers are inserted in emergency departments and
critical care units in emergency situations.
 They provide a bridge to insertion of a permanent pacemaker or until the underlying
cause of the dysrhythmia is resolved.
o Epicardial
 Leads placed on epicardium during heart surgery
 Passed through chest wall and attached to external power source as needed
o Transcutaneous
 For emergency pacing needs
 Noninvasive
 Bridge until transvenous pacer can be inserted
 Use lowest current that will “capture”
 Patient may need analgesia/sedation
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Pacemakers Cont.
 ECG monitoring for malfunction
 Failure to sense
o Causes inappropriate firing
 Failure to capture
o Lack of pacing when needed leads to bradycardia or asystole
 Monitor for other complications
o Infection
o Hematoma formation
o Pneumothorax
o Atrial or ventricular septum perforation
o Lead misplacement
 Postprocedure care
o OOB once stable
o Limit arm and shoulder activity
o Monitor insertion site for bleeding and infection
o Patient teaching important
 Patient and Caregiver Teaching
o Follow-up appointments for pacemaker function checks
o Incision care
o Arm restrictions
o Avoid direct blows
o Avoid high-output generator
o No MRIs unless pacer approved
o Microwaves OK
o Avoid antitheft devices
o Travel not restricted
o Monitor pulse
o Pacemaker ID card
o Medic Alert ID
Radiofrequency Catheter Ablation Therapy
 Electrode-tipped ablation catheter “burns” accessory pathways or ectopic sites in the atria, AV node,
and ventricles
 Nonpharmacologic treatment of choice for several atrial dysrhythmias
 Postcare similar to cardiac catheterization
ECG Changes Associated With Acute Coronary Syndrome
(ACS)
 The 12-lead ECG is a major diagnostic tool used to
evaluate patients with ACS.
 The ECG changes are in response to ischemia,
injury, or infarction (necrosis) of myocardial cells.
 The leads facing the area of involvement
demonstrate the definitive ECG changes.
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The leads facing opposite the area involved in ACS often demonstrate reciprocal (opposite) ECG
changes.
In addition, the pattern of ECG changes among the 12 leads provides information on the coronary
artery involved in ACS (Table 35-14).
Ischemia
o ST-segment depression and/or T wave inversion
o ST-segment depression is significant if it is at least 1 mm (one small box) below the isoelectric
line
o Changes reverse when adequate blood flow is restored to myocardium
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Injury
o ST-segment elevation occurs
 Significant if >1 mm above the isoelectric line
o If treatment is prompt and effective, may avoid or limit infarction
 Absence of serum cardiac markers confirms no infarction
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Infarction
o Physiologic Q wave is the first negative deflection following the P wave
 Small and narrow (<0.04 second in duration)
o Pathologic Q wave is deep and >0.03 second in duration
ECG Finding With Anterolateral Wall MI
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ECG findings with anterolateral wall myocardial infarction. Normally, leads I, aVL, and V 1 to V3 have
positive R wave. Note the pathologic Q waves in these leads and the ST-segment elevation in leads V 2 to
V5 (arrows).
Syncope
 Brief lapse in consciousness accompanied by a loss in postural tone (fainting)
 Noncardiovascular causes
o Stress
o Hypoglycemia
o Dehydration
o Stroke
o Seizure
 Cardiovascular causes
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o Cardioneurogenic or “vasovagal” syncope
 Carotid sinus sensitivity
o Dysrhythmias (tachycardias, bradycardias)
o Prosthetic valve malfunction
o Pulmonary emboli
o HF
Diagnostic studies
o Echocardiography
o Stress test
o EPS
o Head-up, tilt test
 To assess for cardioneurogenic syncope
 Abnormal response to position change causes paradoxic vasodilation and bradycardia
(vasovagal response)
Med Surg 2 Exam #1 Study Guide
Chapter 34: Heart Failure
Heart Failure
 Complex clinical syndrome resulting in insufficient blood supply/oxygen to tissues and organs
o Involves diastolic or systolic dysfunction
o Ejection fraction (EF) is amount of blood pumped by LV with each heart beat
 Associated with CVDs
o Particularly long-standing hypertension, coronary artery disease (CAD), and myocardial
infarction (MI)
 ↑ In incidence and prevalence
o Better survival after cardiac events
o Aging population
o Costly
 Most common cause for hospital admission in adults over age 65
o Keep coming back
 This places a significant economic burden on the health care system
 HF is primarily a disease of older adults
o The incidence is similar in men and women.
Risk Factors
 Primary risk factors
o Hypertension --#1 Modifiable risk factor
 Properly treated and managed, incidence of HF can be reduced by 50%
o CAD (2nd)
 Co-morbidities contribute to development of HF
o Such as diabetes, metabolic syndrome, advanced age, tobacco use, and vascular disease
Etiology of Heart Failure
 Anything that interferes with mechanisms that regulate cardiac output (CO)
o CO depends on (1) preload, (2) afterload, (3) myocardial contractility, and (4) heart rate (HR).
o Any changes in these factors can lead to decreased ventricular function and HF.
o Ex. Sudafed (causes vasoconstriction =increased cardiac workload)
 Primary causes
o Conditions that directly damage the heart
 Hypertension, including hypertensive crisis
 Coronary artery disease, including myocardial infarction
 Rheumatic heart disease
 Congenital heart defects (e.g., ventricular septal defect)
 Pulmonary hypertension
 Cardiomyopathy (e.g., viral, postpartum, substance abuse)
 Hyperthyroidism
 Valvular disorders (e.g., mitral stenosis)
 Myocarditis
 Precipitating causes
o Conditions that increase workload of ventricles
 Anemia (decreased oxygen supply increases workload of heart to meet the demand)
 Infection (increased oxygen demand)
 Thyrotoxicosis (increased heart rate and workload)
 Hypothyroidism (increased risk for atherosclerosis)
 Dysrhythmias (decreased CO and increased workload)
 Bacterial endocarditis (infection increases workload, can also cause valvular disorders)
 Obstructive sleep apnea
 Pulmonary embolism (increased workload to pump blood into lungs)
 Paget’s disease (increased workload secondary to increased vasculature bed)
 Nutritional deficiencies (decreased cardiac function increases workload)
 Hypervolemia (increased preload increases workload)
Classification of Heart Failure
 Left-sided HF
o Most common form of HF
o Results from inability of LV to
 Empty adequately during systole
 Fill adequately during diastole
o Further classified as (tx differently)
 Systolic
 Diastolic
 Mixed systolic and diastolic
Left-Sided Heart Failure
 Left-sided HF results from left ventricular dysfunction.
 Blood backs up into left atrium and pulmonary veins
 Increased pulmonary pressure causes fluid leakage →→ pulmonary congestion and edema
o Crackles in the bases of lungs
Pathophysiology: Systolic HF
 HFrEF – HF with reduced EF
o EF =ejection fraction
o Normal EF is 55% to 60%. Patients with HFrEF generally have an EF less than 45%. It can be as
low as 5% to 10%
 Inability to pump blood forward
o Body tries to pump MORE blood
 Treatment tries to counteract this
 Caused by
o Impaired contractile function
o Increased afterload
o Cardiomyopathy
o Mechanical abnormalities
 Decreased LV ejection fraction (EF)
 The LV in systolic failure loses its ability to generate enough pressure to eject blood forward through
the aorta.
o Over time, the LV becomes dilated and hypertrophied.
 The weakened heart muscle cannot generate adequate stroke volume, which affects CO.
o
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Because the LV cannot effectively push blood forward, end diastolic volumes and pressures in
the LV increase.
When the LV fails, blood backs up into the left atrium.
o This causes fluid accumulation in the lungs.
o The increased pulmonary hydrostatic pressure causes fluid leakage from the pulmonary
capillary bed into the interstitium and then the alveoli.
o This results in pulmonary congestion and edema.
Pathophysiology: Diastolic HF
 HFpEF – HF with preserved EF
 Impaired ability of the ventricles to relax and fill during diastole, resulting in decreased stroke volume
and CO
o The end result of diastolic failure is the same as systolic failure (e.g., pulmonary congestion).
 Result of left ventricular hypertrophy from hypertension, older age, female, diabetes, obesity
 HFpEF is diagnosed by the following criteria: (1) signs and symptoms of HF, (2) normal EF, and (3)
evidence of LV diastolic dysfunction by echocardiography or cardiac catheterization.
 Therapies for HFpEF are targeted at reducing underlying risk factors and treating comorbidities.
Pathophysiology: Mixed Heart Failure
 Mixed systolic and diastolic failure
o Seen in disease states such as dilated cardiomyopathy (DCM)
o Poor EFs (<35%)
o High pulmonary pressures
o Biventricular failure
 Both ventricles may be dilated and have poor filling and emptying capacity
 Transplant only way to save (cure)
Pathophysiology: Right-Sided Heart Failure
 RV fails to pump effectively
 Fluid backs up in venous system
 Fluid moves into tissues and organs
o Causing peripheral edema, abdominal ascites, hepatomegaly, jugular venous distention
 Left-sided HF is most common cause of right-sided HF
o As the LV fails, fluid backs up into the pulmonary system, causing increased pressures in the
lungs
o The RV has to work harder to push blood to the pulmonary system
o Over time, this increased workload weakens the RV and gradually it fails
 Other causes include RV infarction, PE, and cor pulmonale (RV dilation and hypertrophy)
Pathophysiology: Heart Failure in General
 Ventricular failure leads to:
o Low blood pressure (BP)
 Cardiogenic shock (emergency)
o Low CO
o Poor renal perfusion
 Abrupt or subtle onset
 Compensatory mechanisms mobilized to maintain adequate CO
o (1) neurohormonal responses: renin-angiotensin-aldosterone-system (RAAS) and the
sympathetic nervous system (SNS), (2) ventricular dilation, and (3) ventricular hypertrophy.
Compensatory Mechanisms
 Renin-Angiotensin-Aldosterone-System (RAAS)
o Homeostatic regulatory system
 BP control and fluid and electrolyte balance
o Fluid and sodium retained in response to stress
 Causes vasoconstriction to ↑ BP
o This is all bad if have HF
 Recurrent activation of the RAAS in HF is what is responsible for the signs and symptoms
that develop
 Neurohormonal response – RAAS
o As CO falls, blood flow to kidneys ↓ and is sensed as ↓ volume
 SNS is activated to ↑ BP and HR
 Release of aldosterone from adrenal cortex results in sodium and water retention
 Peripheral vasoconstriction and ↑ BP
 Pituitary gland releases ADH which results in water reabsorption
o The outcome of the cascade results in further water and sodium retention in an already
overloaded state, and increased workload of the failing heart.
 Other factors contributing to development of HF
o Endothelin is produced inside arteries
 Causes further arterial vasoconstriction and ↑ cardiac contractility and hypertrophy
 Now have endothelin blockers (new)
o Cytokines are released
 Further depress heart function by causing hypertrophy, contractile dysfunction, and cell
death
 Neurohormonal response - SNS
 Inadequate stroke volume and CO
o Release of catecholamines (epinephrine and norepinephrine)
 ↑ HR
 ↑ Myocardial contractility
 Peripheral vasoconstriction
o Initially helpful but then harmful
 Over time these factors become harmful and counterproductive, as they increase the
workload, preload (volume), and oxygen requirement in an already failing heart
 Stress heart –want to calm down
 Beta blocker!!!
 Ventricular remodeling
o Continuous activation of neuro-hormonal responses (RAAS and SNS)
o Hypertrophy of ventricular myocytes
o Ventricles larger but less effective in pumping
o Can cause life-threatening dysrhythmias and sudden cardiac death
 Drug therapies to prevent or reverse remodeling and decrease mortality are
recommended
 These include ACE-inhibitors, β-adrenergic blockers (β-blockers), and aldosterone
antagonists
 Dilation
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o Enlargement of chambers of heart that occurs when
pressure in left ventricle is elevated
o Initially effective (increased CO and maintenance of BP)
o Eventually this mechanism becomes inadequate and CO
decreases
 elastic elements of the muscle fibers are
overstretched and can no longer contract effectively
o Note the enlarged heart chambers with cardiac dilation 
Hypertrophy
o Increase in muscle mass and cardiac wall thickness
o Initially effective
o Over time leads to poor contractility, increased O2 needs, poor
coronary artery circulation, and risk for ventricular dysrhythmias
o Note the thickened ventricular walls with hypertrophy 
Natriuretic peptides
o Atrial natriuretic peptide (ANP),
b-type natriuretic peptide (BNP)
 Causes vasodilation, diuresis, decreases BP
 Synthetic BNP replaced with nitropreside and
nitroglycerine
o Released in response to increased blood volume in heart
o Causes diuresis, vasodilation, and lowered BP
o Counteracts effects of SNS and RAAS
Nitric oxide (NO) and prostaglandin
o Released from vascular endothelium in response to compensatory mechanisms
o NO and prostaglandin relaxes arterial smooth muscle, resulting in vasodilation and decreased
afterload
o Compensated HF occurs when compensatory mechanisms succeed in maintaining an adequate
CO that is needed for tissue perfusion.
o Decompensated HF occurs when these mechanisms can no longer maintain adequate CO and
inadequate tissue perfusion results.
Acute Decompensated Heart Failure (ADHF): Clinical Manifestations
 ADHF
o Sudden onset of signs and symptoms of HF
o Requires urgent medical care
o Pulmonary and systemic congestion due to ↑ left-sided and right-sided filling pressures
 LASIX AND VASODILATORS = SAVE THEM
 Early → increased pulmonary venous pressure
o Increase in the respiratory rate
o Decrease in Pao2
 Later → interstitial edema
o Tachypnea
 Further progression → alveolar edema
o Respiratory acidemia
 Can manifest as pulmonary edema
 Life-threatening situation – alveoli fill with fluid (rapid response)
 Most commonly associated with left-sided HF
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As pulmonary edema progresses, it inhibits oxygen and carbon dioxide exchange at the alveolarcapillary interface.
o A. Normal relationship.
o B. Increased pulmonary capillary hydrostatic pressure causes fluid to move from the vascular
space into the pulmonary interstitial space.
o C. Lymphatic flow increases in an attempt to pull fluid back into the vascular or lymphatic space.
o D. Failure of lymphatic flow and worsening of left heart failure result in further movement of
fluid into the interstitial space and into the alveoli.
Pulmonary Edema: Clinical Manifestations
o Anxious, pale, cyanotic
o Cool and clammy skin
o Dyspnea
o Orthopnea
o Tachypnea
o Use of accessory muscles
o Cough with frothy, blood-tinged sputum
o Crackles and wheezes
o Tachycardia
o Hypotension or hypertension
o Abnormal S3 or S4
Based on hemodynamic and clinical status, patients can be categorized into one of four groups
o Dry-warm
o Dry-cold
o Wet-warm (most common)
o Wet-cold
Worse as go down (wet and cold in shock)
Chronic Heart Failure: Clinical Manifestations
 Dependent on age, underlying type and extent of heart disease, and which ventricle is affected
 FACES
o Fatigue
o Limitation of Activities
o Chest congestion/cough
o Edema
o Shortness of breath
 Fatigue
o Fatigue is one of the earliest symptoms of chronic HF
 Dyspnea
o Dyspnea is a common manifestation of chronic HF
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Orthopnea
Paroxysmal nocturnal dyspnea
Tachycardia
Edema
o Dependent, liver, abdominal cavity, lungs
o Edema may be pitting in nature
o Sudden weight gain of >3 lb (1.4 kg) in 2 days may indicate ADHF, an exacerbation of chronic HF
o 500 ml = lb
Nocturia
Skin changes (dusky, shiny, swollen, diminished hair growth)
Behavioral changes (restlessness, confusion, and decreased attention span or memory)
Chest pain
Weight changes (fluid attention, ascites, hepatomegaly)
Heart Failure: Complications
 Pleural effusion
o Occurs when excess fluid builds up in the pleural cavity of the lungs secondary to increasing
pressure in the pleural capillaries
 Dysrhythmias – atrial and ventricular
o Enlargement of heart chambers
 Left ventricular thrombus
o Once a thrombus has formed, it may also decrease left ventricular contractility, decrease CO,
and worsen the patient’s perfusion.
o The development of emboli from the thrombus also places the patient at risk for stroke
 Hepatomegaly
o The liver becomes congested with venous blood. The hepatic congestion leads to impaired liver
function
 Eventually liver cells die, fibrosis occurs, and cirrhosis can develop
 Renal failure
o Get 25% of CO, will have elevated creatinine (not getting oxygen)
o Decreased perfusion to the kidneys and can lead to renal insufficiency or failure
Diagnostic Studies
 Determine and treat underlying cause
 Echocardiogram
o Provides information on EF, heart valves and heart chambers
 ECG, chest x-ray, 6-minute walk test, MUGA scan, cardiopulmonary exercise stress test, heart
catheterization, EMB
 BNP levels (normal around 60)
o Higher the number longer they’ve been in HF
ADHF: Interprofessional Care
 Continuous monitoring and assessment
o VS, O2 saturation, urinary output
 Hemodynamic monitoring if unstable
 Supplemental oxygen
 Mechanical ventilation if unstable
o If they need it!
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High Fowler’s position
o This position helps decrease venous return because of the pooling of blood in the extremities.
o This position also increases the thoracic capacity, allowing for improved breathing
Ultrafiltration (aquapheresis) for patients with volume overload and resistance to diuretics
Circulatory assist devices for patients with deteriorating HF
o Intraaortic balloon pump (IABP)
o Ventricular assist devices (VADs)
Left Ventricular Assist Device
ADHF Drug Therapy
 Diuretics
o Decrease volume overload (preload)
 Loop diuretics - Furosemide (Lasix)
 Onset: 3-5 min
 Vasodilators
o Reduce circulating blood volume and improve coronary artery circulation
 IV nitroglycerin
 Reduces preload, slightly reduces afterload (in high doses), and increases
myocardial oxygen supply
 Sodium nitroprusside
 Potent IV vasodilator that reduces both preload and afterload, thus improving
myocardial contraction, increasing CO, and reducing pulmonary congestion.
 Morphine
o Reduces preload and afterload
o Relieves dyspnea and anxiety
 Not for pain
 Positive inotropes
o β-agonists (dopamine, dobutamine, norepinephrine [Levophed])
o Phosphodiesterase inhibitor (milrinone)
o Digitalis
 Digitalis increases contractility but also increases myocardial oxygen consumption
Chronic HF: Interprofessional Care
 Main treatment goals
o Treat the underlying cause and contributing factors
o Maximize CO
o Reduce symptoms
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o Improve ventricular function
o Improve quality of life
o Preserve target organ function
o Improve mortality and morbidity
NO nitro if have had ED drugs (Viagra)
CardioMems system
Implantable cardioverter-defibrillator (ICD)
Biventricular pacing/cardiac resynchronization therapy (CRT)
IABP and VADs as bridge to transplant (BTT) or as destination therapy (DT)
o WATCH VIDEO TO GET THESE EXPLAINED
Placement of Pacing Leads in Cardiac Resynchronization Therapy
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ONLY MRI IF NEW
Chronic HF: Drug Therapy
 Diuretics
o Reduce edema, pulmonary venous pressure, and preload
o Promote sodium and water excretion
o Loop diuretics
 Start with Lasix typically
o Thiazide diuretics (don’t work if GFR less than 20)
 Hydrochlorazide
o Monitor potassium levels (hypokalemia)
 RAAS inhibitors
o ACE inhibitors
 Primary drug of choice for blocking the RAAS system in HF patients with systolic failure
o Angiotensin II receptor blockers
 For patients who are unable to tolerate ACE inhibitors
o #1 side effect: angioedema for ACE and ARBs
o Aldosterone antagonists
 Inspra and Aldactone
 Block aldosterone so don’t retain Na+
o Monitor potassium levels (hyperkalemia)
 β-Blockers
 Vasodilators
o Nitrates
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Combination therapy
o BiDil (hydralazine and isosorbide dinitrate)
Positive inotropic agents
o Digitalis (only oral inotropic agent)
 Increase the force of cardiac contraction
Inhibitor of cardiac sinus node
o Ivabradine (Corlanor)
 New category of oral drug that inhibits the sinus node and reduces HR
o Must be in sinus rhythm with resting HR of > 70 bpm and taking highest dose β-blockers
 Inhibits sinus node
 Reduces HR
 Decreases risk of hospitalization for worsening HF
Chronic HF: Nutritional Therapy
 Low sodium diet (<2 gram a day)
o Individualize recommendations and consider cultural background
(www.nhlbi.nih.gov/health/index.htm#recipes)
o Recommend Dietary Approaches to Stop Hypertension (DASH) diet
o Sodium is usually restricted to 2 g/day
 Fluid restriction not generally required
 If required, < 2L/day
o Ice chips, gum, hard candy, ice pops to help thirst
 Daily weights important
o Same time, same clothing each day
 Weight gain of 3 lb (1.4 kg) over 2 days or a 3- to 5-lb (2.3 kg) gain over a week should be reported to
HCP
Chronic HF: Nursing Assessment
 Objective Data
o Serum electrolytes (especially Na+ and K+)
o Increased BUN, creatinine
o Liver function tests
o Increased NT-proBNP or BNP
o Chest x-ray
 Demonstrating cardiomegaly, pulmonary congestion, and interstitial pulmonary edema
o Echocardiogram
 Showing increased chamber size, decreased wall motion, decreased EF or normal EF
with evidence of diastolic failure
o ECG
o Decreased O2 saturation
Chronic HF: Nursing Implementation
 Health Promotion
o Interprofessional communication and decision-making with patient and caregiver
o Identify and treat risk factors for HF to prevent or slow progression
Heart Transplantation
 Treatment of choice for patients with refractory end-stage HF, inoperable CAD, and cardiomyopathy
(only CURE)
o 3,000 on list; average 2,000 available
o Survival rate of 85%-90% at 1year; 75% at 3
 Selection process identifies patients who would most benefit from a new heart
 Candidates must undergo physical, diagnostic, and psychologic evaluation
 ** If live long enough with transplant will end up with cancer due to immunosuppressants
 Transplant candidates are placed on a list
o Stable patients wait at home and receive ongoing medical care
o Unstable patients may require hospitalization for more intensive therapy
o Overall waiting period for a heart is long; many patients die during this time
 Donor and recipient matching is based on body and heart size, and an immunologic evaluation
o The immunologic assessment includes ABO blood type, antibody screen, panel-reactive
antibody (PRA) level, and human leukocyte antigen typing
 Heart retrieval first step
 Second step is removal of recipient’s heart except for portions of atria (2 different approaches) and
venous connections
 Final step is implantation of donor heart
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Human heart prepared for transplantation into a patient.
Denervated so watch for bradycardia
Posttransplantation monitoring
o Acute rejection
o Infection
o Malignancy
o Cardiac vasculopathy
Immunosuppressive therapy
o Include corticosteroids, calcineurin inhibitors (cyclosporine [Sandimmune, Neoral], tacrolimus
[Prograf]), and antiproliferative drugs (mycophenolate mofetil [CellCept]
Endomyocardial biopsy (EMB)
Endomyocardial biopsies are obtained from right ventricle weekly for the first month, monthly for
following 6 months, and yearly thereafter to detect rejection
Nursing care focuses on
o Promoting patient adaptation to the transplant process
o Monitoring cardiac function
o Managing lifestyle changes
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o Providing ongoing teaching
The newly transplanted heart is ‘denervated’ When removed from the donor, all nervous system
control is cut, therefore, the heart may not respond to normal Sympathetic Nervous System control.
Bradycardia much more dangerous than tachycardia.
Audience Response Question
A patient with a history of chronic heart failure is hospitalized with severe dyspnea and a dry, hacking cough.
Assessment findings include pitting edema in both ankles, BP 170/100 mm Hg, pulse 92 beats/minute, and
respirations 28 breaths/minute. Which explanation, if made by the nurse, is most accurate?
a. “The assessment indicates that venous return to the heart is impaired, causing a decrease in cardiac
output.”
b. “The manifestations indicate impaired emptying of both the right and left ventricles, with decreased
forward blood flow.”
c. “The myocardium is not receiving enough blood supply through the coronary arteries to meet its
oxygen demand.”
d. “The patient’s right side of the heart is failing to pump enough blood to the lungs to provide systemic
oxygenation.”
Answer: B
Rationale: The patient is experiencing acute decompensated heart failure with symptoms of both right- and
left-sided heart failure. Left-sided heart failure prevents normal, forward blood flow and causes pulmonary
congestion. Right-sided heart failure causes a backup of blood and results in venous congestion.
A patient with left-sided heart failure is prescribed oxygen at 4 L/min per nasal cannula, furosemide (Lasix),
spironolactone (Aldactone), and enalapril (Vasotec). Which assessment should the nurse complete to best
evaluate the patient’s response to these drugs?
a. Observe skin turgor
b. Auscultate lung sounds
c. Measure blood pressure
d. Review intake and output
Answer: B
Rationale: Left-sided heart failure will prevent normal blood flow and will cause blood to back up into the left
atrium and into the pulmonary veins. The increased pulmonary pressure causes fluid extravasation from the
pulmonary capillary bed into the interstitium and then the alveoli, which manifests as pulmonary congestion
and edema. The most important assessment to determine if the drugs are improving the patient’s condition is
to auscultate lung sounds. The other assessments are important, but the best indicator of improvement of left
ventricular function is a reduction in adventitious lung sounds (crackles).
The home care nurse visits a patient with chronic heart failure who is taking digoxin (Lanoxin) and furosemide
(Lasix). The patient complains of nausea and vomiting. Which action is most appropriate for the nurse to take?
a. Perform a dipstick urine test for protein.
b. Notify the health care provider immediately.
c. Have the patient eat foods high in potassium.
d. Ask the patient to record a weight every morning.
Answer: B
Rationale: Administration of furosemide increases excretion of potassium and may cause hypokalemia. The risk
for digitalis toxicity increases if potassium levels are below normal and digoxin is administered. Signs and
symptoms of digitalis toxicity include anorexia, nausea and vomiting, visual disturbances (such as “yellow”
vision), and dysrhythmias.
Med Surg 2 Exam #1 Study Guide
Chapter 36: Valvular Heart Disease
Valvular Heart Disease
 Heart has
o Two atrioventricular valves
 Mitral
 Tricuspid
o Two semilunar valves
 Aortic
 Pulmonic
 When taking blood pressure you are hearing turbulence
o Should not hear racket unless something making turbulence (BP cuff or faulty valve)
Normal Valve
Valvular Heart Disease
 Types of valvular heart disease depend on
o Valve(s) affected
o Type of dysfunction
 Stenosis
 Regurgitation
 Stenosis (constriction/narrowing)
o Valve orifice is smaller
o Forward blood flow is impeded
o Pressure differences reflect degree of stenosis
o More common in older people
o Heart has to work extra hard to push (replace to fix)
o forward
 Regurgitation (incompetence/insufficiency)
o Incomplete closure of valve leaflets
o Results in backward flow of blood
o Relationship to problem with valve (vegetations or something else)
o Backward
o Pt feeling tired (narrow pulse pressure) –need to replace
Valvular Stenosis and Regurgitation
Open position of a stenosed valve (left) and position of closed regurgitant valve (right).

Mitral Valve Stenosis
 Majority of adult cases result from rheumatic heart disease
o Don’t see much in U.S. now because tx strep
 ASO titer (for antibodies) these are what attack
o Scarring of valve leaflets and chordae tendineae
o Contractures develop with adhesions between commissures
of the leaflets
 Results in decreased blood flow from left atrium to left ventricle
 ↑ Left atrial pressure and volume
o Left atrium is BIG
o CO in the tank
 ↑ Pressure in pulmonary vasculature
 Risk for atrial fibrillation
o All wires stretched (resistant to tx)
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Mitral Valve Stenosis and Vegetation
What causes vegetations? IE (IV drug abusers get blood stream infection, valves sensitive to this)
Mitral Valve Stenosis with “Fish Mouth Orifice”
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The stenotic mitral valve takes on a “fish mouth” shape because of the thickening and shortening of the
mitral valve structures.
Mitral Valve Stenosis: Clinical manifestations
 #1 Exertional dyspnea (reduced lung compliance)
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Loud S1 (Lub of “lub dub”)
Murmur
Fatigue
Palpitations
o From atrial fibrillation may also occur.
Hoarseness
o From atrial enlargement pressing on the laryngeal nerve
Hemoptysis
o From pulmonary hypertension
Chest pain, seizures/stroke
o From decreased CO and coronary perfusion
o Emboli can form in the left atrium secondary to atrial fibrillation causing a stroke.
Mitral Valve Regurgitation
 Normal valve function depends on intact:
o Mitral leaflets
o Mitral annulus
o Chordae tendineae
o Papillary muscles
 Damage caused by:
o MI
o Chronic rheumatic heart disease
o Mitral valve prolapse
o Ischemic papillary muscle dysfunction
o IE (most common today)
 Incomplete valve closure
 Backward flow of blood
 Acute MR
o Pulmonary edema (HF)
 Chronic MR
o Left atrial enlargement, ventricular hypertrophy →
decrease in CO
 Acute clinical manifestations
o Thready peripheral pulses and cool, clammy extremities
o A low CO may mask a new systolic murmur.
o Rapid assessment (e.g., heart catheterization) and intervention (e.g., valve repair or
replacement) are critical.
 Chronic clinical manifestations
o Asymptomatic for years until development of some degree of left ventricular failure (body
compensates)
 Weakness, fatigue, palpitations, progressive dyspnea
 Peripheral edema, S3, murmur
o Patients with asymptomatic MR must be monitored carefully.
 Surgery (valve repair or replacement) should be considered before significant left
ventricular failure or pulmonary hypertension develops.
Mitral Valve Prolapse
 Abnormality of mitral valve leaflets and the papillary muscle or chordae
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Leaflets prolapse back into left atrium during systole
It is the most common form of valvular heart disease in the United
States.
Usually benign with valve closing effectively
o Common in women –usually benign
Potential complications (including MR, IE, SCD, HF, and cerebral
ischemia)
Unknown cause but genetic link in some
This figure shows the mitral valve prolapsing (buckling) when
closed. Looks like a “hood.” Left atrium stretched out   
o More risk for heart attack
Confirmed with echocardiography
o Mechanical problem (structural)
o EKG would not show this because shows electrical problem
Clinical manifestations
o Most patients asymptomatic for life
o Only 10% with symptoms
o Murmur d/t regurgitation
o MVP does not alter S1 or S2 heart sounds.
o Severe MR uncommon
o Dysrhythmias can cause palpitations, light-headedness, and dizziness
 A-fib most common
o Infective endocarditis
o Chest pain unresponsive to nitrates
 Dyspnea, palpitations, and syncope may occasionally accompany the chest pain and do
not respond to antianginal treatment (e.g., nitrates).
Treat symptoms with β-blockers
o Control chest pain and palpitations
o Encourage the patient to stay hydrated, exercise regularly, and avoid caffeine.
Valvular surgery for MR (do a lot of this today)
o More and more hospitals doing these because people need them
Patient teaching important
o Antibiotic prophylaxis if MR present
 Pulling teeth, or other invasive procedures (dental hygiene related to heart problems)
o Take drugs as prescribed
o Healthy diet; avoid caffeine
o Avoid OTC stimulants (Sudafed)
o Exercise
o When to call HCP or EMS
 If symptoms develop or worsen (e.g., palpitations, fatigue, shortness of breath, anxiety)
Aortic Valve Stenosis
 Congenital stenosis usually discovered in childhood, adolescence, or young adulthood
 Can also be degenerative or caused by rheumatic fever (in older adults)
o Most valve stenosis today
 AS due to rheumatic heart disease accompanies mitral valve disease.
 Isolated AS is usually nonrheumatic in origin.
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o The incidence of rheumatic aortic valve disease has been decreasing, but degenerative stenosis
is increasing as the population ages.
Treat only is symptomatic
Obstruction of flow from left ventricle to aorta
Left ventricular hypertrophy and ↑ myocardial oxygen consumption
o Longer you weight larger valve gets
Leads to ↓ CO, pulmonary hypertension, and HF
o Significant mortality rate if untreated
Clinical manifestations
o Angina (left ventricular size will cause chest pain)
o Syncope
o Exertional dyspnea
 This triad reflects left ventricular failure.
Auscultatory findings (don’t have to memorize heart sounds, just know they are not normal)
o Normal to soft S1
o Diminished or absent S2
o Systolic murmur
o Prominent S4
Poor prognosis if symptomatic and not corrected
Use nitroglycerin cautiously to treat angina (look at VS, pulse pressure, pass out?)
o Reduces preload and BP
o Can worsen chest pain
o Can give but have to tx what happens next
Audience Response Question
The nurse is caring for a patient with aortic stenosis. For what should the nurse assess the patient?
a. Systolic murmur
b. Pericardial friction rub
c. Diminished or absent S4
d. Low-pitched diastolic murmur
Answer: A
Rationale: Clinical manifestations of aortic stenosis include angina, syncope, dyspnea on exertion, heart failure,
normal or soft S1, diminished or absent S2, systolic murmur, and prominent S4.
Aortic Valve Regurgitation
 Acute AR
o IE, trauma, or aortic dissection
o Life-threatening emergency
 Chronic AR
o Rheumatic heart disease, congenital bicuspid aortic valve, syphilis, chronic rheumatic conditions
(such as ankylosing spondylitis or reactive arthritis)
 Backward blood flow from ascending aorta into left ventricle (This results in volume overload)
 With chronic AR, left ventricular dilation and hypertrophy
 ↓ Myocardial contractility, and blood volume in the left atrium and pulmonary bed increases
 Pulmonary hypertension and right ventricular failure
 Clinical manifestations of acute AR
o Severe dyspnea
o Chest pain
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o Hypotension
o Cardiogenic shock (widened mediastinum)
o Life-threatening emergency
Clinical manifestations of chronic AR
o May be asymptomatic for years (body compensates)
o Exertional dyspnea, orthopnea, paroxysmal dyspnea
o Angina
o “Water-hammer” pulse if severe (a strong, quick beat that collapses immediately)
o Soft or absent S1
o S3 or S4
o Soft, high-pitched diastolic murmur
Tricuspid Valve Stenosis
 Occurs in patients with RF and IVDA (IV drug abuse)
o Right side = venous
 Right atrial enlargement and ↑ systemic venous pressure
 Clinical manifestations
o Peripheral edema
o Ascites
o Hepatomegaly
o Murmur
Pulmonic Valve Stenosis
 Almost always congenital (infants)
 Causes right ventricular hypertension and hypertrophy
 Clinical manifestations
o Fatigue
o Loud murmur
Valvular Heart Disease: Diagnostic Studies
 Patient’s history/physical exam
 CT scan of chest
o Gold standard for evaluating aortic disorders
 Echocardiogram
o Transesophageal echocardiography and Doppler color-flow imaging help diagnose and monitor
valvular heart disease progression.
 Chest x-ray
o Reveals the heart size, altered pulmonary circulation, and valve calcification
 ECG
o Identifies heart rate, rhythm, and any ischemia or ventricular hypertrophy
 Heart catheterization
o Detects pressure changes in the heart chambers, records pressure differences across the valves,
and measures the size of valve openings
Valvular Heart Disease: Interprofessional Care
 Conservative Management
o Prophylactic antibiotic therapy to prevent recurrent RF and IE
o Dependent on valve involved and disease severity
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o Prevent exacerbations of HF, pulmonary edema, thromboembolism, and recurrent endocarditis
o Drugs to treat/control HF
 Vasodilators (e.g., nitrates, ACE inhibitors)
 Positive inotropes (e.g., digoxin)
 Diuretics
 β-blockers
o Sodium restriction
o Anticoagulation therapy prevents and treats systemic or pulmonary emboli. It is used
prophylactically in patients with atrial fibrillation
 Warfarin (coumadin)
 Noax and doax for NO valve problem (CAN’T TAKE IF VALVE PROBLEM)
o Anti-dysrhythmic drugs
 Calcium channel blockers, β-blockers, anti-dysrhythmic drugs, or electrical cardioversion
 For A-Fib!!!
Percutaneous transluminal balloon valvuloplasty (NOT opening chest)
o Split open fused commissures
o For mitral, tricuspid, and pulmonic stenosis (NOT aortic, such a stiff valve)
o Balloon-tipped catheter inserted via femoral artery
 Try to stretch out valve (invasive, need consent, RN can’t get)
o Inflated to separate valve leaflets
A single- or double-balloon technique may be used for the PTBV procedure.
Currently, the use of a single Inoue balloon with hourglass shape allows sequential
inflation.
This technique is the most popular because it is easy and has good results with few
complications (e.g., left ventricular perforation).
The PTBV procedure is generally indicated for older adults and for those who are
poor surgery candidates.
The long-term results of PTBV are similar to surgical commissurotomy.
o Will have murmur after
Surgical Therapy
o The procedure that is used depends on the (1) valves involved, (2) pathology and severity of the
disease, and (3) patient’s clinical condition (can tolerate being on bypass???)
o Valve repair
 Surgical procedure of choice
 Lower mortality
 May not restore total valve function
o Valve replacement
Valve repair (procedure of choice)
o Commissurotomy (valvulotomy)
 Closed
 Open (more common)
o Valvuloplasty
 Open
 Minimally invasive
o Annuloplasty
 Involves reconstruction of the annulus, with or without the aid of prosthetic rings
Valve replacement
o Mechanical (artificial)
 Last longer
 Risk of thromboembolism
 Require long-term anticoagulation
 WON’T USE ON OLDER PERSON
o Biologic (tissue)
 Bovine, porcine, and human
 No anticoagulation required
 Less durable
 Can recover heart valves after person dies (they are avascular)
Types of Prosthetic Valves



A, Starr-Edwards caged ball valve; B, St. Jude bi-leaflet valve; C, Carpentier-Edwards porcine; D,
CoreValvetranscatheter aortic valve .
A wide variety of prosthetic valves are available for use. Desirable valves are nonthrombogenic and
durable, and create minimal stenosis.
Prolonged waiting time for aortic valve replacement is associated with greater mortality, and should be
done on a semi-urgent basis.
Nursing Assessment
 Subjective Data (what PT TELLS YOU)
o Past medical history
o IVDA, fatigue
o Palpitations, weakness, activity intolerance, dizziness, fainting
o DOE, cough, hemoptysis, orthopnea, PND
o Angina or atypical chest pain
 Objective Data (they look like crap)
o Fever (IE)
o Diaphoresis, flushing, cyanosis, clubbing, peripheral edema
o Crackles, wheezes, hoarseness
o S3 and S4
o Dysrhythmias
o ↑ or ↓ in pulse pressure; hypotension
 Depending on which valve it is can be widened or narrow
o Water-hammer or thready peripheral pulses
o Hepatomegaly, ascites
o Weight gain
Nursing Diagnoses
 Decreased cardiac output



o related to valvular incompetence as evidenced by murmurs, dyspnea, dysrhythmias, and/or
peripheral edema
Excess fluid volume
o related to fluid retention secondary to valvular-induced heart failure as evidenced by peripheral
edema, weight gain, adventitious breath sounds, and/or neck vein distention
Activity intolerance
o related to insufficient oxygenation secondary to decreased cardiac output and pulmonary
congestion as evidenced by weakness, fatigue, shortness of breath, increase or decrease in
pulse rate, and/or BP changes
Deficient knowledge
o related to lack of experience and exposure to information about disease and treatment process
as evidenced by verbalization of misconceptions about measures to prevent complications and
requests for information
Planning
 Patient Goals
o Normal cardiac function
o Improved activity tolerance
o Understanding of the disease process and health maintenance measures
Nursing Implementation
 Health Promotion
o Diagnosing and treating streptococcal infection
 Test with culture and then treat
o Prophylactic antibiotics for patients with history
o Encourage compliance
o Teach patient when to seek medical treatment
 Individualize rest and exercise
 Avoid strenuous activity
 Discourage tobacco use
 Ongoing cardiac assessments to monitor drug effectiveness
 Monitor INR
o The patient on anticoagulation therapy (e.g., warfarin [Coumadin]) after surgery for valve
replacement must have the international normalized ratio (INR) checked regularly to determine
proper dosage and adequacy of therapy.
o INR values of 2.5 to 3.5 are therapeutic for patients with mechanical valves.
 Patient teaching
o Drug actions and side effects
o Importance of prophylactic antibiotic therapy
o Information related to anticoagulation therapy
o When to seek medical care
 Follow-up care
o Notify HCP for
 Signs of infection (FEVER, intense shivers), HF, or bleeding
 Planned invasive or dental work
 Medical-alert device
Evaluation




Adequate tissue and organ perfusion
Fluid and electrolyte balance
Optimal level of activity
Verbalizes understanding of disease process and measures to prevent complications
Audience Response Question
A 19-year-old patient with rheumatic heart disease is admitted to the hospital with a recurrence of rheumatic
fever. In planning care for the patient, which nursing diagnosis should the nurse include?
a. Ineffective coping related to refusal to carry out health promotion activities
b. Risk for infection related to recent exposure to group A β-hemolytic streptococci
c. Impaired adjustment related to unsuccessful lifestyle modifications, goal setting, and problem solving
d. Ineffective health management related to lack of knowledge about long-term prophylactic antibiotic
therapy
Answer: D
Rationale: A patient with a history of rheumatic fever and rheumatic heart disease will need long-term or lifelong continuous prophylactic antibiotics to prevent recurrence of the disease.
Med Surg 2 Exam #1 Study Guide
Chapter 36: Infective Endocarditis
Infective Endocarditis (IE)
 Infection of inner layer of heart, including the cardiac valves
 Improved prognosis with antibiotic therapy
 10,000–15,000 new cases diagnosed in the United States each year (rising significantly)
What lab values indicate inflammation?
 ESR, WBC, CRP
 How to diagnose IE? #1 sign is of IE BRAND NEW MURMUR
Layers of the Heart
 The endocardium is the innermost layer of the heart and heart valves. Therefore, IE affects the valves.
Classification of IE
 Subacute form
o Preexisting valve disease (bad valve somewhere)
o Longer clinical course (may extend over months)
 Acute form
o Healthy valves
o Rapidly progressive
o Extremely ill, can come in full blown HF and septic
 Also classified by cause or site of involvement
o IE is more often classified based on the cause (e.g., intravenous drug abuse IE [IVDA IE], fungal
endocarditis) or site of involvement (e.g., prosthetic valve endocarditis [PVE]).
Causative Organisms of IE
 Bacterial most common
o Streptococcus viridans
o Staphylococcus aureus (IVDA)
 Viruses
 Fungi
 Only cure is transplant***
Etiology and Pathophysiology of IE
 Occurs when blood flow within heart allows causative organism to infect previously damaged valves or
other endothelial surfaces
 Vegetation
o Fibrin, leukocytes, platelets, and microbes
o Adhere to the valve or endocardium
o Parts break off and enter circulation (embolization)
Risk Factors
 Cardiac, noncardiac, procedural
 Principal risk factors
o Age (calcified aortic stenosis)
o IV drug abuse (IVDA)
o Prosthetic valves
o Use of intravascular devices (resulting in infection such as MRSA)
 VAD, dialysis
o Renal dialysis
o WHAT ELSE TO ASSESS FOR? New murmur, fever, WBC
 Rheumatic heart disease was the most common cause of IE, now it accounts for less than 20% of cases.
Bacterial Endocarditis of Mitral Value
 This is a picture of vegetations growing on the mitral
valve.
Mitral Stenosis and Vegetation
Pathogenesis of Infective Endocarditis
 This diagram depicts the
pathogenesis of IE. Once
vegetations occur, they can break
off, causing embolization (as
discussed on previous slide).
 Many persons with IE will develop
systemic embolization. This occurs
when left-sided heart vegetation
moves to various organs (e.g.,
brain, kidneys, spleen) and to the
extremities, causing limb
infarction.
 Right-sided heart lesions embolize
to the lungs, resulting in
pulmonary emboli.
 The infection may spread locally
and damage the valves or their
supporting structures. This causes
dysrhythmias, valve dysfunction, and eventual invasion of the myocardium, leading to heart failure
(HF), sepsis, and heart block.
Clinical Manifestations of IE
 Flu-like symptoms
 NEW murmur
 Nonspecific
 Fever
 Chills
 Weakness
 Malaise
 Fatigue
 Anorexia
 Subacute form
o Arthralgias (ache all over)
o Myalgias
o Back pain (kidneys being embolized)
o Abdominal discomfort
o Weight loss
o Headache
o Clubbing of fingers
 Vascular manifestations
o Splinter hemorrhages in nail beds (black longitudinal streaks)
 Related to the strep
o Petechiae
 A result of fragmentation and microembolization of vegetative
lesions.
They can occur on the conjunctivae, lips, buccal mucosa and palate, and over the ankles,
feet, and antecubital and popliteal areas.
o Osler’s nodes on fingertips or toes (painful, tender, red or purple, pea-size lesions)
 Suggestive of IE
o Janeway’s lesions on pads of the fingers and toes (lesions (flat, painless, small, red spots)
 Directly linked to IE, not seen as much
o Roth’s spots (hemorrhagic retinal lesions)
New or worsening systolic murmur in most patients
o The aortic and mitral valves are most often affected
Heart failure
o HF occurs in up to 80% of patients with aortic valve endocarditis and in approximately 50% of
patients with mitral valve endocarditis.
Manifestations secondary to embolism
o Spleen
 Embolization to the spleen may cause sharp, left upper quadrant pain and splenomegaly,
local tenderness, and abdominal rigidity.
o Kidneys
 Embolization to the kidneys may cause flank pain, hematuria, and renal failure.
o Limbs
 Emboli may lodge in small peripheral blood vessels of the arms and legs, and may cause
ischemia and gangrene.
o Brain
 Embolization to the brain may cause neurologic damage resulting in hemiplegia, ataxia,
aphasia, visual changes, and change in mental status.
o Lungs
 Pulmonary emboli may occur in right-sided endocarditis and cause dyspnea, chest pain,
hemoptysis, and respiratory arrest.
Mostly SUPPORTIVE CARE (all we can do)





Diagnostic Studies for IE
 History
o Ask patients if they have had any recent (within the past 3 to 6 months) dental, urologic,
surgical, or gynecologic procedures, including normal or abnormal obstetric delivery.
o Note any previous history of IVDA, heart disease, recent heart catheterization, heart surgery,
intravascular device placement, renal dialysis, or infections (e.g., skin, respiratory, urinary tract)
—risk factors already discussed.
 Laboratory tests
o Blood cultures (2 cultures 1 hour apart from different sites)
 Want to maximize the efficacy of antibiotics
o CBC with differential
o ESR, C-reactive protein (CRP), CMP
o Troponin (sure why not)
 Echocardiography
o Transesophageal echocardiogram and two- or three-dimensional (3-D) transthoracic
echocardiograms can detect vegetation on the heart valves.
 Chest x-ray (to detect cardiomegaly (an enlarged heart).
 ECG


o may show first- or second-degree atrioventricular (AV) block. Heart block occurs because the
heart valves lie close to conductive tissue, especially the AV node.
Heart catheterization
o may be used to assess valve function and the coronary arteries when surgery is being
considered.
Major criteria to diagnose IE include at least two of the following: two positive blood cultures 12 hours
apart, nonvalvular regurgitation, or intracardiac mass or vegetation noted on echocardiography.
Interprofessional Care
 Prophylactic antibiotic treatment for select patients having
o Certain dental procedures
o Respiratory tract infections
o Tonsillectomy and adenoidectomy
o Surgical procedures involving infected skin, skin structures, or musculoskeletal tissue
 People with the following heart conditions should have prophylactic antibiotics when they have the
conditions or procedures listed below.
o Prosthetic heart valve or prosthetic material used to repair heart valve
o Previous history of infectious endocarditis
o Congenital heart disease (CHD)
o Unrepaired cyanotic CHD (including palliative shunts and conduits)
o Repaired congenital heart defect with prosthetic material or device for 6 months after the
procedure
o Repaired CHD with residual defects at the site or adjacent to the site of prosthetic patch or
prosthetic device
o Heart transplantation recipients who develop heart valve disease
 Accurate identification of organism
 IV antibiotics (long-term) (Vanco, 6 weeks)
 Repeat blood cultures
 Valve replacement if needed (if symptomatic, HF)
 Antipyretics (reduction of fever)
 Fluids
 Rest, rest, rest (very important to rest organ and hopefully reduce injury)
Nursing Assessment
 Subjective Data
o Health history
 Valvular, congenital, or syphilitic heart disease
 Previous endocarditis, childbirth
 Staph or strep infection, hospital-acquired bacteremia
o Drugs – Immunosuppressive therapy
 Cancer, COPD, autoimmune diseases
o Recent surgeries and procedures
 Recent obstetric or gynecologic procedures; invasive procedures, including
catheterization, cystoscopy; recent dental or surgical procedures; GI procedures (e.g.,
endoscopy)
 Subjective Data: Functional Health Patterns
o IVDA
o Alcohol abuse

o Weight changes
o Malaise
o Anorexia
o Diaphoresis
o Chills
o Hematuria (bloody urine)
o Exercise intolerance, weakness, fatigue
o Cough, DOE, orthopnea, palpitations
o Night sweats
o Pain, headache, joint or muscle tenderness
Objective Data
o Fever (give Tylenol NOT aspirin, no blood thinners)
o Osler’s nodes
o Splinter hemorrhage
o Janeway’s lesions
o Petechiae, purpura
o Peripheral edema, clubbing
o Tachypnea, crackles
o Dysrhythmia, tachycardia, murmurs, S3, S4
o Retinal hemorrhages
Nursing Diagnoses
 Decreased cardiac output
o related to altered rhythm, valvular insufficiency, and fluid overload as evidenced by heart
murmur, S3, tachycardia, diminished peripheral pulses, adventitious breath sounds, decreased
urine output, unexplained weight gain and/or restlessness
 Hyperthermia
o related to infection of cardiac tissue as evidenced by temperature elevation, diaphoresis, chills,
malaise, tachycardia, and tachypnea
 Impaired comfort
o related to illness symptoms including generalized weakness, arthralgia, anorexia, and/or
expressed anxiety and frustration concerning prolonged intravenous antibiotic therapy as
evidenced by fatigue, malaise, weakness, painful joints, dyspnea, dysrhythmias, cardiac
murmurs and reports of anxiety, anger, and/or fear
 Activity intolerance
o related to generalized weakness, arthralgia, and alteration in O2 transport secondary to valvular
dysfunction
 Deficient knowledge
o related to lack of experience and exposure to information about disease and treatment process
as evidenced by verbalization of misconceptions about desired or prescribed health behaviors as
well as requests for information
Planning
 Patient will
o Have normal cardiac function
o Perform ADLs without fatigue
o Understand therapeutic regimen to prevent recurrence
Nursing Implementation
 Health Promotion
o Identify those at risk (everyone technically at risk)
o Assess history and understanding of disease process
o Teach importance of adherence to treatment regimen
 Patient teaching
o Stress need to avoid infectious people
o Avoidance of stress and fatigue (REST heart)
o Rest
o Hygiene
o Prophylactic antibiotics
o Drug rehabilitation (if IVDA, need contract sign)
 Ambulatory Care
o Antibiotic therapy for 4–6 weeks (minimum of 4 weeks)
 Cultures negative AND feeling better!
o Assess home setting
o Monitor laboratory data, including blood cultures
o Assess IV lines
o Coping strategies
o Adequate rest
o Moderate activity
o Compression stockings
o ROM exercises
o Deep breath and cough every 2 hours
 Patient teaching
o Monitor body temperature
o Signs and symptoms of complications
o Nature of disease and reducing risk of reinfection
 Keep clean!
o Stress follow-up care, good nutrition, early treatment of common infections
o Signs and symptoms of infection
o Need for prophylactic antibiotic therapy
Evaluation
 Adequate tissue and organ perfusion
 Normal body temperature
 Activity tolerance
 Comfort
 Verbalizes understanding
Med Surg 2 Exam #1 Study Guide
Chapter 66: Systemic Inflammatory Response Syndrome (SIRS) and Multiple Organ
Dysfunction Syndrome (MODS)
Notes:
Tachypnea: first sign of sepsis and SIRS
Microcirculation clots: distal and works up
ON EXAM: DIFFERENTIATE 4 TYPES OF SHOCK (scribd)
All shock first tx: give oxygen!
SIRS



Systemic inflammatory response syndrome (SIRS) is a systemic inflammatory response to a variety of
insults
Generalized inflammation in organs remote from the initial insult
o Entire body gets involved in chain reaction
 Bacterial –antibiotic
 Shock –treat shock
 If virus –supportive care
o Insults resulting in SIRS include infection (referred to as sepsis), ischemia, infarction, and injury
Triggers
o Mechanical tissue trauma: burns, crush injuries, surgical procedures
o Abscess formation: intraabdominal, extremities
o Ischemic or necrotic tissue: pancreatitis, vascular disease, MI
o Microbial invasion: bacteria, viruses, fungi
o Endotoxin release: gram-negative bacteria (the worst!)
o Global perfusion deficits: postcardiac resuscitation, shock states
 WHY we give oxygen!
o Regional perfusion deficits: distal perfusion deficits (clot off a limb/crush injury)
o Anything can trigger it!
o This pt will be on ICU floor (not stable)
o No evidence for using steroids now
 Decrease ability to fight infection
o Want to interrupt here before get to MODS
MODS
 Multiple organ dysfunction syndrome (MODS) is failure of two or more organ systems
o Homeostasis cannot be maintained without intervention
o Results from SIRS
o Recovery is very poor (losing situation)
 These two syndromes represent the ends of a continuum.
 Transition from SIRS to MODS does not occur in a clear-cut manner.
Relationship of Shock, SIRS, and MODS

Goal: prevention!
SIRS and MODS: Pathophysiology
 Consequences of inflammatory response
o Release of mediators
o Direct damage to endothelium
o Hypermetabolism
o Increase in vascular permeability (edema)
 Allows mediators and protein to leak out of the endothelium and into the interstitial
space
 Albumin can plug the hole so can keep fluid in vascular system
o Activation of coagulation cascade
 Organ and metabolic dysfunction
o Hypotension
o Decreased perfusion
o Formation of microemboli
o Redistribution or shunting of blood (compromises organ perfusion)
 Brain and heart priority organs
 Respiratory system
o Alveolar edema
 Can try Lasix if stable
o Decrease in surfactant
 Makes lungs stiff (noncompliant)
o Increase in shunt






o V/Q mismatch (ventilation/perfusion)
 Mismatch –does not cross over
o End result: ARDS (acute respiratory distress syndrome)
Cardiovascular system
o Myocardial depression and massive vasodilation
 Drugs to use: Levafed, norepinephrine (pressors)
o Results in SVR and BP
o Baroreceptors respond to enhance CO
o Albumin and fluid move out of blood vessels
 Reducing venous return and thus preload
o Other signs include decreased capillary refill, skin mottling, increased CVP and PAWP, and
dysrhythmias.
Neurologic system
o Mental status changes due to hypoxemia, inflammatory mediators, or impaired perfusion
o Often early sign of MODS
o Most SENSITIVE (mental status changes)
Renal system
o Acute kidney injury (AKI)
 Hypoperfusion
 Release of mediators (makes work)
 Activation of renin-angiotensin-aldosterone system
 Nephrotoxic drugs, especially antibiotics
 Don’t give Gent and vanco (nephrotoxic drugs)
o In the early stages of SIRS and MODS, blood is shunted away from the GI mucosa, making it
highly vulnerable to ischemic injury.
o No bowl sounds
Hypermetabolic state
o Hyperglycemia-hypoglycemia
 Depends on whether have glucagon or not
o Insulin resistance
 Catecholamines and glucocorticoids are released, resulting in hyperglycemia and insulin
resistance
o Catabolic state
 The net result is a catabolic state, and lean body mass (muscle) is lost
o Liver dysfunction
o Lactic acidosis
 Lactate level (higher, the worst lactic acidosis)
Hematologic system
o DIC
 Tx: heparin
 DIC causes simultaneous microvascular clotting and bleeding caused by depletion of
clotting factors and platelets, combined with excessive fibrinolysis
Electrolyte imbalances
o Potassium high or low?
 Kidneys dead = low
 If not dead = high
 These changes exacerbate mental status changes, neuromuscular dysfunction, and
dysrhythmias

Metabolic acidosis
o Also lactic acidosis
o Metabolic acidosis results from impaired tissue perfusion, hypoxia, and a shift to anaerobic
metabolism with a resultant increase in lactate levels
SIRS and MODS: Interprofessional Care
 Prognosis for MODS is poor
 Goal: prevent the progression of SIRS to MODS
 Vigilant assessment and ongoing monitoring to detect early signs of deterioration or organ dysfunction
are critical
 MODS mortality rates are 70% to 80% when three or more organ systems fail.
 Survival improves with early, goal-directed therapy.
 Interprofessional care for patients with MODS focuses on
o Prevention and treatment of infection
 WASH HANDS (PRIMARY)
o Maintenance of tissue oxygenation
o Nutritional and metabolic support
o Appropriate support of individual failing organs
 Lungs =ventilator
 Prevention and treatment of infection
o Aggressive infection control strategies to decrease risk for nosocomial infection
 Strict asepsis
 Assess need for invasive lines
o Once an infection is suspected, institute interventions to control source
 If central line suspected: pull it and culture it!
 Maintenance of tissue oxygenation
o Decrease O2 demand and increase O2 delivery
 Sedation (reduce hypermetabolism, increase O2 to tissues/decrease O2 demand)
 Mechanical ventilation
 Analgesia
 Rest
 Nutritional and metabolic needs
o Goal of nutritional support: preserve organ function
o Total energy expenditure is often increased 1.5 to 2.0 times
o Use of the enteral route is preferred to parenteral nutrition (PTN)
o Monitor plasma transferrin and prealbumin levels to assess hepatic protein synthesis
o Provide glycemic control
 Higher blood sugar harder to control infection
 Jaundice indicates an increased bilirubin level that is related to impaired liver function.
 The petechiae could indicate disseminated intravascular clotting (DIC).
 A priority is aggressive treatment of the infection.
 Maintenance of oxygenation—intubation and use of mechanical ventilator.
 Assessment of all body systems and support as needed.
 Support of failing organs
o ARDS: aggressive O2 therapy and mechanical ventilation
o DIC: appropriate blood products (FFP/clotting factors & heparin)
o Renal failure: continuous renal replacement therapy or dialysis
o Continuous renal replacement therapy is better tolerated than hemodialysis, especially in a
patient with hemodynamic instability.
o It is important to maintain communication between the health care team and, in most cases,
the patient’s caregiver regarding realistic goals and likely outcomes for the patient with MODS.
o Withdrawal of life support and starting end-of-life care may be the best options for the patient.
Audience Response Question
A patient with a history of alcoholism is admitted to the ICU with hemorrhage from esophageal varices.
Admission VS are BP 84/58 mm Hg, HR 105, and RR 32 breaths/min. The nurse recognizes the onset of
systemic inflammatory response syndrome (SIRS) upon finding
a. pulmonary edema.
b. cardiac dysrhythmias.
c. absent bowel sounds.
d. decreasing blood pressure.
Answer: A
Rationale: The respiratory system is often the first system to show signs of dysfunction in systemic
inflammatory response syndrome. Increases in capillary permeability facilitate movement of fluid from the
pulmonary vasculature into pulmonary interstitial spaces. The fluid then moves to the alveoli, causing alveolar
edema and pulmonary edema.
A patient admitted to the hospital from a long-term care facility appears to be in the late stage of shock with
systemic inflammatory response syndrome (SIRS). Which order implemented by the nurse has the highest
priority?
a. Insert an indwelling urinary catheter.
b. Insert two large-bore intravenous catheters.
c. Administer 0.9% normal saline at 100 mL/hr.
d. Administer 100% oxygen by non-rebreather mask.
Answer: D
Rationale: A patient in the irreversible stage of shock (late stage) will demonstrate profound hypotension and
hypoxemia. If the condition progresses to systemic inflammatory response syndrome, the patient may
experience profound hypoxemia. Oxygenation is a priority and should be initiated first with a 100% oxygen
delivery method such as a non-rebreather mask.
Med Surg 2 Exam #1 Study Guide
Chapter 66: Shock
Notes:
How much epi in epi-pen? 0.3 mg (IM injection)
• What is shock in general?
• What are the different types of shock?
• Give 100% O2
Shock






Syndrome characterized by decreased tissue perfusion and impaired cellular metabolism
Imbalance in supply/demand for O2 and nutrients
The exchange of oxygen and nutrients at the cellular level is essential to life.
When a cell experiences a state of hypoperfusion, the demand for oxygen and nutrients exceeds the
supply at the microcirculatory level.
Classification of shock
o Cardiogenic –pump failed
 Inotrope drug
o Hypovolemic –bled out
 Give volume!
o Distributive –volume in wrong place
 Only 1 liter circulating
 Pressors
o Obstructive –something blocking blood getting back to heart
Types of shock
o
o Hypovolemic:
 Absolute: had leg cut off
 Relative: related to mediators (have volume inside but not in vascular space)
Low Blood Flow: Cardiogenic Shock
 Definition
o Systolic or diastolic dysfunction
 Primarily affects the left ventricle, because systolic pressure is greater on the left side of
the heart
 When systolic dysfunction affects the right side of the heart, blood flow through the
pulmonary circulation is reduced




o Compromised cardiac output (CO)
 Pump has failed
o Don’t give fluid!!!
o Lasix, pressors, inotropes, balloon pump or VAD
Precipitating causes
o Myocardial infarction
o Cardiomyopathy
o Blunt cardiac injury (hit steering wheel_
o Severe systemic or pulmonary hypertension
 Starts in right side and moves to left
o Cardiac tamponade
o Myocardial depression from metabolic problems
Whether the first event is myocardial dysfunction, a structural problem (e.g., valvular disorder,
ventricular septal rupture), or dysrhythmias, the physiologic responses are similar.
The patient experiences impaired tissue perfusion and cellular metabolism because of cardiogenic
shock.
Early manifestations
o Tachycardia
o Hypotension
o Narrowed pulse pressure
o ↑ Myocardial O2 consumption
o The early clinical presentation of a patient with cardiogenic shock is similar to that of a patient
with acute decompensated heart failure.

o The heart’s inability to pump blood forward will result in a low CO (<4 L/min) and cardiac index
(<2.5 L/min/m2).
Physical assessment
 Tachypnea, pulmonary congestion
 Pallor and cool, clammy skin
 Decreased capillary refill time
 Anxiety, confusion, agitation
o ↑ Pulmonary artery wedge pressure
o Decreased renal perfusion and urinary output
Low Blood Flow: Hypovolemic Shock
 Absolute hypovolemia: loss of intravascular fluid volume
o Hemorrhage (most common cause)
o GI loss (e.g., vomiting, diarrhea)
o Fistula drainage
o Diabetes insipidus
o Hyperglycemia
o Diuresis
 Relative hypovolemia
o Results when fluid volume moves out of the vascular space into extravascular space (e.g.,
intracavitary space)
o Termed third spacing
o Alcoholics known for this
o One example of relative volume loss is leakage of fluid from the vascular space to the interstitial
space from increased capillary permeability, as seen in burns.
 Pathophysiology of Hypovolemic Shock

Response to acute volume loss depends on:
o Extent of injury



o Age (younger you are better you can tolerate)
o General state of health
Clinical manifestations
o Anxiety
o Tachypnea
o Increase in CO, heart rate
o Decrease in stroke volume, PAWP, urinary output
If loss is >30%, blood volume is replaced
o If volume loss is greater than 30%, compensatory mechanisms may fail and immediate
replacement with blood products should be started.
o Loss of autoregulation in the microcirculation and irreversible tissue destruction occur with
loss of more than 40% of total blood volume.
Common laboratory studies and assessments that are done include serial measurements of
hemoglobin and hematocrit levels, electrolytes, lactate, blood gases, central venous oxygenation
(SvO2), and hourly urine outputs.
Distributive Shock: Neurogenic Shock
 Hemodynamic phenomenon
 Can occur within 30 minutes of a spinal cord injury at the fifth thoracic (T5) vertebra or above (SNS
here)
 Can last up to 6 weeks
 Can occur in response to spinal cord injury or spinal anesthesia
 Results in massive vasodilation, leading to pooling of blood in vessels, tissue hypoperfusion, ultimately
impaired cellular metabolism
 Depression of the vasomotor center of the medulla from drugs (e.g., opioids, benzodiazepines) also can
lead to decreased vasoconstrictor tone of the peripheral blood vessels, resulting in neurogenic shock
 Neurogenic shock has two classic findings:
o Parasympathetic response: HR 40 (only time
you have shock with LOW HR)
o Vagus stimulated (sympathetic doesn’t work
because spinal cord severed)
 Clinical manifestations
o Hypotension and bradycardia
o Inability to regulate body temperature
(resulting in heat loss)
o Dry skin
o Poikilothermia- taking on temperature of
environment
 Cover pt up!!
Distributive Shock: Anaphylactic Shock
 Acute, life-threatening hypersensitivity (allergic) reaction
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o (e.g., drug, chemical, vaccine, food, insect venom).
o Massive vasodilation
o Release of vasoactive mediators
o ↑ Capillary permeability
o Low BP, high HR
o Angioedema, tightening of airway (swollen)
Clinical manifestations
o The patient experiences sudden onset of symptoms
o Anxiety, confusion, dizziness
 Brain not being perfused
o Sense of impending doom
o Chest pain
o Incontinence
o Swelling of lips and tongue, angioedema
o Wheezing, stridor due to laryngeal edema
o Flushing, pruritus (itching), urticaria (hives)
o Respiratory distress and circulatory failure
Distributive Shock: Septic Shock
 Sepsis: systemic inflammatory response to documented or suspected infection
 Severe sepsis: sepsis complicated by organ dysfunction
o In as many as 10% to 30% of patients with sepsis, the causative organism is not identified.
o Severe sepsis is diagnosed in more than 750,000 patients per year with mortality rates as high as
28% to 50%.
 Septic shock
o Presence of sepsis with hypotension despite fluid resuscitation (BP stays low)
o Presence of inadequate tissue perfusion resulting in hypoxia
 Confusion, skin cold and clammy
 Lactate can measure
hypoxia too
o The main organisms that
cause sepsis are gramnegative and gram-positive
bacteria. Parasites, fungi, and
viruses can also cause the
development of sepsis and
septic shock.
 Septic shock has three major
pathophysiologic effects:
vasodilation, maldistribution of blood
flow, and myocardial depression.
 MEWS –monitor for sepsis
 Clinical manifestations
o ↑ Coagulation and
inflammation
o ↓ Fibrinolysis
 Formation of microthrombi
 Obstruction of microvasculature
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o Hyperdynamic state: increased CO and decreased SVR
When a microorganism enters the body, the normal immune/inflammatory responses are started.
o Severe sepsis and septic shock, the body’s response to the microorganism is exaggerated
Endotoxins from the microorganism cell wall stimulate the release of cytokines, including tumor
necrosis factor (TNF), interleukin-1 (IL-1), and other proinflammatory mediators that act through
secondary mediators such as platelet activating factor, IL-6, and IL-8.
The release of platelet activating factor results in the formation of microthrombi and obstruction of the
microvasculature.
Three major pathophysiologic effects
o Vasodilation
o Maldistribution of blood flow
o Myocardial dysfunction
 Decreased ejection fraction
 Ventricular dilation
Clinical manifestations
o Tachypnea/hyperventilation
 Results in respiratory alkalosis
 Once the patient can no longer compensate, respiratory acidosis will develop
 Respiratory failure develops in 85% of patients
o These patients may need to be intubated and mechanically ventilated
o ↓ Urine output
o Altered neurologic status
o GI dysfunction, GI bleeding, paralytic ileus
Obstructive Shock
 Develops when physical obstruction to blood flow occurs with decreased CO
o Caused by restricted diastolic filling of right ventricle from compression
o Abdominal compartment syndromeabdominal pressure compresses inferior
vena cava (blood stays in legs and don’t go
back to heart)
 Other causes include abdominal compartment
syndrome in which increased abdominal pressures
compress the inferior vena cava, thus decreasing
venous return to the heart
 Pulmonary embolism and right ventricular
thrombi cause an outflow obstruction as blood
leaves the right ventricle through the pulmonary
artery.
 This leads to decreased blood flow to the lungs, as
well as decreased blood return to the left atrium.
 Notes
o Put foley catheter in bladder to measure
o Open up incision if volume measures 10
o Tension pneumo: needle chest then chest
tube
 Patient will experience:
o Decreased CO
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o Increased afterload
o Variable left ventricular filling pressure
o Other clinical signs include jugular vein distention and pulsus paradoxus.
Rapid assessment and immediate treatment are important
o They are dead with no CO
Stages of Shock
 Shock is categorized into 4 overlapping stages: ** Be able to differentiate
o Initial = may not see sx yet
o Compensatory =when you can intervene
 Compensatory mechanisms starting to fail
o Progressive =when can intervene
o Refractory = dead
Stages of Shock Initial Stage
 Usually not clinically apparent
 Metabolism changes at cellular level from aerobic to anaerobic
o Lactic acid builds up and must be removed by liver
o Process requires O2, unavailable due to decreased tissue perfusion
o Lactate will diagnose
o 100% first line of tx
Stages of Shock: Compensatory Stage
 Compensatory mechanisms
o Neural (ans and sns)
o Hormonal
o Biochemical
 Attempt to overcome consequences of anaerobic
metabolism and maintain homeostasis
 The patient’s clinical presentation begins to reflect
the body’s responses to the imbalance in oxygen
supply and demand.
 Baroreceptors in carotid and aortic bodies activate
SNS in response to ↓ BP
o Vasoconstriction while blood to vital organs
maintained
 Heart (tachycardia)
 Brain
o Most primal receptors
 Blood flow to the most essential (vital) organs, the
heart and brain, is maintained, while blood flow to
the nonvital organs, such as the kidneys, GI tract,
skin, and lungs, is diverted or shunted.
 SNS stimulation increases myocardial O2 demands
(epinephrine from adrenal medulla)
 Shunting blood from lungs increases physiologic
dead space
o V/Q mismatch (ventilation-perfusion)
Some areas of the lungs participating in ventilation that will not be perfused because of
the decreased blood flow to the lungs
o ↓ Arterial O2 levels
o Increase in rate/depth of respirations (#1 tool)
Impaired GI motility
o Risk for paralytic ileus
Cool, clammy skin (decreased blood flow to skin)
o Except septic patient who may feel warm and flushed due to a hyperdynamic state.
↓ Blood to kidneys activates renin–angiotensin system
o Angiotensin I converted to angiotensin II
 Vasoconstriction (most potent vasoconstrictor)
 ↑ Venous return to heart & increase in BP
 Stimulates release of aldosterone
 Makes you retain fluid and sodium and excrete potassium
 Increased sodium reabsorption stimulates ADH
 ADH increases water reabsorption by the kidneys, thus further increasing blood
volume
 The increase in total circulating volume results in an increase in CO and BP
Body is able to compensate for changes in tissue perfusion
If cause of shock is corrected, patient recovers with little or no residual effects
If cause of shock is not corrected, patient enters progressive stage
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Stages of Shock: Progressive Stage
 Begins when compensatory mechanisms
fail
o Crashing, HR high, BP low
 Patient moved to ICU for advanced
monitoring and treatment
o Hopefully get to ICU before this
 Distinguishing features of ↓ cellular
perfusion and altered capillary permeability
o Leakage of protein into interstitial
space
o ↑ Systemic interstitial edema
 The cardiovascular system is profoundly
affected in the progressive stage of shock
o CO begins to fall, resulting in a
decrease in BP and coronary artery,
cerebral, and peripheral perfusion
 Anasarca: diffuse profound edema
o Fluid leakage affects solid organs
and peripheral tissues (liver, spleen,
GI tract, lungs)
o ↓ Blood flow to pulmonary
capillaries
 Sustained hypoperfusion
o Weak peripheral pulses
o Ischemia of distal extremities
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Myocardial dysfunction results in
o Dysrhythmias
o Myocardial ischemia
o Possible myocardial infarction
o End result: complete deterioration of cardiovascular system
o CPR will not be effective
o Epi ineffective in face of acidosis
Movement of fluid from pulmonary vasculature to interstitium
o Pulmonary edema
o Bronchoconstriction
o ↓ Functional residual capacity
Fluid moves into alveoli
o Alveolar Edema
o Decreased surfactant production
o Impaired gas exchange
o Worsening V/Q mismatch
o Tachypnea
o Crackles
o Increased work of breathing
Mucosal barrier of GI system becomes ischemic
o Ulcers
o GI bleeding
o Risk of migration of bacteria
o Decreased ability to absorb nutrients
Hypoperfusion leads to renal tubular ischemia
o May result in acute kidney injury
 Worsened by nephrotoxic drugs (e.g., certain antibiotics, anesthetics, diuretics)
o Decreased urine output
o Elevated BUN and serum creatinine
o Metabolic acidosis
 Occurs from the kidneys’ inability to excrete acids (especially lactic acid) and reabsorb
bicarbonate
Liver fails to metabolize drugs and waste
o Jaundice (accumulation of bilirubin)
o Elevated enzymes
 (e.g., alanine aminotransferase [ALT], aspartate aminotransferase [AST], γ-glutamyl
transferase [GGT]).
o Loss of immune function
 Bacteria from the GI tract longer destroyed by the Kupffer cells  they are released into
the bloodstream  increasing the possibility of bacteremia
o Risk for disseminated intravascular coagulation (DIC) and significant bleeding
 Liver produces clotting factors (can’t produce enough now)
Stages of Shock: Refractory Stage
 Exacerbation of anaerobic metabolism
 Accumulation of lactic acid
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↑ Capillary permeability
o Increased capillary permeability
allows fluid and plasma proteins to
leave the vascular space and move to
the interstitial space
Blood pools in the capillary beds secondary to
the constricted venules and dilated arterioles
Profound hypotension and hypoxemia
Tachycardia worsens
Failure of one organ system affects others
o Failure of liver, lungs, and kidneys will
result in accumulation of waste
products such as lactate, urea,
ammonia, and carbon dioxide
Recovery unlikely
o If they do they will have disability
Diagnostic Studies
 Thorough history and physical examination
o History of recent events (e.g., surgery,
chest pain, trauma) provides valuable
data
 No single study to determine shock
o Blood studies
 Elevation of lactate
 How to draw? Release
tourniquet, get new
stick
 Base deficit (too many
acids and bases losing)
o 12-lead ECG, continuous ECG monitoring
 Try to determine is cardiogenic
o Chest x-ray
 Looking for pulmonary edema
o Hemodynamic monitoring
 Only can do this in ICU
 Allows you to carefully treat fluid
o Continuous pulse oximetry
Interprofessional Care
 Successful management
o Identification of patients at risk for developing shock
o Integration of patient’s history, physical examination, and clinical findings to establish a
diagnosis
o Interventions to control or eliminate cause of decreased perfusion
o Protection of target and distal organs from dysfunction
o Provision of multisystem supportive care
 General management strategies
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o Ensure patient is responsive
o Ensure a patent airway
o Maximize oxygen delivery
Oxygen and ventilation
o Increase supply
 Space activities that increase oxygen consumption (e.g., endotracheal suctioning,
position changes) appropriately for oxygen conservation
o Optimize CO with fluid replacement or drugs
o Increase hemoglobin by transfusion
o Increase arterial oxygen with supplemental oxygen and mechanical ventilation
Cornerstone of therapy for septic, hypovolemic, and anaphylactic shock = volume expansion
o One or two large-bore IV catheters (e.g., 14- to 16-gauge), intraosseous access device, or central
venous catheter
o Isotonic crystalloids (e.g., normal saline, lactated Ringers, dextrose) and colloids (e.g., albumin,
blood)
o *** Volume expansion for every shock EXCEPT cardiogenic
Volume expansion
o Fluid responsiveness is determined by clinical assessment
 Vital signs
 Cerebral and abdominal pressures
 Capillary refill (end perfusion)
 Skin temperature
 Urine output
 Use an indwelling bladder catheter to monitor urine output during resuscitation
o Two major complications of large volumes
 Hypothermia (make sure blood/fluid warmed up)
 Coagulopathy (DIC)
o Persistent hypotension after adequate fluids
 Vasopressor may be added
 Vasopressor (e.g., norepinephrine [Levophed], dopamine [Intropin]) and/or an
inotrope (e.g., dobutamine [Dobutrex]) may be added
 Never add until tank is full
Fluid resuscitation
o Warm crystalloid and colloid solutions
o Replace clotting factors
Primary goal of drug therapy = correction of decreased tissue perfusion
o Vasopressor drugs (e.g., norepinephrine)
 Achieve/maintain MAP >60 to 65 mm Hg
 Means organs are being perfused
 Reserved for patients unresponsive to fluid resuscitation
 Continuously monitor end-organ perfusion
 These drugs have the potential to cause severe peripheral vasoconstriction and an
increase in SVR
 The increased SVR increases the workload of the heart
 This can harm a patient in cardiogenic shock by causing further myocardial
damage
o Vasodilator therapy (e.g., nitroglycerin, nitroprusside)
 Decrease afterload
Achieve/maintain MAP >65 mm Hg
The vasodilator agent most often used for the patient in cardiogenic shock is
nitroglycerin (Tridil).
 Vasodilation may be enhanced with nitroprusside (Nipride) or nitroglycerin in
noncardiogenic shock.
Nutrition is vital to decreasing morbidity from shock
o Start enteral nutrition within first 24 hours
o Parenteral nutrition used only if enteral feedings contraindicated
o Start trophic feeding- slow drip of small amounts of enteral nutrition
o Weigh patient daily
o Monitor serum protein, total albumin, prealbumin, BUN, glucose, electrolytes
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Interprofessional Care: Cardiogenic Shock
 Overall goal: restore blood flow to myocardium by restoring balance between O2 supply and demand
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Cardiac catheterization is performed as soon as possible after the initial insult
Angioplasty with stenting
Emergency revascularization
Valve replacement
o Help restore hearts blood flow
Until these interventions are performed, the heart must be supported to optimize stroke volume and
CO to achieve optimal perfusion
Hemodynamic monitoring
Drug therapy
o Nitrates to dilate coronary arteries
o Diuretics to reduce preload
o Vasodilators to reduce afterload
o β-adrenergic blockers to reduce HR and contractility
Circulatory assist devices
o Balloon pump or VAD
o Decrease SVR and left ventricular workload
o Intraaortic balloon pump
o Ventricular assist device (VAD)
Heart transplantation
o Unlikely (small select group of patients with cardiogenic shock)
Interprofessional Care: Hypovolemic Shock
 Management focuses on stopping loss of fluid and restoring the circulating volume
 Fluid resuscitation is calculated using a 3:1 rule (3 mL of isotonic crystalloid for every 1 mL of estimated
blood loss)
Interprofessional Care: Septic Shock
 Fluid replacement to restore perfusion
o Hemodynamic monitoring
 Vasopressor drug therapy
 Exogenous vasopressin for patients refractory to vasopressor therapy
 IV corticosteroids for patients who cannot maintain an adequate BP with vasopressor therapy despite
fluid resuscitation
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o NOT INDICATED UNTIL PT NEARLY DEAD
Antibiotics should be started within first hour
o After cultures are obtained (e.g., blood, wound exudate, urine, stool, sputum)
Broad-spectrum antibiotics are given first
o ALWAYS CULTURES FIRST
More specific antibiotics may be ordered once the organism identified
Glucose levels <180 mg/dL (tight control increases mortality)
Stress ulcer prophylaxis with proton pump inhibitors (e.g., pantoprazole [Protonix])
Deep vein thrombosis prophylaxis (e.g., heparin, enoxaparin [Lovenox])
Interprofessional Care: Neurogenic Shock
 In spinal cord injury: spinal stability
o Treatment of hypotension and bradycardia with vasopressors and atropine
 Sometimes atropine can be effective
o Fluids infused cautiously as hypotension generally is not related to fluid loss
o Monitor for hypothermia
o If the cause is spinal cord injury, general measures to promote spinal stability (e.g., spinal
precautions, cervical stabilization with a collar) are initially used
 Spinal fusion to stabilize
Interprofessional Care: Anaphylactic Shock
 Epinephrine, diphenhydramine, ranitidine (Zantac) H2 blocker
o Want to block both receptors just in case
 Maintain a patent airway
o Nebulized bronchodilators
o Aerosolized epinephrine
o Endotracheal intubation or cricothyroidotomy may be necessary
 Aggressive fluid replacement
o Usually crystalloids (didn’t lose blood)
 IV corticosteroids if significant
o Suppress immune system
 Hypotension persists after 1–2 hours of aggressive therapy
o Results from leakage of fluid out of the intravascular space into the interstitial space as a result
of increased vascular permeability and vasodilation.
Interprofessional Care: Obstructive Shock
 Primary strategy is early recognition and treatment to relieve obstruction
o Mechanical decompression
 For pericardial tamponade, tension pneumothorax, and hemopneumothorax may be
done by needle or tube insertion
o Thrombolytic therapy (if massive PE)
o Radiation, debulking, or removal of mass (for superior vena cava syndrome)
o Decompressive laparotomy (for abdominal compartment syndrome)
Nursing Management: Shock Nursing Assessment
 ABCs
o Airway
o Breathing
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o Circulation
Focused assessment of tissue perfusion
o Vital signs
o Peripheral pulses
o Level of consciousness
o Capillary refill
o Skin (e.g., temperature, color, moisture)
o Urine output
Brief history
o Events leading to shock (cause)
o Onset and duration of symptoms
Health history
o Medications
o Allergies
o Vaccinations, recent travel
Nursing Management: Shock Nursing Diagnoses
 Ineffective peripheral tissue perfusion and risk for decreased cardiac tissue perfusion, ineffective
cerebral tissue perfusion, ineffective renal perfusion, impaired liver function, and ineffective GI
perfusion
 Anxiety
Nursing Management: Shock Planning
 Goals
o Evidence of adequate tissue perfusion
o Restoration of normal or baseline BP
o Recovery of organ function
o Avoidance of complications from prolonged states of hypoperfusion
Nursing Management: Shock Nursing Implementation
 Health Promotion
o Identify patients at risk
 Older patients
 Those who are immunocompromised
 Those with chronic illness
 Surgery or trauma patients
 Hemorrhage, sepsis, spinal cord injury
o Planning to prevent shock (KEY)
 Intervene in earliest stages
 Monitoring fluid balance to prevent hypovolemic shock
 Maintenance of hand washing to prevent spread of infection
 Acute Care
o Monitor patient’s ongoing physical and emotional status
o Identify trends to detect changes in patient’s condition (MEWS tool)
o Plan and implement nursing interventions and therapy
o Evaluate patient’s response to therapy
o Provide emotional support to patient and caregiver
o Collaborate with other members of interprofessional team to coordinate care
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Neurologic status (prevent ICU psychosis)
o Assess orientation and level of consciousness, clinical manifestations
o Orient to person, place, time, events
o Reduce noise and light levels in ICU
o Keep a day-night cycle
Cardiovascular status
o Continuous ECG , BP, CVP, PA pressures
 CO, SVR, SVV
 Monitor for dysrhythmias
 Do not treat hypotension with Trendelenberg position
o Heart sounds: murmurs, S3, S4
  HF
Respiratory status
o Respiratory rate, depth, and rhythm
o Breath sounds
o Continuous pulse oximetry
o Arterial blood gases
o Many patients will be intubated and on mechanical ventilation
Renal status
o Urine output ( <0.5 mL/kg/hr may indicate inadequate perfusion of the kidneys)
o Serum creatinine (assess renal function)
o Body temperature and skin changes
o Core temperature (e.g., urinary, central line, PA catheter).
o Skin: temperature, pallor, flushing, cyanosis, diaphoresis, piloerection
Gastrointestinal status
o Auscultate bowel sounds
o NG drainage/stools for occult blood
 Check for blood anywhere leaking
Personal hygiene
o Perform bathing, nursing measures carefully
o Turn every 1 to 2 hours
o Passive/active range of motion
Emotional support and comfort
o Assess level of anxiety, fear, pain
 Drugs PRN
 Talk to patient
 Give simple explanations of all procedures
 Visit from clergy
 Caregiver involvement
 Privacy
 Call light within reach
Shock: Ambulatory Care
 Rehabilitation of patient requires
o Correction of precipitating cause
o Prevention or early treatment of complications
o Teaching focused on disease management or prevention of recurrence
Nursing Management: Shock Evaluation
 Adequate tissue perfusion with restoration of normal or baseline BP
 Normal organ function with no complications from hypoperfusion
 Decreased fear and anxiety and increased psychologic comfort
Audience Response Questions
a. normal cardiac output in cardiogenic shock.
b. increase in central venous pressure in hypovolemic shock.
c. increase in systemic vascular resistance in all types of shock.
d. variations in cardiac output and decreased systemic vascular resistance in septic shock.
Answer: D
Rationale: Septic shock has three major pathophysiologic effects: vasodilation, maldistribution of blood flow,
and myocardial depression. Patients may be normovolemic, but because of acute vasodilation, relative
hypovolemia and hypotension may occur. The ejection fraction is decreased for the first few days after the
initial insult. Because of a decreased ejection fraction, the ventricles will dilate to maintain stroke volume. The
ejection fraction typically improves and ventricular dilation resolves over 7 to 10 days. Persistence of a high CO
and a low SVR beyond 24 hours is an ominous finding and is often associated with increased development of
hypotension and MODS. Systemic vascular resistance (SVR) increases in cardiogenic and hypovolemic shock;
SVR decreases in neurogenic, anaphylactic, and septic shock. Cardiac output decreases in cardiogenic shock.
Central venous pressure decreases in hypovolemic shock.
The nurse is caring for a critically ill patient. The nurse suspects that the patient has progressed beyond the
compensatory stage of shock if what occurs?
a. Increased blood glucose levels
b. Increased serum sodium levels
c. Increased serum calcium levels
d. Increased serum potassium levels
Answer: D
Rationale: Hyperkalemia occurs in the progressive phase of shock when cellular death liberates intracellular
potassium. Hyperkalemia will also occur in acute kidney injury and in the presence of acidosis.
The nurse is caring for a patient in septic shock. Which hemodynamic change would the nurse expect?
a. Increased ejection fraction.
b. Increased mean arterial pressure.
c. Decreased central venous pressure.
d. Decreased systemic vascular resistance.
Answer: D
Rationale: Patients in septic shock will have a decreased systemic vascular resistance, decreased ejection
fraction, and decreased mean arterial pressure. Decreased central venous pressure (preload) is expected in
hypovolemic or obstructive shock.
Med Surg 2 Exam #1 Study Guide
Chapter 37: Disorders of the Aorta
Aorta
 Largest artery (2-3 cm normally)
 Responsible for supplying oxygenated blood to essentially all vital organs
 In RETROperitoneal space
o Need to know to know symptoms
Disorders of the Aorta
 Most common vascular problems of aorta
o Aneurysms (#1)
 When do they develop? During fetal development
 Anywhere with bifurcation is a an area of weakness
 If DON’T get hypertension
 Size of aneurism determines if going to fix it (watchful waiting)
 Mostly found by going in for something else and finding it
 On very thin people can see it pulsing
o Aortoiliac occlusive disease (#2)
 Atherosclerosis (fatty streaks)
 Most have this started by age 5
o Aortic dissection
Aortic Aneurysms
Aortic Aneurysms: Definition
 Outpouching or dilation of arterial wall
 Common problems involving aorta
 Occur in men more often than in women and in whites more often than African Americans
 Incidence ↑ with age
 Abdominal aortic aneurysms (AAA)
o ¾ occur in abdominal aorta (better outcome)
o ¼ occur in thoracic aorta
o Most occur below renal arteries
o The larger aneurysm, the greater risk of rupture
Abdominal Aortic Aneurysm
 Angiography demonstrating fusiform abdominal aortic
aneurysm.
 Note calcification of the aortic wall (arrows) and extension of the
aneurysm into the common iliac arteries.
Aortic Aneurysms: Etiology and Pathophysiology
 Dilated aortic wall becomes lined with thrombi that can embolize
o Leads to acute ischemic symptoms in distal branches
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Causes
o Degenerative
o Congenital
o Mechanical
 Penetrating or blunt trauma
o Inflammatory
o Infectious
o The most common cause of descending AAAs is atherosclerosis
Aortic Aneurysms: Risk Factors
 Age
 Male gender
 High BP
 Coronary artery disease
 Family history (big deal, highly genetic if female)
 High cholesterol
 Lower extremity PAD
 Carotid artery disease
 Previous stroke
 Tobacco use ** most important modifiable risk factor
 Being overweight or obese
Aortic Aneurysms: Genetic Link
 The familial tendency is related to a number of congenital anomalies
o Bicuspid aortic valve
o Coarctation of aorta
o Turner’s syndrome
o Autosomal dominant polycystic kidney disease
o Ehlers-Danlos syndrome
o Loeys-Dietz syndrome
o Marfan’s syndrome (big one, connective tissue disorder)
Aortic Aneurysms: Classification
 Two basic classifications
o True
 Wall of artery itself forms aneurysm
 At least one vessel layer still intact
 Further subdivided
 Fusiform
o Circumferential, relatively uniform in
shape
 Saccular
o Pouchlike with narrow neck
connecting bulge to one side of
arterial wall
o False
 Also called pseudoaneurysm
 Not an aneurysm
Disruption of all layers of arterial wall
 Results in bleeding contained by surrounding structures
 Still need to fix, but not the normal
 May result from trauma or infection, or may occur after peripheral artery bypass graft
surgery at the site of the graft-to-artery anastomosis.
 They also may result from arterial leakage after removal of cannulae (e.g., lower
extremity arterial catheters, intraaortic balloon pump devices).
A, True fusiform abdominal aortic aneurysm. B, True saccular aortic aneurysm. C, False aneurysm or
pseudoaneurysm. D, Aortic dissection.
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Aortic Aneurysm: Clinical Manifestations
 Thoracic aorta aneurysm (TAA)
o Often asymptomatic
o Most common manifestation
 Deep diffuse chest pain (BP high; last thing we want)
 Bring BP down! Treat pain with morphine and beta blockers or nitroprusside
 Pain may extend to interscapular area
 Ascending aorta/aortic arch
o Angina (from decreased blood flow to the coronary arteries)
o Transient ischemic attacks (attacks from decreased blood flow to the carotid arteries)
o Coughing and shortness of breath
 Compression on superior vena cava
o Hoarseness and/or dysphagia
 From pressure on the laryngeal nerve
o If presses on superior vena cava
 Decreased venous return
 Distended neck veins
 Edema of face and arms
 Abdominal aortic aneurysms (AAA)
o Often asymptomatic
 Bruits may be auscultated over the aneurysm
 A pulsatile mass in the periumbilical area slightly to the left of the midline may be
present
o Frequently detected
 On routine physical exam
 Physical findings may be more difficult to detect in obese individuals
 When patient examined for unrelated problem (i.e., CT scan, abdominal x-ray)
o May mimic pain associated with abdominal or back disorders
o May cause back pain, epigastric discomfort, altered bowel elimination, intermittent claudication
(pain in calves, lack of blood flow, vessels spasming, pain when walking, relieved with rest)
 Random symptoms and often dismissed
o May spontaneously embolize plaque
 Causing “blue toe syndrome”
 Patchy mottling of the feet and toes in the presence of palpable pedal pulses
Aortic Aneurysm: Complications
 Rupture—serious complication

o Rupture into retroperitoneal space
 Bleeding may be tamponaded by surrounding structures, thus preventing
exsanguination and death.
 Severe back pain
 May/may not have back/flank ecchymosis (Grey Turner’s sign)
o Rupture is more likely to occur in people who smoke tobacco
Rupture—serious complication related to untreated aneurysm
o Rupture into thoracic or abdominal cavity (most don’t survive)
 Massive hemorrhage
 Most do not survive long enough to get to the hospital
 The patient who reaches the hospital will be in hypovolemic shock with
tachycardia, hypotension, pale clammy skin, decreased urine output, altered
level of consciousness, and abdominal tenderness.
 Simultaneous resuscitation and immediate surgical repair are necessary!!!
Aortic Aneurysm: Diagnostic Studies
 X-rays
o Chest – demonstrate mediastinal silhouette and any abnormal widening of thoracic aorta
o Abdomen – may show calcification within wall of AAA
 ECG – to rule out MI
o Since thoracic aneurysm or dissection symptoms can mimic angina
 Echocardiography
o Assists in diagnosis of aortic valve insufficiency
 Ultrasonography
o Useful in screening for aneurysms
o Monitors aneurysm size
 CT scan (1 CT equal to 100 x-rays; it’s the best!)
o Most accurate test to determine
 Anterior-to-posterior length
 Cross-sectional diameter
 Presence of thrombus
 Best type of surgical repair
 What are they eligible for? EVAR or TEVAR
 MRI
o Diagnose and assess location and severity
 Angiography
o Anatomic mapping of aortic system using contrast
o Not reliable method of determining diameter or length
o Can provide accurate information about involvement of intestinal, renal, or distal vessels
o Angiography is also useful if a suprarenal or thoracoabdominal aneurysm is suspected
Aortic Aneurysm: Interprofessional Care
 Goal – prevent aneurysm from rupturing
 Early detection/treatment imperative
 Once detected
o Studies done to determine size and location
 A careful review of body systems is necessary to identify any co-morbidities, especially of the lungs,
heart, or kidney, because they may influence the patient’s surgical risk.
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Small aneurysm (4- 5.4 cm)
o Conservative therapy used (better to not crack chest)
 Risk factor modification
 Tobacco cessation, decreasing BP, optimizing lipid profile, and annual monitoring
of aneurysm size using ultrasound, CT, or MRI
 ↓ blood pressure
 Growth rates may be lowered with β-adrenergic blocking agents (e.g.,
propranolol [Inderal]), ACE inhibitors (e.g., captopril [Capoten]), and angiotensin
II receptor blockers (e.g., losartan [Cozaar]), statins (e.g., simvastatin [Zocor]),
and antibiotics (e.g., doxycycline [Acticlate])
 Ultrasound, MRI, CT scan monitoring every 6 to 12 months
 Monitoring by ultrasound every 2 to 3 years is recommended for patients with
AAAs smaller than 4.0 cm in diameter.
5.5 cm is threshold for repair
o Intervention at >5 cm in women with AAA
Surgical intervention may occur earlier in
o Patients with a genetic disorder (e.g., Marfan’s, Ehlers-Danlos syndrome)
o Rapidly expanding aneurysm
o Symptomatic patients
o High rupture risk
o Correction of existing carotid and/or coronary artery blockages may be needed before the
aneurysm is repaired.
Surgical therapy
o If ruptured, emergent surgical intervention required
 90% mortality with ruptured AAAs
o Preop
 Hydration
 Stabilize electrolytes, coagulation, and hematocrit
Surgical technique
o Open aneurysm repair (OAR)
 Inserting synthetic graft
 Dacron or polytetrafluoroethylene (PTFE)
 Suturing native aortic wall around graft
 Acts as protective cover
o Incising diseased segment of aorta
o Removing intraluminal thrombus or plaque
Autotransfusion reduces need for blood transfusion during surgery
AAA resection
o Require cross-clamping of aorta proximal and distal to aneurysm
o Can be completed in 30 to 45 minutes
o Clamps are removed and blood flow to lower extremities is restored
If extends above renal arteries or if cross-clamp must be applied above renal arteries
o Check for adequate renal perfusion after clamp removal and before closure of incision
o Risk of postop renal complications ↑ significantly when repair is above renal arteries
Endovascular graft procedure (EVAR)
o Alternative to conventional surgical repair
o Involves placement of sutureless aortic graft into abdominal aorta inside aneurysm
 Held in with size
o Minimally invasive
 Done through femoral artery cutdown
o Graft
 Constructed from Dacron cylinder
 Surface supported with rings of flexible wire
 Delivered through sheath to predetermined point
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Delivered through a femoral artery catheter
 Deployed against vessel wall by balloon inflation
 Anchored to vessel by series of small hooks
o Blood then flows through graft, preventing expansion of aneurysm
o Aneurysm wall will begin to shrink over time
o Must meet strict eligibility criteria to be a candidate
o Benefits
 Don’t have to crack chest or abdomen
 ↓ Anesthesia and operative time
 Smaller operative blood loss
 ↓ Morbidity and mortality
 More rapid resumption of physical activity
 Shortened hospital stay
 Quicker recovery
 Higher patient satisfaction
 Reduction in overall costs
o Potential complications
 Endoleak (the seepage of blood back into the old aneurysm)
 This may be due to an inadequate seal at either graft end, a tear through the
graft fabric, or leakage
between overlapping graft
segments, and may require
coil embolization (insertion of
beads) for hemostasis
 Aneurysm growth
 Aneurysm rupture
 Aortic dissection
 Bleeding
 Stent migration
 Renal artery occlusion
 Graft thrombosis
 Incisional site hematoma
 Site infection
o Graft dysfunction may require traditional
surgical repair
o Need for long-term follow-up
Surgical Repair of Aneurysm
 Surgical repair of an abdominal aortic aneurysm. A,
Incising the aneurysmal sac. B, Insertion of synthetic
graft. C, Suturing native aortic wall over synthetic graft.
EVAR
 Bifurcated (two branched) endovascular stent grafting of an aneurysm.
 A, The insertion of a woven polyester tube (graft) covered
by a tubular metal web (stent).
 B, The stent graft is inserted through a large blood vessel
(e.g., femoral artery) using a delivery catheter. The
catheter is positioned below the renal arteries in the area
of the aneurysm.
 C, The stent graft is slowly released (deployed) into the
blood vessel. When the stent comes in contact with the
blood vessel, it expands to a preset size. D, A second stent
graft can be inserted in the contralateral (opposite) vessel
if necessary.
 E, Fully deployed bifurcated stent graft.
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Aortic Aneurysm: Interprofessional Care Cont.
 Intraabdominal hypertension (IAH)
o Potentially lethal complication in emergency repair
o Associated with abdominal compartment syndrome (ACS)
 Reduces blood flow to viscera
 End-organ perfusion impaired
o Treatment
 Open surgical compression
 Percutaneous drainage
 Percutaneous drainage combined with tPA infusion
 Conservative measures such as intubation, ventilation, patient positioning, gastric
decompression, cautious fluid resuscitation, pain management, and temporary
hemofiltration are also used
Nursing Management: Assessment
 Thorough history and physical exam
o Disorientation, hypoxia, anxiety, or age
 Watch for signs of cardiac, pulmonary, cerebral, and lower extremity vascular problems
 Establish baseline data to compare postoperatively
o Pedal and radial pulses (arterial circulation)
o Vital signs elevated related to pain
 Note quality and character of peripheral pulses and neurologic status
o may indicate poor peripheral perfusion
 Mark/document pedal pulse sites and any skin lesions on lower extremities before surgery
 Monitor for indications of rupture (Crash/shock)
o Diaphoresis
o Pallor
o Weakness
o Tachycardia
o Hypotension
o Abdominal, back, groin, or periumbilical pain
o Changes in level of consciousness (if conscious hasn’t ruptured yet)
o Pulsating abdominal mass
Nursing Management: Planning
 Overall Goals
o Normal tissue perfusion
o Intact motor and sensory function
o No complications related to surgical repair
 Thrombosis
 Infection
 Rupture
Nursing Management: Nursing Implementation
 Health Promotion
o Alert for opportunities to teach health promotion to patients and their caregivers
o Encourage patient to reduce cardiovascular risk factors
 These measures help ensure graft patency after surgery
 Examples of risk factors include BP control, smoking cessation, increasing physical
activity, and maintaining normal body weight and serum lipid levels.
 Acute Care
o Patient/caregiver teaching
 Don’t smoke
o Providing emotional support for patient/caregiver
o Careful assessment of all body systems
o Preop teaching
 Brief explanation of disease process
 “You have weakness in the wall and its at risk for rupture we are going to go in a
fix”
 Planned surgical procedure
 Preop routines
 Bowel prep
 NPO
 Shower
 IV antibiotics right before incision made
o 30 min prior to surgery
o Cephalosporin
 Expectations after surgery
 Recovery room, tubes, drains
 ICU
 β – blocker
o Patients with a history of CVD usually receive a beta blocker (e.g.,
metoprolol [Lopressor]) preoperatively
o Reduces BP
o Postop
 ICU monitoring
 Arterial line
 Central venous pressure (CVP) or pulmonary artery (PA) catheter
 Mechanical ventilation
 Peripheral IV lines
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 Urinary catheter (30ml/hr; 0.5ml/kg/hr)
 NG tube
 ECG
 Pulse oximetry
 Pain medication
Aortic surgery patients typically go to an ICU for 24 to 48 hours for close monitoring
 Head to toe assessment!
Maintain graft patency
 Normal blood pressure
o Prolonged low BP may result in graft thrombosis
 IV fluids and blood components
 CVP or PA pressure monitoring
 Urinary output monitoring
 Avoid severe hypertension
o Drug therapy may be indicated
o Drug therapy for severe hypertension consists of IV diuretics (e.g.,
furosemide [Lasix]) or IV antihypertensive agents (e.g., nitroprusside
[Nipride], esmolol [Brevibloc], labetalol [Normodyne])
Cardiovascular status
 Continuous ECG monitoring
 Electrolyte monitoring
 Arterial blood gas monitoring
 Oxygen administration
o Myocardial ischemia or infarction may occur in the perioperative period
due to decreased myocardial oxygen supply or increased myocardial
oxygen demands
 Antidysrhythmic and antihypertensive meds
o Cardiac dysrhythmias may occur due to electrolyte imbalances,
hypoxemia, hypothermia, or myocardial ischemia
 Pain control
 Resume heart medications
Infection
 Antibiotic administration
 Assessment of body temperature
 Monitoring of WBC
 Adequate nutrition
 Observe surgical incision for signs of infection
GI status
 Record amount and character of NG tube output
 Abdominal assessment
 Passing of flatus = return of bowel function
 Assess for signs of bowel ischemia
o Clinical manifestations of bowel ischemia include absent bowel sounds,
fever, abdominal distention, diarrhea, and bloody stools
Neurologic status
 Level of consciousness
 Pupil size and response to light
 Facial symmetry
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 Speech (or ask to lift arms/hands if on ventilator)
 Ability to move upper extremities
 Quality of hand grasps
 Peripheral perfusion status
 Pulse assessment (hourly)
o Mark pulse locations with felt-tip pen
 When the ascending aorta and the aortic arch are involved, assess the carotid,
radial, and temporal artery pulses. For surgery of the descending aorta, assess
the femoral, popliteal, posterior tibial, and dorsalis pedis pulses
 Extremity assessment
o Temperature, color, capillary refill time, sensation, and movement of
extremities
o May need to use a Doppler to assess
 Occasionally, lower extremity pulses may be absent for a short
time after surgery as the result of vasospasm and hypothermia.
o A decreased or absent pulse together with a cool, pale, mottled, or
painful extremity may indicate embolization or graft occlusion. Report
these findings to the physician immediately.
 Renal perfusion status
 Urinary output (hourly recording; 30ml/hr or 0.5ml/kg/hr)
 Fluid intake
 Daily weight
 CVP/PA pressure
 Blood urea nitrogen/creatinine
Ambulatory Care
o Encourage patient to express concerns
 Medication management must be controlled!
o Instruct patient to gradually increase activities
o No heavy lifting
o Teach about signs and symptoms of complications
 Infection
 Neurovascular changes
o Fatigue, poor appetite, and irregular bowel habits are common.
o Any redness, swelling, increased pain, drainage from incisions, or fever greater than 100° F
(37.8° C) should be reported to a HCP.
o Sexual dysfunction in male patients is common after aortic surgery
 Could get penile implant
o Preoperatively, document baseline sexual function and recommend counseling as appropriate.
o A referral to a urologist may be useful if erectile dysfunction occurs.
Nursing Management: Evaluation
 Expected Outcomes
o Patent arterial graft with adequate distal perfusion
o Adequate urine output
o No signs of infection
Aortic Dissection
Aortic Dissection
 Often misnamed “dissecting aneurysm”
 Not a type of aneurysm
o BE ABLE TO DIFFERENTIATE BETWEEN DISSECTION
AND ANEURYSM
 Dissection is a tear
 Nothing inherently wrong/MVA or other
type of blunt trauma
 Result of a false lumen through which blood flows
Classification of Aortic Dissection
 Aortic dissection is classified based on location of
dissection and duration of onset
o Type A dissection affects the ascending aorta and
arch
o Type B dissection begins in the descending aorta
Aortic Dissection
 Affects men more often than
women
 Occurs most frequently in sixth
and seventh decades of life
 Predisposing factors include age,
aortic diseases (e.g., aortitis,
coarctation, arch hypoplasia),
atherosclerosis, blunt or
iatrogenic trauma, tobacco use,
cocaine or methamphetamine use, congenital heart disease (e.g., bicuspid aortic valve), connective
tissue disorders (e.g., Marfan's or Ehlers-Danlos syndrome), family history, history of heart surgery,
male gender, pregnancy, and poorly controlled hypertension.
 Nearly half of all acute aortic dissections in patients younger than 40 years of age occur in patients with
Marfan’s syndrome
Aortic Dissection: Etiology and Pathophysiology
 Due to degeneration of the elastic fibers in the arterial wall
 Chronic hypertension hastens the process
 Tear in inner layer allows blood to “track” between inner and middle layer
 If the blood-filled channel ruptures through the outside aortic wall, aortic dissection is often fatal
 As heart contracts, each systolic pulsation ↑ pressure on damaged area
o Further ↑ dissection
o May occlude major branches of aorta
 Cutting off blood supply to brain, abdominal organs, kidneys, spinal cord (may end up
paralyzed), and extremities
Aortic Dissection: Clinical Manifestations
 Depend on location of intimal tear and extent of dissection
o Acute Type A aortic dissection
 Abrupt onset of excruciating anterior chest pain
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 So acute about to pass out
o Acute Type B aortic dissection
 More likely to report pain located in their back, abdomen, or legs
Pain characterized as
o Sudden, severe pain in anterior part of chest, or intrascapular pain radiating down spine to
abdomen or legs
o Described as “sharp” and “worst ever”
o May mimic that of MI
 Dissection pain can be differentiated from MI pain that is more gradual in onset and has
increasing intensity. As the dissection progresses, pain may migrate and follow the path
of the dissection.
o Older patients are less likely to present with abrupt onset of chest or back pain and are more
likely to present with hypotension and vague symptoms.
Cardiovascular, neurologic, and respiratory signs may be present
If aortic arch involved
o Neurologic deficiencies may be present
 May include altered level of consciousness, weakened or absent carotid and temporal
pulses, and dizziness or syncope
Type A
o Disruption of blood flow in coronary arteries and aortic valve insufficiency
o The patient may develop angina; MI; and a new high-pitched, heart murmur. In severe cases,
these complications can result in left heart failure (e.g., dyspnea, orthopnea, pulmonary
edema), cardiogenic shock, and death
Aortic Dissection: Complications
 Cardiac tamponade
o Severe, life-threatening complication
o Occurs when blood escapes from dissection into pericardial sac
 Usually can go in and drain
o Clinical manifestations include:
 Hypotension
 Narrowed pulse pressure
 Distended neck veins
 Muffled heart sounds
 Pulsus paradoxus (most accurate method to determine tamponade; pump up BP cuff
and get BP on exhalation, pump back up again and watch their breathing—if greater
than 10 point difference on inhalation)
 Aorta may rupture
o Results in exsanguination and death
 Hemorrhage may occur in mediastinal, pleural, or abdominal cavities
 Occlusion of arterial supply to vital organs
Aortic Dissection: Diagnostic Studies
 ECG to rule out MI
 Chest x-ray (may show a widening of the mediastinum and pleural effusion)
 3-D CT scan (standard of care)
 MRI
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o Can provide more detailed information on the severity of the dissection and related
complications (e.g., pericardial effusions, carotid dissection
Transesophageal echocardiography for clots (standard of care)
Aortic Dissection: Interprofessional Care
 Initial goal
o HR and BP control
 ↓ BP and myocardial contractility to diminish pulsatile forces within aorta
o Pain management
 Drug therapy
o IV β-adrenergic blocker
 Esmolol (Brevibloc)
o Other antihypertensive agents
 Calcium channel blockers
 Nitroprusside
 Angiotensin-converting enzyme inhibitors
o Morphine
 Decreases sympathetic nervous system stimulation as well as relieving pain
 Give as much as they need
 Conservative therapy
o If no symptoms
 Can be treated conservatively for a period of time
o Pain relief, HR, and BP control
o CVD risk factor modification
o Close surveillance with CT or MRI
 Thoracic endovascular aortic repair
o TEVAR
 A temporary lumbar drain may be inserted for cerebrospinal fluid removal to reduce
spinal cord edema and help prevent paralysis.
 If a lumbar drain is used, strict aseptic techniques are essential to avoid introducing
infection.
o Standard to treat acute and chronic Type B aortic dissections with complications
o Similar to EVAR
 Surgical therapy
o Emergency surgery for acute Type A aortic dissection
o When drug therapy is ineffective or when complications of aortic dissection are present
o Surgery is delayed to allow edema to decrease and permit clotting of blood
o Involves resection of aortic segment and replacement with synthetic graft material
o In-hospital mortality and neurologic complications are high
 Open surgical repair is recommended for patients with a chronic dissection that have a
connective tissue disorder, and a descending thoracic aortic diameter greater than 5.5
cm.
 Causes of death include aortic rupture, mesenteric ischemia, MI, sepsis, stroke, and
multiorgan failure.
Aortic Dissection: Nursing Management
 Preoperative
o Semi-Fowler’s position
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o Maintaining a quiet environment
o Anxiety and pain management
 Opioids and tranquilizers as ordered
o Continuous IV administration of antihypertensive agents
o These measures help to keep the HR and systolic BP at the lowest possible level that maintains
vital organ perfusion (typically HR less than 60; systolic BP between 110-120 mm Hg).
 To prevent the extension of the dissection, manage pain and anxiety because they can
cause elevations in the HR and systolic BP.
o Continuous ECG and intraarterial pressure monitoring
o Observation of changes in quality of peripheral pulses
o Frequent vital signs
o If the arteries branching off the aortic arch are involved, monitor the patient's level of
consciousness, cranial nerve functions, and limb movement, sensation, and strength.
Postoperative
o See aneurysm postop care (discussed earlier)
Discharge teaching
o Therapeutic regimen (lifelong)
 Antihypertensive drugs and side effects
o If pain returns or symptoms progress, instruct patient to seek immediate help
Audience Response Question
Following an aortic aneurysm repair, the patient suddenly develops severe pain in the right lower extremity.
The right pedal pulse is decreased and the right foot is cool and pale. Which complication should the nurse
suspect?
a. Hypothermia
b. Wound infection
c. Bleeding from the graft site
d. Embolization or graft occlusion (threw a clot)
Answer: D
Rationale: A decreased or absent pulse together with a cool, pale, mottled, or painful extremity may indicate
embolization or graft occlusion.
Med Surg 2 Exam #1 Study Guide
Chapter 37: Peripheral Artery Disease of the Lower Extremities
Description
 Involves progressive narrowing and degeneration of arteries of upper and lower extremities
 Atherosclerosis is leading cause in majority of cases
 Patients with PAD are more likely to have coronary artery disease and/or cerebral artery disease
 Typically appears at ages in sixth to eighth decades of life
o In persons with diabetes mellitus, PAD occurs much earlier
 PAD prevalence is higher in those of lower socioeconomic status, women and African Americans.
 Largely underdiagnosed
 Risk factors
o Tobacco use
 vasoconstrictor and tobacco smoke impairs transport and cellular use of oxygen, and
increases blood viscosity and homocysteine levels
o Chronic kidney disease
o Diabetes mellitus
o Hypertension
o Hypercholesterolemia
o Other risk factors include elevated C-reactive protein, family history, hypertriglyceridemia,
increasing age, hyperhomocysteinemia, hyperuricemia, obesity, sedentary lifestyle, and stress
 Peripheral artery disease (PAD) may affect
o Iliac artery
o Femoral artery
o Popliteal artery (most common in nondiabetic pts)
o Tibial artery
o Peroneal artery
Common Sites of Atherosclerotic Lesions
 Common anatomic locations of atherosclerotic lesions
(shown in yellow) of the abdominal aorta and lower
extremities.
 Atherosclerosis more commonly affects certain segments of
the arterial tree. These include the coronary (see Chapter 33),
carotid (see Chapter 57), and lower extremity arteries.
 Clinical symptoms occur when vessels are 60% to 75%
blocked.
Clinical Manifestations
 Classic symptom of PAD –intermittent claudication
o Ischemic muscle pain that is caused by a constant
level of exercise
 Want to exercise to develop their own collateral circulation
o Resolves within 10 minutes or less with rest
o Reproducible
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o PAD of the iliac arteries produces claudication in the buttocks and thighs, whereas calf
claudication indicates femoral or popliteal artery involvement.
o As many as one third of patients with PAD report classic claudication symptoms
 Like angina but in legs
o The remaining either have no symptoms or present with atypical leg symptoms (e.g. burning,
heaviness, pressure, soreness, tightness, weakness) in atypical locations (e.g. ankle, foot,
hamstring, hip, knee, shin). Older women experience classic claudication less often than men.
Paresthesia
o Results from nerve tissue ischemia.
o Numbness or tingling in the toes or feet
o Produces loss of pressure and deep pain sensations
o Injuries often go unnoticed by patient
Thin, shiny, and taut skin
Loss of hair on the lower legs
Diminished or absent pedal, popliteal, or femoral pulses
Pallor of foot with leg elevation
Reactive hyperemia of foot with dependent position
Pain at rest
o As PAD progresses
o Occurs in feet or toes
o Aggravated by limb elevation (LOWER LEGS)
o Occurs from insufficient blood flow
o Occurs more often at night (May sleep in chair or legs off bed)
Critical Limb Ischemia (CLI)
 Characterized by:
o Chronic ischemic rest pain lasting more than 2 weeks
o Arterial leg ulcers or gangrene
 Patients with PAD who also have diabetes, heart failure, and a history of a stroke are at increased risk
for critical limb ischemia.
Complications
 Atrophy of skin and underlying muscles
 Boney prominences most affected
 Delayed healing
 Wound infection
 Tissue necrosis
 Arterial ulcers
 Nonhealing arterial ulcers and gangrene are most serious complications
 May result in amputation
o If adequate blood flow is not restored
o If severe infection occurs
Diagnostic Studies
 Doppler ultrasound
o When palpation of a peripheral pulse is difficult because of severe PAD
o A palpable pulse and a Doppler pulse are not equivalent
o Segmental blood pressure
Obtained (using Doppler ultrasound and a sphygmomanometer) at the thigh, below the
knee, and at ankle level while the patient is supine.
 A drop in segmental BP of greater than 30 mm Hg suggests PAD.
Ankle-brachial index (ABI) (NOT ON TEST BECAUSE DON’T DO MUCH ANYMORE)
o Done using a hand-held Doppler
o Calculated by dividing the ankle systolic BPs by the higher of the left and right brachial systolic
BP
o 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
Angiography and magnetic resonance angiography
o Location and extent of PAD
Duplex imaging
o Bidirectional, color Doppler
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Interprofessional Care: Risk Factor Modification
 MAKE WALK!
 Tobacco cessation
 Glycosylated hemoglobin <7.0% for diabetics
 Aggressive treatment of hyperlipidemia
o Both dietary interventions and drug therapy are needed
 Statins (e.g., simvastatin [Zocor]) lower LDL and triglyceride levels and reduces CVD
morbidity and mortality risks
 BP maintained <140/90
Interprofessional Care: Drug Therapy
 ACE inhibitors
o Ramipril (Altace)
 ↓ Cardiovascular morbidity
 ↓ Mortality
 ↑ Peripheral blood flow
 ↑ ABI
 ↑ Walking distance
 Antiplatelet agents
o Aspirin (75-325 mg daily).
 Aspirin intolerant patients may take clopidogrel (Plavix) 75 mg daily
o Clopidogrel (Plavix)
o DRUG ALERT—Clopidogrel (Plavix) and Omeprazole (Prilosec)
 Antiplatelet effect of clopidogrel is reduced by about half when given with omeprazole.
 This increases the risk of myocardial infarction and stroke.
 Drugs prescribed for treatment of intermittent claudication
o Cilostazol (Pletal)
 Inhibits platelet aggregation
 ↑ Vasodilation
o Pentoxifylline (Trental)
 Improves deformability of RBCs and WBCs (Makes more flexible)
 Decreases fibrinogen concentration, platelet adhesiveness, and blood viscosity
o Drug Alert: Cilostazol (Pletal)

Contraindicated in patients with heart failure of any severity
Interprofessional Care: Exercise Therapy
 Exercise improves oxygen extraction in legs and skeletal metabolism
 Walking is most effective exercise for individuals with claudication
o 30 to 45 minutes daily, 3 times/week
Interprofessional Care: Nutritional Therapy
 BMI <25 kg/m2
 Waist circumference <40 inches for men and <35 inches for women
 Recommend reduced calories and salt for obese or overweight persons
 Even modest, sustained weight loss of 3% to 5% yields important reductions in triglycerides, glucose,
A1C, and the risk of developing type 2 diabetes. Greater weight loss produces greater benefits.
 Patients taking antiplatelet agents, nonsteroidal antiinflammatory agents (NSAIDs) (e.g., ibuprofen
[Motrin]), and anticoagulants (e.g., warfarin) should consult with their health care provider before
taking any dietary or herbal supplements due to potential interactions and bleeding risks.
Interprofessional Care: Leg With Critical Limb Ischemia
 Revascularization via bypass surgery (optimal therapy)
 Percutaneous transluminal angioplasty (PTA)
 IV prostanoids (iloprost [Ventavis]) (not surgical candidate)
 Spinal cord stimulation (manage pain)
 Angiogenesis
o Growth factors and gene and stem cell therapy may be used to stimulate blood vessel growth
 Conservative Treatment
o Protect from trauma
o Decrease ischemic pain
o Prevent/control infection (systemic antibiotics)
o Improve arterial perfusion
Interprofessional Care: Interventional Radiology Procedures
 Indications
o Intermittent claudication symptoms become incapacitating
o Pain at rest
o Ulceration or gangrene severe enough to threaten viability of the limb
 Percutaneous transluminal angioplasty (PTA)
o Involves insertion of a catheter through femoral artery
o Catheter contains a cylindrical balloon
o Balloon is inflated dilating the vessel by compressing atherosclerotic intimal lining
o Stent is placed
 Expandable metallic devices, are positioned within the artery immediately after the
balloon angioplasty is done.
 The stent acts as a scaffold to keep the artery open.
 Atherectomy
o Removal of obstructing plaque
o Performed using a cutting disc, laser, or rotating diamond tip
 Cryoplasty
o Combines percutaneous transluminal angioplasty and cold therapy
o Liquid nitrous oxide
 Changes from liquid to gas as it enters the balloon
 Expansion of the gas results in cooling to 14° F (−10° C). The cold temperature limits
restenosis by reducing smooth muscle cell activity
Interprofessional Care: Surgical Therapy
 Most common surgical approach
o Peripheral artery bypass surgery with autogenous vein or synthetic graft to bypass blood around
the lesion
o PTA with stenting may also be used in combination with bypass surgery
 Endarterectomy (involves opening the artery and removing the obstructing plaque)
 Patch graft angioplasty (opening the artery, removing plaque, and sewing a patch to the opening to
widen the lumen)
 Amputation
o If tissue necrosis is extensive, gangrene or osteomyelitis develops, or all major arteries in the
limb are blocked, precluding the possibility of successful surgery
Bypass Grafts
 A, Femoral-popliteal bypass graft around an occluded superficial femoral artery.
 B, Femoral-posterior tibial bypass graft around occluded superficial femoral, popliteal, and proximal
tibial arteries.
Nursing Management: Nursing Assessment
 Past health history
o Diabetes mellitus
o Smoking
o Hypertension
o Hyperlipidemia
o Obesity
 Exercise intolerance
 Loss of hair on legs and feet
 Decreased or absent peripheral pulses

Intermittent claudication
Nursing Management: Nursing Diagnoses
 Ineffective peripheral tissue perfusion
o related to deficient knowledge of contributing factors
 Activity intolerance
o related to imbalance between oxygen supply and demand
 Chronic pain
o related to ischemia, inflammation, and swelling
 Ineffective health management
o related to lack of knowledge of disease and self-care measures
Nursing Management: Planning
 Overall goals for patient with PAD
o Adequate tissue perfusion
o Relief of pain
o Increased exercise tolerance
o Intact, healthy skin on extremities
o Increased knowledge of disease and treatment plan
Nursing Management: Nursing Implementation
 Health Promotion
o Identification of at-risk patients
o Diet modification (reduce the intake of cholesterol, saturated fat, and refined sugars)
o Proper care of feet
o Avoidance of injuries
o Encourage patients with positive family histories of cardiac, diabetic, or vascular disease to
obtain regular follow-up care.
 Acute Care
o Frequently monitor after surgery (every 15 min then hourly)
 Skin color and temperature
 Capillary refill
 Presence of peripheral pulses distal to the operative site
 Loss of palpable pulses and/or a change in the Doppler sound over a pulse
requires immediate notification of the HCP and prompt intervention
 Sensation and movement of extremity
o Continued circulatory assessment
o Monitor for potential complications
o Knee-flexed positions should be avoided except for exercise
o If edema develops, position the patient supine and elevate the leg above heart level
o Turn and position frequently
o Walking even short distances is desirable. The use of a walker may be helpful, especially in frail,
elderly patients.
 Ambulatory Care
o Management of risk factors
 Continued tobacco use dramatically decreases the long-term patency rates of grafts and
stents, and increases the risk of an MI or stroke
o Long-term antiplatelet therapy
o
o
o
o
o
 Don’t want to clot off the stents
Importance of supervised exercise training after revascularization
 Decreases CVD risk factors, including hypertension, hyperlipidemia, obesity, and glucose
levels
Importance of meticulous foot care
 Especially in diabetic patients
Daily inspection of the feet
Comfortable shoes with rounded toes and soft insoles
Shoes lightly laced
Nursing Management: Evaluation
 Adequate peripheral tissue perfusion
 Increased activity tolerance
 Effective pain management
 Knowledge of disease and treatment plan
 Plans for walking program
 Increased activity tolerance
 Verbalize key elements of
o Therapeutic regimen
o Knowledge of disease
o Treatment plan
o Reduction of risk factors
o Proper ulcer/foot care
Audience Response Question
A patient with peripheral artery disease has marked peripheral neuropathy. An appropriate nursing diagnosis
for the patient is
a. Risk for injury related to decreased sensation.
b. Impaired skin integrity related to decreased peripheral circulation.
c. Ineffective peripheral tissue perfusion related to decreased arterial blood flow.
d. Activity intolerance related to imbalance between oxygen supply and demand.
Answer: A
Rationale: Peripheral neuropathy is caused by diminished perfusion to neurons and results in loss of both
pressure and deep pain sensations. The patient may not notice lower extremity injuries. Neuropathy increases
susceptibility to traumatic injury and results in delay in seeking treatment.
The nurse teaches a patient with peripheral arterial disease. The nurse determines that further teaching is
needed if the patient makes which statement?
a. “I should not use heating pads to warm my feet.”
b. “I should cut back on my walks if it causes pain in my legs.”
c. “I will examine my feet every day for any sores or red areas.”
d. “I can quit smoking if I use nicotine gum and a support group.”
Answer: B
Rationale: Patients should be taught to exercise to the point of discomfort, stop and rest, and then resume
walking until the discomfort recurs. Smoking cessation and proper foot care are also important interventions
for patients with peripheral arterial disease.