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1. Left-sided heart failure is characterized by
a. pulmonary congestion.
b. decreased systemic vascular resistance.
c. jugular vein distention.
d. peripheral edema.
ANS: A
Left-sided heart failure is characterized by pulmonary congestion and edema. Right-sided
heart failure is characterized by congestion in the systemic venous system that increases
systemic vascular resistance. Jugular vein distention is a classic sign of right-sided heart
failure. Peripheral edema is seen in right-sided failure.
2. The therapy that most directly improves cardiac contractility in a patient with systolic heart
failure is
a. afterload reduction.
b. -antagonist agents.
c. preload reduction.
d. digitalis.
ANS: D
Digitalis may be used for symptom management of heart failure. Cardiac glycosides directly
inhibit the sodium-potassium pump present in the cell membrane of all cells. The intracellular
changes allow more calcium to remain in the cell, thus strengthening myocardial contraction.
Contractility is not improved through afterload reduction. Beta-blockers inhibit the effects of
sympathetic activation and have the potential to reduce cardiac output. Preload reduction is
not the therapy of choice in improving cardiac contractility.
3. Hypertrophy of the right ventricle is a compensatory response to
a. aortic stenosis.
b. aortic regurgitation.
c. tricuspid stenosis.
d. pulmonary embolus.
ANS: D
Right ventricular hypertrophy is the direct result of pulmonary disorders that increase
pulmonary vascular resistance and impose a high afterload on the right ventricle such as
pulmonary embolism. Aortic stenosis does not lead to right ventricular hypertrophy. Aortic
regurgitation is not associated with right ventricular hypertrophy. Hypertrophy of the right
ventricle is not a compensatory response to tricuspid stenosis.
4. The common denominator in all forms of heart failure is
a. poor diastolic filling.
b. reduced cardiac output.
c. pulmonary edema.
d. tissue ischemia.
ANS: B
The common manifestation of all forms of heart failure is the failure of the heart to pump
blood adequately. The clinical presentation may differ depending on which ventricle fails (left
or right, or both). Poor diastolic filling is not seen in all forms of heart failure. Pulmonary
edema is seen in left-sided failure. Tissue ischemia is directly related to myocardial infarction,
which may induce heart failure.
5. Cor pulmonale refers to
a. biventricular failure.
b. left ventricular hypertrophy secondary to lung disease.
c. right ventricular hypertrophy secondary to pulmonary hypertension.
d. right ventricular failure secondary to right ventricular infarction.
ANS: C
Pulmonary disorders that result in increased pulmonary vascular resistance impose a high
afterload on the right ventricle. The resultant right ventricular hypertrophy known as cor
pulmonale may progress to right ventricular failure as the lung disease worsens. Biventricular
failure is most often the result of primary left ventricular failure that progresses to the right.
Cor pulmonale is not associated with left ventricular hypertrophy. Only 3% of MIs occur in
the right ventricle.
6. Lusitropic impairment refers to
a. poor contractile force.
b. impaired diastolic relaxation.
c. altered action potential conduction rate.
d. altered automaticity.
ANS: B
Lusitropic impairment refers to an energy-requiring process that removes free calcium ions
from the cytoplasm by pumping them back into the sarcoplasmic reticulum and across the cell
membrane into the extracellular fluid. Ischemia interferes with this process in the active phase
of diastolic relaxation. Poor contractile force is not associated with lusitropic impairment. The
conduction rate is not associated with the energy-requiring process known as lusitropy.
Automaticity is not a factor in lusitropy.
7. First-degree heart block is characterized by
a. prolonged PR interval.
b. absent P waves.
c. widened QRS complex.
d. variable PR interval.
ANS: A
First-degree block is generally identified by a prolonged PR interval (more than 0.20 second)
on ECG. P waves are not absent in first-degree heart block. A widened QRS complex is
associated with a particular dysrhythmia, but not first-degree heart block. A variable PR
interval is found in type I second-degree block.
8. Second-degree heart block type I (Wenckebach) is characterized by
a. absent P waves.
b. lengthening PR intervals and dropped P wave.
c. constant PR interval and dropped QRS complexes.
d. no correlation between P waves and QRS complexes.
ANS: B
Type I second-degree block is associated with progressively lengthening PR intervals until
one P wave is not conducted and becomes a dropped beat. Second-degree block is not
characterized by an absence of P waves. Type II second-degree block is associated with a
consistent PR interval and dropped beats. The ECG of third-degree block shows regularly
occurring P waves that are independent of the ventricular rhythm.
9. Which dysrhythmia is thought to be associated with reentrant mechanisms?
a. Second-degree AV block
b. Sinus bradycardia
c. Junctional escape
d. Preexcitation syndrome tachycardia (Wolf-Parkinson-White syndrome)
ANS: D
Reentry is a complex process in which a cardiac impulse continues to depolarize in a part of
the heart after the main impulse has finished its path and the majority of the fibers have
repolarized. Wolff-Parkinson-White syndrome is caused by accessory pathways that
originate in the atria, bypass the AV node, and enter a site in the ventricular myocardium. This
causes the ventricles to contract prematurely, resulting in a reentrant tachycardia.
Second-degree block is a conduction failure between the sinus impulse and its ventricular
response. Sinus bradycardia is a slowed impulse generation by the sinus node. A junctional
escape rhythm originates in the AV node.
10. In which dysrhythmias should treatment be instituted immediately?
a. Asymptomatic sinus bradycardia at a heart rate of 50 beats/minute
b. Fever-induced tachycardia at 122 beats/minute
c. Premature atrial complexes occurring every 20 seconds
d. Atrial fibrillation with a ventricular rate of 220 beats/minute
ANS: D
Atrial fibrillation is a completely disorganized and irregular atrial rhythm accompanied by an
irregular ventricular rhythm of variable rate. Atrial fibrillation causes the atria to quiver rather
than to contract forcefully. This allows blood to become stagnant in the atria and may lead to
formation of thrombi. This condition requires resuscitation because of the reduction in cardiac
output. The cause of the bradycardia should be investigated, but is not treated emergently
when an individual is not exhibiting any symptoms. Fever-induced tachycardia will correct
itself once the fever is lowered. Dysrhythmias are treated if they produce significant
symptoms or are expected to progress to a more serious level.
11. An abnormally wide (more than 0.10 second) QRS complex is characteristic of
a. paroxysmal atrial tachycardia.
b. supraventricular tachycardia.
c. junctional escape rhythm.
d. premature ventricular complexes.
ANS: D
The QRS of the premature complex is prolonged (greater than 0.10 second) and bizarre in
appearance. Paroxysmal atrial tachycardia does not display a QRS complex that is greater
than 0.10 seconds. Supraventricular tachycardia does not display a wide QRS complex.
Escape rhythms may have a P wave that is inverted and located before, during, or after the
QRS.
12. A laboratory test that should be routinely monitored in patients receiving digitalis therapy is
a. serum sodium.
b. albumin level.
c. serum potassium.
d. serum calcium.
ANS: C
Digitalis slows the heart rate through parasympathetic system activation and promotes sodium
and water excretion through improved cardiac output to the kidney. Depletion of serum
potassium (hypokalemia) may potentiate digitalis toxicity. Sodium and water excretion is
activated through the parasympathetic system because of improved cardiac output to the
kidneys. Albumin level is not affected by digitalis. Digitalis allows more calcium to remain in
the cell through a slowing of the sodium-dependent calcium pump.
13. After sitting in a chair for an hour, an older patient develops moderate lower extremity edema.
His edema is most likely a consequence of
a. arterial obstruction.
b. isolated left-sided heart failure.
c. right-sided heart failure.
d. peripheral arterial disease.
ANS: C
The backward effects of right-sided heart failure are as a result of congestion in the systemic
venous system and lead to lower extremity edema. Arterial obstruction is not associated with
dependent edema of the lower extremities. Left-sided heart failure is associated with
pulmonary symptoms. Peripheral arterial disease would lead to cool, pale extremities lacking
hair and with weak pulses.
14. A patient is exhibiting severe dyspnea and anxiety. The patient also has bubbly crackles in all
lung fields with pink, frothy sputum. This patient is most likely experiencing
a. right-sided heart failure.
b. cardiomyopathy.
c. a medication reaction.
d. acute cardiogenic pulmonary edema.
ANS: D
Acute cardiogenic pulmonary edema is a life-threatening condition requiring immediate
treatment. It is associated with left ventricular failure that severely impairs gas exchange, and
produces dramatic signs and symptoms including anxiety, severe dyspnea, an upright posture
to breathe effectively, and pink frothy sputum. Right-sided heart failure produces systemic
venous congestion. Cardiomyopathy is not associated with bubbly crackles and pink frothy
sputum. A medication reaction is not the reason for the patient to exhibit severe dyspnea,
anxiety, bubbly crackles, and frothy sputum.
15. A patient with pure left-sided heart failure is likely to exhibit
a. jugular vein distention.
b. pulmonary congestion with dyspnea.
c. peripheral edema.
d. hepatomegaly.
ANS: B
Left-sided heart failure includes ineffective pumping of the left ventricle, resulting in an
accumulation of blood within the pulmonary circulation. As a result, pulmonary congestion
with dyspnea is an expected finding. Jugular vein distention is more often associated with
right-sided failure. Peripheral edema is associated with right-sided failure. Hepatomegaly is
not seen in pure left-sided edema.
16. Beta-blockers are advocated in the management of heart failure because they
a. increase cardiac output.
b. inhibit SNS activation.
c. enhance sodium absorption.
d. reduce blood flow to the kidneys.
ANS: B
Beta-blockers are advocated in the management of heart failure to inhibit the cardiac effects of
sympathetic activation. Sympathetic activation is a compensatory response in the short term,
but over time, it leads to remodeling and worsening heart failure. Beta-blockers do not affect
sodium reabsorption. Angiotensin II and aldosterone enhance sodium and water reabsorption
by the kidney, contributing to an elevated blood volume.
17. A patient with heart failure who reports intermittent shortness of breath during the night is
experiencing
a. orthopnea.
b. paroxysmal atrial tachycardia.
c. sleep apnea.
d. paroxysmal nocturnal dyspnea.
ANS: D
Dyspnea that occurs at night is known as paroxysmal nocturnal dyspnea. Orthopnea is
shortness of breath when lying down. Intermittent shortness of breath at night is not known as
paroxysmal atrial tachycardia. Sleep apnea is an absence of breathing during sleep.
18. Low cardiac output to the kidneys stimulates the release of from juxtaglomerular cells.
a. aldosterone
b. norepinephrine
c. angiotensinogen
d. renin
ANS: D
When cardiac output is reduced, juxtaglomerular cells in the kidney release renin and initiate
the renin-angiotensin-aldosterone cascade leading to salt and water retention by the kidney.
Aldosterone is not released from juxtaglomerular cells. Norepinephrine is not released by cells
within the kidney. Angiotensin is not involved in the process of cellular release within the
kidneys.
19. A patient with heart failure has had significant improvement with a blocker, but has a
resting heart rate in the 90s. What medication might be indicated for this patient to add to the
regime?
a. Digitalis
b. Dobutamine
c. Furosemide
d. HCN channel blocker
ANS: D
HCN channel blockers are a new classification of medication that causes rate-dependent
inhibition of the pacemaker cells. This class of medications is indicated as add-on therapy for
a heart rate greater than 70 bpm after optimization of blockers. Digitalis and dobutamine are
positive inotropes. Furosemide is a loop diuretic.
20. The majority of tachydysrhythmias are believed to occur because of
a. triggered activity.
b. enhanced automaticity.
c. defective gap junctions.
d. reentry mechanisms.
ANS: D
Reentry is thought to be the culprit in most tachydysrhythmias. Reentry is a complex process
in which a cardiac impulse continues to depolarize in a part of the heart after the main impulse
has finished its path. Triggered activity occurs when an impulse is generated during or just
after repolarization. Alterations in automaticity create electrolyte imbalances. Defective gap
junctions are not related to tachydysrhythmias.
21. A patient who reports dizziness and who has absent P waves, wide QRS complexes, and a
heart rate of 38 beats/minute on an ECG is most likely in which rhythm?
a. Third-degree heart block
b. Junctional tachycardia
c. Ventricular escape rhythm
d. Sinus bradycardia
ANS: C
A ventricular escape rhythm originates in the Purkinje fibers, has a rate of 15 to 40
beats/minute, and is characterized by a wide QRS complex. An important clue to identifying
escape rhythms is the absence of normal P waves and PR intervals. The rhythm involved in
third-degree heart block includes regularly occurring P waves. Junctional tachycardia has a
heart rate between 70 and 140 beats/minute. P waves are preceding, following, or buried in
the QRS complex. Sinus bradycardia has a normal pattern on the ECG, but with a rate of less
than 60 beats/minute.
22. A patient is diagnosed with heart failure with preserved ejection fraction (HFpEF). This
patient is most likely described as a(n)
a. elderly woman without a previous history of MI.
b. middle-aged man with a previous history of MI.
c. young female athlete with cardiomegaly.
d. young sedentary male with a high-stress job.
ANS: A
Heart failure with preserved ejection fraction (HFpEF) is particularly likely to develop in the
elderly, in women, and in those without a history of MI. A middle-aged man with a previous
history of MI may have heart failure, but the older woman fits the criteria of heart failure with
normal ejection fraction. A young female athlete with cardiomegaly may experience heart
failure, but is not the normal patient profile for this condition. A young sedentary male with a
high-stress job may experience heart failure, but this patient does not fit the normal profile for
this condition.
23. Increased preload of the cardiac chambers may lead to which patient symptom?
a. Decreased heart rate
b. Decreased respiratory rate
c. Edema
d. Excitability
ANS: C
Preload reduces glomerular filtration resulting in fluid conservation, or edema. Increased
preload may lead to an increased, not decreased, heart rate. Increased preload may lead to
shortness of breath and an increased respiratory rate. Increased preload may lead to fatigue,
not excitability, as the heart works harder to circulate blood.
1. Which statement is true about the incidence of heart failure? (Select all that apply.)
a. Heart failure affects about 2 million Americans.
b. Heart failure is the cause of increasing hospitalizations each year.
c. There are more than 400,000 new cases of heart failure diagnosed each year in the
United States.
d. The increasing incidence and hospitalization rates of heart failure reflect the aging
population in the United States.
e. The incidence of heart failure is 21 per 1000 population after age 65.
ANS: B, D, E
Heart failure is one of the fastest growing cardiac disorders at this time. The incidence and
hospitalization rates associated with heart failure are reflective of the aging population in the
United States. The incidence of heart failure is 21 per 1000 population in people over 65.
Heart failure affects about 6.2 million Americans. More than 670,000 new cases of heart
failure are diagnosed in the United States each year.
2. Right-sided heart failure is usually a consequence of which conditions? (Select all that apply.)
a. Elevated right ventricular afterload
b. Right ventricular infarction
c. Tricuspid valve defects
d. Congenital anomalies
e. Pulmonary embolus
ANS: A, B, E
Because the right and left ventricles function in tandem, left ventricular failure eventually
increases the workload on the right ventricle. Consequently, the right ventricle may fail
causing infarction. Pulmonary disorders create a high afterload on the right ventricle and may
cause a progression to right ventricular failure. Tricuspid valve defects are not the cause of
right-sided heart failure. Congenital anomalies are not generally associated with right-sided
failure.
3. A patient has heart failure with a preserved ejection fraction. Which findings are most likely
found in this patient? (Select all that apply.)
a. High cardiac output
b. Pulmonary congestion
c. Edema
d. Ejection fraction greater than 50%
e. Ejection fraction less than 45%
ANS: B, C, D
Pulmonary congestion is a hallmark sign of heart failure. Edema is also a hallmark sign of
heart failure. An ejection fraction greater than 50% indicates preserved ejection fraction. Low
cardiac output, not high cardiac output, is a sign of heart failure. An ejection fraction of less
than 45% indicates an abnormal ejection fraction.
4. The most common causes of heart failure include which of the following? (Select all that
apply.)
a. Myocardial ischemia
b. Hypertension
c. Dilated cardiomyopathy
d. High-fat diet
e. Urinary retention
ANS: A, B
The most common causes of heart failure are myocardial ischemia from coronary artery
disease, followed by hypertension. Dilated cardiomyopathy is less common cause of heart
failure. A high-fat diet can contribute to coronary artery disease, which is a contributor to
heart failure, but a high-fat diet is not one of the most common causes of heart failure. Urinary
retention is not a common cause of heart failure.
5. A patient with forward effects of heart failure may present with which symptoms? (Select all
that apply.)
a. Impaired memory
b. Mental fatigue
c. Stupor
d. Confusion
e. Aggression
ANS: A, B, D
The forward effects of heart failure cause inadequate perfusion of the brain and may lead to
restlessness, mental fatigue, confusion, anxiety, impaired memory, generalized fatigue,
activity intolerance, and lethargy. Stupor is not a symptom of the forward effects of heart
failure. Aggression is not a symptom of the forward effects of heart failure.
6. Dysrhythmias are significant for which reasons? (Select all that apply.)
a. An indicator of life span
b. Indicate an underlying disorder
c. Can impair venous return
d. Increase the severity of heart murmurs
e. Can impair cardiac output
ANS: B, E
Dysrhythmias can be indicative of an underlying pathophysiologic disorder. Dysrhythmias
can impair normal cardiac output and lead to serious patient complications. Dysrhythmias are
not an indicator of life span, but they may certainly shorten a patient's life span. Dysrhythmias
do not impair venous return, but they do impair cardiac output. Alone, dysrhythmias do not
increase the severity of heart murmurs.
7. A patient's ECG lacks recognizable waveforms and is deemed to represent sinus arrest. What
conditions could have caused this condition? (Select all that apply.)
a. Myocardial infarction
b. Electrical shock
c. Electrolyte disturbance
d. Acidosis
e. Alkalosis
ANS: A, B, C, D
Sinus arrest may result from MI, electrical shock, electrolyte disturbances, acidosis, and
extreme parasympathetic activity. Alkalosis is not a cause of sinus arrest.
8. The Renin-Angiotensin-Aldosterone System (RAAS) has which effects on the heart? (Select
all that apply.)
a. Increases cardiac afterload
b. Decreases cardiac output
c. Causes fibrosis of cardiac cells
d. Leads to cardiac remodeling
e. Can be beneficial in low cardiac output
ANS: A, C, D, E
The RAAS plays an important role in regulation of blood pressure and serves as a beneficial
compensatory mechanism for heart failure in the short term by increasing cardiac output via
increased afterload. However, its deleterious effects include causing fibrosis of cardiac cells
and remodeling