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Quizzes > Health & Medicine

Heart Failure Quiz: Check Your Knowledge of Core Concepts

15 quick questions with instant feedback. A concise heart failure knowledge test.

Editorial: Review CompletedCreated By: Nile WrightUpdated Aug 26, 2025
Difficulty: Moderate
Questions: 20
Learning OutcomesStudy Material
Colorful paper art representing a heart for a Heart Failure Knowledge Assessment Quiz

This heart failure quiz helps you review key signs, treatments, and care basics in a simple case format. Studying for exams or a clinical shift? Try our congestive heart failure practice questions, follow up with a cardiac nursing NCLEX quiz, and round out your study with a cardiovascular system quiz.

What happens to ejection fraction in systolic heart failure?
Varies unpredictably
Decreases
Increases
Remains unchanged
Systolic heart failure involves impaired contractility leading to a reduced fraction of blood ejected from the ventricle. The ejection fraction therefore decreases below normal values.
In left-sided heart failure, fluid backs up into which circulation?
Systemic veins
Pulmonary circulation
Lymphatic system
Coronary arteries
Left ventricular dysfunction raises pressure in the pulmonary veins and capillaries, causing pulmonary edema. Systemic venous congestion occurs in right-sided heart failure rather than left-sided failure.
A primary symptom of right-sided heart failure is:
Peripheral edema
Dyspnea on exertion
Orthopnea
Hemoptysis
Right-sided heart failure leads to systemic venous congestion and fluid accumulation in peripheral tissues. Dyspnea and orthopnea are more characteristic of left-sided failure.
Jugular venous distention indicates increased pressure in which chamber?
Right atrium
Left ventricle
Left atrium
Right ventricle
Elevated jugular venous pressure reflects high right atrial and central venous pressures. This finding is a sign of right-sided or biventricular failure.
Which medication class is first-line to reduce afterload in systolic heart failure?
Nitrates
Digoxin
ACE inhibitors
Loop diuretics
ACE inhibitors lower systemic vascular resistance, reducing afterload and improving cardiac output in systolic heart failure. Diuretics mainly relieve congestion, nitrates primarily reduce preload, and digoxin improves contractility but not mortality.
According to the NYHA classification, which class describes patients with symptoms at rest?
Class I
Class III
Class IV
Class II
NYHA Class IV patients experience heart failure symptoms even at rest. Class I patients have no limitation, Class II have symptoms with ordinary activity, and Class III with less than ordinary activity.
In diastolic heart failure, which hemodynamic parameter is primarily elevated?
Heart rate
Mixed venous oxygen saturation
Left ventricular end-diastolic pressure
Cardiac output
Diastolic dysfunction impairs ventricular filling, leading to increased LV end-diastolic pressure. Cardiac output often remains normal until advanced stages.
Which of the following drugs has been shown to improve survival in HFrEF?
Digoxin
ACE inhibitors
Loop diuretics
Nitrates alone
ACE inhibitors reduce ventricular remodeling and mortality in heart failure with reduced ejection fraction. Loop diuretics and digoxin relieve symptoms but do not demonstrate a mortality benefit on their own.
An ejection fraction of 45% is classified as:
High-output heart failure
Heart failure with reduced EF (HFrEF)
Heart failure with preserved EF (HFpEF)
Heart failure with mid-range EF (HFmrEF)
Heart failure with mid-range ejection fraction (HFmrEF) is defined as EF between 40 - 49%. HFrEF is below 40% and HFpEF is 50% or greater.
Beta-blockers are beneficial in chronic heart failure because they:
Enhance sodium excretion in kidneys
Directly increase myocardial contractility
Increase heart rate to improve output
Reduce sympathetic activity and improve ventricular remodeling
Beta-blockers blunt excessive sympathetic drive, lower heart rate, and counteract adverse remodeling in heart failure. They do not directly increase contractility or cause diuresis.
The pulmonary capillary wedge pressure reflects which cardiac pressure?
Right atrial pressure
Right ventricular pressure
Left atrial pressure
Left ventricular systolic pressure
Pulmonary capillary wedge pressure, measured via a balloon-tipped catheter, approximates left atrial pressure and thus left ventricular filling pressure. It does not measure right-sided pressures directly.
Which feature is characteristic of diastolic heart failure?
Reduced ejection fraction due to weak contractions
Preserved ejection fraction despite filling impairment
Dilated left ventricle with thin walls
High-output state with normal chambers
Diastolic heart failure involves stiff, noncompliant ventricles with normal or preserved EF and impaired relaxation. Systolic failure shows reduced EF and often dilation.
Brain natriuretic peptide (BNP) levels are elevated in heart failure because they:
Increase in response to ventricular wall stretch
Decrease when cardiac preload rises
Are released directly by the kidneys
Reflect decreased renal function
BNP is secreted by ventricular myocytes in response to increased wall tension and stretch. It serves as a biomarker for severity of volume overload.
In African-American patients with HFrEF still symptomatic on ACE inhibitors and beta-blockers, which add-on therapy improves outcomes?
Spironolactone
Calcium channel blockers
Hydralazine with isosorbide dinitrate
Digoxin
Hydralazine plus isosorbide dinitrate provides combined preload and afterload reduction and has been shown to improve mortality in this population. Spironolactone and digoxin have different roles.
A physical exam finding of crackles in lung bases most directly indicates:
Bronchospasm from asthma
Atelectasis from pleural effusion
Consolidation from pneumonia
Pulmonary edema due to left-sided heart failure
Crackles or rales indicate fluid in the alveoli from elevated pulmonary capillary pressures seen in left-sided heart failure. Other conditions have different auscultation findings.
Activation of the renin-angiotensin-aldosterone system in chronic heart failure primarily leads to:
Sodium retention, vasoconstriction, and fluid overload
Vasodilation and reduced preload
Decreased aldosterone release and diuresis
Increased natriuresis and hypotension
RAAS activation attempts to maintain perfusion pressure but causes vasoconstriction and promotes sodium and water retention, worsening volume overload. This is maladaptive in chronic HF.
According to ACC/AHA stages of heart failure, a patient with structural heart disease and prior symptoms but currently asymptomatic is in stage:
C
B
D
A
Stage C includes patients with known structural heart disease and current or prior symptoms of HF, even if they are presently asymptomatic. Stage A is at risk, B has structural changes without symptoms, and D is refractory.
A hemodynamic profile showing decreased cardiac output, increased pulmonary capillary wedge pressure, and increased systemic vascular resistance is characteristic of:
Diastolic heart failure with normal output
High-output heart failure
Advanced systolic heart failure
Pericardial tamponade
In systolic HF, weakened contractility leads to low output, pulmonary congestion raises wedge pressure, and compensatory vasoconstriction increases SVR. Tamponade also raises filling pressures but usually reduces SVR.
In a patient with chronic HFrEF and renal insufficiency (eGFR 25 mL/min), which diuretic is most appropriate for symptomatic volume control?
Furosemide
Spironolactone
Hydrochlorothiazide
Metolazone
Loop diuretics like furosemide are effective even at low GFR and are first-line for volume control in renal insufficiency. Thiazides lose efficacy, and spironolactone has risks in renal failure.
The combination of hydralazine and nitrates benefits heart failure patients by:
Increasing heart rate
Only reducing afterload
Reducing both preload and afterload
Only reducing preload
Hydralazine is an arterial vasodilator that reduces afterload, while nitrates venodilate to lower preload. Their combined effect improves cardiac performance in HF.
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Learning Outcomes

  1. Analyze hemodynamic changes in heart failure
  2. Identify clinical signs and symptoms of heart failure
  3. Evaluate treatment strategies for systolic and diastolic dysfunction
  4. Demonstrate knowledge of pharmacologic management options
  5. Apply diagnostic criteria to classify heart failure stages
  6. Interpret ejection fraction values accurately

Cheat Sheet

  1. Hemodynamic changes in heart failure - Imagine your heart as a water pump that's losing strength: when cardiac output drops, your body cranks up the heart rate and squeezes blood vessels to compensate. These quick fixes might help short-term but end up overworking the heart and creating a vicious cycle.
  2. Recognizing clinical signs and symptoms - Spotting shortness of breath, fatigue, and swelling is like reading the heart's distress signals. These clues show when blood isn't circulating well and fluid starts pooling in the lungs and tissues.
  3. Systolic vs. diastolic dysfunction - In systolic dysfunction the heart can't squeeze hard enough (low ejection fraction), while in diastolic dysfunction it can't relax properly (normal ejection fraction). Knowing the difference helps tailor treatments and gives insight into what's going wrong mechanically.
  4. Pharmacologic management options - Drugs like ACE inhibitors, beta-blockers, diuretics, and aldosterone antagonists each tackle different parts of heart failure's complex puzzle. From reducing fluid overload to calming an overexcited heart, these medications help break harmful feedback loops.
  5. Diagnostic criteria and classification - The NYHA functional classes and ACC/AHA stages act like report cards, grading heart failure severity from mild to severe. Understanding these scales guides treatment choices and predicts outcomes.
  6. Interpreting ejection fraction values - A normal ejection fraction falls between 50 - 70%, reduced is under 40%, and preserved is 50% or higher despite symptoms. Matching EF numbers to patient presentations helps determine the exact heart failure subtype.
  7. Role of biomarkers (BNP & NT-proBNP) - These blood tests are like smoke detectors for heart stress: higher levels mean more pressure in the heart chambers. Tracking them over time helps monitor treatment success and spot flare-ups early.
  8. Lifestyle modifications - Simple tweaks - like cutting back on sodium, managing fluids, and adding gentle exercise - can make a big difference in daily energy and comfort. Think of these changes as adding supportive crew members to help your heart sail smoothly.
  9. Advanced therapies: CRT & ICDs - For some patients, devices like cardiac resynchronization therapy and implantable defibrillators act as mechanical sidekicks correcting rhythm and electrical coordination. Knowing who benefits most is key to boosting quality of life and survival.
  10. Common comorbidities - Conditions like hypertension, diabetes, and kidney issues often tag along with heart failure, complicating treatment plans. Recognizing and managing these buddies is crucial for a holistic approach.
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