Congestive cardiac failure: pathophysiology and pharmacotherapy MCQs With Answer

Introduction

Congestive cardiac failure: pathophysiology and pharmacotherapy MCQs With Answer is designed for M.Pharm students to consolidate advanced knowledge of heart failure mechanisms and current drug therapies. This set blends core pathophysiology—neurohormonal activation, hemodynamic alterations, and molecular remodeling—with therapeutics including ACE inhibitors, ARNI, beta-blockers, diuretics, inotropes, SGLT2 inhibitors and device-related considerations. Each question targets clinical pharmacology, mechanism of action, evidence-based indications, adverse effects and practical treatment decisions. These 20 MCQs with precise answers will help refine understanding for exams and practice, emphasizing depth and application rather than superficial facts.

Q1. Which statement best differentiates heart failure with reduced ejection fraction (HFrEF) from heart failure with preserved ejection fraction (HFpEF)?

• HFrEF is primarily due to impaired diastolic relaxation with normal LVEF
• HFrEF is characterized by reduced left ventricular ejection fraction (LVEF <40%) due to impaired systolic contraction
• HFpEF always progresses to HFrEF within 1 year
• HFpEF is treated exclusively with inotropes

Correct Answer: HFrEF is characterized by reduced left ventricular ejection fraction (LVEF <40%) due to impaired systolic contraction

Q2. How is the Frank–Starling relationship altered in chronic systolic heart failure?

• Enhanced slope with increased stroke volume at low preload
• Flattening of the curve producing reduced stroke volume for a given preload
• Leftward shift with higher stroke volume at lower filling pressures
• No change in curve but increased heart rate compensates

Correct Answer: Flattening of the curve producing reduced stroke volume for a given preload

Q3. Which effect is a principal maladaptive consequence of chronic RAAS activation in heart failure?

• Decreased preload due to natriuresis
• Vascular smooth muscle relaxation and reduced afterload
• Aldosterone-mediated sodium and water retention and myocardial fibrosis promoting remodeling
• Reduced sympathetic tone and HR slowing

Correct Answer: Aldosterone-mediated sodium and water retention and myocardial fibrosis promoting remodeling

Q4. B-type natriuretic peptide (BNP) in heart failure is primarily secreted by which cardiac chamber and why is it clinically useful?

• Left atrium; it indicates valvular stenosis severity
• Right ventricle; it predicts pulmonary embolism only
• Ventricles; secreted in response to increased wall stretch and used to diagnose and assess severity of heart failure
• Atrial appendage; it identifies supraventricular tachycardia

Correct Answer: Ventricles; secreted in response to increased wall stretch and used to diagnose and assess severity of heart failure

Q5. What is the primary mechanism by which ACE inhibitors improve outcomes in HFrEF?

• Direct positive inotropic effect increasing contractility
• Inhibition of angiotensin-converting enzyme reducing angiotensin II levels, decreasing afterload, aldosterone, and ventricular remodeling
• Blocking beta-1 receptors to reduce heart rate
• Inhibiting neprilysin to increase natriuretic peptides

Correct Answer: Inhibition of angiotensin-converting enzyme reducing angiotensin II levels, decreasing afterload, aldosterone, and ventricular remodeling

Q6. Sacubitril/valsartan (ARNI) combines which two pharmacologic actions?

• ACE inhibition and beta-blockade
• Neprilysin inhibition (increasing natriuretic peptides) plus angiotensin II receptor blockade
• Direct renin inhibition and aldosterone antagonism
• PDE3 inhibition and alpha-1 blockade

Correct Answer: Neprilysin inhibition (increasing natriuretic peptides) plus angiotensin II receptor blockade

Q7. Which statement correctly summarizes the role of evidence-based beta-blockers in chronic HFrEF?

• They are contraindicated because they reduce contractility and increase mortality
• Short-acting beta-2 agonists are preferred over beta-blockers
• Long-term use of specific beta-blockers (e.g., bisoprolol, carvedilol, metoprolol succinate) reduces mortality and improves remodeling
• Beta-blockers are only used acutely in decompensated heart failure

Correct Answer: Long-term use of specific beta-blockers (e.g., bisoprolol, carvedilol, metoprolol succinate) reduces mortality and improves remodeling

Q8. For rapid symptomatic relief of volume overload in decompensated heart failure which diuretic class is preferred and why?

• Thiazide diuretics because they block NKCC2 in the loop of Henle
• Loop diuretics because they provide potent natriuresis by inhibiting the Na+-K+-2Cl− cotransporter in the thick ascending limb
• Aldosterone antagonists because they produce immediate diuresis
• Carbonic anhydrase inhibitors as first-line agents for pulmonary edema

Correct Answer: Loop diuretics because they provide potent natriuresis by inhibiting the Na+-K+-2Cl− cotransporter in the thick ascending limb

Q9. What is the primary clinical benefit of adding spironolactone or eplerenone in selected HFrEF patients?

• Immediate increase in systolic blood pressure
• Reduction in morbidity and mortality through aldosterone antagonism, but with a risk of hyperkalemia
• Replacement for ACE inhibitors in all patients
• Primary therapy for acute pulmonary edema

Correct Answer: Reduction in morbidity and mortality through aldosterone antagonism, but with a risk of hyperkalemia

Q10. Digoxin exerts its positive inotropic effect mainly by which mechanism and what is a key clinical caveat?

• Beta-adrenergic stimulation; safe at any potassium level
• Inhibition of Na+/K+ ATPase increasing intracellular Na+ and Ca2+; narrow therapeutic index and toxicity risk enhanced by hypokalemia
• ACE inhibition; causes hyperkalemia primarily
• PDE5 inhibition; contraindicated with nitrates

Correct Answer: Inhibition of Na+/K+ ATPase increasing intracellular Na+ and Ca2+; narrow therapeutic index and toxicity risk enhanced by hypokalemia

Q11. Milrinone is used as an inotrope in advanced heart failure — what is its mechanism and main adverse effect concern?

• Beta-1 agonist; causes severe hyperkalemia
• PDE3 inhibition leading to increased cAMP, inotropy and vasodilation; increased arrhythmia risk and hypotension
• ACE inhibition; causes cough
• Calcium channel blockade; leads to bradycardia

Correct Answer: PDE3 inhibition leading to increased cAMP, inotropy and vasodilation; increased arrhythmia risk and hypotension

Q12. Recent trials show SGLT2 inhibitors (e.g., empagliflozin, dapagliflozin) provide which benefit in heart failure patients?

• Only glucose lowering with no cardiovascular benefit
• Reduced hospitalization for heart failure and mortality in HFrEF irrespective of diabetes status
• Major increase in blood pressure limiting their use
• Primary effect is potent negative inotropy

Correct Answer: Reduced hospitalization for heart failure and mortality in HFrEF irrespective of diabetes status

Q13. Hydralazine combined with nitrates is particularly recommended in which clinical scenario in HFrEF?

• As first-line therapy replacing ACE inhibitors in all patients
• As add-on therapy in self-identified African-American patients with advanced HFrEF on optimal therapy, or when ACEi/ARB/ARNI cannot be used
• Only for heart failure with preserved ejection fraction
• To treat bradycardia in heart failure

Correct Answer: As add-on therapy in self-identified African-American patients with advanced HFrEF on optimal therapy, or when ACEi/ARB/ARNI cannot be used

Q14. According to NYHA functional classification, what defines Class IV heart failure?

• Ordinary physical activity does not cause symptoms
• Symptoms occur only during intense exertion
• Symptoms are present at rest and any physical activity leads to discomfort
• No symptoms and no limitation of activity

Correct Answer: Symptoms are present at rest and any physical activity leads to discomfort

Q15. Cardiorenal syndrome in chronic heart failure primarily arises from which sequence?

• Excess renal perfusion causing diuresis and improved cardiac output
• Decreased cardiac output → reduced renal perfusion → neurohormonal activation (RAAS, sympathetic) → sodium/water retention and worsening congestion
• Increased GFR leading to electrolyte loss and hypotension
• ACE inhibitor overuse causing immediate renal recovery

Correct Answer: Decreased cardiac output → reduced renal perfusion → neurohormonal activation (RAAS, sympathetic) → sodium/water retention and worsening congestion

Q16. Orthopnea in left-sided heart failure is best explained by which mechanism?

• Decreased venous return when lying flat
• Lying flat increases venous return and pulmonary capillary hydrostatic pressure causing redistribution of fluid into the lungs
• Right ventricular failure reducing lung perfusion when upright
• Improved lymphatic drainage while standing

Correct Answer: Lying flat increases venous return and pulmonary capillary hydrostatic pressure causing redistribution of fluid into the lungs

Q17. Which commonly used drug class is known to exacerbate heart failure and is generally avoided or used with caution?

• ACE inhibitors
• Nonsteroidal anti-inflammatory drugs (NSAIDs) due to sodium retention and prostaglandin inhibition
• SGLT2 inhibitors
• Loop diuretics

Correct Answer: Nonsteroidal anti-inflammatory drugs (NSAIDs) due to sodium retention and prostaglandin inhibition

Q18. Ivabradine is indicated in chronic HFrEF for which specific patient profile?

• Patients with atrial fibrillation and bradycardia
• Patients in sinus rhythm with resting heart rate ≥70 bpm despite maximally tolerated beta-blocker therapy to reduce hospitalizations
• All HFrEF patients as first-line instead of beta-blockers
• Only for acute decompensated heart failure requiring immediate inotropy

Correct Answer: Patients in sinus rhythm with resting heart rate ≥70 bpm despite maximally tolerated beta-blocker therapy to reduce hospitalizations

Q19. In acute decompensated heart failure with pulmonary congestion but adequate perfusion, which immediate pharmacologic therapy is most appropriate?

• Oral spironolactone as first-line
• Intravenous loop diuretics to rapidly reduce intravascular volume and relieve congestion
• High-dose inotropes as routine initial therapy
• Long-term ACE inhibitor initiation without diuresis

Correct Answer: Intravenous loop diuretics to rapidly reduce intravascular volume and relieve congestion

Q20. Which biomarker is most specific for increased myocardial wall stress and commonly used to assist diagnosis and prognosis in heart failure?

• Serum troponin I as a marker of chronic wall stress
• BNP/NT-proBNP as markers of ventricular wall stress and heart failure severity
• CRP as a direct marker of intracardiac pressure
• Serum creatinine as a heart failure biomarker

Correct Answer: BNP/NT-proBNP as markers of ventricular wall stress and heart failure severity

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