Questions: Heart Failure: Systolic and Diastolic Dysfunction

Question 1

A 68-year-old patient with longstanding hypertension presents with shortness of breath on exertion and elevated BNP. An echocardiogram shows an ejection fraction of 58% (normal). What is the most likely mechanism of their heart failure?

• A. Systolic dysfunction — the ventricle is too weak to eject blood adequately.
• B. Diastolic dysfunction — the ventricle is stiff and cannot relax fully, requiring elevated filling pressures to accept a normal stroke volume.
• C. Valvular disease — the mitral valve is leaking, reducing effective forward flow.
• D. High-output failure — the heart cannot meet the body's elevated metabolic demands.

Answer: (B)

A preserved ejection fraction (≥50%) rules out systolic (HFrEF) as the primary mechanism. This is HFpEF: the ventricle contracts normally but is abnormally stiff — chronically elevated blood pressure causes concentric left ventricular hypertrophy and fibrosis. Impaired relaxation means the ventricle needs higher filling pressures to accept the same stroke volume, and those elevated pressures back up into the pulmonary veins, causing exertional dyspnea and pulmonary edema despite normal contractility. BNP elevation reflects ventricular wall stress from those high filling pressures.

Question 2

In systolic heart failure (HFrEF), the renin-angiotensin-aldosterone system (RAAS) is activated as a compensatory mechanism. However, sustained RAAS activation ultimately worsens the disease primarily by:

• A. Reducing heart rate below the level needed to maintain cardiac output.
• B. Promoting maladaptive ventricular remodeling — the ventricle dilates, becomes more spherical, and wall stress increases by the law of Laplace, further impairing ejection efficiency.
• C. Directly suppressing myocardial contractility through angiotensin receptor effects.
• D. Depleting serum potassium to dangerously low levels, causing arrhythmias.

Answer: (B)

RAAS increases sodium and water retention (boosting preload) and causes vasoconstriction (increasing afterload). Initially, the Frank-Starling mechanism uses the higher preload to maintain stroke volume. Over time, chronic volume overload and neurohormonal stimulation cause pathological cardiac remodeling: the ventricle dilates and assumes a more spherical shape. By the law of Laplace (wall tension = pressure × radius / 2 × wall thickness), dilation increases wall stress, forcing the myocardium to work harder with each beat — accelerating dysfunction. ACE inhibitors and ARBs that block RAAS improve survival by reversing this remodeling.

Question 3

In HFpEF (heart failure with preserved ejection fraction), the left ventricle's contractility is normal, but elevated filling pressures back up into the pulmonary circulation, causing exertional dyspnea even though the ejection fraction is preserved.

• T. True
• F. False

Answer: True

This is the defining physiology of HFpEF. The stiff, non-compliant ventricle cannot relax properly during diastole (impaired lusitropy). To fill adequately, it requires higher end-diastolic pressures — these elevated pressures are transmitted backward through the pulmonary veins and capillaries, causing fluid to leak into the alveoli (pulmonary edema) and producing dyspnea. The systolic function — the squeezing — is intact, so the ejection fraction is normal. The problem is filling, not emptying.

Question 4

A patient with an ejection fraction of 30% (well below normal) but no symptoms of fatigue, dyspnea, or fluid retention has compensated heart failure and does not have true cardiac dysfunction.

• T. True
• F. False

Answer: False

Low ejection fraction does not always cause symptoms — many patients with significantly reduced EF (even <40%) remain asymptomatic for years through neurohormonal compensation (RAAS, sympathetic activation) and cardiac remodeling. This is 'asymptomatic left ventricular dysfunction.' These patients still have cardiac dysfunction and are at high risk for developing symptomatic heart failure and sudden death. Screening and early treatment (ACE inhibitors, beta-blockers) in asymptomatic patients with reduced EF reduces progression to overt heart failure.

Question 5

Why is the neurohormonal compensation in systolic heart failure — specifically sympathetic activation and RAAS — ultimately considered maladaptive, even though it initially helps maintain cardiac output?

Model answer: The compensatory response is designed for acute, short-lived crises (hemorrhage, acute volume loss). In chronic heart failure, sustained activation causes harm: sympathetic stimulation increases afterload and promotes pathological hypertrophy; RAAS-driven sodium retention causes chronic volume overload and ventricular dilation. By the law of Laplace, a dilated, spherical ventricle has greater wall stress, making each contraction less efficient and accelerating failure. Chronically elevated catecholamines also cause myocyte apoptosis and fibrosis. The system designed to rescue cardiac output instead drives the structural remodeling that worsens it — compensation becomes the disease.

This explains why the most effective treatments for HFrEF (ACE inhibitors, beta-blockers, aldosterone antagonists) work by blocking the neurohormonal response rather than directly stimulating the heart. Reducing the maladaptive compensation allows partial reversal of remodeling (reverse remodeling) and improves survival, even in patients who feel better with diuretics alone.