Pathophysiology Quiz: Systolic Vs Diastolic Hf
20 questions · exam conditions
0:00
Systolic Vs Diastolic HfQuestion 1 of 20

A new investigational drug is found to promote the phosphorylation of phospholamban. In which type of heart failure would this mechanism be most specifically targeted to improve the primary pathophysiologic defect?

Systolic heart failure, by increasing the calcium sensitivity of troponin C.
Diastolic heart failure, by improving the rate of myocardial relaxation.
Systolic heart failure, by directly inhibiting the maladaptive fibrosis stimulated by angiotensin II.
Diastolic heart failure, by causing peripheral vasodilation to reduce ventricular afterload.
← Back to quizzes

Pathophysiology Quiz

Pathophysiology Quiz: Systolic Vs Diastolic Hf

Practice Systolic Vs Diastolic Hf in Pathophysiology with focused quiz questions that help you check what you know, review explanations, and build confidence with test-style prompts.

What this quiz covers

This quiz focuses on Systolic Vs Diastolic Hf, giving you a quick way to practice the rules, question types, and explanations that matter most for Pathophysiology.

How to use this quiz

Try each quiz question before looking at the correct answer. Use the explanations to review missed ideas, then come back to similar questions until the pattern feels familiar.

All questions

Question 1

A new investigational drug is found to promote the phosphorylation of phospholamban. In which type of heart failure would this mechanism be most specifically targeted to improve the primary pathophysiologic defect?

  1. Systolic heart failure, by increasing the calcium sensitivity of troponin C.
  2. Diastolic heart failure, by improving the rate of myocardial relaxation. (correct answer)
  3. Systolic heart failure, by directly inhibiting the maladaptive fibrosis stimulated by angiotensin II.
  4. Diastolic heart failure, by causing peripheral vasodilation to reduce ventricular afterload.
Explanation: Phospholamban (PLN) is a key regulator of SERCA2a, the pump that returns calcium to the sarcoplasmic reticulum. In its dephosphorylated state, PLN inhibits SERCA2a. Phosphorylation of PLN relieves this inhibition, accelerating calcium re-uptake and thereby enhancing the rate and completeness of myocardial relaxation (lusitropy). This directly addresses the core mechanism of impaired relaxation in diastolic heart failure.

Question 2

A medical student incorrectly states that 'since the ejection fraction is preserved in diastolic heart failure, the patient's stroke volume must be normal.' Why is this statement pathophysiologically incorrect?

  1. Ejection fraction is calculated as stroke volume divided by end-systolic volume, which is abnormally high.
  2. The Frank-Starling mechanism is pathologically suppressed in diastolic failure, invalidating the ejection fraction measurement.
  3. In diastolic failure, end-systolic volume is significantly increased, which directly lowers the calculated stroke volume.
  4. Stroke volume is often reduced because the end-diastolic volume is abnormally low due to impaired filling. (correct answer)
Explanation: When evaluating heart failure with preserved ejection fraction (HFpEF), you need to understand that ejection fraction and stroke volume are related but distinct measurements that can change independently under pathological conditions. The correct answer is D because diastolic heart failure fundamentally involves impaired ventricular filling. The stiff, non-compliant ventricle cannot adequately relax during diastole, resulting in a reduced end-diastolic volume (EDV). Since stroke volume equals EDV minus end-systolic volume (ESV), when EDV decreases significantly while ESV remains relatively unchanged, stroke volume falls. The ejection fraction (EF = stroke volume ÷ EDV) can remain normal because both the numerator (stroke volume) and denominator (EDV) are proportionally reduced. Option A incorrectly describes the ejection fraction formula - it's stroke volume divided by end-diastolic volume, not end-systolic volume. Option B misrepresents the pathophysiology; the Frank-Starling mechanism isn't "suppressed" in diastolic failure, and ejection fraction measurements remain valid. The mechanism simply operates on a shifted curve due to altered preload conditions. Option C contradicts the actual pathophysiology - in diastolic failure, end-systolic volume typically remains normal or may even be reduced, not increased. Remember this key distinction: ejection fraction measures the percentage of blood pumped out, while stroke volume measures the absolute amount. In HFpEF, think "small but efficient" - the heart ejects a normal percentage of a smaller volume, resulting in reduced cardiac output despite preserved ejection fraction.

Question 3

Both systolic and diastolic heart failure are associated with elevated levels of B-type natriuretic peptide (BNP). Which statement provides the most accurate explanation for the significant BNP elevation seen in a patient with pure diastolic dysfunction (HFpEF)?

  1. The stiff, non-compliant ventricle experiences high wall stress during diastolic filling, which is the primary stimulus for BNP release. (correct answer)
  2. BNP is released primarily in response to low systemic arterial pressure, a common finding in HFpEF.
  3. BNP is released from atrial myocytes in response to the volume overload caused by preserved systolic function.
  4. Impaired renal clearance of BNP is the main reason for its elevation, as renal dysfunction is universal in HFpEF.
Explanation: When you encounter questions about BNP elevation in heart failure, focus on the fundamental stimulus for its release: ventricular wall stress. BNP is primarily secreted by ventricular myocytes when they experience mechanical stretch or increased wall tension. In HFpEF (heart failure with preserved ejection fraction), the ventricle becomes stiff and non-compliant due to processes like fibrosis, hypertrophy, or infiltrative disease. During diastolic filling, this rigid ventricle cannot accommodate blood volume easily, creating high intracavitary pressures. According to LaPlace's law, wall stress increases with both pressure and chamber size. Even though the chamber may not be dramatically enlarged in HFpEF, the elevated filling pressures create significant wall stress, triggering BNP release. This makes option A correct. Option B is wrong because HFpEF patients typically have normal or elevated blood pressure, not low arterial pressure. BNP responds to ventricular stretch, not systemic pressure changes. Option C incorrectly identifies the source and mechanism - while atrial stretch can contribute to natriuretic peptide release (specifically ANP), the primary source of BNP elevation in heart failure is ventricular myocytes responding to wall stress, not atrial volume overload. Option D overstates renal dysfunction's role; while kidney disease can reduce BNP clearance, it's not universal in HFpEF, and the primary driver of elevation is increased production due to ventricular stress. Remember: BNP questions often test whether you understand that mechanical stress on ventricular walls - not just reduced ejection fraction - drives BNP release in all forms of heart failure.

Question 4

A clinician is evaluating two patients with classic symptoms of heart failure. Patient A has an LVEF of 35%. Patient B has an LVEF of 55%. Which of the following pathophysiological findings is most likely to be a prominent feature in Patient A but not in Patient B?

  1. Elevated brain natriuretic peptide (BNP) levels.
  2. Evidence of pulmonary congestion on chest x-ray.
  3. A significant increase in left ventricular end-systolic volume. (correct answer)
  4. Presence of a fourth heart sound (S4) on auscultation.
Explanation: Patient A has HFrEF (systolic failure), while Patient B has HFpEF (diastolic failure). The defining hemodynamic abnormality in systolic heart failure is impaired contractility, resulting in the ventricle's failure to empty effectively. This leads to a significant increase in the amount of blood left in the ventricle after contraction (end-systolic volume). In diastolic heart failure, the primary problem is filling, and the end-systolic volume is typically normal or near-normal.

Question 5

In the progression of systolic heart failure following a myocardial infarction, the initial drop in cardiac output triggers neurohormonal activation, including the renin-angiotensin-aldosterone system (RAAS). How does the resulting chronic elevation of angiotensin II contribute to maladaptive ventricular remodeling?

  1. By promoting myocyte relaxation through increased nitric oxide synthesis, improving diastolic function.
  2. By causing systemic vasodilation, which reduces cardiac afterload and decreases myocardial oxygen demand.
  3. By directly stimulating myocyte hypertrophy and interstitial fibrosis via AT1 receptor activation. (correct answer)
  4. By increasing renal sodium excretion and reducing circulating volume via suppression of aldosterone.
Explanation: While initially compensatory, chronic RAAS activation is detrimental. Angiotensin II has direct trophic effects on the heart, mediated by AT1 receptors. It promotes myocyte hypertrophy and stimulates cardiac fibroblasts to produce excess collagen, leading to interstitial fibrosis. This remodeling process further stiffens the ventricle and contributes to the progressive decline of cardiac function in systolic heart failure.

Question 6

A pressure-volume loop analysis is performed on a patient with heart failure. The loop shows a normal end-systolic volume and a preserved ejection fraction. However, the end-diastolic pressure-volume relationship (EDPVR) is shifted upward and to the left compared to normal. This finding is most indicative of:

  1. A primary defect in myocardial systolic force generation.
  2. Chronically elevated cardiac preload from renal failure.
  3. Decreased left ventricular compliance. (correct answer)
  4. A reduction in cardiac afterload due to sepsis.
Explanation: The EDPVR represents the passive stiffness (or compliance) of the ventricle during filling. An upward and leftward shift of this curve means that for any given diastolic volume, the pressure is significantly higher. This is the definition of decreased ventricular compliance or increased stiffness, which is the fundamental mechanical defect in diastolic heart failure (HFpEF).

Question 7

In heart failure with preserved ejection fraction (HFpEF), impaired diastolic relaxation is a key feature. Alterations in which of the following intracellular calcium handling proteins is most directly responsible for this impaired lusitropy?

  1. Increased expression of ryanodine receptor 2 (RyR2), leading to excessive sarcoplasmic reticulum calcium release.
  2. Reduced activity or expression of the sarco/endoplasmic reticulum Ca2+-ATPase (SERCA2a). (correct answer)
  3. Downregulation of the sarcolemmal Na+/K+ ATPase pump, leading to intracellular sodium accumulation.
  4. Constitutive phosphorylation of troponin I, decreasing myofilament sensitivity to calcium.
Explanation: Lusitropy, or myocardial relaxation, is an active, energy-dependent process that largely relies on the re-uptake of cytosolic calcium into the sarcoplasmic reticulum by the SERCA2a pump. In many forms of diastolic dysfunction, the activity or expression of SERCA2a is reduced. This leads to slower removal of calcium from the cytosol, which impairs and prolongs myocyte relaxation, a core mechanism of diastolic heart failure.

Question 8

An S3 gallop is heard in early diastole, while an S4 gallop is heard in late diastole. How do the underlying mechanisms of these two sounds relate to systolic and diastolic heart failure?

  1. An S3 is from atrial contraction against a stiff ventricle (diastolic HF); an S4 is from rapid filling into a dilated ventricle (systolic HF).
  2. Both S3 and S4 are caused by turbulent flow across stenotic valves and are not specific to either type of heart failure.
  3. An S3 reflects rapid filling into a dilated, volume-overloaded ventricle (systolic HF); an S4 reflects atrial contraction into a non-compliant ventricle (diastolic HF). (correct answer)
  4. An S3 is a sign of high afterload common in both HF types; an S4 is a sign of reduced preload and is rare in heart failure.
Explanation: The S3 gallop is generated by the deceleration of blood rushing into a dilated, overly compliant, and volume-overloaded ventricle, a state characteristic of systolic heart failure. The S4 gallop is generated by the forceful contraction of the atrium pushing blood into a pathologically stiff, non-compliant ventricle, which is the hallmark of diastolic dysfunction. Therefore, S3 is associated with systolic HF and S4 with diastolic HF.

Question 9

A 65-year-old male with a history of a large anterior myocardial infarction presents with progressive dyspnea. An echocardiogram reveals a left ventricular ejection fraction (LVEF) of 30% and significant left ventricular dilation. Which of the following best describes the primary pathophysiologic mechanism for his heart failure?

  1. Decreased ventricular compliance causing impaired diastolic filling and pulmonary congestion.
  2. Impaired myocardial contractility leading to a reduced forward stroke volume. (correct answer)
  3. Excessive afterload from systemic hypertension leading to concentric hypertrophy.
  4. Increased preload due to primary mitral valve regurgitation causing left atrial enlargement.
Explanation: The patient's history of myocardial infarction, low ejection fraction (<40%), and dilated ventricle are classic features of systolic heart failure (HFrEF). The fundamental mechanism in HFrEF is the loss of functional myocytes, which leads to impaired myocardial contractility (systolic dysfunction). This inability of the ventricle to pump effectively results in a reduced stroke volume and a high end-systolic volume.

Question 10

A patient with chronic hypertension develops heart failure. Biopsy of the ventricular myocardium shows extensive interstitial fibrosis and an increase in collagen cross-linking. This structural change would most directly impair which phase of the cardiac cycle and contribute to which type of heart failure?

  1. Isovolumetric contraction; Systolic HF.
  2. Ventricular ejection; Systolic HF.
  3. Diastolic filling; Diastolic HF. (correct answer)
  4. Isovolumetric relaxation; Systolic HF.
Explanation: Interstitial fibrosis and collagen cross-linking significantly increase the passive stiffness of the myocardium. This directly impedes the ability of the ventricle to relax and expand to accept blood during diastole. This impairment of ventricular filling is the cardinal feature of diastolic dysfunction, which leads to diastolic heart failure (HFpEF). While relaxation is impaired, the most significant functional consequence is on the overall filling phase.

Question 11

A 72-year-old female with a 20-year history of poorly controlled hypertension complains of exertional dyspnea. Her echocardiogram shows a normal ejection fraction of 58% but reveals significant left ventricular hypertrophy and left atrial enlargement. Which mechanism best explains her symptoms?

  1. Reduced cardiac output at rest due to a primary failure of systolic function.
  2. Elevated left ventricular end-diastolic pressure due to decreased ventricular compliance. (correct answer)
  3. Inadequate ventricular filling time caused by a primary sinus node dysfunction.
  4. A decrease in total blood volume leading to compensatory neurohormonal activation.
Explanation: This clinical picture is characteristic of diastolic heart failure (HFpEF). Chronic hypertension causes pressure overload, leading to concentric left ventricular hypertrophy. This makes the ventricle stiff and non-compliant, impairing its ability to relax and fill during diastole. Consequently, the left ventricular end-diastolic pressure (LVEDP) rises significantly, which is transmitted backward to the left atrium and pulmonary circulation, causing pulmonary congestion and dyspnea, especially on exertion.

Question 12

A patient with well-compensated diastolic heart failure (HFpEF) and concentric hypertrophy is asked to walk briskly on a treadmill. Which of the following mechanisms best explains why they rapidly develop dyspnea?

  1. The exercising muscles extract excessive oxygen, causing systemic hypoxia and a reflex increase in respiratory rate.
  2. The exercise-induced tachycardia shortens diastolic filling time, which a non-compliant ventricle cannot tolerate, causing a sharp rise in left atrial pressure. (correct answer)
  3. The drop in systemic vascular resistance during exercise causes profound hypotension and coronary malperfusion.
  4. Catecholamine release during exercise paradoxically decreases myocardial contractility, leading to acute systolic failure.
Explanation: In HFpEF, the stiff, non-compliant left ventricle requires adequate time to fill. During exercise, the heart rate increases, which shortens the duration of diastole more than systole. This reduced filling time is poorly tolerated, leading to a smaller end-diastolic volume and thus a limited ability to increase stroke volume. Simultaneously, the increased venous return against a stiff ventricle causes a rapid rise in left atrial and pulmonary venous pressures, leading to acute pulmonary congestion and dyspnea.

Question 13

In heart failure with preserved ejection fraction (HFpEF), impaired diastolic relaxation is a key feature. Alterations in which of the following intracellular calcium handling proteins is most directly responsible for this impaired lusitropy?

  1. Increased expression of ryanodine receptor 2 (RyR2), leading to excessive sarcoplasmic reticulum calcium release.
  2. Reduced activity or expression of the sarco/endoplasmic reticulum Ca2+-ATPase (SERCA2a). (correct answer)
  3. Downregulation of the sarcolemmal Na+/K+ ATPase pump, leading to intracellular sodium accumulation.
  4. Constitutive phosphorylation of troponin I, decreasing myofilament sensitivity to calcium.
Explanation: Lusitropy, or myocardial relaxation, is an active, energy-dependent process that largely relies on the re-uptake of cytosolic calcium into the sarcoplasmic reticulum by the SERCA2a pump. In many forms of diastolic dysfunction, the activity or expression of SERCA2a is reduced. This leads to slower removal of calcium from the cytosol, which impairs and prolongs myocyte relaxation, a core mechanism of diastolic heart failure.

Question 14

A clinician is evaluating two patients with classic symptoms of heart failure. Patient A has an LVEF of 35%. Patient B has an LVEF of 55%. Which of the following pathophysiological findings is most likely to be a prominent feature in Patient A but not in Patient B?

  1. Elevated brain natriuretic peptide (BNP) levels.
  2. Evidence of pulmonary congestion on chest x-ray.
  3. A significant increase in left ventricular end-systolic volume. (correct answer)
  4. Presence of a fourth heart sound (S4) on auscultation.
Explanation: Patient A has HFrEF (systolic failure), while Patient B has HFpEF (diastolic failure). The defining hemodynamic abnormality in systolic heart failure is impaired contractility, resulting in the ventricle's failure to empty effectively. This leads to a significant increase in the amount of blood left in the ventricle after contraction (end-systolic volume). In diastolic heart failure, the primary problem is filling, and the end-systolic volume is typically normal or near-normal.

Question 15

A patient with well-compensated diastolic heart failure (HFpEF) and concentric hypertrophy is asked to walk briskly on a treadmill. Which of the following mechanisms best explains why they rapidly develop dyspnea?

  1. The exercising muscles extract excessive oxygen, causing systemic hypoxia and a reflex increase in respiratory rate.
  2. The exercise-induced tachycardia shortens diastolic filling time, which a non-compliant ventricle cannot tolerate, causing a sharp rise in left atrial pressure. (correct answer)
  3. The drop in systemic vascular resistance during exercise causes profound hypotension and coronary malperfusion.
  4. Catecholamine release during exercise paradoxically decreases myocardial contractility, leading to acute systolic failure.
Explanation: In HFpEF, the stiff, non-compliant left ventricle requires adequate time to fill. During exercise, the heart rate increases, which shortens the duration of diastole more than systole. This reduced filling time is poorly tolerated, leading to a smaller end-diastolic volume and thus a limited ability to increase stroke volume. Simultaneously, the increased venous return against a stiff ventricle causes a rapid rise in left atrial and pulmonary venous pressures, leading to acute pulmonary congestion and dyspnea.

Question 16

A pressure-volume loop analysis is performed on a patient with heart failure. The loop shows a normal end-systolic volume and a preserved ejection fraction. However, the end-diastolic pressure-volume relationship (EDPVR) is shifted upward and to the left compared to normal. This finding is most indicative of:

  1. A primary defect in myocardial systolic force generation.
  2. Chronically elevated cardiac preload from renal failure.
  3. Decreased left ventricular compliance. (correct answer)
  4. A reduction in cardiac afterload due to sepsis.
Explanation: The EDPVR represents the passive stiffness (or compliance) of the ventricle during filling. An upward and leftward shift of this curve means that for any given diastolic volume, the pressure is significantly higher. This is the definition of decreased ventricular compliance or increased stiffness, which is the fundamental mechanical defect in diastolic heart failure (HFpEF).

Question 17

A new investigational drug is found to promote the phosphorylation of phospholamban. In which type of heart failure would this mechanism be most specifically targeted to improve the primary pathophysiologic defect?

  1. Systolic heart failure, by increasing the calcium sensitivity of troponin C.
  2. Diastolic heart failure, by improving the rate of myocardial relaxation. (correct answer)
  3. Systolic heart failure, by directly inhibiting the maladaptive fibrosis stimulated by angiotensin II.
  4. Diastolic heart failure, by causing peripheral vasodilation to reduce ventricular afterload.
Explanation: Phospholamban (PLN) is a key regulator of SERCA2a, the pump that returns calcium to the sarcoplasmic reticulum. In its dephosphorylated state, PLN inhibits SERCA2a. Phosphorylation of PLN relieves this inhibition, accelerating calcium re-uptake and thereby enhancing the rate and completeness of myocardial relaxation (lusitropy). This directly addresses the core mechanism of impaired relaxation in diastolic heart failure.

Question 18

A patient is diagnosed with restrictive cardiomyopathy due to cardiac amyloidosis. They present with signs of severe heart failure, but their echocardiogram shows a normal ejection fraction. The fundamental mechanism of their heart failure is most similar to that seen in:

  1. Heart failure secondary to a large, acute myocardial infarction.
  2. Heart failure caused by chronic, severe aortic regurgitation.
  3. Heart failure associated with long-standing, untreated hypertension. (correct answer)
  4. High-output heart failure from a large arteriovenous fistula.
Explanation: Restrictive cardiomyopathy, caused by infiltration of the myocardium by substances like amyloid, results in extremely stiff, non-compliant ventricular walls. This severely impairs diastolic filling, leading to HFpEF. This underlying mechanism—impaired filling due to pathologic stiffness—is the same fundamental problem as in the most common form of diastolic heart failure, which is caused by the concentric hypertrophy resulting from long-standing hypertension.

Question 19

A medical student incorrectly states that 'since the ejection fraction is preserved in diastolic heart failure, the patient's stroke volume must be normal.' Why is this statement pathophysiologically incorrect?

  1. Ejection fraction is calculated as stroke volume divided by end-systolic volume, which is abnormally high.
  2. The Frank-Starling mechanism is pathologically suppressed in diastolic failure, invalidating the ejection fraction measurement.
  3. In diastolic failure, end-systolic volume is significantly increased, which directly lowers the calculated stroke volume.
  4. Stroke volume is often reduced because the end-diastolic volume is abnormally low due to impaired filling. (correct answer)
Explanation: When evaluating heart failure with preserved ejection fraction (HFpEF), you need to understand that ejection fraction and stroke volume are related but distinct measurements that can change independently under pathological conditions. The correct answer is D because diastolic heart failure fundamentally involves impaired ventricular filling. The stiff, non-compliant ventricle cannot adequately relax during diastole, resulting in a reduced end-diastolic volume (EDV). Since stroke volume equals EDV minus end-systolic volume (ESV), when EDV decreases significantly while ESV remains relatively unchanged, stroke volume falls. The ejection fraction (EF = stroke volume ÷ EDV) can remain normal because both the numerator (stroke volume) and denominator (EDV) are proportionally reduced. Option A incorrectly describes the ejection fraction formula - it's stroke volume divided by end-diastolic volume, not end-systolic volume. Option B misrepresents the pathophysiology; the Frank-Starling mechanism isn't "suppressed" in diastolic failure, and ejection fraction measurements remain valid. The mechanism simply operates on a shifted curve due to altered preload conditions. Option C contradicts the actual pathophysiology - in diastolic failure, end-systolic volume typically remains normal or may even be reduced, not increased. Remember this key distinction: ejection fraction measures the percentage of blood pumped out, while stroke volume measures the absolute amount. In HFpEF, think "small but efficient" - the heart ejects a normal percentage of a smaller volume, resulting in reduced cardiac output despite preserved ejection fraction.

Question 20

Both systolic and diastolic heart failure are associated with elevated levels of B-type natriuretic peptide (BNP). Which statement provides the most accurate explanation for the significant BNP elevation seen in a patient with pure diastolic dysfunction (HFpEF)?

  1. The stiff, non-compliant ventricle experiences high wall stress during diastolic filling, which is the primary stimulus for BNP release. (correct answer)
  2. BNP is released primarily in response to low systemic arterial pressure, a common finding in HFpEF.
  3. BNP is released from atrial myocytes in response to the volume overload caused by preserved systolic function.
  4. Impaired renal clearance of BNP is the main reason for its elevation, as renal dysfunction is universal in HFpEF.
Explanation: When you encounter questions about BNP elevation in heart failure, focus on the fundamental stimulus for its release: ventricular wall stress. BNP is primarily secreted by ventricular myocytes when they experience mechanical stretch or increased wall tension. In HFpEF (heart failure with preserved ejection fraction), the ventricle becomes stiff and non-compliant due to processes like fibrosis, hypertrophy, or infiltrative disease. During diastolic filling, this rigid ventricle cannot accommodate blood volume easily, creating high intracavitary pressures. According to LaPlace's law, wall stress increases with both pressure and chamber size. Even though the chamber may not be dramatically enlarged in HFpEF, the elevated filling pressures create significant wall stress, triggering BNP release. This makes option A correct. Option B is wrong because HFpEF patients typically have normal or elevated blood pressure, not low arterial pressure. BNP responds to ventricular stretch, not systemic pressure changes. Option C incorrectly identifies the source and mechanism - while atrial stretch can contribute to natriuretic peptide release (specifically ANP), the primary source of BNP elevation in heart failure is ventricular myocytes responding to wall stress, not atrial volume overload. Option D overstates renal dysfunction's role; while kidney disease can reduce BNP clearance, it's not universal in HFpEF, and the primary driver of elevation is increased production due to ventricular stress. Remember: BNP questions often test whether you understand that mechanical stress on ventricular walls - not just reduced ejection fraction - drives BNP release in all forms of heart failure.