7: Pathophysiology of Heart Failure

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Questions and Answers

Which of the following best describes heart failure?

A condition where blood flow to the heart is completely blocked.

A condition where the heart pumps blood at an accelerated rate.

A state in which the heart is unable to pump blood at a sufficient rate to meet the body's demands. (correct)

A condition where the heart muscle is excessively strong.

What is the primary characteristic of systolic heart failure (HFrEF)?

Increased filling of the ventricle during diastole.

Reduced stiffness of the ventricular wall.

Impaired ability of the ventricle to contract effectively. (correct)

Increased ventricular compliance.

How does diastolic dysfunction (HFpEF) primarily affect the heart?

It has no effect on the heart's ability to fill during diastole.

It increases the end-systolic volume.

It increases the heart's contractility.

It reduces the heart's ability to relax and fill with blood. (correct)

How does systolic dysfunction typically alter the Frank-Starling curve?

The curve shifts downward and to the right. (A) Signup and view all the answers

Which of the following best describes a consequence of neurohumoral compensatory responses in heart failure?

They initially help maintain cardiac output but can become harmful over time. (D) Signup and view all the answers

How is the cardiovascular response to exercise typically affected by heart failure?

Exercise capacity is reduced due to limited increases in cardiac output. (C) Signup and view all the answers

What is the primary characteristic of heart failure with reduced ejection fraction (HFrEF)?

Decreased ability of the heart to contract effectively. (C) Signup and view all the answers

Which of these is a common cause of heart failure with preserved ejection fraction (HFpEF)?

Ventricular concentric hypertrophy due to chronic hypertension (C) Signup and view all the answers

Which of the following is NOT a direct effect of the activation of the Renin-Angiotensin-Aldosterone System (RAAS) in heart failure?

Vasodilation of systemic blood vessels. (C) Signup and view all the answers

What triggers the release of atrial natriuretic peptide (ANP)?

Sympathetic activation, atrial stretch, and angiotensin II. (B) Signup and view all the answers

Which of the following is a consequence of increased blood volume in heart failure?

Increased venous pressures leading to edema. (B) Signup and view all the answers

What is a direct consequence of acute systolic dysfunction on the Frank-Starling curve?

Decrease in stroke volume at a given ventricular preload. (D) Signup and view all the answers

What is a characteristic change observed in pressure-volume loops as a result of acute systolic dysfunction?

A reduction in the area within the P-V loop, indicating a reduction in stroke work (A) Signup and view all the answers

Which of the following physiological responses is NOT a compensatory mechanism for acute systolic dysfunction?

Decreased heart rate due to parasympathetic activation (B) Signup and view all the answers

Which of the following best describes the relationship between cardiac 'stiffness' and ventricular compliance?

Compliance is inversely related to cardiac stiffness. (D) Signup and view all the answers

In the context of ventricular filling, what does increased ventricular compliance imply?

A lower end-diastolic pressure (EDP) for a given end-diastolic volume (EDV). (A) Signup and view all the answers

What is the immediate effect of acute ventricular dysfunction on the ventricular compliance curve?

It shifts the curve up and to the left, leading to higher EDP. (A) Signup and view all the answers

What is a key consequence of chronic ventricular dysfunction on ventricular structure?

Increased compliance and increased EDV. (A) Signup and view all the answers

How does chronic ventricular remodeling affect the end-diastolic pressure (EDP) relative to the increase caused by acute dysfunction?

It attenuates the increase in EDP that was caused by acute dysfunction. (C) Signup and view all the answers

What effect does loss of intrinsic inotropy have on the end-systolic pressure-volume relationship (ESPVR) in chronic systolic dysfunction?

Depresses the ESPVR. (D) Signup and view all the answers

In chronic systolic dysfunction, what is the relationship between the increase in end-systolic volume (ESV) and the increase in end-diastolic volume (EDV)?

Increase in ESV is greater than the increase in EDV. (B) Signup and view all the answers

Compared to a normal stroke volume of 70 mL, what is a typical stroke volume in chronic systolic dysfunction, according to the content?

Approximately 50 mL. (C) Signup and view all the answers

How does chronic systolic dysfunction affect the ejection fraction (EF) compared to a normal EF?

Leads to lower ejection fraction. (C) Signup and view all the answers

What is a cardinal sign of chronic systolic dysfunction according to the content?

Decreased ejection fraction due to an increase in end-systolic volume and a decrease in stroke volume. (B) Signup and view all the answers

What primarily leads to increased filling pressures in heart failure with preserved ejection fraction (HFpEF)?

Reduced diastolic compliance (B), Increased blood volume (D) Signup and view all the answers

Which of the following best describes the relationship between end-diastolic volume (EDV) and end-diastolic pressure (EDP) during diastolic dysfunction?

EDV decreases and EDP increases (A) Signup and view all the answers

What is the net effect of combined systolic and diastolic dysfunction on stroke volume (SV) and ejection fraction (EF)?

Decreased SV and decreased EF (C) Signup and view all the answers

How are the exercise responses of a heart failure patient at rest compared to a normal individual?

Heart failure patients have a lower resting stroke volume (D) Signup and view all the answers

What is primarily responsible for the impaired exercise response in heart failure patients?

Reduced inotropic responsiveness (A) Signup and view all the answers

What does an increase in end-systolic volume (ESV) due to systolic dysfunction primarily indicate?

Decreased peak systolic pressure (C) Signup and view all the answers

Study Notes

Pathophysiology of Heart Failure

Heart failure is the inability of the heart to deliver adequate blood flow and oxygen to organs, or to do this only at elevated filling pressures.

Learning Objectives

Define heart failure and list major causes
Differentiate between systolic (HFrEF) and diastolic dysfunction (HFpEF)
Explain how systolic dysfunction affects Frank-Starling curves, pressure-volume loops (EDV, ESV, EF), and ventricular compliance
Explain how diastolic dysfunction affects ventricular compliance and pressure-volume loops (EDV, ESV, EF)
Describe the beneficial and deleterious effects of neurohumoral compensatory responses to heart failure
Describe how heart failure impairs the cardiovascular responses to exercise

Definition of Heart Failure

Inability of the heart to deliver adequate blood flow and oxygen to organs or perform this task only at elevated filling pressures.

Two Major Categories of Heart Failure

Heart Failure with Reduced Ejection Fraction (HFrEF):
- Systolic dysfunction: Loss of the heart's ability to contract, resulting in decreased forward flow and clinical symptoms. Ejection Fraction (EF) ≤40%.
Heart Failure with Preserved Ejection Fraction (HFpEF):
- Diastolic dysfunction: Impaired ventricular filling with elevated filling pressures leading to decreased forward flow and clinical symptoms. Ejection Fraction (EF) ≥50%.

Causes of Heart Failure

HFrEF:
- Ischemic heart disease and infarction
- Dilated cardiomyopathies
- Myocarditis
- Persistent tachycardia
- Chronic volume and pressure overload
- Valve disease
- Chronic hypertension
- Congenital cardiac defects
- Pregnancy
HFpEF:
- Ventricular concentric hypertrophy caused by:
  - Chronic hypertension
  - Aortic valve stenosis
  - Genetic defect (hypertrophic cardiomyopathy, HCM)
- Restrictive cardiomyopathy
- Cardiac tamponade
- Impaired relaxation (e.g., ischemia)

Neurohumoral Compensation in Heart Failure

Sympathetic nerves and catecholamine release are activated by:
- Baroreceptor reflex (acute failure)
- Cardiac stretch receptors
- Chronic, central sympathetic activation
- Increased circulating angiotensin II (peripheral and central effects)
RAAS activated by:
- Reduced renal perfusion
- Increased sympathetic activity
- Enhanced release of vasopressin (stimulated by sympathetic activation and angiotensin II) and ANP (stimulated by atrial distension)

Summary of Neurohumoral Responses to Heart Failure

Increased systemic vascular resistance, arterial pressure and blood volume, and venous pressures
Increased blood volume leads to pulmonary and systemic edema.
This response of the body’s systems causes the heart to work harder.

Sympathetic Activation and Catecholamine Release

Acute heart failure:
- Hypotension causes decreased firing of arterial baroreceptors, leading to reflex sympathetic activation.
- Sympathetic stimulation releases adrenal catecholamines.
Chronic heart failure:
- Central activation of the sympathetic system is stimulated by angiotensin and cardiopulmonary receptors.

Renin-Angiotensin-Aldosterone System (RAAS) Activation

Activated by:
- Reduced renal perfusion
- Sympathetic stimulation
Causes:
- Renal retention of sodium and water
- Increased blood volume and venous pressures
- Vascular constriction
- Stimulates vasopressin (ADH) release
- Enhance sympathetic activity
- Cardiac remodeling

Natriuretic Peptides (ANP)

Release:
- Synthesized and released by atria
- Release stimulated by atrial stretch
- Sympathetic stimulation
- Angiotensin II (AII)
Actions:
- Inhibits RAAS system, promoting natriuresis and diuresis.
- Causes arterial and venous vasodilation
- Lowers arterial and venous pressures

Vasopressin (ADH) Release

Activated by:
- Sympathetic stimulation
- Increased angiotensin II
- Hyperosmolarity
- Decreased atrial receptor firing
Causes:
- Renal reabsorption of water (H2O)
- Increased blood volume and venous pressures
- Arterial constriction

Benefits of Neurohumoral Activation

Increased blood volume helps maintain stroke volume via the Frank-Starling mechanism.
Cardiac stimulation and systemic vasoconstriction help maintain arterial pressure to support vital organ perfusion.
Cardiac remodeling

Deleterious Effects of Neurohumoral Activation

Increased blood volume causes increased venous pressures, leading to pulmonary and systemic edema.
Systemic vasoconstriction increases afterload and impairs ventricular ejection.
Stimulates molecular and biochemical changes that promote cardiac dysfunction over time.
Promotes arrhythmias.

Heart Failure Signs and Symptoms

Cause(s):
- Exertional dyspnea: Pulmonary edema, affecting gas exchange; chemoreceptor responses
- Exercise intolerance: Impaired oxygen delivery to muscles.
- Cognition deficits, Fatigue: Impaired brain and peripheral blood flow
- Cough or wheezing: Pulmonary edema caused left heart failure, increased blood volume
- Swelling of legs, abdomen: Systemic edema, caused by right heart failure, increased blood volume.
- Arrhythmias: Remodeling of cardiac chambers (stretching, hypertrophy); myocardial ischemia.
- Cardiac murmurs : Chamber dilation, causing valve regurgitation

Systolic Dysfunction

Acute loss of inotropy reduces Stroke Volume (SV) and Ejection Fraction (EF) at a given ventricular preload.
Cardiac compensation includes ventricular dilation (may not involve remodeling), increased end-diastolic volume and pressure, and increased heart rate.
Acute systolic dysfunction results in reduced SV, resulting in a decreased stroke work.

Effects of Acute Systolic Dysfunction on Pressure-Volume Loops

Loss of intrinsic inotropy (↓ESPVR) causes a reduction in stroke volume.
This is followed by a decrease in systolic and diastolic aortic pressures
Cardiac compensation includes ventricular passive dilation (not remodeling), increased end-diastolic volume and pressure, and increased heart rate.

Acute vs. Chronic Systolic Dysfunction and Ventricular Compliance

Ventricular compliance is inversely related to cardiac stiffness.
Acute dysfunction moves up the normal ventricular compliance curve, resulting in an elevated end-diastolic pressure.
Chronic dysfunction leads to increased compliance and end-diastolic volume, but reduces the increase in end-diastolic pressure

Effects of Chronic Systolic Dysfunction on Ventricular Pressure-Volume Relationship

Loss of inotropy leads to decreased systolic pressure reserve (ESPVR).
Chronic dilation (remodeling) increases compliance but results in a decreased end-diastolic volume/pressure reserve.

HFrEF: Cardiopulmonary & Systemic Changes

Reduced stroke volume (SV) and Ejection Fraction (EF).
Increased filling pressures (elevated LVEDV, LVEDP, LAP, RVEDP, and RAP, pulmonary pressures).
Pulmonary congestion and edema
Increased blood volume
Systemic edema

Diastolic Dysfunction

Reduced ventricular compliance leads to increased end-diastolic pressure (EDP).
A given EDV leads to increased pressure.
Diastolic dysfunction often increases end-diastolic pressure (EDP).

Effects of Diastolic Dysfunction on Ventricular Pressure-Volume Relationship

Reduced ventricular compliance leads to lower preload volume (EDV) and higher preload pressure (EDP).
Reduced stroke volume (SV) may result from reduced afterload.
Ratio of stroke volume to EDV may not change significantly

HFpEF: Cardiopulmonary & Systemic Changes

Reduced Stroke Volume (SV), but normal Ejection Fraction (EF).
Increased filling pressures (elevated LVEDV, LVEDP, LAP, RVEDP, and RAP, pulmonary pressures).
Pulmonary congestion and edema.
Increased blood volume.
Systemic edema.

Combined Systolic and Diastolic Dysfunction

Decreased ejection (systolic dysfunction) leads to increased End-systolic Volume (ESV) and reduced peak systolic pressure.
Decreased filling (diastolic dysfunction) leads to decreased End-diastolic volume (EDV) and reduced preload pressure.
Results in reduced stroke volume (SV) and ejection fraction (EF), increased end-diastolic pressure (EDP), and reduced stroke work.

Impaired Exercise Responses in Heart Failure

Maximal cardiac output is reduced, limited by dyspnea and fatigue.
Normal increases in stroke volume are reduced.
Impaired inotropic responses in heart failure patients.
Dyspnea and muscle fatigue limit exercise.
Impaired gas exchange, caused by pulmonary congestion/edema and impaired pulmonary perfusion, coupled to respiratory fatigue.
Skeletal muscle fatigue caused by insufficient oxygen delivery.

CV responses in CHF patients

Maximal cardiac output is reduced.
Maximal heart rate is limited by dyspnea and fatigue.
Normal increases in stroke volume are reduced.
Impaired inotropic responses (particularly in HFrEF patients).
Dyspnea and muscle fatigue limit exercise response and causes impaired gas exchange, caused by pulmonary congestion and edema and impaired pulmonary perfusion/coupled to respiratory fatigue.
Skeleteal muscle fatigue resulting from insufficient oxygen delivery to contracting muscles.

Answers to Questions

Q1: Decreased ventricular compliance (D) causes ESV to increase and SV to decrease during systolic dysfunction.
Q2: Reducing afterload with arterial vasodilation helps improve left ventricular ejection during systolic dysfunction because it increases myocyte shortening velocity and ejection velocity, which then decreases ESV and ultimately increases stroke volume (SV). (D)
Q3: Left ventricular diastolic dysfunction causes pulmonary edema because it leads to increases in LVEDP and LVEDV, thus increasing pulmonary capillary hydrostatic pressure. (C)

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Description

Test your knowledge on heart failure and its mechanisms with this quiz. Learn about the characteristics of systolic and diastolic dysfunction, neurohumoral responses, and the effects of the Renin-Angiotensin-Aldosterone System. This quiz is essential for understanding cardiovascular health.