Heart Failure

Heart failure (HF) is a clinical–pathophysiological syndrome in which the heart is unable to pump blood at a rate sufficient to meet the metabolic demands of tissues, or can do so only at the expense of elevated filling pressures. Heart failure may develop acutely or chronically and results from structural or functional abnormalities affecting ventricular filling, contraction, or ejection.

From a pathophysiological perspective, heart failure arises due to impaired myocardial contractility, abnormal loading conditions, or altered ventricular compliance, leading to reduced cardiac output and/or increased intracardiac pressures.

Classification of Heart Failure (Pathophysiological Perspective)

Heart failure can be classified according to several pathophysiological criteria:

• Acute vs chronic
• Left-sided vs right-sided
• Systolic vs diastolic dysfunction
• Low-output vs high-output heart failure

These forms often coexist and evolve over time.

Causes of Heart Failure

The causes of heart failure can be grouped according to the primary pathophysiological mechanism involved.

1. Myocardial Dysfunction

a) Ischemic heart disease

Ischemic heart disease is the most common cause of heart failure in developed countries. Myocardial ischemia and infarction lead to:

• loss of functional cardiomyocytes,
• replacement fibrosis,
• impaired contractility,
• ventricular remodeling.

Acute myocardial infarction may result in acute heart failure, while repeated ischemic injury leads to chronic ischemic cardiomyopathy.

b) Cardiomyopathies

• Dilated cardiomyopathy → systolic dysfunction
• Hypertrophic cardiomyopathy → diastolic dysfunction
• Restrictive cardiomyopathy → impaired ventricular filling

These conditions alter myocardial structure and compliance, leading to progressive heart failure.

2. Pressure Overload

Chronic pressure overload increases ventricular afterload and leads to concentric hypertrophy.

Common causes include:

• systemic arterial hypertension,
• aortic valve stenosis,
• pulmonary hypertension (right ventricular overload).

Initially adaptive hypertrophy eventually becomes maladaptive, resulting in:

• reduced coronary reserve,
• impaired relaxation,
• myocardial fibrosis,
• diastolic and later systolic dysfunction.

3. Volume Overload

Volume overload leads to eccentric ventricular hypertrophy and chamber dilation.

Typical causes include:

• valvular regurgitation (mitral or aortic insufficiency),
• intracardiac shunts,
• chronic fluid retention.

Progressive ventricular dilation increases wall stress and reduces mechanical efficiency, ultimately leading to heart failure.

4. Diastolic Dysfunction (Impaired Ventricular Filling)

Diastolic heart failure occurs when ventricular filling is impaired despite preserved systolic function.

Major causes include:

• ventricular hypertrophy,
• myocardial fibrosis,
• aging-related loss of compliance,
• restrictive cardiomyopathies.

Elevated filling pressures lead to pulmonary or systemic congestion despite normal ejection fraction.

5. Arrhythmias

Arrhythmias may precipitate or worsen heart failure by:

• reducing ventricular filling (tachyarrhythmias),
• causing loss of atrial contribution to ventricular filling,
• producing bradycardia with inadequate cardiac output.

Atrial fibrillation is a frequent contributor to decompensation in chronic heart failure.

6. Pericardial Disease

Conditions such as:

• constrictive pericarditis,
• cardiac tamponade,

limit ventricular filling and reduce cardiac output, resulting in low-output heart failure.

Pathophysiological Mechanisms of Heart Failure

1. Reduced Cardiac Output

Primary myocardial dysfunction or excessive loading conditions reduce stroke volume and cardiac output, leading to:

• tissue hypoperfusion,
• fatigue,
• organ dysfunction.

2. Increased Ventricular Filling Pressures

To maintain cardiac output, ventricular filling pressures rise, resulting in:

• pulmonary congestion (left heart failure),
• systemic venous congestion (right heart failure)

3. Ventricular Remodeling

Structural changes in ventricular geometry include:

• hypertrophy,
• dilation,
• fibrosis.

Although initially compensatory, remodeling ultimately worsens systolic and diastolic function.

4. Neurohumoral Activation

Reduced cardiac output activates compensatory systems:

• sympathetic nervous system,
• renin–angiotensin–aldosterone system (RAAS),
• antidiuretic hormone (ADH).

Chronic activation leads to:

• increased afterload,
• sodium and water retention,
• myocardial toxicity,
• progression of heart failure.

5. Altered Peripheral Circulation

Heart failure causes:

• redistribution of blood flow to vital organs,
• reduced skeletal muscle perfusion,
• impaired renal function,
• worsening fluid retention.

Acute vs Chronic Heart Failure

Acute Heart Failure

• sudden reduction in cardiac output,
• pulmonary edema or cardiogenic shock,
• common causes: myocardial infarction, acute valve failure, arrhythmias.

Chronic Heart Failure

• gradual progression,
• structural remodeling,
• long-term neurohumoral activation,
• episodes of acute decompensation.

Summary

Heart failure results from diverse etiologies that converge on common pathophysiological mechanisms:

• impaired myocardial function,
• abnormal loading conditions,
• maladaptive compensatory responses.

Understanding these mechanisms is essential for explaining both the clinical manifestations and the progressive nature of acute and chronic heart failure.

References

• Kumar V, Abbas AK, Aster JC. Robbins and Cotran Pathologic Basis of Disease. Elsevier.
• Hammer GD, McPhee SJ (eds.). Pathophysiology of Disease: An Introduction to Clinical Medicine. McGraw-Hill Education.
• Maruna P. Examination Tests from Pathological Physiology. Karolinum.