Heart failure (HF)

Clinical syndrome caused by structural and functional defects in myocardium resulting in impairment of ventricular filling or the ejection of blood.

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Epidemiology

Global distribution:

Rule of halves:

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Classification

Based on functional status of heart:

Based on left ventricular ejection fraction (LVEF)

• HF with preserved ejection fraction (HFpEF): Normal LVEF (≥ 50%)
  • Normal LV volume , but LV wall is thickened and stiff; hence ↑ ratio of LV mass/end-diastolic volume
• HF with reduced ejection fraction (HFrEF): ↓ LVEF (< 40%)
  • Dilated LV, and normal/↓ LV mass/end-diastolic volume ratio
• HF with mid-range ejection fraction (HFmrEF): LVEF 40-49%
  • LV cavity is typically dilated, and the ratio of LV mass/end-diastolic volume is either normal or reduced.

New York Heart Association (NYHA) functional classification:

Classifies heart failure by symptom severity

American College of Cardiology (ACC)/American Heart Association (AHA) working group classification:

Describes stages of evolution of heart failure

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Etiology

Low output failure (common):

Characterized by insufficient forward cardiac output, particularly during times of increased metabolic demand.

• LV dysfunction d/t large MI
• RV dysfunction d/t acute pulmonary embolus
• Biventricular dysfunction

High-output failure (uncommon):

This occurs as a result of ineffective blood volume and pressure, which stimulate the sympathetic nervous system and renin-angiotensin-aldosterone system (RAAS), causing the release of antidiuretic hormone (ADH), which all together ultimately lead to ventricular enlargement, negative ventricular remodeling and HF.

Characterized by resting cardiac index > 2.5–4.0 L/min/m² and low systemic vascular resistance.

• Severe anemia
• Vascular shunting
• Hyperthyroidism
• Vitamin B1 deficiency

More than two-thirds of all cases of HF are attributable to ischemic heart disease, COPD, hypertensive heart disease, and rheumatic heart disease.

Coronary artery disease (CAD): > 70% of cases

Chronic and acute ischemia causes direct damage to myocardium leading to remodeling and scar formation, resulting in inadequate relaxation in diastole and impaired contraction in systole, which decreases contractility and cardiac output (CO)

• Myocardial infarction (MI): Causes dyssynchronous contraction of the infarcted segment, subsequent remodeling of the ventricle, ventricular dilatation with annular dilation, and mitral regurgitation that predispose to HF and decrease the CO
• Tachyarrhythmias (atrial fibrillation/atrial flutter or non sustained ventricular tachycardia) is common in patients with CAD and can deteriorate the cardiac function more

Hypertension (HTN):

HTN is an independent risk factor for CAD. HTN increases vascular resistance and activates the renin-angiotensin-aldosterone system (RAAS) resulting in a higher afterload, which increases myocardial mass as a compensatory mechanism to maintain a normal CO and that causes left ventricular hypertrophy (LVH). If blood pressure (BP) remains uncontrolled, apoptosis and fibrosis may result. LVH increases the myocardial stiffness and can cause ischemia, which leads to HFpEF or HFrEF.

Chronic obstructive pulmonary disease (COPD):

COPD increases the risk of CAD and other smoking-related illnesses, cardiac dysrhythmias, and can cause pulmonary hypertension and right heart failure.

Valvular heart disease:

Aortic and pulmonary stenosis increases the ventricular afterload and may cause HF. In valve regurgitation, a persistent volume overload can cause ventricular enlargement and functional impairment that may lead to HF.

• Degenerative valve disease (developed countries)
• Rheumatic valve disease (low-income countries)

Cardiomyopathies (CMP):

Functional and structural heart muscle abnormalities in the absence of CAD, HBP, valvular, or congenital heart disease. CMP can cause HFrEF, HFpEF, or HFmrEF.

• Dilated cardiomyopathy (DCM)
• Hypertrophic cardiomyopathy (HCM)
• Restrictive cardiomyopathy (RCM)
• Arrhythmogenic right ventricular cardiomyopathy (ARVC)
• Unclassified cardiomyopathies (isolated noncompaction of the left ventricle [INLV] and Takotsubo syndrome).

Other precipitating causes:

• Infections (especially pneumonia)
• Anaemia
• Alcohol excess
• Iatrogenic cause (eg. postoperative fluid replacement or administration of steroids or NSAIDs)
• Poor drug compliance, especially in antihypertensive treatment
• Thyrotoxicosis
• Pregnancy

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Pathophysiology

Left-sided heart failure:

Right-sided failure:

Neurohormonal activation:

Neurohormonal systems, which are normally stimulated under conditions of acute volume depletion, are activated by the low cardiac output and arterial pressure. However, sustained and chronic activation of these systems, as occurs in congestive heart failure (CHF), can cause progressive ventricular remodeling and worsening heart failure.

Principal neurohumoral systems involved in the response to HF:

• Sympathetic (adrenergic) nervous system (SNS)
• Renin–angiotensin–aldosterone system (RAAS): Maintain cardiac output through increased retention of salt and water,
• Antidiuretic hormone (ADH)

Systolic dysfunction	Diastolic dysfunction
↓ EF	Preserved EF
↑ EDV	Normal EDV
↓ contractility often 2° to ischemia/MI or dilated cardiomyopathy.	↓ compliance (↑ EDP) often 2° to myocardial hypertrophy.

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Presentation

Typical features:

Symptoms are more severe with exertion

• Symptoms secondary to fluid accumulation:
  • Dyspnea, orthopnea
  • Oedema
  • Abdominal discomfort (hepatic congestion)
  • Ascites (in the setting of right heart failure)
• Symptoms due to decreased cardiac output:
  • Fatigue, anorexia, and weakness

Atypical symptoms:

• Nocturnal cough
• Loss of appetite
• Wheezing
• Palpitations
• Depression
• Dizziness, syncope
• Bendopnea (short of breath while bending forward)

Left-sided failure	Failure of either side	Right-sided failure
Tachypnea   Tachycardia Cough Wheezing Rales in chest	Cardiac enlargement   Gallop rhythm (S3) Peripheral cyanosis Small volume pulse Lack of weight gain (children)	Hepatomegaly (nutmeg liver)   Jugular venous engorgement Peripheral oedema

Physical examination:

• Resting sinus tachycardia, diaphoresis, narrow pulse pressure (< 25 mmHg d/t ↓ CO)
• Peripheral vasoconstriction (cool and pale extremities d/t ↓ perfusion)
• Volume overload manifestations:
  • Peripheral edema (extremities edema, ascites, scrotal edema, and hepatosplenomegaly)
  • ↑ Jugular venous pressure (JVP)
  • Pulmonary congestion (rales on examination and pleural effusions)
• Sign of LV enlargement: Displaced apical impulse (laterally past the midclavicular line)
• Sign of RV enlargement: Parasternal lift
• S3 gallop

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Complications

Arrhythmias:

• Atrial fibrillation
• Ventricular arrhythmias (ventricular tachycardia/fibrillation)
• Bradyarrhythmias

Thromboembolism

• Stroke
• Peripheral embolism
• Deep venous thrombosis (DVT)
• Pulmonary embolism

Gastrointestinal complications:

• Hepatic congestion
• Hepatic dysfunction
• Malabsorption

Musculoskeletal complications:

• Muscle wasting

Respiratory complications:

• Pulmonary congestion
• Respiratory muscle weakness
• Pulmonary hypertension (rare)

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Diagnosis

Chest X-ray:

Useful in evaluating heart size, pulmonary congestion and to detect alternative cardio-pulmonary diseases that may cause or contribute to the patient’s symptoms

Transthoracic echocardiography (TTE):

Useful in providing immediate information, including systolic and diastolic function of LV and right ventricle (RV), chamber size, wall thickness, and valve abnormalities.

Differential diagnosis:

• Cardiac arrest and asystole: No cardiac output at all → Sudden death (without treatment)
• Myocardial infarction (“Heart attack“): Heart muscle damage due to insufficient blood supply, usually as a result of a blocked coronary artery. 
• Cardiomyopathy: Problems within the heart muscle, resulting in heart failure.
  • Ischemic cardiomyopathy: Cause of muscle damage is coronary artery disease. 
  • Dilated cardiomyopathy: Muscle damage has resulted in enlargement of the heart. 
  • Hypertrophic cardiomyopathy: Enlargement and thickening of the heart muscle

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Management

Four-pronged management principle:

1. Reducing cardiac load
2. Augmenting myocardial contractility
3. Improving cardiac performance
4. Correcting underlying cause

Medical management:

First-line: Diuretics (↓ volume overload to improve symptoms) + [angiotensin system blocker (ACEi, ARB, or ARNI) or hydralazine + nitrate] + beta-blocker

• Diuretics (thiazides, loop diuretics and potassium sparing) + salt restriction: Reduce oedema by reduction of blood volume and venous pressure for symptomatic relief
• Angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin receptor blockers (ARBs): Neuro-hormonal modification, vasodilatation and improvement in LVEF
  • Alternative (if unresponsive): Hydralazine ± nitrates
• β-adrenergic blockers: Neuro-hormonal modification, improvement in symptoms and LVEF, survival benefit, arrhythmia prevention and control of ventricular rate
• Aldosterone antagonists: Adjunct to other drugs for additive diuresis, heart failure symptom control, improved heart rate variability, decreased ventricular arrhythmias, reduction in cardiac workload, improved LVEF and an increase in survival
• Digoxin: Small increase in cardiac output, improvement in heart failure symptoms and a decreased rate of heart failure hospitalizations
• Anticoagulants: Decrease risk of thromboembolism
• Inotropic agents: Restore organ perfusion and reduce congestion in patients with heart failure with reduced ejection fraction, so as to increase in cardiac output and reduce neuro-humoral activation