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Chronic Heart Failure

Q: What diuretic classes are used in chronic heart failure?

Management of chronic heart failure utilizes: Loop diuretics — used for rapid elimination of excess fluid.Potassium-sparing diuretics, including aldosterone antagonists — used in combination therapy alongside loop diuretics.Aldosterone antagonists reduce sodium and water retention; examples include spironolactone and eplerenone.

Q: What adverse effects are characteristic of ACE inhibitors?

ACE inhibitors can cause specific adverse drug reactions. Dry cough (tussis) — a specific side effect occurring in five to twenty percent of patients due to bradykinin accumulation; it does not resolve with continued therapy and warrants drug discontinuation.

For medical students2 min readUpdated 2026-10-10

Chronic heart failure is a progressive impairment of the heart's pumping function, leading to peripheral hemodynamic disorders and congestion. The core pathogenesis involves myocardial injury and sustained hyperactivation of neurohormonal systems.

Prevalence1.5–2% in the general population, increasing to 10% in individuals over 65 years of age.

Main ManifestationCongestive syndrome and pathological left ventricular remodeling.

Key SystemsHyperactivation of the sympathetic nervous system (SNS) and the renin-angiotensin-aldosterone system (RAAS).

PharmacotherapyPriority is given to blocking neurohormonal mechanisms and breaking the vicious cycle.

Pathology and Types of Dysfunction

Heart failure develops due to the myocardium's inability to maintain adequate blood flow. There are two main types of impaired contractile and relaxation capacity:

Systolic dysfunction is characterized by a primary decrease in myocardial contractility and a reduced left ventricular ejection fraction. Causes include coronary artery disease, myocardial infarction, myocarditis, and cardiomyopathies.
Diastolic dysfunction develops from secondary myocardial overload while contractility remains preserved. It is triggered by arterial hypertension, valvular heart disease, and arteriovenous shunts, eventually progressing to a mixed form.

Hemodynamic Alterations and Clinical Features

The clinical presentation directly depends on the predominantly affected chambers of the heart:

Left-sided heart failure is accompanied by pulmonary congestion. The acute form presents as pulmonary edema, and dyspnea arises from elevated pulmonary capillary pressure and impaired gas exchange.
Right-sided heart failure causes systemic venous congestion. Clinically, it manifests as tissue hypoxia, acrocyanosis, and dependent peripheral edema.

The disease follows a progressive course accompanied by left ventricular remodeling, including hypertrophy, dilatation, and mitral regurgitation.

Neurohormonal Mechanisms and the Vicious Cycle

Disease progression is sustained by the hyperactivation of compensatory systems. Reduced renal perfusion and a drop in pressure within the vessels of the juxtaglomerular apparatus trigger renin release.

A self-reinforcing loop of interconnected activation is established:

The sympathetic nervous system (SNS) stimulates cardiac adrenergic receptors, causing tachycardia and hypoxia, constricts blood vessels via alpha-receptors, and stimulates renal renin production.
The renin-angiotensin-aldosterone system (RAAS) synthesizes angiotensin II under the action of renin and ACE.
Angiotensin II and subsequent aldosterone production cause potent vasoconstriction, sodium and water retention, and stimulate myocardial fibrosis.

As a result, cardiac preload and afterload increase, worsening congestion.

Principles of Pharmacotherapy

Modern treatment approaches aim to break the pathogenetic vicious cycle and slow myocardial remodeling:

Beta-blockers reduce the impact of the SNS on the heart and block renin secretion.
ACE inhibitors prevent angiotensin II formation, reducing vascular tone and aldosterone levels.
Diuretics effectively eliminate excess sodium and water, reducing edema and lowering preload.
Cardiac glycosides are used for their direct positive inotropic effect to enhance contractility.

Mnemonic

CHF Vicious Cycle: SNS and RAAS engage kidneys and vessels $\rightarrow$ renin, angiotensin, and aldosterone cause congestion, which is treated with blockers, ACE inhibitors, and diuretics.

Frequently asked questions

What drug classes are used for baseline pharmacotherapy in chronic heart failure?

The management of chronic congestive heart failure relies on primary medications that target components of the pathogenetic vicious cycle.

Angiotensin-converting enzyme inhibitors (ACE inhibitors) — block the formation of angiotensin II and affect remodeling.
Diuretics (water pills) — used to reduce edema and decrease cardiac preload.
Beta-blockers — block the influence of the sympathetic nervous system on the myocardium and inhibit renin secretion.
Cardiac glycosides — exert a direct positive inotropic effect on the myocardium.
Vasodilators — belong to the primary drug groups used to treat chronic congestive heart failure.

What is the full mechanism of action of ACE inhibitors in chronic heart failure?

ACE inhibitors effectively slow the progression of heart failure by blocking the ACE enzyme and preventing the conversion of angiotensin I into active angiotensin II, thereby disrupting key pathogenetic links.

Hemodynamic effects (hemodynamics) — reducing the vascular effects of angiotensin II lowers afterload via vasodilation, while reducing adrenal stimulation decreases secondary hyperaldosteronism, lessening fluid retention.
Cardioprotective effect (cardioprotection) — reducing cardiac overload slows myocardial remodeling and structural alterations.

Which specific drugs belong to the cardiac glycosides group?

In pharmacological classification, cardiac glycosides are divided into three groups based on their plant source.

Digitalis glycosides (Digitalis) — include digoxin, acetyldigoxin B, lanatoside C, and digitoxin.
Strophanthus glycosides (Strophanthus) — represented by ouabain or strophanthin G.
Lily of the valley glycosides (Convallaria) — include corglycon and convallatoxin.

What is the mechanism of action of beta-blockers in heart failure?

Beta-blockers are used in combination therapy for heart failure to protect the myocardium from excessive neurohormonal stimulation.

SNS blockade (beta-adrenoreceptors) — these drugs directly block the effects of the sympathetic nervous system on the heart via beta-1 adrenergic receptors.
Reduction of renin secretion (reninum) — they block renin secretion in the kidneys, disrupting the pathological link between the sympathetic nervous and renin-angiotensin systems.

What diuretic classes are used in chronic heart failure?

Management of chronic heart failure utilizes:

Loop diuretics — used for rapid elimination of excess fluid.
Potassium-sparing diuretics, including aldosterone antagonists — used in combination therapy alongside loop diuretics.
Aldosterone antagonists reduce sodium and water retention; examples include spironolactone and eplerenone.

What adverse effects are characteristic of ACE inhibitors?

ACE inhibitors can cause specific adverse drug reactions.

Dry cough (tussis) — a specific side effect occurring in five to twenty percent of patients due to bradykinin accumulation; it does not resolve with continued therapy and warrants drug discontinuation.

What is the difference between systolic and diastolic dysfunction?

Systolic dysfunction is associated with a primary decrease in contractility and a drop in left ventricular ejection fraction. Diastolic dysfunction develops with preserved contractility, but in the setting of increased preload or afterload on the myocardium.

Why is the RAAS activated in heart failure?

A drop in cardiac output leads to systemic congestion and reduced renal perfusion. Decreased pressure in the renal juxtaglomerular vessels, along with SNS stimulation, triggers the release of renin into the blood.

What are the main goals of chronic heart failure pharmacotherapy?

Treatment aims to block neurohormonal systems using beta-blockers and ACE inhibitors, reduce congestion and preload using diuretics, and enhance myocardial contractility with inotropic agents.

Go deeper

NYHA functional classification of heart failure (Classes I–IV)
Role of the vasopressin system and natriuretic peptides in volume regulation
Effects of angiotensin II via AT1 receptors and the development of tissue fibrosis
Myocardial metabolic features and the phenomenon of cardiomyocyte hibernation
Involvement of the endothelin system in vascular tone regulation