Essence of the pathology and types of dysfunction
Heart failure develops due to the inability of the myocardium to provide adequate blood flow. There are two main types of impaired contractility and relaxation:
- Systolic dysfunction is characterized by a primary decrease in myocardial contractility and a reduced left ventricular ejection fraction. Its causes include coronary artery disease, myocardial infarction, myocarditis, and cardiomyopathies.
- Diastolic dysfunction develops with secondary myocardial overload against the background of preserved contractility. It is triggered by arterial hypertension, valvular heart disease, and arteriovenous shunts, eventually progressing to a mixed form.
Hemodynamic disorders and clinical presentation
The clinical picture directly depends on the predominant involvement of the heart chambers:
- Left ventricular failure is accompanied by congestion in the pulmonary circulation (in the lungs). The acute form manifests as pulmonary edema, and dyspnea occurs due to increased pressure in the pulmonary capillaries and impaired gas exchange.
- Right ventricular failure causes congestion in the systemic circulation. Clinically, it is expressed by tissue hypoxia, acrocyanosis, and the appearance of dependent peripheral edema.
The disease has a progressive course accompanied by left ventricular remodeling—its hypertrophy, dilatation, and mitral regurgitation.
Neurohumoral mechanisms and the vicious circle
The progression of the pathology is sustained by the hyperactivation of compensatory systems. Decreased renal perfusion and a drop in pressure in the vessels of the juxtaglomerular apparatus trigger the release of renin.
A closed loop of interrelated activation is formed:
- Sympathoadrenal system (SAS) stimulates cardiac adrenoceptors, causing tachycardia and hypoxia, constricts blood vessels via alpha receptors, and stimulates renin production in the kidneys.
- Renin-angiotensin-aldosterone system (RAAS) synthesizes angiotensin II under the action of renin and ACE.
- Angiotensin II and the resulting aldosterone cause powerful vasoconstriction, sodium and water retention, and stimulate myocardial fibrosis.
As a result, cardiac preload and afterload increase, exacerbating congestive symptoms.
Principles of pharmacotherapy
The modern treatment approach aims to break the pathogenetic vicious circle and slow down myocardial remodeling:
- Beta-blockers reduce the effect of the SAS on the heart and block renin secretion.
- ACE inhibitors prevent the formation of angiotensin II, reducing vascular tone and aldosterone levels.
- Diuretics effectively remove excess sodium and water, reducing edema and decreasing preload.
- Cardiac glycosides are used as agents with a direct positive inotropic effect to enhance contractility.
Briefly: answers to topical questions
Which drug groups are used for the basic pharmacotherapy of chronic heart failure?
For the treatment of chronic congestive heart failure, basic medications are used that target the links of the pathogenetic vicious circle.
- Angiotensin-converting enzyme inhibitors (ACE inhibitors) block the formation of angiotensin II and affect remodeling.
- Diuretics (diuretic agents) are used to reduce edema and decrease cardiac preload.
- Beta-blockers block the effect of the sympathoadrenal system on the myocardium and renin secretion.
- Cardiac glycosides exert a direct positive inotropic effect on the myocardium.
- Vasodilators belong to the main groups of drugs for the treatment of chronic congestive heart failure.
What is the complete mechanism of action of ACE inhibitors in chronic heart failure?
ACE inhibitors effectively slow down the progression of heart failure by blocking the ACE enzyme and preventing the conversion of angiotensin I into active angiotensin II, which disrupts key pathogenetic links.
- Hemodynamic effects (hemodynamics)—reducing the effect of angiotensin II on blood vessels decreases afterload via vasodilation, and reducing the effect on the adrenal glands decreases secondary hyperaldosteronism, mitigating fluid retention.
- Cardioprotective effect (cardioprotection)—reducing cardiac overload slows down the processes of myocardial remodeling and structural restructuring.
Which specific drugs belong to the cardiac glycosides group?
In pharmacological classification, cardiac glycoside drugs are divided into three groups depending on the source plant.
- Foxglove glycosides (Digitalis) include digoxin, acetyldigoxin B, lanatoside C, and digitoxin.
- Strophanthus glycosides (Strophanthus) are 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 the complex therapy of heart failure to protect the myocardium from excessive neurohumoral stimulation.
- Blockade of SAS influence (beta-adrenoreceptors)—drugs directly block the effect of the sympathoadrenal system on the heart via beta-1 adrenoreceptors.
- Reduction of renin secretion (reninum)—they block renin secretion in the kidneys, which breaks the pathological connection between the sympathoadrenal and renin-angiotensin systems.
Which groups of diuretics are used in chronic heart failure?
In chronic heart failure, the following are used:
- Loop diuretics are used for rapid elimination of excess fluid.
- Potassium-sparing diuretics, including aldosterone antagonists, are used in combination therapy with loop diuretics.
- Aldosterone antagonists reduce sodium and water retention; these include spironolactone and eplerenone.
What adverse effects are typical for ACE inhibitors?
During the use of ACE inhibitors, specific adverse reactions from the body may develop.
- Dry cough (tussis) is a specific adverse effect that develops in five to twenty percent of patients due to bradykinin accumulation, does not stop with continued therapy, and serves as an indication for drug withdrawal.
The vicious circle of CHF: SAS and RAAS involve the kidneys and blood vessels $\rightarrow$ renin, angiotensin, and aldosterone create congestion, which is treated with blockers, ACE inhibitors, and diuretics.
Class and exam questions
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 against the background of myocardial overload by preload or afterload.
Why is the RAAS activated in heart failure?
A drop in cardiac output leads to systemic congestion and decreased renal perfusion. A drop in pressure in the vessels of the renal juxtaglomerular apparatus, as well as stimulation by the sympathoadrenal system, causes the release of renin into the blood.
What are the main directions in the pharmacotherapy of CHF?
Treatment aims to block neurohumoral systems using beta-blockers and ACE inhibitors, reduce congestion and preload using diuretics, and enhance myocardial contractility with cardiotonic agents.
What else to study on this topic
- Functional classification of heart failure by NYHA (classes I–IV)
- Role of the vasopressin and natriuretic peptide systems in volume regulation
- Effects of angiotensin II via AT1 receptors and the development of tissue fibrosis
- Myocardial metabolism characteristics and the phenomenon of cardiomyocyte hibernation
- Involvement of the endothelin system in the pathogenesis of vascular tone
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