Definition and Classification of CHF
Chronic heart failure (CHF), or congestive heart failure, is a syndrome in which the heart is unable to provide adequate perfusion of organs and tissues. Clinically, left-ventricular and right-ventricular failure are distinguished, which is important for understanding symptoms and management tactics.
From a pathophysiological standpoint, systolic and diastolic forms are distinguished. In clinical practice, classification is based on the ejection fraction (EF) measured by echocardiography:
- HFrEF (heart failure with reduced ejection fraction) — with reduced EF (<40%);
- HFpEF (heart failure with preserved ejection fraction) — with preserved EF (≥50%);
- intermediate variant HFmrEF — with mildly reduced EF (40–49%).
Causes and pathogenesis
Systolic left-ventricular failure (HFrEF) develops when myocardial contractility decreases. Main causes:
- Myocardial infarction with scar formation and loss of the contractile zone;
- Myocarditis with inflammation and fibrous replacement;
- Dilated cardiomyopathy with wall thinning and flaccidity.
Diastolic failure (HFpEF) occurs when afterload increases and relaxation of the hypertrophied myocardium is impaired. Key causes are aortic stenosis and arterial hypertension. Contractility is preserved, EF is normal, but the chamber lumen is reduced due to hypertrophy.
Right-ventricular failure develops in right ventricular infarction (systolic variant) or when afterload on the right heart increases — pulmonary valve stenosis and pulmonary hypertension. Five groups of causes of pulmonary hypertension: idiopathic, secondary to left-sided heart disease, associated with COPD and other chronic lung diseases, PE, and infiltrative/tumor lung diseases.
A separate form is high-output heart failure. It occurs with a sharp drop in systemic vascular resistance: sepsis, beriberi (vitamin B1 deficiency), thyrotoxicosis, arteriovenous fistulas, severe anemia.
Compensatory mechanisms
When cardiac output decreases, mechanisms to maintain blood pressure are activated, which in the long term exacerbate the pathology.
- Activation of the sympathetic nervous system via aortic arch and carotid sinus baroreceptors: stimulation of β1-receptors increases heart rate, α1-receptors in arteries increase afterload, and in veins — preload.
- Activation of the RAAS: angiotensin II causes vasoconstriction, aldosterone retains sodium and water.
- Elevated antidiuretic hormone levels with additional fluid retention.
Normally, natriuretic peptides (BNP, NT-proBNP) are secreted, counteracting the RAAS, but as CHF progresses, their effect is insufficient.
Complications
In left-ventricular failure, blood congests in the left atrium and pulmonary veins, leading to pulmonary edema: fluid transudates across the alveolar wall. Characteristic features are orthopnea, paroxysmal nocturnal dyspnea, moist rales. A marker is an elevated pulmonary capillary wedge pressure (PCWP) >18 mmHg.
Cardiogenic shock is a critical drop in cardiac output with centralization of blood flow. Manifestations: cold mottled extremities, pallor, confusion, oliguria, rising creatinine, decreased saturation. Multiple organ dysfunction syndrome develops: ischemic encephalopathy, acute kidney injury, myocardial and intestinal ischemia, strokes. Cardiorenal syndrome is highlighted, involving mutual damage to the heart and kidneys.
In right-ventricular failure, pressure in the venae cavae rises: jugular venous distension, peripheral edema, ascites, hepatic congestion resulting in cardiac cirrhosis.
Diagnostics
- Physical examination: jugular venous distension, edema, ascites, moist rales.
- Chest radiography: cardiomegaly, signs of venous congestion, pleural effusion.
- BNP / NT-proBNP: low levels practically rule out CHF; high levels support the diagnosis but are nonspecific (also elevated in CKD, pulmonary hypertension).
- Echocardiography is the gold standard: evaluation of EF, chamber dimensions, valves, diastolic function.
- ECG: signs of ischemia, prior infarction, hypertrophy, arrhythmias, blocks.
- Right heart catheterization with PCWP measurement is the most accurate method when the etiology of dyspnea is unclear.
- Coronary angiography — if ischemic etiology is suspected.
Treatment
The goal of therapy is to break the vicious cycle of neurohormonal activation. Basic therapy for HFrEF includes four drug classes:
- Beta-blockers (bisoprolol, carvedilol, metoprolol succinate) — reduce heart rate, oxygen consumption, and prevent remodeling.
- ACE inhibitors or ARBs; if intolerant or to enhance the effect — ARNI (sacubitril/valsartan), which inhibits BNP degradation.
- Mineralocorticoid receptor antagonists (spironolactone, eplerenone) — with preserved renal function.
- SGLT2 inhibitors (dapagliflozin, empagliflozin) — effective even in the absence of diabetes mellitus.
Symptomatically, loop diuretics (furosemide, torasemide) and thiazides are prescribed. If tachycardia persists, ivabradine is added. An alternative for ACE inhibitor/ARB intolerance is the hydralazine + isosorbide dinitrate combination. Digoxin is used in concomitant atrial fibrillation.
Devices and surgery: cardiac resynchronization therapy (CRT) for left bundle branch block and low EF; implantable cardioverter-defibrillator (ICD) for risk of life-threatening arrhythmias; LVAD and heart transplantation — in end-stage disease.
In cardiogenic shock, inotropes (dobutamine, milrinone, digoxin), intra-aortic balloon counterpulsation, ECMO, and non-invasive ventilation (BiPAP) for pulmonary edema are used. Inotropes do not improve survival and are used as a temporary measure.
Key points
- CHF is divided into left- and right-ventricular, systolic and diastolic; by EF — into HFrEF, HFmrEF, and HFpEF.
- HFrEF is most commonly caused by infarction, myocarditis, dilated cardiomyopathy; HFpEF — by arterial hypertension and aortic stenosis.
- Compensatory activation of the SNS and RAAS in the long term exacerbates myocardial remodeling.
- Left-ventricular failure leads to pulmonary edema and cardiogenic shock, right-ventricular failure — to venous congestion, ascites, and cardiac cirrhosis.
- Diagnostic minimum: echocardiography, BNP/NT-proBNP, ECG, radiography; confirmatory — right heart catheterization with PCWP measurement.
- Basic therapy for HFrEF — four classes: beta-blockers, ACE inhibitors/ARBs/ARNI, aldosterone antagonists, SGLT2 inhibitors.
- Diuretics are used symptomatically, ivabradine — for persistent tachycardia.
- In end-stage cases, CRT, ICD, LVAD, and heart transplantation are used.