Congestive Heart Failure

Congestive Heart Failure

• Cardial decompensation occurs due to a decrease in cardiac output (CO), leading to a deterioration of blood supply to tissues.
• Preload is determined by the tone of the venous system, while afterload is determined by the arterial system and peripheral resistance (PR).

Cardial Decompensation Reasons

• Systolic dysfunction: muscle strength decreases, leading to decreased cardiac output and perfusion, often caused by coronary stenosis, arrhythmia, or cardiomyopathy.
• Diastolic dysfunction: inability to relax due to left ventricular stiffness, leading to pulmonary blood flow disorders and peripheral edema, often caused by hypertension, valvular dysfunction, or pericarditis.

Compensatory Processes

• Increased sympathetic activity: increased heart rate (β1 receptor) and vasoconstriction (α1 receptor), which worsens the condition further.
• RAAS (Renin-Angiotensin-Aldosterone System): increased angiotensin II activity leads to vasoconstriction, remodeling, and left ventricular hypertrophy, and aldosterone mobilization causes Na and water retention, resulting in edema.

NYHA Classification

• Divided into 4 stages based on the onset of symptoms:
  • I: physical activity does not cause symptoms
  • II: physical activity causes mild symptoms, which disappear at rest
  • III: even mild physical activity causes shortness of breath
  • IV: symptoms of heart failure occur even at rest

Treatment

• Lifestyle changes, diet, and regular exercise
• Drug treatment:
  • In milder cases (NYHA I, II): aim to stop compensatory processes
    • Beta1 receptor blockers (bisoprolol, nebivolol): reduce increased sympathetic activity
    • ACE inhibitors (perindopril, telmisartan): prevent vasoconstriction and remodeling effect
    • Diuretics (indapamide, eplerone): reduce preload
  • In more severe cases:
    • Cardiac glycosides (digitalis preparations): increase contractility, positive inotropic effect, and negative chronotropic effect

Digitalis Preparations

• Mechanisms of action:
  • Inhibit Na/K-ATPase, increasing Na and Ca levels, and contractility
  • Decrease renin release in the kidney
  • Negative dromotropic effect: slow conduction in the atrial chamber
  • Increase heterotropic stimulation: can cause ventricular arrhythmias
• Side effects:
  • Loss of appetite, nausea, vomiting, headache, fatigue, dizziness, bradycardia, extrasystole, bigeminia, AV block, and ventricular tachycardia
• Treatment of overdose:
  • Drug withdrawal
  • Potassium replacement
  • ECG control
  • Treatment of arrhythmias
  • Antibody (Digibind) to bind to free digoxin molecules and reverse cardiotoxic effects