Congestive Heart Failure

Study Notes

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).

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.

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.

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

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