Comprehensive Overview on Congestive Heart Failure (CHF) and Inotropic Drugs

 Introduction to Congestive Heart Failure (CHF)

  • Definition: CHF is a chronic condition where the heart is unable to pump sufficient blood to meet the body's needs.
  • Epidemiology: Affects millions worldwide, commonly in elderly populations.
  • Pathophysiology: Results from conditions like hypertension, coronary artery disease, and cardiomyopathy.

Types of CHF

1.    Left-Sided Heart Failure:

o   Symptoms: Dyspnea, pulmonary congestion, fatigue.

o   Causes: Hypertension, aortic valve disease, ischemic heart disease.

2.    Right-Sided Heart Failure:

o   Symptoms: Peripheral edema, hepatomegaly, ascites.

o   Causes: Chronic lung disease, left-sided heart failure.

3.    Biventricular Heart Failure:

o   Symptoms of both left and right-sided failure.

Classification of CHF Drugs

  • Inotropic Drugs (e.g., Digoxin, Dobutamine) – Increase cardiac contractility.
  • Diuretics (e.g., Furosemide, Spironolactone) – Reduce fluid overload.
  • Vasodilators (e.g., ACE inhibitors, ARBs, Hydralazine) – Decrease afterload.
  • Beta-blockers (e.g., Metoprolol, Carvedilol) – Reduce myocardial oxygen demand.

Inotropic Drugs – Digoxin

  • Definition: A cardiac glycoside that increases myocardial contractility.
  • Source: Extracted from Digitalis purpurea (Foxglove plant).
  • Uses: Mainly for CHF and atrial fibrillation.

Pharmacokinetics of Digoxin

  • Absorption: 60-80% oral bioavailability.
  • Distribution: Large volume of distribution; binds to cardiac tissues.
  • Metabolism: Minimal hepatic metabolism.
  • Excretion: Primarily renal (unchanged form).
  • Half-life: ~36-48 hours.

Pharmacodynamics of Digoxin

  • Primary Action: Inhibition of Na+/K+ ATPase pump.
  • Effects:
    • Increases intracellular calcium leading to increased cardiac contractility.
    • Slows AV node conduction, beneficial in atrial fibrillation.
    • Increases vagal tone, reducing heart rate.

 

 Mechanism of Action of Digoxin

1.    Inhibits Na+/K+ ATPase → Increases intracellular Na+.

2.    Na+/Ca2+ exchanger activity increases intracellular Ca2+.

3.    Increased Ca2+ enhances myocardial contractility.

4.    AV node depression leads to a slower heart rate.

Indications of Digoxin

  • Congestive heart failure (CHF) – Mainly in patients with systolic dysfunction.
  • Atrial fibrillation and atrial flutter – To control ventricular rate.

Adverse Effects of Digoxin

  • Cardiac Effects: Arrhythmias, bradycardia, heart block.
  • Gastrointestinal: Nausea, vomiting, diarrhea.
  • Neurological: Confusion, dizziness, visual disturbances (yellow vision).

Contraindications of Digoxin

  • Hypokalemia (increases toxicity risk).
  • AV block (risk of worsening conduction defects).
  • Ventricular fibrillation.
  • Digoxin hypersensitivity.

Drug Interactions of Digoxin

  • Increased Digoxin Toxicity:
    • Diuretics (cause hypokalemia → increase digoxin effect).
    • Calcium channel blockers (reduce renal clearance of digoxin).
    • Quinidine, Amiodarone (increase plasma digoxin levels).
  • Reduced Efficacy:
    • Rifampin, St. John’s Wort (increase digoxin metabolism).
Presentation for Congestive Heart Failure (CHF) and Inotropic Drugs




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