Congestive Heart Failure (CHF)

Here are the updated study notes

• Congestive Heart Failure (CHF)

Definition

• A chronic progressive condition where the heart cannot pump enough blood to meet the body's needs for oxygen and nutrients.
• Results in the heart being unable to fill with enough blood or pump with enough force.

Common Causes

• Coronary artery disease (CAD): Reduced blood flow to the heart muscle.
• High blood pressure (hypertension): Increases the workload on the heart.
• Heart valve problems: Affect blood flow in and out of the heart.
• Cardiomyopathy: Damage to the heart muscle.
• Congenital heart defects: Structural heart problems present at birth.

Risk Factors

• Age: Risk increases with age.
• Family history: Genetic predisposition.
• Obesity: Increases the heart's workload.
• Diabetes: Increases risk of heart disease.
• Smoking: Damages blood vessels.
• Excessive alcohol consumption: Can weaken the heart muscle.

Symptoms

• Shortness of breath (dyspnea): Especially during exertion or when lying down.
• Fatigue and weakness: Reduced blood flow to muscles.
• Swelling (edema): In ankles, feet, legs, and abdomen due to fluid buildup.
• Rapid or irregular heartbeat: Heart compensates for reduced function.
• Persistent cough or wheezing: Fluid buildup in the lungs.
• Sudden weight gain: Due to fluid retention.
• Lack of appetite or nausea: Reduced blood flow to the digestive system.
• Difficulty concentrating: Reduced blood flow to the brain.

Pathophysiology

• Cardiac Output Reduction: Heart's inability to pump enough blood.
• Neurohormonal Activation: The body's compensatory mechanisms are activated.
  • Activation of the sympathetic nervous system (SNS): Increases heart rate and vasoconstriction.
  • Activation of the renin-angiotensin-aldosterone system (RAAS): Promotes sodium and water retention, increasing blood volume.
  • Release of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP): Counteract RAAS by promoting vasodilation and diuresis.
• Ventricular Remodeling: Changes in the size, shape, and function of the ventricles.
  • Hypertrophy: Enlargement of the heart muscle, which may initially compensate but eventually impairs function.
  • Fibrosis: Stiffening of the heart muscle due to collagen deposition.
• Fluid Retention: Due to RAAS activation and impaired kidney function.
• Reduced Oxygen Delivery: Insufficient blood flow leads to inadequate oxygen supply to tissues.

Classification

• New York Heart Association (NYHA) Functional Classification:
  • Class I: No limitation of physical activity. Ordinary physical activity does not cause undue fatigue, dyspnea, or palpitations.
  • Class II: Slight limitation of physical activity. Comfortable at rest, but ordinary physical activity results in fatigue, dyspnea, or palpitations.
  • Class III: Marked limitation of physical activity. Comfortable at rest, but less than ordinary activity causes fatigue, dyspnea, or palpitations.
  • Class IV: Unable to carry on any physical activity without discomfort. Symptoms of heart failure at rest.
• American College of Cardiology/American Heart Association (ACC/AHA) Stages:
  • Stage A: At high risk for developing heart failure but without structural heart disease or symptoms of HF.
  • Stage B: Structural heart disease but without signs or symptoms of HF.
  • Stage C: Structural heart disease with prior or current symptoms of HF.
  • Stage D: Refractory HF requiring specialized interventions.

Diagnosis

• Physical Examination:
  • Listening for abnormal heart sounds (murmurs, gallops).
  • Checking for signs of fluid retention (edema, jugular venous distension).
  • Assessing lung sounds for crackles (rales).
• Echocardiogram: Assesses heart structure and function.
  • Measures ejection fraction (EF), the percentage of blood pumped out of the left ventricle with each contraction.
• Electrocardiogram (ECG): Detects arrhythmias and signs of heart damage.
• Chest X-ray: Reveals heart enlargement and fluid in the lungs.
• Blood Tests:
  • BNP (B-type natriuretic peptide) levels: Elevated in heart failure.
  • Kidney and liver function tests: Assess organ function.
  • Electrolyte levels: Detect imbalances.

Treatment Goals

• Relieve symptoms.
• Improve quality of life.
• Slow the progression of the disease.
• Reduce hospitalizations.
• Prolong survival.

Non-Pharmacological Treatment

• Lifestyle Modifications:
  • Dietary changes: Low-sodium diet, fluid restriction.
  • Regular exercise: Moderate physical activity as tolerated.
  • Weight management: Maintain a healthy weight.
  • Smoking cessation.
  • Limit alcohol consumption.
• Cardiac Rehabilitation: Supervised exercise and education programs.

Pharmacological Treatment

• Diuretics: Reduce fluid overload.
  • Loop diuretics (e.g., furosemide, bumetanide): Inhibit sodium and chloride reabsorption in the loop of Henle.
  • Thiazide diuretics (e.g., hydrochlorothiazide): Inhibit sodium reabsorption in the distal convoluted tubule.
  • Potassium-sparing diuretics (e.g., spironolactone, eplerenone): Block aldosterone receptors, reducing sodium and water retention.
• Angiotensin-Converting Enzyme (ACE) Inhibitors: Block the conversion of angiotensin I to angiotensin II.
  • Actions: Vasodilation, reduced aldosterone production, decreased sodium and water retention.
  • Common drugs: Enalapril, lisinopril, ramipril.
  • Adverse effects: Hypotension, cough, hyperkalemia, angioedema.
• Angiotensin II Receptor Blockers (ARBs): Block angiotensin II receptors.
  • Actions: Similar to ACE inhibitors but without the cough side effect.
  • Common drugs: Valsartan, losartan, candesartan.
  • Adverse effects: Hypotension, hyperkalemia, angioedema (less common than with ACE inhibitors).
• Angiotensin Receptor-Neprilysin Inhibitors (ARNIs): Combine an ARB with a neprilysin inhibitor.
  • Neprilysin: An enzyme that breaks down natriuretic peptides.
  • Actions: Vasodilation, reduced sodium and water retention, increased natriuretic peptide levels.
  • Common drug: Sacubitril/valsartan (Entresto).
  • Adverse effects: Hypotension, hyperkalemia, angioedema.
• Beta-Blockers: Block the effects of adrenaline on the heart.
  • Actions: Reduce heart rate, blood pressure, and myocardial oxygen demand.
  • Common drugs: Metoprolol, bisoprolol, carvedilol.
  • Adverse effects: Bradycardia, hypotension, fatigue, bronchospasm.
  • Cautions: Start at low doses and titrate slowly.
• Mineralocorticoid Receptor Antagonists (MRAs): Block aldosterone receptors.
  • Actions: Reduce sodium and water retention, prevent potassium loss.
  • Common drugs: Spironolactone, eplerenone.
  • Adverse effects: Hyperkalemia, gynecomastia (spironolactone).
• Sodium-Glucose Co-transporter 2 (SGLT2) Inhibitors: Inhibit glucose reabsorption in the kidneys.
  • Actions: Reduce blood glucose, blood pressure, and weight; improve cardiovascular outcomes.
  • Common drugs: Dapagliflozin, empagliflozin.
  • Adverse effects: Genital infections, urinary tract infections, dehydration.
• Hydralazine and Isosorbide Dinitrate: Vasodilators.
  • Hydralazine: Arterial vasodilator.
  • Isosorbide dinitrate: Venous vasodilator.
  • Actions: Reduce afterload and preload, improve cardiac output.
  • Common use: In patients who cannot tolerate ACE inhibitors or ARBs, particularly African Americans.
  • Adverse effects: Hypotension, headache, dizziness.
• Digoxin: Cardiac glycoside.
  • Actions: Increases myocardial contractility, slows heart rate.
  • Use: Primarily to control heart rate in patients with atrial fibrillation.
  • Adverse effects: Arrhythmias, nausea, vomiting, vision changes.
  • Monitoring: Narrow therapeutic index; monitor serum digoxin levels.

Device Therapy

• Implantable Cardioverter-Defibrillator (ICD): For patients at risk of sudden cardiac death due to ventricular arrhythmias.
• Cardiac Resynchronization Therapy (CRT): Biventricular pacing to improve coordination of ventricular contractions.
• Left Ventricular Assist Device (LVAD): Mechanical pump to support heart function in advanced heart failure.

Monitoring

• Regular follow-up appointments with a cardiologist.
• Monitoring weight, blood pressure, and heart rate.
• Blood tests to assess kidney function, electrolytes, and drug levels.
• Echocardiograms to assess heart function.

Complications

• Arrhythmias: Irregular heartbeats.
• Sudden cardiac death.
• Renal failure: Reduced blood flow to the kidneys.
• Liver damage: Congestion of the liver due to fluid buildup.
• Pulmonary hypertension: Increased pressure in the pulmonary arteries.
• Thromboembolism: Blood clot formation.

Prognosis

• Heart failure is a progressive condition with a variable prognosis.
• Prognosis depends on the severity of the disease, underlying causes, and response to treatment.
• Multidisciplinary care, including lifestyle modifications, medications, and device therapy, can improve outcomes.