Heart Failure PDF

Congestive heart failure CHF Heart failure Learning Objectives • Causes of heart failure • Signs and symptoms • Classifications of HF • The physiology of muscle contraction • The compensatory responses in CHF • The different between pulmonary and systemic edema • Classification of Pharmacological...

Congestive heart failure CHF Heart failure Learning Objectives • Causes of heart failure • Signs and symptoms • Classifications of HF • The physiology of muscle contraction • The compensatory responses in CHF • The different between pulmonary and systemic edema • Classification of Pharmacological therapy • Mechanism of actions and side effects What is Heart Failure? It is a condition in which the heart is unable to pump sufficient blood to meet the needs of the body. CHF can be caused by: -impaired the ability of the cardiac muscle to contract Or -increased workload imposed on the heart. CHF major causes are: CHF is accompanied by: • Ventricular dysfunction • Reduced cardiac output • Chronic hypertension • Valvular disease • Coronary artery disease (CAD) • Congenital heart disease • Insufficient tissue perfusion • Fluid retention CHF Classification Symptoms of CHF • Class I (asymptomatic) Think FACES... Fatigue Activities limited No limitation of ordinary physical activity • Class II (mild) Slight limitation of physical activity with normal activity produces fatigue, dyspnea, palpitations • Class III (moderate) Chest congestion Edema or ankle swelling Shortness of breath (dyspnea) Marked limitation of physical activity with mild activity produces symptoms as class II • Class IV (severe) Symptoms occur at rest 1-Action potential PHYSIOLOGY OF MUSCLE CONTRACTION 2- Calcium Concentration Agents that increase these calcium levels result in an increase in the force of contraction (inotropic effect). Compensatory responses in CHF Sources of free intracellular calcium: 1) Increased sympathetic activity a) From outside the cell, where opening of calcium channels causes an immediate rise in free cytosolic calcium. b) From the release of calcium from the sarcoplasmic reticulum and mitochondria, which further increases the cytosolic level of calcium. 2) Fluid retention 3) Myocardial hypertrophy: Therapeutic strategies in CHF Lifestyle changes – Stop smoking – Lose weight Pharmacological Therapy – Avoid alcohol – Avoid or limit caffeine – low-fat, low-sodium diet – Mild regular physical activity I. Vasodilators I. Vasodilators 1.1. Angiotensin converting enzyme (ACE) inhibitors 1.2.Angiotensin II blockers 1.3. Direct smooth muscle relaxants 1.1. Angiotensin converting enzyme (ACE) inhibitors (captopril,enalopril,fosinopril, lisinopril, quinapril) 2. Diuretics 3. Inotropic drugs 3.1. Digitalis 3.2. β-Adrenergic agonists 3.3. Phosphodiesterase inhibitors • The use of ACE inhibitors in the treatment of CHF has significantly decreased both morbidity and mortality. Mechanism and actions on heart Adverse effects: • • • • postural hypotension renal insufficiency Hyperkalemia persistent dry cough. • The potential of symptomatic hypotension with ACE inhibitor therapy requires careful monitoring. • ACE inhibitors should not be used in pregnant women. 1.2. Angiotensin II antagonist 1.3. Direct smooth muscle relaxants (Losartan, telmisartan, valsartan and candesartan) (hydralazin, isosorbide, minoxidil, sodiumnitroprusside) ➢ Its pharmacological effects are similar to ACE inhibitors in that it ▪ Dilation of venous blood vessels leads to a decrease in cardiac produces vasodilation and blocks aldosterone secretion. preload by increasing venous capacitance; arterial dilators reduce systemic arteriolar resistance and decrease afterload. ➢ Its main adverse effects is hyperkalemia. ▪ If the patient is intolerant of ACE inhibitors, the combination of hydralazine and isosorbide dinitrate is most commonly used. 2. Diuretics (hydrochlorothizide, metolazone, furosemide and bumetanide) ➢ Diuretics relieve pulmonary congestion and peripheral edema. ➢ These agents are useful in reducing the symptoms of volume overload. 3. Inotropic drugs 3.1. Cardiac glycosides (Digitalis) (Digitoxin and digoxin) Positive inotropic agents enhance cardiac muscle contractility, due to increased cytoplasmic calcium concentration that enhances the contractility of ❖ The cardiac glycosides are often called digitalis or digitalis glycosides because most of the drugs come from the digitalis (foxglove) plant. cardiac muscle. ❖ They are a group of chemically similar compounds that can increase the contractility of the heart muscle and are therefore widely used in treating heart failure. Mechanism of action a) Regulation of concentration cytosolic calcium b) Increased contractility of the cardiac muscle An increased myocardial contraction leads to a decrease in end diastolic volume, thus increasing the efficiency of contraction (increased ejection fraction). Therapeutic uses ✓ Digoxin therapy is indicated in patients with severe left ventricular systolic dysfunction after initiation of diuretic and vasodilation therapy. Adverse effects • Severe dysrhythmia • Anorexia, nausea, and vomiting • Headache ✓ Patients with mild to moderate heart failure will often respond to treatment with ACE inhibitors and diuretics and do not require digoxin. • Fatigue, confusion • Blurred vision • Alteration of color perception, and yellow-tinted vision or yellow corona-like spots. Yellow-tinted vision or yellow corona-like spots Factors predisposing to digitalis toxicity a. Electrolytic disturbances Hypokalemia which can be prevented by use of a potassium sparing diuretic or supplementation with potassium chloride. b. Drug ❖ Quinidine ❖ Verapamil They can increase digoxin levels by 50 to 75%, this may require a reduction in the dose of digoxin. 3.2. β-Adrenergic agonists ➢ β-Adrenergic stimulation improves cardiac performance by positive inotropic effects and vasodilation. ➢ Dobutamine is the most commonly used inotropic agent other than digitalis. MOA Dobutamine leads to an increase in intracellular cAMP, which results in the activation of protein kinase led to phosphorylation of calcium channel and increase calcium entrance 3.3. Phosphodiesterase inhibitors ➢ Amrinone and milrinone are phosphodiesterase inhibitors that increase the intracellular concentration of cAMP. ➢ This results in an increase in intracellular calcium, and therefore cardiac contractility