Congestive Heart Failure Lecture Notes PDF

CONGESTIVE HEART FAILURE REAGAN KABUKA (B.PHARM, MPH) DEFINITION Congestive Heart Failure is a clinical syndrome in which the heart is unable to pump enough blood to meet the body’s needs, to dispose of systemic or pulmonary venous return adequately This m...

CONGESTIVE HEART FAILURE REAGAN KABUKA (B.PHARM, MPH) DEFINITION Congestive Heart Failure is a clinical syndrome in which the heart is unable to pump enough blood to meet the body’s needs, to dispose of systemic or pulmonary venous return adequately This may be as a result of an inability of the heart to fill or pump blood CAUSES Metabolic abnormalities Hyperthyroidism Heart block (ass with structural heart defects) Severe anemia Dilated cardiomyopathy Viral Myocarditis Rheumatic valvular heart disease Classification of C.H.F according to Symptomatology Class I: - Symptoms occur with greater than ordinary exercise Class II: - Symptoms occur on ordinary exercise Class III: - Symptoms occur at minimal activity Class IV: - Symptoms occur even at rest SIGNS AND SYMPTOMS RIGHT SIDED LEFT SIDED Facial edema Tachypnea Hepatomegaly Tachycardia Jugular venous Cough enlargement Wheezing Edema in feet Chest crepitations PATHOPHYSIOLOGY Cardiac output is determined by preload, afterload, myocardial contractility and heart rate Increase in preload Increase in afterload Decrease in contractility (Causing accumulation of blood in the ventricles Ventricular distention causing exhaustion and failure to work) Increase heart rate Compensatory Mechanisms 1. Activation of Sympathetic nervous system- caused by increased adrenal secretion of circulating epinephrine and increased neural release of norepinephrine 2. Renin-angiotensin-aldosterone system- Due to reduced renal perfusion and GFR. Angiotensin II causes vasoconstriction and myocardial hypertrophy attempting to restore wellness to normal DRUGS USED IN HEART FAILURE 1. Diuretics 2. Vasodilators 3. Inotropic drugs 4. Beta blockers Diuretic drugs in Heart failure Used to reduce extracellular fluid volume and ventricular filling pressure (Preload). Therefore, they are effective in controlling congestive symptoms (dyspnea, edema) Patients should be advised to limit dietary intake of Na+ to 2-3 grams/day. 1- Thiazide diuretics: Useful for therapy of mild Heart failure 2- Loop diuretics: Useful for therapy of moderate and severe Heart failure. Dose 3- Potassium sparing diuretics (Aldosterone antagonists): Not effective as diuretics when used alone. Useful in limiting renal K+ and Mg++ loss induced by other diuretics. Low dose of Spironolactone improves survival in advanced Heart failure Vasodilator drugs used in C.H.F I-Arterilar and venodilators- ACEIs in C.H.F Arteriolar dilatation leading to decreased afterload and improve Cardiac output resulting in decreased fatigue Decreased renovascular resistance (decreases renal vasoconstriction of AT- II) resulting in increased renal blood flow Decreases Aldosterone secretion. II- Veno-dilators-Organic Nitrates e.g. Isosorbide dinitrate, Nitroglycerine Venodilators decrease preload resulting in decreased venous and pulmonary congestion thereby relieving edema and dyspnea III- Arteriolar-Hydralazine, Minoxidil and nicorandil Arterial vasodilator leading to decreased afterload and increased cardiac output thereby decreasing fatigue Effective in increasing renal blood flow Most effective when combined with organic nitrates therefore useful in patients who can not tolerate ACEIs POSITIVE INOTROPIC AGENTS 1- Sympathomimetic amines- Dobutamine and Dopamine: Stimulate myocardial contractility Dopamine has renal vasodilator effect resulting in diuresis. Not active orally. Reserved for management of acute Heart failure or refractoriness to oral agents 2- Phosphodiesterase inhibitors (Inamrinone and Milrinone): Selective inhibitors of Phosphodiesterase enzyme resulting in increased cAMP Stimulate myocardial contractility Induce arterial and venous dilatation Used I.V. for short term support in advanced heart failure Milrinone is preferred because it reduces risk of thrombocytopenia and liver toxicity. CARDIAC GLYCOSIDES (Digitalis) Digoxin and Digitoxin are active orally. Molecular mechanism of action of Digitalis: 1. Digitalis inhibits membrane Na+/K+ ATPase responsible for the Na+ pump 2. Inhibition of this enzyme increases intracellular Na+ and consequently increases free intracellular Ca++ through increasing Na+/Ca++ exchange mechanism Digitalis also facilitates Ca++ entry through the voltage gated Ca++ channels facilitating excitation-contraction coupling. Pharmacological actions: 1. Mechanical effects: - Positive inotropic effect: The main action of Digitalis is to increase the force of contraction of the heart in patients with heart failure. Increased force of contraction increases Cardiac output increasing blood flow to various organs and inhibiting the compensatory sympathetic and renin-angiotensin system activation 2. Electrophysiological effects: Digitalis increases vagal tone and decreases sympathetic activity resulting in: 1- Decreased heart rate. 2- Decreased conduction in AV node 3- Decreased refractory period in atrial and ventricular tissues Therapeutic uses of Cardiac glycosides 1- Congestive heart failure: - Reserved for patients with heart failure who are in atrial fibrillation or remain symptomatic despite therapy with ACEI For initiating Digoxin therapy, begin with 0.125 – 0.25mg/day 2- Atrial fibrillation with rapid ventricular response: Blocks AV node thereby protects ventricle from rapid atrial rate. Loading dose 1mg over 24 hours i.e. 0.25mg/6hrs I.V. Maintenance dose 0.125mg daily. 3- Atrial flutter: - It may convert Atrial flutter to Atrial fibrillation (shorten Effective Refractory Period), which may return to normal rhythm on withdrawal of Digoxin BETA BLOCKERS Bisoprolol, carvedilol, metoprolol Reduce the heart rate and keep the heart from overworking Cardiac protectionfrom beta-1 adrenoceptor overstimulation, arrhythmic effects, reduction in heart rate and positive energetic effects CCF patients treated with beta blockers if they are in a compensated state Contraindicated in ADHF (sudden worsening of signs and symptoms of HF) due to acute inotropic effects and thus potential worsening of hemodynamics TREATMENT ALGORYTHM Class I: - Most patients do not require medicine but lifestyle modifications Class II: - ACEI + (HCTZ OR FUROSEMIDE) + BBLOCKER Class III: - ACEI + FUROSEMIDE + DIGOXIN + ASPIRIN 75 + (ISDN+HYDRALAZINE if patient cannot tolerate ACEIs) Class IV: - ACEI + FUROSEMIDE + DIGOXIN + ASPIRIN 75 + SPIRONOLACTONE + (ISDN+HYDRALAZINE if patient cannot tolerate ACEIs) THANK YOU!!