Title 19. DRUGS USED FOR THERAPY OF CONGESTIVE HEART FAILURE.pdf ✅

PHARMD GURU Page 1 DEFINITION: Congestive heart failure (CHF) is a clinical syndrome during which the center is unable to pump ample blood to fulfill the metabolic necessities of the body, or will do thus solely at an elevated filling pressure. CLASSIFICATION OF CHF: BASED ON AMOUNT OF CARDIAC OUTPUT: BASED ON THE POSITION OF HEART FAILURE: DRUGS USED FOR THERAPY OF CONGESTIVE HEART FAILURE
PHARMD GURU Page 2 PATHOPHYSIOLOGY OF CONGESTIVE CARDIAC FAILURE (C.C.F): COMPENSATORY MECHANISMS OF CHF: To enhance the cardiac output, body compensates for the intrinsic cardiac effects in the following manner. 1. Increased sympathetic discharge. 2. To complete the remittent B.P., baroreceptors set within the arch of artery arterial blood vessel sinuses and walls of the center get excited and causes activation of beta-adrenergic receptors resulting in an increase in rate and force of contraction of heart. 3. An increase in blood vessel comes back (preload) is additionally seen because of the activation of alpha adrenergic receptors. 4. Increased rate associated force of contraction at the side of the enhanced preload ends up in an initial increase within the flow. 5. Vasoconstriction of the arteries due to alpha stimulation also causes an increase in after load, leading to fall in ejection fraction.
PHARMD GURU Page 3 ACTIVATION OF RENIN ANGIOTENSIN ALDOSTERONE (RAA):  Fall within the flow decreases the urinary organ perfusion rate; as a result the RAA system gets activated.  Angiotensin II may cause atrophic response in vascular smooth muscle (with vasoconstriction) and myocardial hypertrophy, attempting to restore wall stress to normal. CARDIAC REMODELING: It is most vital mechanism by that body stipendiary for the intrinsic internal organ effects.  It involves changes within the form of the center (from traditional to spherical) because of cardiac muscle hypertrophy.  During cardiac remodeling, the connective tissue cells as well as the abnormal myocardial cells undergo proliferation and dilation instead of stretching under the influences of angiotensin-2.  In the early stages, the remodeled heart maintains the cardiac performances.  But later on, hypertrophy may exert certain adverse effects like ischaemic changes, decrease in the rate and force of contraction of heart. After certain period of time the antagonistic mechanisms get exhausted and worsen the cardiac performances. The stress on heart increases and a stage is reached where these mechanisms fails to maintain the adequate cardiac output. CLINICAL MANIFESTATIONS/SIGNS AND SYMPTOMS:  Fluid retention  Pulmonary congestion  Dyspnoea and orthopnoea CVS MANIFESTATIONS:  Resting tachycardia  Ventricular arrhythmias  Enlargement of heart
PHARMD GURU Page 4 RENAL MANIFESTATIONS:  Nocturia  Oliguria OTHER MANIFESTATIONS:  Reduced cardiac output lead to poor perfusion of skeletal muscle resulting in fatigue.  Reduced flow result in poor perfusion of muscle leading to fatigue.  Reduced perfusion to brain results in altered mental states and confusion.  Reduced perfusion might also cause the patient to seem pale with cold and perspiring hands. TREATMENT: Non drug treatment/ non pharmacological approach:  Physical exercise  Salt intake  Fluid intake  Alcohol consumption  Liquorice PHARMACOLOGY/ DRUG THERAPY: CLASSIFICATION: 1. DIURETICS: (a) Loop diuretics: Furosemide, bumetanide, torsemide. (b) Thiazide diuretics: Chlorothiazide, hydrochlorothiazide, metolazone. (c) Aldosterone antagonists: Spironolactone, eplerenone. 2. VASODILATORS: (a) Arteriolar and venodilators: - ACE inhibitors: Enalapril, lisinopril, ramipril, fosinopril, trandolapril. - Angiotensin receptor blockers (ARBs): Losartan, candesartan. - Direct renin inhibitor: Aliskiren. - Sodium nitroprusside.