Diuretics and Vasodilators in Heart Failure PDF

█ Diuretics Mechanism in heart failure  They ↓ fluid retention and pulmonary congestion leading to improvement of tissue oxygenation  They ↓ preload & afterload so improve myocardial function.  Spironolactone antagonizes the effect of aldosterone tha...

█ Diuretics Mechanism in heart failure  They ↓ fluid retention and pulmonary congestion leading to improvement of tissue oxygenation  They ↓ preload & afterload so improve myocardial function.  Spironolactone antagonizes the effect of aldosterone that is increased in CHF due to secondary stimulation of RAS. Recent evidence showed that it reduces mortality rates in patients with advanced heart failure (NYHA class III and IV). Disadvantages of diuretics  Excessive use of diuretics will ↓ ECF volume → ↓ COP.  Diuretic-induced acid-base imbalance may impair cardiac function.  Diuretic-induced hypokalemia can ↑ digitalis toxicity and cardiac arrhythmia. These adverse effects could be minimized by diuretic combination (loop diuretics plus K+ sparing diuretics) to minimize hypokalemia and acid-base imbalance. █ Vasodilators (nitrates and hydralazine)  Nitrates and hydralazine have complementary hemodynamic actions:  Nitrates are primarily venodilators, →↓ preload.  Hydralazine is a direct arterial dilator →↓ systemic vascular resistance and afterload.  Recent evidence showed that combination of nitrates and hydralazine reduces mortality and hospitalizations for patients with HF.  A fixed-dose combination product is available (USA and Europe) that contains isosorbide dintrate 20 mg and hydralazine 37.5 mg.  Guidelines recommend addition of hydralazine and nitrates to moderate to severe HF despite therapy with ACE inhibitors, diuretics, and β-blockers.  The combination is also appropriate as first-line therapy in patients unable to tolerate ACE inhibitors or ARBs due to any contraindication. █ ACEIs and ARBs Beneficial effects in heart failure:  They ↓ arterial BP → ↓ afterload.  They ↓ aldosterone → ↓ Na & H2O retention → ↓ preload.  They prevent myocardial wall thickening and cardiac remodeling. 180 █ Beta a-blockerrs High ddoses of β-blockerrs are ge enerally not recommmended in heart failuref be ecause the ey producce –ve inotropic effec ct and mayy precipita ate cardiac c decompe ensation, but b small doses hav ve some bbenefits in heart failure: Beneficial effectts in heartt failure:  β-b blockers reduce tachyca ardia an nd mpathetic overactivity sym o y.  β-b blockers redduce BP → ↓ ventricu ular strain associated a d with HF.  β-b blockers inhhibit renin release → ↓ cardiac remodeling r g caused bby RAAS.  Carrvedilol is a new beta-blocker with additional VD and antioxid dant prope erties. Accord ding to currrently ava ailable eviddence, bis ol, and carrvedilol soprolol, metoprolo m have sh hown the most m usefu ul effects in n patients with chron nic HF. █ MAN NAGEMENT T OF ACUT TE CARDIO OGENIC PU ULMONARY Y EDEMA Pathop physiology y of APE Acute c cardiogenic pulmonary edema a (APE) is accumula ation of fluuid (transudate) in the lun ng interstiitium and alveoli aas a result of incre eased cap pillary hydrostatic pressure seconda ary to LV dysfunction d n. Manife estations – Dysspnea, orth hopnea and d wheezess. – Cheest x-ray: patchy p or diffuse d alve eolar filling (haziness). ( 181  Manag gement  Hosspitalization and sitting or sem mi-sitting po osition.  High-flow oxyygen (hypo oxia causess pulmona ary VC and incrreased card diac load).  Furrosemide (20-80 ( mg IV): to ↓ ve enous returrn and pulm monary con ngestion. It is the mosst importantt trea atment.  Morphine (2-4 mg IV): – T To ↓ stresss and anxieety. – V Venodilatattion → ↓ VR R → ↓ lung co ongestion. – It ↓ pulmon ch reflex → ↓ tachypnea & work nary stretc o of breathin ng.  Nitrroglycerin ne (sublingual or i.v.).  Hem modynamic c support according to systolic c BP: – Maintain systolic s BP P >100 mmmHg. – If the SBP is