CHF Flashcards
Classes of drugs
Vasodilator, loop diuretics, digitalis
Nitroprusside/SNP (vasodilator)
Acts as NO supplier –> NO has vasorelaxation properties such as decrease preload, afterload to decrease cardiac load
SE of nitroprusside
Hypotension (NO), cyanide poisoning, cellular hypoxia [Cyanide & methaemoglobin are by-products of SNP breakdown]
MoA of Furosemide (loop diuretics)
Selective inhibition of Na/K/2CL transporter in thicken ascending limb of LoH –> decrease Na, H2O retention reduces fluid overload
Induce renal PG synthesis
Increase renal perfusion, increase filtration, decrease fluid volume in body
PK of loop diuretics
Rapid absorption, rapid diuretic effect —use for acute situations (APO, hyperK, renal failure)
MoA of digitalis
Inhibit Na/K ATPase –> increase intracellular Na –> decrease Ca efflux –> stronger systolic contraction
Mechanical: increase contractility –> baroreflex, decrease AngII –> decrease preload & afterload –> decrease cardiac workload
Electrical: Increase PNS, decrease AV conduction, increase PR interval, decrease ventricular rate
(Decrease QT, ST intervals, T-wave inversion)
Toxic: Decrease Ca efflux increase intracellular [Ca] –> automaticity, extrasystole, tachycardia, fibrillation, PVB
Use of digitalis
Systolic dysfunction, A-fib
SE of digitalis
Dysrhythmia (AV block, AF, VF), GI (anorexia, N&V), CNS (H/a, confusion)
Digitoxin vs digoxin
Digitalis is metabolized in liver, excreted in faeces — + in renal impaired
Digoxin is 2/3 excreted unchanged in kidney — (-) for renal impaired
Digitalis toxicity
Triggers: hypoK/Mg, hyperCa, verapamil, steroids, K+ depleting diuretics (loop, thiazides)
Tx: stop digitalis, correct Mg/K deficiency
Anti-arrhythmics: lidocaine, propranolol
Digoxin antibody: FAB fragment, digibind