Congestive Heart Failure Flashcards
what is CHF
CO below normal range
Symptoms of CHF
Decreased exercise tolerance Tachycardia Oedema (left ankle especially) Dyspnoea Cardiomegaly (larger but thinner walls so less effective)
Treatments
Diuretics ACE inhibitors ARBs Beta blockers Cardiac glycosides (inotropes) Vasodilators Beta-1 agonists (inotropes), acute CHF PDE-III inhibitors (inotrope)
Cardiac Glycosides MOA
Digitoxin (long-acting)/digoxin (med-acting) inhibits Na/K ATPase by competing with K, higher intracellular Na slows Na/Ca exchange at other transporter so intracellular Ca rises, inc force of contraction and vagal tone increases
Does hypokalaemia affect digoxin’s action
increases block, opposite for hyperkalaemia
Cardiac glycoside types and t1/2
Digitoxin t1/2 7 days, eliminated in liver
Digoxin t1/2 40 hours, eliminated in kidney
Ouabain t1/2 20h used in labs only, eliminated in kidney
*all have low therapeutic index so radioimmunoassay used to monitor plasma conc
Cardiac glycoside SE
Arrhythmias, anorexia, DNV, rarely confusion/psychosis, ectopic beats, AV block due to vagal/depolarising effects
beta-1 agonist MOA
dobutamine inc cAMP and therefore Ca currents, inc contraction force
Used in acute HF
PDE III inhibitor MOA
Milrinone inhibits PDE III which breaks down cAMP, acts in heart for contraction and relaxation of vascular smooth muscle
Given slow i.v.
beta-1 antagonists MOA
Carvedilol/bisoprolol reduces sympathetic drive to heart
Carvedilol also an alpha-1 antagonist - vasodilation
Diuretics (thiazide + loop) MOA
bendroflumethiazide, bumetanide/furosemide, aldosterone antagonist (eperonone/spironolactone) reduce pre-load, reduce EDV for more efficient contraction
ACE inhibitors MOA
Ramipril/enalapril also switch off angiotensin system, decrease pre-load and EDV so more efficient contraction
Vasodilators
Isosorbide denitrate and hydralazine reduce afterload so inc SV and therefore CO
Gold standard heart failure treatment
Carvedilol (/bisoprolol), ACE inhibitor and spironolactone
