Heart failure treatment Flashcards
systolic dysfunction due to frank starling law
if the muscle of a healthy heart is stretched it will contract with greater force and pump out more blood but in failing or damaged heart this is lost as circulatory volume increases the heart dilates, the force of contraction weakens and cardiac output drops further. cardiac output then activates the sympathetic and RAAS which leads to further salt and water retention
main choice of drug for patients with salt and water retention
loop diuretics (furosemide)
loop diuretics
reduce symptoms of tiredness, fatigue, improve exercise capacity, induce profound diuresis by inhibiting the sodium, potassium, chlorine transporter in the loop of henle. works at low glomerular filtration rates. some patients resistant- use in combination with thiazide diuretics then
adverse drug reactions of loop diuretics
dehydration, hypotension, hypokalaemia, hyponatraemia, gout, impaired glucose tolerance
negative drug drug interactions with loop diuretics
aminoglycosides, lithium, NSAIDs, antihypertensives, vancomycin
neurohormonal inhibitors
ACE inhibitors, beta blockers, mineralocorticoid blockers, combined angiotensin blockade plus ANP/BNP enhancement
ACE inhibitors
ramipril, enalapril, lisinopril, block angiotensin converting enzyme, prevent the conversion of angiotensin I to angiotensin II, reduce preload and after load on heart. reduce morbidity and mortality of heart failure patients. first after diuretics.
angiotensin receptor blockers
block the angiotensin II to AT1 receptor, effective but not consistently proven to reduce mortality in patients with HFrEF and use is restricted to people intolerant to ACE inhibitors
Valsartan- sacubitril (ARNI)
combined valsartan and ARB and neprilysin inhibitor, new, ARB blocks AT1 inhibitor, neprilysin inhibit stops break down of ANP and BNP by neutral endopeptidases. reduces mortality. most effective
when to use valsartan sacubitril
in patients with symptomatic chronic heart failure and reduced ejection fraction (less than 35%), who have NYHA class II to IV and who are taking a dose of ACE inhibitors or angiotensin II blockers but still symptomatic
beta blockers
block sympathetic system, reduce mortality and morbidity in mild-severe heart failure by 30%, only used when stabilised not during acute presentation as precipitate severe deterioration in chronic heart failure is patient is fluid overloaded. carvedilol, bisoprolol
mineralcorticoid receptor antagonist
bind aldosterone and other steroid hormone receptors, spironolactone or eplerenone are recommended in all symptomatic patients with HErEF and LVEF less than 30% to reduce mortality and hospitalisation, reduces mortality in combination with ACEIs
ivabradine
slows the heart rate through inhibition of the I channel in the sinus node and therefore should only be used for patients in sinus rhythm. can be beneficial to reduce HF hospitalisation for patients with symptomatic stable chronic HErEF who are receiving standard therapy, including beta blocker at max tolerated dose and who are in sinus rhythm with a hr of 70bpm or greater at rest
positive ionotropes
digoxin, increases availability of calcium in myocyte, reduces hospitalisations, no effect on mortality, arrhythmias, nausea, confusion, narrow therapeutic index
therapeutic regime
furosemide +- thiazide, furosemide + pulsed metalozone, ACE inhibitor, angiotensin receptor blocker, ARNI, beta blocker +- ivabradine, MRA spironolactone, digoxin, warfarin