29 BBs and Inotropes in HF Flashcards
describe the compensatory mechanism of systolic heart failure
- heart cant pump blood as well for any number of reasons
- greedy kidney has a tantrum, boosting renin-angiotensin system until it gets its perfusion
- heart fails even more due to neurohormonal overload
long term effects of sympathetic overstimulation on myocardium during heart failure
direct toxicity to myocytes
bad proliferative signaling – hypertrophy/fibrosis
death of muscle cells
beta blocker with activity on b1,b2 and a1
carvedilol
beta blockers that are b1 selective
metoprolol, bisoprolol
only documented beta blockers with increased survival for HF
metoprolol
bisoprolol
carvedilol
why do we think beta blockers are beneficial long term in heart failure?
they sheild the heart from SNS overstimulation
long term proven benefits of BBs for HF
33% improved survival
improved Left ventricular EF
decreased sudden death
when should you be cautious about giving beta blockers to heart failure patients
decompensated patients should probably wait to get BBs
you should always start low and work up to higher doses
be more sensitive to the more severe HF patients when starting BBs
b1 effects on heart
enhanced inotropy(contractility)
enhanced lusitropy(relaxation)
positive chronotropy(HR)
increased AV conduction velocity
increased arrhythmogenicity(BAD)
dopamine vs dobutamine as inotropes in heart failure
dopamine has more of an affect on HR and vasopression than dobutamine so is reserved for patients with loooooow BP and HF
dobutamine is more of a pure inotrope. can have much more positive effects on contractility without the same spike in HR and vasoconstriciton as dopamine
milrinone
PDE3 inhibitor
keeps cAMP high by inhibiting PDE3
inotropic function
describe digoxin’s function as an inotrope
what are its non-inotropic effects
binds Na/K pump
indirectly reverses Na/Ca pump(starts moving Ca in and sodium out)
more Ca in cell = increased contractility, relaxation
non-inotropic effects - increased vagal tone
adverse effects of digoxin
arrhythmias – increased automaticity
bradycardia
hypokalemia increases binding to Na/K pump; more likely to be toxic
Na/K pumps are in many cell types
- GI: cramping/vomiting
- eye: green/yellow halos
- brain: confusion
indications for digoxin
atrial fibrillation, atrial flutter
HF patients in NORMAL sinus rhythm who are still symptomatic on standard therapy
how long do BBs take to start having a postitive effect on EF in HF
about 3 months
the first week after therapy starts is the hardest
