Digoxin & Inotropes Flashcards
(90 cards)
use of digoxin
- CHF
- slow ventricular response of pts with supraventricular tachydysrhytmias (PAT, afib, aflutter)
digoxin decreases the risk of death due to heart failure but still might make the patient die because of what adverse effect?
increased incidence of sudden death d/t arrhytmias
digoxin can be combined with what other drug class in the treatment of SVT
what is the benefit of this?
beta antagonist
can give smaller doses of each and yet obtain more rapid control
contraindications for digoxin
- Wolff-Parkinson White (WPW)
- Hypertrophic cardiomyopathy
- Acute MI
why is digoxin contraindicated in pts with WPW?
30% develop Vfib from increased conduction down alternate path
why is digoxin contraindicated in pts with hypertrophic cardiomyopathy?
increased contractility = increased obstruction
why is digoxin contraindicated in acute MI?
increases O2 demand and contractility
T/F - Digoxin is effective for patients with normal LV systolic function
false - may not be effective
when might digoxin be used in a patient with mild to moderate heart failure?
pt doesn’t respond to ACE inhibitor or beta blocker
patient comorbidities that must be considered when dosing digoxin
renal failure
patients who benefit the most from digoxin
patients with severe heart failure, an enlarged heart, and a third heart sound gallop
MOA of digoxin
- Inhibits Na+/K+-ATPase ion transport system (more Na+ inside cell)
- Increased intracellular Na+ then affects the Na+/Ca2+ exchanger (more Ca2+ inside the cell for increased force of contraction)
how does digoxin affect resting membrane potential
why?
decreases
(less negative, increased automaticity)
d/t changes in K+ gradient
how does digoxin affect phase 4 of cardiac action potential?
increases slope
(increased automaticity)
how does digoxin affect the duration of action potential?
decreased duration d/t shortening of phase 2
(corresponds to ventricular contraction)
effect of digoxin on cardiac output
what effects does this have?
increases
- increased renal perfusion
- diuresis of newly mobilized edema
how does digoxin affect ANS activity?
- enhanced PNS activity
- SA node activity decreased
- slowed conduction through AV
effect of digoxin on contractility
how does this affect SV, preload, and LVEPD?
increased contractility
- increased SV
- decreased heart size (decreased preload)
- decreased LVEDP
effect of digoxin on tissue perfusion
improved
how does digoxin affect SVR
decreases (leading to even better stroke volume)
how does digoxin affect HR?
why?
slowed HR d/t negative chronotropic and dromotropic effects
(increased PNS activity)
how is increased contractility offset in a normal heart?
how does digoxin affect CO in a normal heart?
decreases in HR and direct vasoconstriction in arterial smooth muscle
CO may be unchanged or even decrease
effects of positive inotropic effects with no change in HR on a failing heart
- decreased preload
- decreased afterload
- decreased wall tension
- decreased O2 consumption
EKG changes assoc. with cardiac glycosides
- prolonged PR
- shortened QT
- ST segment depression
- smaller or inverted T wave