Digoxin & Inotropes Flashcards
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
dose of digoxin
up to 10 mcg/kg over 30 min
onset and elimination ½ life of digoxin
onset 5-30 minutes
elim. ½ life: 31-33 hours
how does renal failure affect elimination time of digoxin?
can be prolonged up to 4.4 days in renal failure pts
how is digoxin excreted
daily via kidneys
protein binding of digoxin
25% bound to protein (skeletal muscle)
therapeutic range of digoxin
0.5 - 2.5 ng/mL
how common is digoxin toxicity?
20% of pts taking it will have some form of toxicity
causes of digoxin toxicity
- renal dysfunction (most common)
- hypokalemia
- increasing myocardial binding of drug
- hypoxemia (increased SNS activity)
- hypercalcemia, hypomagnesemia
- decreased muscle mass (elderly)
for every 10 mmHg increase in PaCO2, serum K decreases an average of:
0.5 mEq/L
most frequent cause of death with digoxin toxicity
Vfib
what EKG change confirms digoxin toxicity?
no 1 specific change confirms toxicity
patient population most likely to have CNS symptoms with digoxin toxicity
elderly
GI symptoms of digoxin toxicity
- N/V
- Diarrhea
- increased salivation
CNS symptoms of digoxin toxicity
- fatigue
- confusion
- delirium
- blurred vision
- green halos
electrolyte imbalance seen with digoxin toxicity
life-threatening hyperkalemia
correctable causes of digoxin toxicity
- hypokalemia
- hypomagnesemia
- arterial hypoxemia
treatment of complete AV block associated with digoxin toxicity
temporary pacemaker
antiarrhythmics used to treat digoxin toxicity
- lidocaine
- atropine
common events under anesthesia that increase risks of digoxin toxicity
- altered renal function
- hyperventilation causing hypokalemia
- increased sympathetic activity
use of prophylactic digoxin in thoracic/abd surgeries
in elderly patients, 1mg over 4 doses the day before and morning of surgery decreased SVT incidence
use of prophylactic digoxin for surgical procedures in pts with cardiac disease
decreased incidence of impaired cardiac function in pts with CAD during recovery
how does digoxin interact with succinylcholine?
additive PNS effects or cause dsrhythmias d/t catecholamine release (theoretical)
how does digoxin interact with beta agonists?
increased dysrhythmias
how does digoxin interact with IV calcium
causes dysrhythmias
how is digoxin affected by diuretics
diuretics causing loss of K+ can lead to digoxin toxicity
which volatile is associated wtih dysrhythmias when used with digoxin?
halothane
due to sensitization of myocardium to catecholamines
2 meds we’ll use a lot that decrease automaticity of digoxin
- fentanyl
- isoflurane
MOA of PDE-3 Inhibitors
decreased hydrolysis of cAMP and cGMP, increasing cAMP & cGMP in myocardium and vascular smooth muscle
effect of PDE-3 inhibitors
positive inotropic effect with diastolic relaxation and vascular smooth muscle relaxation
clinical use of PDE-3 inhibitors
acute cardiac failure
how does increased cAMP affect the myocardium vs. vascular smooth muscle?
- myocardium: increases intracellular Ca2+
- vascular smooth muscle: decreases intracellular Ca2+ by facilitating uptake into sarcoplasmic reticulum (smooth muscle relaxation and dilation)
PDE-3 inhibitors
- Amrinone
- milrinone (Primacor)
nonselective PDE3 inhibitor
theophylline
effects of amrinone?
- inotropic effect, vasodilation
- increases CO within 5 minutes
side effects of amrinone
- hypotension d/t vasodilation
- thrombocytopenia
- dysrhytmogenic
advantage of amrinone over cardiac glycosides
therapeutic index is 100:1 vs. 1.2:1
effects of milrinone
- inotropic effect, vasodilation
- little effect on HR and myocardial O2 consumption
uses of milrinone
- acute LV dysfunction after cardiac surgery
- weaning from CBP
PDE-3 inhibitor that has 30x the inotropic potency of amrinone with less side effects
milrinone
dosing of milrinone for bolus vs. infusion
bolus 50 mcg/kg
infusion 0.5 mcg/kg/min
uses of theophylline
treatment of bronchospasm
(recommended to reserve use after beta 2 agonists and steroids have been tried)
side effects of theophylline
- may relax GE sphincter
- can cross placenta
- toxic effects: dysrhytmias
metabolism of theophylline
what things can negatively or positively affect its metabolism?
- liver metabolism
- negatively affected by alcoholism, cimetidine, or age extremes
- smoking speeds metabolism
CV effects of IV calcium admin
- inotropic effect of increased SV, decreased LVEDP (especially in patients with hypocalcemic)
- HR and SVR decrease
which contains more calcium - CaCl or CaGluconate?
CaCl
AE of giving IV calcium to pts receiving digoxin and also hypokalemic
arrhytmias
what is inotropy?
the intrinsic ability of the myocardium to pump in the absence of changes in preload or afterload
contractility is related to the rate of myocardial muscle shortening, which is dependent on:
intracellular Ca2+ concentration during systole
MOA of glucagon
- stimulates cAMP production
- causes catecholamine release
positive chronotropic effects of glucagon are useful for what treatment?
symptomatic bradycardia, especially in cases of calcium blocker or beta blocker overdose
increases HR and contractility
AE of glucagon
tachycardia - can be significant enough to interfere with filling and offset ability to increase CO (causing heart failure)
dose and elimination ½ time of glucagon
- 1-5 mg rapid bolus
- elim ½ time 3-6 min
adverse effects of glucagon
- N/V
- hyperglycemia
- paradoxical hypoglycemia
- hypokalemia
how does glucagon cause smooth muscle relaxation
increased cAMP in smooth muscle decreases intracellular Ca2+
decreased intracellular Ca2+ by facilitating uptake into SR, leading to smooth muscle relaxation
MOA of methylene blue
potent NO synthase inhibitor in vascular endothelial cells
binds to guanylate cyclase in vascular smooth muscle, blocking cGMP action
how does methylene blue increase SVR
by inhibiting NO synthase release in vascular endothelial cells
decreased NO release = increased SVR
uses of methylene blue
- septic shock
- endocarditis
- transplant
- protamine reaction
- post CPB to counteract excessive vasodilation of vasoplegic syndrome
methylene blue dose
2 mg/kg over 30 min followed by 0.5-1 mg/kg/hr if needed
why does digoxin cause a prolonged PR interval
delay through AV node
why does digoxin shorten the QTc
soo the book says more rapid repolarization and her notes say depolarization..at this moment I do not have the brain cells to know which is correct
why does digoxin cause ST segment depression
decreased slope of phase 3 depolarization of cardiac action potential
~of note phase 3 is repolarization so i think she had a typo?~
why does digoxin cause a smaller or inverted T wave
decreased slope and duration of phases 2 & 3
T/F - if your pt who takes digoxin has ST segment or T wave changes, no need to be alarmed because that’s a normal change with digoxin
(info from book)
false - changes in ST and T don’t correlate with therapeutic plasma concentrations of cardiac glycosides
may indicate myocardial ischemia
what is the most frequent cause of digoxin toxicity in the absence of renal dysfunction?
(book)
concurrent admin. of diuretics that cause K+ depletion
how can supplemental potassium help in digoxin toxicity?
(book)
decreases binding of digoxin to cardiac muscle - directly antagonizes cardiotoxic effects
(still check a K+ before you give!)
what is digibind?
(book/google)
digoxin antibodies that decrease plasma concentration of digoxin
used to treat life-threatening digoxin toxicity
