S15C187 - Digoxin toxicity Flashcards
Digoxin Pharmacology
- increases intracellular Na, by blocking Na/K ATPase pump leading to increase in intracellular calsium resulting in increased inotropy
- allso decreases AV node conduction and therefore can treat SVT but leads to bradycardia
- normal dose: 125-250mcg
- toxic dose: 1-2mg (fatalities seen at 10mg adults 4mg children)
Digoxin toxicity: clinical picture
- syncope, dysrhythmia
- GI Sx, dizzy, h/a, weak, Sz
- confusion, disorientation, delirium, hallucinations
- see yellow-green halos around objects
Dig Tox DDx
-other toxins that cause bradyarrhythmias:
CCB
BB
class IA antiarrhythmics (procainamide, quinidine)
Clonidine
Organophosphate poisonoinng
Plants: rhododendron, monkshood, tobacco, false hellebore, yew berry
SSS
ECG findings of a pt on digoxin (therapeutic)
- T wave flattening or inversion
- QT shortening
- Scooped ST segment with ST depression
- increased U wave amplitude
Dig Toxicity and K
- hyperkalemia occurs d/t inhibition of Na/K ATPase pump in acute ingestions
- K may be normal in a chronic toxicity
Dig levels
- do not rely on level for toxicity, clinical picture more important
- therapeutic levels: 0.5-2 nanograms/ml
Dig Tox: Tx
-asymptomatic: cardiac monitor, charcoal, have digi-fab ready if needed
-symptomatic:
ABC (monitor)
D: charcoal
F: digiFab
bradyarrhythmia: atropine 0.5-2mg IV, PM
ventricular dysrhythmia: MgSO4- 2-4g IV, lidocaine, phenytoin, DC CV
arrest: ACLS
hyperkalemia: AVOID CALCIUM (stone heart), glucose-insulin, sodium bicarb, digiFab, kayexalate, HD
hypomagnesemia: MgSO4
- if given digiFab, send to ICU
- if asymptomatic monitor for 12h