Tox: Cardiac Meds Flashcards
(45 cards)
Non-cardiac SE of propranolol
Can cause delirium in absence of cardiovascular effects, seizures due to lipophilicity
Normal function of beta receptors
B1: Cardiac effects (inc HR, contractility, conduction), kidney (inc renin secretion), eyes (inc aqueous humor).
B2: Smooth muscle relaxation (esp lung)
B3: lipolysis in adipose tissue
Symptoms of beta blocker overdose
CVD: hypoTN, bradycardia, cardiogenic shock, QRS/QTc prolongation.
Pulm: resp depression, apnea, bronchospasm.
Neuro: AMS, coma, seizures w/ lipophilic agents (propranolol)
Endo: HYPERK, HYPOGLYCEMIA (not always, more likely in kids)
DDx for BB overdose
CCB, clonidine, dig toxicity
Tx of BB overdose
Decontam:
1) AC if within 1hr
2) Consider GL if presenting within 1hr after ingestion of large quantity of potentially lethal agents that lack effective antidote (e.g. verpamil, diltiazem, propranolol).
3) WBI: if large OD of modified release preparation and patent airway.
Additional Meds for brady/hypoTN:
1) Atropine 1mg IV if bradycardia (repeat up to 3mg)
2) Calcium gluconate: 3-6g
3) Glucagon 1-5mg IV push (max 15 mg)
4) High dose insulin R: 1U/kg IV bolus followed by infusion at 1U/kg/hr (with dextrose)
5) Lipid emulsion as last resort
6) Levophed prn
Non-pharma:
Cardiac pacing, intra-aortic balloon pump, ECMO if pharma fails
Specific additional treatment for propranolol
Sodium bicarb as can cause QRS widening due to Na channel blockade
Specific additional treatment for atenolol OD
Hemodialysis
Mxn of glucagon in BB/CCB OD
bypasses beta-adrenergic receptors to increase cAMP resulting in increased calcium influx into the cell (requires high doses, 5-10mg IV)
Mxn of CCB toxicity
Blockade of voltage gated Ca channels –> reduced Ca influx into cells.
In cardiac cells, decreased SA node activity, contractility and slowed AV conduction.
In smooth muscles (periph vasc) -> relaxation and vasodilation.
Panc beta cells –> reduced insulin release.
Agent specific toxicities for: verapamil, diltiazem, dihydropyridines (e.g. nifedipine)
Verapamil: Major effect at SA and AV nodes
Diltiazem: Intermediate activity at both cardiac and peripheral vasculature.
DHPs: Major effect on peripheral vasculature.
**Specificity between peripheral vs central cardiovascular effects may be lost in overdose.
Symptoms/exam findings CCB OD
CVD: hypoTN, bradycardia, cardiogenic shock. May see QRS widening, QTc prolongation.
Neuro: AMS, seizures, coma, respiratory depression.
Endo: HYPERglycemia.
How can BG levels aid in differentiating CCB and BB OD?
BB OD typically euglycemic, CCB OD usually hyperglycemic.
DDx CCB OD
BB, digoxin, clonidine OD
GI decontam options for CCB OD
GL: only if presenting within 1hr ingestion and lack of effective antidote (verapamil, dilt, propranolol).
AC: If within 1hr presentation and airway protected.
WBI: large overdose of SR preparation and protected airway.
Mgmt of bradycardia and hypoTN in CCB OD
Initial: atropine, vasopressors (e.g. levo, epi).
Calcium (inc intracellular Ca/contractility).
Glucagon (may be less successful than with BB toxicity).
High-dose insulin (to inc cardiac output, 1U/kg bolus, then 0.5U/kg infusion with dextrose)
Non-pharma: pacing, intra-aortic balloon pump, ECMO if pharma fails.
What is digoxin/purpose
Cardiac glycoside, derived from foxglove.
Used to increase the force of contraction in HFrEF and reduce AV conduction in AF.
Narrow therapeutic window
How is digoxin excreted
renally
MOA digoxin
inactivates Na/K ATPase on cardiac cell membrane -> increased intracellular Ca, extracellular K.
Increases automaticity.
Reduces conduction through AV node via increased vagal tone.
Compare acute vs chronic dig toxicity
Acute:
Severe Na/K ATPase pump inhibition –> hyperK (predictor of poor outcome w/o tx).
Chronic:
Caused by increase in dose or decreased GFR.
Hypokalemia may enhance chronic toxicity (tox at lower dig levels).
Higher overall mortality (generally sicker population at baseline).
Symptoms of dig toxicity
Onset insidious if chronic.
CVD:
Acute –> more bradycardia, AV blocks.
Chronic –> ventricular dysrhythmias. Bidirectional VT, slow AF, almost any dysrhythmia other than SVT or TdP.
GI: n/v, AN.
Neuro: visual disturbance (scotoma, yellow halos around lights), HA, generalized weakness, AMS.
What specific visual changes may be seen with dig toxicity?
Scotoma, yellow halos around lights.
What ECG finding is fairly specific for cardiac glycoside toxicity (e.g. dig)?
Bidirectional VT
Diagnosis of dig toxicity
Serum concentration may not correlate with symptoms and may take 4-6hrs to reach steady state in acute ingestion.
(so how to dx??)
Tx of dig toxicity
Supportive.
Ok to use Ca++ if hyperK (previously thought not to).
Brady: atropine, pacing.
Tachydysrhythmias: cardioversion/defib may induce VF/VT. Phenytoin and lidocaine to be safest (phenytoin can increase AV conduction).
DigiFab if indicated.
