Beta Blocker Toxicity
In the setting of presumed toxic ingestion, the differential diagnosis of a patient presenting with bradycardia and hypotension should include: beta-blockade, calcium channel blockade, digoxin toxicity, and clonidine toxicity - Erica Simon DO
HWN Suggests
Beta blocker overdose
Glucagon has traditionally been considered the first line antidote treatment, but this tradition is based on anecdotes and elder authority... High dose insulin euglycaemic therapy is becoming the new favourite, but is still based largely on case reports and animal studies (Woodward et al, 2014). Also, nobody really knows how it works... Atropine is worth a try, but probably won't work... Vasopressors and inotropes may be useful in some cases, but there will always be the possibility of disaster.
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Beta Blocker Toxicity
Many centers throughout the country are becoming much more comfortable with high dose insulin (hyperinsulinemia-euglycemia therapy). All emergency physicians, intensivists, and pharmacists should discuss its use in beta-blocker poisoning with their regional poison center if considering its use. Dosing, monitoring, and dextrose supplementation recommendations may vary. Sadly, pacing is rarely effective. The reason for this is thought to be that the clinical state of sick beta-blocker poisoned patients is not only dependent on the heart rate. In beta-blocker poisoned patients with characteristic vital sign abnormalities, glucagon is absolutely my first choice medication.
High Dose Insulin/Euglycemia Regimen
Bolus 1 IU/kg along with 25 g dextrose. Avoid insulin bolus if glucose < 150. Avoid dextrose bolus if glucose > 400. Start 0.5 IU/kg/hr drip with IV glucose replacement as needed – aim for a blood glucose of 100-250 with accuchecks every 30 minutes. Always use central access for these infusion, in order to use higher concentration glucose and avoid volume overload. Monitor potassium closely while giving insulin.
Articles of Interest
Beta Blockers Overdose
High-dose insulin (HDI) therapy improves cardiac function without increasing myocardial work. Early initiation of HDI therapy (start when vasopressors are started)is recommended as response may take 30-90 minutes. Start with 1 unit/kg insulin bolus with 50 mL D50W, followed by a continuous infusion of 1 unit/kg/hour, titrating by 0.5-1 unit/kg/hour every 20-30 minutes to achieve a systolic blood pressure of 90-100 mm Hg). Intravenous dextrose should be infused at 0.5 g/kg/h (Usually D10W at 100-200 mL/h).
Beta-Blocker Overdose
Two beta-blockers require special consideration: — propanolol -> causes sodium channel blockade -> QRS widening -> treat with NaHCO3. — sotalol -> causes potassium efflux blockade -> long QT -> monitor for Torsades.
Calcium Channel Blocker (CCB) & Beta-Blocker (BBl) overdose
Pitfalls: Delayed initiation of high-dose insulin. Reliance on therapies that are unlikely to work (e.g., atropine, IV calcium, and glucagon). Early focus on placing a transvenous pacemaker (this wastes time, often doesn't capture the myocardium). Note that traditional algorithms for bradycardia don't work for these patients.
Does Glucagon Really Work for Beta Blocker Overdose?
There is a paucity of studies on the efficacy and safety of glucagon in beta blocker toxicity in the literature, and we commend the authors for their thoughtful undertaking of a difficult task.
EM@3AM – Beta-Blocker Toxicity
Bradycardia (most common initial sign), hypotension, altered mental status, respiratory arrest, dysrhythmias (atrioventricular block (AV) (beta-blockers capable of fast sodium channel blockade), or ventricular fibrillation. Hypoglycemia is more common in the pediatric population. Seizures are often witnessed following toxic propranolol exposure.
