Ep 155 Treatment of Bradycardia and Bradydysrhythmias

In Part 1 of our 2-part series on bradycardia and bradydysrhythmias we discussed a practical approach with electrophysiologist Paul Dorian and EM doc Tarlan Hedayati. In this, part 2, we discuss details of treatment. We answer questions such as: When should pacing be prioritized over medications and vice versa? What are the latest recommendations about dosing of atropine and when is atropine likely to be detrimental? How is the treatment of bradycardia different in the patient with hypothermia? Cardiac ischemia? Myxedema coma? AV nodal blocker overdose? What are the most common pitfalls in utilizing transcutaneous and transvenous pacing? and many more... Podcast production & editing by Anton Helman, sound design by Yuang Chen Written Summary and blog post by Anton Helman April 2021 Cite this podcast as: Helman, A. Dorian, P. Hedayati, T. Episode 155 Treatment of Bradycardia and Bradydysrhythmias. Emergency Medicine Cases. April, 2021. https://emergencymedicinecases.com/treatment-bradycardia-bradydysrhythmias. Accessed [date] Go to part 1 of this 2-part podcast on bradycardia and bradydysrhythmias Suggested Treatment Algorithm for Crashing Bradycardic Patient Without an Obvious Cause * For the crashing patient administer drugs/fluids and start transcutaneous pacing simultaneously * There is a paucity of randomized trials for medications to treat bradycardia; these recommendations are based on the ACLS guidelines, weak observational data and expert opinion * The underlying cause needs to be taken into consideration (i.e., for B-blocker overdose or Calcium channel blocker overdose, consider high dose insulin, for digoxin overdose consider digiFab, for the hypothermic patient rewarming is usually required before consideration of medications or pacing, for myxedema coma, consider thyroxine) Atropine for bradycardia and bradydysrhythmias Atropine essentially fires up the SA node by poisoning the vagus nerve; it therefore is effective only if the distal conduction system is conducting normally. Overall, only 28% of patients with bradycardia have been shown to respond to atropine. Appropriately dosed atropine is usually effective for proximal AV block, sinus bradycardia and junctional rhythms but is not useful (nor particularly harmful) in distal AV block (idioventricular rhythms and second-degree type II and third-degree AV block). In the latest 2020 AHA update the recommended single dose administration of atropine was increased from 0.5 mg to 1 mg based on data suggesting that at low doses, atropine may cause paradoxical bradycardia. At low doses, atropine decreases heart rate by blocking M1 acetylcholine receptors in the parasympathetic ganglion controlling the SA node. At higher doses, atropine increases heart rate by blocking M2 acetylcholine receptors on the myocardium itself. Atropine-induced bradycardia may be especially difficult to manage in patients who are morbidly obese or post cardiac transplantation. Atropine dosing: 1mg IV q3 mins, max 3mg (cholinergic poisoning may require higher doses using a doubling approach: 1mg, then 2mg, 4mg, 8mg etc.) Beware: cardiac transplant patients may have paradoxical worsening of bradycardia with atropine; atropine should generally be avoided in cardiac transplant patients Most sick bradycardia patients will not respond to atropine, so it is important to move quickly to chronotropic drugs such as epinephrine if atropine is not effective. Pitfall: underdosing atropine and waiting for it to work too long before moving onto a chron...