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Kusumoto et al 2018 Bradycardia Clinical Practice Guidelines August 20, 2019 Circulation. 2019;140:e382–e482. DOI: 10.1161/CIR.0000000000000628 e408 CLINICAL STATEMENTS AND GUIDELINES trials or observational series data to support or discourage its use in this setting. Because isoproterenol increases myocardial oxygen demand through beta-1 effects while decreasing coronary perfusion attributable to beta-2 effects, it is best avoided in settings where there is concern for coronary ischemia.S5.3.2.1-25,S5.3.2.1-26 From a clinical standpoint, it is predominantly used in the electrophysiology laboratory (1-20 mcg/ min intravenously) and has only a second-line role in treatment of bradycardia in the setting of resuscitation.S5.3.2.1-27 Two RCTs of isoproterenol as adjunctive therapy in the setting of cardiac arrest did not show improved return of spontaneous circulation or survival to hospital discharge.S5.3.2.1- 28,S5.3.2.1-29 A trial of 82 patients presenting with unstable bradycardia refractory to intravenous fluid bolus and atropine randomized to transcutaneous pacing or dopamine at doses of 5 mcg/ kg/min, titrated every 2 minutes by 5 mcg/kg/min to a maximum of 20 mcg/kg/min, showed no difference in survival to hospital discharge or serious adverse events.S5.3.2.1-11 3. In a study of 25 patients who had undergone heart transplant, atropine at standard clinical doses resulted in paradoxical heart block or less commonly sinus arrest in 20%.S5.3.2.1-12 Although sympathetic reinnervation can be observed after long-term follow-up after orthotopic heart transplant, evidence for parasympathetic reinnervation is far less common: 34% versus 11% in 1 series that used heart rate variability response to neck suction to test autonomic responses.S5.3.2.1-30 5.3.2.2. Therapy of Beta Blocker and Calcium Channel Blocker Mediated Bradycardia Attributable to SND or Atrioventricular Block Recommendations for Therapy of Beta Blocker and Calcium Channel Blocker Mediated Bradycardia Referenced studies that support recommendations are summarized in Online Data Supplement 12. COR LOE Recommendations IIa C-LD 1. In patients with bradycardia associated with symptoms or hemodynamic compromise because of calcium channel blocker overdose, intravenous calcium is reasonable to increase heart rate and improve symptoms.S5.3.2.2-1–S5.3.2.2-3 IIa C-LD 2. In patients with bradycardia associated with symptoms or hemodynamic compromise because of beta-blocker or calcium channel blocker overdose, glucagon is reasonable to increase heart rate and improve symptoms.S5.3.2.2-4,S5.3.2.2-5 IIa C-LD 3. In patients with bradycardia associated with symptoms or hemodynamic compromise because of beta-blocker or calcium channel blocker overdose, high-dose insulin therapy is reasonable to increase heart rate and improve symptoms.S5.3.2.2-6,S5.3.2.2-7 Synopsis Cardiovascular effects of beta-blocker and calcium channel blocker toxicity are systemic and can be fatal because of profound negative chronotropic and inotropic effects, as well as vasodilation.S5.3.2.2-8 Pharmacotherapy is supportive and directed toward improving hemodynamic stability.S5.3.2.2-8 Shock often requires adrenergic pressor support.S5.3.2.2-3,S5.3.2.2-6–S5.3.2.2-9 The evidence base and specific treatment considerations for beta-blocker and calcium channel blocker mediated bradycardia are the same for SND and atrioventricular block (Table 8). Recommendation-Specific Supportive Text 1. Case reports and small series show variable results in response to calcium infusion in the treatment of calcium channel blocker overdose, and no randomized trial data are available to support its use.S5.3.2.2-1,S5.3.2.2-10–S5.3.2.2-12 Because of improvements in heart rate and blood pressure, coupled with low risk of adverse effects, intravenous calcium is often recommended as a first-line therapy if central or reliable peripheral venous access is present.S5.3.2.2-2,S5.3.2.2-13 A systematic review of treatment for calcium channel blocker poisoning not specific to SND found 7 animal studies demonstrating reduced mortality and hemodynamic improvement with intravenous calcium.S5.3.2.2-3 Hemodynamic benefits in humans were less consistent in 11 case series and 21 case reports, but adverse effects, primarily hypercalcemia, were rare.S5.3.2.2-3 Both calcium chloride and calcium gluconate (to minimize peripheral vein irritation) are commonly used.S5.3.2.2-3,S5.3.2.2-13 2. Glucagon is a vasoactive polypeptide, which counteracts the effects of beta blockers by activation of hepatic adenyl cyclase that promotes glycogenesis.S5.3.2.2-14 Although scores of case reports and case series (the largest comprised of 9 patientsS5.3.2.2-5) have been published showing increased heart rate in settings of beta-blocker and calcium channel blocker overdose, no clinical trials have been performed.S5.3.2.2-4 The standard therapy in cardiac arrest is a bolus of 3 to 10 mg given over 3 to 5 minutes. Because effects are transient, an infusion of 3 to 5 mg/h is also initiated.S5.3.2.2-9 Side effects of glucagon therapy include nausea and vomiting, which is of particular concern when ability to protect the airway is compromised. 3. High-dose insulin therapy, using a bolus of 1 unit/ kg followed by an infusion of 0.5 units/kg/h, has been studied in patients with severe beta-blocker Downloaded from http://ahajournals.org by on October 7, 2026