Today, we discussed the case of a middle-aged man with a history of HIV and HCV cirrhosis who presented with symptomatic, sinus bradycardia, likely secondary to metoprolol poisoning!
- Atropine works well for conduction abnormalities above or at the level of the AV node.
- Approach sinus bradycardia by thinking about intrinsic vs extrinsic causes!
- Hemodialysis has a minimal role in treatment of beta blocker overdose. Only hydrophilic beta blockers (atenolol, nadolol, sotalol) are removed by HD, but metoprolol, propranolol, and timolol are not.
APPROACH TO BRADYCARDIA (AND MORE ON BETA-BLOCKER POISONING)
STEP 1: Stabilize the patient!
- Is airway secure? Is ACLS needed?
- Atropine can be given early. Give in dose of 0.5 to 1 mg every 3-5 minutes for a total of 0.03 to 0.04 mg/kg (Remember that Atropine works above or at the level of the AV node, and does not work for conductional abnormalities below the His)
- If symptoms do not improve with atropine, consider dopamine or epinephrine.
- If still symptomatic despite pharmacologic agents, do transcutaneous pacing!
- Treat hypotension with IV fluids (but not if patient is in heart failure!)|
STEP 2: After buying yourself more time, determine the etiology behind the bradycardia
- Intrinsic Causes
– Ischemia: always think about this and rule-out. Acute MI vs chronic ischemia.
– Collagen vascular disease
– Viral myocarditis
– Lyme Disease
– Inherited: Neuromuscular disorder, Friedreich ataxia, X-lined muscular dystrophy
– Idiopathic degenerative disorder
- Extrinsic Causes
– Medication effect: anti-arrhythmics, calcium channel blockers, beta blockers, amiodarone, clonidine, lithium, amitriptyline, and many more!
– Electrolyte deranagements: Hyperkalemia
– Endocrinopathy: hypothyroidism
– Intracranial hypertension
– Autonomically mediated: vasovagal, carotid sinus hypersensitivity
STEP 3: Treat the underlying cause – We will focus on Beta-blocker poisoning here.
- Glucagon: first-line treatment for beta-blocker overdose!
- Give 5 mg IV bolus over 1 minute; may repeat the bolus if there is no increase in pulse or BP after 10-15 minutes (you should see an effect within 1-3 min, with a peak response at 5-7 min!)
- Note, vomiting is common following glucagon administration. Can give prophylactic or concurrent anti-emetics.
- Mechanism of action: Activates the cAMP at a site independent of beta agonist à leads to increase in intracellular Calcium à augments cardiac contractility
- Calcium: A few case reports have shown efficacy of IV calcium in treating beta-blocker toxicity.
- Beware of iatrogenic overdose!
- Insulin and glucose: Mechanism of action is not entirely understood, but the current thought is beta blockers inhibit pancreatic insulin release à reduction in available glucose à diminished cardiac output. Insulin and glucose improve inotropy by providing substrate for aerobic metabolism within the myocyte!
- GI decontamination: activated charcoal