The hypotensive and bradycardic patient

Notes from Ben Sandefur Grand Rounds "The hypotensive and bradycardic patient"

By Damian Baalmann, M.D.

Broad Differential for Hypotensive + Bradycardic Patient

1. Toxic
   1. CCB
   2. Beta Blocker
   3. Cardiac Glycodisde (Digoxin)
   4. Alpha-2 Agonist (Clonidine)
   5. Organophosphate
2. Cardiac
   1. Cardiac Conduction Disease
      1. Infarction
      2. Primary Conduction Disease
      3. Pacemaker Failure
      4. Infectious: Lyme Carditis/ Chaga’s Disease
3. Electrolyte
   1. Hyperkalemia
4. Endocrine
   1. Hypoadrenalism
   2. Hypothyroidism
5. Environmental
   1. Hypothermia
6. Gastrointestinal
   1. Massive GI Bleed (vaso-vagal response)
7. Neurogenic
   1. Neurogenic Shock

• Remember that often the presentation is multifactorial. Additionally, bradycardia + hypotension is often the final common pathway for dying patient, regardless of etiology.

Calcium Channel Blockers

• Classic Non-Dihyhdropyridine CCB overdose: Hypotensive, Bradycardic, and Hyperglycemic

Beta-Blockers

• Pharmacology: G-Protein Linked Receptor→Adenylyl cyclase→cAMP→PKA
• Beta-Blocker Overdose: Hypotensive, Bradycardic, Hypo- or Normoglycemic
  • CNS effects with propranolol (b/c it crosses the BBB)

Therapeutic Options for CCB or Beta-Blocker Toxic Patient

• Give Calcium!
  • Calcium Gluconate: PIV, dose: 3-6g
  • Calcium Chloride: Central access, dose: 1-2g
• Glucagon
  • Activates G-protein and bypasses B-blocker
• Amrinone
  • Increases cAMP in the cell
• Vasopressors
  • Works on Beta receptor
• Insulin
  • Overcomes hypoglycemia of CCB
  • Glucose entry in the Myocytes →increase ionotropy
  • Bolus 1U/kg, infusion 1-10U/kg/hr, D10 @100mL/hr, replete K+, avoid vasopressors
• Intralipid Therapy
  • 1.5 mL/kg of 20% solution of 2-3min; 0.25-0.5 mL/kg/min drip for 30-60 min
  • Data not quite as robust as hyperinsulinemia therapy
• Also think of Transvenous Pacemaker, Intra-aortic balloon pump, ECMO, Cardioplumonary Bypass

Summary

• Think broadly with differential of hypotension and bradycardia
• Animal data strongly supports using insulin for increasing survival in CCB and beta-blocker; vasopressors ↑SVR and may be counterproductive
• Glucagon, Vasopressors, and Amrinone all display tachyphylaxis because they rely on cAMP pathway which eventually is depleted
• Consult Poison Control Center Early: 1-800-222-1222
• High-dose insulin therapy has emerged as an effective therapy for CCB and beta-blocker toxicity
• Lipid Emulsion Therapy may be helpful in cardiotoxicity or cardiac arrest from lipophilic cardiotoxic medications, but the data is not as compelling