Pharmacology · Year 2 · from Pharmacology
Case 3: Beta-Blocker Overdose
Clinical Scenario
A 65-year-old male presents to the emergency department after intentional ingestion of his propranolol prescription.
Patient Demographics
- Age: 65 years
- Sex: Male
- Weight: 82 kg
Chief Complaint
Found lethargic with an empty pill bottle
History of Present Illness
The patient has a history of hypertension, migraine prophylaxis, and depression. His wife found him minimally responsive with an empty bottle of propranolol 80 mg (90 tablets dispensed 3 days ago). He was recently diagnosed with terminal cancer and expressed suicidal ideation. Last seen normal 3 hours prior.
Physical Examination
- Vital Signs: BP 70/45 mmHg, HR 38 bpm, RR 8, T 35.8C, SpO2 91% on room air
- General: Obtunded, responds only to painful stimuli
- Cardiovascular: Severe bradycardia, weak pulses
- Respiratory: Shallow respirations, mild wheezes bilaterally
- Neurological: GCS 7 (E2V2M3), pupils 3 mm reactive
- Skin: Cool, pale, mottled
- Glucose (bedside): 52 mg/dL
Workup and Results
| Test | Result | Reference Range |
|---|---|---|
| ECG | Sinus bradycardia 38 bpm, first-degree AV block, QRS 88 ms | - |
| Glucose | 48 mg/dL | 70-100 mg/dL |
| Potassium | 5.4 mEq/L | 3.5-5.0 mEq/L |
| Lactate | 6.2 mmol/L | 0.5-2.0 mmol/L |
| Troponin I | 0.12 ng/mL | <0.04 ng/mL |
Diagnosis
Severe beta-blocker toxicity with cardiogenic shock, bradycardia, bronchospasm, and hypoglycemia
Autonomic Pharmacology Principles Illustrated
- Beta-1 blockade (cardiac): Negative chronotropy (bradycardia) and negative inotropy (decreased contractility).
- Beta-2 blockade (bronchial): Bronchospasm from unopposed parasympathetic tone - significant with non-selective blockers like propranolol.
- Beta-2 blockade (metabolic): Hypoglycemia from impaired glycogenolysis and gluconeogenesis.
- CNS effects: Propranolol is lipophilic and crosses BBB, causing sedation, seizures.
- Hyperkalemia: Beta-2 receptors normally promote potassium uptake into cells.
Treatment
- Airway management: Intubation for airway protection
- IV fluids: Bolus crystalloid for hypotension
- Atropine: 1 mg IV for bradycardia (limited efficacy)
- Glucagon: 5-10 mg IV bolus, then 2-10 mg/hr infusion - first-line specific antidote
- High-dose insulin/euglycemia therapy: Regular insulin 1 unit/kg bolus, then 0.5-1 unit/kg/hr with dextrose
- Calcium gluconate: 3 g IV for inotropy
- Vasopressors: Norepinephrine if refractory
- Lipid emulsion: 1.5 mL/kg 20% intralipid for lipophilic beta-blockers
- Dextrose: For hypoglycemia
- Consider transcutaneous pacing for refractory bradycardia
Key Learning Points
- Beta-blocker toxicity causes the triad of bradycardia, hypotension, and hypoglycemia
- Non-selective agents (propranolol) also cause bronchospasm
- Glucagon works by activating adenylyl cyclase independent of beta-receptors
- High-dose insulin improves cardiac contractility through enhanced glucose utilization
- Lipid emulsion therapy is effective for lipophilic beta-blockers