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Stem
A 26-year-old woman is brought to the emergency department by ambulance four hours after a deliberate overdose. She took forty tablets of sustained-release verapamil 240 mg (9.6 g) that belonged to her mother, along with an unknown quantity of alcohol. She is drowsy but rousable.
On examination: pulse 38/min (junctional rhythm), blood pressure 74/45 mmHg, respiratory rate 14/min, oxygen saturation 96 percent on air, GCS 13, cool peripheries, capillary refill 5 seconds, blood glucose 14 mmol/L. 12-lead ECG shows junctional bradycardia with 2:1 AV block and a normal QRS duration. Venous gas: pH 7.18, lactate 6.2 mmol/L.
Questions
a) What is the diagnosis, and which TWO features in the stem distinguish this from a beta-blocker overdose? (2 marks)
Diagnosis: severe sustained-release verapamil (calcium-channel blocker) overdose with cardiogenic shock. Distinguishing features (any two): (1) HYPERGLYCAEMIA (glucose 14 mmol/L) with metabolic acidosis (pH 7.18, lactate 6.2) — verapamil blocks L-type calcium channels on pancreatic beta cells, inhibiting insulin release; a beta-blocker overdose does NOT cause hyperglycaemia (and may cause hypoglycaemia). (2) The sustained-release formulation and the 4-hour delay to severe toxicity — sustained-release verapamil produces a delayed, prolonged, biphasic course; immediate-release BB toxicity would typically have declared itself within 1-2 hours.
b) Outline the mechanism by which verapamil produces BOTH its cardiac AND its metabolic (hyperglycaemic) effects. (3 marks)
Verapamil is a non-dihydropyridine calcium-channel blocker that directly blocks the L-type voltage-gated calcium channel. In the heart, this channel carries the slow inward calcium current (I_Ca-L) responsible for the upstroke of the action potential in the SA and AV nodes (slow-response tissue) and for the plateau-phase calcium influx that drives excitation-contraction coupling in working myocytes. Blockade therefore produces negative chronotropy (bradycardia), negative dromotropy (AV block) and negative inotropy (cardiogenic shock) — explaining the junctional bradycardia, 2:1 AV block and hypotension in this patient. In the pancreatic beta cell, the L-type calcium channel mediates the calcium influx that triggers insulin granule exocytosis; verapamil blocks this calcium entry -> insulin release is impaired -> hyperglycaemia, and impaired cardiac carbohydrate metabolism plus shock produces the metabolic (lactic) acidosis. This combination of hyperglycaemia + acidosis is the discriminator from beta-blocker overdose.
c) Describe the stepwise management of this patient, with drug doses. (4 marks)
- ABCDE + immediate measures — airway (intubate early if GCS drops further — sustained-release verapamil patients deteriorate suddenly), high-flow oxygen, two large-bore IV cannulae, continuous cardiac monitoring, arterial blood gas. Cautious IV crystalloid boluses (250-500 mL aliquots — the myocardium is failing; avoid overload).
- Decontamination — whole-bowel irrigation with polyethylene glycol 1-2 L/h via nasogastric tube (this is a sustained-release ingestion — continue until rectal effluent clear). Activated charcoal is of limited benefit at 4 h.
- IV CALCIUM — calcium chloride 10% 10-20 mL (1 g) IV via a central line over 5-10 min, OR calcium gluconate 10% 30-60 mL via a peripheral line; repeat every 10-20 min to effect, then an infusion. This provides supraphysiological calcium to overcome the channel blockade.
- High-dose insulin euglycaemia therapy (HIET) — the most effective inotrope — regular insulin 1 unit/kg IV bolus then 0.5-1 unit/kg/h infusion (titrate up to 10 U/kg/h in severe), with concurrent dextrose (her glucose is already 14 mmol/L, so the initial dextrose bolus can be withheld and glucose monitored every 30 min, starting dextrose when glucose falls below 10 mmol/L). Supplement potassium to keep serum K+ above 2.5-2.8 mmol/L (insulin drives K+ into cells).
- Vasopressors — noradrenaline 0.05-1 microgram/kg/min (vasoplegia) and/or adrenaline (inotropy + chronotropy), titrated to MAP over 65 mmHg. High doses in combination are expected.
- Escalation — if refractory, intravenous lipid emulsion (20% lipid 1.5 mL/kg bolus then 0.25 mL/kg/min) and early referral for VA-ECMO (bridge to drug clearance). ICU admission for at least 24 h.
d) State the disposition principle for this ingestion, and ONE treatment that should be avoided if digoxin co-ingestion is suspected, with the reason. (1 mark)
Disposition: admit to ICU for at least 24 hours of continuous monitoring because sustained-release verapamil produces a delayed, prolonged, biphasic course — the patient can deteriorate again at 12-24 h despite initial stabilisation. If digoxin co-ingestion is suspected, AVOID IV calcium (the classic 'stone heart' teaching holds that calcium worsens the already calcium-overloaded digoxin-toxic myocardium) — use digoxin Fab fragments instead for the digoxin component.