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Refractory Shock After a Massive Verapamil Overdose

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Refractory Shock After a Massive Verapamil Overdose

A 34-year-old man is brought in 2 hours after ingesting roughly 40 sustained-release verapamil tablets of 240 mg each (about 9.6 g) in a suicide attempt, along with a pint of vodka. He is drowsy but protects his airway. Heart rate 44 and irregular, blood pressure 72/40 mmHg, respiratory rate 18, SpO2 99% on 4 L, temperature 36.4 degrees C, and point-of-care glucose 232 mg/dL. ECG shows a junctional rhythm with a QRS of 132 ms. Venous gas: pH 7.24, lactate 7.4 mmol/L, potassium 4.1 mmol/L. He has received 3 L of crystalloid, two doses of atropine 1 mg, and calcium gluconate 3 g IV without a change in heart rate or blood pressure. Transcutaneous pacing is capturing electrically at 70/min, but he remains hypotensive at 76/44 mmHg with no improvement in palpable femoral pulse. A norepinephrine infusion is running at 12 mcg/min. The nearest ECMO center is 25 minutes away and accepts patients on peripheral VA-ECMO for poisoning.

1. Why is he refractory to the measures given, and what is the next-line therapy? Give agents, doses, monitoring, and mechanism.

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Why he is refractory. Verapamil blocks L-type calcium channels in vascular smooth muscle and myocardium, producing vasodilation, negative inotropy, and negative chronotropy. At this dose he is in a calcium-channel-blocker shock state: high-dose calcium can be overwhelmed, atropine has no residual vagal target (the block is at the channel, not the vagus), and pacing often yields electrical capture without mechanical contraction because contractility itself is calcium-dependent. Norepinephrine alone frequently fails.

Next line: high-dose insulin euglycemia therapy (HIET)

  • Regular insulin 1 unit/kg IV bolus with 25 g dextrose (0.5 g/kg) to prevent hypoglycemia.
  • Infusion starting at 0.5-1 unit/kg/hr, titrated every 30 minutes by 0.5-1 unit/kg/hr to a maximum of about 10 units/kg/hr for refractory shock.
  • Run D10 at 100-150 mL/hr and titrate to keep glucose roughly 100-250 mg/dL; check glucose every 15-30 minutes initially, then every hour.
  • Check potassium hourly; insulin shifts potassium intracellularly and hypokalemia is a real complication. Replace as needed.
  • Mechanism: insulin improves myocardial glucose uptake and carbohydrate delivery to a starved, stunned myocardium, and acts as a positive inotrope in this setting. Onset is often 30-60 minutes, so it does not replace vasopressors.

Continue and repeat calcium every 15-20 minutes while watching ionized calcium, aiming for roughly 1.5-2 times normal. Watch for extravasation injury with calcium chloride and prefer a central line if available.

2. How do you sequence further interventions, and what is your threshold for ECMO? What should you avoid?

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Sequencing in the next 30 minutes

  1. Start HIET while maintaining norepinephrine; add epinephrine if he remains hypotensive, and use a second vasopressor early rather than pushing a single agent to an extreme.
  2. Repeat calcium gluconate 3 g as above.
  3. Obtain central access, arterial line, and a urinary catheter, and correct acidosis in terms of perfusion rather than by giving bicarbonate routinely.
  4. Call the ECMO center now. The threshold for refractory cardiogenic shock after calcium-channel-blocker overdose is failure to achieve adequate perfusion despite calcium, HIET, and vasopressors. Do not wait for cardiac arrest; survival with VA-ECMO in poisoning is markedly better when patients are cannulated before arrest.
  5. Turn off the pacer if it is producing capture without perfusion, and let the team focus on inotropy; continued pacing has little value and can distract from HIET.

Avoid

  • More atropine; it will not work.
  • Class IA or III antiarrhythmics and further AV nodal blockers.
  • Flumazenil, which has no role and may precipitate seizures.
  • Interpreting electrical capture as adequate perfusion without confirming a pulse and end-organ perfusion.

What to monitor. Lactate clearance, mentation, urine output, ionized calcium, glucose, and potassium. Improving lactate and mentation are more meaningful than a heart rate number. Discuss the overdose with the ECMO service, and prepare the patient for transfer even if he transiently responds.

3. What decontamination and disposition decisions follow, given the sustained-release formulation?

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Decontamination. Activated charcoal 1 g/kg may be considered if he is within 1-2 hours of ingestion and the airway is protected; it is not a rescue therapy and does not replace HIET. Sustained-release verapamil can remain in the gut for many hours, so a delayed presentation does not automatically exclude charcoal, but the airway must be secure or the risk of aspiration in a drowsy, hypotensive patient outweighs benefit. Whole bowel irrigation with polyethylene glycol has weak evidence and should not be used in a hemodynamically unstable or ileus-prone patient; it is not a priority here.

What will not work. Hemodialysis and hemoperfusion do not meaningfully clear verapamil, which has a large volume of distribution and high protein binding.

Disposition. ICU admission with continuous cardiac monitoring and serial ECGs for at least 24 hours, longer if there is any hemodynamic instability or if the patient required HIET or pressors. The sustained-release formulation routinely produces prolonged and sometimes biphasic toxicity, so a patient who looks well at 6 hours is not yet safe.

Other necessary steps

  • Repeat glucose and potassium after stopping HIET gradually, watching for rebound hyperglycemia and hyperkalemia as insulin wears off.
  • Assess for coingestants, including acetaminophen and salicylates, and check an ethanol level given the history.
  • Involve psychiatry and poison control, and document capacity assessment; this was a suicide attempt and he needs a safe disposition plan, not just medical clearance.
  • Discuss the prognosis and the possibility of a prolonged ICU course with his family.