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[Diltiazem poisoning: hemodynamic aspects].
C Beauvoir1, D Passeron, G du Cailar
1Département d'Anesthésie-Réanimation A, Hôpital Lapeyronie, Montpellier.
Annales Francaises D'Anesthesie Et De Reanimation
|January 1, 1991
Summary
A massive overdose of diltiazem and benzodiazepines in a post-myocardial infarction patient caused severe cardiac issues. Aggressive vasopressor and inotropic support ultimately restored sinus rhythm and improved hemodynamics.
Area of Science:
- Cardiology
- Clinical Toxicology
- Pharmacology
Background:
- A 50-year-old male with a recent myocardial infarction (MI) presented with a massive overdose of diltiazem, potassium clorazepate, and nordazepate.
- The patient's history of MI complicated the management of the overdose.
Observation:
- On admission, the patient exhibited severe hypotension (80 mmHg systolic), bradycardia with irregular rhythm (60 bpm), superficial tachypnea (40 cpm), and hypoxia (PaO2: 63.5 mmHg).
- Electrocardiogram (ECG) showed complete sinus arrest in addition to signs of previous MI.
- Initial treatments including gastric lavage, activated charcoal, atropine, and calcium chloride failed to correct the cardiac dysrhythmia.
Findings:
- Mechanical ventilation and intensive hemodynamic support with isoproterenol, dobutamine, and noradrenaline were required to manage cardiovascular collapse and restore sinus rhythm.
- A combination of noradrenaline and dobutamine, followed by adrenaline, was crucial in stabilizing the patient's hemodynamics.
- Spontaneous sinus rhythm returned after 7 hours of intensive vasopressor and inotropic therapy.
Implications:
- This case highlights the critical management of massive calcium channel blocker overdose, particularly in patients with compromised cardiac function.
- The successful use of combined vasopressor and inotropic agents underscores their importance in managing severe overdose-induced cardiovascular collapse.
- Understanding the interplay between cellular calcium dynamics and the adrenergic system is vital for treating such complex toxicological emergencies.