INTRODUCTION: Cardiac dysrhythmias, other than sinus tachycardia, rarely occur with salicylate poisoning. When dysrhythmias do occur, they are typically a terminal event. CASE REPORT: A 45-year-old woman presented an unknown amount of time after an intentional ingestion of aspirin and acetaminophen. On presentation her vital signs were T 39 degrees C, P 125 beats/minute, R 26 breaths/minute, and BP 153/79 mmHg. She was initially obtunded, but minutes after presentation had a generalized tonic-clonic seizure lasting approximately two minutes, which ceased after 2 mg of intravenous lorazepam. She was sedated, intubated and treated with sodium bicarbonate. Her peak salicylate concentration was 152 mg/dL. Her course was complicated by seizures and dysrhythmias, including monomorphic ventricular tachycardia and Torsades de Pointes. With bicarbonate therapy, hemodialysis, and veno-venous hemofiltration, she survived neurologically intact. DISCUSSION: The etiology of these dysrhythmias is likely multifactorial. Metabolic derangements typically encountered with severe salicylism, including insensible water losses, respiratory alkalosis, and metabolic acidosis, may contribute. Iatrogenic causes, especially sodium bicarbonate therapy, may cause hypokalemia, hypocalcemia, and hypomagnesemia. Additionally, animal data suggests that high salicylate concentrations may have direct deleterious effects on the electrophysiology of cardiac cells, specifically by its action on the SA node and on the action potential of atria and Purkinje fibers. CONCLUSIONS: Non-fatal ventricular dysrhythmias associated with salicylate toxicity are rare in patients who survive. The causes of dysrhythmias in salicylate may include electrolyte abnormalities and a direct effect of salicylate on myocardial membrane permeability.
INTRODUCTION:Cardiac dysrhythmias, other than sinus tachycardia, rarely occur with salicylate poisoning. When dysrhythmias do occur, they are typically a terminal event. CASE REPORT: A 45-year-old woman presented an unknown amount of time after an intentional ingestion of aspirin and acetaminophen. On presentation her vital signs were T 39 degrees C, P 125 beats/minute, R 26 breaths/minute, and BP 153/79 mmHg. She was initially obtunded, but minutes after presentation had a generalized tonic-clonic seizure lasting approximately two minutes, which ceased after 2 mg of intravenous lorazepam. She was sedated, intubated and treated with sodium bicarbonate. Her peak salicylate concentration was 152 mg/dL. Her course was complicated by seizures and dysrhythmias, including monomorphic ventricular tachycardia and Torsades de Pointes. With bicarbonate therapy, hemodialysis, and veno-venous hemofiltration, she survived neurologically intact. DISCUSSION: The etiology of these dysrhythmias is likely multifactorial. Metabolic derangements typically encountered with severe salicylism, including insensible water losses, respiratory alkalosis, and metabolic acidosis, may contribute. Iatrogenic causes, especially sodium bicarbonate therapy, may cause hypokalemia, hypocalcemia, and hypomagnesemia. Additionally, animal data suggests that high salicylate concentrations may have direct deleterious effects on the electrophysiology of cardiac cells, specifically by its action on the SA node and on the action potential of atria and Purkinje fibers. CONCLUSIONS: Non-fatal ventricular dysrhythmias associated with salicylate toxicity are rare in patients who survive. The causes of dysrhythmias in salicylate may include electrolyte abnormalities and a direct effect of salicylate on myocardial membrane permeability.