A Collapse, A Clue, A Comeback: Solving a Deadly Mystery

Background: Ventricular tachycardia arrest can arise from metabolic disturbances, electrolyte depletion, and physiological stress. In this case, severe hypokalemia and hypomagnesemia, exacerbated by diabetic ketoacidosis and precipitous proton pump inhibitor use, lead to cardiac arrest. Post-resuscitation complications, included acute respiratory distress syndrome necessitating venovenous extracorporeal membrane oxygenation for stabilization.

Methods: A 32-year-old woman presented to the ED after collapsing with worsening epigastric pain, nausea, and vomiting. Witnessed by her husband, she experienced a 5-minute pulseless VT arrest en route, achieving ROSC after defibrillation and CPR. In the ED, she suffered a second VT arrest, stabilized with defibrillation and IV antiarrhythmics. Labs revealed severe hypokalemia (1.8 mmol/L), hypomagnesemia (0.9 mg/dL), high-anion gap metabolic acidosis (pH 7.1, bicarbonate 8 mmol/L), and hyperglycemia (520 mg/dL), consistent with DKA. ECG showed inferior ST elevations and prolonged QT, prompting emergent angiography, which revealed Normal coronary anatomy, with no evidence of obstructive disease; transient RCA vasospasm attributed to metabolic stress and hypokalemia, with preserved LVEF (55%) on echocardiogram.
The patient’s pulmonary status deteriorated, with follow-up chest X-rays revealing bilateral infiltrates consistent with aspiration pneumonitis, likely secondary to emesis preceding her VT arrest requiring VV-ECMO initiation on day 2. By day 7, pulmonary function improved, allowing ECMO decannulation, and she was extubated by day 8. She was transferred out of the ICU by day 10 with stable cardiac and neurological function and discharged on day 14 with follow-up in cardiology, endocrinology, and gastroenterology for long-term management of vasospasm, DKA, and PPI safety.

Outcome: Chronic PPI use disrupts electrolyte homeostasis by inhibiting renal H(+),K(+)-ATPase, leading to increased urinary potassium and magnesium excretion. Hypomagnesemia further impairs intracellular potassium uptake and renal potassium reabsorption, exacerbating hypokalemia. In the setting of DKA, where potassium shifts extracellularly due to acidosis, this depletion is masked until fluid resuscitation drives potassium back into cells, revealing severe total-body potassium deficiency. The result is myocardial instability, prolonged QT intervals, and a high risk of ventricular arrhythmias. Additionally, metabolic stress and catecholamine surges can induce coronary vasospasm, as seen in this case with transient RCA spasm mimicking ischemia. The subsequent VT arrest led to aspiration of gastric contents, triggering ARDS.

Conclusion: PPIs, although common, can precipitate severe hypokalemia and hypomagnesemia, especially in stressed metabolic states, which can precipitate life-threatening arrhythmias. DKA should heighten suspicion for potassium depletion, emphasizing the need for aggressive early repletion. Timely VV-ECMO use in ARDS secondary to aspiration pneumonitis allowed for lung recovery and prevented additional complications.