SUN-515 - When pH Becomes Lethal: Profound Metabolic Acidosis as a Reversible Cause of Cardiac Arrest in Severe DKA

Background: Arrhythmias in diabetic ketoacidosis (DKA) are typically linked to potassium derangements. However, cardiac arrest directly precipitated by severe acidosis is rarely reported. We describe a case of profound metabolic acidosis in the setting of severe DKA, complicated by cardiac arrest with return of spontaneous circulation (ROSC) occurring after sodium bicarbonate administration, suggesting acidosis as a reversible precipitating factor.

Case Description: A 64-year-old male with latent autoimmune diabetes in adults (LADA) managed as type 1 diabetes mellitus, poorly controlled on insulin presented with progressive lethargy and persistent vomiting. On arrival, he was lethargic but oriented, with marked hemodynamic instability: blood pressure of 67/48 mmHg and temperature 94.7°F. Heart rate was 89 bpm, respiratory rate 18/min, and oxygen saturation 99% on room air. Point-of-care glucose exceeded 600 mg/dL. Venous blood gas revealed severe acidosis (pH 6.86). Laboratory evaluation showed bicarbonate 3.6 mmol/L, potassium 6.8 mmol/L, chloride 77 mmol/L, beta-hydroxybutyrate >114 mg/dL, and a calculated serum osmolality of 376 mOsm/kg, consistent with severe DKA. Additional findings included leukocytosis (20.1 ×10⁹/L), lactate 6.1 mmol/L, and acute kidney injury, raising suspicion for concurrent septic shock. Broad-spectrum antibiotics were initiated.
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Shortly after arrival and before initiation of continuous insulin therapy, the patient became unresponsive and developed pulseless electrical activity. Advanced cardiac life support was initiated, and he was intubated. A single intravenous bolus of 10 units of regular insulin was given. The rhythm then converted to pulseless ventricular tachycardia, requiring defibrillation, amiodarone, and epinephrine, without immediate ROSC. Administration of 50 mEq sodium bicarbonate and calcium gluconate, along with additional epinephrine, was followed by ROSC after 12 minutes of downtime. Post-arrest electrocardiogram showed sinus rhythm.

He was admitted to the intensive care unit for management of post-arrest care, septic shock, and severe DKA, requiring vasopressors, insulin infusion, and bicarbonate-containing fluids, with subsequent resolution of DKA.

Conclusion: This case highlights that, beyond hyperkalemia, profound acidosis may directly impair myocardial contractility, reduce vascular tone, blunt the catecholamine response, and increase the risk of arrhythmias. The temporal association between bicarbonate administration and ROSC supports severe acidosis as a key reversible contributor to cardiac arrest. Recognition of severe acidosis as a potential cause of cardiovascular collapse in DKA is critical, particularly when compounded by septic physiology.

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