Pseudo-Ischemic ECG Changes in a Patient With Profound Mixed Metabolic Acidosis Due to Metformin Use

BACKGROUND: Metformin-induced lactic acidosis can cause electrocardiographic (ECG) changes and precipitate cardiac arrest. CASE SUMMARY: A 58-year-old woman presented to the emergency department after a ventricular fibrillation arrest. Laboratory findings on admission showed severe lactic acidosis, and ECG showed ischemic changes concerning for a ST-segment elevation myocardial infarction. After treatment of the patient's sepsis, urinary tract infection, and acute kidney injury, she improved, and the pseudo-ischemic ECG changes resolved. DISCUSSION: Metformin is a known instigator of lactic acidosis, particularly in patients with renal failure. On rare occasion, such lactic acidosis secondary to metformin can produce lethal arrhythmias. This case demonstrates the need for providers to consider metabolic derangements in patients with ventricular fibrillation arrest and subsequent ECG changes. TAKE-HOME MESSAGE: It is crucial for providers to recognize metabolic acidosis as a precipitator of cardiac arrest and to identify patients who take metformin who are at risk for metformin-associated lactic acidosis.

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Publication Details

Journal
JACC Case Reports
Published
2026-03-31
DOI
https://doi.org/10.1016/j.jaccas.2026.107733
Primary Topic
Renal function and acid-base balance
Type
article
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article

Pseudo-Ischemic ECG Changes in a Patient With Profound Mixed Metabolic Acidosis Due to Metformin Use

John Schindler, John J. Grant, David P. Wilson
JACC Case Reports
Renal function and acid-base balance
article

Pseudo-Ischemic ECG Changes in a Patient With Profound Mixed Metabolic Acidosis Due to Metformin Use

John Schindler, John J. Grant, David P. Wilson
article en

Abstract

BACKGROUND: Metformin-induced lactic acidosis can cause electrocardiographic (ECG) changes and precipitate cardiac arrest. CASE SUMMARY: A 58-year-old woman presented to the emergency department after a ventricular fibrillation arrest. Laboratory findings on admission showed severe lactic acidosis, and ECG showed ischemic changes concerning for a ST-segment elevation myocardial infarction. After treatment of the patient's sepsis, urinary tract infection, and acute kidney injury, she improved, and the pseudo-ischemic ECG changes resolved. DISCUSSION: Metformin is a known instigator of lactic acidosis, particularly in patients with renal failure. On rare occasion, such lactic acidosis secondary to metformin can produce lethal arrhythmias. This case demonstrates the need for providers to consider metabolic derangements in patients with ventricular fibrillation arrest and subsequent ECG changes. TAKE-HOME MESSAGE: It is crucial for providers to recognize metabolic acidosis as a precipitator of cardiac arrest and to identify patients who take metformin who are at risk for metformin-associated lactic acidosis.

JACC Case ReportsVol. 31(18)
Gaston Memorial Hospital (US), Edward Via College of Osteopathic Medicine (US)
Zero hunger
Openalex Percentile: Top 37%
Renal function and acid-base balance
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