# Cardiac Arrest Secondary to Hypercapnia in an Obese Patient: A Case of Unresponsiveness With Preserved Awareness

## TL;DR

A 58-year-old obese woman with sleep apnea experienced cardiac arrest due to high carbon dioxide levels, showing awareness during the event and highlighting the need for vigilance in similar cases.

## Contribution

This case highlights the rare occurrence of hypercapnia-induced cardiac arrest with preserved awareness in obese patients with obstructive sleep apnea.

## Key findings

- The patient showed awareness during a cardiac arrest episode despite being unresponsive.
- Hypercapnia was identified as a trigger for the cardiac event through arterial blood gas analysis.
- Bilevel positive airway pressure therapy improved the patient's clinical condition.

## Abstract

In rare circumstances, hypercapnia can precipitate life-threatening cardiac events, particularly in patients with obesity hypoventilation syndrome and obstructive sleep apnea (OSA). Awareness during such episodes of unresponsiveness is uncommon, underscoring the complex interaction between respiratory and neurologic physiology. A 58-year-old Caucasian female with a body mass index of 37.4 kg/m², OSA, and a history of recurrent syncope presented to the emergency room with chest pain and shortness of breath. During hospitalization, she received sublingual nitroglycerin, after which she developed bradycardia and was administered atropine. She subsequently progressed into ventricular tachycardia and required two defibrillations to restore sinus rhythm. Remarkably, during resuscitation, she reported awareness despite unresponsiveness, hearing staff, and feeling defibrillation shocks. A comprehensive cardiac evaluation, including catheterization, troponin trends, ECG, imaging, echocardiography, Doppler studies, cultures, and laboratory tests, revealed no acute coronary pathology. She was admitted to the intensive care unit, underwent implantable cardioverter-defibrillator (ICD) placement, and was later discharged. Several days after discharge, she experienced another syncopal episode at home, this time with complete unresponsiveness and no awareness. On readmission, arterial blood gas analysis revealed significant hypercapnia, prompting initiation of bilevel positive airway pressure therapy. She improved clinically and was discharged on continuous positive airway pressure therapy for OSA, along with weight management counseling. This case emphasizes the importance of recognizing hypercapnia-induced cardiac events in obese patients with severe OSA. Identifying this mechanism, particularly when presenting as unresponsiveness with preserved awareness, highlights the diagnostic challenges and the necessity for vigilant monitoring, non-invasive ventilation, ICD support, and lifestyle modification to prevent recurrence and improve long-term outcomes.