Sedation, Sleep, and Sudden Death: How ICU Sedation Alters Cardiac Rhythmicity and Autonomic Tone

📖 Top 50% JournalJan 6, 2026Cardiology in review

How ICU Sedation Changes Heart Rhythm and Nerve Control Linked to Sleep and Sudden Death

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Abstract

Deeper or prolonged sedation is associated with increased incidences of atrial fibrillation, bradyarrhythmias, and QT interval abnormalities in critically ill patients.

Propofol, dexmedetomidine, benzodiazepines, and ketamine have distinct effects on autonomic regulation.
Sedative agents may alter heart rate variability, baroreflex sensitivity, and ventricular repolarization.
Sleep disruption and circadian misalignment can reduce vagal dominance and increase sympathetic activation.
Emerging monitoring techniques may help detect early signs of neuro-cardiac instability.
Sedation practices could be optimized to enhance neuro-cardiac homeostasis and reduce arrhythmia risk.

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Sedation is essential for modern intensive care management, yet its effects on autonomic regulation, circadian biology, and cardiac electrophysiology remain incompletely understood. This review synthesizes current evidence on how commonly used sedative agents influence autonomic tone, sleep architecture, and electrophysiologic stability in critically ill patients. Mechanistic data indicate that propofol, dexmedetomidine, benzodiazepines, and ketamine exert distinct autonomic signatures that alter heart rate variability, baroreflex sensitivity, and ventricular repolarization. Clinical studies show that deeper or prolonged sedation is associated with increased incidences of atrial fibrillation, bradyarrhythmias, ventricular ectopy, and QT interval abnormalities, particularly in the context of sepsis, hypoxia, or metabolic derangements. Sleep disruption and circadian misalignment further diminish nocturnal vagal dominance, heighten sympathetic activation, and contribute to arrhythmogenic vulnerability. Advances in physiologic monitoring, including heart rate variability metrics, QT variability, T-wave alternans, and electroencephalogram-electrocardiogram coupling, offer emerging tools to detect early neuro-cardiac instability and guide individualized sedation strategies. Collectively, current evidence supports viewing sedation as a modifiable determinant of neuro-cardiac homeostasis. Optimizing sedation depth, preserving circadian cues, and integrating multimodal physiologic monitoring may reduce arrhythmia risk and improve outcomes in the intensive care unit, although further research is required to address substantial gaps in physiologic characterization and high-risk populations.

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