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Updated: Mar 29, 2026

Preoxygenation Techniques for Tracheal Intubation in Critically Ill Adults Utilizing Oxygen Mask and Noninvasive Ventilation
Published on: December 5, 2025
The hemodynamics of tracheal intubation in critically ill patients: a narrative review
Yuki Kotani1, Takatoshi Koroki1, Yoshiro Hayashi1
1Department of Intensive Care Medicine, Kameda Medical Center, Kamogawa, Japan.
Background:
Tracheal intubation is a ubiquitous but high-risk procedure in critically ill patients, often required in the setting of severe hypoxemia, shock, or metabolic acidosis. Despite being a life-saving procedure, it is associated with a high incidence of peri-intubation adverse events. In a large international study (INTUBE), more than 40% of intubations in critically ill patients were complicated by cardiovascular instability, approximately 10% by severe hypoxemia, and over 3% by cardiac arrest, highlighting the magnitude of risk in this population. Among these complications, cardiovascular instability-particularly hypotension-emerges as the most frequent and most consequential, being independently associated with increased intensive care unit (ICU) and 28-day mortality. However, robust randomized evidence to guide optimal peri-intubation hemodynamic management remains scarce, leaving clinicians to rely largely on physiologic reasoning.
Main Body:
Hemodynamic physiology during intubation is highly dynamic and influenced by cumulative and interacting threats. Critically ill patients often present with an endogenous catecholamine surge that temporarily preserves perfusion but reflects a fragile reserve. The administration of induction agents rapidly abolishes this sympathetic drive, leading to abrupt decreases in systemic vascular resistance and cardiac output. Apnea introduces hypoxemia, hypercapnia, and acidosis, all of which further impair myocardial contractility and catecholaminergic response, with increased arrhythmogenic risk. The subsequent initiation of positive-pressure ventilation raises intrathoracic pressure, reduces venous return, and increases right ventricular afterload, especially in the context of acute respiratory distress syndrome with hypoxic pulmonary vasoconstriction or pulmonary microthrombosis. Finally, post-intubation sedation, ventilator settings, and vasopressor therapy continue to shape the hemodynamic trajectory.
Conclusions:
This narrative review synthesizes current evidence and physiological insights into a structured timeline extending from induction to post-intubation care.
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