Emergency intubation is not just an airway procedure. It is a major hemodynamic event.
Many critically ill patients are maintaining blood pressure through high sympathetic tone, spontaneous negative-pressure breathing, and a narrow reserve of venous return. Induction, paralysis, and positive-pressure ventilation can remove those supports within seconds.
Several mechanisms can contribute to post-intubation hypotension.
Induction medications may reduce sympathetic tone and vascular resistance. Positive-pressure ventilation increases intrathoracic pressure, which can reduce venous return. Loss of spontaneous breathing removes the negative intrathoracic pressure that was helping blood return to the heart.
The right ventricle is especially vulnerable. If the patient has pulmonary hypertension, severe hypoxemia, acidosis, PE, ARDS, or high PEEP requirements, positive pressure may increase RV afterload and worsen RV output.