Pulmonary Embolism (PE)

Recognize it intraoperatively - A sudden drop in end-tidal CO2 with hypoxemia, hypotension, and tachycardia should raise PE (among other embolic and obstructive causes). The abrupt end-tidal CO2 fall is a key clue.

Protect the right ventricle - The RV fails from acute pressure overload. Support coronary perfusion with a vasopressor such as norepinephrine, maintain preload without overloading, and avoid anything that raises pulmonary vascular resistance.

Avoid raising PVR - Hypoxia, hypercarbia, acidosis, and hypothermia all worsen pulmonary hypertension and RV strain — keep each corrected.

Anticoagulation and timing - Balance thrombosis against bleeding risk; the timing of holding or resuming anticoagulation and any neuraxial technique is case-specific and coordinated with the team.

Support and diagnose - For suspected massive PE, support hemodynamics, give 100% oxygen, and pursue diagnosis — TEE can show RV strain or clot. Definitive therapy ranges from anticoagulation to thrombolysis or embolectomy.

Pulmonary embolism is obstruction of the pulmonary arterial tree, usually by thrombus from a lower-extremity deep vein thrombosis. The clot raises pulmonary vascular resistance abruptly, and the thin-walled right ventricle — unaccustomed to high afterload — dilates and can fail.

Obstruction also creates dead-space ventilation and V/Q mismatch, producing hypoxemia and a fall in end-tidal CO2. A large (saddle) embolus causes obstructive shock and cardiac arrest. Intraoperatively, PE can present as sudden hypoxemia, a drop in end-tidal CO2, hypotension, and tachycardia — easily mistaken for other causes, so it demands a high index of suspicion.