Intraoperative Oxygen Desaturation Following Nitroglycerin Administration
The oxygen saturation drop to 91% after starting nitroglycerin was most likely caused by pulmonary vasodilation leading to increased ventilation-perfusion (V/Q) mismatch, as nitroglycerin dilates pulmonary vessels in poorly ventilated lung regions, shunting blood away from well-oxygenated areas.
Mechanism of Nitroglycerin-Induced Hypoxemia
Nitroglycerin causes both systemic and pulmonary vasodilation through its direct action on vascular smooth muscle. 1 While this is beneficial for reducing preload and afterload in cardiac conditions, it has important pulmonary consequences during general anesthesia.
Primary Mechanism: V/Q Mismatch
Nitroglycerin abolishes hypoxic pulmonary vasoconstriction (HPV), a protective reflex that normally diverts blood away from poorly ventilated lung regions toward better-ventilated areas. 2
When HPV is inhibited, blood flows to atelectatic or hypoventilated lung zones, creating increased intrapulmonary shunting and worsening oxygenation. 2
This effect is particularly pronounced during general anesthesia, where patients already have reduced functional residual capacity and areas of dependent atelectasis, especially in the supine position required for LAVH. 3
Supporting Evidence from Clinical Studies
A study comparing nitroglycerin to nitroprusside during general anesthesia found that both drugs significantly decreased PaO2 at comparable blood pressure reductions, confirming the pulmonary effects of nitroglycerin. 2
The rapid onset (3-4 minutes) of nitroglycerin's effects matches the timeline described in your case, where desaturation occurred within 5 minutes of starting the infusion. 4
Additional Contributing Factors in This Case
Pneumoperitoneum Effects During Laparoscopy
If pneumoperitoneum was already established for the laparoscopic portion of LAVH, this further compromises respiratory mechanics by elevating the diaphragm, reducing lung compliance, and worsening V/Q matching.
The combination of pneumoperitoneum-induced respiratory compromise plus nitroglycerin-induced pulmonary vasodilation creates a particularly high-risk scenario for desaturation.
Excessive Preload Reduction
Nitroglycerin's primary mechanism is venous capacitance vessel dilation, which reduces venous return and cardiac preload. 1
Excessive preload reduction can decrease cardiac output by 13% or more, potentially reducing oxygen delivery despite adequate arterial oxygen content. 4
The FDA label specifically warns that severe hypotension and shock may occur with even small doses of nitroglycerin, particularly in volume-depleted patients. 1
Clinical Management Approach
Immediate Actions
Stop or reduce the nitroglycerin infusion immediately when oxygen saturation drops below 92-94%.
Increase FiO2 to 100% to maximize oxygen delivery and overcome the increased shunt fraction. 3
Apply recruitment maneuvers (sustained inflation to 30-40 cmH2O for 30 seconds) to re-expand atelectatic lung regions and improve V/Q matching.
Ensure adequate intravascular volume before resuming nitroglycerin, as hypovolemia exacerbates the hypotensive effects. 1
Alternative Agents for Intraoperative Hypertension
For sudden intraoperative hypertension in this clinical scenario, consider alternative agents that don't impair HPV:
Esmolol (short-acting beta-blocker) is particularly useful for managing intraoperative tachycardia and hypertension without pulmonary vasodilation effects. 3
Labetalol or nicardipine are effective alternatives recommended by guidelines for intraoperative blood pressure control. 3
Clevidipine is specifically mentioned for perioperative hypertension management without the pulmonary complications of nitroglycerin. 3
Dosing Considerations
The dose used in your case (1 mL in 500 mL RL at 60 drops/min) likely delivered approximately 2-4 mcg/min, which is within the typical starting range but may have been excessive given the patient's response. 1
When using non-absorbing tubing, initial dosing should start at 5 mcg/min with careful titration in 5 mcg/min increments every 3-5 minutes. 1
Important Caveats
Nitroglycerin is often an agent of choice in patients with coronary ischemia, so if this patient had active ischemia, the risk-benefit calculation changes. 3
The desaturation may resolve spontaneously within 27 ± 8 minutes after stopping the infusion, as nitroglycerin has a very short half-life of approximately 3 minutes. 1, 4
Monitor for rebound hypertension after discontinuing nitroglycerin, which may require alternative antihypertensive therapy. 1