(197) A Puzzling Case of Reversible Hypoxemia

Introduction: Hypoxemia is a prevalent problem in the critically ill patient with a broad differential. Dihydropyridine calcium channel blocker (DHP CCBs) infusion is a common antihypertensive therapy used for multiple indications including blood pressure control in aortic dissection and hemorrhagic stroke and may also inadvertently cause hypoxemia.

Description: A 57-year-old male with history of tobacco use presented with sudden tearing chest pain. On examination, blood pressure was 158/72, respiratory rate 22, SpO2 on room air 100% with well-perfused extremities, clear lungs to auscultation, and left > right radial pulses. Laboratory results revealed a high-sensitivity troponin of 12 and 13 ng/mL. Inferolateral T-wave inversions were non-dynamic on ECGs. CT angiography of the chest, abdomen, and pelvis showed intimal irregularity in the ascending aorta suggestive of ulcerated plaque with intramural hemorrhage and thrombosed dissection extending from the distal ascending aorta to the iliac bifurcation consistent with a type B aortic dissection. Clevidipine (DHP CCB) and esmolol infusions were started to target systolic blood pressure < 120 mmHg and heart rate < 60 bpm. SpO2 steadily decreased from 100 to 87% and 4L of supplemental oxygen were initiated to maintain SpO2 >92%. Esmolol was titrated off by hospital day 2 and he continued to require 2 to 6L of nasal cannula oxygen while on clevidipine. Chest x-ray on hospital day 2 demonstrated pulmonary edema and diuresis with furosemide had no effect on oxygen requirement. On hospital day 5, he achieved goal blood pressure on oral clonidine, hydralazine, metoprolol and nifedipine, and was titrated off clevidipine with simultaneous weaning to room air.

Discussion: One cause for hypoxemia is pulmonary shunting, a type of ventilation-perfusion mismatch where a lung segment receives blood flow without oxygen delivery. Shunting is mitigated by hypoxic pulmonary vasoconstriction (HPV), the ability of pulmonary vasculature to restrict blood flow to poorly ventilated regions. DHP CCBs antagonize vascular constriction causing vasodilation in pulmonary vascular beds disrupting HPV, which can result in shunting and hypoxemia. In the patient with new hypoxemia after intravenous CCB therapy, consider medication effect and if switching agents is warranted.