Nicardipine-induced acute respiratory failure: Case report and literature review

Hypoxic pulmonary vasoconstriction (HPV) is a major physiological mechanism that prevents the development of hypoxemia secondary to a regional decrease in the ventilation-perfusion ratio (the intrapulmonary shunt effect). Calcium plays a critical role in the cellular response to hypoxia and the regulation of the pulmonary vascular tone. Therefore, calcium channel antagonists such as nicardipine have the potential to interfere with the pulmonary response to hypoxia, increasing intrapulmonary blood shunt and thus worsening underlying hypoxemia. This article reports the case of a 40-year-old man suffering from lobar pneumonia, who developed a rapidly progressing hypoxemia after starting nicardipine infusion for blood pressure control. After ruling out all major causes of hypoxemic respiratory failure, the involvement of the calcium channel antagonist was strongly suspected. Hypoxemia caused by HPV release is an underreported side effect of calcium channel blockers. There are few clinical reports that describe the occurrence of this adverse event, and to our knowledge, only one other publication describes a patient suffering from infectious pneumopathy. In this article, we discuss the cellular mechanisms behind the HPV, as well as the pharmacology of calcium channel antagonists and their involvement in the development of acute respiratory failure. The purpose of this report is to remind clinicians dealing with patients affected by acute hypoxemia that pharmacologic HPV inhibition should be considered as part of the differential diagnosis, thus avoiding unnecessary costly and time-consuming assessments.