Abstract

Interruption of the aortic arch is a rare anomaly affecting 1% of children with congenital heart disease. The systemic circulation is ductal dependent and is determined principally by the ratio of the resistances in the systemic and the pulmonary vascular bed. Any increase in the pulmonary vascular resistance may increase the dead space ventilation due to acute pulmonary hypoperfusion. We report a case where sudden decreases in the end-tidal carbon-dioxide due to pulmonary hypoperfusion mimicked accidental endotracheal tube extubation in an infant undergoing repair of interrupted aortic arch.

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