Acute Hypoventilation

An obese, middle-aged woman was undergoing laparoscopic cholecystectomy. After a routine induction and orotracheal intubation, low-flow anesthesia was initiated, and the ventilator was set to provide a tidal volume of 700 mL at a rate of 10 breaths/min (measured exhaled tidal volume was 560 mL). Ten minutes after induction of anesthesia, the PCO₂ was 35 mm Hg, and the peak airway pressure was 28 mm Hg. Arterial blood gas determinations showed pHa = 7.43, PaCO₂ = 35 mm Hg, bicarbonate = 22.4, and BE = -1 mEq/L. Thirty minutes into the procedure, the peak airway pressure was 48 mm Hg, the end-expired PCO₂ was 49 mm Hg, and the measured exhaled tidal volume was 380 mL. Repeat blood gas analysis showed pHa = 7.27, PaCO₂ = 55 mm Hg, bicarbonate = 24.9, and BE = -1 mEq/L. The principal abnormality was a marked respiratory acidosis with no metabolic acidosis. It is characteristic of an acute respiratory disturbance.

The rise in PaCO₂ can be attributed to two factors: uptake of the inflating gas (CO₂ ) in the abdomen and reduction of effective ventilation due to raised airway pressure required to overcome abdominal distention. The discrepancy between end-tidal PCO₂ and arterial blood gas PaCO₂ is typical and results from the patient's temperature being slightly less than that of the analyzer, lack of time between breaths to reach true end-tidal equilibration, normal pulmonary maldistribution, and the slight loss occurring on the length of the tubing.