Ventilation-perfusion inequality in patients undergoing cardiac surgery.

BACKGROUND: Impaired gas exchange is a major complication after cardiac surgery with the use of extracorporeal circulation. Blood gas analysis gives little information on underlying mechanisms, in particular if the impairment is multifactorial. In the current study we used the multiple inert gas technique with recordings of hemodynamics to analyze the separate effects of intrapulmonary shunt (QS/QT), ventilation-perfusion (VA/Q) mismatch, and low mixed venous oxygen tension on arterial oxygenation during cardiac surgery.
METHODS: VA/Q distribution was studied in nine patients undergoing coronary artery revascularization surgery. The obtained data related to VA/Q distribution were perfusion of lung regions with VA/Q < 0.005 (QS/QT), perfusion of lung regions with 0.005 < VA/Q < 0.1 ("low"-VA/Q regions), ventilation of lung regions with 10 < VA/Q < 100 ("high"-VA/Q regions), and ventilation of lung regions with VA/Q > 100 (dead space [VD/VT]). In addition, arterial and mixed venous oxygen and carbon dioxide tensions and systemic and pulmonary hemodynamics were analyzed. Recordings were made before and after induction of anesthesia, after sternotomy, 45 min after separation from extracorporeal circulation, 4 h postoperatively during mechanical ventilation, and on the 1st postoperative day during spontaneous breathing.
RESULTS: In the awake state, QS/QT was 4 +/- 4%, and perfusion of low-VA/Q regions was 3 +/- 5%. The sum of QS/QT and low-VA/Q units correlated with the alveolar-arterial oxygen tension gradient (PA-aO2) (r = 0.63, P < 0.05). After induction of anesthesia, QS/QT increased to 10 +/- 9% (P = 0.069). Sternotomy had little effect on shunt, but QS/QT increased to 22 +/- 8% (P < 0.01) after separation from extracorporeal circulation, which was correlated with a significantly higher PA-aO2 (r = 0.77, P < 0.05). Postoperatively, gas exchange improved rapidly, as assessed by a decrease of PA-aO2 from 341 +/- 77 to 97 +/- 36 mmHg (P < 0.01) and a reduced QS/QT (5 +/- 4%, P < 0.05). On the 1st postoperative day, arterial oxygen tension was significantly lower than preanesthesia values (58 +/- 6 vs. 68 +/- 8 mmHg, P < 0.05). QS/QT had increased to 11 +/- 6% (P < 0.05), but little perfusion of low-VA/Q units was observed. A correlation was found between PA-aO2 and QS/QT (r = 0.82, P < 0.03).
CONCLUSIONS: QS/QT is a major component of impaired gas exchange before, during, and after cardiac surgery. QS/QT increases after induction of general anesthesia, probably because of development of atelectasis. After separation from extracorporeal circulation, accumulation of extravascular lung water or further collapse of lung tissue may aggravate QS/QT. Postoperatively, oxygenation improves, possibly because of recruitment of previously nonventilated alveoli or resolution of extravascular lung water. During spontaneous breathing, additional mechanisms such as altered mechanics of the chest, perfusion of low-VA/Q regions, and decreased mixed venous oxygen tension may contribute to impaired gas exchange.