Adverse hemodynamic effects of pericardial closure soon after open heart operation

Abstract

The short-term hemodynamic effects of pericardial closure on cardiac function were studied during steady-state anesthesia and ventilation in 10 patients (6 men) (mean age, 59 ± 9 years) who underwent an open-heart valve operation. Observations were made after the heart was decannulated, both while the pericardium was open and after it had been closed, and then after closure of the chest after the pericardium had been reopened by removing the pericardial soture through the chest wall. The effect of closing the pericardium before closing the chest was an immediate reduction in cardiac output (thermodilution) of 1.39 ± 0.24 L/min from 5.09 ± 0.40 L/min ( p < 0.001). The heart rate remained stable, but there was a decrease in stroke volume of 29% and an increase in systemic vascular resistance of 34% (both, p < 0.01). The mean arterial pressure increased slightly by 2% (not significant). Opening the pericardium (1.5 to 2 hours after the end of the operation) while the chest remained closed was followed by an increase in cardiac output of 1.33 ± 0.15 L/min from 4.12 ± 0.62 L/min ( p < 0.001). As the heart rate and the mean blood pressure changed insignificantly, there was an increase in stroke volume of 15 ± 3 mL from 53 ± 5 mL and a reduction in systemic vascular resistance of 473 ± 83 dyne · s · cm −5 from 1,721 ± 181 dyne · s · cm −5 (both, p < 0.01). The data suggest that pericardial closure early after an open heart operation consistently lowers stroke volume and cardiac output; mean blood pressure is maintained by an increase in systemic vascular resistance. Thus, monitoring blood pressure alone is not a reliable guide to decisions on whether to close the pericardium or leave it open in individual patients.