Closed mitral valvotomy and elective ventilation in the postoperative period: effect of mild hypercarbia on right...

It is customary to extubate patients immediately after closed mitral valvotomy. These patients often have deranged respiratory function caused by chronic lung congestion. The left ventricular function may also be subnormal after valvotomy in some patients. Therefore, elective ventilation for some duration in the postoperative period can be beneficial to these patients. This work is an attempt to find whether elective ventilation should be preferred over immediate extubation in these patients.

A prospective randomized study.

The study was performed in a tertiary care hospital, and the patients are referred from the northern states of India.

One hundred patients undergoing elective closed mitral valvotomy were included in the initial part of the study. Ten more patients were studied to evaluate the effect of mild hypercarbia on right ventricular function after closed mitral valvotomy.

One hundred patients were divided into two groups of 50 each. Group 1 consisted of patients in whom the neuromuscular blockade was reversed at the end of surgery with neostigmine and atropine and the trachea was extubated. In group 2, the residual neuromuscular paralysis was not reversed and the patients were electively ventilated in the postoperative period for an average duration of 5 hours and 29 minutes +/- 1 hour and 58 minutes. In all the patients in both the groups, electrocardiogram, direct arterial blood pressure, and oxygen saturation were continuously monitored, and arterial blood gases were measured intermittently throughout the study period. Because the results showed that there was mild hypercarbia, 30 minutes after extubation in group 1, 10 more patients were studied to evaluate the effect of mild hypercarbia on right ventricular function after surgery. Patients were ventilated after surgery (F1O2 = 1) to maintain normocarbia (PaCO238.6 +/- 3.4 mmHg). Mild hypercarbia PaCO251.5 +/- 3.7 mmHg) followed by normocarbia (PaCO2 40 +/- 2.5 mmHg) was induced by adjusting the ventilator rate with a constant tidal volume. Standard hemodynamic measurements were performed at each stage.

Although all the patients maintained satisfactory and stable hemodynamics in the postoperative period, the PaCO2 at the end of 30 minutes of extubation was significantly higher in group 1 (48.1 +/- 5.3 mmHg) as compared with group 2 (40.2 +/- 4.3 mmHg, p < 0.001). Mild hypercarbia significantly increased pulmonary vascular resistance (p < 0.01), mean pulmonary arterial pressure (p < 0.001), right ventricular stroke work (p < 0.01), right ventricular systolic pressure (p < 0.01), and right ventricular end-diastolic pressure (p < 0.001). The effect was not totally reversible with CO2 washout as all parameters except right ventricular end-diastolic pressure and pulmonary vascular resistance continued to remain significantly higher when normocarbia was restored. The significant changes in systemic hemodynamics produced by hypercarbia were increases in cardiac index, mean arterial pressure, and pulmonary capillary wedge pressure.

Avoidance of even mild hypercarbia, therefore, appears advisable in the early postoperative period because of potential impedence to right ventricular ejection. Continuous monitoring of end-tidal CO2 and frequent blood gas analyses should be practiced, and elective ventilation should be considered in patients with long-standing disease and pulmonary hypertension.