In Response

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Excerpt

We thank Sanfilippo et al1 for their astute insights regarding our recently reported case of a perimembranous ventricular septal defect, complicated by a likely infective aorto-right ventricular fistula.2 This lesion presented a diagnostic dilemma that was not fully resolved until a comprehensive, intraoperative echocardiographic examination was undertaken: specifically, the presence of an apparently large, left-to-right shunt on differential oxygen saturation (Qp/Qs of 1.4:1) with preserved right ventricular function and apparently normal pulmonary artery pressures.
The readers submit that a full evaluation of the lesion should be undertaken before midline sternotomy or incision of the pericardium. The principal concern articulated is that the sudden drop in intrathoracic or intrapericardial pressure associated with chest opening will lead to a similar fall in right ventricular pressure, thereby increasing the pressure gradient and flow across the ventricular septal defect and leading to acute right ventricular failure.
The described phenomenon is often used to the advantage of cardiac surgeons and anesthesiologists: in the patient without an interventricular communication, delayed chest closure and open chest management in the intensive care unit are associated with substantial benefits in cardiac output and systemic blood pressure. However, these same data also suggest that the intracavity pressures do not change with chest opening and closure.3,4 What this scenario likely demonstrates are the consequences of improved diastology: the reduction in intrathoracic pressure allows a greater degree of filling for a given chamber pressure. In the patient with an impaired right ventricle and coexistent pulmonary hypertension, it is possible that a sudden increase in filling could lead to acute decompensation and the need for a precipitous transition to cardiopulmonary bypass.
In the case we have described, neither sternotomy nor pericardotomy was associated with an appreciable change in hemodynamics. Pulmonary artery pressures did not increase, and right ventricular function on trans-esophageal echocardiography did not appear to deteriorate. This likely reflects the fact that our patient presented for surgery before meaningful degradation in right ventricular function, and before the development of pulmonary hypertension. Consequently, the heart was able to absorb any increase in flow that was entailed in intrathoracic decompression.
Given the time constraints often associated with cardiac surgery, performance of a full echocardiographic examination before surgical intervention is not always feasible. However, surgeons and anesthesiologists who are managing a patient with an interventricular communication and severely impaired right ventricular function would be wise to heed Sanfilippo’s warning, as it is plausible that a sudden increase in the filling of the ventricle already precariously positioned on the Frank-Starling curve could prove catastrophic.
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