Changes in the Electrocardiogram After Open Heart Surgery

Summary This is a study of the electrocardiograms of 23 patients who had undergone open heart surgery— repair of an atrial septal defect in 10, and in 13 closure of a ventricular septal defect, some with and some without an associated pulmonary infundibulectomy. A variety of supraventricular arrhythmias were noted after the repair of an atrial septal defect. Possible ætiological factors include atrial irritability, pericarditis and electrolyte changes. Arrhythmias noted after the closure of a ventricular septal defect consisted of ventricular fibrillation during or immediately after the operation. This could be more clearly attributed to the direct trauma of surgery or to electrolyte shifts at the time of surgery. There were decreases in the height of the P waves and a diminution of the P‐R interval after the repair of atrial septal defects. These changes appear to be related to improved atrial conduction and the decreased size of the right atrial chamber. Elimination of the left‐to‐right shunt after operation probably explains these findings. The proximity of a defect of the ventricular septum to the known anatomical pathway of conduction along the right bundle correlates with the right bundle branch block or delay in the activation of the right ventricle which is noted after the repair of these defects. This study confirms the association of pulmonary infundibulectomy with the appearance of a type of right bundle branch block. However, this association did not occur when a lateral excision of tissue from the pulmonary outflow tract was performed. This emphasizes the importance of damage to the superiorly located crista supraventricularis in the genesis of right bundle branch block after infundibulectomy. The occurrence of the major QRS vector change after the completion of the first 0.04 second of the complex suggests that the later portions of the QRS complex are inscribed after a surgically imposed block has been encountered. The presence of S‐T segment elevation after surgery for both atrial and ventricular septal defect repair probably correlates with the pericardial reaction and inflammation which one might expect. We learn that the electrocardiographic evidence of such change may last from four to at least 14 days after surgery. The changes noted in the mean T wave vector suggest that the repolarization of the ventricles is altered in a fairly consistent fashion after the repair of an atrial septal defect, and in a varied manner after the repair of a ventricular septal defect. The T wave changes in precordial leads after surgery are probably due to a number of factors, including anoxia and injury.