Marked ST-T Electrocardiographic Changes After Retrosternal Reconstruction of the Esophagus

We observed marked ST-T changes in electrocardiography (ECG) recorded after reconstructive surgery for esophageal cancer. These changes disappeared abruptly after expulsion of a large amount of air that had been retained in the reconstructed esophagus posterior to the sternum. In this case report, we attempt to explain the mechanism of these ST-T changes in order to differentiate them from changes associated with ischemic heart disease. Case Report A 75-yr-old male developed dysphagia 6 mo before his first visit to our hospital. His condition was diagnosed as esophageal cancer, and he was treated by esophagectomy and retrosternal reconstruction with the stomach. The patient did not exhibit preoperative ischemic heart disease, diabetes, or hypertension. Preoperative ECG was within the normal range. The operation was completed without any circulatory complications or any noticeable changes in ECG monitored by lead II. The patient was transferred to an intensive care unit (ICU) and ventilation was controlled. A 12-lead ECG revealed significant elevation of the ST-T segment from leads V1 to V4 and slight depression of the ST-T segment in leads II, III, and aVF Figure 1. We were unable to perform echocardiography because of the presence of the reconstructed esophagus posterior to the sternum. Myocardial ischemia was suspected, and continuous administration of diltiazem and nitroglycerin was started. Despite the therapy, the ST-T changes persisted. Two hours later, the range of these ST-T changes tended to increase during expiration and decrease during inspiration Figure 2a. Then 7.5 h later, after coughing, a large amount of air was expelled from the drainage tube in the reconstructed esophagus. The ECG at that time showed complete disappearance of the ST-T changes Figure 2b, which were not observed again despite frequent follow-up examinations by 12-lead ECG. The chest radiograph taken after the patient entered the ICU had shown a large volume of air trapped in the reconstructed esophagus. During the patient's course, his circulatory state was stable and the creatine kinase-MB titer remained low. No subjective symptoms, such as chest pain or dyspnea, were observed after the patient emerged from anesthesia. He was removed from the ICU 5 days later without complications.Figure 1: Electrocardiogram immediately after entering the intensive care unit. Slight depression of ST-T in leads II, III, and aVF, and significant elevation of ST-T in leads V1-V 4 were observed.Figure 2: (a), Electrocardiogram (ECG) 6 h after entering the intensive care unit (ICU) (leads V2-V 3). The ST-T level shifts according to the respiratory cycle. (b), ECG (leads V2-V 3) taken 7.5 h after entering the ICU. After the expulsion of air in the reconstructed esophagus, the ST-T changes disappeared.Discussion Myocardial ischemia and injury of the epicardial membrane were suspected as the causative factors underlying this significant ST-T change. However, both of these factors were ruled out by the range of fluctuations of ST-T elevation that were synchronized with the respiratory phase, and by the stable vital signs, the absence of creatine kinase-MB increase, and the sudden disappearance of the ST-T changes after air was expelled from the reconstructed esophagus. Periodic occurrence of spasm or compression of the coronary artery was negated by the fact that 30 s to 4 min would be needed for complete or partial obstruction, respectively, of a coronary artery to cause ECG changes [1]. The mechanism of ST-T changes in this case may be explained as follows. During cardiac systole, a recoil force produced by ejection of blood into the aorta thrusts the left ventriculum against the chest wall in the anterior direction [2]. A large volume of air in the reconstructed esophagus increases the space between the sternum and the heart, resulting in more dynamic cardiac movement. The heart moved toward the sternum during systole and away from it during diastole. Therefore, in the anterior chest leads, the ECG changed in accordance with the cardiac cycle. The positive wave generated during systole corresponded to the ST-T elevation Figure 3a. In contrast, the negative wave or a return to the baseline occurred during diastole Figure 3b. As it approached the thoracic wall, the heart moved away from the caudal side, resulting in the recording of an ST-T depression in leads II, III, and aVF, resembling the reciprocal changes in cardiac infarction.Figure 3: The mechanism of the ST-T changes, which shifted according to the respiratory cycle. (a), Expiratory phase, systolic period of the heart. With the recoil force of the blood stream ejected from the heart, the heart moves forward. (b), Expiratory phase, diastolic period of the heart. The heart returns to its original position, moving away from the anterior thoracic wall. (c), Inspiratory phase. The inflated lung restricts the pendicular movement of the heart.During inspiration, the inflated lung restricted the pendicular motion of the heart toward the anterior thoracic wall. Thus the ST-T changes became smaller than those during expiration Figure 3c, which caused fluctuations in the range of ST-T elevation in synchrony with the respiratory phase. When the air space between the heart and the anterior chest wall disappeared after frequent coughing, the pendicular motion of the heart ceased, resulting in abrupt restoration of the ECG to normal. Figure 4a shows leads V1-V3 when mechanical ventilation was terminated. The patient was apneic and expiration was sustained. Figure 4b shows the same leads when the lung was kept inflated with positive airway pressure generated by holding the air bag. The ST-T elevation was reduced by the inflated lung, a finding that supports the explanation shown in Figure 3.Figure 4: Leads V1-V 3 during (a) expiration and (b) inspiration. ST-T elevation is restricted by the inflated lung.The ST-T changes caused by this mechanism are characteristic of retrosternal reconstruction and cannot be produced by a retrocardiac maneuver, because the latter does not cause pendicular motion of the heart. Perioperative cardiac complications occur frequently in thoracic and upper abdominal surgery [3,4], particularly of the esophagus [5]. It is important to note that ST-T changes can occur by the above-described mechanism as an artifact, and may be confused with myocardial ischemia in the setting of retrosternal reconstruction of the esophagus. The changes may also occur under certain circumstances, such as thoracotomy or mediastinotomy, when air enters the space between the heart and the chest wall. To identify this artifact, the existence of the cyclic change of the ST-T segment or air retention in the reconstructed esophagus should be noted.