Thoracic Cavity Irrigation: An Unusual Cause of Acute ST Segment Increase

Abstract

One goal of electrocardiographic (ECG) monitoring is to detect myocardial ischemia, which often presents as ST segment depression (subendocardial ischemia) or ST segment increase (transmural injury). However, not all ST segment increase occurs because of myocardial injury (1). The patient we describe in this report had no cardiac risk factors but developed focal ST segment increase after irrigation of an open chest with warm saline. Case Report A 55-yr-old, 170-cm, and 61-kg woman presented for right extrapleural pneumonectomy for mesothelioma. Her medical and surgical history was unremarkable. She was a nonsmoker and had no significant risk factors for coronary artery disease. Apart from decreased breath sounds on auscultation of the right lung base, physical examination was normal. Pulmonary function tests were normal. Preoperative ECG showed a ventricular rate of 68, normal sinus rhythm, and was interpreted by a staff cardiologist as normal. A transthoracic echocardiogram was performed at the request of her primary physician as part of her preoperative evaluation. Left ventricular size and function were normal, ejection fraction was 65%, and no abnormalities were seen. After placement of standard monitors, the patient received midazolam (2 mg) and fentanyl (100 μg) before placement of an epidural catheter at the T5–6 interspace. The catheter was subsequently fitted with a bupivacaine bolus (0.25%; 5 mL). General anesthesia was induced with propofol (2 mg/kg) and fentanyl (150 μg), and muscle relaxation was achieved with vecuronium (0.1 mg/kg). A 37F left-sided double-lumen endotracheal tube was placed, and anesthesia was maintained with inhaled isoflurane and an infusion (10 mL/h) of epidural bupivacaine (0.075%) and fentanyl (5 μg/mL). The anesthetic course was unremarkable until the surgeon irrigated the right hemithorax with warm saline to assess the integrity of the right mainstem bronchial stump suture line. The irrigant solution was taken from a warm but nonactive autoclave located in the operating room. The temperature of the solution was not directly measured, and the temperature inside the autoclave was unknown. There was no intention for the irrigation process to aid in assessment of hemostasis or for chemotherapeutic effect. Instantaneous, significant, and inferior ST segment increase (6 mm, leads II and III) and anterior ST segment depression (anterior precordial lead) occurred upon thoracic cavity irrigation (Fig. 1). The anterior precordial lead’s morphology correlated with that of the V2 lead on her preoperative ECG. The V lead was not moved during the operation, and therefore no other precordial leads were monitored. There was no evidence of a new bundle branch block. Esophageal temperature increased from 35.5°C to 42.4°C, indicating an irrigant temperature of at least 42.4°C. The patient’s hemodynamic variables did not change (heart rate, 80 bpm; blood pressure [BP], 110/55 mm Hg), and she remained well oxygenated (Spo2, 98%) during the period of ST segment increase. Nitroglycerine (NTG) (800 μg) was administered as an IV bolus. The patient became mildly hypotensive (BP, 80/40 mm Hg), and BP returned to baseline after the phenylephrine administration (50 μg IV). No reduction in the degree of ST segment increase occurred in response to NTG. The irrigant was then removed from the right hemithorax, and over the course of 4 min, the esophageal temperature and ST segment returned to their baseline levels. Laboratory data obtained during the period of ST segment increase were unremarkable (Pao2, 461 mm Hg; Paco2, 39 mm Hg; pH value, 7.44; HCO3, 26 mEq/L, hemoglobin, 12.5 g/dL; Spo2, 99%; K+, 4.2 mEq/L; iCa2+, 4.8 mg/dL).Figure 1: Electrocardiograph (ECG) leads II and V at (A) baseline, (B) during open chest irrigation, and (C) after removal of chest irrigation.A second episode of ST segment (4 mm) increase occurred during subsequent thoracic cavity irrigation with warm saline before closure of the thoracotomy incision. The solution used for the second irrigation was the remainder of the initial irrigant, which had been placed at the side of the surgical field. The irrigant was thought to have cooled sufficiently, however its temperature was not measured. An increase in esophageal temperature to 40.3°C was noted, indicating an irrigant temperature of at least 40.3°C. IV NTG was not administered. The patient again remained hemodynamically stable, and the ST segment and esophageal temperature returned to baseline levels 5 min after removal of the warm irrigant solution. The remainder of the anesthetic course was unremarkable. The postoperative ECG was unchanged from baseline, and serial relative creatine kinase (CPK) indices were within institutional normal values (CPK-MB/CPK <1.3). Troponin I concentrations were not measured. The remainder of her hospital course was unremarkable. She was discharged to home 7 days later. Discussion Abnormal ST segment and T-wave changes are the most common ECG abnormalities, accounting for approximately one half of abnormal recordings in hospitalized patients (2). ECG changes in the ST segment can be seen in both ischemic and nonischemic states. Ischemic ST segment increase reflects a transmural injury pattern caused by rapid repolarization of the ischemic myocardium (3). ST segment increase is usually caused by acute occlusion of an epicardial coronary vessel because of plaque rupture and occlusive thrombus formation or coronary spasm. The management of acute myocardial injury consists of measures to restore antegrade blood flow, such as thrombolytic therapy or catheter-based intervention, which carry substantial risk in the intraoperative or postoperative patient. Consequently, it is important to consider nonischemic causes when ST changes occur. Overall, ST segment increase is usually nonischemic in nature (1). Chronic benign early repolarization, often seen in young women, is the most common type of ST segment increase. Other chronic conditions associated with ST segment increase include left ventricular hypertrophy, left bundle branch block, hypertrophic cardiomyopathy, and invasion of the heart by neoplastic or infiltrative tissue (1). Nonischemic acute ST segment changes may occur with cor pulmonale, hyperkalemia, cerebrovascular accidents, and both total body and focal myocardial temperature changes. Systemic hypothermia is associated with ST-increase (Osborne waves) (4) and hyperthermia with ST segment depression (5). Local myocardial temperature changes or temperature gradients also alter the rate of myocardial repolarization (6,7). Focal warming results in a more rapid/earlier efflux of potassium along its electrochemical gradient leading to early repolarization (8). The differential diagnosis for acute ST segment increase in this patient included acute hyperkalemia, an intracranial process, myocardial injury from occlusive arterial thrombus formation or coronary spasm, and focal myocardial warming. Serum potassium and acid-base status were normal. Upon emergence from anesthesia, no neurologic changes were observed. Despite the magnitude of electrocardiographic changes, the patient remained hemodynamically stable, and evidence of myocardial infarction by postoperative ECG or CPK-MB/CPK criteria was absent. The ST segment increase in lead II along with ST-depression in the anterior precordial lead were temporally associated with open chest irrigation. One can see reciprocal changes (ST depression) in V2–3 leads when ST increase occurs in inferior frontal leads. In this case report, the ST segment depression present in the precordial lead may have been related to either (a) reciprocal changes in the precordial lead that most resembled the morphology of the V2 lead on her preoperative 12 lead ECG or (b) myocardial ischemia occurring in the V2 distribution. Although coronary spasm could account for the ST segment changes seen, we feel this is less likely given the hemodynamic stability throughout both episodes and the lack of improvement in ST segment changes in response to the IV NTG administration. Notably, both episodes of ST segment increase resolved in a similar time frame after removal of the warm irrigant regardless of whether or not NTG was administered. ST segment changes are not seen when the thoracic cavity is irrigated with normothermic saline. Therefore, we cannot attribute this patient’s ECG changes to an alteration in electrical impulse conduction as a result of the fluid filled hemithorax. The ECG changes seen in this case seem to have been caused by focal myocardial warming. Acute intraoperative temperature-related ST segment changes mimicking myocardial ischemia have not been reported. Westover and Saidman (9) presented a case of acute increased T-wave amplitude in a patient undergoing thoracotomy at the time of open chest irrigation that they attributed to warm irrigation fluid. However, the representative ECG tracing presented in their case report, whereas clearly abnormal and different from baseline, did not mimic the changes most often associated with acute myocardial ischemia, specifically ST segment increase. In summary, we present an unusual case of a patient without cardiac risk factors who developed acute ST segment changes consistent with myocardial ischemia during warm saline irrigation of the open chest without subsequent evidence of myocardial infarction. The history, clinical course, and temporal relation with irrigation suggest that these changes were secondary to a warm irrigant-induced myocardial temperature gradient resulting in early focal myocardial repolarization. The temperature of saline used to irrigate the thoracic cavity should be measured to assure that it is approximately that of the patient’s body temperature. Failure to do so can result in focal myocardial warming-induced ST segment increase interpreted as myocardial injury, leading to potentially harmful therapeutic interventions. Prompt communication with surgical colleagues regarding these findings is crucial to appropriate intra- and postoperative management.