Anesth Analg 1999;88:332
© 1999 International Anesthesia Research Society
CARDIOVASCULAR ANESTHESIA
Acute Myocardial Infarction During Lung Volume Reduction Surgery
Charles W. Hogue, Jr, MD*,
Thomas Stamos, MD*,
Kenneth J. Winters, MD ,
Michael Moulton, MD ,
Peter E. Krucylak, MD*, and
Joel D. Cooper, MD
Departments of
*Anesthesiology,
Medicine,
Surgery, Washington University School of Medicine, St. Louis, Missouri
Address correspondence and reprint requests to Charles W. Hogue, Jr, MD, Department of Anesthesiology, Washington University School of Medicine, 660 South Euclid Ave., Box 8054, St. Louis, MO 63110. Address e-mail to hoguec{at}notes.wustl.edu
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Introduction
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Emphysema is a chronic progressive disease with a high mortality and no effective medical treatments for advanced disease (1,2). Lung volume reduction surgery (LVRS) was successfully introduced at our institution in 1993 as a novel therapeutic intervention for selected patients with severe emphysema (3,4). In this procedure, targeted areas of overventilated but poorly perfused lung are removed, leading to augmented chest wall mechanics, reduced dyspnea, improved pulmonary function, and enhanced quality of life (3,4). Because of older age and prior tobacco abuse, patients undergoing LVRS are at risk of coronary artery disease (4–6). Experience with LVRS has been confined to small series thus far, and the true surgery-specific risk for cardiovascular complications of this procedure are unknown. We describe a patient undergoing bilateral LVRS who developed a myocardial infarction during surgery.
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Case Report
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A 77-yr-old man with smoking-related obstructive lung disease presented for bilateral LVRS. The patient's 1-s forced expiratory volume was 0.61 L, forced vital capacity was 1.59 L, and arterial blood gas values (room air) were: pH 7.37, PaCO2 44 mm Hg, PaCO2 and 62 mm Hg. His chest radiograph showed heterogeneous emphysema. A coronary angiography performed 6 mo before surgery for atypical chest pain revealed mild plaque of the proximal left anterior descending (LAD) artery and a 70% stenosis of the extreme distal LAD. Ventricular function was normal, and there was no history of myocardial infarction. Based on these findings, negative adenosine-thallium imaging results the day before surgery, and cardiology consultation, it was concluded that the patient was an acceptable cardiac risk for LVRS.
On arrival in the operating room, a thoracic epidural catheter was placed, the position was confirmed with fluoroscopy, and an anesthetic level was established with 0.5% bupivacaine from T1 to T10. General anesthesia was then induced with thiopental supplemented with fentanyl (150 µg), isoflurane, and rocuronium. A left-sided double-lumen endobronchial tube was inserted. Monitoring included direct radial arterial blood pressure; continuous electrocardiogram (ECG) ST segment analysis of leads V5, II, and aVF, and transesophageal echocardiography (TEE). Throughout anesthesia induction and the start of surgery, the patient's heart rate ranged from 64 to 84 bpm—the latter immediately after endobronchial intubation—and the systolic blood pressure ranged from 110 to 120 mm Hg. After median sternotomy, the left lung was deflated, and the emphysematous target areas were excised using a bovine pericardium reinforced stapling device. Shortly after completion of the left LVRS, when the patient's heart rate was 62 bpm and blood pressure was 112/58 mm Hg, marked ST-segment increase was noted in all ECG leads, along with TEE-detected akinesis of the anterior and anterior-septal left ventricular myocardial segments. Systolic blood pressure decreased to 80 mm Hg, and three episodes of ventricular tachycardia occurred. The patient was treated with direct electrical cardioversion, phenylephrine, lidocaine, and nitroglycerin, which resulted in sinus rhythm, normalization of the ST segments, and improvement in regional myocardial dysfunction. Because of the reversible nature of the myocardial ischemic event, and in light of the patient's underlying, severe obstructive lung disease, it was decided to proceed with right LVRS. However, shortly after beginning right LVRS, ST-segment increase and akinesis of the same myocardial segments recurred but resolved after an IV infusion of nicardipine. After two further episodes of myocardial ischemia, an intraaortic balloon catheter was inserted, and counterpulsation was started. After chest closure and replacement of the endobroncheal tube with a single-lumen endotracheal tube, the patient was transported to the cardiac catheterization laboratory. Coronary angiography revealed total thrombotic occlusion of the proximal LAD coronary artery, which partially recanalized after heparin was given (Figure 1). Balloon angioplasty was then performed, and an intracoronary stent was placed. Ventriculography at the conclusion of the procedure revealed normal left ventricular function. Throughout the cardiac catheterization, the patient received a continuous IV infusion of propofol, intermittent doses of rocuronium, and 6 mL/h 0.15% bupivacaine epidurally, and his lungs were adequately ventilated with 15 cm H2O pressure-controlled ventilation. The patient was transferred to the intensive care unit anesthetized; his trachea was extubated 2 h later, after restoration of normothermia. Arterial blood gas values after tracheal extubation were (fraction of inspired oxygen 0.40) pH 7.37, PaCO2 41 mm Hg, and PaO2 307 mm Hg; there was no evidence of pleural air leaks. IV heparin infusion, aspirin, and clopidrogel were given with the partial thromboplastin time maintained 2 times control for the first 3 postoperative days. Serum troponin I concentrations increased to 6.9 ng/mL (normal <1.4 ng/mL) at 5:00 AM the next day, but there were no new Q waves on the postoperative 12-lead ECGs. The epidural catheter was removed on Postoperative Day 4 after heparin was stopped. The patient's postoperative course was complicated by a temporary increase in serum creatinine (peak 2.7 mg/dL) and transient atrial fibrillation, but he was discharged from the hospital on Postoperative Day 7.
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Figure 1. Coronary angiograms obtained 6 mo preoperatively (A), immediately after lung volume reduction surgery (B), after intracoronary heparin "flush" (C), and after angioplasty and intracoronary stent placement (D). The arrows highlight the same region of the left anterior descending (LAD) coronary artery that showed minimal disease before surgery (A), then developed thrombotic occlusion perioperatively (B).
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Discussion
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Myocardial infarction is a leading cause of mortality and cost after noncardiac surgery, which has prompted intensive research to develop strategies of identifying before-surgery patients at risk of adverse cardiac outcomes (7,8). In this report, our patient had undergone extensive preoperative testing and was believed to be a suitable surgical candidate, yet he developed acute thrombosis of the proximal LAD coronary artery that was previously shown to have only mild plaque (Figure 1). Acute progression of coronary disease in the months before surgery cannot be excluded, but this seems unlikely because of our patient's stable clinical course. Rapid expansion of coronary stenosis results from plaque fissuring, hematoma formation, and an inflammatory repair process (9,10). More likely, our patient developed acute plaque rupture and thrombosis of an insignificant (i.e., <50% narrowing) stenosis, as has been observed in nonsurgical patients with acute coronary thrombosis and in small autopsy series of surgical patients with perioperative myocardial infarction (9,11,12). These findings underscore the limitations of current diagnostic methods in identifying lipid-laden coronary plaques vulnerable to rupture and thrombosis, regardless of the severity of obstruction (9,11).
In our patient, the development of the initial myocardial ischemic episodes was not preceded by acute increases in myocardial oxygen demand, as heart rate and blood pressure were unchanged. Coronary vasospasm plays a role in acute plaque rupture, and spontaneous vessel contraction or vasospasm resulting from inadvertent cardiac traction at the time of surgery could possibly explain the development of the acute coronary syndrome in our patient (13,14). Nonetheless, despite our understanding of the relationship between perioperative myocardial ischemia and infarction, there is little information regarding the management of intraoperative myocardial infarction (7,15). Primary angioplasty is the treatment of choice for acute myocardial infarction when thrombolytic therapy is contraindicated, such as immediately after surgery (16,17). This treatment in our patient minimized the size of the infarction, as documented by the small increase in troponin I concentrations, the absence of new ECG Q waves, and preserved left ventricular function.
Several issues related to the complexities of LVRS required consideration in managing this patient's acute coronary event. Because pulmonary air leaks are a major source of morbidity and prolonged hospitalization after LVRS, avoidance of high airway pressures and smooth tracheal extubation immediately after surgery are fundamental goals (3,4). The potential risk of postoperative mechanical ventilation if our patient's pulmonary function had been only marginally improved by partial LVRS was a consideration for continuing an elective procedure after the patient's initial, albeit reversible, myocardial ischemic episode. At the conclusion of surgery, we elected to leave the trachea intubated to facilitate immediate coronary angiography and to avoid increases in myocardial oxygen demand during emergence from anesthesia. To minimize the risk of high airway pressures that could promote disruption of the lung staple line, we chose pressure-controlled, as opposed to volume-controlled, lung ventilation. An additional concern was the need for unexpected anticoagulation and antiplatelet drug therapy in a patient with a thoracic epidural catheter. Systemic heparinization after epidural catheter placement has been reported to be safe in vascular surgical series, but anticoagulation in our case was for a longer duration (18,19).
In summary, acute coronary thrombosis developed at an arterial site documented before surgery not to have significant coronary stenosis. This case highlights the necessity for urgent communication and coordination among the anesthesiologist, surgeon, and cardiologist when an acute coronary event is suspected intraoperatively. The management of patients undergoing LVRS requires special consideration after surgery, especially in minimizing airway pressures to avoid pulmonary air leaks when unexpected postoperative mechanical ventilation is required. Our management approach proved successful, as major myocardial damage was averted and LVRS was judged successful.
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Accepted for publication November 18, 1998.
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Introduction
Case Report
