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CARDIOVASCULAR ANESTHESIA

Acute Hemodynamic Collapse After Induction of General Anesthesia for Emergent Pulmonary Embolectomy

Peter Rosenberger, MD^*, Stanton K. Shernan, MD^*, Prem S. Shekar, MD, Jayshree K. Tuli, Sc, Thomas Weissmüller, MD, Sary F. Aranki, and Holger K. Eltzschig, MD, PhD

*Department of Anesthesiology, Perioperative and Pain Medicine, Division of Cardiac Surgery, Department of Neurosurgery, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts; Department of Anesthesiology and Intensive Care Medicine, Tübingen University Hospital, Tübingen, Germany

Address correspondence and reprint requests to Holger K. Eltzschig, MD, PhD, Assistant Professor of Anesthesiology, Department of Anesthesiology and Intensive Care Medicine, Tübingen University Hospital, Hoppe-Seyler-Str. 3, D-72076 Tübingen, Germany. Address e-mail to heltzschig{at}partners.org.

	Abstract

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Patients undergoing pulmonary embolectomy often experience hemodynamic deterioration during induction of general anesthesia (GA). Therefore, we studied the incidence and possible risk factors for hemodynamic deterioration during GA induction. Fifty-two consecutive patients undergoing emergent pulmonary embolectomy at our institution were included. Hemodynamic collapse after GA induction was defined as hypotension refractory to vasopressor, inotrope, or fluid administration, requiring cardiopulmonary resuscitation followed by urgent institution of cardiopulmonary bypass (CPB). Demographic variables, comorbidities, specific location of thromboemboli, preoperative inotropic support, and anesthetic drugs used for GA induction were evaluated as possible risk factors. After GA induction, hemodynamic collapse occurred in 19% of patients (n = 10). However, the occurrence of hemodynamic instability was not predicted by any of the evaluated risk factors. In addition, the incidence of in-hospital mortality did not differ between hemodynamically stable or unstable patients (10%; 4 of 42 versus 10%; 1 of 10 patients, respectively). In conclusion, hemodynamic deterioration after GA induction develops frequently during emergent pulmonary embolectomy. On the basis of our experience from this study and the unpredictable nature of hemodynamic deterioration, we suggest that patients undergoing pulmonary embolectomy should be prepared and draped before GA induction, and a cardiac surgical team should immediately be available for emergent institution of cardiopulmonary bypass.

	Introduction

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Pulmonary embolism (PE) occurs in more than 600,000 patients annually in the United States (1). Severe PE is frequently associated with hemodynamic instability and has a mortality rate of 30% that increases to 70% if cardiac arrest occurs (2,3). Treatment options include anticoagulation, thrombolysis, placement of a vena caval filter, and pulmonary embolectomy (4,5). Recently, some studies suggest a more favorable outcome for surgical pulmonary embolectomy compared with conventional, noninvasive pharmacological intervention when PE is severe, particularly in regard to intracerebral hemorrhage (6,7).

Anesthetic management of patients undergoing pulmonary embolectomy may be challenging as a result of their hemodynamic instability. In these patients, systemic blood pressure becomes predominantly dependent on compensatory increases in systemic vascular resistance and heart rate (8). Many anesthetic drugs used to induce general anesthesia (GA) are associated with varying degrees of myocardial depression and direct or indirect systemic vasodilation (9,10). In healthy patients, cardiac output is maintained after GA induction by an increase in cardiac output that, at least partially, compensates for systemic hypotension. However, patients with massive PE often present with tachycardia, decreased left ventricular preload, and compromised systolic function, which limits their ability to adjust to the physiological consequences associated with the induction of GA.

The incidence of hemodynamic collapse after the induction of GA and the need for urgent cardiopulmonary bypass (CPB) is not known. Therefore, we investigated 52 consecutive patients undergoing emergent pulmonary embolectomy to determine the incidence and risk factors for the development of hemodynamic instability requiring cardiopulmonary resuscitation (CPR) and the need for emergent CPB on induction of GA.

	Methods

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The study population consisted of all patients who underwent emergent pulmonary embolectomy at the Brigham and Women's Hospital in Boston between January 1995 and December 2004. Approval for the retrospective analysis of the patients' medical records was obtained from the hospital's IRB. Patients who required preoperative tracheal intubation or were receiving active CPR before the induction of anesthesia were not included in the analysis. Hemodynamic collapse after GA induction was defined as acute hypotension refractory to vasopressor, inotrope, or IV fluid administration, and requiring CPR followed by the urgent institution of CPB.

Patients' medical records were reviewed to obtain demographic data including age, body mass index, gender, and comorbidities (i.e., history of systemic hypertension, myocardial infarction, congestive heart failure, chronic obstructive pulmonary disease, malignancy, deep venous thrombosis, previous PE). Detailed anesthesia records were reviewed to determine perioperative hemodynamic variables, GA induction drugs, and inotropic requirements. Surgical operative notes were reviewed to identify the technical details pertaining to the initiation of CPB and the definitive location of pulmonary thromboemboli. In addition, the intraoperative transesophageal echocardiography reports were reviewed to document the exact presence and location of extrapulmonary thromboemboli.

GA was induced in the operating room (OR) after obtaining venous access and placing a radial or femoral arterial cannula. Choice of the anesthetic medication was made at the discretion of the attending anesthesiologist involved in the care of each individual patient. A cardiac surgery team was present during induction of GA in anticipation of the potential requirement for emergent institution of CPB. Hemodynamic collapse after GA induction that was refractory to vasopressor, inotrope, or fluid administration was treated by immediately initiating CPR, administration of IV heparin, sternotomy, arterial cannulation of the ascending aorta, and venous cannulation of the caval veins, and initiation of CPB.

After systemic heparinization, cannulation of the ascending aorta, inferior vena cava (IVC), and superior vena cava (SVC) were performed. Normothermic CPB using vacuum-assisted venous drainage was used in all patients. Pulmonary embolectomy was performed through a Y-shaped incision, which extended from the terminal portion of the pulmonary trunk into the proximal aspect of both pulmonary arteries.

Statistical analyses including descriptive statistics, bivariate analysis, and multiple regression on the covariates analyzed as risk factors for hemodynamic instability, was performed using JMP software (SAS, Cary, NC). Means and standard deviations were obtained for the continuous variables and frequencies for the categorical variables. Bivariate analysis included the use of the Fisher's exact test (with two-tailed P values) for categorical variables and the Wald ² test for continuous variables. All covariates that reached a statistical significance of P < 0.2 were entered into the multivariable analysis. Multivariable analysis was performed using logistic regression to determine the significance of the covariates in predicting death. A P < 0.05 was used to reject the null hypothesis that the regression coefficient equates to zero. The Wald statistic was used to define the significance of the regression coefficients. The odds ratios and their 95% confidence intervals were obtained. A parsimonious model was adhered to by maintaining the number of variables incorporated into the model at a 10 to 1 ratio (number of outcomes to the number of variables).

	Results

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The study population consisted of 57 consecutive patients who underwent pulmonary embolectomy between January 1995 and October 2004. Five patients who were tracheally intubated preoperatively or received active CPR before the induction of anesthesia were excluded from the study. Therefore, 52 patients were considered for analysis in the present study. Hemodynamic collapse after induction of GA was reported in 10 of 52 patients (19%). This occurred with a systolic blood pressure of 35 ± 28 mm Hg on average (Fig. 1). The rate of in-hospital mortality (mean length of stay, 12 days; range, 1–82 days) did not differ between the hemodynamically stable patients (10%; 4 of 42 patients) versus the hemodynamically unstable patients (10%; 1 of 10 patients). Demographic data including descriptive variables and medical history did not differ between groups (Table 1).

View larger version (15K): [in this window] [in a new window]   Figure 1. Systolic and diastolic blood pressure measurements of patients undergoing surgical pulmonary embolectomy. Of the 52 patients included in the present study, 10 patients developed acute hypotension on induction of general anesthesia that was refractory to fluid, inotrope, or vasopressor administration, and required emergent institution of cardiopulmonary bypass ("hemodynamically unstable" group). In contrast, the other 42 patients tolerated induction of general anesthesia without hemodynamic compromise ("hemodynamically stable" group, *P < 0.01).

Preoperative transthoracic echocardiography was obtained in 38 patients and revealed severe right ventricular dysfunction in 19 of 32 hemodynamically stable patients compared to 5 of 6 hemodynamically unstable patients (P > 0.05) (Table 1). Left ventricular function was normal in all transthoracic echocardiography examinations (Table 1). The location of pulmonary artery and extrapulmonary thromboemboli (i.e., superior vena cava, inferior vena cava, right ventricle, or right atrium) diagnosed by intraoperative transesophageal echocardiography, did not predict the occurrence of hemodynamic instability (Table 2). Furthermore, differences between hemodynamically stable and unstable patients in the requirement for preoperative inotropic drugs were not statistically significant (Table 3).

The use of anesthetics, opioids, and muscle relaxants is detailed in Table 3. Midazolam was administered as premedication to 4 of 10 patients (40%) in the group of the hemodynamically unstable patients and to 25 of 42 patients (59%) in the group of hemodynamically stable patients. Fentanyl was used during the induction of GA in 8 of 10 patients (80%) in the group of unstable patients and in 35 of 42 (83%) of the stable patients. The combination of midazolam and fentanyl was used in 4 of 10 patients (40%) in the unstable group and 23 of 42 (54%) patients in the stable group. Succinylcholine was used in 5 of 10 patients (50%) in the unstable patients and in 28 of 42 stable patients (67%). All patients received pancuronium, either as sole muscle relaxant, or proceeded by succinylcholine as outlined above. Etomidate was used for the induction of GA in all patients.

	Discussion

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Pulmonary embolectomy is an evolving surgical technique for patients with severe PE. Hemodynamic instability may develop during GA induction in these patients as the result of changes in loading conditions and myocardial contractility in combination with pulmonary artery obstruction and arrhythmias. In the present series of 52 consecutive patients undergoing pulmonary embolectomy, 10 (19%) developed severe hypotension on GA induction that was refractory to fluid administration, vasopressor, and inotropic therapy, and consequently required CPR and urgent institution of CPB. Although we could not demonstrate specific risk factors that could predict the development of hemodynamic instability in this setting, our results show that hemodynamic deterioration occurs frequently in this clinical setting. Therefore, all patients undergoing surgical pulmonary embolectomy should be prepared and draped before GA induction, and a cardiac surgical team should be present in the OR ready to initiate CPB.

Reported risk factors for the development of PE include gender, advanced age, increased body mass index, arterial hypertension, and a history of deep venous thrombosis. Although these factors are associated with a more frequent incidence for the development of PE and may influence hemodynamic stability, we could not demonstrate a correlation between any of these risk factors and the occurrence of hemodynamic instability during GA induction. Among the anesthetic drugs administered during GA induction, the combination of midazolam and fentanyl may produce a vasodilatory effect (10,11). Midazolam is known for its potential to reduce systemic blood pressure by blunting endogenous catecholamine release, even in doses administered only for sedation (12). The potential of succinylcholine to produce bradycardia (13) or the ability of pancuronium to decrease cardiac filling pressures and pulmonary vascular resistance (14) are probably more trivial in these critically ill patients with high endogenous catecholamine levels. We could not demonstrate a significant independent impact of the dose of these drugs on the occurrence of hemodynamic instability, nor did we observe a relative protective effect from other anesthetics, such as etomidate. This is consistent with previous studies that failed to clearly demonstrate a protective effect from etomidate against hemodynamic instability (15).

Patients with PE often develop additional extrapulmonary thromboemboli within the right heart chambers or caval veins (16). These thromboemboli can potentially dislodge during central venous catheter insertion or patient positioning or even spontaneously embolize into the pulmonary arterial circulation causing hemodynamic instability and cardiac arrest (5,17). Cannulation of the femoral vessels, a technique used in patients with chronic pulmonary hypertension, is not advisable in these patients because this could also dislocate these thromboemboli (18). We were unable to demonstrate a correlation between the presence of extrapulmonary thromboemboli and hemodynamic collapse after GA induction. Furthermore, the specific location of thromboemboli within the pulmonary artery had no significant impact on the occurrence of hemodynamic instability after GA induction. Thus, hemodynamic instability during GA induction seems unpredictable by the anatomic location or extent of the underlying disease process.

The fact that hemodynamic instability occurs frequently and is not predictable in patients undergoing pulmonary embolectomy warrants consideration of alternative strategies to conventional GA induction. For example, successful cannulation of the femoral vessels under local anesthesia and institution of CPB before GA induction has been described in patients with difficult airways (19–21). However, cannulation of the femoral vessels may present an additional risk in patients with deep venous thromboembolism, which is often present in patients with PE. Alternatively, emergent institution of CPB via sternotomy may be required in patients who experience hemodynamic collapse immediately after GA induction. Before this study, it was common practice at the author's institution to have the surgeon in the OR during the induction of GA for pulmonary embolectomy (16,22). This is also common practice at many cardiac surgery services in the United States (23). However, after we recognized the frequency and unpredictable nature of hemodynamic deterioration of patients during GA induction for pulmonary embolectomy, we changed our own practice. In fact, it has since become our practice to prepare and drape patients before GA induction for pulmonary embolectomy with the surgeon standing by, ready for incision. Thus, we now have a similar setting for the induction of GA in these patients as, for example, a ruptured abdominal aortic aneurysm (24,25). However, it should be pointed out that hemodynamic instability was not associated with an adverse outcome in the present study. This suggests that the management of hemodynamic instability with emergent institution of CPB was efficient in preventing major complications in this setting.

Limitations of the present study include the fact that an exact dose range, especially of the vasopressor therapy, can be variable in an emergency situation. Because of the retrospective character of the present study, we are not able to define exact dose ranges that were used for resuscitation, thus we cannot prove that patients were adequately resuscitated before the emergent institution of CPB. In addition, the induction of GA, the rate of drug administration, and ventilation patterns used by individual anesthesiologists were not standardized, and therefore could have independently influenced the development of hemodynamic instability. In addition, the impact of anesthetic drugs other than those given by the attending anesthesiologist (e.g., ketamine) has yet to be determined. Hypoxemia, hypocarbia, hypercarbia, and changes in pH can also all influence systemic and pulmonary vascular resistance and therefore could have an impact on hemodynamics during induction of GA. Finally, it is possible that we were not able to identify risk factors for hemodynamic instability because of a lack of statistical power and a limited number of patients in each study group. Nevertheless, the present study is among the largest case studies on pulmonary embolectomy that have been published.

In conclusion, hemodynamic instability after GA induction in patients undergoing pulmonary embolectomy occurs relatively frequently, yet remains unpredictable. Based on our experience, the critical nature of this procedure warrants preparing and draping the patient before GA induction. In addition, the presence of a cardiac surgical team ready for incision to initiate CPB in an efficient manner is recommended.

	Footnotes

 
Accepted for publication January 19, 2006.

Support was provided solely from institutional and/or departmental sources.

	References

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Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999