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Ann Thorac Surg 1996;61:1506-1509
© 1996 The Society of Thoracic Surgeons


Original Articles: General Thoracic

Symptomatic Tachydysrhythmias After Esophagectomy: Incidence and Outcome Measures

David Amar, MD, Michael E. Burt, MD, PhD, Manjit S. Bains, MD, Denis H. Y. Leung, PhD

Departments of Anesthesiology and Critical Care Medicine, Surgery, and Biostatistics, Memorial Sloan-Kettering Cancer Center and Cornell University Medical College, New York, New York

Accepted for publication February 1, 1996.


    Abstract
 Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
Background. Supraventricular tachydysrhythmias (SVT) after esophageal operations for carcinoma occur frequently and may be associated with increased morbidity. Prospective data on the etiology, incidence, and importance of these dysrhythmias are sparse.

Methods. In 100 consecutive patients undergoing esophagectomy without prior history of atrial dysrhythmias or receiving antiarrhythmics, we prospectively examined the effects of predefined risk factors by history and pulmonary function on the 30-day incidence of symptomatic postoperative SVT, need for intensive care unit admission, and mortality rate.

Results. Symptomatic postoperative SVT occurred in 13 (13%) of the 100 patients studied at a median of 3 days after operation and was accompanied by hypotension in 9/13 (69%). Univariate correlates of SVT were older age (p = 0.03), perioperative use of theophylline (p = 0.044), and a low carbon monoxide diffusion capacity (measured in 56% of patients) on preoperative pulmonary function. Patients in whom SVT developed had a higher rate of intensive care unit admission (p = 0.0001) and a longer hospital stay (p = 0.036). Although patients in whom SVT developed had a higher (p = 0.013) 30-day mortality rate, SVT was not the direct cause of death.

Conclusions. These prospective data show that the true incidence of symptomatic SVT within 30 days of esophagectomy is lower than previously reported. Occurrence of SVT was associated with significant morbidity. Older age was the strongest predictor of SVT after esophagectomy. In high-risk patients, continued monitoring (48 to 72 hours) and early interventions to decrease the incidence of postoperative SVT may improve overall surgical outcomes.


    Introduction
 Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
Supraventricular tachydysrhythmias (SVT) occur frequently after noncardiac thoracic operations [13]. Most studies have reported the incidence of SVT after pulmonary resection with little emphasis on the incidence after esophagectomy. In a retrospective study of 77 patients undergoing esophageal operations for carcinoma, the incidence of SVT was 47% [4]. Two prospective reports [5, 6] that examined the efficacy of digoxin prophylaxis to prevent SVT after esophageal operations for carcinoma found a 32% incidence of dysrhythmias and no added benefit to the use of digoxin. It is difficult, however, to establish the true incidence of symptomatic SVT after esophagectomy from the above reports due to varying study designs, patient selection, and dysrhythmia definition. Little is known about whether the type of surgical approach influences dysrhythmia occurrence and whether other clinical conditions such as advanced age, theophylline use, or preexisting medical conditions predispose patients to these events.

The aim of this prospective study was to define the frequency and cardiovascular effects of symptomatic SVT after esophagectomy and to determine whether patients in whom SVT develop have worse surgical outcomes. We also evaluated the effects of surgical approach, namely, transhiatal or thoracoabdominal, and other clinical characteristics on the incidence of dysrhythmias.


    Material and Methods
 Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
Study Population
Consecutive patients scheduled for elective esophagectomy were prospectively studied. Patients with a known history of atrial dysrhythmias or those receiving digoxin were excluded from analysis but followed up in the same fashion. One hundred consecutive patients who had resection were studied from February 1994 to July 1995. During the same time period 7 patients with a prior history of atrial fibrillation were also followed up, 5 of whom were in sinus rhythm at the time of operation. Preoperative evaluation consisted of routine blood tests, 12-lead electrocardiogram, and pulmonary function testing (56% of patients). A standard nomogram [7] adjusting for sex, age, and height was used to calculate the percent of predicted values of the forced expired volume in 1 second and the percent of predicted values of the forced vital capacity in patients who had pulmonary function studies.

Anesthetic and Postoperative Care
All patients received routine anesthetic management and were monitored with continuous intraarterial and central venous pressure catheters. Pulmonary artery catheterization was not employed routinely in this study. Postoperatively, patients were monitored overnight in the postanesthesia care unit and returned to the thoracic surgical floor on the first postoperative day. Continuous ambulatory electrocardiographic monitoring was not employed. No patient received chest percussion, which has been associated with cardiac dysrhythmias. Satisfactory postoperative pain relief was achieved in all patients with either continuous epidural fentanyl administration or intravenous morphine patient-controlled analgesia. Benzodiazepines were usually avoided.

Intraoperative blood loss and fluid replacement, daily weights, and the use of theophylline or inhaled ß-agonist bronchodilators were recorded. Postoperative complications were also recorded throughout the hospital stay, and patients were monitored for complications as outpatients for 30 days. Clinically significant dysrhythmias were defined as new-onset atrial fibrillation, atrial flutter, or paroxysmal supraventricular tachycardia associated with acute cardiovascular or pulmonary symptomatology or with the presence of an irregular heart rate on physical examination and documented by electrocardiography. Presence or absence of hemodynamic compromise (systolic blood pressure <90 mm Hg or a >=20% decrease in systolic blood pressure) or ST-segment changes at the time of the dysrhythmia were noted.

Statistical Analysis
Statistical analysis was performed with the SAS software version 6.04. To determine the association of patient-specific and pulmonary function-specific factors with new-onset SVT, all variables were examined by two-tailed univariate analysis (Student's t test or Fisher's exact test). After log transformation of data (due to nonnormal distribution), t tests were done for hospital stay, estimated blood loss, and fluid requirement.

In a second step, all variables showing a univariate association with SVT occurrence or those that may be correlated with SVT according to theoretic considerations or clinical experience were entered into a stepwise logistic regression model. The final model showed the variables with independent influence on the incidence of SVT. A p value less than 0.05 was considered significant. Data are presented as mean value ± standard deviation unless otherwise indicated.


    Results
 Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
Incidence of Supraventricular Tachydysrhythmias
Patient characteristics and type of operation are shown in Table 1Go and preoperative pulmonary function in Table 2Go. Supraventricular tachydysrhythmias developed in 13/100 patients: 9 had atrial fibrillation, 1 had paroxysmal supraventricular tachycardia later converting to atrial fibrillation, and 3 had atrial flutter. Of the 13 documented episodes, four occurred during night hours between 12:00 midnight and 5:00 AM, and nine episodes occurred during the day between 9:00 AM and 7:00 PM. The onset of SVT occurred a median of 72 hours after arrival in the postanesthesia care unit, with a range of 16 to 576 hours. The mean heart rate at the onset of the dysrhythmia was 160 ± 14 beats/min (range, 135 to 180 beats/min). Late-onset SVT (postoperative days 10 and 28) occurred in 2 patients in whom sepsis developed. Data were reanalyzed with the exclusion of these 2 patients and showed no new findings or differences.


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Table 1. . Patient Characteristics and Operation Type
 

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Table 2. . Preoperative Pulmonary Function
 
Supraventricular tachydysrhythmia was associated with hemodynamic compromise in 9 (69%) of the 13 episodes and acute myocardial ischemia in 4/13 (31%), and most patients complained of palpitations. Direct-current cardioversion was required to interrupt rapid atrial flutter in a patient with a systolic arterial pressure less than 70 mm Hg. Once the ventricular response was controlled (most commonly with intravenous diltiazem), no patient had evidence of myocardial ischemia or infarction. Sinus rhythm was restored in all patients within 24 to 48 hours.

The group of patients with prior history of atrial fibrillation (n = 7) had a mean age of 66 ± 10 years (range, 50 to 76 years). Of these, two were in atrial fibrillation before operation and 5 were in sinus rhythm. Of the latter group of patients, 2 of 5 (40%) had development of atrial fibrillation after operation. When compared with the patients without history of atrial fibrillation there was no significant difference in the frequency of new-onset SVT between the two groups (13/100 versus 2/5; p = 0.15 by Fisher's exact test).

Association of Supraventricular Tachydysrhythmias With Other Outcomes
Patients in whom SVT developed had a significantly higher intensive care unit admission rate, a longer hospital stay, and a higher 30-day mortality (Table 3Go). In the patients in whom SVT developed the reasons for intensive care unit admission included respiratory failure and management of arrhythmias (n = 4) and infection/sepsis (n = 3). The cause of 30-day mortality in the entire patient population was sepsis in 2, pulmonary embolism in 1, and acute myocardial infarction in 1, and 1 patient suffered a sudden death a week after discharge from the hospital. The total 60-day mortality was 6% due to another case of sudden death of unknown cause.


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Table 3. . Supraventricular Tachydysrhythmias and Outcome
 
The frequency of other serious postoperative complications was not associated with SVT occurrence; such complications included anastomotic leak (n = 8), renal failure (n = 3) or insufficiency (n = 1), deep venous thrombosis and pulmonary embolism (n = 3), pericarditis (n = 1), wound infection (n = 1), and a prolonged air leak (n = 1).

Clinical Correlates of Supraventricular Tachydysrhythmias
Univariate correlates of SVT were older age and perioperative use of intravenous theophylline (see Table 1Go). The SVT group had a significantly lower carbon monoxide diffusion capacity on baseline pulmonary function studies when compared with the no-SVT group (see Table 2Go). The SVT group did not have a greater operative blood loss (0.8 ± 0.9 versus 0.8 ± 0.6 L) or greater intraoperative fluid requirement (6.4 ± 5.6 versus 5.5 ± 2.1 L) than the patients without SVT, respectively. No difference was seen in the perioperative weight change from baseline in patients in whom SVT did or did not develop. The correlates of SVT entered into the stepwise logistic regression model also identified older age and use of theophylline as risk factors. Because theophylline was used in a few patients only, age remained as the strongest predictor of SVT in this multivariate model.


    Comment
 Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
The 13% (13/100) incidence of SVT in this prospective study is considerably lower than that described by others [4, 6]. This difference is most likely due to differences in study design, patient selection, and dysrhythmia definition. Supraventricular tachydysrhythmia in our patient population was accompanied by disabling symptoms in 69% of patients. Although patients in whom SVT developed had a longer hospital stay and higher 30-day mortality, SVT was not the direct cause of death. We prospectively studied consecutive patients with biopsy-proven esophageal carcinoma without prior history of atrial dysrhythmias and followed up those with prior history of dysrhythmias as a separate subset of patients. We considered only clinically significant dysrhythmias defined by electrocardiography and their association with hemodynamic changes, whereas others [4, 6] considered nonsustained dysrhythmias or those without any hemodynamic sequelae. A possible limitation of our study is that continuous electrocardiographic monitoring was not employed to detect asymptomatic dysrhythmias or silent myocardial ischemia. However, our study was designed to evaluate clinically significant dysrhythmias that are the focus of patients' complaints and need for therapeutic interventions. Our conclusions, however, do not apply to the occurrence of asymptomatic dysrhythmias after esophageal operations for carcinoma.

We observed a significant association between the occurrence of SVT and greater age, perioperative theophylline use, and a lower carbon monoxide diffusion capacity. Because few patients received perioperative theophylline and only 56% of our patients had pulmonary function testing, we urge caution in the interpretation of these results. Nevertheless, due to the known serious arrhyhthmogenic effects of theophylline even at serum concentrations considered to be therapeutic [8], its use should be carefully weighed against its potential harmful effects. The effect of age on the incidence of SVT in our patients, however, was significant both when examined as a continuous variable and when dichotomized to less than 70 years or 70 or more years. Konno and associates [4] identified age of 66 years or greater as a cutoff point for a higher rate of postoperative dysrhythmias; however, caution should be used to only employ cutoff points that have been established from large trials. Surgical approach did not significantly influence the incidence of postoperative SVT in our experience as in that of others [4, 6]. Ritchie and colleagues [6] found no association between onset of dysrhythmia and hypoxia or serum potassium abnormalities. These authors [6] also reported a 52% incidence of intraoperative dysrhythmias and a 24% incidence of dysrhythmias occurring within the first 6 hours postoperatively. In contrast, we saw no episodes of sustained dysrhythmias requiring intervention in the operating room, and clinically significant SVT developed in 9/13 patients (69%) between 16 and 72 hours postoperatively but not before. Although inhaled anesthetics if given in high concentrations during the operation may sensitize the myocardium to circulating catecholamines to the development of dysrhythmias, this is highly unlikely to be a mechanism of postoperative dysrhythmias due to the rapid wash-out of these agents (<30 minutes).

The observation that SVT after esophagectomy occurs most commonly on postoperative days 2 through 4, as does SVT after major thoracic operations [13] and coronary artery bypass grafting [9, 10], is intriguing. Advanced age, right coronary artery stenosis, and lower use of postoperative ß-blocker therapy [9] and prolonged signal-averaged P-wave duration [10] were shown to predict the onset of atrial fibrillation after coronary artery bypass grafting. Whether some of the above predictors may apply to patients undergoing esophagectomy is unknown. It is not surprising that advanced age is a strong predictor of postoperative supraventricular dysrhythmias, because by 75 years of age only approximately 10% of normal sinus node pacemaker cells remain [11, 12]. Consistent with our previous observation [3], most SVT episodes after esophagectomy also occurred during wakefulness, supporting an important sympathetic contribution to the development of this complication [13]. Thus, we speculate that SVT after esophagectomy is precipitated by the resolution of an inflammatory response following blunt or sharp surgical trauma to sympathovagal nerve fibers supplying the heart (cardiac plexus) 1 to 4 days postoperatively, which alters the autonomic modulation of atrial myocardial cells to endogenous catecholamines. Whether this reasoning applies to late (>7 days) postoperative SVT occurrence is unknown.

Digoxin has been used extensively after thoracic operations. Its efficacy in this setting, however, has not been proved in prospective trials, and its use may be associated with untoward effects [5, 6]. Digoxin's predominant action on the atrioventricular node is mediated by enhanced vagal tone [14], which would explain digoxin's lack of efficacy after thoracic operations, a period when vagal influences are withdrawn and adrenergic output is high [15]. It is well known that increased sympathetic tone can shorten the atrial refractory period and cause atrial reentry or promote triggered automaticity to produce SVT [16]. It is not known whether it is optimal to treat SVT after esophagectomy with drugs that attenuate the adrenergic response (ie, ß-blockers), with those that prolong atrioventricular conduction (ie, calcium-channel blockers), or both.

In view of the increased morbidity associated with SVT occurrence it is possible that, once likely triggers of SVT after esophageal operations are characterized, future studies can focus on continuous postoperative monitoring for 48 to 72 hours and early therapy to improve overall outcome in older patients.


    Acknowledgments
 Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
We thank Ilana Ginsburg, RN, for technical assistance; Robert J. Downey, MD, Patricia M. McCormack, MD, Valerie W. Rusch, MD, and Alan D. Turnbull, MD, for their help; Robert J. Ginsberg, MD, and Roger S. Wilson, MD, for reviewing the manuscript; and Ms Barbara Viets for preparing the manuscript.


    Footnotes
 Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
Address reprint requests to Dr Amar, Department of Anesthesiology and Critical Care Medicine, Memorial Sloan-Kettering Cancer Center, 1275 York Ave, New York, NY 10021.


    References
 Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 

  1. Krowka MJ, Pairolero PC, Trastek VF, et al. Cardiac dysrhythmias following pneumonectomy: clinical correlates and prognostic significance. Chest 1987;91:490–5.[Abstract/Free Full Text]
  2. Von Knorring J, Lepantalo M, Lindgren L, et al. Cardiac arrhythmias and myocardial ischemia after thoracotomy for lung cancer. Ann Thorac Surg 1992;53:642–7.[Abstract/Free Full Text]
  3. Amar D, Roistacher N, Burt M, et al. Clinical and echocardiographic correlates of symptomatic tachydysrhythmias after noncardiac thoracic surgery. Chest 1995;108:349–54.[Abstract/Free Full Text]
  4. Konno O, Tezuka T, Muto A, et al. Postoperative arrhythmia after operation for esophageal cancer. J Jpn Assoc Thorac Surg 1993;41:45–51.
  5. Ritchie AJ, Bowe P, Gibbons JRP. Prophylactic digitalization for thoracotomy: a reassessment. Ann Thorac Surg 1990;50:86–8.[Abstract/Free Full Text]
  6. Ritchie AJ, Tolan M, Whiteside M, McGuigan JA, Gibbons JRP. Prophylactic digitalization fails to control dysrhythmia in thoracic esophageal operations. Ann Thorac Surg 1993;55:86–8.[Abstract/Free Full Text]
  7. Morris JF, Koski A, Johnson LC. Spirometric standards for healthy nonsmoking adults. Am Rev Respir Dis 1971;103: 57–67.[Medline]
  8. Bittar G, Friedman HS. The arrhythmogenicity of theophylline: a multivariate analysis of clinical determinants. Chest 1991;99:1415–20.[Abstract/Free Full Text]
  9. Mendes LA, Connelly GP, McKenney PA, et al. Right coronary artery stenosis is an independent predictor of atrial fibrillation after coronary artery bypass surgery. J Am Coll Cardiol 1995;25:198–202.[Abstract]
  10. Steinberg JS, Zelenkofske S, Wong SC, Gelernt M, Sciacca R, Menchavez E. Value of the P-wave signal-averaged ECG for predicting atrial fibrillation after cardiac surgery. Circulation 1993;88:2618–22.[Abstract/Free Full Text]
  11. Davies MJ. Pathology of the conduction system. In: Caird FL, DaUe JLC, Kennedy RD, eds. Cardiology in old age. New York: Plenum, 1976:57–9.
  12. Wei JY. Age and the cardiovascular system. N Engl J Med 1992;327:1735–9.[Medline]
  13. Chernow B, Alexander HR, Smallridge RC et al. Hormonal responses to graded surgical stress. Arch Intern Med 1987;147:1273–8.[Abstract/Free Full Text]
  14. Gillis RA, Quest JA. The role of the nervous system in the cardiovascular effects of digitalis. Pharmacol Rev 1979;31: 19–97.[Medline]
  15. Falk RH, Leavitt JJ. Digoxin for atrial fibrillation: a drug whose time has gone? Ann Intern Med 1991;114:573–5.[Abstract/Free Full Text]
  16. Josephson ME, Kastor JA. Supraventricular tachycardia: mechanisms and management. Ann Intern Med 1977;87:346–58.[Abstract/Free Full Text]



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