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Ann Thorac Surg 1995;60:1081-1086
© 1995 The Society of Thoracic Surgeons

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Original Articles: Cardiovascular

Right Ventricular Dysfunction in Low Output Syndrome After Cardiac Operations: Assessment by Transesophageal Echocardiography

Cardiovascular Division, Washington University School of Medicine, St. Louis, Missouri

Accepted for publication May 17, 1995.

	Abstract

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

 
Background. Low output syndrome after cardiac operations is associated with high morbidity and mortality rates. The contribution of right ventricular dysfunction to this syndrome has not been fully characterized. The purpose of this study was to evaluate the utility of transesophageal echocardiography to identify the frequency and the in-hospital mortality from right ventricular dysfunction in patients with this syndrome.

Methods. Seventy-five consecutive patients undergoing transesophageal echocardiography for low output syndrome early after cardiac operations were evaluated. The findings from transesophageal echocardiography were correlated with the type of surgical procedure, cross-clamp time, right heart hemodynamics, and coronary angiography.

Results. Right ventricular systolic dysfunction occurred in 36 patients (42%); in 17 patients it was isolated and in 19 patients it occurred in combination with left ventricular dysfunction. Postoperative right ventricular dysfunction was not uniformly associated with important right coronary artery disease or with prolonged ischemic time during cardiopulmonary bypass. Hemodynamic data were not useful to distinguish the group with postoperative right ventricular dysfunction. Patients with right ventricular dysfunction had a high (44%) in-hospital mortality rate.

Conclusions. Right ventricular dysfunction occurs frequently in patients with low output syndrome after cardiac operations and is associated with a high in-hospital mortality rate. Better understanding of the mechanisms causing postoperative right ventricular dysfunction may provide insight for preventing this complication.

	Introduction

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

 
Low output syndrome after cardiac operations is associated with high morbidity and mortality rates [1]. This syndrome, defined as a cardiac index less than 2.0 L•min^-1•m^-2, may be attributed to one of a number of factors, including myocardial dysfunction, cardiac tamponade, hypovolemia, or valvular dysfunction. Although left ventricular systolic dysfunction is often the cause of a postoperative low output state, the frequency of concomitant or isolated right ventricular dysfunction in this syndrome is unknown. Right ventricular dysfunction is associated with decreased cardiac output in a variety of clinical situations, such as acute right ventricular infarction, acute pulmonary emboli, and chronic conditions that cause right ventricular pressure or volume overload [2–4]. The frequency of right ventricular dysfunction in the postoperative low output syndrome has not been fully characterized, in part because of technical limitations of noninvasive imaging techniques, such as transthoracic echocardiography, to provide adequate visualization of the right ventricle early after cardiac operations. The utility of transesophageal echocardiography (TEE) for the assessment of cardiac function in intensive care units has been documented [5–7]. Because of the proximity of the imaging probe to cardiac structures, TEE provides excellent images of these structures and is particularly suited to the evaluation of right and left ventricular and valvular function.

In this study, we used TEE to evaluate the cause of low output syndrome (cardiac index of 2.0 L•min^-1•m^-2 or less) in patients within 48 hours after cardiac operations. Specifically, in patients with low postoperative output syndrome, we sought to determine: (1) the frequency of right or left ventricular systolic dysfunction, (2) the potential causes of right ventricular dysfunction, and (3) the in-hospital mortality rate.

	Material and Methods

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

 
Patient Population
The study population included 75 consecutive patients undergoing TEE for low output syndrome within 48 hours (66 patients within the first 24 hours) after cardiac operations over a 12-month period. Low output syndrome was defined as a cardiac index less than or equal to 2.0 L•min^-1•m^-2 that persisted despite the use of inotropic drugs or intraaortic balloon counterpulsation support. Thirty-three women and 42 men with a mean age of 65 ± 12 years (range, 31 to 88 years) met the study entry criteria. Right atrial, pulmonary artery, and pulmonary capillary wedge pressures were measured at the time of postoperative TEE; the ratio of right atrial to pulmonary capillary wedge pressure was calculated for each patient. The ischemic aortic cross-clamp time was obtained from the anesthesiologist's record. Preoperative coronary angiograms of all patients who underwent arteriography (n = 65) were reviewed. Important coronary artery disease was defined as that causing a 50% or greater reduction in cross-sectional luminal diameter in the proximal region of any of the major epicardial coronary arteries. All but 6 of the patients had preoperative echocardiograms that showed normal right ventricular function. Data on in-hospital deaths were obtained by one of the investigators, who reviewed the medical records after each patient's hospital discharge or death.

Echocardiographic Analysis
Transesophageal echocardiography was performed with a single-plane, 5-MHz, 64-element transducer. Quantitative and semiquantitative measurements were obtained in all patients from digitized end-systolic and end-diastolic images acquired from the transgastric short-axis plane. End-systolic and end-diastolic endocardial boundaries of both ventricles were traced off-line for calculation of the fractional area change (FAC), as follows: FAC = [(end-diastolic area - end-systolic area)/end-diastolic area] x 100. Segmental wall motion was scored using a modification of the recommendations by the American Society of Echocardiography [8]. Each segment was graded visually with a semiquantitative scoring system, such that 1 = normal or hyperdynamic; 2 = hypokinetic; 3 = akinetic; and 4 = dyskinetic.

Right ventricular systolic dysfunction was present if the following findings were seen on TEE: severe hypokinesis or akinesis in two or more right ventricular segments (inferior, septal, or right ventricular free wall), right ventricular fractional area change of 25% or less, and right ventricular dilatation (right ventricular cavity end-systolic diameter of 3 cm or greater, mid-septum to right ventricular free wall) [4]. Left ventricular systolic dysfunction was present if the following findings were seen on TEE: severe hypokinesis or akinesis in at least two of five left ventricular segments (septum, anterior, lateral, posterior, or inferior wall), left ventricular fractional area change of 25% or less, and left ventricular dilatation (left ventricular end-systolic diameter of 4 cm or greater) [3, 4, 6]. By the use of these criteria, moderate to severe or severe ventricular dysfunction can be differentiated from normal or mild dysfunction. For the purpose of this study, right or left ventricular function was considered normal if the above criteria were not met.

Color flow imaging was performed in the four-chamber view for detection of tricuspid or mitral valve regurgitation. Valvular regurgitation was graded based on the ratio of the visual estimation of the relative jet area to atrial size, with a ratio less than or equal to 30% considered unimportant and greater than 30% pronounced. The analysis of right and left ventricular systolic function and valvular regurgitation was assessed by two experienced, independent observers. There was complete agreement in the grading of right ventricular dysfunction, left ventricular dysfunction, and severe mitral and tricuspid regurgitation in 95%, 93%, 96%, and 92% of cases, respectively. All discrepancies were settled by consensus.

For the purpose of analysis, the patients were divided into four groups based on the TEE findings with regard to ventricular function: group 1 comprised patients with right ventricular systolic dysfunction and normal left ventricular function; group 2 included those with both right and left ventricular systolic dysfunction; group 3 included those with normal right ventricular systolic function but with left ventricular systolic dysfunction; group 4 consisted of those with normal right and left ventricular function.

Statistical Analysis
All values are expressed as mean ± standard deviation. Differences between the groups in the hemodynamic indices and ischemic cross-clamp times were determined by analysis of variance. A p value less than 0.05 was considered statistically significant.

	Results

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

 
The cardiac surgical procedures performed in the 75 patients are listed in Table 1. Thirty-one of the 75 patients (41%) underwent coronary artery bypass graft surgery (CABG) alone; 28 patients (37%) underwent valvular procedures with or without concomitant CABG. The remaining 22% underwent other cardiac procedures.

Isolated CABG or CABG combined with valve repair/replacement was the surgical procedure performed most often in those with combined right and left ventricular dysfunction (15 of 19), isolated left ventricular dysfunction (15 of 18), or normal biventricular function (12 of 21). In the group with isolated right ventricular dysfunction, only 4 of 17 patients underwent CABG.

Table 2 lists data on age, intraoperative aortic cross-clamp time, and postoperative hemodynamic indices (at the time of the TEE study) for each group. Patients with isolated left ventricular dysfunction were significantly older than those with isolated right ventricular dysfunction or those with normal right and left ventricular function. The ischemic cross-clamp times were significantly longer in patients with right and left ventricular dysfunction than in those with isolated right ventricular dysfunction or those with normal right and left ventricular function. The right atrial pressures were significantly higher in the group with combined right and left ventricular systolic dysfunction than in any other group. Pulmonary artery systolic pressures were lower in the patients with normal right and left ventricular function than in patients in the three other groups, but this difference was not statistically significant. The pulmonary artery capillary wedge pressures were similar among the four groups. The ratio of right atrial pressure to pulmonary artery capillary wedge pressure was significantly higher in patients with right and left ventricular dysfunction than in patients with isolated right ventricular dysfunction or isolated left ventricular dysfunction.

Thirty-four patients (44%) died while in the hospital. The causes of death included intractable cardiac failure in 5, sepsis in 2, acute renal failure in 2, cardiac tamponade in 1, ventricular fibrillation in 1, and multisystem failure in the other 23. The in-hospital mortality rate by group was highest in those with isolated left ventricular dysfunction (63%), followed by the rate in those with combined right and left ventricular dysfunction (53%) and in those with isolated right ventricular dysfunction (47%).

When the patients were grouped according to whether they had left ventricular systolic dysfunction (regardless of right ventricular function) or right ventricular systolic dysfunction (regardless of left ventricular function), the in-hospital mortality rate was 57% in the 37 patients with left ventricular dysfunction and 50% in the 36 patients with right ventricular dysfunction. Survival was best in those with normal right and left ventricular function, although 4 patients (19%) in this group died during their hospitalization.

Five patients with low output syndrome were treated with mechanical assistance with left or right ventricular assist devices (VAD): a right VAD was inserted in 2 patients with isolated right ventricular dysfunction, and right and left VADs were inserted in 3 patients with combined right and left ventricular systolic dysfunction. Among these patients, 4 died during their hospitalization.

	Comment

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

 
Echocardiographic Assessment of Cardiac Function in the Early Postoperative Period
The utility of TEE in the assessment of postoperative complications after cardiac surgical procedures has been well documented [5–7]. Accurate assessment of ventricular size and function can be obtained from the transgastric short-axis view, and measurements obtained from this view have been shown to correlate with measurements of global ventricular function [9]. In this study, we used TEE to evaluate the cause of low output syndrome within 48 hours after cardiac operations and found that a large number of patients had substantial right or left ventricular dysfunction. Our findings confirm those of previous reports in which low output syndrome, regardless of cause, was associated with a high in-hospital mortality rate [1, 7, 10]. In our study, the in-hospital mortality rate was high despite the use of inotropic agents or mechanical support.

Postoperative Ventricular Dysfunction
Ventricular dysfunction after cardiac surgery has been described in both clinical and animal studies [11–15]. Breisblatt and colleagues [11] obtained serial hemodynamic and radionuclear angiography studies in 24 patients undergoing uneventful CABG and observed that transient right and left ventricular dysfunction developed in 96% a mean of 4 ± 2 hours after operation, which was partially reversible by 8 to 10 hours after operation. Royster [12] proposed several potential mechanisms as contributors to postoperative ventricular dysfunction, such as ischemic insult during aortic cross-clamping, inadequate myocardial protection during cardioplegia, severe atherosclerotic coronary artery disease, inadequate surgical revascularization, and reperfusion injury.

Low output syndrome after cardiac surgery is frequently associated with hypovolemia, left ventricular dysfunction, valvular dysfunction, and mechanical complications such as cardiac tamponade. Substantial right ventricular systolic dysfunction (isolated or combined with left ventricular dysfunction) occurred in nearly half of our study population, and nearly one quarter had isolated right ventricular dysfunction. The importance of right ventricular systolic dysfunction has been described recently by Reichert and co-workers [7] in a small group of patients. These investigators studied 30 patients after cardiac operations and found that 21 (70%) had right ventricular dysfunction; however, their study population included 10 patients with ventricular septal rupture, a group known to have right ventricular dysfunction and an excessively high perioperative mortality rate. In the patients in our study population, none of whom had septal rupture, we also found a high in-hospital mortality rate associated with right ventricular dysfunction.

The presence of right coronary artery disease may contribute to right ventricular dysfunction, particularly during ischemic arrest when delivery of cardioplegia may be inadequate for right ventricular myocardial perfusion [16–18]. Laster and associates [19] suggested that a brief period of right ventricular ischemia (less than 1 hour of right coronary artery occlusion) followed by reperfusion results in an almost immediate return to normal right ventricular function; late reperfusion (more than 4 hours of right coronary artery occlusion) leads to minimal acute recovery of right ventricular function, but significant improvement occurs over time. Thus, even after prolonged periods of ischemia, right ventricular function tends to improve if reperfusion is established. It has been postulated that postischemic ventricular dysfunction or myocardial stunning can result from abnormalities of excitation-contraction coupling [20]. These abnormalities can occur early after weaning from cardiopulmonary bypass, particularly after revascularization via CABG. Myocardial stunning may have accounted for right ventricular dysfunction in some of our patients, particularly those with important right coronary artery disease; 19 of 33 patients (58%) with right ventricular dysfunction had pronounced disease of the right coronary artery. However, 22 of 31 patients (71%) without right ventricular dysfunction did have notable right coronary artery disease. Moreover, 10 patients with isolated right ventricular dysfunction had normal coronary arteries, but no patients with isolated left ventricular dysfunction had normal coronary arteries. In addition, ischemic cross-clamp times in those with or without right ventricular dysfunction were not significantly different (85 ± 39 versus 73 ± 32 minutes; p = not significant). Thus, even though right coronary artery disease is associated with postoperative right ventricular dysfunction, the majority of cases could not be explained on the basis of atherosclerotic disease of the right coronary artery, prolonged ischemic cross-clamp time, or myocardial stunning occurring after cardiopulmonary bypass.

Because of its anterior position, the right ventricle may be particularly susceptible to ischemic insults that result from coronary embolism of air, thrombi, or particulate matter (ie, aortic atheroma or macroaggregates) or from inadequate cooling during operation. Inadequate preservation of the right ventricle during cardiopulmonary bypass as a result of poor myocardial cooling has been suggested as another cause of postoperative right ventricular dysfunction [16, 21]. Although in many of our patients myocardial temperatures were not uniformly available, it is possible that inadequate myocardial cooling could have been responsible for the right ventricular dysfunction that we observed. Because the operation in 24 of 36 patients (67%) with right ventricular dysfunction involved manipulation of the left ventricle or the ascending aorta, embolization to the right coronary artery may have occurred. Air embolism usually occurs early after the operative procedure, and the resulting right ventricular dysfunction resolves within a short period without lasting effects [22]. On the other hand, embolization of particulate matter such as macroaggregates or atheromatous debris is more likely to cause severe and prolonged right ventricular dysfunction [23, 24]. This possibility, although intriguing, is difficult to prove unless postmortem examination of the heart is performed [23].

Hemodynamic Indices of Right Ventricular Dysfunction
Some investigators have advocated the use of hemodynamic measurements in the assessment of acute right ventricular dysfunction [25]. Elevations in right atrial and right ventricular diastolic pressures with equalization of pulmonary artery capillary wedge pressure are often present in right ventricular infarction. Similar hemodynamic findings were observed in this study, particularly in the group of patients with right and left ventricular dysfunction. This group had the highest elevation in right atrial pressure and an increased ratio of right atrial to pulmonary artery capillary wedge pressure. However, right atrial pressures in the group with isolated right ventricular dysfunction were similar to those in the group with isolated left ventricular dysfunction and the group with normal right and left ventricular function. Pulmonary artery capillary wedge pressures were similar among the four groups. Thus, the ratio of right atrial to pulmonary artery capillary wedge pressure was not helpful in differentiating patients with isolated right ventricular systolic dysfunction from those in the other groups. These results contrast with the findings of Lopez-Sendón and associates [25], who reported that a right atrial pressure of 10 mm Hg and within 1 to 5 mm Hg of the pulmonary capillary wedge pressure occurred in 73% of patients with right ventricular infarction. In our study, the lack of specificity of this ratio may be due to altered hemodynamics resulting from changes in intravascular volume status, the administration of multiple drugs, or interactions between the right and left ventricle. Right ventricular systolic dysfunction can also be caused by elevated pulmonary artery systolic pressures, which cause increased afterload to the right ventricle, but this abnormality was not found in a large number of patients in this study.

Substantial tricuspid regurgitation was present more often in patients with right ventricular dysfunction (78%); important mitral regurgitation was present more often in patients with left ventricular dysfunction (74%). The presence of regurgitation in these patients is likely secondary to ventricular dilatation associated with ventricular dysfunction. In those patients with normal right or left ventricular function, as measured by echocardiography, artifactually low measurements of cardiac output may have been due to important tricuspid regurgitation, because of its effects on the accuracy of the thermodilution estimation of this measurement.

Limitations of the Study
The assessment of right and left ventricular function was for the most part based on the semiquantitative wall motion score, as recommended by the American Society of Echocardiography. There are no established guidelines for the quantitation of right ventricular function using echocardiography. We therefore used a combination of quantitative measurements (ie, fractional area change) and semiquantitative assessment (ie, segmental wall motion score).

This study was a retrospective investigation of consecutive patients undergoing TEE for evaluation of low output syndrome after cardiac operations, and is subject to all of the limitations inherent in this type of investigation. Because some patients with this syndrome improved shortly after initial treatment (ie, intravenous fluids, inotropic agents, or mechanical support with intraaortic balloon counterpulsation) but before the TEE study was performed, there was a selection bias (mostly dictated by the surgeon) as to which patients underwent TEE. Thus, our study population was highly selected, comprising only those with postoperative low output syndrome that persisted despite aggressive initial therapy. The overall incidence of untreated low output syndrome or the incidence of right ventricular dysfunction after cardiac operations, particularly in patients with normal or nearly normal cardiac index, remains undetermined.

	Conclusions

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

 
Low output syndrome after cardiac operations, regardless of its cause, carries a high in-hospital mortality rate. Even though left ventricular dysfunction is the most common cause of postoperative low output syndrome, in this study we found an unexpectedly high frequency of right ventricular dysfunction (either isolated or associated with left ventricular dysfunction) after cardiac operations. Postoperative right ventricular dysfunction was not uniformly associated with important right coronary artery disease or prolonged ischemic time during cardiopulmonary bypass, and hemodynamic variables such as right atrial pressure and the ratio of right atrial to pulmonary capillary wedge pressure were not helpful in establishing its presence or absence. Right ventricular dysfunction identified by TEE after cardiac operations provides prognostic information regarding in-hospital mortality. Better understanding of the mechanisms causing postoperative right ventricular dysfunction may provide insight for preventing this complication of cardiac operations.

	Acknowledgments

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

 
This work was supported in part during the tenure of a Minority Scientist Development Award from the American Heart Association and by the National Institutes of Health HL-17646 (SCOR in Coronary and Vascular Diseases) Minority Investigator Research Grant (MIRS), both to Dr Dávila-Román.

	Footnotes

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

 
Address reprint requests to Dr Dávila-Román, Cardiovascular Division, Washington University School of Medicine, Box 8086, 660 S Euclid Ave, St. Louis, MO 63110.

	References

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

 

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This Article Abstract Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): William E. Hopkins Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Dávila-Román, V. G. Articles by Barzilai, B. Search for Related Content PubMed PubMed Citation Articles by Dávila-Román, V. G. Articles by Barzilai, B.