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Anesth Analg 2002;94:774-780
© 2002 International Anesthesia Research Society

CARDIOVASCULAR ANESTHESIA

Segmental Wall Motion Abnormalities During Telerobotic Totally Endoscopic Coronary Artery Bypass Grafting

Stephan Mierdl, MD*, Christian Byhahn, MD*, Selami Dogan, MD{dagger}, Tayfun Aybek, MD{dagger}, Gerhard Wimmer-Greinecker, MD, PhD{dagger}, Paul Kessler, MD, PhD*, Dirk Meininger, MD*, and Klaus Westphal, MD, PhD*

Departments of *Anesthesiology, Intensive Care Medicine and Pain Control and {dagger}Thoracic and Cardiovascular Surgery, J. W. Goethe-University Hospital Center, Frankfurt, Germany

Address correspondence and reprint requests to Klaus Westphal, MD, PhD, Head of the Department of Anesthesiology, Katharina-Kasper Kliniken, Richard-Wagner Str. 14, D-60318 Frankfurt, Germany. Address e-mail to klaus.westphal{at}em.uni-frankfurt.de


   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 References
 
In addition to single-lung ventilation (SLV), intrathoracic CO2 insufflation is mandatory for adequate exposure during totally endoscopic coronary artery bypass grafting. With transesophageal echocardiography, we investigated biventricular myocardial wall motion in 25 patients with isolated disease of the left anterior descending coronary artery who underwent totally endoscopic coronary artery bypass grafting with the "Da Vinci" robotic surgical system. At distinct time points during the operation, a cine loop of both ventricles was registered from a transgastric mid-short-axis view. Myocardial wall motion analysis was performed according to an established segmentation model of the left ventricle and to an established five-point scale for wall motion (1, normal; 5, dyskinesia). Significant alterations from preoperative baseline wall motion were visible in the septal, inferior, and anterior segments of the left ventricle at some time during the prebypass period, combined with a markedly decreased PaO2 under SLV and increased intrathoracic pressure. The same findings applied to the right ventricle; however, wall motion abnormalities were more pronounced here. After myocardial revascularization, weaning from cardiopulmonary bypass, CO2 deflation, and return to double-lung ventilation, myocardial wall motion recovered to baseline values. Clinically significant hemodynamic instability did not occur. The data suggest that robot-assisted coronary artery bypass grafting leads to significant prebypass alterations of biventricular segmental wall motion. On the basis of our data, it cannot be definitively stated whether the observed results were due to reduced oxygenation during SLV and thus "real" myocardial ischemia, intrathoracic CO2 insufflation with positive pressure leading to mechanical compromise of the heart, absolute or relative hypovolemia, or a combination of these factors. However, in this cohort, which consisted of patients with single-vessel disease and good ventricular function, these changes were of limited clinical relevance.

IMPLICATIONS: Segmental myocardial wall motion was evaluated with transesophageal echocardiography during robot-assisted totally endoscopic coronary artery bypass grafting. Significant biventricular segmental wall motion abnormalities occurred before cardiopulmonary bypass under single-lung ventilation and carbon dioxide insufflation. The changes in myocardial wall motion were of limited clinical relevance.


   Introduction
Top
 Abstract
 Introduction
Methods
 Results
 Discussion
 References
 
Within the last few years, there has been a rapid increase in minimally invasive procedures, including endoscopic techniques, in cardiothoracic surgery (1). To overcome the limitations of traditional endoscopic techniques, robotic systems have recently been designed and used to render totally endoscopic coronary artery bypass grafting (TECAB) possible. Special considerations are required for this technique: single-lung ventilation (SLV) is mandatory during the period of internal thoracic artery (ITA) preparation. In addition, exposure is optimized by intrathoracic insufflation of CO2 with positive pressure, similar to laparoscopic procedures (2,3).

Although a number of studies have described hemodynamic compromise during artificially augmented intrathoracic pressure of 10 or 15 mm Hg (4,5) or hypoxemia from SLV (6,7), there are no reports of the effect of this combination on myocardial function. The aim of this study was to elucidate the effect of this new surgical technique on global and regional myocardial function.


   Methods
Top
 Abstract
 Introduction
 Methods
Results
 Discussion
 References
 
After approval by the IRB, 25 adults with symptomatic single-vessel disease of the left anterior descending coronary artery (LAD) who underwent TECAB were studied. All patients received IM premedication with 0.06 mg of fentanyl and 3 mg of droperidol 30 min before the induction of anesthesia. Upon arrival in the preoperative holding area, IV access, five-lead surface electrocardiogram (ECG), and noninvasive blood pressure monitoring were established. In addition, direct arterial blood pressure monitoring was instituted by using the left radial artery.

After the induction of anesthesia with sufentanil (25 µg), etomidate (0.2 mg/kg), and succinylcholine (1 mg/kg), the patients were intubated with a left endobronchial 37–41F double-lumen tube (Kendall, Neustadt, Germany). Correct positioning of the tube was verified by both auscultation and fiberoptic bronchoscopy. Once the patient was anesthetized, a second arterial catheter was introduced into the right radial artery. A pulmonary vent catheter for cardiopulmonary bypass (CPB) with the Port-Access technique (Heartport, Redwood City, CA) was inserted via the right internal jugular vein and positioned by transesophageal echocardiographic (TEE) guidance. Pulse oximetry, ECG, invasive arterial blood pressure, and central venous pressure were recorded continuously.

Anesthesia was maintained with an end-tidal concentration of 1.1 to 1.4 vol% enflurane with air in oxygen (fraction of inspired oxygen [FIO2], 0.5). The respiratory rate was set to 10 breaths/min, and tidal volume was set to 8–10 mL/kg and adjusted by means of repeated arterial blood gas analyses to achieve PaCO2 and pH within ranges of 32 to 45 mm Hg and 7.34 to 7.47, respectively. During the period of SLV, initial respiratory rate, tidal volume, and inspired oxygen concentration were maintained unless the arterial oxygen saturation as measured by pulse oximetry decreased to <92% or if arterial blood gas analyses performed in 15-min intervals throughout SLV showed PaO2 <100 mm Hg. If one or both conditions applied, the FIO2 was increased to 100%, and continuous positive airway pressure of 5 cm H2O was added to the nonventilated lung. The next step was to add 5 cm H2O positive end-expiratory pressure to the dependent ventilated lung. Both continuous positive airway pressure and positive end-expiratory pressure were incrementally increased to a maximum of 10 cm H2O if necessary. Similar to double-lung ventilation (DLV), respiratory rates and tidal volumes were adjusted to achieve pH as described previously and PaCO2 of approximately 40 mm Hg.

During mildly hypothermic (32°C–33°C) CPB, anesthesia was maintained by continuous administration of 4 mg · kg-1 · h-1 of propofol, supplemented by pancuronium for muscle relaxation. In addition, 25 µg of sufentanil was administered for analgesia when deemed necessary. All patients received continuous infusions of dopamine (3 µg · kg-1 · min-1) and diltiazem (3 mg/h).

The surgical procedure was performed by the use of the "Da Vinci" computer-enhanced telemanipulator system (Intuitive Surgical, Mountain View, CA) through a left-sided transthoracic approach, with patients in the supine position and the left chest slightly elevated. After institution of SLV and under continuous CO2 insufflation, the left ITA was dissected, and then CPB was instituted via the femoral artery and vein. ITA harvesting was finished after initiation of CPB. After occlusion of the ascending aorta with an endoaortic balloon catheter and application of antegrade cardioplegia, the left ITA was grafted onto the LAD. Weaning from CPB was achieved under SLV after reperfusion and rewarming, which consumed at least one third of the aortic cross-clamp time. DLV was reinstituted after surgical hemostasis and CO2 release from the thoracic cavity. At the end of the operation, the double-lumen tube was replaced with a single-lumen tube, and the patient was transferred to the intensive care unit.

To evaluate PaO2, PaCO2, and serum lactate levels, arterial blood gas analyses were performed immediately before incision during DLV as a baseline value; 30, 90, and 120 min after institution of SLV; and 5 min after DLV was restarted after weaning from CPB (Fig. 1). In every instance, the samples were immediately analyzed in a laboratory next to the operating room (ABL, Acid Base Laboratory/Hemoxymeter; Radiometer, Copenhagen, Denmark). At the same time points, FIO2, intrathoracic CO2 pressure, and automated ST segment analysis at J + 60 ms for leads I, II, and V5 were recorded (Hellige Marquette Solar 8000 Patient Monitor; Marquette Medical Systems, Milwaukee, WI). An ST segment alteration of >=1 mm (0.1 mV) from baseline that persisted longer than 60 s was considered evidence of ischemia.



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  		Figure 1. Time line of the data sampling points (not to scale). DLV = double-lung ventilation; SLV = single-lung ventilation.

 
All examinations were performed with the patient in the supine position with the left chest slightly elevated. A Vingmed System Five (GE Vingmed, Horten, Norway) echocardiography device with a multiplane 5- to 7-MHz TEE probe was used. Device settings were as follows: frequency 6.7 MHz, power 4 dB, depth 14 cm, and frame rate 70–80/min. A transgastric mid-short-axis view of the left and right ventricles at the level of midpapillary muscles was chosen. An ECG-triggered cine loop of three cardiac cycles of each ventricle was acquired at the previously mentioned intervals and was directly stored on the image processing system (Echo PAC v. 6.1; Vingmed) for off-line analysis. During data acquisition, the patient was disconnected from ventilation in end expiration. Analysis of segmental wall motion was performed by dividing the left ventricle into six segments according to the guidelines of the American Society of Echocardiography and the Society of Cardiovascular Anesthesiologists (8). Because there is no established model for segmentation of the right ventricle, the right ventricle observed at the transgastric mid-short-axis view was divided into two segments. The posterior segment adjacent to the liver and diaphragm was named "diaphragmatic," whereas the anterior segment with no contact to structures other than pericardium was named "free." The ventricular septum was considered a part of the left ventricle.

Analysis of left and right ventricular function was based on a qualitative visual assessment of the motion and thickening of a given segment during systole and graded according to a scale for wall motion which has been used extensively in the intraoperative echocardiography literature. The qualitative grading for wall motion is 1, normal (>30% thickening); 2, mildly hypokinetic (10% to 30% thickening); 3, severely hypokinetic (<10% thickening); 4, akinetic (no thickening); and 5, dyskinetic (paradox movements during systole). Because most patients were receiving myocardial depressants, such as ß-adrenergic blockers, and because of the negative inotropic effects of anesthesia itself, grades of 1 and 2 were defined as normal myocardial function, and grades of 3, 4, or 5 were classified as myocardial dysfunction.

Right (RVEF) and left (LVEF) ventricular ejection fraction and fractional shortening were also registered from the M-mode loop. Ejection fractions were calculated with the Teichholz formula, which shows the best agreement of all M-mode calculations when compared with angiographic results (9). All examinations were performed by two independent, experienced echocardiographers. Whereas the first echocardiographer performed the intraoperative TEE monitoring and therefore was not blinded to patient identity and clinical data, the second echocardiographer had no information regarding hemodynamic or clinical data of the patients and was blinded to the time points, but not to the study purpose. With grades derived from a study by Rouine-Rapp et al. (10), agreement between the investigators was defined as independently assigned grades within the normal (grades 1 and 2) or abnormal (grades 3–5) range. The classification assigned to segments when the echocardiographers independently agreed was considered final. When one investigator classified function as normal and the other abnormal, or when the classification differed by two or more points, the investigators met and assigned a class of function by consensus. If the investigators could not agree on a consensus classification, the respective segment was examined by a third echocardiographer and classified according to the majority opinion of all three investigators.

All data are presented as mean ± SD. Calculation and data analysis were performed by using a statistical package (GraphPad InStat 3.0; GraphPad Software, San Diego, CA). Data were compared with baseline values, and statistical significance was determined with the Friedman test and Dunn’s multiple comparisons test (nonparametric data), one-way analysis of variance with the Bonferroni multiple comparisons test (parametric data), or Wilcoxon’s matched-pairs test, as appropriate. Differences were considered to be statistically significant if P < 0.05.


   Results
Top
 Abstract
 Introduction
 Methods
 Results
Discussion
 References
 
Twenty-five patients (16 men and 9 women; mean age, 56 ± 8 yr) were included in the study. No patient had a history of myocardial infarction, and preoperative LVEF was calculated as >50% in all patients with angiography and transthoracic echocardiography. No segmental wall motion alterations (SWMAs) were visible during the preoperative examinations. Seventeen patients had arterial hypertension, four had a history of obstructive pulmonary disease (however, preoperative pulmonary function testing was normal), and another three had diabetes. Twenty-three patients were receiving ß-adrenergic blockers. The total operating time was 492 ± 129 min, including a 175 ± 56-min period of SLV. CPB lasted for 171 ± 68 min, with 83 ± 36 min of aortic cross-clamping.

After initiation of SLV and CO2 insufflation, PaO2 decreased significantly as compared with the mean PaO2 for DLV, which remained unchanged during SLV and returned to baseline after resumption of DLV. In contrast, a significant increase of the PaCO2 was observed during insufflation with intrathoracic CO2 pressures maintained between 9 and 11 mm Hg. Heart rate increased significantly during the procedure, accompanied by a stable mean arterial blood pressure. Central venous pressure was increased during SLV and CO2 insufflation (Table 1). Episodes of ST segment alteration of ±1 mV from baseline were observed in leads I (n = 10), II (n = 4), and V5 (n = 14) at least once during SLV and CO2 insufflation but returned to baseline at the end of surgery.


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  		Table 1.  Intrathoracic CO2 Pressure, Gas Exchange, and Hemodynamics (mean ± sd)
 
Serum lactate (institutional reference value <20 mg/dL) was not increased during SLV or before CPB (baseline level, 9.5 ± 3.3 mg/dL) and increased to 35.6 ± 28.9 mg/dL after weaning from CPB (P < 0.05). Postoperatively, creatinine kinase (CK) levels (institutional reference value <80 U/L for CK and CK-muscle/brain fraction [MB] <10% of CK) increased from 39 ± 27 U/L (preoperative baseline value) to 1287 ± 1094 U/L (P < 0.05), whereas the postoperative CK-MB fraction did not exceed 43 ± 39 U/L. Preoperatively, the MB fraction was not determined, because total CK was <100 U/L in all patients.

Biventricular ejection fraction and fractional shortening did not change significantly throughout the procedure. Nevertheless, new SWMAs occurred, especially in the right ventricle and in the left ventricular inferior, septal, and anterior segments.

Significant alterations from baseline in left ventricular wall motion were visible 30 min after the onset of SLV in the septal segment and also occurred in the inferior and anterior segments after 90 min of SLV (Table 2). In two patients, akinesia developed during the procedure in the septal and anteroseptal segments, but it was only mildly hypokinetic at baseline.


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  		Table 2.  Scores of Segmental Wall Motion Alterations (SWMAs) of the Left Ventricle (mean ± sd) and Number of Patients with an Increase in SWMA Score of at Least Two Points from Baseline
 
After 30 min of SLV, significant SWMAs were visible in the free right ventricular segment. SWMAs also occurred in the diaphragmatic segment of the right ventricle at 90 and 120 min of SLV (Table 3). Two patients whose free right ventricular segment was defined as mildly hypokinetic at baseline developed dyskinesia during SLV and CO2 insufflation, and in six patients either akinesia or dyskinesia was observed in the diaphragmatic segment of the right ventricle, which was mildly hypokinetic in all these patients at baseline.


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  		Table 3.  Scores of Segmental Wall Motion Alterations (SWMAs) of the Right Ventricle (mean ± sd) and Number of Patients with an Increase in SWMA Score of at Least Two Points from Baseline
 
Except for continuous small-dose dopamine infusion, no patient received further inotropic or vasopressor support because of hemodynamic instability during the operation or the immediate postoperative course. The median time of assisted ventilation after surgery was 540 min. Although two patients were extubated upon arrival at the intensive care unit, another patient required respiratory support for 29 days because of severe postoperative cerebral ischemia.


   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
References
 
Minimally invasive surgical methods have become more prevalent in the field of cardiac surgery. Recently, computer-enhanced telemanipulation systems have been introduced to enable totally endoscopic myocardial revascularization. However, SLV and intrathoracic CO2 insufflation with positive pressure are required for adequate exposure of the intrathoracic structures. In the past, several investigators demonstrated significantly impaired oxygenation or even hypoxemia during SLV (6,7). Relevant hemodynamic disturbance after intrathoracic CO2 insufflation has also been shown (4,5). The effect of combined SLV and CO2 insufflation on myocardial performance in coronary patients has not been studied.

The development of new SWMAs represents a marker of myocardial ischemia with very high sensitivity (11–13). SWMA analysis can be used for perioperative ischemia monitoring in patients at coronary risk. The accuracy of SWMA is based on interdisciplinary guidelines that allow exact interpretation of the extent of SWMA as an indirect scale of ischemia (8). Nonetheless, there are also nonischemic causes of SWMA (14,15). Conduction abnormalities, anesthetics, acute changes in adrenergic tone, or hypovolemia can cause false-positive results. In addition, hibernating or stunned myocardium can show impaired systolic function even though the ischemia-producing event is no longer present (16).

This study demonstrates that new segmental alterations of myocardial wall motion develop during SLV before the onset of CPB. After institution of SLV and intrathoracic CO2 insufflation with positive pressure, significant SWMAs of the left ventricular anterior and inferior wall, as well as of the ventricular septum and the free and diaphragmatic segments of the right ventricle, became visible. These myocardial regions are perfused by the LAD but also by the nondiseased right coronary artery. With increasing duration of CO2 insufflation, and SLV with markedly decreased PaO2, SWMAs become more pronounced and associated with an increased heart rate that we attribute to the relative hypovolemia caused by reduced venous return and poor cardiac filling due to augmented intrathoracic pressure. Absolute hypovolemia may have also been present, because baseline LVEF and RVEF were relatively high. These alterations were more pronounced in the right ventricle but developed simultaneously in the left ventricle. Although the thin muscular wall of the right ventricle is less resistant to positive intrathoracic pressure, mechanical shift may play a major role in right ventricular SWMAs, whereas ischemia may be one of the main reasons for the increase in left ventricular SWMAs. After weaning from CPB and reconstitution of DLV, biventricular wall motion normalized, and there was no statistical difference between baseline and the final postoperative examination.

Well designed and extensive studies have been performed by Leung et al. (17), who used a similar TEE method. This group defines a change in SWMA score of at least two points as a sign of myocardial ischemia. Compared with the data from Leung et al., the SWMAs in this study represent mild alterations in wall motion pattern, because changes of at least two points from baseline were visible in only seven patients (diaphragmatic right ventricle segment, n = 4; diaphragmatic and free right ventricle segments, n = 1; diaphragmatic and free right ventricle segments and left ventricle segments, n = 1; left ventricle segments, n = 1). In addition, these SWMA changes were observed before CPB and—except for one patient with persistent akinesia of the diaphragmatic wall of the right ventricle—were not observed in the crucial post-CPB period as reported by other investigations (17,18). This may be due to different patient populations. Leung et al. examined patients with multivessel disease and unstable angina, whereas the TECAB procedures were performed in patients with single-vessel disease. It should nonetheless be stated that in our cohort, only the transgastric mid-short-axis view was applied. Rouine-Rapp and Cahalan (19) found that 43% of SWMAs may be missed by using this view alone, without additional transverse or longitudinal planes. We were aware of this problem, but keeping the probe in stable position during the entire study period was thought to generate reproducible TEE results of high reliability. Furthermore, the transverse mid-short-axis view allows evaluation of all regions of myocardium perfused by each of the major coronary arteries. The number of patients who developed SWMAs at any time during the course of surgery may have been almost twice as much, provided that the use of additional planes would have detected any other SWMAs, as proposed by Rouine-Rapp and Cahalan (19).

There was no change in biventricular ejection fraction or fractional shortening. This is consistent with findings of other studies conducted on patients undergoing conventional coronary artery bypass graft. We agree with other investigators that these variables do not adequately reflect acute myocardial ischemia, as do eventual hemodynamic changes (20,21). Furthermore, it must be acknowledged that it may be difficult to differentiate whether some of the observed SWMAs in our patients actually represent episodes of reversible myocardial ischemia that disappear after reperfusion on CPB or whether they were—at least to some extent—false-positive results, as previously discussed.

Intermittent ST segment alterations occurred irregularly and independently of SLV time, CO2 pressure, or operating time. They normalized completely at the end of the operation. As shown elsewhere, similar to hemodynamic changes, these ST segment changes were rarely correlated with intraoperative SWMAs (18,22) and thus do not reflect myocardial ischemia. Serum lactate concentrations as evidence of tissue hypoxia or ischemia remained stable despite occasionally low PaO2 during SLV. They increased only after weaning from CPB. Twelve hours after surgery a massive increase of CK was observed that was not accompanied by a marked increase of CK-MB, and this finding allows exclusion of relevant myocardial damage. The increase in CK is most likely caused by limb ischemia caused by femoral cannulation for CPB with the Port-Access system.

The SWMAs observed may be due to a multitude of factors. The mean PaO2 of 90 mm Hg during SLV is an unlikely explanation for SWMAs; however, it is conceivable that patients whose PaO2 during SLV decreased markedly below the normal range experienced transient myocardial ischemia, as shown by SWMAs in the region perfused by the stenotic left coronary artery. A considerable number of patients developed arterial hypercapnia during CO2 insufflation. In contrast to hypoxemia, acute hypercapnia was demonstrated not to induce coronary steal from collateral-dependent myocardium, but to increase global coronary blood flow, making it an unlikely cause of the observed SWMAs (23). More severe SWMAs in the right ventricle seem to reflect positive intrathoracic pressure with resulting right heart compromise because of less wall thickness and muscle mass in the right ventricle. The SWMAs in the right ventricular segments do not advocate hypoxia as a cause of this problem. In addition, should SWMAs be associated with hypoxia, more pronounced SWMAs would be expected in left ventricular segments perfused by the stenotic LAD branches. Acute pulmonary hypertension from hypoxic pulmonary vasoconstriction caused by SLV could also explain the right ventricular SWMAs to some extent; however, no pulmonary artery pressures were obtained during our study to prove or disprove this assumption. Another possible mechanism for SWMAs could be an acute change in loading conditions. Artificially created positive intrathoracic pressure may result in decreased venous return to the heart, mimicking hypovolemia. The increased heart rate during SLV and CO2 insufflation may also contribute to false-positive, nonischemic SWMAs. In summary, the cause of the SWMAs observed could not be identified with certainty and requires additional research in robot-assisted coronary artery surgery.

Our data show that TECAB procedures are accompanied by significant SWMAs during SLV. These alterations can easily be quantified by routine TEE. Because wall motion rapidly returns to baseline after weaning from CPB and neither caused hemodynamic instability nor required inotropic or vasopressor support, there is only a minor (if any) increase in perioperative risk for the patient with isolated single-vessel disease and with good ventricular function. Nevertheless, the risk of hemodynamically relevant perioperative ischemia should not be underestimated, especially if this surgical technique will be applied to patient groups experiencing multivessel coronary artery disease, significant comorbidity, or both.


   References
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 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 

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Accepted for publication November 30, 2001.




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Lippincott, Williams & Wilkins 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 HighWire Press