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*Service d’Anesthésie-Réanimation Chirurgicale and Service de Chirurgie Digestive, Assistance Publique-Hôpitaux de Paris Hôpital Henri Mondor and Université Paris XII, Créteil, France
Address correspondence and reprint requests to François Stéphan, MD, PhD, Département d’Anesthésie-Réanimation, Hôpital Henri Mondor, 51 avenue du Maréchal de Lattre de Tassigny, 94010 Créteil Cedex, France. Address e-mail to francois.stephan{at}hmn.ap-hop-paris.fr.
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Introduction |
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Methods |
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Between March 2000 and May 2001, 10 consecutive patients scheduled for liver resection via an abdominal incision (open group) and 15 consecutive patients scheduled for laparoscopic liver resection (laparoscopic group) were prospectively enrolled in the study. Appropriate candidates for laparoscopic liver resection were patients with peripheral lesions requiring limited hepatectomy (1,8). Anesthetic management and intraoperative care were standardized throughout the study. General anesthesia was induced with propofol 2.5 mg/kg and sufentanil 0.3 µg/kg. After orotracheal intubation facilitated by atracurium 0.5 mg/kg, anesthesia was maintained with 0.5%–1.5% end-tidal isoflurane together with a continuous infusion of sufentanil 0.3 µg · kg–1 · h–1, and muscular relaxation was maintained with continuous infusion of atracurium 0.5 mg · kg–1 · h–1. Crystalloids were infused during the operation at a basal rate of 10 mL · kg–1 · h–1. The inspired oxygen fraction was set at 50% in air, and minute ventilation adjusted to maintain arterial carbon dioxide less than 45 mm Hg.
After the induction of general anesthesia, one radial artery was cannulated, and a luminal central venous catheter was introduced via the right internal jugular vein. Both arterial and central venous pressures were measured after calibration by zeroing to atmospheric pressure and using the mid chest as a reference. The carbon dioxide pneumoperitoneum was induced with 14 mm Hg intraabdominal pressure in the supine position before a 20° head-up tilt in the laparoscopy group. Intermittent clamping was applied with 15-min clamping and 5-min release periods (1). The first PTC period of the surgical procedure was investigated. Hemodynamic and TEE data were collected 5 min before PTC (T1), 5 min after clamping (T2), and 5 min after clamp release (T3) in the two groups. In the laparoscopic group, hemodynamic data were also recorded before and 5 min after the end of peritoneal insufflation.
In the postoperative period, electrocardiography (ECG) recording and measurement of troponin Ic were routinely performed for 48 h in all patients. The normal troponin Ic values ranged from 0.00 to 0.15 ng/mL.
Echocardiographic measurements were performed (128XP10; Acuson Corporation, Mountain View, CA) by a single trained operator (FD). A TEE biplane probe (5 MHz; Acuson) was introduced into the esophagus after the induction of anesthesia and before surgery. From T1 to T3, we successively recorded a LV short-axis view at the midpapillary level and a long-axis view of the LV outflow tract to measure aortic diameter at the level of the aortic annulus. Doppler aortic flow was obtained at the level of the aortic annulus by a transgastric, long-axis approach. LV diameters were measured from the M-mode echocardiogram according to the standards of the European Society of Cardiology (9). Stroke volume, by using a pulsed Doppler two-dimensional method, was calculated by the formula time-velocity integrals x cross-sectional area of the aortic annulus and was indexed by body-surface area (10). All echographic measurements were performed at the end of expiration and were averaged over three consecutive cardiac cycles. The LV end-systolic and the LV end-diastolic areas were measured by manual planimetry of the area circumscribed by the leading edge of the LV endothelial border and were indexed by body-surface area (LVESAi and LVEDAi, respectively). From these measurements, the LV fractional area change (FAC) was computed:
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End diastole was indicated by the peak of R wave, and end systole was defined as the smallest endocardial area. The end-systolic posterior and anterior wall thickness were also determined with M-mode. The LV end-systolic wall stress (LVESWSi) was calculated according to the formula proposed by Grossman et al. (11):
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in which LV wall thickness is represented by the average of the anterior and posterior wall thickness measurements. LVESWSi was also indexed to body-surface area.
Diagnosis of RWMA required observation of RWMA on the midpapillary transverse view and subsequent confirmation on a longitudinal transgastric view. In brief, the midpapillary cross section was divided into four segments, and each segment was evaluated for inward endocardial motion and myocardial thickening. According to previously published definitions (12), five classes of wall motion and thickening were defined: normal, mild hypokinesis, severe hypokinesis, akinesis, and dyskinesis. The midpapillary long-axis view was analyzed by using the same TEE definitions after it was divided into six segments (apical, middle, and basal segments on both the inferior and anterior walls). All RWMAs diagnosed were submitted to another investigator (YH) for confirmation.
Recordings were stored on a videotape recorder. Videotapes were reviewed on an offline analyzer system that allowed slow frame imaging or static image viewing. A random sample of eight patients was submitted twice for analysis to test the reproducibility of the readings. In these cases, the other investigator (YH) was blinded to the type of procedure allocated.
Data were computerized and analyzed with StatView 5.0 (SAS Institute Inc., Cary, NC). We report continuous variables as the mean ± sd or as the median and 25th–75th percentiles when appropriate. The Mann-Whitney U-test was used to analyze continuous variables that were not normally distributed, and 
2 tests or Fisher’s exact test were used to compare proportions and rates. Changes in hemodynamic variables during PTC within the two groups were analyzed with repeated-measures analysis of variance followed by the Scheffé F test, as appropriate. On the basis of a relevant 30% increase in wall stress, we calculated that 10 patients could test the null hypothesis at 0.05 significance with a power of 0.80. A P value <0.05 was considered significant.
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Results |
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Demographic characteristics, duration of surgery before PTC, blood loss, and IV fluid infused until PTC are summarized in Table 1. Patients in the laparotomy group were younger and more likely to be women. For all patients except one in the open group, levels of troponin were in the normal range, and ECG tracings were unchanged during the 48 h postsurgery. No severe perioperative cardiopulmonary complications were observed in this series of patients.
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Hemodynamic and Echocardiographic Data During PTC in the Open Group
At the time of data recording, mean body temperature was 35.0 ± 0.50°C, mean airway pressure was 14 ± 3 mm Hg, mean Paco2 was 35 ± 4 mm Hg, and pH values ranged from 7.39 to 7.47. The mean hemoglobin value was 12.6 ± 0.7 g/dL and remained stable throughout the PTC period. End-tidal isoflurane concentrations were 0.9 ± 0.2%.
Hemodynamic and echocardiographic data before, during, and after PTC are summarized in Table 2. Hemodynamic changes were sustained throughout the PTC but returned to their baseline levels 5 min after clamp release. Changes in percentages are summarized in Table 3. No vasoactive drugs were used during PTC, and no gas embolism was recorded in any patient.
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Evidence of RWMA was demonstrated in only one patient (severe hypokinesis in anterior and septal walls; immediate recovery after clamp release), who recovered uneventfully without significant increases of troponin and modification of ECG tracing. A slight increase in troponin level on the second postoperative day (0.67 ng/mL) without modification of the ECG tracing was noted in another patient.
Hemodynamic and Echocardiographic Data During PTC in the Laparoscopic Group
Five minutes after peritoneal insufflation, mean arterial blood pressure increased by 18 ± 26%, and stroke volume index decreased by 16 ± 10%. LVEDAi remained stable. LVESWSi increased by 32 ± 25%, and FAC decreased by 19 ± 8%. No RWMAs were observed. All measured variables returned to preinsufflation values after 30 min of pneumoperitoneum (Table 4).
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At the time of PTC, mean body temperature was 35.0 ± 0.50°C, mean airway pressure was 21 ± 5 mm Hg, mean Paco2 was 38 ± 6 mm Hg, and pH values ranged from 7.32 to 7.46. The mean hemoglobin value was 13.3 ± 1.9 g/dL and remained stable throughout the PTC period. The end-tidal isoflurane concentration was 0.8 ± 0.2%.
Hemodynamic and echocardiographic data are summarized in Table 4. Hemodynamic changes were sustained throughout PTC but returned to their baseline levels 5 min after clamp release. Changes in percentage are summarized in Table 3. No vasoactive drugs were used during PTC, and no gas embolism was recorded in any patient.
Evidence of RWMA was demonstrated in five patients, who recovered uneventfully without significant increases of troponin or modifications of the ECG tracing. All RWMAs were classified as mild hypokinesis and were located in the anterior and septal walls for three patients, the septal wall for one, and the inferior and lateral walls for another patient. For all RWMAs, immediate recovery was noted after clamp release. Comparisons of echocardiographic changes during PTC between the laparoscopic and open groups are shown in Table 3.
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Discussion |
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Monitoring of cardiac function under pneumoperitoneum conditions was challenging, as illustrated by the poor data recording in one excluded patient. Investigator reliability was the other cornerstone condition for this study. The intraobserver variability reported here (6%) was less than the 8% previously reported (13) and was in accordance with most published studies. Likewise, interobserver variability was less than 8%.
During open surgery, PTC typically increased mean arterial blood pressure and systemic vascular resistance and decreased cardiac output (2,4,5), whereas central venous pressure and pulmonary artery occlusion pressure did not change significantly (2,4,5). In our study, LVEDAi significantly declined after PTC and was a reliable index of LV preload (14,15). A decrease in LV preload is therefore the main mechanism involved in the decrease of cardiac index. Surprisingly, although systemic vascular resistance increased during PTC, LV afterload (assessed by the LVESWSi) did not increase significantly. In fact, systemic vascular resistance is an unreliable index of LV afterload; it reflects only peripheral vasomotor tone, rather than LV systolic wall force (16).
The cardiovascular consequences of laparoscopic surgery have been well documented either by right heart catheterization or by echocardiography. We found the same results as those previously reported (6,17,18). Pneumoperitoneum caused an increase in mean arterial blood pressure and systemic vascular resistance (6,17,18), as well as for LVESWSi (17,18). Changes in cardiac output were variable, consistent with the Starling resistor concept of abdominal venous return (19). For some authors, the hemodynamic, neuroendocrine, and renal changes induced by the pneumoperitoneum even resemble heart failure (7). However, these hemodynamic changes were not sustained throughout the period of pneumoperitoneum (6,18).
In previous studies using right heart catheterization as a tool (2,4), hemodynamic changes were similar when PTC was performed during open or laparoscopic procedures. However, in this study, a significant increase in LV afterload was demonstrated and was probably associated with a decrease in LV preload. Indeed, LVEDAi was expected to increase as a normal response to an increase of LVESAi. Head-up tilt also probably influenced the changes of LV dimensions. Such positioning has been described to be associated with a decrease in indices of LV preload, presumably reflecting a gravitational effect on venous return (17). Finally, LV function was altered, in contrast with the open procedure. This suggested an imbalance between the adequacy of preload and the ability of the heart to pump against an increased afterload. Interestingly, post hoc analysis of echocardiographic data demonstrated the occurrence of RWMAs in 50% of patients during PTC with pneumoperitoneum, as compared with only 10% of patients during PTC without pneumoperitoneum. While some authors did not observe RWMAs during laparoscopy (18), others have reported this occurrence (20). Acute LV loading and afterload changes have been shown to induce RWMAs (12,21), and the combination of both was probably the main cause for the RWMAs detected in our study. A reduction in filling as small as 14% compared with baseline can induce RWMAs (12). However, changes in myocardial perfusion (22) could also have contributed to this phenomenon. Several factors argued for the absence of myocardial ischemia: first, the absence of preexisting cardiac disease in this young patient population; second, the probable preservation of coronary perfusion pressure; third, the occurrence in segments adjacent to normally functioning myocardium; and finally, the immediate recovery after clamp release. Moreover, in the immediate postoperative period, the level of troponin was in the normal range, and the ECG tracing was unchanged. Of note, all RWMAs were mild and did not necessitate stopping the procedure or releasing the PTC.
The major limitation of our study is the small sample size, which provides only limited statistical power for the comparison between groups. Thus, this study was primarily designed to evaluate intragroup hemodynamic changes after PTC. A prospective randomized study of open versus laparoscopic liver resections would be ideal, but the number of potential candidates is still too limited to feasibly undertake such a study.
In conclusion, TEE in this study provided additional insight about the sequence, magnitude, and duration of the cardiovascular responses that occur during PTC performed under open or laparoscopic surgery. Although a decrease in preload was the main important change during PTC in open liver surgery, our results also demonstrated a decrease in LV function that is likely a consequence of decreased LV preload and increased LV afterload during laparoscopic liver resections. In a young patient population without cardiac disease, PTC during a laparoscopic procedure could be performed safely despite the hemodynamic modifications reported. However, consequences in patients with preexisting cardiac disease and altered LV function are unknown and need further investigation.
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  C-C. Balick-Weber, P. Nicolas, M. Hedreville-Montout, P. Blanchet, and F. Stephan Respiratory and haemodynamic effects of volume-controlled vs pressure-controlled ventilation during laparoscopy: a cross-over study with echocardiographic assessment Br. J. Anaesth., September 1, 2007; 99(3): 429 - 435. [Abstract] [Full Text] [PDF]
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