The laparoscopic approach has become widely accepted for many gynecological and general surgical procedures, with well documented benefits for the patient [1-4]. The cardiovascular effects of intraperitoneal insufflation of carbon dioxide (CO2) during laparoscopic cholecystectomy and gynecological procedures have been extensively investigated and found to be relatively mild in patients of good physical status [5-7].
More recently, laparoscopic approaches have been introduced for renal and adrenal surgery [8,9]. These procedures may influence cardiopulmonary function differently from other laparoscopic procedures, because laparoscopic urological surgery takes longer, requires patients to be placed in the lateral position, and involves CO2 insufflation both retroperitoneally and intraperitoneally. Although the effects of head-down and head-up positions on cardiopulmonary functions during intraperitoneal CO2 insufflation have been described [1,5-7], the effects of intra- and retroperitoneal insufflation in the lateral position have not been reported. Therefore, we studied the effects of CO2 insufflation during transperitoneal laparoscopic urological surgery in the lateral position. We also investigated whether there were differences in these effects between the right and left lateral positions.
We studied 15 patients, ASA physical status I or II, who underwent laparoscopic urological procedures. Surgery consisted of nine nephrectomies (three for renal tumors, four for hydronephroses, and two for atrophic kidneys) and six adrenalectomies (three for aldosteronisms and three for nonfunctional tumors). Our institutional research ethics committee approved the study, and informed consent was obtained from each patient.
Famotidine 20 mg and diazepam 5 or 10 mg were given orally 2 h before the induction of anesthesia. In the operating room, noninvasive blood pressure monitoring (NIBP), electrocardiograph (ECG), and a pulse oximeter were attached. An IV cannula was inserted into a forearm vein, and lactated Ringer's solution was given IV throughout surgery. Anesthesia was induced with thiamylal 3-4 mg/kg, and muscle relaxation was obtained with pancuronium. The trachea was intubated, and the lungs were mechanically ventilated with a tidal volume of 10-12 mL/kg and a respiratory rate of 10-12 breaths/min. An inline capnograph was connected between the tracheal tube and breathing circuit, and end-tidal carbon dioxide concentration was monitored. Peak inspiratory airway pressure (PIP) was measured by using an airway pressure gauge incorporated in the anesthetic machine. After the induction of anesthesia, a pulmonary artery catheter, radial artery cannula to the dependent arm, nasogastric tube, and urinary catheter were inserted. Anesthesia was maintained with droperidol 0.1-0.15 mg/kg; buprenorphine 2-3 [micro sign]g/kg, and isoflurane in a mixture of oxygen and air (fraction of inspired oxygen [FIO2] 0.5). Isoflurane was titrated to end-tidal concentrations <or=to2% to keep systolic blood pressure within 20% of baseline values.
After the induction of anesthesia, the patient was positioned in either the right or left lateral position, depending on the site of surgery. The patient was placed in a 70-80[degree sign] semilateral position. A pneumoperitoneum was produced using a Veress needle through the subumbilical region. The retroperitoneal space was opened through an incision in the hepatocolic ligament (right lateral group) or in the retroperitoneum along the line of Toldt, lateroconal fascia (left lateral group). The intraabdominal pressure (IAP) was initially set at 15 mm Hg using a CO (2) insufflator until another four trocars were inserted; then it was maintained automatically at 10 mm Hg for the duration of surgery.
The pressure transducers for arterial, central venous and pulmonary arterial pressures were adjusted to the level of the left atrium after lateral positioning of the patients as defined by Kennedy et al. , i.e., at the level of the fourth intercostal space anteriorly in the sternal midline. Heart rate (HR), mean arterial pressure (MAP), mean pulmonary artery pressure (MPAP), pulmonary capillary wedge pressure (PCWP), and central venous pressure (CVP) were recorded. Cardiac output was measured by thermodilution (Explorer; Baxter, Irvine, CA) in triplicate at the end-expiratory phase. Cardiac index (CI), systemic vascular resistance (SVR), pulmonary vascular resistance (PVR), and the right and left ventricular stroke work index (RVSWI and LVSWI) were calculated. Arterial and mixed venous blood gases were analyzed using a blood gas analyzer (ABL 500; Radiometer, Copenhagen, Denmark).
Alveolar oxygen tension (PAO2) was estimated as follows: Equation 1 where PB = barometric pressure and PH2 O = vapor pressure of water. Respiratory index (PaO2/PAO2) was calculated using the formula above.
Intrapulmonary shunt (Qs/Qt) was calculated from the following equation. Equation 2 where Hb = hemoglobin concentration, CaO2 = total oxygen content in arterial blood, and CvO2 = total oxygen content in mixed venous blood. These measurements were made before insufflation; 5, 30, 60, and 120 min after the beginning of insufflation; and 10 min after deflation.
Data are presented as means +/- SD. Differences in the hemodynamic and respiratory data within each group were determined by using analysis of variance for repeated measures with Fisher's protected least significant difference for post hoc comparison. Student's t-test for independent samples was applied for the assessment of significant group differences (right lateral group versus left lateral group). A P value <0.05 was considered statistically significant.
Eight patients were placed in the right and seven in the left lateral position. There was no significant difference between the right and left lateral groups in the age, body weight, height, urine volume, and the duration of pneumoperitoneum and anesthesia (Table 1). No patient was receiving drugs that might have influenced the hemodynamic results. In all patients, percutaneous oxygen saturation was always >98%, and there were no arrhythmias at any time. Results in cardiovascular variables are shown in Table 2.
Before insufflation, MAP, CVP, MPAP, and PCWP were significantly higher in patients in the right lateral position than those in the left lateral position. Five minutes after CO2 insufflation (15 mm Hg of IAP), MAP significantly increased in both study groups. In addition, significant increases in CI, CVP, MPAP, PCWP, RVSWI, and LVSWI were observed in the right lateral group, but not in patients in the left lateral position.
During CO2 insufflation (10 mm Hg of IAP) in the right lateral group, CI, CVP, MPAP, and PCWP remained significantly increased at all time points compared with control values; in addition, HR, RVSWI, and LVSWI became significantly increased at some but not all the time points. By contrast, SVR significantly decreased and MAP remained unchanged in this group. In the left lateral group, MAP, MPAP, CVP, and PCWP significantly increased at one or more time points during this period compared with control values, but other hemodynamic variables did not change. At several time points, CVP, MPAP, PCWP, and RVSWI in the right lateral group were significantly higher than those observed in the left lateral group.
After deflation in both groups, CI, MAP, MPAP, RVSWI, and LVSWI were all significantly increased compared with control. In the right lateral group, only HR remained significantly increased while CVP and PCWP were unchanged, whereas HR, CVP, and SVR remained unchanged in the left lateral group compared with control.
HR in the left lateral position and PVR in both groups did not show any significant changes at any time point. Results in respiratory variables are shown in Table 3. Before insufflation, respiratory alkalosis was observed in both groups.
Five minutes after CO2 insufflation (15 mm Hg of LAP), PaCO2 significantly increased in both right and left lateral positions. pH decreased in the right lateral group. PCO2 in mixed venous blood (PvCO2) significantly increased in patients in the left lateral position. PIP increased in both positions. During CO2 insufflation (10 mm Hg of IAP) PaCO2 and PvCO2 increased, and pH decreased in both groups. PIP increased during this period in both groups.
After deflation in both groups, pH remained lower than the baseline values. Although PaCO2 and PvCO2 decreased to control levels in the right lateral group, values in the left lateral group remained significantly increased.
There were no significant changes in Qs/Qt and PaO2/PAO2 at any point in the study.
In this study, there was a difference in hemodynamic effects between the right and left lateral positions in patients undergoing laparoscopic urological surgery. Baseline MAP and indices of preload were higher in the right compared with left lateral position. CI, indices of preload, and RVSWI increased and SVR decreased during pneumoperitoneum in the right lateral group, whereas pneumoperitoneum induced similar but lesser changes in these hemodynamic variables in the left lateral group.
When the position of the transducer is remote from that of the pressure measuring site, the pressure obtained may be inaccurate. We leveled the transducer at the junction of the fourth intercostal space and the sternal midline, which is the left atrial level in the lateral position as described by Kennedy et al. . Because we measured MAP using the radial artery on the dependent side in all cases, differences in the effect of hydrostatic pressure between right and left lateral positions did not influence MAP in the present study. The hydrostatic pressure could affect MPAP and PCWP when the tip of pulmonary artery catheter was positioned in a different side of the pulmonary artery. This possibility was not excluded in the present study because we did not examine the position of a pulmonary artery catheter with a radiograph in each patient. However, we consider that the effects of pneumoperitoneum on intravascular pressures were accurately represented because the position of the transducer was constant during the study.
Although it is not clear why there were differences in preload indices between the right and left lateral positions before CO2 insufflation, a few possibilities can be considered. First, the heart, being located in the left hemithorax, shifts to the dependent side to a differing extent with gravity when the patient is placed in the lateral position. We should consider the effects of hydrostatic pressure mentioned above and shifts of the axis of the heart and the interventricular septum. Second, because of the right-sided anatomical position of the right atrium, the venous return via the inferior and superior vena cavae to the right atrium may be more favorable in the right lateral position.
We did not measure hemodynamic variables in the supine position and could not study the effects of postural changes in the same individuals. There are a few studies describing the hemodynamic effects of postural changes from the supine to the lateral positions. Eggers et al.  reported a lower MAP and SVR without change in CI in the right lateral position, and a higher SVR in the left lateral position than in the supine position. Nakao et al.  reported that a change from supine to either lateral position significantly increased intracardiac pressures and cardiac output, and that an increase in hydrostatic pressure might be responsible for the increase in intracardiac pressure because radiographic studies showed that a difference in height of the right ventricle relative to the inferior vena cava was greater in both lateral positions than when supine. They also found that systolic and end-diastolic right ventricular pressures were higher in the right lateral position than in the left lateral position in dogs and pigs.
The introduction of pneumoperitoneum increased CI and preload and decreased SVR in the present study, which is at variance with previous reports [5-7]. Although cardiac output responses during the introduction of pneumoperitoneum are conflicting in different studies, increases in SVR and MAP are reported in most [5-7]. There are several possible factors in the present study to explain why our results differ from the previous investigations [5-7]. First, the laparoscopic procedures previously reported were performed in supine, Trendelenburg, or reverse Trendelenburg positions, whereas our patients were placed in the lateral position. Second, the IAP was set at 10 mm Hg in the present study, whereas the IAP was set at a much higher pressure in the previous investigations [5,13]. Third, although previous investigations were performed under general anesthesia with nitrous oxide [2,13,14], we did not use this drug. Fourth, in this study, the retroperitoneal tissue was also exposed to CO2. Fifth, the ventilation was not adjusted to produce normocarbia, and PaCO2 increased as a result of CO2 insufflation in the present study.
Increased IAP during CO2 insufflation has biphasic effects on hemodynamics [13,15]. When IAP increases to approximately 40 cm H2 O (29.4 mm Hg), the inferior vena cava is compressed and impedes venous return from abdominal organs and legs; thus, the central venous reservoir decreases. When the IAP is relatively low (<or=to20 cm H2 O, 14.7 mm Hg), blood moves more readily from both the abdominal organs and inferior vena cava to the right atrium. Furthermore, the effects of an increase in IAP on venous return may be dependent on the baseline CVP. Kashtan et al.  showed that a high IAP (40 mm Hg) augmented venous return when the CVP was high but reduced it when the CVP was normal or low. We believe that the higher baseline preload values seen in the right lateral position and the lower IAP used in our study resulted in the increased venous return and cardiac output figures observed. The number of subjects we studied was small, but there were statistically significant differences in preload values between different sides of lateral position.
Anesthetics affect hemodynamic changes. We used isoflurane and droperidol, both of which have vasodilating actions and inhibit activity of the sympathetic nervous system [17,18]. The use of nitrous oxide, which has some sympathetic effects, may enhance sympathoadrenal stimulation associated with hypercarbia . The use of anesthetics having vasodilating actions and the absence of nitrous oxide may explain why SVR did not increase during pneumoperitoneum in our study.
Exposure of extraperitoneal tissue to CO2 would increase CO2 absorption . Because the minute ventilation was maintained constant, PaCO (2) increased further with CO2 insufflation. An increase in PaCO2 dilates vessels directly and stimulates the sympathetic nervous system [21,22], but this effect was also equal in both groups.
Intrathoracic pressure  and PIP might affect venous return and increase during the pneumoperitoneum. Because there was no significant difference in PIP between the right and left lateral positions, it can therefore be eliminated as a cause of the differences in preload and CI between the sides.
Although the reports of the effects of intraperitoneal insufflation on PaO2 during laparoscopic cholecystectomy are inconsistent, healthy patients usually maintain a stable PaO2[1,6,7]. PaO2 can also be influenced by changes in pulmonary and cardiovascular function, and increased cardiac output and MPAP increase intrapulmonary shunt [23,24]. Because PVR did not change despite increases in cardiac output and MPAP in our study, the calculated intrapulmonary shunt did not increase, resulting in unchanged pulmonary oxygenation. PaO2 can be influenced by the patient's posture, IAP, and PaCO2 during laparoscopic procedures [1,5-7]. The lateral position itself might displace the diaphragm cephalad, reducing the functional residual capacity of the lungs and inducing a mismatch between ventilation and perfusion . Pneumoperitoneum is likely to further displace the diaphragm cephalad and reduce functional residual capacity [1,5-7].
In our study, PvCO2 remained high in the left lateral position after deflation. Mullet et al.  studied pulmonary CO2 elimination during intra- and extraperitoneal CO2 insufflation and found that CO2 diffusion into the body was greater during extraperitoneal insufflation compared with intraperitoneal insufflation. The time required to reach a plateau of pulmonary CO2 elimination during insufflation and to return to the preinsufflation values of end-tidal CO2 after CO2 insufflation were longer during extraperitoneal than intraperitoneal CO2 insufflation. We consider that high values of PaCO2 and PvCO2 after deflation in the left lateral position were probably related to the retroperitoneal insufflation. Although we cannot explain why these were observed only in the left lateral group, we suppose that the differences in hemodynamics observed between the right and left lateral positions may form part of the explanation. Further investigation is required to elucidate the mechanism.
In conclusion, insufflation of CO2 in the right lateral position increased both cardiac output and venous return and decreased SVR under general anesthesia without nitrous oxide. The extent of these changes was less in the left lateral position. Intraperitoneal insufflation of CO2 with retroperitoneal exposure in the lateral position did not affect the pulmonary oxygenation in healthy patients.
We thank Dr. Peter Jackson, Consultant Anaesthetist and Honorary Senior Clinical Lecturer, University of Birmingham, for his valuable help in translation, advice, and critical reading of our manuscript.
1. Aissa I, Hollande J, Clergue F. Pulmonary function during and following laparoscopy. Curr Opin Anesthesiol 1994;7:548-53.
2. Joris J, Cigarini I, Legrand M, et al. Metabolic and respiratory changes after cholecystectomy performed via laparotomy or laparoscopy. Br J Anaesth 1992;69:341-5.
3. Neugebauer E, Troidl H, Spangenberger W, et al. Conventional versus laparoscopic cholecystectomy and the randomized controlled trial. Br J Surg 1991;78:150-4.
4. Grace PA, Quereshi A, Coleman J, et al. Reduced postoperative hospitalization after laparoscopic cholecystectomy. Br J Surg 1991;78:160-2.
5. Cunningham AJ, Brull SJ. Laparoscopic cholecystectomy: anesthetic implications. Anesth Analg 1993;76:1120-33.
6. Wahba RWM, Beique F, Kleiman SJ. Cardiopulmonary function and laparoscopic cholecystectomy. Can J Anaesth 1995;42:51-63.
7. Odeberg-Wernerman S, Sollevi A. Cardiopulmonary aspects of laparoscopic surgery. Curr Opin Anaesthesiol 1996;9:529-35.
8. Clayman RV, Kavoussi LR, Soper NJ, et al. Laparoscopic nephrectomy: initial case report. J Urol 1991;146:278-82.
9. Matsuda T, Terachi T, Yoshida O. Laparoscopic adrenalectomy: the surgical technique and initial results of 13 cases. Miner Invas Ther 1993;2:123-7.
10. Kennedy GT, Bryant A, Crawford MH. The effects of lateral body positioning on measurements of pulmonary artery and pulmonary artery wedge pressures. Heart Lung 1984;13:155-8.
11. Eggers GWN Jr, deGroot WJ, Tanner CR, Leonard JJ. Hemodynamic changes associated with various surgical positions. JAMA 1963;185:81-5.
12. Nakao S, Come PC, Miller MJ, et al. Effects of supine and lateral positions on cardiac output and intracardiac pressures: an experimental study. Circulation 1986;73:579-85.
13. Kelman GR, Swapp GH, Smith I, et al. Cardiac output and arterial blood-gas tension during laparoscopy. Br J Anaesth 1972;44:1155-62.
14. Joris JL, Noirot DP, Legrand MJ, et al. Hemodynamic changes during laparoscopic cholecystectomy. Anesth Analg 1993;76:1067-71.
15. Wolf JS, Jr, Stoller ML. The physiology of laparoscopy: basic principles, complications and other considerations. J Urol 1994; 152:294-302.
16. Kashtan J, Green JF, Parsons Equation HolcroftJW. Hemodynamic effects of increased abdominal pressure. J Surg Res 1981;30:249-55.
17. Hickey RF, Eger EI II. Circulatory effects of inhaled anaesthetics. In: Prys-Roberts C, ed. The circulation in anaesthesia. Oxford: Blackwell, 1980:441-57.
18. Roberts JG. Intravenous anesthetic agents. In: Prys-Roberts C, ed. The circulation in anaesthesia. Oxford: Blackwell, 1980: 459-89.
19. Hornbein TF, Martin WE, Bonica JJ, et al. Nitrous oxide effects on the circulatory and ventilatory responses to halothane. Anesthesiology 1969;31:250-60.
20. Mullet CE, Viale JP, Sagnard PE, et al. Pulmonary CO2
elimination during surgical procedures using intra- or extraperitoneal CO2
insufflation. Anesth Analg 1993;76:622-6.
21. Price HL. Effects of carbon dioxide on the cardiovascular system. Anesthesiology 1960;21:652-63.
22. Viles PH, Shepherd JT. Evidence for dilator action of carbon dioxide on the pulmonary vessels of the cat. Circ Res 1968;22:325-32.
23. Cheney FW, Colley PS. The effect of cardiac output on arterial blood oxygenation. Anesthesiology 1980;52:496-503.
24. Yamamura H, Kaito K, Ikeda K, et al. The relationship between physiologic shunt and cardiac output in dogs under general anesthesia. Anesthesiology 1969;30:406-13.
25. Rehder K, Hatch DJ, Sessler AD, Fowler WS. The function of each lung of anesthetized and paralyzed man during mechanical ventilation. Anesthesiology 1972;37:16-26.