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Anesth Analg 2006;102:1304-1310 © 2006 International Anesthesia Research Society doi: 10.1213/01.ane.0000202473.17453.79
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Abstract |
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The effect of laparoscopy on cardiac function is controversial. We hypothesized that cardiac dysfunction related to increased afterload could be predominant in patients undergoing elective abdominal aortic repair. To test this hypothesis, we conducted a transesophageal echocardiographic study in 15 patients during laparoscopic aortic surgery. We systematically assessed left ventricular (LV) and right ventricular (RV) functions. Measurements were obtained in the supine position without pneumoperitoneum and with an intraabdominal pressure of 14 mm Hg. Then, patients were turned to the right lateral position without pneumoperitoneum and intraabdominal pressure was increased to 7 mm Hg and to 14 mm Hg. Pneumoperitoneum induced a 25% arterial blood pressure increase and a 38% increase in LV systolic wall stress. A 25% decrease in LV ejection fraction and an 18% decrease in LV stroke volume were observed, associated with an increase in LV end-systolic volume. LV diastolic function impairment was observed without change in LV end-diastolic volume. Respiratory alterations in superior vena cava diameter were never observed, suggesting that volume status remained optimal. Respiratory changes in RV stroke volume were increased according to intraabdominal pressure and body position, reflecting an increase in RV afterload. In conclusion, peritoneal CO2 insufflation in patients scheduled for laparoscopic aortic surgery could impair LV and RV systolic functions as a consequence of increased afterload.
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Introduction |
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A cardiac output decrease can be associated with intraperitoneal CO2 insufflation during laparoscopic surgery (1,2). Intraabdominal pressure increase has been reported to induce a mechanical impairment of venous return as the result of inferior vena cava compression (3). Also, a cardiac output decrease is usually attributed to a preload mechanism. According to this hypothesis, a head-up tilt position (4,5) or a hypovolemic status (6) could aggravate the hemodynamic effects of the pneumoperitoneum insufflation. Conversely, a head-down tilt position (7) or an intermittent compression of the lower limbs (8) could re-establish pre-insufflation stroke volume values. However, many of these previous studies were performed in healthy patients (3,9–15).
Mean arterial blood pressure is significantly increased with CO2 pneumoperitoneum (2,11,12), leading to left ventricular (LV) afterload increase (11). In this regard, a decrease in cardiac output observed during laparoscopic surgery may be related to cardiac dysfunction induced by an increased afterload. Moreover, this mechanism could be especially important in a population with frequent cardiovascular comorbidity.
Identifying mechanisms of cardiac output decrease during surgery is important because it definitely influences perioperative care management. For instance, administration of excessive intravascular volume to a patient with cardiac output decrease as a result of systolic dysfunction could be harmful. Conversely, administration of a vasodilator to a hypovolemic patient could be deleterious. Another issue is the frequent incidence of postoperative myocardial ischemia in patients scheduled for major aortic surgery (16). In this case, occurrence of systolic dysfunction related to peritoneal CO2 insufflation could indicate that caution should be exercised in the use of pneumoperitoneum for these patients. In other words, cardiac status should be precisely defined during the preoperative period and/or occurrence of cardiac dysfunction during pneumoperitoneum will necessitate more cardiac monitoring during the postoperative period.
A totally laparoscopic infra-renal aortic surgery was recently developed in our hospital (17) and the aim of our study was to establish the influence of intraperitoneal CO2 insufflation on cardiac preload and afterload during the procedure. For this, we used transesophageal echocardiography (TEE) to provide a complete and noninvasive analysis of cardiac function and blood volume status. We hypothesized that cardiac output decrease is related more to a cardiac workload increase than to a venous return impairment. Because the surgical procedure required that patients be placed in a lateral position, we also evaluated whether position could influence right ventricular (RV) function by decreasing respiratory system compliance.
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Methods |
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The study was approved by the Ethics Committee of the Société de Réanimation de Langue Française (Paris, France) and informed consent was obtained from the patients. A TEE study was prospectively conducted in 16 consecutive patients scheduled for totally laparoscopic infra-renal aortic surgery over a 6-mo period (November 2002–April 2003). One patient was excluded from the study because of the poor quality of TEE. Physical and medical characteristics of the remaining 15 patients are summarized in Table 1. During the preoperative period, a cardiologist assessed cardiac function at baseline by means of echocardiography. All patients underwent stress echocardiography with dobutamine plus coronary angiography in the case of a positive test.
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All usual cardiovascular drugs were taken with the anesthetic premedication, except for angiotensin-converting enzyme inhibitors and angiotensin receptor blockers. Before induction of anesthesia, 10 mL/kg Ringer's lactate solution was given. General anesthesia was induced with thiopental and maintained with isoflurane in air and oxygen mixture. Depth of anesthesia was adjusted to obtain a bispectral index between 40 and 60. Heart rate and systemic arterial blood pressure from an indwelling radial artery catheter and pulse oximetry were continuously recorded. The oxygen inspired fraction was continuously adjusted to obtain a Spo2 value more than 95%. After anesthesia induction, ventilatory variables were adjusted to keep end-tidal CO2 less than 34 mm Hg and were not modified throughout the study. Pneumoperitoneum pressure was adapted between 0 and 14 mm Hg with a variable-flow insufflator of CO2.
The surgical procedure has been previously described (18). Briefly, throughout the intraabdominal procedure, the patient was placed in right lateral and rotated decubitus position. After introduction of the endoscope and various trocars, a left retrocolic dissection was conducted and the small bowel and left mesocolon moved into the right part of the abdomen, thus exposing the infrarenal aorta.
TEE was performed with a Toshiba "CoreVision" model SSA-350A (Toshiba Corporation, Otawara-Shi, Japan) equipped with a multiplane 5-MHz transducer. The probe was inserted into the esophagus after patients were anesthetized and their lungs were mechanically ventilated. TEE images were recorded on videotape and reviewed for single-frame, stop-motion analysis by a blinded and trained observer unaware of the time of measurement. Under each set of experimental conditions, the TEE study was completed after 5 min of stabilization. Evaluations were first obtained in the supine position without pneumoperitoneum (Sp 0) and with a stable intraabdominal pressure of 14 mm Hg (Sp 14). Then, patients were turned in a strict right lateral decubitus position without pneumoperitoneum (Lp 0) and intraabdominal pressure was progressively increased to 7 mm Hg (Lp 7) and to 14 mm Hg (Lp 14).
A short-axis cross-sectional view of the LV at the mid-papillary muscle level was obtained by a transgastric approach. LV end-diastolic (ED) and end-systolic (ES) diameters (D) were measured from M-mode recording, permitting calculation of LV ED and ES volumes (V) using the formula of Teicholz: V = 7D3/(2.4 + D). LV stroke volume (LVSV) and LV ejection fraction (LVEF) were calculated using LVEDV and LVESV. Cardiac output was calculated by multiplying LVSV by heart rate. In the same view, LV wall thickness at end-systole (ThES) was also measured from M-mode recording. LV systolic wall stress (LVSWS) was calculated using the formula of Reichek et al. (19): LVSWS = 0.334 SAP (LVESD)/ThES (1 + ThES/LVESD), where SAP indicates systolic arterial blood pressure and LVESD is LV end-systolic diameter.
Using an esophageal approach, we also obtained a four-chamber view of the cardiac cavities. From this view, pulsed-Doppler at the mitral annulus was performed and peak velocities of E and A waves were measured and expressed as E/A ratio (20). Velocity-time integral (VTIM) of mitral flow was also measured to estimate LV SV (21) and to corroborate LV SV variations measured from M-mode recording.
Doppler pulmonary VTI (VTIP) was recorded at the level of the RV outflow tract, together with pulmonary artery diameter (Dp), permitting calculation of RV stroke volume, as RVSV = VTIP x 
DP 2/4 (22). As previously reported (23), maximal RVSV at end-expiration and minimal RVSV at end-inspiration were collected, permitting calculation of decrease in RVSV related to tidal insufflation (
RVSV = maximal RVSV – minimal RVSV/maximal RVSV).
The superior vena cava (SVC) was examined from a long-axis view, using the two-dimensional view to direct the M-mode beam across the maximal diameter. Thus, we measured SVC diameter at end-expiration and at end-inspiration (24).
On the basis of a 15% decrease in LV SV, we calculated that 15 patients could test the null hypothesis at 0.05 significance with a power of 0.90. Statistical calculations were performed using the Statgraphics plus package (Manugistics, Rockville, MD). Data are expressed as means ± sd. Doppler echocardiographic measurements and clinical parameter changes under the five sets of experimental conditions were compared with repeated-measures analysis of variance and a Fisher's exact test for post hoc comparison. P values < 0.05 were considered significant.
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Results |
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Overall results with P values are reported in Table 2. Measurements at Sp 14, Lp 0, Lp 7, and Lp 14 were respectively performed 5, 15, 25, and 35 min after Sp 0. Pneumoperitoneum induced a significant increase in SAP (from 111 ± 5 mm Hg at Sp 0 to 144 ± 8 mm Hg at Lp 14) and in mean arterial blood pressure (from 77 ± 4 mm Hg to 102 ± 7 mm Hg, respectively). Heart rate was also significantly increased, according to peritoneal insufflation, whereas cardiac output was not modified.
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Pneumoperitoneum induced a significant increase in LVSWS (Fig. 1), associated with a marked increase in LV ESV. Significant decreases in LV EF (Fig. 1) and LV SV (Fig. 2) were also found. LV EDV did not change significantly, whereas a significant reduction in E/A ratio at the mitral annulus was observed (Fig. 3). Individual values of LV EF recorded during the preoperative period, at baseline (Sp0), and during pneumoperitoneum are reported in Figure 4. Abnormalities in the motion of the LV infero-posterior wall were observed in 2 patients with a history of myocardial infarction. New wall motion abnormalities were never noted during the study. We observed a significant increase in RVSV induced by pneumoperitoneum and right lateral position together, and RVSV at Lp 14 was significantly higher than at Sp 14. SVC diameter during respiration remained constant, with no change observed between end-inspiration and end-expiration. On the other hand, a significant increase in SVC diameter was observed related to pneumoperitoneum and body position. The intra- and inter-observer variabilities of our main echocardiographic measurements are reported in Table 3.
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Discussion |
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In our study, peritoneal CO2 insufflation produced a decrease in LV SV that was related to an LV afterload increase. Impairment in venous return was never observed. The decrease in LV SV did not produce a significant change in cardiac output because it was associated with a significant increase in heart rate. Tachycardia compensatory to LV SV decrease has been previously reported (25) and also demonstrated during laparoscopy in patients with previously diagnosed cardiac or pulmonary disease (26). We also demonstrated that LV diastolic dysfunction could be partially induced by a significant increase in RV afterload.
We did not find an effect of pneumoperitoneum on venous conductance. Yet the significant increase in SVC diameter suggests a better venous conductance and a progressive increase in central venous pressure. Moreover, a significant change in SVC diameter related to tidal ventilation is effective in detecting hypovolemia (24) and in predicting cardiac output increase after blood volume expansion (27). The fact that SVC diameter was not influenced by tidal ventilation throughout the study suggests that intravascular volume status of all patients was adequate. Finally, LV preload, evaluated with LV EDV, was not modified during the study in our patients. However, LV preload decrease and caval vein zone 2 condition have been reported during peritoneal gas insufflation (3,4,9,10).
There are various explanations for the differences between our results and previous findings. In some studies, pneumoperitoneum was insufflated in a head-up tilt position (1,28), which induces a decrease in systemic venous return. In these cases, cardiac function was normalized after the patient's placement in a head-down tilt position (7). Impact of pneumoperitoneum on LV preload condition is highly dependent on preinsufflation blood volume status (6). In our study, all patients received 10 mL/kg before anesthesia induction and, thus, blood volume status was optimized before surgery.
Mean arterial blood pressure was increased by 25% with peritoneal CO2 insufflation. This was in accordance with values usually reported in healthy subjects (12). The association of arterial blood pressure and LV ESV increases strongly suggested an increased LV afterload produced by peritoneal CO2 insufflation. Indeed, we observed a significant increase in LV SWS, an index of LV afterload (29). In healthy patients, LV afterload increase did not affect LV systolic function (11–13) or produced only a transitory effect of no clinical relevance (14,15). By contrast, we observed impairment of LV systolic function, marked by a 25% decrease in LV EF. Thus, in the present study, LV systolic function was significantly affected by a significant increase in LV afterload as a result of peritoneal pressure increase with CO2 insufflation. Although all patients had a preoperative LV EF above 50%, 8 of them exhibited a decrease to less than 50% after peritoneal CO2 insufflation. Our specific population could partially explain discrepancies between previous studies in healthy patients and our results. Indeed, a majority of our patients had preexisting cardiovascular disease, i.e., chronic hypertension, and were probably extremely sensitive to LV afterload changes (1,30).
Changes observed in the LV filling pattern, exhibited by a modification of mitral flow, i.e., a decrease in E/A ratio, demonstrated LV relaxation impairment (20). A progressive increase in SVC diameter suggested that blood return might be augmented from the abdominal cavity toward the thoracic cavity by the increase in abdominal pressure. Despite this potential augmentation, we did not observe any increase in LV diastolic dimensions, suggesting a high ventricular elastance. Moreover, a normal LV is unable to dilate abruptly in response to acute systolic dysfunction (31). Thus, LV diastolic function appeared to be impaired by pneumoperitoneum and was explained by increase in LV afterload (4).
Another factor that potentially can affect LV relaxation is a sudden increase in RV outflow impedance (32). Cyclic changes in RV SV during mechanical ventilation, including a decrease during pulmonary inflation and a progressive return to preinflation value during pulmonary deflation, have been found to result from cyclic changes in RV afterload resulting from cyclic changes in transpulmonary pressure (23). These respiratory variations are accentuated in hypovolemic patients (24). In the present study, amplitude of these respiratory changes was enlarged by an increase in abdominal pressure and posture changes from supine to lateral position. Although small changes were observed at baseline, RV SV decreased by 40% at each tidal ventilation when pneumoperitoneum was inflated with the patient in the lateral position. Thus, peritoneal pressure increase and positional changes may affect inspiratory RV ejection by way of hypovolemia and/or by RV afterload increase. We noted above the absence of preload effect. End-inspiratory airway pressure was progressively increased during peritoneal insufflation and posture changes. The fact that this increase occurred despite an unchanged tidal volume suggested that the compliance of lung and chest wall was reduced. Of course, chest wall compliance is reduced when a positive abdominal pressure is exerted on the diaphragmatic part of the chest wall. Such a compliance decrease, related to pneumoperitoneum and lateral position, has previously been described (33,34). But this mechanical effect would not change transpulmonary pressure because a reduced chest wall compliance would preferentially increase pleural pressure (23). In a previous report, Joris et al. (35) found a 9 mm Hg increase in intrathoracic pressure during a pneumoperitoneum of 14 mm Hg. However, reducing the apico-basal dimension of the lung by displacing the diaphragm toward the apex would also reduce functional residual capacity and decrease lung compliance (36). In the same manner, lateral position would also reduce functional residual capacity by modifying gas distribution (37) and thus would decrease lung compliance. Both resulted in an increased transpulmonary pressure for delivering the same tidal volume, responsible for an increase in RV afterload.
For ethical reasons, and as in many other studies exploring the effect of peritoneal CO2 insufflation, measurements were done according to the surgical timing. A limitation on the interpretation of our results is that the different sets of measurements were not randomized. Also, we could not exclude that our findings are not simply the result of hemodynamic changes during surgery. However, arterial blood pressure and cardiac variables were modified in a similar fashion during pneumoperitoneum and data recorded during periods without pneumoperitoneum (Sp0 and Lp0) were also comparable. All these observations indicate that peritoneal CO2 insufflation is probably the main factor in creating hemodynamic disturbances during laparoscopic surgery.
Our results demonstrate that laparoscopic surgery in patients undergoing abdominal aortic repair induces a significant increase in workload of the LV and RV. The first clinical implication is that fluid infusion is not a good option when a decrease in stroke volume is observed during this kind of surgery and that strict control of systemic blood pressure probably plays a key role. Also, these results suggest that cardiac events, such as perioperative myocardial ischemia, could be facilitated in patients who often present various cardiac comorbidities. Our observational study in a small number of patients was only designed to verify a hypothesis concerning hemodynamic variations induced by peritoneal CO2 insufflation. We cannot draw firm conclusions about the possible occurrence of postoperative cardiac events in relation to laparoscopic surgery. A larger study is required to answer this question.
In conclusion, laparoscopic surgery in patients undergoing abdominal aortic repair may produce a marked impairment in LV systolic function by way of increased LV afterload. Cardiac preload effect was never observed. This major hemodynamic dysfunction is also associated with enhancement of RV afterloading by mechanical ventilation.
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Footnotes |
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Accepted for publication December 12, 2005.
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References |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
- Safran D, Sgambati S, Orlando R 3rd. Laparoscopy in high-risk cardiac patients. Surg Gynecol Obstet 1993;176:548–54.[Web of Science][Medline]
- Joris JL, Noirot DP, Legrand MJ, et al. Hemodynamic changes during laparoscopic cholecystectomy. Anesth Analg 1993;76:1067–71.
[Abstract/Free Full Text] - Giebler RM, Behrends M, Steffens T, et al. Intraperitoneal and retroperitoneal carbon dioxide insufflation evoke different effects on caval vein pressure gradients in humans: evidence for the starling resistor concept of abdominal venous return. Anesthesiology 2000;92:1568–80.[Web of Science][Medline]
- Dorsay DA, Greene FL, Baysinger CL. Hemodynamic changes during laparoscopic cholecystectomy monitored with transesophageal echocardiography. Surg Endosc 1995;9:128–33.[Web of Science][Medline]
- Rist M, Hemmerling TM, Rauh R, et al. Influence of pneumoperitoneum and patient positioning on preload and splanchnic blood volume in laparoscopic surgery of the lower abdomen. J Clin Anesth 2001;13:244–9.[Medline]
- Diamant M, Benumof JL, Saidman LJ. Hemodynamics of increased intra-abdominal pressure: Interaction with hypovolemia and halothane anesthesia. Anesthesiology 1978;48:23–7.[Web of Science][Medline]
- Harris SN, Ballantyne GH, Luther MA, Perrino AC Jr. Alterations of cardiovascular performance during laparoscopic colectomy: a combined hemodynamic and echocardiographic analysis. Anesth Analg 1996;83:482–7.[Abstract]
- Alishahi S, Francis N, Crofts S, et al. Central and peripheral adverse hemodynamic changes during laparoscopic surgery and their reversal with a novel intermittent sequential pneumatic compression device. Ann Surg 2001;233:176–82.[Web of Science][Medline]
- Derouin M, Couture P, Boudreault D, et al. Detection of gas embolism by transesophageal echocardiography during laparoscopic cholecystectomy. Anesth Analg 1996;82:119–24.[Abstract]
- Decailliot F, Streich B, Heurtematte Y, et al. Hemodynamic effects of portal triad clamping with and without pneumoperitoneum: an echocardiographic study. Anesth Analg 2005;100:617–22.
[Abstract/Free Full Text] - Cunningham AJ, Turner J, Rosenbaum S, Rafferty T. Transoesophageal echocardiographic assessment of haemodynamic function during laparoscopic cholecystectomy. Br J Anaesth 1993;70:621–5
[Abstract/Free Full Text] - Myre K, Buanes T, Smith G, Stokland O. Simultaneous hemodynamic and echocardiographic changes during abdominal gas insufflation. Surg Laparosc Endosc 1997;7:415–9.[Web of Science][Medline]
- Odeberg S, Ljungqvist O, Svenberg T, et al. Haemodynamic effects of pneumoperitoneum and the influence of posture during anaesthesia for laparoscopic surgery. Acta Anaesthesiol Scand 1994;38:276–83.[Web of Science][Medline]
- Branche PE, Duperret SL, Sagnard PE, et al. Left ventricular loading modifications induced by pneumoperitoneum: a time course echocardiographic study. Anesth Analg 1998;86:482–7.[Abstract]
- Larsen JF, Svendsen FM, Pedersen V. Randomized clinical trial of the effect of pneumoperitoneum on cardiac function and haemodynamics during laparoscopic cholecystectomy. Br J Surg 2004;91:848–54.[Medline]
- McFalls EO, Ward HB, Santilli S, et al. The influence of perioperative myocardial Infarction on long-term prognosis following elective vascular surgery. Chest 1998;113:681–86.
[Abstract/Free Full Text] - Coggia M, Javerliat I, Di Centa I, et al. Total laparoscopic bypass for aortoiliac occlusive lesions: 93-case experience. J Vasc Surg 2004;40:899–906.[Web of Science][Medline]
- Coggia M, Bourriez A, Javerliat I, Goeau-Brissonniere O. Totally laparoscopic aortobifemoral bypass: a new and simplified approach. Eur J Vasc Endovasc Surg 2002;24:274–5.[Medline]
- Reichek N, Wilson J, St John Sutton M, et al. Noninvasive determination of left ventricular end-systolic stress: validation of the method and initial application. Circulation 1982;65:99–108.
[Free Full Text] - Cohen GI, Pietrolungo JF, Thomas JD, Klein AL. A practical guide to assessment of ventricular diastolic function using Doppler echocardiography. J Am Coll Cardiol 1996;27:1753–60.[Abstract]
- Lewis JF, Kuo LC, Nelson JG, et al. Pulsed Doppler echocardiographic determination of stroke volume and cardiac output: clinical validation of two new methods using the apical window. Circulation 1984;70:425–31.
[Abstract/Free Full Text] - Maslow A, Comunale ME, Haering JM, Watkins J. Pulsed wave Doppler measurement of cardiac output from the right ventricular outflow tract. Anesth Analg 1996;83:466–71.[Abstract]
- Vieillard-Baron A, Loubieres Y, Schmitt JM, et al. Cyclic changes in right ventricular output impedance during mechanical ventilation. J Appl Physiol 1999;87:1644–50.
[Abstract/Free Full Text] - Vieillard-Baron A, Augarde R, Prin S, et al. Influence of superior vena caval zone condition on cyclic changes in right ventricular outflow during respiratory support. Anesthesiology 2001;95:1083–8.[Web of Science][Medline]
- Ho HS, Gunther RA, Wolfe BM. Intraperitoneal carbon dioxide insufflation and cardiopulmonary functions: laparoscopic cholecystectomy in pigs. Arch Surg 1992;127:928–32.
[Abstract/Free Full Text] - Wittgen CM, Andrus CH, Fitzgerald SD, et al. Analysis of the hemodynamic and ventilatory effects of laparoscopic cholecystectomy. Arch Surg 1991;126:997–1000.
[Abstract/Free Full Text] - Vieillard-Baron A, Chergui K, Rabiller A, et al. Superior vena caval collapsibility as a gauge of volume status in ventilated septic patients. Intensive Care Med 2004;30:1734–9.[Web of Science][Medline]
- Hein HA, Joshi GP, Ramsay MA, et al. Hemodynamic changes during laparoscopic cholecystectomy in patients with severe cardiac disease. J Clin Anesth 1997;9:261–5.[Web of Science][Medline]
- Noble MI. Left ventricular load, arterial impedance and their interrelationship. Cardiovasc Res 1979;13:183–98.[Web of Science][Medline]
- Irwin MG, Ng JK. Transoesophageal acoustic quantification for evaluation of cardiac function during laparoscopic surgery. Anaesthesia 2001;56:623–9.[Medline]
- Colucci WS. Pathophysiology of heart failure. In: Braunwald E, Zipes P, Libby P, eds. Heart disease: a textbook of cardiovascular medicine. Philadelphia: WB Saunders Company, 2001:503–23.
- Jardin F, Dubourg O, Bourdarias JP. Echocardiographic pattern of acute cor pulmonale. Chest 1997;111:209–17.
[Free Full Text] - Sharma KC, Brandstetter RD, Brensilver JM, Jung LD. Cardiopulmonary physiology and pathophysiology as a consequence of laparoscopic surgery. Chest 1996;110:810–5.
[Free Full Text] - Tanskanen P, Kytta J, Randell T. The effect of patient positioning on dynamic lung compliance. Acta Anaesthesiol Scand 1997;41:602–6.[Medline]
- 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.
[Abstract/Free Full Text] - Tokics L, Hedenstierna G, Brismar B, et al. Thoracoabdominal restriction in supine men: CT and lung function measurements. J Appl Physiol 1988;64:599–604.
[Abstract/Free Full Text] - Nunn JF. Elastic resistance to ventilation applied respiratory physiology, 2nd ed. London: Butterworths and Co., 1977:63–93.
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