BJA Advance Access originally published online on July 10, 2007
British Journal of Anaesthesia 2007 99(3):429-435; doi:10.1093/bja/aem166
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Respiratory and haemodynamic effects of volume-controlled vs pressure-controlled ventilation during laparoscopy: a cross-over study with echocardiographic assessment
1 Service of Anaesthesiology
2 Service of Cardiology
3 Service of Urology, Pointe-à-Pitre Hospital, BP 465, 97159 Pointe-à-Pitre Cedex, France
* Corresponding author. Service of Anaesthesiology, Pointe-à-Pitre Hospital, BP 465, 97159 Pointe-à-Pitre Cedex, France. E-mail: francois.stephan{at}chu-guadeloupe.fr
Accepted for publication April 4, 2007.
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Abstract |
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Background: The effects of pressure-controlled (PC) ventilation on the ventilatory and haemodynamic parameters during laparoscopy procedures had not been carefully assessed. This prospective cross-over study was undertaken to compare how volume-controlled (VC) and PC modes could affect pulmonary mechanics, gas exchange, and cardiac function in patients undergoing laparoscopy.
Methods: Twenty-one patients undergoing laparoscopic urological procedures had their lungs ventilated at the beginning with VC ventilation. PC ventilation was instituted at the end of the VC sequence. Ventilator settings were adjusted to keep tidal volume, respiratory rate, and FIO2 constant in every mode. A complete set of ventilatory, haemodynamic, and gas exchange parameters was obtained under VC after 40 min of pneumoperitoneum and 20 min after switching for PC. Transoesophageal echocardiography was performed in order to evaluate systolic and diastolic function of the heart.
Results: When VC was switched to PC, peak airway pressure decreased [mean (SD) 32 (6) vs 27 (6) cm H2O; P < 0.0001], peak inspiratory flow increased [17 (3) vs 48 (8) litre min–1; P < 0.0001), and dynamic compliance improved [+15 (8)%]. No difference was noted for static airway pressure, static compliance, and arterial oxygenation. No significant change could be demonstrated in the systolic [left ventricular end-systolic wall stress 66 (16) vs 63 (14)·103 dyn cm–2 m–2] or diastolic function [early diastolic velocity 10.3 (2.5) vs 10.5 (2.7) cm s–1].
Conclusions: In this study, no short-term beneficial effect of PC ventilation could be demonstrated over conventional VC ventilation in patients with pneumoperitoneum.
Keywords: airway, pressure; echocardiography; lung, gas exchange, respiratory; surgery, laparoscopy; ventilation, mechanical
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Introduction |
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Laparoscopic surgery has increasingly been used during the last decade in many surgical procedures.1–3 Cardiopulmonary physiology and pathophysiology of pneumoperitoneum is now well understood.4 Besides cardiovascular effects, one of the most obvious ventilatory consequences is the increased peak airway pressure (Ppeak). In order to limit this increase in Ppeak, the anaesthetist could change the respiratory rate (RR), tidal volume, or change from volume-controlled (VC) to pressure-controlled (PC) ventilation; PC ventilation is now frequently used in the operating room in the management of patients with elevated Ppeak, despite an incomplete understanding of its ventilatory and haemodynamic effects, or its potential complications.1 5
The PC ventilation is a time-cycled mode in which square waves of pressure are applied and released by means of a decelerating flow.6 The decelerating flow often results in a higher mean inflation pressure when compared with constant flow.7 8 Therefore, with the concomitant presence of pneumoperitoneum, a complex cardiopulmonary response can occur.9 In acute lung injury, PC vs VC ventilation has been well studied.10–13 Although a decrease in Ppeak has been reported by all the studies, no difference has been found for plateau pressure (Pplat), or for respiratory system compliance, when the tidal volumes are kept constant.10–12 Likewise, there was only minimal differences in gas exchange and haemodynamics studied by right heart catheterization.10–12
As far as we know, the effects of PC ventilation on the ventilatory and haemodynamic parameters during laparoscopy procedures have not been assessed carefully by controlled studies. The aim of this study was, therefore, to compare how VC and PC modes could affect pulmonary mechanics, gas exchange, and cardiac function in patients undergoing laparoscopy. We used transoesophageal echocardiography (TOE) for non-invasive evaluation of systolic and diastolic function.
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Methods |
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This study was approved by our hospital ethics committee (Comité de Protection des Personnes se Prêtant à la Recherche Biomédicale, CHU de Pointe-à-Pitre, Pointe-à-Pitre, France; reference no. 06-04), and informed consent was obtained from the patients. All data used in subsequent analyses were anonymized.
During a 3-month period, 23 consecutive patients undergoing radical prostatectomy or lymphadenectomy by laparoscopy were prospectively enrolled in the study. Patients with left atrial dilation (>4.0 cm), left ventricular (LV) dilation [LV end-diastolic (ED) internal dimensions > 5.7 cm], decreased shortening fraction (<31%), regional wall motion abnormalities, valvular heart disease, dilated cardiomyopathy, and pericardial disease were excluded from the study. Patients who were ASA III or IV, or had oesophageal disease or dysphagia, were also excluded. Patients with intraoperative bleeding defined as the need for rapid volume expansion or blood transfusion before completion of the protocol and with haemodynamic instability defined as mean arterial pressure variation > 10% before completion of the protocol were excluded.
Anaesthesic management and intraoperative care were standardized. Premedication, hydroxyzine, was given orally 2 h before induction of anaesthesia, and all cardiovascular drugs, except angiotensin receptor blockers, were taken with the premedication. Propofol was infused using a target-controlled infusions system (Diprifusor-TCI©, ZenecaTM). Target plasma concentration for induction and maintenance of anaesthesia was 4–6 µg ml–1. Analgesia was provided by sufentanil 0.3 µg kg–1 i.v. bolus followed by a continuous infusion of 0.3 µg kg–1 h–1. Orotracheal intubation was facilitated by cisatracurium besylate 0.15 mg kg–1, and the muscle relaxation was maintained with continuous infusion of 0.15 mg kg–1 h–1. All patients received 500 ml of colloids before induction of pneumoperitoneum; crystalloids were then infused during operation at a basal rate of 10 ml kg–1 h–1. Inspired oxygen fraction (FIO2) was set at 60% in air and minute ventilation adjusted to maintain end-tidal CO2 (PE'CO2) between 3.7 and 4.2 kPa. Carbon dioxide pneumoperitoneum was induced with 14 mm Hg intra-abdominal pressure in the supine position after a 20° Trendelenburg position. This position was maintained throughout the surgical procedure.
The patients were first studied during VC with a constant square waveform and an inspiratory/expiratory (I:E) ratio of 1:2 without inspiratory plateau. Respiratory and echocardiographic data were collected 10 min after induction of anaesthesia (VCbaseline, T1), 15 min after pneumoperitoneum (VCpno, T2), and 40 min after pneumoperitoneum which was the period retained for comparison with PC (VCprotocol, T3). PC ventilation with a decelerating flow waveform and an I:E ratio 1:2 was started at the end of the VC sequences (PCprotocol, T4). Peak pressure was set to match expired Vt measured during VCprotocol. Because PC allows some variability in Vt with changes in impedance, a value of ±5% was tolerated. After a stabilization period of 20 min, respiratory and echocardiographic data were collected.
All patients were ventilated with a Horus 4 ventilator (Taema, Antony, France). During the study period, FIO2, RR, I:E, and tidal volume (Vt) were held constant. External positive end-expiratory pressure (PEEP) was not added.
The magnitude of Ppeak and mean airway pressure (Pmean) was obtained directly from the ventilator. Static lung compliance was measured during a 2 s inspiratory and expiratory hold for calculation of Pplat and intrinsic PEEP. Total respiratory compliance (Cst) was calculated with the following equation: Cst = Vt/(Pplat – total PEEP). Total respiratory dynamic compliance (Cdyn) was calculated with the following equation: Cdyn = Vt/(Ppeak – total PEEP). Arterial blood was sampled for measurement of PaO2, PaCO2, and pH and lactates only at VCprotocol T3 and PCprotocol T4 time intervals. Physiologic dead space (Vd/Vt) was estimated according to the Hardman and Aitkenhead equation: Vd/Vt = 1.14 x (PaCO2 – PE'CO2)/PaCO2 – 0.005.14
TOE was performed with an HDI® 5000 imaging system model (ATL ultrasound, Bothell, WA, USA) equipped with a multiplane 4.0–7.0 MHz probe. The probe was inserted into the oesophagus, after the induction of anaesthesia and before surgery. To minimize the risk of gastro-oesophageal mucosal injury from pressure of the transducer probe, flexion of the probe was intermittently released and the transducer probe inactivated.
Standard transgastric and upper and lower oesophageal views were obtained. LV diameters were measured from the M-mode echocardiogram according to the standards of the European Society of Cardiology.15 All echocardiographic measurements were performed at the end of expiration and averaged over three consecutive cardiac cycles. LVED and LV end-systolic (ES) diameters (D) were measured from M-mode recording, permitting calculation of LVED and LVES volumes (V) using the formula of Teicholz: V = 7D3/(2.4 + D). LV wall thickness at end-systole was also measured from M-mode recording. LV end-systolic wall stress (LVESWS) was calculated according to the formula proposed by Grossman and colleagues:16 [0.334 cuff arterial systolic pressure (LVESD)]/[LVPWT (1 + LVPWT/LVESD)], where PWT is the posterior wall thickness. Velocity–time integral of pulmonary flow (VTIP) was recorded at the level of the right ventricular (RV) outflow tract, together with pulmonary artery diameter (Dp), permitting calculation of RV stroke volume (SV), as RVSV = VTIP x [
]DP2/4. The mean acceleration of the flow in the pulmonary artery (Acmean) was calculated as peak velocity/acceleration time.17 All echocardiographic measurements were indexed to body-surface area. Pulsed-Doppler at the mitral annulus was performed; peak early (E) and peak late (A) velocities were measured and expressed as the E/A ratio.18 A Doppler tissue imaging (DTI) at the corner of the mitral annulus was also performed and the early diastolic velocity (Ea) was recorded (Fig. 1).19 20
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Recordings were stored on a videotape recorder. Videotapes were reviewed on an off-line analyser system that allowed slow-down or stop of the picture. A random sample of 10 patients was submitted twice for analysis in order to test the reproducibility of the measurements.
Statistical analysis
Data were computerized and analysed using the Statview 5.0 statistical packages (SAS Institute Inc., Cary, NC, USA). Normality of the distribution of data was assessed by the Kolmogorov–Smirnov test. We expressed continuous variables as the mean (SD). Changes in haemodynamic and respiratory parameters during VC sequences and PCprotocol were analysed using repeated measures analysis of variance (ANOVA) followed by the Scheffe f-test, as appropriate. Otherwise, normally distributed continuous variables were compared using the Student's t-test. When PC was applied instead of VC ventilation, airway pressure was expected to change.7 8 The cardiovascular effects were related to the degree to which applied airway pressure was transmitted to the pleural space. Thus, we chose to focus on the LVESWS, which reflected systolic function. Taking into account the preliminary results for the first 10 patients and on the basis of a relevant 20% change in wall stress, we calculated that 18 patients could test the null hypothesis at 0.05 significance with a power of 0.90. A P-value of <0.05 was considered significant.
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Results |
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Among the 23 patients initially enrolled, only 21 could be studied: in one patient, a severe bronchospasm occurred after induction of anaesthesia and the quality of the echocardiographic records was inadequate in the other. Intraobserver and interobserver reproducibility were 9.1 (4.8)% and 8.9 (6.1)%, respectively, for wall thickness, and 3.2 (1)% and 5.0 (4.0)%, respectively, for Ea. Demographic characteristics, duration of surgery, and blood loss are summarized in Table 1. Eleven patients (52%) had BMI of >25 kg m–2 and 11 patients suffered from arterial hypertension. Lactate values at T3 and T4 periods were 1.0 (0.2) mmol litre–1 (range 0.3–1.5). The normal lactate values ranged from 0.5 to 2.0 mmol litre–1.
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Ventilatory parameters measured at each ventilation period are shown in Table 2. During all the study periods, RR and Vt were comparable, but the peak inspiratory flow was very different between the two modes of ventilation. When compared with VC, Ppeak was lower in PC whereas Pmean was slightly increased. Dynamic compliance significantly improved after switching VC to PC [+15 (8)%] (Fig. 2). However, static airway pressures (Pplat and intrinsic-PEEP) and static compliance were not different between the two modes. No patient presented an intrinsic PEEP > 5 cm H2O. Effects on oxygenation also did not reveal significant changes. End-tidal CO2 underestimated PaCO2 levels with a mean gradient of 12 (4) mm Hg in both modes.
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The overall results are reported in Table 3. Pneumoperitoneum induced a significant increase in LVESWS and LVESV. A significant decrease in RVSV was also found [–15 (13)%], without any change in RV output impedance estimated by Acmean obtained at end-expiration. There was no significant variation of filling pressures, estimated by the E/Ea ratio. When the two modes of ventilation were compared, no significant change could be demonstrated in the systolic or diastolic function.
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Discussion |
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Our study demonstrated that, during laparoscopy, PC ventilation decreased Ppeak and increased Pmean slightly when compared with VC ventilation. Dynamic compliance significantly improved after switching from VC to PC. No other significant respiratory change could be noted. Likewise, switching from VC to PC did not lead to modification in systolic or diastolic function. Interpretation of echocardiographic results should be taken into account that 50% of our patients suffered from slight obesity and arterial hypertension.21
One expected advantage of PC ventilation could be related to its effect on volotrauma. Thus, in no part of the lung could the pressure be higher than the pre-set pressure.6 When compared with VC, the association between PC and a lower Ppeak was a constant finding in all previous studies.5 10–12, 22 This was achieved because of the decreasing flow pattern with PC and an earlier dissipation of flow resistance.22 However, Pplat was not modified by PC. Similar Pplat values suggest that the high flow meeting the endotracheal tube during the use of the constant square waveform was the cause of the elevated Ppeak. Therefore, during VC, the higher Ppeak did not reflect a change in lung mechanics or end-inspiratory alveolar peak pressure, and was probably not associated with any ventilatory harm.13 23 However, peak inspiratory flow was very different between the two modes of ventilation, and the ventilatory consequences are still a matter of controversy. In a rabbit model, high peak inspiratory flow in PC ventilation induced significantly more severe lung damage than lower peak inspiratory flows in the VC mode.24 In addition, limiting inspiratory flow and altering its pattern of delivery to a constant rate significantly reduced lung injury in normal lung of sheep.25 On the contrary, in patients with acute lung injury, the decelerating flow of PC could reduce lung strain.23 Another potential advantage of PC was to aid recruitment and to improve distribution of inspired gas.12 26 The change in Cdyn was of interest here because it was associated with a change in gas distribution.27 However, in isovolumetric conditions, variation of Cdyn depended not only on the elastic properties of the respiratory system but also on the resistive (flow-dependent) component of the airways and the endotracheal tube. Thus, neither the PaCO2 nor the estimated Vd/Vt ratio was different between PC and VC. Interestingly, Pmean was slightly higher during PC. Such a result was not surprising. In fact, using a decelerating flow waveform could result in a higher Pmean according to the mathematical models.7 8 Increases in Pmean appeared to be directly related to increases in oxygenation.28 However, the low Pmean generated during all steps of our study may have contributed to minimize its positive effect on oxygenation.
The main disadvantage of PC ventilation included variability in delivered Vt.6 In contrast to VC, PC ventilation resulted in a smaller delivered Vt when respiratory system compliance was decreased.29 A smaller Vt might lead to atelectasis and might go undiagnosed because there would be no change in Ppeak as PC ventilation would be used.29
Monitoring of cardiac function under pneumoperitoneum condition was challenging2 3 as illustrated by the poor data recorded in one excluded patient. Investigator's reliability was the other cornerstone condition. The intraobserver and interobserver variabilities reported here (between 3% and 9%) was in accordance with previous published studies.2 3 20
Cardiovascular consequences of laparoscopic surgery have been well documented by TOE. Pneumoperitoneum during VC ventilation caused an increase in mean arterial pressure and in LVESWS.2 3 We found the same results as reviously reported, but changes were less pronounced.2 3 These haemodynamic changes were not sustained throughout the period of pneumoperitoneum.2 Our study also showed that filling pressures were stable during the protocol as the ratio of the transmitral E velocity to Ea was significantly related to the filling pressures.19
Changes in cardiac output are sometimes variable, consistent with the Starling resistor concept of abdominal venous return.30 A significant but small decrease in RVSV was noted 15 min after pneumoperitoneum. As discussed earlier, we failed to detect a significant decrease in preload. We were also unable to show a decrease in Acmean at the end of expiration, which reflects changes in RV output impedance.17 Interestingly, elevation of RV afterload was demonstrated during inspiration, whereas no change was observed during expiration.17 Unfortunately, we have not studied beat-to-beat variations of RV outflow impedance according to the respiratory cycle.17 However, the pneumoperitoneum led to a decrease in respiratory compliance.3 4 This resulted in an increased transpulmonary pressure for delivering the same Vt.3 An increase in RV afterload during inspiration was, therefore, expected3 17 as transpulmonary pressure was its main determinant factor. Some authors also reported a decrease in the E/A ratio after pneumoperitoneum.3 However, we did not find an impairment in LV relaxation. In our study, the induction of pneumoperitoneum was performed when the patients were in a 20° Trendelenburg's position and after an infusion of 500 ml of colloids. These two actions should be taken into account to explain some differences between studies.4 18 In order to be unaffected by fluid loading, we used a DTI (Fig. 1).19 20 Unlike the E/A ratio which was influenced by loading conditions,18 the Ea is a preload-independent index of LV relaxation.19 Thus, Ea did not change during the different steps of our protocol.
When switching from VC to PC ventilation, the cardiovascular effects of PC ventilation should be related to airway pressure, through its effects on pleural pressure.9 We reported a slight increase in Pmean. Expected effects would have been a decrease in RVSV, LV preload, and LVESWS.9 However, no echocardiographic change was noted during our study. The most plausible explanation was the absence of a significant increase in intrathoracic pressure after the slight increase in Pmean. For the same Vt, RV afterload did not change at the end of expiration. Once again, the main determinant of RV afterload was transpulmonary pressure and not airway pressure in its strict sense at the end of inflation.17 Interestingly, evaluation of LV relaxation did not show any significant difference between the two modes of ventilation.19 20 In summary, our echocardiographic results indicated a lack of association of Ppeak and inspiratory flow pattern on cardiac function.
There were several limitations of our study. The patients were not randomized to the starting mode of ventilation. However, our intention was to study a ventilatory strategy commonly used in clinical practice. To our knowledge, physicians always started mechanical ventilation with a VC mode. The ventilation in VC or PC mode was maintained for a relatively short time. However, changes in respiratory mechanics, haemodynamics, and gas exchange are usually completed within this time period.10 12 Another potential limitation was the lack of pleural pressure measurement.9 However, pleural pressure variations would have been minor, taking into account the small changes in respiratory mechanics.
In conclusion, we found no advantage of PC ventilation over VC ventilation regarding respiratory mechanics, gas exchange, or on cardiac function. Specifically, the risk of barotrauma was not decreased by PC ventilation.
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