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*Department of Anesthesiology, Mayo Clinic, Rochester, Minnesota;
Department of Anesthesiology, The Cleveland Clinic Foundation, Naples, Florida;
Department of Obstetrics and Gynecology, Minimally Invasive Surgery,
The Cleveland Clinic Foundation, Cleveland, Ohio; and
||Department of Anesthesiology, University of Maryland, and Veterans Administration Medical Center, Baltimore, Maryland
Address correspondence to Denis L. Bourke, MD, University of Maryland, Anesthesiology Service, Baltimore VA Medical Center, 10 North Greene St., Baltimore, MD 21201. Address e-mail to bourkedenisl{at}aol.com Address reprint requests to Juraj Sprung, MD, PhD, Mayo Medical School, Department of Anesthesiology, Saint Mary’s Hospital, MB 2-752, 200 First St. SW, Rochester, MN 55905. Address e-mail to sprung.juraj@mayo.edu.
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Abstract |
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IMPLICATIONS: Morbid obesity decreases arterial oxygenation and respiratory system compliance. During laparoscopy, arterial oxygenation is affected only by the patient’s body weight. Increases in tidal volume or respiratory rate do not improve arterial oxygenation.
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Introduction |
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Under anesthesia, MO patients’ closing volume can exceed their functional residual capacity (FRC), causing airway closure and resulting in an increased alveolar-arterial difference in oxygen tension (AaDO2). In the 1970s, several authors showed that during mechanical ventilation, large tidal volumes (VT) could improve oxygenation in MO patients (3,4). Another strategy to improve oxygenation is the use of positive end-expiratory pressure (PEEP). However, PEEP has not proven to be the answer. A number of authors (5–11) have shown that PEEP in normal or lung-injured patients, under anesthesia or not, is not a reliable tool for improving gas exchange. Using PEEP for MO patients, Pelosi et al. (8) were able to obtain only slight improvements in PaO2 (from 110 to130 mm Hg). Salem et al. (4) found that removing 10–12 cm H2O PEEP in MO patients reduced the AaDO2 by 44 mm Hg. Horton and Cheney (12) suggested that PEEP may fail to improve oxygenation because increased alveolar pressure increases the shunt fraction. As an alternative, large VT have been advocated for improving oxygenation in MO patients (13,14).
Because of the difficulty in maintaining oxygenation in MO patients, particularly during laparoscopic surgery (1,2), we investigated the effects of increasing either VT or respiratory rate (RR). The effects of these strategies have not been quantified in MO patients during laparoscopy. We studied these effects in the various positions (supine, Trendelenburg, and reverse Trendelenburg) frequently used during laparoscopic surgeries.
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Methods |
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All the patients received premedication with IV midazolam, 2–4 mg. After preoxygenation, anesthesia was induced with 2 mg/kg propofol and 10 µg/kg alfentanil. Tracheal intubation (8.0-mm inside diameter endotracheal tube) was facilitated with succinylcholine 1–2 mg/kg. Total IV anesthesia was maintained with 150 µg · kg-1 · min-1 propofol and 2 µg · kg-1 · min-1 alfentanil. Drug doses were based on calculated ideal body weight. Thereafter, doses adjusted to deep hypnotic effect with automated encephalogram analysis, maintaining the bispectral index between 45 and 55 (BIS monitor—bispectral index). Throughout the study period, rocuronium was used to assure muscle relaxation as evidenced by no train-of-four response with neuromuscular stimulation. The lungs were ventilated with a FIO2 = 0.5 using a mixture of oxygen and air with volume-controlled ventilation (Servo-Siemens 300 ventilator). In addition to standard anesthetic monitoring, arterial blood pressure was monitored with a radial arterial line. A Paratrend 7® continuous blood gas monitor was used to monitor on-line arterial blood gases: PaO2, PaCO2, and pHa. To perform this measurement, an ultrathin sensor, a part of the Paratrend 7® monitoring system, was inserted through the standard 20-gauge arterial catheter.
A Servo Screen 390 V2.0 (Siemens-Elma AB, Solna, Sweden) pulmonary monitor was used to calculate the following variables: static respiratory system compliance (Cst,rs, mL/cm H2O) and inspiratory resistance (RI,rs, cm H2O · L-1 · s-1). Respiratory system compliance was calculated by dividing the expiratory VT by the difference between the plateau pressure and the end-expiratory pressure: Cstat = VTexp/(Ppause - PEEPtotal). Inspiratory system resistance was calculated from the difference between peak inspiratory pressure and plateau pressure, divided by end-inspiratory flow: Rinsp = (Ppeak - Ppause)/(end-inspiratory flow). The minute ventilation (volume-controlled mode) was initially adjusted to maintain the PaCO2 between 38 and 40 mm Hg. All measurements were performed before surgery was initiated. All manipulations of the patient were halted during the measurement of respiratory mechanics. We used an inspiratory/expiratory ratio of 1:2.5 and a PEEP of 5 cm H2O. Measurements (Cst,rs, RI,rs) were recorded in supine, Trendelenburg (30° head-down), and reverse Trendelenburg (30° head-up) positions before CO2 insufflation and in the same positions after CO2 insufflation to 20 mm Hg (Storz Electronic Endoflator model 26012, Charlton, MA). In each body position, before and after pneumoperitoneum, the following ventilatory sequence was used: (a) normal VT and RR (VT 600–700 mL, RR 10 breaths/min), (b) double VT and normal RR (VT 1200–1400 mL, 10 breaths/min), and (c) normal VT and double RR (VT 600–700 mL, RR 20 breaths/min). At each condition, we ventilated the patients’ lungs for 5 min before observations were recorded. Oxygenation was assessed by AaDO2 according to the following equation: AaDO2 = (FIO2)(PB - pH2O) - (PaCO2/RQ) - (PaO2), where PB is the barometric pressure, pH2O is the water vapor tension at 37°C, and RQ is the respiratory quotient set at 0.8.
Data are means ± SD. Effects of body position, weight, abdominal insufflation, and mode of ventilation were analyzed by the repeated measures analysis of variance. Statistical significance was accepted at a 0.05 level. A Bonferroni correction was applied to ensure the P < 0.05 significance for all pairwise comparisons (for these data, a P value < 0.02 was accepted as a significance level).
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Results |
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At baseline conditions (supine, normal VT, and 10 breath/min), MO patients had on average 29% lower Cst,rs than the NW patients (44 versus 62 mL/cm H2O P < 0.05) (Fig. 1). Changing the position from supine to Trendelenburg or reverse Trendelenburg did not significantly affect Cst,rs in either group. Compared with baseline, ventilation at double VT before pneumoperitoneum moderately increased Cst,rs in both groups (P < 0.05). Pneumoperitoneum induced 43% decreases in Cst,rs in both groups (P < 0.001), in NW to 34 and in MO to 25 mL/cm H2O. Changing the body position or mode of ventilation during pneumoperitoneum did not further affect Cst,rs in either group (P > 0.7).
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Discussion |
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Under baseline conditions, FIO2 = 0.5, VT = 10 mL/kg ideal body weight, RR = 10 breaths/min, PaO2 was significantly worse in MO patients than in NW patients, PaO2 = 172 ± 47 mm Hg versus 260 ± 21 mm Hg. Surprisingly, oxygenation was not further adversely affected either by body position, pneumoperitoneum, or a combination of both. Under each of these conditions, increasing the minute ventilation by either doubling the VT or the RR failed to produce any improvement in oxygenation. Others have found similar results (15–17). Conversely, Visick et al. (3) found that increasing VT improved oxygenation. An explanation for this discrepancy may be that their initial VT was only 5 mL/kg, whereas our initial VT was 10 mL/kg with 5 cm H2O PEEP. Our settings were probably closer to optimal values and thus little improvement could be expected with increases in either VT or RR.
Decreased PaO2 in MO patients is probably explained by the disproportionally large reduction of FRC under anesthesia compared with NW patients. Under anesthesia, the FRC of MO patients frequently decreases to less than the closing capacity (1,18–22). However, if decreases in FRC were the primary cause of the decrement in oxygenation, then restoring lung volume with larger VT would be expected to improve oxygenation. In our study, large VT (1000–1200 mL) failed to improve oxygenation in both MO and NW patients, suggesting that poorly ventilated (but perfused) lung areas were not recruited. It may have been that our initial conditions, RR 10 breaths/min, VT 600–700 mL, and PEEP 5 cm H2O, were near to ideal and further, clinically significant, alveolar recruitment could not be obtained with larger VT.
A somewhat different mechanism may explain the findings of Salem et al. (4) that increased levels of PEEP (10–12 cm H2O) failed to improve oxygenation in MO patients and that discontinuing PEEP resulted in an increase in arterial oxygen tension. The beneficial effects of PEEP result from alveolar recruitment; however, when using larger PEEP, the benefits may be cancelled by the deleterious effect of continuous increased pressure on pulmonary and systemic hemodynamics (23). In our study, the intermittent increased pressure of large VT did not prove beneficial; however, it did not adversely affect oxygenation.
A criticism of our study design may be that the five-minute equilibration periods were too short to permit significant changes to be observed. However, Salem et al. (4) observed statistically significant decreases in AaDO2 within only two minutes of discontinuing PEEP. Burns et al. (5) were also able to detect significant changes in PaO2 within five minutes of changing PEEP or VT. Furthermore, Figure 4, regardless of the conditions, does not even suggest changes in AaDO2. Therefore, we believe that our results are clinically valid in that if one must improve a patient’s oxygenation and increasing VT, for example, does not produce a clinical improvement within five minutes, it is unlikely to result in useful clinical improvement given more time.
In this study, we observed, as have others, that MO anesthetized supine patients have 30% less respiratory system compliance than their NW counterparts (17,18,24). We found that respiratory system compliance decreased on average 40% with pneumoperitoneum (Fig. 1). Similar results have previously been reported (16,17). Furthermore, we confirmed others’ findings that ventilation with large VT before pneumoperitoneum resulted in small, clinically insignificant, increases in static compliance (3,16,25).
Before pneumoperitoneum, inspiratory resistance in MO anesthetized patients was almost 70% higher than for NW patients (Fig. 2). Only the NW patients had a slightly higher inspiratory resistance after doubling the VT. Before pneumoperitoneum, doubling the RR did not affect inspiratory resistance in either group under any of our study conditions. During pneumoperitoneum, inspiratory resistance increased significantly in the Trendelenburg and reverse Trendelenburg positions but not while supine (Fig. 2). Interestingly, despite the appearance of a positive trend, a 30° reverse Trendelenburg position did not have any beneficial effects on breathing mechanics. Casati et al. (26) have reported similar results.
In our MO patients, ventilation with large VT, especially during pneumoperitoneum, resulted in large end-inspiratory (plateau) pressures (Fig. 3). NW patients under all study conditions and MO patients during conditions other than double VT had end-inspiratory pressures approximately 30 cm H2O. The end-inspiratory pressure is considered to reflect average peak alveolar pressure and it is believed that the acceptable upper limit is approximately 35 cm H2O (27,28). Large end-inspiratory pressure correlates closely with large end-inspiratory volume which can result in parenchymal stretch and ventilator-induced lung injury (29,30). End-inspiratory pressures exceeded 50 cm H2O in our MO patients when ventilated with double VT; however, their considerably lower compliance may have had a protective role in limiting parenchymal distention (Figs. 1 and 3). Although we did not encounter pulmonary complications during our short-term ventilatory trials with large end-inspiratory pressures, this does not mean that these ventilatory pressures are safe. In addition to the degree of parenchymal stretch, the duration of such ventilation may have an important role in lung injury (31,32). Because large VT did not improve PaO2 either in MO or NW patients under any of the conditions we studied, they cannot be advocated as a means of correcting high AaDO2 gradients in MO patients under anesthesia.
In conclusion, oxygenation may be compromised in MO patients during laparoscopy and should be monitored closely. We found that PaO2 was adversely affected primarily by increased body weight and not by body position and/or pneumoperitoneum. Increases in VT to >1 L or RR up to 20 breaths/min had no beneficial effect on PaO2 during laparoscopy in either NW or MO patients. Additionally, it does not seem that PEEP >5 cm H2O will reliably improve PaO2 (4,8). Increasing the inspired oxygen concentration may be the most reliable treatment for hypoxemia in MO patients.
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Acknowledgments |
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References |
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  P. Cadi, T. Guenoun, D. Journois, J.-M. Chevallier, J.-L. Diehl, and D. Safran Pressure-controlled ventilation improves oxygenation during laparoscopic obesity surgery compared with volume-controlled ventilation Br. J. Anaesth., May 1, 2008; 100(5): 709 - 716. [Abstract] [Full Text] [PDF]
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D. Henzler, R. Rossaint, R. Kuhlen, J. Sprung, and D. L. Bourke Is There a Need for a Recruiting Strategy in Morbidly Obese Patients Undergoing Laparoscopic Surgery? * Response Anesth. Analg., January 1, 2004; 98(1): 268 - 269. [Full Text] [PDF]
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