Maintenance of adequate pulmonary ventilation and oxygenation is often a major problem in obese patients during general anesthesia. Abundant chest wall fat and protruberant abdomens alter pulmonary mechanics both by weighting the chest wall [1,2] and by exerting increased upward pressure on the diaphragm . The compliance of the respiratory system (CRS) in obese individuals is half of that of normal-weight patients at any respiratory volume  as a result of reduced compliance of both the chest wall and the lungs. Morbidly obese patients have reduced functional residual capacity and expiratory reserve volume (ERV) while awake, which is further aggravated in the supine position and during anesthesia [4,5]. As a consequence, PaO2 may be lower than expected. In order to improve arterial oxygenation, controlled mechanical ventilation with large (15-20 mL/kg ideal body weight) tidal volumes (VTS) is recommended [5-7]. However, the use of large VTS may induce decreases in PaCO2 tension and may result in high inspiratory airway pressures, which may cause parenchymal damage even in normal lungs . In view of these possible problems, we reassessed the effects on PaO2 of short-term ventilation with high VTS in anesthetized obese patients.
Eight morbidly obese patients undergoing gastric bypass surgery were studied after having given their informed consent. The study was approved by the Ethics Committee of our University Hospital. The criteria of morbid obesity was a body mass index greater than 35, calculated as: [body mass (kg) divided by height (2) (m2)].
The investigations were performed prior to the surgical procedures. Electrocardiogram, direct radial arterial blood pressure, and arterial oxygen saturation were monitored continuously. Propofol (1 mg/kg) and fentanyl (100 micro gram) were given intravenously to induce general anesthesia. Endotracheal intubation was performed after relaxation with pancuronium (0.1 mg/kg), and anesthesia was maintained by a continuous infusion of propofol (6-10 mg centered dot kg-1 centered dot h-1); inhaled anesthetics were omitted. The patients' lungs were ventilated via a Siemens Servo 900C ventilator (Siemens AB, Solna, Sweden) with constant inspiratory flow. The ventilator was calibrated before each study.
Inspiratory and expiratory VT, ventilatory rate (RR), peak inspiratory airway pressure (Ppeak), end-inspiratory pressure (Pplateau), end-expiratory pressure, and CRS were monitored continuously by means of the Capnomac Ultima Trademark respiratory monitor (Datex Instrumentarium, Helsinki, Finland), with the flow sensor placed at the proximal end of the endotracheal tube. The respiratory monitor was calibrated with a 1000-mL syringe and its accuracy was verified before each series of measurements. Detailed validation of the respiratory monitor and the characteristics of the bidirectional flow sensor have been described previously . Controlled mechanical ventilation was initiated with a baseline VT of 13 mL/kg ideal body weight, calculated by subtracting 105 cm from the height of the patient . Ventilatory frequency was set at 10 breaths/min (total cycle time 6 s), inspiratory time (TI) was 2 s, and end-inspiratory pause was 0.6 s. Positive end-expiratory pressure was not administered.
Baseline VT of 13 mL/kg was increased sequentially to 16 mL/kg, 19 mL/kg, and to 22 mL/kg, while TI, RR, and FIO2 were kept constant. Arterial blood samples were drawn and ventilatory data recorded after 15 min ventilation at each VT levels. Pulmonary gas exchange was assessed by calculating the following indices: Alveolar-arterial oxygen tension difference (P(A-a)O2) was calculated as (P(A-a)O2 = PIO (2) - PaCO2/0.8 - PaO2, where 0.8 is the respiratory quotient. PIO2 (partial pressure of inspired O2) was calculated by the formula, PIO2 = FIO2 (PB - 47), where FIO2 is the fractional concentration of O2 in the inspired gas. The barometric pressure (PB) was 760 mm Hg and alveolar water vapor partial pressure was 47 mm Hg. Arterial-alveolar oxygen tension ratio was calculated as a/A ratio = PaO2/PO 2 in the alveoli.
Two sets of ventilatory data were recorded in each setting and the means of the two were used for statistical analysis with the Friedman's two-way analysis of variance test, and the two-sample t-test. Linear regression analysis was used to discern the degree of correlation between associated variables. P < 0.05 was considered significant. Data are presented as mean +/- SD.
General characteristics of the patients are summarized in Table 1. The calculated ideal weight of the patients was 63 +/- 7 kg (range 55-75 kg). As expected, increasing VT with fixed TI and RR resulted in significantly increased Ppeak (P < 0.008) and Pplateau (P < 0.01) Figure 1. Progressively larger VT resulted in improved CRS, but this increase only reached the level of statistical significance (P < 0.01) at VT of 19 mL/kg Table 2.
The magnitude of preoperative functional residual capacity and ERV were influencing the baseline value of CRS, Ppeak, and Pplateau measured at the 13 mL/kg tidal volume level. Preoperatively measured ERV was highly dependent on the weight of the patient (R = -0.85, P = 0.01) and in turn influenced significantly the value of CRS (R = 0.785, P = 0.03) during mechanical ventilation. The baseline P(A-a)O (2) gradient showed a negative correlation with the preoperative ERV (R = -0.729). The P(A-a)O2 during mechanical ventilation of our obese patients was correlated with the weight of the patient at all VT levels (R = 0.711). In comparison to the initial 13 mL/kg VT, PaO2 changed insignificantly due to incremental increases in VTS. PaCO2 and PETCO2 tensions were reduced significantly (P < 0.008) Table 3. Increasing the VT to 22 mL/kg did not significantly change either the P(A-a)O2 or the a/A ratio.
Incremental increases in tidal volume of 15 min duration in morbidly obese patients induced significant hyperventilation with marked hypocapnia. Although compliance also increased, suggesting recruitment of alveolar units, there was no significant improvement in oxygenation.
Among the ventilatory variables measured by the respiratory monitor, the compliance value represents the combined compliances of the lungs and chest wall (CRS). It is calculated by the monitor as the ratio between the expiratory VT and the difference of the end-inspiratory (Pplateau) and end-expiratory pressure. It provides a reasonable estimate of true static compliance and is termed quasi-static compliance .
At the initial (13 mL/kg) ventilatory settings low CRS was found in our obese patients, which improved after the applications of larger VT. Despite the improved compliance, high Ppeak and Pplateau were necessary to deliver the larger VTS Table 2, partly owing to the sheer weight of the rib cage and the abdomen, and partly a result of delivering a greater VT in the same fixed time interval, i.e., a higher inspiratory flow rate.
Peak airway pressure measured at the proximal end of the endotracheal tube is primarily influenced by the flow-resistive characteristics of the endotracheal tube. In our study, tidal volumes were increased with unaltered TI, therefore inspiratory gas flow rate was higher with the larger VTS Table 2. It is reasonable to assume that the flow resistance of the endotracheal tube was responsible for most of the increased Ppeak. On the contrary, the plateau pressure reflects average peak alveolar pressure [11,12] and is not influenced by the flow resistive characteristics of the endotracheal tube, if the end-inspiratory pause time is adequate. In our study, increasing VT resulted in significant increase in Pplateau before any surgical manipulation. During periods of surgical retraction Pplateau may increase further, close to the upper limit of 30 cm H2 O accepted during mechanical ventilation . In agreement with the results of previous studies [13,14] there were no significant overall differences in the PaO2, P(A-a)O2, and a/A ratio when VTS were increased sequentially from 13 mL/kg to 22 mL/kg Table 3.
Tidal volume of 22 mL/kg resulted in a significant decrease in PaCO2 to 28.1 +/- 3.1 mm Hg. Hypocapnia due to hyperventilation shifts the oxygen-hemoglobin curve to the left, increasing the hemoglobin affinity for O2 . Hyperventilation may cause increased intrathoracic pressure , thereby a decrease in cardiac output [8,15] and reduced oxygen availability . In addition, there is evidence in the literature that ventilation with large VTS and high distension pressures is harmful for the healthy lung parenchyma . As factors affecting susceptibility are unknown at present, cyclic overstretching of lung tissue may be best avoided.
Our study has several shortcomings. Firstly, to study the effect of large VTS, hypocapnia could have been circumvented by decreasing the ventilatory rate. This approach was not reasonable in our study because RR of less than 10/min should have caused excessively high inspiratory pressures. Secondly, the effect of different VTS on oxygenation may not be fully expressed in the short-term evaluation performed in our study. Finally, although changes in PaO2 were characterized by the lack of meaningful amelioration in each patient, the small sample size may have reduced the power to detect a significant improvement. It would be reasonable to question whether our findings would persist in a larger study or with a longer period of ventilation.
In summary, we did not find the administration of large VTS during short-term mechanical ventilation of morbidly obese patients beneficial under the circumstances of our study. Increasing the VT from 13 to 22 mL/kg (based on ideal body weight) did not improve oxygenation, but resulted in severe hypocapnia. As high VT-high airway pressure ventilation may be intrinsically deleterious to lung parenchyma, it may be more rational to use a VT that results in an acceptable PaO2 and PaCO2 at the lowest Pplateau.
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