Laparoscopy presents many problems because abdominal distension and head-down positioning have a considerable influence on hemodynamic and respiratory function (1). Increasing intraperitoneal pressure (IPP) from 3 to 15 cm H2O decreases functional residual capacity (2). Carbon dioxide (CO2), widely used to establish a pneumoperitoneum, leads to a decrease in PaO2 and absorption of a significant quantity of CO2, resulting in hypercapnia, acidosis, and a hyperdynamic circulation (3). These effects are mainly caused by CO2, not by the intraabdominal pressure itself (4). Both, CO2 pneumoperitoneum and positive end-expiratory pressure (PEEP) affect cardiac performance. Kraut et al. (5) found a significant reduction in cardiac output when 10 cm H2O of PEEP and an IPP of 15 cm H2O were applied simultaneously. The use of PEEP during intraperitoneal CO2 insufflation increases ventricular afterload, and cardiac index is reduced (6). However, the precise mechanism underlying the decrease in PaO2 during CO2 pneumoperitoneum remains unclear. We therefore sought to determine whether CO2 pneumoperitoneum at a pressure of 15 cm H2O causes ventilation/perfusion ratio (VA/Q) heterogeneity, which can be reversed by PEEP. Specifically, we hypothesized that PEEP values of 15 and 20 cm H2O result in marked decreases in VA/Q heterogeneity and an improvement in pulmonary gas exchange compared with 5 cm H2O of PEEP.
This investigation was approved by the Animal Care Committee of the Austrian Ministry of Science in August, 1998. We studied 13 12–16-wk-old pigs weighing 35.6 ± 1.2 kg (mean ± SD). Anesthesia was introduced IM with ketamine (15 mg/kg) and maintained by infusion of fentanyl (0.8 mg/h) and midazolam (8 mg/h). A 3% gelatin solution (4 mL · h-1 · kg-1) was administered continuously. Depth of anesthesia was monitored by means of arterial blood pressure and heart rate. All pigs were placed supine with 15° head-down tilt. The tracheas were intubated by using endotracheal tubes (inside diameter, 6.5–7.5 mm). The lungs were ventilated by using a time-cycled, volume-controlled mode (Servo 900 D; Siemens, Elema, Sweden) at a respiratory rate of 15 breaths/min with a fraction of inspired oxygen of 0.4. During the preparatory phase, minute volume was adjusted to maintain a PaCO2 of 40 mm Hg. Ten minutes before intraabdominal gas insufflation, minute volume was increased to achieve a PaCO2 of 30 mm Hg. This minute volume was then maintained for all subsequent measurements. Two inspiratory holds of 20 s each were performed before each set of measurements to prevent atelectasis. Body temperature was maintained between 38.0°C and 39.0°C by using a heating blanket. Nine animals were subjected to incremental increases of PEEP (PEEPincre; 5–20 cm H2O, increments of 5 cm H2O). A control group, consisting of four animals, was treated with a constant PEEP (PEEPconst) of 5 cm H2O throughout the study. All animals were investigated in four different study phases. In both groups the abdominal cavity was inflated with CO2 at a pressure of 15 cm H2O (IPP 15). After 30 min of stabilization, baseline measurements were made. In the PEEPincre group, PEEP was increased stepwise by 5 cm H2O, and measurements were performed 30 min after each single increase. In the PEEPconst group, measurements were taken in the same mode. Each set of measurements included heart rate and mean arterial, central venous, pulmonary arterial, and pulmonary capillary wedge pressures, and the respiratory measurements described below. Inert gas, as well as arterial and mixed venous, samples were collected at the same time. A 7F thermistor-tipped, flow-directed pulmonary artery catheter was inserted directly into the right internal jugular vein and advanced into a main pulmonary artery by using direct-pressure monitoring. This permitted measurements of cardiac output, pulmonary arterial pressure, pulmonary capillary wedge pressure, mixed venous blood sampling, and collection of inert gas blood samples. Finally, the left femoral artery was cannulated for measurement of systemic arterial pressure, arterial blood gas sampling, and collection of inert gas blood samples. The peritoneal cavity was punctured and inflated with purified dry CO2. The pressure in the abdominal cavity was measured by using a manometer, which had been originally designed to assess the cuff-pressure of tracheal tubes. IPP was maintained at 15 cm H2O in all animals. Mean arterial, central venous, pulmonary arterial, and pulmonary capillary wedge pressures were measured by using an intensive care unit monitor (Servomed; Hellige GmbH, Freiburg, Germany) and standard pressure transducers. The transducers had been zeroed to the level of the right atrium. Measurements were taken before each collection of blood and expired samples for inert gas determination. Cardiac output was measured by using the thermodilution technique; the mean of three subsequent determined values was recorded. Arterial and mixed venous blood samples (2 mL each) were collected after collection of each set of inert gas arterial and mixed venous samples and analyzed for PO2 and PCO2, by using a Ciba Corning 806 blood gas analyzer (Ciba-Geigy, Basel, Switzerland). Values were corrected to body temperature. The distributions of ventilation and perfusion were determined by using the multiple inert gas elimination technique as described before (7,8). A mixture of six inert gases, including sulfur hexafluoride, ethane, cyclopropane, halothane, diethyl ether, and acetone was dissolved in saline and infused via a peripheral vein at a rate of 3 mL/min. This infusion was started 1 h before the first set of measurements. Duplicate 10-mL blood samples were collected in heparinized glass syringes from the pulmonary artery and the left femoral artery. Thirty-milliliter mixed expired gas samples were obtained from a heated mixing chamber and placed in warmed gas-tight glass syringes. All samples were kept at a temperature of 39°C and immediately prepared for analysis. Inert gas extraction was performed according to Wagner et al. (7). Concentrations of inert gases were measured by using gas chromatography (HP-5890, Series II; Hewlett-Packard, Avondale, PA). Ventilation-perfusion distributions were then determined from inert gas data by using the 50-compartment model of Wagner et al. (8) and Evans and Wagner (9). Inert gas shunt, log standard deviation of the Q, log standard deviation of VA, mean VA/Q values of VA and Q distributions, and dead space were calculated from this 50-compartment model. Distributions of VA and Q are presented as follows:
- 1. blood flow to unventilated lung units, shunt (VA/Q < 0.005);
- 2. blood flow to poorly ventilated lung units (low VA/Q, 0.005–0.1);
- 3. blood flow to normally ventilated lung units (normal VA/Q, 0.1–10);
- 4. ventilation of poorly perfused lung units (high VA/Q, 10–100);
- 5. ventilation of unperfused lung units, dead space (VA/Q > 100).
The residual sum of squares was used as an indicator of fit of the experimental data to this 50-compartment model (10). Mixed arterial oxygen pressure was calculated from compartmental end capillary values and compared with the measured value (11). In addition, the alveolar-arterial PO2 difference was calculated. Airway pressures, expiratory tidal volume, respiratory minute volume, and respiratory rate measurements were measured by using a pneumotachograph (CP-100; BiCore Monitoring System, Irvine, CA), placed between the endotracheal tube and the breathing circuit. Values were recorded by using a pulmonary mechanics computer. Results are shown as mean ± SEM. Intergroup and intragroup differences comparing animals treated with constant PEEP with animals treated with incremental PEEP were examined by a two-factor repeated measurement analysis of variance (two-tailed). Post hoc comparisons were conducted by using the Scheffé test. P < 0.05 was considered significant.
Inert Gas Measurements
Values are shown in Table 1 and Figure 1. At baseline (PEEP 5/IPP 15), blood flow to areas with normal VA/Q was 72% of cardiac output in the PEEPincre group. By increasing PEEP to 10 cm H2O (PEEP 10/IPP 15), the blood flow to areas of low VA/Q was significantly reduced (P < 0.01) and directed to areas of normal VA/Q. By adjusting PEEP to 15 cm H2O (PEEP 15/IPP 15), blood flow to areas of low VA/Q was further reduced and so was blood flow to areas of zero VA/Q. By setting PEEP to 20 cm H2O (PEEP 20/IPP 15), a smaller amount of blood flow to areas of zero VA/Q was shifted to areas of normal VA/Q. In the 60- and 90-min measurement (PEEP 15/IPP 15 and PEEP 20/IPP 15), blood flow to areas with a zero VA/Q was significantly smaller (P < 0.007 and P < 0.02) in the PEEPincre group than in the PEEPconst group, and blood flow to areas of normal VA/Q was significantly higher (P < 0.006 and P < 0.007). The incremental increases in PEEP did not cause significant increases in ventilation of areas with high VA/Q or in alveolar dead space ventilation. The overall intrasubject variation for log standard deviation of the Q and log standard deviation of VA was below 5% by using the mean of duplicate measurements. An indication of acceptable quality of the VA/Q distribution is a residual sum of squares of 5.3 or less in half of the experimental runs (50th percentile) or 10.6 or less in 90% of the experimental runs (90th percentile) (10). In the present study, 92% of the residual sum of squares was <5.3 and 100% was <10.6.
Arterial Blood Gas Data
Values are shown in Table 2. With respect to PaO2, no significant intergroup difference could be detected. Also, comparing baseline (PEEP 5) with PEEP 10 showed no significant difference (P = 0.59). Comparing PEEP 5 with PEEP 15 displayed a significant difference in arterial PO2 (P < 0.05), and a highly significant difference could be found by comparing PEEP 5 with PEEP 20 (P < 0.01).
Values are shown in Table 2. No significant difference could be found in central venous pressure, pulmonary artery pressure, pulmonary capillary wedge pressure, or mean arterial pressure. Stroke volume index was reduced (P < 0.02) when 20 cm H2O was applied compared with 5 cm H2O.
Compared with the PEEPconst group, mean airway pressure was notably elevated (P < 0.001) when applying PEEP values ≥10 cm H2O in the PEEPincre group. Other ventilatory variables did not change significantly.
The principal finding of this study was that a PEEP of 15 or 20 cm H2O significantly improves pulmonary gas exchange during CO2 pneumoperitoneum. The increase from 10 to 15 cm PEEP led to a redistribution of blood flow from areas with low and zero VA/Q to areas with normal VA/Q. This improved both arterial oxygenation and CO2 elimination. In animals kept at 5 cm H2O PEEP during pneumoperitoneum, low VA/Q and shunt perfusion remained high, and therefore, normal VA/Q perfusion persisted with low values. During laparoscopy, diaphragmatic excursion is impaired, and CO2 pressure increases in mixed venous blood. However, in our experiment, because all animals were moderately hyperventilated, CO2-associated effects on pulmonary circulation were not apparent. Applying 5, 10, or 15 cm H2O of PEEP caused practically no difference in alveolar dead space as measured with the multiple inert gas elimination technique. PEEP decreases cardiac output by reducing ventricular preload (12) and by other factors. IPP per se reduces left ventricular preload (13). IPP and PEEP should have additive effects on reducing preload, as both superior and inferior venae cavae are compressed and provide less blood to the right atrium. Moreover, Moffa et al. (6) found that CO2 increases ventricular afterload and exacerbates the adverse effects of PEEP. PEEP plus IPP should greatly reduce cardiac performance. When applying increasing PEEP values in our study, cardiac index was not significantly changed; nevertheless, there was a trend for a decrease as soon as 10 cm H2O was exceeded. Stroke volume index was depressed (P < 0.02) when applying 20 cm H2O of PEEP compared with 5 cm H2O of PEEP.
Three limitations of this study should be mentioned. First, all animals studied had proper fluid replacement before baseline measurements were taken. Patients listed for elective abdominal surgery are generally fasted overnight. Usually, pneumoperitoneum is established within a few minutes after anesthesia has been induced. Some patients may then still be hypovolemic, and PEEP values above 10 cm H2O are likely to cause marked depressions in blood pressure and cardiac output. Secondly, anatomical and physiological differences between healthy young pigs and the average human adult have to be remembered. The pig’s abdomen, which relative to its thorax is bigger than in humans, is possibly more distensible, as well. There might, therefore, be a larger peritoneal surface available for CO2 resorption in pigs as compared with humans. Finally, in our experiment, four different PEEP-levels, but only one IPP, were studied. This restriction was accepted, as 15 cm H2O IPP resemble clinical reality.
PEEP, 15 cm H2O, resulted in significantly less blood flow to lung areas with zero VA/Q and significantly more blood flow to lung areas with normal VA/Q. Because cardiac index was only slightly less than with 10 cm H2O, 15 cm H2O PEEP was the better setting in this model. We conclude that PEEP of 15 H2O during pneumoperitoneum resulted in modest hemodynamic depression but significant gas exchange augmentation in our experiment.
The writers thank Prof. Dr. W. Seeger and Dr. D. Walmrath for introducing Dr. A. Loeckinger to the multiple inert gas elimination technique during the years 1997 and 1998 in Giessen, Germany.
1. Makinen MT, Yli-Hankala A. Respiratory compliance during laparoscopic hiatal hernia repair. Can J Anaesth 1998; 45:865–70.
2. Mutoh T, Lamm WJ, Embree LJ, et al. Abdominal distension alters regional pleural pressures and chest wall mechanics in pigs in vivo. J Appl Physiol 1991; 70:2611–8.
3. McDermott JP, Reagan MC, Page R, et al. Cardiorespiratory effects of laparoscopy with and without gas insufflation. Arch Surg 1995; 130:984–8.
4. Ho HS, Saunders CJ, Gunther RA, Wolfe BM. Effector of hemodynamics during laparoscopy: CO2
absorption or intra-abdominal pressure? J Surg Res 1995; 59:497–503.
5. Kraut EJ, Anderson JT, Safwat A, et al. Impairment of cardiac performance by laparoscopy in patients receiving positive end-expiratory pressure. Arch Surg 1990; 134:76–80.
6. Moffa SM, Quinn JV, Slotman GJ. Hemodynamic effects of carbon dioxide pneumoperitoneum during mechanical ventilation and positive end-expiratory pressure. J Trauma 1993; 35:613–8.
7. Wagner PD, Naumann PF, Laravuso RB. Simultaneous measurement by eight foreign gases in blood using gas chromatography. J Appl Physiol 1974; 36:600–5.
8. Wagner PD, Saltzman JA, West JB. Measurement of continuous distributions of ventilation-perfusion ratios: theory. J Appl Physiol 1974; 36:588–99.
9. Evans JW, Wagner PD. Limits on VA
/Q distributions from analysis of experimental inert gas elimination. J Appl Physiol 1977; 42:889–98.
10. Roca J, Wagner PD. Principles and information content of the multiple inert gas elimination technique. Thorax 1993; 49:815–24.
11. West JB. Ventilation-perfusion inequality and overall gas exchange in computer models of the lung. Respir Physiol 1969; 7:88–110.
12. Labermont B, Detry O, D’Orio V, et al. Effects of PEEP on systemic venous capacitance. Arch Physiol Biochem 1998; 105:373–8.
© 2000 International Anesthesia Research Society
13. Marathe US, Lilly RE, Silvestry SC, et al. Alterations in hemodynamics and left ventricular contractility during carbon dioxide pneumoperitoneum. Surg Endosc 1996; 10:974–8.