Measurement of respiratory mechanics can be useful for examining patients whose lungs are mechanically ventilated, and some techniques are suitable to evaluate anesthetized patients; we used one of these techniques, i.e., the rapid occlusion during constant flow inflation.
As previously mentioned, the maintenance of an adequate pulmonary ventilation and oxygenation may still be a major problem in anesthetized obese patients, because anesthesia significantly affects respiratory function. The decrease of FRC is one of the main side effects of anesthesia on respiratory function, and this change is particularly marked in morbidly obese patients (2,8,9,11–13). Pelosi et al. (14) demonstrated that the reduction of FRC is closely related to body mass index.
A cranial shift of the diaphragm has been identified as an important factor causing decrease of FRC in obese patients undergoing general anesthesia (8,14); the loss of tone of this muscle may determine the reduction in lung volume because of unopposed intra-abdominal pressure (8,14). However, also atelectasis seems related to a number of interacting factors that include the shape of chest wall structures, volume, and distribution of blood (14). In clinical practice, some morbidly obese patients do not tolerate the supine posture, and it may even be fatal to them (2,7,15).
Large TVs (15–20 mL/ideal body weight) are often recommended for these patients to move tidal ventilation higher than the closing volume and consequently increase arterial oxygen tension (2,5,7,16). This traditional approach to mechanical ventilation intends to aggressively recruit and ventilate atelectatic lung units, but may risk overdistention of the normal lung units. Thus, large TVs may cause a decrease in Paco2, respiratory alkalosis, cardiovascular impairment, and excessive stretch of nondependent lung regions (2,16,17). Furthermore Bardoczky et al. (16) demonstrated that very large TVs do not improve oxygenation in obese patients.
However, even the use of positive end-expiratory pressure to increase FRC and improve oxygenation in obese patients is questionable (2,5). Although the use of positive end-expiratory pressure is of proven value for improving oxygenation in many situations involving respiratory failure, its role in anesthetized patients is controversial. In normal subjects, positive end-expiratory pressure can reduce the atelectasis but not necessarily the shunt (18); however, recently Pelosi et al. (19) claimed that positive end-expiratory pressure can improve oxygenation and respiratory mechanics in obese patients. Nevertheless, a possible detrimental effect of positive end-expiratory pressure on the oxygenation of obese patients has been described by Salem (20).
In this study performed during upper abdomen surgery, we used the RTP to counteract the weight of the abdominal contents and the effects of the retractors on the diaphragm. A wide P(A−a)o2 was observed in all of our patients in every phase, with a further significant increase during Phase 3; this worsening seems related to the application of subcostal retractors, which may cause a further decrease of FRC and a more limited movement of the diaphragm during mechanical ventilation. In Phase 4, with the patients placed in RTP without removing the retractors, oxygenation indexes improved, and P(A−a)o2 returned toward the baseline values.
As for respiratory mechanics, RTP determined a significant increase in the compliance that reached a level higher than baseline; the slopes of volume-pressure relationships in supine postures were less than that in RTP (Table 3). The increased compliance obtained by RTP and steeper volume/pressure regression lines suggest a recruitment of alveolar units and therefore an increase of FRC; thus the operating compliance could be improved by increasing end expiratory volume toward the more compliant range.
A limitation of our study might be the lack of the direct measure of FRC. However, because the reduction in FRC is most likely responsible for the decreased Ctot during general anesthesia, it is reasonable to argue that the increase of Ctot obtained with RTP can be related to an increased FRC (13,18). However, despite this significant increase in compliance, well above baseline values, P(A-a)o2 did not decrease much.
A weak correlation was found between compliance and P(A−a)o2 (r = −0.32;P <0.05; r = −0.45;P <0.05), meaning that other factors play a significant role in determining gas exchange efficiency.
As for hemodynamic factors, it is possible that RTP may compromise cardiovascular function by reducing venous return. Therefore, the beneficial effects of RTP on Pao2 could be offset by a decreased cardiac output. However, obese subjects show a reduced venous compliance and a smaller decrease of the central blood volume and of the cardiac stroke volume during orthostatic stress (21). Moreover, even if extensive hemodynamic monitoring has not been performed, no clinically relevant cardiovascular change was noted in our study.
Another reasonable explanation for this weak relationship between compliance and P(A−a)o2 could be the redistribution of pulmonary blood flow toward less-ventilated dependent zones along a gravitational gradient (22); so reversing the decrease in lung volume with RTP meets with limited success. In this regard, Heneghan et al. (23) showed that there was no improvement in oxygenation when lung volumes were increased significantly by RTP (head up 30°) in normal anesthetized subjects.
However, in our series, other than P(A−a)o2 values significantly wider than those found by Heneghan et al. (23) in normal subjects (P < 0.01), we found a correlation between P(A−a)o2 values of Phase 3 and the improvement in oxygenation obtained with RTP (r = −0.64;P < 0.001) (Figure 3); so the improvement in oxygenation obtained with RTP is greater when P(A−a)o2 is wider. This relationship, as well as the different type of patients, could explain the difference with Heneghan et al’s (23) study.
Moreover, in upper abdomen surgery of obese subjects, the exposure of the operative field creates major problems, and the use of a fixed-support retractor system greatly facilitates the surgeon (10). Like any procedure that increases the subdiaphragmatic pressure, it may make a further decrease in FRC and pulmonary compliance leading to hypoxemia (2). In this regard, the RTP offers potential advantages; it ameliorates the oxygenation indexes, exposes at best the subdiaphragmatic region, and allows mechanical ventilation with safe levels of airway pressures.
In conclusion, our data suggest that RTP is a simple and safe intraoperative posture for obese patients and offers some cardiorespiratory advantages during upper abdominal surgery.
We express our thanks to Dr. A. Ceccarelli for his statistical analysis of original data presented in this article.
1. Winer J, Brodsky JB, Merrell RC. Massive obesity and arterial oxygenation. Anesth Analg 1981; 60: 691–3.
2. Øberg B, Poulsen TD. Obesity: an anesthetic challenge. Acta Anaesthesiol Scand 1996; 40: 191–200.
3. Hickey RF, Visick WD, Fairley HB, Fourcade HE. Effects of halothane on functional residual capacity and alveolar-arterial oxygen tension difference. Anesthesiology 1973; 38: 20–4.
4. Rehder K, Marsh M. Respiratory mechanics during anesthesia and mechanical ventilation. In: Macklem PT, Head J, eds. Handbook of physiology section 3, volume III: Mechanics of breathing part 2. Bethesda MD: American Physiological Society, 1986: 737–52.
5. Shenkman Z, Shir Y, Brodsky JB. Perioperative management of the obese patient. Br J Anaesth 1993; 70: 349–59.
6. Buckley FD. Anaesthesia for the morbidly obese patient. Can J Anaesthesiol 1994; 41: R94–100.
7. Dumont L, Mattis M, Mardirosoff C, et al. Changes in pulmonary mechanics during laparoscopic gastroplasty in morbidly obese patients. Acta Anaesthesiol Scand 1997; 41: 408–13.
8. Pelosi P, Croci M, Ravagnan I, et al. Respiratory system mechanics in sedated, paralyzed, morbidly obese patients. J Appl Physiol 1997; 82: 811–8.
9. Damia G, Mascheroni D, Croci M, Tarenzi L. Perioperative changes in functional residual capacity in morbidly obese patients. Br J Anaesth 1988; 60: 574–8.
10. Buchwald H. Three helpful techniques for facilitating abdominal procedures, in particular for surgery in the obese. Am J Surg 1998; 175: 63–4.
11. Roothen HU, Sporre B, Engberg G, et al. Atelectasis and pulmonary shunting during induction of general anaesthesia: can they be avoided? Acta Anaesthesiol Scand 1996; 40: 191–200.
12. Nunn JF. Effects of anaesthesia on respiration. Br J Anaesth 1990; 65: 54–62.
13. Nunn JF. Respiratory aspects of anaesthesia. In: Nunn JF, eds. Applied physiology. 4th ed. Oxford: Butterworth-Heinemann, 1993: 384–417.
14. Pelosi P, Croci M, Ravagnan I, et al. The effects of body mass index on lung volumes, respiratory mechanics, and gas exchange during general anesthesia. Anesth Analg 1998; 87: 654–60.
15. Tsueda K, Debrand M, Zeok SS, et al. Obesity supine death syndrome: reports of two morbidly obese patients. Anesth Analg 1978; 58: 345–7.
16. Bardoczky GI, Yernault JC, Houben JJ, d’Hollander AA. Large tidal volume ventilation does not improve oxygenation in morbidly obese patients during anaesthesia. Anesth Analg 1995; 81: 385–8.
17. MacIntyre NR. Minimizing alveolar stretch injury during mechanical ventilation.
18. Tockics L, Hedenstierna G, Strandberg Å, et al. Lung collapse and gas exchange during general anesthesia: effects of spontaneous breathing, muscle paralysis, and positive end-expiratory pressure. Anesthesiology 1987; 66: 157–67.
19. Pelosi P, Ravagnan I, Giurati G, et al. Positive end-expiratory pressure improves respiratory function in obese but not in normal subjects during anesthesia and paralysis. Anesthesiol 1999; 91: 1221–31.
20. Salem MR. Does PEEP improve intraoperative arterial oxygenation in grossly obese patients? Anesthesiology 1978; 48: 280–2.
21. Stepniakowsky K, Egan BM. Additive effects of obesity and hypertension to limit venous volume. Am J Physiol 1995; 268: R562–8.
22. Pelosi P, Croci M, Calappi E., et al. Prone positioning improves pulmonary function in obese patients during general anesthesia. Anesth Analg 1996; 83: 578–83.
© 2000 International Anesthesia Research Society
23. Heneghan CPH, Bergman NA, Jones JG. Changes in lung volume and (PAO2
) during anaesthesia. Br J Anaesth 1984; 56: 437–45.