Intraoperative Arterial Oxygenation in Obese Patients ROBERT W. VAUGHAN, M.D.,* LESLIE WISE, M.D.t
Although obese patients have been shown to represent a particularly high risk group with respect to hypoxemia both pre and postoperatively, no data exist to delineate the intraoperative arterial oxygenation pattern of these patients. Furthermore, no one has studied the effects of a change in operative position or a subdiaphragmatic laparotomy pack on arterial oxygenation (Pao2). Sixty-four adults undergoing jejunoileal bypass for morbid exogenous obesity, with a mean weight of 142.0 + 31.4 kg and a mean age of 33.3 + 10.4 years, were studied. Twentyfive patients (Group I) were maintained in the supine position throughout the operative procedure, while the remaining 39 patients (Group II) were changed to a 15° head down position 15 minutes after a control blood sample was taken. Four additional markedly obese patients were studied to determine the effect of an abdominal pack of Pao2 values. The following findings were demonstrated: 1) 40%o oxygen did not uniformly produce adequate arterial oxygenation for intraabdominal surgery in otherwise healthy obese patients; 2) placement of a subdiaphragmatic abdominal laparotomy pack without a change in operative position resulted in a consistent fail in Pao2 in each patient to less than 65 mm Hg even though 40% oxygen was being administered; and 3) a change from supine to a 15° head down operative position resulted in a significant (P < 0.001) reduction in mean Pao, (73.0 + 26.3 mm Hg). Seventy-seven per cent of these patients demonstrated Pao2 values of less than 80 mm Hg on 40% oxygen. Because of these findings, serious consideration should be given to the routine use of the Trendelenberg position intraoperatively in obese patients. However, if one elects this posture, prudence would dictate careful monitoring and maintenance of arterial oxygenation. Certainly, in obese patients, the intraoperative combination of the head down position and a subdiaphragmatic laparotomy pack should be avoided. In addition, since our data were collected in obese but otherwise healthy, young patients free of cardiorespiratory disease, special attention should be directed at the continuous measurement of arterial oxygenation in the older obese patient with either intrinsic Submitted for publication November 10, 1975. * Department of Anesthesiology, University of Arizona Medical Center, Tucson, Arizona, 85724. t Department of Surgery, Long Island Jewish-Hillside Medical Center, New Hyde Park, New York, 11040 and the State University of New York at Stoney Brook, Stony Brook, New York.
35
From the Departments of Anesthesiology and Surgery, Washington University School of Medicine, St. Louis, Missouri, 63110
dysfunction of vital organs (heart, lung, liver, kidney) or surgical disorders (peritonitis, sepsis).
IN A PREvious communication we have shown that obese patients are prone to develop severe reductions in arterial oxygenation (Pao2) following intra-abdominal operations. This postoperative hypoxemia may reach dangerous levels during postoperative days one through four.28 Subsequently, we have demonstrated that in obese patients the type of abdominal operative incision is an important factor influencing the postoperative hypoxemia. There was a more significant and prolonged reduction in arterial oxygen tension in the vertical as opposed to the transverse incision group.29 In addition, we have studied the effect of position on postoperative gas exchange. There was a statistically significant decrease in the PaO2 in the supine versus the semirecumbent position on postoperative days one and two.30 To our knowledge, this is the first study on the intraoperative arterial oxygenation pattern in obese patients undergoing abdominal operations; also included in the study is the effect of change in operative position and the effect of subdiaphragmatic laparotomy packs on arterial oxygenation. Clinical Material and Methods
Sixty-four morbidly obese adult patients without clinical evidence of cardiopulmonary disease were studied while undergoing elective jejunoileal bypass. Morbid obesity was defined as at least 125 pounds in excess of the ideal weight for the particular height.21 Informed consent was obtained from each patient. Twenty-five patients
VAUGHAN AND WISE
36
Ann. Surg. * July 1976
TABLE 1. Physical Characteristics of 64 Obese, Adult Patients Sex
Group I (supine position) A (transverse incision) B (vertical incision) 11 (15° head down position) A (transverse incision) B (vertical incision) *
Mean
+
Weight/Height
Number
(M/F)
Age* (yrs)
11 14
2/9 0/14
29.3 ± 2.2 33.2 ± 2.1
148.0 ± 10.5 136.2 ± 5.3
169 ± 4 167 ± 1
0.87 ± .05 0.81 ± .03
22 17
3/19 2/15
33.1 ± 1.6 37.4 ± 1.9
144.0 ± 5 139.7 ± 5.7
167 ± 1 164 ± 2
0.87 ± .03 0.85 ± .03
Weight*
(kg)
Height*
(cm)
Ratio* (kg/cm)
SEM.
(Group I) were maintained in the supine position throughout the operative procedure, while the remaining 39 patients (Group II) were changed to a 150 head down position (legs remaining straight) 15 minutes after the control blood sample was taken. Each group was further subdivided on the basis of the type of abdominal operative incision as follows: transverse (A) or vertical (B). The distribution of patients in these four groups, according to physical characteristics, is presented in Table 1. Anesthesia was induced intravenously with 2.5% sodium thiopental (dose range 250 to 600 mg) following premedication with intramuscular Innovar (1.5-2 ml) and diphenhydramine (50-75 mg). Each patient was pretreated with a nondepolarizing muscle relaxant (gallamine 20 mg), placed in a 100 head up position and given a rapid intravenous induction sequence with cricoid pressure (Sellick maneuver25). All patients were intubated with cuffed endotracheal tubes to insure an airtight fit. Intubation was facilitated by succinylcholine (120-140 mg). Anesthesia was maintained with a semiclosed system using nitrous oxide and oxygen of known concentrations (Beckman 02 analyzer); muscle relaxation was provided by intermittent injections of pancuronium. Halothane (0.5 per cent inspired) was used for anesthesia. Ventilation was controlled with a Hopkins Emerson ventilator. The tidal volume in these patients ranged from 700 to 1,000 ml, at respiratory frequencies ranging from 16 to 22 per minute. Fresh gas flow in liters per minute remained constant at 3:2 (nitrous oxide: oxygen). Paco2 was set after anesthetic induction at 40 mm Hg (S.D. 2.0) by adjusting respiratory frequency. Once adjusted at the beginning of the procedure, the pattern of ventilation (tidal volume and rate) remained constant throughout the study period. The constancy of tidal volume delivered was periodically checked with a ventilometer. No deep breaths were administered before the study period. However, at the end of the study period of constant ventilation, passive hyperinflation of the lungs (sighs) were carried out with the anesthesia rebreathing bag, always using the anesthetic mixture given at the time. An airway pressure of 25 to 30 cm H20
maintained for approximately 10 seconds for each sigh, usually resulting in exhaled tidal volumes of 1500 ml. Five minutes after the three consecutive inflations, which were two or three minutes apart, arterial blood samples were drawn. Body temperature was measured continuously with a tympanic membrane thermistor. By clinical criteria the circulatory status as assessed continuously by electrocardiogram and intra-arterial pressure remained stable in all patients during the study period. The depth of anesthesia was monitored by the usual clinical guides of blood pressure, pulse, and response to operation. An attempt was made to keep the depth of anesthesia as was
light as possible. In all patients the period of study began after the self-retaining intra-abdominal retractors had been in position for 20 minutes, usually 30 minutes after the skin incision had been made. Thus anesthesia and artificial ventilation had been administered for approximately 45 to 60 minutes prior to the start of the study period. Nitrous oxide uptake was considered constant at this time.14 Abdominal packings were not used during this study except for the four additional patients described in Table 3. After each gas mixture had been administered for 10 minutes, 3 ml of arterial blood was withdrawn from an indwelling radial artery cannula into a plastic syringe wet with heparin. Syringes were capped and stored in ice for approximately 15 to 30 minutes before analysis by the same research technician in our laboratory. Arterial pH, oxygen tension, and carbon dioxide were analyzed in each sample. The arterial PO2, PCO2 and pH determinations were performed at 37 C and where appropriate, values were corrected to the patient's temperature.18 Four additional markedly obese patients were studied to determine the effect a laparotomy pack positioned between the undersurface of the diaphragm and dome of the liver (subdiaphragmatic) on PaO2 values. A cotton pack measuring 45 cm square of dry weight 30 gm was employed. These individuals were undergoing an incidental cholecystectomy prior to jejunoileal bypass;
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ARTERIAL OXYGENATION IN OBESE PATIENTS
37
TABLE 2. Arterial Oxygen Tension (Mean + S.D. ) Measured in mm Hg for 64 Morbidly Obese Patients During Surgery While Breathing 40 Per Cent Oxygen. Time in Minutes is With Reference to Position Change (0 Time): Before (-) and After (+) -15
Time (min.)
(control)
0
+10
+45
Group I Peritoneum Open Incision: No Position Change A (transverse) 139 33 135 ±41 B (vertical) 119 41 111±37 Group II Incision: Position Change A (transverse) 79 29+ 123 ±33 B (vertical) 114 28 68 12+
+ 115*
Post-sigh
Peritoneum Closed 154 127
46 40
135 124
36 42
158 164
45+ 38+
122 110
30 30
114 105
27 28
142 148
31+ 45+
* Mean time after position change (S.D. = 16 minutes). Statistically significant (P < 0.001) from control value using Student's paired t test.
+
performed with the patient supine without change in operative position. Control Pa02 values were obtained in a similar fashion to the previously described 64 obese patients. Each Pa,0 value was determined after 10 minutes equilibration at the desired oxygen concentration. In each patient, the period of study began after the self-retaining intra-abdominal retractors had been in position for 20 minutes, usually 30 minutes after the skin incision had been made. Statistical analysis was conducted using Student's t test for paired data. Control Pao, values were defined as those obtained 15 minutes prior to change to the 15° head down position. Each patient served as his own control. Student's t test for means of two sample groups was used to compare physical characteristics between surgery was
a
the actual operative times were remarkably uniform. Probably this finding reflects the identical operative procedure being performed by the one team. The "postsigh" sample was obtained before abdominal wall closure
completed. Except for the post-sigh samples, the Pao, values with the vertical incision were consistently lower than with the transverse incision in both groups (Table 2). This relationship persisted throughout the study, but was never statistically significant. In Group I Pan, values showed no significant change with time except post-sigh. This latter value was statistically above control PaO, value was
Meons± SE.M.
groups. 170
Results
Physical characteristics and patient groupings are as shown in Table 1. One should note that this patient sample is quite young (overall mean age: 33.3 years) and markedly obese (overall mean weight: 142 kg) with a mean weight/height ratio (0.85) of more than twice the normal. 10 Both within and between groups the physical characteristics shown in Table 1 are statistically similar (P > 0.1). Table 2 reveals that the overall mean control Pao, in the supine position is 124 mm Hg. This value is lower than would be predicted for non-obese patients under comparable anesthetic conditions.3 Pao, values intraoperatively with time are presented numerically in Table 2 and graphically in Figure 1. "0" times refers to a change in position in Group II patients. The + 115 minute time represents the mean value taken 10 minutes after peritoneal closure. It should be noted in Table 2 that the preinflation (sigh) sample reveals a variability in time from "0" time. Obviously, both the time for the surgical procedure and abdominal wall closure varied among the 64 patients. It is interesting, however, that
160 150
140
60
810
So 60 50
-15
0
10
45
Time (rrinutes)
115+
post
sigh
FIG. 1. Arterial oxygen tension (mean + S.E.) in 64 morbidly obese patients during anesthesia and surgery. All values were obtained at 40%o inspired oxygen concentration. Solid lines present Pao, values with time for Group I patients (i.e. no change in operative position); interrupted lines are comparable values for those patients in Group II (i.e. position changed to 15' head down at "O" time). Operative incision is indicated by circles: closed circle = transverse, open circle = vertical. The solid horizontal line at 80 mm Hg (Pao0) represents the lower limits of normal oxygenation intraoperatively.2f Change in operative position (interrupted lines) resulted in a statistically significant (P < 0.001) fall in Pao, values independent of the operative incision.
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Ann. Surg. * July 1976
TABLE 3. Influence of a Subdiaphragmatic Abdominal Laparotomy Pack on Arterial Oxygenation in Four Additional Obese Supine Anesthetized Patients During Cholecystectomy Abdominal Pack
Case no.
Age (yrs)
1 2 3 4
26 31 32 23
Remove Pack
Weight (kg)
Control
Sex
Height (cm)
40%o 02
40%o 02
99.5% 02
40%o 02
99.5% 02
F F M M
0.75 1.03 0.85 1.18
97 82 123 98
58 60 64 63
78 88 85 97
83 86 94 100
210 260 253 250
(P < 0.001) in both the transverse and vertical incision
to less than 80 mm
Hg when measured 10 minutes after position change. Although this level may be acceptable pre- or postoperatively with the patient breathing room air, intraoperatively many variables supervene which may further reduce arterial oxygenation. Certain of these variables (age, physical status, abdominal packing, type of surgery, and inspired oxygen concentration) were purposely controlled for this study. This selection is not possible in the usual surgical patient. Considering the variables of age and physical status, our subjects were young, otherwise healthy obese patients without associated cardiopulmonary disease. Although retractors were in place, no abdominal packs were used to facilitate surgical exposure; packing as described in this paper, however, may be helpful to expose the gall bladder in an obese patient during cholecystectomy. Indeed, during this investigation four additional patients underwent cholecystectomy; in these patients an abdominal laparotomy pack was placed above the liver to simultaneously facilitate exposure and evaluate its effect on arterial oxygenation. Abdominal packing even in the supine position resulted in precipitous falls in Pa02. With only one abdominal pack, Pa02 values were all less than 65 mm Hg on 40% oxygen. At this range of PaO2, hemoglobin saturation begins to function on the lower, steep portion of the hemoglobin-oxygen dissociation curve. Small decreases in Pac2 cause large falls in arterial oxygen content (Ca02).3 Changing to 99.5 per cent inspired oxygen allowed an improvement in Pa02 (Table 3), and thereby increased C502. However, tissue oxygen delivery depends not only on the Cac,, but also on the level of cardiac output.23 By Discussion changing to 99.5% oxygen and excluding nitrous oxide, Our results show that in 64 adult, morbidly obese, one is forced to increase the dose of potent inhalation supine patients the mean control Pao, value (124 + 43 agent (halothane) required for maintenance of anesthesia. mm Hg) was less than the predicted value for non- While an increased Ca02 may be gained with the added obese patients (i.e. 200-240 mm Hg).3 Fourteen per inspired oxygen, the price to the patient in terms of cent of these supine, anesthetized patients had Pao2 reduced tissue oxygen delivery due to the decreased values of less than 80 mm Hg during ventilation with 40 cardiac output13 may be unacceptable. per cent oxygen. With the assumption of 150 head down position, there was a further marked fall in Pao2 to a Mechanism of Hypoxemia: Abdominal Packs mean value of 73 mm Hg. (S.D. 26.3). Seventy-seven In this study, the insertion of an abdominal pack per cent of Group II patients experienced a fall in Pao2 under the diaphragm resulted in a fall of PaO2 from subgroups. In group II the post-sigh Pao2 values were again significantly elevated (P < 0.001) above control in both the vertical and transverse incision subgroups. In addition, in Group II patients 10 minutes after a change to the 150 head down position, there was a statistically significant (P < 0.001) fall in Pao2 values. This reduced Pao, value was independent of the operative incision being used. By 45 minutes after position change, the Pao2 value for both incision subgroups in Group II had returned to control value. Since Groups I and II were shown to have statistically comparable physical characteristics, the observed difference between the groups is due to the position change. Table 3 presents the effect of an abdominal pack interposed between the undersurface of the diaphragm and dome of the liver on the Pao, values in four additional markedly obese patients. Packing alone without any change in operative position markedly reduced arterial oxygenation. Pao2 measurements on 40%o oxygen 10 minutes after packing consistently fell in each patient to less than 65 mm Hg. Although there was a significant improvement in Pao2 with 99.5% oxygen, these latter values still represent a large intrapulmonary shunt. Return to control Pao2 values on 40% oxygen was only possible with pack removal. Judged by Paco2 criteria, ventilation was adequate throughout the study period. There was no statistically significant difference from control with time in either Paco2, pH, or temperature in either groups.
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ARTERIAL OXYGENATIION IN OBESE PATIENTS
control levels. A possible explanation for this finding could be a fall in cardiac output with an increase in arterial to venous oxygen content difference. Although cardiac output was not measured, by clinical criteria the circulatory status remained stable in these four patients. A more likely explanation for impaired oxygenation in the presence of adequate ventilation with oxygen-enriched mixtures is venous admixture (physiologic shunting).5 Three possible mechanisms may be responsible for this phenomenon. First, blood is known to bypass gas exchange areas via normal anatomic shunts which include the bronchial, pleural, and Thebesian veins. Normally, this constitutes only about 3 per cent of the cardiac output,2 and is not influenced during operation. A second possible mechanism is the occurrance of regional hypoventilation in relation to pulmonary capillary blood flow. When 100% oxygen is given, these ventilation-perfusion (V/Q) abnormalities no longer contribute to the venous admixture effect.17 Consequently, V/Q could not be responsible for the total reduction in Pao2 demonstrated. The third possible cause of a right-to-left shunt is atelectasis (continued perfusion of these non-ventilated alveoli). When atelectatic areas are perfused they must contribute to shunt whatever the inspired mixture. The added effect of abdominal packing to reduce PaO2 intraoperatively is apparent. Although atelectasis (perfusion without ventilation) is the most likely explanation, one cannot rule out changes in cardiac output or the distribution of blood flow incidental to pack placement. Nevertheless, whatever the cause of the arterial hypoxemia secondary to packs, one should be cognizant of the physiologic consequences of placing packs above the liver in the obese patient. It should be noted that all the operations in this study were elective procedures on obese patients. An emergency operative procedure with possible associated fluid and electrolyte disturbances, peritonitis, and preexistent cardiopulmonary dysfunction may all exacerbate the observed hypoxemia. However, even without these variables to further reduce arterial oxygenation, when operative position was changed to 150 head down (Table 2), 23% of our patients (9/39) had PaO2 values below 60 mm Hg. In addition, one 47-year-old woman (weight/ height ratio = 1.07) with change in position experienced a fall in Pao, to 45 mm Hg. Also, two patients with the position change and placement of retractors necessary for surgical exposure experienced a precipitous fall in mean systolic blood pressure from 128 to 50 mm Hg. Each of these episodes was relieved by repositioning of the retractors away from the inferior vena cava. For adequate surgical exposure and adequate blood pressure maintenance, it was necessary in each patient to return them to the supine position. Clearly, no margin for PaO2
39 changes intraoperatively is allowed at values below 80 mm Hg. Although arbitrary, this value has been stated previously to represent the borderline value between normal and abnormal oxygenation for non-obese
patients intraoperativelyA26
The levels of arterial oxygen tension measured in our study give some cause to question the practice of administering 30 to 33% oxygen during intra-abdominal operations in obese patients. Slater26 previously suggested a minimum of 33% oxygen administration during intraabdominal surgery. However, the weights and heights of the patients in his study were not given. Our findings demonstrate impaired gas exchange in obese patients when 40o oxygen concentration is administered, even with large-tidal-volume ventilation and maintenance of normocarbia. Previous studies have shown already the adverse effects of hypocapnia on cardiac output27 and thereby the reduced arterial oxygenation.15
Mechanism of hypoxemia: Postural Change The final question that arises from our results is the mechanism of the demonstrated hypoxemia. Impaired gas exchange during spontaneous and controlled ventilation has been demonstrated in anesthetized patients compared with the unanesthetized state.16'24 Although the mechanisms producing this defect are not clear, functional residual capacity (FRC) during anesthesia is known to be diminished compared with the values before induction.10'19 As lung volume is reduced from total lung capacity, a volume at which airways start to close [the closing volume (CV)] is reached. Behind the closed airways, gas will be trapped6 and will come into equilibrium with venous blood, producing venous admixture in the pulmonary circulation. The relationship of FRC to CV, therefore, is critical to gas exchange and thereby arterial oxygenation. This phenomenon is important during surgical operations because both anesthesia10 and the supine position9 reduce FRC. General anesthesia of obese subjects, who preoperatively tend to have small FRC's,4 and also older individuals, in whom CV is increased,11 will be associated with a greater likelihood of airway closure and gas trapping. In addition, Couture et al.7 have shown that in conscious subjects in the supine position the degree of airway closure and gas trapping is greater in obese subjects. Presumably, this is because the weight of the thoracic cage reduces lung volume. Therefore, in some obese subjects, the reduction of FRC accompanying anesthesia might place FRC below CV, cause increased trapped gas, and thereby result in arterial hypoxemia due to this venous admixture. Don11 further clarified the effect of body configuration on gas exchange. He showed that an individual with an increased wieght/height ratio (i.e. relatively obese)
40
VAUGHAN AND WISE
would be at a particular disadvantage in the supine position; CV would increase in relation to FRC as the ratio of weight to height increased. Our further consideration of pulmonary gas exchange in the obese, anesthetized patient involved a change from the supine to a 150 head down position. Arterial oxygen tension measured 10 minutes after position change with 40% inspired oxygen revealed a mean decrease from control of 43 mm Hg. Three previous communications involving unsedated, conscious, non-obese subjects should be examined when looking at this effect of position change (from seated to supine) on lung volumes and gas exchange. In 80 normal subjects, LeBlanc et al.20 have shown important alterations in the relationship of airway closure to FRC associated with the change from the seated to the supine position. They pointed out that in the supine position, which is regularly accompanied by a fall in FRC, closing volume (CV) is within the tidal range from the age of 44 years onward. Craig et al.8 further considered closing volume and its relationship to gas exchange in seated and supine positions. He showed that FRC fell in the supine position, whereas CV was unchanged. When CV involved tidal volume to a greater extent in the supine posture, gas exchange deteriorated. While age and weight have both been considered as factors affecting gas exchange, Craig's data suggest that they do so by way of their effects on CV. Finally, Don et al." studying 30 normal subjects were able to show that the supine position, as compared with the sitting position, was associated with a reduced FRC and a greater volume of trapped gas when CV was greater than FRC. Therefore, the reality of airway closure and its detrimental effect on gas exchange in the supine position were confirmed. The further effect of a change from supine to 150 head down position on airway closure and lung volumes was studied by Craig.9 In 10 normal, unanesthetized, non-operated males with position change, there was a statistically significant additional reduction in total lung capacity and FRC; no change occurred in closing volume. Body position, therefore, has an important effect on the critical relationship between the CV and FRC, and hence on the functional consequences of airway closure. Consequently, our findings of impaired gas exchange with position change in obese, anesthetized patients is understandable.
Ann.
Surg. * July 1976
would imply that in obese patients with a greater likelihood of airway closure and gas trapping,7 the effect of obesity on gas exchange under the conditions of this study is partially reversible with passive, sustained hyperinflations. Don et al,'2 studying non-obese, anesthetized patients, questioned the value of intermittent hyperinflation to restore lung volume. In that study sighs did not affect FRC, nor did the volume of trapped gas increase significantly. Perhaps obese patients can better benefit from a sigh to restore more optimum ventilation-perfusion relationships and thereby arterial oxygenation. We have established that there is no progressive decrease in arterial oxygenation with time during anesthesia with large-tidal-volume ventilation, unless one alters the surgical position (Table 2, Fig. 1). Don et al.12 have shown in supine, anesthetized, adults during spontaneous ventilation that there is no progressive decrease in FRC with time, and therefore, the intrapulmonary shunt should not progressively increase. Nunn22 found minimal temporal changes in arterial oxygenation during anesthesia when normocarbia was maintained. Visick et al.31 employing controlled ventilation with small to large tidal volumes in anesthetized adults observed a slight but significant improvement in arterial oxygenation with time; this finding was regardless of the sequence of ventilatory patterns. They postulated these findings represent a combination of increasing cardiac output,'3 and less oxygen consumption due to falling body temperature (mean temperature change throughout their study: 1.6 C). Although the former possibility may pertain in our study, the latter explanation is not tenable. The mean temperature change from 37°C throughout the present study was 0.30C. A more plausible explanation for our observed improvement in mean Pa0. with time after position change would be the effect of controlled, large volume ventilation on re-expanding partially collapsed alveoli. An overall improvement in the distribution of ventilation with respect to perfusion would reduce venous admixture. Visick's study3' comparing the effects of tidal volume and end-expiratory pressure on pulmonary gas exchange during anesthesia lends credence to this postulate. Small volume ventilation (5 ml/kg or V5) decreases PaO2 by permitting airway closure. By exceeding closing volume at end inflation, large tidal volume (15 ml/kg or V15) or V5 plus continuous positive pressure (i.e. V5 + CPP) ventilates alveoli which otherwise would be Restoration of arterial oxygenation perfused but not ventilated. In addition, his finding of We employed passive hyperinflations (sigh) at the com- a positive correlation of decreasing Pao with increasing pletion of the study period. In spite of the 150 head degrees of obesity (i.e. elevated weight/height ratio) is down position, sighs improved arterial oxygenation; compatible with this explanation, since airway closure Pao2 was statistically elevated above control levels. This does increase with obesity.7 The beneficial effect of
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ARTERIAL OXYGENATION IN OBESE PATIENTS
41
V5 + CPP will be partially offset by the reduction in Acknowledgment cardiac output produced by the greater intrathoracic The authors wish to thank Miss Dorothy Hollander for technical pressure. Moreover, arterial oxygenation should and assistance and Mrs. Mary Rogers for her competent preparation of actually does improve when V15 replaces V5 + CPP. the manuscript. Therefore, the detrimental effects on oxygenation in the obese of spontaneous or small tidal volume (V5) ventilaReferences tion could be anticipated. 1. Anscombe, A. R.: Pulmonary Complications of Abdominal SurFinally, it has long been appreciated that breathing gery. 1st Ed. London, Lloyd-Luke (Medical Books), 1957, Chap. VIII. at low lung volumes secondary to obesity,3 pain,' or S. M., Criscitiello, A. and Grabovsky, E.: Components during general anesthesia,10'19 may be associated with 2. Ayres, of Alveolar-arterial 02 Difference in Normal Man. J. Appl. deficient pulmonary gas exchange. Atelectasis has been Physiol., 19:43, 1964. suggested as the likely mechanism affecting gas exchange, 3. Bates, D. V. and Christie, R. V.: Respiratory Function in Disease. An Introduction to the Integrated Study of the Lung. 1st Ed. although supporting evidence for this diagnosis has often Philadelphia and London, W. B. Saudners and Co., 1964, been lacking. Atelectasis can clearly cause the defects pp. 58, 65-66, 100-101. noted in these situations, but airway closure rates con- 4. Bedell, G. N., Wilson, W. R. and Seebohm, P. M.: Pulmonary Function in Obese Persons. J. Clin. Invest. 37:1049-1060, 1958. sideration as either the sole mechanism responsible, or 5. Bendixen, H. H., Egbert, L. D., Hedley-Whyte, J., et al.: as perhaps a primary mechanism which. then leads to Respiratory Care. St. Louis, C. V. Mosby Company, 1965; pp. 12-17. secondary atelectasis. E. J., Jr. and Macklem, P.: Airway Closure: DemonstraThe following conclusions are apparent from this 6. Burger, tion by Breathing 100 per cent Oxygen at Low Lung Volumes paper in morbidly obese patients: 1) Forty per cent and by N2 Washout. J. Appl. Physiol., 25:139-148, 1968. oxygen may not be adequate for intraabdominal surgery 7. Couture, J., Picken, J. J., Ruff, F., et al.: Demonstration of Airway Closure and Trapping of Air in the Recumbent Position in otherwise healthy obese patients; 2) A subdiaphragin Normal and Obese Subjects. Am. Roy. Coll. Phys. Surg. matic abdominal laparotomy pack without a change in Canada, 3:25, 1970. operative position seriously interferes with arterial 8. Craig, D. B., Wahba, W. M., Don, H. F. et al.: "Closing Volume" and Its Relationship to Gas Exchange in Seated and oxygenation; 3) Change from supine to a 150 head down Supine Positions. J. Appl. Physiol., 31:717-721, 1971. operative position resulted in a significant reduction 9. Craig, D. B., Wahba, W. M. and Don, H.: Airway Closure and Lung Volumes in Surgical Positions. Canad. Anaesth. Soc. J., in arterial oxygenation.
Clinical Implications
Serious consideration should be given to the routine use of the Trendelberg position intraoperatively in obese patients. It is recognized that a 150 head down position may facilitate surgery in these patients during some operative procedures (pelvic, genitourinary, jejunoileal bypass). However, if one elects this posture for the obese patient, prudence would dictate careful monitoring of arterial blood gases. If arterial hypoxemia ensues, supplementation with higher inspired oxygen concentration is mandatory. Certainly the combination of the Trendelenberg position and a subdiaphragmatic laparotomy pack should be completely avoided. Finally, since our data were collected in otherwise healthy, young, obese patients free of cardiorespiratory disease, special attention should be directed at the continuous measurement of arterial oxygenation in the older, obese patient. These individuals with either intrinsic dysfunction of vital organs (heart, lung, liver kidney) or surgical diseases (peritonitis, sepsis) would be a particularly high risk group with reference to oxygenation. Any intraoperative position change should be carefully considered and arterial oxygenation continuously assessed.
18:92-99, 1971. 10. Don, H. F., Wahba, M., Curadrado, L. and Kelkar, K.: The Effects of Anesthesia and 100 Per Cent Oxygen on the Functional Residual Capacity of the Lungs. Anesthesiology, 32:521529, 1970. 11. Don, H. F., Craig, D. B., Wahba, W. M. and Couture, J. G.: The Measurement of Gas Trapped in the Lungs at Functional Residual Capacity and the Effects of Posture. Anesthesiology, 35:582-590, 1971. 12. Don, H. F., Wahba, W. M. and Craig, D. B.: Airway Closure, Gas Trapping, and the Functional Residual Capacity during Anesthesia. Anesthesiology, 36:533-539, 1972. 13. Eger, E. I., II, Smith, N. T., Stoelting, R. K. et al.: Cardiovascular Effects of Halothane in Man. Anesthesiology, 32: 396-409, 1970. 14. Eger, E. I., II: A Mathematical Model of Uptake and Distribution, In Uptake and Distribution of Anesthetic Agents, Edited by Papper, E. M. and Kitz, R. J. New York, McGrawHill, 1963, Ch. 7. 15. Fairley, H. B.: The Effect of Hyperventilation on Arterial Oxygen Tension: A Theoretical Analysis. Can. Anaesth. Soc. J., 14: 87-93, 1967. 16. Froese, A. B. and Bryan, A. C.: Effects of Anesthesia and Paralysis on Diaphragmatic Mechanics in Man. Anesthesiology, 41: 242255, 1974. 17. Hedley-Whyte, J., Corning, H., Laver, M. B. et al.: Pulmonary Ventilation-Perfusion Relationships After Heart Valve Replacement or Repair in Man. J. Clin. Invest., 44:406, 1965. 18. Kelman, G. R. and Nunn, J. F.: Normograms for Correction of Blood Po2, PCO2, pH, and Base Excess for Time and Temperature. Appl. Physiol., 21:1484-1490, 1966. 19. Laws, A. K.: Effects of Induction of Anesthesia and Muscle Paralysis on Functional Residual Capacity of the Lungs. Can. Anaesth. Soc. J., 15:325-331, 1968. 20. LeBlanc, P., Ruff, F. and Milac-Enmili,- J.: Effects of Age and
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21. 22. 23. 24.
25. 26.
Body Position on "Airway Closure" in Man. J. Appl. Physiol., 28:448-451, 1970. Metropolitan Life Insurance Co., Table of Desirable Weights in Adults. In Documenta Geigy, Scientific Tables, (6th Edition), 1962; p. 624. Nunn, J. F., Bergman, N. A. and Coleman, A. J.: Factors Influencing the Arterial Oxygen Tension During Anesthesia with Artificial Ventilation. Br. J. Anaesth., 37:898-914, 1965. Nunn, J. F. and Freeman, J.: Problems of Oxygenation and Oxygen Transport during Haemorrhage. Anaesthesia, 19:206, 1964. Price, H. L., Cooperman, L. H., Warden, J. C. et al.: Pulmonary Hemodynamics during General Anesthesia in Man. Anesthesiology, 30:629-636, 1969. Sellick, B. A.: Cricoid Pressure to Control Regurgitation of Stomach Contents during Induction of Anesthesia. Lancet, 2:404-406, 1%1. Slater, E. M., Nilsson, S. E., Leake, D. M. D. et al.: Arterial
27. 28. 29. 30.
31.
Ann. Surg. * July 1976
Oxygen Tension Measurements during Nitrous Oxide-Oxygen Anesthesia. Anesthesiology, 26:642-647, 1965. Theye, R. A., Milde, J. M. and Michenfelder, J. D.: Effect of Hypocapnia on Cardiac Output during Anesthesia. Anesthesiology, 27:778-782, 1966. Vaughan, R. W., Engelhardt, R. C. and Wise, L.: Postoperative Hypoxemia in Obese Patients. Ann. Surg., 180:877, 1974. Vaughan, R. W. and Wise, L.: Choice of Abdominal Operative Incision in the Obese Patient: A Study Using Blood Gas Measurements. Ann. Surg., 181:829-835, 1975. Vaughan, R. W. and Wise, L.: Postoperative Arterial Blood Gas Measurements in Obese Patients: Effect of Position on Gas Exchange. Ann. Surg., 182:705-709, 1975. Visick, W. D., Fairley, H. B. and Hickey, R. F.: The Effects of Tidal Volume and End-expiratory Pressure on Pulmonary Gas Exchange during Anesthesia. Anesthesiology, 39:285-290, 1973.
Erratum The list of references following "Portosystemic Shunting in Patients with Primary Biliary Cirrhosis: A Good Risk Disease," by Joel L. Bauer, et al., Ann. Surg., 183:3:324, 1976, should have appeared as follows. References 1. Addison, T. and Gull, W.: On a Certain Affection of the SkinVitilgoidea a plana, B. Tuberosa. Guys Hosp. Rep., 7:265, 1851. 2. Ahrens, E. H., Jr., Payne, M. A. and Kunkel, H. G.: Primary Biliary Cirrhosis. Medicine, 29:299, 1950. 3. Child, C. G.: The Liver and Portal Hypertension. Philadelphia, W. B. Saunders Co., 1964. 4. Hanot, V.: La Cirrhosis Hypertrophique avec Icteric Chronique. Paris, Reuff and Cie, 1892. 5. Popper, H., and Schaffner, F.: Liver- Structure and Function. N.Y., Toronto, and London, McGraw Hill, 1957.
6. Popper, H., Elias. H. and Petty, D. E.: Vascular Pattern of the Cirrhotic Liver. Am. J. Clin. Pathol., 22:717, 1952. 7. Rubin, E., Schaffner, F. and Popper, H.: Primary Biliary Cirrhosis. Am. J. Pathol., 46:387, 1965. 8. Sherlock, S.: Primary Biliary Cirrhosis (Chronic Intrahepatic Obstructive Jaundice) Gastroenterology, 37:574, 1959. 9. Walker, J. G., Doniach, D., Roitt, I. M. and Sherlock, S.: Lancet 1:827, 1965. 10. Zeegen, R., Stansfeld, A. G., Dawson, A. M. and Hunt, A. H.: Bleeding Oesophageal Varices as the Presenting Feature in Primary Biliary Cirrhosis. Lancet, 2:9, 1969.
Although obese patients have been shown to represent a particularly high risk group with respect to hypoxemia both pre and postoperatively, no data exist to delineate the intraoperative arterial oxygenation pattern of these patients. Furthermore, no one has studied the effects of a change in operative position or a subdiaphragmatic laparotomy pack on arterial oxygenation (Pao2). Sixty-four adults undergoing jejunoileal bypass for morbid exogenous obesity, with a mean weight of 142.0 + 31.4 kg and a mean age of 33.3 + 10.4 years, were studied. Twentyfive patients (Group I) were maintained in the supine position throughout the operative procedure, while the remaining 39 patients (Group II) were changed to a 15° head down position 15 minutes after a control blood sample was taken. Four additional markedly obese patients were studied to determine the effect of an abdominal pack of Pao2 values. The following findings were demonstrated: 1) 40%o oxygen did not uniformly produce adequate arterial oxygenation for intraabdominal surgery in otherwise healthy obese patients; 2) placement of a subdiaphragmatic abdominal laparotomy pack without a change in operative position resulted in a consistent fail in Pao2 in each patient to less than 65 mm Hg even though 40% oxygen was being administered; and 3) a change from supine to a 15° head down operative position resulted in a significant (P < 0.001) reduction in mean Pao, (73.0 + 26.3 mm Hg). Seventy-seven per cent of these patients demonstrated Pao2 values of less than 80 mm Hg on 40% oxygen. Because of these findings, serious consideration should be given to the routine use of the Trendelenberg position intraoperatively in obese patients. However, if one elects this posture, prudence would dictate careful monitoring and maintenance of arterial oxygenation. Certainly, in obese patients, the intraoperative combination of the head down position and a subdiaphragmatic laparotomy pack should be avoided. In addition, since our data were collected in obese but otherwise healthy, young patients free of cardiorespiratory disease, special attention should be directed at the continuous measurement of arterial oxygenation in the older obese patient with either intrinsic Submitted for publication November 10, 1975. * Department of Anesthesiology, University of Arizona Medical Center, Tucson, Arizona, 85724. t Department of Surgery, Long Island Jewish-Hillside Medical Center, New Hyde Park, New York, 11040 and the State University of New York at Stoney Brook, Stony Brook, New York.
35
From the Departments of Anesthesiology and Surgery, Washington University School of Medicine, St. Louis, Missouri, 63110
dysfunction of vital organs (heart, lung, liver, kidney) or surgical disorders (peritonitis, sepsis).
IN A PREvious communication we have shown that obese patients are prone to develop severe reductions in arterial oxygenation (Pao2) following intra-abdominal operations. This postoperative hypoxemia may reach dangerous levels during postoperative days one through four.28 Subsequently, we have demonstrated that in obese patients the type of abdominal operative incision is an important factor influencing the postoperative hypoxemia. There was a more significant and prolonged reduction in arterial oxygen tension in the vertical as opposed to the transverse incision group.29 In addition, we have studied the effect of position on postoperative gas exchange. There was a statistically significant decrease in the PaO2 in the supine versus the semirecumbent position on postoperative days one and two.30 To our knowledge, this is the first study on the intraoperative arterial oxygenation pattern in obese patients undergoing abdominal operations; also included in the study is the effect of change in operative position and the effect of subdiaphragmatic laparotomy packs on arterial oxygenation. Clinical Material and Methods
Sixty-four morbidly obese adult patients without clinical evidence of cardiopulmonary disease were studied while undergoing elective jejunoileal bypass. Morbid obesity was defined as at least 125 pounds in excess of the ideal weight for the particular height.21 Informed consent was obtained from each patient. Twenty-five patients
VAUGHAN AND WISE
36
Ann. Surg. * July 1976
TABLE 1. Physical Characteristics of 64 Obese, Adult Patients Sex
Group I (supine position) A (transverse incision) B (vertical incision) 11 (15° head down position) A (transverse incision) B (vertical incision) *
Mean
+
Weight/Height
Number
(M/F)
Age* (yrs)
11 14
2/9 0/14
29.3 ± 2.2 33.2 ± 2.1
148.0 ± 10.5 136.2 ± 5.3
169 ± 4 167 ± 1
0.87 ± .05 0.81 ± .03
22 17
3/19 2/15
33.1 ± 1.6 37.4 ± 1.9
144.0 ± 5 139.7 ± 5.7
167 ± 1 164 ± 2
0.87 ± .03 0.85 ± .03
Weight*
(kg)
Height*
(cm)
Ratio* (kg/cm)
SEM.
(Group I) were maintained in the supine position throughout the operative procedure, while the remaining 39 patients (Group II) were changed to a 150 head down position (legs remaining straight) 15 minutes after the control blood sample was taken. Each group was further subdivided on the basis of the type of abdominal operative incision as follows: transverse (A) or vertical (B). The distribution of patients in these four groups, according to physical characteristics, is presented in Table 1. Anesthesia was induced intravenously with 2.5% sodium thiopental (dose range 250 to 600 mg) following premedication with intramuscular Innovar (1.5-2 ml) and diphenhydramine (50-75 mg). Each patient was pretreated with a nondepolarizing muscle relaxant (gallamine 20 mg), placed in a 100 head up position and given a rapid intravenous induction sequence with cricoid pressure (Sellick maneuver25). All patients were intubated with cuffed endotracheal tubes to insure an airtight fit. Intubation was facilitated by succinylcholine (120-140 mg). Anesthesia was maintained with a semiclosed system using nitrous oxide and oxygen of known concentrations (Beckman 02 analyzer); muscle relaxation was provided by intermittent injections of pancuronium. Halothane (0.5 per cent inspired) was used for anesthesia. Ventilation was controlled with a Hopkins Emerson ventilator. The tidal volume in these patients ranged from 700 to 1,000 ml, at respiratory frequencies ranging from 16 to 22 per minute. Fresh gas flow in liters per minute remained constant at 3:2 (nitrous oxide: oxygen). Paco2 was set after anesthetic induction at 40 mm Hg (S.D. 2.0) by adjusting respiratory frequency. Once adjusted at the beginning of the procedure, the pattern of ventilation (tidal volume and rate) remained constant throughout the study period. The constancy of tidal volume delivered was periodically checked with a ventilometer. No deep breaths were administered before the study period. However, at the end of the study period of constant ventilation, passive hyperinflation of the lungs (sighs) were carried out with the anesthesia rebreathing bag, always using the anesthetic mixture given at the time. An airway pressure of 25 to 30 cm H20
maintained for approximately 10 seconds for each sigh, usually resulting in exhaled tidal volumes of 1500 ml. Five minutes after the three consecutive inflations, which were two or three minutes apart, arterial blood samples were drawn. Body temperature was measured continuously with a tympanic membrane thermistor. By clinical criteria the circulatory status as assessed continuously by electrocardiogram and intra-arterial pressure remained stable in all patients during the study period. The depth of anesthesia was monitored by the usual clinical guides of blood pressure, pulse, and response to operation. An attempt was made to keep the depth of anesthesia as was
light as possible. In all patients the period of study began after the self-retaining intra-abdominal retractors had been in position for 20 minutes, usually 30 minutes after the skin incision had been made. Thus anesthesia and artificial ventilation had been administered for approximately 45 to 60 minutes prior to the start of the study period. Nitrous oxide uptake was considered constant at this time.14 Abdominal packings were not used during this study except for the four additional patients described in Table 3. After each gas mixture had been administered for 10 minutes, 3 ml of arterial blood was withdrawn from an indwelling radial artery cannula into a plastic syringe wet with heparin. Syringes were capped and stored in ice for approximately 15 to 30 minutes before analysis by the same research technician in our laboratory. Arterial pH, oxygen tension, and carbon dioxide were analyzed in each sample. The arterial PO2, PCO2 and pH determinations were performed at 37 C and where appropriate, values were corrected to the patient's temperature.18 Four additional markedly obese patients were studied to determine the effect a laparotomy pack positioned between the undersurface of the diaphragm and dome of the liver (subdiaphragmatic) on PaO2 values. A cotton pack measuring 45 cm square of dry weight 30 gm was employed. These individuals were undergoing an incidental cholecystectomy prior to jejunoileal bypass;
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ARTERIAL OXYGENATION IN OBESE PATIENTS
37
TABLE 2. Arterial Oxygen Tension (Mean + S.D. ) Measured in mm Hg for 64 Morbidly Obese Patients During Surgery While Breathing 40 Per Cent Oxygen. Time in Minutes is With Reference to Position Change (0 Time): Before (-) and After (+) -15
Time (min.)
(control)
0
+10
+45
Group I Peritoneum Open Incision: No Position Change A (transverse) 139 33 135 ±41 B (vertical) 119 41 111±37 Group II Incision: Position Change A (transverse) 79 29+ 123 ±33 B (vertical) 114 28 68 12+
+ 115*
Post-sigh
Peritoneum Closed 154 127
46 40
135 124
36 42
158 164
45+ 38+
122 110
30 30
114 105
27 28
142 148
31+ 45+
* Mean time after position change (S.D. = 16 minutes). Statistically significant (P < 0.001) from control value using Student's paired t test.
+
performed with the patient supine without change in operative position. Control Pa02 values were obtained in a similar fashion to the previously described 64 obese patients. Each Pa,0 value was determined after 10 minutes equilibration at the desired oxygen concentration. In each patient, the period of study began after the self-retaining intra-abdominal retractors had been in position for 20 minutes, usually 30 minutes after the skin incision had been made. Statistical analysis was conducted using Student's t test for paired data. Control Pao, values were defined as those obtained 15 minutes prior to change to the 15° head down position. Each patient served as his own control. Student's t test for means of two sample groups was used to compare physical characteristics between surgery was
a
the actual operative times were remarkably uniform. Probably this finding reflects the identical operative procedure being performed by the one team. The "postsigh" sample was obtained before abdominal wall closure
completed. Except for the post-sigh samples, the Pao, values with the vertical incision were consistently lower than with the transverse incision in both groups (Table 2). This relationship persisted throughout the study, but was never statistically significant. In Group I Pan, values showed no significant change with time except post-sigh. This latter value was statistically above control PaO, value was
Meons± SE.M.
groups. 170
Results
Physical characteristics and patient groupings are as shown in Table 1. One should note that this patient sample is quite young (overall mean age: 33.3 years) and markedly obese (overall mean weight: 142 kg) with a mean weight/height ratio (0.85) of more than twice the normal. 10 Both within and between groups the physical characteristics shown in Table 1 are statistically similar (P > 0.1). Table 2 reveals that the overall mean control Pao, in the supine position is 124 mm Hg. This value is lower than would be predicted for non-obese patients under comparable anesthetic conditions.3 Pao, values intraoperatively with time are presented numerically in Table 2 and graphically in Figure 1. "0" times refers to a change in position in Group II patients. The + 115 minute time represents the mean value taken 10 minutes after peritoneal closure. It should be noted in Table 2 that the preinflation (sigh) sample reveals a variability in time from "0" time. Obviously, both the time for the surgical procedure and abdominal wall closure varied among the 64 patients. It is interesting, however, that
160 150
140
60
810
So 60 50
-15
0
10
45
Time (rrinutes)
115+
post
sigh
FIG. 1. Arterial oxygen tension (mean + S.E.) in 64 morbidly obese patients during anesthesia and surgery. All values were obtained at 40%o inspired oxygen concentration. Solid lines present Pao, values with time for Group I patients (i.e. no change in operative position); interrupted lines are comparable values for those patients in Group II (i.e. position changed to 15' head down at "O" time). Operative incision is indicated by circles: closed circle = transverse, open circle = vertical. The solid horizontal line at 80 mm Hg (Pao0) represents the lower limits of normal oxygenation intraoperatively.2f Change in operative position (interrupted lines) resulted in a statistically significant (P < 0.001) fall in Pao, values independent of the operative incision.
VAUGHAN AND WISE
Ann. Surg. * July 1976
TABLE 3. Influence of a Subdiaphragmatic Abdominal Laparotomy Pack on Arterial Oxygenation in Four Additional Obese Supine Anesthetized Patients During Cholecystectomy Abdominal Pack
Case no.
Age (yrs)
1 2 3 4
26 31 32 23
Remove Pack
Weight (kg)
Control
Sex
Height (cm)
40%o 02
40%o 02
99.5% 02
40%o 02
99.5% 02
F F M M
0.75 1.03 0.85 1.18
97 82 123 98
58 60 64 63
78 88 85 97
83 86 94 100
210 260 253 250
(P < 0.001) in both the transverse and vertical incision
to less than 80 mm
Hg when measured 10 minutes after position change. Although this level may be acceptable pre- or postoperatively with the patient breathing room air, intraoperatively many variables supervene which may further reduce arterial oxygenation. Certain of these variables (age, physical status, abdominal packing, type of surgery, and inspired oxygen concentration) were purposely controlled for this study. This selection is not possible in the usual surgical patient. Considering the variables of age and physical status, our subjects were young, otherwise healthy obese patients without associated cardiopulmonary disease. Although retractors were in place, no abdominal packs were used to facilitate surgical exposure; packing as described in this paper, however, may be helpful to expose the gall bladder in an obese patient during cholecystectomy. Indeed, during this investigation four additional patients underwent cholecystectomy; in these patients an abdominal laparotomy pack was placed above the liver to simultaneously facilitate exposure and evaluate its effect on arterial oxygenation. Abdominal packing even in the supine position resulted in precipitous falls in Pa02. With only one abdominal pack, Pa02 values were all less than 65 mm Hg on 40% oxygen. At this range of PaO2, hemoglobin saturation begins to function on the lower, steep portion of the hemoglobin-oxygen dissociation curve. Small decreases in Pac2 cause large falls in arterial oxygen content (Ca02).3 Changing to 99.5 per cent inspired oxygen allowed an improvement in Pa02 (Table 3), and thereby increased C502. However, tissue oxygen delivery depends not only on the Cac,, but also on the level of cardiac output.23 By Discussion changing to 99.5% oxygen and excluding nitrous oxide, Our results show that in 64 adult, morbidly obese, one is forced to increase the dose of potent inhalation supine patients the mean control Pao, value (124 + 43 agent (halothane) required for maintenance of anesthesia. mm Hg) was less than the predicted value for non- While an increased Ca02 may be gained with the added obese patients (i.e. 200-240 mm Hg).3 Fourteen per inspired oxygen, the price to the patient in terms of cent of these supine, anesthetized patients had Pao2 reduced tissue oxygen delivery due to the decreased values of less than 80 mm Hg during ventilation with 40 cardiac output13 may be unacceptable. per cent oxygen. With the assumption of 150 head down position, there was a further marked fall in Pao2 to a Mechanism of Hypoxemia: Abdominal Packs mean value of 73 mm Hg. (S.D. 26.3). Seventy-seven In this study, the insertion of an abdominal pack per cent of Group II patients experienced a fall in Pao2 under the diaphragm resulted in a fall of PaO2 from subgroups. In group II the post-sigh Pao2 values were again significantly elevated (P < 0.001) above control in both the vertical and transverse incision subgroups. In addition, in Group II patients 10 minutes after a change to the 150 head down position, there was a statistically significant (P < 0.001) fall in Pao2 values. This reduced Pao, value was independent of the operative incision being used. By 45 minutes after position change, the Pao2 value for both incision subgroups in Group II had returned to control value. Since Groups I and II were shown to have statistically comparable physical characteristics, the observed difference between the groups is due to the position change. Table 3 presents the effect of an abdominal pack interposed between the undersurface of the diaphragm and dome of the liver on the Pao, values in four additional markedly obese patients. Packing alone without any change in operative position markedly reduced arterial oxygenation. Pao2 measurements on 40%o oxygen 10 minutes after packing consistently fell in each patient to less than 65 mm Hg. Although there was a significant improvement in Pao2 with 99.5% oxygen, these latter values still represent a large intrapulmonary shunt. Return to control Pao2 values on 40% oxygen was only possible with pack removal. Judged by Paco2 criteria, ventilation was adequate throughout the study period. There was no statistically significant difference from control with time in either Paco2, pH, or temperature in either groups.
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ARTERIAL OXYGENATIION IN OBESE PATIENTS
control levels. A possible explanation for this finding could be a fall in cardiac output with an increase in arterial to venous oxygen content difference. Although cardiac output was not measured, by clinical criteria the circulatory status remained stable in these four patients. A more likely explanation for impaired oxygenation in the presence of adequate ventilation with oxygen-enriched mixtures is venous admixture (physiologic shunting).5 Three possible mechanisms may be responsible for this phenomenon. First, blood is known to bypass gas exchange areas via normal anatomic shunts which include the bronchial, pleural, and Thebesian veins. Normally, this constitutes only about 3 per cent of the cardiac output,2 and is not influenced during operation. A second possible mechanism is the occurrance of regional hypoventilation in relation to pulmonary capillary blood flow. When 100% oxygen is given, these ventilation-perfusion (V/Q) abnormalities no longer contribute to the venous admixture effect.17 Consequently, V/Q could not be responsible for the total reduction in Pao2 demonstrated. The third possible cause of a right-to-left shunt is atelectasis (continued perfusion of these non-ventilated alveoli). When atelectatic areas are perfused they must contribute to shunt whatever the inspired mixture. The added effect of abdominal packing to reduce PaO2 intraoperatively is apparent. Although atelectasis (perfusion without ventilation) is the most likely explanation, one cannot rule out changes in cardiac output or the distribution of blood flow incidental to pack placement. Nevertheless, whatever the cause of the arterial hypoxemia secondary to packs, one should be cognizant of the physiologic consequences of placing packs above the liver in the obese patient. It should be noted that all the operations in this study were elective procedures on obese patients. An emergency operative procedure with possible associated fluid and electrolyte disturbances, peritonitis, and preexistent cardiopulmonary dysfunction may all exacerbate the observed hypoxemia. However, even without these variables to further reduce arterial oxygenation, when operative position was changed to 150 head down (Table 2), 23% of our patients (9/39) had PaO2 values below 60 mm Hg. In addition, one 47-year-old woman (weight/ height ratio = 1.07) with change in position experienced a fall in Pao, to 45 mm Hg. Also, two patients with the position change and placement of retractors necessary for surgical exposure experienced a precipitous fall in mean systolic blood pressure from 128 to 50 mm Hg. Each of these episodes was relieved by repositioning of the retractors away from the inferior vena cava. For adequate surgical exposure and adequate blood pressure maintenance, it was necessary in each patient to return them to the supine position. Clearly, no margin for PaO2
39 changes intraoperatively is allowed at values below 80 mm Hg. Although arbitrary, this value has been stated previously to represent the borderline value between normal and abnormal oxygenation for non-obese
patients intraoperativelyA26
The levels of arterial oxygen tension measured in our study give some cause to question the practice of administering 30 to 33% oxygen during intra-abdominal operations in obese patients. Slater26 previously suggested a minimum of 33% oxygen administration during intraabdominal surgery. However, the weights and heights of the patients in his study were not given. Our findings demonstrate impaired gas exchange in obese patients when 40o oxygen concentration is administered, even with large-tidal-volume ventilation and maintenance of normocarbia. Previous studies have shown already the adverse effects of hypocapnia on cardiac output27 and thereby the reduced arterial oxygenation.15
Mechanism of hypoxemia: Postural Change The final question that arises from our results is the mechanism of the demonstrated hypoxemia. Impaired gas exchange during spontaneous and controlled ventilation has been demonstrated in anesthetized patients compared with the unanesthetized state.16'24 Although the mechanisms producing this defect are not clear, functional residual capacity (FRC) during anesthesia is known to be diminished compared with the values before induction.10'19 As lung volume is reduced from total lung capacity, a volume at which airways start to close [the closing volume (CV)] is reached. Behind the closed airways, gas will be trapped6 and will come into equilibrium with venous blood, producing venous admixture in the pulmonary circulation. The relationship of FRC to CV, therefore, is critical to gas exchange and thereby arterial oxygenation. This phenomenon is important during surgical operations because both anesthesia10 and the supine position9 reduce FRC. General anesthesia of obese subjects, who preoperatively tend to have small FRC's,4 and also older individuals, in whom CV is increased,11 will be associated with a greater likelihood of airway closure and gas trapping. In addition, Couture et al.7 have shown that in conscious subjects in the supine position the degree of airway closure and gas trapping is greater in obese subjects. Presumably, this is because the weight of the thoracic cage reduces lung volume. Therefore, in some obese subjects, the reduction of FRC accompanying anesthesia might place FRC below CV, cause increased trapped gas, and thereby result in arterial hypoxemia due to this venous admixture. Don11 further clarified the effect of body configuration on gas exchange. He showed that an individual with an increased wieght/height ratio (i.e. relatively obese)
40
VAUGHAN AND WISE
would be at a particular disadvantage in the supine position; CV would increase in relation to FRC as the ratio of weight to height increased. Our further consideration of pulmonary gas exchange in the obese, anesthetized patient involved a change from the supine to a 150 head down position. Arterial oxygen tension measured 10 minutes after position change with 40% inspired oxygen revealed a mean decrease from control of 43 mm Hg. Three previous communications involving unsedated, conscious, non-obese subjects should be examined when looking at this effect of position change (from seated to supine) on lung volumes and gas exchange. In 80 normal subjects, LeBlanc et al.20 have shown important alterations in the relationship of airway closure to FRC associated with the change from the seated to the supine position. They pointed out that in the supine position, which is regularly accompanied by a fall in FRC, closing volume (CV) is within the tidal range from the age of 44 years onward. Craig et al.8 further considered closing volume and its relationship to gas exchange in seated and supine positions. He showed that FRC fell in the supine position, whereas CV was unchanged. When CV involved tidal volume to a greater extent in the supine posture, gas exchange deteriorated. While age and weight have both been considered as factors affecting gas exchange, Craig's data suggest that they do so by way of their effects on CV. Finally, Don et al." studying 30 normal subjects were able to show that the supine position, as compared with the sitting position, was associated with a reduced FRC and a greater volume of trapped gas when CV was greater than FRC. Therefore, the reality of airway closure and its detrimental effect on gas exchange in the supine position were confirmed. The further effect of a change from supine to 150 head down position on airway closure and lung volumes was studied by Craig.9 In 10 normal, unanesthetized, non-operated males with position change, there was a statistically significant additional reduction in total lung capacity and FRC; no change occurred in closing volume. Body position, therefore, has an important effect on the critical relationship between the CV and FRC, and hence on the functional consequences of airway closure. Consequently, our findings of impaired gas exchange with position change in obese, anesthetized patients is understandable.
Ann.
Surg. * July 1976
would imply that in obese patients with a greater likelihood of airway closure and gas trapping,7 the effect of obesity on gas exchange under the conditions of this study is partially reversible with passive, sustained hyperinflations. Don et al,'2 studying non-obese, anesthetized patients, questioned the value of intermittent hyperinflation to restore lung volume. In that study sighs did not affect FRC, nor did the volume of trapped gas increase significantly. Perhaps obese patients can better benefit from a sigh to restore more optimum ventilation-perfusion relationships and thereby arterial oxygenation. We have established that there is no progressive decrease in arterial oxygenation with time during anesthesia with large-tidal-volume ventilation, unless one alters the surgical position (Table 2, Fig. 1). Don et al.12 have shown in supine, anesthetized, adults during spontaneous ventilation that there is no progressive decrease in FRC with time, and therefore, the intrapulmonary shunt should not progressively increase. Nunn22 found minimal temporal changes in arterial oxygenation during anesthesia when normocarbia was maintained. Visick et al.31 employing controlled ventilation with small to large tidal volumes in anesthetized adults observed a slight but significant improvement in arterial oxygenation with time; this finding was regardless of the sequence of ventilatory patterns. They postulated these findings represent a combination of increasing cardiac output,'3 and less oxygen consumption due to falling body temperature (mean temperature change throughout their study: 1.6 C). Although the former possibility may pertain in our study, the latter explanation is not tenable. The mean temperature change from 37°C throughout the present study was 0.30C. A more plausible explanation for our observed improvement in mean Pa0. with time after position change would be the effect of controlled, large volume ventilation on re-expanding partially collapsed alveoli. An overall improvement in the distribution of ventilation with respect to perfusion would reduce venous admixture. Visick's study3' comparing the effects of tidal volume and end-expiratory pressure on pulmonary gas exchange during anesthesia lends credence to this postulate. Small volume ventilation (5 ml/kg or V5) decreases PaO2 by permitting airway closure. By exceeding closing volume at end inflation, large tidal volume (15 ml/kg or V15) or V5 plus continuous positive pressure (i.e. V5 + CPP) ventilates alveoli which otherwise would be Restoration of arterial oxygenation perfused but not ventilated. In addition, his finding of We employed passive hyperinflations (sigh) at the com- a positive correlation of decreasing Pao with increasing pletion of the study period. In spite of the 150 head degrees of obesity (i.e. elevated weight/height ratio) is down position, sighs improved arterial oxygenation; compatible with this explanation, since airway closure Pao2 was statistically elevated above control levels. This does increase with obesity.7 The beneficial effect of
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ARTERIAL OXYGENATION IN OBESE PATIENTS
41
V5 + CPP will be partially offset by the reduction in Acknowledgment cardiac output produced by the greater intrathoracic The authors wish to thank Miss Dorothy Hollander for technical pressure. Moreover, arterial oxygenation should and assistance and Mrs. Mary Rogers for her competent preparation of actually does improve when V15 replaces V5 + CPP. the manuscript. Therefore, the detrimental effects on oxygenation in the obese of spontaneous or small tidal volume (V5) ventilaReferences tion could be anticipated. 1. Anscombe, A. R.: Pulmonary Complications of Abdominal SurFinally, it has long been appreciated that breathing gery. 1st Ed. London, Lloyd-Luke (Medical Books), 1957, Chap. VIII. at low lung volumes secondary to obesity,3 pain,' or S. M., Criscitiello, A. and Grabovsky, E.: Components during general anesthesia,10'19 may be associated with 2. Ayres, of Alveolar-arterial 02 Difference in Normal Man. J. Appl. deficient pulmonary gas exchange. Atelectasis has been Physiol., 19:43, 1964. suggested as the likely mechanism affecting gas exchange, 3. Bates, D. V. and Christie, R. V.: Respiratory Function in Disease. An Introduction to the Integrated Study of the Lung. 1st Ed. although supporting evidence for this diagnosis has often Philadelphia and London, W. B. Saudners and Co., 1964, been lacking. Atelectasis can clearly cause the defects pp. 58, 65-66, 100-101. noted in these situations, but airway closure rates con- 4. Bedell, G. N., Wilson, W. R. and Seebohm, P. M.: Pulmonary Function in Obese Persons. J. Clin. Invest. 37:1049-1060, 1958. sideration as either the sole mechanism responsible, or 5. Bendixen, H. H., Egbert, L. D., Hedley-Whyte, J., et al.: as perhaps a primary mechanism which. then leads to Respiratory Care. St. Louis, C. V. Mosby Company, 1965; pp. 12-17. secondary atelectasis. E. J., Jr. and Macklem, P.: Airway Closure: DemonstraThe following conclusions are apparent from this 6. Burger, tion by Breathing 100 per cent Oxygen at Low Lung Volumes paper in morbidly obese patients: 1) Forty per cent and by N2 Washout. J. Appl. Physiol., 25:139-148, 1968. oxygen may not be adequate for intraabdominal surgery 7. Couture, J., Picken, J. J., Ruff, F., et al.: Demonstration of Airway Closure and Trapping of Air in the Recumbent Position in otherwise healthy obese patients; 2) A subdiaphragin Normal and Obese Subjects. Am. Roy. Coll. Phys. Surg. matic abdominal laparotomy pack without a change in Canada, 3:25, 1970. operative position seriously interferes with arterial 8. Craig, D. B., Wahba, W. M., Don, H. F. et al.: "Closing Volume" and Its Relationship to Gas Exchange in Seated and oxygenation; 3) Change from supine to a 150 head down Supine Positions. J. Appl. Physiol., 31:717-721, 1971. operative position resulted in a significant reduction 9. Craig, D. B., Wahba, W. M. and Don, H.: Airway Closure and Lung Volumes in Surgical Positions. Canad. Anaesth. Soc. J., in arterial oxygenation.
Clinical Implications
Serious consideration should be given to the routine use of the Trendelberg position intraoperatively in obese patients. It is recognized that a 150 head down position may facilitate surgery in these patients during some operative procedures (pelvic, genitourinary, jejunoileal bypass). However, if one elects this posture for the obese patient, prudence would dictate careful monitoring of arterial blood gases. If arterial hypoxemia ensues, supplementation with higher inspired oxygen concentration is mandatory. Certainly the combination of the Trendelenberg position and a subdiaphragmatic laparotomy pack should be completely avoided. Finally, since our data were collected in otherwise healthy, young, obese patients free of cardiorespiratory disease, special attention should be directed at the continuous measurement of arterial oxygenation in the older, obese patient. These individuals with either intrinsic dysfunction of vital organs (heart, lung, liver kidney) or surgical diseases (peritonitis, sepsis) would be a particularly high risk group with reference to oxygenation. Any intraoperative position change should be carefully considered and arterial oxygenation continuously assessed.
18:92-99, 1971. 10. Don, H. F., Wahba, M., Curadrado, L. and Kelkar, K.: The Effects of Anesthesia and 100 Per Cent Oxygen on the Functional Residual Capacity of the Lungs. Anesthesiology, 32:521529, 1970. 11. Don, H. F., Craig, D. B., Wahba, W. M. and Couture, J. G.: The Measurement of Gas Trapped in the Lungs at Functional Residual Capacity and the Effects of Posture. Anesthesiology, 35:582-590, 1971. 12. Don, H. F., Wahba, W. M. and Craig, D. B.: Airway Closure, Gas Trapping, and the Functional Residual Capacity during Anesthesia. Anesthesiology, 36:533-539, 1972. 13. Eger, E. I., II, Smith, N. T., Stoelting, R. K. et al.: Cardiovascular Effects of Halothane in Man. Anesthesiology, 32: 396-409, 1970. 14. Eger, E. I., II: A Mathematical Model of Uptake and Distribution, In Uptake and Distribution of Anesthetic Agents, Edited by Papper, E. M. and Kitz, R. J. New York, McGrawHill, 1963, Ch. 7. 15. Fairley, H. B.: The Effect of Hyperventilation on Arterial Oxygen Tension: A Theoretical Analysis. Can. Anaesth. Soc. J., 14: 87-93, 1967. 16. Froese, A. B. and Bryan, A. C.: Effects of Anesthesia and Paralysis on Diaphragmatic Mechanics in Man. Anesthesiology, 41: 242255, 1974. 17. Hedley-Whyte, J., Corning, H., Laver, M. B. et al.: Pulmonary Ventilation-Perfusion Relationships After Heart Valve Replacement or Repair in Man. J. Clin. Invest., 44:406, 1965. 18. Kelman, G. R. and Nunn, J. F.: Normograms for Correction of Blood Po2, PCO2, pH, and Base Excess for Time and Temperature. Appl. Physiol., 21:1484-1490, 1966. 19. Laws, A. K.: Effects of Induction of Anesthesia and Muscle Paralysis on Functional Residual Capacity of the Lungs. Can. Anaesth. Soc. J., 15:325-331, 1968. 20. LeBlanc, P., Ruff, F. and Milac-Enmili,- J.: Effects of Age and
VAUGHAN AND WISE
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Body Position on "Airway Closure" in Man. J. Appl. Physiol., 28:448-451, 1970. Metropolitan Life Insurance Co., Table of Desirable Weights in Adults. In Documenta Geigy, Scientific Tables, (6th Edition), 1962; p. 624. Nunn, J. F., Bergman, N. A. and Coleman, A. J.: Factors Influencing the Arterial Oxygen Tension During Anesthesia with Artificial Ventilation. Br. J. Anaesth., 37:898-914, 1965. Nunn, J. F. and Freeman, J.: Problems of Oxygenation and Oxygen Transport during Haemorrhage. Anaesthesia, 19:206, 1964. Price, H. L., Cooperman, L. H., Warden, J. C. et al.: Pulmonary Hemodynamics during General Anesthesia in Man. Anesthesiology, 30:629-636, 1969. Sellick, B. A.: Cricoid Pressure to Control Regurgitation of Stomach Contents during Induction of Anesthesia. Lancet, 2:404-406, 1%1. Slater, E. M., Nilsson, S. E., Leake, D. M. D. et al.: Arterial
27. 28. 29. 30.
31.
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Oxygen Tension Measurements during Nitrous Oxide-Oxygen Anesthesia. Anesthesiology, 26:642-647, 1965. Theye, R. A., Milde, J. M. and Michenfelder, J. D.: Effect of Hypocapnia on Cardiac Output during Anesthesia. Anesthesiology, 27:778-782, 1966. Vaughan, R. W., Engelhardt, R. C. and Wise, L.: Postoperative Hypoxemia in Obese Patients. Ann. Surg., 180:877, 1974. Vaughan, R. W. and Wise, L.: Choice of Abdominal Operative Incision in the Obese Patient: A Study Using Blood Gas Measurements. Ann. Surg., 181:829-835, 1975. Vaughan, R. W. and Wise, L.: Postoperative Arterial Blood Gas Measurements in Obese Patients: Effect of Position on Gas Exchange. Ann. Surg., 182:705-709, 1975. Visick, W. D., Fairley, H. B. and Hickey, R. F.: The Effects of Tidal Volume and End-expiratory Pressure on Pulmonary Gas Exchange during Anesthesia. Anesthesiology, 39:285-290, 1973.
Erratum The list of references following "Portosystemic Shunting in Patients with Primary Biliary Cirrhosis: A Good Risk Disease," by Joel L. Bauer, et al., Ann. Surg., 183:3:324, 1976, should have appeared as follows. References 1. Addison, T. and Gull, W.: On a Certain Affection of the SkinVitilgoidea a plana, B. Tuberosa. Guys Hosp. Rep., 7:265, 1851. 2. Ahrens, E. H., Jr., Payne, M. A. and Kunkel, H. G.: Primary Biliary Cirrhosis. Medicine, 29:299, 1950. 3. Child, C. G.: The Liver and Portal Hypertension. Philadelphia, W. B. Saunders Co., 1964. 4. Hanot, V.: La Cirrhosis Hypertrophique avec Icteric Chronique. Paris, Reuff and Cie, 1892. 5. Popper, H., and Schaffner, F.: Liver- Structure and Function. N.Y., Toronto, and London, McGraw Hill, 1957.
6. Popper, H., Elias. H. and Petty, D. E.: Vascular Pattern of the Cirrhotic Liver. Am. J. Clin. Pathol., 22:717, 1952. 7. Rubin, E., Schaffner, F. and Popper, H.: Primary Biliary Cirrhosis. Am. J. Pathol., 46:387, 1965. 8. Sherlock, S.: Primary Biliary Cirrhosis (Chronic Intrahepatic Obstructive Jaundice) Gastroenterology, 37:574, 1959. 9. Walker, J. G., Doniach, D., Roitt, I. M. and Sherlock, S.: Lancet 1:827, 1965. 10. Zeegen, R., Stansfeld, A. G., Dawson, A. M. and Hunt, A. H.: Bleeding Oesophageal Varices as the Presenting Feature in Primary Biliary Cirrhosis. Lancet, 2:9, 1969.
