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Revista Brasileira de Anestesiologia

Print version ISSN 0034-7094On-line version ISSN 1806-907X

Rev. Bras. Anestesiol. vol.54 no.4 Campinas July/Aug. 2004 



PETCO2 and SpO2 allow adequate ventilatory adjustment in morbidly obese patients*


PETCO2 y SpO2 permiten ajuste de ventilación adecuada en pacientes obesos mórbidos



Fábio Ely Martins Benseñor, M.D.I; José Otávio Costa Auler Júnior, TSA, M.D.II

IMédico Assistente, Doutor em Anestesiologia - FMUSP
IIProfessor Titular da Disciplina de Anestesiologia - FMUSP





BACKGROUND AND OBJECTIVES: Ventilation strategies for anesthesia in morbidly obese patients have been investigated, but an agreement has not been achieved yet. This study aimed at clinically evaluating ventilation adjustments based on oximetry and capnography readings in these patients during anesthesia.
METHODS: Consent was obtained from the Institutional Ethics Committee and from patients. Smokers and respiratory or cardiac disease patients were excluded. Eleven patients with Body Mass Index (BMI) of 59.2 ± 8.3 undergoing gastroplasty under general anesthesia were studied (Group O), with a control group (NO) composed of 8 non-obese patients (BMI 20.2 ± 3.9) submitted to gastrectomy. Ventilator was adjusted to keep PETCO2 below 40 mmHg and SpO2 above 95%. PEEP was not used. Through a CO2SMO Plus respiratory monitor, airway, alveolar and physiologic dead spaces (respectively VD aw, VD phy and VD alv), as well as alveolar tidal volume (TV alv) were measured. Arterial and central venous blood samples were used to calculate PaO2/FIO2 and VD phy/TV relationships. Data were compared and evaluated by ANOVA (p < 0.05).
RESULTS: Tidal volume was 4.2 ± 0.4 in Group O and 7.9 ± 2.3 in Group NO for measured weight, and 11.5 ± 1.8 in Group O and 6.6 ± 1.1 in Group NO for ideal weight. PaO2 was lower and TV alv was higher in Group O (p < 0.008 and 0.0001, respectively). No difference was found in PaCO2, VD phy, VD alv and VD aw.
CONCLUSIONS: SpO2 and PETCO2 seem to assure adequate ventilation, which can be achieved in morbidly obese patients with tidal volumes adjusted to ideal weight.

Key Words: DISEASES: morbid obesity; VENTILATION: controlled mechanical


JUSTIFICATIVA Y OBJETIVOS: A pesar de las diversas propuestas de ventilación para anestesia en pacientes obesos mórbidos, un consenso no fue establecido. Este estudio evaluó el ajuste de ventilación en estos pacientes durante anestesia fundamentado en la oximetria y capnografia.
MÉTODO: El consentimiento previo fue obtenido de la Comisión de Ética y de los pacientes. Fueron excluidos fumantes y portadores de enfermedad cardíaca o pulmonar. Fueron estudiados once pacientes con índice de masa corpórea (IMC) de 59,2 ± 8,3 sometidos a gastroplastia bajo anestesia general (Grupo O). Ocho no obesos (IMC 20,2 ± 3,9) sometidos a gastrectomia formaron el grupo control (NO). Se ajustó la ventilación visando el dióxido de carbono expiratorio final (PETCO2) menor que 40 mmHg y saturación periférica de oxígeno (SpO2) mayor que 95%. No se utilizó PEEP. A través de monitor respiratorio CO2SMO Plus, se midió espacios muertos fisiológico, alveolar y de vías aéreas (VD phy, VD alv y VD aw) y el volumen corriente alveolar (VT alv). Muestras de sangre arterial y venoso central permitieron calcular PaO2/FIO2 y VD phy/VT. Los datos fueron comparados y analizados por ANOVA (p < 0,05).
RESULTADOS: Volúmenes corrientes fueron de 4,2 ± 0,4 en el Grupo O y 7,9 ± 2,3 en el Grupo NO para el peso medido, y de 11,5 ± 1,8 en el Grupo O y 6,6 ± 1,1 en el Grupo NO para el peso ideal. La PaO2 se mostró menor y el VT alveolar se mostró mayor en los obesos (p < 0,008 y 0,0001, respectivamente). No fue encontrada diferencia en PaCO2, VD phy, VD alv o VD aw.
CONCLUSIONES: La SpO2 y la PETCO2 parecen garantir ventilación adecuada, la cual puede ser obtenida en pacientes con obesidad mórbida con volúmenes corrientes ajustados al peso ideal.




Exaggeratedly or not, obesity has been considered a major 21st Century epidemics1.

Although there is no specific information on the prevalence of obesity in Brazil, including those individuals classified as morbidly obese (Body Mass Index - BMI - > 40), an expressive increase in their number has been observed in major centers among the population submitted to elective or emergency procedures. This impression confirms previous studies2,3.

The high prevalence of perioperative complications4,5 and pre-existing chronic diseases, including diabetes mellitus, systemic hypertension, vascular and cardiopulmonary diseases in such patients6,7 are issues to be considered when providing perioperative care to morbidly obese patients.

The tidal volume to be used during anesthesia for obese patients and the search for its optimal value have generated discussions in the medical literature. Bardoczky et al.8 have compared ventilation with tidal volumes between 13 and 22 mL per kg of ideal weight and have shown that high volumes during anesthesia have generated hypocapnia, not followed by significant partial oxygen tension increase though. Tidal volumes between 15 and 20 mL per kg of ideal weight have also been proposed as adequate5.

Aiming at establishing parameters to safely guide anesthesiologists during intraoperative care of morbidly obese patients, this study has evaluated, through ventilation and perfusion analysis, the safety of relatively low cost/complexity methods (pulse oximetry, capnography and arterial gases analysis) to determine adequate ventilatory adjustment during morbidly obese patients anesthesia.



The Institutional Ethics Committee has approved the study and patients gave their written consent the day before surgery. Exclusion criteria were smokers in the last 12 months and patients with clinical evidence of heart or lung disease.

Patients were divided in two groups according to body mass index (BMI): Obese Group (O), with BMI ³ 40, and Non-Obese Group (NO), with BMI < 30.

Group O included 11 morbidly obese female patients, submitted to gastroplasty through laparotomy. Group NO consisted of 8 patients (5 males and 3 females), seven of them undergoing open gastric surgery due to neoplastic disease, and one to open colon resection.

All patients were submitted to general anesthesia. Anesthetic doses were calculated based on ideal weight (ideal weight = height in centimeters less 100 for males and less 105 for females)10.

Patients were premedicated with muscular midazolam (0.1 45 minutes before surgery. In the operating room, patients were monitored with continuous ECG (CS-5 lead), noninvasive blood pressure and pulse oximetry. After spontaneous ventilation with 100% oxygen, anesthesia was induced with etomidate (0.3 and fentanyl (5 µ, followed by tracheal intubation facilitated by pancuronium (0.08 to group NO and succinylcholine (1 to Group O. Monitoring after induction consisted of invasive blood pressure, right atrium pressure and esophageal temperature. Alveolar ventilation variables were measured with ventilatory monitor combining infrared capnographer, pressure differential flow sensor through fixed hole and red/infrared pulse oximetry (CO2SMO Plus respiratory profile monitor, Novametrix, CT, USA).

Patients were ventilated with Linea (Intermed, São Paulo, Brazil) anesthesia machine in volume-controlled mode through a ventilatory system open to the room thru a unidirectional valve. Predetermined protocol conditions required that patients be ventilated with tidal volume equal to 8 mL per kg of ideal weight and respiratory rate of 10 cycles per minute. If end tidal CO2 (PETCO2) was above 40 mmHg or oxygen peripheral saturation was below 95%, respiratory rate and/or tidal volume would be adjusted at the anesthesiologist's discretion. Positive end expiratory pressure (PEEP) was not used.

Anesthesia was maintained with 2% to 4% sevoflurane in a mixture of air and oxygen in equal parts. Inspired and expired gases were analyzed with Capnomac Ultima respiratory monitor (Datex Instrumentarium, Helsinki, Finland).

Gases exchanges evaluation and arterial/venous blood samples collection were performed with patients in the supine position during surgical procedure pauses, at five moments: first sample (AI: after anesthetic induction) was collected 15 minutes after tracheal intubation and before surgical incision; second sample (PO: after peritoneum opening), was collected immediately after abdominal wall opening; third sample (PO1h) was collected one hour after abdominal opening; fourth sample (PC: peritoneum closing) was collected immediately after peritoneum closing; fifth and last sample (SC: surgery completion), was collected immediately after surgical incision dressing.

Before each sampling, muscle relaxation was checked by means of a neuromuscular function monitor (TOF-GUARD, Organon-Tecnika NV, Turnhout, Belgium) and, when necessary, additional pancuronium doses were given. After 5 respiratory cycles with fresh gases flow closed, a set of measurements was performed by CO2SMO Plus, checking airways dead spaces (VD aw), alveolar tidal volume (TV alv), mean expired CO2 in one minute adjusted to patient's weight (VCO2/kg) and partial CO2 pressure (PeCO2), and the amount of CO2 in one expiration divided by expired volume.

Arterial and central venous blood samples were simultaneously collected and analyzed by i-Stat portable clinical analyzer (i-Stat Corporation, East Windsor, NJ, USA) measuring arterial oxygen and carbon dioxide pressures (PaO2 and PaCO2), as well as arterial pH, which allowed for the calculation of physiological dead space (VD phy), alveolar dead space (VE alv), relationship between physiological dead space and tidal volume (VD/TV phy) and relationship between arterial oxygen pressure and oxygen inspired fraction (PaO2/FIO2).

Values are presented in mean ± standard deviation (SD). Non-paired Student's "t" test (p < 0.05) was used to compare demographics of obese and non-obese patients, as well as surgery duration. Fisher's Exact test was used to check patients distribution by gender between groups. To verify differences between the five sampling moments, either within the same group or between groups in the same moments, Analysis of Variance (ANOVA) for repetitive measures was used, followed by Tukey's test. Significance level was established to 5%.



All patients evolved normally after surgery and were discharged according to schedule. No study-related complication has been observed and there were no complaints about participating in the study.

There were no statistical differences between groups in age (45.4 ± 14.3 years for obese and 38.6 ± 8.4 years for non obese, p = 0.21), height (160 ± 9 cm for obese and 163 ± 13 cm for non obese) and surgery duration (325.6 ± 150.4 minutes and 325 ± 42.7 minutes respectively for Groups O and NO, p = 0.991). However, Groups O and NO have differed in weight (151 ± 16.6 kg for obese and 55.1 ± 13.7 kg for non obese, p < 0.001), BMI (59.2 ± 8.3 kg.m-2 for obese and 20.6 ± 4 for non obese, p < 0.001) and gender distribution (11 females in Group O, 5 males and 3 females in Group NO, p < 0.001).

Results were grouped into three different aspects, according to the variables used to evaluate respiratory function: 1) tidal volume and oxygenation, including PaO2 and PaO2/FiO2 ratio; 2) carbon dioxide production, including PaCO2, VCO2/kg and PETCO2; 3) ventilation-perfusion ratio, including VD aw, TV alv, VD phy, VD alv and VD/TV phy ratio.

For tidal volume and oxygenation, Group O patients were ventilated with mean tidal volume of 4.2 ± 0.4 of measured weight or 11.51 ± 1.8 of ideal weight, while Group NO was ventilated with 7.9 ± 2.3 of measured weight, or 6.6 ± 1.1 of ideal weight to remain within previously established limits for SpO2 and PETCO2.

PaO2 has not changed during surgery for both groups when the five moments were compared. Group NO, however, has shown statistically higher PaO2 in all measurements as compared to Group O (respectively 238.3 ± 50.6 and 157.6 ± 48 mmHg for AI, 216.1 ± 68.1 and 145.5 ± 47.5 mmHg for PO, 202.9 ± 69.7 and 158.3 ± 56.3 mmHg for PO1h, 219.1 ± 55.5 and 179.8 ± 40 mmHg for PC, 236.6 ± 51.6 and 180.1 ± 49 mmHg for SC, p = 0.08). There have been no changes in PaO2/FiO2 ratio among moments for Group NO. Group O has shown significant increases between initial and final moments (respectively 261.7 ± 76.9 and 316.1 ± 88.4 mmHg, p = 0.02). When both groups were compared for PaO2/FiO2 ratio, Group O had statistically higher values in moments AI (411.7 ± 92.2 and 261.7 ± 76.9 mmHg, p = 0.0008), PO (374 ± 123.5 and 249.2 ± 81.3 mmHg, p = 0.01) and SC (413.8 ± 95.5 and 316.1 ± 88.4 mmHg, p = 0.02). Oxygenation data are shown in figure 1.

CO2 production and excretion analysis, as expected, has shown no differences between groups in all five comparisons, probably due to the research protocol which required ventilatory parameters adjustments to maintain PETCO2 below 40 mmHg. Nevertheless, PaCO2 was significantly increased in Group NO between moments AI and PO (p = 0.02), PO and PO1h (p = 0.007) and AI and SC (p = 0.005). PaCO2 values measured in such moments were 34 ± 5.1 mmHg in AI, 36.5 ± 5.2 mmHg in PO, 39.7 ± 7.2 mmHg in PO1h and 38.8 ± 6.4 mmHg in SC.

VCO2/kg has shown lower values for Group O as compared to Group NO (respectively 1.2 ± 0.2 and 1.9 ± 0.3 in AI, 1.3 ± 0.1 and 1.8 ± 0.4 in PO, 1.2 ± 0.2 and 1.9 ± 0.4 in PO1h, 1.3 ± 0.3 and 1.8 ± 0,3 in PC and 1.3 ± 0.2 and 1.9 ± 0.4 in SC, p = 0.0001). When comparing moments within the same group, no differences were detected among Group NO patients, while in Group O such differences were significant between moments PO and PO1h and PO1h and PC (p = 0.02 and 0.03, respectively). PeCO2 has not changed for both groups throughout the procedure, but levels were higher for Group O in the five moments: 27.8 ± 2.3 and 22.3 ± 4 in AI, 26.9 ± 1.8 and 22.7 ± 3.4 in PO, 26.1 ± 2.8 and 22.9 ± 2.3 in PO1h, 26.4 ± 1.7 and 21.3 ± 3.4 in PC and 27.2 ± 3.4 and 22.4 ± 3.1 in SC, p = 0.0001 for al moments. CO2 production data are shown in figure 2.

Ventilation-perfusion variables have not shown differences between groups in airways dead space (VD aw). Nevertheless, both groups have shown increased VD aw between moments AI and PO (75.6 ± 22 and 84.6 ± 24 mL in Group O, 90.6 ± 15.5 and 98.3 ± 19.4 mL in Group NO, p = 0,01) and between moments PO and PO1h, being PO1h values equal to 91.4 ± 20.5 and 103.8 ± 19.4 mL respectively for Groups O and NO (p = 0.02). On the other hand, both groups had decreased VD aw between moments PC and SC (97.8 ± 19.4 and 84.91 ± 18.8 mL for Group O and 109 ± 26.4 and 104.4 ± 24.6 mL for Group NO, p = 0.004).

There have also been significant increases between moments AI and SC (p = 0.004). Alveolar dead space (VD alv) was not different between groups or among moments in the same group, the same being true for physiological dead space (VD phy). Alveolar tidal volume (TV alv), which is really involved in gaseous exchanges, was calculated by CO2SMO Plus by subtracting expired volume from airways dead space. TV alv was statistically higher in Group O as compared to Group NO in the five sampled moments, respectively 439.7 ± 104.3 and 309.6 ± 59.3 in AI, 443.4 ± 95.6 and 291.2 ± 58.3 in PO, 425.3 ± 88.3 and 290.4 ± 69.7 in PO1h, 425.9 ± 72.9 and 318 ± 84.8 in PC, 404.2 ± 85.2 and 293.2 ± 62.6 in SC (p = 0.0001 in all moments). There have been no differences among moments in both groups. VD/BT phy ratio was higher in Group NO in the five moments, respectively 0.35 ± 0.1 and 0.25 ± 0.1 in AI, 0.38 ± 0.1 and 0.26 ± 0.1 in PO, 0.42 ± 0.1 and 0.25 ± 0.1 in PO1h, 0.45 ± 0.1 and 0.27 ± 0.1 in PC, 0.40 ± 0.1 and 0.26 ± 0.1 in SC (p = 0.002 in all moments). There have been no differences among moments in both groups. Ventilation/perfusion ratio data are shown in figure 3.



Standard ventilation monitoring based on pulse oximetry, capnography and periodic blood gases analyses has shown to be safe and enough during morbidly obese patients care. Ventilator adjustment based on those two variables has shown that adequate intraoperative respiratory rate and tidal volume for obese patients can be achieved in a similar manner to that used for patients with lower BMI, provided ideal weight is used as reference.

The first part of this analysis was related to adequate oxygenation via tidal volume adjustment. Both groups have received adequate oxygen supply during the five evaluation moments. In spite of statistically higher PaO2 and PaO2/FiO2 values in Group NO, in line with the literature4,5,9,11, it is worth highlighting that values collected in the five moments for both groups are within normal ranges. As to oxygen supply, the conclusion was that morbidly obese patients may be adequately ventilated with 11 mL per kg of ideal weight, value similar to that used by several anesthesiologists for patients with lower BMI.

High oxygen fractions in the gaseous mixture administered during anesthesia promote atelectasis12 and such effect seems to be exacerbated in obese patients, specially morbidly obese ones13. Hedenstierna et al.14 have described decreased functional residual capacity (FRC) promoted by general anesthesia and muscle paralysis under mechanical ventilation caused by diaphragm relaxation. Pelosi et al.13 have proposed that decreased oxygenation and pulmonary volume are inversely related to BMI. They have also proposed that such decrease could also be true for FRC. Better safety margin in anesthesia for morbidly obese patients would be obtained with positive end expiratory pressure (PEEP) due to alveolar recruitment that it promotes15. This way, PEEP would allow even lower oxygen expired fractions than those used in this study, what would be desirable to prevent intra and postoperative atelectasis.

The analysis of CO2 production and excretion has shown that morbidly obese patients have produced more carbon dioxide according to PeCO2 evaluation, which is in line with the literature11. However, PeCO2 values were within normal ranges for both groups. VCO2/kg ratio has shown that morbidly obese patients produce less CO2 as compared to non-obese after weight adjustment, probably because increased body mass is predominantly made up of poorly perfused fatty tissue. Higher tidal volumes in Group O patients have certainly interfered with VCO2 values. Despite of higher CO2 production in Group O, this increase does not seem to be clinically important, provided limits proposed in this study for expired CO2 are respected.

The final part of respiratory function evaluation has studied ventilation/perfusion ratio variables. Results were very similar for both groups. Hedenstierna et al.11 have shown increased alveolar dead space during obese patients anesthesia, but have stressed that such effect is also seen in individuals with normal BMI. Our study has confirmed such similarity. Alveolar ventilation results were not statistically different for both groups and should not be a reason for concern during morbidly obese patients anesthesia. So, in terms of ventilation/perfusion ratio, monitoring including expired CO2 analysis, periodic central and/or arterial blood gases analysis, pulse oximetry and desirably, however not imperatively, circuit gases and vapors analysis, are safe indicators for morbidly obese patients anesthesia.

A final caveat is related to the nature of the control group. By including a patient with BMI below 18 and another with BMI above 25, characterizing malnutrition and overweight respectively, it could be prone to criticism. Our aim in maintaining such patients was to compare the population of morbidly obese patients to the general population, which includes patients who could not be characterized as eutrophic.

In conclusion, tidal volumes close to those usually employed and PEEP values still to be determined seem to be an adequate strategy for intraoperative ventilation of morbidly obese patients when associated to pulse oximetry and capnography, in addition to other alternatives used in previous studies4. Future studies assessing pulmonary recruitment, maybe through airway pressure versus volume curves analysis, would be useful to determine adequate PEEP values during ventilation of such patients.



We acknowledge Dr. Jorge Bonassa, Electronic Engineer, Doctor in Pneumology, and Mr. Anderson Silva, Technician in Anesthesia and Engineering Student for their cooperation in adjusting and maintaining equipment during data collection stage; Karine Savalli Redigolo and Lilian Natis, from the Statistics Department, Heart Institute, Hospital das Clinicas, Faculdade de Medicina, USP, for helping in the statistical analysis; Joaquim Edson Vieira, M.D., for helping in the statistical analysis and final text review.



01. Halpern A - A epidemia da obesidade. Arq Bras Endocrinol Metab, 1999;43:175-176.        [ Links ]

02. Monteiro CA, Conde WL - A tendência secular da obesidade segundo estratos sociais: Nordeste e Sudeste do Brasil, 1975-1989-1997. Arq Bras Endocrinol Metab, 1999;43: 186-194.        [ Links ]

03. Martins IS, Velásquez-Melendez G, Cervato AM. - Estado nutricional de grupamentos sociais da área metropolitana de São Paulo, Brasil. Cad Saúde Publica, 1999;15:71-78.        [ Links ]

04. Øberg B, Poulsen TD - Obesity: an anaesthetic challenge. Acta Anaesthesiol Scand, 1996;40:191-200.        [ Links ]

05. Shenkman Z, Shir Y, Brodsky JB - Perioperative management of the obese patient. Br J Anaesth, 1993;70:349-359.        [ Links ]

06. Rosenbaum M, Leibel RL, Hirsch J - Obesity. N Engl J Med, 1997;337:396-407.        [ Links ]

07. Waaler HT - Hazard of obesity - the Norwegian experience. Acta Med Scand, 1988;723:(Suppl):17-21.        [ Links ]

08. Bardoczky GI, Yernault JC, Houben JJ et al - Large tidal volume ventilation does not improve oxygenation in morbidly obese patients during anaesthesia. Anesth Analg, 1995;81:385-388.        [ Links ]

09. Buckley FP - Anaesthesia for the morbidly obese patient. Can J Anaesth, 1994;41:R94-R100.        [ Links ]

10. Auler Jr JO, Miyoshi E, Fernandes CR et al - The effects of abdominal opening on respiratory mechanics during general anesthesia in normal and morbidly obese patients: a comparative study. Anesth Analg, 2002;94:741-748.        [ Links ]

11. Hedenstierna G, Santesson J - Breathing mechanics, dead space and gas exchange in the extremely obese, breathing spontaneously and during anaesthesia with intermittent positive pressure ventilation. Acta Anaesthesiol Scand, 1976;20:248-254.        [ Links ]

12. Kufel TJ, Grant BJB - Arterial Blood-Gas Monitoring: Respiratory Assessment, em: Tobin MJ - Principles and Practice of Intensive Care Medicine. 1st Ed, New York: McGraw-Hill, 1998;197-215.        [ Links ]

13. Pelosi P, Croci M, Ravagnan I et al - The effects of body mass on lung volumes, respiratory mechanics, and gas exchange during general anaesthesia. Anesth Analg, 1998;87:654-660.        [ Links ]

14. Hedenstierna G, Strandberg Å, Brismar B et al - Functional residual capacity, thoracoabdominal dimensions, and central blood volume during general anaesthesia with muscle paralysis and mechanical ventilation. Anesthesiology, 1985;62:247-254.        [ Links ]

15. Pelosi P, Ravagnan I, Giurati G et al - Positive end-expiratory pressure improves respiratory function in obese but not in normal subjects during anaesthesia and paralysis. Anesthesiology, 1999;91:1221-1231.        [ Links ]



Correspondence to
Dr. Fábio Ely Martins Benseñor
Address: Rua Mauá, 934/936
ZIP: 01028-000 City: São Paulo, Brazil

Submitted for publication July 22, 2003
Accepted for publication October 27, 2003



* Received from Disciplina de Anestesiologia do Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, São Paulo, SP; Financiado pela Fundação de Amparo à Pesquisa do Estado de São Paulo, FAPESP, sob o número 97/11311-2

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