Objectives. We examined the relationship between partial end-tidal CO2 (pet) and mean arterial pressure in patients with traumatic hemorrhagic shock, who were receiving constant minute ventilation.
Methods. In 61 patients we continuously measured pet CO2 with a capnograph, direct arterial pressure via a cannula, oxygen levels via pulse oximetry and body temperature.
Results. We observed significant changes in pet CO2 (increase) after volume resuscitation and a quantitative linear relationship between pet CO2 and mean arterial pressure.
Conclusions. Partial end-tidal CO2 can be used as a reliable non-invasive monitoring device in patients with hemorrhagic shock when minute ventilation is relatively constant. The monitoring of pet CO2 might also be a useful guide for volume resuscitation in hemorrhagic shock, especially in the pre-hospital setting.

Keywords: end- tidal CO2, mean arterial pressure, hemorrhagic shock, relationship


Partial end-tidal CO2 pressure (pet CO2) is normally determined by CO2 production (metabolism), alveolar ventilation, pulmonary perfusion (circulation) and V/Q matching. (1)
Pet CO2 has been shown to be a reliable and non-invasive prognostic indicator of the success of cardiac resuscitation, (2,3) and highly correlates with cardiac index. (4-6) Additionally, investigators have confirmed on animal models that pet CO2 can be used for non-invasive and continuous monitoring of cardiac output in circulatory shock. (7-10) Some authors reported the use of pet CO2 as a predictor of mortality and as a useful intraoperative tool for assessing the physiological conditions of the patient. (11,12) The aim of this study was to examine the relationship between mean arterial pressure (MAP) and pet CO2 in patients with hemorrhagic shock in the presence of constant minute ventilation end tidal (Et) CO2 monitoring be considered a technically simple, non-invasive and rapid quantitator of severity of circulatory shock states.

Patients and methods

Intraoperative data were acquired in 61 patients who underwent emergency surgery for massive haemorrhage. Data were gathered prospectively (16 measurements of MAP and pet CO2) in the Department of anesthesiology, intensive care medicine and for the treatment of pain, University Clinical Centre Maribor from June to December 2006. The operative procedures were: 21 laparotomies, 19 explorations of the extremities and/or major fractures, 12 craniotomies, 9 thoracotomies and 1 neck exploration. On admission we calucalated for all patients (with the standard protocol) the value of two trauma scores: Injury Severity Score (ISS) and Trauma Score (TS). (13,14) Patients with lung trauma were excluded by CT scan and CT angiography. Routine intraoperative monitoring (continuous electrocardiography, pulse oxymetry, direct arterial pressure via cannula and body temperature measured in the bladder) was performed. Systemic vascular resistance was measured with a Swan Ganz catheter. We used intermittent positive pressure ventilation (with sedation, analgesia and relaxation). Pet CO2 was continuously measured at the tip of the endotracheal tube by using a previously calibrated capnograph (Propaq encore – Model 202 EL, Protocol Systems INC, Beaverton, Oregon, USA). MAP was measured using the invasive method (Schiller Physiogard, TM 910, France). Arterial blood gasses were obtained every 30 – 60 minutes during the procedure. For fluid resuscitation we used 0,9% saline, Ringer solution, plasma expanders (6% HES and Voluven), fresh frozen plasma and concentrated erythrocytes. We compared initial data on admission to the operating room with those collected after adequate hemodynamical stability for each patient was achieved. Unless otherwise indicated, summary values are expressed as the mean +/- SD (standard deviation). The measurements of MAP and pet CO2 were distributed normally. Categorical variables were compared using the Fisher exact test and continuous variables using the Wilcoxon rank sum test. To quantify the association between two variables (relationship between MAP and pet CO2 and between pet CO2, HCO3- and base excess (BE) we determined the Pearson correlation coefficient (r).
We considered p < 0.05 to be significant.
Statistical calculations were performed using SAS version 8.2 (SAS Institute, Cary, NC) Systemic vascular resistence wasn’t determined in the early stage of treatment.
The study was approved by the Ethical Committee of the Ministry of Health in Slovenia.


A total of 216 simultaneous measurements were analyzed (61 patients; 45 male patients). The mean ISS (see methods section) was 24,3 +/- 11,3, and mean Trauma Score (see methods section) was 8,6 +/- 2,2. The average MAP on admission (95 +/-16 mmHg) was significantly lower than the average MAP after adequate hemodynamic stability was achieved (final value after surgical treatment: 131 +/- 18 mmHg; p=0.03. The average partial pressure of pet CO2 on admission (31 +/- 5 mmHg) was significant lower than the average pet CO2 after adequate hemodynamic support (final value after surgical treatment: 44 +/- mmHg; p=0.02).
The average ΔEt CO2 was 5,3 ± 2,8 mmHg and the average ΔMAP was 28,8 +/-12,8 mmHg. The average difference in MAP of 61 patients was: (ΔMAP) = 5.94 (+/-0.85 ) X Δ pet CO2 (r=0.68; p=0.001) The average Δ BE was -3,1 +/- -1,2 and average Δ HCO3- was 1,5 +/- 0,6 (between value on admission and value after surgical treatment). Pet CO2 correlated with BE (r = 0,73; p=0.001) and HCO3- (r = 0,64; p=0.01).


In steady state conditions alveolar CO2 elimination and therefore pet CO2 depend on CO2 production and on alveolar ventilation and pulmonary perfusion (cardiac output). (4,15) Previous studies have found that pet CO2 correlates with cardiac output. (4-7) In the setting of cardiac arrest it can aid identifying restoration of spontaneous circulation. (2,16) In addition pet CO2 has been shown to be a prognostic indicator of outcome following resuscitation from cardiac arrest. (3,17) Other investigators have demonstrated that pet CO2 effectively tracks hemodynamic changes in low flow conditions. (8,10,18) However, little is known about pet CO2 during resuscitation from hemorrhagic shock in clinical situations. In our study we observed the significant changes in pet CO2 (increase) after volume resuscitation and the quantitative relationship between pet CO2 and MAP (linear relationship). Guzman et al. (8) observed a rapid increase in pet CO2 immediately after reinfusion of blood and restoration of oxygen delivery in an experimental study with dogs. They concluded that this increase in pet CO2 reflects CO2 washout and repayment of oxygen debt in addition to re-establishment of normal aerobic metabolism following restoration of systemic perfusion.
Jin et al. (7) in animal models of hemorrhagic shock, concluded that decreases in pet CO2 were accompanied by decreases in Pa CO2, MAP and cardiac index during bleeding. After reinfusion of blood pet CO2, cardiac index, MAP and Pa CO2 returned to approximately baseline concentrations. Tybursky et al. (11,12) concluded that pet CO2 can be useful in predicting survival and may have utility to guide intraoperative resuscitation efforts. We concluded that pet CO2 can be used as a reliable non-invasive monitoring device in patients with hemorrhagic shock (especially in pre-hospital conditions) and correlates with HCO3-, pet CO2, pO2, pH and BE. In our investigation the correlation between pet CO2, HCO3- and BE was confirmed. We find pet CO2 an important adjuvant in monitoring patients with hemorrhagic shock. In addition to conventional monitoring of heart rate, blood pressure, respiratory rate, body temperature and blood oxygen saturation we suggest pet CO2 as a vital sign that should be monitored. On the basis of the results of these small pilot observational studies in hospital, we have started a large prospective study in the pre-hospital setting.
Limitations. Changes in alveolar ventilation can affect results. In patients with altered ventilation/perfusion ratios (cheonic obstructive pulmonary disease, atelectasis, chronic congestive heart failure, respiratory distress syndrome) the difference between pet CO2 and arterial pCO2 may increase up to 20 mmHg or more because of a decrease in pet CO2 stemming from non -perfused areas. (19) In addition pet CO2 is typically decreased after administration of vasopressor drugs (an increase of the veno-arterial mismatch, whereby CO2 returns to the arterial circuit after shunting the alveoli).
Conclusions. The present study supports on-line pet CO2 monitoring as a reliable, non-invasive and continuous methods for measuring perfusion failure in the setting of hemorrhage (when minute ventilation is relatively constant). In the future, research should be done to determine accurate parameters – the values of pet CO2 for each stage of haemorrhagic shock -in the pre-hospital setting.


01. West JB. Ventilation-perfusion relationship. Am Rev Respir Dis 1977;116:919-43.
02. Grmec Š, Klemen P. Does the end-tidal carbon dioxide (Et CO2) concentration have prognostic value during out-of-hospital cardiac arrest. Eur J Emerg Med 2001;8:263-9.
03. Grmec Š, Kupnik D. Does the Mainz Emergency Evaluation Scoring (MEES) in combination with capnometry (MEESc) help in the prognosis of outcome from cardiopulmonary resuscitation in a prehospital setting. Resuscitation 2003;58:89-96.
04. Isserles SA, Breen PH. Can changes in end-tidal pet CO2 measure changes in cardiac out-put? Anesth Analg 1991;73:808-14.
05. Ornato JP, Garnet AR, Glauser FL. Relationship between cardiac output and the end-tidal carbon dioxide tension. Ann Emerg Med 1990;19:1104-6.
06. Weil MH, Bisera J, Trevino RP, Rackow EC. Cardiac output and end-tidal carbon dioxide. Crit Care Med 1985;13:907-9.
07. Jin X, Weil MH, Tang W, Povoas H, Pernat A, Xie J, et al. End-tidal carbon dioxide as a noninvasive indicator of cardiac index during circulatory shock. Crit Care Med 2000;28:2415-9.
08. Guzman JA, Lacoma FJ, Najari A, Kruse JA. End-tidal partial pressure of carbon dioxide as a noninvasive indicator of systemic oxygen supply dependency during hemorrhagic shock and resuscitation. Shock 1997;8(6):427-31.
09. Dubin A, Murias G, Estenssoro E, Canales H, Sottile P, Badie J, et al. End-tidal CO2 pressures determinants during hemorrhagic shock. Intensive Care Med 2000;26(11):1619-23.
10. Dubin A, Silva C, Calvo G, Valli J, Faruna O, Estenssoro E, et al. End-tidal CO2 pressure in the monitoring of cardiac output during canine hemorrhagic shock. J Crit Care 1990;5:42-6.
11. Tyburski JG, Collinge JD, Wilson RF, Carlin AM, Albaran RG, Steffes CP. (2002) End-tidal CO2 derived values during emergency trauma surgery correlated with outcome: A prospective study. J Trauma 2002;53:738-43.
12. Tyburski JG, Carlin AM, Harvey EHS, Steffes C, Wilson RF. End-tidal CO2 – arterial CO2 differences: a useful intraoperative mortality marker in trauma surgery. J Trauma 2003;55:892-7.
13. Copes WS, Champion HR, Sacco WJ, Lawnich MM, Keast SL, Bain LW. The injury severity score revised. J Trauma 1988;28:69-77.
14. Champion HR, Sacco WJ, Carnazzo AJ, Copes WS, Fouty WJ. Trauma Score. Crit Care Med 1981;9:672-6.
15. Ward KR, Yealy MD. End Tidal Carbon Dioxide Monitoring in Emergency Medicine, Part 1: Basic Principles. Acad Emerg Med 1998;5:628-38.
16. Falk JL, Rackow EC, Weil MH. End-tidal carbon dioxide concentration during cardiopulmonary resuscitation. N Engl J Med 1988;318:607-11.
17. Sanders AB, Kern K, Otto CW, Milander MM, Ewy GA. End-tidal carbon dioxide monitoring during cardiopulmonary resucitation. A prognostic indicator for survival. J Am Med Assoc 1989;262:1347-51.
18. Gazmuri RJ, von Planta M, Weil MH, Rackow EC. Arterial pCO2 as an indicator of systemic perfusion during cardiopulmonary resuscitation. Crit Care Med 1989;17:237-40.
19. Trillo G, von Planta M, Kette F. Et CO2 monitoring during low flow states: clinical aims and limitis. Resuscitation 1994;27:1-8.

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