Partial pressure of end-tidal carbon dioxide successful predicts cardiopulmonary resuscitation in the field: a prospective observational study

Introduction

Prognosis in patients suffering out-of-hospital cardiac arrest is poor. Higher survival rates have been observed only in patients with ventricular fibrillation who were fortunate enough to have basic and advanced life support initiated soon after cardiac arrest. An ability to predict cardiac arrest outcomes would be useful for resuscitation. Changes in expired end-tidal carbon dioxide levels during cardiopulmonary resuscitation (CPR) may be a useful, noninvasive predictor of successful resuscitation and survival from cardiac arrest, and could help in determining when to cease CPR efforts.

Methods

This is a prospective, observational study of 737 cases of out-of-hospital cardiac arrest. The patients were intubated and measurements of end-tidal carbon dioxide taken. Data according to the Utstein criteria, demographic information, medical data, and partial pressure of end-tidal carbon dioxide (Pet CO ₂) values were collected for each patient in cardiac arrest by the emergency physician. We hypothesized that an end-tidal carbon dioxide level of 1.9 kPa (14.3 mmHg) or more after 20 minutes of standard advanced cardiac life support would predict restoration of spontaneous circulation (ROSC).

Results

Pet CO ₂ after 20 minutes of advanced life support averaged 0.92 ± 0.29 kPa (6.9 ± 2.2 mmHg) in patients who did not have ROSC and 4.36 ± 1.11 kPa (32.8 ± 9.1 mmHg) in those who did (P < 0.001). End-tidal carbon dioxide values of 1.9 kPa (14.3 mmHg) or less discriminated between the 402 patients with ROSC and 335 patients without. When a 20-minute end-tidal carbon dioxide value of 1.9 kPa (14.3 mmHg) or less was used as a screening test to predict ROSC, the sensitivity, specificity, positive predictive value, and negative predictive value were all 100%.

Conclusions

End-tidal carbon dioxide levels of more than 1.9 kPa (14.3 mmHg) after 20 minutes may be used to predict ROSC with accuracy. End-tidal carbon dioxide levels should be monitored during CPR and considered a useful prognostic value for determining the outcome of resuscitative efforts and when to cease CPR in the field.     

呼气末二氧化碳监测在心肺复苏中的应用进展

分析通过测定呼气末二氧化碳分压(PetCO2)可以反映肺的气体交换状况、通气血流分布情况及循环状态等指标.PetCO2监测广泛应用于麻醉、危重症监护及急救医学等领域.2010年美国AHA心肺复苏(CPR)指南推荐连续PetCO2监测用于CPR整个过程以确认气管插管的位置,监测CPR的质量,并指导通气治疗.     

Measurement of end-tidal carbon dioxide concentration during cardiopulmonary resuscitation.

End-tidal carbon dioxide concentrations were measured prospectively in 12 cardiac arrest patients undergoing cardiopulmonary resuscitation (CPR) in an accident and emergency department. The end-tidal carbon dioxide (CO2) concentration decreased from a mean (+/- SD) of 4.55 +/- 0.88% 1 min after chest compression and ventilation was established, to values ranging from 2.29 +/- 0.84% at 2 min to 1.56 +/- 0.66% following 8 min of CPR. Spontaneous circulation was restored in five patients. This was accompanied by a rapid rise in end-tidal CO2 which peaked at 2 min (3.7 +/- 1.08%). Changes in end-tidal CO2 values were often the first indication of return of spontaneous cardiac output. There was a significant difference in the end-tidal CO2 in patients undergoing CPR before return of spontaneous circulation (2.63 +/- 0.32%) and patients who failed to develop spontaneous output (1.64 +/- 0.89%) (p < 0.001). We conclude that measurement of end-tidal CO2 concentration provides a simple and non-invasive method of measuring blood flow during CPR and can indicate return of spontaneous circulation.     

潮气末二氧化碳分压对心肺复苏结果的指导和预测作用

目的 探讨潮气末二氧碳(PetCO2)监测在心肺复苏(CPR)期间的临床意义并寻求定值以指导临床抢救.方法 采用回顾性研究方法,选择2003年5月至2009年3月解放军第四五一医院急诊科院内外非外伤性心搏骤停已明确原因的患者124例,监测心搏骤停患者在CPR过程中PetCO2的变化.结果 ①恢复自主循环(ROSC)的71例与未恢复的53例气管插管后性别、年龄、抢救时间比较P值分别为＜0.05,＜0.05,＜0.01,差异具有统计学意义,说明上述因素与复苏成功正相关,但性别和年龄与最终存活率无相关性.②最终存活者PetCO2水平高于未复苏成功者和虽复苏成功但最终院内死亡者,并与施救时间相关.③经过20 min的高级生命支持没有恢复自主循环者PetCO2平均水平在(6.7±1.2) mmHg(1mmHg =0.133 kPa),恢复自主循环者在(33.9±7.8) mmHg (P＜0.01),以20 min高级生命支持后PetCO2水平高于14.4 mmHg作为参考值预期死亡,阳性率和阴性率均为100％.结论 CPR过程中PetCO2的监测对复苏有指导和预测作用.     

Prediction of outcome of cardiopulmonary resuscitation from end-tidal carbon dioxide concentration

Capnography is a valuable tool in the management of cardiac arrest, since end-tidal CO2 (PetCO2) correlates well with cardiac output and there are no other suitable noninvasive ways to measure this important variable during resuscitation. Animal studies also suggest that PetCO2 correlates well with the likelihood of resuscitation, but this has never been confirmed in humans. We prospectively studied 55 adult, nontraumatic prehospital cardiac arrest patients. PetCO2 was monitored with an in-line sensor on arrival in the ED and throughout the arrest, which was managed by the usual advanced cardiac life-support treatment guidelines. Chest compression was carried out mechanically. Patients were assessed for return of spontaneous pulse as evidence of initial resuscitation; hospital discharge and long-term survival were not examined. Fourteen patients developed spontaneous pulses and were resuscitated, and 41 were not. The length and aggressiveness of treatment and CPR were not different between the two groups, nor were there differences in down time, resuscitation time, or other factors known to affect outcome. Patients who developed a pulse had a mean PetCO2 of 19 +/- 14 (SD) torr at the start of resuscitation, and those who did not had a mean PetCO2 of 5 +/- 4 torr (p less than .0001). This difference was significant both in nonperfusing rhythms (asystole and ventricular fibrillation) and in potentially perfusing rhythms (electromechanical dissociation). An initial PetCO2 of 15 torr correctly predicted eventual return of pulse with a sensitivity of 71%, a specificity of 98%, a positive predictive value of 91%, and a negative predictive value of 91%. A receiver operating curve was generated for sensitivity and specificity of the test at varying PetCO2 thresholds.     

Effect of cardiopulmonary resuscitation compression rate on end-tidal carbon dioxide concentration and arterial pressure in man

The optimal rate of chest compression during CPR in man has been debated. Recently, the end-tidal carbon dioxide concentration (PetCO2) has been shown to correlate with cardiac output during CPR in experimental animals. Eighteen prehospital cardiac arrest patients were studied to determine the effect of external chest compression rate on the PetCO2 and BP in man when ventilation rate, ventilation inspiration time, applied compression force, and a 50:50 downstroke:upstroke ratio were held constant using a microprocessor-controlled CPR Thumper. Compression rate was increased from 60 to 140/min in 20 beat/min increments. The PetCO2 was 1.7 +/- 0.2% at a compression rate of 60/min and did not change significantly at increased rates. Systolic BP fell progressively from 59 +/- 5 mm Hg at 60/min to 46 +/- 4 mm Hg at 140/min. Diastolic BP remained approximately 23 mm Hg at all rates studied. Using a CPR manikin, we found that greater Thumper compression force was necessary to sustain the same sternal displacement and to achieve the same applied sternal pressure when the rate was increased due to a rate-limited fall in the compression duration.     

Utility of colorimetric end-tidal carbon dioxide detector for monitoring during prehospital cardiopulmonary resuscitation

The purpose of this study was to evaluate a colorimetric end-tidal CO2 (ETCO2) detector (EASY CAP) as a monitor during prehospital cardiopulmonary resuscitation (CPR) without tracheal intubation. This detector was used for 121 patients during CPR with a laryngeal mask airway or face mask by authorized emergency lifesaving technicians. At 7 to 15 minutes after the initiation of CPR, ETCO was <0.5% in 30 cases (group A), 0.5% to 2.0% in 46 cases (group B) and >2.0% in 45 cases (group C). The rate of return of spontaneous circulation was 17% in group A, 24% in group B, and 48% in group C (groups A v C, P < .01). There was a significant difference in the rate of hospital admission between groups A and C. The ETCO2 value may be useful for monitoring during prehospital CPR with a laryngeal mask airway or face mask.     

Changes of end-tidal carbon dioxide during cardiopulmonary resuscitation from ventricular fibrillation versus asphyxial cardiac arrest

BACKGROUND:

Partial pressure of end-tidal carbon dioxide (P_ETCO₂) has been used to monitor the effectiveness of precordial compression (PC) and regarded as a prognostic value of outcomes in cardiopulmonary resuscitation (CPR). This study was to investigate changes of P_ETCO₂ during CPR in rats with ventricular fibrillation (VF) versus asphyxial cardiac arrest.

METHODS:

Sixty-two male Sprague-Dawley (SD) rats were randomly divided into an asphyxial group (n=32) and a VF group (n=30). P_ETCO₂ was measured during CPR from a 6-minute period of VF or asphyxial cardiac arrest.

RESULTS:

The initial values of P_ETCO₂ immediately after PC in the VF group were significantly lower than those in the asphyxial group (12.8±4.87 mmHg vs. 49.2±8.13 mmHg, P=0.000). In the VF group, the values of P_ETCO₂ after 6 minutes of PC were significantly higher in rats with return of spontaneous circulation (ROSC), compared with those in rats without ROSC (16.5±3.07 mmHg vs. 13.2±2.62 mmHg, P=0.004). In the asphyxial group, the values of P_ETCO₂ after 2 minutes of PC in rats with ROSC were significantly higher than those in rats without ROSC (20.8±3.24 mmHg vs. 13.9±1.50 mmHg, P=0.000). Receiver operator characteristic (ROC) curves of P_ETCO₂ showed significant sensitivity and specificity for predicting ROSC in VF versus asphyxial cardiac arrest.

CONCLUSIONS:

The initial values of P_ETCO₂ immediately after CPR may be helpful in differentiating the causes of cardiac arrest. Changes of P_ETCO₂ during CPR can predict outcomes of CPR.KEY WORDS: Partial pressure of end-tidal carbon dioxide, Cardiac arrest, Cardiopulmonary resuscitation, Return of spontaneous circulation, Rats     

Kinetics of carbon dioxide during cardiopulmonary resuscitation

CO2 kinetics during CPR was investigated in 15 anesthetized piglets. BP, blood gases, and acid-base balance were monitored through catheters in the carotid artery and a central vein, as well as in cerebrospinal fluid. Cardiac arrest was induced by a transthoracic direct current shock. CPR was begun immediately by artificial ventilation and simultaneous external chest compressions. Epinephrine was administered after 8 min of CPR. One group (n = 5) of animals received no buffer treatment while another (n = 5) received an infusion of 75 mmol sodium bicarbonate and a third group (n = 5) received an equivalent amount of tris-buffer mixture. The results of these experiments, as well as previously described circulatory variables during CPR, were analyzed using a computer model describing the CO2 kinetics of the pig. Our main finding was that PaCO2 was positively correlated to cardiac output during CPR; improved cardiac output during CPR resulted in more efficient tissue CO2 elimination and was associated with increased survival rates. PaCO2 was also somewhat reduced by efficient alveolar hyperventilation. The arterial PCO2 and pH did not reflect the acid-base balance in peripheral tissues. During CPR, bicarbonate and tris-buffer mixture both quickly passed through the blood-brain barrier. When buffer treatment is indicated during CPR, a buffer which does not increase tissue PCO2 may be the drug of choice.     

Effects of epinephrine and vasopressin on end-tidal carbon dioxide tension and mean arterial blood pressure in out-of-hospital cardiopulmonary resuscitation: an observational study

Introduction  

Clinical data considering vasopressin as an equivalent option to epinephrine in cardiopulmonary resuscitation (CPR) are limited. The aim of this prehospital study was to assess whether the use of vasopressin during CPR contributes to higher end-tidal carbon dioxide and mean arterial blood pressure (MAP) levels and thus improves the survival rate and neurological outcome.     

The effects of epinephrine/norepinephrine on end-tidal carbon dioxide concentration, coronary perfusion pressure and pulmonary arterial blood flow during cardiopulmonary resuscitation

End-tidal CO2 concentration correlates with pulmonary blood flow during cardiopulmonary resuscitation and has been claimed to be a useful tool to judge the effectiveness of chest compression. A high concentration of end-tidal CO2 has been related to a better outcome. However, most authors have noticed a decrease in end-tidal CO2 concentration after administration of epinephrine, concomitant with an increase in coronary perfusion pressure and an increased incidence of return of spontaneous circulation. This study was performed to evaluate changes in end-tidal CO2 concentration after injection of vasopressors during cardiopulmonary resuscitation and to investigate the time-course of the response and possible explanations for it. After 1 min of electrically induced cardiac arrest and 5 min of chest compressions, 18 pigs were randomly assigned to receive 0.045 mg kg(-1) epinephrine, 0.045 mg kg(-1) norepinephrine or no drug. After another 4 min of chest compressions the pigs were defibrillated. End-tidal CO2, pulmonary blood flow and coronary perfusion pressure decreased immediately after the induction of cardiac arrest, increased slightly during chest compressions and increased initially to supernormal levels after the return of spontaneous circulation. Injection of epinephrine or norepinephrine during chest compressions decreased end-tidal CO2 51 +/- 2%, (mean +/- S.E.M.), and 43 +/- 1%, respectively, and pulmonary blood flow by 134 +/- 13 and 125 +/- 16%, respectively, within 1 min, simultaneously increasing coronary perfusion pressure from 10 +/- 2 to 45 +/- 5 mm Hg and from 11 +/- 1 to 38 +/- 5 mm Hg, respectively. The coronary perfusion pressure slowly fell, but the effects on end-tidal CO2 and pulmonary blood flow were prolonged. In conclusion, vasopressors increased coronary perfusion pressure and the likelihood of a return of spontaneous circulation, but decreased end-tidal CO2 concentration and induced a critical deterioration in cardiac output and thus oxygen delivery in this model of cardiopulmonary resuscitation.     

Monitoring end-tidal carbon dioxide

Learn how a simple colorimetric device helps verify correct endotracheal tube placement.     

Continuous monitoring of gastric intraluminal carbon dioxide pressure, cardiac output, and end-tidal carbon dioxide pressure in the perioperative period in patients receiving cardiovascular surgery using cardiopulmonary bypass

OBJECTIVE: To verify the hypothesis that the gastric intraluminal PCO2 (PgCO2) changes independently of the change in cardiac output (CO) during and after cardiovascular surgery using cardiopulmonary bypass (CPB), and that the elevation of PgCO2 affects the patients' morbidity. DESIGN: Prospective, noninterventional study. SETTING: Medical/surgical intensive care unit and operating theater of a university hospital. PATIENTS: Sixteen adults patients receiving elective cardiovascular surgery using CPB. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: After induction of anesthesia, the patients were fitted with a gastric tube equipped at the tip with a CO2 sensor (ion-selective field effect transistor) that can continuously measure real-time PgCO2, and a pulmonary artery catheter capable of monitoring continuous CO (CCO) and end-tidal CO2. Data from the devices was uploaded to a personal computer every 2 mins until the catheter was pulled off based on clinical judgment (PgCO2 values were blinded to everyone except the investigator). One patient expired as a result of multiple organ failure subsequent to sepsis, and postoperative morbidity assessed by the peak SOFA (sequential organ failure assessment) score (mean +/- SD 6.9 +/- 3.5; range, 2-13) was correlated with the peak PgCO2 during intensive care unit stay (mean +/- SD 74.1 +/- 30.7 mm Hg; range, 45-169 mm Hg) (p < .01, by regression analysis). The peak PgCO2 during surgery (mean +/- SD 71.1 +/- 18.1 mm Hg; range, 44-115 mm Hg) had no correlation with the postoperative morbidity. From analysis of CCO before, during, and after returning from the above 60 mm Hg of PgCO2, PgCO2 changed independently of CCO. CONCLUSIONS: PgCO2 changed independently of CCO, and its postoperative elevation was related to morbidity, even in the group of patients with a good outcome. Continuous monitoring of PgCO2 is useful for the detection of morbidity and can be expected to help elucidate the pathophysiology of change of PgCO2.     

Noninvasive monitoring of carbon dioxide: A comparison of the partial pressure of transcutaneous and end-tidal carbon dioxide with the partial pressure of arterial carbon dioxide

This study compares two noninvasive techniques for monitoring the partial pressure of carbon dioxide (Pco2) in 24 anesthetized adult patients. End-tidal PCO₂ (PETCO₂) and transcutaneous Pco₂ (PtcCO₂) were simultaneously monitored and compared with arterial Pco₂ (PaCO₂) determined by intermittent analysis of arterial blood samples. PETCO₂ and PtcCO₂ values were compared with PaCO₂ values corrected to patient body temperature (PaC0_2T) and PaCO₂ values determined at a temperature of 37°C (PaCO₂). Linear regression was performed along with calculations of the correlation coefficient (r), bias, and precision of the four paired variables:PETCO₂ versus PaCO₂ and PaCO_2T (n = 211), and PtcCO₂ versus PaCO₂ and PaCO_2T (n = 233). Bias is defined as the mean difference between paired values, whereas precision is the standard deviation of the difference. The following values were found forr, bias, and ± precision, respectively.PetCO₂ versus PaCO₂: 0.67, ?7.8 mm Hg, ±6.1 mm Hg;PETCO₂ versus PaCO_2T: 0.73, ?5.8 mm Hg, ±5.9 mm Hg;PETCO₂ versus PaCO₂: 0.87, ?1.6 mm Hg, ±4.3 mm Hg; PtcCO₂ versus PaC0_2T: 0.84, +0.7 mm Hg, ±4.8 mm Hg. Although each of thesePCO ₂ variables is physiologically different, there is a significant correlation (P < 0.001) between the noninvasively monitored values and the blood gas values. Temperature correction of the arterial values (PaCO_2T) slightly improved the correlation, with respect toPETCO₂, but it had the opposite effect for PtcCO₂. In this study, the chief distinction between these two noninvasive monitors was thatPETCO₂ had a large negative bias, whereas PtcCO₂ had a small bias. We conclude from these data that PtcCO₂ may be used to estimate PaCO₂ with an accuracy similar to that ofPetCO₂ in anesthetized patients.     

Cardiac output and end-tidal carbon dioxide

Previous studies demonstrated selective increases in mixed venous carbon dioxide tension (PvCO2) during CPR in a porcine model of cardiac arrest. This was associated with a decrease in end-tidal carbon dioxide concentration (ETCO2), possibly due to a critical reduction in cardiac output and therefore pulmonary blood flow during CPR. We investigated the relationship between ETco2 and cardiac output before cardiac arrest and during CPR. Observations in 19 minipigs confirmed a high linear correlation between ETco2 and cardiac output. We conclude that the increase in Pvco2 and the concurrent decrease in ETco2 reflect a critical reduction in cardiac output, which reduces alveolar blood flow to the extent that carbon dioxide clearance by the lung fails to keep pace with systemic CO2 production.     

The gradient between arterial and end-tidal carbon dioxide predicts in-hospital mortality in post-cardiac arrest patient

Purpose

We investigated the predictive value of the gradient between arterial carbon dioxide (PaCO₂) and end-tidal carbon dioxide (ETCO₂) (Pa-ETCO₂) in post-cardiac arrest patients for in-hospital mortality.

Accuracy of end-tidal carbon dioxide tension analyzers

Substantial mean differences between arterial carbon dioxide tension (PaCO₂) and end-tidal carbon dioxide tension (PetCO₂) in anesthesia and intensive care settings have been demonstrated by a number of investigators. We have explored the technical causes of error in the measurement ofPetCO₂ that could contribute to the observed differences. In a clinical setting, the measurement ofPetCO₂ is accomplished with one of three types of instruments, infrared analyzers, mass spectrometers, and Raman spectrometers, whose specified accuracies are typically ±2, ±1.5, and ±0.5 mm Hg, respectively. We examined potential errors inPetCO₂ measurement with respect to the analyzer, sampling system, environment, and instrument. Various analyzer error sources were measured, including stability, warm-up time, interference from nitrous oxide and oxygen, pressure, noise, and response time. Other error sources, including calibration, resistance in the sample catheter, pressure changes, water vapor, liquid water, and end-tidal detection algorithms, were considered and are discussed. On the basis of our measurements and analysis, we estimate the magnitude of the major potential errors for an uncompensated infrared analyzer as: inaccuracy, 2 mm Hg; resolution, 0.5 mm Hg; noise, 2 mm Hg; instability (12 hours), 3 mm Hg; miscalibration, 1 mm Hg; selectivity (70% nitrous oxide), 6.5 mm Hg; selectivity (100% oxygen), −2.5 mm Hg; atmospheric pressure change, <1 mm Hg; airway pressure at 30 cm H₂O, 2 mm Hg; positive end-expiratory pressure or continuous positive airway pressure at 20 cm H₂O, 1.5 mm Hg; sampling system resistance, <1 mm Hg; and water vapor, 2.5 mm Hg. In addition to these errors, other systematic mistakes such as an inaccurate end-tidal detection algorithm, poor calibration technique, or liquid water contamination can lead to gross inaccuracies. In a clinical setting, unless the user is confident that all of the technical error sources have been eliminated and the physiologic factors are known, depending onPetCO₂ to determine PaCO₂ is not advised. An erratum to this article is available at .     

Accuracy of end-tidal carbon dioxide tension analyzers

Substantial mean differences between arterial carbon dioxide tension (PaCO₂) and end-tidal carbon dioxide tension (PetCO₂) in anesthesia and intensive care settings have been demonstrated by a number of investigators. We have explored the technical causes of error in the measurement ofPetCO₂ that could contribute to the observed differences. In a clinical setting, the measurement ofPetCO₂ is accomplished with one of three types of instruments, infrared analyzers, mass spectrometers, and Raman spectrometers, whose specified accuracies are typically ±2, ±1.5, and ±0.5 mm Hg, respectively. We examined potential errors inPetCO₂ measurement with respect to the analyzer, sampling system, environment, and instrument. Various analyzer error sources were measured, including stability, warm-up time, interference from nitrous oxide and oxygen, pressure, noise, and response time. Other error sources, including calibration, resistance in the sample catheter, pressure changes, water vapor, liquid water, and end-tidal detection algorithms, were considered and are discussed. On the basis of our measurements and analysis, we estimate the magnitude of the major potential errors for an uncompensated infrared analyzer as: inaccuracy, 2 mm Hg; resolution, 0.5 mm Hg; noise, 2 mm Hg; instability (12 hours), 3 mm Hg; miscalibration, 1 mm Hg; selectivity (70% nitrous oxide), 6.5 mm Hg; selectivity (100% oxygen), –2.5 mm Hg; atmospheric pressure change, <1 mm Hg; airway pressure at 30 cm H₂O, 2 mm Hg; positive end-expiratory pressure or continuous positive airway pressure at 20 cm H₂O, 1.5 mm Hg; sampling system resistance, <1 mm Hg; and water vapor, 2.5 mm Hg. In addition to these errors, other systematic mistakes such as an inaccurate end-tidal detection algorithm, poor calibration technique, or liquid water contamination can lead to gross inaccuracies. In a clinical setting, unless the user is confident that all of the technical error sources have been eliminated and the physiologic factors are known, depending onPetCO₂ to determine PaCO₂ is not advised.