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Original Contribution

Capnography as a Predictor of the Return of Spontaneous Circulation

August 2004

Capnography, which has become an integral part of monitoring in the prehospital environment, helps to prevent life-threatening events. Monitors available for prehospital care use infrared spectrography technology to measure carbon dioxide in respiratory gases, then give a numerical reading (capnometry) and a waveform (capnography). The capnogram provides information about respiratory rate and effectiveness, and end-tidal carbon dioxide values. Expired carbon dioxide reflects changes in metabolism, circulation, respiration, the airway and the breathing system. Thus, capnography has clinical relevance as a tool for cardiopulmonary status, including return of spontaneous circulation (ROSC) following cardiac arrest.

Introduction to Capnography

Carbon dioxide is produced in the tissues by metabolism and transported in blood to the lung by venous return, which is essentially equal to cardiac output. Carbon dioxide is then eliminated from the lung by minute ventilation. To understand the significant value of EtCO2, one needs to be familiar with the following: normal physiology of CO2, principle determinants of EtCO2, CO2 gradient with normal VQ relationship, EtCO2 analyzer (capnometer) and limitations of EtCO2 measurements.1

EtCO2 represents the partial pressure or maximal concentration of CO2 at the end of exhalation. There are four main stages of normal CO2 physiology: production, transport, buffering and elimination. CO2 production occurs in cells. As intracellular CO2 increases, CO2 diffuses out into the tissue capillaries and is carried by venous circulation to the lungs, where it diffuses from pulmonary capillaries into the alveoli. The partial pressure of CO2 (PaCO2) of venous blood entering pulmonary capillaries is normally 45 mmHg; the partial alveolar pressure of CO2 (PACO2) is normally 40 mmHg.2 The pressure difference of 5 mmHg will cause all the required CO2 to diffuse out of pulmonary capillaries into the alveoli.

The second stage is CO2 transport, which is a way of maintaining the CO2 tension of arterial blood at approximately 35–45 mmHg despite high CO2 production due to increased metabolism. Transport is typically a function of cardiac output and venous return.

The third stage is where the buffer action of hemoglobin and pulmonary blood flow maintains the normal level of CO2 tension by eliminating excess CO2. CO2 can either be carried, dissolved or combined with water (H2O) to form carbonic acid (H2CO3), which can dissipate to hydrogen ions (H+) and bicarbonate ions (HCO3-). The hydrogen ions are buffered by hemoglobin, and the bicarbonate ions are transported into the blood. This mechanism accounts for 90% of CO2 transport.

The fourth stage involves CO2 elimination by alveolar ventilation under the control of the respiratory center. This process allows the diffusion of CO2 from blood to the alveoli, where the partial alveolar pressure of CO2 is lower than tissue pressure. During normal cardiopulmonary circulation, the PaCO2 is closely comparable to EtCO2; therefore, PaCO2 can be considered equivalent to EtCO2. This relationship may be significantly altered in the prehospital patient with significant pre-existing lung disease.

The principal determinants of EtCO2 are alveolar ventilation, pulmonary perfusion (cardiac output) and CO2 production. During an acutely low cardiac output state, as in cardiac arrest, decreased pulmonary blood flow becomes the primary determinant, resulting in abrupt decrease of EtCO2. Changes in alveolar ventilation can also influence EtCO2. If ventilation and chest compressions are constant, with the assumption that CO2 production during cardiac arrest is constant, then the change in EtCO2 reflects changes in systemic and pulmonary blood flow. Ultimately, EtCO2 can be used as a quantitative index for evaluating adequacy of ventilation and pulmonary blood flow during CPR.3

Capnography Technology and Implementation

Capnography is a safe, noninvasive test associated with few hazards. With mainstream analyzers, using too-large a sampling window may introduce a small amount of dead space into the breathing system. Care must be taken to minimize the amount of additional weight placed on the artificial airway by adding the sampling window or sampling line. Capnography, in both sidestream and mainstream applications, has few limitations.

Mainstream Capnography

The main advantage of the mainstream analyzer is its rapid response, because the measurement chamber is part of the breathing circuit. The sample cuvette lumen, through which inspired and expired gases pass, is large in order to minimize the work of breathing, and pulmonary secretions generally do not interfere with carbon dioxide analysis. However, compared with sidestream sampling, the airway cuvette is relatively bulky and can add dead space. But within the past few years, lighter and smaller airway cuvettes have been developed to reduce the impact of these issues. The analyzer is warmed to prevent condensation on the sample chamber window. The monitoring of EtCO2 in nonintubated patients is more difficult with mainstream sampling, although this does not typically present as a problem during prehospital cardiac arrest situations.

Sidestream Capnography

The sidestream EtCO2 analyzer adds only a light T-adapter to the breathing circuit and can be easily adapted to nonintubation forms of airway control. Because the sampling tubing is small-bore, it can be blocked by secretions. During sidestream capnography, the dynamic response, the steepness of the expiratory upstroke and inspiratory downslope, tends to be blunted because of the dispersive mixing of gases through the sampling line, where gas of high CO2 concentration mixes with gas of low CO2 concentration. In addition, a washout time is required for the incoming sampled gas to flush out the volume of the measuring chamber mounted at the endotracheal tube. The overall effect is an averaging of the capnogram, resulting in a lowered alveolar plateau and elevated inspiratory baseline. EtCO2 may be underestimated in this situation. These problems are exacerbated by high ventilatory rates and the use of long sampling tubing. In addition, the capnogram is delayed in time by transport delay—the time required to aspirate gas from the airway opening adapter through the sampling tubing to the sampling chamber within the monitor.

Prior to implementation of capnography in an EMS system, training must be provided and all prehospital clinicians must demonstrate knowledge and skills to correctly initiate, calibrate and evaluate capnography, assess the patient and patient-ventilator system, and exercise appropriate clinical judgment. Capnography is not a difficult topic to learn, but it requires a specific educational program for proper use and to gain maximum benefit for the patient.

Predicting Survival in Cardiopulmonary Arrest

Prediction of survival, as measured by return of spontaneous circulation (ROSC) during cardiopulmonary resuscitation, is difficult. The potential for survival in field resuscitation is dependent upon several factors, including ROSC. Other factors include judgment of causal factors surrounding the cardiac arrest, patient-defined limits to resuscitation, response to resuscitation efforts, length of time from onset of cardiac arrest, and length of time since initiation of resuscitation efforts. Objective methods for assessment of ROSC (pulse detection by Doppler, invasive blood pressure measurement, etc.) are often limited to hospital use. Continuous assessment of EtCO2 during prehospital CPR allows differentiation between patients with ROSC and without ROSC.

The quantitative measurement of PETCO2 may have predictive value during CPR. This was recognized as early as 1939, when Eisenmenger wrote, “If, during a resuscitation attempt, the analysis of the expired air, performed about twice per hour, still shows plenty of carbon dioxide, then continuation of artificial respiration (and circulation) would be indicated.” Exhaled CO2, specifically EtCO2, is a noninvasive indicator of cardiac output. The lower the cardiac output, the lower the EtCO2. If EtCO2 is less than 10 mmHg after 20 minutes of CPR, the resuscitation effort is almost always unsuccessful.4 The higher the EtCO2, the more effective the resuscitation effort.5-7

In most human and animal studies of CPR, ventricular fibrillation is the mode of arrest. They show a characteristic pattern of a sudden drop in CO2 that increases with effective CPR. The most common cause of pediatric cardiac arrest is respiratory arrest. The initial EtCO2 has been shown to be markedly elevated, decreased to low levels during CPR and finally increased at ROSC. This is due to accumulation of CO2 in the lungs after respiratory arrest and prior to cardiac arrest.

An important and relatively successful application of capnography in the nonsteady-state clinical setting has been during CPR. As a cardiac arrest occurs, the abrupt decrease in cardiac output results in a reduction in carbon dioxide transport from the tissues to lungs, with a subsequent reduction in carbon dioxide elimination from the lungs. Capnography is also a useful noninvasive index of the adequacy of pulmonary perfusion during closed-chest cardiac compression. With effective CPR, the increase in cardiac output restores some pulmonary blood flow and carbon dioxide transport, and thus increases pulmonary elimination of carbon dioxide. This will produce a measurable increase on the capnometer. In fact, capnography may be used to compare the efficacy of different modes of chest compression.8,9

A dramatic increase in exhaled carbon dioxide is the best signal of return of spontaneous circulation.

Capnography in the Field

Analysis of PaCO2 is not available in the field, but it correlates well with EtCO2 in most patients. Capnography functions as an excellent adjunct to other monitoring methods. While EtCO2 levels in very ill patients should be interpreted with caution, trends in EtCO2 correlate with changes in PaCO2 and can provide an early warning of metabolic or cardiorespiratory problems, such as shunting, dead space, bronchoconstriction or pulmonary embolism. Capnography allows for trending of the EtCO2 value.

Although capnographs can be used with pulse oximeters, and are often combined with them in single units, these instruments present different views of oxygenation and ventilation. Pulse oximeters require the presence of a pulse and measure oxygen saturation of hemoglobin in arterial blood (SpO2) at the sensor site, thereby providing additional information about the adequacy of lung perfusion and oxygen delivery to tissues. Capnography continuously measures pulmonary ventilation and is able to detect small changes in cardiorespiratory function rapidly, before oximeter readings change.

Trauma and Resuscitation

Respiratory assessment and monitoring of the trauma patient are of critical importance, as changes in vital signs and patient symptoms pose an increased risk to the patient’s stability. Trauma-patient monitoring may result in significant and immediate changes, as obtaining other vital signs may be difficult in the immediate resuscitation period. In addition to conventional monitoring of heart rate, blood pressure, respiratory rate and arterial oxygen saturation, EtCO2, as the sixth vital sign, should be monitored.10

Using clinical measures only, predicting survival after cardiac arrest, as measured by the return of spontaneous circulation, is difficult. Capnography has the potential to assist in making that prediction.11 The potential for survival is dependent upon several factors, including the cause of cardiac arrest, the patient’s response to resuscitation efforts, length of time elapsed from the onset of cardiac arrest and length of time since the initiation of resuscitation efforts. Objective methods for assessing return of spontaneous circulation (Doppler pulse detection and invasive blood-pressure measurement) are often limited to the ability to detect a pulse and circulation.

At the other end of the patient timeline, capnography is an objective assessment tool for predicting survival at the end of a period of cardiac arrest. EtCO2 levels correlate well with cardiac output, perfusion of peripheral tissues and pulmonary circulation. As cardiac output increases, perfusion of peripheral tissue beds improves, sweeping carbon dioxide from the peripheral circulation and returning it to the pulmonary capillary membrane for exhalation. The concentration of carbon dioxide in the exhaled gases increases as cardiac output increases. In patients with return of spontaneous circulation, the level of EtCO2 increases with cardiac output. Conversely, cardiac arrest can manifest itself as a sudden drop in EtCO2 from normal levels to near zero.

Capnography monitoring during resuscitation efforts has a potential ability to predict CPR outcomes, but there are several limitations. Manual ventilation and chest compressions could cause EtCO2 to fluctuate with the effort of compression and rate of ventilation. Ideally, the minute ventilation should be controlled during quantitative monitoring of EtCO2 in cardiac arrest since ETCO2 is affected by the alveolar ventilation. Administration of epinephrine may cause reduced end-tidal carbon dioxide readings.

Capnography in Shock and Low Perfusion

Respiratory assessment and monitoring of the critically ill or near-arrest patient are of critical importance, as capnography monitoring would be additive to changes in vital signs and patient symptoms as a measure of the patient’s stability. Capnography monitoring in near-arrest patients may result in significant and immediate changes, as obtaining other vital signs may be difficult in the immediate resuscitation period. In addition to conventional monitoring of heart rate, blood pressure, respiratory rate and arterial oxygen saturation, EtCO2, as the sixth vital sign, should be monitored.10

EtCO2 monitoring is widely used for various clinical practices, such as verification of endotracheal tube placement, assessment of conscious sedation safety and evaluation of mechanical ventilation. EtCO2 monitoring can guide prehospital clinicians in providing adequate oxygenation and ventilation to unstable patients, such as those with head injuries, if capnography is used correctly. A fall in EtCO2 may mean decreased lung perfusion. If ventilation has not changed, the decrease in EtCO2 may indicate early signs of shock;12 however, EtCO2 must be interpreted in the context of other information about the patient’s clinical status.

Summary

EtCO2 monitoring is a valuable tool for clinical management of patients in cardiac arrest, near-arrest and post-arrest. During cardiac arrest, EtCO2 levels fall abruptly at the onset of cardiac arrest, increase after the onset of effective CPR and return to normal at return of spontaneous circulation (ROSC). During effective CPR, end-tidal CO2 has been shown to correlate with cardiac output, coronary perfusion pressure, efficacy of cardiac compression, ROSC and even survival.

Colorimetric detectors (shown to correlate with infrared capnometry) have been shown to have prognostic value in both adult and pediatric CPR. The higher the initial value of EtCO2, the greater was short-term survival.13 EtCO2 is a useful tool during patient resuscitation for evaluating the current and potential effects of treatment, and could be potentially useful in determining when to terminate resuscitation efforts.

References

1. Szaflarski NL, Cohen NH. Use of capnography in critically ill adults. Heart Lung 20:363–372, 1991.
2. Prause G, Hetz H, Lauda P, et al. A comparison of the end-tidal CO2 documented by capnometry and the arterial pCO2 in emergency patients. Resuscitation 35:145–148, 1997.
3. White RD, Asplin BR. Out-of-hospital quantitative monitoring of end-tidal carbon dioxide pressure during CPR. Ann Emerg Med 23:25–30, 1994.
4. Domsky M, Wilson RF, Heins J. Intraoperative end-tidal carbon dioxide values and derived calculations correlated with outcome: prognosis and capnography. Crit Care Med 23:1497–1503, 1995.
5. Grmec S, Lah K, Tusek-Bune K. Difference in end-tidal CO2 between asphyxia cardiac arrest and ventricular fibrillation/pulseless ventricular tachycardia cardiac arrest in the prehospital setting. Crit Care 7(6):R139–44, Dec 2003.
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8. Ward KR, Menegazzi JJ, Zelenak RR, et al. A comparison of chest compressions between mechanical and manual CPR by monitoring end-tidal PCO2 during human cardiac arrest. Ann Emerg Med 22:669–674, 1993.
9. Koetter K, Maleck WH. Effectiveness of mechanical versus manual chest compressions in out-of-hospital cardiac resuscitation [letter]. Am J Emerg Med 17:210, 1999.
10. Helm M, Schuster R, Hauke J, Lampl L. Tight control of prehospital ventilation by capnography in major trauma victims. Br J Anaesth 90(3):327–332, Mar 2003.
11. Sehra R, Underwood K, Cheecchia P. End-tidal CO2 is a quantitative measure of cardiac arrest. Pacing Clin Electrophysiol 26(1, Pt 2):515–517, Jan 2003.
12. Callaham M, Barton C, Matthay M. Effect of epinephrine on the ability of end-tidal carbon dioxide readings to predict initial resuscitation from cardiac arrest. Crit Care Med 20(3):337–343, Mar 1992.
13. Ahrens T, Schallon L, Bettorf K, et al. End-tidal carbon dioxide measurements as a prognostic indicator of outcome in cardiac arrest. Am J Crit Care 10(6):391–398, Nov 2001.

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