Elsevier

Resuscitation

Volume 132, November 2018, Pages 73-77
Resuscitation

Review
Capnography during cardiac arrest

https://doi.org/10.1016/j.resuscitation.2018.08.018Get rights and content

Abstract

Successful resuscitation from cardiac arrest depends on provision of adequate blood flow to vital organs generated by cardiopulmonary resuscitation (CPR). Measurement of end-tidal expiratory pressure of carbon dioxide (ETCO2) using capnography provides a noninvasive estimate of cardiac output and organ perfusion during cardiac arrest and can therefore be used to monitor the quality of CPR and predict return of spontaneous circulation (ROSC). In clinical observational studies, mean ETCO2 levels in patients with ROSC are higher than those in patients with no ROSC. In prolonged out of hospital cardiac arrest, ETCO2 levels <10 mmHg are consistently associated with a poor outcome, while levels above this threshold have been suggested as a criterion for considering patients for rescue extracorporeal resuscitation. An abrupt rise of ETCO2 during CPR suggests that ROSC has occurred. Finally, detection of CO2 in exhaled air following intubation is the most specific criterion for confirming endotracheal tube placement during CPR. The aetiology of cardiac arrest, variations in ventilation patterns during CPR, and the effects of drugs such as adrenaline or sodium bicarbonate administered as a bolus may significantly affect ETCO2 levels and its clinical significance. While identifying ETCO2 as a useful monitoring tool during resuscitation, current guidelines for advanced life support recommend against using ETCO2 values in isolation for decision making in cardiac arrestmanagement.

Introduction

End-tidal carbon dioxide (ETCO2) is the partial pressure of carbon dioxide (PCO2) in the exhaled air measured at the end of expiration. CO2 is produced in perfused tissues by aerobic metabolism, it diffuses from the cells into the blood and is transported by the venous return to the lungs, where it is removed by ventilation. The major determinants of ETCO2 therefore include CO2 production, cardiac output (CO), lung perfusion and alveolar ventilation [1].

Capnography represents a continuous, non-invasive measurement of PCO2 in the exhaled air during the breathing cycle. The correspondent waveform is called a capnogram (Fig. 1).

In the typical capnogram ETCO2 is the value recorded at the end of the plateau phase and it is the one which better reflects the alveolar PCO2. Normally, ETCO2 is around 5 mmHg lower than PCO2 in the arterial blood (PaCO2). This gradient increases when there is a ventilation/perfusion mismatch in the lung that may occur because of pulmonary embolism or lung hypoperfusion during cardiac arrest [2].

Section snippets

ETCO2 for monitoring the effectiveness of cardiopulmonary resuscitation

In patients with cardiac arrest, cardiopulmonary resuscitation (CPR) temporarily restores CO. Both experimental [3,4] and clinical [5] studies have shown that survival from cardiac arrest depends on provision of adequate perfusion to vital organs. However, direct measurement of organ blood flow during CPR is not clinically feasible. ETCO2 represents a non-invasive measurement of the effectiveness of CPR in terms of blood flow that is generated and the potential of successful resuscitation.

In an

ETCO2 to confirm endotracheal tube placement during CPR

Performing a rapid and successful endotracheal intubation during resuscitation from cardiac arrest is important. Detection of CO2 in exhaled air using waveform capnography is the most specific method for confirming endotracheal tube placement.

A study [19] from Grmec et al. on 246 OHCAs who underwent prehospital intubation showed that capnography had 100[97–100]% specificity and 100[98–100]% sensitivity for detecting correct endotracheal tube placement. In a study [20] on 81 OHCAs who were

ETCO2 to detect ROSC

ROSC is associated with a significant increase of ETCO2 (Fig. 2), which raises up to a level three times above the values during CPR and then slowly declines to a stable value in all patients that maintain ROSC [24]. ETCO2 monitoring can therefore help detect ROSC during resuscitation to avoid continuing unnecessary chest compression. On the other side, however, inappropriate interruptions of CPR should also be avoided, since they are detrimental to defibrillation success and survival [19,25,26

ETCO2 to predict survival from cardiac arrest

Since ETCO2 is expected to reflect organ perfusion during CPR, it may not only represent a target of resuscitation, but also a predictor indicating when prolonged CPR is futile. In 1997, Levine et al. [30] investigated on the association between ETCO2 measured after 20 min of ALS and survival to hospital admission in 150 adults with OHCA from primary cardiac cause associated to pulseless electrical activity (PEA). Results showed that no patient with ETCO2 ≤10 mmHg after 20 min of ALS survived

Confounding factors

When interpreting ETCO2 values during CPR a series of confounding factors need to be taken into account. As mentioned above, in patients with a respiratory cause of arrest, ETCO2 may initially be high [35,46] as a result of hypercapnia and may therefore not reflect cardiac output generated by CPR.

Conversely, hyperventilation decreases ETCO2 levels during CPR. In a pig model of cardiac arrest Gazmuri et al. [47] demonstrated that increasing either respiratory rate from the recommended value of

Conclusion

Measurement of ETCO2 is currently the only noninvasive clinical tool for estimating organ perfusion during CPR. During experimental CPR, ETCO2 has shown a significant positive correlation with cardiac index and with coronary and cerebral perfusion pressures. In observational studies on pre-hospital cardiac arrest, ETCO2 levels below 10 mmHg after 20 min of ALS were highly predictive of pre-hospital mortality. However, accuracy of ETCO2 as a predictor of ROSC is lower when it is measured earlier

Conflict of interest statement

We wish to confirm that there are no known conflicts of interest associated with this publication and there has been no significant financial support for this work that could have influenced its outcome.

We confirm that the manuscript has been read and approved by all named authors and that there are no other persons who satisfied the criteria for authorship but are not listed. We further confirm that the order of authors listed in the manuscript has been approved by all of us.

We confirm that we

Acknowledgment

None.

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