A 68 year-old gentleman was admitted to the Emergency Department in cardiac arrest. He had complained of sudden onset upper abdominal pain to his wife immediately prior to a collapse, and bystander cardiopulmonary resuscitation (CPR) was commenced whilst emergency services were called. He had a background of ischaemic heart disease, insulin-dependent diabetes, peripheral vascular disease and hypertension.

On arrival, the Paramedic crew found him to be in ventricular fibrillation was the predominant rhythm. Despite appropriate advanced life support with defibrillation and administration of adrenaline and amiodarone over multiple cycles. His airway was supported with an I-Gel supraglottic airway device, and he was transferred to hospital urgently.

Ischaemic heart disease is the leading cause of death in the world, and sudden cardiac arrest is responsible for more than 60% of adult deaths from coronary heart disease. Early and effective CPR, early defibrillation and physiological support post-resuscitation form the chain of survival [1].

Assessment of the patient’s airway on arrival in the Emergency Department revealed evidence of vomit in the pharynx, and endotracheal intubation was performed. Vomitus was aspirated from his endotracheal tube, indicating pulmonary aspiration either at the time of collapse or during the resuscitation attempts. Sidestream capnography was connected to a self-inflating bag administering high-concentration oxygen. The initial capnography indicated a flattened end tidal carbon dioxide (EtCO2) trace with a highest partial pressure of 1.5 kPa. Chest auscultation was performed and air entry was confirmed as being equal bilaterally.

Chest compressions continued uninterrupted and by this stage the overall resuscitation attempt had been ongoing for 45 minutes. The rhythm had changed to pulseless electrical activity, and despite effective CPR, administration of adrenaline and fluids, there was no return of spontaneous circulation (ROSC). Blood gas analysis revealed a severe metabolic acidosis (pH 6.8, lactate 15.2 mmol/L) and by this stage the highest EtCO2 recorded was 0.9 kPa. Following discussion with the team, and on the grounds of futility, the resuscitation attempt was abandoned.

What is the role of capnography in cardiac arrest?

Measurement of EtCO2 has become gold-standard monitoring in anaesthesia and critical care, and provides an insight into cardio-respiratory function in the critically ill. Low cardiac output is reflected by low EtCO2 by two mechanisms. Firstly, there is reduced delivery of carbon dioxide to the lung, and secondly there is an increase in alveolar deadspace as a consequence of a high ventilation-to-perfusion ratio. EtCO2 has been shown to be closely- related to cardiac output in experimental models of shock, and it offers a non-invasive alternative for the continuous assessment of cardiac output during low-flow circulatory shock states [2].

The use of waveform capnography during cardiac arrest is recommended in the 2010 International Consensus on Cardiopulmonary Resuscitation Science with Treatment Recommendations. The Advanced Life Support Group confirm the superiority of waveform capnography over disposable colorimetric EtCO2 detectors and non-waveform devices. The use of waveform capnography has also been advocated by the Royal College of Anaesthetists 4th National Audit Project findings, as the primary method for confirming correct placement of an endotracheal tube (or other airway device) [3]. The sensitivity and specificity of capnography for endotracheal tube confirmation is superior to both auscultation and capnometry.

An attenuated (rather than absent) capnography trace is seen during CPR. Complete absence of expired CO2 during ventilation of the lungs can occur in certain circumstances. It can occur if the lungs are not being ventilated, for example by a misplaced or obstructed airway. It can also occur if the pulmonary arteries are not being perfused, for example by a massive pulmonary embolus, during cardiac arrest without CPR or in a deceased patient [4]. Monitoring error or failure may also account for an apparent absence of expired CO2.

Capnography has further uses in cardiac arrest, including early detection of poor-quality chest compressions, early indication of ROSC (by an immediate and sustained increase in EtCO2) and may guide termination, as an EtCO2 value of <10 mmHg after twenty minutes of resuscitation is strongly predictive of poor outcome [5]. High quality chest compressions will result in typical EtCO2 values of 2.0-2.5 kPa (15-20 mmHg) [6].

A retrospective review of capnography data in 575 non-traumatic out-of-hospital cardiac arrest (OOHCA) patients in Norway found that capnography distinguished between patients with or without ROSC. It was found that OOHCA of respiratory aetiology had a significantly higher EtCO2 in comparison with cardiac causes. Presence or absence of bystander CPR, as well as time from cardiac arrest until capnography measurement influenced EtCO2 values. It was commented that these complicating variables might limit interpretation of capnography as an accurate prognostic tool [7].

In 2014 a systematic review and meta-analysis of EtCO2 values associated with ROSC during CPR was undertaken [8]. Twenty studies were included to determine mean EtCO2 values. In participants with ROSC this was 25.8 ± 9.8 mmHg, versus 13.1 ± 8.2 mmHg in those without ROSC. Nineteen studies were included in a meta-analysis that revealed a mean difference of 12.7 mmHg between the two groups. This difference was not modified by administration of sodium bicarbonate, uncontrolled minute ventilation, or era of resuscitation guidelines.

In both studies there is no standardisation of minute ventilation delivered during cardiac arrest. In the absence of protocolised intermittent positive pressure ventilation through a mechanical ventilator, EtCO2 values will vary from case to case and values are less reliable as a predictor of outcome

---

 

Lessons Learnt

Capnography is a useful tool to guide treatment in cardiac arrest. Current evidence indicates higher EtCO2 in cardiac arrest with ROSC. An EtCO2 concentration of 25 mmHg might be an appropriate target during resuscitation, indicating the need for optimally effective chest compressions. However, factors determining EtCO2 are complex and rates of minute ventilation and CO2 production need to be considered when interpreting this.

Further research is needed to define appropriate EtCO2 targets during resuscitation, in an effort to improve outcome following cardiac arrest. With increasing cardiac arrest capnography data accumulating, there is reasonable hope that predictors of outcome and determining CPR duration will become more accurate in the future.

---

 

References

1. Advanced Life Support 6th Edition January 2011 ISBN 978-1903812228
2. JinX,WeilMH,TangW,PovoasH,PernatA,XieJ,etal.End-tidalcarbondioxide as a noninvasive indicator of cardiac index during circulatory shock. Crit Care Med. 2000;28:2415–9.
3. ScarthE,CookT.Capnographyduringcardiopulmonaryresuscitation. Resuscitation. 2012 Jul;83(7):789-90. doi: 10.1016/j.resuscitation.2012.04.002. Epub 2012 Apr 12.
4. CookTM,NolanJP.Useofcapnographytoconfirmcorrecttrachealintubation during cardiac arrest. Anaesthesia. 2011 Dec;66(12):1183-4. doi: 10.1111/j.1365- 2044.2011.06964.x.
5. HeradstveitBE,HeltneJK.PQRST-Auniqueaide-memoireforcapnography interpretation during cardiac arrest. Resuscitation 2014; 85:1619-20.
6. AdvancedLifeSupportAppendixE:WaveformCapnography185-187. https://www.resus.org.uk/pages/IOaccess.pdf
7. HeradstveitBE,SundeK,SundeGA,Wentzel-LarsenT,HeltneJK.Factors complicating interpretation of capnography during advanced life support in cardiac arrest–a clinical retrospective study in 575 patients. Resuscitation. 2012 Jul;83(7):813-8. doi: 10.1016/j.resuscitation.2012.02.021. Epub 2012 Feb 25.
8. HartmannSM,FarrisRW,DiGennaroJL,RobertsJS.SystematicReviewand Meta-Analysis of End-Tidal Carbon Dioxide Values Associated With Return of Spontaneous Circulation During Cardiopulmonary Resuscitation. J Intensive Care Med. 2014 Apr 22.