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 .
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?
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
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.
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