‘Life like’ end-tidal CO2 production has been reported in frozen cadaver during intubation training. We report the same phenomenon in a non-frozen cadaveric model used to undertake CT postmortem, with the additional findings of an increase in CO2 with chest compressions and an increase in CO2 after a pause in ventilation.
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Measurable end-tidal CO2 has been previously reported in a frozen cadaveric model used for intubation training.1 We made the same observation in a non-frozen cadaver undergoing ‘ABC’ interventions as part of a research project into the use of postmortem CT (PMCT) compared with physical postmortem. As part of the PMCT procedure, the cadaver is intubated, and ventilation and chest compressions are used to circulate injected contrast for a contrast-enhanced CT scan to aid the diagnosis of the cause of death. This procedure may also allow the comparison of different methods of cardiopulmonary resuscitation (CPR). The project had Research Ethics Committee approval and was supported by a Resuscitation Council (UK) grant. Consent was obtained from relatives.
The patient was an elderly female without known abnormality of the airway, who had been in a temperature-controlled environment at 4°C for 32 h after death with no other preservation. She was intubated and approximately 60 min later ventilation was commenced. End-tidal CO2 was measured from the start of ventilation using continuous waveform capnography (Propaq CS Monitor, Model 246, Software V.3.7X, Welch Allyn). After 8 min of ventilation, a venous injection of contrast was given via the right antecubital fossa and 2 min of chest compressions performed using a Lucas device. Ventilation was then stopped on an inspiratory hold and whole body CT was undertaken.
The configuration of the CO2 trace obtained was similar to that seen in a live patient (figure 1). The initial end-tidal CO2 levels were high (at about 6 kPa), then decreased rapidly (figure 2)—confirming findings previously reported in a frozen cadaver. A novel observation was that the level of CO2 rose again (although at low levels) when CPR was started, presumably due to effective circulation. The PMCT confirmed that some circulation had been achieved as contrast had travelled into the pulmonary vasculature, and also confirmed that the endotracheal tube was situated in the trachea. A further novel finding was that end-tidal CO2 was again higher after the pause in ventilation required for the CT scan, presumably due to diffusion of CO2 down a concentration gradient created by the ventilation-induced fall in alveolar partial pressure, or ongoing bacterial activity.
These novel findings will be further investigated to establish whether or not measurement of end-tidal CO2 in cadavers has a role: (a) in a protocol for PMCT (as it may indicate effective ventilation and circulation of contrast) or (b) in the comparison of the effectiveness of different methods of CPR.
Contributors TJC drafted the manuscript. All the authors reviewed and revised the draft.
Funding Resuscitation Council UK.
Competing interests None declared.
Ethics approval REC Nottingham 1.
Provenance and peer review Not commissioned; externally peer reviewed.
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