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I ran a bit of an unusual cardiac arrest this AM and thought I'd run a couple questions by the forum. In short, we witnessed the arrest but have no history from the patient or anyone else. A third party caller from another town contacted 911 and advised the patient had contacted her and complained of "difficulty breathing." We arrived a short time later and found the patient seated, unresponsive, gasping, extremely hypoxic, and with clenched muscles and rightward gaze. She had palpable (but weak) radial pulses at a rate of ~45. Before we were able to perform further assessment or any intervention, she began to brady down into an agonal rhythm and lost carotid pulses.
In the course of working this code, we placed a capnography EtCO2 cannula on her during our ventilations with a BVM per our standard policy. We had excellent compliance and easy ventilations with effective chest rise and fall noted during a period of ROSC, but our capnography output was quite low at ~5 mm Hg. I didn't think much of it as NC EtCO2 readings during arrests are understandably a bit hit or miss. I was far more surprised after I intubated the patient and still only had an EtCO2 reading of 5 mm Hg during ventilations through the ETT. Tube placement was confirmed again with video laryngoscopy and the cuff was noted to be inflated. As the patient was jostled during some movement, the EtCO2 gradually increased (no rhythm change from asystole) and then remained at ~40 mm Hg. At this point, the EtCO2 baseline remained high. I've attached a picture to demonstrate what I mean here. I'm accustomed to being able to visualize LUCAS compressions on the EtCO2 waveform, but typically the waveform returns to zero between ventilations.
This picture shows three waveforms and displays lead II on top in black, SpO2 pleth in the middle in blue, and the EtCO2 waveform on the bottom in orange. The LP15 calibrated and zeroed itself with the EtCO2 numeric at the end of ventilation being ~50 mm Hg at this point. You can see the compressions on the EtCO2 waveform along with a slightly higher and prolonged wave during ventilations.
Our best guess was that the patient may have suffered from a PE causing the arrest and then possibly dislodged the clot during compressions and jostling causing the rise in EtCO2 values. I remain a bit confused as to why the baseline would not return to zero or why she seemed to continually be exhaling some CO2 (or at least reading that way on the monitor). We had a brief period of ROSC and mechanical capture with pacing in which compressions were discontinued and the EtCO2 readings looked the same, so we don't believe it was caused by the continuous compressions not allowing the lungs to fully exhale. I haven't seen anything quite like it before. Any other ideas or additional experience with anything similar?
In the course of working this code, we placed a capnography EtCO2 cannula on her during our ventilations with a BVM per our standard policy. We had excellent compliance and easy ventilations with effective chest rise and fall noted during a period of ROSC, but our capnography output was quite low at ~5 mm Hg. I didn't think much of it as NC EtCO2 readings during arrests are understandably a bit hit or miss. I was far more surprised after I intubated the patient and still only had an EtCO2 reading of 5 mm Hg during ventilations through the ETT. Tube placement was confirmed again with video laryngoscopy and the cuff was noted to be inflated. As the patient was jostled during some movement, the EtCO2 gradually increased (no rhythm change from asystole) and then remained at ~40 mm Hg. At this point, the EtCO2 baseline remained high. I've attached a picture to demonstrate what I mean here. I'm accustomed to being able to visualize LUCAS compressions on the EtCO2 waveform, but typically the waveform returns to zero between ventilations.
This picture shows three waveforms and displays lead II on top in black, SpO2 pleth in the middle in blue, and the EtCO2 waveform on the bottom in orange. The LP15 calibrated and zeroed itself with the EtCO2 numeric at the end of ventilation being ~50 mm Hg at this point. You can see the compressions on the EtCO2 waveform along with a slightly higher and prolonged wave during ventilations.
Our best guess was that the patient may have suffered from a PE causing the arrest and then possibly dislodged the clot during compressions and jostling causing the rise in EtCO2 values. I remain a bit confused as to why the baseline would not return to zero or why she seemed to continually be exhaling some CO2 (or at least reading that way on the monitor). We had a brief period of ROSC and mechanical capture with pacing in which compressions were discontinued and the EtCO2 readings looked the same, so we don't believe it was caused by the continuous compressions not allowing the lungs to fully exhale. I haven't seen anything quite like it before. Any other ideas or additional experience with anything similar?
