I came back from a week off the other day and was greeted with a cardiac arrest on my first call and then another arrest the next day. Both codes were asystole, although we managed to get pulses back briefly on the second one. I had my preceptee with me on both calls. He got some good experience, including getting a successful intubation, and did a fine job orchestrating the second call.
On the first code we had excellent capnography (30-40) with CPR, but could never get any kind of rhythm going. The patient was last seen breathing an hour before. The initial capnography on intubation was 64, but it went down to the 30s as soon as the excess carbon dioxide was ventilated off. The high reading indicated a likely respiratory cause of arrest as the still beating heart carried CO2 to the lungs where it could not be ventilated off. After some ventilation, the excess removed, the number dropped.
Three years ago I wrote a post called Compressions about an new EMT doing his first code. That same EMT was on this call with us, and, now a seasoned EMT (and notorious “shit magnet”) he did an awesome job on the compressions — so much so I thought the patient was in VT, although as soon as he stopped compressions, the lines went flat again. He also did a fine job in instructing our newest EMT in the proper method of compression.
Here’s the difference between the two compressions:
We worked the patient for 30 minutes, but with no change from flatline, we called it.
As an experiment, once we stopped working the patient, I had the crew stop CPR first and I kept bagging for a minute to see the effect on the end tidal. As we stopped CPR, the ETCO2 dropped precipitously. 35, 29, 15, 9, 3. No cardiac output, no ETCO2.
The second code was at a nursing home, a patient with a significant medical history (IDDM, HTN, MI, cancer, amputee, respiratory failure) complete with foley, colostomy, huge freshly zipped scar running vertically up his chest and of course a full code. I figured he would also be a 20 minute ACLS and out. While my preceptee prepared the tube, and our crew did CPR, as an experiment I applied a nasal capnography cannula to the patient to see how well we were ventilating with just CPR and bagging. I have heard it suggested that this is an excellent way to assess ventilation in cardiac arrest and or the need for intubation or the ability to delay it while concentrating on compressions or drug administration. The ETCO2 didn’t even register, which was either due to poor bagging technique or just the plain difficulty of effectively ventilating someone in arrest by bagging. I would like to try this experiment again on a patient when we have more hands to help and a better seal with proper head positioning.
My preceptee sunk the tube quickly. The ETCO2 was an unpromising 8. We had brought in our new EZ-IO and one look at this guy showed no quick IV access, so I grabbed the EZ-IO and elbows up, told my preceptee, “Me first!” Having never done an EZ-IO, I felt I was entitled. It truly is as advertised — an easy IO. Pop the needle on the drill, press against the skin and squeeze the drill. Brrrrup. Instant access. I have to say this, along with CPAP, are two of the most amazing innovations I have seen in all my years in EMS.
We gave some epi and atropine and my other partner and I switched off between bagging and doing CPR. I was really pounding the CPR, but couldn’t get it above 8. I noticed my partner would get it to 10 when he did it. We switched back and forth a couple times and he was consistently a few points higher than I was. I was going much faster than he was, but maybe not as deep. The next switch, I slowed down and went much deeper and concentrated on full recoil of the chest and slowly the ETCO2 started to rise and it just kept going. I got it up into the high 30’s.
Some more epis and atropines and we had a wide complex rhythm and even pulses and a blood pressure back a couple times, but we had trouble maintaining it. Almost every time when we stopped compressions, the ETCO2 dropped. It was probably just the epi talking. We ended up transporting and the patient was called dead at the hospital. All told we had worked him almost an hour. We all had sore backs. I don’t do CPR that often, p[articuarly not in a moving ambulance or going down the hall in the hospital — I am usually managing the airway, but since on this day it was my preceptee’s job, I did the compressing. With the new CPR, it is vitually impossible to do it properly in a moving vehicle or even going down the hallway. The old I’m just doing compressions and we all know they don’t work method just doesn’t cut it anymore, particularly when the capnography shows an instant drop off in compression effectiveness.
It was a good precepting call and a good educational call all around. I love the ETCO2 as an indicator of how well CPR is being done, and as instant feedback to your technique. Now I know sometimes it is hard to know whether to credit the rise to the technique or maybe the effects of the drugs finally working, but it is certainly something to consider.
Where I continue to have some confusion is when the ETCO2 rises into the 30’s and 40’s and maintains it there at least temporarily without compressions, but you still cannot find a pulse. I have been told by experts and have told others that it is impossible to maintain an ETCO2 in the 30s and 40’s without cardiac output, and I agree with that. But the question is just how effective is that output? Is this PEA or just a really low pressure? Does it represent a pressure of say, 40 or 50, and wouldn’t it be better to just do CPR? (much in the way we do CPR on infants with low heart rates). My final answer is you just have to judge on a patient by patient basis. I would say if you have what looks to be a perfusing rhythm with a good ETCO2, and the patient is pinking up, but no palpable pulses (sometimes I can’t palpate pulses on a talking person), then maybe hold back on the CPR, try to get a pressure either manually or with the automatic cuff. Maybe try some dopamine if you can’t. But if you don’t have a rhythm you believe capable of perfusing and or the patient does not look as if there is life, there, then by all means, keep pounding away. This is really inadequately chartered territory. I have witnessed the sudden rise in ETCO2 attributed to return of spontaneous circulation and felt pulses and I have seen rises without being able to feel pulses. Some patients I have been comfortable witholding CPR on (and the ED BP machine has validated my decision with solid pressures) and others, no way. And forget trying to explain to an ED doctor why you are not doing compressions because of a non compression assisted capnography reading in the 30’s or above. It is, at least for now, (unle
you have an exceptional and I would say narrow complex rhythm)a tenuous limb. Until the ED docs (and the literature) are more on board, it is a little risky.