How long does it take ETCO2 to drop after an arrest?

[wanderingmedic]

I was thinking about this the other day, and I wanted to see if anyone knew of any literature/answers here. Here is the question: How long does it take for ETCO2 to fall after cardiac arrest, assuming CPR is not being provided? If ETCO2 remains high or WNL (>45) w/o CPR, is it safe to assume the pt still has a pulse?

Patient is intubated and is in extremis secondary to new onset CHF. BP is in the gutter (lets say MAP of 48, NiBP BP 63/40), NSR 80, SPO2 90% after intubation w/ FiO2 100%, and 3 of PEEP. ETCO2 is 52, and shows a good persistent waveform.

During your 30 minute transport, BP remains low, it is hard to palpate a pulse, however you think you can feel a faint carotid pulse. How long would it take ETCO2 values to fall, reflecting cardiac arrest?

My assumption is that the relatively high ETCO2 indicates the pt still has pulmonary perfusion, even if pulses are difficult to palpate because of the BP. Thoughts?

 

[VFlutter]

Somewhat of a complex question. Post-arrest ETC02 can be influenced by many factors such as current perfusion and ventilation status, potential V/Q mismatch, as well as potential hypercapnia or acidosis from the arrest. If ETC02 is 45, without recent Bicarb administration, I would assume patient probably has a pulse even if peripheral pulses are not palpable.

Pulmonary Edema potentially creates a V/Q mismatch which can skew ETC02.

Do you have a Ventilator or was the patient being bagged? What did the ETCO2 waveform look like?

ETC02 tends to drop fairly abruptly, within a few ventilations, with perfusion changes.

Our company did a retrospective review of our cardiac arrests and ETC02 <20 and SBP <80 will arrest within 8 mins if not improved over those thresholds.

If there is a question if a pulse is palpable and the ETC02 <20 I would probably just start CPR. I have seen Academic centers start CPR on patients with an arterial waveform but significant hypotension and ETC02 < 20. The rationale being that it is an impeding arrest and that starting resuscitation with some perfusion is better than waiting until they are completely pulseless.

 

[wanderingmedic]

There was not really a V/Q mismatch once I got the patient intubated. The situation really seemed more like the SNF let the pt sit for over a day with low SPO2 because "we did not want to give him more oxygen because he might have CPOD and go apneic." I think by the time we were called, the patient was so tired from working to breathe that he had lost his airway from fatigue. Depending on the nurse/CNA at the SNF, the patient had been struggling to breathe for 12-36 hours. There was new +4/+4 pitting edema in all extremities, and rales in all lung fields. Deep suction via ballard following intubation revealed pink frothy sputum.

Following intubation SPO2 improved and ETCO began to come down into the high 40's. We do not carry vents, so I was providing BVM ventilations at a moderate volume, about 1/4 to 1/3 a squeeze of an adult bag at about 14/min, rate titrated to a targeted ETCO2 of 45 or less. ETCO2 waveform looked like a pretty normal plateau waveform. No shark fin or other present abnormality on the waveform. ETCO2 remained 45 or greater throughout the transport.

No Bicarb was given. The only drugs I gave were: 1 mg of Versed and 100 mcg of Fentanyl for induction. 500 mL NS bolus per OLMC. 10-20 mcg PDP Epi PRN.

 

[E tank]

In true circulatory arrest, the wave tanks within one breath, certainly within one screen sweep. If the arrest comes after a gradual decline in cardiac output, there will be that 'stair step' pattern as the CO falls.

I can't think of a reason that a patient with an ETCO2 of 45 would not have some cardiac output. There might be a reason for him not to have a pulse, but thats a different discussion

 

[wanderingmedic]

In true circulatory arrest, the wave tanks within one breath, certainly within one screen sweep. If the arrest comes after a gradual decline in cardiac output, there will be that 'stair step' pattern as the CO falls.

I can't think of a reason that a patient with an ETCO2 of 45 would not have some cardiac output. There might be a reason for him not to have a pulse, but thats a different discussion

If the patient no longer had palpable carotid pulses and NiBP was no longer reading, but you still had an ETCO2 of 45-50, would you have started compressions and traditional ACLS?

The patient had a single lumen PICC which had good blood return when I initiated access. When pulses became questionable I repeated my PDP Epi at 20 mcg and saw an increased HR and pulses became barley palpable again.

Any thoughts on emiric Bicarb?

 

[VFlutter]

If the patient no longer had palpable carotid pulses and NiBP was no longer reading, but you still had an ETCO2 of 45-50, would you have started compressions and traditional ACLS?

The patient had a single lumen PICC which had good blood return when I initiated access. When pulses became questionable I repeated my PDP Epi at 20 mcg and saw an increased HR and pulses became barley palpable again.

Any thoughts on emiric Bicarb?

Tough call. Hard to defend not starting CPR with non-palpable carotid and failed NIBPs. The normal ETC02 is evidence of perfusion but not definitive.

Why push does pressors and not a drip? PDP are a bridge to something definitive. I

IMO only reason to give Bicarb is confirmed pH less than ~7.0 or refractory hypotension on pressors with known acidosis.

 

[wanderingmedic]

Tough call. Hard to defend not starting CPR with non-palpable carotid and failed NIBPs. The normal ETC02 is evidence of perfusion but not definitive.

Why push does pressors and not a drip? PDP are a bridge to something definitive. I

IMO only reason to give Bicarb is confirmed pH less than ~7.0 or refractory hypotension on pressors with known acidosis.

We only have PDPs in our standing orders. I was going to call for a drip, but we don’t carry pumps and we were reasonably close to the hospital at that point.

 

[E tank]

If the patient no longer had palpable carotid pulses and NiBP was no longer reading, but you still had an ETCO2 of 45-50, would you have started compressions and traditional ACLS?

The patient had a single lumen PICC which had good blood return when I initiated access. When pulses became questionable I repeated my PDP Epi at 20 mcg and saw an increased HR and pulses became barley palpable again.

Any thoughts on emiric Bicarb?

Hard to say why or how your ETCO2 was where it was, but pulseless is pulseless and compressions are called for. Would not step outside of hard stop pre-hospital protocols for a zebra on a monitor. I personally only give bicarb if I can fix the reason for the acidosis or if pressors are not working and the patient is circling the drain. You only have a couple of boluses anyway until you cause a hypernatremia in a lot of patients so, no, I don't give bicarb empirically.

And yeah, I agree with above, an inotrope infusion would be called for if it were in your wheelhouse. I'd start with epi at .05mcg/kg/min and move up aggressively