explain this?

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caligas

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EP lab. O/W healthy 50 yo female for fib ablation. Normal preop echo. GA, ett, radial a line W Cuff on opposite arm. Smooth sailing for 2 hours. No drips just Des. No recent iv drugs. Abrupt loss of a line tracing and pulse ox. Co2 peters out. Ekg is normal sinus at 60 as it has been since admit (afib is paroxysmal). No carotid pulse on a thin patient. As I announce the situation i feel a week pulse followed by increasingly robust pulses and I see the pulse ox and a line come back. Nobody was leaning on the arm or sampling the line. Intracardiac echo and floro cxr normal. Vent normal. Abg normal.

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Temporary loss of cardiac output during the Case. Perhaps, one of our Cardiac superstars could speculate on all the physiological effects of the EP study and ablation on the heart which would explain this brief drop in cardiac output.
 
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Europace. 2012 Feb;14(2):204-8. doi: 10.1093/europace/eur314. Epub 2011 Sep 20.
Clinical characteristics of massive air embolism complicating left atrial ablation of atrial fibrillation: lessons from five cases.
Kuwahara T, Takahashi A, Takahashi Y, Kobori A, Miyazaki S, Takei A, Fujii A, Kusa S, Yagi****a A, Okubo K, Fujino T, Nozato T, Hikita H, Sato A, Aonuma K.
Source
Cardiovascular Centre, Yokosuka Kyousai Hospital, 1-16, Yonegahama-dori, Yokosuka, Kanagawa, Japan. [email protected]
Abstract
AIMS:
This study aimed to elucidate the clinical characteristics of massive air embolism occurring during atrial fibrillation (AF) ablation.
METHODS AND RESULTS:
Of 2976 patients undergoing AF ablation, 5 patients complicated by serious air embolism were examined. Atrial fibrillation ablation was performed with the use of three long sheaths for circular mapping and ablation catheters under conscious sedation. Two patients had air spontaneously introduced through a haemostasis valve of the long sheaths, at the end of long apnoea caused by the sedation, even though the catheters were placed within the long sheaths. The remaining three patients, all of whom also exhibited long apnoea, had air entry at the circular mapping catheter exchanges. Air accumulated in the right and left ventricles, left atrial appendage, right coronary artery, and ascending aorta. Haemodynamic collapse and hypoxaemia occurred in all and two patients, respectively, and supportive treatment and the accumulated air were aspirated. ST elevation, haemodynamic collapse, and hypoxaemia persisted for 10-35 min; however, all patients recovered completely. After we changed the sedative to one with less respiratory depressive effects and the timing of the saline flush at the circular mapping catheter exchanges, we never experienced such serious complications any further.
CONCLUSION:
Serious air embolism can occur in patients with long apnoea under sedation during AF ablation with the use of long sheaths. Supportive therapy and air aspiration were effective in resolving the complication. A sedative that causes less respiratory depression and the timing of the saline flush were important for preventing air embolism.
 
Transient PEA, i suspect an air embolism wouldn't have a ROSC so fast

PEA from air embo is the most likely explanation. No other cause of PEA would resolve in this timeframe without intervention.
 
Less common during AFib ablation, compared to VT, but sometimes the EP induces a rhythm that is non-perfusing briefly. Typically the a-line doesn't flatline altogether, though.
 
PFO? Bubbles generated by heating the atria slipping into the left circulation/coronaries? I'd expect pre and post arrest ST segment changes to go along with that scenario. The complete loss of pressure tracings and quick resolution is unusual for right-sided air embolism in the few cases that I have had.
 
Interesting.

What were the EP guys doing at the time? Had they done a trans-septal puncture? Anything in the coronary sinus? If they had done a trans-septal, were they working on the right or the left at the time of the event?

My first thought is coronary artery air embolism of the right main. They are acute, resolve quickly and spontaneously, would not reveal ST changes in the standard monitoring leads if at all, and could give you this exact clinical scenario.

A massive pulmonary embolism could give you a similar picture, but likely would not resolve quite as quickly.

- pod
 
Was ICE done during the event? If so, looking at what structures? ICE would be extremely sensitive for air.

I agree it smells like air down the RCA, but if ICE was in active use it would essentially rule that out.
 
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EP lab. O/W healthy 50 yo female for fib ablation. Normal preop echo. GA, ett, radial a line W Cuff on opposite arm. Smooth sailing for 2 hours. No drips just Des. No recent iv drugs. Abrupt loss of a line tracing and pulse ox. Co2 peters out. Ekg is normal sinus at 60 as it has been since admit (afib is paroxysmal). No carotid pulse on a thin patient. As I announce the situation i feel a week pulse followed by increasingly robust pulses and I see the pulse ox and a line come back. Nobody was leaning on the arm or sampling the line. Intracardiac echo and floro cxr normal. Vent normal. Abg normal.

I would say you lost the a line tracing because you had an a line in the first place.

I don't put a lines for healthy a fibs.

Any changes in capnogaphy?

Were they pushing adenosine?

Were they pacing?

How was the EKG when pulse was lost?

I imagine you were listening to the pulse ox and missed it for a few secs, then looked at the EKG. That's how it always goes. Chances are we will never know what happened.
 
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