chbare Posted November 21, 2009 Share Posted November 21, 2009 As stated earlier, we need to seriously consider the cause of the arrest. The differential for PEA includes multiple considerations. Getting crazy with amiodarone will not be helpful if we are dealing with an overdose of a med known to increase the QTc. Additionally, we need to consider other medical and trauma causes. I alway consider electrolyte imbalances. We can actually do something about hyperkalemia in the field. The key is index of suspicion and identification. Take care, chbare. Link to comment Share on other sites More sharing options...
tniuqs Posted November 21, 2009 Share Posted November 21, 2009 (edited) As stated earlier, we need to seriously consider the cause of the arrest. The differential for PEA includes multiple considerations. Getting crazy with amiodarone will not be helpful if we are dealing with an overdose of a med known to increase the QTc. Additionally, we need to consider other medical and trauma causes. I alway consider electrolyte imbalances. We can actually do something about hyperkalemia in the field. The key is index of suspicion and identification. Take care, chbare. Agreed unless one has the bigger picture in this situation basically one is shooting in the dark, I find it very curious that mentioned in the "scenario" a PEA (so what was the rhythm prior to return of pulses ?) And without a possible cause or PMHX to the OP you are treating a monitor and talking about hanging dopamine, very curious as well. Cardilogists typically refer to a "stunned heart" and with crazy reperfusion rhythms as stated my kevkie (put your hands in your pockets hold the rx) Then a rate of 80 during recovery quite curious again (thinking Beta Blockers?) typically a resuscitated arrest are far more tachycardic, that said a relative slow but wide complex could be Ventricular Flutter or perhaps a BBB? Quite a stab in the dark without a strip to look at, or proper Hx of incident, akin to buying a mail order bride. A little story, in Hospital, Patient 36 y/o female O pmhx, just delivered first child, some post partum hemorrhage, Ergonovine Malate IM .... then a sudden arrest .... Code Team responded <insert heavy breathing> ECG observed by experianced RNs a very wide ventricular appearing complex and a slow response ~ 80 bpm. Paddles pulled like a gunslinger's in an old duster, BUT some one noticed a tiny little "hick up" buried in the complex ;>) initially appearing to be artifact, NOT ... stat to angio an nitro squirted directly into coronary artery. PRESTO the huge ischemic T waves disappeared and was determined that the epithelium of the coronary arteries was hyper sensitive to Ergot ... go figure. Point being without a history ... Edited November 21, 2009 by tniuqs Link to comment Share on other sites More sharing options...
Kiwiology Posted November 21, 2009 Share Posted November 21, 2009 Ordinarily I would consider cardioverting VT or any WCT that is causing significant comrpomise (the ass-pucker factor) and maybe hanging some amiodarone. However given the possiblity of transiet reperfusion dysrhythmia I would concur I'm not keen to go cardioverthing this guys poor broken down old ticker or getting crazy and prolonging his QTc with amiodarone. I would be interested in a history and some rhythm strips or a 12 lead ECG. Link to comment Share on other sites More sharing options...
Arctickat Posted November 21, 2009 Share Posted November 21, 2009 (edited) Chuckle...this thread reminds me of a doc I gave grief to a few weeks back...in hindsight, I probably should have reported her. She was a locum at a nearby hospital which called my ALS service for transfer of a post arrest patient. When we arrived to transport her she was tubed with a King tube because the doc was too uncomfortable in using an ETT. The report I got was that the woman came in by ambulance after losing consciousness at the breakfast table. Just after arrival at the hospital it was determined she was in PEA. (She still had a blood pressure of 170/90 and sats of 97% on high flow O2) The doc runs the code and administers 1mg 1:10,000 epi IV. Remarkably, she has a pulse!! Go figure. The patient's heart rate hits 150 so the doc turns around and slams her with adenosine.... When I assessed the patient I notice her fixed and dilated right pupil and ask the doc if her diagnosis happened to include the cerebral hemorrhage this lady was having and if she was being sent to the neurologist instead of the CCU. She died the next day. Edited November 21, 2009 by Arctickat Link to comment Share on other sites More sharing options...
zzyzx Posted November 21, 2009 Author Share Posted November 21, 2009 Guys, this is a fictional scenario. As I stated in my original post, I did have something similar in my experience. I saw a patient with a massive MI go from a sinus brady rhythm to what was probably VT but at a rate of about 120. I didn't do anything for about a minute, and the patient self converted back to a sinus rhythm. I'm just trying to get your opinion on what you would do in the scenario as presented. Good discussion so far! Link to comment Share on other sites More sharing options...
P_Instructor Posted November 21, 2009 Share Posted November 21, 2009 I'm just trying to get your opinion on what you would do in the scenario as presented. Ultimately you are going to base your treatment on the clinical picture of the patient, however, you better get all the information needed to make that decision on which treatment modality/pathway you are deciding on. It comes down to fully understanding the pathophysiology of what is going on with the patient. Although fictional, there are many variables that need to be thought of prior to just slamming or bamming (meds/shock). If this was a true situation, your knowledge and experience would hopefully promote a fast clinical decision to the proper treatment regime. One must remember that not all thought out processes will work, and you must always be prepared for the possible unwanted outcome. This could have many factors involved, but my opinion would be in in line with chbare, if the patient was previously in PEA, we need to consider all the H/T's, and could be electrolyte problem. Good scenario. 1 Link to comment Share on other sites More sharing options...
zzyzx Posted November 23, 2009 Author Share Posted November 23, 2009 P Instructor wrote, "If this was a true situation, your knowledge and experience would hopefully promote a fast clinical decision to the proper treatment regime. One must remember that not all thought out processes will work, and you must always be prepared for the possible unwanted outcome." Well said. Link to comment Share on other sites More sharing options...
medic82942003 Posted November 23, 2009 Share Posted November 23, 2009 (edited) I tend to simplify it, is it stable or unstable? Stable use drugs, unstable- cook em, or cardiovert. Edited November 23, 2009 by medic82942003 Link to comment Share on other sites More sharing options...
mobey Posted November 23, 2009 Share Posted November 23, 2009 unstable- cook em, or cardiovert. Really?? Cook em? Link to comment Share on other sites More sharing options...
chbare Posted November 23, 2009 Share Posted November 23, 2009 I tend to simplify it, is it stable or unstable? Stable use drugs, unstable- cook em, or cardiovert. However acting without considering the big picture or causes that can be corrected or treated is myopic and potentially harmful IMHO. If this were a post resus renal failure patient who missed dialysis for a week, would your treatment modalities be different? Treating patients with blanket statements in a vacuum should be avoided if at all possible. This is why I continue to question patient history. A simple cardiovert/no cardiovert scenario is meaningless without history and additional considerations. Take care, chbare. Link to comment Share on other sites More sharing options...
Recommended Posts