FIREMEDIC-CCRN

All I am saying is that one should not consider atrial fibrillation a non dangerous heart condition. If a-fib were so benign then there would not be cardioversion, anticoagulation, rate and rhythm control, and a-fib would not cause stroke, heart failure, and death. One should not say, oh, they are just in a-fib, no big deal, we will deal with it in the morning. At least that is the attitude of a pretty big heart center in Cleveland.

I agree, there are millions of people walking around with a-fib, but some of those same people will not tolerate a-fib with rvr, and most know when they switch into that, and seek treatment. I din't think we were talking about everyday a-fib, the poster stated the patient was placed on amiodarone and cardizem drip, sounds like they were trying to control his rvr, not letting him walk the halls.

I would argue that a-fib actually is a dangerous condition to the heart, maybe not to the degree that v-tach/v-fib is, yet still dangerous. A-fib with rvr can certainly decrease your hemodynamic stability and stress an already weakened heart muscle. Add that to the fact that most people with chronic a-fib are placed on anti-coagulation like coumadin and the leading cause of trauma is falls, makes a-fib in my opinion somewhat dangerous. Now newer drugs are coming to the market like pradaxa which make measuring bleeding times very difficult if not impossible and the only way to reverse the effects is to do dialysis, or wait it out, it will be interesting to see the trauma papers on this population. Did you ever look for a cause as to why your patient was running 140's for 24 hours, in my experience it has usually been related to a intravascular hypovolemic fluid imbalance, just wondering what you found, also wondering what his Magnesium level was, and did you give IV amiodarone or just start with PO.

I wonder if the reason the military is having so much success with ECMO is because their patient population are soldiers who are young, healthy, and fit with limited medical conditions, I would imagine it has decreased success the older the patient is and the more medical conditions one already brings to the table.

I believe the first poster was correct, Levophed dilates the coronary arteries and vasoconstricts peripherally.

You also have to remember that ACLS guidelines are not just for hospital patients who already have an IV established, numerous staff, and crash carts right next to their rooms, ACLS is vital in the prehospital care of these patients. Time and time again studied have shown that acls meds have little value in code situations without quality CPR, that is why you have seen such a big push to get away from medications and intubation as the priority things and concentrate on what works, that being good quality CPR and defib. It is not usually the meds that are bringing these people back in the hospital but the fact that we can intervene within a minute or so. It used to be unacceptable to bring a cardiac arrest into the ER without attempting to intubate the patient, now it is almost standard that we quickly drop a king LT or do basic BVM and concentrate on CPR/Defib.

I don't think you did anything wrong, things just happen sometimes. I would think if his pneumothorax expanded into what you suspected was a tension pneumothorax you would have certainly noticed when you were bagging him because that would have gotten much harder for you to squeeze the BVM, and the pneumo expanding or the chest tube out still doesn't explain the belly getting bigger. You think you would have to go with the ET tube being dislodged.

Did you happen to see what your Ventilator displayed during this time. It is very possible that the ET tube was dislodged, but between the ET tube securing device and alarms/settings on the ventilator you would have thought that it would be unlikely, but patient bradying down and then CPR is classic ET tube dislogement . What was his/her SP02 at this time? Doesn't seem like things always go wrong during an MRI.

I thought I was a strong applicant as well, GRE 1140/4.0, BSN 3.5, 7 years experience as firefighter/paramedic at busy 911 service, skilled at intubations, acls, and IV's, 4.5 years experience as RN, MICU/SICU at level 1 trauma center, ER RN, and RN at cardiovascular ICU, certs in CCRN, Cardiac Medicine- CCRN, CEN, TNCC, ACLS, PALS, NRP, EMT-P, honestly I am not arrogant at all but if there are two classes full of people more qualified than I am then god bless that program

I called today and the secretary stated that they were still finalizing the list. I have heard a few say that they have been accepted, a few say they were rejected, and a bunch who have heard nothing, anyone else have any contact with others who have gotten in or rejected.

I heard one person say they got an acceptance phone call yesterday, so that makes a grand total of 2 people I have heard of who have gotten in so far, who knows what is going on, as for me I have gotten no letter, no phone call. ***

Big Deal, is it really that important? Was your patient stable? Was your patient alive and progressing when you handed care over at shift change? Did they get all of their meds? It amazes me to see nurses who get so wrapped up in dirty sheets and hygiene but fail to trend vital signs and other important events. From my experience I have never had a patient die from a bloody sheet or from body odor. Don't be so hard on yourself, you are going to make thousands of mistakes, and you are going to learn from mistakes. Mistakes are unavoidable, and they are the things that make life worth living. Embrace your failures and mistakes, they are wonderful teaching tools and moments.

I was wondering if anyone has heard from Pitt. I interviewed back in December and was told that we would either get a letter or a call about our status. I know they have more interviews set up in March for the CRNA program. Haven't really seen anything posted on the message boards either way.

I was wondering if anyone could given me some information about the University of Pittsburgh CRNA interview process. I have a December interview date and was just wondering if anyone has had any experience with Pitt.

Happy, About a year ago I had a women go into flash pulmonary edema secondary to CHF which led to asystole by the time we arrived on scene. We use a LUCAS automated CPR machine that we hooked up and started CPR, I intubated the patient with a large amount of that frothy blood tinged sputum in her airway and ET tube, end tidal co2 turned yellow, good breath sounds, and we placed our capnography device on the ET tube with a reading of 5, good waveform. The reading all of a sudden started to increase rapidly and went from 5 to the 60's and 70's. The reason for this huge jump was we got her pulse back and now her heart was pumping again and perfusing and expelling all of that built up CO2. I would have to believe that she was just not perfusing that well, CPR, let alone CPR by individuals and/or a machine is not that adequate to perfuse the body sometimes. Just look at how much the atrial kick contributes to cardiac output, and the fact that it was a traumatic arrest, I think you did the best you could do. But I would have to say that it was probably due to lack of perfusion like some of the other posters have said.