TopherSRN

I apologize if you're confusing a teaching opportunity with belittling. I was trying to offer insight as to why he turned the corner(the amio) and the advantage of biphasic defibs and discuss those issues. If you'd rather me just say 'gj on flogging the guy for 4 hrs and letting the IABP fix everything'. I can, but that does neither of us any good, and its not why I read this board.

I apologize if you're confusing a teaching opportunity with belittling. I was trying to offer insight as to why he turned the corner(the amio) and the advantage of biphasic defibs and discuss those issues. If you'd rather me just say 'gj on flogging the guy for 4 hrs and letting the IABP fix everything'. I can, but that does neither of us any good, and its not why I read this board.

I don't think the balloon 'solved' your VT, as it doesn't 'open' the coronaries, rather it facilitates their filling. An IABP isn't a substitute for PTCA. There was some other etiology, and Im sure the amiodarone gtt you started solved your arrhythmias.

I don't think the balloon 'solved' your VT, as it doesn't 'open' the coronaries, rather it facilitates their filling. An IABP isn't a substitute for PTCA. There was some other etiology, and Im sure the amiodarone gtt you started solved your arrhythmias.

Why would you want a monophasic? Biphasic has been proven more effective and you can crank a biphasic to 360. We do it very often.

Why would you want a monophasic? Biphasic has been proven more effective and you can crank a biphasic to 360. We do it very often.

"Calcium (chloride) is indicated for hyperkalemia during a code. And, it is indicated first line for severe hyperkalemia." Why do you keep repeating this? Its cookbook medicine and not even the point I was making. You were incorrect in saying that Ca corrects hyperkalemia, when it in fact does NOT. Its a bandaid fix that treats the symptoms, and not the problem. Im well aware of its indications. Gluconate can be used, its largely MD preference (one of our surgeons preferred it in a non-emergent situation), but CaCl has roughly 3x the elemental Ca.

"Calcium (chloride) is indicated for hyperkalemia during a code. And, it is indicated first line for severe hyperkalemia." Why do you keep repeating this? Its cookbook medicine and not even the point I was making. You were incorrect in saying that Ca corrects hyperkalemia, when it in fact does NOT. Its a bandaid fix that treats the symptoms, and not the problem. Im well aware of its indications. Gluconate can be used, its largely MD preference (one of our surgeons preferred it in a non-emergent situation), but CaCl has roughly 3x the elemental Ca.

So a Sa02, Abgs, ETCO2, EBBS and a PCXR (ALL done in a pt Why not just go for a CT to check ETT placement? Thats just as pragmatic as your bronch comment.

Your 2 quotes are contradictory. Ca has absolutely 0 effect on the potassium level. It only acts to normalize the normal resting membrane potential thereby rturning myocyte excitability to a more normal level. It is more of a cardioprotective measure than a corrective. You can give all the calcium in the world to a pt with a K of 8.1 and their K will stay 8.1, you will only help to prevent arrythimias steming from the hyperkalemia. Intracellular shifting agents such as NAHCO3, Insulin and High dose albuterol are the quickest and most effective way to get a K down. Exchange resins (kayexalate) are a more protracted treatment and not appropriate in a code. And there is STILL a lot of misinformation in this thread.

Your 2 quotes are contradictory. Ca has absolutely 0 effect on the potassium level. It only acts to normalize the normal resting membrane potential thereby rturning myocyte excitability to a more normal level. It is more of a cardioprotective measure than a corrective. You can give all the calcium in the world to a pt with a K of 8.1 and their K will stay 8.1, you will only help to prevent arrythimias steming from the hyperkalemia. Intracellular shifting agents such as NAHCO3, Insulin and High dose albuterol are the quickest and most effective way to get a K down. Exchange resins (kayexalate) are a more protracted treatment and not appropriate in a code. And there is STILL a lot of misinformation in this thread.

You 'coded' a person for 5 hours and 25 min s/p code they wer AAOx3? And 10 tries to get a fem cvl? No wonder it took 5 hours.

You 'coded' a person for 5 hours and 25 min s/p code they wer AAOx3? And 10 tries to get a fem cvl? No wonder it took 5 hours.

The decline of PACs probably has more to do with MDs than RNs.

I don't think it necessary for me to go browsing pubmed to 'prove' that PAd approximates PAWP in a NORMAL heart. That is common knowledge and I am far too busy. This text was handy so on pg. 211 of "Hemodynamic Monitoring: Invasive and Noninvasive Clinical Application 3rd Ed" by Gloria Obkouk Darovic it states: "During systole, no correlation between pulmonary artery pressure and left atrial pressure exists because of the systolic thrust of blood from the right ventricle. PAd pressure, however, is normally 1 to 4 mm Hg higher than left atrial pressure because of the slight resistance to diastolic runoff imposed by the friction of flowing blood against the highly distensible pulmonary vascular walls." I never said 'DONT EVER MEASURE PAWP BECAUSE PAD IS THE SAME'. Im saying PAWP is a reflection of LAP, it isnt even an exact measurement. And in a cardiopulmonary system with near normal physiology PAd closely correlates. Yes I know when stenotic or regurgitant valves are involved it won't. Hell I could probably find 10 articles citing that PACs increase morbiity and mortality and should be used sparingly. Nice abstract, you bother to notice it was from 1988?

thank you both :icon_roll :icon_roll :icon_roll any other pearls of wisdom you wish to impart on me? i've been doing open heart for years taking care of vads, double valves, triple valves,robotic valves, thoracic aneurysms, aaa, cabgs with efs in the teens, aortic roots, heart and heart + double lung xplants, you name it and have never wedged. yes it has its place, but i don't lay awake at night crying because i can't wedge. a wedge won't tell me much i can't figure out other ways, though i am spoiled by the laps i see so often now.

Why do people want to wedge so badly? The PAD usually correlates and if it doesnt and they're that sick I get a LA line at my new gig. I guess thats the one advantage to the ivory tower. I just don't understand the romanticism with wedging :/ PS: To stay on topic. The PP hosp i worked at used swans on 90% of their cases except softball cases where they didn't even bother placing epicardial wires. The academic hospital I'm now at uses them somewhat but often times they come back with LAs.

Its called ACLS protocol. if pt is dead -> give drugs. Do you not have protocols in place for repleting electrolytes? xfuse for Hct 38.3 give tylenol? Protocols are not dx'ing its cook book medicine that a monkey could carry out. You really don't want any kind of autonomy do you? Id also suggest not renewing your acls and working in a less acute area if it puts you out to follow protocol on a dead (pulseless/apneic) person. Would you rather call the attending with "uh mrs. jones doesnt have any QRS complexes, isn't breathing, has no pulse, is blue as a smurf. What do you want me to do?"

Its probably 7 months too many.

This blows my mind. You have a fresh heart with wires and the first thing thats done is pound on his chest instead of hook his wires up to the pacer that should be at the bedside of EVERY open heart pt with wires. What about atropine, you know a vagolytic, for someone who is 'vagaling'???? Maybe im just lazy, but id rather pace someone/push atropine/robinul than do CPR. You probably will get mad and think im trying to be an @$$, but CPR isnt the best option for symptomatic bradycardia in this patient. Always, always use your wires. I've seen much sicker people walk out of the hospital, you wernt even maxxed on vaso or dopa (not sure on epi as every hosp i've worked at weight based it). Renal failure isn't a death sentence, crrt in the unit then hemo when stable. You're right i dont know everything that went on. Im just making observations based on my experiences and what you posted. You can take my post as constructive criticism and see how things could have been handled differently or as I suspect you'll just get defensive and insult me. :) :) :)

They are not going to just give up after they do a cabg/valve on someone. To be honest those gtts and support devices (iabp/crrt) are pretty run of the mill in CVI. As far as him dropping his rate, did he not have epicardial wires?

Your getting Transmyocardial Revascularization (TMR) and a MAZE confused. TMR is where a laser is used to 'drill' holes through the myocardium in order to promote collateral capillary beds as a method of perfusion. A MAZE is a procedure where the atria and the pulmonary veins are surgically manipulated in order to reorganize the internodal pathways. And YES you will see asystole, junctional, a flutter and EVEN afib in someone s/p MAZE. A fib will persist for up to 6 months. Its akin to seeing the wierd conductions in valves. She told you to look it up because you will remember it better than if she had just told you. How hard is it to look things up these days with google?

If they are on high enough doses of pressors to develop mottled/hypoperfused extremities the odds of them walking out of the hospital are slim; so they don't need the toes/extremeities anyway. The whole levophed - leave em dead philosophy has fallen out of vogue(levo is now the first line pressor for sepsis) so I would hesitate to perpetuate that kind of thinking. Some ignorant people still spout that mantra anytime someone mentions levo. I've never seen even marked mottling of extremeities on

they meant trying to pace and get capture first rather than immediately starting compressions. you'd be surprised how often peope forget about their wires. Though oftentimes you wont capture anyway :/ To not do compressions on a pt. with a non-perfusing rhythm is assinine. CPR can be done on a sternotomy pt, it just needs to be done differently. There are very few cases in which you're gonna do a re-entry at the bedside, and hopefully the surgeon is smart enough to take them back before it gets to that point. Why would acls be any different on a fresh heart? If anything its more liberal.

I would looove to work at a facility where balloons are mandated 1:1. While I have had sick balloons that were 1:1, they would have been 1:1 with or without the IABP. We get pre-op balloons and they are a breeze and it would be stupid to single them. An IABP isnt all that much additional paperwork/monitoring. Then again I see them frequently, so driving them is second nature.