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?