Right-side heart failure.

[NR_Paramedic]

CPAP def. to lead off, as far as the failure treat what will kill them first, the left sided failure. As far as the A-fib goes dont assume the beta agonist caused it. If the rate is high enough to cause the failure then maybe that is the underlying cause....the telltale sign there would be hypertensive vs. hypotensive....Also the ASA is not a bad idea and for sure will not hurt this pt. the pt is not circulating a whole lot of blood (therefore peripheral edema)....great time for clots to form...esp. w/ the a-fib. Also w/ the NTG, personnaly I would give it and not worry about the "right sided MI"...however in this case I would make sure that I had an IV est. prior to NTG admin. if the pt. became hypotensive then I would elevate the legs, drop the head and administer a 1-200 cc bolus monitor the pt. I would def. give the lasix, and lots of it....we do double the daily dose in my system...(most I have ever given was 200 mg...however that pt. could have gotten 480 mg per protocol). One more thing I didnt see anyone mention which suprises me is MS04, morphine works excellent for CHF pts. (esp. for those w/ renal failure where lasix may not work as well)...just consider that this pt. needs the preload reduced...you can scare yourself into not treating this pt. by thinking to much. Don't get me wrong, you need to consider the ramifications of your treatment...however...you also need to treat what will kill them first...and in this case it is left sided failure. But remember the underlying cause (a-fib etc...)...maybe treating according the CHF/Pulm. Ed. protocol is wrong, maybe the arrythmia protocol is the way to go. anyway...just my thoughts...g'night and good luck....

Conrad

[NR_Paramedic]

regarding the life to NTG...its also very short acting...nitroprusside is great...but if you dont have it use the next best thing...may be the NTG or MS....obviously doesnt hurt to consult a doc if you have questions...(try to see what they have to say when you talk to your med-com doc.)....I'll ask mine and see what he has to say...

Conrad

[als_medic_uk]

First of all congestive heart failure will cause an enlarged [and] or pulsatile liver, the dyspnoea is often very worrying, I would have given the vasodilating agent, as people with CHF need to maintain a euvolaemic state and the Nitroglycerine will help this. I would have also given a beta blocker and a positive inotropes. Did this person have a CRT fitted?

And no 12 lead, tut tut

[Ace844]

First of all congestive heart failure will cause an enlarged [and] or pulsatile liver, the dyspnoea is often very worrying, I would have given the vasodilating agent, as people with CHF need to maintain a euvolaemic state and the Nitroglycerine will help this. I would have also given a beta blocker and a positive inotropes. Did this person have a CRT fitted?

And no 12 lead, tut tut

Can you please clarify for me how NTG causes failure pt's to be euvoluemic? Also, what's CRT?

out here,

Ace844

[als_medic_uk]

Nitroglycerine (NTG) is the most effective medication available for preload reduction. Think of the loop effect when dilating blood vessels.

[als_medic_uk]

Sorry that wasn't very explanatory, should I say reducing venous pressure decreases proximal capillary hydrostatic pressure, which reduces capillary fluid filtration and edema formation.

[Doczilla]

Rales halfway up, I would have given the NTG. Yes, there is concern about giving NTG to patients with suspected RVI, but this guy clearly has LEFT sided heart failure, and most right HF is as ERDoc said, due to LHF. My priority here would be taking the preload off the LV and getting the fluid out of the lungs. If the pressure dropped, then it's time for dopamine or dobutamine. I think that withholding the NTG for the remote possibility of RV infarct while the patient is hypoxic, tachycardic, and severely dyspneic from CHF is not the right thing to do.

'zilla

[Ace844]

Nitroglycerine (NTG) is the most effective medication available for preload reduction. Think of the loop effect when dilating blood vessels.

IIRC, I understand that premise, yet in a patient who is HYPERvolemic, there is little NTG action in achieving EUvolemia, unless of course you are considering the increase of Renal perfusion as a benefit to increased preload, from NTG admin...then perhaps, but I'm not quite sure I agree with your assertion..

You can learn more about this here:: http://www.emtcity.com/phpBB2/viewtopic.php?t=2639 , http://www.emtcity.com/phpBB2/viewtopic.php?t=2496..

hope this helps,

Ace844

[als_medic_uk]

High hydrostatic pressure of the veins, leading to poor reabsorption of fluid is the classical problem for hypervolaemia, hence you need to reduce the proximal pressure, which is what a vasodilator does.

[Ace844]

High hydrostatic pressure of the veins, leading to poor reabsorption of fluid is the classical problem for hypervolaemia, hence you need to reduce the proximal pressure, which is what a vasodilator does.

Still this doesn't solve the oncotic pressure gradient that remains present..