Congestive Charlie

[Kiwiology]

This pt still needs GTN but prefer to have a higher BP before using it. If he starts to deteriorate then inotropes, fluid, CPAP/BiPAP and possibly fluid bolus are what he needs.

I am not in favour of GTN because it will reduce cardiac output and worsen fluid mismatch/cardiogenic shock.

Having said that GTN may have a role in reducing myocardial workload and demand which may benefit his knackered conduction system.

Lasix is pretty much on the way out as most of these patients are actually dehydrated and since this guy has been sick with a fever for a few days he most likely needs fluid but first his heart needs help moving the fluid in the right direction. If you gave too much fluid right now he would probably deteriorate pretty rapidly.

Hence why I don't think fluid or frusemide will be of benefit here.

What he needs is, as you say, help to shift the fluid out of the interstitium and into the intravascular space which should fix up his edema and shortness of breath. If we can move the fluid into the arterial circulation by way of pumping it out of the left ventricle then this will help.

Now, not being an Intensivist and having not stayed at a Holiday Inn last night (Hostel California $29 a night FTW!), I would immagine some sort of vasopressor and inotropic support is in order.

And leave Stanley in the pasture as this guy most likely has a horse (or zebra) galloping around in his chest rather than an elephant sitting on it! If Stanley develops pachydermitis let me know as I know a few people who know a few people...if you know what I mean! (nudge, nudge, wink, wink!)

He's out in the front yard at the moment and it's raining again, blast, I wish summer were not bipolar. I couldn't find a big enough tarp at Home Depot or Bunnings to cover him. I may have to build a barn or something.

I am not following you about ACE inhibitors and inotropy. Could you please explain?

Hmm I am not either. ACE inhibitors lower blood pressure through preventing angiotensin 1 being converted to angiotensin 2 by blocking angiotensin converting enzyme (gosh whodathunkit?) which lowers Na/H2O rebsorption, sympathetic vascular tone and the release of ADH/aldosterone.

If anything I would think that ACE inhibitors would have a negative inotropic effect!

Not following you either Kiwi. I cannot find the drug Isporel, which I assume is Isuprel.

Isuprel rather

So, I am not getting this either. How can you screw up heart tones, then kill somebody with heart tones? How can listening to heart tones extend your scene time dramatically? How can they take away heart tones? Doesn't make much sense to me...

How often do you have the quiet to listen to heart tones? What do you do with the findings once you have them; do we introduce a new treatment based upon them or just write them down in a purely extrinsic exercise that will be repeated 20 minutes later in the ER?

Somebody, somewhere would find a way to screw up spending a lot of time on scene with a time critical cardiac patient trying to listen to heart sounds; I almost guarentee it.

It could be useful but IMHO it has limited benefit in the out of hospital setting with the current state of the system. It's kind of like saying well we want to measure if the patient hears better in one ear than the other.

[melclin]

There are a few potentially exciting studies out about ACEI's and acute CHF treatment. The results show rather substantial hemodynamic improvements over traditional modalities such as nitroglycerine. I am talking class III and IV CHF. While the base of evidence is still rather small, I suspect this to become very popular with subsequent studies of large numbers. Perhaps large studies now exist? ACEI's are also very popular for AMI salvage type therapy. Even more so than beta blockers. In fact, beta blockade is being somewhat emphasized as an immediate core measure in the ER management of the AMI patient. The evidence is so compelling, my medical direction and clinical gurus are looking at a possible ACEI guideline to be integrated into our practice.

That's interesting, I'll have to have a look at some of that evidence base.

I agree, the pressor debates are all over the place and I am not sure I would consider a pressor or adrenergic based agent with any of the given blood pressures. I guess if you really had a hardon for increased B1 effects for the patient with a systolic B/P in the 90's, you could look at dobutamine; however, I am more of a conservative fella. Yet, the argument of augmenting inotropic activity and perhaps augmenting coronary perfusion is valid when considering dobutamine or even variable doses of other agents such as dopamine.

Take care,

chbare.

I agree with you. This guy is just not sick enough to need pressors in the prehospital environment. If a consultant EM or intensivist reckons its a good idea with considered assessment then maybe, but Charlie doesn't need me to mess around with those kinds of things in the 15 or so minutes I'm with him.

[Mateo_1387]

Isuprel rather

...

How often do you have the quiet to listen to heart tones? What do you do with the findings once you have them; do we introduce a new treatment based upon them or just write them down in a purely extrinsic exercise that will be repeated 20 minutes later in the ER?

Somebody, somewhere would find a way to screw up spending a lot of time on scene with a time critical cardiac patient trying to listen to heart sounds; I almost guarentee it.

It could be useful but IMHO it has limited benefit in the out of hospital setting with the current state of the system. It's kind of like saying well we want to measure if the patient hears better in one ear than the other.

So why Isuprel rather than Dopamine when they both have effects on heart rate?

...

I asked the questions first, where are my answers dude?

Honestly, I can make arguments for listening to heart tones and checking hearing, both can be of benefit to certain patient. I guess that is the difference between training and education.

Matty

[Kiwiology]

So why Isuprel rather than Dopamine when they both have effects on heart rate?

I thought isuprel had less chronotropic effect than dopamine?

Perhaps I am wrong.

Honestly, I can make arguments for listening to heart tones and checking hearing, both can be of benefit to certain patient. I guess that is the difference between training and education.

So can I however I am just not convinced it's of a great deal of benefit when given to the masses of ambo's.

[chbare]

I thought isuprel had less chronotropic effect than dopamine?

Perhaps I am wrong.

So can I however I am just not convinced it's of a great deal of benefit when given to the masses of ambo's.

Isuprel is a highly potent nonselective beta agonist. It's use is commonly associated with tachycardias and tachyarrhythmias. It has profound chronotropic effects. While tachycardias are a concern with dopamine, isuprel pretty much takes the cake in the chronotropic department.

Take care,

chbare.

[Kiwiology]

Perhaps we should go with some dopamine then

[DartmouthDave]

Hello,

Really, if your transport time is short the prudent option would supportive care until you get to the ED. Just be ready if things go down hill during the 15-20 minute transport.

I am not saying 'scoop' and 'run' with everything and let the ED sort it out. But, EMS should be an extension of the ED. In the ED he would get supportive care and a work up to see what is going on. Why should the EMS standard be different?

He has signs if right sided failure (edema and JVD) and signs of left sided failure (rales and pulmonary edema). Signs of a infectious process (general malaise x 5 days with a fever). Cardiac issues as well (1st degree block/bigeminy with an elevated DBP).

Plus, a solid list of unknows.....

Renal...what is going on? Any failure? Urine output?

Lytes? K+ Mg+ Phos? et al.... Fluid status? In he dry intavascular?

CBC? Hgb?

LFT?

Tn-I

Blah...blah.... =)

So, Kiwimedic.....what is going on here?

Cheers,

David

[Kiwiology]

Dave;

I don't have blood work sorry; don't have an iSTAT machine on the truck just yet

The problem was myocarditis however it presents in such a way that one could take it as "chest pain" and load the patient up on morphine and GTN, or "pulmonary edema" and go with GTN, lasix and morphine. The low BP might be in the minds of some, an indicator for IV fluids, when in reality none of these are clinically appropriate in my mind.

Wouldn't suprise me if some out there looked right past the obvious signs of a cardiac infection and RVF e.g. fever, pedal edema, JVD etc and just saw a person with "chest pain" or "pulmonary edema" or maybe even "short of breath" and went down the respective recipe for each. My ALS textbook mentions RVF in one paragraph and doesn't mention anything about withholding nitrates or fluid, it even states to establish an IV at KVO rate!

[Aussieaid]

Dave;

I don't have blood work sorry; don't have an iSTAT machine on the truck just yet

The problem was myocarditis however it presents in such a way that one could take it as "chest pain" and load the patient up on morphine and GTN, or "pulmonary edema" and go with GTN, lasix and morphine. The low BP might be in the minds of some, an indicator for IV fluids, when in reality none of these are clinically appropriate in my mind.

Wouldn't suprise me if some out there looked right past the obvious signs of a cardiac infection and RVF e.g. fever, pedal edema, JVD etc and just saw a person with "chest pain" or "pulmonary edema" or maybe even "short of breath" and went down the respective recipe for each. My ALS textbook mentions RVF in one paragraph and doesn't mention anything about withholding nitrates or fluid, it even states to establish an IV at KVO rate!

Note the treatment section.

[Kiwiology]

Note the treatment section.

It notes that left ventricular failure should be treated in-hospital with IV nitrates, duiretics and vasodialstors where feasible.

Note here its right ventricular failure or could be complete heart failure but it's not like we can do an echo or other cardiac imaging to differentiate betweeen complete heart failure and cardiogenic shock caused by right ventricular failure.