CHF - no more Lasix?

[ccmedoc]

As it should be. It is part of the national curriculum as is OG/NG tubes and central lines.....

I agree with NG/OG in the field, Foley is marginal (sterile). I think maybe we have differing opinions on what constitutes a central line, but where in any national curriculum is a central line advocated for a field paramedic???

And yes, we have seen a shift from the diuretics and towards NTG and ACEIs in a few areas..CPAP or BiPAP is very nice, but how many areas have a true CPAP or BiPAP or vent setup in their ambulances??

[HellsBells]

So I don't have a lot of expierence with lasix, being that I'm in an urban setting. However, I think the point of having a foley is a good one in the rural setting. If your far enough out for it to take effect, then you should have a good idea of what type of output is happening. The issue of a sterile field may be a problem, but I think if your well organized then it is entirely possible.

Our trucks are still running with lasix, but only if our SL nitro is having no effect. Sadly, it looks as though CPAP isn't even on the distant horizon at this point, judging fro

the outright dismissive response from a field trainer when I suggested it.

[armymedic571]

I agree with NG/OG in the field, Foley is marginal (sterile). I think maybe we have differing opinions on what constitutes a central line, but where in any national curriculum is a central line advocated for a field paramedic???

And yes, we have seen a shift from the diuretics and towards NTG and ACEIs in a few areas..CPAP or BiPAP is very nice, but how many areas have a true CPAP or BiPAP or vent setup in their ambulances??

http://www.nhtsa.dot.gov/people/injury/ems/EMT-P/index.html

Here is the link. Goto disk 1-8, page 4

I am not saying this is a skill whck all systems should perform, but one that could be considered in some of the very rural systems. I said should be considered. Not mandatory....

But that is just my opinion.

[HERBIE1]

http://www.nhtsa.dot...MT-P/index.html

Here is the link. Goto disk 1-8, page 4

I am not saying this is a skill whck all systems should perform, but one that could be considered in some of the very rural systems. I said should be considered. Not mandatory....

But that is just my opinion.

In most settings, an indwelling Foley would never be needed. I would however say that for longer transports, if you are monitoring I/O's, why not a Texas Catheter for a male? No need for a "sterile field". Anyone in an urban setting would never need this, but for folks who routinely have 30 minute+ transports it's a possibility, I guess.

[armymedic571]

In most settings, an indwelling Foley would never be needed. I would however say that for longer transports, if you are monitoring I/O's, why not a Texas Catheter for a male? No need for a "sterile field". Anyone in an urban setting would never need this, but for folks who routinely have 30 minute+ transports it's a possibility, I guess.

That is my point exactly.

[Paramagic]

There is more to the removal of furosemide than purely the risks involved in misdagnosing pneumonia.

Patients with acute cardiogenic pulmonary edema (ACPE) have traditionally been treated for having too much fluid - after all, there is fluid in the lungs, so they must have too much fluid everywhere. Hence the use of diuretics in the acute setting. However we know that this is not actually the case. ACPE occurs not because there is too much fluid, but because there is fluid in the wrong place. It is at it's heart a problem with pressure - innappropriate systemic vascular resistance leads to a redistribution in fluid and the subsequent vicious circle of decreased oxygenation, increased sympathetic response aggravating SVR, decreased contractility aggravating back-flow, leading to further decreased oxygenation. Eventually the right heart gets in on the action too, with a RV afterload mismatch caused by hypoxic shunt from increased pulmonary cascular resistance. Bad news.

Most ACPE patients are not in fact fluid overloaded, but euvolemic and in many cases they are actually dry, so diuresis is not going to provide anything beneficial. Whilst some may argue that there is a degree of vasodilation that occurs due to furosemide administration (and this is true) the degree of dilation and the time it takes to happen is extremely variable and not clinically relevant when superior agents such as nitrates are available to achieve the same ends. THere may be some call for furosemide in certain cohorts of patients, such as those with a history of fluid overload, however it should be used with caution if at all.

Now, on top of all of that, there may actually be a place for the use of furosemide in the setting of a patient with pulmonary edema, just not in the acute or pre-hospital setting. It seems that patients who recieve positive pressure ventilation for more than about 24s have a subsequent inappropriate production of anti-diuretic hormone and their fluid balance and CVP and so forht needs to be monitored carefully (which of course will be done in the ICU, not the ambulance)

There are a number of good papers and text books out there that discuss this issue that are not too hard to find if you look for them.

Paramagic

[armymedic571]

There is more to the removal of furosemide than purely the risks involved in misdagnosing pneumonia.

Patients with acute cardiogenic pulmonary edema (ACPE) have traditionally been treated for having too much fluid - after all, there is fluid in the lungs, so they must have too much fluid everywhere. Hence the use of diuretics in the acute setting. However we know that this is not actually the case. ACPE occurs not because there is too much fluid, but because there is fluid in the wrong place. It is at it's heart a problem with pressure - innappropriate systemic vascular resistance leads to a redistribution in fluid and the subsequent vicious circle of decreased oxygenation, increased sympathetic response aggravating SVR, decreased contractility aggravating back-flow, leading to further decreased oxygenation. Eventually the right heart gets in on the action too, with a RV afterload mismatch caused by hypoxic shunt from increased pulmonary cascular resistance. Bad news.

Most ACPE patients are not in fact fluid overloaded, but euvolemic and in many cases they are actually dry, so diuresis is not going to provide anything beneficial. Whilst some may argue that there is a degree of vasodilation that occurs due to furosemide administration (and this is true) the degree of dilation and the time it takes to happen is extremely variable and not clinically relevant when superior agents such as nitrates are available to achieve the same ends. THere may be some call for furosemide in certain cohorts of patients, such as those with a history of fluid overload, however it should be used with caution if at all.

Now, on top of all of that, there may actually be a place for the use of furosemide in the setting of a patient with pulmonary edema, just not in the acute or pre-hospital setting. It seems that patients who recieve positive pressure ventilation for more than about 24s have a subsequent inappropriate production of anti-diuretic hormone and their fluid balance and CVP and so forht needs to be monitored carefully (which of course will be done in the ICU, not the ambulance)

There are a number of good papers and text books out there that discuss this issue that are not too hard to find if you look for them.

Paramagic

Magic,

Welcome to the city.

I like your post. I think this another example of why assessment and history are so important. I believe that was the point I was trying to make with discussing the mis-diagnosis of pneumonia.

But, I am against taking this medication (furosemide) out of the tool box. We need to start increasing educational standards and stop dumbing down this profession.

[Paramagic]

Magic,

Welcome to the city.

I like your post. I think this another example of why assessment and history are so important. I believe that was the point I was trying to make with discussing the mis-diagnosis of pneumonia.

But, I am against taking this medication (furosemide) out of the tool box. We need to start increasing educational standards and stop dumbing down this profession.

Thanks, long time lurker, first time poster....

At this stage, generally speaking, I would be in favour of removing lasix from the drug box, at least for the setting of suspected pulmonary edema - nitrates, CPAP and ACE Inhibitors are first line treatment for this, and irrespective of the difficulties with differentiating ACPE from pneumonia, it probably leads to worse outcomes. However, while there seems to be less and less of a role for it in the setting of ACPE, that is not to say that it does not have uses elswhere in pre-hospital care (hyperkalemia for example) although these instances may be rare, and a cost/benefit analysis should probably be undertaken.

I am, however, firmly against protocolisation (is that a word?) of emergency medicine as the sole form of clinical risk management. The first line of clinical risk management should always be education. In some cases further protocolisation may be required, but it shoud be a last resort.

Something else we need to be careful of is being against losing 'skills' or drugs for reasons other than patient care (ie. ego). There often seems to be an attitude that removal of a particular drug or procedure somehow reflects badly on us as paramedics (not that I am trying to imply that this is your stance; this is just a general observation) Now, if this has occured because, say we have been unable to differentiate between the decapitated/non-decapitated patient, then fair enough, we should be ashamed. However if it has occured because the best available evidence demonstrated no benefit, or even harm from using it, then we should happily wave it goodbye and maybe give it a Viking Burial at sea. We need to practice emergency medicine, not massive egotism.

The studies quoted earlier in the thread seem to me to relate to a systemic problem in the diagnosis and management of a particular cohort of patients in a particular service. One needs to be careful with making generalisations regarding our own practice or service from these kinds of studies without having read and understood the study in it's entirety, including any methodological errors before making decisions regarding it's applicability to our own specific circumstances. When we just read abstracts we end up with blanket statements being made like "RSI is bad, mmmmkay" that may not be appropriate depending on ones circumstances.

[armymedic571]

Thanks, long time lurker, first time poster....

At this stage, generally speaking, I would be in favour of removing lasix from the drug box, at least for the setting of suspected pulmonary edema - nitrates, CPAP and ACE Inhibitors are first line treatment for this, and irrespective of the difficulties with differentiating ACPE from pneumonia, it probably leads to worse outcomes. However, while there seems to be less and less of a role for it in the setting of ACPE, that is not to say that it does not have uses elswhere in pre-hospital care (hyperkalemia for example) although these instances may be rare, and a cost/benefit analysis should probably be undertaken.

I am, however, firmly against protocolisation (is that a word?) of emergency medicine as the sole form of clinical risk management. The first line of clinical risk management should always be education. In some cases further protocolisation may be required, but it shoud be a last resort.

Something else we need to be careful of is being against losing 'skills' or drugs for reasons other than patient care (ie. ego). There often seems to be an attitude that removal of a particular drug or procedure somehow reflects badly on us as paramedics (not that I am trying to imply that this is your stance; this is just a general observation) Now, if this has occured because, say we have been unable to differentiate between the decapitated/non-decapitated patient, then fair enough, we should be ashamed. However if it has occured because the best available evidence demonstrated no benefit, or even harm from using it, then we should happily wave it goodbye and maybe give it a Viking Burial at sea. We need to practice emergency medicine, not massive egotism.

The studies quoted earlier in the thread seem to me to relate to a systemic problem in the diagnosis and management of a particular cohort of patients in a particular service. One needs to be careful with making generalisations regarding our own practice or service from these kinds of studies without having read and understood the study in it's entirety, including any methodological errors before making decisions regarding it's applicability to our own specific circumstances. When we just read abstracts we end up with blanket statements being made like "RSI is bad, mmmmkay" that may not be appropriate depending on ones circumstances.

HHmmmm. I see your point, especially about reading abstracts.

However, I have a question in regards to ACPE. Would it be correct to state that diuretics have been used in the past (not necessarily by pre-hospital, but by MD's) to help reverse the shift of fluid in these cases? And if so, what is the potential benefit/risk in patients with well documented history of heart failure who are suffering from acute exacerbation?

[Paramagic]

<br />HHmmmm.  I see your point, especially about reading abstracts.   <br /><br />However, I have a question in regards to ACPE.   Would it be correct to state that diuretics have been used in the past (not necessarily by pre-hospital, but by MD's) to help reverse the shift of fluid in these cases?  And if so, what is the potential benefit/risk in patients with well documented history of heart failure who are suffering from acute exacerbation?<br />

<br /><br /><br />

That's a good question. They certainly have been used to deal with the fluid shift, but on the erroneous assumption that there is an overload of fluid. The key term is 'fluid shift'. Eliminating the fluid in the system does not necessarily correct the fluid shift (it's not systemic overload we are usually worried about with ACPE - it's fluid in the wrong place, not too much fluid) and can lead to further problems with electrolytes (K+ in particular of course) and long term poor outcomes. Nitrates and ACEI's all serve to better correct the imbalance between hydrostatic and colloid oncotic forces that are the main problem to allow the fluid to shift back (or rather be taken up by the lymphatic system) and CPAP splints alveoli open to improve oxygenation and the problems that come from the V/Q mismatch (and shunt if really bad) (hopefully someone else can explain that better than me)

Regarding long term CHF patients with an exacerbation, there are two schools of thought. One is that diuretics are appropriate as this may at least in part be a problem that has overload as a contributing factor. The other is that in the face of the sometimes quite substantial amounts of furosemide that these patients are taking alreadsy, a small amount may just be peeing into the wind and not achieving anything.

To be honest, I am not sure how much data there is or isn't to support either of these positions. I currently am coming down in favor of giving the frusemide to these patients, but really, I'm not sure whether that is to make them feel better or me feel better... And it is only in cases of documented fluid overload that I consider it. I certainly would like to think that the potential to do harm with furosemide that we have in the true acute cases is not there for the acute on chronic cases. I stand to be corrected on this though, so if anyone else has a position, or better some data to support one way or another I would love to see it.

That probably doesn't help a great deal though does it?

I'll have a fossick around tomorrow and dig up some studies to support my ramblings.

Paramagic