CHF?

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jaksasquatch

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Hello all,

I"m currently in Semester I of Paramedic and I have about 7 months of EMT-B experience in a rural 911 system (3 to 4 calls a 12 hours shift) under my belt. I had a call the other night that puzzled me. Sorry for the broken history, the medic was getting the history while I was working on the patient, this was also near midnight and fatigue was setting in for sure.

Dispatched to respiratory difficulties, arrived on scene to find one 53 y/o female patient laying supine in her bed (that happened to be in an extremely small room). Patient speaking in one word sentences with family around. Family stated that patient has CHF and if I'm not mistaken COPD (not sure on this one, again apologize for the crappy history). SPO2 was in the crapper (<50), HR 125 with obvious work of breathing, 12 lead ekg showed no other abnormalities, BP 102/64. Capnography initially 39 with a RR in the 40's if I'm not mistaken. Patient looked jaundiced, not warm to touch, no diaphoresis. Breath sounds revealed crackles/fine rales in the upper and lower lobes with stridor in the lower lobes. Patient was given a duo neb and 125mg of Solumedrol. Patient was stable after a few minutes with a SPO2 of 81, HR never came down, Sys BP got up in the 160's. Not sure if the medic gave NTG enroute. Patient was probably intubated in the hospital later.

I didn't think about this call until I got off shift. I understand stridor reveals that the airway is closing up but the rales would be revealing CHF w/ obvious L sided heart failure due to history and symptoms. If I was the one running this call I would have gone with CHF w/ pulmonary edema and given NTG w/CPAP immediately and possibly bumex later. Any comments/concerns about my logic here?
 
I'm also a student... I'll be interested to see what experienced people think.

I would really like to know more history... Kind of surprised to find a 53 female in this condition, but I guess some people get old fast (especially if they smoke, had/have cancer, etc). Is the patient on oxygen at home? How many pillows does she normally sleep on? Peripheral edema? Distended neck veins? Any evidence of old MI's on the EKG?

A hypotensive CHF patient seems to be about as hard to manage as it gets. I'd love to give her nitro, but that BP is concerning. Fortunately she's CAOx4 (I assume, since you say she's speaking), so you can use CPAP, but CPAP is also going to lower her blood pressure... Would love to give fluids, but pulmonary edema... She's already a bit shocky and atropine really isn't going to help... Dopamine might do some good but that's a med control option for me.

First things first, I get her sitting up a bit and put her on O2 at 15Lpm via NRB. Get her on the stretcher and see how she's doing. Hopefully just positioning and oxygen will do her a lot of good. Considering CPAP, nitro and/or a call to med control to ask for dopamine orders depending on her condition by the time we're in the truck.



FWIW I don't think "stridor in the lower lobes" is a thing - stridor comes from obstruction of central airways (IE, the trachea from foreign body obstruction or something like that). Probably you were just hearing wheezing. Cardiac wheezing is a thing. Basically fluid in the lungs makes sounds similar to wheezes: http://www.mayoclinic.org/diseases-...re/expert-answers/cardiac-asthma/faq-20058447
 
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O2 at home I'm not sure. She was sleeping on 2 pillows, barely any peripheral edema, JVD was a negative, no evidence of old MI on the EKG. The bp started coming up once we got her upright and to the truck. CAO X4 for sure. With her weight (120 lbs) I don't consider her bp really that hypotensive especially with the trend up in the truck. We put her on 8 lpm nebulizer mask in the truck. You are also correct in that it had to be wheezes. My paramedic called it stridor and I was just copying his terms. Didn't make any sense to me. My guess is that it was such a high pitched wheeze (this being a bad thing) that it sounded continuous like stridor.

With regards to atropine or dopamine I really don't have a great understanding of using that in CHF. With the heart rate at 123 bpm and a stable bp I wouldn't consider it based on our local protocols.
 
Why was the neb given? Lets exacerbate them more.

It is common for CHF exacerbation to present with hypertension. It may have been the neb that shot their BP up.

Was this sudden onset? Was CPAP not initiated? You say they were jaundice -- where? Guessing without a decent history isn't going to solve much. My guess is they have other chronic issues going on (i.e. liver failure) and pulmonary edema resulting.
 
jaksasquatch said:
With regards to atropine or dopamine I really don't have a great understanding of using that in CHF. With the heart rate at 123 bpm and a stable bp I wouldn't consider it based on our local protocols.
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I don't know why atropine was mentioned; that would make an already bad issue worse. Dopamine isn't a great choice in CHF -- dobutamine would be a better option. The goal is to use an inotrope as contractility is often severely diminished with CHF.
 
teedubbyaw said:
Why was the neb given? Lets exacerbate them more.

It is common for CHF exacerbation to present with hypertension. It may have been the neb that shot their BP up.

Was this sudden onset? Was CPAP not initiated? You say they were jaundice -- where? Guessing without a decent history isn't going to solve much. My guess is they have other chronic issues going on (i.e. liver failure) and pulmonary edema resulting.
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Unfortunately my medic continued with the nebulizer, CPAP wasn't initiated, jaundiced look was over the whole body, not so much in the eyes like you usually see. I'll ask him about it later. Upset with myself that I didn't pay more attention to the history, pretty sure just chronic CHF. Probably what made my medic perform the neb was the "stridor" which I can now identify as cardiac wheezes.

Dopamine is all we have so I would only consider it if I saw legit cardiogenic shock (dropping bp, ashen look, diaphoretic, slight tachycardia with dips in the hr etc...). Giving fluids for cardiogenic shock would be a no no in this case so it would be the only tool in the toolbox I would think.
 
This is a case where capnography waveforms can help you determine treatment modalities. If the patient presents with wheeze, a glance at the waveform can help you determine obstructive etiology vs cardaic wheeze, which would show a flat expiratory plateau. I'd certainly put this patient on CPAP and possibly a concurrent albuterol/ipratroprium neb. The old nuggest about CHFers flashing as soon as you touch them with albuterol is unfounded. Treat what you can treat in a priority order and then manage your patient logically, ruling out and honing your differential as you go.
 
DEmedic said:
This is a case where capnography waveforms can help you determine treatment modalities. If the patient presents with wheeze, a glance at the waveform can help you determine obstructive etiology vs cardaic wheeze, which would show a flat expiratory plateau. I'd certainly put this patient on CPAP and possibly a concurrent albuterol/ipratroprium neb. The old nuggest about CHFers flashing as soon as you touch them with albuterol is unfounded. Treat what you can treat in a priority order and then manage your patient logically, ruling out and honing your differential as you go.
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Looking back on it I have no clue why he didn't. Possibly trying to see if the neb helped to form a differential. Still the highest her saturation got to was 86%, still pitiful. She was also tiring out by the time we got to the ER, should have been on CPAP immediately.
 
History of CHF and COPD. Wheezes doesn't mean it's strictly one or the other. In fact, you can have CHF and COPD happening at the same time, one exacerbating the other. Duoneb is not exactly ''wrong'' as they have a history of both and it just depends on presentation and what the medic thinks is going on (and since we don't have a complete picture, we don't know either).


Stridor is an upper airway sound, caused by an upper airway issue. Sure, you can ''hear'' stridor in the lobes when auscultating however the issue is above the carina. If the patient did have ''stridor'' I'd be leaning further away from CHF.
 
I agree with DEmedic.
Of course local protocols may vary a little with treatment options, (what meds you carry and devices that are available to you).
If you're a crew of two - a paramedic student - not being able to continue participating with the patient assessment and treatments, because maybe you have to drive - makes things difficult for a learning environment. Sounds like you're definitely trying to grasp the ALS side of EMS and trying to put the pieces of the puzzle together. Keep looking for answers to questions.
Good luck in your Paramedic course.
 
Pop quiz...what's a side effect of CPAP/BiPAP that could be concerning in this patient? Especially if you're using it in conjunction with NTG as was previously stated.

Most CHF patients are volume depleted so fluids aren't a bad idea. Also see Starling's Law.

Also, and EtCO2 number was given, was the waveform obstructive?
 
CPAP can cause hypotension. Also concerned with air trapping with CPAP and COPD patients.

My question is what did they do to make the BP go from 102 systolic to 160's systolic?
 
jaksasquatch said:
I didn't think about this call until I got off shift. I understand stridor reveals that the airway is closing up but the rales would be revealing CHF w/ obvious L sided heart failure due to history and symptoms. If I was the one running this call I would have gone with CHF w/ pulmonary edema and given NTG w/CPAP immediately and possibly bumex later. Any comments/concerns about my logic here?
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All I can say is that it can be really difficult to differentiate between COPD and CHF exacerbations in patients who have an established history of both, and there are certainly no rules saying that they can't both be acting up at the same time.

FWIW, remember that wheezing can be the primary presenting sign in a CHF exacerbation. It's not always the classic "wet" sounds and nothing else.

It's hard to go wrong with albuterol. It will help or it won't, and it isn't going to hurt. It's also hard to go wrong with NTG.

It'd be nice to have the ED docs chime in on this topic.....
 
Remi said:
All I can say is that it can be really difficult to differentiate between COPD and CHF exacerbations in patients who have an established history of both, and there are certainly no rules saying that they can't both be acting up at the same time.

FWIW, remember that wheezing can be the primary presenting sign in a CHF exacerbation. It's not always the classic "wet" sounds and nothing else.

It's hard to go wrong with albuterol. It will help or it won't, and it isn't going to hurt. It's also hard to go wrong with NTG.

It'd be nice to have the ED docs chime in on this topic.....
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(I'm an EM intern and only on my 3rd month in the adult ED)

It's easier in patients with history of one over the other only because you can play the odds if the clinical picture isn't clear. But just because one has a history of COPD doesn't mean that they cannot develop CHF, and certainly because someone has CHF but not COPD, doesn't mean that they can't develop it (e.g. the pt. with extensive smoking history), and there are some zebras out there that can cause wheezing (e.g. Carcinoid syndrome, Churg-Straus syndrome) in addition to chemical irritation (e.g. aspiration pneumonia), obstruction due to tumors, etc., etc.

In the ED, the chest X-ray can help and so can some labs, but it all depends. Its a classic trick for a radiologist to put up 3 chest x-rays from 3 different patients and ask their resident to determine if the X-rays show CHF, pneumonia, or atelectasis - inevitably one will be chosen as CHF, another as pneumonia, and the last as atelectasis only for the radiologist to say "nope, they're all [CHF or pneumonia or atelectasis]". This is why I occaisionally will get a call from a radiology resident for more clinical information as it will help guide their interpretation. BNP may not be elevated in flash pulm edema or may be mildly elevated at baseline for many patients without CHF. All other labs and imagine have limitations, too.

CPAP should definitely help CHF, and often helpful for COPD or asthma (though BiPAP is preferred). Albuterol has association with harm (or more probably, use in more severe presentations), but there are no RCTs to confirm or refute this. NTG is certainly helpful in CHF, but could be detrimental in COPD if they're exacerbated due to pneumonia, thus potentially dehydrated or septic.

A good middle ground is likely albuterol and CPAP. Maybe NTG if they're hypertensive.
 
I totally agree with medicsb. It can be impossible to accurately distinguish between copd vs chf vs pneumonia, or a combination of these, based on clinical s&s alone. Even with a BNP and chest xray, it may not be possible. When it is an obvious diagosis, then I treat aggressively with the appropriate treatments. When I am not sure, then I use more basic treatments, with CPAP being an obvious go-to Tx.
 
Awesome assessment by the OP, by the way.
 
this may be a difference in protocol, but why was solumedrol given ? to my understanding solumedrol could make the situation worsen in time
 
Handsome Robb said:
Pop quiz...what's a side effect of CPAP/BiPAP that could be concerning in this patient? Especially if you're using it in conjunction with NTG as was previously stated.

Most CHF patients are volume depleted so fluids aren't a bad idea. Also see Starling's Law.

Also, and EtCO2 number was given, was the waveform obstructive?
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On the contrary, most CHF patients are in a chronic state of fluid OVERLOAD. The renin-angiotensin-aldostersterone-system is provoked when kidney perfusion is inadequate, as is typical in heart failure. The activation of the RAAS is an important adaptation for regulating blood volume and SVR in response to hemorrhage or excess fluid loss, but it is detrimental in the case of CHF—creating complications such as pulmonary edema. It's neat that you mentioned Starling's law, however it is not particularly applicable to a heart in a state of failure (See Laplace's law). Sure, for a healthy heart, contractility increases in proportion to the increase in preload—though a failing heart lacks the ability to compensate for increased preload (factors such as: fibrosis, hypertrophy, ventricular dilation, et. al); the sarcomeres of cardiac myocytes are over-stretched, impairing contractility and worsening pump function—which, in the case of left ventricular failure, forces the 'back-up' of fluid into the lung parenchyma. This is precisely why nearly all of the drugs prescribed for CHF (ACE-inhibitors, diuretics, vasodilators, etc.) function to decrease fluid volume and cardiac preload.
 
TXmed said:
this may be a difference in protocol, but why was solumedrol given ? to my understanding solumedrol could make the situation worsen in time
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I also am wondering about the steroid use here. If the provider had determined this is a reactive airway disease issue then that would be appropriate, but if he was treating pulmonary edema primarily I'd be a bit dubious. I was always taught that when you have a dual diagnosis such as COPD/asthma and CHF, and that you're not sure which one is causing the acute condition, go the safe route and treat the CHF. nothing in a CHF treatment (cpap, nitro) is going to make your asthma/COPD worse, however treating the reactive airway issues (aka solu medrol, albuterol, epi), all will cause increased strain on the heart, which can greatly accelerate the effects of CHF.

I've seen my fair share of older folks out of the "skilled" nursing facilities, with both CHF and COPD on their diagnosis list, on their second or third duoneb, prescribed by the doctor, administered by a nurse, with lungs that sound like a dishwasher that you could hear in another state if you wanted to. it just pays to be careful and thorough. "do no harm" and all that.
 
SixEightWhiskey said:
I also am wondering about the steroid use here. If the provider had determined this is a reactive airway disease issue then that would be appropriate, but if he was treating pulmonary edema primarily I'd be a bit dubious. I was always taught that when you have a dual diagnosis such as COPD/asthma and CHF, and that you're not sure which one is causing the acute condition, go the safe route and treat the CHF. nothing in a CHF treatment (cpap, nitro) is going to make your asthma/COPD worse, however treating the reactive airway issues (aka solu medrol, albuterol, epi), all will cause increased strain on the heart, which can greatly accelerate the effects of CHF.

I've seen my fair share of older folks out of the "skilled" nursing facilities, with both CHF and COPD on their diagnosis list, on their second or third duoneb, prescribed by the doctor, administered by a nurse, with lungs that sound like a dishwasher that you could hear in another state if you wanted to. it just pays to be careful and thorough. "do no harm" and all that.
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After asking my paramedic about this he still believes that stridor can be heard in the lower lobes (after research and a commonsense analysis I believe it to be a cardiac wheeze). If I'm correct COPD doesn't present with fine rales all that often (more wheezing than anything) and with the history and the low SPO2 saturation it all seems to confirm CHF as the primary problem. Solumedrol seems to be his version of candy, I haven't done much study on solumedrol (I'm still first semester medic and we haven't touched on it quite yet) but I know it's a smooth muscle relaxant, something a CHF patient wouldn't need. He wasn't treating pulmonary edema because he saw that as secondary to a reactive airway disease. My belief is that the assessment was off therefore the treatment was off.
 
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