Back when I was in paramedic school, the text we used was “Emergency Care In The Streets” by Nancy Caroline MD. It was a pretty good text book, although not written at the college level. In fact, the original paramedic program that Dr. Caroline ran was intended to provide inner city youths with a job that didn’t involve flipping hamburgers or selling drugs. As such, it was written at, I think, the Eigth Grade level. Some people scoffed at the level of writing used and in fact, we used a number of supplemental texts, but Emergency Care… was our main text book.
One of the things that Dr. Caroline wrote about was what she termed “Cardiac Asthma”. She also used the phrase that I used for this post title. Her point was that wheezing is a sign of airway restriction, not necessarily of bronchoconstriction. All too many people jumped (and sadly still do) to the conclusion that a wheeze must be caused by COPD or Asthma. They then immediately throw nebulized medications at the patient.
People used to laugh at the term “Cardiac Asthma” and in truth it’s not very accurate. Like “The Golden Hour”, it was a conceptual tool to help people get that it’s dangerous (to the patient) to assume that a wheeze can only be caused by Asthma or COPD. At various points in the evolution of a Congest Heart Failure exacerbation one can hear any number of breath sounds. Or one can ominously hear no breath sounds which can fool people into believing they are hearing clear breath sounds.
The point here is that it’s easy to be fooled if 1) You want to believe one particular thing, and 2) You don’t do a thorough exam.
All of which is preamble for rest of the post.
We were dispatched to a call for an elderly man having trouble breathing. No details in the call, not that they are always helpful. Nothing but his age, gender, and the fact that he was having breathing problems.
We arrived behind the fire department and the BLS ambulance, gathered our equipment, and proceeded into the house. Up to the second floor (what else?), and into a tiny, cramped bed room.
The BLS crew arrived a couple of minutes before we had, but had not released the fire company, which just made it more crowded. Turns out the BLS crew had an oops with their portable oxygen tank which left it empty. So, they used the fire department’s oxygen while one EMT ran down stairs to get a fresh tank. What his partner was doing in the mean time is a mystery, since it didn’t involve taking a pulse, blood pressure, asking any questions, or doing even one thing to help figure out what was going on with the patient. Harsh, I know, but for this particular EMT it’s the norm. She’s a wealth of information on a call, none of it useful.
Such is my lot in life.
My partner took a set of vital signs while I asked the patient a few questions.
His story was that he had got out of bed to use the bathroom and upon returning to his bed felt out of breath. This was not normal for him, which is what prompted him to ask his son to call 9-1-1. His son wasn’t particularly helpful, although he was pleasant and tried. He did tell us that his father had inhalors prescribed and had for years, but never used them. Not surprising since his Dad is a veteran and gets his care at a VA clinic. Nothing they do surprises me, although if they did something right, that would in fact surprise me.
While the EMT wrote down an incorrect list of medications, I listened to the patient’s lungs. Normal, except for a fairly localized area of wheezing on one side. Odd, but not concerning… yet. My partner gave me the vital signs which were pulse 120, BP, 200/100, RR 40. O2 saturation on a non rebreather was only 96%. Hmmm. ETCO2 was 45. The plot was thickening.
My early thought was Congestive Heart Failure. I’ll be honest. With most patients over the age of 50 or so, new onset dyspnea, with suddent onset, and no history to suggest otherwise, and after midnight, my early thought is always CHF. As a very wise doctor told me when I was a new paramedic, “People do not suddenly develop Asthma in the middle of the night, but they do suddenly develop CHF in the middle of the night.” I’ve followed that advice for almost 20 years and it’s always held me in good stead.
The 12 Lead, which I include because people like to look at them, was non informative. Which is to say that nothing jumped right out at us.
I suppose you could split hairs and say that V1 and V2 are “suggestive” of an MI, but I wasn’t and still am not convinced. At least not convinced enough that I’d insist on going to a PCI capable hospital. Wouldn’t do to have Rogue Medic accuse me of kidnapping a patient, would it?
I asked the patient’s son if his father seemed to be having trouble breathing or was working harder than normal to breath. He couldn’t really answer, but the grandson offered that the patient was in fact working to breath and looked pale. Hmmm.
The wave form was more instructive, at least I thought so. While I have often said that a O2 saturation of 100% is pretty meaningless, an O2 saturation of 96% on high flow O2 is informative, at least to me.
When looking at pulse oximeter readings, it’s important to make sure that the pulse wave form is good as that affects the accuracy of the readings. This is a good wave form, so I had no reason to doubt the accuracy of the reading. The ETCO2 waveform was similarly informative, showing me that there was no hint of CO2 retention or a “shark fin” wave form. The clinical picture was becoming more clear, but as is usually the case, the numbers were more confirmatory than diagnostic.
You’ll notice that the time on this is later than on the 12 Lead. We had the monitoring probes on much earlier than the print out, but you have to print about six seconds of waveform out for the readings to be set into the Code Summary. Which I constantly have to remind my technophobic partner. Well, oddly technophobic when it comes to some things like a monitor that we’ve been using since about 1998.
Sigh.
My gut feeling was that this was very early Congestive Heart Failure, but I really had nothing to pin that to. The patient wanted to go to the hospital that was the furthest away from us (of course). I wasn’t particularly comfortable with that non only because of the distance, but because care in that ER is marginal on a good day. We had a little bit of discussion and agreed to transport that patient to a closer hospital. Not my first choice, but my role in determining destination is limited in most cases.
The next task was to get the patient into the chair for the carry down stairs. This is actually a good diagnostic test, although that might seem odd. It might even seem a bit cruel, but it often helps to confirm clinical suspicion. If the patient can stand and pivot 90 degrees without difficulty, it’s a positive sign. If he can’t, it’s not so good. Maybe that sound cruel, or like I’m lazy, but it often helps clarify a murky case such as this. Being a paramedic often means being a detective.
Think about that for a minute. If a person who normally can stand and walk without assistance or difficulty suddenly gets short of breath standing, there is a clinical clue for the alert practitioner.
The patient stood (with me holding his arms) pivoted and sat down. And was short of breath. The diagnosis was clinched in my mind.
We carried him down the long wooden stairs and out to the ambulance.
The rest of the call was pretty routine. In the ambulance we listened to his breath sounds again, which were without change. We started an IV and gave some Nitroglycerin. The Nitroglycerin worked as it should, lowering his blood pressure, reducing his preload, and helping his breathing. We stabilized him enough so that the hospital could continue his care and he’d be fine.
Well they could once I convinced them that the wheezing was not due to his non existent COPD or Asthma. The nurse persisted in asking me if he used his nebulizer at home before calling us. This, despite the medication list print out from his clinic which I brought with us and which showed NO, I repeat NO, medications of any sort for Asthma or COPD. At which point the doctor told the nurse that the wheezing was probably cardiac wheezing, not Asthma. Which, as I had pointed out repeatedly, the patient did not have.
At least the doctor had paid attention to my report. Or maybe she had been a paramedic in a previous life. Either way, she ordered CPAP, not a nebulizer and she didn’t even wait for the Chest Xray to come back. She did what we did, only probably better. She used good clinical judgement to determine what was going on with the patient.
That’s some good detective work right there. Good job!
Thanks. I’m a freak of nature or something. What was going on jumped out at me as clear as day. Most everything else we did to diagnose was confirmatory in nature. Then again, I’ve seen it a couple of thousand times, so I should know it by now.
This was a good learning experience for me, previously I did 2 years on a med surg floor, I have never heard of Cardiac Asthma. Thanks for sharing…as a RN working psych, it never hurts to expand my horizons.
This is a VERY good article. Thank you, I enjoyed it very much. Your assessment and treatment were spot on.
I would like to point out a couple of other things that would point towards CHF and not COPD.
1. The pt’s B/P was 200/100…………Classic sign of most CHF pt’s I’ve encountered.
2. The 12 lead EKG shows LVH……………..along with 60 cycle artifact on the frontal leads…..lol
The fact that the patient is not showing typical shark fin appearing capnography wave form is a good sign since the alveoli are still somewhat emptying equally. In the COPD or Asthma patient, the alveoli are emptying unequally which we see as a shark fin capnography wave form. The PetCO of 45 is not a tell tale sign, especially if the patient is tachypneic @ 40/min……that is worrisome. You would expect the CO2 level to be below the lower range of 35 with such rapid respirations (blowing it off). Low CO2 levels happen frequently with COPD and Asthma patients because they are tachypneic. But as the airways swell and constrict more, the pt losses the ability to get the air out, and the CO2 levels start to rise rise. It’s kind of a good tool to weigh at what stage the COPD or Asthma patient is in. I think the higher level in the CO2 with such a tachypneic pt is secondary to the fluid in the intersitial space and alveoli……..can’t get out.
Our protocols also give us the ability to place the pt on CPAP right away. CPAP with help then if it is CHF or COPD. Because the mask is sealed and the pt can’t have SL NTG this way, we start a NTG gtt instead starting @ 10 mcg/min and titrating up to 200 mcg/min…………or 1-2 inches of NTG paste. We’ll also give the pt 40mg of Lasix IV.
I like to think of it this way………….The heart is congested from the fluid overload and the HTN. We give the Lasix to vasodilate the vessels which drops the preload, and there fore the overall pressure. with this vasodilation, we are giving the fluid in the lungs a place to go, and then give the Lasix so they can pee the extra fluid out. Boom….done.
Great comments Nick, thank you very much for sending them.
1) Yes, that was a pretty good clue, but by itself not definitive. I’m sure you’ve seen patients with COPD and Hypertension. Although COPD didn’t enter my differential at all. The question, at least in my mind, was CHF or something less pernicious.
2) LVH certainly, but I’d expect that in a patient as elderly as this one. I don’t know if that was 60 cycle artifact, or just that the patient’s skin was so dry so as to be poorly conductive.
3) The patient isn’t blowing off CO2 because no gas exchange is taking place at the cellular level. Again, I know that you know that, but I just wanted to clarify. What I have seen in patients that we have treated for CHF is that when the treatment starts to work ETCO2 rises. This is more dramatic when we put a patient on CPAP. Which might seem counter intuitive, but makes sense when you think through the physiology of the process. CPAP is within our protocols and when to use it is within our discretion. In this case we didn’t because the patient responded well to NTG sprays. We don’t have NTG IV in our protocols which I’ve been lobbying for for a while but without success so far. There was a small but interesting study, referenced by Rogue Medic, out of Pittsburgh using 2mg boluses with good effect. That was an in hospital study, but I can’t see why it couldn’t be done in the field. We have short transport times, so it would seem to be a good tool to use. Oh well. We have the option of NTG paste, but our medical director doesn’t like it, so we don’t use it as a rule. While Lasix is within our protocols, it’s not used in the field very much, at least not by most of the medics.
Acutely, we go for reducing preload, hence the NTG and CPAP, both are excellent at that. We let the hospital titrate the Lasix as they see fit. If we had longer transport times, we’d probably give IV Lasix.
Again, thanks for the comments.
A few years back, I had a medic student riding with me and we ran a trouble breathing. Much like you, I tend to look past “trouble breathing = asthma”. This one wasn’t a CHF issue and the lungs were completely clear. The 12 lead showed an anterior ischemia (STE V2, V3, V4) without reciprocal changes or a generalized ischemia pattern.
My treatment was the unstable angina/STEMI that we were running at the time (MONA). My student was suitably impressed, although she later had her training program field coordinator questioning “her” treatments as being “completely inappropriate” to “asthma”. /eye roll/ I got to go have a sit down with said coordinator and explain the reality of alternate cardiac ischemia symptomologies.
I have a two part post titled “Anginal Equivalents” that you might find interesting. Or not. Much the same scenario although my “trainee” wasn’t a trainee he was a Spare-o-medic assigned to my unit for one shift. Which was more than enough for me to decide that standards have lowered at my agency. It’s amazing how many people in EMS and EM can’t seem to grasp the concept that not all cardiac events involve chest pain, pressure, or discomfort. Many of them involve other symptoms, foremost among them dyspnea.
I really enjoyed those posts and had read them when I was a new Paramedic. I really wish this post would have been around when I was brand new because three years ago I likely would have been freaking out in my head about this sort of patient (prior to reading such posts as yours)!
Is it asthma?! COPD?! CHF?! What if I give him nitro and its not CHF?! What if I give him albuterol and its CHF?!
Am I looking too hard or is the B-C segment sloped a bit more than is normal suggesting some inhibition of expiration? Not as pronounced as in asthmatics or COPD Pts, but still relevant & may support the CCF diagnosis
I think you’re looking to hard.
One thing to note is it is not unexpected to have that sort of rounding initially when using the nasal EtCO2 detectors, especially when they’re as markedly tachypneic as your patient!