Hoping to followup on this patient

Epi-do

Epi-do

I see dead people
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Had a run for a female in her late 50's c/o CP/SOB. Hx of diabetes, htn, MI x 1, heart disease. Can't recall what exact meds she was on, but takes oral meds for her diabetes, htn med, water pill, and a couple other things. Is not currently prescribed any inhalers.

BBS=clear. SR without ectopy at a rate of 88-104 throughout transport. 12 lead showed inverted Ts in V4-V6. Blood sugar was 112. BP initially 120s/70s. RR 18-20 throughout the transport.

Patient stated she was having chest pain & felt as if she just couldn't catch her breath. This episode began around breakfast time, after taking her morning medications. One of her medications was changed from name brand to generic due to insurance changes and she had taken the generic for the first time this morning.

Her chest pain has been unchanged throughout the day, but her shortness of breath has gotten progressively worse. She now feels dizzy when she attempts to walk even a couple steps. When the episode began, she had dizziness, diaphorisis, and nausea but no vomitting. She denies a fever, HA, or having been around anyone who has been sick recently.

When we got to her, it was around 4 in the afternoon. She was no longer diaphoretic or nauseous. She still felt dizzy when she attempts to stand. She has no allergies, so she is given 162 mg ASA and nitro 0.4 mg SL x 3, q5 min. Her BP drops to roughly 90/60, so nitro is d/c'ed. I looked for an IV, but she had absolutely no veins to speak of, so I was unable to obtain one. Throughout the entire transport, her chest pain remained a 7-9/10. It was nonradiating and constant. There was no change in it with a deep breath, movement, or palpation.

To look at the patient, her color is normal, she is speaking in complete sentences with ease, and overall she "looks" good, despite saying she can't catch her breath. I put the pulse ox on her and get an SpO2 of 77%. I mess with it, putting it on different fingers, making sure I have a good connection with the monitor, and even putting it on my finger to see what reading I get. Everything checks out ok, so it appears the patient really is 77% on room air. She is put on a NC at 4 lpm and SpO2 comes up to 85. Better, but still not great. The patient states the O2 does seem to be helping though. We go ahead and move on up to a NRB at 12 lpm. SpO2 comes up to 94. The patient states her nausea is completely gone at this point and her dizziness is much better, almost completely gone. To physically look at her, she looks no different than when I first walked in the door of her house and saw her. Her BBS remained clear and equal throughout transport to the ER.

As we were pulling into the ER, the patient states that even though she took her water pill today, she has not been going to the bathroom as frequently as she typically does. She has no edema.

I feel as if I treated her well. As I continued to treat her, I really didn't believe she was having a cardiac episode. I am just not really sure what was going on with her. Was she possibly beginning to have CHF or renal failure and was still early enough into the episode that I wasn't seeing the "typical" signs/symptoms I would expect to see? What other possibilities are there as to what might have been going on? I am really hoping we end up back downtown so I can find out what the ER did for her and to get some answers.
 
PE maybe??? Not sure.
 
I'd want to say PE as well. Did she complain of any pain in any other part of her body that would lead you to such a conclusion?
 
Diabetic females in their 50s are going to be hard to diagnose without labs and a CXR as well as a couple more 12-lead ECGs.
 
Shame on you for giving nitroglycerine without IV access. I would have also given oxygen before any drugs. With those ischemic changes in the anterior and lateral leads I would like to see a 15 lead. It's unlikely that she is having an isolated posterior episode but it will only take about 20 seconds and a few more electrodes to find out. I would also like to know if this episode has any similarities to her last MI. You said her EKG was SR, but was there any blocks? If she had a LBBB her dizziness could be from a reduced ejection fraction which is dropping cardiac output. This could also by why she became hypotensive after NTG and also why she improves with O2.
 
fma08 & Linuss - I didn't think of possibly a PE. However, she didn't "look" like the PE patients I have seen in the past. Although she was complaining of not being able to catch her breath, she didn't look panicked or stressed, like the PE patients I have seen in the past. In fact, if she hadn't told you she was having problems breathing, you never would have suspected it. She just didn't physically look like she was having issues.

Vent - I understand where you are coming from and completely agree with what you are saying. I was just looking for some other ideas of more "common" possibilities of what could have been wrong with this patient. Just additional info I could keep in the back of my mind while assessing similar patients in the future.

emtbill - re: nitro w/o an IV, there have been countless discussions over this. I know the arguments on both sides. I also know the risks involved. That being said, I have to play within the rules set forth by my medical director. He has said on more occassions than I can count, in various trainings that as long as the patient's SBP is above 90 and they appear to be having a cardiac event, he wants nitro onboard every 3-5 (a he prefers every 3) min. While we are to get a 12 lead prior to nitro, he wants the IV to come after. He is always quick to point out and comment on runs where an IV was started first. It is not something that he wants done. His stance is that the nitro is doing the patient more good than the IV and he wants the chest pain decreased, and hopefully stopped ASAP.

As for the EKG of this patient, there were no blocks. At least none that I was able to detect. Furthermore, the chest pain did not improve with O2. It was only her complaint of not being able to catch her breath and the dizziness that improved with O2. Also, I apologize for my post being somewhat scattered. This patient was put on O2 prior to any medications being given to her. She did state that the pain she was having with this current episode was more intense than with her previous MI.
 
Interesting case, and definitely worth a follow up. I think I would have gone down the same pathway as you, treating as per cardiac cause. Her SpO2 is interesting given a lack of any abnormal breath sounds and would certainly make you suspicious of a PE. Did she have much in the way of risk factors for PE? She certainly has plenty for ACS and shows abnormal T waves in lateral leads/antero-lateral leads along with a good description for the most part of an ACS. Was the pain the same kind of pain as with her previous AMI (I realise it was more intense, but did she use the same descriptors?)

Labile heart rate is interesting. Sinus tach, the second most dangerous rhythm in ACS :)

Perhaps a sneaky little bit of pulmonary oedema creeping up on her during an ACS?

IV access would be nice obviously, but we've all had those patients where it isn't going to happen, for love nor money!

Anyway, it's quacking like a duck, waddling like a ducking, pooping like a duck. It's a duck I think, unless something else obvious pops up.
 
Normal but not normal

Cardiomyopathy? One of the most common resultants of infarct. Plus she has a history of hypertension also leading in that direction. Would explain exercise intolerance, bouts of dizziness, SOB, ischemic pain, no energy etc.

Still speculative of course. CXR would likely show a big fat floppy heart given her unfortunate history at age 50.

More info from ED would be interesting. Agree about supplementing O2 as a first step.

MM
 
Melbourne MICA said:
Cardiomyopathy? One of the most common resultants of infarct. Plus she has a history of hypertension also leading in that direction. Would explain exercise intolerance, bouts of dizziness, SOB, ischemic pain, no energy etc.
Click to expand...

Data is now being published and we have also found in our CardioPulmonary stress labs that women who are given a blanket dx of Chronic Fatique Syndrome actually have had some cardiac hx that went undiagnosed.

This woman would be the perfect candidate for more serious failure including that of some of the heart structures.

Epi, what about heart sounds?
 
We never made it back to the ER (at least, that ER) last shift. If we get down there tomorrow I will try to follow-up.

Vent, one of the shortcomings of my education is that we were never taught heart tones. I can listen, but I have no idea if what I am hearing is abnormal, or what it would be called. Because of that, I did not listen, or even think of listening to heart sounds.

Also, I will try to remember to print out a copy of the strip tomorrow so I can scan and post it for everyone to see as well.
 
The T wave inversion I'm betting is the old infarct.

I'd go with probable PE or cardiac episode secondary to the ischemic damage caused by the old MI.

... at best, it's like one of our Advanced Paramedics said; he looks at the patient, at the ECG, shrugs and just perfectly said "he's probably had some sort of cardiac event" :P
 
Epi-do said:
Vent, one of the shortcomings of my education is that we were never taught heart tones. I can listen, but I have no idea if what I am hearing is abnormal, or what it would be called. Because of that, I did not listen, or even think of listening to heart sounds.
Click to expand...

From Marieb's A&P 7e chapter 18

During each heartbeat, two sounds can be distinguished when the thorax is auscultated (listened to) with a stethoscope. These heart sounds, often described as lub-dup, are associated with closing of heart valves. (The timing of heart sounds in the cardiac cycle is shown in Figure 18.20a.)
The basic rhythm of the heart sounds is lub-dup, pause, lub-dup, pause, and so on, with the pause indicating the quiescent period. The first sound, which occurs as the AV valves close, signifies the point when ventricular pressure rises above atrial pressure (the beginning of ventricular systole, discussed in the next section). The first sound tends to be louder, longer, and more resonant than the second, which is a short, sharp sound heard as the SL valves snap shut at the beginning of ventricular relaxation (diastole). Because the mitral valve closes slightly before the tricuspid valve does, and the aortic SL valve generally snaps shut just before the pulmonary valve, it is possible to distinguish the individual valve sounds by auscultating four specific regions of the thorax (Figure 18.19). Notice that these four points, while not directly superficial to the valves (because the sounds take oblique paths to reach the chest wall), do handily define the four corners of the normal heart. Knowing normal heart size and location is essential for recognizing an enlarged (and often diseased) heart.

Abnormal heart sounds are called heart murmurs. Blood flows silently as long as the flow is smooth and uninterrupted. If it strikes obstructions, however, its flow becomes turbulent and generates heart murmurs that can be heard with a stethoscope. Heart murmurs are fairly common in young children (and some elderly people) with perfectly healthy hearts, probably because their heart walls are relatively thin and vibrate with rushing blood. Most often, however, murmurs indicate valve problems. If a valve is incompetent, a swishing sound is heard as the blood backflows or regurgitates through the partially open valve, after the valve has (supposedly) closed. A stenotic valve, in which the valvular opening is narrowed, restricts blood flow through the valve. In a stenotic aortic valve, for instance, a high-pitched sound or click can be detected when the valve should be wide open during systole, but is not.
Click to expand...
 
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I believe this link is actually written for the lay person but it has some useful info.
http://www.chfpatients.com/faq/s3s4.htm

It might be interesting to listen for these sounds on patients with known conditions. This would especially apply to those who work those "boring and uninteresting" IFTs. Every patient can be your lab.

This site has other interesting information also.
http://www.chfpatients.com/
 
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Heart Sounds

I'd be interested to hear arguments for it but listening for heart sounds by EMS personnel doesn't seem like a productive exercise to me. In the pre-hospital environment how often will you have the quiet needed to listen carefully as you must. You would also need a quality stethoscope and most importantly, you may well hear particular heart sounds, or think you did, but how many Paramedics let alone EMT-I's or B's would have the cardiology skills to interpret them correctly so as to align treatments with specificity.

Then there is the problem of adding new treatment regimes to guidleines aligned with heart sound ausculation findings, education issues and of course in-field quality and assurance maintenence and auditing.

If you're talking about treatments used on the basis of heart sounds we're getting into some pretty dangerous meds or alternately procedures and therapies impractical or impossible in the pre-hospital environment.

To me the idea sounds like a potentially dangerous distraction from more important endeavours especially when dealing with the time critical cardiac patient.

I'm certainly interested in alternative viewpoints however.

MM
 
Heart tones are a really useful skill but has limited use in the pre-hospital setting.
 
Interesting case, I do have a couple of thoughts:

We were taught that any CP was cardiac in nature until proven otherwise. You started down the
 
I listen for s1 and s2 over the four valves, and note any murmurs. I listen with the bell for gallops. I do this no so much to make a diagnosis or change a treatment, but to get a good ear for the future, as I plan on pursuing medical education.

Read about it in Bates or DeGowins and than go online and listen to samples.
 
We made it back to the ER tonight. I wasn't able to get alot of details because they were swamped, however, this lady was admitted and is still in the hospital. She was diagnosed with a PE.
 
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