I guess he read the textbook!

[AZCEP]

The presence of hypotension is a good indicator that some fluid replacement is needed. Even with a strict cardiogenic origin, patients tend to be volume depleted and will respond favorably to a challenge of fluid.

Atropine might be considered, but it's use in the presence of AF isn't really warranted. Perhaps application of pacer pads in preparation of what might be needed would be a better option.

[WelshMedic]

AZCEP,

Whilst your message is clear to me, I wonder how what constitutes " reacting favorably" in this scenario. Although this pt is clearly sick, I still stand by my conclusion that fluids are not the answer. A systolic pressure of 90 mmHg is fine in the majority of cardiac pts, as you are probably aware. I know that here the CCU uses beta-blockers to reduce pressure to a 90 mmHg level in the MI patient.

Or was it maybe that you are making a general statement and I'm only referring to the case at hand? A case of crossed wires, as it were....

WM

[emt322632]

With the new onset of a-fib I'm more inclined to lean toward a cardiac condition than a heat related one. What is his normal BP? (If he knew it that is?)

Any improvment in his condition after ASA, O2 and the fluid bolus?

[Mateo_1387]

Any Idea why his heart rate is 60? How healthy did the patient appear? Did he take any medicine at all?

Just thinking out loud, I figure that someone having new onset of a-fib usually does not know so until their heart rate becomes uncontrollable to the point it causes chest pain. Most people do not have problems with the a-fib, usually not more than palpitations or discomfort.

Questions that raise concern for me. Why a slow heart rate? Although his ventricles are doing the "work", what is possibly causing them to reduce contractility? For someone who has hypertension, and as far as I can tell no meds, why such a low blood pressure.

Some things I would consider, Right sided MI, Pulmonary Embolism, Stroke affecting the Vagus nerve causing the bradycardia.

I am not convinced this man has new onset a-fib, and I am not convinced it is his problem at the moment, but rather the cause of his problem at the moment.

Just a guess, but maybe a clot got away from his a-fib that is two weeks old, traveled to his brain, and is affecting the stimulation of the vagus nerve causing the man to have bradycardia, and subsequent reduced blood pressure. This would explain sudden onset, and the chest pressure 10/10 can be due to reduced coronary artery flow causing chest pressure.

Of course an MI may be causing the refractory period of the AV node to lengthen, thus causing the bradycardia, and subsequent signs and symptoms. (Totally a wierd moment, but wouldn't it be interesting if the man had a heart block without the presence of p waves?)

Did you have any follow up information? Did a neurological assessment reveal anything? Were there any other abnormalities with the 12 at the hospital, even though there was no presence of ST elevation?

As far as treatment, I agree with oxygen, IV fluids ( because of dehydration from working outside, and Hypotension) atropine 0.5 mg I think could be indicated due to brady cardia, hypotension, significant chest pain (which technically may indicate need for pacing), as well as Firedoc's treatment of pain.

[zzyzx]

Sorry if I gave the impression that I dumped a ton of fluid into him. I ran the two IV's wide open, but only gave him about 500 cc of fluid on the short ride to the ER; then TKO'd them.

Doesn't happen often, but this patient read the textbook.

[Chief1C]

A&O? Confusion? Too many HTN pills?; BGL? I start to have similar vitals when I work out on a hot day w/ out snacking periodically.

[letmesleep]

Ok, so how did his BP respond to the challenge?

At this point I too am on board with the ASA, O2, and some fluid..........

Atropine I would agree is out, and besides a CYA issue, I'm not ready to pull out the old pacer pads just yet......

I would also buy the new onset AF due to the fact that his Meds don't reflect a Hx of such........

[zzyzx]

His BP had come up a bit when we brought him into the ER, but I forgot what it was. We continued to run the IV's TKO.

I'm surprised that some posters say that starting two large-bore IV's was unjustified.

I don't know why we waited so long for a bed. The staff at this hospital is wonderful and I have great respect for them. I made sure they were fully aware of what was going on with this patient. I have never worked in an ER, so I can't say whether they were negligent. I was certainly disappointed that we had to wait so long after we made every effort to limit our on-scene time and went code 3.

[letmesleep]

Looking through this post again I'm guessing some possible heat related event/ dehydration. Was he working in the heat prior to the episode? how long (hours and/or days)? Clothing? The decreased HR wouldn't fit necessarily until you figure in maybe a Potassium deficiency (cramping noted on the OP), as well as the sudden onset rhythm change. I agree with the fluids as stated above, and without sounding judgemental, based on what I have read so far, I might not have "hit" him with 2 lines, but that is more of a pototo/ potato issue.

Just a guess!

[zzyzx]

I thought this call was interesting for a couple of reasons.

Our patients don't always read the same textbook that we do, but this one seems to have! It doesn't often happen that you get something that is such a textbook presentation. Crushing chest pain radiating to his left arm, skins signs, etc.. It's been a while since I've had a patient who was so obviously having an MI.

Not only was it a textbook presentation of an MI, but he also had the classic signs of an MI with right-ventricular involvement: hypotension with clear lungs sounds, borderline bradycardia, and a new onset of AF.

The other interesting thing about this call was that he did not have ST elevation an hourinto the event. I was expecting to see elevation in the inferior leads. It's possible that only the right ventricle was involved and not the inferior wall, but from what I understand that would be very unusual.

I know that often MI's won't show up with ST elevation, but I really expected to see it in this case.

A few days later I had a chance to talk to the nurse who had taken care of the patient. He said that his labs had come back with elevated cardiac enzymes, and he was taken to the cath lab where he was found to have "a big MI." Unfortunately the nurse did not know any other details, such as the location of the infarct.