Please Tell Me What You Would've Done?

[TXmed]

The fact that his temp was that low and he had hypotension not responsive to fluid therapy shows that he Was very septic. If you carried levophed it would be good to start it at low dose but fluids and early anti-biotics are the key in terms of the emergency setting. As for the ECG I'm sure the PH and potassium was messing with it so I try not to get tunnel visioned on that. Great assessment with the etco2 by the way

 

[Doczilla]

I didn't mean to bring this thread to a screeching halt. It was hopping in the wee hours of the morning but suddenly died. I like seeing other people's opinions on these interesting calls. Please don't let my hypothetical diatribe be the last post on this very interesting thread. I keep hitting refresh, and it's making me sad.

That's an interesting theory. Too bad people don't listen to heart sounds in EMS. (Might be because it wouldn't change our treatment save for maybe becks triad) Let's play the rheumatic heart fever game. If it was caused by group A strep, there would most likely be severe consequences to the kidneys as well (post-streptococcal glomerulonephritis), and possibly would have reflected in the history.

I believe that hypotension (especially below the limits of autoregulation) will cause ECG changes regardless of structural heart disease.

It also seems that if the stenosis was severe enough chop away most of the stroke volume, he would likely have coded from the deleterious effects of the compensatory tachycardia; whether it be from distributive causes or volume depletion. Or, at the very least, an arrhythmia would have gotten him before the sepsis evolved to full on septic shock.

If we're going down the sepsis route (with no left shift, that still bothers me), I would vote for ARDS before pulmonary edema.

Great thought provoking post though.

 

[Rykielz]

Nova1300- I've been finishing up some last minute Christmas shopping so I'm just now checking the thread. That sounds like an interesting theory but it's probably one of the last things i'd have been thinking about on the call just because the assessment findings were pointing so strongly towards sepsis. The pt had been pretty healthy throughout his life up to this point and did not have an accent, which to me says he's at least been living in this country for a decade or more. The lung sounds were also clear in the bases bilaterally and with adequate tidal volume. The rhonchi in the upper lobes sounded coarse (probably due to dehydration) but was definitely rhonchi and not rales. Nevertheless, it's definitely a differential diagnosis to consider. I'll keep you posted as soon as I hear something new.

 

[Carlos Danger]

So, Im going to go out on a limb and be the contrarian on this case. I don't think this was sepsis. I think this was volume depletion from gastroenteritis, but I dont think this gentleman had this syndrome for 3 days and suddenly became septic. He is afebrile, he is mentating, he is not tachycardic and he is not really hypothermic. I think if he was septic with that blood pressure, you would have been dealing with a much sicker patient than you present.

Instead, I would suggest there were possibly two processes going on here. This sounds like run-of-the-mill gastroenteritis to me. But I wonder if this guy had undiagnosed aortic stenosis. First, you say he was of Indian descent. If he had been in the states his whole life, it makes my diagnosis a little less likely. However, outside of first-world countries, rheumatic fever remains prevalent and is the number one cause of aortic valve disease.

Because of the stenotic valve, these patients have fixed cardiac output. They are exquisitely sensitive to volume depletion and when depleted experience hypotension and subsequently syncope. They can increase their peripheral resistance to a point, but without the ability to increase cardiac output, there is a ceiling to their ability to compensate and once that is reached, hypotension ensues.

You mention he had a non-productive cough and you heard noisy breath sounds. I would suggest that what you found was actually the effect of mild pulmonary edema. A heart rate in the high 80's may actually be a relative tachycardia for this man. Because the valve is stenotic, the heart is not able to empty with each systole since the HR has increased (decreased ejection time through a tight valve = incomplete ejection). This causes backup of blood into the pulmonary circulation and leads to the pulmonary edema. And because the heart doesnt have time to empty with each ejection, the cardiac output is actually decreased despite the increase in heart rate. This, combined with the hypotension probably decreased his coronary perfusion pressure and may be the cause of your EKG changes. These patients are exquisitely sensitive to decreases in their coronary perfusion pressures.

Most patients with aortic stenosis have what is called pulsus parvus et tardus. This means that the carotid pulsation is both weaker and slower than it would be in most patients. However, in the face of a blood pressure like this, it may be the only pulse you can palpate because the carotids come off the aortic arch. By the time the slow and weak pulse wave reaches the periphery, it is probably dampened enough to be non-palpable.

If this was the case, you saved this man's life. Fluids are most certainly the answer, despite the possible pulmonary edema. By restoring the patient's volume, you will increase the systemic blood pressure and thus perfuse the coronaries. This will likely slow the heart rate and allow the heart more time to eject blood through that stenotic valve, and likely resolve the pulmonary edema by relieving the backup into the pulmonary circulation.. Vasoconstrictors such as phenylephrine or vasopressin would also be options, though it may seem counterintuitive to raise the afterload on a stenotic valve. But, volume and coronary perfusion pressure are the key factors in treating patients with aortic stenosis. The worst thing you can do to these folks is put them on positive chronotropic drugs. Dopamine may very well have made this patient much worse.

All supposition, but food for thought.

Really interesting. Would not have been on my list of differentials, but makes sense.

 

[EpiEMS]

Shame we don't have a case of the month competition, 'cause this seems like the one!
Really insightful posts, guys!

 

[teedubbyaw]

What was so strange about this call?

 

[medicsb]

That's an interesting theory. Too bad people don't listen to heart sounds in EMS. (Might be because it wouldn't change our treatment save for maybe becks triad) Let's play the rheumatic heart fever game. If it was caused by group A strep, there would most likely be severe consequences to the kidneys as well (post-streptococcal glomerulonephritis), and possibly would have reflected in the history.

Heart sounds aren't that useful. I listen to them on nearly every patient I see, but I can't think of a time where it changed my management. There are MANY times where I listen and do not hear anything abnormal and then read an echo report that shows stenosis or regurg of different valves. I've had patients with known aortic stenosis and in many could not hear a murmer (probably in part to ambient noise - EDs are not quiet places). Also PSGN is not inevitable with GAS (its actually pretty rare).

I believe that hypotension (especially below the limits of autoregulation) will cause ECG changes regardless of structural heart disease.

It also seems that if the stenosis was severe enough chop away most of the stroke volume, he would likely have coded from the deleterious effects of the compensatory tachycardia; whether it be from distributive causes or volume depletion. Or, at the very least, an arrhythmia would have gotten him before the sepsis evolved to full on septic shock.

If we're going down the sepsis route (with no left shift, that still bothers me), I would vote for ARDS before pulmonary edema.

A left shift is not always present. I see multiple sepsis patients a week, and many (most?) do not have a significant bandemia.

 

[k9Dog]

Just fluid resuscitation.. And obtain a more accurate auscultation blood pressure.

 

[Doczilla]

Heart sounds aren't that useful. I listen to them on nearly every patient I see, but I can't think of a time where it changed my management. There are MANY times where I listen and do not hear anything abnormal and then read an echo report that shows stenosis or regurg of different valves. I've had patients with known aortic stenosis and in many could not hear a murmer (probably in part to ambient noise - EDs are not quiet places). Also PSGN is not inevitable with GAS (its actually pretty rare).



A left shift is not always present. I see multiple sepsis patients a week, and many (most?) do not have a significant bandemia.

Thanks for the response! That's very useful.

 

[jwk]

Just fluid resuscitation.. And obtain a more accurate auscultation blood pressure.

THIS!! Thank you!

Nobody will be alert and oriented and talking to you with a BP of 40/23. Any time you get a reading like that, use those things you have hanging around your neck and take a real blood pressure.

 

[johnrsemt]

I have had patient alert and talking at 52/20 (manual cuffs, stethoscopes, 3 different people). At a blood center, ready to donate, but they wouldn't let person donate due to too low blood pressure.

I was the person, I walked in, checked out, walked out

Fairly awake, talking, alert

 

[chaz90]

I have had patient alert and talking at 52/20 (manual cuffs, stethoscopes, 3 different people). At a blood center, ready to donate, but they wouldn't let person donate due to too low blood pressure.

I was the person, I walked in, checked out, walked out

Fairly awake, talking, alert

I would still wager something was wrong in their technique, equipment, or bias since they were told you were hypotensive.

52/20 in an adult is going to be pathological and symptomatic.