Case Study: Sepsis and Tachycardia (with EKGs)

[medic001918]

Fiznat,

You and I spoke about this call the other night. I have to agree that adenocard probably wasn't the best case treatment for this patient. I think we've all agreed that the tachycardia was not a true cardiac tach, but compensatory for some other underlying pathophysiology. This is a patient with a poor history, and a poor ability to compensate due to their underlying conditions. The brain cysts raise a curious point too. We had talked about if they were ever biopsied, but you weren't sure. I still wonder if she had something going on with her cysts causing the dysfunction. Possibly increasing numbers, growing, etc.

In this case, since the tachycardia was compensatory the adenonsine wouldn't have been expected to work. As you know, adenosine is a "chemical cardioversion" allowing the heart to reset itself. If the patient is compensating, they will reset right back to the rate needed in order to compensate.

Someone made a valid point that sepsis takes liters of fluid to begin to take effect. Another IV would have been a good start. I'm not sure that with the short transport time that I would have initiated pressor therapy. But definatly fluid challenges. Another IV would have been helpful, although you did say the patient was a poor stick at best.

All in all, it's a learning experience. Like we talked about, I think that with time you'll actually find yourself less aggressive with pharmacological therapies...and more accepting that not every issue needs to be addressed prehospitally. Sometimes being aware of the issue is enough in itself.

You are already starting to grow termendously as a paramedic. And you have a better start as an entry level paramedic than most. Keep up the strong work. It will only get better as you continue to gain knowledge, and more importantly experience.

Feel free to talk to me any time about calls you have questions on. I'm happy to listen.

Shane

NREMT-P

[fiznat]

Dwayne and others, thank you. It is a bit embarrassing sometimes-- especially with cases like this, and the previous one with the other (?wide) tachycardia, where things tend to be much clearer in hindsight. I put this stuff up here because it is extremely valuable to me to hear what you guys have to say, and I hope at the same time that it will be equally valuable to other people as well. Thank you for the compliments (even in the face of my sometimes questionable medicine, haha)-- but I have no doubt that many of you guys would do the same thing. (Post threads, that is :wink:)

I did get a chance to follow up on the patient a little bit though today. The doc who had the patient wasn't in, but I got a chance to talk with the nurse. Apparently they did a head CT which was unremarkable, and tried to do some other kind of scan (unsure what he called it) to identify a possible PE but they were unable because the patient's renal function was so low. I guess he couldnt metabolize contrast dye or something? Not sure about that. Anyways, the guy's WBC count was just over 30k-- everyone seemed to be thinking sepsis, as I/we had originally suspected. The patient was sent up to the ICU, extubated, and put on CMO orders with a morphine drip only. The nurse didnt know for sure but he thought the patient had already died. I'll try and get a better, more specific followup next time I run into the doc.

[chbare]

Perhaps a Helical/Spiral CT to look for PE? Unfortunately, the problem with altered renal function is impaired ability to clear certain types of contrast media. What was the differential on the WBC? This can at least give you a general idea of the organism involved. (Bacteria, virus, parasite.)

Take care,

chbare.

[AnthonyM83]

Giving adenosine to a sinus tach is probably not what I would have done. What are you looking to achieve? If you think its an ectopic rythm, then sure, try and break it, but if your idea is to slow it down to improve filling time, adenosine is not the drug to do that. Adenosine has a half life of around 10 seconds (someone will correct me with the actual half life) so even if you slow this down, your only slowing it for about 10 seconds and then the sinus tach will resume. Sustained rate control is not the role of adenosine, and in this particular patient, volume resus seems to be the best course of action, imho.

Could we throw in a little education for the BLS providers?

I was under the impression, both from class and seeing it used in the field, that while adeonsine had a short half-life, its effects lasted more than the half-life. We just want to get the drug to heart quickly, then its effects EVEN THOUGH TRANSIENT last more than a few seconds.

I was also taught SVT was rate over 150 coming from above the ventricles (aka not a wide NR? Was I given an oversimplified definition?

[crazycanuck]

AnthonyM83:

Could we throw in a little education for the BLS providers? Smile

I was under the impression, both from class and seeing it used in the field, that while adeonsine had a short half-life, its effects lasted more than the half-life. We just want to get the drug to heart quickly, then its effects EVEN THOUGH TRANSIENT last more than a few seconds.

I was also taught SVT was rate over 150 coming from above the ventricles (aka not a wide NR? Was I given an oversimplified definition?

Here's a few references for adenosine:

http://www.drugs.com/pro/adenosine.html

anesthesia.slu.edu/pdf/keywords/ADENOSINE%20PHARMACOLOGY.pdf

(cut and paste, I dont know how to make it clicky)

Everyone is going to have a different definition for SVT, some will cite it as any atrial rhythm >100bpm if there is no reason for sinus tachycardia such as illness, stress, exercise, compensatory response. For most patients, it will not become hemodynamically unstable until it reaches a much higher rate so it really isn't so much the semantics of what you will define SVT as, but more so about when it becomes a rate that you want to treat as symptomatic.

As for the rapid push to get it in as quickly as possible, this is debatable too and I'll leave that for someone else...I'm not sure of the longterm effects of the drug, I believe the half life and mechanism of action are short. Half life less than 10sec, and action on the AV node is short too, the specific amount of time I do not have the answer....

[fiznat]

SVT = SupraVentricularTachycardia

Supra = above

Ventricular = the ventricles

Tachycardia = fast heart rate

Strictly speaking, a SVT is any tachycardia that originates from above the ventricles. This includes both atrial and junctional foci.

People have come to use the term "SVT" more specifically, though, generally referring to reentry tachycardias, ectopic atrial tachycardias, junctional tachycardias, etc. A-fib, A-flutter, sinus tachycardia, etc, although they are technically SVTs, are usually considered to be separate as the treatments are different.

Adenosine has a very short half life and a very short duration of action, but that doesn't mean that it's effects dont last longer. Adenosine is a kind of chemical cardioversion-- think of it as defibrillation in a syringe. The goal is break the rhythm into something else, "reset" the heart to a safer rhythm. The drug does it's thing and then goes away very quickly, with the hopes that the heart will do the rest of the work on it's own. That's why Adenosine only works with a few specific tachyarrhythmias: only some rhythms can actually be "broken" back into normal sinus.

[AZCEP]

SVT is a default rhythm interpretation when you are unable to isolate any of the other specific narrow-complex tachycardias.

If P-waves are present, the rhythm is not SVT. If flutter waves are discernible, again, no SVT. When the rate is so fast that an underlying focus is indiscernible, then it is reasonable to identify the tachycardia as SVT. Any other time, it is the sign of a lazy provider.

Adenosine has a half-life of up to 30 seconds, but it's duration of action can last 2-3 minutes depending on the patient's tolerance/sensitivity to it. Patient's on methylxanthines (caffeine, theophylline) have a reduced response to Adenosine. Tegretol (carbamazepine) potentiates the effects.

[Dustdevil]

Adenosine was not the indicated treatment for this patient. Second IV or not, using a rate control medication on a patient that is trying to compensate for widespread vasodilation is not recommended anywhere. Your second IV should have been in the biggest vein you could find, including an IO site. This patient needed fluids and pressors.

Yep.

But if it makes you feel any better, I've watched physicians make the same mistake. Recently, even.

[AZCEP]

Yep.

But if it makes you feel any better, I've watched physicians make the same mistake. Recently, even.

Shoot, we've probably all watched physicians do things that were worse than this. That's an entirely different discussion though. :roll:

[brentoli]

in the moving, lights + sirens ambulance

Just curious. What prompted the priority transport? From what I can gather, the patient was on that fine line of stability? Not completely stable, but not exactly circling the drain?

This is just a personal curiosity of mine. I know there are many factors to take into account with a priority response. If I have a suspected MI and we are loaded to meet the medic enroute, I won't run emergent to meet them. Some medics will hop on, and tell us to light er up. Others will run with traffic. I have read, and personally belive that a calmer response is probably better for the suspected cardiac that is conscious.

Anyways. Sorry to take this on an unintended tangent, just a curiosity.