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Case Study: Sepsis and Tachycardia (with EKGs)

58 posts in this topic

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Dispatched:

Intercept with BLS crew for shortness of breath. The patient is a 45 y/o male:

Hx: "Brain Cysts," HIV+, Unknown other (family not the best reporters)

Rx: Family remembers only Morphine and Ativan

All: NKDA

The patient presents unresponsive, GCS 4 (1 point for occasional moans). Family says (through the BLS crew, I intercepted enroute) that this mental status is baseline x 1 week. I have a hard time believing that, but thats the story. They called 911 "because it looked like he was having troube breathing."

VS:

RR: 48

HR: 190

BP: Unobtainable. Maybe a radial pulse, hard to tell.

SPO2: Wont read (?hypotension/perfusion issue)

ETCO2: 10, with good waveform

Lung sounds with diffuse rhonchi, no JVD/distal edema. Skin is warm/pink/dry at the core but mottled and somewhat cyanotic to the extremities. Pupils are sluggish to react, 3mm, with a disconjugurate gaze to the upper left (unknown baseline). Rapid trauma assess negative for DCAPBTLS. Blood Glucose is 146.

EKG:

adeno3lead.jpg

adeno12lead.jpg

SVT at 175-190 without ectopy, generalized ischemia.

My treatment:

I direct assisted vents with BVM+OPA+O2. Reassessment of the lungs finds good expansion on each vent from the BVM, ETCO2 trending upward as the tachypenia is slowed down.

IV with NS wide open

Trendelenburg position

I made a decision here to give Adenosine 6mg. I felt that the heart rate was too fast to be compensatory, and that reduced refilling time could be accounting for at least some of the hypotension. I realized that this patient was probably not having a primary cardiac problem, but I felt that the rate was something that needed to be addressed.

6mg didnt touch the guy-- no changes on the EKG or otherwise. We arrived at the ED before I had time to draw up 12mg.

**

In the hospital the patient was intubated with RSI, and promptly coded 4 times, recuscitated each time from the various (VF, VT, PEA, asystole) rhythms. When I turned in my paperwork the patient had a blood pressure in the 70s systolic, and they were mixing up an epi drip in the hopes that it would bump the pressure up. I havnt been able to follow up since, but it didnt look good.

Discussion:

The crossroads here was really the decision to go with adenosine. I was working with a primary clinical impression of septic shock, but believed that the heart rate was way too fast to be helping. I felt I did what I was able to.

I could also have spent my time attempting to intubate, but the patient was biting on the OPA and the BVM vents seemed to be working just fine. I didnt think it would be successful and at the moment, the airway was secure.

I suppose I could have also spent the time attempting a 2nd IV.

I would like to hear what you guys think.

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Posted · Report post

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.

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The assumption is that the rhythm was ectopic. I know that the LP12 printout says "sinus tach" on it, but that readout is often incorrect, and with an unknown rhythm onset I really had very little to distinguish between sinus tach and ectopic SVT. If for nothing else, the adenocard may have helped make that differentiation.

Attempting to break the rhythm was not my only treatment. As I mentioned above, I was running fluids as well, along with the airway stuff.

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I agree. I am not sure adenosine would have been the best choice with this patient. When looking at tachycardias, one must consider the cause and correct if possible. If you thought his unstable condition was in fact because of his heart rate, cardioversion would have been a therapy to consider. I understand your thinking regarding ventricular filling time as it relates to decreased cardiac output with extreme cases of tachycardia; however, I think this patients tachycardia was part of a bigger picture.

I applaud the fact that you are willing to put yourself on the stand in front of your peers and take both the praise and criticism. I do not see this as a recurring theme with EMS providers. Many people are too prideful and self absorbed to even think about attempting to learn from their actions, bad or good. In addition, you seem quite willing to own up to your decisions right or wrong. (Not that I am telling you that what you did was incorrect, this is simply how I viewed the situation given the information.)

Take care,

chbare.

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I think this patients tachycardia was part of a bigger picture.

I agree. ...Although at the same time I felt that the rate was possibly a problem in and of itself. Sure, it may be part of some other pathology, but that doesn't make the rate benign. Like I said before, I worried that it was contributing to the hypotension. I couldnt/wouldnt assume that it was the only cause.

I agree that cardioversion was indicated considering the patient's condition, but to be honest I sissied out on it a little bit-- mostly because I knew in the back of my mind that the tachycardia was probably not the primary problem. I decided to do a brief trial of medication first and see how that worked out. Meanwhile, I did the fluid boluses and maintained the airway.

As far as putting myself out there, thank you. I am new, I admit, and there is a lot I have yet to learn. The same is probably true of many members here. Hopefully we can all learn from these calls.

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In paramedic school we learned that basicly anything > than a rate of 150 was SVT if you could not see P-waves. I have since learned a formula that is 220 - age = sinus tachy. This means that this 45 y/o man could achieve a sinus tachy of roughly 185 under certian circumstances. With the ronchi and supressed immune system I would have given the fluid challenge a chance to take effect, after all sepsis requires several litters of fluid to correct if that was a possibility you had considered early on. I feel your pain for the lack of information on BLS report, we see this all to often as well with a few of the agencies we assist.

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I wouldn't let it bother you too much, its only one of several possible causes. Given the history of this onset and symptoms you found right away its just a possible cause, we have all been there after a call or several for that matter scratching our heads wondering what we should have done different. :D

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I understand your thinking. I would not have gone the route of adenosine with this patient; however, that is not to say you were in the wrong. Medicine is pretty complex in this way, you can arrive at a plan to treat people by taking many paths. No one path may be more or less beneficial than the others. I imagine you are starting to see this outside of school. Providers can differ in the way they look at their patients and their treatment modalities may differ as well. However, we agree on the major points: His airway and breathing was addressed and he was receiving a fluid challenge.

Take care,

chbare.

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I feel your pain for the lack of information on BLS report, we see this all to often as well with a few of the agencies we assist.

The BLS report wasn't the problem here. The family just didn't know anything. BLS can't invent information.

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You have a patient with a clearly discernible sinus tachycardia. Even if you do not use the machine's interpretation, which is a good move, your own eyes should tell you that there are P-waves preceding each QRS complex. There is no other interpretation that this could be. It is sinus, the rate is due to a compensatory mechanism.

Adenosine is not indicated for this situation. Pressors and enormous amounts of fluid replacement are needed. Not rate control.

I apologize for the harshness that is probably coming out of this post, but I've had to run through this same progression a number of times recently. :roll: It would seem that some providers are missing a couple of days of class.

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I would have given the patient a 500 ML bolus of NS first and then re-assessed the patient. If the lung sounds were clear after the first bolus then I would have given a second 500 ML bolus.

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You have a patient with a clearly discernible sinus tachycardia. Even if you do not use the machine's interpretation, which is a good move, your own eyes should tell you that there are P-waves preceding each QRS complex. There is no other interpretation that this could be. It is sinus, the rate is due to a compensatory mechanism.

Wait a minute. Correct me if I am wrong here (I may very well be), but just because there are p waves doesn't mean that the rhythm is coming from the sinus node. All it means is that the rhythm has a single atrial focus. I admit that the morphology of the p waves is pretty consistent, but that would also be true if the rhythm was from a single, irritable ectopic focus. It is simply not true that "there is no other interpretation that this could be." I'm not seeing anything there that tells me that the rhythm is NOT an ectopic atrial tachycardia. In fact, the rate might even suggest it. It could be sinus, too, but I felt that the rate was too fast and I took a shot.

Dont worry about the perceived harshness-- its all good. I expect that from you guys, especially if I screwed up! :wink:

I would have given the patient a 500 ML bolus of NS first and then re-assessed the patient. If the lung sounds were clear after the first bolus then I would have given a second 500 ML bolus.

That would be nice if I had a half hour with the patient. I had 10 minutes, and probably only 5-6 minutes of actual time to run fluids in once I got the line and everything else all set up. The IV was wide open. Theres your bolus.

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Your rationale is correct regarding the fact that p waves can originate from areas other than the SA node; however, is this really the case with the patient in the scenario above? Is this really the patient's primary problem? There is a significant amount of evidence that supports the hypothesis that the tachycardia is related to the patients underlying condition. You will have to convince us that using adenosine to rule out other problems was in fact the most appropriate course of therapy with this patient.

Take care,

chbare.

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There is a significant amount of evidence that supports the hypothesis that the tachycardia is related to the patients underlying condition. You will have to convince us that using adenosine to rule out other problems was in fact the most appropriate course of therapy with this patient.

Yeah, and there it is.

Like I've said a few times now, I never really thought that this patient had a primary cardiac problem. I used adenocard because I felt strongly that a rate of 180-190 was too fast to be compensatory or singly mediated by infection, and the patient was profoundly hypotensive. I had already done everything else that I could have to help with pressure (fluids wide open, trendelenburg), and I had maybe two minutes to do something else. The choices were (I think we agree): intubate, 2nd IV, or drugs. I went with drugs because I felt intubation would be difficult if not impossible (and the BVM was working nicely), and the patient was a very tough stick-- I didnt think I'd be able to get another line, leaning over the patient to his right arm in the moving, lights + sirens ambulance. Adenosine was diagnostic, yes, but could also have turned out to be an effective treatment. In the unlikely event that this rhythm was originating from an irritated ectopic focus, I might have been able to break the rate and help contribute to a more reasonable blood pressure. Given the amount of time I had, and the complications with my other options, I felt it was the best thing to do at the time.

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What does ectopic atrial tachycardia look like if this is what you think this rhythm could be?

It is irregular, and the p-waves have different morphology from beat to beat. Yes, we are making an assumption that this is sinus, but with the strip provided it is the best interpretation you will get.

Regular rhythm, identical p-waves in front of each QRS, normal PR interval for each of them. This is sinus. The likelihood of it originating regularly from an ectopic atrial focus is slim, at best.

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.

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What does ectopic atrial tachycardia look like if this is what you think this rhythm could be?

It is irregular, and the p-waves have different morphology from beat to beat. Yes, we are making an assumption that this is sinus, but with the strip provided it is the best interpretation you will get.

I think you're thinking of multifocal atrial tachycardia (MAT), not simply ectopic atrial tachycardia, which can be from a single focus and therefore maintain a regular rhythm and a single p-wave morphology. You are right, though, that this rhythm is probably fairly rare (although I am unsure of the real statistics), and my patient's rhythm was more likely sinus. You are probably also right that adenosine was not indicated.

Given all that, though, at the time I felt that it was worth a try. If the rhythm was truly compensatory, the adenosine would do nothing. If it was ectopic, there is a chance the drug could have helped. I am not putting the patient at risk, but simply attempting a treatment that may or may not work.

Will I do it next time? Probably not.

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fiznat,

The fact that you brought it to us for our discussion, and your willingness to learn, shows that The Force is strong with you.

Your patient is septic. 220-age=highest sinus tachycardia possible.

If it was an SVT, chances are your patient woulda been cool/pale/diaphoretic. Remember that in immunocompromised patients, a fever may not be necessarily present in infection.

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[quote="fiznat

If the rhythm was truly compensatory, the adenosine would do nothing. If it was ectopic, there is a chance the drug could have helped. I am not putting the patient at risk, but simply attempting a treatment that may or may not work.

Will I do it next time? Probably not.

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fiznat, You're my hero.

Two things about you stand out.

1) It takes major brass testes to march yourself out here naked time and time again. Often I think "man, he could have said that a little different, it would have still been the truth, but he would have looked better!" But you never do that! You just march out, warts and all...If this site can give people nothing else, just one simple tool, it's to see the educational value in that. You've inspired me in many ways, I hope I am brave enough to do the same when the time comes.

2) I can't remember (though I didn't run back your history here) a single thread that you've been involved in that wasn't completely focuse on improving yourself, and the rest of us, as a medics and professionals. Thread after thread shows you to be kind, focused, and to always have your eye on the ball. Amazing.

Plus (bonus point) I hope you notice that only the smartest people on the board reply to your posts...that speaks volumes to me...thanks for what you do.

I return you to your previously scheduled thread...

Dwayne

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You know, Dwayne is spot on. For some reason, medics tend to be very sensitive about having someone critique there medicine. Doctors do rounds, and residents get put on the spot time and time again, its the way you learn. There is no one "right"way to treat a patient, and there is plenty of room for debate. Anyone who has been doing this job for more than 10 minutes has made mistakes, and in hind sight may have done things differently. We have very little time in some instances to make very big decision, with very limited information and no access to labs, imageing, etc...Good for you for putting yourself out there, most wouldn't have the "balls" to do the same.

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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

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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.

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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.

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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?

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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....

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