Cardioversion of tachycardic septic patient

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engineeredout

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So I got into a discussion with a few of my attendings the other day about a patient and there were some differences of opinion.

85-year-old male brought in by EMS unresponsive in his home, intubated in the field. In the ED patient hypotensive and tachycardic to 150. Patient also febrile. Initial labs show a white count of 29 with significant bandemia. We get a line in him, start fluid resuscitation and antibiotics. Patients pressure still sucks. Heart rate gradually goes up to 180s, occasionally 190s, appears regular on 12 lead. Do a bedside echo, the heart itself looks a little globally hypo kinetic but overall seems to be ok.

I end up starting the patient on levophed, but then I pretty much switch over to phenylephrine because I didn't want to jack the heart rate up further. I ended up getting a decent blood pressure with him and he went up to the unit. From what I understand they still haven't found a particular source, just that there's gram-positive's in his blood. My question is, in talking with others after-the-fact I had one attending who said that due to this patient's age he could not possibly have mounted a sinus tachycardia with that rate and thus I should have cardioverted the patient on that basis. Another one said no the rhythm with sinus, no reason to cardiovert, the high heart rate was due to sepsis. What are your guys thoughts on this?

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For a patient who is 85 years old, a heart rate of 180-190 beats per minute is almost undoubtedly too fast. There isn't enough time to allow for appropriate filling, and his cardiac output is compromised by how fast his rate is. You indicated that it was regular on a 12-lead ECG (and presumably narrow). In the intubated patient with a rate that fast, in my mind it would definitely have been reasonable to attempt chemical cardioversion with adenosine. Extremely short-acting, can see if the patient corrects, and if you are wrong there is no downside (e.g., if you see the sinus pause and then the tachycardia restarts, either it was sinus or the impetus for the supraventricular tachycardia has restarted anyway). Remember that when the rate is that fast as well, it may be difficult to see if it is truly regular (I use calipers for this) because the beat-to-beat variation is less given how fast the rate is and in a septic patient, atrial fibrillation with rapid ventricular response is not uncommon. If you can remove the identifying information, it might be an interesting ECG to discuss -- at a rate of 190 making the definite determination of sinus rhythm is difficult.
 
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So these patients bedeviled me when I first came out. Playing the odds the actual rhythm was A.fib > SVT >>sinus tach. I'm not necessarily eager to give adenosine to an old, sick hypotensive patient but it would make your diagnosis. You can try cardioverting, if it's SVT it should break easily. In an n ~20 at my first shop, cardioverting hypotensive a.fib with concomitant sepsis does not result in restoration of sinus rhythm. Fluids, vasopressors, and antibiotics are the order of the day.
 
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Agree with posters above. Adenosine may help you identify the underlying rhythm, but the source is irritation from sepsis. I would not intervene if you had decent perfusion with your above managements. Adenosine or cardioverting have low likelihood of working long term in this patient, but may work if not perfusing.

http://emcrit.org/podcasts/crashing-a-fib/



Sent from my iPhone using Tapatalk
 
Agree with arcan. 180 is too fast, and fluids abx's and getting the BP are important. However, I give a rate control med like amio, bolus and drip to try and slow the rate down and cardiovert. My colleagues in the unit will sometimes place the patient on esmolol within the first 24 hours (not sure where I stand). Also neo is not a very potent vasopressors, if I have problems with tachycardia I use vasopressin early and levophed if needed. If the dose is > 5 I add hydrocortisone continuous infusion.

I have run into the problem after giving amio and cardioversion of now having relative sinus bradycardia on my hand (HR in the 50's in a guy whose map is 55 is not appropriate.) Which means i switch around vasopressors and try to find the sweet spot.

Also in patients with pacemakers who are 100% A-V paced at a rate of 70, and come in septic and hypotensive I do just the opposite; I call in the EP nurse and change his rate to 90, which should improve inotropy (Bowditch effect) and CO and maybe reduce need for vasopressors.
 
I had two patients that came into my ED yesterday with completely different history and presentations with tachycardia:

  • A mid to late 50s patient with a history of an immune-suppressed history with a similar scenario including tachycardia into the 160-180s, hypotensive 50/30s, hypoxic on room air, and mottled throughout. He appeared septic and was given 30ml/kg of normal saline with broad spectrum antibiotics, norepinehprine and then dopamine (both maxed out on the infuser), and intubated. There's no way I'm cardioverting these patients as the tachycardia is there secondary to another cause, namely sepsis.
  • A late 60s to 70s patient with multiple co-morbidities including COPD, diabetes mellitus, atrial fibrillation who presented with "weakness and shortness of breath" for one week, tachydysrhythmia on the EKG possibly concerning for SVT wth aberrancy vs SVT vs VT but it was difficult to tell what was the actual underlying rhythm, normotensive, and AOx3. I was debating to give adenosine when the BMP comes back with hypokalemia (potassium 2.0) and magnesium 1.2 which can precipitate a tachydysrhythmias including VT. Replete electrolytes and give fluids. Didn't give adenosine or attempt cardioversion.
 
Like others have responded, I'd favor afib and SVT over ST. The rate is too high for the age. I've seen otherwise healthy patients go into tachydysrhthmias from hypovolemic and septic shock. Appropriate fluids, targeted infection control via Abx, and vasopressors are your primary therapies. Levophed is first choice in this situation. I've only used Neo in spinal shock, where the heart and vasculature is working normally (neither is the case in sepsis).

Once that's done, in this patient I'd attempt electrical cardioversion/defibrillation (as appropriate), given the patient was hemodynamically unstable and already intubated. Ca++ and beta blockers will drop one's pressure. I've also done an amio drip in this situation, but it can sometimes drop someone's pressure and/or heart rate, and can take awhile to have an effect (amio also has Ca++ blocker effects). Dig is sometimes used in this situation, but there are downsides to using it as well.
 
Wow. Good thread. Need more like this'n on here instead of endless matchitis and "my job is teh SUX0Rz, Lolz" threads.
 
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So these patients bedeviled me when I first came out. Playing the odds the actual rhythm was A.fib > SVT >>sinus tach. I'm not necessarily eager to give adenosine to an old, sick hypotensive patient but it would make your diagnosis. You can try cardioverting, if it's SVT it should break easily. In an n ~20 at my first shop, cardioverting hypotensive a.fib with concomitant sepsis does not result in restoration of sinus rhythm. Fluids, vasopressors, and antibiotics are the order of the day.
This.
 
Traxus - with regards to the first patient, yes, the tachydysrhthmia is likely secondary to the patient's sepsis, but if they are still hypotensive after fluids and pressors, it is reasonable to attempt cardioversion. EDIT: this assumes you have an EKG showing afib or SVT.

In the second patient, I would not give adenosine. I practice as if SVT with aberrancy does not exist. I would use procainamide or amio in a patient with VT who was HDS.
 
Also - I'd rather increase the EKG paper speed than give adenosine to something I can't identify.
 
[QUOTE="Hair Police, post: 15843164, member: 303064"

Once that's done, in this patient I'd attempt electrical cardioversion/defibrillation (as appropriate), given the patient was hemodynamically unstable and already intubated. Ca++ and beta blockers will drop one's pressure. I've also done an amio drip in this situation, but it can sometimes drop someone's pressure and/or heart rate, and can take awhile to have an effect (amio also has Ca++ blocker effects). Dig is sometimes used in this situation, but there are downsides to using it as well.[/QUOTE]


Amio can drop someones blood pressure, or it can significantly improve it by returning atrial kick and allowing diastolic relaxation after removal of a malignant dysrhythmia into sinus rhythm. If you give it you just need to be able to deal with the consequences.

Dig is a good alternative, its peak effect will take a few hours, but many will see some result within 30 minutes. We usually bolus 0.5 mg and add 0.125 Q 4-6ish. I think the ICU uses this more as I rarely saw this done in the ed when I was training.
 
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So there have been a few studies showing benefit of esmolol drips in septic patients with tachycardia. Ive used it a few times in the septic tachycardic pt, it has negligible effect on BP, and bring the HR into a better range. This cannot be generalized to other beta blockers though.
http://www.ncbi.nlm.nih.gov/pubmed/24108526
http://pulmccm.org/2013/randomized-...s-reduced-septic-shock-mortality-60-rct-jama/


this was used after the patient was stabilized for 24 hours of resus, just FYI not necessarily applicable to the ed.

Also this study had ridiculously good results...like on the order of using penicillin for infections in the 1940's kind of results.
 
Amio can drop someones blood pressure, or it can significantly improve it by returning atrial kick and allowing diastolic relaxation after removal of a malignant dysrhythmia into sinus rhythm. If you give it you just need to be able to deal with the consequences...
I agree with everything you said. I would just give electricity a chance or two before I give a med. Especially since you can't take it away and amio has a half life of 9-36 days.

The beta blocker studies are redonkulous and they have not changed my practice. Strangely high mortality, small numbers, ICU and not ED patients, already after maximal therapy, and the results are too good without a sufficiently good explanation.
 
So there have been a few studies showing benefit of esmolol drips in septic patients with tachycardia. Ive used it a few times in the septic tachycardic pt, it has negligible effect on BP, and bring the HR into a better range. This cannot be generalized to other beta blockers though.
http://www.ncbi.nlm.nih.gov/pubmed/24108526
http://pulmccm.org/2013/randomized-...s-reduced-septic-shock-mortality-60-rct-jama/

The thought of this did cross my mind, but I don't have the cojones to try it out in the ED on a septic as **** patient.

Taking that septic-as-**** patient and electrically cardioverting them scares me too. I was just watching this guy get progressively more acidotic and I wonder if shocking him would have just sent him into some wide complex tachyarrhythmia that would have been difficult to recover from.

I love the discussion and everyone's input and it's great to see that there are many different points of view and different ways to handle this.

I'm still working on getting a copy of the initial EKG. I can't access the EKG image remotely so the next time I'm there I'll try to get a copy.

For an update on this patient: He never got cardioverted or even got anything for his rate. He grew out MSSA in his blood but nobody is sure of the source. His TTE didn't show any heart vegitations, I don't know if they're planning on performing a TEE. He apparently does get antivascular injections in his eyes for macular degeneration so maybe that is the source?

Most importantly: He got extubated yesterday. Off all pressors. Someone who I couldn't leave his bedside for almost two hours because I was sure was going to code is off the vent. Sure, actually leaving the hospital is still another goal that needs to be reached, but still pretty cool to know that we must have done something right.
 
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Sure, actually leaving the hospital is still another goal that needs to be reached, but still pretty cool to know that we must have done something right.

No matter what you do, some people are going to die, and, no matter what you do...some people are going to live.

Do everything right...box.

Do everything wrong...save.

Go figure!

But, congrats! That's why we're here.
 
I'd be very certain as to what I have in front of me before juicing a septic pt with tachyarrythmia. Don't forget the myocardial stunning effect after electrical cardioversion (and chemical... but to a lesser degree). They are going to need all the LVEF they can muster for their sepsis.

Interesting discussion, though. I personally think it would be an extremely rare occurrence that I could convince myself to electrically cardiovert sepsis.
 
Traxus - with regards to the first patient, yes, the tachydysrhthmia is likely secondary to the patient's sepsis, but if they are still hypotensive after fluids and pressors, it is reasonable to attempt cardioversion. EDIT: this assumes you have an EKG showing afib or SVT.

In the second patient, I would not give adenosine. I practice as if SVT with aberrancy does not exist. I would use procainamide or amio in a patient with VT who was HDS.

Even if the EKG shows "sinus tach" you can be sure that it is not sinus tach and is more likely an a-tach. This guy should get shocked or at least chemically cardioverted if he's going 190 and hypotensive
 
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Even if the EKG shows "sinus tach" you can be sure that it is not sinus tach and is more likely an a-tach. This guy should get shocked or at least chemically cardioverted if he's going 190 and hypotensive
What post are you responding to? My comment, the one you quoted, was in response to Traxus' post, where he described a septic pt in his 50s. With the case as presented and without an EKG, it's likely ST and the pt gets a fluid challenge. If there's something obvious on the EKG, ACLS says that get treated first with electricity in the unstable patient.

In the OP's post, 150 is right out for a 80-90 yo, let alone 180-190, I agree there has to be some dysrhythmia. In fact, I was the fifth guy in a row who thought there was an atrial tachycardia and that an attempt at cardio version should be made.
 
What post are you responding to? My comment, the one you quoted, was in response to Traxus' post, where he described a septic pt in his 50s. With the case as presented and without an EKG, it's likely ST and the pt gets a fluid challenge. If there's something obvious on the EKG, ACLS says that get treated first with electricity in the unstable patient.

In the OP's post, 150 is right out for a 80-90 yo, let alone 180-190, I agree there has to be some dysrhythmia. In fact, I was the fifth guy in a row who thought there was an atrial tachycardia and that an attempt at cardio version should be made.
Please, Hair Police. Stop.

You can't win this argument. You're arguing with someone who is a fellow, and is therefore still learning to be an expert in "something" and as a result, therefore clearly knows everything about this one thing. I went through his/her post history by the way, and he's already used the words "stupid," "*****," "ridiculous" and other choice words multiple times in only the past 10 days of posting. So don't even try. You'll likely end up in one of those buckets, very soon.

But on a slightly less sarcastic note, personally, I feel you can't definitively tell someone else how to manage a patient let alone be certain enough to criticize, based on little snippets read on the Internet and certainly not without seeing the patient, seeing the chart, or the ekg. Only malpractice plaintiffs attorneys have that God-given right.

But I don't know, because after all, I'm not a fellow. (That's been years ago, now.) And I'm not a resident or board certified for the first time. (That was over a decade ago.)

So what I can't do, is to know EVERYTHING. I had that ability once, but I lost it, quite some time ago. And I'm glad I did.
 
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wait so we're cardioverting unstable tachydysarrhythmias now?

they just told me in residency that if the HR ever shows up red in the VS I should just call the cardiology fellow.
 
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Please, Hair Police. Stop.

You can't win this argument. You're arguing with someone who is a fellow, and is therefore still learning to be an expert in "something" and as a result, therefore clearly knows everything about this one thing. I went through his/her post history by the way, and he's already used the words "stupid," "*****," "ridiculous" and other choice words multiple times in only the past 10 days of posting. So don't even try. You'll likely end up in one of those buckets, very soon.

But on a slightly less sarcastic note, personally, I feel you can't definitively tell someone else how to manage a patient let alone be certain enough to criticize, based on little snippets read on the Internet and certainly not without seeing the patient, seeing the chart, or the ekg. Only malpractice plaintiffs attorneys have that God-given right.

But I don't know, because after all, I'm not a fellow. (That's been years ago, now.) And I'm not a resident or board certified for the first time. (That was over a decade ago.)

So what I can't do, is to know EVERYTHING. I had that ability once, but I lost it, quite some time ago. And I'm glad I did.
But but but, someone is wrong on the internets!

Ya. I responded before I read the Stress Test thread. A little spectrum bias, anyone?
 
wait so we're cardioverting unstable tachydysarrhythmias now?

they just told me in residency that if the HR ever shows up red in the VS I should just call the cardiology fellow.
I think it's an Obamacare mandate now, too. For all ekg's. Even normals. Cards fellow must be called and given a "heads-up."
 
What post are you responding to? My comment, the one you quoted, was in response to Traxus' post, where he described a septic pt in his 50s. With the case as presented and without an EKG, it's likely ST and the pt gets a fluid challenge. If there's something obvious on the EKG, ACLS says that get treated first with electricity in the unstable patient.

In the OP's post, 150 is right out for a 80-90 yo, let alone 180-190, I agree there has to be some dysrhythmia. In fact, I was the fifth guy in a row who thought there was an atrial tachycardia and that an attempt at cardio version should be made.

Not responding to you, just responding in general. I just happened to quote you.
 
For a patient who is 85 years old, a heart rate of 180-190 beats per minute is almost undoubtedly too fast. There isn't enough time to allow for appropriate filling, and his cardiac output is compromised by how fast his rate is. You indicated that it was regular on a 12-lead ECG (and presumably narrow). In the intubated patient with a rate that fast, in my mind it would definitely have been reasonable to attempt chemical cardioversion with adenosine. Extremely short-acting, can see if the patient corrects, and if you are wrong there is no downside (e.g., if you see the sinus pause and then the tachycardia restarts, either it was sinus or the impetus for the supraventricular tachycardia has restarted anyway). Remember that when the rate is that fast as well, it may be difficult to see if it is truly regular (I use calipers for this) because the beat-to-beat variation is less given how fast the rate is and in a septic patient, atrial fibrillation with rapid ventricular response is not uncommon. If you can remove the identifying information, it might be an interesting ECG to discuss -- at a rate of 190 making the definite determination of sinus rhythm is difficult.

I'd argue it is simple in this age group.

Max heart rate = 220 - age, therefore, the max sinus conduction should be about 135.

Ok yes with all the changes of sepsis maybe the nodal system can conduct 'a little' faster. Let's say 140 or maybe even 160.

Still nowhere near 190. That's the max heart rate of a 30 year old! As long as it isn't wide and irregular I agree and think a trial of adenosine makes sense. If the patient is super hypotension then you have to cardiovert him.

Regardless, even after doing that you still need to fix the underlying problem (the sepsis) that caused the tachyarrhythmia in the first place.
 
I'd argue it is simple in this age group.

Max heart rate = 220 - age, therefore, the max sinus conduction should be about 135.
That's a crude estimate and not reliable. Max HR is highly variable patient to patient. It's kind of like the old adage of picking an ET tube by looking at the patient's little finger or body mass index being an accurate measure of health, or assuming your patient's weight by their height.
 
Just remember in the setting of a.fib and septic shock that if you do decide to cardiovert that you need to be prepared for the strong possibility that you're going to shock them and they're going to jump right back into a.fib. Especially if it's chronic a.fib. The only study I've been able to find on this was from 2010 and excluded chronic a.fib and was in an ICU setting. They restored sinus in the majority of patients but everyone that got shocked also got meds (usually amiodarone) and they didn't give a time frame for when they converted.
 
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That's a crude estimate and not reliable. Max HR is highly variable patient to patient. It's kind of like the old adage of picking an ET tube by looking at the patient's little finger or body mass index being an accurate measure of health, or assuming your patient's weight by their height.

I agree but we aren't debating 135 vs 136 vs 145.

The patients heart rate is nearly 55 beats above the predicted amount. If it was 200 or 220 or 240 would you still question if it could be sinus?

I would approach the above scenario as a non-sinus tachydysrhythmia till proven otherwise.
 
I agree but we aren't debating 135 vs 136 vs 145.

The patients heart rate is nearly 55 beats above the predicted amount. If it was 200 or 220 or 240 would you still question if it could be sinus?

I would approach the above scenario as a non-sinus tachydysrhythmia till proven otherwise.

Agree.

Age is very strongly related to max HR (very impressive R value of 0.9). When you're 80, your sinus node just isn't going to be able to go that fast.

So whether you use the normal 220-age or some of the other equations, they're pretty reliable. As Link2swim said, it's not going to estimate exactly but usually pretty good.
 
I'd bolus 2 L then consider dig. I like that in the hypotensive fib'ers - takes a little longer, but I've had good success the few times I've used it. Defintely wouldn't give adenosine - I don't see it fixing the problem, and could lead to cardiovascular collapse. Electricity could be OK when they are intubated/sedated, but I think IVF and patience are the ticket.
 
Max heart rate = 220 - age

This is just a made up formula with little scientific merit:


"The common formula was devised in 1970 by Dr. William Haskell...
On an airplane traveling to the meeting, Dr. Haskell pulled out his data and showed them to Dr. Fox. ''We drew a line through the points and I said, 'Gee, if you extrapolate that out it looks like at age 20, the heart rate maximum is 200 and at age 40 it's 180 and at age 60 it's 160,'' Dr. Haskell said."

http://www.nytimes.com/2001/04/24/health/maximum-heart-rate-theory-is-challenged.html?pagewanted=2


This study states the 220-age formula is way off and the real one may be closer to 211-0.64 x age, with >10 beat error +/- on top of that:

"HRmax was univariately explained by the formula 211 − 0.64·age (SEE, 10.8), and we found no evidence of interaction with gender, physical activity, VO2max level, or BMI groups. There were only minor age-adjusted differences in HRmax between these groups. Previously suggested prediction equations underestimated measured HRmax in subjects older than 30 years. HRmax predicted by age alone may be practically convenient for various groups, although a standard error of 10.8 beats/min must be taken into account. "

http://onlinelibrary.wiley.com/doi/10.1111/j.1600-0838.2012.01445.x/abstract


Or is the real formula something entirely different?

"The age-predicted HRmax equation (i.e., 220 - age) is commonly used ... Despite its importance and widespread use, the validity of the HRmax equation has never been established... The real formula may be closer to HRmax is 208 - 0.7 x age in healthy adults."

http://www.ncbi.nlm.nih.gov/m/pubmed/11153730/


"Consequently, the formula HRmax=220-age has no scientific merit for use in exercise physiology and related fields." -Journal of Exercise Physiology

http://www.cyclingfusion.com/pdf/220-Age-Origins-Problems.pdf
 
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Excellent thread about a challenging situation. Made me think of the article referenced by the journal watch summary copied below.
For what it's worth, personally I would be leery of adenosine or amiodarone (or electricity) further decreasing cardiac output, but thought dig sounded reasonable.

What Should We Do About A-Fib/Flutter when There Is Another Acute
Condition?
Daniel J. Pallin, MD, MPH
[Emergency Medicine | Summary and Comment | Subscription Required]
Reviewing Scheuermeyer FX et al., Ann Emerg Med 2014 Nov 6;
A retrospective study suggests that rate or rhythm control may bring
unintended consequences.
http://www.jwatch.org/content/2015/NA36664?query=etoc_jwem


Rapid atrial fibrillation or flutter (A-fib/flutter) can be managed by rate
or rhythm control, but prior studies have focused on A-fib/flutter
occurring in isolation. Now, investigators have retrospectively compared
the incidence of adverse events in patients with A-fib/flutter and aYe
serious underlying acute condition who either did or did not undergo rate
or rhythm control.

During the 1-year study period, 416 patients at two Canadian emergency
departments had A-fib/flutter and other complex acute medical issues. Among
135 patients with attempted rate or rhythm control, 41% had adverse events
such as hypotension or intubation. Among 281 patients with no attempted
rate or rhythm control, 7% had adverse events. The two groups were similar
at baseline in terms of type of acute illness and comorbidities.

Comment
We already know that sinus tachycardia should never be suppressed, but
rather its underlying etiology should be treated. In the case of
A-fib/flutter, it is difficult to disentangle cardiogenic tachycardia
(which we'd like to suppress) from tachycardia due to physiological needs
(which we'd like to allow). This retrospective study does not provide any
specific recommendation for practice change, but rather reminds us of the
importance of recognizing and addressing intravascular volume and other
noncardiac determinants of a rapid ventricular response in A-fib/flutter.
When we believe the tachycardia is an appropriate response of the heart to
a noncardiac problem, we should be reluctant to suppress it.
 
Excellent thread about a challenging situation. Made me think of the article referenced by the journal watch summary copied below.
For what it's worth, personally I would be leery of adenosine or amiodarone (or electricity) further decreasing cardiac output, but thought dig sounded reasonable.

What Should We Do About A-Fib/Flutter when There Is Another Acute
Condition?
Daniel J. Pallin, MD, MPH
[Emergency Medicine | Summary and Comment | Subscription Required]
Reviewing Scheuermeyer FX et al., Ann Emerg Med 2014 Nov 6;
A retrospective study suggests that rate or rhythm control may bring
unintended consequences.
http://www.jwatch.org/content/2015/NA36664?query=etoc_jwem


Rapid atrial fibrillation or flutter (A-fib/flutter) can be managed by rate
or rhythm control, but prior studies have focused on A-fib/flutter
occurring in isolation. Now, investigators have retrospectively compared
the incidence of adverse events in patients with A-fib/flutter and aYe
serious underlying acute condition who either did or did not undergo rate
or rhythm control.

During the 1-year study period, 416 patients at two Canadian emergency
departments had A-fib/flutter and other complex acute medical issues. Among
135 patients with attempted rate or rhythm control, 41% had adverse events
such as hypotension or intubation. Among 281 patients with no attempted
rate or rhythm control, 7% had adverse events. The two groups were similar
at baseline in terms of type of acute illness and comorbidities.

Comment
We already know that sinus tachycardia should never be suppressed, but
rather its underlying etiology should be treated. In the case of
A-fib/flutter, it is difficult to disentangle cardiogenic tachycardia
(which we'd like to suppress) from tachycardia due to physiological needs
(which we'd like to allow). This retrospective study does not provide any
specific recommendation for practice change, but rather reminds us of the
importance of recognizing and addressing intravascular volume and other
noncardiac determinants of a rapid ventricular response in A-fib/flutter.
When we believe the tachycardia is an appropriate response of the heart to
a noncardiac problem, we should be reluctant to suppress it.
I like the message but there's all sorts of problems in looking at this retrospectively. Similar types of illness is not the same as same disease severity and without controlling for severity you have no way of knowing if you caused the adverse events or they were a function of a sicker population. But again, it feels right based on my clinical experience.
 
I like the message but there's all sorts of problems in looking at this retrospectively. Similar types of illness is not the same as same disease severity and without controlling for severity you have no way of knowing if you caused the adverse events or they were a function of a sicker population. But again, it feels right based on my clinical experience.

Yeah, as noted in the reviewer's comments you can't really draw any conclusions on which to base practice. Confounding by indication etc. But I think it's interesting to know how our patients do, even if we don't have a ton of evidence supporting practice decisions. Gotta start somewhere.
 
Yeah, as noted in the reviewer's comments you can't really draw any conclusions on which to base practice. Confounding by indication etc. But I think it's interesting to know how our patients do, even if we don't have a ton of evidence supporting practice decisions. Gotta start somewhere.
Agreed. With 7 million patients in the US with A. fib (why do you think we see all those Eliquis commercials?), sepsis in the setting of a.fib seems like it would be a niche that would support an academic career. Maybe in Canada since there wouldn't be any drug company support.
 
I'd bolus 2 L then consider dig. I like that in the hypotensive fib'ers - takes a little longer, but I've had good success the few times I've used it. Defintely wouldn't give adenosine - I don't see it fixing the problem, and could lead to cardiovascular collapse. Electricity could be OK when they are intubated/sedated, but I think IVF and patience are the ticket.

This. (except the electricity part)

I don't see the benefit of adenosine...and I certainly see complete cardiovascular collapse as a huge risk. The described patient sounds so tenous to me that even 5-10 seconds without cardiac output (no ventricular contraction) -- nevermind the possibility of "stunning" -- is likely to lead to full arrest. ...this isn't even considering the effect on diastolic flow to the coronaries. There would be no ROSC if full arrest.

As someone else said, if you want to know if this is a regular or irregular underlying rhythm, increased the "speed of the paper" on your EKG and measure.

Fluids, pressors, determine the rhthym, bedside limited ECHO, consider dig vs. amio prn...then after re-assesment consider electricity very cafefully (if Afib, it is unlikely to covert and maintain sinus in such a diseased state...and a state that likely kicked in the Afib or RVR in the first place).

That's what I would do, but I am just a friendly fellow (who doesn't know everything)...

HH
 
Let me fix that for you, "Please do. I'll tell you what to do unhappily."

Now let me augment it for you.

"Please do. I'll tell you what to do unhappily, and I'll do so without actually seeing the patient."
 
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