NIGHT FLOAT CASE #12

[VA Hopeful Dr]

You will always have free air in a fresh post op, whether laparotomy or laparoscopy.

Shall I give the answer? Don't want to spoil it for the students...

Heh, fair enough. I guess that's why the right answer is "make the surgeon come examine the patient"

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[anbuitachi]

Is this not a leak until proven otherwise? The a-flutter is secondary to what's going on internally?

Bariatric surgery - Meaning Roux en Y? Sleeve Gastrectomy? Look at the OP note. Risk of leak is not zero.

Also, I'm calling the surgery staff (resident, attending, whoever) to let them know about their patient.

Whats happening could be due to a leak, but i'd say you'd have to lower that HR first

 

[sozme]

Update #3

Everyone wants a chest X-ray... here it is: NORMAL

Also check update #1 NIGHT FLOAT CASE #12

Minimal surgical blood loss (though you couldve figured that out from several days of stable hemoglobin, with the most recent one checked within the last hour).
Isolated chest pain with high blood pressure shouldnt make you think of hemorrhage.
He's been anticoagulated now for over a day. Does this lower his risk of PE?


Still has chest pain. Tachy at 150. I already gave you the rhythm = atrial flutter. What's the treatment? What are you going to do besides order more tests?

 

[Xurros]

Patient is hemodynamically stable based on vitals. Would go for rate control at this point-- either IV dilt or metoprolol. He's hypertensive so we don't have to worry too much about lowering his BP. If these work, we can give a drip to control the rate.

If these don't work, we can go to either rhythm control (like amiodarone drip) or cardiovert (with a TEE to see if he has any thrombi-- given his history of obesity he is at risk for paroxysmal afib/aflutter).

Would rule out any potential inciting causes (like leak, PE, MI, etc). He's gotten DVT prophylaxis but that doesn't mean his chance of having a DVT/PE is zero-- I think a CT PE is warranted due to his weight and being post-op with new onset aflutter.

But these are just my thoughts so feel free to correct me if I'm wrong.

 

[Redpancreas]

Patient is hemodynamically stable based on vitals. Would go for rate control at this point-- either IV dilt or metoprolol. He's hypertensive so we don't have to worry too much about lowering his BP. If these work, we can give a drip to control the rate.

If these don't work, we can go to either rhythm control (like amiodarone drip) or cardiovert (with a TEE to see if he has any thrombi-- given his history of obesity he is at risk for paroxysmal afib/aflutter).

Would rule out any potential inciting causes (like leak, PE, MI, etc). He's gotten DVT prophylaxis but that doesn't mean his chance of having a DVT/PE is zero-- I think a CT PE is warranted due to his weight and being post-op with new onset aflutter.

But these are just my thoughts so feel free to correct me if I'm wrong.

Agreed, he’s showing up with A-flutter now, but who knows how long this has been going on for in the past so I think a CT-PE is justified as anticoagulation for a day is not going to prevent what may have already been occurring.

Also, the PE could have also caused the rhythm with RA dilation.

 

[operaman]

Yeah rate control - I tend to try metop first and then dilt. We can’t do new dilt drips on the floor so I don’t start many of those. Thankfully our floor patients don’t often have these issues.

In my hands this guy is still getting a CTA chest to look for PE.

For the students and soon to be terns - I view night float as a very unique situation where you practice a very narrow style of medicine. You’re usually by yourself managing a lot of patients at a time when the house is at minimum staffing and getting anything done is painful.

My general approach is usually determining as quickly as possible who is sick and who is not sick. Does someone need to go to a higher level of care? Does someone need an advanced airway? Do they need to go back to the OR? Some of those things are beyond your ability as an intern and you are trying to figure out whether or not you need to call in the calvary. There’s not usually time for thorough diagnostic work ups and pontification. It’s more about keeping everyone alive until morning. Sometimes you just rule out the life threatening things and leave it to the day team to continue the workup when they have time and manpower.

In this guy we’ve ruled out all the scary causes of his symptoms other than a PE. One he’s rate controlled and scanned, he either goes down the PE treatment pathway or the “don’t know why this happened but you’re not gonna die tonight” pathway.

 

[cbrons]

So this is a subtle EKG - but there's a good lesson to be learned here. Anybody with a tachycardia at around 150bpm needs to have Atrial Flutter on the differential diagnosis. You can't chalk all these up to sinus tach vs. SVT.

1) Always go see the patient and perform a physical exam.

2) Stable vs. Unstable. This patient is stable. Yes, chest pain/discomfort is concerning, but this patient is perfusing well and protecting his airway. You have time to think.

3) Get repeat EKGs or watch this rhythm on the monitor for a while. While it doesn't appear on this EKG, most cases of 2:1 Atrial Flutter will degenerate briefly into 3:1 at some point, and then the diagnosis becomes much more clear.

4) Treatment of Atrial Flutter is going to be just like that of Atrial Fibrillation. I prefer calcium channel blockers (i.e. Diltiazem drip) as a rate control method over beta blockers (Metoprolol push doses) but you may be in a setting on the floor where starting a drop is not possible, in which case stick with the metoprolol pushes. There's some school of thought towards giving chemical/electrical cardioversion instead of rate control in isolated afib/flutter like this case (especially if he was on a monitor and we can definitely see the onset of this rhythm, so thrombus and anticoagulation are not concerns) but that probably goes beyond the purpose of this exercise. Stick with rate control when in doubt.

I agree with most of this except 2; sharp substernal chest pain and diaphoresis scream ischemia, which makes him unstable by definition. In this context the ischemia is very likely demand ischemia from the a flutter.

If there wasn't a component of active chest pain, I might try a beta blocker, probably a bolus of esmolol. But in this case, I would probably seriously consider shocking this person (using adequate procedural sedation of course). Curious to know if any one else would do this... maybe @Instatewaiter is around to give his opinion...

 

[anbuitachi]

I agree with most of this except 2; sharp substernal chest pain and diaphoresis scream ischemia, which makes him unstable by definition. In this context the ischemia is very likely demand ischemia from the a flutter.

If there wasn't a component of active chest pain, I might try a beta blocker, probably a bolus of esmolol. But in this case, I would probably seriously consider shocking this person (using adequate procedural sedation of course). Curious to know if any one else would do this... maybe @IMreshopeful is around to give his opinion...

Nah disagree. We are talking about now, not in the future. You can certainly become UNSTABLE in the future due to this ongoing ischemia. But currently he's stable. I would wheel this patient down to CT if i thought it was a PE
Similarly you can get stabbed on the arm and bleed with some tachycardia but otherwise normal vitals. Stable? Yea. However if you dont stop that bleed you'll be dead, so at some point you'll be unstable. Just not now

 

[cbrons]

I would also add that sending this person for a CTPA or CT with PE protocol seems like a fairly insane thing to do without first addressing the dysrhythmia and chest pain. Even on the off chance this person does have a massive PE (no great reason to think that's the case), most people with PE die from hemodynamic collapse usually as a result of RV failure... reduced ventricular preload from an atrial dysrhythmia can lead to hemodynamic collapse, and is the most pressing issue to address. After that issue is stabilized, you can then try to convince yourself they need to be scanned.

 

[Redpancreas]

I would also add that sending this person for a CTPA or CT with PE protocol seems like a fairly insane thing to do without first addressing the dysrhythmia and chest pain. Even on the off chance this person does have a massive PE (no great reason to think that's the case), most people with PE die from hemodynamic collapse usually as a result of RV failure... reduced ventricular preload from an atrial dysrhythmia can lead to hemodynamic collapse, and is the most pressing issue to address. After that issue is stabilized, you can then try to convince yourself they need to be scanned.

Point taken, at what point would you say it would be safe to take the patient to the CT? When the patient is NSR?

Also, can atrial flutter due to increased workload mimic cardiac ischemic pain (demand ischemia)? Does this apply to most dysrhythmias?

 

[IMreshopeful]

I agree with most of this except 2; sharp substernal chest pain and diaphoresis scream ischemia, which makes him unstable by definition. In this context the ischemia is very likely demand ischemia from the a flutter.

If there wasn't a component of active chest pain, I might try a beta blocker, probably a bolus of esmolol. But in this case, I would probably seriously consider shocking this person (using adequate procedural sedation of course). Curious to know if any one else would do this... maybe @IMreshopeful is around to give his opinion...

I think it depends on the definition of “unstable”. ACLS algorithm defines it primarily as hypotension or really bad symptoms. I have emergently shocked flutter before but in the setting of hypotension.

I agree that flutter alone unlikely to cause a plaque rupture. Prob demand mediated ischemia. Wouldn’t treat it as an ACS and look for causes of possible ischemia - blood loss post op, pneumothorax, pleural or pericardial effusion, infectious, etc. I got called about this all the time on consults - a few times it turned out to be something serious that wasn’t primarily cardiac.

Also pro tip is that the HR being pinned at 140-150 is highly suspicious for an atrial tachycardia - if the atrial rate is double that (assuming 2:1 conduction) then it’s more likely flutter, even if you don’t see classic flutter waves as in this example. This is why for future interns telemetry monitoring is so helpful to see heart rate trends

I would also consider slowing the flutter and seeing what his symptoms do. Try IV metop

 

[IMreshopeful]

Point taken, at what point would you say it would be safe to take the patient to the CT? When the patient is NSR?

Also, can atrial flutter due to increased workload mimic cardiac ischemic pain (demand ischemia)? Does this apply to most dysrhythmias?

Sure can

 

[quickfeet]

Sure can

Would modified Valsalva maneuveur work in a flutter?

Also is there any case where giving adenosine in narrow-complex tachycardia is dangerous?

 

[IMreshopeful]

Would modified Valsalva maneuveur work in a flutter?

Also is there any case where giving adenosine in narrow-complex tachycardia is dangerous?

I mean adenosine lasts a few seconds so doubt there’s any lasting effect. It can cause heart block and a ventricular escape rhythm if you give it in a person who is in sinus but it’s temporary

Valsalva can unmask flutter, sure

 

[anbuitachi]

I think it depends on the definition of “unstable”. ACLS algorithm defines it primarily as hypotension or really bad symptoms. I have emergently shocked flutter before but in the setting of hypotension.

I agree that flutter alone unlikely to cause a plaque rupture. Prob demand mediated ischemia. Wouldn’t treat it as an ACS and look for causes of possible ischemia - blood loss post op, pneumothorax, pleural or pericardial effusion, infectious, etc. I got called about this all the time on consults - a few times it turned out to be something serious that wasn’t primarily cardiac.

Also pro tip is that the HR being pinned at 140-150 is highly suspicious for an atrial tachycardia - if the atrial rate is double that (assuming 2:1 conduction) then it’s more likely flutter, even if you don’t see classic flutter waves as in this example. This is why for future interns telemetry monitoring is so helpful to see heart rate trends

I would also consider slowing the flutter and seeing what his symptoms do. Try IV metop

The go to for seeing the underlying rhythm is adenosine. Adenosine is rapid onset and offset. In situations where you are not sure what is going on, always go for short acting medications.
But it's important to figure out what may have caused the patient to go into A flutter before you go crazy with long acting meds like IV metoprolol. You wouldn't want to give this guy IV metoprolol if his flutter is caused by PE

 

[deleted245139]

A bedside ultrasound, if available, can be of utility with PE in a differential if there is ever a stability concern for leaving a unit. US eval for RV strain (normotensive, so this can be present, but subtle). With a new onset tachydysrythmia and polarity change on EKG in a post op patient, PE would be up there for my differential. DVT ppx isn't 100% effective

 

[anbuitachi]

I mean everyone with a prolonged hospital stay will be on DVT ppx unless contraindicated. Every patient i've seen who developed massive PE in the hospital were on DVT ppx

 

[NITRAS]

M1 taking a stab. Seems like cardiac, pe VS hypovolemic shock.
What was the post op blood loss?
What type of bariatric procedure?
Any vomiting blood or bowel movements with blood or blood products?
What day is this post op? Were his home meds dced during the hospital stay?
Hematocrit?

Never trust Op Note estimated blood loss. Odds are the whole note is copy and pasted and hasn’t changed for the past 5 years if coming from a training center.

 

[anbuitachi]

Never trust Op Note estimated blood loss. Odds are the whole note is copy and pasted and hasn’t changed for the past 5 years if coming from a training center.

At our hospital, there is a template and each note is filled out after the surgery. The surgeons estimated blood loss is usually underestimated, so it's better to look at the anesthesiologists note. Then again if you have a stable crit it's all good

 

[doc05]

At our hospital, there is a template and each note is filled out after the surgery. The surgeons estimated blood loss is usually underestimated, so it's better to look at the anesthesiologists note. Then again if you have a stable crit it's all good

Bariatric surgery? EBL should be nil. That doesn't rule out a postop bleed.

 

[doc05]

Also no one addressed why this patient is still in the hospital on POD 3!

 

[anbuitachi]

Bariatric surgery? EBL should be nil. That doesn't rule out a postop bleed.

No, surgery in general.

Also no one addressed why this patient is still in the hospital on POD 3!

Not tolerating diet i guess

 

[IMreshopeful]

The go to for seeing the underlying rhythm is adenosine. Adenosine is rapid onset and offset. In situations where you are not sure what is going on, always go for short acting medications.
But it's important to figure out what may have caused the patient to go into A flutter before you go crazy with long acting meds like IV metoprolol. You wouldn't want to give this guy IV metoprolol if his flutter is caused by PE

Agree, usually want to see what’s causing it. Rarely have I seen people crump purely as the result of an atrial flutter - it’s organized so often reasonably well tolerated.

That being said the ED still loves to use metoprolol on SVT... even though it’s clearly not indicated as the first line in the ACLS algorithm ...

 

[IMreshopeful]

A bedside ultrasound, if available, can be of utility with PE in a differential if there is ever a stability concern for leaving a unit. US eval for RV strain (normotensive, so this can be present, but subtle). With a new onset tachydysrythmia and polarity change on EKG in a post op patient, PE would be up there for my differential. DVT ppx isn't 100% effective

Agree but not all PE cause RV strain or McConnell sign or what have you. And some people are, let’s say, overconfident about their bedside echo skills

If you’re that worried get a CTA

 

[deleted245139]

Oh I agree ^... Specific yes, not sensitive.

 

[quickfeet]

Paging @Instatewaiter

 

[nlax30]

Agree, usually want to see what’s causing it. Rarely have I seen people crump purely as the result of an atrial flutter - it’s organized so often reasonably well tolerated.

That being said the ED still loves to use metoprolol on SVT... even though it’s clearly not indicated as the first line in the ACLS algorithm ...

ACLS is a general guideline and not a strict set of rules for physicians to use when they are treating a specific entity. If they think they’re treating a flutter or AF then certainly a BB/CCB is reasonable to use.

 

[nlax30]

Would modified Valsalva maneuveur work in a flutter?

Also is there any case where giving adenosine in narrow-complex tachycardia is dangerous?

Don’t use adenosine if you are dealing AFib or flutter in the setting of WPW/Accessory pathway, “pre-excited AFib”. When you block the AV node you risk that rapid flutter/AF conducting rapidly down the accessory pathway.

Otherwise for a narrow complex SVT or even REGULAR wide complex arrhythmia then adenosine reasonable to try.

If it’s AF, AT or Flutter then you’ll just see either nothing or underlying flutter waves. It won’t terminate it.

If it’s an AV node dependent tachycardia such as AVNRT or AVRT (either orthodromic or antidromic) then it should terminate when there’s AV node block.

 

[BigRedBeta]

Update #2


The lack of biphasic P-wave in V1 suggests this not sinus rhythm.

for the record I didn't watch the video...

The above is a good rule of thumb. The other thing you can look for is + P-waves (ie upgoing) in I and AVF for sinus rhythm. Not having those suggests a pacemaker that is not your SA node.

 

[cbrons]

Don’t use adenosine if you are dealing AFib or flutter in the setting of WPW/Accessory pathway, “pre-excited AFib”. When you block the AV node you risk that rapid flutter/AF conducting rapidly down the accessory pathway.

Otherwise for a narrow complex SVT or even REGULAR wide complex arrhythmia then adenosine reasonable to try.

If it’s AF, AT or Flutter then you’ll just see either nothing or underlying flutter waves. It won’t terminate it.

If it’s an AV node dependent tachycardia such as AVNRT or AVRT (either orthodromic or antidromic) then it should terminate when there’s AV node block.

How about a stable patient with a wide complex tachycardia... is there any situation where beta blockers are unsafe?

 

[Instatewaiter]

This is 2:1 atrial flutter or a 2:1 atrial tach. There are a few leads that you can see this in but it is probably best seen in lead 1 (also in II, and aVL). There are 2 humps in the T wave and the first hump is the other P wave. This would be atypical atrial flutter and is notoriously difficult to rate control.

To evaluate a narrow complex tachycardia you need to start with the EKG. Regular or irregular ?
Irregular?- most commonly AF but also atrial flutter with variable block and MAT- EKG is all you need
If regular, Look for P waves- is it a long RP tachycardia or short RP tachycardia. -sometims more than the EKG is needed

Here this is a long RP tachycardia which means it is very unlikely to be AVNRT and more likely to be either sinus tach, atrial tach or atrial flutter (along with a handful of rarer things). So it would be smart to look for burried P waves within the T wave or QRS complex. If you find them, make sure them march out as the atrial rate is usually fixed and you'd have Atrial flutter/tach (what we have here). Because the T waves are not the classic sawtooth it is atypical. This impacts where the EP guy will have to ablate. Tip: You can often double the gain on the EKG which will allow you to see the P waves better

Sometimes you can't find the other P waves to tell what the long-RP tachycardia. To tell the mechanism of atrial activity I find adenosine works well (tip). In my exerience valsalva works in a very very small percentage of patients with a long RP tachycardia specifically because most are either atrial flutter or atrial tachs which don't respond to vagal maneuvers well. But do it anyway.

So next when that doesn't work you give adenosine 6 and then 12 mg WITH AN EKG RHYTHM STRIP (TIP). The adenosine will usually block the AV node and your QRS complexes dissappear. In this case would reveal only atrial activity with a atrial rate of ~320. In a few seconds the node will come back and you will go right back to your fast atrial flutter.

Treatment:
The next question becomes what will you use to treat it. If stable, I favor rate control as the first attempt post-op and if that doesn't work cardioversion. If unstable just get them out of it quickly. Synchronized cardioversion at 200J (go big or go home)

The patient is having chest pain which some will say is "unstable" which is dubious. However, it does confuse what is going on to cause the pain and what further evaluation needs to happen. If you get rid of the flutter and the patient is still having chest pain, it is very different than if the pain goes away when you cardiovert them. Here I say cardiovert them and see what the symptoms are.

Evaluation:
In my experience fib/flutter that is causing ischemic pain usually also causes marked ST depressions which we don't see here. Is it possible this could be ischemic mediated? Yeah. But I also have the ability to do and interpret a pretty reasonable bedside echo... There is a new left axis deviation. The inferior waves technically don't meet criteria for Q waves as only III has Q waves which is allowed. So the person needs serial troponins, an echo and an eventual ischemic eval- the speed at which this done and what is done will be determined by the enzymes. At this time, doesn't need to go right to the cath lab.

Next, new atrial flutter after surgery in my mind has a high enough pre-test probability a PE that it warrants further eval. D dimer is useless. Echo is not sensitive enough. If the renal function is ok, pull the trigger on PE protocol CT.

 

[Crayola227]

side note, be very careful about patients in whom you have reason to suspect sepsis or shock, with rate control

sometimes the tachy is in fact part of their compensation, and if you take it away, they decompensate very very fast

I saw a post-op patient very much like this killed by metoprolol

I would just want to be pretty sure about what was going on in his chest first, night float absolutely has a flavor of EM-style medicine, not saying you ignore the flutter or don't treat it, and surely you want to deal with that particularly in what looks like a picture of demand ischemia, but by definition demand ishchemia has a cause, and that cause might have a cause, meaning dealing with slowing flutter alone isn't sufficient to me

yes, don't pontificate, and yes, a lot of stuff has to wait for day team, however potential post-op complication leading to potential new onset tachyarrythmia leading to potential demand ischemia and necessitating rate control, in my view is not one of them

leak in this setting, pneumomediastinum and such, is so immediately and quickly deadly, while most bariatric surgeries are NBD (no big deal), when it is a big deal it's a huge big deal and very emergent

also, while you would expect air on a CXR s/p lap, I would think there are questions of amount, someone mentioned concern for pneumothorax which I think is low, but point is while maybe using CXR in a binary manner of +/- of air is not useful, where and how much is still diagnostically useful, not to mention what else you can see

I think bedside echo is a great idea overall, FAST or the modified FAST that includes looking for signs of pleural effusion/pneumothorax (can't recall the name), besides just looking for PE you can see lots of other conditions related to too much air/fluid in places you don't want but could happen in a surgery like this

TLDR
I don't consider this case handled from a NF perspective. Having identified the a flutter and cardioverting/rate controlling, work up on the case as given was not complete, and most of the tests mentioned in this thread looking at what is going on in his chest, including contacting the surgical team, was appropriate in my view

possible leak or infection driving all this has to be addressed as well before you go back to sleep

 

[anbuitachi]

This is 2:1 atrial flutter or a 2:1 atrial tach. There are a few leads that you can see this in but it is probably best seen in lead 1 (also in II, and aVL). There are 2 humps in the T wave and the first hump is the other P wave. This would be atypical atrial flutter and is notoriously difficult to rate control.

To evaluate a narrow complex tachycardia you need to start with the EKG. Regular or irregular ?
Irregular?- most commonly AF but also atrial flutter with variable block and MAT- EKG is all you need
If regular, Look for P waves- is it a long RP tachycardia or short RP tachycardia. -sometims more than the EKG is needed

Here this is a long RP tachycardia which means it is very unlikely to be AVNRT and more likely to be either sinus tach, atrial tach or atrial flutter (along with a handful of rarer things). So it would be smart to look for burried P waves within the T wave or QRS complex. If you find them, make sure them march out as the atrial rate is usually fixed and you'd have Atrial flutter/tach (what we have here). Because the T waves are not the classic sawtooth it is atypical. This impacts where the EP guy will have to ablate. Tip: You can often double the gain on the EKG which will allow you to see the P waves better

Sometimes you can't find the other P waves to tell what the long-RP tachycardia. To tell the mechanism of atrial activity I find adenosine works well (tip). In my exerience valsalva works in a very very small percentage of patients with a long RP tachycardia specifically because most are either atrial flutter or atrial tachs which don't respond to vagal maneuvers well. But do it anyway.

So next when that doesn't work you give adenosine 6 and then 12 mg WITH AN EKG RHYTHM STRIP (TIP). The adenosine will usually block the AV node and your QRS complexes dissappear. In this case would reveal only atrial activity with a atrial rate of ~320. In a few seconds the node will come back and you will go right back to your fast atrial flutter.

Treatment:
The next question becomes what will you use to treat it. If stable, I favor rate control as the first attempt post-op and if that doesn't work cardioversion. If unstable just get them out of it quickly. Synchronized cardioversion at 200J (go big or go home)

The patient is having chest pain which some will say is "unstable" which is dubious. However, it does confuse what is going on to cause the pain and what further evaluation needs to happen. If you get rid of the flutter and the patient is still having chest pain, it is very different than if the pain goes away when you cardiovert them. Here I say cardiovert them and see what the symptoms are.

Evaluation:
In my experience fib/flutter that is causing ischemic pain usually also causes marked ST depressions which we don't see here. Is it possible this could be ischemic mediated? Yeah. But I also have the ability to do and interpret a pretty reasonable bedside echo... There is a new left axis deviation. The inferior waves technically don't meet criteria for Q waves as only III has Q waves which is allowed. So the person needs serial troponins, an echo and an eventual ischemic eval- the speed at which this done and what is done will be determined by the enzymes. At this time, doesn't need to go right to the cath lab.

Next, new atrial flutter after surgery in my mind has a high enough pre-test probability a PE that it warrants further eval. D dimer is useless. Echo is not sensitive enough. If the renal function is ok, pull the trigger on PE protocol CT.

Nicely explained! Are you a surgeon??

 

[doc05]

Way too much pontificating. There are just a few big postop complications that you see in bariatric surgery...

 

[cbrons]

Nicely explained! Are you a surgeon??

Hes a cardiologist

 

[nlax30]

How about a stable patient with a wide complex tachycardia... is there any situation where beta blockers are unsafe?

Stable wide complex tachycardia....

Probably a topic for another thread BUT, my approach would probably depend on the patient and the characteristics of the QRS on the EKG itself. In most cases just closely looking at the morphology I’ll have a good idea of if this is VT or SVT aberrancy which is the big decision to make.

I also consider the type of patient.

A young patient with known or presumably structurally normal heart then I’m thinking of SVT w/ aberrancy or an idiopathic VT (Outflow tract VT, fascicular VT, etc). Regular and wide, and especially if I’m thinking an SVT w/ aberrancy (AVNRT or AVRT) then I’ll try adenosine.

An older patient or one with known structural heart disease then you should be thinking VT if you just play the odds. If the morphology just screams aberrant SVT to me (known prior bundle block) then I may try adenosine. If I’m pretty sure it’s VT form the start then I won’t and go down the VT pathway.

As far as beta blockers go.... the times to avoid it would be again if you are dealing with Pre-excited AF or flutter (in setting of WPW). In the case of AF you may see an IRRegular wide complex tach and in that case avoid nodal blockers and go straight to cardioversion or something like procainimide for chemical conversion.

That’s probably the only real time I would NOT use beta blockers. Obviously if they’re “shocky” then avoid but then we’re getting into more unstable tachycardias.

As an aside, back to this case with the atrial flutter..... I don’t suggest this without speaking with cardiology but I like using Ibutilide for these stable atrial flutters that I want to try and convert on the floor chemically.

 

[agnes5]

This is 2:1 atrial flutter or a 2:1 atrial tach. There are a few leads that you can see this in but it is probably best seen in lead 1 (also in II, and aVL). There are 2 humps in the T wave and the first hump is the other P wave. This would be atypical atrial flutter and is notoriously difficult to rate control.

To evaluate a narrow complex tachycardia you need to start with the EKG. Regular or irregular ?
Irregular?- most commonly AF but also atrial flutter with variable block and MAT- EKG is all you need
If regular, Look for P waves- is it a long RP tachycardia or short RP tachycardia. -sometims more than the EKG is needed

Here this is a long RP tachycardia which means it is very unlikely to be AVNRT and more likely to be either sinus tach, atrial tach or atrial flutter (along with a handful of rarer things). So it would be smart to look for burried P waves within the T wave or QRS complex. If you find them, make sure them march out as the atrial rate is usually fixed and you'd have Atrial flutter/tach (what we have here). Because the T waves are not the classic sawtooth it is atypical. This impacts where the EP guy will have to ablate. Tip: You can often double the gain on the EKG which will allow you to see the P waves better

Sometimes you can't find the other P waves to tell what the long-RP tachycardia. To tell the mechanism of atrial activity I find adenosine works well (tip). In my exerience valsalva works in a very very small percentage of patients with a long RP tachycardia specifically because most are either atrial flutter or atrial tachs which don't respond to vagal maneuvers well. But do it anyway.

So next when that doesn't work you give adenosine 6 and then 12 mg WITH AN EKG RHYTHM STRIP (TIP). The adenosine will usually block the AV node and your QRS complexes dissappear. In this case would reveal only atrial activity with a atrial rate of ~320. In a few seconds the node will come back and you will go right back to your fast atrial flutter.

Treatment:
The next question becomes what will you use to treat it. If stable, I favor rate control as the first attempt post-op and if that doesn't work cardioversion. If unstable just get them out of it quickly. Synchronized cardioversion at 200J (go big or go home)

The patient is having chest pain which some will say is "unstable" which is dubious. However, it does confuse what is going on to cause the pain and what further evaluation needs to happen. If you get rid of the flutter and the patient is still having chest pain, it is very different than if the pain goes away when you cardiovert them. Here I say cardiovert them and see what the symptoms are.

Evaluation:
In my experience fib/flutter that is causing ischemic pain usually also causes marked ST depressions which we don't see here. Is it possible this could be ischemic mediated? Yeah. But I also have the ability to do and interpret a pretty reasonable bedside echo... There is a new left axis deviation. The inferior waves technically don't meet criteria for Q waves as only III has Q waves which is allowed. So the person needs serial troponins, an echo and an eventual ischemic eval- the speed at which this done and what is done will be determined by the enzymes. At this time, doesn't need to go right to the cath lab.

Next, new atrial flutter after surgery in my mind has a high enough pre-test probability a PE that it warrants further eval. D dimer is useless. Echo is not sensitive enough. If the renal function is ok, pull the trigger on PE protocol CT.

What is your opinion on using rhythm control if rate control doesn't work? I've seen some cardio attendings/fellows put patients on amio drips if rate control is ineffective as opposed to cardioverting them.

 

[evilbooyaa]

We're all pontificating about the a-flutter and nobody wants to figure out why this guy has the a-flutter in the first place.

He's leaking or has a PE. I agree that given he's POD#3 and still in the hospital, likely a mild, progressive leak that isn't causing fever and peritonitis (yet). Do we have a recent CBC?

Again, if you don't tell the operating surgeon (or his staff), ASAP in this situation as the night float person, you're gonna be in trouble. As someone else said, bariatric surgery goes very well 99% of the time, and the 1% it doesn't, it has the potential to be catastrophic.

 

[operaman]

We're all pontificating about the a-flutter and nobody wants to figure out why this guy has the a-flutter in the first place.

He's leaking or has a PE. I agree that given he's POD#3 and still in the hospital, likely a mild, progressive leak that isn't causing fever and peritonitis (yet). Do we have a recent CBC?

Again, if you don't tell the operating surgeon (or his staff), ASAP in this situation as the night float person, you're gonna be in trouble. As someone else said, bariatric surgery goes very well 99% of the time, and the 1% it doesn't, it has the potential to be catastrophic.

Huh I could swear it originally said day 1 post op — was there an edit at some point? Yeah day 3 and leak is definitely up there on the ddx, though PE definitely still looms larger in my mind.

When I was a surgical intern this would definitely be a phone call to the senior/chief. Nobody wants to walk into a surprise like this on morning rounds.

 

[nlax30]

What is your opinion on using rhythm control if rate control doesn't work? I've seen some cardio attendings/fellows put patients on amio drips if rate control is ineffective as opposed to cardioverting them.

That's a reasonable approach. These atrial flutters can be difficult to rate control and in this case if I knew the onset I wouldn't hesitate to jump to using something like IV ibutilide or amio to try and convert.

In general the 1a, 1C and class III anti-arrhythmic agents can be used for these flutters.

 

[doc05]

We're all pontificating about the a-flutter and nobody wants to figure out why this guy has the a-flutter in the first place.

He's leaking or has a PE. I agree that given he's POD#3 and still in the hospital, likely a mild, progressive leak that isn't causing fever and peritonitis (yet). Do we have a recent CBC?

Again, if you don't tell the operating surgeon (or his staff), ASAP in this situation as the night float person, you're gonna be in trouble. As someone else said, bariatric surgery goes very well 99% of the time, and the 1% it doesn't, it has the potential to be catastrophic.

Thank you for the common sense. All this debate over antiarrthymic drugs is lunacy.

 

[IMreshopeful]

ACLS is a general guideline and not a strict set of rules for physicians to use when they are treating a specific entity. If they think they’re treating a flutter or AF then certainly a BB/CCB is reasonable to use.

Sure agreed. But metop is still not the FIRST line for an SVT, especially if you aren’t sure if it’s flutter. It’s also mostly harmless - IV beta blockers not so much.

And yes obvi you would want to use procainamide for someone with an accessory pathway like WPW. That’s a zebra diagnosis though

 

[IMreshopeful]

That's a reasonable approach. These atrial flutters can be difficult to rate control and in this case if I knew the onset I wouldn't hesitate to jump to using something like IV ibutilide or amio to try and convert.

In general the 1a, 1C and class III anti-arrhythmic agents can be used for these flutters.

Ibutilide is a fantastic drug - underutilized to some extent. I’ve seen it work well

 

[IMreshopeful]

Way too much pontificating. There are just a few big postop complications that you see in bariatric surgery...

This isn’t a real patient. It’s worth going through treatment algorithms or arrhythmias irrespective of what is actually happening to the patient. At this point I would hope the NF intern has tried to rule out a PE

 

[nlax30]

Sure agreed. But metop is still not the FIRST line for an SVT, especially if you aren’t sure if it’s flutter. It’s also mostly harmless - IV beta blockers not so much.

And yes obvi you would want to use procainamide for someone with an accessory pathway like WPW. That’s a zebra diagnosis though

I’ll clarify the procainamide usage for WPW part; for pre-excited AF/flutter with WPW yes, for AVRT no.

I’m assuming you’re cardio as well so wasn’t directed toward you, more for the education of others in the thread.

 

[Zebra Hunter]

This is an easy one. With an isolated complaint of chest pain, afebrile, normal labs, normal sats, the treatment is simple, fluids and diltiazem. This ECG very clearly demonstrates a-flutter, although I frequently see people missing this IRL all the time. If you want a better look at the atrial activity, rearrange the monitor leads to Lewis leads or do the same with the ECG leads. If the patient remains symptomatic following being rate or rhythm controlled then you can start going down the sepsis/PE/surgical catastrophe algorithm. If he tells he feels amazing and goes to sleep, so should you after speaking with the surgery team.

 

[Instatewaiter]

What is your opinion on using rhythm control if rate control doesn't work? I've seen some cardio attendings/fellows put patients on amio drips if rate control is ineffective as opposed to cardioverting them.

In this circumstance, I would use rhythm control preferentially and would cardiovert. I want to get to the heart of the chest pain and if it is from the arrhythmia or something underlying the arrythmia. So here, cardioversion would be my choice rather than wait for an antiarrhythmic to work.

I use amio, sotalol, and flec a lot. I use tikosyn a moderate amount. I rarely ibutilide because I usually feel like there are better options.

Ibutilide is a fantastic drug - underutilized to some extent. I’ve seen it work well

I feel like there are rare times when ibutilide is the right choice. The main problem with ibutilide is it has a 5% rate of torsade and it is really rare that the risk of flutter is that high. Especially since this guy has probably gotten zofran already, a QT prolonger would not be my first choice... and almost never is. For flutter it is usually both easy to cardiovert and very easy to ablate. Pretty sure the attending surgeon would be pretty pissed if this guy had Torsade from a medication you gave.

 

[cbrons]

In this circumstance, I would use rhythm control preferentially and would cardiovert. I want to get to the heart of the chest pain and if it is from the arrhythmia or something underlying the arrythmia. So here, cardioversion would be my choice rather than wait for an antiarrhythmic to work.

I use amio, sotalol, and flec a lot. I use tikosyn a moderate amount. I rarely ibutilide because I usually feel like there are better options.




I feel like there are rare times when ibutilide is the right choice. The main problem with ibutilide is it has a 5% rate of torsade and it is really rare that the risk of flutter is that high. Especially since this guy has probably gotten zofran already, a QT prolonger would not be my first choice... and almost never is. For flutter it is usually both easy to cardiovert and very easy to ablate. Pretty sure the attending surgeon would be pretty pissed if this guy had Torsade from a medication you gave.

What kind of sedation do you use for a circumstance like this

 

[IMreshopeful]

In this circumstance, I would use rhythm control preferentially and would cardiovert. I want to get to the heart of the chest pain and if it is from the arrhythmia or something underlying the arrythmia. So here, cardioversion would be my choice rather than wait for an antiarrhythmic to work.

I use amio, sotalol, and flec a lot. I use tikosyn a moderate amount. I rarely ibutilide because I usually feel like there are better options.




I feel like there are rare times when ibutilide is the right choice. The main problem with ibutilide is it has a 5% rate of torsade and it is really rare that the risk of flutter is that high. Especially since this guy has probably gotten zofran already, a QT prolonger would not be my first choice... and almost never is. For flutter it is usually both easy to cardiovert and very easy to ablate. Pretty sure the attending surgeon would be pretty pissed if this guy had Torsade from a medication you gave.

This guy I agree although you could potentially just premedicate with a ton of mag. I’ve had refractory flutter and fib which have worked with Ibutilide but of course those are the minority. It’s a bit cowboy but I’ve seen EP guys push it

 

[sozme]

RESOLUTION​

(Will update this specific post as more responses/valuable insight becomes available)

This is a patient 3-days post-bariatric surgery. The specific kind of surgery e.g. REY vs. GBL isn't as relevant; sure there could be some operative complication here, but the primary goal of the exercise is to deal with the emergency first, namely the fast HR and possible on-going ischemia. You were given enough information to realize that the tachydysrhythmia wasn't due to acute blood loss anemia, hence the answer to stabilization isn't to give blood or IV fluids.

Again, picture yourself in this scenario as a resident overnight. You only have the information presented. You are at bedside. There's 7 or 8 other people in room waiting for you to tell them what to do. You have a patient with relatively stable vital signs except for a regular narrow complex tachycardia in the 150s complaining of severe chest pain. You actually have to ***do*** something here.

One of the important steps you could've made here was to identify the rhythm itself, as that offers insight into what effective (or safe) interventions could be. But if you are ever doubt about the actual rhythm, here is a good rule to remember:

When in doubt: Pace a slow rhythm. Shock a fast rhythm (try not to shock sinus tachycardia - but it will likely be OK if you do).

Initial actions for this case:

• Stat team basics
  [Things you should ask for when you are paged]
  • Ask for latest set of vital signs
  • Ask for continuous telemetry and pulse oximetry
  • Ensure placement of 2 large-bore IVs
  • Order stat 12-lead EKG
• Determine patient stability
  • Look at vital signs
  • Assess for the presence of serious symptoms
    [Presence of any of the below suggest instability]
    • Chest pain?
      [Usually represents demand ischemia from the fast HR itself]
    • Dyspnea?
      [If lungs are “wet” – possibly acute decompensated heart failure from dysrhythmia-induced pulmonary edema]
    • Decreased level of consciousness
      [Represents poor cerebral perfusion]
    • Signs of shock (hypotension, cold and clammy skin)
  • Determine if above symptoms/signs are due to rapid HR or if rapid HR (and above symptoms/signs) are due to something else
    [E.g. sinus tachycardia: Sepsis, hemorrhage, pulmonary embolism, cardiac tamponade, dehydration]
  • 
    
  • Review EKG to determine rhythm (or at least determine if it is wide or narrow
• o Wide or narrow
  
  o P-waves present?
  
  o Regularity (regular vs. regularly irregular vs. irregularly irregular)
  
  o Rate?
  
  o Rate changes: sudden or gradual?
  [Gradually decreases with IV fluids – e.g. sinus tachycardia, always 150? – atrial flutter]

Appropriate intervention:

In this case, I likely would have cardioverted this patient emergently. That being said, there have been some good arguments for a rate-control strategy (which might be what most residents are more comfortable with overnight). If you go the rate-control route, you need to be ready to cardiovert if that doesn't work out (in this case, if patient's chest pain continues or BP bottoms out, etc.).

Rate-control options

Electrical cardioversion: requires procedural sedation in this case (because patient is stable).

Post-stabilization testing
Some people have said this patient requires a "stat CTPE" because he has new-onset atrial flutter and chest pain. I'm not sure that's necessary. If you cardiovert him and he no longer has any chest pain, then that obviates the need to look for a PE. I also am not aware of any research showing that new onset SVT in post surgical patients is associated with PE. Given that he has been on prophylactic Lovenox for 24-hours, I also wonder how much that lowers his pre-test probability for PE. But you've read other arguments for testing him, so you should make-up your own decision. I will say that sending him to the scanner before stabilizing his HR and chest pain issue is probably a bad idea.

I do believe a post-stabilization troponin, electrolyte panel, and transthoracic echocardiogram are reasonable tests. The troponin for the chest pain, the electrolytes because he had a dysrhythmia, and the echo because of the newly diagnosed atrial flutter (which is a standard test for this indication).

Concluding notes

Here is my very simplified algorithm for what I would do if I was dealing with a tachyarrhythmia that I couldn't identify (more than willing to change this based on any helpful input from our experts in this thread

Simplified Adult Tachydysrhythmia Algorithm
(Assumes you do NOT know the exact rhythm you are dealing with)​

**In case you are wondering, the Modified Valsalva maneuver is the only kind of vagal maneuver i do in these circumstances. Carotid massage is potentially dangerous. Regular Valsalva rarely works. I try to keep my memorization to interventions that are high effectiveness and relatively safe (Modified Valsalva's only contraindication that I know of is in pregnant women, in whom it may induce premature labor).

Remaining questions for research:
1. To what extent does prophylactic-dose LMWH reduce one's chance of developing a VTE while in the hospital?
2. What is the association between new-onset SVT and PE in medical patients (and surgical patients)?