1) The Story.
You respond to a call about a 56 year old male who is having some shortness of breath and is dizzy when he stands.
On arrival the story you get from EMS is:
EMS was called to the patients house. They are BLS only as this is a very rural area. The patient presented with near syncopal episodes and SOB.
They quickly placed him on 15L NRM and laid the fellow down. They are not your typical EMTs and are well versed in how to place and print a 12 lead. On your arrival they hand you one (see below).
Lung sounds are clear and equal.
2) History
Patient says he has "heart problems"
3) Meds
Digoxin
lasix
ASA
4) Allg.
None
5) Obvious Pertinent Physcial findings
- Pt appears in mild resp. distress
- Pt looks a little pale and diaphoretic
- Pt gets dizzy on standing
Vitals On arrival:
BP: 81/55 HR: as in EKG RR: 20 Sat: 95% on NRM
6) Images
All examples not actual patient.
The EKG
7) Discussion Points
The discussion points are:
Facility appropriateness
Possible secondary Differential Diagnosis
Concerns
Treatment plan
Issues:
Nearest Cardiac center is 1 hour by rotor.
hi Mike,
Can you try reposting the 12 lead again...I can't get the link to open, thx.
Same as Canuck, the image link is wrong... no EKG... uhggg!
I couldn't get the EKG link to open either, but I'm going to "use the force" and guess that it is showing rapid A-fib...seeing that the patient is taking ( or supposed to be taking) digoxin. This, combined with the lasix, I'll bet his Na and K are all out of whack and his heart is just a bit cranky. The rapid A-fib is acting like SVT, decreasing his filling time, thus giving us the low BP ( and orthostatic, too).
Now, I reserve the right to COMPLETELY change my mind once I see the EKG....and knowing Mike's case studies, this will be FAR more involved than just a "routine" rapid A-fib
Fly safe everyone.....
OOpps
Sorry
Should work now let me know
Mike the mistyper!
Damn, not A-fib. Where's my MGS04?
Quick questions:
1. What was he doing at the onset of his complaint?
2. How long has this been going on? Anything aggravate/alleviate it?
3. Any previous similar events?
4. Could he possibly have taken more dig than he needed?
5. How alert and oriented is he?
6. Can I palpate a peripheral pulse consistent with each complex on the monitor?
To me, the tracing looks like underlying rhythm of a-fib with multi-focal ventricular ectopy. Rate around 125-140. The septal leads look like they've got some elevation too. I know that digitalis toxicity produces some arrythmias that are unique to it and that's the fist thing I'd suspect here.
Is his cardiologist an attending at the nearest cardiac center? Knowing your cases, Mike, I'm doubting this guys BP will hold up for an hour flight!!!
For now, keep him on the NRB. 2 IVs, labs, repeat 12 lead, prepare combo-patches in case we need them, Maybe ask him if he can "bear down", see if that slows his rate a little and helps him feel less syncopal. I"m assuming he has no dependent edema, has taken his meds as scheduled and denies anything other than dyspnea and pre-syncope.
Actually, it is A-fib...look at the leads below and I believe you'll see the underlying rhythm is irregular and narrow. The patient is also having runs of V-Tach...fun, fun. We have a pathologic left axis deviation as well, which gives us a block of the left anterior hemifasicle---the patient is only working on 2 of the three electrical pathways in the ventricles ( RBBB, and only one of the 2 branches of the Left Bundle).
Wierd progression through the V leads...V1 should normally have a negative deflection ( it does), as should V2, but it doesn't; notice V2 is has a positive deflection. V6 should normally have a positive deflection, but it doesn't in this EKG.
My initial thoughts:
1. Calm the patient as best you can...anxiety is NOT our friend right now.
2. Get control of the UNDERLYING rhythm and that may take care of the runs of V-tach.
3. Get a good hx: make sure the patient is compliant with the meds.
4. Although this looks narrow, double check with the measurements on the 12 lead. I get a good chuckle sometimes with the interpretations that these things spit out, but the measurements are reliable. I would check the QRS duration and the PR interval...Again, I don't SEE 'P' waves, and if the machine didn't/couldn't measure for them it just confirms my thoughts.
5. Hard to see any hard and fast AMI ST changes, but the rate may be too fast to see any subtle changes. Get the rate under control and we may see something....then again, that may help a number of things.
I learned to take care of things like this in this order: Rate, Rhythm, BP. Getting control of the Rate may help the Rhythm, which hopefully then takes care of the BP. If not, start "fixing" things at the beginning....
So, for now....
High flow O's
2 lines
Fluid challenges as long as the lungs stay clear
Cardizem ( or your flavor of choice) for the rapid A-fib
Serial 12 leads ( if you have the capability)
Have the fast patches VERY close....
Fly to a place with interventional cardiology
And as with ALL pt's like this ( especially Mike's cases ) BE READY FOR ANYTHING!!!!
Fly safe everyone....
Facility appropriateness: cardiac center is 1 hr. away, I'd transport to the nearest facility that can handle his condition
Differential Diagnosis: Accelerated Idioventricular Rhythm with hemodynamic compromise; under lying problem could be myocardial ischemia, digoxin toxicity, some electrolyte imbalance (such as hypokalemia), or hypoxemia. Hard to tell without more info.
Concerns: For me #1 concern is that the patient is hemodynamically unstable with a systolic BP of less the 90. This patient is going into cardiogenic shock.
Treatment: O2 via NR (consider RSI), IV of NS (fluid challenge), and Atropine 0.6-1.2 mg via IV or Isoproterenol @ 0.5-2.0 mcg/min via IV of course. The atropine should increase the sinus rate and allow the sinus to resume its normal pacemaking function if AV conduction is intact. This will have little to no influence on the rate of the accelerated AV junction focus which appears to be in the ventricals. If the atropine or isoproterenol is non-reactive then I'd consider pacing.
Goal should be to improve conduction through the AV node by reducing the vagal tone. This should make the patient hemodynamically stable. If the patient has a positive response to this then transporting to the cardiac center is an option because definitive treatment for this patient needs to be in a cardiac center.
Hey all,
Somewhat new to the forum, and my first post in the case studies, so like others have asked, go easy!!! OK, so BLS did a good thing, supine with 100% oxygen. Medicflyt kinda covered my thought process well, but in addition, we've got a wide complex tachyarrhythmia, looking extremely atrial, aberrancy...hmm.....BP 81/26.....kinda qualifies as unstable.......cardioversion? He is conscious, and a more conservative approach may be better.....fluid challenges, antiarrhythmics....(how 'bout Procainamide if Cardizem doesn't work?.....has both ventricular and atrial antiarrhythmic properties?)
Reassess lungs after boluses, get going to interventional center, how he responds to any of these treatments gives a better idea of what's goin on. I am ready to cardiovert however...... I'm thinking A-fib with RVR, aberrancy, ischemia/infarct? possible electrolyte and medication level abnormalities....?dig level, NA, K,(but not for us to know.....yet)...concerns... degradation of the rhythm, sustained low cardiac output, cardiogenic shock.....knowing Mike's cases....well...... Peace, Steve
Although nervous, and perhaps off in the bushes with the derailing....my thought process is....
How long has this guy been on his cardiac meds? How long since the dx was made?
Is there a chance that he may have been mislead into thinking this was a-fib, when in fact, it could have been WPW?
I think a cardiology consult, even with a 1 hour trip by rotor would be justifiable in case we've gotten to the point of a difficult rhythm to get out of.
As far as the basics, I would continue NRB O2, monitor airway status, give the volunteers a great Attaboy! for good management thus far., Get loaded, fluid bolus, if lungs stay clear; if the b/p stays low while supine and the SOB continues, it's either edison medison time or try the old amiodarone 150mg over 10min IV. Rate control definately a priority and perhaps that would be enough to fix his presenting symptoms.
If this is WPW, any other drug than amiodarone and procainamide would be contraindicated, and these two are a safe bet (procainamide with cardiac output issues addressed)
Just a thought,
epi
Hey again all....
Epi raises a good observation....could very well be a delta wave on that leading QRS complex; looking at lead I especially. Someone asked about how long ago this dx was made, ie how long has he been on digoxin. As I said before some more digging into his history might lead us to find that his "heart problems" may have been tachy-arrythmias. Cardizem in WPW is very much a bad thing....
One question for the group: Am I wrong in thinking that WPW is still fairly regular? This rhythm isn't....
At any rate, I still believe that the complexes are narrow so the decision would have to be made: rapid A-fib vs. WPW. Given the two I would much rather give procainamide to A-fib than a calcium channel blocker to WPW.....
I might watch the tracing ( or 12 leads) for a few more seconds to try to get a firm handle on the underlying rhythm, then treat with one of the above ideas.
So Mike.....any history of tachy problems? What interventions or office visits have led to his "heart problems"?
Intriguing about why he's on ASA too.....previous AMI or chronic A-Fib? Hmmmm.........
This is fun!!!! Fly safe everybody....
So we all meet again.........at another one of mike's cases.
The only comment I have so far is slow waaaaaaaaay down on the thought process about giving procainamide!
Procainamide takes on average about 40 minutes to 1 hour to convert stable monomorphic V-tach (an example arrhythmia). It also is notorious (VERY NOTORIOUS) for causing hypotension.
Not a big fan of giving someone who is hypotensive a drug that will likely make him more hypotensive as well as take about an hour to work.
Procainamide works AWESOME for very stable (ie no chest pain, no dyspnea, good BP stable monomorphic V-tach). Otherwise it takes way to long to work and will drop his BP.
Of course you could look at it another way......give the procainamide get his pressure around 60/P then you have a real good excuse to light 'em up with the juice.
Would we be wrong for wanting to "light him up with the juice" now? He is hemodynamically unstable. I would feed him 100% O2, start 2 lines,slap on the pads,consider cardioversion and maybe a little Versed and I mean a little Versed to help him forget being lit up.
I would also head for the closest interventional facility.
I may be crazy, but if I am wrong, at least we are learning here...and we are getting along!
Sue
No you would not be wrong to light 'em up at all.
Matter of fact you could make a great argument for cardioverting him.
Pale/diaphoretic, resp distress, dizzy, hypotensive......sounds like a good argument to me.
However, if he's alert and oriented, cooperative, and appears to be tolerating it relatively well you do have a little play time to try some things, but you could absolutely zap him and be correct.
just don't forget the versed.
I agree with Stobey with the cardioversion,.
You could consider some pharmicalogical intervention if an IV has been established PTA but, I guess you can argue the time factor involved.
I would consider this pt unstable:
-SOB
-Dizzy
-Mild resp distres
-Pale/diaphoretic skin
-BP 81/55 (if you do the CPP formula that less than 53 mmHg not much cerebral flow)
also, if you did orthostatic V/S I'd bet they'd be worse.
But, that would be too easy of a treatment
This appears to be an unstable tachycardia (Rapid A- fib with runs of V-tach) with significant hemodynamic compromise. I would prefer to use Etomidate for brief sedation (0.1mg/kg ) due to the fact the patient is hypotensive. Then I would light em' up. If this brakes the unstable tachycardia i would go to an antiarrthymic infusion ( cardizem or amiodarone ).
Im new to this forum these are great case studies
well here goes nothing.
all the std questions as far as hx goes,
any similar episodes, how long ago did it start. and cardiac surgeries
is there any edema in the extremities?
i would also do another 12 lead of my own to make sure lead placement is correct.
DD- possible dig tox ? is the pt seeing yellow?
im pretty fresh so im definately going to cardiovert to control the rate and treat for possible AMI. position for bp, if there is no edema then bolus for bp as well. maybe a right sided 12 lead as well. transport to nearest cardiac center.
if you get the rate under control and can get a better interp of a 12 lead could you use Lidocaine for irratibility?
The pt is clearly symptomatic, so you can put him on a NRB mask with high flow O2. Looking at his EKG you could make an argument for torsades or maybe WPW. Does look like maybe a delta wave on the leading edge of the QRS.
Either way you could give him some mag and if that does not work amiodorone or cardiovert. If the guy is still looking at me and coherent I would opt for pharm intervention. If he is not then he gets the electricity.
Clearly this guy needs a facility that can do cardiovascular intervention and should have an EP lab.
I admit it...my biggest weakness as a clinician is EKG interpretation...sure, I can pick out an obvious AMI, but other than that I'm just learning how to read them now.
No need to be an expert at EKG's however, to know that this guy needs to be cardioverted. He has a hemodynamically unstable tachycardia, and that always = synchronized cadioversion. A little etomidate and ZAP 'EM (unless of course he's REALLY unstable - which it doesn't sound as though this guy is - then skip the meds and just ZAP 'EM).
After we zap him, some amiodarone would probably be appropriate.
Do his lungs sound wet? Is he edemetous? Has he been peeing? Any history or signs of renal dysfunction?
Before I do too much with this guy I would want to see his dig level and a chemistry, specifically K, Na, Mg, CK, troponin, BUN, and creatinine. Do we have an i-Stat by any chance?
I think you can make a decent case for going to a closer facility than the cardiac specialty center. This guy probably just needs to be watched for a day or two and have some electrolytes replaced and meds adjusted. Any hospital with a cardiologist or good intensivist can do that, and if it is decided he needs a cath or EP lab or other specialist consult then he can be transported to the city non-emergently.
However, we don't know for sure, so I would definitely just take him to the cardiac center.
And for once, I DON'T think I'd intubate him...depending on how he looks after the cardioversion, of course. If it turns out that he needs it for some reason I'd forgo the sux for rocuronium, given that his K may already be through the roof.
Hey All
Before i post answers I have a question.
How many people call someone who is mentating "unstable" and justify it.
Isnt it the pervue of medicine to intervene with the least invasive option when a patient is stable?
While everyone is looking at this as unstable, the definition of an elective cardioversion (where someone has to sign an informed consent form) is a patient who is mentating isnt it? So isnt he stable?
If you were to decide to cardiovert a guy who is mentating i would assume you would give a med like etomidate (mentioned here). If there is time to give a sedative isnt there time to attempt a less invasive intervention like medication for the rhythm?
Just putting it out there. what do you think?
Ill be answering the questions on the case later tonight!
I believe you are right on Mike...
perform least invasive procedures such as administering meds then take it up a notch from there if the is either no change or the patient is getting worse. I'd pace/cardiovert as a last resort after the meds if needed.
As stated in my previous post I believe this is a simple accelerated idioventricular rhythm, nothing more. Digoxin toxicity can cause this if the pt. accidently OD'd on his Digoxin.
Lidocaine is a strong possiblility but you need a NSR underlying the accelerated idioventricular rhythm otherwise the patient can get a lot worse.
My definition of unstable is the irritablitly, runs of vtach, and at any moment he could possibly arrest, i would be all for administering an anti arrythmic that a) isnt contraindicated by hypotension or AMI, or doesnt take 5 minutes to setup and even longer to drip in.
i choose electricity to control the rate, then go from there.
however my mind is young, fresh and ready for molding.
I always read these posts and answer tentatively. Mike's scenarios have me paranoid about the unseen and next turn in the bend.
The mentation question is a good issue to bring up. A person who is mentating well does have the power to refuse any part of any care we render.....HOWEVER.....tis our jobs to be influential enough to talk him into treatment however bizarre it may seem to the layman.
I know as well that we tend to be gun-shy when it comes to pulling out the big guns to a person looking back at your paddle/patch wielding self. I remember a case I had very similar to this one:
A lady who presented on all fours in the floor, scared because "whenever I sit up, I pass out". Very similar presentation-pale, diaphoretic, short of breath and of course a similar EKG. I wanted to go to cardioversion, my partner did not. We did every non-zapping way of treating only to have the doc waiting on us at the ED, paddles in hand. Maybe we just ruled out everything for him. I just gave my partner "the look" after it was over, but we both learned from it.
Unstable? I guess it really is subject for interpretation. The bottom line is how does this patient look? If you walk into the room and he looks bad (severe SOB, chest pain-not listed with this patient, diaphoresis, sudden onset, etc) then question answered. If he looks ok maybe you have time to play with meds. My lady looked bad, yet I let my partner talk me out of immediate cardioversion.
My reaction with this guy would be to get him supine, then trendelenburg, a fluid bolus, amiodarone because I'm not convinced he's not WPW, and take it from there.
Etomidate BTW is a great idea for sedation, but I would give "a whiff" compared to its more traditional dosing and see how well the patient tolerates it. Though if my patient is very unstable, I will go to the "ask forgiveness later" way of thinking and proceed to immediate cardioversion.
My thoughts on going the distance to the cardiac center is that if things aren't easily remedied, we haven't wasted any time-he's already at the final stop for complete care.
Ok, back under my rock.
Ok
Ill give more time for the discussion on stabe vs unstable and cardioversion but will definitly come back to it at the end of this case. It may surprise some of you
Next question.
Lets consider the pharmacology for a sec
We have 5 potential Dx here:
1) WPW
2) Afib with runs of Vtach
3) Runs of Vtach (polymorphic maybe)
4) Or is it an SVT with abbarency like a LBBB?
5) Or is it some combination?
So.....
Adenosine for SVT
Amiod. for Vtach
CCB for afib
Procainamide
Depending on the Dx some of these drugs could kill the guy. Which ones and why? He is also on some meds which dont work so well with some listed here. Which would they be and whats the mechanism?
If we had to make a decision how would you know one rhythm from another? The evidence is there, but what is it?
Bwhahhahaha Muhahahahhahahah
Ahem.. couldnt help it.
In reply to Mike's question regarding the stable vs. unstable question. If you have a systolic bp of 60 and are perfusing your head and heart and can still mentate and talk would that still be considered stable because you can mentate? talk? This is if I remember correctly a scene call, so signing a consent for cardioversion as you would in a controlled setting is not concern number one. Being able to justify cardioversion should it be needed with objective and subjective info might have to be good enough this time.
I think in this situation even though your patient can talk and mentate, doesn't he have what the ACLS handbook would call "serious signs or symptoms" that determine that unstable vs. stable question? Shortness of breath, dizzy, hypotensive, near syncope, cardiac hx and arrhythmia hx, pale and diaphoretic, and an ugly looking ekg. Enough stuff that cumulatively adds up in my book to qualify as unstable.
Having said that,I'm personally not quite ready to spark him yet . I do agree that we have some time to try some medication first. I might be inclined to try amiodarone in case this is a wpw related rhythm. That as you would say is my .02 on the matter.
I like SVT with LBBB and a run of VT. I still vote for amiodorone since he is looking at us and has a SBP >80. If that does not work then he gets some sedative and some electricity.
Good question rod
ACLS actually looks at unstable in different measures. So there is alot of "grey" area. Its boxes for the masses and not critical thinking like it used to be.
Strickly speaking, it is less important what the vitals are and more important to assess the patient. If the goal of BP is to cause neuro (end organ) perfursion hen mentating is stable. So who cares what the BP is if they are mentating laying flat.
However, a BP of 60 systolic is not compatible with mentating. A MAP of > 55 is typically needed to be mentating. A systolic of 60 would be a MAP of about 45.
Back to "treat the patient not the monitor" eh
As for a signed consent, its the principal. You cannot intubate a patient (or cardiovert one) who looks at you and says "you cant do it". Signing isnt needed, informed consent certainly is for an elective procedure (which this is if he can mentate).
What if you were to weld him to the stretcher (which has signifigant risks associated with it) and caused an iatrogenic degredation to Vfib then death. It wouldnt go over well in court when another provider testified that it isnt standard of care to "shock" people who are talking to you as a first intervention.
Obviously I know you are not saying you would. Im just pointing out that the definition of Stable goes well beyond a vital sign set and really rests with the patients mentation (a true indication). Now it may be that they will only be "stable" for a very short period of time, but shouldnt the less invasive plan be attempted first?
There are times when a patient may appear stable and be cardioverted as the initial intervention, but this would have to be justified with science and backed by standard of care to take such a risk.
Is this one of them?
[QUOTE BY= rodekingdz] In reply to Mike's question regarding the stable vs. unstable question. If you have a systolic bp of 60 and are perfusing your head and heart and can still mentate and talk would that still be considered stable because you can mentate? talk? This is if I remember correctly a scene call, so signing a consent for cardioversion as you would in a controlled setting is not concern number one. Being able to justify cardioversion should it be needed with objective and subjective info might have to be good enough this time.
I think in this situation even though your patient can talk and mentate, doesn't he have what the ACLS handbook would call "serious signs or symptoms" that determine that unstable vs. stable question? Shortness of breath, dizzy, hypotensive, near syncope, cardiac hx and arrhythmia hx, pale and diaphoretic, and an ugly looking ekg. Enough stuff that cumulatively adds up in my book to qualify as unstable.
Having said that,I'm personally not quite ready to spark him yet . I do agree that we have some time to try some medication first. I might be inclined to try amiodarone in case this is a wpw related rhythm. That as you would say is my .02 on the matter.
[/QUOTE]
Mike,
I agree with you as far as 1. I'm not ready to shock this guy, 2. there's time to try other thing's i.e. meds, fluid challenge, etc.. 3. that acls gives you guidelines, not absolute black and white. The point I was really getting at is that given the complex scenario, complicated patient condition, limited history, and the prospect of further patient condition deterioration, cardioversion is certainly part of the decision tree and could be considered. It's not what I would try first, but I understand the rationale that the previous posts have used to come to that decision.
As far as mentation goes with low bp, I will go with experience of taking care of patients who are alert and oriented at a reliable systolic of 60. Not by any means feeling good in that condition, mind you, but knowing exactly whats going on.
Good discussion points for a complicated patient. Still leaning to Amiodarone, and possible dig toxicity issues.
We used to determine stable vs. unstable by the rate, if the rate was over 150 then they were considered unstable. Obviously that is not the case anymore, but I would still say this guy is right on the line, leaning a tad more towards stable. Now if we were to use that outdated rule defined by rate, it appears that his rate actually varies from about 150 to, at times, 300! So, then it would go to reason that he is stable sometimes and unstable sometimes, hence possible the period of syncope. A key point here, though, is that the rate VARIES. Therefore, I am going to hang it out there and say AFIB with rapid ventricular respone and go with the CCB (calcium channel blockers), maybe diltiazem 0.25 mg/kg.
"Depending on the Dx some of these drugs could kill the guy."
....which is EXACTLY why cardioversion is a better option than any medication, IMO.
Stability is not necessarilly defined by whether or not someone is mentating. Just because they are perfusing their squash RIGHT THIS MOMENT means nothing in terms of what might happen a couple minutes from now. Some of the sickest, most traumatized people I've seen were quite lucid, but with lethal injuries that hadn't quite manifested themselves yet, they were anything but stable.
First off, electrical therapy IS less "invasive" than pharmacologic therapy, hands down.
IMO, anyone in a dysrythmia that is clearly affecting their perfusion AND which clearly has the potential to deterioriate quickly meets the definition of "unstable".
Plus, even if we were to stick to the "able to mentate" definition, this guy is dizzy, right? So his cerebral perfusion is likely compromised at least somewhat (he's probably very orthostatic, so I'll just stand him up quick and when he passes out then he won't be mentating and we can cardiovert him ).
I've heard many cardiologists and ED docs say that electrical therapy is safer (if not more effective) in most any acute case than pharmacologic therapy.
[QUOTE BY= Mike MacKinnon] Ok
Ill give more time for the discussion on stabe vs unstable and cardioversion but will definitly come back to it at the end of this case. It may surprise some of you
Next question.
Lets consider the pharmacology for a sec
We have 5 potential Dx here:
1) WPW
2) Afib with runs of Vtach
3) Runs of Vtach (polymorphic maybe)
4) Or is it an SVT with abbarency like a LBBB?
5) Or is it some combination?
So.....
Adenosine for SVT
Amiod. for Vtach
CCB for afib
Procainamide
Depending on the Dx some of these drugs could kill the guy. Which ones and why? He is also on some meds which dont work so well with some listed here. Which would they be and whats the mechanism?
If we had to make a decision how would you know one rhythm from another? The evidence is there, but what is it?
Bwhahhahaha Muhahahahhahahah
Ahem.. couldnt help it. [/QUOTE]
Hey SM
We usually agree on just about everything, but we have a difference of opinion here.
[QUOTE BY= supermedic] "Depending on the Dx some of these drugs could kill the guy."
....which is EXACTLY why cardioversion is a better option than any medication, IMO. [/QUOTE]
This is true. However, I would suggest that this may be the case in every patient. In order to use this as a reason one would have to know the whys. What drugs? Why? What is the rhythm that may make cardioversion the first line intervention?
[QUOTE BY= supermedic]
Stability is not necessarilly defined by whether or not someone is mentating. Just because they are perfusing their squash RIGHT THIS MOMENT means nothing in terms of what might happen a couple minutes from now. Some of the sickest, most traumatized people I've seen were quite lucid, but with lethal injuries that hadn't quite manifested themselves yet, they were anything but stable.[/QUOTE]
Good response. However, i would say that as long as a patient is mentating they are stable at that time. Now we all know the clinical circumstances they are in may cause them to degrade quickly. I use mentation as the prime vital sign which goes along with my use of permissive hypotension.
The other potential complication with electrical therapy is if, by chance, his underlying rhythm is AFIB, you could send an embolus from his atria. I could be heading down the wrong path...
Hey Mike, good discussion indeed. Great job as always with this case.
As far as meds being safer than cardioversion: I recall learning that cardioversion is normally safer when it is an option. Dont know if I can back that up, but I know I've heard/read that numerous times. At any rate it's definitely safer than giving a drug you aren't sure is the right one because you aren't 100% sure of the rhythm...as you said, the wrong drug can kill this guy.
As far as stability for cardioversion: I would concede that he doesn't need it right now. I would be cool with just applying the fast-patches and zapping him if he deteriorates any further.
If we can decide with confidence what rhythm he's in, then great, we can give him the right drug, but I thought we weren't sure yet...
I don't know. I guess I'll have to wait and see how this one pans out.
Hoss
There is no doubt this is an issue and may well make you reconsider a cardioversion until you feel it just has to be done.
Not the wrong path, just critical thinking
[QUOTE BY= Hoss] The other potential complication with electrical therapy is if, by chance, his underlying rhythm is AFIB, you could send an embolus from his atria. I could be heading down the wrong path... [/QUOTE]
We are on the same page
So... How do we know what they rhythm is? Before we treat it would be good to know for sure.
If you have a theory, explain why you think you see it.
So far alot of people think its underlying afib with Vtach. If thats true, how do you know?
Alot of people mentioned WPW. Is WPW ever irregular? Are you sure you see delta waves? Is there a time when WPW may well be irregular?
Dont worry, i have the EKG all done up with indicators so ill make it as visual as i can at the end
[QUOTE BY= supermedic] Hey Mike, good discussion indeed. Great job as always with this case.
As far as meds being safer than cardioversion: I recall learning that cardioversion is normally safer when it is an option. Dont know if I can back that up, but I know I've heard/read that numerous times. At any rate it's definitely safer than giving a drug you aren't sure is the right one because you aren't 100% sure of the rhythm...as you said, the wrong drug can kill this guy.
As far as stability for cardioversion: I would concede that he doesn't need it right now. I would be cool with just applying the fast-patches and zapping him if he deteriorates any further.
If we can decide with confidence what rhythm he's in, then great, we can give him the right drug, but I thought we weren't sure yet...
I don't know. I guess I'll have to wait and see how this one pans out.[/QUOTE]
One could place on O2, IV's, and apply shock patches. Then ask the pt. to walk to the bird. When he passes out, light his ass up. Then reevaluate and recheck EKG. Just kidding
I would start with Mag SO4 to bring up his level. Then slow his conduction with amiodarone. Also, maintain BP with boluses. Package and head to the closest cardiac facility.
Actually, now that you mention it, WPW can be irregular with AFIB. Also, I don't think Vtach can reach the high rates that we are seeing here, about 300bpm, whereas WPW definitely can. So, maybe this is WPW, if so he needs a cardiac center for possible ablation therapy.
Ok Ill take a shot at this after mesuring R-R with my trusty paper calipers I see that the complexes are pretty regular, aside from the run of Vtac it fairly looks regular (sorry I forgot the calipers) I would be hesitant to call this Afib with RVR, I would need a cleaner strip, Am I seeing P waves in lead 1 in those complexes perhaps buried at times or not at all? WPW is a great possibility here Delta wave preceeding the QRS with LAD also, again is there a bundle branch block (EKG) ? I agree with the pre tx O2 Iv's placed I would place the pads on him although he is able to mentate well hemodynamicaly Considering, SOB, hypotensive Diaphoretic ,as precautionary are there Rales inthe chest there Mike???? Definate Baby ASA as someone mentioned before I would start Heparin too. I know a mirade of cardiologist who would Cardiovert here, But I agree with foregoing the procedure for now... Does this patient know if he has WPW? CCB's adenosine, B Blockers and digoxin could be hazardous to the patient, How long has this been going on for less than or greater than 48 hours?? I would go forth with Amiodarone and take the wait and see approach all though AHA recommends DC cardioversion due to posssibility of thrombus. And to answer Yes to AF with WPW it can happen. I await... Oh yea the Mag Sulfate great Idea and transport to the closest Cardiac interventional facility would be most appropriate and.... Mike Did they do any Labs here???
Not having read through all the replies, I'll apologize if this has been asked already:
Mike, how are the heart sounds? Anything funky? Like, say, a click after S1?
Great point Jeff! Mitral Valve Rupture could account for this too any hx of endocarditits and if it wasnt said by now, Is there a Balloon Pump available???
Hey Getoverit
Lemme answer some of your questions:
Ooo good question.
In fact he has had "fast heart", as he calls it, a few times, he has never gone to the doctor about it because it always went away
[QUOTE BY= medicflyt] Hey again all....
Epi raises a good observation....could very well be a delta wave on that leading QRS complex; looking at lead I especially. Someone asked about how long ago this dx was made, ie how long has he been on digoxin. As I said before some more digging into his history might lead us to find that his "heart problems" may have been tachy-arrythmias. Cardizem in WPW is very much a bad thing....
One question for the group: Am I wrong in thinking that WPW is still fairly regular? This rhythm isn't....
At any rate, I still believe that the complexes are narrow so the decision would have to be made: rapid A-fib vs. WPW. Given the two I would much rather give procainamide to A-fib than a calcium channel blocker to WPW.....
I might watch the tracing ( or 12 leads) for a few more seconds to try to get a firm handle on the underlying rhythm, then treat with one of the above ideas.
So Mike.....any history of tachy problems? What interventions or office visits have led to his "heart problems"?
Intriguing about why he's on ASA too.....previous AMI or chronic A-Fib? Hmmmm.........
This is fun!!!! Fly safe everybody....[/QUOTE]
Lung sounds are normal. No labs since we are at his house
[QUOTE BY= supermedic] I admit it...my biggest weakness as a clinician is EKG interpretation...sure, I can pick out an obvious AMI, but other than that I'm just learning how to read them now.
No need to be an expert at EKG's however, to know that this guy needs to be cardioverted. He has a hemodynamically unstable tachycardia, and that always = synchronized cadioversion. A little etomidate and ZAP 'EM (unless of course he's REALLY unstable - which it doesn't sound as though this guy is - then skip the meds and just ZAP 'EM).
After we zap him, some amiodarone would probably be appropriate.
Do his lungs sound wet? Is he edemetous? Has he been peeing? Any history or signs of renal dysfunction?
Before I do too much with this guy I would want to see his dig level and a chemistry, specifically K, Na, Mg, CK, troponin, BUN, and creatinine. Do we have an i-Stat by any chance?
I think you can make a decent case for going to a closer facility than the cardiac specialty center. This guy probably just needs to be watched for a day or two and have some electrolytes replaced and meds adjusted. Any hospital with a cardiologist or good intensivist can do that, and if it is decided he needs a cath or EP lab or other specialist consult then he can be transported to the city non-emergently.
However, we don't know for sure, so I would definitely just take him to the cardiac center.
And for once, I DON'T think I'd intubate him...depending on how he looks after the cardioversion, of course. If it turns out that he needs it for some reason I'd forgo the sux for rocuronium, given that his K may already be through the roof.[/QUOTE]
Goof question Jeff
Nothing obvious on the heart sounds.
[QUOTE BY= JeffBro] Not having read through all the replies, I'll apologize if this has been asked already:
Mike, how are the heart sounds? Anything funky? Like, say, a click after S1?
[/QUOTE]
OK
So it looks like many people are questioning the EKG but not wanting to come out and give the specifics
Here is the EKG with some pointers i made to show some things:
The EKG Review
So on the EKG we see two things.
1) an R-R that isnt equidistant which = irregular
With his history this should make you think A fib. Vtach is always regular so its quickly ruled out.
2) Rates > 300 at times which very very rare for Vtach. > 300 is indicitive of an accesory pathway conduction problem.
Some other things you will note is that Josephson's sign and Brugada's sign (not the syndrome thing) are not there. These are two cardinal Vtach Signs.
Josephson's = Presence of a notch on the downstroke of the S wave. Its used to distinguish an abbarently (LBB conducted SVT vs Vtach
Brugada's = A distance of 0.10 seconds from onset of QRS comples to the very bottom of the S wave that is present in complexes of ventricular origin.
So... We have ruled out Vtach with abbarency (like a BB. We have an irregularly Irregular rhythm with an accesory pathway conduction problem where we have identified delta waves. That means WPW until proven otherwise.
So now the EKG is cleared up (At the end i have one post conversion thats shows his normal rhythm).
What drugs are appropriate and why? What are absolutely not appropriate?
Why is cardioversion in this case where the patients appears to be "stable", considered the first line tx when if it was any other combination it wouldnt be?
What do you mean by any other combination? I am guessing because this has the high potential to decompensate to VFIB. Also, would not want to give IV dig, verapamil, or lido because of the same reason by potentially increasing the ventricular response, could end up in decompensation by increased lengths of very high ventricular rates.
Hey Hoss
What i meant was that in any other case where you had a stable patient with a rhythms that made you unhappy (and them) you would consider pharmacology before electricity. In this particular combo. of Afib and WPW there is some danger in meds.
You are totally correct about those Rx as they would increase rates and worsen this guy!
When we think of the basic treatment principle in WPW AFib is to prolong the anterograde refractory period of the accessory pathway relative to the AV node. This slows the rate of impulse transmission through the accessory pathway and, thus, the ventricular rate. This is in direct contradistinction to the goal of treatment of non-WPW AFib, which is to slow the refractory period of the AVN.
Currently, the meds of choice are in contraversy. Amiod vs Procainamide. Procainamide blocks the accessory pathway, but it has the added effect of increasing transmission through the AV node. So, although procainamide may control the AFib rate through the accessory pathway, it may create a potentially dangerous conventional AFib that may require treatment with other medications and/or cardioversion.
Essentially, the current reccomendation is that patients with Afib/WPW who are somewhat stable or not, should be cardioverted to fix both rhythm issues. Consideration of medical management for this combo should only be in the presence of a cardiologist.
Scary stuff but it highlights the need to know they "whys" eh?
[QUOTE BY= Hoss] What do you mean by any other combination? I am guessing because this has the high potential to decompensate to VFIB. Also, would not want to give IV dig, verapamil, or lido because of the same reason by potentially increasing the ventricular response, could end up in decompensation by increased lengths of very high ventricular rates. [/QUOTE]
Ahhh, yes. Thx, good case! So, are you ready to tell us what you did and how it went? How did this guy do? Did you go to the cardiac center, etc...
"Essentially, the current reccomendation is that patients with Afib/WPW who are somewhat stable or not, should be cardioverted to fix both rhythm issues. Consideration of medical management for this combo should only be in the presence of a cardiologist."
Mike,
Could you please touch a bit more on concerns of cardioversion/rhythym converion in a patient who may have been in persistant A-Fib for a long period of time. I see that he is not on an anticoagulant (unless you consider ASA one).
Is there a grave risk of conversion to sinus rhythym and the R Atrium pumping clots into the lungs/coronary arteries/brain?
Please let me know your thoughts on this.
Thanks,
SFM
Hey
SooperFLTMedic:
huhuh. You are the only one who noticed that! Actually, i forgot to put that in the meds section! He has a Hx of afib so he was on coumadin! Nice catch!
If this was a random new afib which cane with a WPW (which can happen) we would still cardiovert as it would be a new afib. Anyone with an old afib should be on anticoagulant as you noted! You have a keen eye!
As for the Final result
This patient was cardioverted as soon as the delta waves with an irregular rhythm was noted. He converted on the first attempt and was absolutely asymptomatic en route to a level 1 cardiac center.
Here is his post EKG:
The Post Cardioversion EKG
Its a bit small, but you can see the underlying delta waves and therefore WPW (which had been undiagnosed. Also, no afib on the monitor.
[QUOTE BY= rnmedic1839] Ok Ill take a shot at this after mesuring R-R with my trusty paper calipers I see that the complexes are pretty regular, aside from the run of Vtac it fairly looks regular (sorry I forgot the calipers) I would be hesitant to call this Afib with RVR, I would need a cleaner strip, Am I seeing P waves in lead 1 in those complexes perhaps buried at times or not at all? WPW is a great possibility here Delta wave preceeding the QRS with LAD also, again is there a bundle branch block (EKG) ? I agree with the pre tx O2 Iv's placed I would place the pads on him although he is able to mentate well hemodynamicaly Considering, SOB, hypotensive Diaphoretic ,as precautionary are there Rales inthe chest there Mike????
Great and interesting case study. The rule for cardioverting Afib with our facility is they have been in Afib more than 2 hours they get anticoagulated before cardioversion. Less than 2 hours they can get the juice.
[QUOTE BY= Irishrn] Great and interesting case study. The rule for cardioverting Afib with our facility is they have been in Afib more than 2 hours they get anticoagulated before cardioversion. Less than 2 hours they can get the juice. [/QUOTE]
Problem with this thinking is that 30% of people who go into A-fib don't know they are in A-fib (ie they are completely asymptomatic) and they wait a week or 2 or more to have any symptoms.
so using patient perception of "my heart is fluttering" or whatever is NOT a good indicator of duration of A-fib. Usually people who go into A-fib don't go right into a RVR they are just in A-fib. They never knew it.
As a person example to illustrate my point. My grandmother had A-fib on a routine physical and had no idea she was in it. never had any symptoms. who knows how long she'd been in it.
However, if a patient is unstable and they're in A-fb you cardiovert without concern for any emboli. Life over possible clot is the rule. Hopefully, you can pharm them to slow down, but if no line or decompensating quickly you have to shock.
WHAT A FANTASTIC CASE STUDY!!!
THESE ARE AMAZING LEARNING TOOLS!!!
THANK YOU MIKE!!!!!!!!!!!!!!
SFM
Im glad everyone likes them
My initial plan for this was simply to setup a way that flight crews could do an interactive review of difficult cases. Essentially, keep fresh on medicine. It also does exactly the same thing for me, and then some!
What it has turned into is an AWESOME way to have excellent clinical discourse with some of the best people in EMS
Special thanks to MDEMT-P and Randy for their input. It is excellent to have physician involvement on this site and i only wish there was more!
Awesome work everyone!
[QUOTE BY= SooperFLTMedic] WHAT A FANTASTIC CASE STUDY!!!
THESE ARE AMAZING LEARNING TOOLS!!!
THANK YOU MIKE!!!!!!!!!!!!!!
SFM[/QUOTE]
Hey Mike ( and anyone else you may want to throw in on this question...)
Although you didn't say he was on coumadin, you did note that he took ASA. Knowing this, is that a proper level of "anticoagulant" therapy? In other words, I would have thought that throwing an embolism had a low chance because of the ASA. Would anyone else be nervous in thinking this way? Please enlighten me everyone!!
Great case, Mike.
Fly safe everyone...
New to the forum. Question. When individuals offer a treatment modality does this suggest that it is done prehospital? For example, this case, are you suggesting this individual be cardioverted prehospital?
Thanks in advance for taking time to school the newbie.
Brush after you Barf!
Hey
just noticed yer post
He actually was on coumadin but i forgot to write it in, super caught it tho. And no, ASA isnt good enough
[QUOTE BY= medicflyt] Hey Mike ( and anyone else you may want to throw in on this question...)
Although you didn't say he was on coumadin, you did note that he took ASA. Knowing this, is that a proper level of "anticoagulant" therapy? In other words, I would have thought that throwing an embolism had a low chance because of the ASA. Would anyone else be nervous in thinking this way? Please enlighten me everyone!!
Great case, Mike.
Fly safe everyone...[/QUOTE]
Hey
Ij this particular case the tx would be to cardiovert pre hospital for sure.
[QUOTE BY= n2b8tm] New to the forum. Question. When individuals offer a treatment modality does this suggest that it is done prehospital? For example, this case, are you suggesting this individual be cardioverted prehospital?
Thanks in advance for taking time to school the newbie.
Brush after you Barf![/QUOTE]
I am way late on this, but I have a comment to Mike's "unstable" vs "stable"
Isn't it what AHA feels is unstable vs stable. If I can remember, if a pt is having chest pain, is diaphoretic, hypotensive etc, these all fit the "unstable" criteria. Granted he is mentating, so i would go with cardioversion.
FlightWeb - Forum
http://www.flightweb.com/forum/viewtopic.php?showtopic=17316
