EKG Interp/scenario take 2
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socalmedic
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will a patinet with a LVAD in vfib will most likely not have very good coronary perfusion due to the insertion of the LVAD higher in the aorta regardless of systemic perfusion. I would treat as "unstable" v-fib.
Hockey
Quackers
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Stupid question and I'll blame this on the excessive studying stress of having to retake it but...with unstable v-fib, that would be the same treatment as unstable vtach? I mean v-fib is usually pulseless apneic patients that I have ran into
Shishkabob
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Vfib will ALWAYS be considered unstable, pulseless and apneac. It's a non-perfusing rhythm. Same algorhythm and essential treatment as pulseless vtach: Shock fast.
socalmedic
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thats why i put "unstable" in quotations. the question was if the person IS perfusing but in v-fib, how do you treat.
Shishkabob
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Are they perfusing adequately?
If so, I say that warrants a call to a doc.
If so, I say that warrants a call to a doc.
jjesusfreak01
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Hmm, clear bigeminy with good P-waves prior to the PVCs (they appear to be from the same focus). Almost makes me want to say WPW or something else with secondary conduction pathways.
The only problem with this is that the beginning of the QRS complexes aren't slurred like I would expect. I would try to brady the patient down just to see what happens, but i'll stick with my original guess for now.
PS: Lack of ST change or Q waves makes me think that the v-fib and v-tach are results of a rhythm disturbance, not an infarction.
The only problem with this is that the beginning of the QRS complexes aren't slurred like I would expect. I would try to brady the patient down just to see what happens, but i'll stick with my original guess for now.
PS: Lack of ST change or Q waves makes me think that the v-fib and v-tach are results of a rhythm disturbance, not an infarction.
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Aidey
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A LVAD is not a pacemaker, the patient must still have a perfusing rhythm to be alive. The LVAD only takes over for the left ventricle, so if the right ventricle isn't beating properly the whole system collapses. Someone with a LVAD may have slightly more blood circulating than someone without one, but not enough to support adequate perfusion.
If you have someone with v-fib who is still walking and talking I suggest checking your monitor to make sure it is working properly
If you had run into someone with a LVAD you would remember, people with them don't exactly travel lightly.
Sinus tachycardia with bigeminal PVCs, possible lateral ischemia.
P waves @ 120/min
Every second complex is wide, occurs with a shorter PR than the previous normally-conducted complex, with a rightward axis. Noncompensatory. These are PVCs, probably originating somewhere in the LV.
Axis for the normally conducted beats is normal, around + 60, give or take a bit.
ST segments are isoelectric. Physiologic q wave in V1, possibly a small physiologic q in aVL (second normally-conducted complex, difficult to see).
T waves are mostly upright, with the exception of aVR (normal), aVL (clear inversion), possibly inverted / biphasic in I (but difficult to see, as the T waves are very small here).
Treatment depends on clinical condition.
P waves @ 120/min
Every second complex is wide, occurs with a shorter PR than the previous normally-conducted complex, with a rightward axis. Noncompensatory. These are PVCs, probably originating somewhere in the LV.
Axis for the normally conducted beats is normal, around + 60, give or take a bit.
ST segments are isoelectric. Physiologic q wave in V1, possibly a small physiologic q in aVL (second normally-conducted complex, difficult to see).
T waves are mostly upright, with the exception of aVR (normal), aVL (clear inversion), possibly inverted / biphasic in I (but difficult to see, as the T waves are very small here).
Treatment depends on clinical condition.
jjesusfreak01
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@systemet
Do you think the wide complex beats are really PVCs? That would be an easy guess if they weren't correlated with the p-waves, which is why I was considering trying a vagal maneuver to rule that out.
Do you think the wide complex beats are really PVCs? That would be an easy guess if they weren't correlated with the p-waves, which is why I was considering trying a vagal maneuver to rule that out.
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I was leaning towards bigeminal PVCs as well seeing as all the intervals seem to be WNL, from what I can tell,but I was under the influence that a PVC covered the P wave...I haven't studied 12 leads very extensively though so take my opinion with a grain of salt.
I think they're PVCs.
(1) The SA node doesn't appear to be reset. If they were PACs or PJCs, I'd expect the P-P interval around the ectopic to be lengthened. This would be a noncompensatory pause (I used the term incorrectly in my previous post --- where I should have said "compensatory"). The P wave morphology also appears identical.
(2) The PR interval for the ectopic is shorter than the PR interval for the previous normally conducting beat. So if this is an aberrantly conducted beat originating in the atria, for some reason AV conduction is improved, at the same time that conduction through the bundle branches is reduced.
(3) The complex only comes a few ms early. While it's possible to have rate-dependent BBB, and it's possible that every second beat could be conducted aberrantly, I don't think this is too likely.
I'm sure someone could take a look at the Brugada criteria for VT versus aberrancy and compare the morphology of the PVCs. I could even be that somebody -- but I'm not sure I want to go and look that stuff up. I just don't keep it in the back of my head
jjesusfreak01
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Right, I wasn't suggesting rate dependent BBB, I was thinking LGL or WPW with possibly a slowly repolarizing AV node or bundle branches (allowing for every other beat to be conducted normally). If it was the AV node that was slow, then it could be either of these, but if it was a bundle branch with slow repolarization it would need to be WPW, because LGL conduction pathways don't bypass the bundle branches. Although I agree this would be unlikely, it explains your #2 bullet point almost completely. I think that PVCs in rhythm with the normal beats and P waves is equally unlikely.
So, you're suggesting it could be either:
- WPW, where one atrial depolarisation passes through the accessory pathway, and one atrial depolarisation passes through the AV node, due to variable conduction in either the accessory pathway or the AV node
OR
- LGN, with every second excitation passing through a BBB system with delayed conduction?
I hope I represented what you were saying accurately. WPW is possible -- but the abnormal complexes have inverted T waves. I'm not sure how many cases of WPW present with altered ventricular repolarisation (I really don't know). With LGN, typically the QRS is narrow, as I'm sure you're aware, but if there's aberrant conduction through the bundle branches, it could become wider.
Both possibilities rely on one atrial depolarisation passing through the AV node, and a subsequent depolarisation passing through an accessory pathway. Again, I'm not sure how frequently this happens.
Yeah. I really don't know. I'd have to do some reading to have a more informed opinion about that. I would have thought that bigeminal PVCs would be much more likely, but I may be wrong.
BTW, this is an awesome site.
jjesusfreak01
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I agree bigeminal PVCs would be more likely, which is why I would try a vagal maneuver to see if the PVCs separate from the P-waves.
I get the idea behind this -- and the idea is good. I'm just not sure doing vagal maneuvers here is going to be safe. If the ventricles are already irritable, and you suppress the sinus node / AV conduction, an ectopic could become some VT.
Just a thought.
If the patient's asymptomatic (granted we have no clinical info here), we're not going to treat anyway, beyond perhaps a nasal cannula.
Sorry, I just realised that the way I wrote that sounds a little condescending. I didn't mean it to come across that way.
socalmedic
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@ systemet, good interpretation you have been studying lately and i like that. however i have one question, maby i missed it, but how are you explaining the the P-waves in front of your "PVC". I think in this case leaving it as Bundle conduction delay would be more appropriate than trying to truly define it. what we have is a wide complex rhythm which came after V-FIB and V-TACH yea the 12 lead is not going to be normal after that... wait 30min to an hour and see what it is then i guarantee it will be different.
here if you have a ventricular rhythm with ROSC you go to the cath lab, and i believe we have found occlusions in 100% of our patients meeting these requirements.
please i am not being a smart ***, but after an arrest there is going to be ischemic, and altered conduction. you have to take the 12 lead at face value and treat you patient.
notice: please disregard any spelling or grammatical errors i dont feel like editing right not
here if you have a ventricular rhythm with ROSC you go to the cath lab, and i believe we have found occlusions in 100% of our patients meeting these requirements.
please i am not being a smart ***, but after an arrest there is going to be ischemic, and altered conduction. you have to take the 12 lead at face value and treat you patient.
notice: please disregard any spelling or grammatical errors i dont feel like editing right not
Sort of. I've been out of the field for a couple of years, going to school. Now I'm thinking about going back to working as a paramedic in a year. It seemed like a good idea to start reviewing things before that!
P waves arise (probably in the ventricles), transmit to the AV node, and undergo AV delay. Around the same time, an ectopic focus in the ventricles fires, creating a PVC. The SA-initiated depolarisation never passes the AV node, the impulse that originates in the ventricles depolarises them, but is blocked from (retrogradely) propagating into the atria by the AV node.
So we see the P wave, as the atria depolarise, but the wide complex that follows originates from an ectopic ventricular focus.
It might be. It's a possibility. Distinguishing ventricular complexes / rhythms from aberrantly conducted sinus/atrial/junctional rhythms is difficult.
I thought this was a new patient? Is this the same patient from the previous ECGs?
This is still a sinus rhythm.
If this is a post-arrest ECG, I agree, there's a good chance it will look different in a while. Treating arrhythmias in the post-arrest period can often cause more problems than it fixes. Without knowing the clinical state of the patient, it's impossible to decide on treatment.
Really?
Perhaps I'm misunderstanding what you've written -- but it sounds like you're saying all of your patients with post-arrest VT have had coronary occlusions on angiography? Is this published anywhere? How many patients is 100%?
Absolutely. I'm not trying to be a d**k either. I agree post-arrest 12-leads may show ischemic changes. I also get that changes on the ECG need to be evaluated on the basis of the patient's clinical condition.
I realise I'm a little rusty, but I do have a little experience. This isn't my first walk in the park
No problem. Please do the same!