90 year old female CC: Seizure

This interesting case is thanks to Dana from Redmond Medic One, we hope you enjoy it as much as we did!

You're dispatched with a nearby engine company to an assisted living facility for a 90 year old female who has had a seizure. Dispatch notes indicate the patient is alert at this time.

You're by the officer off the engine outside, who leads you in to the dining area. You see an awake elderly female, seated in a chair, being assessed by the engine company. Her husband states she had a seizure which, "lasted maybe 10-15 seconds, her arms and legs were jerking the entire time."

While your partner gets a report from the firefighters, you introduce yourself and ask the patient how she feels.

"Well, I felt ok earlier. Never had this happen before."

  • PMHx: COPD, diabetes, "heart attack", CABG, dementia, "mass in my lung"
  • Allergies: NKDA
  • Medications: Coumadin, "nebulizer"
  • Last ins/outs: was eating dinner when this happened
  • Events: sudden onset, tonic/clonic activity, no apparent post-ictal period

Your partner relays the initial vitals:

  • Skin: pale, cold, dry
  • Pulse: 123, irregular
  • BP: 94/64
  • Resps: 24, unlabored
  • SaO2: 96% on 3 L/min via NC
  • BGL: 188 mg/dL (10.4 mmol/L)
  • Temp: 99.7° F tympanic

As the monitor is turned on it begins chiming. Electrodes are quickly added for a 12-Lead.

When asked about the rapid heart rate, her husband states, "she's had a fast heart before when she takes her nebs, but never this fast."

One of the firefighters obtains a repeat set of vitals:

  • Pulse: 200, weak radials
  • BP: 92/68
  • Resps: 16
  • SaO2: 98% on 3 L/min via NC

You're less than 10 minutes from 2 hospitals, including a PCI capable facility.

Your patient states dryly, "I feel pretty tired."

What is your interpretation of the rhythm and do you agree with the monitor's interpretation?

Is this a load and go situation?

What do you do next?

51 Comments

  • TidalMedic says:

    VTach, decreased BP, MS change, light ‘em up! Take pt to PCI facility, antidysryhthmics, additional electricity as needed.

  • Lucas says:

    I think it favors vtach as it appears to show some left axis deviation and it appears to be fairly regular when viewing on my phone. The rate is a little over 150bpm. Treat with high flow o2, iv, monitor, amiodarone bolus since her pressure is tolerable (alert while sitting up). If conversion start amoodarone drip. If not consider synchronized cardio version. After conversion repeat twelve lead to look for signs of ischemia or infarct and transport to pci per protocol. I would say this is not a load and go situation since we have the tools to treat this patient. If signs and symptoms of acs are noted after conversion treat accordingly

  • Newer EMT-I says:

    Vtac.  Due to age/assisted living home/PMH…I would ask if there are any DNR's or Advanced Directives.  Load and go.  IV, O2/NC ok, Have the pads on and ready as well as a BVM and airway kit open and ready, Amioderone drip, I wouldn't cardiovert since I's are not allowed in our system to do that (but I would want to based on she seems unstable).  Emergent to the closest appropriate facility.  

  • Do Cottle says:

    It is worth noting that in stable monomorphic VT, procainamide is the preferred agent. It's in the AHA guidleines for the managment of vantricular arrythmias, but apparently it's a well-hidden secret.
    If it turns out that this IS AF w/ aberrancy, procainamide would be preferable if there was any concern for WPW.
    Alas, no one is trying to sell you an expensive brand of procainamide anymore!

  • Bobby says:

    I do not agree with the monitor, but I do believe the pt normal rhythm is Afib. The now Vtach is in response to the low pressure and dehydration. The seizure was induced under the same conditions.
    RX is load and go, position pt supine, current O2 delivery is fine based on Sats, IV access. Fluid bolus to effect and prepare for cardioversion. Attempt to vagal pt down, 150 mg Amioderone on standby, 4 mg of Ativan on standby. 
    Based on pt Hx, this has the potential to go bad fast, so I reiterate, load and go.
     

  • LindseyP says:

    I see it as a wide complex tachycardia.  Pale, cool, "I feel pretty tired", BP systolic in the 90s… go to the Emergency Room patient is not tolerating it well.  The next one:  Pulse is 200 and perfusion is decreased with weak peripherals. 
    While in transit keep the cardioversion in arms reach in case it goes to PEA because the pulses are getting weaker.
    Seizure could be caused by lots of things, but the post-ictal makes me think that it is metabolic and not originating from the brain.  She's at a long term facility… perhaps a med mixup or OD of some sort?  If she has dementia, maybe she has a fluid and electrolyte imbalance of some sort. 
    And I have a question.  Why would you not use Adenosine in this situation?  People are suggesting procainamide and amio, but I thought Adenosine would "reset" the AV node?

  • Bill says:

    V-Tach, unstable due to decreased perfusion and mental status. Apply pads and cardiovert. Maintain or increase oxygen. Load and go. IV and meds during transport.

  • Prehospital RN says:

    Monitor shows VT … I would begin transport immediately and treat with 150 mg amiodarone bolus.  If the rhythm is in fact afib with RVR the amiodarone can also help with rate control but I am pretty certain we are dealing with VT.  I guess the pt could be considered "unstable" due to the apparent syncopal episode (based on hx I don't believe it was true seizure activity) but she is alert and talking to me now so I would rather not light her up if I don't have to … would have the pads in place just in case.  Also sedation prior to cardioversion is an option, but the pt already has some compromised hemodynamics going on so it wouldn't be without additional risks especially in an elderly pt that might be especially sensitive to sedatives, which is why I am going with the amiodarone. 

  • Lance from Raleigh, NC says:

    Hey LindseyP (the first paragraph's the only one addressed to you… the rest is my humble opinion),
         I think that most of the people looking at this are paying attention to the pt's QRS width and axis, which I think the LP has interpreted incorrectly. The 12-lead appears to be 'extreme right axis deviation'. When added to a positive deflection in v1, a negative deflection in v6 and a QRS > 180, ERAD typically leads the prehospital providers (myself included) down the VT route (even though it's not 'technically' tachycardic… perhaps "fast and idioventricular" is more appropriate), which is generally best resolved with K+ and/or Na+ blockade. That being said, I've got a little different perspective in thinking about this patient. Adenosine is not 'incorrect' however. Just remember, we can reset the SA all we like, but "IF" (and I am insinuating my perspective here) the ventricles are where the ectopic beats are originating, it may not have any effect. I teach it kind of like giving atropine to a symptomatic heart block. "It won't hurt, but it's not likely to help"… – if that makes any sense… sorry, it's part of a lecture on a different problem, but I felt like it might fit there :-P
         It's important to remember that this is an EXTREMELY DIFFICULT CASE to objectively QA, but a VERY SIMPLE CASE to arm-chair-quarter back, knit-pick, insinuate-circumstances-within or critique. Remember: The best way to get 10 completely correct and totally different opinions on ONE 12-lead is to set it down in front of 5 cardiologists and listen ;-)
         As far as the seizure's concerned, I'd be interested if hubby's able to relay whether the pt had any complaints immediately preceeding her seizure. It doesn't seem like she had any identifiable postictal period, which leads me to suspect some sort of metabolic or 'mechanical' problem. It almost sounds like it was a seizure that was anoxic in nature, rather than epileptic. Complaints of being dizzy, light-headed, nauseous or having a sudden decrease in vision, hearing or skin color might help me feel more confident in that general impression. They're more common in kids, but I've taken care of more than a handful of adults that have had such (brief) seizures that have been a direct result of a sudden drop/complete-interruption-of blow flow to the brain. Over stimulation of the vagal nerve and VT that causes a sudden drop/stop in BP are documented causes. Personally, I've had more experience with such seizures in the acute, witnessed VT/VF arrests. I actually got into the habit of calling them 'Fib seizures'. I'm not trying insinuate that the seizure would be my primary focus though; it appears to be more of a symptom.
         This pt's above her 'max. sinus HR' (220-90 = 130) and I think that would need to be corrected, as it doesn't appear there was an airway/breathing problem. The reasons that I noted above would lead me toward the treatment of a relative VT that would need to be adressed immediately. Her BP, while technically higher than "90", may not be enough to perfuse her brain adequately. I'd base that completely off of the fact that she's lethargic, has pale/cool skin and likely has some degree of increased ICP from the seizure (I'm not sure of how significant that'd be though after an undisclosed amount of recovery time; just rationalizing my position). My treatment of choice would be a quick initial dose of 'Edison-Medicine' followed promptly by cautiously treating this pt for her midazolam deficiency ;-P
         I'd have a tough time, however, disagreeing with a partner who, after all considered, decided to go the pharmacological route. I'd just emphasise that the pt's heart is '90 and tired' and be sure to put the pads on her chest before we got started.
         Disposition-wise, I don't view this pt's problem to be one most effectively addressed by utilizing the 'load and go' methodology. I think this pt's problem, at the moment, is her rhythm, which appears to be lethal. I'm not sure that whisking her off to the ambulance and attempting to fix her rate while screaming toward the hospital is in the best interest of this pt.
         - And I do have to agree with 'NEWER EMT-I' that this pt's code status and adv. directives are VERY important to discern, but I think we ought to remember to effectively delegate the retrival of those items; The ALS providers in this scenario should be completely focused-on and attending-to this urgent pt. If Hubby's able to provide an accurate, objective pt history, he should (and I am insinuating here) be able to provide a quick 'yay' or 'nay' on her code status. If he's unable and the pt has no problems with her mentation aside from the noted lethargy, ask her something tactful like 'Have you and your family ever talked about what to do if your heart stops?'. If she isn't quick enough to respond or you don't think you can trust her answer, then you're absolutely correct: at our first opportunity, we need to track those down… preferably before heading to the hospital, but certainly not before administering the life-saving interventions neccessary. I know that goes without saying, just remember that a DNR only applies after her heart stops and Adv. Directives typically only address 'manual compressions' and 'intubation'/other life support (though they certainly can include 'electricity').
         This is a great case review – thanks so much for sharing!! I'm really interested in seeing what the rest of her work-up revealed and what her outcome. I can't wait to hear some more perspectives to put into my bag of tricks. It's one of the primary ways I like to get my learn-on!
         

  • Cody says:

    Anyone consider hyperkalemia? Lol

  • Lance from Raleigh, NC says:

    That'd be hysterical, wouldn't it?! lol

  • LindseyP says:

    I understand that it's probably originating in the ventricles somewhere which is why I called it a wide complex tachycardia instead of a sinus tachycardia.  To be quite honest, I never really understood the difference between accelerated idioventricular and wide complex tachycardia.  Perhaps just the rate?  I don't know.  I don't understand deviations from the axis at all.  I am in last semester RN school, and we don't get quite in depth with 12 leads.  We do measurements of PR interval, T wave peaking, STEMI in 2 or more concurrent leads, mirroring, and identification of different types of rhythms.  I would love to learn more about it, and if you have any suggestions on where to learn more, I'd really appreciate it. 
    I didn't think hyperkalemia would result in seizures.  The only electrolyte imbalances I am aware of that cause seizures are hypo and hypernatremia and maybe low calcium, but they said she was eating at the time so I don't see why she would have a nutritional deficit of hydration problem. 
    I had to do a clinical presentation over amiodarone and I think it's really strange that it isn't even FDA approved, but it's use is becoming more prevalent.  I can see it for life threatening scenarios, but the longer term problems associated with it are really strange.  But then again, I've never seen it in the codes I've been in or any other "real life" experience with it.  The EMS are always doing stuff before hospitals.. same thing with IO.. I've only seen it upon arrival and never seen one inserted. 

  • LindseyP,

    "Wide Complex Tachycardia" is like "Supraventricular Tachycardia"; both are just broad categories in which to place rhythms. By definition, sinus tachycardia with a left bundle branch block is a wide complex tachycardia. However, in emergent situations we primarily care about WCT's that are not sinus in origin.

    You're correct that the distinction between V-Tach and Accelerated Idioventricular rhythm is based on rate alone (by the "rules"). VT is usually greater than 140bpm and AIVR is usually greater than 40 but less than 120 bpm.

    I would add the easiest way to differentiate the two is based on circumstance. AIVR is the most common rhythm after reperfusion, e.g. after thrombolytics are given. You can also see AIVR when "slow V-Tach" is present, e.g. a slower wide complex tachycardia during hyperkalemia.

    I hope this helps!

  • V-Tach. Patient is sypmtomatic. Accelerated transport to the PCI facility. IV wide open, O2, ASA. Attempt to vagal her down, if it's unsuccessful, sedate and cardiovert. Be prepared to intubate. If time, get a second line for drugs or pressors in the event that it's needed. Continue to monitor. Contact medical control for further orders. 
    (My system requires an order for antidysrhythmics in this situation) 

  • LindseyP says:

    Thanks C. Watford!  Out of all the stuff they teach us about hyperkalemia and "peaked T waves" they have never said anyting about a slower WCT during hyperkalemia.  Can you explain deviations or a good reference for such?

  • Dana says:

    So Much Fun!! giggle giggle :-)
    You should all be sharing your cases, its a totally different perspective to watch others work it out…

  • Dana says:

    Strong work Lance.

  • woody says:

    puzzled that the computer called this rapid a fib.  it looks like a regular rhythm which would exclude fib quickly.  One reference I like by Ken Grauer, gives a list of common causes of a regular wide complex tachycardia of uncertain etiology.  He asserts that "VT must ALWAYS be assumed as the diagnosis until PROVEN otherwise."  He lists SVT with preexisting bundle branch block and SVT with aberrant conduction as other possible, but unlikely causes.

  • ToddB says:

    @LindseyP-
    A good place to start with toxicologic and electrolyte abnormalities as related to EKG/cardiac arrest is the ACLS-EP course manual.  It can be found at the link below
    http://shop.aha.channing-bete.com/onlinestore/storeitem.html?iid=176477 

  • Rob says:

    VT w/ serious signs & symptoms = unstable (despite an "acceptable" BP).  Load & go, IV access, transmit the strip, consult for versed, & sync cardiovert.  Consider a fluid bolus if the pressure is still low.  Repeat 12-lead if there's conversion…if not apply high-flow diesel to the PCI facility.  Treat according to the repeat 12's & other ongoing assessment findings.

  • Firemedic24 says:

    I am shocked at how many people are so quick to cardiovert. To me she seems pretty stable.

    Only current pt complaint is feeling tired. She is 90 years old and had a seizure. I think anyone would be tired. No mention of chest pain, no mention of SOB. MAP is greater than 70 and she is alert and oriented. While it is important to anticipate cardioversion, I think it might be more pertinent to try amio/lido/procain or correcting the underlying problem.

    I think the computer is off. I see ERAD and VTACH, and I would consider this emergent, but I would also take the time to get a full history and try to find out what the underlying problem is. I don’t think cardioversion is wrong, but I would not jump to it so quickly in this patient. If the patient deteriorates, then I would not hesitate to cardiovert.

  • Medic6595 says:

    V-Tach currently stable. The "seizure" activity is suspect. Lack of postictal activity, no mention of voiding
    IV, O2, Monitor, Amiodarone drip, transport to PCI-capable facility. Be prepared with sedation and electricity in case the patient degrades to instability (AMS, chest pain, hypotension, etc.).
    I would wait to light her up. You may want to avoid sedating a 90 yo with a respiratory history.  Her pressure if probably due to the fact that her rate isn't sustainable. If you can break the rhythm with drugs its probably better. Electricity should be a last resort especially in patients with extensive histories.
    Cool case.

  • Texas Rabbi says:

    Let me play devils advocate for a moment. I’ll take the opposite side of the fence just to bring up a possible point. If she has a history of a CABG, an old infarct, and COPD, she could very well have a wide QRS for her “normal” presentation. Given her age, and the fact a palpable pulse is reported as irregular, she could in fact be in AFib with RVR. Combine that with the “normal” wide QRS, it could appear to be V-Tach. If we look at the history of a reported seizure, and the possibility of A-Fib, it’s very possible she broke loose a small clot from within her heart, and had a CVA. The fact she’s on Coumadin, supports the possibility that she’s predisposed to having them. If her levels are sub-therapeutic, she may have developed a clot.
    So, since I’m very old school, I’d hold off the knee jerk reaction to cardiovert her or even medicate her at this time. If she deteriorates, then I’d consider it, but until that time, a ten minute trip to a Cath lab facility, is what I’d consider.
    Just my two cents worth.

  • cher says:

    "seizure" w/ no post-ictal — does she have an AICD?

  • Christina says:

    I agree with Firemedic, this patient does appear to be stable enough to go the medication route. Obviously if Amiodarone or whatever first line medication your system uses doesnt work or the patients condition deterioates then cardioversion would be appropriate. The patient is 90 years old with a cardiac history cardioversion may lead to no rythym at all. I don't believe the patient had a seizure. She was not post ictal and had no urinary incontinence. Bystanders confuse seizure activity with syncope all the time. She probably had a syncopal because she was having an episode of Vtach causing her to be hypotensive. Someone mentioned Adenoside which doesnt usually work on rythyms originating from the atria or ventricles thus why it is used for rhythms involving the AV node such as SVT. At first glance of the 12 lead it looked like a RAF with abberancy, but either way Amidorone is intended for both. After conversion to a normal rhythm 12 lead would need to be repeated to look for ST abnormalities indicative of a STEMI. I think its time this patient got a pacer/defib and some cardizem to go.

  • Christina says:

     Never trust what the monitor diagnoses the 12 lead as.

  • Emt824 says:

    It does look like v-tach. But the 12-lead is reading a-fiv with rvr. Load and go. She is unstable so the staffest thing might be to sync-cardiovert. Pre medicate with ativan. Do all enroute. No playing on scene.

  • DapDan says:

    Lots of good comments. I agree with Firemedic that the patient appears more stable than unstable. With any WCT I think it is more important to rule in V-Tach than rule out anything else. If it is wide and fast, V-Tach in. With the patient's stability, you can look at things like ERAD, morphology and the like, and neg deflection in I, II, III and positive in V1, more likely V-Tach.
    I have had many docs tell me that Amiodarone for unstable V-Tach is off lable, but what I have found is that is really the only indication other than VF. Either way, I know Amio is extremely toxic and I am an "old school" medic (2005 AHA Guidelines, LOL) so I like my Lidocaine. Must be careful with the geriatric patient's, but a side effect of Amio is it potentates coumadin, I wouldn't want the patient to have bleeding issues in 2 or 3 days.
    So I would continue the oxygen 3lpm NC, establish IV, fluid bolus while administering Lido 1.5mg/kg. Of course defib pads are in place just in case. If conversion, lido drip, another 12 Lead and Tx.
    In looking at causes, can't previous MI/CABG be a precursor to VTACH? I would agree with LindseyP that anoxia might be the culprit of the seizure and the anoxia was a result of the VT.

  • Christina says:

    I forgot this little tip for determining VT vs another wide complex tachycardia. If you have ventricular concordance in your percordial leads its Vtach.

  • Thomas O'Hagan NREMT-P says:

    CALL A CODE, GET THE CART !

  • Thomas O'Hagan NREMT-P says:

    And another thing, whether this is VT or AF w/ Aberrancy, high flow O2 is indicated. I don’t care what her SATS are, you treat the pt not the monitor. This be requires a high amount of stress on the myocardium which in turn needs a lot of O2.

  • Lance from Raleigh, NC says:

    Lindsey P – I've got plenty of stuff for axis, etc… if you wanna look me up on FB, it's lancelynch22@gmail.com. In terms of good instructors, Bob Page (the best), Tim Phalen and Dr. Stephen Smith are a couple of my favorites. Also, check out hqmeded.com for more sweet case reviews. In one of Bob's lectures, he has video clips of teaching various 5 year olds to read axis after spending 5 minutes with the information he gives, lol. Of course, they're all tips/tricks and not 100% accurate, but have specificities over 95%. 
    My advice though, says to get through the nursing stuff FIRST, then SMOKE everyone on the floors/units with your cardiac knowledge ;-) I only say that b/c I'm a few classes away from completing the RN stuff as well and that crap is 'tough', for lack of better.
    As far as being quick to electrically cardiovert this pt, cardioversion's the only treatment we have that won't interfere with other medications, has no half-life and offers immediate improvement. If I were 90 and had a HR of 200, I'd appreciate it if you all would just light me up :-) – One of the things that I try my absolute best to remember in situations like these is that Versed has a very impressive retrograde amnesiac effect, as well as antegrade for subsequent treatment ;-) If BP's a concern after cardioversion (it shouldn't be, BUT), fentanyl's also a strong sympatholytic with little/no BP effect. Another sweet trick to put in the back of your minds is morphine WITH 50mg of benadryl (blunts histamine release, which causes the hypotensive response). I used that one with VERY good luck before fentanyl got big on the prehospital side of the lines.
     
    - So when do we get the low-down on how this scenario played-out?!? :-P

  • WCT. have to put eyes on her to decide between stable and unstable.

  • Jimmy B says:

    Hmmm my guess is VTACH. and since the patient is alert and oriented ; i would suggest drugs and than electricity as needed. Load and Go and Lights/Siren to hospital. High flow O2 instead of NCannula. 

  • Andy J says:

    I'm astounded that so many people think this pt is 'stable'. We have a 90 you pt who has had a previous AMI and CABG. She is in a rhythm that has high metabolic demands and she is in a low output state. A BP of 94/64 in an elderly pt is rubbish!! How much longer do you think the pt is going to be able to compensate? She's not going to be able to vasoconstrict like a 20 year old.
    This pt will end up being cardioverted either now or when she decompensates. If I were in front of this pt I'd give her a sniff of Midazolam (0.5-1mg) just to get some amnesia then sync cardiovert. There's no way I'd be giving this lady any boluses of Amiodaone, run it as an infusion post reversion to aviod any unwanted hypotensive effects.

  • ToddB says:

    @Lance-  no disrespect at all with my comment, just a differing viewpoint.  I believe you have just pinpointed a large part of the problem with EMS education today.  No one (5 or 95) can truly learn axis in 5 minutes.  They may know a quadrant to put stuff into….but they have no idea what it all means.  I have had students come back from national conferences and indicate they now understand BBB – V1 up it's RBBB, V1 down its LBBB.  That's great, but they still have no clue what's going on in the heart or the significance of it. Ask them which ventricle depolarizes last in a RBBB and WHY the terminal deflection is up…. –  silence, crickets chirping….no response.  I would personally rather see folks being educated rather and edutained.
     

  • Lance from Raleigh, NC says:

    Hey Todd, First – No disrespect taken, anyone that wants to try to argue with your reasoning is doing so foolishly. Secondly – I didn't mean to insinuate that one could 'truly' learn axis… in 5 minutes or outside of studying nothing-but axis for much longer than myself or most that I work with care to. I was expecting anyone who was interested to read between the lines and interpret that information as "a great place to look for information that'd introduce one to axis is…(fill in the blank)"

    You eluded to the fact that you're an educator as well. In saying thing, I'm sure you've heard things like 'when are we going ot need this' or 'this is way to much info for me to remember on scene'. I try to remember that when lecturing on 'axis' and other 'dry' subjects. If it's only necessary for providers to understand how to relate a pathologic left axis to an anterior hemi-block and an upright, wide RS complex in v1 to a RBBB and recognize that both together equal a bi-fasicular block, then why gunk up (for lack of better) their heads with more information than they 'need' (or are able to process) at present. After experience and a certain comfort level with the material have set in, I think it's appropriate to further their education.
    I do, again, totally agree with your statement that we need more providers 'digging deeper' and trying to relay the information that they learn back to 'the rest' – which I think is the general goal of Bob Page, Tim Phalen and our other friends.
     
    Forgive any typos that make me look like a two year old…. my keyboard's acting up.

  • Robyn says:

    Is anyone thinking about that low grade fever? 

  • woody says:

    i think the temp of 99.7 is a red herring.  if it's >=100.4 then you've got my attention.
    thinking more about the original irregular pulse of 123, I first assumed due to afib.  it's certainly possible that irregularity could have been due instead to frequent PVCs or short runs of vtach prior to the tracing we see.

  • Frankie says:

    I love this Dana Yost guy… Good work.  Call me if you ever get to San Fran!
     

  • johan theunis says:
    • O2 15l NRMask
    • fluid bolus
    • fentanyl and etimidate small doses
    • cardiovert 200J synchronized
    • magnesium 2gr over 15'

    DD:
    Vtach
    Afib -Aflutter with aberrancy
    beware electrolytes
     

  • ToddB says:

    @Lance – agreed….education should be an evolution based on experience. I’m in Raleigh too…might contact you offline.

    Apologies to the moderators for topic diversion.

  • ToddB/Lance,

    Your sidebar is a common one most EMS educators have at one point or another. "How much is too much?" or "When is teaching the trick right (or wrong)?"

    Sometimes a trick is a great segue into knowing why, sometimes it keeps you from having to learn why. My only fault with Bob Page lectures are they lean heavily on tricks. Same goes for Dubin's EKG book.

    I think the only trick for this patient is knowing just how many joules do we start with?

  • Lance, from Raleigh, NC says:

    Todd – Absolutely; my e-mail's in an earlier post, I'd be happy to get up with you!
    Watford – Well-said, bro!
    My same to the moderators: – Sorry… – and on with the show!! :-)

  • Firemedic24 says:

    The problem with the stable or unstable argument is that it is never quite that black and white.
    I am of the opinion that there is a whole lot of grey area between pre arrest and asymptomatic.
    I don't think cardioversion is wrong, I would just prefer to use antiarrhythmics and treat the underlying problem first.  When I ask myself the question cardioversion or antiarrhythmics I think; 1. Does this patient currently have hypoperfusion leading to anaerobic cellular metabolism and subsequent cellular death. 2. Will this patient decompensate to the point of hypoperfusion causing cellular death in the next 10 minutes.  3. Finally what do I think the underlying etiology is and how will my intervention affect the problem.
    In my mind the patient is not currently hypoperfused to the point of cellular death.  The pt does have less ability to compensate, and I expect her condition to deteriorate.  However, I think I can spare 10 mins to get a loading dose of procain (my preference in this instance) or another antiarrhythmic.  Now for the underlying problem…  Judging from the history and previous MI the most likely cause is myocardial scarring causing a circuit around the old infarct.  An electrolyte imbalance is also possible.  And while a new, acute MI is possible… it is a little lower on my list due to the absence of CP.
    In the first two cases the antiarrhythmics will likely work, in the case of MI antiarrhythmics might work, but I can understand quickly cardioverting to get a clearer picture and terminating the rhythm earlier.  If there is an electrolyte imbalance than cardioversion is just a temporizing measure and the pt is likely to go back into VTACH.
    I think you could go either way, but I try to avoid cardioversion it if I can.  If the pt is deteriorating too quickly or antiarrhythmics are not working you can always change your mind, but if you go down the path of cardioversion sometimes the subsequent choices are made for you.  Also it is really hard to make a determination without seeing the patient.

  • Rob says:

    Clearly VTACH. Apply pads, PT has history of dementia so compared to norm is mental status changed? Establish IV if time allows. Synchronized Cardioversion should be indicated although vitals seem to be somewhat stable, as cardioversion is what this pt needs. along with 150 mg Amiodarone IV over 10 minutes. If IV access is available, sedation would be indicated prior to Synchronized Cardioversion. Monitor PT rhythm for changes as well as overall condition. treatment should be initiated prior to transport, however notify receiving PCI capable hospital of PT. Second IV should be established enroute if PT condition allows. 

  • Medic Student says:

    Pulsed v-tach. Get your Iv established. She is still hemodynamically stable per algorithm. so you can first start with a amiodarone drip 150mg IVPB 100cc bag over 10 minutes, or Procainamide 20-50 mg/min IVPB.  If that does not work then go to sync cardiovert with sedation. Transport to the appropriate facility. Also rule out H's and T's. I guess seeing the pt would help also to know if she seems stable or not. Treat the pt not the monitor.

  • Keith says:

    Guys, this is VT and…. Its stable enough to warrant pharmacological intervention. This is not abarrantly conducted A-fib. The seizure, assuming no history of seizures, was probably second to a brief period of cerebral hypoperfusion second to a short period of marked hypotension following an acute onset of VT before the body pressed.
    Treatment should consist of normal assessment and supportive care and Amiodarone 150 mg over 10 minutes. Dont be surprised if the BP drops some during administration of Amiodarone and it tends to be transient and responsive to a fluid bolus.
    While you can certainly repeat the Amiodarone, for those of you not very experienced with cardioversion…. dont be afraid of it! If at any point this patient becomes unstable or she doesnt respond to a couple of amiodarone infusions a synchronised shock at 100j would probably be highly effective. Yea the patient is alert….. the answer, 10 mg of etomidate slow iV before the shock. We have been doing this for years and its very effective and safe!

  • Anthony says:

    I would call this VT.  Wide, seems to be A-V dissociation and Josephson's sign in the inferior leads which favours VT.  Also the patients age and cardiac Hx give a great then 95% chance of this being VT. 
    The "seizure" was not a seizure, it was myoclonic activity from a syncope related to the rhythm.  Also no prodrome of syncope and no post-ictal period.  Not sure why some people would have midaz ready to treat another seizure.  this is clearly NOT a true seizure.
    The patient should recive from O2, nasal cannula would be fine, aspirin in case of ACS and an amiodarone infusion.  Cardiovert if becomes unstable.  Not sure why some people want to just load and go and the pt only needs PCI if there is any suggestion of ACS causing the rhythm. 
    Lastly, that monitor needs replacing as it is clearly manfunctioning. 
    Cheers
     
     

  • Greg says:

    This is vtac. Pt is unstable from what is described. In my humble opinion I think the “seizure” was not a seizure but a syncopal episode which can many times mimic seizure like activity. I also don’t think it mentions the pt was postictal anywhere.

  • Dane Friley says:

    Def vt. Monophasic r in avr also see some av dissociation there as well!

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