41 year old female CC: Chest pain

Here’s a case submitted by Bob Sullivan from New Castle County EMS.

EMS is called to the residence of a 41 year old female with chest pain.

Onset: Sudden while sweeping the floor
Provoke: Nothing makes the pain better or worse
Quality: Tightness
Radiate: The pain does not radiate
Severity: 8/10
Time: 20 minutes prior to EMS arrival

Past medical history: MI, Pacemaker/ICD
Medications: amiodarone

Vital signs:

RR: 22
Pulse: Very rapid
BP: 150/80
SpO2: Not registering

The cardiac monitor is attached.

A 12-lead ECG is captured.

The patient is placed on O2 via NRB @ 15 LPM and IV access is established.

What do you think the paramedics should do next?

*** UPDATE ***

Paramedics give 150 mg amiodarone over 10 minutes via piggyback infusion.

The patient’s BP drops to 90/48 and the patient’s clinical status is observed to deteriorate.

Synchronized cardioversion is performed.

The rhythm is now narrow complex but extremely fast and unstable.

The ICD delivers a shock and the patient is observed to be in VF.

After waiting a few seconds (to see what the ICD is going to do) paramedics shock the VF.

The rhythm starts to stabilize and the patient’s BP comes up to 142/74.

Are you ready to drop this patient off at the emergency department?

41 Comments

  • Aharon Oppenheimer says:

    that patiant need to cardiovrsion with 100J for the biging with Medazolam befor and after Amiodoron Push of 150 mg and after it dreep 1-4mg/min after to try to make AKG to be shore that she don’t have MCI.

  • Christopher says:

    Fluid bolus (her age predicted MHR is 180, so maybe this is compensatory), if able to transmit her ECG get a consult.

    WCT @ 170, probably VT given QRSd of 0.16 (not 0.25 as calculated), probably 2ndary ischemic heart disease.

    Pharmacological options:
    – Procainamide 20mg/min
    – Amiodarone 150mg
    – Lidocaine 1.5mg/kg
    – Later, magnesium 1-2g

    Orrr electricity. His BP is holding, which given the poor SpO2 readings, leads me to believe she is clamped down and shunting to create that pressure. Depending on transport time we may just hang out and talk.

  • Patrick says:

    Looks like VTach to me, and it looks like this patient has a history of it. Rapid transport sounds good to me. After the O2 and the IV I would go with Amiodarone or another antiarrhythmic, attach the pads, and be prepared for synchronized cardioversion if necessary. If I had the time I’d get an order for some premedication before the cardioversion since she is stable, for the time being.

  • isaiah says:

    I’d say a cardioversion and rapid transport..

  • Royce M. Worrell says:

    Why didn’t the ICD zap that prior to arrival???…or did it???

  • Christopher says:

    Royce,

    Perhaps the tachycardia settings on the pacer are higher than his current rate?

  • Jeff C says:

    I agree looks like VTach to me as well, BP seems to be ok so I would give an Amiodarone drip and transport.

  • Coyotemedic says:

    I’m leaving a comment before I read everyone else’s so forgive me if I repeat a treatment.
    1. If pt is lucid start with medications. Amioderone at 1mg/minute drip. Or maybe lidocaine if allowed.
    2. Apply pads in case pt gets all loosey goosey on us and starts to lose the BP she is working so hard to maintain. Diesel bolus to the hospital with killing us, the pt, or anyone else in the process.

  • Coyotemedic says:

    Oops, comment above should say “Diesel bolus to hospital withOUT killing us.” Please don’t confuse me with the grim reaper.

  • Aaron L. EMT-LP says:

    A-fib w/ Rapid Ventricular Response. Too fast for V-Tach. Irreuglarly irregular in V-1/V-2. Pt is stable, mildly hypertensive. Cardioversion if pt begins to decompensate. O2 w/ capnography, IV access. Amiodirone 150mg bolus or consider Calcium channel blocker.

  • Hillis says:

    Monomorphic ventricular tachycardia .
    Agree with the rest.. Amiodarone 150 mg iv , MgSO4 1-2 iv if the rythm is converted to SR the maintaince dose of amiodarone is 1mg /min for 6 h. followed by 0,5mg/ min for 18h. If not responding then sync. cardioversion.

  • Rose says:

    I agree with Aaron that this is A-Fib. There are definite P waves seen in Lead I and V2. and there is a ventricular beat after the P wave.

  • Billy says:

    I have a question? If you have distinguishable P waves doesn’t that rule out your A-Fib theory? The rate is consistant with V-tach. It also looks perty regular to me, the “irregularly irregular” in V1 and V2 just isn’t there. I would like to point out that the QRS is wide suggesting it originates in the ventricles, I’m not an EMT I just watch Grey’s Anatomy. I could be wrong about most of that? I would agree with the Amiodarone 150mg or Lidocaine 1-1.5mg/kg depending on protocol and if she goes down hill well I hope she likes electricity!

  • Marc says:

    VT by the looks of things!

    In England, A Paramedic would continue with 02 therapy, Cannulate and put a stand by in, and rapid transport. We do not carry drugs for cardioversion or the likes…..

    Continuous reassessment while transporting, and be prepared for the worst….

  • DaveO says:

    This looks like v-tach but I think I’m also seeing p waves in Ld. I (on the 12 Ld)which would beg the question is this possibly a sinus tach with a BBB and the p waves are hidden in the other leads ????…….also on the rhythm strip, the first couple of beats (particularly in avL)appear to be sinus and then the rest have the v-tach morphology.

  • a good rule is that true QRS duration is the longest duration you can find out of all 12 leads, and following that convention, whatever deflections you may see, P waves or not, are part of the QRS, even if in certain leads the complexes are narrow.

    to assume that this is anything but wide-complex tachycardia consistent with VT is a little risky.

  • Hodgie says:

    Not so sure about the VT, possibly A-fib c RVR and abberancy, or SVT c abberancy, mostly because there is no concordance in the precordial leads and the ICD hasn’t gone off. So, either the ICD is flawed or it’s not ventricular in origin. Either way, if unstable cardiovert and call for orders for a drip. If stable, transmit the 12 lead and rapid transport!!!! In the end though, it’s always VT until proven otherwise.

  • M says:

    P waves in A-Fib?
    Looks like VT

  • VinceD says:

    Most assuredly v-tach. Perfectly regular wide complex tachycardia that is slow to reach it’s nadir. Hx also fits, with both known CAD and an implantable defibrillator. The flaw in some people’s thinking is that they are using criteria designed to rule-IN ventricular tachycardia to rule it out. For example, if V1-6 are all positively or negatively concordant, yes, that does increase the likelihood of v-tach, but the opposite does not apply. You cannot say that just because it moves from a positive to negative QRS across the precordials that it is NOT v-tach.
    Anyway, the patient’s chest pain makes them symptomatic, but in my book that doesn’t make them “unstable” or warrant electrical cardioversion just yet. I’d give 150mg amiodarone over 10min, keep a close eye on her, and transport expeditiously. Hopefully she’d respond to pharmacological cardioversion in route and we could make sure she didn’t have a STEMI triggering the arrhythmia before arrival.

  • Ben says:

    I see that the 12-Lead was taken at 23:47 and cardioversion took place at 01:08. At what point during this 1 hour 21 minute interval did the Amiodarone go in? Was it at the beginning, end, or what? And did the patient remain in V-Tach for this entire hour and a half?

  • Christopher says:

    I too wonder what occurred during that time period, but it could just be a looong transport. Sometimes folks can tolerate VT for a good period of time, and the rate on the VT was just about at her age predicted MHR. Granted, if you’ve had an MI in the past your MHR is probably lower.

    I wouldn’t be surprised if the diluent in the amiodarone caused the BP drop and not the VT. My gut says if the VT caused the hypotension there would be a more gradual decline.

    Also, the post shock rhythm is 250+ bpm, weee! The AICD kicked in for that rate, which leads me to believe the original 170ish rate was too slow for the device to initiate therapy. Perhaps her settings need adjusting?

    Post VF rhythm looks to be sinus tach or NSR (maybe accelerated junctional, little bit of artifact).

  • Aaron L. EMT-LP says:

    Sorry guys and girls, I was half asleep when I posted yesterday and I was horrified at what I wrote! A-fib with aberrant conduction I what I was thinking and instead I wrote A-Fib with RVR…sorry! Treatment would be the same.

  • harrison says:

    cardioversion

  • Dave B says:

    For a regular, wide complex tachycardia, is it not wise to assume VT until proven otherwise, since there are no ECG findings that rule out VT? VT morphologies can vary greatly, and assuming anything other than VT until proven otherwise for a regular WCT may be harmful to your patient’s health.

  • nba says:

    as 4 me the 1st ecg trace is vt need xylocard 2% bulus and then followed by 20% and preferd 4 cardio version…

  • Hillis says:

    I should admit amazing work done by the paramedics in this case that makes me wonder what was the role of ED physicion 😛

  • firemedic50537 says:

    Abbarent SVT (RAFIB x/RVR) but would like a better 4lead strip, strong work on their part. Steal the Beta1 affect from Amio. BP drops with Amio. Lay her back and give fluid. Serial 15-leads to ER. If I was lucky enough to have POC testing, check trop, CKMB and electrolytes.

  • Aaron L EMT-LP says:

    I agree with firemedic, definitely atrial in origin. Not sure about SVT vs Atrial Fib, but you can’t go wrong with an Amio bolus and a drip. Just monitor closely.

  • Robert says:

    I have a little question about why everyone is so adamant about calling this V-Tach. Initial 12 lead is showing a QRS axis of -81, Pathological Left. V1 looks as if there’s a right bundle branch block, which leads me to believe moreso that this is an abberantly conducted bifasicular block than ventricular tachycardia. Granted, my treatment would’ve been similar with the exception of perhaps attempting 6mg adenocard before the amiodarone.

    Also, after the first cardioversion, she goes into a rapid, narrow complex tachycardia. I’m REALLY suspect now that the initial rhythm was abberantly conducted rather than SVT suddenly following a V-Tach.

    I’d also agree that the amio caused the decompensation more than the wide complex tachycardia, she seemed like she was compensating well up until the medication infusion, and once she decompensated, ACLS algorithms take over. Great job by the paramedics that treated this patient.

  • Christopher says:

    Applying various criteria to this.

    Clinical findings:
    1). Age > 35? VT (85% PPV): yes
    2). Male sex? VT (78% PPV): no
    3). Hx MI? VT (98% PPV): yes
    4). Hx CHF? VT (100% PPV): no
    5). Hx CABG? VT (92% PPV): yes
    6). Hx angina? VT (100% PPV): yes

    ECG Criteria

    Wellens (3 of 6 match):
    1). AV Dissociation: unclear
    2). LAD: present
    3). Capture or fusion beats: not present
    4). QRSd > 140ms: present
    5). Precordial QRS concordance: not present
    6). RSR’ in V1, mono-/biphasic QRS in V1, monophasic QS in V6: present

    Kindwall’s (2 of 4 match):
    1). R wave in V1 or V2 of > 30ms: present
    2). Any Q in V6: present
    3) Duration of >60ms from the onset to nadir of S in QRS in V1/V2: difficult to assess
    4). Notching on the downstroke of the S wave in V1/V2: difficult to assess

    Brugada’s 4 step (2 of 4):
    1). If RS complex absent from all precodials, then VT: no
    2). If RS present, and the longest precordial RS interval > 100ms in one or more precordials, then VT: YES
    3). If AV dissociation present, then VT: not appreciable
    4). If morphological criteria for VT present both in precordial V1-2/V6, then VT: YES

    Morphological criteria (using V1(V2) positive):
    1). V1 mono- or biphasic QRS = VT: YES
    2). V1 Rabbit ear sign with R > R’ = VT: potentially yes
    3). V1 rSR’ = SVT + RBBB: no
    4). V6 QS or deep S (R/S ratio 1.0 = SVT + RBBB: no

    Pretty certain this is VT given these rules.

    – Baerman JM, et al. Differentiation of VT from SVT with Aberration: Value of the Clinical History. Ann Emerg Med (1987) 16: 40-43.
    – Brugada P, et al. A New Approach to the Differential Diagnosis of Regular Tachycardia with a Wide QRS Complex. Circ (1991) 83: 1649-1659.
    – Garmel GM. Wide Complex Tachycardias: Understanding this Complex Condition Part 1 – Epidemiology and Electrophysiology. W J Emerg Med (2008) 9: 28-39.

  • Robert says:

    Christopher, according to your morphology rules in Brugada’s 4 step, this is an abberrantly conducted SVT, not V-tach. I’m not sure where you’re looking, but in V1, there are only 2 beats with RSR’, and both of them (one most definitely, one is left to interpretation) rSR’. I’m also fairly certainly V6 is a 1:1 ratio QS wave.

    Also, your only options with any wave is either monophasic or biphasic. Using that as criteria doesn’t make much sense, can you clarify what you mean in Wellens?

    I’m also not sold on Kindwall’s criteria either. Based off of what you posted and my interpretation, I’m still seeing SVT with a bifasicular block (RBBB and anterior hemiblock), and Brugada’s seems to agree with me.

  • Christopher says:

    My apologies, rule 4/5 got cut off due to HTML encoding (as a software engineer I should have considered that while writing…) and instead should read:

    4). V6 QS or deep S (R/S ratio < 1.0) = VT: YES
    5). V6 qRS (triphasic) with R/S ratio > 1.0 = SVT + RBBB: no

    As far as V1, it is either RS or RSr’, certainly not rSR’. Left ear is much larger than right ear.

    As for Wellen’s:
    – If it is RSR’ in V1
    – Or, monophasic in V1
    – Or, biphasic in V1
    – Or monophasic QS in V6
    it is VT.

    nb: these criteria use capitalization to denote size of complexes.

    Do my corrections to Brugada’s criteria change your conclusion? I apologise for any confusion.

  • Tom B says:

    You are right on the money, Christopher. This is 100% VT. Not even marginal. This is only bifascicular morphology to the extent that the QRS complex is mostly positive in lead V1 with a left axis deviation. It is certainly not typical in morphology or appearance. Keep in mind, a wide complex tachycardia with (RBBB/LAFB) morphology is consistent with VT that originates in the left posterior fascicle of the left ventricle. Likewise, a wide complex tachycardia with (RBBB/LPFB) morphology is the expected morphology of VT originating in the left anterior fascicle of the left ventricle. So there is no reason this can’t be VT, and in fact it hits many of the rule-in criteria that Christopher articulated (and one would be more than enough for me). Of course, you can make life a lot simpler by adopting the principle that “wide and fast” is VT until proven otherwise (and morphology “tricks” that are prone error and inter-observer disagreement do not constitute proof). They just put patients at risk.

    Tom

  • Travis says:

    I must applaud everyone for the in-depth analysis of this case, and I can only hope that one day I can perform such a thorough diagnosis in the back of my rig. However lets keep it simple (when you hear hooves look for horses not zebra’s), bottom line is wide complex tachycardia- initially stable go with Amio (the only thing I like about this drug in the field is it will work on both atrial and ventricular arrhythmias). Pt condition gets worse, maybe from Amio or maybe because she has been compensating for so long and no longer can. Once again wide complex tachy and unstable = electricity. I can’t see changing anything the medic in this case did. I think they where right on.

  • Christopher says:

    Tom/Travis: agreed! Here is a good lecture on Wide Complex Tachycardias from William Nelson MD, a no-nonsense cardiologist at the Texas Heart Institute. He covers a bunch of cases and by the end you’ll be pretty strong in your powers of ruling in VT.

  • it’s quite interesting how many proponents of non-VT there are here.

  • Gary says:

    Looks more like Afib with an aberrant conduction…V1 does not look like V-Tach, pathological left axis. I am guessing a runaway WPW. Would not give cardizem of course, consider adenisone to slow down the ventricular response and get a better look. Placing the pads always a good option, IV w/fluid bolus.

  • chris says:

    well as a monmorphic vt with sob/ cx pain go with 100 j cardioversion, but there is no pacemaker spikes in the inital 12 lead. The post shock is not vt or a psvt so why cardiovert this ?? If pt did not have cx pain or sob go with lido 1mg/kg then .5 mg/kg q 10 min to 3 mg/kg, not a polymorphic vt so no mag sulfate then do a quick check and she if she can have enoxaparin and tenecteplase and then straight the ccu for a new pacemaker/icd

  • Chris says:

    Gary. I may be at error but you may want to look over contraindications to adenosine. I am sure that you will find that given your thoughts od WPW adensine could produce refractory asystole.
    I too am supprised that there is so many differences. VT heck yes. Shock or drugs, pt was stable BP but pt is symptomatic, i am Amioderone 150mg over 10min fan, titrate slower if BP is dropping and since I usually have two lines on these patients open up one line NS or arrange it as piggyback. I too would have been patient with VF after ICD shock then defib. Is this patient ready to go to the ED, at this point at the end of the scenario, yup im happy.

  • William says:

    I would go..OH BOY..silently. This is VT clear as day. I would place to patient on O2 and get and IV right away. I would go with Lidocaine 1mg/kg of body weight. If that did not work and the patient did deteriorate I would shock it like the Medics did.

  • Pendell says:

    Is it just me or are the synchronization marks on the synchronized defibrillation monitor strip almost exactly on the T-wave instead of the QRS complex?

    I would not have pressed shock with the monitor showing this, as I would have thought it was likely to induce VF. I have seen this phenomenon work with amazing reliability in the EP lab when they are testing to make sure the defibrillator that they just implanted does what its supposed to do when the patient goes into VF.

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