Should you ever give a calcium channel blocker to a wide complex tachycardia?

Some of you are probably wondering whether or not I’d ever condone giving a calcium channel blocker to a wide complex tachycardia in the field.

A recent case submitted by Robert Bees demonstrates a situation where I might consider it (or at least not criticize someone for considering it).

EMS is called to a 90 year old female with a chief complaint of difficulty breathing and weakness.

On arrival, the patient is alert and oriented to person, place, and time.

Vital signs:

Resp: 20 and non-labored
Pulse: 80 and regular
BP: 180/82
SpO2: 96 on RA

BGL: 121

Breath sounds are clear bilaterally.

Past medical history: HTN, asthma

Medications: prednisone, albuterol

The patient states that she used her inhaler prior to EMS arrival with no relief.

The patient denies chest discomfort. She states that she is not nauseated and she has not vomited.

The cardiac monitor was attached and a 12-lead ECG was captured.

The patient is placed on oxygen via NC @ 2 LPM and loaded for transport.

An IV is established in the left arm and 0.9% NS is run KVO.

Shortly after leaving the scene, a rhythm change is noted on the monitor.

Another 12-lead ECG is captured.

The patient became markedly more tired and went from alert to responsive to verbal stimuli.

What do these ECGs show?

The second 12-lead ECG shows a rhythm that is wide (QRS > 120 ms) and fast (HR > 100).

Is it ventricular tachycardia?

How do you know?

How would you treat this patient?


  • Mark says:

    I think I'd do another 12 lead w/ leads V8 and V9 (15 lead). It looks like the Pt. has a Left BBB as well as the Anterior hemi block. With the ST depression in leads V5, V6, and AVL, it appears to be reciprocal ectopy from a possible posterior MI. I don't believe it's V-Tach due to lead I having a positive deflection.

  • Mark says:

    As I looked into this more V1-V4 show ST depression in Posterior MI's. So what does V5, V6, and AVL show?

  • Tom B says:

    Mark – It's a foregone conclusion that when the left bundle branch is blocked, so are both fascicles on the left side (including the left anterior fascicle of the left ventricle).If you think this is a left bundle branch block, then ST-depression in leads aVL, V5, V6 is a normal finding! (Rule of appropriate T-wave and ST-segment discordance).Just out of curiosity, why would a positive QRS complex in lead V1 rule out VT? Why couldn't VT show a normal axis or left axis deviation?Tom

  • Tom B says:

    Mark – I agree that ST-depression in leads V1-V3 (and probably V4) would be "bad" in the setting of LBBB! The ST-segment should be deflected opposite the terminal deflection of the QRS complex, but not more than 0.25 the depth!That means we'd expect ST-elevation in the right precordial leads.Tom

  • Mark says:

    Okay, so I'm going with ischemia to the lateral area of the heart (ST depression V5, V6, AVL. The Left BBB shows there is blockage and also could mask any ST elevation.

  • Tom B says:

    Mark – One of the coolest things I have ever learned about ECG interpretation is to understand the expected appearance of a "normal" bundle branch block (either RBBB or LBBB).There are a lot of people walking around with a bundle branch block who are not experiencing an acute blockage of an epicardial coronary artery! In LBBB, if the QRS complex is positive, then the ST-segment and T-wave should be negative (within reason — the ST-segment should not be deflected more than 0.25 the main deflection of the QRS complex). In this case, the ST-depression in lead aVL and V5, V6 is well within normal parameters for LBBB.In other words, it's a normal finding for LBBB! Tom

  • Jared says:

    Tom, to answer your question about V1…the answer should be in V6. Any negative deflection in V6 is VT. There is a "Key 3 Criterion" in determining VT. 1st is Extreme Right Axis deviation and Upright V1. If this is true, then you have VT, if not go on to 2nd criteria which is Lead V1 Morphology Criteria. If V1 is an upright complex look to see if 1.Taller left peak than right, “BIG mountain little mountain”2. Single upright peak, “steeple sign”3. Single peak with a slur, “fireman’s hat." If you see one of these then there is a 94% likely hood of this being VT. The final criteria is the negative deflection in V6. Aside from the simple fact that this is way to irregular to be VT, it doesn't meet the criteria. Likely cause is A-fib with a LBBB.

  • Mark says:

    I'm still thinking it's not V-tach because Lead I is upright, VI is downward and V6 is upward. None of this fits w/ VT. Don't V1 – V6 need to be in concordance too. They aren't. V1-V4 are downward and V5 and V6 are upward. Doesn't seem to me to be a rhythm originating in the ventricles.

  • Tom B says:

    Jared -Agreed this is AF w/ LBBB (first 12-lead ECG shows same morphology during sinus rhythm).But let's pretend we didn't have an previous ECG for comparison, and let's pretend this rhythm was regular instead of irregular.Click HERE for an example.What would you call this rhythm and why?Tom

  • Tom B says:

    Mark – This is my #1 complaint with using morphology criteria for the differential diagnosis of wide complex tachycardias.Failure to "rule-in" VT does not "rule-out" VT! VT should always be the default diagnosis for a wide complex tachycardia.Tom

  • I agree that CCBs is a consideration, in that this time (bery unusual in EMS) we have a 12 Lead previous to the decompensated state. I agree that this rythmn chnage is most probably SVT of AF origin oweing to the irregular nature of the rythmn, the concistency between the vectors of the previous 12 Lead (1st being NSR and subsequently same vector and morphology) suggesting that the rythmn chnage still remains SVT and irregular therfore AF. Also going back to the arguement of a few days ago that lack of concordnace ( appproriate discoredance) in the chest leads suggest an SV origin. Probably what is lacking of importance is th rest of the vital signs and the presence of ischemic changes, though the lateration of MS is suggesated of hemodynamicaly significant disminishment

  • Tom B says:

    Thanks for the comment, Bostonmedic109! I don't know if you saw, but I clarified what I meant by discordance in the previous case.I was referring to "appropriate T-wave discordance" as opposed to positive or negative concordance of the QRS complexes in the precordial leads.I know that can get confusing! Tom

  • Geoff says:

    I'm late with my reply, but I'm also going with rapid afib w/ LBBB. Based on B/P and past history of the complaint, I'm leaning towards cardioversion because we don't have calcium channel blockers. At 90 years old though, I'd be worried about someone w/ chronic afib and breaking loose a clot…On the example you showed on comment 9… I hate being the first to comment, I'll call it WCT. Appears very regular. Rate seems to be around 240. Accessory pathway of some sort?

  • Rogue Medic says:

    Failure to "rule-in" VT does not "rule-out" VT! That is an extremely important concept – and not just in this part of EMS. For example – failure to rule in an ACS does not rule out an ACS.Failure to rule in asthma, or CHF, or hysterical hyperventilation, or anything else as a cause of respiratory distress, does not rule out that as the cause of respiratory distress.This applies to everything in EMS/medicine.PS While this is extremely unlikely to be VT, the irregularly irregularity does not rule out VT. I have not unpacked most of my books, but I am pretty sure that Marriott has at least one example of irregularly irregular VT.Since the rhythm changed in front of us, I wonder if this rhythm has been going back and forth between slow and fast, between AF and rapid apparent AF. Were her symptoms present when you arrived and she was in the slow rhythm?Have her symptoms changed at all since they began? When did the symptoms begin?Has she ever had similar symptoms before?Is she taking aspirin, Plavix, coumadin, or any other blood thinner?Digoxin?Any halos around lights or other signs of digoxin toxicity? Does she know what atrial fibrillation is?Has she been diagnosed with AF?And so on. The patient became markedly more tired and went from alert to responsive to verbal stimuli. I am hoping that I already asked these questions (yes, they are questions I would ask this patient even without the rhythm change) before the change in level of consciousness.

  • Hillis says:

    Am thinking about wide complex supraventricular tachycardia .I would start the therapy by valsalva manuever , if no respond Adenosine 6mg iv followed by 20ml saline flush . Reapeat with 12 mg adenosine if required.

  • tbern says:

    I would consider a CCB based on the fact that we already have a baseline ECG that shows a LBBB pattern. The second strip appears to be AFib w/ RVR and the patient is obviously symptomatic which means we are going to have to manage it. Is the CCB the best drug of choice? What other options do we have? In my toolbox, Adenosine, Lidocaine, Diltiazem or cardioversion. I would want to rule out or rule in VT right off the bat, it would warrant the most aggressive management. I'm not sure if this choice is the right one but i'd probably go with Diltiazem 15mg slow IVP and go from there. I hate to just throw a drug at a patient but based on my choices, I feel that the CCB would be the most appropriate.Great case!

  • Scott says:

    Assuming her lung sounds are still clear and her change in mental status is from loss of blood pressure due to the loss of atrial kick as well as decreased ventricular filling time, I'd like to place her in a low-fowlers/ supine position, increase the amount of O2 we're giving her, give her a small fluid bolus and wait for the side effects of the albuterol to wear off.

  • Christopher says:

    She might have had a run of AF w/ RVR prior to our arrival, or she might be having some SOB that irritated her heart to cause it to go into AF w/ RVR.I'm confident given initial 3L and 12L, that upon seeing the WCT that it is coming down the same way and not an accessory pathway. Nearly identical in every way.High flow O2. Since she's not really with it enough for valsalva I'm going to consider sync cardioversion immediately, however if we have a line and her BP is still pretty solid, diltiazem 0.25 mg/kg slow slow slow IVP.

  • Tom B says:

    Geoff -Your comment made me realize that I didn't post enough information to make an intelligent decision with regard to making the stable/unstable determination here.A repeat set of vital signs is certainly indicated.I almost always show restraint when dealing with AF. In fact, I can count the number of times I've given diltiazem on one hand. I might even have fingers left over.Why? Simple. If you're reaching for IV medications, the patient is hemodynamically stable. As you mentioned, there's a possibility of the patient thowing a clot with a conversion to sinus rhythm, particularly when symptom onset is greater than 48 hours (sometimes it's difficult to make this determination).What's the rush?As for my link to the wide complex tachycardia with LBBB morphology, I agree the ventricular rate is up there, but it's well within the range for VT.I certainly don't fault you for considering the possibility of an accessory pathway when rates approach 250, but my default dx would be VT.To give you some background, this patient was unstable.The treatment? Synchronized cardioversion. The outcome? Sinus rhythm with a nice, narrow QRS complex.Tom

  • Tom B says:

    RM – I agree that VT can rarely present as an irregular wide complex tachycardia.However, I feel very confident in this case we are dealing with AF/LBBB/RVR simply on the basis that we have a 12-lead ECG showing LBBB with the same morphology in sinus rhythm.You know I'm not a huge proponent of prehospital antiarrhythmics, and there's an excellent chance I would treat this patient with nothing more than supportive care.Having said that, this is one occasion where I could understand someone giving a calcium channel blocker (assuming the patient is hemodynamically stable).So the evidence that this wide complex tachycardia isn't VT or complicated by WPW:1.) It's irregularly irregular (with the shortest R-R interval > 6 small blocks and an absence of delta waves).2.) ECG in sinus rhythm showing typical LBBB and virtually identical morphology with the tachycardia.If you're going to risk the patient's life, you better know with certainty that a calcium channel blocker is indicated.Tom

  • Tom B says:

    Dr. Hillis – I agree this tachycardia has a supraventricular (or non-ventricular) mechanism.However, I would probably forego the vagal maneuvers and trial of adenosine since I feel certain the patient is in atrial fibrillation.That being the case, I would be more inclined to try diltiazem (in the field as an EMS provider).I know you physicians have access to other options! Tom

  • Tom B says:

    tbern – Good comments! Just out of curiosity though, when you say the first thing you'd do is "rule out VT" is that something you'd feel confident doing with a regular wide complex tachycardia (with no prior ECG for comparison)?Tom

  • Tom B says:

    Scott -Very prudent! I'm very conservative myself.Tom

  • Tom B says:

    Christopher – This patient would have to be very unstable for me to cardiovert in the field! Diltiazem? I agree it's an option. Then again, I'm forced to question its usefulness in the prehospital setting.Yes, I've given it. But looking back, was it really necessary?Tom

  • Christopher says:

    Tom,Her acute mental status change prompted me to consider field interventions beyond expeditious transport. Given we had evidence that the AF is new (or at least we had a non-AF rhythm upon arrival), I would feel comfortable about not breaking off a clot.Although, rereading the post, I think I should have considered that her mental status change is related to throwing a clot, esp if her BP remained elevated in the face of AMS.Good clinical case, lots to chew on!

  • Tom B says:

    Christopher – You will recall that the patient's chief complaint included weakness.After the onset of AF the patient reportedly became "markedly more tired and responsive to verbal stimuli".I wasn't there, but this could simply mean she didn't feel well, was exhausted, and preferred to keep her eyes closed, but opened them and answered questions appropriately when questioned.Sometimes you need to see something with your own eyes! Tom

  • Tony D says:

    I think that is Afib with a left BBB (or incomplete LBBB) and since its irregular it shows that its not V tach. if patient has good BP I would go with cardizem. But since here she is unstable already, I would cardiovert.

  • RobertB says:

    A few things to bear in mind with this patient.. (1) No known cardiac history (by her or by her visiting caregiver) (2) She has had 'weak spells' in the past, often put down by family to being overtired, which could be interpreted as previous AF which spontaneously converted to sinus rhythm (3) transport time is 35 minutes to closest facility. Her rhythm/mental status changes occurred right as we left the scene, and very suddenly.

  • tbern says:

    Tom:I just went back and read the thread again and noticed the comment you made about assuming the rhythm is regular, etc. In that case, I would never be confident in ruling out VT. I agree, we should default back on VT until proven otherwise. In the original case, I was more comfortable in doing so based on the previous EKG along with the irregular rhythm. If that makes sense… 🙂

  • Tom B says:

    tbern – Makes perfect sense to me! Tom

  • Jason Primrose says:

    Hi TomWhen I look at this, I see a wide QRS combined with an irregular rhythm, then when you add a young person with a history of fainting spells, that says "WPW" to me. In this case, my biggest worry would be that this VT is really an A fib being super-conducted down an access tract. Now, if this is the case, CCB's are likely to be lethal. Why? because the only hoper for this patient to regain a stable rhythm is for the normal conduction pathway to be able to go fast enough that it can keep the ventricles beating in a somewhat orderly manner, because the His pathway is so much faster than the ventricular cell-to-cell conduction that it can override the extrememly fast impulses coming down the accessory tract. (same idea as overdrive pacing, really). A CCB would knock out the normal conduction system altogether, allowing the extrememly fast atrial rate coming down the access tract to be unopposed => instant VF. While this is rare, it's deadly. So, giving a CCB to ANY rhythm that is wide, fast AND irregular is a bad idea for me.

  • Jason Primrose says:

    Never mind, looked at the first ECG again, no delta waves. Also not young. whoops.

  • Chris T says:

    irreg, not v tach even without abbarancy. No one has suggested amiodarone. if medication is what we are reaching for in one service im with its the only choice.
    unstable sync cardiovert.
    stable amiodarone. 150mg/50D5w over ten min
    If dilt is available, prepare med, and patient isnt totally crashing med control consult with ekg findings.

  • Chris T says:

    Yes i know its not a CCB just wondering if it would be an option and what you thought

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