Unconscious late 50s male with bizarre wide complex rhythm and ICD – Part 1

EMS is called to the residence of a late 50s male who was found unconscious at the bottom of the stairs by the spouse.

The patient responds to painful stimuli with a grimace.

Past medical history and medications

Past medical history: MI, pacemaker/ICD, renal insufficiency

Medications: Numerous – unable to locate at the time of evaluation

Vital signs

  • RR: 12 shallow
  • HR: 40 and irregular (radial pulses absent)
  • NIBP: Not assessed
  • Temp: Not assessed
  • SpO2: 79% on room air

The cardiac monitor is attached and wide, bizarre complexes.

By the appearance of the ECG paramedics are surprised that the patient is not in cardiac arrest.

They prepare the patient for immediate transcutaneous pacing (TCP).

Paramedics report capture at 60 PPM and 80 mA.

The patient regains consciousness but is not alert.

He is not conversant but nods his head to simple questions and manages to mouth the word, “Sick.”

What do you think is wrong with this patient?

What do you think about the current course of treatment?

For the conclusion click HERE.


  • Troy says:

    I believe those are hyperkalemia waves. Patient is obviously symptomatic for his hyperkalemia so i would start an iv, place O2, continue to pace, and push either 500-1000mg Calcium ro 50mEq Bicarb (I would prefer the calcium). Drive fast!! This guy needs some serious help and will probably end up in the ICU on an insulin/glucose drip.

  • Patrick says:

    I agree with Troy.

  • Hillis says:

    The first thing comes to my mind when i saw the first ECG is malignant hyperkalaemia (very nice typical apperance of hyperkalaemia in this ECG )as the cause of this malignant arrythmia the history of renal insuff. makes me pretty sure of this diagnosis . So as soon as possibe rush the patient to the nearest hospital meanwhile try to stabilize the patient reassure the IV lines , Calcium gluconate i.v has a cardioprotective effect ,measure firslty the BGL then give glucose insufion with insulin the insulin shift K intacellularly.

  • VinceD says:

    I’m also gonna say hyperK. Give him a gram of calcium and ask the med control doc if they would like bicarb. Now here’s the real problem… I’m seriously doubting there is electrical capture with the TCP because the pacing spikes march right through the underlying rhythm and show no T-waves. Coincidentally enough, there are a couple beats that look like they have a nice repolarization wave, but it’s actually just the underlying rhythm lining up just after the spike. The patient probably became more responsive simply because he was now being electrocuted 60 times a minute. Crank those mA’s, you’re not gonna do more damage, and really scrutinize the pulse you’re feeling. The rhythmic contractions of the patient’s muscles can really feel like a pulse, I’ve seen it in 3 of the 5 patients on TCP I’ve encountered, but unless you have electrical capture, you don’t have mechanical capture.

  • Brian H. says:

    Agree with calcium, calcium, calcium, but don’t forget you’ve got an unresponsive patient at the bottom of the stairs. C-collar and log roll precautions would be prudent.

  • Dave B says:

    i don’t know… something isn’t clicking for me… wide bizarre QRS, but no signs of any discordance… and the morphology pre-pacing looks a lot like the morphology of T waves post pacing.. in the original strip, is it possible that they are not wide qrs at all, but giant T waves possibly from MI? just saying… it looks weird to me… i would want to see a 12 lead before treating for hyperkalemia… and what about the patient’s own pacemaker, why isn’t it firing? or is it only visible in non limb leads? seems like a lot of unknowns for me.

  • Christopher says:

    Low and slow…not good. Prepare for CPR. Also I do not believe they have capture. Looks like the underlying rhythm is breaking through. Up the mA or consider an epi drip?

  • Troy says:

    Dave B,

    I was thinking the same thing about the pacemaker. My guess is it’s a low mEv pacemaker and the hyperkalemia has increased the threshold on the cardiac cells so much that the pacemaker can’t fire high enough to reach the threshold potential. I work for a CCEMT-P company (and i’m not a CCEMT-P…yet) but when we transfer patient’s from ICU’s who are on an insulin/glucose drip with hyperkalemia their have been a few that have had some pretty screwy pacemaker rhythms. But thats just my guess 🙂

  • Tim says:

    Although further assesment is neccsary, I agree with the hyperkalemia. Although he is at a low/normal rate it has the wide sine pattern consitent with severly elevated K. Agree pretty much with most treatment so far. I would probably go with calcium chloride before gluconate just because of the higher availability of calcium. Albuterol updraft and a fluid challenge(as appropriate with further assesment). I probably wouldn’t be pacing at this point. I also would want to avoid the bicarb. Although yes, it is a treatment and does work if nothing else is available, it can create its own problems. Ultimately the patient will probably end up on a insulin/glucose drip and a couploe doses of kayexalate.

  • Mark says:

    @ Vince, I’m still just a student @ this point, but one thing harped on us is checking a femoral pulse to check capture. Also, I’m a little curious about whether or not they have capture, since the pacer spikes do seem to be marching through

  • Todd Mills says:

    They have electrical capture (pacer spike before every qrs and the arrows on the bottom show he’s being paced) but do they have mechanical? Maybe they need to increase his pressure by increasing milliamps, rate, a little fluid or on ionotropic med if all else fails. I want to see what he’s showing in all leads and get a bgl. Could be an MI the second ECG is a little clearer looks almost like a LBBB

  • Mitch D says:

    Agreed with Brian H. Let’s not forget C-spine.

  • Bob S. says:

    I disagree with your treatments to this point. With the fall first consideration needs to be c-spine and correction of the shallow respirations. Nothing tells me skin color on how negative an effect there is due to the shallow respirations. His altered mental status could be from a fall down the steps. Those should be done before the monitor gets applied. Underlying rhythm is a sinus brady but he has dropped one whole complex (which would march out). Symptomatic sinus brady would get an IV and I would start with .5mg of atropine. His renal hx. isnt defined enough, is he a dialysis pt? Either way, with renal insuff. I would be hesitant on bicarb. Does he need to be dialized? As I was pushing the atropine I would definately be preparing him for TCP. If first .5mg of atropine had no effect I’d repeat it. With MI hx. would also want to see a 12 lead. If his oxygenation is impared by his shallow resp. correcting that may go a long ways to correcting the bradycardia. I dont think “diagnosing” a problem off the 3 lead EKG is our job. We interpret the rhythm and treat it, which is sinus brady.

  • Kathi R says:

    How about a TCA overdose?

  • Josh says:

    Looks like pacer stopped working and subsequently, acidosis from inadequate profusion. C-spine, bag em, pacer doesn’t appear to be working so dope drip or epi drip, and definitely some bicarb, rapid transport to facility with cardiac capabilities

  • Denise C. says:

    Kathi I was wondering about an OD – not being able to find meds.

  • Ben says:

    In regards to the pacing, I disagree that electrical capture is present. On the ECG given that shows “capture”, I do not see a QRS after the 1st, 4th, 6th or 8th pacing spike, therefore there is not a QRS for each pacing spike. Further, the inherent QRS marches right through the middle of the 2nd pacing spike.

    I disagree that the notion that the pacer doesn’t appear to be working. The pacer is only at 80mA. Why not add a little more current?

  • Royce M. Worrell says:

    I agree with placing a c-collar first and protecting the spine (does the initial assessment make you believe he tumbled down the stairs or that he simply collapsed at the base of the stairs…when in doubt, I provide spinal motion restriction). I don’t think I would have called this sinus brady though…I am leaning more towards junctional/accelerated junctional since the p-waves seem too close to the QRS or non-existent to be sinus based. I don’t see a missed beat, just a delay in conduction between the second and third beats on the initial strip…every other R-R is regular. BGL and 12 lead would be nice, as well as the initial BP. Since I do not feel this is a heart block I would have used Atropine prior to the pacing. As the call rolled on, I would regroup with the changing assessment(s) and treat according to our protocol…very interesting seeing everyones course of treatment…thanks.

  • Stuart Hensley says:

    He is hyperkalemic. That is a sine wave EKG and his K is prolly 8 or higher. Def need CA++, Bicarb and albuterol to drive the K+ back into the cells. Once he is treated in the field he will most likely stabilize and not need emergent (RLS) transport. A cold or non RLS transport will be safer. Stay safe and Merry Christmas.

  • Wade H. says:

    Spinal Immobilization is definitely imperative here. Let’s not forget our ABC’s(Airway, Breathing, Circulation)either. A detailed head to toe physical exam(especially the head). Pulse Oximetry and B/P. Everybody keep up the good work and stay safe.

  • margie says:

    I’m fascinated with everyone seeing large t waves when what I saw was super side qrs with byphasic p wave I’m still a student so this is great learning tool for me thanks for all the comments

  • Kevin N says:

    Looks like you are all pretty much right on. A-Fib is the original ECG. K+ is out of wack, lots of good ideas for stop gap, Ca+, BiCarb, Epi, Insulin Glucose, Proventol, all will work to a degree. Patient is shallow breathing, and renal insufficency, consider CHF/PE…as the patient is probably hypoxic. Thus High flow oxygen and Proventol most likely will increase his alertness and heart rate. Transport patient ASAP and work on the way. Dont forget if you have wet lung sounds and a decent BP, treat the CHF. We can start the treatment for high K+, but without a lab result to confirm it, we may just push him the wrong way.

  • Royce M. Worrell says:

    My first impression at a glance was A-Fib, but when you actually measure it, it is NOT A-Fib…

  • Patrick F says:

    Well i think that you must got right to TCP because he is symptomatic. The first thing c-spine and long board for transport then i would IV 12 lead and give a fluid bolus high flow 02 and would contact medical control. In my state there is not a protocol for hyperkalemia. medics said they had capture with pacing and pts MS is now imporved how about other vitals? But i would try to find out pt meds and also allergies. Contact med control and get the pt to hospital for labs.

  • Troy says:

    As far as the underlying rhythm goes, there is no way to accurately say what it is. Remember with hyperkalemia the following happens when K+ levels increase: P waves dissapear, PR is normal or prolonged (as long as there’s a P wave), QRS widens, ST segment disappears, T wave goes from tall to peaked to tented to flat, and the heart rate slows. Now that being said can you make an accurate rhythm recognition?

  • Christopher says:

    Troy’s right on, anything that low, slow, and fat had better be pulled pork and not a heart rhythm. A likely rhythm interpretation is sinus arrest from all the K+ w/ an idioventricular escape. I think the external pacer is running at almost an even multiple of the escape rhythm which gives rise to the apparent electrical capture.

  • Troy says:

    mmmmmm…….pulled pork 😛

  • VinceD says:

    Just to build off of what Troy said: All of those signs he listed are great to know for increasing our suspicion of hyperK, but don’t fall into the trap that just because someone has only minor ECG changes like peaked t-waves that they are less sick than someone with the classic sine wave pattern from a high K+. I was originally taught, and many people still teach, that there is a nice progression from peaked T’s to a widened QRS to dropped p-waves to the sine patten (or something like that), but in practice you will almost never see that. A patient with hyperK exhibiting only peaked T’s can go into arrest just like someone with the sine wave pattern. There is also little correlation between someone’s serum K+ level and the changes seen on the ECG, so don’t even play the game of guessing the potassium from the ECG.
    The take-home point is the if the ECG looks bad and you think hyperK, treat the patient like they are sick, but if you suspect hyperK for some reason, don’t be reassured just because the ECG looks fairly normal.

  • VinceD says:

    @Mark – Definitely check femoral pulses when attempting TCP, and while in class go along with what your instructors are saying, but personally, I wouldn’t trust a palpated pulse as the gold standard of checking capture. In my vast experience of only 5 TCP patients, the pulse ox actually does a pretty good job of following the physical pulse. When there isn’t capture, the HR monitor may read at 60 or 70, but you’ll see a pulse ox waveform cruising along at 30. In 3 of those 5 pts, when they arrived at the ED, the medics (and nurses, and even docs), would swear they felt a pulse, even though the monitor showed signs there wasn’t electrical capture and the pulse ox waveform didn’t match the pacing rate. Pacing someone is a stressful situation that can affect our perceptions of what is happening, which is why we need an objective measure of whether our treatment is working. (Mental status is rarely that measure. Start zapping many people who are altered and they’ll perk up, even when their pulse doesn’t increase)
    I’ve never actually read into the topic, but it makes intuitive sense to me that there will never be a case of mechanical capture without electrical capture (and if there was, it wouldn’t be sufficient to create any real cardiac output), but it is plausible to have electrical capture without a mechanical response. For that reason, my ideal steps are to try and palpate a slow pulse before TCP starts, keep my hand in that exact spot until I see electrical capture, and hope that I’ll also feel the pulse jump up when that occurs. If you move your hand, it’s easy to get fooled by the large muscle contractions of the torso as the pt is shocked and be unable to find the original pulse. Then I’ll check the pulse ox waveform and see if that agrees with what the pulse should be. If everything isn’t matching up (good electrical capture, good pulse, good pulse ox waveform), it’s time to take a deep breath, step back, and most likely, turn up the mA’s.
    note: while I’ll pretend to know it all, I’m by no means a source of great experience or knowledge, so always defer to your senior instructors and medics who know how to really get things done in the field.

  • VinceD says:

    @ Bob S. – I disagree regarding our role in diagnosing a pt. off their ECG. While the ECG is often not very sensitive, it can be fairly specific for certain conditions when coupled with a patient’s history and physical findings. I definitely agree, we always want to start with the ABC’s and avoid over-treating pts when they could wait until arrival at the ED (a good example is the overuse use of lasix for suspected CHF, it’s not the answer in the field). However in this case, with a high suspicion for hyperkalemia based off the patient’s history and fairly specific ECG, we could anticipate that he will not be responsive to atropine and immediately get an order for calcium and maybe albuterol, which may actually help him. If we’re lucky and his rhythm and rate prettied up a bit, we wouldn’t have to waste time with (ineffective) pacing, and could focus on transporting the patient and monitoring his status, not playing with our monitors.

  • Arthur says:

    Imagine, paramedics jumping right into diagnostics? NOWHERE inody that cannot be healed because you overlooked the basic ten the intial scenario, and or evaluation have I seen the simple stuff…as in SPINAL STABLIZATION? One note even says that he "nods his head."  The one rule I learned in 1976 is to "ASSUME NOTHING." I realize this is an ECG primer, and you will doubtless think me the Village Moron. I just felt that it's worth stating the obvious (the guy fell down the steps) in the overall patient asessment. Wade H. caught what I was thinking. Slow your roll cowboys! You're smart guys from what I can tell, but if you fix a heart in a broken body, that might never heal because you overlooked the obvious, what good have you done? Review the definition for malpractice.

  • Joe pichler says:

    Oxygen, Collar, spine board, IV line, put your foot down, get a set of obs, CPR might be required. With the pacemaker not working, we will have to provide mechanical help (chest compressions) to achieve some sort of output. I think the wide thingy is a wide QRS and a p wave way in front so heartblock as well. Atropine wont hurt. But the interesting thing will be when the patient wakes because someone is jumping up and down on his chest, do you then sedate? Get him to hospital quick, he needs pacing. THE FALL MIGHT HAVE CAUSED THE PACEMAKER TO BREAK, is my guess anyway.

  • Nick Adams says:

    Hey guys (and gals)…..take it easy….geeesh.  This is supposed to be a fun learning exercise.  I think most people are on-board with the diagnosis of hyperkalemia.  The first ECG shows clear sine wave activity with the absence of PW's.  This, with the pt's history of renal isufficiency, is enough to treat for such a condition.  With such wide bizzar QRS's, no PW's and bradycardic rhythm…..there is no reason to NOT give CaCl.  It wont hurt them.  With the suspicion of hyperkalemia, the patient should also receive some sort of sympathomimetic (Albuterol Neb),  NaHCO3 (they will be acidotic with such a high serum K), and when you get to the hospital Dextrose and Insulin.  As far as the other treatments are concerned, such as full spinal precautions, oxygenation and ventilation, IV, ECG (3) (12)….they should always be done when necessary.  Most people had omitted these things because this is a cardiac scenerio and people are concentrating on the cardiac diagnoses and treatment, not because they wouldn't do it.  If the patient fell before he got to the stairs, he may not need full spinal precations……maybe he was going to go up stairs and not down……lol.  As far as the pacing goes, it can be done until the treatments are given (quick fix).  I would say in the second strip, they definately got electrical capture with a QRS after each pacer spike best seen in leads I and III.  What I would do is increase the mV until I got electrical capture, and then ensure you maintain it by increasing the mV by 10%……then check for a femoral pulse away from the jerking chest.

  • VinceD says:

    @Nick – Usually you're spot on, but in this case I disagree with your acceptance of TCP capture in the second tracing. Here's my reasoning:

    – If you ignore that "narrow QRS" complexes, the rhythm is basically unchanged. You still have giant, WIDEEEE QRS complexes wandering across the strip and doing their own thing. With true capture, the underlying rhythm with usually be supressed (as in overdrive pacing).
     – The "paced" complexes are exceptionally narrow considering the disgusting state the heart was in beforehand. I'm not saying it would be impossible for the paced rhythm to appear cleaner than the patient's intrinsic conducion, but it's certainly a piece of the puzzle pointing away from success.
     – The "paced" complexes also lack any real T-waves. There's a slight deflection of the baseline as it returns to isoelectric after each, but we've come to associate paced rhythms with large T-waves and discordent ST-deviations, especially when in monitor mode on Lifepacks.
     – It looks a lot like false capture cases that I've encountered and have been on this site before.

    The rest of your plan is just dandy in my mind.

  • porrohman says:

    The initial rhythm is not sinus. The rate is about 38. We spend a lot of times on wide tacchys, but not brady. I'm going with 3rd degree and a failed pacemaker.
    No, they do not have capture. Look at lead II. Every pacing spike should have a QRS after it. While partner is trying for capture, get a line and start fluids wide open, then try some epi with consideration of dopamine. I'd stay far away from atropine without a 12 lead..
    Get him packaged depending on secondary assesment, number of steps fallen etc as appropriate and get him the hell out of there.

  • O Berthiaume says:

    Very wide complex … To wide … Probably hyperkaliemia or toxine 
    Pacing is good, Calcium and bic should be use too 

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