59 Year Old Male: Unwell

**UPDATE** The conclusion to this case is now posted here.

It’s the middle of the afternoon when you are dispatched to the residence of a 59 year old male with a chief complaint of general illness.

When you arrive on scene you encounter a middle-aged man in obvious distress, lying on a couch. He is pale, gray, diaphoretic, and drowsy. He states that he has felt drained for the past 8 hrs—unable to catch his breath or get up off the couch—with a heavy sensation in his chest. 30 minutes prior to your arrival he vomited and felt like he was going to pass-out so he decided to call 911.

His radial pulse is faint, rapid, and irregular, while his skin cold and moist.

  • HR – 150 bpm, irregular
  • SpO2 – Unable to get a clear waveform
  • BP – 72/42 mmHg
  • RR – 26, labored
  • Temp – 36.6 C (97.9 F)

Breath sounds reveal crackles bilaterally.

Multiple 12-lead ECG’s are performed but suboptimal due to the patient’s increased work of breathing and inability to stay still. This is the best of the bunch:

Initial 12-Lead

BGL is 156 mg/dL.

He is a bit lethargic but properly oriented and answers questions appropriately, albeit slowly.

  • S – As above
  • A – No known drug allergies
  • M – None
  • P – Appendectomy @ 24yo
  • L – Soup 45 min prior, which he vomited soon after
  • E – Can’t recall—states he has felt terrible “all day.”

Regarding the chest heaviness…

  • O – Gradually through the morning
  • P – Nothing makes it better or worse
  • Q – Heaviness
  • R – None
  • S – Unable to quantify
  • T – Worsening x 8 hrs

What are your management priorities for this patient?

What is your interpretation of the ECG?

 

 ***UPDATE (2015/6/29/ 14:00 EDT)***

After carefully transferring the patient to the ambulance and finding him a position of comfort (head-of-bed at 60 degrees—he doesn’t like to lie flat), you succeed in obtaining a cleaner EKG. Does this change your approach to the case?

02 - 12-Lead 02

68 Comments

  • KIM HYEON SU says:

    I think that’s EKG is VT

  • BMB says:

    This is almost certainly VT, although there is a slight chance of it being hyperkalemia there is nothing in his hx to point to that.

    But I am 96% sure this is VT based on aVR being positive and the morphology of the precordial leads, especially v6 being negative and the reverse R wave progression.

    Lead I and aVL both look like there is ST elevation but the baseline is not flat at all so it is hard to say….I guess it could be Spodicks sign and perhaps a slight chance of VT + pericarditis, but I really doubt it.

    I think there is ST depression in the inferior leads as well.

    But I am not in love with the idea of actually saying this is a STEMI until we slow the rate down a bit. Is this demand ischemia from being in VT for 8 hours or is it an MI that caused VT ? Either way we need to slow down the rate.

    I really want to give him amiodarone 150mg rather than synch cardiovert but he is too far gone for that. His BP is pretty bad and he is now in cardiogenic shock.

    I would give ASA 325, a little versed and give it a try to see if synchronized cardioversion works. If it doesn’t I think I would consider amiodarone and a vasopressor to treat the shock and potential worsening hypotension.

    I would also throw in some zofran and probably on to two liters of O2 as I can’t get a spo2 but I think he likely is hypoxic with the pulmonary edema. if I get an spo2 of >94% then no O2. I might even consider a small dose of fentanyl for him.

  • Bryan says:

    Agree with the above with the exception that I would consider a dose Calcium gluconate prior to synch cardioversion. This seems to me a really wide tachycardia so treat as electrolyte/toxic etiology first. Etco2 reading?

  • dan says:

    I’d love to see the numbers on this. I’m going to go out on a limb and say an Abarently conducted afib, probably MI and deteriorating over the 8 hours. I know I’ll probably get hammered but it’s a gut feeling. There is a lot of irregularity to the rhythm and I’d like a bit faster rate than 150 to be completely satisfied with vtach. That being said…treatment wise he is getting cardioversion either way. He’s obviously in failure and too unstable for medication except possibly a pressor depending on how he reacts to the cardioversion.

  • Dean says:

    I also lean towards this being A Fib with BBB instead of V tach. Fortunately the treatment for either in this patient is cardioversion. I would like to have a line and sedate then sync at 100j.

  • Olivier says:

    Got to agree with everyone above on this one, especially when it comes to defining the rhythm as VT: the axis is basically “Northwest” (aVR and aVL positive) and in the so-called ‘z-axis’, the depolarization wave seems to travel from the lateral wall towards the anteroseptal wall (Huge positive QRS wave in right-sided leads V1, V2 and V3).

    There is something weird as it proves quite difficult to me to determine the QRS length – I’ve got trouble to determine the exact J-point in several leads and therefore pointing to the diagnosis of severe hyperkalemia – however the QTc seems a bit long, around 600 ms if I don’t miscalculate.

    Also couldn’t it be a case of double tachycardia, i.e concurrent atrial fibrillation and VT ?

  • Spencer says:

    This is a tricky EKG. I can see why V-Tach is a populR answer, it’s a wide and fast at about 150bpm. But it’s not really regular which makes me nervously move away from V-Tach. But I’m pretty sold on STEMI. I see concordent ST elevation in lead 1, avL, and V4. I also saw that the QRS duration seems wider than it should and am curious as to what electrolyte imbalance may exist?

    With the fast rate and low BP I can synchronized cardiovert the patient. I would follow that with a fluid challenge to try to maintain a decent MAP. ASA would be important and some O2 administration via nasal cannula seems prudent given the unreadable sat monitor. Ultimately, we’re traveling fast to get to a hospital with cath lab capabilities.

    • Spencer says:

      Forgive the spelling errors!

      Also I missed the lung sounds my first read through. This might be a good case for a pressor to help push fluid though. Possibly CPAP if I can get the pressure high enough to use it.

    • Spencer says:

      Addendum: I shared this case with a colleague of mine and he agreed with my assessment of STEMI and resulting heart failure. He then asked why I would be cardioverting the patient? It’s a very valid question.
      I am not cardioverting because I think it’s V-tach. I actually don’t believe this is v-tach as its not regular. The rate is fast but is the fast rate the cause of the heart failure or is the occlusion and resulting failure of the ventricles the cause? My money is on the occlusion given the concordant ST elevation in the leads I mentioned above. The resulting high heart rate is probably the heart trying to compensate for its awful perfusion. I suspect that by sticking to the things that will help augment ventricular clearing and coronary perfusion that will be the best bet.

      So though I put it in my treatment plan for the original post I am going to remove it. This man doesn’t need electricity, he needs to be taken to the cath lab (now) and he needs pressors, some oxygen, some ASA, and ultimately a stent placed.

      I would have the pads placed though. I’m afraid his condition will deteriorate en route.

      (Thanks to Seth C. for the assist!)

  • Spencer S says:

    Afib w/ rvr, abberrent due to LAFB. Primary tx- CCB vs. Cardioversion. Consider dopamine before and after tx. Wish there was a better 12-lead 🙂

  • Xander Loubser says:

    The patient is heanodynamically unstable and requires immediate intervention. According to AHA Guidelines you would Syncronize Cardiovert this patient on 100 Joules. If not responsive you will increase your Joules in a stepwise fashion. This would follow a Rapid Infusion of 150mg of Amiodarone Hydrochloride over 10 minutes then another Maintainance Infusion over 6 Hours (1mg per minute) of Amiodarone Hydrochloride.

    Inotropic Infusion (2-10 mcg per minute) for increased Cardiac Output to retain intrapulmonary fluids building up. Once the Blood Pressure is stable, a diuretic can also be administered.

    CPAP / IPPV to displace fluids back into systemic circulation.

  • JFP says:

    Afib. Complete arryhtmia.
    Wide QRS with R in V1 plus ST elevation. Proximal LAD occlusion and cardiogenic shock. More clues in I and aVL. T- in V1 to V3. Probably more than 6 hours of STEMI.
    Norepinefrine to rise blood pressure without rise pulse rate and emergent coronariography.
    Bad prognosis.

  • Dean says:

    Update ECG: Looking slower and more like an Anterior STEMI with the orthopnea being due to heart failure. No P waves seen so still think A fib,BBB. I would LOVE to see vitals when this was taken. TREATMENT: conservative use of pressors. If Zofran can control nausea give ASA, PLAVIX, HEPERAN..

  • Jordan says:

    Push that calcium! Close up those QRS’s, give him some O2 and get another 12 lead.. He obviously has ischemic changes, so that could make everyone lean towards STEMI, but it doesnt have the reverse lead depression, so im not comfortable reaching for nitro or ASA. I’d say Calcium, O2, versed to calm him down, grab another strip. It honestly looks like a nasty a-fib thats gotten out of hand. Chances are at the ER, he’ll be cardioverted.

  • Bryan says:

    I’m not sure that Sgarbossa’s applies to a vtach/RRW tachycardia or aberrant conduction? Based on my observation of the EKG, there is ERAD indicating pure ventricular activation. Narrow out the QRS complex, then reasses for appropriate treatment. In this case it is problematic to assign causality to the patient’s chest ‘discomfort’ without ascertaining the cause of the tachycardia. Keep in mind AMI rarely presents with tachycardia!

    • Kori says:

      There’s the point! There is are no P waves, and the rhythm is irregulary-irregular-atrial fibrillation.
      If you look, it is rsR phenomen-RBBB, BUT there are huge ST elevations on all leads from V1-V5 (that’s why the QRS complexes look so broad). I and aVL is clearly ST elevation suggesting STEMI. In limb leads you can see the “mirror” ST depressions as well.
      I guess there is a proximal LAD occlusion (extensive anterior MI) and cardiogenic shock. ASA, heparin, morphine, oxigen (if possible arterenol). Straight to cath lab, IABP could be usefull as well! What was the lab’s finding?

  • Katie says:

    Anteroseptal MI with lateral extension. Reciprocal depression in II,III, aVF. Underlying rhythm is rapid AFib c RBBB.

    Treatment—> rapid transport to cath lab, ASA, O2, levophed, zofran

  • Ernie says:

    This is inferior wall MI in the presence of a LBBB and rapid afib. Its easy to over think these and we often do. I would like to see a more regular rhythm before I call VTACH. The qrs is wide in all leads suggestive of a block. The BP is tanked suggesting a right sided event. I would bet that this is a new LBBB for this patient. I would work up for a right sided AMI…THOUGHTS?

    • doobis says:

      yes, it is good to be knowledgeable and think though this but we can easily over think it, too. Dont look for zebras in a herd of horses, leave that to expert consultation once all the more likely things have been ruled out. Also, in the field with a pt like this, you really on a practical level do not have the time to over think as we do in these postings.

  • Andrew Merelman says:

    This is a tough EKG. I would say this is VT with obvious ST elevation in leads I, AVL, and V1-V4. There is reciprocal depression in the inferior leads. This could also be atrial fibrillation with a right bundle branch block. Either way, initial treatment is synchronized cardioversion. Aspirin, oxygen as needed, heparin, IV fluids, transport to STEMI facility. After cardioversion, if his hemodynamic situation has improved, I would consider amiodarone and nitroglycerin as tolerated. I would consider norepinephrine if pressure remains low after cardioversion.

  • Terry says:

    Looks like a fib with a RBBB. I also think he is in CHF from an anterior septal wall MI. Very nice and difficult EKG. Cath Lab.

  • Adam says:

    Anyone saying VT desperately needs to attend another ACLS course. This is clearly a fib with rvr and abberant conduction. Not to mention screaming evidence of a high lateral STEMI, and if you don’t know how to identify that, you should not be interpreting ECGs.

    • Steve says:

      Afib is a possibility but the differentials for a wide complex tachycardia have always been said to be:

      1:VT
      2; VT
      3: VT
      4:VT
      5: abberency

      Especially since he has no reported history of afib.

      Show a 12lead to 5 cardiologist and get 6 different readings. Stop with the elitist attitude.

      • John K says:

        No one knows they have afib until someone finds it. Never discount the possibility simply because you were the first to DX the condition.

    • doobis says:

      completely agree. afib rvr lbbb lat stemi and cardiogenic shock.

      • doobis says:

        oh yeah and also anter stemi.

        these scenerios are a good learning tool but really do not equate to actually being on scene with this pt. remember this guy is relatively young and has no medical hx or takes meds. he does not have a hx of chf but his symptoms started 8 hrs prior. wiyh the stemi starting 8 hrs ago, he likely developed the bbb and possibly afib as well as the cardiogenic shock as a result.
        tx depends on protocols and while it maybe difficult to obtain a good SpO2 reading, usually with some manipulation and placing the sensor in other areas you will be able to get a brief reading.
        at any rate, O2, ASA, Dopamine. Emerg xport to Cath hospital. If he beging to stabilize you maybe able to go down other tx paths. If not and it is in your protocols, RSI is a possibility for poor oxygenation sec to the pul edema. Perhaps with dopamine u will be able to better assess SpO2 levels maybe and cautiously give NTG.
        Why cardiovert given the relatively stable rate – most people that are not excessive in age can tollerate 150 bpm for a while. If u do cardiovert and it does not work after a few tries reconsider what u r thinking.
        My guess he will end up intubated and sent for cath if his bp increases enough.
        Oh, and definately place the quick combo defib pads on this pt regardless.

  • Kevin says:

    I would cardiovert this pt ASAP, rales, hypotension, and chest heaviness.. I would also call this an antero- high lateral MI.. Anterior decending, and circumflex..definitely not VT, it’s irregular..

  • Rick G says:

    Afib RVR, with RBBB with AnterioLateral wall MI

  • Casey says:

    Afib with RBBB and LAHB. Extensive Antero-lateral STEMI with reciprocal changes seen in inferior leads.

    The rate is obviously a concern but this has been developing for 8 hours (possibly with an acute decline starting 30 mins ago), so I feel comfortable getting an IV and fluid started before shocking his angry heart.

    My initial focus would be IV, careful aliquots of fluid (monitoring lungs), ASA, activate cath lab, confirm with the doc that cardioversion is the appropriate next step if perfusion remains poor, cardiovert, if no improvement or decline. Otherwise supportive care and serial 12-leads.

  • Not VT. This is atrial fib with RVR and anterolateral STEMI in the presence of RBBB/LAFB. Possible superimposed hyperK. Needs cardioversion, then repeat ECG. STEMI can sometimes be due to demand ischemia and one must repeat the ECG after rapid rate is slowed.

    • Laurie says:

      Good thinking, Martin! Sometimes the best thing to do is nothing but treat the patient, not the monitor!!

  • Martin says:

    Had a very similar case and EKG just the other day. Docs called it BBB. They pushed calcium chloride and Bicarb and it started to narrow down after 20mins. Luckily I was 3 mins to ER “didn’t push anything cause I didn’t have time.” aka..i didn’t know what it was.

  • Steve says:

    The differentials for a wide complex tachycardia.

    1:VT
    2; VT
    3: VT
    4:VT
    5: sinus with abarency

    Since he’s the right age, doesn’t have history of afib, and MIs can cause VT, I’m leaning towards VT. Luckily treatment for unstable tachycardiaI is the same : shock. If it IS afib, it’s doubtful he’s been in it long enough to have any clots in the atria.

  • Kris Johns says:

    O2. Monitor. IV. 324mg ASA. Diesel. STEMI. elevation in avL, v4, & v5.

  • dan says:

    It’s not V Tach people. I see P waves….. It’s an anterolateral MI, Afib, and RBBB. Establish 2 IV’s give 1L fluid bolus and recheck pressure and transport to the appropriate PCI center. oh yeah ASA if tolerated P.O. and no nitro. No CPAP because you don’t want to increase the pressure in the thoracic cavity.

  • Grady ATL says:

    I think a fib right bundle with septal MI. suspecting STEMI due to elevation in v3-v5. don’t think it is vtach because the precordial leads show near normal r wave progression. asa, fluids, fentanyl, iv, oxygen.

  • Shay says:

    I’ll go with A-fib with RVR, and an Anterior/Septal/Inferior MI. TX the MI since it’s the worst of the evils, and I’m willing to bet the A-Fib may be a result of irritation from the MI. ASA, IV x 2, 1000mL bolus, Nitro when his BP finally supports it (though I doubt it ever will, may consider a low dose Dopamine drip), CPAP. My company is pretty fortunate that our transport times are relatively short…

  • Rob says:

    LBBB. Unknown if it’s normal or not, so with S/S treat per ACS protocols/cardiogenic shock. IV, ASA, lung sounds w/ possibly a 250cc-500cc fluid bolus and/or dopamine at 5-10 mcg/kg. Continue lung sound assessments and rapid transport to Cath Lab!!!!

  • Matthew says:

    First of all we can all agree that this guys ECG is messed up and this guy is sick, the heart rate is irregular so it’s an a-fib issue, lots of what looks like elevation, so I’m going to call this a stemi and rapid transport and follow ami Protocols, oxygen, Asa, morphine, can’t give nitro because his pressure sucks, I’m thinking because it’s rate related, don’t want to do a bolus because the lungs are wet, so 20mg cardiezm to control rate, hopefully will bring his pressure up and we can put him on cpap and give him some nitro. So that’s what I would do, been a paramedic only for 6 months any constructive comments would be aprciated.

    • doobis says:

      would u give rate controlling meds for someone in shock? electricity is painful but if used correctly , ie synch the defibrillator, it is safer than meds because it is short duration nd can be controlled.
      Not saying I woukd try to control his rate however. I think his rate is secondary to anxiety, shock, and the inability to breath. I wiuld focus on other aspects well before I went down that path.

  • Horace says:

    Lots of trap doors in this one.
    My first thought is hyperK+. Very wide, on the slow side, irregularly irregular. Began with generalized symptoms. I’m not confident in VT or STEMI. Perhaps a trial of calcium (chloride or gluconate – we carry the latter). IV fluid, inotropes if indicated. I want to know more about the degree to which this is sudden or gradual, over what time, “all day”? Hmm.

    Looking forward to outcome.

  • Eric says:

    I disagree with most of you. I don’t believe this is V-Tach. If you look in the best rhythm leads (II or III) you will see the QRS is clearly under 120ms. Combine that with the irregularity and I’m going to call it a rapid A-Fib until proven otherwise. The most concerning thing for me is the inferior depression, with Anterior and Septal elevation, as well as Wellens syndrome. I have a large suspicion for an LAD occlusion and would treat him as such. Pads, MONA as appropriate and blood pressure permitting, fluids, and lots of diesel to the cath lab.

  • Floyd Miracle says:

    @Stephen Smith, what would be your treatment of choice to cardiovert this patient?

  • William Lansford says:

    Rapid ventricular Response STEMI.. O2 @2lpm/nc. Continual CM.. IV access, NS@75ML/HR.. NTG SL X3.. immediate transport to closest ER, preferably a Chest Pain Center with cardiac cath team.. And prayers

  • Eric says:

    This is A-Fib with anteriolateral STEMI. I’d give 324mg ASA, 500ml bolus and recheck lung sounds, consider norepinephrine if bolus didn’t improve BP or caused more pulmonary edema, start with a nasal cannula @ 6 LPM. cardioverting this guy would be my absolute last resort because I think it would send him right into arrest.

    His main problem is the MI and Cardiogenic shock not the arrhythmia… ASA supportive care and get him to a cath lab

  • Jenny says:

    Am very happy that my job is to get this guy to y’all!!! And why I think I will stay a basic emt, with some endorsements!!! Will learn how to put the leads on pt, recognized what is bad versus very bad, and of course what is good…… .

  • DudeBro says:

    We cant jump so quickly at shocking this patient.

    It is a fast irregular rhythm, with ST depression in your inferior leads, and elevation 1, aVL, V1-V5.

    YOU HAVE TO CONSIDER, IS HIS TACHYCARDIA CAUSING HIS PROBLEM, OR IS HIS PROBLEM CAUSING THE TACHYCARDIA.

    He is in cardiogenic shock. If you attempt to slow down his rhythm, he will stop perfusing. With no Hx of A Fib, it may be new onset due to the stressed heart. He also states he is not a diabetic, has no Hx of renal issues, i’d consider Hyper K but its low on the differential list.

    Call med control. Then ABC. Airway is clear, lungs filled with fluid. He is hypotensive, but apply CPAP at low level while attempting small fluid bolus. Heart is already stressed, but if the hypotension is effecting mental status, consider Dopamine. Again med control, and cath lab.

  • Scott says:

    Lead II you got no clue, add a 15 lead to see what else you can find out ….

  • CV says:

    SVT w/aberrancy treatment w/adenosin otherwise w/amiodarone!! See Brugada criteria

  • Thomas says:

    VT is dead regular (pun intended). This is A-fib with a rapid ventricular response and aberrancy. He feels crappy due to decreased cardiac output and he has SOB due to pulmonary congestion. CPAP is a good choice me thinks.

    • Nicole says:

      Looks like acute MI and possible aspiration. I say intubate to protect airway and give meds to calm pt and regulate BP with fluids and pressors. Get pt to nearest hospital to stabalize and they can fly him/her to closest Cath lab. Time is life….or death. just do what you know! ABC’s…or I guess its CAB until They decide to change it again.

  • Billy says:

    Interesting case study. I’m leaning toward an inferior wall MI. For those of you who advised NTG with a systolic of 70, you failed, big time. I’m calling it a STEMI. Oxygen, ASA x324 mg, IV access a call to a PCI telling them what I have, transmit ECG and have the cath lab on standby. This is a massive MI with associated cardiogenic shock. He has lost a lot of tissue because it has been going on for hours, that is the key. Look at ii, iii, and AVF. No matter what else is going on here, inferior leads dictate he has lost any preload and his increased heartrate and low systolic are due to that, Frank Starling mechanism, remember? Just my guess, but I’m glad I’m usually close to a PCI.

  • Matt King says:

    This is A-Fib(irregularly irregular) with aberrancy(RBBB) coupled with a STEMI. There is ST elevation in lead I, avL, v4-v5 with reciprocal changes in II, III, & avF. Taking the assessment into account and PMH, this is not a rate/rhythm issue, this is a dying heart issue. That said I still wouldn’t treat the rate or rhythm, as this would probably kill him. This guy needs his MAP to be raised a little(however you choose to do that) and a cathlab now.

    HyperK was mentioned earlier, but nothing in his PMH or assessment suggests HyperK. That said, HyperK is considered the syphilis of EKGs, but would still not treat for it in this patient. Maybe I’m wrong and would like to hear expert opinion on my approach.

    Matt

  • Todd Ellingson says:

    Being irregular argues against VT, though first glance it does look like that. This is likely afib with aberrancy. One could consider WPW with afib with antidromic conduction down accessory pathway, however WPW is usually dx’d when someone is younger – unlikely to be 59 and not know this. Electrolytes, especially high K, is a risk with 8 hours of symptoms including vomiting, however by the time the QRS is wide, the person is typically brady. Still, it would be worth checking. There is some lateral ST changes worrisome for STEMI, and the aberrancy has a RBBB look to it, so activating a cath lab is a good consideration. The treatment for this is electricity – synchronized cardioversion. Meds such as adenosine, CCB and BB are contra-indicated, and amiodarone could be argued to be dangerous if antidromic WPW was a real consideration. Code 3 with call to med control to discuss cath lab as VTach is typically treated currently with cath lab activation (as this is on DDx), there is sign of STEMI (though not definite), and the patient is deteriorating with a likely cardiac cause meaning the Emergency Doc and Cardiologist may decide to take to cath lab regardless. It’s a tough EKG – unsure why so many “negative comments” towards people’s interpretations. Seems a little lack of professionalism.

  • Josh says:

    Looks like anterior lateral STEMI with BBB. Possibly LAD infarct. Positive Avr indicative of a Proximal LAD.

    Clear elevation to high and low lateral leads. I, AVL, V3,4,5,6.

    Reciprocal inferior ST Depression in II, III and AvF.

    Tachycardia could be secondary to hypotension, anxiety, pain or tachyarrythmia caused by hypoxic excitation.

    Descernable P waves, ST segments, Irregularity and inconsistency across all leads rules out AF and VT.

    My stab in the dark would be Sinus tachyarrythmia with anteriolateral STEMI and BBB.

  • Bryan says:

    Calcium has little to no side effects, given the first EKG I think it is reasonable to consider it for first line treatment. Repeat EKG after 5 mins and reassess.

  • James says:

    This is a ugly EKG. Wide complex irregular tachycardia around 150’s. A-fib and a-flutter are possibilities. He’s severely symptomatic. At this point, all treatment is same, electricity. If A fib, it may not want to “shock out” easily. This may be a case where initial cardioversion at max joules would be prudent. Pulmonary edema likely due to pump failure vs volume overload. Careful fluid boluses of 250-500ml likely to be helpful. If non responsive to shock and fluid and still hypotensive, norepinephine would be first choice as pressor (less arrythmogenic effects than dopamine). As for the sgarbossa criteria with the tachycardia, I recall seeing a studying stating in tachycardia you can not relibly call a stemi due to potential for demand ischemia. I would hesitate to call stemi here until rate slowed down some. Hyperkalemia is a possibility, but with info given there is not enough to really look at that angle yet. Maybe before pressors its worth a shot (calcium likely low risk intervention). If after cardioversion, you feel very certain afib or a flutter is cause, 1-2 grams magnesium may be of benefit depending on hemodynamics

  • Holden says:

    I’ve only studied cardiology for a few months and have read Dubin’s book 1.5 times so I’m not an expert by any means. However, can a possible interpretation be a junctional tachycardia with aberrant ventricular conduction and a STEMI? No P waves and aberrancy causing a slightly wide QRS (but not wide enough for V-Tach).

  • Brian Brubaker says:

    At a quick glance it looks like tombstones (R on T). At closer look without calipers, it appears to be accelerated ideoventricular rhythm due to complete heart block. Not enough information to go off of, so cardioverting or pacing might just kill the patient quicker than anything. Transport immediately since his sick heart could stop compensating soon. Support with high-flow oxygen en route. This guy needs a cath lab standing by upon arrival.

  • Jonas says:

    CPAP. IV. Nitro if BP can be controlled. Kidneys may be in acute failure causing extra fluid, or CHF, or both. Big ole triangular looking t-waves would have me thinking calcium. Monitor to see if conditions improve with CPAP. Place pads on patient, and have help with you in the ambulance.

  • Jared says:

    Field Dx: Uncompensated cardiogenic shock. Tachycardia caused by compensation mechanism.
    Probable cause: Complete heart block due to the global nature of the changes.
    Tx: O2 @ 15 lpm NRB and possibly CPAP if pressure rises enough, 324 ASA, amio drip, possible norepi, and diesel. Put pads on in case he tanks.
    Definitive Tx: Needs cathed.

  • Stephen Williams says:

    AFIB, RBBB, Ant/Lat STEMI
    Not VTACH
    NOT AFIB with WPW

    RIde the lightning and see what happens

  • Jason says:

    AF RBBB Ant Lat STEMI (I, aVL also elevated) Prox LAD occlusion

  • Ken Graurer says:

    Just getting to this now …. (BEFORE I look at Vince’s answer). I agree with those who call this rapid AFib with RBBB/LAHB + acute anterior STEMI. These types of tracings ARE tricky — but there ARE several clues: i) the definite irregular irregularity (much more than is generally seen for VT); ii) several leads suggesting that the QRS is really not overly wide; iii) LACK of extreme axis deviation (there IS a tiny-but-real initial r in each of the inferior leads — so Axis is of NO HELP in distinguishing between SVT vs VT in this case; and iv) the “telltale” ST elevation that is subtle-but-very-real in leads I,aVL and V4 in association with subtle-but-real reciprocal ST depression in each of the inferior leads. The presence of marked ST deviation in association with a fast supraventricular rate is a known mimic of VT, when in reality this is most probably ALL supraventricular.

1 Trackback

Leave a Reply

Your email address will not be published. Required fields are marked *