68 year old male CC: Chest Pain

Here’s another great case submitted by Robert Bees.

EMS is called in the very early morning to a 68 year old male complaining of chest pain and shortness of breath.

On arrival, the patient is anxious and appears acutely ill. He is oriented to person, place, and time.

Skin is cool, pale, and diaphoretic.

The patient feels light-headed and admits to nausea but has not vomited.

Onset: While sleeping
Provoke: Nothing makes the pain better or worse
Quality: Poorly localized heavy pressure
Radiate: The pain does not radiate to the arms, back, neck or jaw
Severity: 8/10
Time: Patient states he occasionally “feels bad” but “not like this”

Past medical history: MI with stents x 2 years ago.

Medications: ASA, Lipitor, Tenormin, NTG

Patient states he took NTG x 1 prior to EMS arrival which made him “feel worse”

Vital signs:

Resp: 22 shallow
Pulse: 140
BP: 88/54
SpO2: 92 on RA

Breath sounds: rales – patient becomes very light-headed sitting up

The cardiac monitor is attached.

A 12-lead ECG is captured.

What now?


  • Right sided MI, MONA and cath lab STAT!!!

  • Ckemtp says:

    I get to be the first?? Thank you Twitter!Although that means that I can't hide behind anyone else either.. Dang you Twitter!Ok, so judging by the 12-lead, this guy's heart isn't so hearty (har!) and it's had some previous damage, which is backed up by his history. The bifasicular block has also messed up the QRS complex substantially, which makes finding the actual ST segment somewhat difficult. I'm not a 12-lead expert by any means, but I am most concerned about the lateral V leads starting at V3, most pronounced at V4, and possibly continuing into that mess that is this guy's EKG. But that's not the important part in my book, and I only put my (rudimentary) interpretation of the EKG first because this is an EKG blog. What really concerns me here is this guy's clinical presentation. His BP is in the crapper and his heart is taching right along trying to compensate for his lack of ventricular output. With his BP as craptacular as it is, it can't be a problem with the afterload so it has to be a lack of left-ventricular effectiveness. Couple that with the EKG interpretation of an anteriorlateral MI and you see a patient in clear cut cardiogenic shock due to Left Ventricular compromise. Since you've got the EKG on him and have vitals already done, one would guess that you're also in the process of performing the other traditional staples of ALS care, o2, and an IV. Do that if you haven't. o2? Medium to high flow. IV? They're so good, why not start 2. You need to aggressively support this guy's LV function. Start with fluid to bump up the BP as much as you can unless the lungs are wet. In fact, if this guy has some form of CHF (which I would guess that he does) you have to be a bit careful with that.. but start it as much as you can get away with. Withhold NTG and Morphine. Give ASA if he hasn't taken it already.Then go to a hospital that can take care of him. In my case, I could take him to the rural community hospital but I would request the helicopter to meet me at the hospital to get the guy to a PCI capable facility. Depending on where I was in my service area, I would consider running to one of the PCI capable facilies within 45min of ground transport.. No use driving 20min to the community hospital only to delay care further. This guy needs a cath, maybe more.Caring for this guy will be a balance of supporting his LV function while taking care not to extend the MI. Expect pulmonary edema but try to support the BP with fluid. Consider dopamine for cardiogenic shock. Drive fast. In my service, I'd consider heparin 5000 units IV. I'd withold Metoprolol unless directed by medical control… because his block and hyptension scare me. I'd like to decrease his cardiac workload which is increased by the rate… but I believe that that's the only thing boosting his cardiac output. Drive fast, support LV function. Give o2 to help the heart tissue survive. Don't give Nitro. Do give ASA. Don't put him into pulmonary edema with too much fluid. Do give enough fluid to boost his BP a bit. Don't waste time. Do give dopamine if you can't boost his BP with fluid.Did I mention drive fast?

  • G.W. says:

    O2, IV, patches, diesel. Transport to cardiac facility and activate cath lab. Consider dopamine. Consider CPAP? Though probably will not be tolerated.That's the best I can do with what I have in the toolbox. Cketmp mentions fluids for the BP. Curious about that with the rales.

  • Ckemtp says:

    Meh.. I actually didn't read that part although I anticipated that they were coming. Here's where you see the Left Vent. insufficiency. CPAP would be good there. Here's something crazy that I heard from a professor from the Univ. of Iowa EMS program say at a conference the other day. Give lasix to vasodilate (yes it does that too) and reduce the total fluid load, then dopamine to support LV function. I was pretty against it when I heard it.. but you've got to decrease the overall LV workload while supporting it's effectiveness. It's a tough call.You've also got to get the BP up. Get this guy to some place that can help him, he might need an LVAD as well.

  • Tom B says:

    johnnyisafrog – Just curious, why do you think ride-sided?Tom

  • Tom B says:

    Ckemtp – Thanks for the reply! I picked up on the bifascicular morphology (RBBB/LAFB) myself.But are you certain it's sinus tach with 1AVB?I know it's a little slow for VT but the instability has me concerned! It could also be some kind of atrial flutter.I'd hate to cardiovert sinus tach, but I have to admit, I'd be thinking about shocking.Tom

  • Tom B says:

    G.W. -I hate to admit it, but my EMS system just got CPAP.Our protocol states that hypotension is a contraindication.I'm assuming this is because increased intrathoracic pressure reduces blood return to the heart.Of course, you've got to balance that against ventilation and oxygenation.Tom

  • Tom B says:

    Ckemtp -It's a tough case, isn't it? There's no easy solution! If I knew for sure it was sinus tach with 1AVB (and bifascicular block) I'd feel more secure that the tachycardia wasn't causing the instability.On the other hand, you hate to give dopamine to a patient who is already tachy and may be having a STEMI.It's a tough call! Tom

  • Ckemtp says:

    Yea, it's scary to increase the cardiac workload with the pressor… however, look at the total coronary perfusion with the diastolic pressure being so low. It's a toss-up… yes you're increasing myocardial oxygen demand, but you're also increasing total coronary blood flow by increasing the blood pressure. Gotta do something, you can't give fluid and the guy's BP has already taken a dive. Same goes for the CPAP. Of course, that may be an academic issue. This low BP is being caused by cardiogenic shock secondary to LV compromise from the anteriolateral MI. The cure for that is a cath-lab. In the cath-lab they're going to put the guy under and intubate him. Sooooo… you might as well do that too. How's your RSI skills?(and yes, I would obtain a V4R, and if it's showing ST elevation this is a HUUUUge STEMI)

  • Tom B says:

    Ckemtp – I have no RSI skills! :)Oh, wait… I'm mediocre at laryngoscopy. Does that count?Tom

  • akroeze says:

    Forget the scope, digital intubation is the best choice in this patient.

  • Ckemtp says:

    Ummmm… ok. Care to explain why? I'm not doubting your opinion, but why would you do a digital intubation on this patient?

  • Jumping in a bit late here, but I don't like the lung sounds coupled with the bp.We're clearly heading to the unstable algorythm unless we get his bp up and his resp effort reduced.Slightly seated up and legs elevated might help us along, regardless of what many say about trendellenberg being useless, it really does work.Certainly a cath lab facility with an early radio report. The old blocks can be distracting at first and do indeed mask the ST segment as my red headed associate mentioned, so I will assume it is masking a STEMI, Anterior moving septal.O2 at 10 on a mask unless we need to chat, then 6 nc.IV tko for now, might try cpap if the lungs get worse, he'll likely feel better and that might get the rate down a touch so I can get a better look at the rhythm.Not doping, no sense shrinking an empty system in my book, sure the bp numbers will change, but I don't think we need it yet, but I've got a 10 minute transport time. Faced with 20 + 'm doing my calc and hanging it to be ready.HM

  • Nicky G says:

    Hmmm, im obviously way out of my league but heres my provisional. Rate 140 junctional tachy, short PR interval, wide QRS, would WPW be out of the question? Could it account for rate related T wave inversion anteroseptal?RBBB/LAFB consistent with hx but serial 12 leads required on route.I dont see the STEMI but at my level the Rx is the same.Elevate legs, aspirin, IV access, high flow 02, morphine (no nitrates due to BP). Call for Intensivist back up (I cant activate cath lab if required).

  • Tom B says:

    HM -Thanks for the comment! Good to see you back.You raise an interesting point. I agree that sometimes, when you fix the respiratory component, the rate will come down by itself (when it's ST or AF).Interestingly, that's one of the reasons my service got rid of Cardizem. A patient with hypertension, shortness of breath, a low SpO2, rales, and AF w/RVR needs NTG and PPV, not Cardizem!It would be nice to slow this rhythm down a little bit and confirm whether or not the bump at the end of the T-waves in lead V1 are in fact P-waves! Sometimes we have to fight the urge to "do something". This patient obviously "needs something" but as a well respected physician on the EKG Club said about these ECGs, "many ems and even some ED treatments would have to be done very carefully as changing rate, volume, preload, afterload may all aid in doing the patient in, keep him in position of comfort/flat, O2, monitor, he is circling the drain we dont want to accidentally pull the stopper out."Tom

  • Tom B says:

    Nicky G. -I hate to say anything's "out of the question" but the rate suggests something other than a reciprocating tachycardia a la WPW.The T-wave inversion in leads V1 and V2 isn't rate-related. It can be explained by the "rule of appropriate T-wave discordance" which basically states that with depolarization abnormalities (like bundle branch blocks and ventricular rhythms) the T-wave will be deflected opposite the terminal (last) deflection of the QRS complex.In leads V1 and V2, the QRS complex ends with an R-wave (RBBB-type morphology). In other words, the terminal deflection is positive. Hence, the T-waves are negative, which is a normal finding for RBBB-type morphology (whether actual RBBB or ventricular rhythm mimicking RBBB).The opposite is true for LBBB-type morphology.Tom

  • Christopher says:

    (repost from EKG Club)Rhythm: VT @ 130. On the 3L I think I've marched out disassociated P waves. Hx of MI also points to VT. Regardless, given he's unstable it is prudent I don't spend much time debating.12L: tough! I think I have concordant STD in inferior leads, concordant STE I/aVL, V1-V4, aVR. Monitor says MI, they're usually pretty good, although the VT may be a confounding factor. [Tom had pointed out on EKG Club that perhaps I was seeing fat slurry rS complexes inferiorly and the ST segments weren't easily interpretable. He also pointed out the GE-Marquette algorithm is confounded by tachycardia, much like myself 🙂]MI or not, very bad. Heart failure is my first thought for VT w/ pulse + rales. The slower rate of VT makes me question which mode of Tx is most appropriate. Sick heart, tired heart, I wonder just how much it can tolerate. Obviously we're heading to a PCI capable facility, transmitting the ECG if possible, early notification with MD consult on this one. The debate raging in my head is heart failure -> pulmonary edema -> hypoxia -> VT versus MI -> pulmonary edema -> hypoxia -> VT. I don't feel like I have enough experience to know exactly how those two paths should change my treatment (if any). Placing pads on the patient, drawing up 150mg amiodarone, and plugging in CPAP if we still have rales.I'm thinking I have three immediate problems for my pt:1. Possible MI2. Heart failure3. Ventricular tachycardiaThe first one I'm not fixing in the field, and of the second two I'm probably going to have to work on the 3rd to get to the 2nd. Eventually any of these three are going to lead to cardiac arrest or cardiogenic shock. I'm selling myself on an Rx plan that begins with sync cardioversion @50J biphasic. If we terminate the VT, we can work on the pulmonary edema. If things are cooperating a good rhythm returns and the LV can start pumping out the fluid in the lungs and fix that for us. If not and we've still got poor LV function, attempt to correct that with CPAP. Also, I'm going to keep in mind we may need to pace them.I'd also hope for a short transport.

  • akroeze says:

    Ckemtp,My comment was tongue in cheek commenting on Tom's comment.

  • Hillis says:

    Am still worry about the cardiac rythm here !! It looks like atrial flutter to me but in anterior leads ( V1-V3 ) and aVL i see P wave !! do you agree with me ? Anyway i think we agreed that this patient is having bifasicular block ( LAFB + RBBB ).I do agree with johnnyisafrog that there is right ventricular MI there is 1mm ST elevation in V4 so confirm the diagnosis with V4R.. Inferior STEMI could also be present.. The clinical presentation of cardiogenic shock strengthen the diagnosis .O2, IV , thrombolytic , antiaggregants and transport the patient to PCI as soon as possible .

  • Tom B says:

    Dr. Hillis – I agree with you that lead V4 looks suspicious (although I would like to see it during sinus rhythm).However, lead V4 is an anterior lead, which I usually associate with a blockage somewhere on the left side (meaning left coronary artery and it's branches).It does not make me automatically think of RV infarction, although anything is possible with this case! :)Tom

  • Anonymous says:

    I'm still a little shaky on whether on not this is VT. I think those just may be P waves in V1 and if you measure out the PRI and apply in to lead II you will notice that there are small but consistent notches on the downslope of the T wave. As far as treatment goes I agree with a previous poster who said they would at least have the dopamine out and ready to go. Other than O2, ASA, IV and pads there aren't a lot of other interventions i'd be too keen on. Good case!

  • Here is my thought, this patient has what appears to me to be significant st depression in leads ii iii and avf on top of that the patient is exhibiting classic signs of right sided mi. The reason the patients bp is in the toilet is from the nitro he took before sms arrived which is a typical reaction to nitro in a r side mi. The rales are another typical sign of a right side where the heart does not have enough ooomph and fluid backs up on the lungs. Nitro to reduce his preload will actually help this, however also typically dumps the bp even more. In a patient like this nitro to help ischemia, fluid wide open to keep the bp up even if you have to intubate from pulmonary edema, lasix and cpap can help prevent the pulmonary edema however you have to be very careful with the cpap as it will reduce cardiac output so make sure you are hemodynamically stable first.

  • Vince says:

    First time posting and I'm still very new at this, but I'm not seeing any depression in the inferior leads. My assessment of the ECG is a bifasicular block (aware of the possibility of VT) with concordant STE in V4. Maybe I missed it in the comments, but does anyone else dislike the T-wave in V3; it looks biphasic with an overall concordance that bugs me. Either way, anterior MI with cardiogenic shock being my worry at the moment, exacerbated by the nitro. Give him some ASA and O2 (BLS capabilities, don't ask why I'd be running/interpreting an EKG on the scene), with expeditious transport to the cath lab where I'm guessing he'll buy himself a balloon pump or LVAD for a bit.Of course I may be completely wrong, I'm not even basic certified yet, sorry if I killed him.

  • Vince says:

    Now I'm figuring that extra bump on V3 is just the only strong sign of atrial activity with V1 and V2 also showing hint as Dr. Hillis said, but I don't think if I'm buying into a-flutter. Doesn't change my treatment or anterior MI diagnosis.

  • Geoff says:

    Way late on this here, I'm cutting and pasting from 12 Lead ECG Blog…don't know how I missed it here.First things I'm thinking on treatment is O2 via non-rebreather, ASA 324 mg, IV, STEMI center. With the rales & decreased B/P I'm worried about cardiogenic shock. All we carry for B/P support is dopamine, but his tachycardia makes me think twice about that. One of our ED docs will still give a fluid bolus to people who are hypotensive w/ rales based on the theory that often times they are not really hypervolemic, especially with diuretics, but he isn't on any. Could the tenormin (B1 blocker) be responsible? Curious as to what he means that he felt worse w/ NTG? Dizziness, chest pressure worsening?In terms of the ECG, to be honest, I am not sure about what to look for in terms of STEMI w/ IVCD. Is there anything specific? Looks like STE maybe in V3, STE V4, abnormally large T Waves V5 & V6. I'm going way out on a limb here, but, w/ the positive R waves in V1 & 2 w/ depressed ST & upright T wave, do we need to worry about posterior involvement (along w/ ST depression II, III, aVF)? Is this a normal pattern kind of similar to a BBB? Is there anything else going on that might cause this? Hyperkalemia? Do we know what is abnormal based on his previous MI?Also drive fast…I have a short transport time, my hat is off to those of you with long transport times. I love this stuff, but honestly I'd be anxious to make him someone else's problem (who can fix him).

  • Tom B says:

    johnnyisafrog -I think what you're interpreting as ST-depression in the inferior leads are actually big fat S-waves.Regardless, we usually associate RV infarction with inferior STEMI which would be ST-elevation and not depression.It's true that NTG must be used cautiously in the setting of RV infarction, but NTG can and will drop the BP in most patients to some degree.If the patient is in cardiogenic shock, NTG is certainly not going to help! As a final note, the lungs will typically be "dry" with RV infarction, since most of the time the left ventricle continues to pump normally. In this case, low BP, tachycardia, and rales points to left-sided heart failure.Tom

  • Tom B says:

    Vince – You're funny, dude!I agree with you with regard to the inferior leads and that this ECG shows bifascicular morphology.It's hard to say what's going on in lead V4 for a couple of reasons.First, if this is sinus tachycardia with 1AVB then our eyes could be deceived by PR-depression. It's hard to say exactly where the "baseline" (isoelectric) line is.Second, this is a transition lead, meaning that the terminal deflection switches to negative in the next lead. I've noticed that the ST-T complex is sometimes concordant in the transitional lead.I do dislike the T-wave (or what appears to be the T-wave) in lead V3, but this is the exact ECG finding that makes me suspect the possibility of atrial flutter!Regardless, I agree with your assessment of possible anterior MI with cardiogenic shock.For not even being basic certified yet, that was one heck of a nuanced interpretation! What's your secret, Vince?TomP.S. The patient died, but you didn't kill him.

  • Tom B says:

    Geoff -This ECG shows a bifascicular pattern similar to right bundle branch block and left posterior fascicular block.It could be a "new" bifascicular block due to acute STEMI. Or it could be an "old" ECG finding. Or, it could be VT! This is a really difficult case, in my opinion!Tom

  • john says:

    sinus tachycardia with RBBB and acute antero-lateral wall MI

  • john says:


  • john says:


  • john says:


  • Jaylene says:

    Was totally stuck until I read this, now back up and rnunnig.

  • Luckie says:

    Information is power and now IÂ’m a !@#$ing dciatotr.

  • Andrew says:

    Very good call. I’m excited to hear the final DX. I’ll keep it simple. Looks like he’s in failure secondary to a decent size STEMI. I’d stick to the basics on this patient. First and formost this is a rapid transport to a cath lab facility. His hypotension will make me avoid nitro. ASA ( the most important med we give for STEMIS) if he could crew. High flow 02. I’d avoid CPAP as well due to the hypotension but could consider trying it and maybe starting at 5cm and not 10cm? Serial 12 leads. 12 lead Transmission to cath lab. He’d be someone I’d probably get the combo pads on in preparation. Two large bore IVs. I’d hold off on fluid as of now. My overall opinion of this call is they are very sick and there is not much we can do for him. He needs a cath lab. Ran a few of these in my 10 years and I can honestly say its difficult on these calls to “sit on your hands” but most of the time it’s the best thing to do. Great post Tom!

  • Baqui says:

    Probably restenosis previously stented arteries. NTG should not be administered because low BP. O2, IV access and slow fluid filling, pain relief, CAT LAB.

  • Satch says:

    Neg in lead I, hard to see on the phone, Neg in II, III, positive in VI, V-tach !

  • Matt says:

    I didn’t see anyone say it but this pt needs dobutrex. He has flash pulmonary edema. Learn from this don’t jump to intubation, you will knock out his drive and kill him. After getting his pressure up treat him accordingly and if nuero status permits you can cpap him while starting the dobutamine.

  • gorgemedic says:

    Yikes…toughie.  I'm leaning away from the interpretation of VT, although there's certainly a great case for calling that.  I think the hemiblock can likewise be explained away by the history, although it's definitely not helping matters clinically.  The things I saw that popped out at me are increased R:S ratio in V1 and ST elevation in aVR and aVL, coupled with the obvious injury patterns in the precordials.  That makes me think of a L mainstem occlusion that's affecting the septal, anterior, and posterior areas.  I have to confess I didn't even consider VT until other posters brought it up; I'm dissuaded by the normal X-Y axis and the QRS interval, although it could totally be an ectopic ventricular focus high in the ventricular wall maintaining some semblence of normal depolarization.  But all that's just head games…definitely going to grab some oxygen, IV access, avoid the fluids and haul a** to the PCI facility.  NICE puzzler of a 12-lead!!!

  • Adrian says:

     Remember ST depression in inferior leads is not inferior ischemia, but rather reciprocal to lateral STEMI.
    RBBB plus LAFB.2:1 Av block, anterolateral STEMI

  • EMTPRN says:

    No doubt this is a hard one call now, nevermind in the back of the rig. I'm not convinced about VT, besides, i think if this pt gets shocked its all over anyway. Personally, talking prehospital, I'd take a less aggressive approach to him. Not enough resourses in the back of an ambulance as the hospital does. He did say he took 1 NTG which probably made matters worse. He probably wasnt as tachy and may have even had a boarderline BP prior to the NTG. So supportive measures, high flow O2, 2 IV's, ASA, and a partner driving like he stole it to PCI center!

  • Bob Smith says:

    Wow, there’s a lot of crazy diagnosis going on here. Seems we’re all amateur cardiologists. My first thought when I looked at the initial lead II was high potassium. After looking at the 12-lead, I still feel the same way. The rate seems a little fast but it looks similar to patients I’ve seen with a potassium around 8.

  • Brodie47 says:

    So I just sat through Bob page’s 12 lead interpretation class. We all learned an amazing amount of knowledge. The pt has a normal axis, assuming correct lead placement. This can be confirmed by the QRS axis displayed on 12 lead. His QRS is wide at 0.138 which help determine it’s ventricular. Although we can not see great p- waves, you can get a sense they are there in a few leads. The 12 lead also gives you a PR interval. Which by the way is just greater than 0.2. This pt has 2 blocks and is in serious condition for arrest. There are multiple criteria for determining VT. I’ll point out the ones I think apply to this pt. Using MCL-1, or v1- Rule 1), he does not have extreme right axis deviation and an upright v1. Although I believe v1 is upright. VT NEEDS both criteria. Rule 2 has three sub criteria of which none are met, therefore I’ll move on. Rule 3-involves v6. Any negative deflection below isoelectic is VT. The newest study sone 2010, and being releases now involves avR. It says an upright R wave in avR is 98% diagnostic for VT. An additional note, we know the pt has had a previous MI… I would be great to know if he had tachycardia after his previous MI. A yes to both would favor VT by 86%. Now that was a lengthy explanation for the reason I think the pt is in VT. Who cares now that we know this about STE! He needs immediate intervention. Dop will not help asystole. The pt I feel has Rales because his EF is less than 40ish %. We can not measure his EF but he/she is in failure because of the crackles. He may mind being shocked due the fact he’s conscious, or not. Amiodarone or lidocaine would be my treatment choice after IV is established with o2 sat maintained at 92% or greater.

  • Beodie47 says:

    That was not by any means an attempt to
    Diagnose the pts condition. Not performing the correct treatment could or would kill the pt. Another change to the AHA guidelines is to use adenocard to slow the rate enough to see if it’s ventricular or an a fib/ flutter. Ten seconds of no rhythm is better than 90 minutes after lidocaine or amiodarone! Those recommendations are coming out this later this year.

  • anonimus says:

    Does anyone considered cardiogenic shock??? Symptoms fit :).

  • weldonado says:

    I’m a brand new medic. Wow! I feel lost. So many of the treatments that have been suggested are contraindicated in my system bp must be over 100 for nitro and cpap. I’m thinking I would be activating the cath lab and running the stemi protocol. When that 12 lead got transmitted I’m asking for orders.

  • Craig Barraclough says:

    Great case. From a quick look i would be considering Inferior infarction query RCA occlusion.

    Treatment plan, STEMI pathway
    Position head elevated
    O2 to maintain SpO2> 94%, 300mg aspirin
    Clopidogrel 600mg PO, IV access and withhold fluids due to rhales. Reconsider if this changes
    Pain relief IV fentanyl
    I would call our clinical desk for advice on transport location as Cath Labs are location dependent in New Zealand and this case needs a Cath lab a helicopter would help l.
    All treatments enroute when possible
    No nitrites Morphine with extreme caution

  • Caleb Seavey says:

    Rate/ Rhythm: Regular Extreme Wide Complex Tachycardia with no P-waves
    Axis: LAD
    Hypertrophy: Not Present
    Blocks: RBBB formation, Absent P waves
    Ischemia: Not Present
    Interpretation: Extreme wide QRS complexes, with an almost sinusoidal formation in lead III. The combination is pathognomonic of Hyperkalemia.
    Note: Auto EKG interpretation of STEMI is because the machine is not recognizing that the complexes are wide (states the QRS is 120ms).

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