79 year old male CC: Shortness of breath

Here’s another interesting case submitted by Geoff Dayne.

79 y/o male c/o non-provoked SOB without CP.

Patient was found sitting upright, tripodding, 1 word dyspnea.

Lung sounds: extremely decreased tidal volume. EMS crew was unable to tell if there was rales or wheezing.

Past medical history: HTN, dyslipidemia, CHF, pacemaker (recently implanted within a week or so), diabetes, emphysema.

Drug allergies: Sulfa

Current meds: Glipizide, Omerprazole, Hydralizine, Lovastatin, Lasix, Albuterol

Vital signs:

B/P: 154/84
Pulse: 134 Strong/Irregular
Resp: 30
SpO2: 84 on RA

They treated w/ O2 and put him on the patient’s home BiPAP and transported.

A 12-lead ECG was captured.



And a rhythm strip.



I think this case is an excellent example of the real-life difficulties paramedics face in the field when it comes to the triage of possible ACS patients.

What would you do next as the treating paramedic?

See also:

Identifying AMI in the presence of LBBB – Sgarbossa’s Criteria Part I

Identifying AMI in the presence of LBBB – Sgarbossa’s Criteria Part II

Discordant ST-segment elevation in LBBB or paced rhythm

Found on the Lifenet Receiving Station (LBBB with concordant ST-depression in leads V3 and V4)

62 year old male CC: Chest pain (LBBB with ST-elevation > 0.2 the QRS complex)

58 year old female CC: Chest pain

58 year old female CC: Chest pain – Conclusion (meets all 3 of Sgarbossa’s criteria)

19 Comments

  • SoCal Medic says:

    Tom,Very difficult for me, I would start first off with the respiratory, sticking with my ABC's. Might try assisting his breathing with a BVM to see what kind of lung sounds present if any with good tidal volume, based on that, either Nitro or Albuterol/Atrovent inline with the CPAP. Since I am not convinced on the 12 Lead (QRS looks wide and computer interpretation is close to the 0.120 ms, left axis deviation present, elevation could be MI or could be manipulated by the wide QRS) and since I don't have transmit capabilities, I would reassess him once we hit the back of the rig, get another set of vitals and EKG and see what changes present based on the treatment modalities. I would certainly call my physician regardless and tell them of my findings and probably put him in a Cardiac Care Center since our ETA's are not that much longer as a fail safe, but doubt the trigger would be pulled for the lab, unless significant findings were noted with the follow up assessment. Now the waiting period, betting you have a repeat of the ekg somewhere, and more insight to the ekg itself.Chris

  • TatonkaDTD says:

    I don't really care for the machine's interpretation…doesn't look like AFib to me…I (think I) see p waves…therefore I'd call it Sinus Tach w/ some ectopy.ST Elevations in V1-V4 without reciprocal changes = anteroseptal MI, right?WRT the rate, has the pt been hammering his albuterol? I'd also like to see if it calmed down with some assited ventilations.For treatment: ASA, SL Nitro… …and shooting from the hip, how about calling for orders for some Lopressor?

  • Christopher says:

    Argh! Tachy AND elevation AND incomplete (or full on) LBBB…que no es bueno for STEMI interpretation :)Rhythm: P-waves on 12L, premature complexes all look roughly the same as normal ones, so probably PACs. Respiratory problems make me call this ST w/ frequent PACs.12L: I see STE V1-V4. The screen I'm on isn't helping me w/ measuring, will check back in the AM. I'm leaning towards significant. He's a CHF'er though so it probably isn't surprising to have a nasty ECG.Rx: NTG, CPAP, med control early, he'd get the PCI capable center in my area only because they'd also be taking most pt's who are in extremis.

  • Smasher says:

    Not easy for a complete noobie like me, but I'll have a go, please correct me as you go: Sinus tachycardia, first degree AV block, LBBB, occassional premature atrial complexes. Is that some concordant ST elevation in Lead I and V6? Discordant ST depression in V1, V2, V3? There doesn't appear to be any elevation >5mm or .2 of the R Wave, so I think this is suggestive of high lateral injury according to Sgarbossa's criteria? I'd like some further leads (V7, V8 and V9) to get a better look at the lateral and posterior walls, and I don't like the look of the complexes in V4, V5 and V6 (Q waves?) BiPAP sounds like a good option, I'd like to open him up a bit as well to hear something, so I would go with treating B first and trying some inline albuterol and ipratropium as he has a history of reactive airways disease and presents with acute SOB and some typical signs/symptoms of this type of patient (tripoding, hypoxemia). If that opens him up a little and gets some air moving we may be able to hear what is actually going on to decide where to go. Nitrates may be in order, but I'll work on B before C at the moment as his BP (systolic and MAP) aren't that far beyond what I would expect to see in this patient. Not that he can't have pulmomary edema of course. I have carte blanche to use IV albuterol, but I would not be going down that route just yet, far too many nasty side effects in COPD patients.I would also like a bit more info on his pace-maker (which seems to be MIA) and some further details like BGL, temperature (sepsis?), GCS (will he need a tube?) and so on.There's a long list of things that could be the problem, I would be leaning towards ACS causing pulmonary edema then triggering bronchospasm. Regardless: keep an eye on A, do what we can for B, see what happens with C before we start treating it, notify the ER and send the ECG for the cardiologists to look at.Looking forward to your reply,Smasher

  • Brandon says:

    Tricky, tricky. This is why I love this site.Based upon the snap short story, one 3 lead & the one 12L, I would lean toward Afib w/ RVR; there only appear to be undulations instead of p-waves; and with a irregular R-R interval and barely acceptable QRS width… I'd feel comfortable defending that interpretation.Based upon the 12 lead findings; I wonder if LVH plays a role in these "elevations". V3 has the most pronounced STE of 4mm, however that is also the lead with the deepest S wave. Looking at V1 &V2;, their elevations also seem dependent upon S wave depth.To further defend my suspicions, I'd rely upon the discordant T waves for an ostensibly non-ventricular rhythm, as well as the concave slope the "STE" in leads V1-V3.Personally, I'd withhold the sympathomimetics & parasympatholytics at this point; this gentelman is certainly taching away already, I'd be hesitant to potentially increase his rate, which IMHO is causing his SOB (further exascerbated by COPD/CHF).O2 12 l/min via NRB for starters, then see how spO2 & dyspnea respond. Keeping in mind this gentleman has hx COPD, I would be VERY satisfied with a spO2 in the low 90's.As much as I hate to do this, this ride would probably be IV/O2/Monitor for me with a PCI capable facility to greet us at the door. This pt needs definitive evaluation and care; I don't see a need to throw any calcium channel blockers or bronchodilators at him until a more confident and higher level of care evaluates the pts condition.

  • Terry says:

    Sinus tach with a LBBB and frequent PACs. I almost went with the A-Fib. I would start him on CPAP right away and and inline neb. If he didn't turn around quickly he would be an RSI candidate. I hate nasal tubes. If you dont't get a handle of his respiratory problem quickly he will be in resp arrest. 1 word dyspnea, extremely diminished breath sounds!! Not good.

  • Tom B says:

    SoCal Medic – That all sounds very reasonable to me! The computer measurement is borderline here at 118 ms but that's close enough for me, especially when you see appropriate T-wave discordance throughout the ECG! It would be a mistake to think of this heart rhythm as "narrow". I also agree with treating the patient's symptoms and transporting to a PCI center without pre-activation of the cardiac cath lab, if that's something that can be done easily in your EMS system.Tom

  • Tom B says:

    TatonkaDTD – Good eye! I would also call this sinus tachycardia with occasional PACs.I'm not sure based on this ECG whether or not the wide QRS complexes are due to an intraventricular conduction defect or ventricular pacing, but either way, remember that ST-elevation in the opposite direction of the QRS complex is normal, as long as it is not excessive.What is excessive? That's the key difficulty in this case, because it appears that the ST-elevation in lead V3 may be excessive. However, it's difficult to say for certain because it's hard to get a baseline for the TP segment and J-point. In addition, the bottom of the QRS complex may be cut off.This is a difficult case! But that's reality out in the field.Tom

  • Tom B says:

    Christopher -You're absolutely right. Tachycardias are known to cause false positive STEMI interpretations and so are wide complex rhythms! With this case it's easy to see why.Once again, it's nice to be in a jurisdiction where you can easily divert borderline patients to a PCI-center "to be on the safe side". It's far more difficult in the rural setting when faced with a patient like this.Tom

  • Tom B says:

    Smasher – I agree with sinus tachycardia but I'm not sure the PR-interval justifies calling it a 1AVB.I don't see any concordant ST-elevation in the 12-lead ECG. Remember, concordant means "in the same direction as" the QRS complex.If I'm not mistaken, what you're calling concordant ST-depression in the right precordial leads (V1-V3) is part of the QRS complex. The ST-segments in these leads are actually elevated, which is normal, as long as it's not excessive.The differential diagnosis of shortness of breath can be difficult in the field, but I agree our treatment should start there! Tom

  • Tom B says:

    Brandon – The undulations in the inferior leads could pass for U-waves, but based on the morphology in the right precordial leads, and the relative regularity of the R-R intervals when the premature complexes are mentally removed, I'm going with sinus tachycardia.It's hard to diagnose LVH based on ECG criteria when LBBB/paced rhythm is present, but most patients with LBBB have LVH. I like the way you're thinking though! Whether LVH is present based on ECG criteria or not, the deepest S-wave should be associated with the most ST-elevation, and that is certainly true in this case! I also agree that there may be a borderline loss of upward concavity with the ST-elevation in leads V1-V4, but with the tachycardia, and the shortness of breath, and no "old" ECG for comparison, to me it's not enough to make the call on this case.Sometimes it's hard to punt, isn't it? But the truth is that we can't always say with certainty whether or not a patient is experiencing STEMI, especially when a baseline abnormality is present. So what they need is further evaluation at the hospital, and that's okay! It's just unfortunate when that hospital is the local non-PCI hospital and various high-risk criteria are present. That's our greatest challenge, and those are the patients most likely to fall through the cracks.Tom

  • Tom B says:

    Terry – No, not good at all! The reason I think this may be paced (DDD pacemaker) is because we have LBBB morphology in lead V1 and left axis deviation, but a atypical looking QRS complex in lead I. I can't tell if it's rSR' or qR but it might even end with a tiny S-wave. In other words, we'd have to call this a non-specific intraventricular condution defect if it's not paced.Tom

  • Terry says:

    Tom,Shouldn't we be treating the pt and not the monitor? The pt is in severe resp distress with 1 word dyspnea, trippoding, decreased tidal volume, pulse ox 84%. He needs to have aggressive treatment of his resp status before resp arrest. I now this is a 12lead blog and I love it but looking at the hx of this pt. 12-lead should come after ABCs. Just saying.Terry

  • Tom B says:

    Terry – "Treating the patient and not the monitor" simply means to me that we interpret the ECG in light of the history and clinical presentation.I agree we should aggressively treat the patient's shortness of breath, but we should also get a 12-lead ECG as quickly as possible, since acute STEMI can cause uncompensated CHF.If you look at the tag line of my blog, it says, "Advanced airway procedures, cardiac rhythm analysis, 12-lead ECG interpretation, pharmacology, and special resuscitation situations."I think of myself as more of a ACLS specialist who happens to knows a lot about 12-lead ECG interpretation.Tom

  • Nick A. says:

    I totally agree with Tom. This is a ST with a ventricular paced rhythm. Not only does the frontal leads indicate a pathological left axis deviation, the precordial leads also show a negative concordance indicating that this is ventricular in nature. A pacemaker is ventricular in nature given the fact that the SA node does not travel down the ventricular fascicles to cause a ventricul depolarization.
    I would concentrate my treatment efforts at:

    Airway and Breathing: First with O2, CPAP or (if needed) assist ventilations with posive pressure with a BVM and In-line Duo-Neb, then PRN Albuterol Nebs. If you open up his aways and get a better Vt in, you may hear better breath sounds and crackles vs. wheezes, then tret accordingly. Sometimes the patient has primary CHF and exacerbation of COPD….so treat for both.

    Circulation: 12 lead EKG, SL NTG or go to a Tridil gtt if on CPAP so you don’t have to break the seal, MSO4 for possible (L)CHF, ACS, also may help a little with CPAP anxiety.

  • Gary says:

    Well he definatly has elevation, however he also has a bifasicular block with the anterior fasicle and the left bundle branch being blocked. This is not a good day regardless and needs to be treated as a STEMI anyway. Would need more patient history, is this new or somewhat old. I am assuming new cause one more little clot or slight change and he is going to be in a complete 3rd degree block. Rx:two IVS, MONA, O2, CPAP if it is working. If his left ventricle is failing then this has been going on for a while and now flooding his lungs.

  • William says:

    As a Medic I would treat the ABC’s first. CPAP with a duel nebulizer treatment. I do now that he is tachy but if I do not fix his breathing it will not matter. He obvious has a LBB Block and wide QRS. I see ST elevation in V1 thru V4. I do not see the afib. I would monitor the patient and repeat the 12 lead. With his extensive cardiac and COPD history I would be FOCUSED on his airway and get him to a cardiac center ASAP. I am just not convinced the 12 lead is right but like others I would not rule it out. I need a MD opinion. Treat the pt not the monitor.

  • Troy says:

    I would call it a septoanterior STEMI using the Sgarbossa criteria. I think this guy is definitely hurting. The main thing with anterior STEMI in my area is HEART RATE control. Possibly some labatolol for the rate. I’d call the underlying rhythm sinus tach with a LBBB. Treatment wise besides the labatolol for the rate would be ASA, hold nitro (due to the extreme tachycardia plus no pain), CPAP, some lasix in conjunction with the CPAP, and possible some low dose MS for the venous pooling effect. Definitely a PCI canidate.

  • Doug Harwood says:

    I am going down the respiratory path. V3 is the only lead that really bothers me for ST elevation with discordance in a LBBB. The rhythm  is irreg and the rate is compensatory. The cardiac output seems ok by the pressure. I would like to know the patients I/E ratio.
    The patient does have a history of COPD. Ventolin with an atrovent nebulizer, CPAP, IV N/S, monitor, and transport in high fowlers.  

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Comments
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Thanks for writing Tyler. They are the same thing. Strain pattern is just the result of increased pressures against the ventricles which alters the way repolarization occurs from epicardium to endocardium. Similar to stepping on a puddle of water. Your show spreads the water away from the area of pressure. The ST segment is slightly…
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The role of 12 lead ECG in Pediatric Pulmonary Hypertension
Can you explain how these ST segment and T wave changes can be differentiated from right strain pattern?
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