83 Year Old Male: Shortness of Breath

You are called to the residence of an 83 year old male with a chief complaint of shortness of breath.

On arrival you find a sick-appearing gentleman working hard to breath. He states that he woke up feeling a bit weak this morning with dyspnea-on-exertion that it has gotten progressively worse over past 12 hours—to the point where his is experiencing respiratory distress at rest. He has also had a productive cough. Noticing that he didn’t sound great on the phone his son came to visit, found him in this state, and called 911.

The patient is in moderate respiratory distress (4-5 word sentences) with a respiratory rate of 28/min and skin that is pale, warm, and diaphoretic. SpO2 is 85% on room air, improving to 92% with a non-rebreather at 15 L/min. Pulse is present at the radials but weak and his NIBP is 97/58 mmHg. Temperature is 38.3 C (oral). Lung sounds show bilateral rales and coarse rhonchi through much of both lung fields.

He denies chest pain, heaviness, tightness—or pain anywhere else for that matter.

His past medical history is significant for CAD with a prior MI, CHF, HTN, DM, dyslipidemia, and GERD.

You obtain the following ECG:

83yo M - SOB, Ill Appearing
 – What do you see?

 – How is this ECG going to affect your management? Do you need to activate the cath lab?

 – Masters Bonus: What fairly common ECG finding is the cause of that unexpectedly tall R-wave in V2?



  • Kevin says:

    Triple Vessel Disease, up in AVR, with widespread st depression.. Equivalent of LAD lesion in about 2 % of cases… With presentation, and this tracing, he would go directly to the cath lab…

  • Khalid says:

    I’m concerned that this patient has significant LM disease or very proximal LAD/LCx stenosis. Take him to cath lab now.

    By the way, Lead V2 is misplaced, no R wave in V1 and then almost no R wave in V3 and in between large R wave, not possible unless V2 is misplaced.

  • William Meyer says:

    Looking at the ECG…first off, you can see the computerized rhythm interpretation is completely wrong.

    Rhythm is sinus with 1st degree AV block, most easily visualized in V3 with obvious P-waves. LAFB is also present.

    Breaking the ECG down further, we see ST depression in I, II, aVL, V4, V5, and V6. We also see ST elevation in aVR and V1. This suggests most likely LMCA occlusion with resultant large anterolateral ischemia/MI.

    Treatment: Supportive, aspirin, depending on severity of rales maybe some lower pressure CPAP with a close eye on B/P, rapid transport, ECG transmission with call to med control to stress STEMI/STEMI equivalent, request cath activation.

  • Vijith says:

    Definitely cath lab has to be activated.. ST elvtn in avr, v1 with St depression in l, ll, avl, v4-v6. Prolonged pr interval. S/o LMCA occlusion. Tall r in v2 is due to posterior wall infarction.

  • I see a regular rhythm at ~ 95/minute with LOTS of baseline artifact. I am not certain if there are P waves or not ….. It does look in leads V3,V4 like there are P waves with a long PR interval – but I cannot be certain in lead II that there is an upright P – so I’d say supraventricular rhythm at 95/minute of uncertain etiology – possibly sinus, but can’t be sure without additional information.

    Lead V2 is OFF. The qR pattern we see in lead V2 just doesn’t make sense … I see a QS in V1 and a fragmented QS in V3 – possibly consistent with this patient’s prior MI. There is LAHB. The most remarkable finding is fairly diffuse ST depression. This is most marked in leads V5,V6. There is ST elevation in aVR and V1.

    Clinically – we know this 83yo has a complex medical history including prior MI & HF. It sounds like he is in Heart Failure at present – though NO chest pain! So apart from the technical problems with this ECG (rhythm? lead V2?) – I sense this is not acute. The diffuse ST dep with ST elevation in aVR & V1 may indeed indicate severe underlying coronary disease (maybe even proximal LAD or left main) – but no acute event.

    I would NOT rush him to the cath lab. Instead, I’d establish if his progressive dyspnea is due to heart failure – and I would treat that. I’d carefully monitor this patient (sounds like he belongs in the ICU) and would repeat his ECG, check troponins, etc – but entirely possible that management can be solely medical (depending of course on how he responds).

  • Adrian says:

    Firstly, the patient is septic, he needs high flow O2 (which he’s already receiving), IV fluids, blood cultures and antibiotics (most likely IV) and needs to be in resus sharpish.

    Secondly, the ECG needs doing again, V2 is wrong and I’m not sure where it’s been placed to get that reading. Assuming the rest of the ECG is correct and inferring poor quality coronary arteries from the PMH, I’m more likely to base the lateral ischaemia on the hypoxia secondary to sepsis before attributing it to a coronary event, although there could well be an element of triple vessel disease. It is possible this is a proximal LMCA occlusion, but this would probably be caused by DIC again secondary to sepsis. Before I go activating the cath lab though, I want to retake the ECG with proper lead placement and begin treating for sepsis.

  • Dustin says:

    I see a very sick and complicated patient.
    12 Lead: ST elevation in AVR and V1 along with depression in I, II, V4-V6 leading me to an LMCA occlusion. The tall R wave in V2 also points me to Posterior involvement. Posterior MIs and LMCA occlusions can and do cause pulmonary edema, which this patient has.
    This seems to be a more rapid onset so I am leaning away from Septicemia but it is on my list of differentials.
    Treatment would include serial 12 leads to monitor the evolution of the possible occlusion. Along with the serial 12 leads, close monitoring of the BP and ensuring the patient is oxygenating would be the most important. The BP is almost too low for CPAP and I would rather have a low BP than none at all. The lungs have fluid so NS bolus is out. If this is in fact is an occlusion Dopamine could make it worse only demanding myocardial work and oxygen which the patient doesn’t have.
    I would call a STEMI Alert on this patient. The 12 lead could be caused by the lack of oxygen because his lung sounds. BUT his lung sounds could be the caused by an LMCA occlusion.
    I think the fastest and best treatment would be to Cath the patient. The Cath would rule in or out the occlusion without delay. If you do not cath the patient and treat for sepsis or other causes of hypoxia and hypotension, you are wasting time while the patient’s left and posterior portions of his heart die. Unfortunately LMCA present hypotensive with Pulmonary Edema and can have a poor prognosis.

  • Brian says:

    I mostly agree with dustin. I believe this is may be an isolated posterior MI. The R wave in V2 points to it being a posterior MI. otherwise it is a 1st degree av block with a LAHB. I am somewhat concerned with the concordant t segment depression noted and in fact if you were to look at (-)leadII I suspect it looks like aVR which in conjunction with the R wave in V2 leads me to a possible isolated posterior MI and acute heart failure.

    I would be interested in knowing what color the sputum is that he is able to cough up, is it pink and frothy?

    The BP isn’t great and with my suspicions of the posterior involvement I dont want to drop the preload with nitro, I might be tempted to try CPAP as I can always stop it if need be.

    Here is where things get weird. Fluids, yep I might give him a little fluid challenge to see if increasing the preload increases his perfusion. maybe 200-300cc and re-assess lungs and BP and dyspnea. ETCO2 would be nice here as well.

    And 324 of ASA

  • Kyle says:

    Well st elevation in avr and v1 associated with anterior and lateral depression would call for possible posterior wall MI. 15 lead would be in order. Also check all the leads for appropriate placing. If v7, v8, and v9 show the elevation i would treat as a STEMI per my protocol. Asprin only until medical control is contacted! With pt hx it would be a mistake to Fluid challenge him. Especially with rales, and the b/p is 97/sys. Some of these answers are scary and im sure some here have many mdr’s, no longer even have a license or simply a know it all parapup!

    • know it all parapup says:

      @ Kyle

      I would question your authority to call out people for not having a license or being a know it all parapup when your tx basically entails “call medical control.”

      I think we can both agree that his cardiac output is not great at all. I assume your reluctance to give him any other meds is that you are worried about a posterior or R ventricle infarct and preload issues? is that correct? you believe there is a preload issue here as his BP and he isnt perfusing all that well with his SPO2.


      so how are you going to fix this? short of the cath lab? you can increase preload and inotropy with vasoactive drugs or a small fluid challenge might do the trick by increasing preload and hence cardiac output. So give a nod to our pal Frank Starling and increase the preload.

      The time to not give fluids is when you have pulmonary edema with a sky high BP, the edema is due to an Afterload issue and nitrates are perfect here. This patient is most likely heading towards cardiogenic shock.

      No matter what dx you go with this patient is most likely dehydrated and/or lost volume from the vascular space due to edema from sepsis (not that I agree with that dx) or has a relative hypovolemia from vasodilation and capillary leakage in sepsis. And most patients with pulmonary edema are in fact dehydrated, just their fluid is in the wrong spot.Unless he has not been taking his lasix or went on a salt binge.

  • Justin says:

    NSR 1st degree AVB
    Pathologic Left Axis Deviation
    Wide QRS
    Incomplete RBBB (Lead 1)
    STE aVR showing 3-vessel disease and STD in 1, aVL, V4, V5 and V6 showing Lateral wall involvement with slight anterior involvement.

    This man needs a CABG greatly and potentially an IABP with his heart being in such bad shape. He’s hypotensive and developing pulmonary edema from his heart being on the border of cardiogenic shock.

    I’d give him ASA, consider Inotropics to bring his BP up if it drops any lower due to the pulmonary edema, keep him on the high flow O2, and transport code to the nearest PCI center. The 12-lead wouldn’t change my treatment options.

    Tall R in V2 shows V2 was placed incorrectly due to the qRS in V1 and QS in V3 and needs to be moved to the correct spot

  • Ben says:

    Now, I know I’m a new medic and I see a lot of very serious treatments so I’m mildly doubtful here but that’s very diffuse st depression with pale skin and poor sats. Obviously this person is sick and probably septic but as far as an MI, couldn’t this st depression be caused by the poor o2 sats alone? I’d try to get the sats up and do a second 12-lead. I’m not convinced cath lab is needed, but I’d speak with med control and leave the decision up the them

  • Naveed says:

    ST elevation in AVR with probably reciprocal changes in lat leads that raises high suspicion of TVD

  • Iliyas says:

    LVH with strain
    1’AV block
    Dwinter’s t wave in lead 2, v4
    Biphasic t wave in v5, v6
    St elevation in avr, v1, v2
    Severe lf main or three vessel dieases

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