90 year old male CC: "Possible stroke"

EMS responds to a 90 year old male with a "possible stroke".

On arrival the patient is found sitting on the toilet (lid down). His spouse states that he had walked outside to retrieve the newpaper when he lost his balance and skinned his knee. She helped him inside and sat him down on the toilet in the bathroom when his eyes rolled back in his head and he started "shaking all over".

At the time of evaluation he is conscious, alert and oriented to person, place and time. He remembers falling while retrieving the newspaper but denies losing consciousness in the bathroom.

His skin is pale and diaphoretic.

He denies chest pain or shortness of breath.

Past medical history: Mild cognitive impairment, HTN, dyslipidemia

Medications: Metropolol, donepezil (Aricept), lovastatin (Mevacor)

Vital signs are assessed.

  • RR: 16
  • Pulse: 116
  • NIBP: 115/53
  • SpO2: 96 on RA

Breath sounds clear bilaterally.

Neuro exam: No facial droop, equal smile, clear speech. Slight pass pointing on the right side.

The cardiac monitor is attached which shows sinus rhythm, borderline sinus tachycardia.

A 12-lead ECG is captured.

What is your impression of this ECG?

See also:

90 year old male CC: "Possible stroke" – Conclusion

33 Comments

  • Trevor says:

    Lateral ST depression and flipped T waves. Investigate more; chest pressure or tightness? N & V? ASA 160mg, IV and transport.

  • Trevor says:

    Forgot to mention the elevation in the anterior septal leads. Whoops

  • CC Medic 537 says:

    Stroke? I suppose the spouse suspected a stroke 2* to the eye rolling and shaking. I suspect a dysrhythmia ( tachycardic ) . further I suspect he is having an acute coronary event. 12 lead is suggestive of an anteroseptal STEMI with 1 mm elev. In V1-3, T wave inversion 1, aVl, V5-6 small amount depression of the ST seg. I would be very interested in a posterior 12-lead…. R/O CVA vs. STEMI. PMHX/Rx and allergies. O2, asa, iv, nitrates. PCI facility. Silent MI??? 90 yo neuropathy. Diabetic? Previous MI or CVA? Just a thought.

  • VinceD says:

    First off, from the history and physical, the patient is sick until proven otherwise; people shouldn't be pale and diaphoretic. My top worries in patients looking ashen with a Hx of seizure vs. syncope include ACS, stroke (ischemic or hemorrhagic), dissection, AAA, PE, and GI bleed.
    My overall impression of the ECG is the old hedge of "non-diagnostic." Patient is in normal sinus at 96 bpm, but in my head I'd consider it equivalent to sinus tach with a rate over 90 and an ill-appearing patient. PRi is normal and I'm measuring the QRSi at about 100 ms with a slight slurring of the upstroke in the lateral leads. P-wave is a little wide, possible left-atrial-enlargment. Somehow I still haven't committed the LVH criteria to memory (probably because there is so little agreement over the correct criteria and they exhibit poor sensitivity/specificity anyway), but the complexes are tall and ellicit a probable strain pattern, so I'd consider LVH quite likely. It also fits with the possible LAE and slight QRS widening.
    The only thing that strikes me as odd is the appearance of the ST-segments and T-waves in the inferior leads. They're a bit depressed with flattened T-waves, but I and aVL aren't that impressive either, so it could be normal for the patient. With LVH an old ECG is almost always helpful. I'd label it "non-specific ST or T-wave abnormality, consider ischemia."

    At this point the patient definitely needs a more thorough history and physical exam, including a neuro check and finding out how long it took him to return to baseline from his shaking fit, but with the given scenario I don't see any need for specialty transport or intervention at this time. I'd want to give him some supplemental O2 (even with a normal Sat), but a 500 mL bolus of NS would probably also be warranted to top off the vasculature of a guy who's pale and diaphoretic with a BP that's low-normal for his age.
    Look forward to seeing what the rest of the world thinks about this case.

  • John says:

    LVH causing ST elevation with WPW indicated

  • Rob says:

    There also looks like a possible delta wave which I can see in leads I & V5. Lots of ST depression & TWI, some anterioseptal elevation, however I’m taking the elevation in V2 & V3 with a grain of salt given the relatively little bit of elevation compared to the large QRS complexes (rule of proportionality). I’d be interested to see what serial 12-leads would show. It would also help to see what his BGL was. Most people get the newspaper early in the AM to read while drinking their coffee & eating breakfast, he could be hypoglycemic which could be contributing to this presentation. Any way you cut it, this guy is sick. Can’t jump & call it one thing or another, but I’m gonna watch him like a hawk because something is going on & it’s only a matter of time before he crashes.

  • mohammed albesh says:

    a picture of lateral ischemia but in combination of convulsion the patien had we can suspect subarachnoid haemorhge or embolic stroke ,  tropinin ck-mb , CT should be  done 

  • Trey says:

    -Agreed: sick until proven otherwise.

    -V1 & V2 look sketchy.  Transmit it & maybe call med control for review and/or orders for NTG/ASA, etc. 
    -Stroke test(s)!
    -Also, does no one else see the possibility of WPW?  There may have been a transient run of an SVT-like rhythm.. thus hypoperfusing the brain and causing an anoxic "seizure" or the syncope.
    -Lastly, I tried doing a QTc two different ways (I don't do it often, so my math may be off), and I came up with 0.65s.  Isn't this extremely long?!  I've recently had a patient with a similar condition, but was extremely altered/combative upon arrival.  ER MD related  his long QTc is associated with Torsades..
    which leads me to say again: he may have had a short and transient episode of a hypoperfusing rhythm (Torsades, WPW/SVT, etc) which caused this.  The long QTc is associated with Torsades.  The WPW is associated with SVT.  Which came first: the chicken or the egg?

  • Trey says:

    (Also, can anyone direct me how to get an account here?  I see some of the same people who respond often with a little avatar thingy.  I'd just like to feel like a member.  Ha!)

  • harrison says:

    Sinus, LBBB by definition, flat T's in inferior, T wave inversion in precordials. Iffy ST segments in v3-6. ST segments beginning to depress in inferiors.
    I agree with trey's differentials. T's could be an after effect of a transient dysryhthmia.
    In this case though the stroke like symptoms > 12 lead ECG.
    If I saw this I would alert the hospital with a cardiac and stroke alert on the same patient. In my region, cardiac alert is one step down from a STEMI, used in suspicion of NSTEMI, or stable vtach, TCP, you get the picture.

  • harrison says:

    no LBBB my bad

  • Craig says:

    I am just going to throw this out there. Signs of lateral ischemia T-wave inversion in 1, AvL as well as V5 V6 with an upright AvR usually indicate LAD involvement as well as multiple vessel disease. I looking at it on a smart phone so it is hard to see everything that I want.

  • saraswathi says:

    could be SAH/ICH .. as the patient s having LVH  prob secondary to hypertension and QTc prolongation which is the most common ecg manifestation in SAH though it can present with st  elevation and t  inversion .. as the patient s not having chest pain i would like to rule out SAH by ct  brain and or DSA ..  

  • Newer EMT-I says:

    Really not sure…but I would go with treat the patient first.  He is pale and diaphoritic…something is going on.  I'm not convinced it's cardiac related though.  I would put O2 on as well as IV access witha fluid challenge and start moving to the hospital.  I would also do a stroke assessment to see if there were any signs of that.

  • The post has been updated with the past medical history, medications and neuro exam. I apologize for the oversight.

  • billy bob says:

    hx points to cardiac or stroke however the possible syncope spell with shaking is pretty vague; that could be anything up to and including an electrolyte imbalance. I would say it was a cardiac problem based on vitals hx and assessment. His neuro was good, his vitals don't really support a bleed (however still could be) and the SAH that Ive seen have produced DRASTIC changes (only seen a few) which I wouldn't call his EKG drastic. As mentioned above perhaps he had a run of SVT or V-tach. As far as the EKG I see a normal sinus rhythm, normal axis, and LVH with a strain pattern; I'm going cardiac  

  • Mel says:

    I would not think stroke here, but def neuro.  Transport to a neuro facility.  I see a sinus rhythm with LVH, T-wave inversion.  I may say there is a hx of mi, I see ischemia here.  But it does not appear to be cardiac to me.  Has anyone considered perhaps early signs of beta blocker toxicity?  I know the ekg dont show enough to prove this (late sign), but Im guessing the "shaking all over" could have been a beta blocker induced seizure… also prolonged qti in the inferior leads, inversion of t waves… its entirely a possibility.

    Any other complaints from the patient, or is he generally asymptomatic?  I would almost want to say beta blocker toxicity.  My treatment would be large IV, NS KVO, O2 @ 2lpm NC.  Cardiac monitor, and treat any other patient symptoms.

  • Igor PT says:

    I agree with VinceD.  There seems to be LVH. Sokolow-Lyon criteria is present: S V1+ R V5 > 35, Specifity 87%, ( in this case around 36/37), Framinghan criteria: S V1 or V2 + R V5 or V6 > 35. Here we have S V2 + R V6 = 27+18= 45. ( Don't know the Spec.)

    ST-T abnormalities and QRS around 100-110 ms  supports LVH. So the ST-T waves abnormalities and the tiny ST  elevation V1- V3 can be normal, due to LVH. But yes, to rule out STEMI we needed to have a prior ECG without any ST elevation V1-V3. 

    Another thing: there's no WPW nor delta wave. At all. What we see in the left leads, that "delta wave" is a consequence of an incomplete LBBB.

    When there's an incomplete LBBB, there's no Q waves in left leads. Remember that Q waves in left leads (and the small R wave in V1/V2) are consequence of the depolarization of the "left septum", which occurs a bit first than the "right septum."  In an incomplete LBBB,  the depolarization of the "left septum" is a bit delayed and when it happens, happens at the same time with the depolarization of the "right septum", so these 2 electrical forces neutralize it self and there's no Q wave. And, for the same reason, there's no R wave  ( or are decreased) in the Right precordial leads, V1 or V2.  And this happens when the delay is around 0,01 second.

    Beside this, specifically, when the delay is larger, between  0,02 and 0,03 seconds, there's also ( or could)  this upstroke of the QRS in left leads! (Complete LBBB is present when the delay is plus than 0,05 seconds )  And the presence of an incomplete LBBB also supports LVH, because LVH it's an excelent cause of Inc-LBBB.

    So, LVH, Inc-LBBB, can explain all these ST-T wave abnormalities. And of course…his age!
    To me, the most worrying detail, is that T wave in V5, +- . Even though it's necessary to rule out ACS and a stroke, this ECG, specially without chest pain, seems harmless!
     

  • Jeff says:

    In my differential I would think about subarachnoid hemorrhage .  I have seen it once in the cath lab.  Inverted T waves, elevated cTnI, and a clean cath.  Towards the end of the cath the patient just wasn't acting right.  Thanks to Dr. Smith's book, I mentioned this fact to the cardiologist.  We got a CT and there was a bleed. 

  • Brian Terzian says:

    The lateral T wave inversions look like a strain pattern 2/2 LVH, which he meets criteria for. Delta waves in the laterals, maybe PSVT that caused syncope? No impressed by the septal j point elevation, probably secondary to the LVH. Also should consider aricept as a cause of transient bradydysrhythmia (e/g/ av block), as it is a chilinesterase inhibitor (therefor it has choliergic effects).

  • Lance says:

     
    I agree with Brian, possible PSVT episode causing a decreased cardiac output that lead to the weakness and CNS hypoxia episode.  It would also explain the paleness and diaphoresis.

  • non – symptomatic  presentation  of  wpw  with  borderline  lvh  , geniuses  ,  check  his  glucose  ,  iv access    observation   transport    nobody  sees  a  delta  wave   huh  look  closely  !!! 

  • johan theunis says:

    You have to consider:
    .short P-R delta wave small qrs–>aberaant conduction dysrythmia and neurological symptoms
    .flipped T waves lateral STE V2-V4 –>LVH

  • doobis says:

    I wouldn't over anaylze the EKG or over think this PT too much.  Could be just about anything given his age, hx, and the 12 lead.  Take him to a capible cardiac and neuro facility, if available (I wouldn't call for air transport based on this if in a rural setting), and continue to monitor the PTs vitals, EKG, and mentation for changes.
    Unless the 12 lead changes, based on the limited info, I'd suspect something like a TIA.  With the P-Pul I think I see, maybe he has a hx of going in and out of A Fib and either had a syncopal episode with the A Fib or threw a little blood clot that resolved on its own.  I have personally seen something similar to this where an elderly man had normal vitals with SR but went into A Fib and became hypotensive when standing.  Orthostatic testing would be in order.

  • Doobis, you do have a point.  I had a patient yesterday as you described.

  • ToddB says:

    He's old, pale, and sweaty. With a history of recent trauma (falling), and the fact he's beta blocked with a hx of HTN I'm betting he's hypovolemic with limited ability to compensate. HR won't be as high on b blockers, BP may not look bad….but he has HTN.  I'd look for outward signs of trauma (belly/pelvis/etc)….but 12 lead doesn't really impress me. Call me crazy…..but I'm leaning toward expediting to a trauma center with appropriate treatment enroute (iv's , o2, cspine, etc). 

  • Chris says:

    Maybe I missed it somewhere, but what was the pt's position at time of pt contact? (laying on the floor?, sitting in a chair?…) If he's sitting up with that presentation I'd probably start by laying him down and seeing if his skin condition improved. I think I'll second Todd's post and say that I'm not super impressed by the ECG alone. ….. though I just did some reading regarding broad T waves and subarrachnoid bleeds… do the Ts on this strip qualify as broad?

  • Brian says:

    No reason to suspect stroke.. 12 lead- STE on V1, V2 (septal leads) and growing elevation in V3 but not yet at the 1mm mark.. There's a conduction disturbance that could be caused by the septal infart. Calling STEMI, take serial EKGs, watch the block since it may cause a dysrhythmia. There's LVH (probably from chronic HTN)..  Wouldn't be concerned with a slightly altered cognitive ability due to PMH. 

  • Sean says:

    He definitely meets LVH criteria, so the ST-elevation in V1-3 is a STEMI mimick, and he definitely looks like an incomplete LBBB, especially with the RSR pattern in Leads III and aVF. One could look at it and say maybe there are Delta waves, but without ECG evidence of the patient being in SVT or Uncontrolled/Rapid A-Fib or anyother type of tachycardia that one is a tough sell, especially since the incomplete LBBB can give the R-wave a slurred look to it.
    The other thing noteable with the LVH is some possible strain pattern, the look of the inverted T-waves has the look of strain patter, I mean this by saying that the T-wave appears to be pulling the ST-segment down, as opposed to the ST segment being depressed.
    Pt definitely has some Right Atrial Enlargment as shown by the wide & peaked P-wave in Lead II, which this could be chronic, or result of a tachycardic event causing fluid backup in the right atrium.
    No noteable axis-deviation, so this patient doesn't appear to be in any type of fasicular block, which if he had that coupled with the incomplete LBBB may cause badness such as V-Tach or other arrhythmias.
    The fact that this patient is Beta-blockaded and has a HR of 116 is extremely concerning, his HR shouldn't be getting much over 60-70, as well there is no tell-tale 1rst degree block notable, so he may have missed taking his Metoprolol, or he could have a small little bleed that could be messing with his sympathetic nervous system causing tachycardia… but I think that is reaching a touch.
    Ultimately we have a patient who had an event causing syncope or a siezure, which caused likely massive norepinepherine and epinepherine release causing his pale/cool/diaphoretic skin. We don't know his normal BP, so it's completely possible that he's hypotensive and compensating with the tachycardia.
    My bet though would be that there is nothing acute on this ECG since he's 90y/o, and it has a LVH with strain pattern (there is an app for the iPhone that makes 12-Lead recognition quite fast… I can't describe why I think this is strain, but it looks like it from looking at multiple 12-Leads with LVH and strain.. pattern recognition I guess), and possibly an incomplete LBBB. So this patient needs to be transported to hospital for cardiac workup, and some neuro workup too, as arrhythmia isn't the only cause of syncope or seizure. Postural V/S would probably be a good idea, and serial ECGs enroute just to ensure there are no changes.

  • Sean says:

    Looks like there was a conclusion to this once I scrolled down… guess I didn't really need to write all that. Meh, good exercise in critical thinking though.

  • Holly says:

    Ok, unless my eye sight is failing me, I dont see some of the things people are diagnosing. I see no BBB, im looking on my cell, but I have a clear picture. Also the diagnostics w/ LVH vs STEMI are quite clear, I dont see either here, Id personally call that early repolerization,but it could be LVH, definitly no ST elevation though. Abd remember that the main cause for LVH is prolonged untreated HTN. With this pt id be more concerned w/ syncope or first time sz. At that age, w/ that PMH, the even described, and findings, Id go w/ first time sz, which is a precursor to CVA in this situation.

  • George says:

    LVH with strain pattern and WPW

  • Chee Yong Chuan says:

    This is a non diagnostic ECG

    The history is actually not typical of a stroke. Sounds more like a pre-syncopal attack, however, a transient ischemic attack cannot be confidently ruled out. There was no neurological deficit upon arrival of the paramedics.

    The ECG shows:
    -Sinus rhythm
    -Regular, QRS complexes narrow, beating at a rate of slightly less than 100 beats per minute
    -Left axis deviation
    -No features of atrial enlargement
    -Features of LVH present
    *R wave in V6 + S wave in V2 >35 mm
    *rS complex in V1 and V2
    * Tall upright R wave in aVL
    *Strain pattern over the lateral leads evidenced by horizontal ST segment depression with T wave invasion over V5,V6 I and aVL
    *1mm ST segment elevation over V1-V3

    Features are consistent with LVH with strain pattern

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