51 year old female CC: Near Syncopal Episode

This case comes from a reader who wishes to remain anonymous, as always details have been changed to protect patient and provider privacy.

You're working an overtime shift at a college football game on a hot Saturday in August, when a man flags down your crew. You head on over and are directed into one of the stadium tunnels to a female laying on the ground with bystanders pouring cold water onto her.

One of her friends reports she felt hot and dizzy while watching the game and came into the tunnel to, "cool off." She then said she felt faint and her legs gave out from underneath her and she fell to the ground.

You introduce yourself and ask the patient how she feels, however, while her eyes track you appropriately she is very lethargic and slow to answer. Her friends are unaware of any medical problems your patient may have.

Your partner obtains a set of vitals while you place the patient on the monitor.

  • LOC: alert to verbal (GCS E3 V5 M6)
  • Pulse: weak radials at 50 bpm
  • BP: 80/50
  • RR: 14, shallow, clear lung sounds
  • SpO2: 92% r/a
  • BGL: 68 mg/dL (3.8 mmol/L)

Your event jump bag lacks all but basic trauma and IV supplies so you request an ALS unit meet you on location. Your partner establishes an IV and hangs a bag of fluids. The rhythm strip prints out.

Wouldn't Want to Miss the Big Game - Initial Rhythm

Noting a difference in rate, you ask your partner to recheck her radial pulses. He confirms they are now at 120/min and weak; you direct him to place a BP cuff around the liter bag and to work on a second line.

Your partner asks, "should we give her anything for her blood sugar?"

A quick history from the patient reveals no major medical problems, takes no medications, has no allergies, and she denies any history of diabetes. You acquire a 12-Lead ECG as the ALS unit checks on scene.

Wouldn't Want to Miss the Big Game - Initial 12-Lead

Multiple rhythm changes are noted on the monitor and a long strip is printed.

Wouldn't Want to Miss the Big Game - Long Rhythm Strip

The ALS crew asks you for a report as you help place her on their stretcher.

  • What is your diagnosis? What are your next steps?
  • What does the first rhythm strip show?
  • What does the 12-Lead show?
  • What does the long rhythm strip show?

37 Comments

  • Darryl Hoke says:

    It could be multifocal atrial tachycardia caused by hypoxia.  I'm surprised they didn't mention high-flow O2 before doing anything else.  BLS before ALS.  Without a hx of hypoglycemia, not too concerning at this point.  Treat the hypoxia, transport in Trendelenberg, treat for shock, monitor, continue fluid resuscitation.  My diagnosis is that it may be heat syncope.

  • Elaina says:

    Anteroseptal STEMI … The longer strip looks like an intermittent AV block secondary to the ischemia … Needs to go to the cath lab NOW!

  • Shalom says:

    How does her skin color look?
    Temperature??
    ECG: the rhythm is what appears to be junctional tachycardia(retrogade p waves buried in the t waves).
    There is incomplete RBBB, STE in the Antero-Septal-Lateral walls, hyperacute T wave and reciprocal STD.
    By the ecg and syncope/dizziness episode we must suspect STEMI (which among women very oftenly doesn't manifest with the classic chest pain and other classic symtoms)

    On the other hand, considering the hot day, lethargia, low BP, and tachycardia I strongly suspect heat stroke which can cause secondary STE(what is her temp.??).
    The long strip seems to show junctional tachycardia with occasional atrial and ventricular escape beats.

  • Mank says:

    according to my opinion the 12 lead of the rythm look like junctional tachicardia with anterior ekstensif ST elevasi, T wave abnormality.  first rythm step show atrial tachicardia, examine the causes of tachicardia, observe 5T, 6H and  give oxygen binasal to threat hypoxia and improve SpO2, to maintain perifer oxygenation adequately. Long rythm strip show junctional tachicardia,

  • Mike Fraser says:

    It appears this patient might be having a cardiac event.
    12Lead ECG shows obvious ST Elevation in V1, V2, V3 & V4 with reciprocol ST Depression in Leads 2, 3 & AVF, inferior leads. ? ST elevation in AVL and V5, lateral leads. A very busy ECG!
    Likely this patient is having a massive Anterior STEMI.
    Absolutely right to treat the C deficit first with high flow Oxygen to bring the O2 saturation up. 
    IV access a must for this lady, large cannula in the ACF  as this patient might require large fluid resuscitation as she is already Hypotensive. Although now the patient is no longer bradycardic, probably the cause of the BP drop, hopefully a BP rise might be observed.
    If the patient has chest pain, obviously treat as ACS, go through the motions of Aspirin, GTN, Entonox, Morphine and convey the patient to the nearest Cath Lab. (Depending on which ambulance service you belong to).
    It might be worth attempting to bring the BGL up with some Hypostop if she is able to maintain a patent airway, but probably the last thing to consider.
     

  • Francis says:

    I am bar far no expert so I may be incorrect in my assesment here but looking at both ECG’s I am seeing what could be LQTS. I am not convinced of RBBB and the wide QRS may suggest heat stroke but I would still run serial ECG’s apply high flow O2 via non rebreather and transport to the Nearest ER for monitoring.

  • Chris R. says:

    We are looking to a anterior STEMI. Probably proximal to the i.m. and septal branch.
    Pseudo-RBBB; there is a retrograde P-wave because of a junctional tachycardia:
    Look at the rhtyhm strip; there is a normal conducted atrial beat with no RBBB, when the rhtyhm change, there is a new broad s-wave (or r-wave, depends on which lead you look at).
    So the rhtyhm strip shows a junctional or atrial tachycardia (don't think its re-entry because of the onset).
    Diagnose: maybe Tako-Tsubo cardiomyopathy because the lady was stressed because of the football game?
     

  • MarkB says:

    Clearly alot of people above forgot what EMS is! HI flow o2, Lg gore IV– get bp up to atleast 90. BLG-60 is the new 80. It is a MI. early warning to hospital of choice. Large bolus of deisel. Quit making this so hard people!

  • gbards says:

    I Agree with MarkB!

  • ST elevation in v1-v2 might be isolated right ventricular infarction which explains the hypotension

  • Chase says:

     I am really not too worried about that spo2. Ya I am going to put her on some O2 but throwing on a NRB @ 15 lpm is not my priority, I would start out with a NC and go from there. I agree on the large bore IV access and fluid. The first EKG looks like Junctional Tach, the 12 lead appears to be an Extensive Anterior/ High Lateral MI (proximal LAD). The long strip looks like Junctional with ectopic atrial beats. The patient's symptoms are atypical and with a large Infarct, as suggested by the 12 lead, I would expect chest pain and possibly some flas pulmonary edema. 

  • doobis says:

    First, with regard to the low SpO2 readings I'd take them with a grain of salt because of the hypotension and SpO2s do not tend to read accurately with lower perfusion states.
    Start with the basics as usual – NC O2 (don't want to flood the body with high O2 which will cause vasoconstriction and can produce free O2 radicals in damaged myocardium).
    Stablize the B/P.  Fluids being the first choice but watch for pulmonary edema formation.  May have to consider a cardiogenic shock state and treat accordingly later on but that is down the road.
    Place the quick patches on in case the PT goes into a fatal rhythm requiring the use of joules (be proactive).
    Lead II appears to be a Sinus Tach with the P waves buried in the T's.  I can see the possible retrograde P's but they seem to occur when the base line is wandering so I am suspect it may just be part of the artifact.
    On the 12 lead, it appears to be a large anterio/septal MI.  I'd prefer to take another 12 lead before I call it though and would prefer there not to be so much movement.  QRS only seems to be around .08 on the EKG, don't see any BBB, etc.
    On the strip – I'll probably mess this up a bit.  But I think it is gonna be something along the lines of SA standstill – not firing.  In responce the ventricles are starting some escape beats. Sometimes these escape beats are fusing with the QRS.
    I'd be expiditing the PT to a cardiac hospital.  Stabilize the PT, give ASA and nitro if not contraindicated.

  • doobis says:

    Looking at the last stip a bit closer I see where it looks clearer that it could be a junctional rhy.  Honestly though it does not affect my treatment of hte PT and I would not be spending my time on this critical PT trying to deterimine if the SA nodes are firing or if it is junctional in nature.
    THe only time I can think where differentiating SA vs junctional is on a simple bradycardia PT and needing to increase the rate with either pacing or atropine.  Even then, it is not that critical on a practical side of things in the field.

  • Brooks Walsh says:

    Goodness, look at that QTc. That's long!
     
    I'll push my chips onto an acute LAD occlusion

  • MarkB says:

    "NC O2 (don't want to flood the body with high O2 which will cause vasoconstriction and can produce free O2 radicals in damaged myocardium)."      Doobis obviously did not read the pt's vitals from above. And what is gonna kill that pt faster– "free O2 radicals" or dead myocardium?
    How do you people think up this crap?
     

  • Christopher says:

    MarkB,
    Usually through scientific literature.

  • Nicky G says:

    Wow MarkB time to get out of bedrock.
    Very tricky case. Firstly she does not have chest pain however the STE that everyone else has commented on definately warrants trip to pPCI capable facility.
    Is the STE due to a lack of perfusion or mild tachycardia she is experiencing? chronic supply demand vs acute thrombus? quite atypical symptoms. 
    Furthermore I am no expert but I wouldnt mind throwing sick sinus syndrome into the mix due the initial bradycardia, now tachycardia and frequent sinus exit blocks. (that is of course if the fluid bolus was not the reason for increased HR….bainbridge reflex etc)
    Im stumped on this one. Unless something further jumps out in the history/VSS treatment as per crew on scene and give some aspirin with early prenotification.

  • doobis says:

    In reply to MarkB:
    First, as I stated in my first reply – I would take the SpO2 readings being low with a grain of salt given his low perfusion state and would focus my attention to other areas first.
    2nd, 92% on RA is not great but is not so bad as to necessairly justify going all in with the O2.  I'd prefer to take smaller steps that could correct the situation rather than take drastic steps such as a low flow NC – don't need to win the SpO2 battle in the field if it worse for the PT in the long run (the pyrrhic victory).  Besides, I didn't read anything that said this occured at a location at sea level.  Maybe it is at a higher elevation which, if I am not mistaken, causes SpO2 to be naturally lower in PTs than if they are found at sea level.
    3rd, I don't claim to know everything.  These were just my thoughts.  How I respond to a few paragraphs and a few EKG strips on here with my thought process does not ncessairly compare to how I'd respond in dynamic real life situation.  Just last week I had a PT with a Inferior STEMI and his SpO2 was in the lower 90's.  I placed him on CPAP along with the usual ACLS treatments.  Why?  Well I figured his DIB secondary to the rales he had as a result of the MI demanded a stronger response so as to force the fluid out that was building in his lungs.  (There was no R sided elevation noted in this PT and he had been experencing CP on and off for several days without treatment.)
    Finally, O2 radicals are potentially highly destructive in stressed and damaged myocardium.  Hence the effort recently to be more judicious with O2 administration.  Of course the O2 radical theory could be thrown out in the future just as so many other treatments and procedures have been in the past.

  • Mike McD says:

    yup, big ST elevation and reciprocal changes. chewed aspirin, maybe oxygen (monitor Sp02, idiots). lay flat. phone call and cath lab. I really didn't even look at the rythm (didn't zoom in on computer), and I never bothered to visualize a p-wave. who cares? it might be nice to give NTG or Metoprolol (even lasix if rales, if you need to, and BP permits).

  • Mike McD says:

    almost forgot: clot busters depending on regulations/protocols in your area 

  • CTMedicA504 says:

    Funny, I saw a similar 12 Lead ECG today that I plan on submitting.  This patient appears to be having a few issues going on.  I agree I want to know her temperature and rule out heat stroke as an additional ailment.  My main focus and priority is to me what is an obvious cardiac event.  She is most like a high proximal LAD occlusion, willing to bet 100% or close to it.  She needs fluids with out overloading her, Aspirin if she can follow directions to chew it.  If we can increase her pressure we need to start juggling the possible use of Nitrates.  She needs an early activation of the Cath Lab and transport to that appropiate PCI facility.

  • MarkB says:

    Hey Nicky and Doobis— K.I.S.S  — Keep it simple, stupid. Unless you are interventional cardioligists, your job is to transport, not diagnose.
     

  • Christopher says:

    MarkB,
    Then why carry a cardiac monitor at all? Should just scoop and run. It is the biggest lie told in EMS that paramedics do not diagnose, and one of the most dangerous too. Many services expect paramedics to properly diagnose cardiac rhythms and 12-Lead ECG's. If your service is not one of them you should push for this, as you're not really a paramedic if you cannot or do not.
    I don't want you to waste your time on this site as it is meant for people looking to learn something. Perhaps you'll find a better fit elsewhere.

  • doobis says:

    MarkB – anyone with or without real training can parrot "O2, Nitro, Morphine, and ASA".  Everyone can also state drive to the hospital quickly.  We know this is the foundation of STEMI/CP care.
    This blog is about learing and seeing new things and critical thinking.
    And if you look, the authors placed four bullet point questions at the end of this case to generate discussion.  This is a thinking and discussion board so people are going to think and discuss.

  • doobis says:

    Also, MarkB, we don't  "diagnose" but we develop an unofficial field diagnosis and treat accordingly using protocols and with medical control.
    And the whole diagnosis thing is a bit stale.  People diagnose themselves all the time.  If that is not the case, why do we have OTC medications?  I don't need a doctor to diagnose my head cold, I dianose it and treat it with ASA on my own.  I don't need a doctor to dianose my open fracture, I just need him to fix it.  If I see a STEMI on the monitor, I "field diagnose" the STEMI and treat.  I defer the final dianosis and treatment to the doctor that has years more training than I in this field as he is the higher level professional.

  • deezy says:

    Doobis, we do diagnose.
    Just not in the manner you're thinking.
     
    BTW it's a clear as day STEMI.

  • Dan says:

    Maybe I’m trippin’ but it looks like a big anteroseptal mi with a sinus 1st degree block. The blood sugar is unremarkable imo. Take to a PCI capable facility.

  • Pelagic says:

    This Pt has a MAP of 60 with inadequate sats. That's a life threatening lack of perfusion and oxygenation to major organs including the heart itself in my book.
    If you don't correct that downward slide – nothing else matters – she's dead anyway.
    High flow O2 and cautiously titrated fluids to restore adequate BP and stroke volume. I don't want to flood her with fluid, she's almost certainly in cardiogenic shock, her heart isn't up to being flooded with salty water, we just want to restore enough BP to keep her viable?
    All this "Oxygen is a vasoconstrictor" is Bovine Scatology in my book. This is an MI not a CVA. Hypoxia will kill this lady. She's obtunded and syncopic:  lack of cerebral perfusion / oxygenation anyone?
    Asprin, Clopidogrel, Morphine if she's in pain and a cath lab on the hurry up
    If it looks like a duck and quacks like a duck…….  : KISS

  • Chase says:

    Pelagic,

    Do you put ever patient with a Spo2 of 92% on high flow O2? And by that I assume you mean a NRB @15 LPM. I would not consider 92% “life threatening” hypoxia in this situation, especially given the hypotension. The hypoxia did not cause the syncope. You are welcome to have your own opinions but the physiological effects of oxygen are well documented. The impending cardiogenic shock is more of a concern.

  • STPEMTP says:

    1.  DDX: Anterior-lateral STEMI, Heat stroke/hypovolemia
    What is this patient's temp and the ambient temp? Based on case it appears we already have 2 IV access.  What is the cap refill in the hands? What does the pleth wave on the Sao2 look like? Is it a "good" waveform or is the Sao2 being a random number generator? O2 via NC at this point and re-address in a couple of minutes (assuming Sao2 showing good waveform).  Apply pacing/defib pads (bradycardic once already, abnormal rhythm, STEMI, and suggestion of intraventricular conduction issue highly suggestive that this maybe a very large infarct.) ASA, NTG (prefer via drip if allowed due to episode of hypotension) via your protocols.  I would hold on beta-blockers if allowed via protocol  (they have already had 1 episode of bradycardia) If reasonable to directly transport to PCI capable facility, definitely going that route with this patient. (may be more reasonable to go to closest facility if nearest PCI facility an hour away).  Have a gram or two of Mag sulfate ready in case this patient does go into a ventricular arrhythmia (definitely NO amiodarone here)
    2.  Initial rhythm strip shows a junctional tachycardia
    3. 1. It appears to be a Anterior-Lateral STEMI. STE AVL, V1-V5 (lead I looks like maybe 1/2mm, but hard to tell with baseline wander). QRS does not appear to be greater than 0.12, calling it incomplete RBBB pattern. V4-V6 QRS complexes look to be very large, suspect LVH. QRS axis appears to be in normal range.  QT interval approx 50-60% of R-R interval = Long QT. (does not preclude STEMI call)  I'm not the best at the fasicular blocks but I would be concerned one is developing/present here (increased mortality and suggests a large infarct present)
    4.  It looks like a junctional tach in the middle of the strip.  As for the "clumps" at the beginning of the strip, not really sure what to call that.  Could be a Sinus brady with junctional escape beats, vs intermittent complete AV block (looks like a junctional complex is dropped before the sinus beat at the start of the "clump")
    As for the blood sugar, it is not considered abnormally low for the "normal" pt.  Check her fingertips for scar tissue or signs of recent lancet punctures along with her lower abdomen for any signs of frequent injections.  Is it abnormally low for this patient?  I don't see any harm in giving some oral glucose here to rule out a hypoglycemic cause for the decreased responsiveness. (I'm heavily leaning toward a cardiac cause for it though)
    Great case, and hats off to the crew on catching this! 

  • Rico says:

    Paramedics don't diagnose? Really? Well, this one does, and so does every other modern day paramedic worthy of the responsibility of calling themselves a paramedic. "Amblance [sic] drivers" disappeared a long, long time ago where I live. If a person worked in any system around my neck of the woods and treated a patient like some suggest (transport with HF O2 while driving like your hair is on fire), they would be disciplined (or fired) for not recognizing this for what it is and treating it appropriately. This is the 21st century folks, let's start acting like paramedicine belongs in this century!

  • Pelagic says:

    @Chase
    It's not just about the sats surely?
    This patient has low blood pressure combined with low sats which adds up to a general lack of perfusion as a time when as we now know with hindsight, the most crucial organ in her body is being starved of oxygen with a 100% LAD occlusion?
    Even if you just want to take the universaly accepted protocol on face value – ACS is "high flow oxygen". Not "a little bit "
    Likewise, you might want to think about "hypoxia did not cause the syncope"? What is syncope?Especially in light of "she is very lethargic and slow to answer"

  • Christopher says:

    Pelagic,

    ACS is actually not a high flow oxygen situation and hasn't been for a while.

    Furthermore, syncope from hypoxia is not the same as syncope from hypovolemia. Our patient's altered mental status is due to hypoperfusion as you correctly noted, but not because her blood is hypoxemic. She has hypoperfusion due to pump failure.

    Correcting the pump failure will correct the hypoperfusion, correcting the hypoperfusion will correct the altered mental status. Addition of high flow oxygen isn't going to correct the pump failure and hyperoxemia will not correct her hypoperfusion.

    Some supplemental O2 while you aggressively treat the pump failure is all that is needed. High flow O2, however, is just not indicated.

  • Pelagic says:

    My bad – I didn't read the original sats correctly – apologies

  • Dave says:

    It’s common for females to have a heart attack without chest pain. Ecg clearly shows STEMI in anterior and septal leads. This lady needs to go to cath lab STAT. Give ASA on the way, heparin bolus and plavix or other antiplatelet if you carry it. I’m not worried about 92% spo2. Even at 100% the oxygen isn’t getting to heart muscle. If you are bored and have time you can put oxygen on while en route but don’t shoot or expect 100%. The long strip looks like mobitz 2 (would like to look at real strip) although this is more likely in inferior MI. There is ST depression in inferior leads so ischimia may be present.

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