60 year old male CC: Syncope

Here is yet another awesome case courtesy of Christopher Watford who writes the My Variables Only Have 6 Letters blog.

One of these days Christopher is going to say (in his best Darth Vader voice), “Once you were the teacher but now I am the master!” and it will be completely justified.

EMS is called to evaluate a 60 year old male patient who experienced a syncopal episode.

On arrival the patient is found sitting in the front seat of his car. He is ashen gray and cold to the touch.

He is in moderate respiratory distress.

Past medical history: Brochitis
Medications: None

Breath sounds: clear bilaterally

Vital signs are assessed.

RR: 30
Pulse: 118 (weak and rapid)
BP: 108/64
SpO2: 88 on RA (increases to 94 on oxygen via NC @ 4 LPM)

BGL: 79

The patient states that he “can’t afford to go to the hospital.”

The cardiac monitor is attached.

A 12-lead ECG is captured.

What do you think is wrong with this guy?

*** Update 12/10/2010 ***

This gentleman was diagnosed with bilateral pulmonary emboli. He was admitted to the hospital on Lovenox (enoxaparin). After almost signing out AHA he was persuaded to stay by a doctor and nurse who informed him in no uncertain terms that he would die if he left.

The most suggestive ECG findings were:

  • Sinus tachycardia
  • S1Q3T3 (S-wave in lead I, Q-wave in lead III, inverted T-wave in lead III)
  • Possible beginnings of an acute right ventricular strain pattern in the right precordial leads

It’s important to note that the most common ECG abnormality associated with PE is sinus tachycardia.

18 Comments

  • Dave B says:

    Sinus tach… P waves in lead II seem somewhat larger and peaked, which could point towards right atrial strain… inverted T waves anteriorly in leads V1-V4.. now, this could be suspicious of anterior ischemia, but there are also inverted T waves inferiorly in II.III and aVF.. this combination is HIGHLY suspicious for a large PE. there is also a hint of an S1Q3T3, but the inverted T’s anteriorly and inferiorly are even more specific for PE…
    does this fit the patient presentation? cardiovascular instability, sinus tach, rapid resps and low o2 sats.. I say yes.

  • Chris says:

    clinic and EKG looks suspicious for Pulmonary embolism.

    Nice blog btw.

    Best regards

    Chris. Sweden.

  • Med student says:

    Sinusal tachycardia, with an S1Q3 aspect(???), an increase of the RR, T wave negative from V1 to V4, SpO2=88% —> high suspicion of Pulmonary Embolism !

    He probably also has an incomplete LBBB ??? but we don’t have a story of chest pain…

  • eric says:

    I read someplace, and I’m trying to remember where, that S1Q3T3 is very non-specific for a PE. I’m not disagreeing with the PE DDx, but curious.

    Why the syncope? Doesn’t sound like he’s profusing well, but he has a MAP of about 78 (right now).

    I’m guessing he has a bit of Hx with the recent bronchitis and “can’t afford to go to hospital” “No meds”… got that, but I bet he should be.

    Tx: VS, Lung sounds again, IV w/ fluid bolus of 250 ml to see what it does, run another 12-lead, keep him on the O2 at a level that keeps him above 94%, get more detail on the Hx, transport.

  • Terry says:

    Would definitely like to know more of a hx about this guy. Would question him more on hx of pulmonary disease heart disease etc etc. Recent travel, surgeries, birth control–just kidding. The EKG and pt presentation leans toward a PE so it would definitely be high on the list but so would MI. IV, O2, Monitor, ETCO2 would be real good with this guy and then scare him into going to the hospital. SIR YOU COULD WAKE UP DEAD!!!!

  • Scott says:

    Initially sinus tach w/ a PVC.

    Sinus mechanism @ ~ 120 w/ ~ axis of 75. There’s S1 Q3 T3, however there is virtually no T wave in II and the T wave in aVF is flipped. Inferior ischemia? and there are flipped T’s in V2-V4 (anterior ischemia). No STE/ STD.

    As far as differentials: I’m thinking VQ mismatch 2′ PE (how long’s he been sitting/ stagnant in the car? And farther down the list and in spite of the clear LS’s…how’s the bronchitis tx going? Is that something he also can’t afford? Then there’s the ischemic conduction system throwing PVCs. Maybe a self limiting run of V-tach?

    TX: as far as the PE goes, not too much you can do pre-hospital aside from continued O2, continued monitoring, IV. Cardiologically, (is that a word?) be aware of more PVCs and where they fall, and be prepared for another run of ???

  • Geoff says:

    I also am leaning towards PE. Sinus Tach, signs of right heart strain (peaked P waves in II (P Pulmonale – right atrial enlargement, inverted T waves in V1-V4 also sign of right heart strain I believe). S1Q3T3 pattern, not very specific, but it is there, syncope, low O2 saturation, looks bad.

    O2, transport and monitor. Terry mentioned etCO2, we are just starting to use that w/ CPAP on a nasal cannula, so work with me here. PE = ventilation w/o oxygenation, I assume our etCO2 readings will be high? Is there any specific waveform to look for?

    Great strip

  • harrison says:

    Initial assessment was good, I would bump up the O2 to 5LPM (per my protocols 94%spo2 isnt an acceptable stopping point) to see where the SpO2 goes.
    I would additionally try to inquire about the onset of the dyspnea, if that was with the syncope.

    Either way, the 12 lead shows sinus tach @ 113, however the patient is likely anxious due to waking up and being surrounded by EMS/lights/sirens after a syncope.
    Inverted T’s in V1-V4. Flattened T’s in V5-V6. I would prefer taking this patient to his ‘usual’ hospital, where they can pull old EKG’s. The T wave inversions are quite deep though, suggesting this is new and further suggesting ischemia.
    The S1 Q3 T3 pattern suggestive of a PE is present. The Q’s aren’t as deep as I would like, but they are still there.

    I would start an 18ga or larger IV lock and transport non-emergency to the patient’s usual hospital. The only difference is I would titrate the O2 to keep the SpO2 to my medical director’s likings.

  • VinceD says:

    Another hint towards PE that nobody’s mentioned yet (I think) is the somewhat slow R-wave progression in the precordials. I’ve heard the point where the S and R waves are of roughly equal amplitudes referred to as the “transition zone,” and usually this occurs around V3 or V4. In this tracing, however, it doesn’t occur until V5. Of course, that can be also due to poor lead placement, but if it was Christopher Watford running the call, I doubt that was the case. Like most ECG manifestations of PE, this finding is neither very sensitive or specific (actually I’d venture a guess it’s much less so than the rest), but combined with all the other signs that people mentioned, it’s a clue that can help solidify our working diagnosis.

  • aaron says:

    just curious why he wasnt put on high flow o2

  • EMT-PinNEPA says:

    Sinus tachycardia with occasional PVCs. T wave inversion in the inferior and anterior leads, physiological left axis, possibly an incomplete left bundle.

    Do we have a 15-lead or right-sided 12-lead?

  • Christopher says:

    Aaron,

    Was hard to get him to agree to the transport, let alone the nasal cannula. It was determined that some O2 was better than him refusing all O2 (e.g. a mask).

  • Matthew says:

    I to would be suspicious of a PE, but a little more on the patient’s history would be great. I would definitely do a 15 lead to rule out any further cardiac issues. Since this patient was sitting in a vehicle was the vehicle outside or in a garage type setting, You can not rule out CO poisoning.

    Treatment From The Info Listed: O2, Fluid, but cautiously not to fluid overload, Repeat 12-15 leads, BGL, Etco2, Repeat Vitals.

  • ML Medic says:

    If he has Chronic Bronchitis, then the RAE plus the low voltage QRS may be a sign of Cor Pulmonale as well. His low sats may be falsely low because of the polycythemia that often accompanies. If this were a true S1Q3T3 then the S wave would be deeper than the r wave is tall in lead one (this a right axis) However this is a low sensitivity item (23%). Though PE can be a differential here, I’d of liked to seen the capnograph. That would help settle this V/Q mismatch idea. With sats increasing with mild oxygenation makes me wonder how a big PE can increase o saturization some easily. Good Call for a 15 lead ECG!
    It has been my experience that if something is wrong and we are stumped, there is something we didn’t assess?. Heart tones? any murmurs, or Gallops that could diminish CO? That is usually why people go syncopal (decreased CO). Great Case

  • This is most likely a large pulmonary embolus. Syncope is common in Pulmonary Embolus, there is classic ECG findings and the story and sat support the Dx.

    I disagree Chronic Bronchitis is an episodic disease and is not likely to cause a cor pulmonale or ecg changes suggestive of that. And you can’t have an incomplete bbb with a QRS of 86 mS.

    At this time, only prehospital ultrasound could give us more information.. ie a dilated right ventricle straining to eject blood would also corroborate the Dx of Pulmonary Embolus.

  • Michael B says:

    Also of note is the beginnings of a prominent terminal R wave and ST elevation in lead aVR. Emerging research about the applications of “the forgotten lead” point to greater value in identifying changes in R heart dynamics in aVR due to the unique view afforded by this lead of the right ventricular outflow tract.

  • Patrick Burnside says:

    Actually prob submassive not that likely to die esp since he was diagnosed. Heparin does drop RVSP but doesn’t really impact mortality so if he made it to the ED his native tPA probably preserved him since no lytics…it’s the next one that could get him….

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