By request I'm trying something new. The 12-lead ECG will be cropped and the computerized interpretation removed until the solution is posted. Let me know if you find this approach to be useful. This is how I used to teach 12-lead ECG interpretation but I started leaving the computerized interpretation because that's reality — you'll have access to it in the field (unless you're one of those few systems that turns the comptuerized interpretation off).
EMS is called to the residence of a 63 year old male with a chief complaint of shortness of breath.
On arrival the patient is found sitting on the edge of his bed. He appears to be in moderate respiratory distress.
Past medical history: HTN, IDDM, CHF
Medications: Numerouos (the spouse hands you a large plastic container full of medications)
On questioning the patient admits that he is also experiencing chest tightness.
- Onset: 30 minutes prior to EMS arrival
- Provoke: Symptoms are worse lying flat
- Quality: "Tightness"
- Radiate: The sensation does not radiate
- Severity: 5/10
- Time: Patient admits to prior episodes.
A prolonged expiratory phase is noted.
Breath sounds: basilar rales
Vital signs are assessed.
- RR: 26
- Pulse: 80
- BP: 179/92
- SpO2: 84 on RA
The cardiac monitor is attached.
A 12-lead ECG is captured.
By request here are the computerized measurements:
- HR: 78
- PR: 206
- QRS: 104
- QT/QTc: 430/490
- P-QRS-T: 23 -39 159
What is your interpretation of these ECGs?
How would you treat this patient and why?
SR with 2 mm of anterior/septal elevation. it is hard to see the actual width of the QRS but i don't think it is wide or LBBB causing this. Possibly anterior hemiblock so try to avoid antiarythmics – none are needed here. Lateral T wave inversion in I and V5, V6= likely reciprocal ischemia. Tx=ASpirin. IV, start sucking on NTG. Titrate 1-3 nitro's at a time based on BP. O2 via NRB. Consider CPAP. If CPAP then add NTG paste. tx sitting up to furthur reduce preload. add Morphine if no improvement from above. Repeat 12lead. transport.
F.
Rate-75..
Rhythem–Sinus..
Lead2&3–Horizontelization of ST Segment
Lead V5&V6–T Inversion..
Lead V1+V6(R amplitude)>/=35mm-LVH
Interpratation–CORONARY INSUFFICIENCY/EVOLVING MI
LVH
I would treat for CHF. 1) High Flow O2, 2) IV 3) Nitro 4) diuretic, 5) Patient in a sitting position 6) serial 12 leads 7) monitor for changes and transport
Initial impression prior to EKG leads me to go one of two ways, pneumonia or CHF, seeing as it’s a sudden onset without support for the pneumonia, I’ll stick with CHF as a start point. So, CPAP, check for any meds for ED, IVx2 if I have time. Meds are going to be nitro drip at 20mcg titrate up at 5mcg unil effect is desired maxing at 100mcg per my protocol.
12 lead shows a possible septal/anterior MI, nitro is on board, now getting 324mg or ASA or balance if he prescribed 81mg QD. get transport started, recheck interventions, notify PCI, get serial 12 leads q5-10 to check for progression or reperfusion. Transport emergent depending on distance from hospital and outcome following interventions.
I’d like to see the QTc though. I like it for a quick judgment on heart strain.
Treat for CHF exacerbation. NSR w/ 1 degree AVB. LAFB. LVH. Discordant ST elevation in V1 through V3 with concave ST segments suggesting a strain pattern. Inverted T waves in the high lateral and lateral leads suggesting possible ischemia. Serial ECG's for sure.
What time was the monitor strip and ecg recorded at?
Did the patient recieve any treatment from the medics before the ecg was performed?
There seems to be some normalization of the ST segments when comparing the montior strip with the ecg…
Seems to be LVH with strain, LAFB, and borderline 1 degree AV Block.(But as I said before there may have been some change..)
Treat the CHF and respiratory distress שמג dont forget serial ecgs!
* Sinus rhythm @ 78 bpm
* 1st degree AV Block
* QRS axis ~ -40 degrees (left axis deviation)
* LVH w. secondary ST and T-wave changes (not unusual w. a Hx of CHF)
* Left atrial enlargement (fits w. LVH)
* Poor R-wave progression (either due to LVH or poor lateral precordial electrode positioning, common in larger patients where it's tough to reach all the way to their axilla, who make up a good poopulation of our CHF patients)
Now for the nuanced stuff:
Most leads exhibit appropriate discordence between the QRS and ST-segments in the face of LVH, except for aVF, where there is none of the expected elevation but rather the ST-segment is isoelectric with the baseline. Given the rest of the findings, I'm willing to let this go as normal, but if there was even half a millimeter more depression then my warning lights might start flashing a bit. There is some LAD deviation, but in the face of LVH I cannot call a LAFB, plus it's not quite the degree of LAD expected for a typical hemiblock, so is likely just secondary to the LVH.
Considering my interperetation above, all of the findings tie nicely into what you would expect for someone with chronic CHF. Additionally, there aren't any signs that seem out of place to me (except for aVF, as discussed), so I see no indication to call this a STEMI. Thankfully, there is also less than 2mm of elevation across the right precordials, so my regional protocols wouldn't have me calling a STEMI Alert either. Phew…
On that note, while I don't see any acute changes on the ECG, his Hx and physical findings are quite worrisome and the fella is indeed sick. Also, his pulse is significantly lower than I would expect given his current status (poss med effect?). He warrants the full ALS workup with serial ECG's, aspirin, nitro, CPAP, and a sugar-check for good measure. Based on the info above, he gets non-emergent transport unless his clinical condition changes.
addendum:
* QRS widening (I'm measuring a QRSi on the wide side of 100, also a secondary finding of LVH)
I'm liking not seeing the computer readout, nice touch.
You can really see the biphasic "P" waves in V1/V2 which indicate IACD and notching in the limb leads point to left atrial enlargement, both support a history of left sided failure.
CPAP in my system is contraindicated in any patient who is showing signs of an possible / active MI. The worry is that you'll put damaging pressure on the coronary arteries which could exacerbate the infarction.
I would err on the side of caution and transmit to our doc (who has to approve any cath lab activation) based on his history of DM, line, ASA, NTG as long as BP supports and transport.
Impression: R/O CHF exacerbation secondary to AMI.
The computerized measurements have been added.
ant mi ………….but what about cardiac enzymes
I can see m mitlale- could be due to left atrial enlargement or mitral stenosis. From the symptoms: this patient can be suffering from acute onset of pulmonary edema secondary to acute hypertention. HTN is suggested by the BP and LVH evidence in ECG
LVH. T waves are asymetrical- non-pathologic . Treat CHF
lvh strainish
LVH treat for CHF