Thanks to Jim Tarro for the following case study
43 year old female presents to EMS with “indigestion-like” chest discomfort.
She states that it “feels like a previous heart attack.”
Onset: Several hours ago
Provoke: Antacids make the pain feel better
Quality: “Indigestion-like” chest pain
Radiate: The pain does not radiate
Severity: She gives the pain a 7/10 at the time of evaluation
Time: The pain comes and goes
Vital signs are assessed.
Resp: 16
Pulse: 107
BP: 226/136
Past medical history: Myocardial infarction, HTN, CAD, NIDDM
Meds: Unkown
Allergies: Unkown
A 12 lead ECG is captured.
Does anything about this 12 lead ECG bother you?
*** UPDATE ***
Here is the 12 lead ECG captured at the emergency department.
Yes, it belongs to a 60 year old male – the patient is a 43 year old female!
angor animi – Interesting observation!
The follow-up ECG taken in the emergency department indicates a 43 year old female.I'm not sure why this one says 60 year old male.Tom
Because on a zoll the software defaults to a 60 year old male unless you remember to change it.
Thanks, medic1488!Tom
Flat/inverted T waves inferior and high lateral leads bother me. Big ole P-waves so RAE, V1 meets LAE criteria, agreed biatrial enlargement; not bothersome but noted. QTc is >440ms, 470ms is borderline for females for prolonged QTc; not bothersome but noted.Also her hypertension is profound, I want to address that after a deeper dive on her PMHx.
Christopher -The downsloping ST segments in leads I and aVL bothered me also the first time I looked at this ECG.Tom
Is she in failure?
Adam – I don't know what you mean by "in failure" but it doesn't appear to me that she's in acute decompensated heart failure (resp rate of 16).Certainly the pressure is high, and she has a history of MI, so there's likely a history of heart failure.The textbook definition of heart failure is the inability of the heart to meet the metabolic demands of the body at normal filling pressures.I do think it's safe to say that her filling pressures aren't normal.Tom
ED 12-L is bothersome too, to say the least. The "LBBB" looks a little weird for LBBB. Mainly the intrinsicoid deflection isn't slurred, but the terminal portion is slurred, which I thought was associated more with RBBB. Regardless, new onset no bueno.As far as a STEMI is concerned all I have is STD high lateral plus V4-V6 and STE in only III (aVF looks it, but when going from the TP segment it is isoelectric). Since the STD is in places which are reciprocal to my inferior leads, I'm going to go ahead and extrapolate that soon I'll see additional changes in II and aVF. Not enough to call a STEMI, but enough to have a high suspicion for IWMI.
Christopher – This is an excellent example of Tomas Garcia MD's advice to "consider the company it keeps." When I see downsloping ST-segments in leads I and aVL I'm already thinking acute inferior STEMI (especially with ST-elevation in lead III).But in this case, we also see a flattening and even slight scooping of the ST-segments in the right precordial leads, a possible new onset incomplete LBBB (as you say, no beuno), and perhaps most importantly, changes in serially obtained ECGs.I would not hesitate to call this a STEMI under the circumstances!Tom
I'm wondering what everyone else thinks of the downward slope of the QRS complexes in II and aVF, as well as the morphology of the top of the QRS complexes in III.I'm also wondering if there could have been a pathologic component of an acute MI that could cause atrial enlargement?
Billy – I'm not aware of any literature to suggest that notched R-waves are anything to worry about. Atrial enlargement usually coincides with ventricular hypertrophy (as does incomplete LBBB).Ventricular hypertrophy coincides with heart failure. MI can cause heart failure, but I don't know whether or not it can trigger ventricular hypertrophy.I'll have to read up on that one!Tom
I guess I should have noted that while I'm thinking STEMI, in order to call a Code STEMI I have to meet a rigid set of criteria. Which, at the moment, doesn't currently allow for these edge cases.
Christopher – Understood! Ours doesn't either. But at least the serial ECGs can allow for a prompt diagnosis on arrival (and ideally rapid transfer to a PCI center).Tom
Tom,I meant heart failure, sorry for being so vague. Just wondering about the atrial hypertrophy and HTN. Maybe an underlined pulmonary disease causing an increase in pulmonary pressure (then cor pulmonale). The ER 12-lead looks indicative of LVH as well. I always teach heart failure the same way. Heart failure in itself is the inability to meet the demands of the body. CHF is caused by the compensatory mechanisms resulting from heart failure. ie. The RAAS system, Norepinephrine release, BNP…I never rely on documented respiratory rates, unless some sort of ETCO2 device is used. It has to be the most fudged VS of them all.
Adam – I'd go even further and say that pulmonary edema is the result of the failure of the body's compensatory mechanisms! I definitely agree with you with regard to respiratory rate being a fudged vital sign. I count mine out and other people on scene find it very confusing!
The hard part is finishing without someone alerting the patient that you're counting his/her respirations! Tom
Biatrial enlargment
LBBB