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Taking a step back , remember that sinus tachycardia is less commonly seen in OMI (except in cases of impending cardiogenicshock). Answer : Bedside ultrasound! Smith : RV infarct may also have this appearance on ultrasound. So hypoxia without B lines on lung ultrasound strongly weights toward PE. Both were wrong.
The patient in today’s case presented in cardiogenicshock from proximal LAD occlusion, in conjunction with a subtotally stenosed LMCA. Another approach is sympathetic chain (stellate ganglion) blockade if you have the skills to do it: it requires some expertise and ultrasound guidance. RCA — 100% proximal occlussion.
Shocked x 2 without effect. Pads were placed with ultrasound guidance, so they were in the correct position. As I discussed and documented in Lesson 1 of My Comment at the bottom of the page in the April 2, 2022 post of Dr. Smith's ECG Blog — certain patients may remain in sustained VT not only for hours — but even for days!
ACS and STEMI generally do not cause tachycardia unless there is cardiogenicshock. Then ACS (STEMI) might be primary; this might be cardiogenicshock. Even if this ECG is the first thing one sees (as it was for me), one should stop and think: "This is an unusual STEMI." Are the lungs clear? Is the patient cool and pale?
Smith comment: This patient did not have a bedside ultrasound. Had one been done, it would have shown a feature that is apparent on this ultrasound (however, this patient's LV function would not be as good as in this clip): This is recorded with the LV on the right. In fact, bedside ultrasound might even find severe aortic stenosis.
Tachycardia is unusual for OMI, unless the patient is in cardiogenicshock (or getting close). ECG 2 Especially in the context of the first ECG, readers of this blog will readily appreciate the ST elevations and hyperacute T waves in II, III, aVF, V6, and to a lesser extent V5. link] I also texted the ECG to Dr. Smith.
Case continued A bedside ultrasound showed diminished LV EF and of course bradycardia. RVMI explains part of the shock. OTHER Examples of Lead Reversal on Dr. Smith's Blog: Technical errors featuring a variety of lead reversal placements remain a surprisingly common “mishap” of everyday practice.
I would do bedside ultrasound to look at the RV, look for B lines as a cause of hypoxia (which would support OMI, and argue against PE), and if any doubt persists, a rapid CT pulmonary angiogram. Among others — See My Comment at the bottom of the page in the September 13, 2024 post of Dr. Smith's ECG Blog ).
Case Continued 2 days later the patient became increasingly tachycardic, hypotensive, ashen, clammy (in cardiogenicshock) and had a new murmur. Rupture can be either free wall rupture (causing tamonade) or septal rupture, causing ventricular septal defect with left to right flow and resulting pulmonary edema and shock.
A bedside cardiac ultrasound was normal, with no effusion. Assessment was severe sudden cardiogenicshock. NOTE: For those interested — I review in detail determination of the artifact “culprit extremity” in My Comment in the September 27, 2019 post of Dr. Smith’s ECG Blog. There is minimal, probably normal STE in V2-V6.
Thirty minutes later the first Troponin I came back elevated at 650 ng/L (normal <26), and bedside ultrasound found anteroseptal akinesia. But by this time the patient went into cardiogenicshock and passed away. But it didn’t meet traditional Sgarbossa criteria so the cath lab was not activated.
Just prior to transport, the patient became confused and agitated and, although blood pressure and pulse were OK, I was worried about cardiogenicshock. Diagnosis : Posterior MI, right? We intubated him. Cath lab The BP was 70/40 on arrival to the cath lab and received a balloon pump and norepinephrine.
I have always said that tachycardia should argue against acute MI unless there is cardiogenicshock or 2 simultaneous pathologies. Sinus tachycardia, which exaggerates ST segments and implies that there is another pathology. We showed this in a recent analysis of UTROPIA data (see abstract below).
An elderly man with sudden cardiogenicshock, diffuse ST depressions, and STE in aVR Literature 1. We’ve presented many variations on this theme on Dr. Smith’s Blog — with today’s case being distinguished by its discovery on abdominal exam ! A emergent cardiology consult can be helpful for equivocal cases. Left main?
Why is the patient in shock? He was in profound cardiogenicshock. They did not have an ultrasound on the ambulance (some local crews are starting to utilize POC limited US in our service areas). There is an obvious inferior STEMI, but what else? This STE is diagnostic of Right Ventricular STEMI (RV MI).
Often, intravascular ultrasound or intravascular optical coherence tomography is requeried to make the diagnosis. were pretty sick, with mostly LM/pLAD lesions and high rates of cardiogenicshock. Type 2 is more difficult to appreciate on angiography than type 1. Lobo et al. where more than 3/4 of cases were NSTEMI).
Whenever there is tachycardia, I am skeptical of OMI unless it has led to severely compromised ejection fracction with cardiogenicshock. I suspect pulmonary edema, but we are not given information on presence of B-lines on bedside ultrasound, or CXR findings. Or I suspect that there is OMI simultaneous with another pathology.
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