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Here is his ED ECG at triage: Obvious high lateral OMI that does not quite meet STEMI criteria. Bedside cardiac ultrasound with no obvious wall motion abnormalities. This confirms that the pain was ischemia and is now resovled. He had a previous ECG on file: Proving the findings are new The cath lab was activated.
This EKG is diagnostic of transmural ischemia of the inferior wall. If it is angina, lowering the BP with IV Nitroglycerine may completely alleviate the pain and the (unseen) ECG ischemia. Transmural ischemia (as seen with the OMI findings on ECG) is not very common with demand ischemia, but is possible.
He was rushed by residents into our critical care room with a diagnosis of STEMI, and they handed me this ECG: There is sinus tachycardia with ST elevation in II, III, and aVF, as well as V4-V6. At first glance, it seems the patient is having a STEMI. ACS and STEMI generally do not cause tachycardia unless there is cardiogenic shock.
This is all suggestive of posterior STEMI, but not definitely diagnostic. mm in only one posterior lead is highly sensitive and specific for posterior STEMI). I performed a bedside cardiac ultrasound and the posterior wall appeared to be contracting and shortening normally. The ECG normalized overnight. Maximum troponin was 2.1
This is a 45 yo male who had an inferior STEMI 6 months prior, was found to have severe LAD and left main disease, and was supposed to be set up for CABG a few weeks later, but did not follow up. But it could be anterior STEMI. 40% of anterior STEMI has upward concavity in all of leads V2-V6. is likely anterior STEMI).
4,5] We have now formally studied this question: Emergency department Code STEMI patients with initial electrocardiogram labeled ‘normal’ by computer interpretation: a 7-year retrospective review.[6] have published a number of warnings about the previous reassuring studies.[4,5]
This suggests diffuse subendocardial ischemia. However, along with that subendocardial ischemia, there is also STE in lead III with reciprocal ST depression in aVL, and some STE in V1. If there is also subendocardial ischemia, the ST depression vector remains leftward, with a reciprocal ST Elevation vector also to the right.
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. What should be done? Should the cath lab be activated?
If this STD were due to LVH or to subendocardial ischemia, rather than posterior OMI, it would be maximal in V5 and V6. A bedside ultrasound was done, with dozens of clips, and was even done with Speckle Tracking. Because we are hypnotized the STEMI paradigm. "If It was not a STEMI) 1. Here are a few clips.
There is ST depression beyond the end of the wide QRS in I, II, aVF, and V4-V6, diagnostic of with subendocardial ischemia. A bedside cardiac ultrasound was recorded: Here is a still image of the echo: The red arrows outline the right ventricle and the yellow arrows outline the left ventricle chamber. There is no ST elevation.
This has been termed a “STEMI equivalent” and included in STEMI guidelines, suggesting this patient should receive dual anti-platelets, heparin and immediate cath lab activation–or thrombolysis in centres where cath lab is not available. His response: “subendocardial ischemia. Anything more on history? POCUS will be helpful.”
The ECG shows obvious STEMI(+) OMI due to probable proximal LAD occlusion. There is no definite evidence of acute ischemia. (ie, Simply stated — t he patient was having recurrent PMVT without Q Tc prolongation, and without evidence of ongoing transmural ischemia. ( The below ECG was recorded.
When the ST vector is primarily posterior, the diagnosis is usually posterior STEMI. Contrary to what Ken stated, the ST vector remains mostly posterior __ What about subendocardial ischemia? Subendocardial ischemia results in ST depression, but unfortunately, and rather mysteriously, it does not localize to the ischemic wall.
Here is the EMS ECG: Obviously massive diffuse subendocardial ischemia, with profound STD and STE in aVR Of course this pattern is most often seen from etoliogies other than ACS. The ECG only tells you there is ischemia, not the etiology of it. This was a point of care ultrasound, not a bubble contrast echo.
This is all but diagnostic of STEMI, probably due to wraparound LAD The cath lab was activated. This was diagnosed by IVUS (intravascular ultrasound) as a ruptured plaque. This was clearly severe subepicardial ischemia causing ST Elevation, but it was not of a long enough duration to result in measurable infarct. But maybe not.
I suspect pulmonary edema, but we are not given information on presence of B-lines on bedside ultrasound, or CXR findings. Supply-demand mismatch can cause ST Elevation (Type 2 STEMI). Also see these posts of Type II STEMI. Truly, the Marquette 12 SL algorithm correctly identifies this STEMI. Management?
Such T-waves are almost always reciprocal to ischemia in the region of aVL (although aVL looks n ormal here) , and in a patient with chest pain are nearly diagnostic of ischemia. An emergency cardiac ultrasound could be very useful. Ischemia on the ECG can be very subtle and is easily missed. Lesson : 1.
This meets "STEMI criteria" However, there is very high voltage, with a very deep S-wave in V2 and tall R-wave in V4. The morphology is not right for STEMI. My interpretation: LVH with secondary ST-T abnormalities, exaggerated by stress, not a STEMI. This is very good evidence that the ST elevation is not due to STEMI.
Down-up T-waves in inferior leads are almost always reciprocal to ischemia in the territory underlying aVL. This is not normal and is a tip off that there is posterior ischemia accompanying the ischemia in aVL. Important Learning Point: "STEMI" is defined by millimeter criteria (1 mm in limb leads), which this does not meet.
The patient was brought to the ED as a possible Code STEMI and was seen directly by cardiology. Similarly, STEMI guidelines call for urgent angiography for refractory ischemia or electrical/hemodynamic instability, regardless of ECG findings. Refractory ischemia or electrical/hemodynamic instability are indications for the PCI.
I do not think this ECG is by itself diagnostic of OMI (full thickness, subepicardial ischemia ), b ut comparison to a previous might reveal this ECG as diagnostic of OMI. Immediate and early percutaneous coronary intervention in very high-risk and high-risk Non-STEMI patients. Lupu L, et al. mg/dL, K 3.5 Abstract 556.
This proves that the first one was, surprisingly, due to ischemia!! After rethinking the case, he remained concerned about ACS and subsequently performed a point-of-care ultrasound in order to evaluate for regional wall motion abnormality. A second troponin had been drawn 3 hours after arrival and was again less than 0.30ng/mL.
This strongly suggests reperfusing RCA ischemia. Troponins, echocardiogram An echocardiogram showed inferobasilar hypokinesis, further supporting a diagnosis of regional ischemia , likely of the area supplied by the RCA. A recent study found that SCAD causes almost 20% of STEMI in young women. There is also a Q-wave in III.
These kinds of cases were excluded from the study as obvious anterior STEMI. --QTc Case 1 Acute anterior STEMI from LAD occlusion, or Benign Early Repolarization (BER)? Appropriately, the physicians repeated the ECG 20 minutes later and it was diagnostic of anterior STEMI. QTc is the computer measurement. 100% LAD occlusion.
Normally, concavity in ST segments suggests absence of anterior ischemia (though concavity by itself is not reassuring - see this study ). His ED cardiac ultrasound (which is not at all ideal for detecting wall motion abnormalities, and is also very operator dependent for this finding) was significant for depressed global EF.
Dr. Nossen performed a bedside ultrasound which was interpreted as normal. Learning Points: Ectopic atrial rhythm can produce atrial repolarization findings that can be confused for acute ischemia, STEMI, or OMI.
I know from reading your blog that you "diagnose pericarditis at your own peril", but are there any signs on that initial ECG that would make you think ischemia? However, in almost every case, one should confirm absence of OMI (Occlusion MI) at least by contrast ultrasound. See this case: Pericarditis, or Anterior STEMI?
Ischemic ST-Segment Depression Maximal in V1-V4 (Versus V5-V6) of Any Amplitude Is Specific for Occlusion Myocardial Infarction (Versus Nonocclusive Ischemia). Recall that air is a poor conductor of electricity and will, therefore, generate smaller amplitudes on posterior leads (hence why STEMI criteria requires only >0.5
This suggests further severe ischemia. The problem is difficult to study because angiographic visualization of arteries is not perfect, and not all angiograms employ intravascular ultrasound (IVUS) to assess for unseen plaque or for plaque whose rupture and ulceration cannot be seen on angiogram. And yet the arteries remain open.
Bedside ultrasound showed no effusion and moderately decreased LV function, with B-lines of pulmonary edema. Here is his ED ECG: There is obvious infero-posterior STEMI. What are you worried about in addition to his STEMI? to greatly decrease risk (although in STEMI, the optimal level is about 4.0-4.5 Learning Points: 1.
In terms of ischemia, there is both a signal of subendocardial ischemia (STD max in V5-V6 with reciprocal STE in aVR) AND a signal of transmural infarction of the inferior wall with Q wave and STE in lead III with reciprocal STD in I and aVL. Now another, with ultrasound. The rhythm is atrial fibrillation. What is the Diagnosis?
This case was provided by Spencer Schwartz, an outstanding paramedic at Hennepin EMS who is on Hennepin EMS's specialized "P3" team, a team that receives extra training in advanced procedures such as RSI, thoracostomy, vasopressors, and prehospital ultrasound. Takotsubo is a sudden event, not one with crescendo angina.
Not quite a STEMI, but same effect.) There is ST elevation in V2-V4 that does not quite meet "STEMI criteria." That is a reasonable thought, but we have shown that if there is one lead of V1-V4 with a T/QRS ratio greater than 0.36, then it is STEMI, not LV aneurysm. These ultrasounds confirm LAD occlusion. How do I know?
A middle aged patient who was 3 weeks s/p STEMI came from cardiac rehab where he developed some chest pain, dyspnea and weakness on the treadmill. There is no acute STEMI. This is diagnostic of recent, reperfused STEMI. This is diagnostic of recent, reperfused STEMI. Acute STEMI would have upright T-waves.
The receiving emergency physician consulted with interventional cardiology who stated there was no STEMI. However the patient continued to have chest pain and bedside ultrasound showed hypokinesis of the septum with significantly reduced LVEF. Is there STEMI? The patient continued having chest pain. What is the rhythm?
It may be difficult to read STEMI in the setting of RBBB. There is, however, a long QT also, with abnormal T-waves, but this is not STEMI. This ECG was recorded prehospital, and the computer read STEMI, so the medics activated the cath lab: What do you think? The ECG is consistent with high lateral STEMI. Called 911.
50% of LAD STEMIs do not have reciprocal findings in inferior leads, and many LAD OMIs instead have STE and/or HATWs in inferior leads instead. The ECG easily meets STEMI criteria in all leads V2-V6, as well. 24 yo woman with chest pain: Is this STEMI? Beware a negative Bedside ultrasound. Pericarditis?
There is ST depression in II, III, and aVF that is concerning for reciprocal depression from high lateral STEMI in aVL, where there is some ST elevation. There is also ST depression in precordial leads, greatest in V3 and V4, concerning for posterior STEMI. What was the inciting factor? The diagnosis is in doubt. Plummer D et al.
A bedside cardiac ultrasound was normal, with no effusion. In a series of 18 patients with COVID and ST elevation, 8 were diagnosed with STEMI, 6 of whom had an angiogram and it showed obstructive coronary disease. 12 All STEMI patients had very high cTn typical of STEMI (cTnT > 1.0 Available from: [link] 9.
There is an obvious inferior STEMI, but what else? Besides the obvious inferior STEMI, there is across the precordial leads also, especially in V1. This STE is diagnostic of Right Ventricular STEMI (RV MI). In fact, the STE is widespread, mimicking an anterior STEMI. EKG is pictured below: What do you think?
They recorded a prehospital ECG and diagnosed STEMI and activated the cath lab prehospital. ALL TROPS WERE UNDETECTABLE A formal ultrasound was done: Normal estimated left ventricular ejection fraction at rest. This ST-T wave appearance in the lateral chest leads of ECG #2 is consistent with L V “ S train” vs ischemia.
She had this ECG recorded: Obvious massive anterior STEMI She was quickly brought to the critical care area and the cath lab was activated. Here is the ECG at 25 minutes: Terrible LAD STEMI (+) OMI So a CT scan was done which of course showed a normal aorta. And almost all of them could be detected by bedside ultrasound.
These ECGs were texted to me by one of our previous ultrasound fellows, Will Smoot An elderly male arrived via EMS for acute substernal chest pain with radiation to left shoulder and arm that awakened him from sleep at 0030. He took two full strength aspirin prior to EMS arrival. The pain was relieved by one prehospital NTG spray.
Case continued A bedside cardiac ultrasound revealed grossly preserved left ventricular function, no appreciable wall motion abnormality, pericardial effusion, or obvious valvular abnormality. A good size infarct that no longer has active ischemia will have continually rising troponins due to the damage that was done hours ago.
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