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This 80 year old with a history of CABG had a cardiacarrest. We did a bedside cardiacultrasound. This is as clear a STEMI as you can get. So this is classic inferoposterior STEMI on the ECG but is NOT acute coronary syndrome! There is concordant ST elevation in all inferior leads.
Primary percutaneous coronary intervention (PPCI) remains the gold-standard treatment for ST-elevation myocardial infarction (STEMI). We present the case of a man in his 50s, admitted with cardiacarrest secondary to inferolateral STEMI.
An emergency cardiacultrasound could be very useful. Appreciation of these subtle ECG findings could have helped to avoid a cardiacarrest and its resulting permanent disability 3. The upright portion of the T-wave in aVF is very large compared to the QRS size. If these remain unchanged, then serial troponins.
He had multiple cardiacarrests with ROSC regained each time. CardiacUltrasound may be a surprisingly easy way to help make the diagnosis Answer: pulmonary embolism. Now another, with ultrasound. This patient arrested shortly after hospital arrival. Submitted by a Med Student, with Great Commentary on Bias!
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? If cardiacarrest from hypokalemia is imminent (i.e., He appeared to be in shock.
A bedside cardiacultrasound 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
Past medical history included RBBB without other cardiac history, but old ECG was not available. The prehospital and ED computer interpretation was inferior STEMI: There’s normal sinus rhythm, first degree AV block and RBBB, normal axis and normal voltages. Vitals were normal except for oxygen saturation of 94%. Vitals were normal.
A bedside cardiacultrasound 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. Second: what does the ultrasound tell us about the condition? The large RV and small LV on ultrasound make this a right ventricular process.
The ECG shows obvious STEMI(+) OMI due to probable proximal LAD occlusion. Another approach is sympathetic chain (stellate ganglion) blockade if you have the skills to do it: it requires some expertise and ultrasound guidance. The pain was 10/10 in intensity radiating bilaterally to the shoulders and also to the left arm and neck.
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.
This is a troponin I level that is almost exclusively seen in STEMI. I suspect this is Type 2 MI due to prolonged severe hypotension from cardiacarrest. So this is either a case of MINOCA, or a case of Type II STEMI. If the arrest was caused by acute MI due to plaque rupture, then the diagnosis is MINOCA.
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. aVR ST segment elevation: acute STEMI or not? aVR ST Segment Elevation: Acute STEMI or Not?
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. On arrival, GCS was 13 and the patient complained of ongoing chest pain.
On arrival, the patient was in shock, was intubated, and had an immediate cardiacultrasound. What does a heart look like on ultrasound when the EKG looks like that? Here you go: It's not the world's greatest cardiacultrasound video, but it does appear to show poor function and low volume. If the patient is at 1.8,
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. She was defibrillated and resuscitated. It can only be seen by IVUS.
Could this be Septal STEMI (STE in V1 and aVR, with reciprocal ST depression in V4-V6?), In Septal STEMI , transmural ischemia of the septum is recorded by the overlying lead V1 as ST Elevation. Lead III is also on the right and might manifest ST Elevation in Septal STEMI. with ADDED STE in III?
He had a previous MI with cardiacarrest 2 years prior. Important Learning Point: "STEMI" is defined by millimeter criteria (1 mm in limb leads), which this does not meet. Therefore it is not a STEMI. The ST depression may be the most visibly obvious sign of STEMI. Some are STEMI-equivalents.
His ED cardiacultrasound (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. The patient's initial troponin I was 2.0 ng/mL (99% reference level = 0.030 ng/mL. His prior EF from an ECHO 6 months prior indicated 35% LVEF.
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. The patient died is spite of resuscitative efforts. It is found on 1% to 3.5%
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.
Further history later: This patient personally has no further high risk features (syncope / presyncope), but her mother had sudden cardiacarrest in sleep. A bedside cardiacultrasound revealed grossly normal to hyperdynamic systolic function with no obvious areas of wall motion abnormalities. And another finding.
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