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for those of you who do not do Emergency Medicine, ECGs are handed to us without any clinical context) The ECG was read simply as "No STEMI." He was started on a heparin drip and CTA of the chest was ordered to rule out pulmonary embolism. Unfortunately, there was a long wait and the patient left before being seen by a provider.
The conventional machine algorithm interpreted this ECG as STEMI. It shows sinus tachycardia with right bundle branch block. Taking a step back , remember that sinus tachycardia is less commonly seen in OMI (except in cases of impending cardiogenic shock). When EMS found her, she was dyspneic and diaphoretic. Both were wrong.
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. Smith comment: before reading anything else, this case screamed pulmonary embolism to me. The prehospital, ED computer, and final cardiology interpretation was STEMI negative.
This certainly looks like an anterior STEMI (proximal LAD occlusion), with STE and hyperacute T-waves (HATW) in V2-V6 and I and aVL. How do you explain the anterior STEMI(+)OMI immediately after ROSC evolving into posterior OMI 30 minutes later? This caused a type 2 anterior STEMI. This prompted cath lab activation.
Smith interpretation: This is highly likely to be due to extreme right heart strain and is nearly diagnostic of pulmonary embolism. She was diagnosed with a Non-STEMI and kept overnight for a next day angiogram. Medics recorded the above ECG and called a STEMI alert. It is of course pulmonary embolism.
Is this an anterior STEMI with LBBB? Explanation : The patient had a worrisome history: 59 yo with significant substernal chest pressure, so his pretest probability of MI (and even of STEMI) is reasonably high. Additionally, appropriate discordance is common in NonSTEMI, but very unusual in coronary occlusion (STEMI).
The morphology of V2-V4 is very specific in my experience for acute right heart strain (which has many potential etiologies, but none more common and important in EM than acute pulmonary embolism). CT angiogram showed extensive saddle pulmonary embolism. He had multiple cardiac arrests with ROSC regained each time. This is a quiz.
The "criteria" for posterior STEMI are 0.5 Is it STEMI or NonSTEMI? The patient had no hypertension, no tachycardia, a normal hemoglobin, no drug use, no hypotension/shock, no murmur of aortic stenosis. The troponin I returned at 4.1 ng/mL (ULN = 0.030 ng/mL) , diagnostic of myocardial injury. mm STE in one lead.
Later, she developed chest pain again, and had this ECG recorded: Obvious Anterior OMI that is also a STEMI Coronary angiogram- --Right dominant coronary artery system --The left main artery was normal in appearance and free of obstructive disease. --The Thus, Wellens' syndrome should be thought of as a transient OMI or transient STEMI.
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 Elevated troponin does not, however, guide any treatment strategies to minimize myocardial injury.
Patients with pulmonary embolism or aortic dissection who have normal variant ST elevation are at high risk of being diagnosed with pericarditis when what they have is far more serious!! normal variant, not pericarditis) A Young Man with Sharp Chest pain (normal variant, not pericarditis) 24 yo woman with chest pain: Is this STEMI?
Third, a slow motion segment showing delayed, brisk filling of the PDA due to dislodgment of a thrombus from contrast injection and distal embolization. A distal RCA lesion ( blue arrow ), Delayed brisk filling of an initially occluded PDA due to a thrombus dislodged during injection which embolized distally.
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