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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 pulmonaryembolism. Unfortunately, there was a long wait and the patient left before being seen by a provider.
We discover that for STEMI/OMI vs subendocardial ischemia, we should look for STEMI(-)OMI, subacute OMI, and OMI in the presence of LBBB and RBBB, and consider the differential for diffuse ST depression with reciprocal ST elevation in aVR.
The conventional machine algorithm interpreted this ECG as STEMI. In patients with narrow QRS ( not this patient), this pattern is highly suggestive of acute pulmonaryembolism. Of course it would also be nice to know about the patients oxygenation: in acute MI there is no hypoxia unless it results in pulmonary edema.
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 pulmonaryembolism to me. Vitals were normal except for oxygen saturation of 94%. Vitals were normal.
In this ECG Cases blog we look at 10 cases of patients with chest pain, including false positive STEMI, false negative STEMI, and other causes to help hone your ECG interpretation skills in time-sensitive cases where those very ECG skills might save a life.
On his physical examination, cardiac and pulmonary auscultation was completely normal. Bi-phasic scan showed no dissection or pulmonaryembolism. Take home messages: 1- In STEMI/NSTEMI paradigm you search for STE on ECG. He has 40 packs-year of smoking history. He denies taking any medication. Turk Kardiyol Dern Ars.
The following ECG was recorded: There is an obvious acute inferior STEMI. Whenever there is inferior STEMI, one should think about Right Ventricular STEMI (RVMI). As 85% of inferior STEMI are due to RCA occlusion [the rest due to occlusion of a "dominant" circumflex (i.e., and STE in lead III > STE in lead II.
It makes pulmonaryembolism (PE) very likely. The small LV implies very low LV filling pressures, which implies low pulmonary venous pressure. Although most cardiac arrest from MI is due to ventricular fibrillation, some is due to high grade AV block, and so this could indeed be due to large acute STEMI. Summary: 1.
Smith interpretation: This is highly likely to be due to extreme right heart strain and is nearly diagnostic of pulmonaryembolism. 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 pulmonaryembolism.
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.
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 pulmonaryembolism). CT angiogram showed extensive saddle pulmonaryembolism. He had multiple cardiac arrests with ROSC regained each time.
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.
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 "criteria" for posterior STEMI are 0.5 Is it STEMI or NonSTEMI? The patient had been on a long drive, suggesting possible pulmonaryembolism (this was unlikely given absence of tachyardia, hypoxia, or any other feature of PE), so we sent a d dimer. Patients with ACS and acute pulmonary edema 3.
Without seeing the patient, my interpretation of the first ECG was: likely normal variant ST-elevation (early repolarization), with a small possibility of pericarditis, and almost no possibility of acute coronary occlusion (STEMI). and therefore highly unlikely to be STEMI. Does subsegmental pulmonaryembolism matter?
In this ECG Cases blog, Jesse McLaren and Rajiv Thavanathan explore how ECG and POCUS complement each other for patients presenting to the emergency department with shortness of breath or chest pain. They explain complementary diagnostic insights into pericardial effusion and cardiac tamponade, occlusion MI and RV strain.
No signs for aortic dissection or pulmonary embolus. --"Results were discussed with the ordering physician. If there are T-wave inversions and elevated trops in the context of persistent pain, think of other pathologies such as pulmonaryembolism. Transient STEMI is at high risk of re-occlusion. CAD-RADS category 1. --No
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. CT angiogram chest: no aortic dissection or pulmonaryembolism. 24 yo woman with chest pain: Is this STEMI?
This is a troponin I level that is almost exclusively seen in STEMI. So this is either a case of MINOCA, or a case of Type II STEMI. If the arrest had another etiology (such as old scar), and the ST elevation is due to severe shock, then it is a type II STEMI. I believe the latter (type II STEMI) is most likely.
and the patient was converted to veno-venous (V-V) ECMO due to persistent pulmonary insufficiency. 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
ECG read as: "Shows T wave inversions in the inferior leads and less than 1mm STE in V2, without STEMI criteria." CT pulmonary angiogram was negative for pulmonaryembolism. All very very subtle. So the patient was placed back in the waiting room like many others. Aspirin was given. Chest x-ray was read as normal.
In this ECG Cases blog we look at 6 patients who presented with cardiorespiratory symptoms, possibly from COVID and illustrate the dangers of anchoring, being hypervigilant for cardiovascular complications, and why testing for COVID in patients being admitted for ACS is important.
In this ECG Cases blog we review 10 cases of possible artifact, lead reversal and lead misplacement. Can you spot the abnormalities and avoid the misdiagnosis? The post ECG Cases 29 Misdiagnosis from Lead Misplacement, Artifact and Lead Reversal appeared first on Emergency Medicine Cases.
Patients with pulmonaryembolism 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?
The limb leads have been removed because there was no ST elevation in those leads, the QRS complexes have been obscured because this is irrelevant to STEMI criteria, and red lines have been added to measure ST segment elevation. But STEMI criteria ignore all this and look at ST segments in isolation.
His initial high sensitivity troponin I returned at 1300 ng/L and given that his cardiac workup was otherwise unremarkable, a CT was obtained to evaluate for pulmonaryembolism and aortic aneurysm or dissection but this too was unrevealing. Also: electrical instability, pulmonary edema, or hypotension.
The cath lab was deactivated by cardiologist on arrival at ED because it was "not a STEMI". No pulmonaryembolism is identified. Pt received 324 ASA and 2 sprays of nitro with improvement. Cath lab was activated by EMS and transported emergent." Further events: The patient continued to have pain and an NTG drip was started.
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