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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. Then ACS (STEMI) might be primary; this might be cardiogenic shock.
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). Answer : Bedside ultrasound!
A male in his 40's who had been discharged 6 hours prior after stenting of an inferoposterior STEMI had sudden severe SOB at home 2 hours prior to calling 911. He had diffuse crackles on exam and B-lines on chest ultrasound, and chest x-ray also confirmed pulmonary edema. Here is his ED ECG: There is sinus tachycardia.
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? See here for management of Polymorphic Ventricular Tachycardia , which includes Torsades.
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. The paramedic notes called STEMI into question: “EMS disagree with monitor for STEMI callout. Vitals were normal except for oxygen saturation of 94%. Vitals were normal.
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." Cardiac Ultrasound may be a surprisingly easy way to help make the diagnosis Answer: pulmonary embolism. Now another, with ultrasound. and tachycardia, 1.8. What is the Diagnosis?
The ECG shows obvious STEMI(+) OMI due to probable proximal LAD occlusion. This progressed to electrical storm , with incessant PolyMorphic Ventricular Tachycardia ( PMVT ) and recurrent episodes of Ventricular Fibrillation ( VFib ). The below ECG was recorded. He required multiple defibrillations within a period of a few hours.
Automatic activity refers to enhanced pacemaking function (typically from a non sinus node source), for example atrial tachycardia. The receiving emergency physician consulted with interventional cardiology who stated there was no STEMI. Is there STEMI? The patient continued having chest pain. What is the rhythm? Moffat, M.
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?
There is sinus tachycardia. Sinus tachycardia, which exaggerates ST segments and implies that there is another pathology. I have always said that tachycardia should argue against acute MI unless there is cardiogenic shock or 2 simultaneous pathologies. Here is that ECG: What do you think?
Prehospital Conventional algorithm interpretation: ANTERIOR INFARCT, STEMI Transformed ECG by PM Cardio: PM Cardio AI Bot interpretation: OMI with High Confidence What do you think? On arrival, lung ultrasound confirmed pulmonary edema (B lines). On arrival, lung ultrasound confirmed pulmonary edema (B lines).
Cardiac Ultrasound may be a surprisingly easy way to help make the diagnosis Answer: pulmonary embolism. Now another, with ultrasound. Tachycardia , especially in association with rapid AFib — is notorious for producing transient ST elevation not due to acute infarction ( that often resolves once heart rate slows ).
Is it ventricular tachycardia (VT) due to hyperK or is it a supraventricular rhythm with hyperK? On arrival, the patient was in shock, was intubated, and had an immediate cardiac ultrasound. What does a heart look like on ultrasound when the EKG looks like that? They transported to the ED. How would you treat?
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?
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
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?
So I immediately left the room to get an ultrasound machine. While calling for some help and arranging to have her transported to our critical care zone, I got this quick ultrasound which confirmed my suspicion: This quick view was all I was able to obtain in the circumstances. mm STE depression in aVL.
normal variant, not pericarditis) A Young Man with Sharp Chest pain (normal variant, not pericarditis) 24 yo woman with chest pain: Is this STEMI? Beware a negative Bedside ultrasound. (normal variant misdiagosed as pericarditis) Other cases: Palpitations and Chest Tightness: Should You Activate the Cath Lab (or Give Thrombolytics)?
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%
There is sinus tachycardia and also a large R-wave in aVR. Drug toxicity , especially diphenhydramine , which has sodium channel blocking effects, and also anticholinergic effects which may result in sinus tachycardia, hyperthermia, delirium, and dry skin. Her temperature was 106 degrees. As part of the workup, she underwent an ECG.
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.
The status of the patients chest pain at this time is unknown : EKG 1, 1300: There is sinus tachycardia and artifact of low and high frequency. However, there is also significant tachycardia , with heart rate of 116, and known hypoxia. Supply-demand mismatch can cause ST Elevation (Type 2 STEMI). An EKG was immediately recorded.
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