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The axiom of "type 1 (ACS, plaque rupture) STEMIs are not tachycardic unless they are in cardiogenic shock" is not applicable outside of sinus rhythm. In some cases the ischemia can be seen "through" the flutter waves, whereas in other cases the arrhythmia must be terminated before the ischemia can be clearly distinguished.
Clinical Course The paramedic activated a “Code STEMI” alert and transported the patient nearly 50 miles to the closest tertiary medical center. DISCUSSION: The 12-lead EKG EMS initially obtained for this patient showed severe ischemia, with profound "infero-lateral" ST depression and reciprocal ST elevation in lead aVR.
There is sinus rhythm with minimal STE in V1-V3, not meeting STEMI criteria. V2 never has this appearance in the absence of full thickness ischemia. The delay between OMI and STEMI sometimes causes unacceptable loss of myocardium or worse. There is a small amount of reciprocal STD in V6 with a negative T-wave.
We have also shown several cases in which atrial flutter hides true, active ischemia. Is this inferor STEMI? Atrial Flutter with Inferior STEMI? The EM provider asked if the cardiologist thought it was a "STEMI." Christmas Eve Special Gift!! Prehospital Cath Lab Activation: What do you think? Tachycardia and ST Elevation.
QOH versions 1 and 2 both say Not OMI, with high confidence, without any clinical context, despite the abnormal STE meeting STEMI criteria. Serial echo monitoring showed increasing pericardial pressures without overt tamponade physiology. That said — I did not interpret these differences as the result of acute ischemia.
The attending crews were concerned for SVT with corresponding ischemic hyperacute T waves (HATW) and subsequently activated STEMI pre-hospital. Then, three minutes later… Crews activated STEMI as she deteriorated into PEA arrest. Chapter 6: Introduction to Myocardial Ischemia and Infarction. Physiology. 2] Birnbaum, Y.,
Here, I do not see OMI (although the ECG is falsely STEMI positive with just over 1 mm STE in V1 and about 2.5 In the days before I learned to look for OMI, back when I was counting ST elevation boxes, I used to save ischemia for last.) I interpret tracings systematically in "real time" ( including my assessment for acute ischemia ).
But it doesn’t meet STEMI criteria, and was not identified by the computer or the over-reading cardiologist. Still no WPW pattern, and more obvious inferoposterior OMI, but still STEMI negative. 2] Conduction through the accessory pathway can be intermittent (with different degrees of pre-excitation), and affected by ischemia.
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. The rhythm is atrial fibrillation. The QRS complex is within normal limits.
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. Is this a transient STEMI? Is it normal ST elevation?
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?
The ECG was incorrectly interpreted as no signs of ischemia. Diagnosis: Acute non-ST segment elevation MI (Non-STEMI, or NSTEMI) Second troponin returned at around 0200: 15,894 ng/L 0245 (unclear if ongoing pain or not) Inferoposterior (and lateral V5-6) reperfusion findings.
But lead V2 has a worrisome amount of ST elevation, and in a chest pain patient, I would be worried about STEMI. My subjective interpretation, and that of Pierre's, is of LVH with secondary repolarization abnormalities, including pseudoSTEMI ST elevation in V1-V3. The Ratios of STE to S-wave: V1: 2.5/16
If you still have not read it, I strongly recommend that you read the following article on the diagnosis of "posterior" MI: Ischemic ST-Segment Depression Maximal in V1-V4 (Versus V5-V6) of Any Amplitude Is Specific for Occlusion Myocardial Infarction (Versus Nonocclusive Ischemia), by Meyers HP et al. J Am Heart Assoc. doi: 10.1161/JAHA.121.022866.
When interpreting ECGs such as the initial tracing in today's case We need to remember that we are not trying to "rule in" an acute STEMI. But the definite ST segment flattening and depression in leads V4 , V5 , V6 is real and given the history of new severe CP this has to be assumed as acute ischemia until proven otherwise.
It is possible there is microvascular dysfunction producing residual transmural ischemia. But this is most common when there is prolonged ischemia, and this patient had the fastest reperfusion imaginable! With regard to the Physiologic Chain Reaction As per Dr. Frick We do not have all the answers.
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