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WPW, previous Q wave MI, and acute coronary occlusion Depending on the location of the accessory pathway, WPW pattern can mimic ventricular hypertrophy (including RVH or LVH) or myocardialinfarction (including anterior, inferior, lateral or posterior MI) [1]. Wolff-Parkinson-White syndrome ‘cured’ by myocardialinfarction?
Sinus bradycardia, normal conduction, normal axis, normal R wave progression, no hypertrophy. Prospective validation of current quantitative electrocardiographic criteria for ST-elevation myocardialinfarction. V5-V6) of any amplitude, is specific for Occlusion MyocardialInfarction (vs. What do you think?
Use of drugs producing bradycardia like beta blockers in stages III and IV may precipitate low output state. 2014 May-Jun;66(3):392-3. Ratio of left ventricular peak E-wave velocity to flow propagation velocity assessed by color M-mode Doppler echocardiography in first myocardialinfarction: prognostic and clinical implications.
Within ten minutes, she developed bradycardia, hypotension, and ST changes on monitor. If this were OMI, I would favor proximal RCA culprit (since that commonly produces inferolateral changes and occasionally produces anterior HATW from RV infarct ), but LAD is also possible. Bradycardia and heart block are very common in RCA OMI.
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