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This EKG is diagnostic of transmural ischemia of the inferior wall. Smith: note also the terminal QRS distortion in lead III (absence of S-wave without a prominent J-wave). . __ Smith comment 1 : the appropriate management at this point is to lower the blood pressure (lower afterload, which increases myocardial oxygen demand).
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. The ECG cannot diagnose the etiology of ischemia; it only the presence of ischemia, from whatever etiology.
Two recent interventions have proven in randomized trials to improve neurologic survival in cardiac arrest: 1) the combination of the ResQPod and the ResQPump (suction device for compression-decompression CPR -- Lancet 2011 ) and 2) Dual Sequential defibrillation. Finally, head-up CPR (which was not used here), makes for better resuscitation.
Troponin T peaked at 38,398 ng/L ( = a very large myocardialinfarction, but not massive-- thanks to the pre-PCI spontaneous reperfusion, and rapid internvention!! ). There is no definite evidence of acute ischemia. (ie, Some residual ischemia in the infarct border might still be present.
When “spot diagnosing” precordial ST-depression I instinctively evaluate aVR for any corresponding ST-elevation to see if an emerging pattern of broad subendocardial ischemia can be appreciated, in which the ST-depression should be otherwise global and demonstrably maximal in Leads II and V5. ST-elevation, etc.) is present. 1] Driver, B.
In most cases, rather, the culprit is gross ischemia due to myocardialinfarction, cardiomyopathy, or advanced coronary artery disease. Unfortunately, today’s case is lacking any such diagnostics, thus I cannot say with certainty that the QT interval is, or is not, culpable in arrhythmogenesis. [1] Elsevier: Philadelphia, PA. [7]
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