Download dr. smith the ecg in acute mi pdf

Nice post again! In some cases LAD wraps around the diaphragmatic surface "long LAD", supplying some part of the inferior wall , and if occluded proximally before the first diagonal then the opposite ST vectors of inferior and high lateral injury may cancel each other, and only anterior ST elevation can be seen.

So inferior and high-lateral injury both remain silent. It came to my mind because there is a sign of nonspecific intraventricular conduction disturbance fragmented QRS in aVF which can be a sign of focal block induced my ischaemia, however, can also be seen in normals , and the inferior and high lateral QRS amplitudes diminished compared to the first tracing.

Maybe just because of technical things, I don't know. Dr Smith, i am getting confused about STe at 60ms. Do we calculate ste at j point in lead V3 because if we calculate it at 60 ms it will be same everytime. Sorry, misunderstanding: 60 milliseconds is on the time x axis. So you go to the right 1. Then measure how many millimeters it is above an imaginary horizontal line which is drawn over from the PR interval. If it does then why the equation doesn't include that as a variable?

Read the study if you want to know all about it. However, data will Many hours to a few days later, T waves begin to not be available for days. Fesmire and Terry L. MacMath begin to return toward the baseline. Over the next few sulting in the net formation of Q waves see Figure zyxwvutsrq days to weeks, Q waves evolve and the ST segment 1Jj. This type of myocardial infarction is classically In , Wilson demonstrated both experimentally thought to involve only the subendocardial wall.

The and clinically that Q waves could be produced in sub- ECG manifestations are felt to be early ST segment endocardial infarction. Cell death results in complete loss ac electrophysiology.

The sequelae are: currents In , Durrer demonstrated in dogs that suben- of injury, repolarization abnormalities, and QRS docardial infarctions involving one fourth the thick- abnormalities.

After demonstrated Q waves. There- tion. Autopsy findings revealed 10 patients with fore, currents flow toward the injured zone resulting transmural infarction, 23 patients with subendocar- in ST segment elevation see Figure 1B. Q waves were seen in from cells ceases, injury currents are lost. Thus abundant experimental and clinical evidence The net effect is T wave inversion see Figure 1C. These terms should be left to the Cellular necrosis forms an electrically silent region by pathologist.

Rather a myocardial infarction should failing to contribute to the generation of electro- be described by the only rational electrocardiographic motive forces.

Thus one sees a summation of the terminology-a description of the morphology of the unopposed electrical forces of the opposite wall re- ECG changes.

Plus and minus signs indicate relative electrical potential within individual cell membranes. Solid arrows within cross sections of myocardial walls represent direction of current as measured by surface ECG leads. Dashed arrows indicate direction of depolarization and repolarization waves respectively.

Q Wave vs Non-Q Wave Infarction ST Segment vs T Wave Infarction Although studies have shown how gross anatomy cannot be predicted electrocardiographically, the Investigators have further subclassified non-Q wave terms Q wave versus non-Q wave infarction appear to infarctions into ST segment and T wave infarction to have clinical utility.

Q wave infarcts have a higher rate look for clinical differences. This provides a more ac- Thus the best terminology in myocardial infarc- curate electrocardiographic terminology. Only 2 patients with a later Figure 2. Lead V, illustrating typical ST segment infarction. Ta- ble 3 summarizes the data concerning the patients with a diagnosis of AMI. Lee also characterized sub- groups of patients using clinical signs and symptoms that in certain instances were found to be superior to the initial ECG.

Lee concluded that no single factor could identify low risk patients as well as a normal ECG. He also stated that identifying patients at low risk for AM1 requires the consideration of many factors including history and the physical examination as well as the ECG and, specifically, that the ECG can be mislead- ing in certain circumstances. Figure Lead V, illustrating typical T wave infarction. Further studies are AM1 and investigated the incidence of life threaten- needed to elucidate the underlying differences be- ing complications and mortality in two different ECG tween ST segment and T wave infarction.

Studies are subgroups. An electro- also needed that investigate non-Q wave infarcts exhi- cardiogram was classified as negative if the initial biting ST segment elevation. The initial ECG is bundle branch block; or paced rhythm. Steve, extremely helpful ; very neatly and clearly presented. Tom, I don't think there is IV Plavix. The recommendation is to give po plavix with lytics. Thanks a lot for a wonderful summary of current guidelines!!

Amazing presentation!! Very helpful to me. Needs to hear this lecture a number of times to absorb the amazing amount of data. Dr Smith, Thank you very much for these amazing and highly informative lectures. I am a Cardiology fellow and your ECG lectures made me feel that now I could do justice to my role as a fellow when reviewing patients. Your ECG blogs are amazing as ever and please continue your great work.

Best Wishes Zia. Therefore, comments will rarely be published any more.