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Conventional algorithm interpretation: SINUS TACHYCARDIA ABNORMAL RHYTHM ECG Confirmed by over-reading physician Transformed ECG by PM Cardio: PM Cardio interpretation: OMI with Low Confidence Dr. Rob Reardon did a bedside echo using Speckle tracking. Mild Plaque no angiographically significant obstructive coronaryarterydisease.
This is ischemic ST depression, and could be due to increasing tachycardia, with a heart rate over 130, but that is unlikely given that the patient is now complaining of crushing chest pain and that there was tachycardia all along. See this post: What do you think the echocardiogram shows in this case?
Here is her ED ECG: Here is the ED physician's interpretation: IMPRESSION UNCERTAIN REGULAR RHYTHM, wide complex tachycardia, likely p-waves. LEFT BUNDLE BRANCH BLOCK [120+ ms QRS DURATION, 80+ ms Q/S IN V1/V2, 85+ ms R IN I/aVL/V5/V6] Comparison Summary: LBBB and tachycardia are new. This is clearly ventricular tachycardia.
Echocardiogram was unchanged from baseline. He was counseled to abstain from cannabis use.Conclusion:At low to moderate doses, cannabis can lead to a surge in sympathetic activity causing tachycardia and hypertension, while parasympathetic activity is predominant at higher doses, causing bradycardia and hypotension.
A 56 year old male with a history of diabetes, dyslipidemia, hypertension, and coronaryarterydisease presented to the emergency department with sudden onset weakness, fatigue, lethargy, and confusion. The conventional computer algorithm called “ sinus tachycardia, otherwise normal EKG ”.
See this case: what do you think the echocardiogram shows in this case? Diffuse ST depression with ST elevation in aVR: Is this pattern specific for global ischemia due to left main coronaryarterydisease? Incidence of an acute coronary occlusion. POCUS showed good LV-function and no pericardial effusion.
He was taken emergently to the cardiac catheterization lab and found to have multi-vessel coronaryarterydisease with a near-occlusive culprit lesion in the RCA, possibly reperfused. Slow TIMI 2 initially with brisk flow status post percutaneous coronary intervention with 18mm drug-eluting stent.
The diagnostic coronary angiogram identified only minimal coronaryarterydisease, but there was a severely calcified, ‘immobile’ aortic valve. A transthoracic echocardiogram showed an LV EF of less than 15%, critically severe aortic stenosis , severe LVH , and a small LV cavity.
An external monitor revealed one episode of non-sustained supraventricular tachycardia, otherwise was unremarkable. Cardiac catheterization revealed non-obstructive coronaryarterydisease. Pre-stress echocardiogram revealed a sigmoid septum with septal wall thickness of 1.6
However, an echocardiogram is a different test, also conducted for heart activity. A fast heartbeat is called tachycardia, while a slow heartbeat is called bradycardia in medical terms. Electrocardiogram, echocardiogram, and some other tests are done for patients with cardiac arrest. ECG and EKG refer to the same thing.
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. The scan showed a bicuspid aortic valve with severe stenosis and coronaryarterydisease.
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