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Paco Dardon (@PacoDardon), and it’s a privilege to present it as a formal review due to the many pathophysiological, and electrophysiological, phenomenon at play. McLaren : ACLS attempts to simplify this process, suggesting cardioversion for unstable tachycardias, and anti-arrhythmics for stable wide complex tachycardias.
Here is his 12-lead: There is a wide complex tachycardia with a rate of 257, with RBBB and LPFB (right axis deviation) morphology. Read about Fascicular VT here: Idiopathic Ventricular Tachycardias for the EM Physician Case Continued He was completely stable, so adenosine was administered. See Learning point 1 below. Learning points 1.
Otherwise vitals after intubation were only notable for tachycardia. An initial EKG was obtained: Computer read: sinus tachycardia, early acute anterior infarct. A formal echocardiogram was completed the next day and again showed a normal ejection fraction without any focal wall motion abnormalities to suggest CAD.
An echocardiogram was done. 2 weeks Here is the final electrophysiology note: It is unclear what precipitated his motor vehicle collision. Sinus Tachycardia ( common in any trauma patient. ). Is there also Brugada? Here is the result: The estimated left ventricular ejection fraction is 50 %. Right ventricular prominence.
Here was his ED ECG: There is sinus tachycardia (rate about 114) with nonspecific ST-T abnormalities. Later, he underwent a formal echocardiogram: Very severe left ventricular enlargement (LVED diameter 7.4 An ECG was recorded: This shows a regular narrow complex tachycardia at a rate of about 160. C (99 °F), Resp (!)
If the patient has Abnormal Vital Signs (fever, hypotension, tachycardia, or tachypnea, or hypoxemia), then these are the primary issue to address, as there is ongoing pathology which must be identified. Electrophysiologic studies were performed in selected patients only as clinically appropriate.
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