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Edited by Bracey, Meyers, Grauer, and Smith A 50-something-year-old female with a history of an unknown personality disorder and alcohol use disorder arrived via EMS following cardiacarrest with return of spontaneous circulation. T wave alternans is a harbinger of cardiac instability and TdP. (3) No ischemic ST changes.
Here was his initial ED ECG: There is sinus tachycardia at a rate of about 140 There is profound ST Elevation across all precordial leads, as well as I and aVL. If a patient presents with chest pain and a normal heart rate, or with shockable cardiacarrest, then ischemic appearing ST elevation is STEMI until proven otherwise.
Here is the ECG: Sinus tachycardia. If cardiacarrest from hypokalemia is imminent (i.e., Document in the patient's chart that rapid infusion is intentional in response to life-threatening hypokalemia." Document in the patient's chart that rapid infusion is intentional in response to life-threatening hypokalemia."
Descriptive analysis of the ECG in today's case reveals a regular, narrow tachycardia at ~130/minute , without clear sign of sinus P waves. But the rate is ~130/minute — which is a bit fast for sinus tachycardia. So IF this is sinus tachycardia with a sinoventricular rhythm — then we have to explain WHY the rate is this fast.
Is it ventricular tachycardia (VT) due to hyperK or is it a supraventricular rhythm with hyperK? Here are other posts on hyperK, large calcium doses for hyperK, and ventricular tachycardia in hyperK Weakness, prolonged PR interval, wide complex, ventricular tachycardia Very Wide and Very Fast, What is it? How would you treat?
His prehospital ECG showed "inferior" ST depression and high voltage, with tachycardia. I suspected no OMI, that this could be due to LVH plus tachycardia. Conclusion: Type II MI probable due to hypoxia and tachycardia from resp arrest and amphetamine use. On arrival to the ED, the patient was diaphoretic, tachycardic.
The ECG shows sinus tachycardia, a narrow, low voltage QRS with alternating amplitudes, no peaked T waves, no QT prolongation, and some minimal ST elevation in II, III, and aVF (without significant reciprocal STD or T wave inversion in aVL). It is difficult to tell if there is collapse during diastole due to the patient’s tachycardia.
See here for management of Polymorphic Ventricular Tachycardia , which includes Torsades. If cardiacarrest from hypokalemia is imminent (i.e., As I indicated above, in our cardiacarrest case, after pushing 40 mEq, the K only went up to 4.2 Could the dysrhythmias have been prevented? mEq/L, from 1.9
A few decades ago all sudden cardiacarrests with documented ventricular fibrillation (VF) and structurally normal hearts were diagnosed as idiopathic ventricular fibrillation (IVF).
This progressed to electrical storm , with incessant PolyMorphic Ventricular Tachycardia ( PMVT ) and recurrent episodes of Ventricular Fibrillation ( VFib ). In both tracings — an exceedingly fast PMVT is documented. The patient improved, and on Day-11 of the hospital stay — he was off inotropes and on a small dose of a ß-blocker.
Otherwise vitals after intubation were only notable for tachycardia. An initial EKG was obtained: Computer read: sinus tachycardia, early acute anterior infarct. Our patient had a Brugada Type 1 pattern elicited by an elevated core temperature, which is also a documented phenomenon.
There is sinus tachycardia and also a large R-wave in aVR. Drug toxicity , especially diphenhydramine , which has sodium channel blocking effects, and also anticholinergic effects which may result in sinus tachycardia, hyperthermia, delirium, and dry skin. Her temperature was 106 degrees. As part of the workup, she underwent an ECG.
There is sinus tachycardia with PVCs displaying various degrees of fusion ( See Ken Grauer's comment for below for a more detailed analysis of this rhythm ). If the ventricular escape rhythm also gives out, the patient has cardiacarrest. After ROSC, EKG 5 was recorded: This was interpreted as showing ventricular tachycardia.
Drug toxicity , especially diphenhydramine , which has sodium channel blocking effects, and also anticholinergic effects which may result in sinus tachycardia, hyperthermia, delirium, and dry skin. Unexplained cardiacarrest or documented VF/polymorphic VT: +3 3. Cardiacarrest. Hyperkalemia 2. Hypothermia.
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