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Discontinue all negative chronotropic agents, since the risk of torsade is much higher with bradycardia or pauses. As described above by Dr. Smith Pacing in today's case is an effective intervention as doing so prevents the bradycardia and pauses that are likely to precipitate additional episodes of Torsades de Pointes. (
RBBB is no longer seen after conversion to sinus rhythm — which supports our suspicion that the intermittent RBBB conduction seen every-other-beat during the tachycardia ( in Figure-1 ) was rate-related. Note that QRS morphology after conversion to sinus rhythm is very similar to QRS morphology of odd-numbered beats during the tachycardia.
Initial ECG in the ED: Presenting ECG : Wide-complex tachycardia at a rate about 200. This is overwhelmingly likely to be ventricular tachycardia, even if only age and medical history are considered. Nevertheless, the widths of both the QRS complex and the RS duration are similar in both the old ECG and the tachycardia.
A 50-something male with unspecified history of cardiomyopathy presented in diabetic ketoacidosis (without significant hyperkalemia) with a wide complex tachycardia and hypotension. Analysis: there is a wide complex tachycardia. This was the interpretation I put into the system: WIDE COMPLEX TACHYCARDIA. It is regular.
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. I said I think there is a fixed stenosis in the LAD and the tachycardia and stress caused a type 2 STEMI.
See this case, where a patient with BTWI morphology and dramatic EKG changes within minutes is diagnosed with myocarditis: [link] com/2019/07/what-does-this- ecg-with-significant-st.html EKG 3 also has a saddleback morphology in V2, which is only rarely due to OMI. Still, such dramatic changes cannot be overlooked. It was stented.
No more abnormal U-waves == MY Comment, by K EN G RAUER, MD ( 11/18/2019 ): == LOTS of great points regarding use of the ECG in association with electrolyte abnormalities. U waves may also be found in patients with LVH and/or bradycardia , or occasionally as a normal variant. N OTE # 1 — U waves are not specific for hypokalemia!
And more cases, if you want, at this link. == My Comment, by K EN G RAUER, MD ( 3/2/2019 ): == The importance of this case lies in recognition of a number of findings, and the differential diagnoses that these findings should evoke. Biphasic T-waves in a Middle-Aged Male with Vomiting Diabetic Ketoacidosis: is there hypokalemia?
Kazmi et al have reported on a case in which chest trauma was transiently associated with development of a Brugada-1 ECG pattern ( J Am Coll Cardiol 73 [9-Supp-1], 2019 ). Sinus Tachycardia ( common in any trauma patient. ). Other Arrhythmias ( PACs, PVCs, AFib, Bradycardia and AV conduction disorders — potentially lethal VT/VFib ).
Both of these features make inferior + RV MI by far the most likely ( Pseudoanteroseptal MI is another name for this ) There is also sinus bradycardia and t he patient is in shock with hypotension. A narrow complex bradycardia without any P-waves is also likely to respond to atropine, as it may be a junctional rhythm.
This progressed to electrical storm , with incessant PolyMorphic Ventricular Tachycardia ( PMVT ) and recurrent episodes of Ventricular Fibrillation ( VFib ). There was no evidence bradycardia leading up to the runs of PMVT ( as tends to occur with Torsades ). He required multiple defibrillations within a period of a few hours.
Figure-1: Reasons for the varied ECG presentation of acute LMain occlusion — excerpted from Dr. Smith’s 8/9/2019 post ( This Table from My Comment in the January 16, 2020 post ). As per Dr. Nossen — today's initial ECG ( LEFT tracing in Figure-2 ) shows sinus bradycardia with QRS widening due to bifascicular block ( RBBB/LAHB ).
ECG is consistent with severe hypokalemia and/or hypomagnesemia causing prolonged QT (QU) at high risk of Torsades (which is polymorphic ventricular tachycardia in the setting of a long QT interval). Polymorphic Ventricular Tachycardia Long QT Syndrome with Continuously Recurrent Polymorphic VT: Management Cardiac Arrest. Is it STEMI?
Otherwise vitals after intubation were only notable for tachycardia. An initial EKG was obtained: Computer read: sinus tachycardia, early acute anterior infarct. She was ventilated by bag-valve-mask by EMS on arrival and was quickly intubated with etomidate and succinylcholine. A rectal temperature was obtained which read 107.9
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. Annals of Noninvasive Electrocardiology 2019. 8, 2019 ) — ( Jan.
Within ten minutes, she developed bradycardia, hypotension, and ST changes on monitor. Bradycardia and heart block are very common in RCA OMI. There was indication of parasympathetic overdrive ( the acute inferior STEMI with profound bradycardia and junctional escape ). He told the patient this horrible news.
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