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He developed cardiacarrest shortly after the ECG in Figure-1 was recorded. IMPRESSION: Given the presence of a wide tachycardia — with 2 distinct QRS morphologies, and no sign of P waves — a presumed diagnosis of B i D irectional Ventricular Tachycardia has to be made. What is the most likely cause of this arrhythmia?
While on telemetry monitoring he suffered cardiacarrest and was resuscitated. What ECG finding may have contributed to (or precipitated) the cardiacarrest? Learning points : Takotsubo can lead to cardiacarrest from ventricular arrhythmia. There are no clear signs of OMI. There is a prolonged QTc.
A 60-something woman presented after a witnessed cardiacarrest. This is commonly found after epinephrine for cardiacarrest, but could have been pre-existing and a possible contributing factor to cardiacarrest. Final Diagnosis: CardiacArrest due to Torsades from long QT of unknown etiology.
Cardiac Troponin Testing in Patients with COVID-19: A Strategy for Testing and Reporting Results. Clin Chem [Internet] 2020;Available from: [link] Smith mini-review: Troponin in Emergency Department COVID patients Cardiac Troponin (cTn) is a nonspecific marker of myocardial injury. Guo T, Fan Y, Chen M, et al.
The ECG in Figure-1 — was obtained from a middle-aged man who presented to the ED ( E mergency D epartment ) in cardiacarrest. The rhythm is regular — at a rate just over 100/minute = sinus tachycardia ( ie, the R-R interval is just under 3 large boxes in duration ). Should you activate the cath lab?
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.
This patient is actively dying from a left main coronary artery OMI and cardiacarrest from VT/VF or PEA is imminent! Complete LMCA occlusion is associated with clinical shock and/or cardiacarrest. The arterial blood gas showed a lactic acidosis with a lactate level of 17mmol/L.
NOTE: The ECGs in today's case are recorded in the Cabrera Format ( See Dr. Grauer Comment in the October 26, 2020 post of Dr. Smith's ECG Blog for review on the Cabrera Format ). The 2019 ESC Guidelines for the management of patients with supraventricular tachycardia indicated that IV Amiodarone should not be considered in these populations.
Blood was drawn , and the patient was promptly placed in a room to be seen — but on entering, the ED physician found her unresponsive in cardiacarrest. Do you see any indication on this ECG of WHY this patient was about to arrest? Is there any indication on this ECG of WHY this patient shortly after had a cardiacarrest?
This progressed to electrical storm , with incessant PolyMorphic Ventricular Tachycardia ( PMVT ) and recurrent episodes of Ventricular Fibrillation ( VFib ). As I review in My Comment in the January 16, 2020 post of Dr. Smith's ECG Blog ( and have reproduced in Figure-2 below ) — the ECG of patients with acute LMCA occlusion may be varied.
A man in his 30s with cardiacarrest and STE on the post-ROSC ECG == MY Comment , by K EN G RAUER, MD ( 12/31 /2023 ): == My only hope about today's tragic case — is that the involved providers learn from mistakes made. KEY Findings in ECG #1 include the following: Sinus tachycardia at ~110/minute. Junctional tachycardia? ).
There is sinus tachycardia (do not be fooled into thinking this is VT or another wide complex tachycardia!) Plus recommendations from a 5-member panel on cardiacarrest. This feature is invaluable for assessing QRS morphology with wide tachycardias in the differentiation between SVT vs VT rhythms. Eur Heart J.
After initiating treatment for hyperkalemia, repeat ECG showed resolution of Brugada pattern: The ECG shows sinus tachycardia. Steve, what do you think of this ECG in this CardiacArrest Patient?" A woman in her 50s with dyspnea and bradycardia A patient with cardiacarrest, ROSC, and right bundle branch block (RBBB).
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.
There was 100% proximal LAD occlusion with TIMI 0 flow, and cardiacarrest in the cath lab. There is sinus tachycardia at ~100/minute. As often emphasized by Dr. Smith — sinus tachycardia is not a common finding with acute OMI unless something else is going on (ie, cardiogenic shock ). As per Dr.
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. Arch Intern Med.
Other than tachycardia, Other than slight tachycardia, vitals were within normal limits (including oxygen saturation). About two hours after admission, he suffered a cardiacarrest (whether it was VF/VT or PEA is not available) and expired. The rhythm in ECG #1 is sinus tachycardia at 115-120/minute.
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.
2020 Sep;31(9):2474-2483. Type 2/3 ECG which gets converted to type 1 pattern with sodium channel blockers have 2 points. Rattanawong P, Kewcharoen J, Kanitsoraphan C, Vutthikraivit W, Putthapiban P, Prasitlumkum N, Mekraksakit P, Mekritthikrai R, Chung EH. J Cardiovasc Electrophysiol. Gourraud JB, Barc J, Thollet A, Le Marec H, Probst V.
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.
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
Series of Prehospital ECGs Showing Reperfusion == MY Comment by K EN G RAUER, MD ( 9/21/2020 ): == I wish those cardiologists who continue to strictly adhere to STEMI millimeter criteria would begin reading Dr. Smith’s ECG Blog. MY Thoughts on ECG #1: The rhythm is sinus tachycardia at 105-110/minute. A mysterious case.
BackgroundInhospital cardiacarrest (IHCA) is associated with significant morbidity and mortality. had ventricular tachycardia/ventricular fibrillation and 73.4% Journal of the American Heart Association, Volume 14, Issue 4 , February 18, 2025. The primary outcome was inhospital mortality.
The relationship between J wave and ventricular tachycardia during Takotsubo cardiomyopathy. Internat J Arrhyth 2020 Uesako H, Fukikawa H, Hashimoto S, et al. The final letter in the SLOWED mnemonic is " D " for "Dead" ( resulting from VT/VF or asystolic cardiacarrest ).
It is a wide complex regular tachycardia at a rate of 120. Is it ventricular tachycardia? I fear that many learners would also not easily recognize where the QRS actually ends, and I fear that some may think that this is ventricular tachycardia due to inability to distinguish QRS from ST segment. The ST Elevation is NOT typical.
This may be a sign of cardiac "stunning" following an MI or cardiacarrest ( See ECG Blog #272 for more on Causes of Low Voltage ). T wave inversion as seen in ECG #2 is not uncommon following a sustained tachyarrhythmia ( sometimes called a "Memory Effect" or "post-tachycardia" syndrome ).
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