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A prehospital 12-lead was recorded: There is a regular wide complex tachycardia. The computer diagnosed this as Ventricular Tachycardia. There is a wide complex regular tachycardia at a rate of 226. Toothache, incidental Wide Complex Tachycardia Could it be fascicular VT or Bundle Branch VT ( i.e., idiopathic VT )?
She also has a hx of paroxysmal atrialfibrillation and is on oral anticoagulant treatment. She had a single chamber ICD/Pacemaker implanted several years prior due to ventricular tachycardia. Are you confident there is no ischemia? Answer : The ECG above shows a regular wide complex tachycardia. Is this: 1.
Chart review confirmed that he had been started on flecainide for atrialfibrillation. This new information makes the diagnosis of atrial flutter far more likely: first, atrialfibrillation and flutter are closely associated and, second, this makes a flutter rate of 200 bpm (with 1:1 conduction) quite likely.
PMH: Known paroxysmal Atrial fib. He is usually is in sinus rhythm as far as he knows, but he cannot subjectively feel atrialfibrillation, so he is never completely certain when he is in sinus or atrial fib. Here is his ECG: Atrial Fib with a Ventricular Response of about 66. He immediately completely recovered.
An Initial ECG was performed: Initial ECG: Sinus tachycardia with prolonged QT interval (QTc of 534 ms by Bazett). She was admitted to the ICU where subsequent ECGs were performed: ECG at 12 hours QTc prolongation, resolution of T wave alternans ECG at 24 hours Sinus tachycardia with normalized QTc interval. No ischemic ST changes.
The ECG shows sinus tachycardia with RBBB and LAFB, without clear additional superimposed signs of ischemia. Atrialfibrillation is also a predictor of worse outcomes in this case (Alborzi). Sinus Tachycardia ( common in any trauma patient. ). He was intubated for altered mental status.
Pediatric exercise testing may be used for evaluation of various disorders of cardiac rhythm rather than for inducible ischemia as in adults. This measurement has been correlated with those made at electrophysiology study and may predict the potential risk of rapid anterograde conduction if the person develops atrialfibrillation.
The first task when assessing a wide complex QRS for ischemia is to identify the end of the QRS. The ST segment changes are compatible with severe subendocardial ischemia which can be caused by type I MI from ACS or potentially from type II MI (non-obstructive coronary artery disease with supply/demand mismatch). What do you think?
Atrial fib may cause Occlusion mimic." ACUTE MI (I allowed Acute MI to be in the report because I knew there would be an elevated troponin from ischemia, which is the definition of acute MI -- but in this case it would most likely be a Type 2 MI from tachycardia) There is also LA-RA lead reversal.
DISCUSSION: The 12-lead EKG EMS initially obtained for this patient showed severe ischemia, with profound "infero-lateral" ST depression and reciprocal ST elevation in lead aVR. The ECG cannot diagnose the etiology of ischemia; it only the presence of ischemia, from whatever etiology.
Remember, in diffuse subendocardial ischemia with widespread ST-depression there may b e ST-E in lead s aVR and V1. There are well formed R-waves with good voltage/amplitude which is uncommon for ischemia. The ECG does not show any signs of ischemia. True Positive ECG#2 : Also sinus rhythm. There is ST depression in V1.
There is a narrow complex tachycardia at a rate of 130. ECGs: there is a regular narrow complex tachycardia still at a rate of exactly 130, with no P-waves and also no change since the prehospital ECG. The patient converted to atrialfibrillation. Sometimes, atrial flutter waves are better described as "dome, dome, dome."
Case submitted and written by Mazen El-Baba MD, with edits from Jesse McLaren and edits/comments by Smith and Grauer A 90-year old with a past medical history of atrialfibrillation, type-2 diabetes, hypertension, dyslipidemia, presented with acute onset chest/epigastric pain, nausea, and vomiting. Anything more on history?
The rhythm is atrialfibrillation. In terms of ischemia, there is both a signal of subendocardial ischemia (STD max in V5-V6 with reciprocal STE in aVR) AND a signal of transmural infarction of the inferior wall with Q wave and STE in lead III with reciprocal STD in I and aVL. The QRS complex is within normal limits.
edits by Meyers A woman in her 60s with a history of chronic atrialfibrillation on Eliquis, ESRD on hemodialysis, type-II diabetes mellitus, prior CVA, hypertension, and hyperlipidemia presented to the emergency department with multiple complaints after missing dialysis. Tachycardia and ST Elevation. She was discharged home.
AtrialFibrillationAtrialfibrillation causes irregular heartbeat, and the heart's normal blood supply is affected. Since atrialfibrillation can also be intermittent, such patients should continuously monitor their heart activity while performing daily activities with a portable ECG device.
They include myocardial ischemia, acute pericarditis, pulmonary embolism, external compression due to mass over the right ventricular outflow tract region, and metabolic disorders like hyper or hypokalemia and hypercalcemia. Atrialfibrillation and Brugada syndrome. mV or R/q ≥ 0.75. Heart Rhythm. 2016 Oct;13(10):e295-324.
We see a regular tachycardia with a narrow QRS complex and no evidence of OMI or subendocardial ischemia. The differential of a regular narrow QRS tachycardia is sinus tachycardia, SVT, and atrial flutter with regular conduction. Now the patient is in sinus tachycardia. Her initial EKG is below.
The ECG there reportedly showed an irregular tachycardia, and the patient was immediately referred to the emergency room. Here is her ECG on arrival: There is a wide complex tachycardia that is irregularly irregular (this is difficult to determine at these very high rates). Lead aVR seems to show the atrial activity clearly.
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.
There is atrialfibrillation. Comments: STEMI with hypokalemia, especially with a long QT, puts the patient at very high risk of Torsades or Ventricular fibrillation (see many references, with abstracts, below). See here for management of Polymorphic Ventricular Tachycardia , which includes Torsades.
Here was his ED ECG: There is sinus tachycardia (rate about 114) with nonspecific ST-T abnormalities. There is a large peaked P-wave in lead II (right atrial enlargement) There is left axis deviation consistent with left anterior fascicular block. There is no evidence of infarction or ischemia. So what is it?
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. Evidence of acute ischemia (may be subtle) vii. Most physicians will automatically be worried about these symptoms. Left BBB vi.
Occurrence of “J Waves” in 12-Lead ECG as a Marker of Acute Ischemia and Their Cellular Basis. The relationship between J wave and ventricular tachycardia during Takotsubo cardiomyopathy. Occurrence of "J waves" in 12-lead ECG as a marker of acute ischemia and their cellular basis. Pacing Clin Electrophysiol.
No evidence for ischemia jumps out. Additionally, the patient had no other apparent reason to have sinus tachycardia (such as volume depletion, bleeding, fever). So the most likely rhythm in ECG 1 is ectopic atrialtachycardia. Therefore the first part of ECG 1 shows ectopic atrialtachycardia with biventricular pacing.
It doesn’t require any extraordinary intelligence to conclude any chronic focal atrialtachycardia can get degenerated to AF in the long run. In that case, the famous atrialtachycardia localizing map from Peter Kistler et al from Australia JACC 2006 holds good for location AF focus too. Reference 1. Aronson JK.
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 patient was started on heparin for possible NSTEMI vs demand ischemia.
It is possible there is microvascular dysfunction producing residual transmural ischemia. But this is most common when there is prolonged ischemia, and this patient had the fastest reperfusion imaginable! Here is the final angiogram following placement of a stent in the ostial RCA. Case discussion: This is a tragic case.
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