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The ECG in Figure-1 — was obtained from a middle-aged woman with positional tachycardia and diaphoresis with change of position from suprine to sitting. My THOUGHTS on the ECG in Figure-1: The rhythm is sinus tachycardia at ~105/minute ( ie, The R-R interval is regular — and just under 3 large boxes in duration ).
The ECG shows severe ischemia, possibly posterior OMI. But cardiac arrest is a period of near zero flow in the coronary arteries and causes SEVERE ischemia. It takes time for that ischemia to resolve. The patient was brought to the ED and had this ECG recorded: What do you think? And what do you want to do?
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 )?
Many of the changes seen are reminiscent of LVH with “strain,” and downstream Echo may very well corroborate such a suspicion, but since the ECG isn’t the best tool for definitively establishing the presence of LVH, we must favor a subendocardial ischemia pattern, instead. Type I ischemia. Type II ischemia.
Shortly after isoprenalin infusion was initiated, there were short runs of ventricular tachycardia. Extensive conduction system abnormalities can have various causes (ischemia, genetic, infectious, amyloid, etc). During the next 24 hours, she experienced periods of complete AV block with a ventricular escape rhythm in the 20s.
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.
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.
And of course Ken's comments at the bottom) An elderly obese woman with cardiomyopathy, Left bundle branch block, and chronic hypercapnea presented hypoxic with altered mental status. I do not see OMI here and all trops were only minimally elevated, consistent with either chronic injury from cardiomyopathy or with acute injury from sepsis.
Given her lack of risk factors for coronary disease, and the fact that she was a 53 year old woman with compatible history and echo findings, stress cardiomyopathy rose to the top of my differential. Of course, stress cardiomyopathy is a diagnosis of exclusion. This proves effective treatment of the recurrent ischemia.
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.
Given the rapid rate of the tachycardia and the amorphous shape of the QRS — the decision was made to sedate the patient and cardiovert. This phenomenon may sometimes be seen following an episode of a sustained tachycardia — in which marked ST-T wave abnormalities not due to infarction may be seen for a period of hours, or even days!
Here was the ECG: There is sinus tachycardia. Our chief of cardiology, Gautam Shroff, interprets it differently and thinks this is indeed ischemia. I have summarized the m ajor e tiologic c ategories of acute myocarditis and inflammatory cardiomyopathies. This was sent by a reader. and K was normal.
A fast heartbeat is called tachycardia, while a slow heartbeat is called bradycardia in medical terms. Poor blood supply Ischemia, or inadequate blood supply to the heart, is an abnormality that can be detected in an ECG test. Arrhythmia In simple words, arrhythmia refers to an irregular heartbeat.
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.
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.
In addition to sinus tachycardia, the only abnormalities listed by the computer were "low voltage, precordial leads" and "anteroseptal infarct, old.Q Cardiologist interpretation: "Technically does not meet STEMI criteria but concerning for ischemia." 4) There is well formed J-point notching. Case 2: What do you think?
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. Said differently, the ECG shows a rather slow ventricular tachycardia with a 2:1 VA conduction. Is this: 1.
The above ECGs show the initiation and continuation of a polymorphic ventricular tachycardia. Polymorphic ventricular tachycardia can be ischemic, catecholaminergic or related to QT prolongation. Most such rhythms in the setting of ischemia are VF and will not convert without defibrillation. Learning points: 1.
Arrhythmogenic cardiomyopathy Long QT syndrome Hypertrophic cardiomyopathy. There is a run of polymorphic ventricular tachycardia — which given the QT prolongation, qualifies as Torsades de Points ( TdP ). There are a number of things to look for in an ECG that can hint at arrhythmia as the cause of an apparent seizure.
NOTE: As discussed in detail in ECG Blog #108 — " A IVR" is an "enhanced" ventricular ectopic rhythm that occurs faster than the intrinsic ventricular escape rate ( which is typically between 20-40/minute ) — but slower than hemodynamically significant Ventricular Tachycardia ( ie, VT at rates >130-140/minute ).
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.
Although as a general rule, there should be no ST elevation in RBBB in the absence of ischemia, there sometimes is ST elevation that looks like this. If the ECG findings are truly new compared to a baseline (unavailable), this could suggest persistent ECG findings of ischemia, meaning poor downstream perfusion ("no reflow" phenomenon).
Use of objective evidence of myocardial ischemia to facilitate the diagnostic and prognostic distinction between type 2 myocardial infarction and myocardial injury. This sinus tachycardia ( at ~130/minute ) — is consistent with the patient’s worsening clinical condition, with development of cardiogenic shock. Available from: [link] 9.
This usually represents posterior OMI, but in tachycardia and especially after cardiac arrest, this could simply be demand ischemia, residual subendocardial ischemia due to the low flow state of the cardiac arrest. This rules out subendocardial ischemia and is diagnostic of posterior OMI. V4-5 continue to show STD.
Here was his ED ECG: There is sinus tachycardia (rate about 114) with nonspecific ST-T abnormalities. There is no evidence of infarction or ischemia. The absence of any wall motion abnormality makes ischemic cardiomyopathy very unlikely. An ECG was recorded: This shows a regular narrow complex tachycardia at a rate of about 160.
September 2024 Approvals Flurpiridaz F 18 Approval Date: September 27, 2024 Indication: A radioactive positron emission tomography (PET) tracer for imaging myocardial ischemia and infarction in adults with suspected or known coronary artery disease. Studies on Supraventricular Tachycardia : 5 studies , a total of 317 adults.
There was never ventricular fibrillation (VF) or ventricular tachycardia (VT), no shockable rhythm. By ECG alone: it is suspicious for stress cardiomyopathy, or takotsubo, due to the diffuse ST Elevation: II, III, aVF AND I and aVL. Here is a similar case: Collapse, Ventricular Tachycardia, Cardioverted, Comatose on Arrival.
Whenever I see PVCs with the morphology and axis seen in todays case I always look for signs of AC ( Arrhythmogenic Cardiomyopathy ). Arrhythmogenic cardiomyopathy often manifests with PVCs from the RV. The ECG in Figure-1 however, shows no signs of arrhythmogenic cardiomyopathy. Therefore A different approach is needed.
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