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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.
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 )?
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?
It should be kept in mind that on occasions, beta-one agonist can result in increased ventricular ectopy e.g., in severe myocardial ischemia (by increasing myocardial demand), or sometimes with congenital long-QT syndrome. Even with tachycardia and a paced QRS duration of ~0.16
This is ischemic ST depression, and could be due to increasing tachycardia, with a heart rate over 130, but that is unlikely given that the patient is now complaining of crushing chest pain and that there was tachycardia all along. They agreed ischemia was likely in the setting of demand given DKA and infection.
At about this point in the process — I like to take a closer LOOK at the 12-lead tracing, to ensure there is no acute ischemia or infarction that might need immediate attention. C ASE C onclusion : I lack detailed follow-up from today's case — other than knowing that the Atrial Tachycardia was controlled.
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 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. Acute ischemia?
In any case, the ECG is diagnostic of severe ischemia and probably OMI. So this could be myocarditis but in my opinion needs an angiogram before making that diagnosis. == Dr. Nossen Comment/Interpretation: Evaluation of ischemia on an ECG can be very challenging. Concordant STE of 1 mm in just one lead or 2a.
While the initial impression might not immediately suggest ventricular tachycardia (VT), a closer examination raises suspicion. Additionally, the qR morphology, particularly in a patient with right bundle branch block (RBBB) type wide QRS complex tachycardia (WQCT), lends further support for VT. What is the rhythm?
Sinus tachycardia has many potential causes. This is especially true for the elderly patient with sinus tachycardia. What is the cause of the sudden tachycardia? She had a very elevated troponin T at 12,335 ng/L at the time of presentation. The patient in today’s case suddenly became tachycardic while sleeping.
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.
During active chest pain an ECG was recorded: Meyers ECG interpretation: Sinus tachycardia, normal QRS complex, STD in V2-V6, I, II, III and aVF. Learning Points: You must learn and recognize the ECG patterns of OMI and subendocardial ischemia to best understand the ECG in acute care medicine.
In the days before I learned to look for OMI, back when I was counting ST elevation boxes, I used to save ischemia for last.) This is sinus tachycardia (rhythm) with complete heart block (AV node function) with ventricular escape rate just below 30. Never forget that sinus tachycardia is the scariest arrhythmia.
This proves effective treatment of the recurrent ischemia. The patient had no further symptoms of ischemia. EKG 3 is diagnostic for developing re-occlusion, and EKG 4 proves that the nitrates relieved the ischemia. = This proves effective treatment of the recurrent ischemia." Here was her final EKG prior to discharge.
This point is particularly relevant regarding ECG #2 — because sinus tachycardia is seen on this earlier ECG. ECG Blog #184 — illustrates the "magical" mirror-image opposite relationship with acute ischemia between lead III and lead aVL ( featured in Audio Pearl #2 in this blog post ). Cardiol 27:674-677, 2004 ).
With normal EF the tachycardia is not compensatory. The same reciprocal relationship is seen in severe subendocardial ischemia, just with opposite vector direction where V1 can show ST elevation) Below you can find the 3D model of the heart and coronary vessels. And the patient has sinus tachycardia. ( HR about 90-100/min.
An EKG was repeated around midnight: By itself, this ECG is not diagnostic of anything besides sinus tachycardia, and could be called normal (although there is ST segment straightening in the anterior leads, which should always prompt suspicion). The conventional computer algorithm called “ sinus tachycardia, otherwise normal EKG ”.
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.
First, we have a narrow-complex, regular tachycardia, with a rate of about 135-140. This narrows our differential for the rhythm down to sinus tachycardia, paroxysmal supraventricular tachycardia (PSVT, or SVT), and atrial flutter. Tachycardia and ST Elevation. She was discharged home. Is this inferor STEMI?
Time 17 minutes Not much different One month earlier This is Left Bundle Branch Block (LBBB) without any sign of ischemia. If so, one would expect that the chest pain is diminishing or gone & that the culprit would be the LAD. It turns out that she spends much of her time in LBBB (see ECGs below) What is going on??? link] Shvilkin et al.
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!
The finding of a fairly regular, wide tachycardia without clear sign of atrial activity ( especially when seen in an acutely symptomatic patient ) — should immediately prompt a diagnosis of VT until proven otherwise. Shark Fin" ST segment elevation is most often a sign of severe transmural ischemia that results from acute coronary occlusion.
The flutter waves can conceal or mimic ischemic repolarization findings, but here I don't see any obvious findings of OMI or subendocardial ischemia. 55 year old woman with chest pain and precordial T-wave Inversions == MY Comment , by K EN G RAUER, MD ( 8/14 /2023 ): == Today's initial tracing is challenging !
Ruling out other potential causes of bradycardia ( ie, recent ischemia-infarction; hypothyroidism ). 2 short runs of SVT ( presumably atrial tachycardia ). 2 short runs of SVT ( presumably atrial tachycardia ). Bradycardia was not limited to nighttime hours. No pause beyond 2.0 Bradycardia was not limited to nighttime hours.
Prior ECG available on file from 2 months before: We do not know the clinical events happening during this ECG, but there is borderline tachycardia, PVCs, and likely some evidence of subendocardial ischemia with small STDs maximal in V5-6/II, slight reciprocal STE in aVR. Notice the normal precordial T waves.
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?
The ECG was incorrectly interpreted as no signs of ischemia. Artificial intelligence can be trained to recognize subtle OMI = My Comment by K EN G RAUER, MD ( 2/6 /2023 ): = The initial ECG in today's case was incorrectly interpreted as, "No signs of ischemia". There is sinus tachycardia at 100-105/minute.
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.
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?
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.
There is a run of polymorphic ventricular tachycardia — which given the QT prolongation, qualifies as Torsades de Points ( TdP ). This patient was having recurrent episodes of polymorphic ventricular tachycardia with an underlying long QT interval ( = Torsades des Pointes ). ECG #2 Interpretation of ECG #2: Underlying sinus rhythm.
MY Interpretation of Today's Initial ECG: I've labeled key findings in Figure-2 for today's initial ECG: The rhythm is sinus tachycardia at ~105/minute. The sinus tachycardia is a definite concern that something acute may be ongoing. Figure-2: I've labeled t he initial ECG. All intervals ( PR, QRS, QTc ) are normal.
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.
Here is the only prehospital 12-lead: Sinus tachycardia, somewhat wide QRS, Ischemia Here is the first ED ECG: What is the rhythm here? Medics found patient in PEA arrest. He was resuscitated into a perfusing rhythm. He went in and out of arrest until arrival at the ED.
Even though they were passed the 12 hour mark traditionally associated with reperfusion benefits, ongoing ischemia requires emergent angiogram On assessment, the patient appeared uncomfortable, leaning forward in his chair. ACS with refractory ischemia and electrical instability are indications for emergent cath regardless of the ECG!
Brugada Syndrome: Diagnosis and Risk Stratification Hello friends, this is the modified version of my talk at Indian Heart Rhythm Society Conference, New Delhi, 2023, on Brugada Syndrome. Hope you will enjoy this session. These are the conditions which have to be considered or excluded as they can sometimes manifest Brugada pattern on ECG.
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 doesn’t require any extraordinary intelligence to conclude any chronic focal atrial tachycardia can get degenerated to AF in the long run. In that case, the famous atrial tachycardia localizing map from Peter Kistler et al from Australia JACC 2006 holds good for location AF focus too. Int J Arrhythm 24 , 7 (2023).
The ECG shows sinus rhythm with normal QRS complex morphology and significant subendocardial ischemia (SEI) pattern (ST depression in many leads, worst in lateral areas including leads II, V5-6, with reciprocal STE in aVR). Here is her ECG within 30 minutes of PCI: Improved, but still with ischemia. Pre-intervention. Post-intervention.
There was never ventricular fibrillation (VF) or ventricular tachycardia (VT), no shockable rhythm. Here is a similar case: Collapse, Ventricular Tachycardia, Cardioverted, Comatose on Arrival. Agitation, Confusion, and Unusual Wide Complex Tachycardia. There is sinus tachycardia at ~115/minute.
During observation in the ED the patient had multiple self-terminating runs of Non-Sustained monomorphic Ventricular Tachycardia (NSVT). That said there were no clinical symptoms or ECG findings suggestive of ongoing ischemia. This patient very likely has some form of idiopathic 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. Among potential conditions that may produce Brugada Phenocopy are infarction and ischemia. Ischemia or infarction. Hyperkalemia 2.
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.
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