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Ventricular tachycardia is a potentially life threatening cardiac arrhythmia. On the ECG, ventricular tachycardia can be defined as three or more ventricular ectopic beats occurring in a sequence at a rate more than 100 per minute. Another rare form of ventricular tachycardia is bidirectional ventricular tachycardia.
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.
This progressed to electrical storm , with incessant PolyMorphic Ventricular Tachycardia ( PMVT ) and recurrent episodes of Ventricular Fibrillation ( VFib ). There is no definite evidence of acute ischemia. (ie, Some residual ischemia in the infarct border might still be present.
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?
Discontinue all negative chronotropic agents, since the risk of torsade is much higher with bradycardia or pauses. 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.
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?
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.
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.
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.
during which sinus bradycardia and arrhythmia are seen but not to a degree that produces symptoms. Thus, there is sinus bradycardia and arrhythmia sinus pauses ( which may be longlasting, ultimately leading to sinus arrest ) and SA nodal block. The indication for pacemaker placement with SSS is symptomatic bradycardia.
Whether these EKGs show myocarditis, a normal variant, or something else, they are overall not typical of transmural ischemia of the anterior or high lateral walls. He had multiple episodes of bradycardia and nonsustained ventricular tachycardia. The patient had none of these conditions. It was stented.
This ECG shows a sinus bradycardia with a normal conduction pattern (normal PR, normal QRS, and normal QTc), normal axis, normal R-wave progression, normal voltages. Hypothermia can also produce bradycardia and J waves, with a pseudo-STEMI pattern. There is marked sinus bradycardia. What do you think? Pacing Clin Electrophysiol.
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.
to 1828 msec. ) — which corresponds to a variation in the rate of sinus bradycardia from 36-to-33/minute. This makes sense given that the underlying rhythm in today's case appears to be marked sinus bradycardia and arrhythmia , with a ventricular escape rhythm appearing when the SA node rate drops below 33/minute.
During the night, while on telemetry, the patient became bradycardic, with periods of isorhythmic AV dissociation (nodal escape rhythm alternating with sinus bradycardia), and there were sporadic PVCs. The above ECGs show the initiation and continuation of a polymorphic ventricular tachycardia.
The ECG shows sinus tachycardia with RBBB and LAFB, without clear additional superimposed signs of ischemia. The Initial ECG in Today's Case: As per Dr. Meyers — the initial ECG in today's case shows sinus tachycardia with bifascicular block ( = RBBB/LAHB ). Sinus Tachycardia ( common in any trauma patient. ).
After initiating treatment for hyperkalemia, repeat ECG showed resolution of Brugada pattern: The ECG shows sinus tachycardia. ST elevation in aVL with reciprocal ST depression in the inferior leads Shock, bradycardia, ST Elevation in V1 and V2. He also received insulin with D50, sodium bicarbonate, and kayexalate for hyperkalemia.
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.
Automatic activity refers to enhanced pacemaking function (typically from a non sinus node source), for example atrial tachycardia. Possible mechanisms of ventricular arrhythmias elicited by ischemia followed by reperfusion. The most common triggered arrhythmia is Torsades de Pointes. Do not treat AIVR. References: Ferrier, G.
A useful classification of WCT ( W ide- C omplex T achycardia ) rhythms — separates them into those that are mono morphic ( with similar QRS morphology during the tachycardia ) vs those that are poly morphic ( in which QRS morphology varies ). Acute ischemia? Use of QT-prolonging drugs?
There is also bradycardia. Bradycardia puts patients at risk for "pause-dependent" Torsades de Pointes. Torsades in acquired long QT is much more likely in bradycardia because the QT interval following a long pause is longer still. See here for management of Polymorphic Ventricular Tachycardia , which includes Torsades.
U waves may also be found in patients with LVH and/or bradycardia , or occasionally as a normal variant. This is often quite challenging to recognize — but the finding of negative U waves in a patient with chest pain is highly suggestive of ischemia ! N OTE # 1 — U waves are not specific for hypokalemia! second ).
Diffuse ST depression with ST elevation in aVR: Is this pattern specific for global ischemia due to left main coronary artery disease? Ischemia b. ST depression: is it ischemia? In my experience, Ive seen U waves not only with low K+/low Mg++ but also in patients with bradycardia, LVH, and sometimes in normal subjects.
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
These include ( among others ) — acute febrile illness — variations in autonomic tone — hypothermia — ischemia-infarction — malignant arrhythmias — cardiac arrest — and especially Hyperkalemia. Sinus Tachycardia ( common in any trauma patient. ).
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.
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. No PVCs are seen.
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.
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