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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.
Monomorphic ventricular tachycardia in the setting of acute myocardial ischemia can also be treated by intravenous lignocaine bolus followed by infusion. Predisposing causes for ventricular tachycardia like ischemia and electrolyte imbalance has to be treated simultaneously to prevent recurrence.
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. She spontaneously converted (Defibrillation was not performed). Acute ischemia? Use of QT-prolonging drugs?
She was never defibrillated. As was seen in this case — defibrillation and/or overdrive pacing may be needed. Instead, antiarrhythmic drugs such as amiodarone or ß-blockers may be needed — and/or treatment targeted to correcting ischemia. Acute ischemia? What do you think? Use of QT-prolonging drugs?
Triage physician interpretation: -sinus bradycardia -lateral ST depressions While there are lateral ST depressions (V5, V6) the deepest ST depressions are in V4. Ischemic ST-Segment Depression Maximal in V1-V4 (Versus V5-V6) of Any Amplitude Is Specific for Occlusion Myocardial Infarction (Versus Nonocclusive Ischemia). 121.022866.
We examined the effect of ibutilide, a class III antiarrhythmic agent, on the energy requirement for atrial defibrillation and assessed the value of this agent in facilitating cardioversion in patients with atrial fibrillation that is resistant to conventional transthoracic cardioversion.
He required multiple defibrillations within a period of a few hours. There is no definite evidence of acute ischemia. (ie, This time, the arrhythmia did not spontaneously terminate — but rather degenerated to VFib, requiring defibrillation. Some residual ischemia in the infarct border might still be present.
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?
Extensive conduction system abnormalities can have various causes (ischemia, genetic, infectious, amyloid, etc). She was given CRT-D (Cardiac Resynchronization Therapy-Defibrillator). Discussion : The initial ECG in today's case is pathological for any patient, especially for a 50-year old previously heathy female.
Soon afterward, the patient’s symptoms return along with lightheadedness, bradycardia, and hypotension. The patient has also developed sinus bradycardia, which may result from right coronary artery ischemia to the SA node. The Queen of Hearts agrees: Around this time his initial high sensitivity troponin I resulted at 231 ng/L.
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. The corrected QT interval is extremely long, about 500 ms.
Followup ECG: No Change Absence of evolution is the best evidence against ischemia as the etiology. I was taught that the tell-tale sign of ischemia vs an electrical abnormality was in the hx, i.e. chest pain for the ischemia and potential syncope for brugada. Ischemia/infarction. Cardioversion/defibrillation.
The patient was put on Extracorporeal Life Support in the ED 3 hours after initial resuscitation, the core temp was 30° C and the patient was defibrillated with a single attempt. On arrival, CPR was continued and core temperature was measured at 18° C (64.4° A 12-lead ECG was recorded: There is sinus rhythm with RBBB and right axis deviation.
The designation Brugada “ P henocopy” is given when an otherwise healthy patient has none of the factors associated with Brugada Syndrome — but only develops a Brugada-1 ECG pattern as a result of one of the above conditions — and, resolves this Brugada-1 pattern once the precipitating condition has been corrected.
Although we lack details of events that followed Dr. Smith makes the key point that had this arrest witnessed by the medic team been the result of an acute cardiac event ( therefore, presumably VT or VFib ) prompt defibrillation by on-the-scene medics would most probably have resuscitated her.
Within ten minutes, she developed bradycardia, hypotension, and ST changes on monitor. Bradycardia and heart block are very common in RCA OMI. It is possible there is microvascular dysfunction producing residual transmural ischemia. She was defibrillated perhaps 25 times. He told the patient this horrible news.
That said there were no clinical symptoms or ECG findings suggestive of ongoing ischemia. Below in Figure-5 is a 10-minute continuous lead II recording on oral Flecainide, now showing sinus bradycardia without a single PVC! You have given IV MgSO4 a fast acting -blocker and IV amiodarone bolus and infusion. No PVCs are seen.
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