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He was defibrillated into VT. He then underwent dual sequential defibrillation into asystole. 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. They started CPR.
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.
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 No wall motion abnormality. J Am Coll Cardiol.
She underwent cardiopulmonary resuscitation for VT/VFib — with ROSC ( R eturn O f S pontaneous C irculation ) following defibrillation and treatment with Epinephrine and Amiodarone. C ASE C onclusion : I lack detailed follow-up from today's case — other than knowing that the Atrial Tachycardia was controlled.
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. She spontaneously converted (Defibrillation was not performed). Below are two ECGs from the telemetry monitoring.
She was successfully revived after several rounds of ACLS including defibrillation and amiodarone. An Initial ECG was performed: Initial ECG: Sinus tachycardia with prolonged QT interval (QTc of 534 ms by Bazett). Alternation in ST segment appearance ( or in the amount of ST elevation or depression ) — is often linked to ischemia.
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.
She was never defibrillated. 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? What do you think?
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). She was given CRT-D (Cardiac Resynchronization Therapy-Defibrillator). The above ECG initially shows AV block.
IMPRESSION: Given the presence of a wide tachycardia — with 2 distinct QRS morphologies, and no sign of P waves — a presumed diagnosis of B i D irectional Ventricular Tachycardia has to be made. Acute myocardial ischemia. Despite prolonged resuscitation with multiple defibrillation attempts — the patient could not be saved. =
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?
This progressed to electrical storm , with incessant PolyMorphic Ventricular Tachycardia ( PMVT ) and recurrent episodes of Ventricular Fibrillation ( VFib ). He required multiple defibrillations within a period of a few hours. There is no definite evidence of acute ischemia. (ie, What do you think?
There is a run of polymorphic ventricular tachycardia — which given the QT prolongation, qualifies as Torsades de Points ( TdP ). This episode self terminated before defibrillation was possible. This run of TdP is initiated by a PVC — but it then self-terminates. Discussion : The patient in today’s case presented with "seizures".
It was reportedly a PEA arrest; there was no recorded V Fib and no defibrillation. 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.
At cath, he immediately had incessant Torsades de Pointes requiring defibrillation 7 times and requiring placement of a transvenous pacer for overdrive pacing at a rate of 80. If there is polymorphic VT with a long QT on the baseline ECG, then generally we call that Torsades, but Non-Torsades Polymorphic VT can result from ischemia alone.
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
After epinephrine, atropine, and defibrillation x 2, there was a return of pulses. However, with widespread ST depression, this could also be due to diffuse subendocardial ischemia. Everything is complicated by the arrest and hypotension: Is the ischemia caused by the instability, or the instability caused by the ischemia?
No evidence for ischemia jumps out. This is the shock coil and identifies this device as a defibrillator. CRT-D is cardiac resynchronization therapy with defibrillation capability, like the CXR above. CRT-P is cardiac resynchronization therapy with pacing only, without the ability to defibrillate. ECG 1 What do you think?
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.
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! She was defibrillated perhaps 25 times. Defibrillation strategies for refractory ventricular fibrillation. McLeod, S.
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