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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.
Edited by Bracey, Meyers, Grauer, and Smith A 50-something-year-old female with a history of an unknown personality disorder and alcohol use disorder arrived via EMS following cardiac arrest with return of spontaneous circulation. Circulation. The described rhythm was an irregular, wide complex rhythm. No ischemic ST changes.
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?
The ECG shows sinus tachycardia with RBBB and LAFB, without clear additional superimposed signs of ischemia. Circulation: Cardiovascular Imaging. 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 ). 2015, March 1). Cramer, M.
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.
DISCUSSION: The 12-lead EKG EMS initially obtained for this patient showed severe ischemia, with profound "infero-lateral" ST depression and reciprocal ST elevation in lead aVR. The ECG cannot diagnose the etiology of ischemia; it only the presence of ischemia, from whatever etiology.
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? Angiography usually reveals an absence of collateral circulation to the infarct zone. The patient in today’s case suddenly became tachycardic while sleeping.
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.
Precordial ST depression may be subendocardial ischemia or posterior STEMI. Notice there is tachycardia. I have warned in the past that one must think of other etiologies of ischemia when there is tachycardia. V4-V6, is much more likely to be posterior than subendocardial ischemia. There is no ST elevation.
Circulation: Cardiovascular Interventions , 7(5), 645–655. 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. = Buller, C. Starovoytov, A., Robinson, S.,
Circulation, Volume 150, Issue Suppl_1 , Page A4119267-A4119267, November 12, 2024. Stress echocardiogram ruled out myocardial ischemia. Repeat TTE and EKG then noted newly enlarged left atrium and atrial tachycardia. EKG, cardiac enzymes, and Initial echocardiogram(TTE) was unremarkable.
Post by Smith and Meyers Sam Ghali ( [link] ) just asked me (Smith): "Steve, do left main coronary artery *occlusions* (actual ones with transmural ischemia) have ST Depression or ST Elevation in aVR?" That said, complete LM occlusion would be expected to have subepicardial ischemia (STE) in these myocardial territories: STE vector 1.
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. Circulation Research , 56 (2), 184–194. Circulation , 63 (2), 333–340. References: Ferrier, G.
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. See here for management of Polymorphic Ventricular Tachycardia , which includes Torsades. If there is a pulse, you would call it Torsades. mEq/L, from 1.9
Otherwise vitals after intubation were only notable for tachycardia. An initial EKG was obtained: Computer read: sinus tachycardia, early acute anterior infarct. Circulation, 117, 1890–1893. [3]: She was ventilated by bag-valve-mask by EMS on arrival and was quickly intubated with etomidate and succinylcholine.
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. An ECG was recorded: This shows a regular narrow complex tachycardia at a rate of about 160. There are nonspecific ST-T abnormalities. This seems to me to be very unlikely.
But two features were concerning: An ECG showing reperfusion indicates high risk for reocclusion – either from a transiently open artery at risk of closing, or an artery that is still occluded but with perfusion tenuously maintained by collateral circulation The patient had ongoing ischemic symptoms, suggesting ongoing occlusion. Shroff, G.
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. Circulation. Left BBB vi. Pathologic Q-waves viii. LVH or RV d.
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.
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! Circulation Research , 114 (12), 18521866. Circulation , 92 (3), 657671. Circulation , 125 (3), 491496.
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