#CHEST FLUTTER VERIFICATION#

On the other hand, more than 50% of patients who remained inducible for a previously undocumented (nonclinical) VT do not experience VT recurrences on short-term follow-up, suggesting that pursuing elimination of nonclinical VTs can lead to overtreatment in a large proportion of patients. Importantly, the predictive value of noninducibility for VT recurrence is limited VT recurs in 26% to 44% of patients who were rendered noninducible by catheter ablation. Furthermore, an aggressive ventricular stimulation protocol at the conclusion of a long procedure in marginally stable patients can potentially lead to hemodynamic compromise. In addition, the inducibility of some VTs may not be reproducible. However, while noninducibility of VT is considered an ideal endpoint of the ablation procedure, it has several limitations. The complete protocol of programmed electrical stimulation is again repeated after a 30-minute waiting period, unless such aggressive stimulation places the patient at risk of cardiopulmonary deterioration. If the initial stimulation protocol required additional LV pacing sites or catecholamine infusion to induce VT, then that protocol should be repeated following ablation.

#CHEST FLUTTER VERIFICATION#

54,91,119,122,123įor verification of VT inducibility, the entire programmed electrical stimulation protocol should be performed and should include up to three VESs delivered from at least two ventricular sites, with the shortest coupling intervals of 180 to 200 milliseconds or to refractoriness. However, the mortality benefit has not been consistent across different studies. In a meta-analysis and a large-scale, multicenter cohort, elimination of inducibility of all SMVTs was found to be associated with a significant reduction in both mortality and recurrence of VT/VF events. Noninducibility of any VT (excluding ventricular flutter, polymorphic VT, and VF) is the preferred and recommended endpoint of the ablation procedure. Zipes MD, in Clinical Arrhythmology and Electrophysiology (Third Edition), 2019 Noninducibility of All Sustained Monomorphic Ventricular Tachycardias Other diseases associated with an increased risk of sudden cardiac death are cardiac hypertrophy, congestive heart disease, valvular heart disease, myocarditis, Wolff-Parkinson-White syndrome, and pulmonary embolic disease.

Traumatic accidents, such as electrocution or drowning, can also precipitate ventricular fibrillation. Other disturbances to homeostatic mechanisms, such as hyper- and hypothermia, hyper- and hypovolemia, and hypoxia contribute to the risk of ventricular fibrillation. Diseases associated with high sympathetic tone, or with hyperthyroidism or pheochromocytoma, increase the risk of ventricular fibrillation.Įlectrolyte disturbances, such as hypokalemia and hyperkalemia, as well as acid base disturbances, increase the risk of ventricular fibrillation. Proarrhythmic conditions, such as long QT syndrome, and a variety of ventricular tachyarrhythmias can lead to ventricular fibrillation. The immediate cause for most cases of ventricular fibrillation is ischemic heart disease, or coronary artery disease, with the ischemia altering electrical events to the point of causing complete lack of an organized rhythm. Other disorders associated with ventricular fibrillation are usually the cause of the condition. The two arrhythmias are classified together.

Its implications, causes, and consequences are very similar to ventricular fibrillation. Ventricular flutter, which is characterized by a sine wave appearance on the electrocardiogram (ECG), is a tachyarrhythmia closely related to ventricular fibrillation. Dowd, in xPharm: The Comprehensive Pharmacology Reference, 2007 Associated Disorders

Chest flutter