Ventricular Tachycardia Research Paper

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Physiological Effects of Monomorphic Ventricular Tachycardia Ventricular tachycardia (VT) is a disease of the heart, in which the heart’s normal rhythmic contraction is altered, changing the heart function (Ideker &Walcott, 1993). It is characterized by having a heartbeat that is too fast, although the disease itself is far more complex (Ideker & Walcott, 1993). Ventricular tachycardia often leads to ventricular fibrillation (VF), and together, they are among the most life threatening cardiac conditions. Although there are limited treatment options for this condition, the treatments available have reduced the mortality rate of people.
Ventricular tachycardia can either be monomorphic, related to organic heart disease or idiopathic occurring in people with normal hearts, or polymorphic, associated with normal or abnormal ventricular repolarization, such as Long QT Syndrome (Pellegrini & Scheinman (2010). Ventricular tachycardia, specifically monomorphic type, occurs in people following a myocardial infarction, also known as a heart attack (Ideker & Walcott, 1993), although a person can develop VT without structural heart disease (Koplan & Stevenson, 2009). When it is developed without structural heart disease it is typically a more benign form (Koplan & Stevenson, 2009) and the prognosis of this disease is
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Typically, ventricular tachycardia is diagnosed by an electrocardiographic (ECG/EKG). An EEG is used in clinical practice to detect cardiac arrhythmias, conduction disturbances, structural changes of the myocardium, and myocardia ischemia, among other things (Yan, Lankipalli, Burke, Musco, & Kowey, 2003). The waveforms of an EEG depend on the properties of transmembrane action potentials of atrial and ventricular myocytes (Yan et al, 2003). Medical professionals use ECGs to decipher where the arrhythmias are originating from and at what

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