The diagnosis of<unk>  is made based on the rhythm seen on either a 12-lead ECG or a telemetry rhythm strip. It may be very difficult to differentiate between<unk>  and a wide-complex supraventricular<unk> ycardia in some cases. In particular, supraventricular<unk> ycardias with aberrant conduction from a pre-existing bundle branch block are commonly misdiagnosed as<unk> . Other rarer phenomena include Ashman beats and antidromic atrioventricular re-entry<unk> ycardias. Various diagnostic criteria have been developed to determine whether a wide complex<unk> ycardia is<unk>  or a more benign rhythm. In addition to these diagnostic criteria, if the individual has a past history of a myocardial infarction, congestive heart failure, or recent angina, the wide complex<unk> ycardia is much more likely to be<unk> . The proper diagnosis is important, as the misdiagnosis of supraventricular<unk> ycardia when<unk>  is present is associated with worse prognosis. This is particularly true if calcium channel blockers, such as verapamil, are used to attempt to terminate a presumed supraventricular<unk> ycardia. Therefore, it is wisest to assume that all wide complex<unk> ycardia is<unk>  until proven otherwise. ECG features of<unk>  in addition to the increased Heart rate are: i) A wide QRS Complex ( Because the ectopics for the generation of the cardiac impulse originates in the Ventricular Myocyte and propagated via the intermyocyte conduction, which is a delayed conduction) ii) A Josephson's sign where there is the notch in the downsloping of the S wave near its nadir.(Considered very specific for the<unk> . iii) Capture beats (Normal QRS complex in between when the Heart pick up the sinus rhythm from the impulses generated by the SA node), fusion beats ( due to the fusion of the Abnormal and the Normal QRS complexes) which has a unique morphology . iv) Positive or negative concordance. v) Extreme Axis deviation or NORTH WEST axis . ( Axis between -90 to +180 degrees) Classification sinus top,<unk>  bottom 12 lead electrocardiogram showing a run of monomorphic<unk>  <unk> <unk>  can be classified based on its morphology: * Monomorphic<unk>  means that the appearance of all the beats match each other in each lead of a surface electrocardiogram (ECG). * Scar-related monomorphic<unk>  is the most common type and a frequent cause of death in patients having survived a heart attack, especially if they have weak heart muscle. * Right ventricular outflow tract (RVOT)<unk> ycardia is a type of monomorphic<unk>  originating in the right ventricular outflow tract. RVOT morphology refers to the characteristic pattern of this type of<unk> ycardia on an ECG. * The source of the re-entry circuit can be identified by evaluating the morphology of the QRS complex in the V1 lead of a surface ECG. If the R wave is dominant (consistent with a right bundle branch block morphology), this indicates the origin of the<unk>  is the left ventricle. Conversely, if the S wave is dominant (consistent with a left bundle branch block morphology, this is consistent with<unk>  originating from the right ventricle or interventricular septum. * Polymorphic<unk> , on the other hand, has beat-to-beat variations in morphology. This may appear as a cyclical progressive change in cardiac axis, previously referred to by its French name torsades de pointes ("twisting of the spikes"). However, at the current time, the term torsades de pointes is reserved for polymorphic<unk>  occurring in the context of a prolonged resting QT interval. Another way to classify<unk> s is the duration of the episodes: Three or more beats in a row on an ECG that originate from the ventricle at a rate of more than 120 beats per minute constitute a<unk> . * If the fast rhythm self-terminates within 30 seconds, it is considered a non-sustained<unk> . * If the rhythm lasts more than 30 seconds, it is known as a sustained<unk>  (even if it terminates on its own after 30 seconds). A third way to classify<unk>  is on the basis of its symptoms: Pulseless<unk>  is associated with no effective cardiac output, hence, no effective pulse, and is a cause of cardiac arrest. In this circumstance, it is best treated the same way as ventricular fibrillation (VF), and is recognized as one of the shockable rhythms on the cardiac arrest protocol. Some<unk>  is associated with reasonable cardiac output and may even be asymptomatic. The heart usually tolerates this rhythm poorly in the medium to long term, and patients may certainly deteriorate to pulseless<unk>  or to VF. Occasionally in<unk> , supraventricular impulses are conducted to the ventricles, generating QRS complexes with normal or aberrant supraventricular morphology (ventricular capture). Or, those impulses can be merged with complexes that are originated in the ventricle and produce a summation pattern (fusion complexes). Less common is<unk>  that occurs in individuals with structurally normal hearts. This is known as idiopathic<unk>  and in the monomorphic form coincides with little or no increased risk of sudden cardiac death. In general, idiopathic<unk>  occurs in younger individuals diagnosed with<unk> . While the causes of idiopathic<unk>  are not known, in general it is presumed to be congenital, and can be brought on by any number of diverse factors.
Ventricular tachycardia
Artificial cardiac pacemaker
Sinus arrhythmia
Electrocardiography
Junctional tachycardia
Supraventricular tachycardia
Torsades de pointes
Tachycardia