Tuesday, August 23, 2016

Ventricular Tachycardia

I have a granddaughter with this disease and it is very heart breaking! If anyone knows or has a family member or friend with this my heart goes out to you. 
Ventricular Tachycardia
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Ventricular tachycardia (V-tach or VT) is a tachycardia, or fast heart rhythm, that originates in one of the ventricles of the heart. The ventricles are the main pumping chambers of the heart. This is a potentially life-threatening arrhythmia because it may lead to ventricular fibrillation, asystole, and sudden death.
12 lead electrocardiogram showing a run of monomorphic ventricular tachycardia (VT)
Ventricular tachycardia can be classified based on its morphology:
  • Monomorphic ventricular tachycardia means that the appearance of all the beats match each other in each lead of a surface electrocardiogram (ECG).
    • Scar related monomorphic ventricular tachycardia is the most common type and a frequent cause of death in patients who have survived a heart attack or myocardial infarction especially if they have weak heart muscle.[1]
    • RVOT tachycardia is a type of monomorphic ventricular tachycardia originating in the right ventricular outflow tract. RVOT morphology refers to the characteristic pattern of this type of tachycardia on an ECG.
  • Polymorphic ventricular tachycardia, on the other hand, has beat-to-beat variations in morphology. This may appear as a cyclical progressive change in cardio ac axis, previously referred to by its French name torsade de pointes ("twisting of the points"). However, currently the term torsade is reserved for polymorphic VT occurring in the context of a prolonged resting QT interval.
Another way to classify ventricular tachycardia 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 100 beats per minute constitute a ventricular tachycardia.
  • If the fast rhythm self-terminates within 30 seconds, it is considered a non-sustained ventricular tachycardia.
  • If the rhythm lasts more than 30 seconds, it is known as a sustained ventricular tachycardia (even if it terminates on its own after 30 seconds).
A third way to classify ventricular tachycardia is on the basis of its symptoms: Pulseless VT 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 VT 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 VT or to VF.
Less common is ventricular tachycardia which occurs in individuals with structurally normal hearts. This is known as idiopathic ventricular tachycardia and in the Monomorphic form appears with little or no incidence of increased risk of sudden cardiac death. In general, idiopathic ventricular tachycardia occurs in younger individuals diagnosed with VT. While the causes of idiopathic VT are MI or cardiomyopathy, it is generally presumed to be congenital, and can be brought on by any number of diverse factors.
The morphology of the tachycardia depends on its cause.
In monomorphic ventricular tachycardia, all the beats look the same because the impulse is either being generated from increased automaticity of a single point in either the left or right ventricle, or due to a reentry circuit within the ventricle. The most common cause of monomorphic ventricular tachycardia is myocardial scarring from a previous myocardial infarction (heart attack). This scar cannot conduct electrical activity, so there is a potential circuit around the scar that results in the tachycardia. This is similar to the re-entrant circuits that are the cause of atrial flutter and the re-entrant forms of supraventricular tachycardia. Other rarer congenital causes of monomorphic VT include right ventricular dysplasia, and right and left ventricular outflow tract VT.
Polymorphic ventricular tachycardia, on the other hand, is most commonly caused by abnormalities of ventricular muscle repolarization. The predisposition to this problem usually manifests on the ECG as a prolongation of the QT interval. QT prolongation may be congenital or acquired. Congenital problems include Long QT syndrome and Catecholaminergic polymorphic ventricular tachycardia. Acquired problems are usually related to drug toxicity or electrolyte abnormalities, but can occur as a result of myocardial ischemia. Class III anti-arrhythmic drugs such as Sotelo and Amiodarone prolong the QT interval and may in some circumstances be pro-arrhythmic. Other relatively common drugs including some antibiotics and antihistamines may also be a danger, particularly in combination with one another. Problems with blood levels of potassium, magnesium and calcium may also contribute. High dose magnesium is often used as an antidote in cardiac arrest protocols.
The diagnosis of ventricular tachycardia 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 ventricular tachycardia and a wide-complex supraventricular tachycardia in some cases. In particular, supraventricular tachycardia with aberrant conduction from pre-existing bundle branch block are commonly misdiagnosed as ventricular tachycardia. Other rarer phenomena include Ashman beats and antedromic atrioventricular re-entry tachycardia.[citation needed]
Various diagnostic criteria have been developed to determine whether a wide complex tachycardia is ventricular tachycardia or a more benign rhythm.[2][3] 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 tachycardia is much more likely to be ventricular tachycardia.[4]
The proper diagnosis is important, as the misdiagnosis of supraventricular tachycardia when ventricular tachycardia 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 tachycardia.[5] It is therefore wisest to assume that all wide complex tachycardia is VT until proven otherwise...
Therapy may be directed at either terminating an episode of the arrhythmia or at suppressing a future episode from occurring. The treatment for stable VT is tailored to the specific patient, with regard to how well the individual tolerates episodes of ventricular tachycardia, how frequently episodes occur, their comorbidities, and their wishes. Patients suffering from pulseless VT or unstable VT are hemodynamically compromised and require immediate cardioversion.
Synchronized electrical cardioversion[edit]
If the patient still has a pulse, it is usually possible to terminate a VT episode with a direct current shock across the heart, that is delivered from one side of the chest to the other, or from the front to the back. This is ideally synchronized to the patient's heartbeat, in order to avoid degeneration of the rhythm to ventricular fibrillation. As this is quite uncomfortable, shocks should be delivered only to an unconscious or sedated patient. As a reminder, this is different from defibrillating the patient; see next paragraph.
A patient with pulseless VT or ventricular fibrillation will be unconscious and treated as an emergency on an ACLS protocol, given high energy (360J with a monophasic defibrillator, or 200J with a biphasic defibrillator) unsynchronized cardioversion (defibrillation).
The shock may be delivered to the outside of the chest using the two pads of an external defibrillator, or internally to the heart by an implantable cardioverter-defibrillator (ICD) if one has previously been inserted.
An ICD may also be set to attempt to overdrive pace the ventricle. Pacing the ventricle at a rate faster than the underlying tachycardia can sometimes be effective in terminating the rhythm. If this fails after a short trial, the ICD will usually stop pacing, charge up and deliver a defibrillation grade shock.
Cardiac ablation[edit]
Catheter ablation is a key therapeutic modality for patients with recurrent VT.[6]
There was consensus among the task force members that catheter ablation for VT should generally be considered early in the treatment of patients with recurrent VT. In the past, ablation was often not considered until pharmacological options had been exhausted, often after the patient had suffered substantial morbidity from recurrent episodes of VT and ICD shocks. Antiarrhythmic medications can reduce the frequency of ICD therapies, but have disappointing efficacy and side effects. Advances in technology and understanding of VT substrates now allow ablation of multiple and unstable VTs with acceptable safety and efficacy, even in patients with advanced heart disease.[7]
Remote magnetic navigation is recognized as an important method for delivery of ablation therapy for these patients due to the ability of the flexible magnetic catheter to carefully map the diseased tissue without inadvertently inducing abnormal ventricular rhythms. In a series of 110 patients that included all morphologies of VT, 85% of patients treated with magnetic ablation were free from VT at one year after the intervention and were exposed to statistically reduced levels of radiation when compared to non-magnetic VT ablations at the same center.[8] In patients with myocardial scarring from a previous heart attack who were receiving excessive shocks from an ICD, magnetic ablation was shown to be successful in reducing these shocks and demonstrated a 67% reduction in imaging radiation needed to complete the procedure compared to a historical non-magnetic group.[9] For monomorphic idiopathic VT which may originate in thin-walled tissues, magnetic ablation offers catheter flexibility, steering accuracy and reproducibility to navigate to a desired location with a low probability of perforating the myocardium.[10]
Antiarrhythmic drug therapy[edit]
Drugs such as amiodarone or procainamide may be used in addition to defibrillation to terminate VT while the underlying cause of the VT can be determined. As hypo magnesia is a common cause of VT, stat dose magnesium sulphate can be given for torsade’s or if hypomagnesemia is found/suspected.
Long term anti-arrhythmic therapy may be indicated to prevent recurrence of VT. Beta-blockers and a number of class III anti-arrhythmias are commonly used. Lidocaine is now being replaced by amiodarone as the first line anti-arrhythmic treatment of VT.

The implantation of an ICD is more effective than drug therapy for prevention of sudden cardiac death due to VT and VF, but may be constrained by cost issues,(RDM) and well as patient co-morbidities and patient preference.

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