Include a number of different rhythms.
Fast heart rhythms that arise entirely within the ventricles.
Heart rates are faster than 100 beats per minute by definition.
Characterized as either monomorphic ventricular tachycardia or polymorphic ventricular tachycardia.
Monomorphic ventricular tachycardia appear on an ECG record with a regular rate and rhythm and fixed shape or morpholology with each beat appearing the same.
Polymorphic ventricular tachycardia typically is irregular in rate and rhythm and has varying shapes on the ECG.
Monomorphic ventricular tachycardia may deteriorate into polymorphic ventricular tachycardia.
Polymorphic ventricular tachycardia, ventricular fibrillation, is the most dangerous type with the ECG being extremely disorganized and often leads to death if not corrected very quickly.
Ventricular tachycardias may be associated with palpitations, shortness of breath, or lightheadedness, depending upon the rate of the arrhythmia, its duration, and the underlying heart disease.
Syncope or sudden death may occur with faster heart rates.
Brief episodes lasting only a few beats may produce no or minimal symptoms.
Tachycardia with rates between 110 and 150 may be tolerated even if sustained for minutes to hours.
Rates greater than 220 may terminate spontaneously and cause decreased cardiac output and hypotension.
Patients with ventricular tachycardia have underlying cardiac disease, the majority of which have coronary artery disease.
Occasional patients with ventricular tachycardia do not have underlying heart disease.
May be associated with acute myocardial infarction or can be related to scarring from previous infarction as a result of oxygen deprivation.
Scarred tissue from a previous myocardial infarction can provide an anatomic boundary from which reentrant pathways can originate
Reentry within circuits arise in response to metabolically-induced changes in impulse conduction or appropriately timed premature beats.
Reentrant VT is typically monomorphic.
VT circuits can also arise from ventricular muscle scarring, atrophy, or hypertrophy.
Right ventricular dysplasia is a rare process that can produce VT in young adult males, and can rarely be seen in both sexes and at any age without overt heart disease: Two forms of ventricular tachycardia are commonly found and they are right ventricular outflow tract and left posterior septal fascicular ventricular tachycardia.
The two forms of ventricular tachycardia seen with right ventricular dysplasia are based on the location of the abnormal focus causing these tachycardias and the resulting morphology on ECG, and these tachycardias are generally well tolerated.
Patients with these forms of ventricular tachycardia complain mainly of episodes of palpitations or fast pulse often triggered by exercise catecholamines.
Unlike the VT associated with coronary artery disease, these VT is not associated with an adverse prognosis, seldom degenerate into ventricular fibrillation, and it is often responsive to drug therapy or RF ablation.
RF ablation has been used for repetitive monomorphic VT and offers the only potential cure for V.
The implantable cardioverter-defibrillator (ICD) is the treatment of choice for patients with life-threatening VT.
In general, drug therapy alone is restricted to patients who have well-tolerated arrhythmias or to those whose life expectancy is poor despite aggressive therapy for their arrhythmias.
Ventricular fibrillation occurs when multiple sites in the ventricles fire impulses very rapidly in an uncoordinated fashion and quivering ventricles cease to pump blood effectively leading to rapid death.
VF is the course for death in most patients experiencing out of hospital cardiac arrest.
VF is most commonly associated with structural heart disease such as coronary artery disease and myocardial infarction or ischemia.
Torsade de pointes is a kind of polymorphic VT, characterized by onset with an early complex that follows a long pause.
Torsades de pointes may be caused as a side effect of certain drugs, including most of the antiarrhythmic drugs.
Long QT syndrome (LQTS) is a syndrome of deafness and sudden cardiac death and associated with a characteristic ECG abnormality, the prolonged Q-T interval.
The victims are mostly children and teenagers.
Deaths are due to ventricular tachyarrhythmia, although most episodes of arrhythmias are usually self-limited
Genetic studies show that different syndromes were due to mutations of different genes localized on chromosomes 3,4,7 & 11.
Involved genes are responsible for the synthesis of membrane channel proteins that are involved in the cellular metabolism and regulation of the electric activity of cardiac cells.
LQTSs are cardiac membrane channel diseases associated with syncope and sudden cardiac deaths due to ventricular arrhythmias.
There are variations of the syndrome, and four factors are associated with an increased risk of sudden cardiac death and include: deafness, history of syncope, males before puberty, sustained menarche, and sustained or very irregular torsades de pointes ventricular tachycardia.
Channel gene mutations do not affect cardiac cell electric activity, but increase heart susceptibility to drugs that prolong the QT interval, such as antiarrhythmic drugs, antifungals, psychotropic drugs, and diuretics that induce hypokalemia.
Treatments are guided by genetic and electrophysiologic studies that divide the different LQTS’s.
Beta-blockers have been the major treatment for LQTSs, but new targeted treatments are presently considered.
LQT3 is associated with an increase in sodium current, so specific drugs that selectively block excess sodium currents are utilized.
LQT1 and LQT2 arise from deficient potassium currents, and agents that activate potassium currents are used.
In some patients with life-threatening arrhythmias, an implanted cardioverter defibrillator (ICD) may be an appropriate therapy.
Intraventricular cardioverter-defibrillator superior to most antiarrhythmic drugs in reducing mortality in patients with life-threatening ventricular tachyarrhythmias.