Ventricular tachycardia

Classified according to duration, morphology and hemodynamic effects.

Nonsustained VT terminates spontaneously without hemodynamic compromise.

Often occurs in life-threatening situations.

Its presence demands rapid diagnosis and treatment.

Most common cause is chronic ischemic heart disease.

Nonischemic causes of VT include: acute myocarditis, genetic cardiomyopathy, arrhythmogenic 12syndromes, illicit drug use, and electrolyte imbalances.

Defined as three or more beats of ventricular origin in succession at a rate of greater than 100 beats/minute.

Sustained VT lasts longer than 30 seconds and requires an intervention for termination or produces severe hemodynamic compromise or syncope before terminating spontaneously.

May be tolerated well hemodynamically or associated with hemodynamic compromise.

QRS complexes do not appear normal.

Sinus P waves can sometimes be recognized in between QRS complexes, but they are not in fixed relation to QRS complexes unless the atrial and ventricular rates are the same.

The rhythm is usually regular , but occasionally is modestly irregular.

Atrial to ventricular conduction is usually prevented because the AV node or ventricular conduction system system is refractory secondary to ventricular depolarizations.

Retrograde conduction from the ventricles to atria may occur with a retrograde P wave related to the QRS complex.

Distinguishing VT from supraventricular tachycardia with ab2242ant ventricular conduction may be difficult.

When each QRS complex resembles the next it is described as monomorphic.

When QRS complexes vary during VT with variation in appearance it is classified as polymorphic VT.

Torsades de pointes is a form of polymorphic VT and is often associated with a prolonged QT interval.

Usually associated with structural heart disease, and most commonly it is ischemic heart disease.

VT in the absence of coronary artery disease seen in cardiomyopathy, mitral valve prolapse, heart valve disease, QT prolongation, sarcoidosis, myxedema treatmet, drug exposure to digitalis, sympathetic amines and antiarrhythmic drugs.

Occasionally VT runs can be seen with changes in posture, exercise emotional distress or vagal stimulation.

Acute coronary artery ischemic is the cause of polymorphic ventricular tachycardia or ventricular fibrillation and is the most common cause of out-of-hospital sudden death.

When ischemia occurs, potassium leaks extracellularly and depolarizes myocytes, causing electrical heterogeneity of conduction and refractoriness and provides a source for reentry, with polymorphic VT or VF as a result.

Hemodynamic consequences depends on the presence or absence of myocardial dysfunction and on the rate of the ventricular tachycardia.

Sustained monomorphic VT is mostly due to reentry involving an area of a myocardial scar, which is usually an old myocardial infarct site.

Reentry monomorphic VT occurs in the absence of acute ischemia.

AV dissociation is usally present, meaning that the sinus node is depolarizing the atria in a manner that is normal, at a rate that is equal to, or slower, than the ventricular rate.

Other ventricular scars that can lead to reentry VT may be related to nonischemic cardiomyopathies of idiopathic dilated cardiomyopathy, hypertrophy cardiomyopathy, infiltrative heart disease, right ventricle dysplasia and following surgical repair of valvular or congenital heart disease.

10% of ventricular tachycardias are idiopathic.

Approximately 90% of idiopathic ventricular tachycardias originate in the right ventricle.

Fascicular ventricular tachycardia is generated in the left ventricle.

Fascicular ventricular tachycardia generally affects young adults ages 15 to 40 years and 60 to 80% of patients are mail.

Fascicular ventricular tachycardia presumed caused by focal reentry circuit tachycardia involving the left bundle branch anterior and posterior fascicles.

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