Ventricular tachycardia: Difference between revisions

Ventricular tachycardia (VT) is defined as a sequence of three or more ventricular beats. The rate is often 110-250 bpm. Ventricular tachycardias often origin around old scar tissue in the heart, e.g. after myocardial infarction. Also electrolyte disturbances and ischemia can cause ventricular tachycardias. The cardiac output is often strongly reduced during VT resulting in hypotension and loss of consciousness. VT is a medical emergency as it can deteriorate into ventricular fibrillation and thus mechanical cardiac arrest.  

*'''Non-sustained VT:''' Three or more ventricular beats with a maximal duration of 30 seconds.  

*'''Sustained VT:''' A VT of more than 30 seconds duration (or less if treated by electrocardioversion within 30 seconds).  

*'''Monomorphic VT:''' All ventricular beats have the same configuration.  

*'''Polymorphic VT:''' The ventricular beats have a changing configuration. The heart rate is 100-333 bpm.  

*'''Biphasic VT:''' A ventricular tachycardia with a QRS complex that alternates from beat to beat. Associated with digoxin intoxication and long QT syndrome.  

'''Hemodynamical instability:'''

 

'''Haemodynamical stability in a regular monomorphic broadcomplex tachycardia (systolic blood pressure >100 mmHg):'''

Ventricular flutter is a ventricular tachycardia that occurs at a very rapid rate (often around 300 bpm) and results from re-entry. The QRS complexes are regular and usually monomorphic and show a typical sinusoidal pattern. During ventricular flutter the ventricles depolarize in a circular pattern at a high rate, which prevents good function. Most often this results in a minimal cardiac output and subsequent ischemia. Often deteriorates into ventricular fibrillation.  

Ventricular fibrillation (VF) is identified by the complete absence of properly formed QRS complexes. Instead of uniform activation of the ventricular myocardium, there are uncoördinated series of very rapid, ineffective contractions of the ventricle caused by many chaotic electrical impulses. In recent onset VF the electrical activity is of higher amplitude at rates greater than 320 bpm, which manifest random changes in morphology, width and height. It appears as a completely chaotic rhythm. If VF continues, the fibrillatory waves become fine and can resemble asystole in these cases.  

VF is lethal if the patient is not treated immediately. It gives rise to a mechanical standstill of the heart, because there is no pump function. Electrocardioversion is the only treatment for ventricular fibrillation.  

Accelerated idioventricular rhythm (AIVR) is a relatively benign form of ventricular tachycardia. It is (mostly) a regular repetitive ventricular rhythm rate around 60-120 bpm, but mostly 80-100. It is the result of an enhanced ectopic ventricular rhythm, which is faster than normal intrinsic ventricular escape rhythm (<40 bpm), but slower than ventricular tachycardia (over 100-120 bpm). It often occurs during reperfusion after a myocardial infarction. AIVR is not a predictive marker for early VF; however, recent debate has started whether among patients with successful coronary intervention, AIVR is a sign of ventricular dysfunction and therefore a slightly worse prognosis. AIVR can also occur in infants. By definition, AIVR is a ventricular rhythm of no more than 20% faster than the sinus rate and occuring in the absence of other heart disease. This arrhythmia typically resolves spontaneously during the first months of life (in contrast to an infant with incessant VT which can be due to discrete myocardial tumors or congenital cardiomyopathy).