Tachycardia: Difference between revisions

Various symptoms are:  

Additional information about drug use is mandatory. Toxic levels of digoxin and cocain can lead to VT's. Also additional information about family history of sudden cardiac death is helpfull, as it is a strong predictor of susceptibility to ventricular arrhythmias and sudden cardiac death.  

*'''Exercise testing:''' Exercise testing is recommended in adult patients with ventricular tachycardias who have an intermediate or greater probability of having coronary heart disease by age, gender and symptoms. It is meant to provoke ischemic changes or ventricular arrhythmias.  

*'''Echocardiography, Cardiac CT, MRI:''' Echocardiography is recommended in patients with ventricular tachycardias who are suspected of having a structural heart disease. If echocardiography does not provide accurate assessment of the left and right ventricular function and/or structural changes, cardiac CT or MRI can be done.  

Ventricular tachycardia (VT) is defined as a sequence of three or more ventricular beats. The frequency 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.  

Determination of the location (or exit site) where a ventricular tachycardia originated, can be helpful in understanding the cause of the VT and is very helpful when planning an ablation procedure to treat a ventricular tachycardia. (new page for localization)  

(Non) sustained VT may be idiopathic, but occurs most frequently in patients with underlying structural heart disease of various types including:  

'''Hemodynamical instability:''''

Ventricular flutter is a ventricular tachycardia that occurs at a very rapid rate (often around 300 bpm), mostly caused by 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, 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 and no obvious P waves. 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 QRS complexes are of high 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 the heart is not able to pump normally anymore. 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 predictive marker for early VF; however, recent debate has started whether among patients with successfull coronary intervention, AIVR is a sign of ventricular dysfunction and therefore a slightly worde prognosis. AIVR can also occur in infants. By this definition, this 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).  

[[File:Torsades_de_Pointes.png|thumb|400px|An example of intermittent Torsades de Pointes]]

Torsades de pointes (TdP) is a ventricular tachycardia associated with a prolonged QTc interval on the resting ECG. It is on the ECG characterized by twisting of the peaks of the QRS complexes around the isoelectric line during the arrhythmia (changing axis). Torsade de pointes is typically initiated by a short-long-short interval. A ventricle extrasystole (first beat: short) is followed by a compensatory pause. The following beat (second beat: long) has a longer QT interval. If the next beat follows shortly thereafter, there is a good chance that this third beat falls within the QT interval, resulting in the R on T phenomenon and subsequent Torsades de pointes.  

Torsades de Pointes is observed in patients with long QT syndrome either acquired or congenital. [[LQTS|See the LQTS chapter for more information on the causes of TdP]].

Electrocardioversion is the first treatment for TdP.  

Additional treatments are:  

*Withdrawal of any offending drugs and correction of electrolyte abnormalities (potassium repletion up to 4.5 to 5 mmol/liter).  

*Intravenous magnesium sulfate for patients with QT prolongation and few episodes of TdP.  

*Beta blockers combined with cardiac pacing as acute therapy for patients with TdP and sinus bradycardia.  

*Isoproterenol as temporary treatment in patients with recurrent pause-dependent TdP who do not have congenital long QT syndrome.

====Narrow complex tachycardia:====

QRS duration < 120 ms.  

A narrow complex tachycardia is most likely to be a SVT. However, also a septal VT or His-tachycardia can appear as a small complex tachycardia.  

====Wide complex tachycardia:====

QRS duration > 120 ms.  

A wide complex tachycardia can be due to a SVT with aberration, pre-exited tachycardia (eg antidrome re-entry tachycardia) or VT.