Tachycardia: Difference between revisions

==History==

Additional information about drug use is mandatory. Toxic levels of digoxin and cocain can lead to VT's. Anti-arrhythmics such as amiodarone can influence VT rate. 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.  

==Physical Examination==

*Cannon "A" waves on the jugular venous pulse in the neck. These represent intermittent retrograde propulsion of blood into the jugular veins during right atrial contraction against a closed AV valve. This is evidence of AV dissociation.  

*'''Ambulatory (Holter) ECG:''' An ambulatory ECG can be necessary if the diagnosis needs to be clarified, by detecting arrhythmias, QT-interval changes, T-wave alternans (TWA) or ST-segment changes.  

*'''Electrophysiological testing:''' Electrophysiological testing can be performed to guide and assess the efficacy of VT ablation in patients with ventricular arrhythmias. It can also be done to clarify the mechanism of broad complex tachycardias in patients with coronary heart disease.

 

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

*Coronary heart disease (CHD) with prior myocardial infarction. This is the most frequent cause in developed countries

*Arrhythmogenic RV cardiomyopathy/dysplasia

Hemodynamical instability:  

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

*Pharmacological treatment can be considered with Procaïnamide or Amiodaron

Electrocardioversion is the only treatment for ventricular flutter.

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 with a 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 worse 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).  

AIVR is generally a transient, self-limiting rhythm and resolves as sinus rate surpasses the rate of AIVR. It rarely causes hemodynamic instability and rarely requires treatment.

[[Image:Torsade_de_Pointes.png|thumb|400px|Torsade de Pointes, preceded by bigemini.]]

Torsade de pointes (TdP) is a ventricular tachycardia associated with a prolonged QTc interval on the resting ECG. The ECG is characterized by twisting of the peaks of the QRS complexes around the isoelectric baseline during the arrhythmia (changing axis). Torsade de pointes is 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.  

===Causes of Torsade de Pointes===

*Aquired long QT syndrome (complete list of drugs causing long QT syndrome: http://www.torsades.org http://www.torsades.org])  

To differentiate between supraventricular tachycardias and ventricular tachycardias a 12 lead ECG is the cornerstone of the diagnostic process. At first, the physician has to make a differentiation between a narrow or wide complex tachycardia.  

 

'''Narrow complex tachycardia:''' QRS duration < 120 ms.  

 

'''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.

'''Haemodynamical instability (systolic blood pressure less than 100 mmHg):'''  

*electrical cardioversion  

'''Haemodynamical stability in a regular small complex tachycardia:'''