Tachycardia: Difference between revisions

Symptoms can arise in every ventricular tachycardia, depending on the heart rate, the presence of underlying heart disease and the degree of systolic and diastolic heart failure.  

 

'''Various symptoms are:'''

The patient’s age and previous medical history are essential. The chance that a wide complex tachycardia in a 70 year old man with previous myocardial infarction is a VT (vs. SVT with aberrancy) is >90%. 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 helpful, as it is a strong predictor of susceptibility to ventricular arrhythmias and sudden cardiac death.  

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

*'''Exercise testing:''' Exercise testing is recommended in adult patients with ventricular tachycardias who are now in sinus rhythm to detect coronary heart disease. 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 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.  

*'''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 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).  

Torsades de pointes (TdP) is a ventricular tachycardia associated with a prolonged QTc interval on the resting ECG. The ECG during TdP is 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 (third beat: short), 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.  

Electrocardioversion is the first treatment for an unconcious patient with incessant TdP.  

'''Additional treatments are:'''

*Withdrawal of any offending drugs and correction of electrolyte abnormalities (potassium repletion up to 4.5 to 5 mmol/liter, the goal should be to make the patient slightly hyperkalemic).  

*Intravenous magnesium sulfate can be helpful to cardiovert TdP in the acute phase in patients with few TdP episodes. If recurrence occurs a continues infusion may be beneficial.

*Beta blockers combined with cardiac pacing as acute therapy for patients with TdP and sinus bradycardia. This prevents extrasystoles and thereby short-long-short sequences.

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

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

 

 

'''Broad complex tachycardia:''' QRS duration > 120 ms.

 

A broad 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:'''