PAROXYSMAL TACHYCARDIA …Here the ectopic pace-maker is located either in atrium, Avn junction or in the ventricle and rapidly discharges impulses varying from 150 to 250 beats per minute. According to the location of the pace-maker the condition is called paroxysmal atrial (PAT), AV junctional or ventricular tachycardia. In atrial and ventricular type the rate varies from 140-240 per minute; but in paroxysmal AV junctional tachycardia it is same as paroxysmal atrial tachycardia i.e. 140-240 per minute. However in non-paroxysmal AV junctional tachycardia the rate is usually less 60-130 per minute. Multifocal atrial tachycardia is called MAT.
MECHANISM OF PAROXYSMAL TACHYCARDIA
The basic mechanism of this dysrhythmia is re-entry phenomenon. The attack is initated or terminated by a timed atrial or ventricular ectopics. The re-entry circuit involves the SA node, AV node or accessory pathway or bundle of kent (33%)
Unknown. PAT occurs in young individuals without any obvious organic heart disease. Supraventricular type may be seen in association with atrial septal defect, Ebstein’s anomaly, mitral valve disease, WPW syndrome, Sick sinus syndrome, Floppy mitral valve syndrome and rarely with ischaemic heart disease. Drugs like Digitalis may also cause it as its toxic effect.
Ventricular type is usually due to ischaemic heart disease or Digitalis intoxication and is dangerous. Cardiomyopathy and thyrotoxicosis also cause paroxysmal tachycardia
This is the commonest type and is seen in young adults. This is divided into atrial and junctional (nodal) types depending on the site of the ectopic focus. Atrial tachycardia may be associated with AV block and is usually seen as a result of digitalis toxicity (PAT with block) associated with hypokalaemia.
Here the pace-maker is located in the ventricular myocardium. It is seen in old age and is serious.
Onset is sudden
- Severe palpitation.
- Fluttering sensation in the chest.
- Sometimes dizziness or syncope.
- Precordial pain.
The heart rate and the pulse rate vary from 140-240 per minute, average being 180 per minute, which is uncountable but is regular. This is a fixed pulse. Sinus massage may abruptly terminate supraventricular tachycardia. In ventricular variety heart sounds are split and occasional cannon pulsations may be felt in the jugular pulse.
ECG is helpful for final diagnosis. In atrial tachycardia the QRS complexes are normal but ‘P’ waves will have abnormal morphology. In paroxysmal AV junctional tachycardia the QRS complexes are normal but retrograde ‘P’ waves may be present which are not always visualized. His bundle electrogram or High right atrial electrocardiogram may be helpful. In ventricular type QRS is wide, bizarre and P waves are not clearly seen. A monophasic QS or R wave pattern in precordial leads with no transitional point and sometimes fusion beats or atrial capture beats may be seen. Torsade de pointes is a special form of VT where QRS morphology varies with typical twisting of the points, RR interval is irregular, ventricular rate may be 200-300 beats per minute. Sometimes the rate may be 400 beats per minute. The amplitude of the complexes vary and may be alternately above and below the baseline. This usually occurs in presence of a prolonged QT interval. It may occur spontaneously or after use of drugs which prolong QT duration e.g., Quinidine or in hypokalaemia, hypomagnesemia.PAROXYSMAL TACHYCARDIA
Benign Ventricular Tachycardia (Benign VT)
Ventricular tachycardia in absence of structural heart disease is called benign VT. Two common types are Right ventricle out flow tract VT and idiopathic left ventricular VT. The former is commonly seen in females and is usually exercise induced with LBBB type morphology in ECG and will respond to B-blockers, lidocaine and adenosine; left ventricular VT will have a RBBB morphology in ECG and will respond to Verapamil. This is well tolerated as there is no structural heart disease and is not associated with sudden cardiac death (SCD). As they are usually focal in origin they will respond very much to radiofrequency ablation treatment. Implantable defibrillators are not required.
Here the rate is not so high (usually upto 160 beats per minute), some underlying cause is present, the rate is influenced by exercise or change of posture but carotid sinus pressure has no effect. ECG is helpful.
The rate is rarely so high, from time to time the rate may be changed due to variation of the AV block, the same may be observed after carotid massage, flutter waves may be visible in the jugular pulse, ECG is helpful.
Idionodal tachycardia (Non-paroxysmal AV junctional tachycardia)
Rate is slow-60-130 beats per minute, rhythm is regular. In the ECG retrograde conduction of P wave may be seen or sometimes there may be complete AV dissociation.
Many attacks settle down spontaneously. Termination is specially required when patient complains of Anginal pain, develops syncope or heart failure or if coexistent heart disease is present.
Physical measures, e.g. carotid sinus massage, induction of vomiting, pressure over the eyeballs, (oculobulbar reflex), valsalva manoeuvre (forced expiration with glottis closed), coughing, breath holding, stretching the arms and body, lowering the head between the knees, and diving reflex may increase the vagal tone. All these procedures delay the atrioventricular conduction, blocks the re-entry mechanism and may terminate an attack. However carotid sinus pressure should not be applied if there is history of TIA or presence of carotid murmur.
When mechanical measures fail, drugs are used. IV Adenosine and Verapamil are effective in 90% of cases, Adenosine is the drug of choice. Inj. Adenosine 6 mg bolus IV to be started and if there is no response in 1-2 minutes then 12 mg IV o be given and repeated again. Flushing and chest discomfort are seen in 20% of cases.
Physical measures are ineffective here.
When there is haemodynamic unstability and the back ground is serious heart diseases, synchronized DC cardioversion with 100-400 j should be done immediately.
When there is haemodynamic stability drugs may be tired. IV Lidocaine 1 mg/kg in bolus may be given. If it does not help then IV Procainamide 20 mg per minute IV 1000 mg IV followed by Bretylium 5 mg/kg for 3-5 minutes repeated after 20 minutes to be followed by a drip of 1-2 mg per minute may be tried. IV Amiodarone 150 mg for 10 minutes in a rapid loading infusion followed by 1 mg/min for 6 hours in a slow infusion and then maintenance of 0.5 mg/min for 18-42 hours may also be tried
Ventricular overdrive pacing is useful when VT is recurrent.