| ID | 75 |
|---|---|
| Name | PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA |
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| Management | Management: Treatment of acute attack-In the absence of structural heart disease, most attacks are recovered spontaneously without medical treatment. In other cases, some efforts should be made to terminate the attack by interrupting at any point of re-entry circuit of conduction. 1. Mechanical measure- some mechanical manoeuvers causing vagal stimulation and cholinergic discharge leading to delay in AV nodal conduction and block the re-entry mechanism and thus terminate arrhythmia. Patient may learn these methods to perform themselves; these include- a. Valsalva’s manoeuver b. Self-induced vomiting c. Ocular pressure d. Stretching the arms & body e. Lowering the head between the knees f. Coughing & breath holding Among these methods, the Valsalva’s manoeuver is the best and easier to the patient to perform successfully. This is usually done when the patient is resting in supine position, thus avoiding elevated background tone. Several seconds after the release of strain, the resulting vagotonic discharge may terminate junctional re-entry tachycardia or may cause sufficient AV block to reveal an underlying atrial tachyarrhythmia. 2. Carotid sinus massage- this is also a vagotonic mechanical manoeuver performed to break junc-tional tachycardia by blocking AV nodal conduction. But, this should not be done if the patient has carotid bruits or a history of transient cerebral ischaemic attack. This should be carried out by skilled medical person. The patient is kept relaxed in semi-recumbent position, carotid sinus is mass-aged by firm but gentle pressure against the transverse process of the third cervical vertebrum; first over the right carotid sinus for 10-20 seconds and then over the left. Generally, pressure or massage on the right carotid sinus tends to slow the sinus rate and pressure on the left one tends to impair AV nodal conduction. During this manoeuver, continuous ECG or auscultatory monitoring of the heart rate is necessary, so that carotid sinus pressure can be released as soon as the attack ceases. 3. Drug treatment- where mechanical manoeuvers are failed to control tachycardia, medical treatment should be started immediately. a. Inj. Adenosine a bolus dose of 6mg (or 0.25mg/kg) is administered i.v rapidly in 1-2 seconds, (as the half-life of the drug is <10 seconds). Intravenous adenosine has a very brief duration of action, so if no response is observed after 1-2 mins. a second and a third (if necessary) bolus dose of 12mg should be given. Adenosine is well tolerated, but about 20% of petients may experience transient flushing and some bronchospasm, chest pain & heaviness of the limbs. In asthmatic patient it is contraindicated. b. Calcium channel blocker- may also induce rapid AV block or break most junctional re-entry tachycardia. Inj. verapamil i.v 2.5mg as bolus followed by 2.5mg to 5mg every 1-3 mins. upto a total of 20mg if blood pressure & rhythm are stable. Oral Verapamil 80-120mg every 4-6 hours may be used in stable patients tolerating the rhythm without difficulty. Verapamil should not be given those patients who have been administered b-blockers previously or patients with broad (>0.14s) QRS complexes, c. p-blockers- a suitable short-acting b-blocker may also be effective, such as esmolol, an initial dose of 0.5mg/kg i.v over 1 min. followed by an infusion of 25-200mgm/min. d. Digoxin- it is also effective in paroxysmal supraventricular tachycardia, but often requires a few hours to administer the required dose safely. Initially 0.5-0.75mg i.v, followed by 0.25mg or 0.125mg increment in every 2-4 hours up to a total of l-1.25mg can be used. 4. Cardioversion- where medical treatment fails or contraindicated, or in an emergency, tachycardia should be terminated by DC cardioversion if the patient is haemodynamically stable. In patient with digitalis toxicity as in the case of paroxysmal tachycardia with block, electrical cardioversion should be avoided. 5. Prophylaxis- to prevent recurrent attack- i. Digoxin orally is the first choice of drug. ii. Verapamil alone or in combination is the second choice of drug (verapamil increases digoxin serum levels), iii. b-blockers are also found effective as prophylactic therapy. Doses- please see in the therapeutic section. |
| Introduction | Paroxysmal supraventricular tachycardia is the commonest paroxysmal tachycardia originated from A.V Junctional tissue. This, usually occurs in patients without structural heart disease. Tachycardial attacks begin abruptly and may last a few seconds to many hours and stop spontaneously or may continue indefinitely until medical intervention. The most common mechanism of paroxysmal supraven-tricular tachycardia (Junctional tachycardia) is re-entry. According to the involvement of re-entry pathway, there are two main varieties of Junctional tachycardia- 1. Intra-AV nodal re-entry tachycardia (AVNRT) 2. Atrioventricular re-entry tachy cardia (AVRT) AVNRT is the most common variety, in which the re-entry circuit is confined to the AV node and its surrounding myocardium. AVRT, which is less common, and re-entry is due to an accessory pathway between the atria & ventricle through an abnormal band of atrial tissue, ‘Kent bundle’ (congenital) by-passing AV node- known as Wolff-Parkinson-White syndrome. |
| History | |
| Etiology | Aetiolgy: 1. Tachycardia often strikes suddenly without any definite provocation. 2. Some factors may induce or aggravate tachy-cardia, such as exertion, coffee, tea, alcohol etc. 3. May result from digitalis toxicity. 4. May be associated with atrioventricular block. |
| Clinical Features | Clinical feature: 1. Sudden attack of tachycardia without obvious cause. The rhythm is rapid 140-280/min. (usually 160-220/min) and regular. 2. Some patients may be asymptomatic, except awareness of rapid heart beat or palpitation and may last a few seconds to many hours. 3. Some patients may experience chest pain, breathlessness or may feel faint or syncope, specially when episodes are prolonged even in the absence of associated cardiac abnormalities. 4. Polyurea (due to release of atrial natriuretic peptide), cardiac pain or heart failure may occur if there is co-existing structural heart disease. 5. ECG shows tachycardia with normal QRS complex, with occasional bundle branch block. |
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