worsened quality of life – anxiety, prolonged tiredness after an episode, fear of dying
paroxysmal SVT can degenerate into ventricular fibrillation – often fatal
incessant SVT – may develop into post-tachycardial cardiomyopathy
tachycardias over 150 bpm dramatically reduce cardiac output and coronary blood flow (diastole is very short), potentially causing myocardial ischaemia. The faster the heart rate, the less well it will be tolerated
A four-step approach to diagnose the underlying rhythm:
The width of the QRS complex during SVT is usually 80–100 ms
QRS can be wide >120ms e.g. in these situations: - if the patient has a permanent LBBB or RBBB - if during tachycardia a functional bundle branch block develops - if AV conduction during tachycardia is over an AV accessory pathway (AVNRT, AVRT)
Is the rhythm regular or irregular?
regular – AVNRT, AVRT, atrial tachycardia or atrial flutter with stable conduction
irregular – atrial fibrillation, multifocal atrial tachycardia or atrial flutter with variable conduction (basically excludes AVNRT and AVRT)
Presence and morphology of the P waves
Duration of RP intervals
by this criteria, we can divide tachycardia to long RP and short RP
Picture 1 Differential diagnosis of narrow complex tachycardia
Initial treatment of SVT depends on hemodynamic stability of the patient.
Hemodynamically unstable patient with narrow or wide complex tachycardia – urgent synchronized cardioversion
Hemodynamically stable patient
Acute therapy of narrow complex tachycardia
Carotid sinus massage - Pressure is applied to one carotid sinus for 5 to 10 seconds. Steady pressure is recommended because it may be more reproducible. If the expected response is not obtained, the procedure is repeated on the other side after a one- to two-minute delay.
Valsalva manoeuvres – patient is instructed to exhale forcefully against a closed glottis (against closed mouth and compressed nose) for 10 – 15s and then release.
Modified Valsalva manoeuvre – patient does classical Valsalva manoeuvre followed by 15 seconds of passive leg raise at 45 degree angle – this may be more successful in restoring sinus rhythm.
If this fails -
Adenosine– through cardiac adenosine A1 receptor > transient AV block
6 mg i.v. as a rapid bolus with saline flush
second dose – 12 mg i.v., safe within 1 min of the last dose
maximum dose = 18 mg
AVNRT, AVRT > termination
atrial flutter, focal atrial tachycardia > demasking atrial rhythm during AV blockade
no response – probably underdosed or ventricular tachycardia
CAVE: contraindication in patients with asthma and patients with preexcitation on resting ECG!
Adenosine may induce a wide range of transient bradycardias as well as atrial fibrillation, SVT and ventricular tachycardia
Adenosine should always be administered with an external pacemaker or defibrillator nearby
If Vagal manoeuvres and adenosine application fails:
Verapamil [0.075 - 0.15 mg/kg i.v. (average 5 - 10 mg) over 2 min] or i.v. diltiazem [0.25 mg/kg (average 20 mg) over 2 min] has been shown to terminate SVT in 64-98% of patients, but is associated with a risk of hypotension
application intravenously over 20 minutes has been shown to reduce the rate of hypotension
Adenosine –if there is no evidence of preexcitation on resting ECG
if ineffective: - Procainamide(i.v.) should be considered if vagal manoeuvres and adenosine fail. - Amiodarone (i.v.) may be considered if vagal manoeuvres and adenosine fail.
If drug therapy fails -synchronized cardioversion– to convert or control the tachycardia.
Picture 2 and 3 Treatment of narrow and wide complex tachycardias as per ESC guidelines
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