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SVT can be paroxysmal or sustained.
Rate is 160–220/min.
There are at least eight different types of SVT with differing risks and responses to treatment.
PSVT commonly presents with a sudden onset in otherwise healthy young people.
Passing copious urine after an attack is characteristic of PSVT.
Look for predisposing factors such as an accessory pathway and thyrotoxicosis.
Approximately 60% are due to atrioventricular (AV) node re-entry and 35% due to accessory pathway tachycardia (e.g. WPW).8
Look for evidence of accessory pathways after reversion because accessory pathways can lead to sudden death (avoid digoxin in WPW).
Consider SSS in a patient with SVT and dizziness.
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Wolff–Parkinson–White syndrome
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The structural basis for the arrhythmia of SVT in WPW syndrome is an accessory pathway that bypasses the AV node. A typical ECG shows a short PR interval and slurred upstroke of the QRS complex (delta wave). Patients are prone to sudden attacks of SVT. Up to 30% of patients will develop atrial fibrillation or flutter. Even one episode of PSVT requires consideration for radiofrequency ablation.9
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Vagal stimulation can be attempted. Carotid sinus massage was the treatment of choice, but it has fallen out of favour because of the potential for stroke. A popular method is to blow hard into the end of an empty 20 mL plastic syringe to move the plunger. Other methods of vagal stimulation include:
Valsalva manoeuvre (easiest for patient)
self-induced vomiting
ocular pressure (avoid)
cold (ice) water to face or swallowing ice
immersion of the face in water
If vagal stimulation fails
give adenosine IV (try 6 mg first over 5–10 seconds, then 12 mg in 2 minutes if unsuccessful, then 18 mg in 2 minutes if necessary and well tolerated). Second-line treatment is verapamil IV 1 mg/min up to 10–15 mg (provided patient is not taking a beta blocker).8
Precautions
Adenosine causes less hypotension than verapamil but may cause bronchospasm in asthmatics
Use only if narrow QRS and BP >80 mm Hg
Carefully monitor blood pressure
AVOID verapamil if taking beta blockers
and
persistent tachycardia with QRS complexes >0.14 s (suggests ventricular tachycardia)
In the rare event of failure of medical treatment, consider DC cardioversion or overdrive pacing.
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Prevention and maintenance
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To prevent recurrences (frequent episodes) use at first atenolol or metoprolol, flecainide (only if no structural heart damage) or sotalol (second line). If these agents fail, consider amiodarone. Do an echocardiograph first to exclude structural heart disease. Radiofrequency catheter ablation, which is usually curative, is indicated for frequent attacks not responding to medical therapy.
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Carotid sinus massage1
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Carotid sinus massage causes vagal stimulation and its effect on SVT is all or nothing. It has no effect on ventricular tachycardia. It slows the sinus rate and breaks the SVT by blocking AV nodal conduction.
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In general, right carotid pressure tends to slow the sinus rate and left carotid pressure tends to impair AV nodal conduction. Never massage both sides simultaneously. As a rule, avoid this method and use one of the simpler alternatives.
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Avoid in the elderly (risk of embolism or bradycardia).
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Ventricular tachycardia
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Management requires special supervision.9,10 It may be non-sustained, where drug treatment such as beta blockers and amiodarone may be used for symptomatic cases, or sustained, which may result in cardiac arrest. An implantable cardioverter defibrillator or radiofrequency catheter ablation may be used.
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This uncommon condition is potentially lethal as it may occasionally be prolonged or jump into ventricular fibrillation with sudden death. It is associated with disorders that prolong the QT interval. Treatment involves cessation of drugs that may prolong the QT interval, correcting electrolyte imbalance (especially potassium), cardiac pacing and IV magnesium sulphate.10
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A common problem (9% incidence in the over-70 age group).
It usually presents with an irregular ventricular rate of about 160–180 beats/minute in untreated patients with a normal AV node.
Apart from acute AF (new onset <48 hrs), it tends to fall into one of the ‘three Ps’ patterns:
– paroxysmal AF: abrupt onset, spontaneous return to normal rhythm (lasts <48 hrs)
– persistent AF: abrupt onset, lasts >7 days
– permanent (chronic) AF: cannot be converted to normal rhythm
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All types appear to have a similar risk for thromboembolism.
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Remember to look for the underlying cause: myocardial ischaemia (15% of cases), mitral valve disease, thyrotoxicosis, hypertension, pericarditis, cardiomyopathy including chronic alcohol dependence, alcohol binge.
No cause is found in 12%—isolated9,10 atrial fibrillation.
All patients should have thyroid function tests and an echocardiograph to help find a cause.
With sustained atrial fibrillation there is a 5% chance per annum of embolic episodes. There is a fivefold risk of CVA overall.
The risk of CVA is greater in those with previous CVA, valvular heart disease, prosthetic mitral valve and cardiac failure.
For reversion anticoagulate with warfarin for 4 weeks beforehand and maintain for 4 weeks afterwards.
Digoxin controls the ventricular rate but does not terminate or prevent attacks.
Sotalol, flecainide and amiodarone are used for conversion of atrial fibrillation and maintenance of sinus rhythm. Flecainide should never be prescribed in patients with reduced LV function.
Evidence basis: RCTs showed that digoxin was beneficial for lowering the ventricular rate in the short term but no better than placebo in restoring rhythm. Beta blockers and calcium-channel antagonists benefited rate control but verapamil was much less effective than amiodarone at restoring cardiac rhythm.11
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The ECG of atrial flutter has a regular saw-tooth baseline ventricular rate of 150 with narrow QRS complexes. This is a 2:1 AV block. It is often misdiagnosed as SVT. Rarely, conduction occurs 1:1, giving a ventricular rate of 300/min.
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Treatment for atrial fibrillation/flutter8,9
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To address rate and rhythm control and prevent stroke it is best to refer or consult a specialist. The treatment needs to control the arrhythmia either as the rate or the rhythm and also from the viewpoint of prophylaxis against thromboembolic complications. Paroxysmal or persistent atrial fibrillation confers a risk of thromboembolism similar to permanent atrial fibrillation.8 The AFFIRM study12 confirmed that there was no statistically significant difference between the rate and rhythm of control groups. However, patients fare marginally better (in terms of mortality) with just rate control rather than trying to get them back into sinus rhythm if they are asymptomatic in atrial fibrillation.
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Aim for a rate <110/minute at rest.8
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Rapid, urgent control of ventricular rate:
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Routine control and maintenance8
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verapamil SR 160–480 mg (o) daily
or
diltiazem CR 180–360 mg (o) daily
or
atenolol or metoprolol 25–100 mg (o) bd
Digoxin still has a place in the elderly, especially with cardiac failure:
digoxin 0.0625–0.25 mg (o) daily according to age, plasma creatinine and digoxin level
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This should be considered if the patient is symptomatic and the arrhythmia is of recent onset—less than 6 months.
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Medical cardioversion
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If the rate cannot be well controlled despite maximal medical therapy, consider AV node ablation and a permanent pacemaker. Atrial fibrillation with a rapid ventricular response over a long period gradually causes left ventricular dysfunction.
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Synchronised electrical DC cardioversion
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This can be given for first-line treatment or for failed medical conversion.
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The use of oral anticoagulation in atrial fibrillation8
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The decision to use an oral anticoagulant or an antiplatelet agent (e.g. aspirin), especially in the younger patient, is difficult and should be made in consultation with a cardiologist. If aspirin is indicated, use:
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aspirin 100–300 mg (o) daily
If oral anticoagulation is indicated, use:
warfarin—start with a low dose (e.g. 2–4 mg) and maintain a relatively low INR of 2–3 with regular checks.
or
a direct-acting oral anticoagulant (DOAC)
e.g. dabigatran