The main causes of supraventricular tachycardia (SVT) are:
• Ischaemic heart disease, often at the time of acute myocardial infarction or in the peri-arrest situation
Tx
Mobitz type 2 block and fixed 2 : 1 AV block may herald complete heart block and so require prophy-lactic pacing.Wenckebach’s phenomenon is usually benign and transient; it is caused by drug toxicity, high vagal tone or an inferior MI involving the AV nodal artery. The heart rate may be increased by atropine. When Wenckebach second-degree block occurs after an anterior infarction, temporary pacing is indicated.
Bundle-branch block
Bundle-branch block (BBB) of recent onset after MI is associated with a less favourable prognosis and, in the case of left BBB (LBBB), is an ECG indication for reperfusion therapy (→ p 182). As a rough guide, a broad RSR (M-shaped) pattern in V1 is caused by right BBB (RBBB) and a similar pattern in V6 indicates LBBB. (For further information about the ECG diag-nosis of BBB → Table 11.4 and Figure 11.8.) The further interpretation of BBB requires an expert opinion.
Bifascicular block
This results when only half of one bundle branch is conducting normally. There is most usually a combi-nation of RBBB with left anterior hemiblock, which appears as left axis deviation on the ECG. A quick way to check for this common type of bifascicular block is to look for a broadened M pattern in V1 and a deep S wave that is bigger than the R wave in lead
Figure 11.8 Differentiation of RBBB and LBBB using morphology of V1.
Right Left
S QS R V1 R
Table 11.4 ECG diagnosis of bundle-branch blocks (also → Figure 11.8.)
RBBB LBBB
QRS >120 ms QRS >120 ms Secondary R wave in
V1, V2 and V3
Broad monophasic R wave and absence of Q wave in I, V5 and V6
Wide S wave in I, V5 and V6
ST and T in opposite direction to QRS
the ECG. After resolution of the tachycardia, the ECG may show a short P–R interval and a delta wave (a slurred upstroke denoting pre-excitation) at the start of the QRS complex.
2 Atrial tachycardias
Atrial tachycardia: An ectopic atrial focus causes an atrial rate of 150–250 beats/min. Often the rate is between 160 and 170 beats/min with a 1 : 1 response but at faster rates 2 : 1 block may occur.
Atrial flutter: The atria flutter at around 300 beats/
min and 2 : 1 or 3 : 1 block occurs to give rates of up to 150–160 complexes/min (→ below). It may be difficult to identify flutter waves on the ECG.
Atrial fibrillation: The heart rate is irregular.
Fast atrial fibrillation → p. 171.
• Congenital abnormalities of conduction (which cause paroxysmal attacks)
• Drugs
• Metabolic disturbances.
The two main types of SVT are outlined below.
1 Junctional tachycardias
Atrioventricular nodal re-entry tachycardia (AVNRT): This is the most common type of regular narrow-complex tachyarrhythmia and also the most common paroxysmal SVT. It often occurs in patients with otherwise normal hearts and is thus relatively benign. The cause is a re-entry circuit within the AV node. Explanation of AV nodal re-entry circuits → Box 11.3. The ECG is regular with no visible atrial activity.
Atrioventricular re-entry tachycardia (AVRT): Re-entry involves an accessory pathway such as the bundle of Kent in Wolff-Parkinson–White (WPW) syndrome. There is usually no visible atrial activity on
Box 11.3 AV nodal re-entry circuits In the normal AV node there are two pathways along which the atrial impulse can travel – a slow pathway with a short refractory period and a fast pathway with a longer refractory period.
The two unite to become the bundle of His.
During normal sinus rhythm, the atrial impulse travels along both pathways but completes its journey via the fast pathway only because the slow pathway has already become refractory.
In AVNRT a premature atrial beat occurs at a crucial time and the impulse finds the fast pathway to be still refractory and so travels along the slow pathway. When it gets to the point where both fast and slow pathways join to form the bundle of His, the fast pathway has recovered from its refractory period and the impulse travels backwards up it. This establishes a re-entry circuit and is the mechanism in 90% of patients with AV nodal tachycardia. In the other 10% of patients, a premature ventricular beat is the source of the problem and a slow–fast circuit is set up – the reverse of the situation described above. As a result of the normal anatomy involved, affected individuals are often young and healthy with no detectable heart disease.
Haemodynamic disturbance accompanying tachycardia often suggests a ventricular origin for the dysrhythmia but does not exclude a supraventricular cause.
Irregular or broad-complex SVT
SVT usually appears as a narrow-complex tachycar-dia on ECG but, if there is aberrant (i.e. abnormal) conduction such as BBB, then broad complexes may be seen. In the peri-arrest situation, SVT may precipi-tate VF. An irregular narrow-complex tachycardia is most likely to be fast AF.
Infants with SVT
Infants with a tachydysrhythmia may present with a sudden onset of poor feeding, tachypnoea, pallor and lethargy. SVT is the most common non-arrest arrhythmia of infancy and may give rise to cardio-genic shock. Heart rates range from 220/min to as high as 300 complexes/min.
Tx of SVT
Resuscitation Council (UK) algorithm for the treat-ment of tachycardia in adults (with a pulse) → Figure 11.9.
Fast atrial fibrillation is a difficult situation requiring expert advice (→ p. 171).
• Vagal manoeuvres such as carotid sinus massage, orbital pressure, Valsalva’s manoeuvre, iced water
Figure 11.9Algorithm for tachycardia (with a pulse) in adults. Reproduced with the kind permission of the Resuscitation Council (UK).
Adult tachycardia (with pulse) algorithm Yes/Unstable
•Assess using the ABCDE approach •Give oxygen if appropriate and obtain IV access •Monitor ECG, BP, SpO2,record 12-lead ECG •Identify and treat reversible causes (e.g. electrolyte abnormalities) •Amiodarone 300 mg IV over 10-20 min and repeat shock; followed by: •Amiodarone 900 mg over 24 h No/Stable NarrowBroad Irregular Narrow Complex Tachycardia Probable atrial fibrillation Control rate with: • β-Blocker or diltiazem •Consider digoxin or amiodarone if evidence of heart failure
Is QRS narrow (< 0.12 s)? IrregularNarrow QRS Is rhythm regular?Regular Possibilities include: •AF with bundle branch block treat as for narrow complex •Pre-excited AF consider amiodarone •Polymorphic VT (e.g. torsade de pointes - give magnesium 2 g over 10 min)
If ventricular tachycardia (or uncertain rhythm): •Amiodarone 300 mg IV over 20-60 min; then 900 mg over 24 h If previously confirmed SVT with bundle branch block: •Give adenosine as for regular narrow complex tachycardia
•Use vagal manoeuvres •Adenosine 6 mg rapid IV bolus; if unsuccessful give 12 mg; if unsuccessful give further 12 mg. •Monitor ECG continuously Probable re-entry paroxysmal SVT: •Record 12-lead ECG in sinus rhythm •If recurs, give adenosine again & consider choice of anti-arrhythmic prophylaxis
Yes
Sinus rhythm restored? No Possible atrial flutter •Control rate (e.g. β-Blocker)
Irregular Regular
Adverse features? •Shock •Syncope •Myocardial ischaemia •Heart failure
Synchronised DC Shock Up to 3 attempts Seek expert help Seek expert help
Broad QRS Is rhythm regular?
! !
2010
Resuscitation Guidelines Resuscitation Council (UK)titration is available, a loading dose of 40 mg (500 mcg/kg) is given intravenously over 1 min, fol-lowed by an infusion of 50–100 mcg/kg per min until the desired effect is achieved. Esmolol may also be used for the treatment of symptomatic sinus tachycardia.
• Digoxin (IV, up to 500 mg over 30 min, repeated if necessary).
• Amiodarone (IV, 300 mg over 20–60 min followed by 900 mg over 24 h).
• Flecainide: this is a potent sodium channel blocker which is indicated in the special SVTs associated with accessory pathways (e.g. WPW syndrome) and AF. The dose is 100–150 mg (2 mg/kg for children) given intravenously over 20–30 min.
Overdrive pacing is a further option (not for AF). In patients who have ventricular pre-excitation (due to WPW syndrome) together with AF or atrial flut-ter, drugs that block the AV node must be avoided because they cause an increase in pre-excitation.
These drugs include adenosine, verapamil, diltiazem and digoxin.
Children with narrow-complex tachycardias
Children are treated along much the same lines as adults. Doses of adenosine and electricity for children
→ Box 11.4.
Atrial flutter
The atria flutter at a rate of between 280 and 320 contractions/min; 2 : 1 or 3 : 1 AV block occurs, result-ing in a ventricular response of around either 150 or 100 beats/min. The ECG shows a characteristic saw-tooth pattern (best seen in lead II), which is accentu-ated by increasing the degree of AV block (e.g. by carotid sinus massage). An irregular narrow-complex to the face can be attempted – with care – in most
patients. Infants can have their faces immersed in iced water for 5 s.
• Adenosine is effectively a ‘chemical shock’ – imme-diate effect, short acting and relatively safe in both stable and unstable patients. The initial dose is 6 mg for an adult which is given as a rapid IV bolus.
If this proves to be ineffective, up to two further doses (each of 12 mg) may be given at 2-min inter-vals. Patients after heart transplantation are very sensitive to the effects of adenosine and should be given an initial dose of 3 mg. Undesirable effects from adenosine may be seen in patients with WPW syndrome or in those who are taking dipyridamole or carbamazepine. Adenosine (or vagal manoeu-vres) will terminate almost all AVNRTs or AVRTs within seconds. Failure to terminate a regular narrow-complex tachycardia with adenosine sug-gests the presence of an atrial tachycardia such as atrial flutter. Adenosine may be repeated if an arrhythmia recurs; an antiarrhythmic prophylactic drug should then be started.
Patients with signs of cardiac or cerebral compromise
For patients with adverse features such as:
• hypotension or shock (systolic BP <90 mmHg)
• symptoms of low blood flow to the brain (dizziness, faintness or syncope)
• symptoms of myocardial ischaemia (chest pain or heart failure)
• heart rate >200 beats/min treatment consists of:
• Sedation and synchronised cardioversion (starting with 120–150 J biphasic or 200 J monophasic shocks)
• IV amiodarone 300 mg over 20–60 min followed by 900 mg over 24 h and repeated shocks if SVT persists.
Stable, alert patients
There is a choice of suitable drugs:
• Verapamil (IV, 5–10 mg): this is hazardous in WPW syndrome, some SVTs of childhood, ventricular tachycardias and in conjunction with β blockers. It must not be used in infants.
• Esmolol: this is an ultra short-acting cardioselec-tive β blocker with a half-life of 9 min; it is con-traindicated in shock, heart failure, heart block, asthma and after verapamil. In SVT, when time for
Box 11.4 Adenosine and synchronised DC shock for narrow-complex tachycardia in children Adenosine
50 mcg/kg, then 100 mcg/kg and then 250 mcg/kg
(To maximum total dosage of 500 mcg/kg or 300 mcg/kg for infants <1 month old) Synchronised DC shock
0.5 J/kg, then 1 J/kg and then 2 J/kg
Tx
Resuscitation Council (UK) algorithm for the treat-ment of tachycardia in adults (with a pulse)
→ Figure 11.9.
For AF, there are three main treatment options:
1 Control of the ventricular rate by drugs
2 Control of the atrial rhythm by pharmacological cardioversion
3 Control of the atrial rhythm by electrical cardioversion.
It is important to treat the underlying causes of both the fibrillation and the tachycardia. In addition, some complications must be prevented (e.g. throm-boembolism) and some must be treated (e.g. heart failure).
Paroxysmal AF usually reverts spontaneously to sinus rhythm within 48 h and so cardioversion is seldom required.
In patients with AF complicating heart failure, digoxin is used to slow AV conduction and thus control the ventricular rate. It has no effect on the underlying dysrhythmia. It may be given orally or intravenously depending on the urgency of the situ-ation. A suitable IV dose of digoxin is 0.75–1 mg made up to 50 mL and infused over 2 or more hours. Too rapid infusion causes nausea and dysrhythmias. Oral digitalisation can be achieved by giving 1–1.5 mg digoxin in divided doses over 24 h.
tachycardia may result from atrial flutter with a vari-able AV block.