3.1 Management of arrhythmias

80 2.3.1 Management of arrhythmias

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2.3.2 Drugs for arrhythmias

2.3.2 Drugs for both supraventricular and ventricular arrhy- Drugs for arrhythmias

thmias include amiodarone, beta-blockers (see p. 86), disopyramide, flecainide, procainamide (available

Anti-arrhythmic drugs can be classified clinically into from ‘special-order’ manufacturers or specialist-import- those that act on supraventricular arrhythmias (e.g.

ing companies, see p. 939), and propafenone, see below verapamil), those that act on both supraventricular

under Supraventricular and Ventricular Arrhythmias. and ventricular arrhythmias (e.g. disopyramide), and those that act on ventricular arrhythmias (e.g. lidocaine (lignocaine)).

ADENOSINE

They can also be classified according to their effects on Indications rapid reversion to sinus rhythm of parox- the electrical behaviour of myocardial cells during activ-

ysmal supraventricular tachycardias, including those ity:

associated with accessory conducting pathways (e.g. Class I: membrane stabilising drugs (e.g. lidocaine,

Wolff-Parkinson-White syndrome); aid to diagnosis of flecainide)

broad or narrow complex supraventricular tachy- Class II: beta-blockers

cardias

Class III: amiodarone and sotalol (also Class II) Cautions atrial fibrillation or flutter with accessory

pathway (conduction down anomalous pathway may Class IV: calcium-channel blockers (includes verap-

increase); heart transplant (see below); interactions: amil but not dihydropyridines)

Appendix 1 (adenosine) This latter classification (the Vaughan Williams classifi-

Contra-indications second- or third-degree AV block cation) is of less clinical significance.

and sick sinus syndrome (unless pacemaker fitted); asthma

Side-effects include transient facial flush, chest pain, Cautions The negative inotropic effects of anti-arrhy-

dyspnoea, bronchospasm, choking sensation, nausea, thmic drugs tend to be additive. Therefore special care

light-headedness; severe bradycardia reported should be taken if two or more are used, especially if

(requiring temporary pacing); ECG may show transi- myocardial function is impaired. Most or all drugs that

ent rhythm disturbances

are effective in countering arrhythmias can also provoke

Dose

them in some circumstances; moreover, hypokalaemia enhances the arrhythmogenic (pro-arrhythmic) effect of

ardiov

. By rapid intravenous injection into central or large

many drugs. peripheral vein, 6 mg over 2 seconds with cardiac

monitoring; if necessary followed by 12 mg after 1–2

ascular

minutes, and then by 12 mg after a further 1–2 minutes; increments should not be given if high

Supraventricular arrhythmias

level AV block develops at any particular dose Important Patients with a heart transplant are very sensi-

syst

Adenosine is usually the treatment of choice for termi- tive to effects of adenosine and should receive initial dose of 3 mg over 2 seconds, followed if necessary by 6 mg after 1–2

em

nating paroxysmal supraventricular tachycardia. As it has a very short duration of action (half-life only about 8

minutes, and then by 12 mg after a further 1–2 minutes. Also, if essential to give with dipyridamole reduce initial dose

to 10 seconds, but prolonged in those taking dipyrid-

to 0.5–1 mg

amole), most side-effects are short lived. Unlike verap- Note Adenosine doses in the BNF may differ from those in amil, adenosine can be used after a beta-blocker. Verap-

product literature

amil may be preferable to adenosine in asthma. Adenocor c (Sanofi-Synthelabo) A Oral administration of a cardiac glycoside (such as

Injection , adenosine 3 mg/mL in physiological saline, digoxin, section 2.1.1) slows the ventricular response

net price 2-mL vial = £4.45 (hosp. only) in cases of atrial fibrillation and atrial flutter. However,

Note Intravenous infusion of adenosine (Adenoscan , Sanofi intravenous infusion of digoxin is rarely effective for

Winthrop) may be used in conjunction with radionuclide myo- rapid control of ventricular rate. Cardiac glycosides are

cardial perfusion imaging in patients who cannot exercise contra-indicated in supraventricular arrhythmias asso-

adequately or for whom exercise is inappropriate—consult product literature

ciated with accessory conducting pathways (e.g. Wolff- Parkinson-White syndrome).

Verapamil (section 2.6.2) is usually effective for supra-

Supraventricular and ventricular

ventricular tachycardias. An initial intravenous dose (important: serious beta-blocker interaction hazard,

arrhythmias

see p. 118) may be followed by oral treatment; hypo- Amiodarone is used in the treatment of arrhythmias tension may occur with large doses. It should not be

particularly when other drugs are ineffective or contra- used for tachyarrhythmias where the QRS complex is

indicated. It may be used for paroxysmal supraventri- wide (i.e. broad complex) unless a supraventricular

cular, nodal and ventricular tachycardias, atrial fibrilla- origin has been established beyond reasonable doubt.

tion and flutter, and ventricular fibrillation. It may also It is also contra-indicated in atrial fibrillation with pre-

be used for tachyarrhythmias associated with Wolff- excitation (e.g. Wolff-Parkinson-White syndrome). It

Parkinson-White syndrome. It should be initiated only should not be used in children with arrhythmias without

under hospital or specialist supervision. Amiodarone specialist advice; some supraventricular arrhythmias in

may be given by intravenous infusion as well as by childhood can be accelerated by verapamil with danger-

mouth, and has the advantage of causing little or no ous consequences.

myocardial depression. Unlike oral amiodarone, intra- Intravenous administration of a beta-blocker (section

venous amiodarone may act relatively rapidly.

2.4) such as esmolol or propranolol, can achieve rapid Intravenous injection of amiodarone may be used in control of the ventricular rate.

cardiopulmonary resuscitation for ventricular fibrilla- cardiopulmonary resuscitation for ventricular fibrilla-

Amiodarone has a very long half-life (extending to several weeks) and only needs to be given once daily (but high doses may cause nausea unless divided). Many weeks or months may be required to achieve steady- state plasma-amiodarone concentration; this is particu- larly important when drug interactions are likely (see also Appendix 1).

Most patients taking amiodarone develop corneal microdeposits (reversible on withdrawal of treatment); these rarely interfere with vision, but drivers may be dazzled by headlights at night. However, if vision is impaired or if optic neuritis or optic neuropathy occur, amiodarone must be stopped to prevent blindness and expert advice sought. Because of the possibility of phototoxic reactions, patients should be advised to shield the skin from light during treatment and for several months after discontinuing amiodarone; a wide-spectrum sunscreen (section 13.8.1) to protect against both long-wave ultraviolet and visible light should be used.

Amiodarone contains iodine and can cause disorders of thyroid function; both hypothyroidism and hyper- thyroidism may occur. Clinical assessment alone is unreliable, and laboratory tests should be performed before treatment and every 6 months. Thyroxine (T4) may be raised in the absence of hyperthyroidism; there- fore tri-iodothyronine (T3), T4, and thyroid-stimulating hormone (thyrotrophin, TSH) should all be measured. A raised T3 and T4 with a very low or undetectable TSH concentration suggests the development of thyrotoxic- osis. The thyrotoxicosis may be very refractory, and amiodarone should usually be withdrawn at least tem- porarily to help achieve control; treatment with carbim- azole may be required. Hypothyroidism can be treated with replacement therapy without withdrawing amio- darone if it is essential; careful supervision is required.

Pneumonitis should always be suspected if new or progressive shortness of breath or cough develops in a patient taking amiodarone. Fresh neurological symp- toms should raise the possibility of peripheral neuro- pathy.

Amiodarone is also associated with hepatotoxicity and treatment should be discontinued if severe liver function abnormalities or clinical signs of liver disease develop.

Beta-blockers act as anti-arrhythmic drugs principally by attenuating the effects of the sympathetic system on automaticity and conductivity within the heart, for details see section 2.4. For special reference to the role of sotalol in ventricular arrhythmias, see p. 86.

Disopyramide may be given by intravenous injection to control arrhythmias after myocardial infarction (includ- ing those not responding to lidocaine (lignocaine)), but it impairs cardiac contractility. Oral administration of disopyramide is useful but it has an antimuscarinic effect which limits its use in patients susceptible to angle-closure glaucoma or prostatic hypertrophy.

Flecainide belongs to the same general class as lido- caine and may be of value for serious symptomatic ventricular arrhythmias. It may also be indicated for junctional re-entry tachycardias and for paroxysmal atrial fibrillation. However, it can precipitate serious arrhythmias in a small minority of patients (including those with otherwise normal hearts).

Propafenone is used for the prophylaxis and treatment of ventricular arrhythmias and also for some supraven- tricular arrhythmias. It has complex mechanisms of action, including weak beta-blocking activity (therefore caution is needed in obstructive airways disease—con- tra-indicated if severe).

Drugs for supraventricular arrhythmias include aden- osine, cardiac glycosides, and verapamil; see above under Supraventricular Arrhythmias. Drugs for ventri- cular arrhythmias include lidocaine; see under Ventri- cular Arrhythmias, p. 84.

Mexiletine and procainamide are both available from ‘special-order’ manufacturers or specialist-importing companies, see p. 939. Mexiletine can be used for life- threatening ventricular arrhythmias; procainamide is given by intravenous injection to control ventricular arrhythmias.