A Textbook of Clinical Pharmacology and Therapeutics

Intranodal supraventricular tachycardia

Fibre tracts in the AV node are arranged longitudinally, and if
differences in refractoriness develop between adjacent fibres
then an atrial impulse may be conducted antegradely through
one set of fibres and retrogradely through another, leading to
a re-entry (‘circus’) tachycardia.

Extranodal supraventricular tachycardia
An anatomically separate accessory pathway is present
through which conduction is faster and the refractory period
shorter than in the AV node. The cardiogram usually shows a
shortened PR interval (because the abnormal pathway con-
ducts more rapidly from atria to ventricle than does the AV
node), sometimes with a widened QRS complex with a slurred
upstroke or delta wave, due to arrival of the impulse in part of
the ventricle where it must pass through unspecialized slowly
conducting ventricular myocytes instead of through special-
ized Purkinje fibres (Wolff–Parkinson–White or WPW syn-
drome). Alternatively, there may be a short PR interval but a
normal QRS complex (Lown–Ganong–Levine syndrome),
if the abnormal pathway connects with the physiological
conducting system distal to the AV node.

VENTRICULAR DYSRHYTHMIAS

• Ventricular ectopic beats: Abnormal QRS complexes
  originating irregularly from ectopic foci in the ventricles.
  These may occur in an otherwise healthy heart or may
  occur as a consequence of organic heart disease, e.g.
  coronary heart disease, hypertrophic cardiomyopathy,
  heart failure from other causes. Multifocal ectopics
  (ectopic beats of varying morphology, arising from more
  than one focus) are likely to be pathological.


• Ventricular tachycardia: The cardiogram shows rapid,
  wide QRS complexes (0.14 seconds or greater) and the
  patient is usually, but not always, hypotensive and poorly
  perfused. This rhythm may presage ventricular
  fibrillation.


• Ventricular fibrillation: The cardiogram is chaotic and
  circulatory arrest occurs immediately.

GENERAL PRINCIPLES OF MANAGEMENT

1. Anti-dysrhythmic drugs are among the most dangerous at
   the clinician’s disposal. Always think carefully before
   prescribing one.
   2.If the patient is acutely ill on account of a cardiac
   dysrhythmia, the most appropriate treatment is almost
   never a drug. In bradydysrhythmia, consider pacing, and
   in tachydysrhythmia consider direct current (DC)
   cardioversion. Consider the possibility of hyperkalaemia
   or other electrolyte disorder, especially in renal disease, as
   a precipitating cause and treat accordingly.
   3.It is important to treat the patient, not the cardiogram.
   Remember that several anti-dysrhythmic drugs can
   themselves cause dysrhythmias and shorten life. When

dysrhythmias are prognostically poor, this often reflects

severe underlying cardiac disease which is not improved

by an anti-dysrhythmic drug but which may be improved

by, for example, an ACE inhibitor (for heart failure), aspirin

or oxygen (for ischaemic heart disease) or operation (for left

main coronary artery disease and valvular heart disease).

4.In an acutely ill patient, consider the possible immediate

cause of the rhythm disturbance. This may be within the

heart (e.g. myocardial infarction, ventricular aneurysm,

valvular or congenital heart disease) or elsewhere in the

body (e.g. pulmonary embolism, infection or pain, for

example from a distended bladder in a stuporose patient).

5.Look for reversible processes that contribute to the

maintenance of the rhythm disturbance (e.g. hypoxia,

acidosis, pain, electrolyte disturbance, including Mg^2 as

well as Kand Ca^2 , thyrotoxicosis, excessive alcohol or

caffeine intake or pro-dysrhythmic drugs) and correct them.

6.Avoid ‘cocktails’ of drugs.

218 CARDIAC DYSRHYTHMIAS

Key points

Cardiac dysrhythmias: general principles

• In emergencies consider:
  DC shock (tachydysrhythmias);
  pacing (bradydysrhythmias).


• Correct pro-dysrhythmogenic metabolic disturbances:
  electrolytes (especially K, Mg^2 );
  hypoxia/acid-base;
  drugs.


• Clinical trials have shown that correcting a dysrhythmia
  does not necessarily improve the prognosis –
  anti-dysrhythmic drugs can themselves cause
  dysrhythmias.

CLASSIFICATION OF ANTI-DYSRHYTHMIC

DRUGS

The classification of anti-dysrhythmic drugs is not very satis-

factory. The Singh–Vaughan–Williams classification (classes

I–IV; see Table 32.1), which is based on effects on the cardiac

action potential, is widely used, but unfortunately does not

reliably predict which rhythm disturbances will respond to

which drug. Consequently, selection of the appropriate anti-

dysrhythmic drug to use in a particular patient remains largely

empirical. Furthermore, this classification does not include

some of the most clinically effective drugs used to treat certain

dysrhythmias, some of which are listed in Table 32.2.

CARDIOPULMONARY RESUSCITATION

AND CARDIAC ARREST: BASIC AND

ADVANCED LIFE SUPPORT

The European Resuscitation Council provides guidelines for

basic and advanced life support (Figures 32.1 and 32.2).