Clinical Pharmacology and Therapeutics

218 CARDIAC DYSRHYTHMIAS
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 conducts
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 specialized
Purkinje fibres (Wolff–Parkinson–White or WPW syndrome).
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 K and Ca 2 , thyrotoxicosis, excessive alcohol or
caffeine intake or pro-dysrhythmic drugs) and correct them.
6. Avoid ‘cocktails’ of drugs.
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 satisfactory.
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 antidysrhythmic
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).