Clinical Pharmacology and Therapeutics
A Textbook of Clinical Pharmacology and ... - clinicalevidence
A Textbook of Clinical Pharmacology and ... - clinicalevidence
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218 CARDIAC DYSRHYTHMIAS<br />
Intranodal supraventricular tachycardia<br />
Fibre tracts in the AV node are arranged longitudinally, <strong>and</strong> if<br />
differences in refractoriness develop between adjacent fibres<br />
then an atrial impulse may be conducted antegradely through<br />
one set of fibres <strong>and</strong> retrogradely through another, leading to<br />
a re-entry (‘circus’) tachycardia.<br />
Extranodal supraventricular tachycardia<br />
An anatomically separate accessory pathway is present<br />
through which conduction is faster <strong>and</strong> the refractory period<br />
shorter than in the AV node. The cardiogram usually shows a<br />
shortened PR interval (because the abnormal pathway conducts<br />
more rapidly from atria to ventricle than does the AV<br />
node), sometimes with a widened QRS complex with a slurred<br />
upstroke or delta wave, due to arrival of the impulse in part of<br />
the ventricle where it must pass through unspecialized slowly<br />
conducting ventricular myocytes instead of through specialized<br />
Purkinje fibres (Wolff–Parkinson–White or WPW syndrome).<br />
Alternatively, there may be a short PR interval but a<br />
normal QRS complex (Lown–Ganong–Levine syndrome),<br />
if the abnormal pathway connects with the physiological<br />
conducting system distal to the AV node.<br />
VENTRICULAR DYSRHYTHMIAS<br />
• Ventricular ectopic beats: Abnormal QRS complexes<br />
originating irregularly from ectopic foci in the ventricles.<br />
These may occur in an otherwise healthy heart or may<br />
occur as a consequence of organic heart disease, e.g.<br />
coronary heart disease, hypertrophic cardiomyopathy,<br />
heart failure from other causes. Multifocal ectopics<br />
(ectopic beats of varying morphology, arising from more<br />
than one focus) are likely to be pathological.<br />
• Ventricular tachycardia: The cardiogram shows rapid,<br />
wide QRS complexes (0.14 seconds or greater) <strong>and</strong> the<br />
patient is usually, but not always, hypotensive <strong>and</strong> poorly<br />
perfused. This rhythm may presage ventricular<br />
fibrillation.<br />
• Ventricular fibrillation: The cardiogram is chaotic <strong>and</strong><br />
circulatory arrest occurs immediately.<br />
GENERAL PRINCIPLES OF MANAGEMENT<br />
1. Anti-dysrhythmic drugs are among the most dangerous at<br />
the clinician’s disposal. Always think carefully before<br />
prescribing one.<br />
2. If the patient is acutely ill on account of a cardiac<br />
dysrhythmia, the most appropriate treatment is almost<br />
never a drug. In bradydysrhythmia, consider pacing, <strong>and</strong><br />
in tachydysrhythmia consider direct current (DC)<br />
cardioversion. Consider the possibility of hyperkalaemia<br />
or other electrolyte disorder, especially in renal disease, as<br />
a precipitating cause <strong>and</strong> treat accordingly.<br />
3. It is important to treat the patient, not the cardiogram.<br />
Remember that several anti-dysrhythmic drugs can<br />
themselves cause dysrhythmias <strong>and</strong> shorten life. When<br />
dysrhythmias are prognostically poor, this often reflects<br />
severe underlying cardiac disease which is not improved<br />
by an anti-dysrhythmic drug but which may be improved<br />
by, for example, an ACE inhibitor (for heart failure), aspirin<br />
or oxygen (for ischaemic heart disease) or operation (for left<br />
main coronary artery disease <strong>and</strong> valvular heart disease).<br />
4. In an acutely ill patient, consider the possible immediate<br />
cause of the rhythm disturbance. This may be within the<br />
heart (e.g. myocardial infarction, ventricular aneurysm,<br />
valvular or congenital heart disease) or elsewhere in the<br />
body (e.g. pulmonary embolism, infection or pain, for<br />
example from a distended bladder in a stuporose patient).<br />
5. Look for reversible processes that contribute to the<br />
maintenance of the rhythm disturbance (e.g. hypoxia,<br />
acidosis, pain, electrolyte disturbance, including Mg 2 as<br />
well as K <strong>and</strong> Ca 2 , thyrotoxicosis, excessive alcohol or<br />
caffeine intake or pro-dysrhythmic drugs) <strong>and</strong> correct them.<br />
6. Avoid ‘cocktails’ of drugs.<br />
Key points<br />
Cardiac dysrhythmias: general principles<br />
• In emergencies consider:<br />
DC shock (tachydysrhythmias);<br />
pacing (bradydysrhythmias).<br />
• Correct pro-dysrhythmogenic metabolic disturbances:<br />
electrolytes (especially K , Mg 2 );<br />
hypoxia/acid-base;<br />
drugs.<br />
• <strong>Clinical</strong> trials have shown that correcting a dysrhythmia<br />
does not necessarily improve the prognosis –<br />
anti-dysrhythmic drugs can themselves cause<br />
dysrhythmias.<br />
CLASSIFICATION OF ANTI-DYSRHYTHMIC<br />
DRUGS<br />
The classification of anti-dysrhythmic drugs is not very satisfactory.<br />
The Singh–Vaughan–Williams classification (classes<br />
I–IV; see Table 32.1), which is based on effects on the cardiac<br />
action potential, is widely used, but unfortunately does not<br />
reliably predict which rhythm disturbances will respond to<br />
which drug. Consequently, selection of the appropriate antidysrhythmic<br />
drug to use in a particular patient remains largely<br />
empirical. Furthermore, this classification does not include<br />
some of the most clinically effective drugs used to treat certain<br />
dysrhythmias, some of which are listed in Table 32.2.<br />
CARDIOPULMONARY RESUSCITATION<br />
AND CARDIAC ARREST: BASIC AND<br />
ADVANCED LIFE SUPPORT<br />
The European Resuscitation Council provides guidelines for<br />
basic <strong>and</strong> advanced life support (Figures 32.1 <strong>and</strong> 32.2).