D Durham1, L I G Worthley. 1. Department of Critical Care Medicine, Flinders Medical Centre, Adelaide, South Australia.
Abstract
OBJECTIVE: To review the diagnosis and management of cardiac arrhythmias in a two-part presentation. DATA SOURCES: Articles and published peer-review abstracts on tachycardias and bradycardias. SUMMARY OF REVIEW: Normal cardiac rhythm originates from impulses generated within the sinus node. These impulses are conducted to the atrioventricular node where they are delayed before they are distributed to the ventricular myocardium via the His-Purkinje system. Abnormalities in cardiac rhythm are caused by disorders of impulse generation, conduction or a combination of the two and may be life threatening due to a reduction in cardiac output or myocardial oxygenation. Cardiac arrhythmias are commonly classified as tachycardias (supraventricular or ventricular) or bradycardias. The differentiation between supraventricular and ventricular tachycardias usually requires an assessment of atrial and ventricular rhythms and their relationship to each other. In the critically ill patient the commonest tachycardia is sinus tachycardia and treatment generally consist of management of the underlying disorder. Other supraventricular tachycardias (SVTs) include, atrial flutter, atrial fibrillation and paroxysmal supraventricular tachycardia (PSVT) all of which may require cardioversion, although to maintain sinus rhythm, antiarrhythmic therapy is often needed. Adenosine is useful in management and treatment many SVTs although its use in PSVT with Wolff-Parkinson-White syndrome is hazardous. Multifocal atrial tachycardia is a characteristic supraventricular tachycardia found in the critical ill patient. While it usually responds to intravenous magnesium sulphate, its management also requires removal of various precipitating factors. Ventricular tachycardia (VT) and ventricular fibrillation (VF) require urgent cardioversion and defibrillation respectively. Torsade de pointes should be differentiated from these ventricular arrhythmias as antiarrhythmic therapy may be contraindicated. CONCLUSIONS: Supraventricular and ventricular tachycardias in the critically ill patient often have underlying disorders that precipitate their development (e.g. hypokalaemia, hypomagnesaemia, anti-arrhythmic proarrhythmia, myocardial ischaemia, etc). While antiarrhythmic therapy and cardioversion or defibrillation may be required to achieve sinus rhythm, correction of the associated abnormalities is also required.
OBJECTIVE: To review the diagnosis and management of cardiac arrhythmias in a two-part presentation. DATA SOURCES: Articles and published peer-review abstracts on tachycardias and bradycardias. SUMMARY OF REVIEW: Normal cardiac rhythm originates from impulses generated within the sinus node. These impulses are conducted to the atrioventricular node where they are delayed before they are distributed to the ventricular myocardium via the His-Purkinje system. Abnormalities in cardiac rhythm are caused by disorders of impulse generation, conduction or a combination of the two and may be life threatening due to a reduction in cardiac output or myocardial oxygenation. Cardiac arrhythmias are commonly classified as tachycardias (supraventricular or ventricular) or bradycardias. The differentiation between supraventricular and ventricular tachycardias usually requires an assessment of atrial and ventricular rhythms and their relationship to each other. In the critically ill patient the commonest tachycardia is sinus tachycardia and treatment generally consist of management of the underlying disorder. Other supraventricular tachycardias (SVTs) include, atrial flutter, atrial fibrillation and paroxysmal supraventricular tachycardia (PSVT) all of which may require cardioversion, although to maintain sinus rhythm, antiarrhythmic therapy is often needed. Adenosine is useful in management and treatment many SVTs although its use in PSVT with Wolff-Parkinson-White syndrome is hazardous. Multifocal atrial tachycardia is a characteristic supraventricular tachycardia found in the critical ill patient. While it usually responds to intravenous magnesium sulphate, its management also requires removal of various precipitating factors. Ventricular tachycardia (VT) and ventricular fibrillation (VF) require urgent cardioversion and defibrillation respectively. Torsade de pointes should be differentiated from these ventricular arrhythmias as antiarrhythmic therapy may be contraindicated. CONCLUSIONS: Supraventricular and ventricular tachycardias in the critically ill patient often have underlying disorders that precipitate their development (e.g. hypokalaemia, hypomagnesaemia, anti-arrhythmic proarrhythmia, myocardial ischaemia, etc). While antiarrhythmic therapy and cardioversion or defibrillation may be required to achieve sinus rhythm, correction of the associated abnormalities is also required.