Correct diagnoses and understanding of arrhythmia mechanisms are crucial to successful arrhythmia management.
The hemodynamic effects of an arrhythmia are important in developing an appropriate treatment strategy.
Predisposing conditions and reversible causes should be recognized and corrected.
Knowledge of antiarrhythmics for prophylaxis, acute management, and long-term management are necessary for successful arrhythmia management.
The proarrhythmic potential of antiarrhythmic drugs must be recognized and preventative measures should be taken whenever possible.
Knowledge of antiarrhythmic drug pharmacokinetics and pharmacodynamics and the impact of multisystem organ disease on these parameters are important in preventing drug toxicity.
The intensivist should be skilled in the implantation of temporary pacing systems, external cardioversion, and defibrillation.
Role of cardiac pacing, electrical cardioversion, and defibrillation should be clear to physicians managing patients with arrhythmias.
Recognition of malfunctioning temporary and permanent implantable pacemakers or cardioverter defibrillators is crucial in the management of patients with such devices.
Cardiac arrhythmias are common in the critical care setting. Many arrhythmias detected are benign, may occur in healthy individuals and require no investigation or treatment, for example, sinus tachycardia, sinus bradycardia, Mobitz type I second-degree AV block or premature atrial and ventricular beats. At times, the arrhythmia may be the clue to a sick patient, such as sinus tachycardia in a patient developing sepsis or atrial fibrillation due to a pulmonary embolus. Correct diagnosis and understanding arrhythmia mechanisms as well as knowledge of antiarrhythmic drug pharmacology and nonpharmacologic therapies of arrhythmias are crucial for successful arrhythmia management. This chapter focuses on the mechanisms, investigation, and management of the most common, clinically significant arrhythmias encountered.
Tachycardia mechanisms have been classified as due to abnormalities of impulse formation or impulse conduction.1-3 Abnormalities of impulse formation may be due to normal automaticity, abnormal automaticity or triggered activity occurring within atrial or ventricular muscle tissue or the specialized conduction system (Fig. 36-1A).1,3 Natural pacemaker cells are found in the sinus node, parts of the atria, the atrioventricular node, and the His-Purkinje system. These cells exhibit phasic spontaneous depolarization during diastole, resulting in an action potential when the threshold potential is reached.1 Although in the normal heart, the sinus node is the dominant pacemaker, subsidiary pacemakers may become dominant under certain conditions, for example, sympathetic stimulation or digitalis toxicity (Fig. 36-1). Normal atrial and ventricular muscle maintains a high negative resting potential (−90 mV) and only depolarizes when stimulated. Under certain pathophysiologic conditions, for example, electrolyte abnormalities or ischemia, the resting membrane potential may decrease (−60 mV) and cells may now spontaneously depolarize.
Mechanisms of cardiac arrhythmias—enhanced or abnormal automaticity, triggered activity or reentry. A. The rate of phase 4 depolarization may increase causing the myocardial cell to reach the threshold potential (TP) earlier and spontaneously depolarize. In diseased tissue, the resting potential (RP) may be elevated and the time ...
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