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  • 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 antiarrhythmic drug therapy, cardiac pacing, electrical cardioversion, and defibrillation are essential to successful arrhythmia management.
  • The proarrhythmic potential of antiarrhythmic drugs must be recognized and preventive measures taken whenever possible.
  • Knowledge of antiarrhythmic drug pharmacokinetics and pharmacodynamics and the effect 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.
  • The intensivist should recognize when temporary and implantable pacemakers or cardioverter defibrillators are not functioning appropriately.
  • Not all arrhythmias require long-term prophylactic treatment.

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 (e.g., sinus tachycardia, sinus bradycardia, Mobitz type I second-degree atrioventricular [AV] block, or premature atrial and ventricular beats). Correct diagnosis and understanding of arrhythmia mechanisms and 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. 24-1A).1,2 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 the sinus node is the dominant pacemaker in the normal heart, subsidiary pacemakers may become dominant under certain conditions, such as sympathetic stimulation or digitalis toxicity (see Fig. 24-1). Normal atrial and ventricular muscles maintain a high negative resting potential (−90 mV) and only depolarize when stimulated. Under certain pathophysiologic conditions, including electrolyte abnormalities and ischemia, the resting membrane potential may decrease (−60 mV) and cells may depolarize spontaneously.

Figure 24–1.

Mechanisms of cardiac arrhythmias: enhanced or abnormal automaticity and triggered activity or reentry. A. The rate of phase 4 depolarization may increase, causing the myocardial cell to reach the threshold potential (TP) sooner and spontaneously depolarize. In diseased tissue, the resting potential (RP) may be elevated and the time to reach TP may then be shortened (not shown). B. Early afterdepolarizations (EADs) develop late on phase 3 of repolarization of the action potential and, if they reach threshold, may trigger a depolarization. This is the mechanism of torsade de pointes ventricular tachycardia. ...

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