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128 Chapter 9 Table 9.3 Effect of antiarrhythmic drugs on pacing thresholds Increase at normal drug levels Flecainide Propafenone Amiodarone Sotalol Increase at toxic drug levels Quinidine Procainamide Disopyramide No increase Lidocaine Mexiletine several ways and is often clinically significant. Two major problems caused by antiarrhythmic drugs are that they can change the en-ergy required for successful defibrillation and they can change the characteristics of the arrhythmia being treated. The effect of antiarrhythmic drugs on defibrillation energy re-quirements is an important consideration because increasing the defibrillation threshold can render an ICD ineffective. The effects of various drugs on defibrillation energy requirements are summarized inTable9.4.Ingeneral,drugsthatblockthesodiumchannelincrease defibrillation energy requirements (thus, Class IC drugs have the most profound effect, and Class IA and Class IB drugs tend to have proportionally lesser effects), and drugs that block the potassium channels (e.g., sotalol) decrease defibrillation energy requirements. Drugsthataffectboththesodiumandpotassiumchannels(i.e.,Class IA drugs and amiodarone) have mixed effects—sometimes they in-crease and sometimes they decrease defibrillation energy require-ments. If one must prescribe a drug that has the potential of increas-ing defibrillation energy requirements for a patient who has an ICD, one should consider retesting defibrillation thresholds after the drug has been loaded to be sure that the ICD is still capable of delivering sufficient energy to reliably defibrillate the patient. Antiarrhythmic drugs can also interact with ICDs by changing the characteristics of a patient’s ventricular tachycardia. By slowing the Table 9.4 Effect of antiarrhythmic drugs on defibrillation thresholds Increase Flecainide Propafenone Lidocaine Mexiletine Mixed effect Quinidine Procainamide Amiodarone Decrease Sotalol Common adverse events with antiarrhythmic drugs 129 rate of ventricular tachycardia, a drug can render the arrhythmia more amenable to antitachycardia pacing, which potentially makes the ICD more effective. On the other hand, by slowing the rate of ventricular tachycardia below the recognition rate of the ICD, a drug can cause the ICD to fail to recognize (and therefore fail to treat) re-current arrhythmias. Antiarrhythmic drugs can also cause reentrant ventricular arrhythmias to recur more frequently or even to become incessant, thus inducing frequent ICD therapy, which, in turn, can cause excessive discomfort and premature battery depletion of the ICD. In general, when one is compelled to add an antiarrhythmic drug to the treatment regimen of a patient with an ICD, one should consider electrophysiologic testing to reexamine the characteristics of the patient’s arrhythmias and to be sure that the ICD is optimally programmed to treat the arrhythmias. Reference 1 Echt DS, Liebson PR, Mitchell B, et al. Mortality and morbidity in patients receiving encainide, flecainide or placebo. N Engl J Med 1991;324:781. Part 3 Antiarrhythmic drugs in the treatment of cardiac arrhythmias CHAPTER 10 Basic principles of using antiarrhythmic drugs The first two sections of the book concerned the mechanisms of car-diac arrhythmias, the mechanism of action of antiarrhythmic drugs, and the features of specific antiarrhythmic drugs. In this final sec-tion, that information is applied to the use of antiarrhythmic drugs in the treatment of specific cardiac arrhythmias. Chapter 10 reviews some basic principles that should be kept in mind when using an-tiarrhythmic drugs. On the basis of the generally limited efficacy of antiarrhythmic drugs as well as their inherent propensity to cause serious problems, the first principle should be completely self-evident; namely, one should avoid using antiarrhythmic drugs whenever possible. Thus, when one has decided to prescribe an antiarrhythmic drug, the final step before actually writing the order should be to ask, “Does this patientreallyneedthisdrug?”Thereareonlytwogeneralconditions in which using an antiarrhythmic drug is entirely appropriate: first, when an arrhythmia needs to be suppressed because it threatens to cause death or permanent harm, and second, when an arrhythmia needs to be suppressed because it produces significant symptoms. Before prescribing an antiarrhythmic drug, the physician should be certain that the arrhythmia meets one of these two conditions. The second basic principle is to keep the goal of treatment clearly in mind and to tailor the aggressiveness of one’s therapy accordingly. If one is treating an arrhythmia to prevent death or permanent in-jury, for instance, a relatively aggressive approach may be appropri-ate and necessary. In theory, if the object is to spare life and limb, one should err on the side of efficacy, perhaps willingly accepting the risk of certain drug toxicities. In practice, however, as we will see in Chapters 11 and 12, there are relatively few instances today where one ought to rely primarily on antiarrhythmic drugs to treat arrhythmias that threaten life and limb. 133 134 Chapter 10 On the other hand, if one is treating an arrhythmia to relieve symptoms, a more circumspect approach is appropriate. In these cases, one generally should use a stepwise strategy, beginning with milder, less risky forms of treatment, and carefully reassessing the risk-to-benefit ratio before each potential escalation of therapy. All too often physicians pursue the treatment of relatively insignificant arrhythmias with Ninja-like intensity, an error that can result in unnecessary injury or death. The final basic principle of using antiarrhythmic drugs is that, if one feels compelled to expose a patient to the risk of the drugs, one should also feel compelled to take every reasonable precaution to reduce the risks. For instance, given the almost universal risk of proarrhythmia, one should often consider placing patients on a cardiac monitor while antiarrhythmic drugs are being initiated be-cause,althoughproarrhythmiacanoccuranytimeduringthecourse of treatment, a significant proportion of these events occur during the first 3 or 4 days of drug usage. Most importantly, one must take great care in deciding which drug to use. The choice must be indi-vidualized. The accompanying tables summarize the factors that should be considered in choosing antiarrhythmic drugs for patients with and without significant underlying cardiac disease. Somedrugsareplainlycontraindicatedforparticularpatients.Pro-cainamide, for instance, should not be used in patients with systemic lupus erythematosus; quinidine should not be used in patients with chronic colitis; patients with severe lung disease (in whom mild drug-inducedpulmonarytoxicitygoesalongway)ideallyshouldnot receive amiodarone; patients with a history of heart failure should not receive drugs with negative inotropic effects. Beyond these obvious individual considerations, the presence or absence of underlying heart disease is the most important variable in choosing an antiarrhythmic drug, because heart disease predisposes patients to reentrant circuits and, therefore, to proarrhythmia. As shown in Table 10.1, beta blockers and Class IB drugs are the safest choice regardless of whether the patient has underlying heart dis-ease. Class IC drugs are reasonably safe for patients with normal hearts, but because they very frequently exacerbate reentrant ven-tricular tachyarrhythmias, they are to be avoided in patients with underlying cardiac disease. Class IA drugs carry a moderate risk of toxicity for patients without cardiac disease because they cause both torsades de pointes and end-organ toxicity; in patients with cardiac ... - tailieumienphi.vn
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