every 6 h

may cause less hypotension, but ventricular ectopy may worsen transiently after each dose.


17 mg/kg

1-4 mg/min

Administer load at 20 mg/min unless patient develops hypotension or excessive widening of QRS.

*Currently unavailable.

*Currently unavailable.

(16,67). The efficacy of prophylactic magnesium infusion requires further investigation. Aggressive measures to ensure reperfusion, limit infarct size, prevent recurrent ischemia, and treat heart failure probably act synergistically to further reduce the incidence of malignant ventricular arrhythmias. Finally, continuous electrocardiographic (ECG) monitoring, coupled with an efficient plan for prompt defibrillation if needed, is a cornerstone of CCU care.


Treatment of VF requires a well-rehearsed, orderly, rapid resuscitation effort. Because the likelihood of successful resuscitation decreases with time (68), immediate electrical defibrillation with a nonsynchronized discharge should be performed. For monophasic defibrillators, an initial energy setting of 200 J is appropriate; up to 360 J can be used if necessary (69). Energy requirements for newer, biphasic defibrillators tend to be lower. Lidocaine and bretylium tosylate are equally effective in preventing recurrences of VF (70); however, bretylium more frequently causes significant hypotension (71). Epinepherine and amiodarone may be beneficial in refractory VF.

Patients who are successfully resuscitated should generally receive iv lidocaine; Table 2 reviews dosing information. The optimal duration of therapy is unknown; lidocaine may generally be discontinued after 6-24 h in patients whose post-VF course is uncomplicated. Careful attention should be paid to metabolic (hypoxia, acidemia, or hypokalemia) and hemodynamic (e.g., ongoing ischemia or heart failure) derangements that may have contributed to the episode of VF. Lidocaine toxicity is common in elderly patients and in those with hepatic and/or left ventricular dysfunction. Signs of lidocaine toxicity include confusion, lethargy, slurred speech, and seizures. Therefore,

Fig. 5. This patient presented with an acute anterior MI and presumed new LBBB. Minutes after arrival in the emergency room, this sustained wide-complex tachycardia was recorded. Note the A-V dissociation in the lead II rhythm, indicative of VT.

the patient's clinical status and serum lidocaine levels should be carefully monitored. During prolonged infusion of lidocaine (greater than 24-48 h), the terminal half-life of elimination may increase, necessitating a reduction in dose. Cimetidine (72) and propranolol (73) have been noted to increase the serum level of lidocaine.

Patients who suffer from recurrent VF despite lidocaine therapy should be treated with amiodarone. Bretylium is not presently available in the United States; it is unclear whether it will become available again in the future. Bretylium increases the VF threshold in normal tissue and averts the decrease in VF threshold usually caused by ischemia (74,75). Standard and alternative dosing regimens are reviewed in Table 2. Although iv amiodarone is of proven benefit in refractory or recurrent VF (76,77), fewer data exist regarding its use in the setting of AMI. In a canine model of acute infarction, iv amiodarone facilitated defibrillation in cases of refractory VF (78).

Ventricular Tachycardia

Ventricular tachycardia (VT) (see Fig. 5, 6) is a potentially fatal arrhythmia in the setting of AMI. The frequently employed broad definition of VT—three or more consecutive ventricular complexes at a rate of at least 100-120 beats per minute (BPM)—encompasses benign as well as life-threatening arrhythmias, and is therefore of limited clinical utility. Several definitions, are useful from a practical perspective. Sustained VT lasts more than 30 s and/or causes hemodynamic collapse requiring countershock; nonsustained VT (NSVT) lasts less than 30 seconds. Primary VT occurs in the absence of significant CHF; secondary VT occurs in the setting of profound pump failure. Finally, VT may be monomorphic or polymorphic (79). Relatively narrow fascicular tachycardias, likely reflecting reentry or abnormal automaticity in Purkinje fibers, have occasionally been noted early in the course of anterior MI (see Fig. 7).

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