The diagnosis is established by the combination of characteristic rhythm distur- bances, ancillary symptoms (visual disturbances, nausea, changes in mentation), and elevated serum concentrations. Potentiating factors may include hypothyroidism, hypokalemia, or renal Treatment of digoxin toxic- ity is based on the severity. In mild cases, dis- continuing the medication, monitoring rhythm, and maintaining normal serum potassium may Intravenous magnesium is often administered if VAs are present.S10.7-12 Occasionally, temporary pacing may be needed for atrioventricular block or asystole.S10.7-13 For more severe intoxication (serum digoxin con- centrations exceeding 4 ng/mL and with serious arrhythmias such as VT), the treatment of choice is digoxin-specific Fab antibody.S10.7-1 In 1 series of 150 severely intoxicated patients, response was rapid (30 minutes to 4 hour), and 54% of patients presenting with a cardiac arrest sur- Adverse effects include worsening of the underlying disease (increased ventricular rate during AF, exacerbation of HF) and hypokalemia. Doses lower (and less expen- sive) than the full neutralizing dose are sufficient as long as cardiac arrest is not imminent.S10.7-2 Recommendations for Medication-Induced Arrhythmias (Continued) COR LOE Recommendations CLINICAL STATEMENTS AND GUIDELINES Digoxin concentration monitoring is unreliable after antidigoxin antibody administration. 2. Monitoring high-risk patients during initiation of QT-prolonging antiarrhythmic medications and recognition of the syndrome when it occurs are the first steps. Temporary pacing is highly effective in managing torsades de pointes that is recurrent after potassium and magnesium supplementation.S10.7-3 Isoproterenol can also be used to increase heart rate and abolish postectopic pauses.S10.7-3 3. 