Digoxin toxicity from

F2. Fogelman, A. M., La Mont, J. T., Finkelstein, S., Rado, E., and Pearce, M. L., Fallibility of plasma-digoxin in differentiating toxic from non-toxic patients. Lancet ii, 727-729 (1971). 

FIGURE 2.3 Superimposed frequency histograms in which serum digoxin concentrations are shown for 131 patients without digoxin toxicity and 48 patients with electrocardiographic evidence of digoxin toxicity. (Reproduced with permission from Smith TW, Haber E. J Clin Invest 1970 49 2377- 6.)... 

A retrospective Bayesian analysis in 60 patients confirmed that age is a major factor in digoxin toxicity (136). However, an analysis of the data from the DIG study (SEDA-20, 173) has shown that while mortaUty in heart failure increases with age, the actions of digoxin are independent of age (137). 

Similar results were found with phenytoin in another study in 3 healthy subjeets. Other eases have also been reported with phenytoin, primidone, pentobarbital and phenobarbital. In one ease, quinidine levels fell by 44% when phenytoin was given with quinidine to a patient with reeurrent ventrieular taehyeardia. In another report quinidine levels increased from a mean of 0.8 to 2.2 mierograms/mL 15 days after pentobarbital was discontinued. Interestingly, in this case the patient was also on digoxin, and stopping phenobarbital precipitated digoxin toxicity by causing an increase in quinidine levels. 

A case-control study using data from healthcare databases in Ontario from 1994 to 2000 identified 1051 patients who had been admitted to hospital with digoxin toxicity. Of these, 5 patients (0.5%) had been exposed to cefuroxime in the preceding 3 weeks when compared with 0.3% of controls, suggesting that digoxin toxicity was not significantly related to cefuroxime exposure. ... 

An established interaction of clinical importance but only moderately documented. Monitor the effects of concurrent use (e.g. for bradycardia) and reduce the digoxin dosage where necessary. Some patients may have a substantial increase in serum digoxin levels whereas others will have only a small or moderate rise. There appear to he no case reports of digoxin toxicity arising from this interaction. 

If shortened, may result from digoxin toxicity or electrolyte imbalances (such as hypercalcemia). 

If prominent, may be from hypercalcemia, hypokalemia, or digoxin toxicity. 

Multiform PVCs look different from one another (see shaded areas) and arise either from different sites or from the same site via abnormal conduction. Multiform PVG may indicate severe heart disease or digoxin toxicity. 

The majority of authors agree that plasma digoxin levels in adequately digitalized but nontoxic patients are lower than those in whom toxic symptoms are present and prominent, but there is considerable overlap. Moreover, precise limits for therapeutic effectiveness and toxicity are, for reasons already discussed difficult or impossible to define. Few patients derive much benefit from digoxin at plasma levels below 0.7 ng/ml, and toxic symptoms do not become unduly frequent until plasma digoxin levels exceed 2 ng/ml. 

Hypercalcemia from any cause predisposes the patient to digitalis toxicity. Calcium, particularly when administered rapidly by the IV route, may produce serious arrhythmias in digitalized patients. On the other hand, hypocalcemia can nullify the effects of digoxin in humans thus, digoxin may be ineffective until serum calcium is restored to normal. 

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