Abstract

digoxin and had frequent nonconducted atrial premature contractions on their electrocardiograms. All blood was drawn before the morning digoxin dose. The serum digoxin values were 0.2, 0.6, 0.7, 0.7, 0.8, 1.6, 1.8, 2.1, 2.8 and 4.2 nglml respectively. The serum digoxin concentrations can effectively differentiate nontoxic from toxic individuals. Smith and Haber' observed that 90 percent of patients with no evidence of digoxin intoxication, had levels of 2.0 nglml or below, while 87 percent of the toxic group had concentrations above 2.0 nglml. Thus, seven of the patients in our present series had serum digoxin levels of 2.0 nglml or below and can therefore be classified as a nontoxic group. Only three of the ten patients had evidence of digitalis intoxication based on elevated serum digoxin levels. However, other workers3 have stated that there can be considerable overlap between serum levels of digoxin in patients considered toxic and in those without toxicity. Further, digoxin levels in the upper limits of normal may be toxic in individuals with low serum potassium levels. An electrocardiographic pathognomonic sign of digitalis intoxication would indeed be extremely useful to the clinician. It would appear that nonconducted atrial premature beats can appear in patients with or without digitalis intoxication.

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