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The clinical importance of delayed afterdepolarizations and resultant triggered activity as a cause of cardiac arrhythmias is uncertain. We studied the response of ouabain-induced delayed afterdepolarizations and triggered activity to a pacing protocol similar to those used clinically in an effort to quantify the types of responses to pacing that occur as a result of this arrhythmogenic mechanism. Isolated canine Purkinje fibers were superfused with 2 X 10(7)M ouabain until delayed afterdepolarizations occurred and attained an amplitude of 5 mV at a paced cycle length of 500 msec. We then studied the induction of triggered activity in these fibers by pacing. We found that: (1) As the pacing cycle length decreased, the coupling interval from the last paced beat to the first triggered beat decreased and 83% of fibers developed triggered activity. (2) The coupling interval of the first triggered beat after single (S2) or double (S2S3) premature beats was in part dependent on preceding pacing cycle lengths. S2 pacing induced triggered activity in 39% of fibers, and S2S3 pacing induced triggered activity in 48% of fibers. We then studied the termination of ouabain-induced sustained rhythmic activity by pacing: 89% of sustained rhythmic activity could be terminated by overdrive pacing at a cycle length less than or equal to 300 msec. The coupling interval of the first beat or first delayed afterdepolarization after the termination of overdrive decreased as pacing cycle length decreased. S2 premature beats reset the sustained rhythmic activity and terminated 14% of sustained rhythmic activity. The coupling interval of the first escape beat or delayed afterdepolarization after S2S3 premature beats decreased as the S2S3 interval shortened, and S2S3 terminated 26% of sustained rhythmic activity. Pacing at an S1S1 cycle length of 400 msec followed by an S2 terminated 50% of sustained rhythmic activity; S1S1 at a cycle length of 400 msec followed by S2S3 terminated 85% of sustained rhythmic activity. This quantitative demonstration of the responses of delayed afterdepolarizations, triggered activity, and sustained rhythmic activity to pacing may be useful in differentiating these from other mechanisms for arrhythmias.