Tachycardia produces subendocardial ischemia and ST segment abnormalities after coronary obstruction. To determine whether a quantitative relationship exists between these ST shifts and transmural blood flow, 19 dogs were studied. Coronary obstruction was produced by ameroid constriction of the left circumflex artery, and tachycardia was generated by atrial pacing at 90 to 210 beats/min. ST shifts were studied by body surface isopotential mapping with an 84-electrode torso grid, and blood flow was quantitated by serial radiolabeled microsphere injections. Isopotential maps at each paced rate, 40 msec into the ST segment, were classified as normal or ischemic based on spatial patterns of voltages. Pacing after 3 weeks of ameroid constriction reduced endocardial/epicardial flow ratios in 11 dogs from 1.16 ± 0.22 at rest to 0.41 ± 0.18 at 210 beats/min. Abnormal ST depression developed in these dogs at a rate of 184.0 + 16.5 beats/min. Endocardial/epicardial ratios with ST depression (0.45 + 0.15) were lower than at those without ST depression (1.05 + 0.19; p < .01). Logistic regression analysis demonstrated that ST depression corresponded to an endocardial/epicardial ratio of 0.67 or less (p < .01). With this model, 95.5% of data sets were correctly classified. Neither heart rate nor perfusion bed size were significant independent predictors of an ischemic electrocardiographic response. The magnitude of abnormal ST segment shift was significantly correlated (r = .87) with the transmural flow ratio. Thus (1) development of electrocardiographic changes indicative of ischemia corresponds to a predictable degree of flow redistribution and (2) the magnitude of the ST shift is correlated with the intensity of the flow abnormality.