Using M-mode echocardiography we found that 0.5, 1.0, and 1.5% end-tidal halothane induced dose-related increases in left ventricular volume and decreases in left ventricular performance in seven normal unpremedicated subjects. During controlled respiration with normocarbia, the diastolic minor axis of the heart, which is related to the cube root of left ventricular volume, increased to a maximum of 107.7 ± 1.9 (% ± SE of control) at 1.5% end-tidal halothane from a control value of 43.5 ± 1.3 (mm ± SE). Two ejection-phase performance variables, percentage shortening and mean velocity of circumferential shortening decreased to 60.1 ± 6.1 (% ± SE of control) and 62.4 ± 6.5, (% ± SE of control) at 1.5% halothane from respective control values of 29.7 ± 2.61 (% ± SE) and 0.94 ± 0.08 (circumferences/second ± SE). Surgical stimulation did not significantly affect these changes. Under these experimental conditions, we conclude that halothane dilates the heart, and that echocardiography can be used to monitor the depressant effect of halothane on the heart.