ABSTRACT. The relationship between changes in heart rate, left ventricular output, and left ventricular stroke volume was studied in 18 preterm infants, with mean gestational age 29 wk (range 26-33 wk) and mean postnatal age 10 d (range 1-21 d). To yield left ventricular output, the blood flow velocity in the ascending aorta was measured by range-gated Doppler technique and multiplied by the aortic cross-sectional area measured by cross-sectional and M-mode echocardiography. Stroke volume was calculated by dividing left ventricular output by heart rate. The individual mean left ventricular output correlated poorly with heart rate ( 3 = 0.17), and, accordingly, there was a closer relationship between stroke volume and left ventricular output. In only four of the 18 infants was a significant correlation between heart rate changes and left ventricular output found. Substantial changes in stroke volume were seen in most infants, and in 1 3 of the 18 infants the changes exceeded 25%. These variations in stroke volume were closely related to left ventricular output. In 15 of the 18 infants, the maximum heart rate change was associated with a stroke volume change in the opposite direction. The group average of the maximum heart rate increase in each individual, 24 bpm (18%), corresponded to a decrease in stroke volume of 0.15 mL.kg-' (9%) (p < 0.05) and an increase in left ventricular output of 22.7 m L min-' .kg-' (9%) (p < 0.05). A reciprocal relationship was seen between afterload and left ventricular output. The findings indicate that the preterm infant has a substantial ability to alter stroke volume and that stroke volume is an important determinant of neonatal left ventricular output. During beat-to-beat fluctuations in heart rate, the stroke volume changes appear to reduce the effect of the heart rate changes on output. (Pediatr Res 31: 117-120,1992 Supported by the Karolinska Institute, the General Maternity Hospital Foundation, the Swedish Society for Medicine, and Sallskapet Barnavird.Studies of the fetal and neonatal heart have provided basic information about the myocardial immaturity on the cellular and subcellular levels. The immature myocardium has been shown to contain more water, less contractile elements per unit weight, and less sarcoplasmic reticulum (1, 2). Furthermore, the cardiac sympathetic innervation is not fully developed at birth (3, 4). In in vitro experiments these differences correspond to reduced compliance and reduced contractile force (1) compared with the mature myocardium. However, the hemodynamic consequences of the myocardial immaturity on the intact circulatory system are, despite extensive investigations, still not clearly delineated. It has been claimed that the fetal heart performs at or near its peak capacity even during normal conditions and has a very limited ability to change (SV) (5, 6). Accordingly, fetal and neonatal cardiac output should be almost entirely dependent on HR. This, however, has been questioned in other fetal and neonatal lamb studies (7-lo), as well as in...