Acharya G, Räsänen J, Mäkikallio K, Erkinaro T, Kavasmaa T, Haapsamo M, Mertens L, Huhta JC. Metabolic acidosis decreases fetal myocardial isovolumic velocities in a chronic sheep model of increased placental vascular resistance. Am J Physiol Heart Circ Physiol 294: H498-H504, 2008. First published November 16, 2007 doi:10.1152/ajpheart.00492.2007.-We hypothesized that acute fetal metabolic acidosis decreases fetal myocardial motion in a chronic sheep model of increased placental vascular resistance (Rua). Eleven ewes and fetuses were instrumented at 118 -122 days of gestation. After 5 days of recovery and 24 h of placental embolization to increase Rua, longitudinal myocardial velocities of the right and left ventricles and interventricular septum (IVS) were assessed at the level of the atrioventricular valve annuli via tissue Doppler imaging (TDI). Ventricular inflow (E and A waves) and outflow velocities were obtained, and cardiac outputs were calculated. All measurements were performed at baseline and during fetal acidosis caused by epidural anesthesia-induced maternal hypotension, which decreased uterine artery volume blood flow, fetal oxygenation, arterial pH, and base excess and increased lactate. Compared with baseline, the peak isovolumic myocardial contraction and relaxation velocities of the ventricles and IVS, early relaxation velocity (EЈ) of the ventricles, and systolic velocity of the IVS decreased during metabolic acidosis. The proportion of isovolumic contraction time of the cardiac cycle increased but the isovolumic relaxation and ejection time proportions and the TDI Tei index did not change. The E-to-EЈ ratio for both ventricles was higher during metabolic acidosis than at baseline. During metabolic acidosis, right and left ventricular cardiac outputs remained unchanged compared with baseline. In sheep fetuses with increased Rua and acute metabolic acidosis, global cardiac function was preserved. However, acute metabolic acidosis impaired myocardial contractility during the isovolumic phase and relaxation during the isovolumic and early filling phases of the cardiac cycle. cardiac function; fetal echocardiography; tissue Doppler IN RESPONSE TO HYPOXEMIA, fetuses generally redistribute more blood toward the myocardium, brain, and adrenal glands at the expense of the lower body and viscera (3,22). The fetal heart is known to have a remarkable ability to withstand hypoxia (10, 30), but progressive hypoxia and acidosis may decrease blood supply to the heart (6) and alter myocardial energy metabolism (18,40). However, despite reduced myocardial contractility, global cardiac function is preserved during moderate acidemia (26). Echocardiography has been applied to assess fetal cardiac function noninvasively in a variety of clinical conditions, such as intrauterine growth restriction (29), hydrops (17), congenital heart disease (38), and twin-twin transfusion syndrome (36). Recently, tissue Doppler imaging (TDI) of myocardial motion has been introduced in clinical practice as a promising new techniqu...
