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This Article Full Text Full Text (PDF) All Versions of this Article: 294/1/H498    most recent 00492.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Acharya, G. Articles by Huhta, J. C. Search for Related Content PubMed PubMed Citation Articles by Acharya, G. Articles by Huhta, J. C.

Metabolic acidosis decreases fetal myocardial isovolumic velocities in a chronic sheep model of increased placental vascular resistance

¹Department of Pediatrics, University of South Florida College of Medicine and All Children's Hospital, Children's Research Institute, St. Petersburg, Florida; ²Department of Obstetrics and Gynecology, Faculty of Medicine, University of Tromsø, and University Hospital of Northern Norway, Tromsø, Norway; Departments of ³Obstetrics and Gynecology and ⁴Anesthesiology, University Hospital of Oulu, Oulu, Finland; and ⁵Department of Pediatric Cardiology, University Hospital Leuven, Leuven, Belgium

Submitted 24 April 2007 ; accepted in final form 12 November 2007

We hypothesized that acute fetal metabolic acidosis decreases fetal myocardial motion in a chronic sheep model of increased placental vascular resistance (R_ua). 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 R_ua, 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 (E') 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-E' 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 R_ua 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