Submitted on April 24, 2007
Accepted on November 12, 2007
Metabolic acidosis decreases fetal myocardial isovolumic velocities in a chronic sheep model of increased placental vascular resistance
Ganesh Acharya1*, Juha Rasanen2, Kaarin Makikallio2, Tiina Erkinaro3, Tomi Kavasmaa3, Mervi Haapsamo2, Luc Mertens4, and James Huhta5
1 Pediatrics, University of South Florida, Children's Research Institute, St. petersburg, Florida, United States
2 Obstetrics and Gynecology, University Hospital of Oulu, Oulu, Finland
3 Anesthesiology, University Hospital of Oulu, Oulu, Finland
4 Pediatric Cardiology, University Hospital of Leuven, Leuven, Belgium
5 Pediatrics and Perinatology, University of Southern Florida, United States; Pediatrics and Perinatology, University of Southern Florida
* To whom correspondence should be addressed. E-mail: ganesh.acharya{at}fagmed.uit.no.
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 hours of placental embolization to increase Rua, the longitudinal myocardial velocities of the right and left ventricles and interventricular septum (IVS) were assessed at the level of the atrioventricular valve annuli using 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 to baseline, the peak isovolumic myocardial contraction and relaxation velocities of ventricles and IVS, early relaxation velocity (E') of ventricles, and the 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/E' ratio for both ventricles was higher during metabolic acidosis compared to baseline. During metabolic acidosis, right and left ventricular cardiac outputs remained unchanged compared to baseline. In sheep fetuses with increased Rua and acute metabolic acidosis, the global cardiac function was preserved. However, acute metabolic acidosis impaired myocardial contractility during the isovolumic phase and relaxation during isovolumic and early filling phases of the cardiac cycle.
