Measuring vital signs and simulating hemodynamic patterns during closure of the patent ductus arteriosus

Complications arising from preterm birth account for one million deaths each year, with preterm birth being a risk factor in over 50% of all neonatal deaths. From fetal to neonatal life complications can arise that undermine maturation of neonates. A common condition within this transition process is the patent ductus arteriosus (PDA). Ductal steal of oxygen rich blood from the aorta leads to abnormal cerebral perfusion and hypoperfusion of the gut circulation, which causes life threatening conditions. Ductal tracking using a patient’s vital signs will enable the continuous monitoring of ductal patency in order to adequately treat the patient before these clinical deterioration take place. Within this thesis vital signs are analyzed for possible patterns related to a PDA which can be used to track ductal patency within preterm patients. Additionally hemodynamic simulations are preformed to study possible blood pressure trends during ductal closure. To characterize vital signs patterns associated with closure of the ductus, vital signs were analyzed during a 6-day window surrounding ductal treatment. Vital sign features were calculated every half hour, and at six hourly intervals the mean trends of these features were determined. A 28 weeks gestational age and 1000 gram birth weight preterm hemodynamic model, with ductal flow segment, was created to simulate blood pressure trends during ductal closure. Ductal patency within this model was varied to simulate closure of the ductal flow segment. Blood pressure trends are given with respect to ductal flow, which makes it possible to compare measured and simulated blood pressure trends during ductal closure. Measured vital signs trends during ductal closure showed patterns which can be linked to the ductal closure occurring within PDA patients. The effect of ductal closure is most pronounced in the systolic pressure increase after successful pharmaceutical treatment of the PDA. Results from the hemodynamic simulations showed that the model was able to correctly stimulate closure of the ductal flow segment. Measured and simulated systolic pressure showed to be within the same range, however measured diastolic pressures were higher than the simulated diastolic pressures during ductal closure. The simulation results showed to have blood pressure trends during ductal closure which are comparable with blood pressure trends reported in literature. Measured and simulated blood pressure were given with respect to an estimated ductal flow, but they did not show the same patterns during ductal closure. This thesis shows that there are possible patterns that can be detected during ductal closure. Tracking ductal patency using these general patterns within individual patients will remain challenging.