Seppänen M P, Kääpä P O, Kero P O, Saraste M
Department of Pediatrics, University of Turku, Finland.
Pediatrics. 1994 May;93(5):769-73.
To determine the course of systolic pulmonary artery pressure (PAP) in association with ductal shunting and cardiac output (CO) in preterm neonates.
During the acute phase of respiratory distress syndrome (RDS) with and without surfactant treatment, serial Doppler ultrasound examinations were performed at the ages of 2, 12, 24, 48, and 72 hours in 51 neonates with RDS and 21 healthy, preterm controls. Twenty-eight of the distressed neonates received two or four doses of synthetic exogenous surfactant at intervals of 12 hours. Measurements of hemodynamic variables in these neonates were performed before and after 8 hours following surfactant treatments. PAP was estimated by the Doppler method from the maximal tricuspid regurgitant flow velocity. Doppler ultrasound was also used to determine simultaneously CO, and the direction and magnitude of the ductal shunting.
The PAP was initially at the same level, but remained significantly higher in distressed than in healthy, preterm control neonates between the ages of 12 to 48 hours. The systolic systemic arterial blood pressures did not differ between the distressed and control neonates, but increased gradually during the study period. Consequently, the ratio of systolic pulmonary and systemic pressure was also higher in neonates with RDS than in controls during the first day of life. Bidirectional ductal shunting disappeared in all neonates studied after 2 days of life. Significant left-to-right shunting through the ductus arteriosus persisted more frequently in distressed neonates, especially those with surfactant treatment, than in control neonates during the study period, and more often caused the need for medical or surgical closure. Doppler-derived CO remained stable throughout the study in the distressed neonates, being significantly higher in surfactant-treated neonates than nontreated distressed neonates or healthy controls at 72 hours of life.
The data of the present study confirms that the postnatal decrease in PAP is delayed in acute RDS. Further, significant patent ductus arteriosus shunting persists longer in RDS and may contribute to elevated CO during the resolution of the disease.
确定早产儿收缩期肺动脉压（PAP）与动脉导管分流及心输出量（CO）的关系。
在有或无表面活性剂治疗的呼吸窘迫综合征（RDS）急性期，对51例RDS新生儿和21例健康早产儿在2、12、24、48和72小时龄时进行连续多普勒超声检查。28例病情严重的新生儿每隔12小时接受两剂或四剂合成外源性表面活性剂治疗。在表面活性剂治疗前及治疗后8小时对这些新生儿进行血流动力学变量测量。通过多普勒方法根据最大三尖瓣反流流速估算PAP。还使用多普勒超声同时测定CO以及动脉导管分流的方向和大小。
PAP最初处于相同水平，但在12至48小时龄时，病情严重的新生儿的PAP仍显著高于健康早产儿对照组。病情严重的新生儿与对照组新生儿的收缩期体循环动脉血压无差异，但在研究期间逐渐升高。因此，RDS新生儿出生后第一天的收缩期肺压与体循环压之比也高于对照组。所有研究的新生儿在出生2天后动脉导管双向分流消失。在研究期间，病情严重的新生儿，尤其是接受表面活性剂治疗的新生儿，动脉导管持续存在明显左向右分流的情况比对照组新生儿更频繁，且更常需要进行药物或手术封堵。在整个研究过程中，病情严重的新生儿通过多普勒测得的CO保持稳定，在出生72小时时，接受表面活性剂治疗的新生儿的CO显著高于未治疗的病情严重新生儿或健康对照组。
本研究数据证实急性RDS患儿出生后PAP下降延迟。此外，RDS患儿动脉导管未闭分流持续时间更长，可能在疾病缓解期导致CO升高。
