Connects the PA to the proximal descending aorta. It allows most of the blood from the RV to bypass the fetus's fluid filled non-functioning lungs. Normally closes within 72 hours of life. In utero it allows blood to be diverted to the placenta for gas exchange. About 90% of RV outflow is through the DA.

Premature infants have an immature response to oxygen so although oxygen is normally a potent stimulant of smooth muscle contraction normally closing the PDA, it doesn't in these infants. Prostaglandins inhibit the closure of ductus. Lack of ductal smooth muscle (due to prematurity) prolongs patency.

Upon closure at birth becomes ligamentum artiosum. This is non-functional and is formed within three weeks of birth. It can play a role in major trauma as it fixes the aorta in place and during rapid recoil can result in a ruptured aorta.

When the ductus arteriosis fails to close. Early symptoms are uncommon but within the first year of life the child will experience increased work of breathing and poor weight gain and ultimately congestive heart failure.

PDA is common in neonates with persistant respiratory problems such as hypoxia. This is due to too little oxygen reaching the lungs and thus not enough bradykinin is produced to close the DA.

The PDA allows a portion of oxygenated blood from the left heart to flow back to the lungs by flowing from the aorta to the pulmonary artery. The infant will become short of breath as the additional fluid returning to the lungs increases the lung pressure to the point that the infant has trouble inflating the lungs, this leads to congestive heart failure. This uses more calories and interferes with feeding.

Incidence:

Inversely related to GA and weight.
Appears in 45% of infants weighing less than 1750g.
Appears in 80% of infants weighing less than 1200g.

Haemodynamics:

As peripheral vascular resistance (PVR) falls and systemic vascular resistance (SVR) increases a left to right shunt via the PDA results in blood flow from the aorta to the PA increasing pulmonary blood flow. The increased PAP ind increased LV pressure and volume lead to bilateral CHF.

Because L to R flow is dependent on a drop in PVR infants with pulmonary disease (eg RDS) will show symptoms when lung disease improves. Before this time, PVR greater than SVR leads to a R to L shunt via the PD (referred to as persistant pulmonary hypertension of the neonate or PPHN).

Manifestations:

Presents at day 4 to 7 of life with inability to wean from the ventilator or needing increased ventilatory or oxygen support.
Apnoea
Bradycardic
Increased pulmonary vasculature and cardiomegaly.
Bounding peripheral pulses and hyperactive precordium.
Widening pulse pressure (>20 mmHg)

	Erstellt von Elaine Henry vor etwa 11 Jahre

Fetal circulation Notiz am Ductus Arteriosis, erstellt von Elaine Henry am 15/08/2013.