Pphn

When I think about PPHN, it helps me to think about it's other name- persistent fetal circulation- because that really does describe what is going on. In utero, the baby's blood supply comes in through their umbilical vein, up to their right atrium, and the majority goes through the foramen ovale, into the left atrium and out to the body through the ductus arteriosus. After the ductus, the blood circulates out to the body and back to the mother via the umbilical artery. Very little blood flows to the lungs via the pulmonary artery because the pressure in the artery as well as pulmonary vascular resistence is very high. So more simply, the blood comes in, bypasses the lungs, goes out to the body and back out to the placenta- round and round and round. When a baby is in utero, this is no big deal because the placenta does the oxygenating for the baby. This is another reason the pO2 of a fetus is so very low- like 20-25.

PPHN occurs when the baby's body doesn't figure out it has to switch from being a fetus to being a "big kid" now. Normally, with the first few breaths, the pulmonary vascular resistance (higher blood pressure in lungs) goes down, and the systemic vascular resistance (blood pressure in the body) goes up. When the higher blood pressure in the lungs goes down, blood can flow to the lungs easily and be oxygenated there. This change, as well as the raising of the systemic pressure helps close the foramen ovale and ductus arteriosus, so blood flows through the heart in what we think of as a normal pattern- right atrium to right ventricle, out to lungs via pulmonary artery, back to left atrium via pulmonary vein, to left ventricle and out to body via aorta. Several things cause the changes in blood pressure I talked about- the raising of the baby's pO2, the mechanical forces of the first breaths, the loss of certain substances from the placenta, even fluid shifts in the body- all normal processes at birth. When the newborn's body does not undergo this transition- boom! You have PPHN.

Babies in certain situations are more likely to have PPHN- those with hypoplastic lungs, meconium aspiration, hypoxia/asphyxia at birth, sepsis, diaphagmatic hernia all come to mind. This is because there are already factors impairing their oxygenation/ventilation/acid base status, etc, so their normal transition does not occur.

Books will tell you the signs and symptoms of PPHN include cyanosis, tachypnea, low pO2 with normal-ish pCO2, possible cardiac murmur, and often a notable difference in their preductal (right hand) SpO2 and their post ductal (either foot) SpO2. From practice, I can say that these kids are often the term/near term kids that were born through mec, normal appearing for the first few hours. Then they seem to crash and burn, requiring way more O2 per hood or cannula, etc. than you would expect for their GA. Their work of breathing increases significantly and they just look crappy!

Treatment often includes placement of UA/UV for good access and careful BP/ABG monitoring- you often end up with multiple drips (sedation, pressors, etc) to run on these kiddos- as well as intubation and ventilation with an oscillator for oxygenation and to help reduce CO2 retention. Nitric oxide, a pulmonary vasodilator, is often used to help promote relaxation of the pulmonary vessels. Minimal stimulation is recommended, with carefully controlled light/sound and sedation, as a stressed or struggling infant can reverse any progress that is being made in relaxing those vessels. We always treat with antibiotics to rule out any possible septic causes. Occasionally, these infants need ECMO to provide their oxygenation until their own body can adapt to the task- finally switching from fetal to regular newborn circulation.

I hope this makes sense! If it doesn't, please PM me and I'll try to help you. I'm doing a study on PPHN for my NNP program right now, so this is a favorite topic of mine.