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Ronnie Falcao, LM MS, a homebirth midwife in Mountain View, CA

Detailed Information from an Expert in Circulatory Physiology

Well, since it has been breathing all along, I'm not sure any new stimulus is needed--just the removal of the physical constriction of the pelvis.

From later in my handout: "It remains unclear what actually stimulates the infant to take its first breath. Two recent reviews suggest that the drop in environmental temperature and sensory stimulation may be important (Rosser, 1993; Johnson, 1996). Prior to parturition, foetal respiratory movements are reduced (Austin & Short, 1990; Case & Waterhouse, 1993). In the days prior to delivery, placental prostaglandins in amniotic fluid may inhibit foetal breathing movements (Johnson, 1996)."

True, passage through the pelvis possibly exerts enough pressure to inhibit expansion of the thorax, but inspiration is the active phase of the breathing cycle - initiated in the inspiratory centre of the pons - while exhalation (except during eg exertion and panting) is the result of passive recoil of elastic components of the lung and respiratory muscles.

Breathing in requires some kind of stimulus to the intercostals etc. that is usually initiated in the brain stem (pontine neurons appear to have an inherent underlying rhythmic firing pattern; some trigger inspiration while some inhibit the inspiratory neurons - the so-called "expiratory centre"; sensory stimuli and the autonomics influence their firing rate). As we all know, sudden exposure to a drop in temperature has a tendency to make us breathe in involuntarily - seems pretty logical to me that it should be the stimulus for first breath. Correct me if I'm wrong - I just haven't yet seen sound evidence that convinces me otherwise.

That is, I'm not sure that the cessation of cord pulsing is really tightly linked in time with the dramatic switch in pulmonary circulation.

I'd be willing to bet (though with zero data) that within 30-60 second of birth in a vigorous baby the great majority of its O2 is coming from breathing air rather than from the placenta.

blood is diverted to the lungs and the systemic circulation and away from the placenta. And as this "shunt" happens, the cord will begin to stop pulsating because placental perfusion with fetal blood is no longer necessary.

Coincidentally, on the ob-gyn list, somebody posted about the speculation that the placenta continues to serve as a depressed infant's major O2 source for several minutes. Somebody else had the same thought that I did, which is to doubt this based on the likely decreased perfusion of the placenta as soon as the uterus collapses with the expulsion of the fetus; it seems that it would lose much of the total surface area of contact, though it retains enough to still be physically "stuck" there.

I admit this is mostly "gut" feeling based on my understanding of how the system works; some of it I know that I could find references for, some of it I'm not sure whether the work has been done. I would refer you to the textbook that I consider to be one of the best for serious students of physiology and which (although now getting out of date) is the one we recommend for our courses: Berne & Levy (1993) Physiology 3rd Edition, Mosby

I think:-

As long as fetal blood is getting to the placenta and the pressures in the umbilical artery are adequate to ensure that blood can leave it, then I tend to agree that gaseous exchange could happen and that SOME oxygen could reach the newborn from the placenta.

I agree (although maybe didn't say it explicitly in my original posting) that after a *vigorous* baby takes its first breath, the majority (maybe in most cases, all) of its O2 will come from air - it's p02 rises towards that of it's mother's (although it takes a matter of days to reach what would be considered "normal" saturation later in life) and so it's unlikely that gas exchange in the placenta is very significant - p02 is already low there because the placenta's such an active organ in its own right.

But if the baby is *NOT* yet breathing air or making any respiratory effort and the cord vessels are still pulsating, then the placenta could continue to be a potential source of O2 for the baby - a different situation entirely. If the cord's been amputated then there's absolutely no possibility of the baby getting O2 from this source. IF even a little fetal blood is circulating to the placenta, then because there is a diffusion gradient for O2 (assuming fetal pO2 is lower than on the maternal/placental side) some gas exchange will happen - so I too think it could be a potential source of O2 for a "flat" baby. Gas exchange would only be expected to cease when/if equilibrium is reached. The anecdotal evidence about naloxone getting to babies when he injects it into the cord suggests that some circulation is happening.

The placenta has a huge surface area because of all the sinuses; like the liver (and the lung) it's a "bloody" organ. It's receiving a very significant proportion of the entire maternal cardiac output until the separation process starts - ie vasoconstriction of uterine vessels and contraction of the uterus to form the "living ligatures" of third stage. I don't think there's the same amount of vasoconstriction on the fetal side in the normal course of events. As I have always understood it perfusion from the fetus/newborn just kinda slows down and ceases when the pulsations stop because of the major fetal systemic/pulmonary pressure and anatomical changes.

On the other hand circulating adrenaline in the newborn might contribute (because of the exposure to relatively cold air, the birth itself etc.). Would depend on whether there are a or b receptors in the precapillary vessels. Must go off and suss that one out, but I don't think its' likely to be a very significant factor ........ except if the baby's very hypoxic. Just "thinking out loud here" but if the baby's hypoxic and there are b receptors then there might actually be vasodilatation going on on the fetal side in a kind of last ditch attempt to improve perfusion to the placenta....... only possible if the cord hasn't yet been clamped, of course......

True, once separation begins there's a reduced surface area for contact between the MATERNAL circulation and the placenta; but until perfusion from the fetal side ceases, I'd expect there would still be quite a large volume of maternal blood in close proximity to some circulating fetal blood. After fetal circulation to the placenta stops (whether naturally or by clamping), well since the placenta's a temporary organ, any residual blood from either side would be left there - and lost to both unless the cord is "stripped". Gail has already posted ECPC's conclusions about the possible effects of early clamping and by-passing physiological equilibration. I agree with them; increased blood volume in the placenta makes it a more "solid" mass; potential problem if the uterus cannot clamp down around it to effect separation. And I have for a long time had concerns about over-transfusion of infants.

Clamping the cord before the newborn has spontaneously taken a breath and/or before pulsations stop will serve to raise arterial CO2 and the newborn will become acidotic and hypoxic. This assumes continued gas exchange at the placenta,

Does this make some kind of sense? I'm only too happy to hear another side of the argument.......... Isn't this amazing - all happening in a matter of minutes at the most!! Far less time than it takes to write about and certainly not really one that bothers us in the natural course of things. Babies just start to breathe. We only worry about it when they don't.

But I still think that it's a pretty important transition in physiological terms.