ASPHYXIA DOES NOT INJURE THE BRAIN
[A] Myers RE. Perinatal brain damage. American Journal of Obstetrics and Gynecology 1972 112:246-276.30 [A]
Tracing [A] is of primate newborn delivered by c-section and immediately asphyxiated. The cord was clamped immediately and the head covered with a rubber bag. The eventual result was death; autopsy showed widespread infarction of brainstem nuclei similar to that seen following recovery from cardiac arrest.
Brain infarction results from loss of blood perfusion as in arterial occlusion (segmental infarct) or cardiac arrest (widespread infarcts of metabolically active areas.) The fetal brain grows and develops on a copious supply of partially oxygenated blood; if well perfused, brain tissue tolerates hypoxia.
However, myocardial contraction (blood pressure) depends on aerobic respiration. Under complete asphyxia [A] heart function gradually fails, the tissue perfusion force (blood pressure) gradually disappears and brain infarction begins.
1. Hypoxic heart failure causes loss of perfusion.
2. Loss of perfusion causes neuron necrosis.
Primate model [A] does not completely replicate the human newborn that develops ischemic neuron necrosis. (HIE or NE) Intrapartum hypoxia /asphyxia is a frequent feature of HIE/NE,  but no human neonate is subjected to the degree of anoxia and hypoxic heart failure seen in [A]. Most HIE victims are not (and never were) significantly hypoxic; however, they all exhibit signs of heart failure, inadequate tissue perfusion and multi-organ failure, and typical ischemic neuron necrosis.
· The prime causal agent in HIE/NE responsible for loss of perfusion is not hypoxia.
The most common cause of birth asphyxia is cord compression (e.g. a tight nuchal cord) that impedes oxygen supply to the fetus; it also acts as a venous tourniquet, impedes venous blood return, engorges the placenta and thus exsanguinates the fetus. The severely cord-compressed child is born limp, areflexic, and ashen white with some blue/black mottling. Routine treatment is immediate cord clamping (ICC) and ventilation.
· The child is hypoxic and EXTREMELY hypovolemic, much of its blood volume is in the engorged placenta.
Ventilation establishes pulmonary blood flow, and the blood volume required to perfuse the lungs is drawn from the systemic circulation; this accentuates the systemic hypovolemia. The child may stabilize in this state, but in many cases deterioration is indicated by an important symptom of extreme hypovolemia retraction respiration. (RR)
Gasping (RR) appears on [A] when blood pressure falls below 50 mms Hg. RR is a reflexive reaction to hypo-volemia, hypotension and low central venous pressure. It generates pulses of negative intra-thoracic pressure (NIP) that pull blood into the right atrium and ventricle. It is an extreme response to forestall cardiac collapse and to fill empty cardiac atria and ventricles. The gasps produce spikes of increase in the heart rate, and similar spiking decreases in the diastolic blood pressure to the zero line.
NIP counteracts aortic arterial pressure during a gasp and reverses the pressure gradient between the thoracic aorta and peripheral arteries. The collapse of diastolic blood pressure seen during gasps [A] indicates reversed blood flow from peripheral arteries (e.g carotid) into the thorax. During these gasps and reverse blood flow there is no perfusion of brain tissue, and diminished perfusion continues until the meager cardiac output regenerates arterial blood pressure.
· A retracting child is in urgent need of a blood transfusion.
RR is usually regarded as a symptom of respiratory distress, however, the appearances of RR in [A] correlate only with hypotensive heart failure, in the first instance with no oxygen in the lungs, in the second with the lungs filled with oxygen. This strongly indicates that hypoxia is not the cause of RR and oxygenation will not cure RR. When RR is recognized as a reflexic attempt to forestall hypovolemic heart failure by drawing systemic blood volume into the heart, the origin of neonatal cerebral ischemia becomes apparent.
· Therefore the ischemic lesions of HIE are not of hypoxic origin, but are of hypovolemic, hypotensive origin.
Doppler studies on carotid blood flow in retracting neonates should readily show defective brain perfusion when compared to carotid blood flow in neonates that have received a physiological placental transfusion.
Cowan  there is no evidence that brain damage occurs before birth. At birth, a pulsating cord indicates that the heart and brain are being adequately perfused with oxygenated blood. After birth, retraction respiration indicates that the heart is not adequately perfusing itself or the brain. The cause of inadequate perfusion and consequent brain damage is blood loss hypovolemia caused by ICC; asphyxia is not a factor.