Any factor that reduces the blood oxygen concentration can cause asphyxia. Neonatal asphyxia is closely related to the fetal environment in the uterus and the delivery process. If hypoxia occurs during labor, carbon dioxide in the fetal blood stimulates the respiratory center, resulting in early strong respiratory movements, loss of the laryngeal sphincter barrier and inhalation of large amounts of amniotic fluid, resulting in intrapartum asphyxia or post-delivery neonatal asphyxia. If the fetal respiratory center is paralyzed, the delivered neonate will not breathe. Maternal factors that cause neonatal asphyxia include gestational hypertension syndrome, pre-eclampsia, inter-eclampsia, acute blood loss, severe anemia, heart disease, acute infectious diseases, tuberculosis, etc., which affects the fetus by reducing the oxygen content of the mother’s blood; multiple births, excessive amniotic fluid, which causes excessive expansion of the uterus or early placental abruption, placenta praevia, placental insufficiency, etc., which affect the blood circulation between the placenta; the umbilical cord is wrapped around the neck, knotted or prolapsed, which can make the umbilical cord blood Prolonged labor, abnormal labor, premature rupture of the amniotic membrane, cephalopelvic disproportion, improper handling of various surgical deliveries such as forceps, internal rotation, and improper application of anesthesia, analgesia, and oxytocic drugs can cause neonatal asphyxia; neonatal airway obstruction, intracranial hemorrhage, immature lung development, severe central nervous system, cardiovascular malformation, and diaphragmatic hernia can also lead to neonatal asphyxia after birth. The main respiratory impairment is often hyperventilation followed by a rapid transition to primary apnea, but rhythmic wheezy breathing can still occur with sensory stimulation. The frequency and intensity gradually decreases and finally enters secondary apnea, and death occurs if not actively resuscitated. The blood circulation and metabolism are normal at the beginning after the appearance of asphyxia, the heart is the first to have a transient increase, the arterial pressure temporarily increases, with the rise of PaCO2, PaO2 and pH rapidly decreases, the blood distribution changes, non-vital organs such as intestines, kidneys, muscles, skin vasoconstriction, while maintaining the blood supply and oxygenation of the brain, heart muscle, adrenal glands and other vital organs, so the skin color changes from cyanotic to reticular pattern and then pale, and the body temperature drops; this is also the factor that causes pulmonary hemorrhage, necrotizing small bowel inflammation, and acute renal tubular necrosis. When hypoxia continues to worsen, heart rate turns slow, cardiac blood output decreases, blood pressure drops, central venous pressure rises, heart enlarges, pulmonary capillaries constrict, resistance increases, pulmonary blood flow decreases, arterial ducts reopen, and return to fetal-type circulation, causing hypoxia to worsen again and heart failure. In the case of insufficient blood oxygen supply to vital organs, brain damage is aggravated and may leave sequelae or death. Low birth weight infants are prone to hypoxic intracranial hemorrhage due to poor vascular development in the presence of elevated PaCO2, cerebral stasis and altered vascular permeability. In early asphyxia, increased blood glucose can occur due to the release of catecholamines, but hypoglycemia can occur quickly due to low neonatal glycogen reserves, which can be depleted. In hypoxia, plasma osmolarity increases, the cellular sodium pump and concentrated potassium ions are affected, and plasma protein and water extravasation leads to cerebral edema. All organs can undergo degenerative changes after hypoxia, and the brain has different susceptibility zones to hypoxia in different developmental periods, thus the lesion sites and morphology are also different. The main lesions of the brain are cerebral edema, brain tissue necrosis and intracranial hemorrhage. Necrosis can be followed by foramen ovale, multicystic brain and cortical laminar necrosis. The smaller the weight of preterm infants, the more fragile the blood vessel walls are and the more likely they are to cause brain hemorrhage. Hemorrhage can be disseminated in the ventricles, brain parenchyma, subarachnoid space and subventricular hemorrhage breaking into the ventricles. Systemic blood circulation disorders lead to venous stasis, right heart enlargement, vasodilation, and bleeding due to increased permeability of the vessel wall. In full-term infants with extreme respiratory struggle after hypoxia, inhalation of amniotic fluid and meconium, upper airway obstruction, increased negative thoracic pressure, and subplasmic bruising of the inner thoracic cavity, lungs, and thymus are correspondingly more common, and respiratory obstruction is related to the nature of the inhalants. The thicker amniotic fluid and larger fecal particles tend to stay below the epiglottis cartilage, above the cricoid cartilage and at the bronchial orifices on both sides of the bifurcation of the trachea, while the thin amniotic fluid is easily inhaled into the deeper part of the respiratory tract. Pulmonary atelectasis may be present in cases of terminal airway obstruction, and emphysema in cases of incomplete obstruction. Longer survival may have inflammatory cell infiltration. On visual examination of the gastrointestinal system, there may be excess meconium amniotic fluid in the stomach, a decrease in the diameter of the colon, and a decrease in the amount of meconium.