Neonatal Homeostasis

Cardiorespiratory Changes at Birth

The transition from fetal to neonatal life requires:

Onset of continuous ventilation – apnea/barotrauma

stimuli include umbilical occlusion, sensory (thermal/painful) stimuli, arousal

Clearance of lung fluid – transient tachypnea of the newborn, TTN

most resorbed by lymphatics and vasculature, some is expressed (perhaps due to squeezing of chest in vaginal canal; explains why TTN is more common in C-section babies)

Pulmonary vasodilation – persistent pulmonary hypertension

Ý pulmonary pressure, ß pulmonary blood flow, Ý resistance

at birth these invert; ß pulmonary resistance helps to Ý amount of blood going to lungs to be oxygenated

fetal PaCO₂ is slightly higher (~50mmHg) making fetal pH a little lower. Fetal PaO₂ is low in the umbilical vein (~30mmHg) and even lower in the umbilical arteries (~20mmHg)

Four shunts in Fetal Circulation – normally close at birth

(1) Ductus venosus – oxygenated blood from the umbilical vein bypasses the liver through this

(2) Ductus arteriosus – bypasses the lungs (only 7% of fetal blood goes to the fetal lungs)

(3) Formen ovale – shunts oxygenated blood from RA to LA so it can be pumped to the developing brain

(4) Umbilical arteries – takes low PaO₂ blood to the placenta to get oxygenated and returned through the umbilical vein

Closure of these Shunts

clamping of umbilical cord at birth Ý resistance and Ý left ventrical end diastolic pressure (LVEDP), resulting in Ý left artrial pressure, which helps to close the Foramen Ovale

at the first breath, the expansion of the lungs ß pulmonary vascular resistance and right atrial output goes through the path of least resistance to the lungs instead of through the Ductus Arteriosus

Asphyxia may alter this process and lead to a persistence of pulmonary vascular tone

Thermal Regulation

Fetal temperature is usually 0.5^oC higher than the maternal temperature (important during maternal fever)

Newborns lose heat via convection, conduction, radiation, and evaporation (dry babies thoroughly to ß evaporation loss)

Babies do not shiver; Brown fat is used to metabolically generate heat

Babies under stress are more prone to hypothermia because they lack the metabolic reserves to generate heat

Meconium

fetal feces; normally sterile

Meconium is present in the amniotic fluid in 10% of all births; 4/1000 births will have meconium aspiration

meconium passage in utero can be induced only if GI system is mature by fetal hypoxia or parasympathetic stimulation
since a mature GI system is required, there is no passage of meconium before week 34

Meconium aspiration is a problem because:

(1) Mechanical obstruction can cause pneumothorax
(2) Chemical irritation and surfactant inactivation can cause atelectasis (leads to intrapulmonary shunting)
both of these lead to hypoxia

Treatment: suction when head appears and avoidance of positive pressure ventilation until suction has been performed

Birthweight, Gestational Age, and Intrauterine Growth

Low birthweight babies – defined as <2500 grams regardless of gestational age

50% survival at 24 weeks, girls > boys (female fetuses are roughly a week more mature than male fetuses)

Growth retarded babies – defined as babies that are small for gestational age (SGA)

gestational age is important because SGA babies are more likely to have hypoglycemia or intercranial hemorrhage, whereas normally grown, premature infants are more prone to respiratory distress syndrome and hyperbilirubinemia
multiples are also small because of competition for nutrients

Three reasons why fetuses don’t grow properly:

(1) Genetic – abnormal genes or karyotypes, big problems in every cell

(2) Congenital "TORCH" Infections – CMV, Rubella, Syphillis, etc.

(3) Placental Insufficiency – not enough nutrients to the fetus or too many toxins (#1 toxin = EtOH)
to differentiate look at weight, length, and head circumference. Symmetric = congenital or infectious, Asymmetric = placental insufficiency because of "brain sparing" (vital areas are more protected than less vital areas, so less affected)

Newborn Asphyxia

Interruption of gaseous exchange across the placenta. ß O₂ results in ß heart rate in infants.

Fetal heart monitoring:

Early deceleration fetal heart rate goes down with contraction and rises afterwards, vagally mediated

Late deceleration – HR goes down later in regards to contraction = uteroplacental insufficiency (fetus is not getting enough O₂)

Variable deceleration – variable in shape and time, usually preceded by an acceleration, often because occlusion of the umbilical cord.

Criteria for Asphyxia by the American College of Obstetrics and Gynecology

(1) Umbilical arterial blood pH < 7.00

(2) APGAR score 0-3 for > 5 minutes

(3) Seizures, coma, hypotonia (seizures in infants mimic normal movts but are persistant, confirm with ECG)

(4) Multiorgan dysfunction

Newborns are more resistant to O₂ deprivation. They conserve ATP better than 10 day old infants or adults. Because of Ý CO₂, fetal Hg, Ý Hct, their mito are used to lower O₂, ability to shunt oxygenated blood to the brain, etc

The degree of organ damage depends on the susceptibility of the organ and its capacity for recovery

Low APGARs = Ý chance of death and Ý chance of cerebral palsy in survivors

< 4 APGAR	Risk of death	Risk of Cerebral palsy
1 min	3%	1%
5 min	8%	1%
10 min	18%	5%
15 min	48%	8%