Perinatal Physiology

Fetal circulation recap.
1. Umbilical vein carries oxygenated blood from placenta to foetus.
  1. Blood shunted away from liver to caudal vena cava by ductus venosus.
    1. Blood loses some oxygen content in mixing with deoxygenated blood in the caudal vena cava
      1. Oxygenated blood passes through the foramen ovale into the left atrium.
      2. Foramen ovale open due to pressure in RA>LA,
2. Umbilical arteries, have delivered oxygenated blood to foetus. Return to placenta to be oxygenated.
3. Deoxygenated blood in caudal vena cava--> RA --> RV--> pulmonary artery.
  1. High pulmonary resistance in lungs as uninflated and hard.
  2. Low pO2 in lungs = ^ prostaglandin E levels = dilates walls of ductus arteriosus.
  3. Blood diverted through ductus arteriosus into branch of aorta--> arteries of pelvis and hind-limbs --> placenta to be oxygenated by maternal lungs.
What happens at birth?
1. High risk of mortality, fetus needs to respond to changes brought about by:
  1. Cessation of placental circulation
    Annotations:
    - No more support from placenta.
  2. The first breath - leading to expansion of the lungs
    Annotations:
    - Fetus born hypoxic -lack of oxygen- causes gasping in first breath.
Fetal Lungs
1. Solid, unexpanded tissue
2. Airways filled with fluid - secretions from alveolar cells and tracheal - bronchial glands
  1. Resistant to expansion, due to surface tension within alveoli eg: two glass plates with water inbetween = hard to seperate.
3. Breathing like movements are seen in the foetus pre-birth- fluid moved in/out of lungs
  1. Stretching 'practice' stimulates growth of lung tissue and production of surfactant.
    Annotations:
    - Experiment with lambs - fetus phrenicoabdominal nerves cut. Diaphragm not innervated so pre-birth lung movement not possible. Lambs born with highly underdeveloped lungs. Supports fact that movement stimulates growth etc..
    1. Production of surfactant crucial during late gestation (premature birth in humans, birth is delayed so surfactant can be infused into fetus). No surfactant can = respiratory distress syndrome.
Surfactant
1. Lipoprotein secreted by TYPE 2 alveolar cells.
  1. Heads sit in fluid film of alveoli, tails in gas. This disrupts hydrogen bonds in the fluid and decreases the surface tension within the alveoli (surface tension acts towards centre of alveolus - pulls edges to centre= favours collapse).
2. Surface active agent so reduces surface tension by approx. 90% in adult.
3. Only produced in late gestation (day 130/144 in lambs).
4. More effective in smaller alveoli as more concentrated.
5. Respiratory distress syndrome = problems with surfactant. eg: born pre-surfactant production - Barker's syndrome
Surface tension and surfactant
1. LaPlace's Law = 2T/r
2. Without surfactant, T is constant, so smaller alveoli have much larger pressure. With surfactant, amount of surfactant changes so that pressure is constant for all alveoli. - eg: smaller alveoli have less surfactant.
Fetal lungs at delivery: clearance of fluid and first breath
1. Compression of thorax during delivery helps clear fluid.
  Annotations:
  - Some fluid is absorbed whilst some is coughed up.
2. On delivery: elastic recoil of ribs = strong inspiratory effect = alveoli inflated = huge increase in SA of lung after 1st breath reduces fluid to a thin layer.
  1. Pressure-volume curves of the human lung at birth (compliance curves) showing high forces required for initial inhalation and exhalation.
Changes in circulation: foramen ovale (after first breath)
1. Pulmonary vascular resistance lowered = increase in pulmonary blood flow.
2. Blood flow from lungs to LA increases, increasing pressure in LA
  1. As blood flow from the placenta ceases, pressure in RA decreases. Pressure in LA>RA.
  2. Functional closure of FO (flap), followed within a few days by anatomical closure forms FOSSA OVALIS.
Changes in circulation: ductus arteriosus (after first breath)
1. Pulmonary vascular resistance decreases, increasing pulmonary blood flow, increasing the pO2 in blood.
  1. Lower pO2 = reduced prostoglandin E levels
    1. Reduced prostoglandin=constriction of ductus arteriosus lumen - blood no longer diverted from lungs into aortic arch.
2. Constriction of smooth muscle in ductus arteriosus begins closure of lumen of artery.
  1. Functional closure followed shortly by anatomical closure forming LIGAMENTUM ARTERIOSUM,
Ductus venosus
1. Allows majority of oxygenated blood from placenta - in umbilical vein - to bypass the liver.
2. At birth, constriction of sphincter of DV forces plood to pass through hepatic sinusoids.
3. In neonate, becomes LIGAMENTUM VENOSUM
Histological classification of placentae (recap)
1. Epitheliochorial
  Annotations:
  - Maternal blood - maternal endothelium - maternal connective tissue - uterine (maternal) epithelium - chorion (fetal) epithelium - fetal connective tissue - fetal endothelium - fetal blood
  1. Maintains 6 layers - mare, sow , ruminants
2. Endotheliochorial
  Annotations:
  - Maternal blood - maternal endothelium - chorion (fetal) epithelium - fetal connective tissue - fetal endothelium - fetal blood. NO MATERNAL EPITHELIUM OR CONNECTIVE TISSUE
  1. Reduced to 4 layers - dog and cat
3. Permeability varies due to layers and transport mechanisms.
  1. Larger molecules (eg: maternal antibodies) can't cross epitheliochorial type, therfore no immediate protection in newborn, hence why colustrum important in these species (sheep, cow, horse etc..)
Colustrum
1. Transmission of passive immunity from dam - offspring.
  1. 1) Horse, pig, ruminant
  2. 2) Dogs, cats
  3. 3) Rodents
  4. 4) Humans, rabbits
  5. Importance of colustrum increases, with decreasing transfer from placenta - colustrum increases the probability of survival in the neonate.
2. Very different composition and look from normal milk.
  1. Contains more fat, minerals and vitamins than regular milk - more nutritious.
  2. High IMMUNOGLOBULIN content - provides protection against infectious agents
    1. (Temporary passive immunity until active immunity starts in new born)
  3. Composition changes rapidly after birth
    1. Dry matter, protein: casein/albumin/globulin, lipids, minerals and carotene percentages in milk decrease vastly 0-5 days post birth.
    2. Lactose and pantothenic acid levels increase in milk 0-5 days post birth. These supposedly cause d+, so smaller levels ensure neonate does not develop this.
3. Intestinal absorption of immunoglobins HIGHEST DURING 6HRS AFTER BIRTH, gradually decreases thereafter and CEASES 1-2 DAYS AFTER BIRTH.
4. Kitten Plams IgG levels - colustrum is valuable in carnivores as well.
  1. No measurable IgG levels in first three weeks of kittens deprived of colustrum even when provided milk replacer (not colustrum replacer).
Maternal care
1. Important as promotes offspring survival
2. Livestock husbandry - focus on nutritional/immunological aspects, but psycological components and oppertunities for social learning also important.
3. Formation of maternal bond crucial. Trigger= vaginal-cervical stimulation at delivery causes release of oxytocin. Sensory cues from lamb also (smell/taste)
  1. New mothers (non pregnant ewes) after selective bonding, can be induced to accept/adopt alien lambs - vaginal stimualation essential or else aggressive behaviour shown.
4. Animals experiencing prolonged or difficult labour (dystocia) more likley to reject offspring
Other adaptations, post natal life
1. thermogenesis - lambs warm after birth - generate heat using BAT
2. Locomotion - lambs either 'nester's or runner's' - latter use locomotive apparatus straight away - aiding ability to run from predators.
3. Feeding and digestion - neonate gut able to absorb antiobodies which prevent adhesion of pathogenic micocrobes to the gut wall. After a few days, gut closure prevents ability to absorb these antibodies.
4. Sight and hearing - nester- eyes and ears tend to remain closed for the first 8 days.

Next up

Perinatal Physiology

Description

Resource summary

Similar

	Created by Florence Papworth about 9 years ago