Physiology of transition period in a neonate (Respiratory System)


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Physiology of transition period in a neonate with regard to Respiratory System and administration of Anesthesia in such a circumstance

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Physiology of transition period in a neonate (Respiratory System)

  2. 2. Prenatal development of the lungs
  3. 3. Some concepts…. Surface Tension Property of the surface of a liquid that allows it to resist an external force. (by virtue of cohesive forces between its molecules) What exactly does surfactant do..? It forms a monolayer that adheres closely to the alveolar interface and prevents the sac from collapsing once the fluid is removed.. How then is the fluid removed..? Most of it is expelled by the upper airways. Rest of it is drained by the lymphatics and capillaries. What provides the force required to force open the partially collapsed fluid filled alveolar sacs..? A negative intrathoracic pressure of -30 to -70 cms of H2O that is created by the first gasp of air. What induces this gasp of air..? Clamping of the cord asphyxiates the baby provoking a violent gasp of air.
  4. 4. Some concepts….(continued) So, does this first gasp of air represent the first breath…? • Boddy & Robinson ((1971) were among the first to demonstrate foetal breathing in-utero. • Patrick et al (1980) demonstrated the presence of fetal breathing >30% of the time in utero and further recorded a increase in movements subsequent to a maternal meal. • Motoyama demonstrated a increase in FRC on inducing hypercapnia in the fetus. So, the traditional concept that the first gasp represents the first breath now stands challenged. Why does the fetus need to breathe when the placenta is breathing for it..? • Unclear. But thought to be as a prenatal practice for postnatal life and probably to act as a stimulus for lung development…
  5. 5. Respiratory rate O2 consumption is neonates is double that of an adult Minute ventilation is very high Minute ventilation is the product of respiratory rate and tidal volume Since tidal volume is almost same as a child/adult on a volume/Kg/body weight measure, the only factor that can be augmented is the rate. This explains why the respiratory rate is so high in a neonate. Analogous to increasing heart rate to compensate for the fixed stroke volume, so that on the whole cardiac output remains maintained.
  6. 6. Respiratory reserve Lung volume of the neonate is disproportionately small in relation to body size Further complicated by the increased metabolic rate (O2 consumption/unit body weight being twice as that of adults) i.e. the respiratory reserve is less This calls for increased ventilatory requirements. Relative to the increased ventilatory requirements the lung surface area available for gas exchange is less Primary reason why neonates become rapidly desaturated with hypoventilation or apnea of relatively short duration Implication
  7. 7. Compliance-ability of the lungs & thorax to expand To not react is to be compliant; To react is to be less compliant; What determines the recoiling nature of the lung & the chest wall..? Elastic fibers in the lung tissue, elastic rib cage architecture, good diaphragmatic effort all of which are either deficient or immature in the neonate. Neonatal lung Adult lung
  8. 8. Compliance …(contd) Neonates have a high compliance because: • Poorly developed intercostal muscles • Pliable rib cage (cartilaginous) • Poor diaphragmatic effort due to abundance of type 2 fast twitch, low oxidative fibers that contract in quick succession but invariably fatigue early. Anaesthetic implication • Under general anesthesia the neonatal lungs are more prone to collapse as skeletal muscle relaxation ensues around the chest wall, what precious little rigidity that prevented the collapse is now lost.
  9. 9. Surfactant • Secreted by type 2 pneumocytes • Chemically: dipalmitoylphosphatidylcholine • maintains distensibility of alveoli by reducing surface tension • Laplace law: The gas pressure (P) needed to keep equilibrium between the collapsing force of surface tension (γ) and the expanding force of gas in an alveolus of radius r is expressed as P = 2 γ/r • decreased levels are seen in premature babies and babies born to diabetic mothers • decreased levels predispose to respiratory distress syndrome (RDS) , which includes: 1. Alveolar collapse 2. Decreased compliance 3. Hypoxia 4. Increased work of breathing 5. Ultimately respiratory failure.
  10. 10. Control of breathing • The respiratory centers are still immature and are unable to control breathing effectively. • Neonatal response to hypercapnia is less compared to a child but none the less is mounted in the form of hyperventilation albeit for short durations. • Under conditions of hypothermia, initial hyperventilatory response may be blunted. • Periodic breathing  breathing is interposed with repetitive short apneic spells lasting 5 to 10 seconds without haemoglobin desaturation or cyanosis  Seen in both REM and NREM sleep.  thought to be due to changes in respiratory mechanics rather than reduced sensitivity to CO2
  11. 11. Control of breathing….(Contd.) •Apnea of prematurity & hypoxia  unexplained cessation of breathing for 15 seconds or longer or a shorter respiratory pause associated with bradycardia (heart rate <100), cyanosis, or pallor  may be related to an immature respiratory control mechanism  thought to be due to changes in respiratory mechanics rather than reduced sensitivity to CO2
  12. 12. Persistent pulmonary hypertension of newborn • Collapsed fluid filled alveoli, collapsed capillaries and decreased perfusion offer resistance to flow of blood through pulmonary vasculature in utero • i.e. pulmonary vascular resistance is high in utero • If the same resistance due to any reason is encountered in the post natal period, then the pressure in the pulmonary artery is elevated to overcome such resistance. • i.e. pulmonary artery hypertension ensues.. Precipitating factors include: 1. Hypoxia 2. Preterm 3. Birth asphyxia 4. Meconium aspiration 5. Sepsis 6. Congenital diaphragmatic hernia 7. Maternal use of NSAIDs.
  13. 13. Persistent pulmonary hypertension of newborn….(Contd) Other risk factors include: 1. Maternal diabetes 2. Asthma 3. Caesarean delivery Increased pulmonary artery pressure Increased right ventricular pressure Increased right atrial pressure Throws open the foramen ovale Blood reaches the aorta as pulmonary artery pressure is Ductus arteriosus is thrown open Hypoxia & normal to elevated PaCO2 • Treatment Increase tissue oxygenation Target PaO2 -50-70 mm of Hg Mechanical ventilation High frequency ventilation Exogenous surfactant Alkalinisation ECMO Sildenafil
  14. 14. Persistent pulmonary hypertension of newborn….(Contd) •Meconium aspiration  this is different from meconium aspiration at labour This happens in utero. Seen when the fetus has been exposed to prolonged periods of hypoxia Can predispose to persistent pulmonary hypertension of newborn.
  15. 15. References…. Ganong’s review of physiology 23rd edition P582, 584 Guyton & Hall’s Text book of Physiology 11th edition P1022, 1023
  16. 16. References…. Clinical Anesthesia by Paul.G.Barash 6th edition P1127, 1129 Miller’s Anesthesia 7th Edition, Vol 1 P889. 890
  17. 17. References…. Physiology for anesthetists Wolters Kluwer Chapter 4 Smith’s anesthesia for infants and children Motoyama and Davis Chapter 6