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Neonatal Adaptations: Physiology and Clinical Implications

Explore the physiological changes in neonates after birth, including circulation, ventilation, and renal function. Learn about potential adaptational problems and acute treatments.

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Neonatal Adaptations: Physiology and Clinical Implications

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  1. Neonatal morphology Tamás Machay MD PhD Professor of Paediatrics and Neonatology First Department of Paediatrics Semmelweis University, Budapest, Hungary

  2. Adaptations after the birth: 1/ eyes, nervous system, muscles, bones, metabolism, circulation, ventilation, kidneys, fluid- and electrolyt homeostasis, etc. 2/ Adaptational problems of circulation and ventillation may sometimes necessitate acute treatment!!!

  3. Schema of water intake and water loss Intake Excretion ECF Intake Loss Cells and bone

  4. Total body water (TBW) is devided into two large parts: intracellular (ICF) and extracellular (ECF) fluid. Their changes from the first trimester to 9 month of age is depicted below % 100 90 80 70 60 50 40 30 20 10 0 Fluid content of the body (%) FETUS NEWBORN Age (months)

  5. Insensible water loss through the skin in neonates (gestational age: 25-27 weeks) during the first week of life mL/day Relative humidity Relative humidity Days of life

  6. Physiologic role of Aquaporin 3 (I.) • Anatomic localization: • Transitoric mucosa of the bladder!!! • Upper and lower tract of the digestive system • Upper tract of the airways • Skin !!! • Localization in the skin: • Lower layer of the stratified epithelium

  7. Physiologic role of Aquaporin 3 (II.) • Intracellular localization: • Basal membrane (epithelial cells) • Function: • Water intake of epithelial cells • Water preservation

  8. Aquaporin 3 induced water intake in epithelial cells H2O H2O

  9. Intrauterin (A), perinatal (C), and postnatal (E) amounts of aquaporin 3 J. Histochem. Cytochem., Oct 1999; 47: 1275 - 1286.

  10. Clinically significant adaptational problems 1/ transpulmonal fluid is not absorbing 2/ no breathing 3/ pulmonary circulation stays in its foetal form 4/ no development of functional residual capacity

  11. Clinically significant adaptational problems 1/ transpulmonal fluid is not absorbing

  12. Fetal and neonatal lung 1. 2. Intrauterine Extrauterine Transpulmonary fluid FRC

  13. Predisposing factors for „wet lung” • Very fast delivery • Prematurity • Elective c-section • Sedation of the mother • Maternal diabetes • Fetal distress • RISK: PTX (5-10%)

  14. Composition of pulmonary and amniotic fluids Ion Pulmonary fluid Interstitium Plasm Amniotic fluid Na (mM/l) 150 147 150 113 K (mM/l) 6,3 4,8 4,8 7,6 Cl (mM/l) 157 107 107 87 HCO3 (mM/l) 3,0 25 24 19 pH 6,30 7,31 7,34 7,02 Protein (g%) 0,03 3,27 4,09 0,10

  15. Absorption of pulmonary fluid I. Pneumocyte interstitial space intravascular space „delivery” (Cl transport) -adrenergic effect lymph circulation Vena cava superior (10 ml/h)

  16. Clinically significant adaptational problems 2/ no breathing

  17. Effect of intrauterine hypoxia on breathing Delivery + hypoxia Breathing Primery apnoe Secundary apnoe + hypoxia

  18. Changes in tidal volumen in hypoxiában (Rigatto)  Tv air 15% O2 Cold environment +20 Thermoneutral environment 0 -20 -40 Time (minutes) 1 2 3 4 5

  19. Regulation of breathing in neonate cortex - hypothalamus + + gl. caroticum cardiorespiratoric centre + + + Blood pressure N.vagus actual Breathing heart rate Dopamine!!! -

  20. Clinically significant adaptational problems 3/ pulmonary circulation stays in its foetal form

  21. Fetal circulation

  22. Normal circulation

  23. Antenatal and postnatal circulation

  24. Changes in pulmonary pefusion after delivery pH  pO2 pCO2 Pulmonary-volume Biochemical changes ml/kg/minute 200 160 100 40 40

  25. Upper: extraalveolar vessels Lower: intraalveolar vessels PVR RV FRC TLC Inspiration Exspiration Total pulmonary vascular resistance is low by optimal pulmonary volume

  26. Role of pulmonary vascular endotheial cells in the production of angiotensin induced Prostaglandin I2 (PGI2) synthesis AA PGI2 AII AA AI : Angiotensin I AII : Angiotensin II ACE : Angiotensin convertase AA: Arachidic acid ACE PGI2 AI

  27. The role of pulmonary vascular endothelial cells in prostaglandin I2 and endothelium derived relaxing factor (NO) evoked vasodilatation Bradikinin AA PGI2 L.Arginine EDRF O2 AA: Arachidic acid EDRF: Endothelium derived relaxing factor (NO) Kininogen

  28. Symptoms of PPNH • Background disorder (MAS, pneumonia, etc) • Cyanosis • Respiratiry disturbances • Hyperventilation hyperoxia test: arterial pO2 • Higher O2 saturation on the right arm • pO2 in the right radial artery pO2 • Ultrasonography • - right-left shunt • - D sign • - tricuspidal insufficience

  29. Evaluation of the degree of the right-left shunt 500 400 FIO2 = 1,0 300 Arterial pO2 (mmHg) 200 100 10 20 30 40 50 60 right-left shunt (%)

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