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Explore the physiological adaptations of neonates after birth and the potential problems they may encounter, such as circulation and ventilation issues. Learn about water intake and loss, pulmonary fluid absorption, breathing regulation, and more.
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Neonatal morphology Tamás Machay MD PhD Professor of Paediatrics and Neonatology First Department of Paediatrics Semmelweis University, Budapest, Hungary
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!!!
Schema of water intake and water loss Intake Excretion ECF Intake Loss Cells and bone
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)
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
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
Physiologic role of Aquaporin 3 (II.) • Intracellular localization: • Basal membrane (epithelial cells) • Function: • Water intake of epithelial cells • Water preservation
Aquaporin 3 induced water intake in epithelial cells H2O H2O
Intrauterin (A), perinatal (C), and postnatal (E) amounts of aquaporin 3 J. Histochem. Cytochem., Oct 1999; 47: 1275 - 1286.
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
Clinically significant adaptational problems 1/ transpulmonal fluid is not absorbing
Fetal and neonatal lung 1. 2. Intrauterine Extrauterine Transpulmonary fluid FRC
Predisposing factors for „wet lung” • Very fast delivery • Prematurity • Elective c-section • Sedation of the mother • Maternal diabetes • Fetal distress RISK: PTX (5-10%)
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
Absorption of pulmonary fluid I. Pneumocyte interstitial space intravascular space „delivery” (Cl transport) -adrenergic effect lymph circulation Vena cava superior (10 ml/h)
Clinically significant adaptational problems 2/ no breathing
Effect of intrauterine hypoxia on breathing Delivery + hypoxia Breathing Primery apnoe Secundary apnoe + hypoxia
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
Regulation of breathing in neonate cortex - hypothalamus + + gl. caroticum cardiorespiratoric centre + + + Blood pressure N.vagus actual Breathing heart rate Dopamine!!! -
Clinically significant adaptational problems 3/ pulmonary circulation stays in its foetal form
Changes in pulmonary pefusion after delivery pH pO2 pCO2 Pulmonary-volume Biochemical changes ml/kg/minute 200 160 100 40 40
Upper: extraalveolar vessels Lower: intraalveolar vessels PVR RV FRC TLC Inspiration Exspiration Total pulmonary vascular resistance is low by optimal pulmonary volume
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
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
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
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 (%)