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Fetal and Neonatal Physiology

Fetal and Neonatal Physiology. 新光醫院 小兒科 穆淑琪醫師. Definitions. Classification Significance. Preterm Infants Not yet matured Incomplete but normal IUG Prone to IRDS, IVH, PDA, apnea, ROP, hypothermia Small for Gestational Age Matured but prone to certain conditions

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Fetal and Neonatal Physiology

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  1. Fetal and Neonatal Physiology 新光醫院 小兒科 穆淑琪醫師

  2. Definitions

  3. Classification Significance • Preterm Infants • Not yet matured • Incomplete but normal IUG • Prone to IRDS, IVH, PDA, apnea, ROP, hypothermia • Small for Gestational Age • Matured but prone to certain conditions • IUGR for varied reasons • Prone to hypoglycemia, infection, pneumonia, seizures (not apnea)

  4. NEONATAL PHYSIOLOGY

  5. The Respiratory System • Airway Differences • Obligate nasal breather • Easy airway obstruction • Anatomic differences complicate ETT intubation • Straight blade, uncuffed ETT preferred

  6. 缺氧窒息(Asphyxia)的生理變化: 胎兒之肺臟(Lung)及血液循環 Fetus

  7. Fetus 胎兒之肺臟及血液循環 Diminished Blood Flow Through Fetal Lungs

  8. 出生時的轉變 • 肺泡之肺液吸收 • 臍靜脈及臍動脈收縮 • 肺血管擴張

  9. 肺液的吸收 • 生產前開始減少 • 有效的初始呼吸可以促進吸收 • 減緩吸收 • 出生時不呼吸 • 淺而無效的呼吸

  10. Birth

  11. Decreased Pulmonary Perfusion

  12. 缺氧窒息(Asphyxia) • 新生兒因活動力不佳,而不能建立有效之呼吸,缺氧狀態可能接續進行而導致缺氧窒息。 • 缺氧窒息的定義: 不斷加重的缺氧、二氧化碳堆積及酸血症(acidosis)。 • 缺氧窒息進行到某個程度會造成永久性腦部傷害或死亡。

  13. 缺氧窒息 • 初始反應 • 肺部、腸、胃、腎臟、肌肉及皮膚的血流量均減少,所保存的血主要用來供應心臟及腦部。 • 後期反應 • 當窒息持續時,心肌也受傷害,心輸出量減少,到重要器官之血流量也減少。

  14. 干擾轉變的因素 • 呼吸不足,呼吸道阻塞。 • 失血過多、心臟收縮力不佳、或缺氧造成心搏緩慢 • 肺血管持續收縮。

  15. Chronological Development of Organs, Systems, and Body form-I • ORGAN CHRONOLOGY OF DEVELOPMENT • Bronchial apparatus and pharyngeal pouches 4th week--ridges and grooves appear over the future neck region • Thyroid gland 4th week--endoderm appears over the floor of the pharynx • Tongue 4th week--primordia appear in the of the pharynx • Face End of 4th week--primordia appear • Palate Begins in the 5th week • Upper respiratory system 4th week--laryngotracheal groove appears

  16. Chronological Development of Organs, Systems, and Body form-II • ORGAN CHRONOLOGY OF DEVELOPMENT • Kidneys,urinary bladder,urethra 5th week, permanent adult kidney begins to develop • Adrenal glands 5th week,primordia of adrenal glands develop • Conads,genital ducts,external genitalia 5th week, gonadal ridges form • Heart3rd week,development of the heart begins • Atria 5th week, the atria are formed • Ventricles 5th week,the ventricles form

  17. ORGAN CHRONOLOGY OF VELOPMENT • Fetal circulation3rd week,embryonic blood vessels develop • Brain and spinal cord End of 4th week,primary vesicles form and walls of the neural tube thicken to form the spinal core • Pituitary 6th week,connection of Rathke’s with oral cavity disappears • Limbs End of 4th week,limb buds appear • Skull 7th week,paired cartilages begin to fuse to form the cranium

  18. Apnea • Absence of respirations for 20 sec, causing cyanosis and bradycardia • At-risk neonates • Preterm and ex-preterm infants to 50 wks PCA • Risk is ~60% at 42 wks PCA, <1% 54 wks PCA

  19. Apnea: Primary Apnea 缺氧窒息(Asphyxia)的生理變化 : 呼吸暫停(Apnea)

  20. Apnea : Secondary Apnea 缺氧窒息(Asphyxia)的生理變化 : 呼吸暫停(Apnea)

  21. The Respiratory System • Thorax and Lungs • Increased O2 consumption (6 ml/kg/min) • Due to high BMR (+100%) • Prone to cyanosis • Lung volumes vs. age – no change • RR is increased • Diaphragmatic breathing • Susceptible to abdominal distension • Fatigable – preterm infants

  22. The Cardiovascular System

  23. The Cardiovascular System • Myocardium • Unable to  SV by contractility • CO is primarily rate-controlled • Non-compliant ventricles • CHF • Bradycardia implies hypotension • High vagal tone at birth • PNS mature (not SNS)

  24. The Cardiovascular System • Pulmonary Vasculature • Reactive, thick muscularis layer • Acidosis, hypercarbia, hypoxemia, stress • Stressors may cause acute CHF • Acidosis results and worsens

  25. Fetal Cardiovascular System • UV →RA (FO) → AO • SVC→PA→(DA)→AO • Ductus Arteriosus (DA) • Foramen Ovale (FO) • Umbilical Arteries and Veins

  26. Perinatal Cardiorespiratory physiology • Fetal lungs • 24 days -arises from the foregut • 26-28 weeks -terminal airways developed • 30-32 weeks -final surface active material (SAM) developed • Plasma ultrafiltrate is a normal part of the lungs • Every day IU (intrauterine) 50-150 ml/kg/day of plasma is produced • Plasma is swallowed in the gut and excreted by kidneys

  27. Perinatal Cardiorespiratory physiology • Plasma ultrafiltrate (2) • 2/3 is expelled during vaginal delivery • 1/3 is removed capillaries, lymphatics, breathing • If fluid is retained into lungs causes TTBN • (transient tachypnea of newborn) • Causes: • Small infants • Preterm infants • Rapidly born • Cesarean section born babies

  28. Perinatal Cardiorespiratory physiology

  29. Perinatal Cardiorespiratory physiology • Normal breathing - 30/min at 90 sec of age (reminder) • Normal breathing - 40-60/min at few minutes of age: • Removal of increased CO2 produced • High metabolic rate • Helps maintain FRC

  30. Perinatal Cardiorespiratory physiology • Circulation of the fetus: • RV ~ 2/3 CO • LV ~ 1/3 CO • Foramen ovale • Ductus arteriosus • Blood is coming from placenta - high O2 content • 95% of the blood coming from placenta goes to LA through foramen ovale

  31. Perinatal Cardiorespiratory physiology • Circulation of the newborn: • PVR is  due to pulmonary expansion, breathing,  pH, and  O2 tension • If neonate is born by CS -  PAP’s and PVR • PVR is : • Hypoxia Acidosis • Hypovolemia Hypoventilation • Atelectasis Cold

  32. Perinatal Cardiorespiratory physiology • Changes in circulation of the newborn: •  PVR -  pulmonary blood flow • Right/left shunting will be decreased • LA pressures are , and seal foramen ovale • Ductus arteriosus closes (10-14 days) in response to • O2 • Ach • Parasympathetic nerve stimulation • PG

  33. Asphyxia  PaO2  PCO2  pH  Uteroplacental blood flow Maternal or Fetal disease (cause)

  34. Asphyxia • Intrauterine asphyxia: • PaO2 decreases from 25-40 to 5 mmHg • Anaerobic metabolism occurs • pH drops < 7.0 : respiratory and metabolic acidosis • Lactate is accumulating in the body • Redistribution of blood flow in the body • CO starting normal is now decreasing • Because of high doses of opioids in the blood fetus may survive severe hypoxia (may reduce total O2 consumption)

  35. Development and maturation of the cardiopulmonary systemThe Fetal Circulation • Four unique shunts Placenta Ductus Venosus Foramen Ovale Ductus Arteriosus

  36. Cardiopulmonary Adjustments at Birth-I • Loss of the placental circulation • Newborn breathe on its own • Mild hypoxia Mild hypercapnia Tactile stimuli trigger the first breath Cold skin

  37. Respiratory Distress Syndrome Etiology-Surfactant deficiency during disease

  38. High risk: Prematurity Asphyxia IDM ( Infant of Diabetic Mother ) Maternal hemorrhage C/S Multiple births Male >female Low risk: IUGR Maternal hypertension Steroids Placental insufficiency Heroin addictive Factors precipitating to HMD

  39. Synthesis of surfactant • Maturation of alveolar type II cells and the subsequent synthesis of surfactant --started since 24 wks’ gestation --complete by 32 wks’ gestation

  40. Pathophysiology • Reduce lung compliance • Reduce FRC • Poor lung distensibility • Poor alveolar stability • Right-to-left shunt • Reduce effective pulmonary blood flow

  41. Clinical signs • Onset near the time of birth • Retraction and tachypnea • Expiratory grunting • Cyanosis • Systemic hypotension • Characteristic chest radiography • Course lasts 3-5 days

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