Presentation is loading. Please wait.

Presentation is loading. Please wait.

Fetal and Neonatal Physiology 新光醫院 小兒科 穆淑琪醫師 Definitions Preterm* Infant< 37 wks GA Extremely LBW< 1000g SGA> 37 wks, < 2.5 kg Newborn< 24 h Neonate<

Similar presentations


Presentation on theme: "Fetal and Neonatal Physiology 新光醫院 小兒科 穆淑琪醫師 Definitions Preterm* Infant< 37 wks GA Extremely LBW< 1000g SGA> 37 wks, < 2.5 kg Newborn< 24 h Neonate<"— Presentation transcript:

1

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

3 Definitions Preterm* Infant< 37 wks GA Extremely LBW< 1000g SGA> 37 wks, < 2.5 kg Newborn< 24 h Neonate< 1 month Infant< 1 year

4 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)

5

6

7 NEONATAL PHYSIOLOGY

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

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

10 胎兒之肺臟及血液循環 Diminished Blood Flow Through Fetal Lungs

11 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

12 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

13

14 Birth

15

16

17 Decreased Pulmonary Perfusion

18 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。

19 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。

20 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。

21 Chronological Development of Organs, Systems, and Body form-I  ORGAN CHRONOLOGY OF DEVELOPMENT  Bronchial apparatus and pharyngeal pouches4th week--ridges and grooves appear over the future neck region  Thyroid gland4th week--endoderm appears over the floor of the pharynx  Tongue4th week--primordia appear in the of the pharynx  FaceEnd of 4th week--primordia appear  Palate Begins in the 5th week  Upper respiratory system4th week--laryngotracheal groove appears

22 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 glands5th week,primordia of adrenal glands develop  Conads,genital ducts,external genitalia5th week, gonadal ridges form  Heart3rd week,development of the heart begins  Atria5th week, the atria are formed  Ventricles5th week,the ventricles form

23 ORGAN CHRONOLOGY OF VELOPMENT  Fetal circulation3rd week,embryonic blood vessels develop  Brain and spinal cordEnd of 4th week,primary vesicles form and walls of the neural tube thicken to form the spinal core  Pituitary6th week,connection of Rathke’s with oral cavity disappears  LimbsEnd of 4th week,limb buds appear  Skull7th week,paired cartilages begin to fuse to form the cranium

24 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

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

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

27 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

28 The Cardiovascular System

29  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)

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

31 Fetal Cardiovascular System  UV →RA (FO) → AO  SVC→PA→(DA)→A O  Ductus Arteriosus (DA)  Foramen Ovale (FO)  Umbilical Arteries and Veins

32

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

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

35 Perinatal Cardiorespiratory physiology

36  Normal breathing - 30/min at 90 sec of age (reminder) ì Normal breathing - 40-60/min at few minutes of age: ì Removal of increased CO2 produced ì High metabolic rate ì Helps maintain FRC

37 Perinatal Cardiorespiratory physiology ìCirculation of the fetus: ì RV ~ 2/3 CO ì LV ~ 1/3 CO ì Foramen ovale ì Ductus arteriosus ì Blood is coming from placenta - high O 2 content ì 95% of the blood coming from placenta goes to LA through foramen ovale

38 Perinatal Cardiorespiratory physiology ìCirculation of the newborn: ì PVR is  due to pulmonary expansion, breathing,  pH, and  O 2 tension ì If neonate is born by CS -  PAP’s and PVR ì PVR is  : ì Hypoxia Acidosis ì Hypovolemia Hypoventilation ì Atelectasis Cold

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

40 Asphyxia   PaO 2 ì  PCO 2 ì  pH ì  Uteroplacental blood flow ì Maternal or Fetal disease (cause)

41 Asphyxia  Intrauterine asphyxia: ì PaO2 decreases from 25-40 to 5 mmHg ì Anaerobic metabolism occurs ì pH drops < 7.0 : respiratory and metabolic acidosis ì Lactate is accumulating in the body ì Redistribution of blood flow in the body ì CO starting normal is now decreasing ì Because of high doses of opioids in the blood fetus may survive severe hypoxia (may reduce total O 2 consumption)

42 Development and maturation of the cardiopulmonary system The Fetal Circulation  Four unique shunts Placenta Ductus Venosus Foramen Ovale Ductus Arteriosus

43

44 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

45 Respiratory Distress Syndrome Etiology-Surfactant deficiency during disease

46 Factors precipitating to HMD  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

47

48 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

49 Pathophysiology  Reduce lung compliance  Reduce FRC  Poor lung distensibility  Poor alveolar stability  Right-to-left shunt  Reduce effective pulmonary blood flow

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

51

52

53

54 Function of surfactant  Stabilize the lung during deflation  Prevent high surface tension pulmonary edema  Protect the lung against epithelial and endothelial injury  Provide a defense against infection

55 Homodynamics of surfactant treatment in RDS  Immediate effect ( up to 10 min after instillation) - related to the mode of administration - transient obstruction of the large airways with fluid  PaCO2↑  cerebral vasodilatation with CBF↑ - PaCO2↑  pulmonary vasoconstriction  reduction in L to R ductal flow

56 Cardiopulmonary Adjustments at Birth- II  Closure of placental circulation- increase systemic vascular resistance  Opening of pulmonary circulation decrease pulmonary vascular resistance  Closure of the ductus venosus within the first three hours of life forces portal blood to perfuse the liver  Left atrial pressure > right atrial pressure causing the foramen ovale to close

57 Closure of the ductus arteriosus completes the separation between pulmonary and systemic circulation

58 Renal System and Fluids  Total Body Water 80% in newborns Diuresis (lower fluid requirements)  First 5 days  Hypovolemia Acidosis, tachycardia, hypotension  Hypervolemia CHF

59 Renal System and Fluids  Renal Function GFR increases rapidly for first 3 mos Tubular function increases over 12 mos Poor tolerance for over / under hydration AgeMax UOsm Newborn525 15-30 d950 12 m1200 (adult)

60 Blood Function  Fetal Hemoglobin High affinity for O 2 at low tensions  80% at 25 mmHg Persists until age 3 mos  replaced by adult Hgb Birth Hgb ~ 17 g/dl  maintains O 2 delivery despite high affinity

61 Temperature Homeostasis  Challenges Larger surface-to-volume ratio Lack of significant fat stores  Adaptations Non-shivering thermogenesis Activity, crying  Consequences Acidosis, apnea, hypotension

62 PREMATURE INFANTS

63 Preterm Respiratory Function  Higher incidence of airway obstruction  Respiratory control is underdeveloped  Increased WOB, O 2 consumption Muscle fiber immaturity Compliant chest wall  Intubation recommended over mask ventilation

64 Bronchopulmonary Dysplasia  BPD Persistent respiratory distress requiring O 2 Sequela of chronic lung disease 10 – 15% of formerly intubated infants  High index of suspicion Present with  Increased: FRC, airway resistance, dead space, A-a gradient and reactive airways  Decreased: lung compliance Medicated with  Corticosteroids, diuretics

65 Retinopathy of Prematurity  Exact cause is not certain Retinal artery vasoconstriction  Retina ischemia, neovascularization, retinopathy Risk factors  prematurity, very low birth weights, mechanical ventilation, PaO 2 > 80 mmHg, < 44 wks PCA Evidence for  FiO 2 causing ROP under GA is lacking

66 Retinopathy of Prematurity  Empirically keep SaO 2 90 – 95% Two pulse oximeter technique Measure at a preductal site (ear, R finger)  Measures retinal perfusion Postductal sites  Effect of PDA reopening, shunt reversal

67 Fetus assessment at birth:

68 Neonatal Resuscitation  Apgar Score Guides Resuscitation ApgarCauseTreatment 8 – 10Normal BirthOropharyngeal suctioning, radiant warmer 5 – 7Mild AsphyxiaExternal stimulation, O2 to face. If inadequate response, start BVM 3 – 6Moderate Asphyxia Start BVM, if inadequate, intubate and analyze cord blood. 0 – 2Severe Asphyxia Immediate intubation ± external compressions ± epinephrine (gluc, bicarb?)

69 Neonatal Physiology  Breast milk  Mobilize glucose and fatty acid soon after delivery  Easy to develop fluid and acid-base imbalance high rates of fluid and turnover and acid production  Nonshivering thermogenesis in brown fat keep the neonates warm

70

71

72

73

74

75


Download ppt "Fetal and Neonatal Physiology 新光醫院 小兒科 穆淑琪醫師 Definitions Preterm* Infant< 37 wks GA Extremely LBW< 1000g SGA> 37 wks, < 2.5 kg Newborn< 24 h Neonate<"

Similar presentations


Ads by Google