Fetal and neonatal physiology

onlyuforu3 20,668 views 30 slides Jul 08, 2017
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About This Presentation

Changes that takes place in a newborn with respect to cardiovascular and respiratory physiology


Slide Content

Fetal and Neonatal Physiology

NEWBORN-first 24 hrs of life NEONATE-from birth to under four weeks(<28 days) TERM NEONATE-between 37 to < 42 gestational week PRETERM NEONATE-<37 gestational week POST TERM NEONATE-> or egual to 42 gestational week LOW BIRTH WEIGHT(LBW)<2500 GRAM VERY LOW BIRTH WEIGHT(VLBW)<150O GRAM EXTREMELY LOW BIRTH WEIGHT(ELBW)< 1000 GRAM Irrespective of birth weight Birth weight dependent

Placenta The  placenta  (also known as  afterbirth ) is an organ that connects the developing  fetus to the  uterus. The placenta functions as a fetomaternal organ with two components: the  fetal placenta  ( Chorion frondosum ), which develops from the same blastocyst that forms the fetus , and the  maternal placenta  (Decidua basalis ), which develops from the maternal uterine tissue.

Placental function Nutrition: The perfusion of the intervillous spaces of the placenta with maternal blood allows the transfer of nutrients and oxygen from the mother to the fetus . Excretion Waste products excreted from the fetus such as urea,  uric acid, and  creatinine  are transferred to the maternal blood by diffusion across the placenta . Immunity IgG antibodies can pass through the human placenta, thereby providing protection to the fetus   in utero.

Placental function Endocrine function The first hormone released by the placenta is called the  human chorionic gonadotropin   hormone. promotes the maintenance of the corpus luteum during the beginning of pregnancy. This allows the corpus luteum to secrete the hormone progesterone  which enriches the uterus with a thick lining of blood vessels and  capillaries so that it can sustain the growing  fetus . Progesterone Estrogen Human placental lactogen – promote fetal growth and development

Why mother’s immune cell do not attack the fetus ?   The placenta uses several mechanisms : It secretes  Neurokinin   B containing   phosphocholine molecules . There is presence of small lymphocytic suppressor cells in the fetus that inhibit maternal  cytotoxic T  cells by inhibiting the response to  interleukin.

Fetal Circulation Yolk sac and placenta Endothelium of fetal blood vessel

Fetal Circulation Umbilical vein carries oxygenated blood and nutrients from the placenta to the fetus . Pair of umbilical arteries carry deoxygenated blood & wastes to placenta .

Umblical vein Liver Portal vein Ductus venosus Inferior vena cava Right Atrium Left Atrium Foramen Ovale Left Ventricle Oxygenated blood from mother Placenta Descending Aorta Deoxygenated blood Superior vena cava Right Ventricle Pulmonary artery Lung Ductus ateriosus Ascending Aorta Supplies head n neck Umblical artery Supplies lower body

Changes in fetal circulation after birth Dec r eas e d Pulmona r y and Increas e d Sys t emic V ascular R esistanc e s at Bi r th: Loss of t h e tremendo u s bloo d fl o w th r ou g h the pl a ce n ta, w hich app r o xim a t ely dou b les the sys t emic v ascular resistance at b i r th. The pulmona r y v ascular resistance greatl y decreases as a result of e xpansion of the lu n gs.

Closing of Shunts Shunt Functional closure Anatomical closure Remnant Ductus arteriosus 10 – 96 hrs after birth 2 – 3 wks after birth Ligamentum arteriosum Formamen ovale Within several mins after birth One year after birth Fossa ovalis Ductus venosus Within several mins after birth 3 – 7 days after birth Ligamentum venosum Umbilical arteries → Umbilical ligaments Umbilical vein → Ligamentum teres

Closur e of the F oramen O v ale Fl o w bac kw a r d th r ou g h the f oramen o v ale l o w rig h t at rial press u re the h i g h le f t a trial pres s ure Sm a ll v al v e that lies o v er the f oramen o v ale on the le f t s ide of the a t rial septum closes

Closur e of the D uctus A r t eriosus increa sed s y s t emic res i s t ance e l e v a t es t h e ao r t i c pres s u re whi l e the decrea s ed p u lmona r y re s i s t a n c e reduces t h e p u lmona r y a r t eri a l pre s s u r e  a f t er bi r t h , blood begi ns t o fl o w back w a r d f r om t h e ao r ta in t o the p u lmona r y a r t e r y t h r ough the d u ct u s a r t erio s u s . 1 t o 8 d a y s - f u n c t i o n al clo s u re of the d u ct u s a r t erio s u s 1 t o 4 m o nth s - d u ct u s a r t erio s u s o r dinari l y bec o mes ana t omical l y occl u ded b y g r o wt h of f ib r ous ti s s u e in t o it s l u men P a t ent d u ct u s a r t erio s u son e - t h e d u ct u s f a i ls t o c lo s e e x cessi v e d u ctu s dil a t i on c a us e d b y v asodi l a t i n g pr o s t a gl an di n s i n the d u ctus w a l l. i n dom e tha c in - blo c ks synthesi s of pr o s t a gl an di n s

Characteristics of new born circulation Blood Volume . - 3 m l - i f th e infa nt is le f t atta c he d t o the placen t a f or a f e w mi nu t e s a f t e r b i r th or i f the umb i l i c al c o r d is s tr i pped t o f or c e blo o d out of its v es s el s in t o the ba b y , an addi t i onal 7 5 m i l l i l i t e r s of blo o d en t e r s the infa nt, t o ma k e a t o tal of 3 7 5 m i l l i l i t e r s . Cardiac Output 5 m l/m i n - is abou t tw i c e a s m u c h i n relat i on t o b o dy w ei g h t a s i n the adul t . Arterial Pressure. The arterial pressure during the first day after birth averages about 70 /50 mm Hg and increases slowly during the next several months to about 90/60.

Neonatal Jaundice and Erythroblastosis Fetalis . In the f e tus bil i rubin c a n c r oss th e pla centa in t o the m o the r a n d be e x c r e t ed th r ough th e li v er of th e m o ther A f t er bi r th t he only mea ns f or ridding t he neon a t e of bil i rubin is t h r ou g h t he neon a t e’s o w n li v er f i r st w eek of l i f e l i v er funct i ons po o rl y - incapa b le of con j ugating si gn i f icant q uantit i es of bi lirubin wi th g l ucu r on i c acid f or e x cr e t i on in t o t h e bi l e  t h e p l asma bi lirubin concentra t ion rises f r om a n o r m al v alue of less t h an 1 m g/ d l t o a n a v erage of 5 m g/ d l d uring the f i r st 3 d a y s of li f e  l i v er be comes functional  grad ually f alls bil i rubin b a ck t o normal P h ysio l ogic al h yperbi lirubinemia mild jaundice ( y el l o w nes s ) of t he infan t ’s skin a n d especially of t he scler ae of i t s e y es f or a w eek or t w o.

T he most important abnormal cause of serious neonatal jaundice is erythroblastosis fetalis . the baby inherits Rh-positive red blood cells from the father, while the mother is Rh negative. The mother then becomes immunized against the Rh-positive factor (a protein) in the fetus’s blood cells, Mothers antibodies destroy fetal red blood cells, releasing extreme quantities of bilirubin into the fetus’s plasma . O ften causing fetal death because of a lack of adequate red blood cells.

Th e most o b viou s e f f ect of bi r th on the ba b y - loss of t h e placen tal co n n e ction wit h the m o ther - loss of Oxygen support One of the most i mpo r tant im m edia t e ad j ustments re q uired of the in f ant i s t o b e g i n breathing. child ordinarily begins to breathe within seconds and has a normal respiratory rhythm within less than 1 minute after birth Cause of Breathing at Birth . A slight asp h yxi a t ed sta t e inciden t t o t h e bi r th p r oc e ss senso r y i m pulse s that origina t e i n the suddenly coo led skin Onset of breathing

Tolerability of hypoxia Adults – 4 minute Neonate – 10 minutes Permanent and serious brain impairment often ensues if breathing is delayed more than 10 minutes.

Expansion of Lung at birth At birth - Alveoli are collapsed due to surface tension of viscid fluid present in them. 25 mm Hg of negative pressure required to open them. T he first inspirations of the normal neonate are extremely powerful; they are usually capable of creating as much as 60 mm Hg negative pressure in the intrapleural space .

Respiratory Distress Syndrome Caused When Surfactant Secretion Is Deficient . premature infants and infants born of mothers with diabetes mellitus are mainly affected. A characteristic finding in respiratory distress syndrome is failure of the respiratory epithelium to secrete adequate quantities of surfactant. Surfactant – secreted by Type II alveolar epithelial cells decreases the surface tension of the alveolar fluid ,. Secretion begins only in the last 1-3 month of gestation.

Body temperature regulation Th e n o rmal m e t a boli c ra t e of t h e ne o na t e i n rela t io n t o b ody w eight i s about twice t h at of t h e ad u l t , body su r fa c e are a i s larg e i n re l a t i on t o body m a ss , hea t i s re adi l y lo s t f r om the body  body t e m p er a t u r e of the n eon a t e, p a r t i cularl y of p rem a ture i n fa n ts, fa l l s easi l y B ody temperature of even a normal infant often falls several degrees during the first few hours after birth but returns to normal in 7 to 10 hours.

The premature infant’s temperature tends to approach that of its surroundings. At normal room temperature, the infant’s temperature may stabilize in the low 90s. Studies show that a body temperature maintained below 96°F (35.5°C) is associated with a particularly high incidence of death This explains the almost mandatory use of the incubator when treating prematurity

Th e ne o na t e inherit s m u ch immu nity f r om t h e m o t h er becau s e ma n y p r o t ein ant i bodies di f f u se f r om t h e m o t h er’s blood t h r ough the p l acenta in t o t h e f e t u s . Ba b y’s o wn imm u nity s y s t em begins t o f orm ant i bodies and t h e gamma globu l in co n ce n t r a t io n r e t u rns es s enti a l l y t o n ormal b y t h e age of 1 2 t o 2 mo n t h s. De spi t e t h e decrea s e i n gamm a globulin s soon a f t er bi r t h , t h e ant i bodie s inheri t ed f r om t h e m o t h er p r o t ect t h e in f ant f or about 6 m o nths ag a ins t most ma j or child h ood in f ect i ous dis e a s es, inclu ding dip h t h eri a , me a s l es, and polio. I n her i t ed ant i bodie s ag a ins t whoopin g cough a r e n orma l ly ins u f f icien t t o p r o t ect t h e ne o na t e- immu niza t ion Imm unity

L i v er F u n ction L i v er fu n ct i on i n the n e on a t e m a y b e q u i t e de fic ie n t, as e v iden ced b y the f o ll o win g e f f ects: Th e l i v er of th e n e o n a t e co n j u ga t es bi l i r ub i n wit h g l uc u r o n i c a cid poo rl y a nd th er e f o r e e x cr e t es b i l i r ubin on l y s l ight l y du r i n g the f ir s t f e w d a y s of l i f e. Th e l i v er of the neo n a t e i s de f ic ie n t i n f o r m i ng p l asma p r o t e ins, so the p l asma p r o t e in conce n t r a t io n f a l l s du r i n g the f ir s t w ee k s of l i f e and the i n f a n t d e v e l ops h ypo p r o t e i n e m i c e d em a . Th e glu coneogen e sis fu n ct i on of th e l i v er i s pa r t icu l a r l y de f ic ie n t. As a r e sul t , the b l ood glu cose l e v el of the u n f ed n e on a t e f a l l s t o about 3 t o 4 mg/dl (abou t 4 p e r cent of no r mal ) a n d the i n f a n t must de p e n d ma i n l y on its s t o r ed f a t s f or e n e r g y u n t i l su f f ic ie n t f eed i ng can occu r . Th e l i v er of the neo n a t e usu a ll y a l so f o rms t oo l i tt l e of the b l ood f ac t ors n e eded f or no r ma l b l ood coagu l a t io n .

N e ed f o r C alcium a n d V i tamin D Th e n eo n a t e i s i n a s t age of rapi d ossi f icat i on of its bo n es at bi r th, so a ready supply of calcium th r ou g hou t in f ancy i s nec e ss a r y . Thi s i s o r dinarily supplied a de q ua t ely b y the usual di e t of mil k . – abso r p ti o n of calciu m b y the ga s t r oin t e s tinal tract i s p o or i n the abse n c e of vitami n D – de f icie n t i nfa nt ca n d e v elop s e v ere r i c k e ts Thi s i s pa r ti c u larly true i n prematur e ba b ies b e cause their gas t r oin t estinal trac t s absorb c alcium e v en less e f f ecti v ely than those of normal in f ants

N e cessity f o r I r o n i n t h e D i e t If t h e m o t h er h a s h a d ade q u a t e amo u nts of i r on i n he r di e t, t h e l i v er of t h e in f ant u s u a l ly h a s s t ored en o ug h i r on t o k eep f orming bloo d cel l s f or 4 t o 6 mo n t h s a f t er bi r t h . Bu t i f t h e m o t h er h a s h a d ins u f f icien t i r on i n he r di e t, s e v ere anemia i s l i k ely t o occ u r i n t h e in f ant a f t er about 3 mo n t h s of li f e. T o pr e v ent t h i s pos s ibi l i t y , early f eeding of t h e in f ant wi t h egg y ol k , whic h co n t a ins rea s o n ably l a rge q u ant i t i es of i r o n , o r t h e adm i nis t ra t io n of i r on i n some o t h er f orm i s des i rab l e b y t h e second or th i r d mo n th of l i f e.