neonatal physiology and transition period
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Transcript of neonatal physiology and transition period
NEONATAL PHYSIOLOGY AND TRANSITION PERIOD
Under guidence of Dr neelam dogra ma’am
Presented by anuradha pandey
LEARNING OBJECTIVE
physiological changes which take place following birth and appreciate the unique aspects of neonatal physiology including:
1) limited reserve capacity for temperature control, cardiovascular and respiratory function
2)variable and individualized fluid requirements
3) implications of hepatic and renal immaturity
NEWBORN-first 24 hrs of life
NEONATE-from birth to under four weeks(<28 days)
TERM NEONATE-between 37 to < 42 gestational weekPRETERM NEONATE-<37 gestational week irrespective ofBWPOST TERM NEONATE-> or egual to 42 gestational week
LOW BIRTH WEIGHT(LBW)<2500 GRAM irrespective of birth weightVERY LOW BIRTH WEIGHT(VLBW)<150O GRAMEXTREMELY LOW BIRTH WEIGHT(ELBW)< 1000 GRAM
INTRODUCTION
FETAL CIRCULATION
AIM
Oxygenated placental blood is preferentially delivered to the brain,myocardium and upper torsolower oxygen tension blood distributed to the lower body and placenta Preferential splitting is achieved via intra- and extracardiac shunts that direct blood into two parallel circulations (the left ventricle providing 35% and the right 65% of cardiac output. )
Fetal cardiacoutput is therefore measured as a combined ventricular output closure of the intracardiac (foramen ovale) and extracardiac shunts (ductus venosus and ductus arteriosus)
FETAL CIRCULATION
Oxygenated blood via umbilical vein either through the liver or via the ductus venosus to reach IVC
blood remains on the posterior wall of the inferior vena cava, allowing it to be directed across the foramenovale into the left atrium by the Eustachian valve
blood passes left ventricle and aorta to supply the head and upper torso.
deoxygenated blood returning from the SUPERIOR vena cava and myocardium via the coronary sinus is directed through the right ventricle and into the pulmonary artery.
Most of this blood is returned to the descending aorta via the ductus arteriosus; ( 8-10%of total cardiac output passes through the high-resistance pulmonary circulation.)
Blood in the descending aorta either supplies the umbilical artery to be reoxygenated at the placenta or continues to supply the lower limbs.
FETAL CIRCULATION (PARALLEL CIRCULATION)
PHYSIOLOGICAL CHANGES AT BIRTH
UMBILICAL VESSELS- IMMEDIATELY AFTER CLAMPING:
constrict in response to stretching and increased oxygen content at delivery
large low-resistance placental vascular bed removed from the circulation
increase SVR
Reduction of blood flow along ductus venosus (passive closure over the following 3-7 days),reduced blood flow in IVC
Lung expansion
drops pulmonary vascular resistance
increase in blood returning to the LA
These two changes reduce right atrial and increase left atrial pressures, functionally closing the foramen ovale within the first few breaths of life
Successful transition from fetal to postnatal circulation requires
clamping of umbilical cord and removal of the placenta
increased pulmonary blood flow,
Shunt closure
TRANSITION AT BIRTH
RESPIRATORY CHANGES
Chemical
Sensory/ Thermal
Mechanical InitiationInitiation ofof BreathingBreathing
What part do each of these factors play in initiation of
respirations in the neonate?
CHANGES AT BIRTH….MECHANICAL
Compression of fluid from the fetal lung during vaginal delivery establishes the lung volume
Negative inspiratory pressures of up to 70-100 cm H2O are initially required to expand the alveoli (LaPlace’s relationships) which facilitate lung expansion by overcoming:
airways resistance
inertia of fluid in the airways
surface tension of the air/fluid interface in the alveolus
As the chest passes through the birth canal the lungs are compressed
Subsequent recoil of the chest wall produces passive inspiration of air into the lungs
CHEMICAL EVENTS
1. With cutting of the cord, remove oxygen supply 2. Asphyxia occurs
3. CO2 and O2 and pH = ACIDOSIS
4. Acidotic state-- stimulates the respiratory center in the medulla and the chemoreceptors in carotid artery
to initiate breathing
SENSORY / THERMAL EVENTS Thermal--the decrease in
environmental temperature after
delivery is a major stimulus of breathing
Tactile--nerve endings in the skin
are stimulated
Visual--change from a dark world to
one of light
Auditory--sound in the extrauterine
environment stimulates the infant
BIOPHYSICAL CHANGE CONTINUED
1)Alveolar distension, cortisol and epinephrine further stimulate type II pneumocytes to produce surfactant
2)Expiration initially active,pressures of 18-115 cm H2O generatedamniotic fluid forced out from the bronchi.
PHYSIOLOGICAL CHANGES LEAD TO-increasing blood flow and initiating the cardiovascular changes
.
physiological reverse shunt from left to right commonly occurs.
FORAMEN OVALE completely closed in 50% of children by 5 years remains probe patent in 30% of adults, can facilitate paradoxical embolus and potential stroke.
DUCTUS ARTERISUS- drop in pulmonary artery pressure and increase in SVR reverses
flow across the ductus arteriosus from L TO R affected by blood oxygen content circulating prostaglandins. E2 Functional closure occurs by 60 hours in 93% of term infants.,4-
8 weeks permanent structural closure occurs via endothelial destruction and subintimal proliferation.
SHUNT CLOSURE
CARDIOVASCULAR CHANGES
1. Pressure in RA decreases
2. Blood flows to the lungs
4. Pressure in the LA increases RT Flow of blood from the lungs
3. Ductus Arteriosusbegins to constrict
5. Increase pressurein the LA forcesthe foramen ovale to close
SHUNT CLOSURE
IMPORTANT-
stimulus such as hypoxia, acidaemia or structural anomaly can increase pulmonary vascular resistance and potentially re-open the ductus arteriosus or foramen ovale. which allows a right-to-left shunt, which worsens hypoxia
. Eg seen in persistent pulmonary hypertension of the newborn.
term neonatal cardiac output is approximately 200 ml/kg/minute
fewer myofibrils in a disordered pattern,
Less mature sarcoplasmic reticulum and transtubular system -nt
dec CA-ATP ACTIVITY,dependent on exogenous ionized calcium
follows the Franke Starling relationship of filling pressure to stroke volume, but on a much flatter section of the curve compared with adults. i.e limited increase in stroke volume for a given increase in ventricular filling volume.
dependent on heart rate to increase cardiac output and cardiac output can respond to increased ventricular filling.3 month parasympathetic vervous system effect more developed than sympathetivBaroreceptors not well developed compared to chemoreceptorsfurther depressed under anaesthesia-bradycardia
NEONATAL MYOCARDIAL FUNCTION
Ventricular maturation and associated ECG changes
The fetal heart - right-side dominant, with the right ventricleresponsible for 65% of cardiac output in utero. The neonatal ECG reflects RAD R wave dominance in lead V1S wave dominance in lead V6.
At 3-6 months the classical LAD pattern established as ventricular hypertrophy occurs in response to increased systemicvascular resistance
LOW CARDIAC RESERVE-
Left ventricle has high tone has limited contractile reserve due to;-
Reduced no of alpha receptorsHigh level of circulating cathecholaminesLimited recruitable stroke volumeImmature calcium transport systemDec ventricular complianceeffect of parasympathetic nervous system is more predominentBeta adrenergic receptors are more developed than alpha thus respond better to dobutamine and isiproterenol
MYOCARDIAL METABOLISM
neonates can tolerate hypoxia better due to
High concentration of glycogen
More effective utilisation of anaerobic metabolism
Hence can be resusitated easily if oxygenation and perfusion are reestablished
Oxygen consumption increases after birth(at neutral temperature )
Full term child
At birth-6ml/kg/min
10 days-7 ml/kg/min
4 week-8 ml/kg/min
CARDIAC VALUES
FETAL RESPIRATORY SYSTEM
ALVEOLAR DEVELOPMENTContinues even after birthAt birth 24 million alveoliincreases fivefold in -300 million by 8 years of ageInitally increases in no ,further increase by inc in size and airway development
Lungs develop from the third week of gestation with completion of the terminal bronchioles by week 16
FETAL RESPIRATORY SYSTEM
SURFACTANT type I and II pneumocytes are distinguishable only by 20-22 weeks
present only after 24 weeks, the watershed time for pulmonary gas exchange and therefore extra-uterine survivalproduction can be increased after 24 weeks by giving betamethasone to the mother, thereby improving neonatal lung function if premature delivery is anticipated
APPLIEDseen preterm babies decreases the compliance
– risk for respiratory distress syndrome
, bronchopulmonary dysplasia
and pulmonary hypertension
.
RESPIRATORY SYSTEM
Diaphragm-two types of fibres
Type 1-slow twitch, highly oxidative ,sustained contraction ,less fatigue
Type 2-fast twitch, low oxidative ,quick contraction and easily fatigued
New born have 25% TYPE-1,(PRETERM 10%),BY AGE OF TWO YRS 55%
APPLIED-risk of diaphragmatic fatigue during hyperventilation
NEONATAL AIRWAY
NEONATAL AIRWAY
Larynx is funnel shaped narrowest portion is cricoid –uncuffed tube
preferred(micro cuff useful ,costly) Large size of the tongue-increases chances of
obstruction and difficult laryngoscopy Higher level of larynx(c3 in preterm,c4 in
term and c5-c6 in adults)-straight blade more useful
Epiglottids- short,stubby,omega shaped, angled over laryngeal inlet-control with laryngeal blade more difficult
Tip of epiglottids lies at c1,with close apposition with soft palate-allows simultaneously sucking and breathing
Vocal cords angled-blind intubation ,tube may lodge at anterior commisure
Large occiput-more flexion may lead to obstruction
Chest wall development
Ribs oriented parallel and unable to increase the thoracic volume during inspiration
At 2 yrs old associated with standing and walking, ribs are oriented oblique
Cartilaginous structure with inward movement during inspiration
DEVELOPMENTAL CHANGES OF RIB CAGE
NEONATAL LUNG MECHANICS
imbalance exists between chest wall rigidity and elastic recoil of neonatal lungs. (CONTAIN IMMATURE ELASTIC FIBRES,thus tendency to recoil)
increase closing capacity to the point of exceeding functional residual capacity (FRC) until the age of 6. To counteract this, neonates produce positive end expiratory pressure(PEEP) via high resistance nasal airways and partial closure of the vocal cordsLimited Inspiratory reserve volume Minute volume is maintained by high respiratory rateRespiratory fatigue common
Neonatal lung mechanics-gas exchange
immature in neonates, total shunt estimate of 24% of the cardiac output at birth, reducing to 10% of cardiac output at 1 week. rapid reduction in shunt fraction improves arterial oxygenation and reduces the effort of breathing.
implications during anaesthesia. effective FRC is reduced( physiological PEEP and intercostal muscle tone is lost) along with an increased shunt fraction and High metabolic rate (6-8ml ofO2/kg/minute), These factors contribute to a potential rapid desaturation in neonates under anaesthesia.
Control of ventilation Peripheral chemoreceptors functional at birth but are initially silent because of high post delivery blood oxygen content.Receptor adaptation occurs over 48 hours,
APNOEA OF PREMATURITYneonates exhibit periodic breathing pattern defined as an apnoea of less than 5 seconds often followed by tachypnoea.,
Premature neonates exhibit apnoeic episodes of more than 15 seconds or a shorter period a/w fall in heart rate due to loss of central respiratory drive improves with maturity may persist up to 60 weeks postconceptual ageAnaemia i.e. haematocrit<30% is any independent risk factor
characterized by 1)an initial increase in ventilation followed by a decrease in ventilation; 2).much rapid than adults due to low resting carbon dioxide
Response Varies with temperature, level of arousal and maturity
.
RESPONSE TO HYPOXIA
PERSISTENT PULMONARY HYPERTENSION OF THE NEW BORN/PERSISTENT FETAL CIRCULATION
PATHOPHYSIOLOGY
hypoxia, acidosis and inflammatory mediators l/t persistent increase in pulmonary artery pressure
persistent fetal circulation
Ppt condition-birth asphyxia,meconium aspiration sepsis,CDH, maternal use of nsaids,GDM,,casearen delivery
Leads to R TO L shunt resulting in profound hypoxia,with elevated PCO2
PERSISTENT FETAL CIRCULATION
Goal-PaCO2-50 TO 55mmhg and Pao2-50-70 mmhgMANAGEMENT:-1)treat precipitating condition eg hypoxia,hypoglycemia2)Inhaled nitric oxide3)Mechanical ventilation4)high frequency ventilation 5)exogenous steroids6)inhaled steroid7)ECMO8)experimental-slidnafil
MECONIUM ASPIRATION
Marker for chronic hypoxia in utero in third trimester due to interferance in maternal circulation
passage of meconium in utero-fetus breathes in meconium mixed amniotic fluid enters in pulmonary circulation
Leads to varying degree of respiratory distress Increase in amount of amount of musle in blood vessels
of distal respiratory units
GUIDELINES FOR MANAGEMENT FOR MECONIUM ASPIRATION
“If the baby is not vigorous (Apgar 1-3): Suction the trachea soon after delivery (before many respirations have occurred) for ≤ 5 seconds. If no meconium retrieved, do not repeat intubation and suction. If meconium is retrieved and no bradycardia present, reintubate and suction. If the heart rate is low, administer PPV and consider repeat suctioning. “
“If the baby is vigorous (Apgar >5): Clear secretions and meconium from the mouth/nose with a bulb syringe or a large-bore suction catheter. In either case, the remainder of the initial resuscitation: dry, stimulate, reposition, and administer oxygen as necessary.”
Thermogregulation
2.5-3.0 times higher surface area BWlimited insulating capacity from subcutaneous fat and the inability of neonates to generate heat by shivering until 3 months of age.
Heat loss1) radiation(39%)2)convection (34%)3)evaporation (24%) and4)conduction(3%).
THERMOGENESIS1)by limb movement and2) by stimulationof brown fat (non-shivering thermogenesis).
C old Items on Bed
C old Walls
C old R oom T emp.
R adiation
C old Blankets
C old X -ray plates
C old Scale
C onduction
Passing T raffi c
Oxygen left on
Bed Near Air Vent
C onvection
T achypnea
Bath
Wet Diaper
E vaporation
Baby
BROWN FAT
6% of term bodyweight (dec in preterm)found in the interscapular region, mediastinum, axillae, vessels of the neck andperinephric fat highly vascular with sympathetic innervationhigh mitochondrial content to facilitate heat generation Non-shivering thermogenesis
.1. Skin receptors perceive a drop in
environmental temperataure
2. Transmit impulses to the central nervous system
3. Which stimulates the sympathetic nervous system
4. Norepinephrine is released at local nerve endings in the brown
5. Metabolism of brown fat
6. Release of fatty acids
7. Release of HEAT!
heat loss minimized by
increasing the temperature of the surrounding environment.
CAREFUL;- the environmental temperature exceeds neonatal temperature then heat will be gained, which can be harmful as the ability to sweat is present only after 36 weeks postconceptual age.)
by warming surrounding air and minimizing air speed across the baby’s skin,
increasing ambient humidity and reducing air speed across the neonate.
Insensible water loss through the skin can be minimized by putting the preterm neonate in a plastic bag or covering the body,and especially the head
HEAT CONSERVATION
Haematology
contains both adult (HbA) and fetal haemoglobin
HbF70-80% upto 90% in pretermfour globin chains alpha2delta2 greater affinity for oxygen and helps maintain the molecular structure and function in a more acidic environmentfacilitates oxygen transfer across the placenta from maternal HbA. replaced with HbA at approximately 6 month of age.
Postdelivery,
increase in 2,3-diphosphoglycerate levels, shifting the oxygen dissociation curve to the right,
HAEMATOPOIESIS
occurs in the liver in utero
but is restricted to bone marrow from 6 weeks post delivery,
thus limiting potential sites for haemoglobin synthesis.
PHYSIOLOGICAL ANAEMIA OF INFANCY
Occcurs around 8-10 week of age
HbF is lost faster than HbA is synthesized.
low levels of erythropoietin due to improved tissue oxygenation after birth
decreased lifespan of HbF-laden red blood cells
relative increase in the blood volume,
These factors contributes to the shrinking cellmass
Hepatic
Most enzymatic pathways are present inactive at birthbecome fully active at 3 monthsAlbumin level low-more free drug in circulationRisk of hypoglycemia-low glycogen stores and dec synthetic function
UNCONJUGATED HYPERBILIRUBINEMIA
Unconjugated bilirubin levels rise during the first 48 hours rapid breakdown of HbF poor conjugating abilities of the immature liver.exacerbated in presence of haemolysis, sepsis, dehydration or excessive bruising; can cross the blood brain barrier kernicterus and subsequent developmental delay. Bilirubin levels gradually fall over the first 2weeks, jaundice in term infants being rare beyond this period
Clotting factors1) do not cross the placenta; 2)factors V, VIII and XIII are at adult concentrations before birth.3)vitaminK-dependent clotting factors (II, VII, IX, X, protein C and S) areinitially low
# because of a lack of vitamin K stores and# immaturehepatocyte function causing a prolongation in prothrombin time
.4)Platelet function diminished due to low levels of serotonin and adeninenucleotides, despite platelet counts in the adult range
VITAMIN K PROPHYLAXIS
#Breast milk is a poor source of vitamin K #Endogenous synthesis by the gut flora is not established for the first few weeksafter birth. #protect against haemorrhagic disease of thenewborn
Renal
EXCRETORY FUNCTION1 million nephrons is present by 34 weeks ’gestation. The glomeruli and nephrons are immature at birth Low GFR and limited concentrating ability. Suseptible to both dehydration and volume overloadLack of renal medulla osmotic gradient and absence of medullary tubules limit urinary concentrating ability,half that of the adult (1200-1400 mOsm/kg)Glycosuria and aminoaciduria are commonly detected because of immature active transport pumps in the proximal tubule.
ENDOCRINOLOGYRenal immaturity affects vitamin D formation and calcium homeostasis. The fetus and neonate have a high calcium and phosphate requirement for bone formation and growth.
75% of TBW,80-85% IN PRETERMReduced to 60-65% BY one yearECF:ICF IS 2:1,The diuresis reduces the extracellular water (30% of TBW) and ICF increases due to growth of cellls-reaches adult value by 1 yr
Blood volume Full term-85 ml /kg Preterm90-100 ml /kg(50 ml/kg is plasma)
important postnatal adaptation to facilitate lung function and reduces the risks of symptomatic patent ductus arteriosus, necrotizing enterocolitis and bronchopulmonary dysplasia
BODY FLUID COMPOSITION
FLUID THERAPY
MAINTAINENCE FLUID-
70,80,90,120 ml/kg on day 1/3/5/7
Rest period-150ml/kg/24hr
Fluid choice
FIRST 48 hrs-10% glucose
Higher in pre term
Na and k 2-3 meq/100 ml
Beyond that-5% glucose(preterm higher glucose requirement)
IMPORTANT-newborn of diabetic mother, small for gestational age, glucose monitoring must
precocious in development ,
continues to develop to achieve a full complement of cortical and brainstem cells by 1 year.
neonatal cerebral circulation receiving one-third of cardiac output compared with one-sixth of cardiac output in adults
The blood brain barrier is immature in the neonatal period
increased permeability to fat-soluble molecules
potentially increasing the sensitivity to certain anaesthetic drugs(
NERVOUS SYSTEM
NERVOUS SYSTEM
Cerebral autoregulation is fully developed at term, maintaining cerebral perfusion down to a mean arterial pressure of 30 mmHg, reflecting the lower blood pressures found in neonates.
ANS better developed to protect against hypertension than hypotension because the parasympathetic system predominates., reflected in the propensity of neonates to bradycardia and relative vasodilation.
Delayed myelination-easier intraneural penetration of LA,short time of onset and diluted conc as effective as concentrated
pathways are developed by 24-28 weeks’ gestation,
The concept of neonatal nociception is now widely accepted, with adultlike
physiological stress and behavioural responses to a noxious Stimulus
Neonates undergoing awake nasal intubation increase mean arterial pressure by 57% and intracranial pressure by a similar amount.
Noxious stimulus exposure in the neonatal period can also affect behavioural patterns in later childhood, suggesting adaptive behaviour and memory for previous experience
NOCICEPTION
IMMUNOLOGIC ADAPTATION
Active acquired immunity Pregnant woman forms antibodies herself
Passive acquired immunity Mom passes antibodies to the fetus Lasts for 4-8 months
Newborn begins to produce own immunity about 4 weeks of age
KEY POINTS
KEY POINTS
THANK YOU