Pediatric Physiology All

Pediatrics Physiology

Definitions

Preterm or Premature Infant: < 37 weeks

Term Infant: 38-42 weeks gestation

Post Term Infant: > 42 weeks gestation

Newborn: up to 24 hours old

Neonate: 1-30 days old

Infant: 1-14 months old

Child: 14 months to puberty (~12-13 years)

Body Size

• The most obvious difference between children & adults is size

• It makes a difference which factor is used for comparison: a newborn weighing 3kg is

– 1/3 the size of an adult in length

– 1/9 the body surface area

– 1/21 the weight

• Body surface area (BSA) most closely parallels variations in BMR & for this reason BSA is a better criterion than age or weight for calculating fluid & nutritional requirements

Body Size

Fetal Development

The circulatory system is the first to achieve a functional state in early gestation

The developing fetus outgrows its ability to obtain & distribute nutrients and O2 by diffusion from the placenta

The functioning heart grows & develops at the same time it is working to serve the growing fetus

At 2 months gestation the development of the heart and blood vessels is complete

In comparison, the development of the lung begins later & is not complete until the fetus is near term

Fetal Circulation

• Placenta– Gas exchange

– Waste elimination

• Umbilical Venous Tension is 32-35mmHg– Similar to maternal mixed venous blood

– Result:• O2 saturation of ~65% in maternal blood, but ~80% in the fetal

umbilical vein (UV)

– Low affinity of fetal Hb (HbF) for 2,3-DPG as compared with adult Hb (HbA)

– Low concentration of 2,3-DPG in fetal blood

• O2 & 2,3-DPG compete with Hb for binding, the reduced affinity of HbF for 2,3-DPG causes the Hb to bind to O2 tighter– Higher fetal O2 saturation

Fetal Circulation

P50 is 27mmHg for adult Hgb, but only 20mmHg for fetal Hb This causes a left shift in the O2 dissociation curve

Because the bridge between arterial & tissue O2 tension crosses the steep part of the curve, HbF readily unloads O2 to the tissue despite its relatively low arterial saturation

Fetal Circulation

Fetal Circulatory Flow

Starts at the placenta with the umbilical vein Carries essential nutrients & O2 from the placenta to

the fetus (towards the fetal heart, but with O2 saturated blood)

The liver is the first major organ to receive blood from the UV Essential substrates such as O2, glucose & amino acids

are present for protein synthesis 40-60% of the UV flow enters the hepatic

microcirculation where it mixes with blood draining from the GI tract via the portal vein

The remaining 40-60% bypasses the liver and flows through the ductus venosus into the upper IVC to the right atrium (RA)


The fetal heart does not distribute O2 uniformly Essential organs receive blood that contains more

oxygen than nonessential organs This is accomplished by routing blood through

preferred pathways From the RA the blood is distributed in two

directions: 1. To the right ventricle (RV) 2. To the left atrium (LA)

Approximately 1/3 of IVC flow deflects off the crista dividens & passes through the foramen ovale of the intraatrial septum to the LA


• Flow then enters the LV & ascending aorta– This is where blood perfuses the coronary and cerebral

arteries

• The remaining 2/3 of the IVC flow joins the desaterated SVC (returning from the upper body) mixes in the RA and travels to the RV & main pulmonary artery

• Blood then preferentially shunts from the right to the left across the ductus arteriosus from the main pulmonary artery to the descending aorta rather than traversing the pulmonary vascular bed– The ductus enters the descending aorta distal to the

innominate and left carotid artery

– It joins the small amount of LV blood that did not perfuse the heart, brain or upper extremities


The remaining blood (with the lowest sat of 55%) perfuses the abdominal viscera

The blood then returns to the placenta via the paired umbilical arteries that arise from the internal iliac arteries Carries unsaturated blood from the fetal heart

The fetal heart is considered a “Parallel” circulation with each chamber contributing separately, but additively to the total ventricular output Right side contributing 67% Left side contributing 33%

The adult heart is considered “Serial”

Cardiac Malformations

The parallel nature of the two ventricles enables fetuses with certain types of cardiac malformations to undergo normal fetal growth & development until term because systemic blood flow is adequate in utero

Complete left to right heart obstruction does not impede fetal aortic blood flow

The foramen ovale & ductus arteriosus provide alternate pathways to bypass obstruction


Summary: Ductus Venosus shunts blood from the UV to

the IVC bypassing the liver Foramen Ovale shunts blood from the RA to

the LA Ductus Arteriosus shunts blood from the PA

to the descending aorta bypassing the lungs Fetal circulation is parallel Blood from the LV perfuses the heart & brain

with well oxygenated blood

Fetal Pulmonary Circulation

Fetal Lungs

Extract O2 from blood with its main purpose to provide nutrients for lung growth

Neonatal Lungs

Supply O2 to the blood

Fetal lung growth requires only 7% of combined ventricular output

Fetal Pulmonary Circulation

Fetal pulmonary vascular resistance (PVR) is high & helps restrict the amount of pulmonary blood flow

If not for the low resistance ductus arteriosus (DA) & adjoining peripheral vascular bed the RV would need to pump against a higher pulmonary resistance than the LV

Instead, both ventricles face relatively low systemic vascular resistance established by the low resistance / high flow from the placenta

Transitional & Neonatal Circulation

There are 3 steps to understanding transitional circulation

1. Foramen Ovale: ductus arteriosus & ductus venosus close to establish a heart whose chambers pump in series rather than parallel

Closure is initially reversible in certain circumstances & the pattern of blood flow may revert to fetal pathways

2. Anatomic & Physiologic: Changes in one part of the circulation affect other parts

3. Decrease in PVR: The principal force causing a change in the direction & path of blood flow in the newborn


Changes that establish the newborn circulation are an “orchestrated” series of interrelated events

As soon as the infant is separated from the low resistance placenta & takes the initial breath creating a negative pressure (40-60cm H2O), expanding the lungs, a dramatic decrease in PVR occurs

Exposure of the vessels to alveolar O2 increases the pulmonary blood flow dramatically & oxygenation improves


Hypoxia and/or acidosis can reverse this causing severe pulmonary constriction

The pulmonary vasculature of the newborn can also respond to chemical mediators such as

Acetylcholine

Histamine

Prostaglandins

**All are vasodilators


Most of the decrease in PVR (80%) occurs in the first 24 hours & the PAP usually falls below systemic pressure in normal infants

PVR & PAP continue to fall at a moderate rate throughout the first 5-6 weeks of life then at a more gradual rate over the next 2-3 years

Babies delivered by C-section have a higher PVR than those born vaginally & it may take them up to 3 hours after birth to decrease to the normal range

Ductus Arteriosus

Closure occurs in two stages

Functional closure occurs 10-15 hours after birth

This is reversible in the presence of hypoxemia or hypovolemia

Permanent closure occurs in 2-3 weeks

Fibrous connective tissue forms & permanently seals the lumen

This becomes the ligamentum arteriosum

Foramen Ovale

Increased pulmonary blood flow & left atrial distention help to approximate the two margins of the foramen ovale

This is a flap like valve & eventually the opening seals closed

This hole also provides a potential right to left shunt

Crying, coughing & valsalva maneuver increases PVR which increases RA & RV pressure

A right to left atrial & intrapulmonary shunt may therefore readily occur in newborns & young infants

Foramen Ovale

• Probe Patency– Is present in 50% of children < 5 years old & in more

than 25% of adults

– Therefore, the possibility of right to left atrial shunting exists throughout life & there is a potential avenue for air emboli to enter the systemic circulation

– A patent FO may be beneficial in certain heart malformations where mixing of blood is essential for oxygenation to occur such as in transposition of the great vessels

– Patients who rely on the patency of the foramen require a balloon atrial septoplasty during a cardiac cath or a surgical atrial septectomy

Ductus Venosus

This has no purpose after the fetus is separated from the placenta at delivery

Cardiovascular Differences in the Infant

There are gross structural differences & changes in the heart during infancy

At birth the right & left ventricles are essentially the same in size & wall thickness

During the 1st month volume load & afterload of the LV increases whereas there is minimal increase in volume load & decrease in afterload on the RV

By four weeks the LV weighs more than the RV

This continues through infancy & early childhood until the LV is twice as heavy as the RV as it is in the adult


• Cell structure is also different

– The myocardial tissues contain a large number of nuclei & mitochondria with an extensive endoplasmic reticulum to support cell growth & protein synthesis during infancy

• The amount of cellular mass dedicated to contractile protein in the neonate & infant is less than the adult

– 30% vs. 60%

• These differences in the organization, structure & contractile mass are partly responsible for the decreased functional capacity of the young heart


Both ventricles are relatively noncompliant & this has two implications for the anesthesia provider

1. Reduced compliance with similar size & wall thickness makes the interrelationship of the ventricular function more intimate

Failure of either ventricle with increased filling pressure quickly causes a septal shift & encroachment on stroke volume of the opposite ventricle


2. Decreased compliance makes it less sensitive to volume overload & their ability to change stroke volume is nearly nonexistent CO is not rate dependent at low filling pressures

but small amounts of fluid rapidly change filling pressures to the plateau of the Frank-Starling length tension curve where stroke volume is fixed

This changes the CO to strictly being rate dependent Additional small amounts of fluid can push the filling

pressure to the descending part of the curve & the ventricles begin to fail

The normal immature heart is sensitive to volume overloading


Functional capacity of the neonatal & infant heart is reduced in proportion to age & as age increases functional capacity increases

The time over which growth & development overcome these limitations is uncertain & variable

When adult levels of systemic artery pressure & PVR are achieved by age of 3 or 4 years the above limitations probably no longer apply

Autonomic Control of the Heart

Sympathetic innervation of the heart is incomplete at birth with decreased cardiac catecholamine stores & it has an increased sensitivity to exogenous norepinephrine

It does not mature until 4-6 months of age

Parasympathetic innervation has been shown to be complete at birth therefore we see an increased sensitivity to vagal stimulation

Circulation

The vasomotor reflex arcs are functional in the newborn as they are in adults

Baroreceptors of the carotid sinus lead to parasympathetic stimulation & sympathetic inhibition

There are less catecholamine stores & a blunted response to catecholamines

Therefore neonates & infants can show vascular volume depletion by hypotention without tachycardia

Cardiovascular Parameters

Parameters are much different for the infant than for the adult Heart rate: higher

Decreasing to adult levels at ~5 years old Cardiac output: higher

Especially when calculated according to body weight & it parallels O2 consumption

Cardiac index: constant Because of the infants high ratio of surface area to

body weight O2 consumption: depends heavily on temperature

There is a 10-13% increase in O2 consumption for each degree rise in core temperature

Circulation Variables in Infants

Respiratory System

Neonatal adaptation of lung mechanics & respiratory control Takes several weeks to complete

Beyond this immediate period the lungs are not fully mature for another few years

Formation of adult type alveoli begins at 36 weeks postconception Represents only a fraction of the terminal air

sacs with thick septa It takes more than several years for

functional and morphologic development to be complete

Respiratory System

• Neural & chemical controls of breathing in older infants & children are similar to those in adolescents & adults– A major exception to this is found in neonates and

young infants, especially in premature infants less than 40-44 weeks postconception• In these infants, hypoxia is a potent respiratory

depressant, rather than a stimulant• This is due either to central mediation or to changes

in respiratory mechanics• These infants tend to develop periodic breathing or

central apnea with or without apparent hypoxia– This is most likely because of immature

respiratory control mechanisms

Respiratory System

During the early years of childhood, development of the lungs continues at a rapid pace

This is with respect to the development of new alveoli

By 12-18 months the number of alveoli reaches the adult level of 300 million or more

Subsequent lung growth is associated with an increase in alveolar size

Respiratory System

Lung volumes of infants is disproportionately small in relation to body size

Since the infant’s metabolic rate, in relation to body weight, is twice that of the adult, more marked differences are seen in respiratory frequency and in alveolar ventilation

The higher level of alveolar ventilation in relation to FRC makes the FRC a less effective buffer between inspired gases & pulmonary circulation

Any interruption of ventilation will lead rapidly to hypoxemia & the function of anesthetic gases in the alveolus will equilibrate with the inspired fraction more rapidly than occurs in adults

Respiratory System

Functional Residual Capacity (FRC)

Determined by the balance between the outward stretch of the thorax & the inward recoil of the lungs

In infants, outward recoil of the thorax is very low

They have cartilaginous chest walls that make their chest walls very compliant & their respiratory muscles are not well developed

Inward recoil of the lungs is only slightly lower than that of an adults

Respiratory System

The FRC of young infants in conditions such as apnea , under general anesthesia and/or in paralysis decrease to 10-15% of TLC

Total Lung Capacity (TLC) is normally ~50% of an adults

10-15% TLC is incompatible with normal gas exchange because airway closure, atelectasis & ventilation/perfusion imbalance result

Awake infants are normally as capable of maintaining FRC as older children & adults

This is important because it limits O2 reserve during apnea and greatly reduces the time before you see a drop in oxygen saturation

Respiratory System

Breathing Patterns of Infants Less than 6 months of age

Predominantly abdominal (diaphragmatic) and the rib cage (intercostal muscles) contribution to tidal volume is relatively small (20-40%)

After 9 months of age The rib cage component of tidal volume increases to

a level (50%) similar to that of older children & adolescents, reflecting the maturation of the thoracic structure

By 12 months Chest wall compliance decreases The chest wall becomes stable & can resist the

inward recoil of the lungs while maintaining FRC This supports the theory that the stability of the

respiratory system is achieved by 1 year of age

Anatomic Differences in the Respiratory System

• Anatomic Airway Differences are Many

• Upper Airway: the nasal airway is the primary pathway for normal breathing

– During quiet breathing the resistance through the nasal passages accounts for more than 50% of the total airway resistance (twice that of mouth breathing)

– Except when crying, the newborns are considered “obligate nose breathers”

• This is because the epiglottis is positioned high in the pharynx and almost meets the soft palate, making oral ventilation difficult

– If the nasal airway becomes occluded the infant may not rapidly or effectively convert to oral ventilation

• Nasal obstruction usually can be relieved by causing the infant to cry


The Tongue: is large & occupies most of the cavity of the mouth & oropharynx

With the absence of teeth, airway obstruction can easily occur

The airway usually can be cleared by holding the mouth open and/or lifting the jaw

An oral airway may also be helpful


Pharyngeal Airway: is not supported by a rigid bony or cartilaginous structure Is easily collapsed by:

The posterior displacement of the mandible during sleep

Flexion of the neck Compression over the hyoid bone

Chemoreceptor stimuli such as hypercapnia & hypoxia stimulate the airway dilators preferentially over the stimulation of the diaphragm so as to maintain airway patency


Laryngeal Airway: this maintains the airway & functions as a valve to occlude & protect the lower airway In the infant the larynx is located high (anterior &

cephlad) opposite C-4 (adults is C-6) The body of the hyoid bone is between C2-3 & in the

adult is at C-4 The high position of the epiglottis & larynx allows the

infant to breathe & swallow simultaneously The larynx descends with growth Most of this descent occurs in the 1st year but the

adult position is not reached until the 4th year The vocal cords of the neonate are slanted so

that the anterior portion is more caudal than the posterior


Laryngeal Reflex: is activated by stimulation of receptors on the face, nose & upper airways of the newborn Reflex apnea, bradycardia & laryngospasm may occur Various mechanical stimuli can trigger response

including: Water Foreign bodies Noxious gases

This response is very strong in newborns


Narrowest area of the airway Adult is between the vocal cords Infant is in the cricoid region of the larynx

The cricoid is circular & cartilaginous and consequently not expansible

An endotracheal tube may pass easily through an infants vocal cords but be tight at the cricoid area

The limiting factor here becomes the cricoid ring This is also frequently the site of trauma during intubation

1mm of edema on the cross sectional area at the level of the cricoid ring in a pediatric airway can decrease the opening 75% vs. 19% in an adult

There should be an audible air leak at 15-20cm H2O airway pressure when applied


Trachea

Infant: the alignment is directed caudally & posteriorly

Adult: it is directed caudally

Cricoid pressure is more effective in facilitating passage of the endotracheal tube in the infant

Anatomic Differences in the Respiratory System Newborn Trachea

Distance between the bifurcation of the trachea & the vocal cords is 4-5cm

Endotracheal tube (ETT) must be carefully positioned & fixed

Because of the large size of the infant’s head the tip of the tube can move about 2cm during flexion & extension of the head

It is extremely important to check the ETT placement every time the baby’s head is moved


Tonsils & Adenoids

Grow markedly during childhood

Reach their largest size at 4-7 years & then recedes gradually

This can make visualization of the larynx more difficult


The compliant nature of the major airways of the infant are also different than adults

The diameter of infant airways changes more easily when exposed to distending or compressing forces

With obstruction at the level of the larynx, stridor will be heard mainly on inspiration

With obstruction at the level of the trachea (foreign body), stridor may be heard during both inspiration & expiration

In contrast, during lower airway obstruction (asthma or bronchiolitis), most of the collapse occurs during expiration thus producing expiratory wheeze


The configuration of the thoracic cage differs in the infant & adult Infant: ribs are horizontal & do not rise as much as an

adult’s during inspiration The diaphragm is more important in ventilation &

the consequences of abdominal distention are much greater

As the child grows (learns to stand) gravity pulls on the abdominal contents encouraging the chest wall to lengthen Now the chest cavity can be expanded by raising

the ribs into a more horizontal position


Lower Airway

Diaphragmatic & intercostal muscles of infants are more liable to fatigue than those of adults

This is due to a difference in muscle fiber type

Adult diaphragm has 60% of type I: slow twitch, high oxidative, fatigue resistant

Newborns diaphragm has 75% of type II: fast twitch, low oxidative, less energy efficient

The same pattern is seen in intercostal muscles

The newborn is more prone to respiratory fatigue & may not be able to cope when suffering from conditions that result in reduced lung compliance (RDS)

Infants & children: the distribution of pulmonary blood flow is more uniform than adults

Adults changes from base to apex because of gravity

Infants & children PAP is relatively high & the effect of gravity is less

Ventilation/Perfusion Ratio (V/Q)

V/Q changes in anesthesia

General anesthesia (GA)

FRC & diaphragmatic movements are reduced

Airway closure tends to be exaggerated & the dependent parts of the lung are poorly ventilated

Hypoxic pulmonary vasoconstriction, which diverts blood flow from areas of the lung that are under ventilated, is abolished during GA

This increases the hypoxic tendency

Physiologics differences in the Respiratory System

In General:

Rate & depth of respiration are regulated to expend the least amount of energy

At their given rates, both the infant & the adult expend about 1% of their metabolic energy in ventilation

Periodic Breathing

Can be observed in the normal newborn infant & frequently occurs during REM sleep

Manifested as rapid ventilation followed by a period of apnea of less than 10secs

During this period arterial oxygenation tension remains in the normal range

Usually not seen in healthy infants after 6 weeks of age


Apneic spells longer than 20secs are frequently seen in premature infants & are frequently associated with arterial desaturation & bradycardia

Episodes of apnea increase in frequency during stressful situations such as respiratory infection or the postanesthetic & postsurgical states

Apneic spells can be central (originating in the CNS) or obstructive (d/t upper airway obstruction)

Treatment with caffeine & theophylline has been show to be effective in reducing both types in preterm infants


Tidal Volume

7-10ml/kg

Dead Space

2-2.5ml/kg

These two measures remain constant between infants & adults


Oxygen Transport

Blood volume of a healthy newborn is 70-90ml/kg

Hemoglobin tends to be high (approx. 19g/dl)

Consisting primarily of HbF

Hb rises slightly in the first few days because of the decrease in extracellular fluid volume

Thereafter, it declines & is referred to as physiologic anemia of infancy

HbF has a greater affinity for oxygen than HgA

After birth, the total Hgb level decreases rapidly as the proportion of HbF diminishes (it can drop below 10g/dl at 2-3 months) creating the anemia

Oxygen Transport

The P-50 rapidly increases at the same time the HbF is replaced by HbA which has a high concentration of 2,3-DPG & so insures efficient oxygen off-loading at the tissues

The gradual decrease in O2 carrying capacity in the first few months of life is thus well tolerated by normal, healthy infants

There is no consensus about the lowest tolerable Hb concentration for an infant

The lowest limit will depend on factors such as duration of anemia, the acuity of blood loss, the intravascular volume & more important the impact of other conditions that might interfere with O2 transport

Oxygen Transport

Key Points

Respiratory control mechanisms are not fully developed until 42-44 weeks postconception

Most alveolar formation & elastogenesis occurs during the first year of life

The thoracic structure is insufficient to support the negative pleural pressure during the respiratory cycle until the infant develops muscle strength from upright posture around 1 year old

Key Points

Weakness of the thoracic structure is partly compensated for by contractions of the intercostal & accessory muscles

Anesthesia abolishes this compensatory mechanism & the end expiratory lung volume (FRC) decreases to the point of airway closure & alveolar collapse

Infants are prone to upper airway obstruction

Due to anatomic & physiologic differences

Anesthesia depresses pharyngeal & other neck muscles which resist the collapsing forces in the pharynx

Key Points

HbF has high oxygen affinity & limits oxygen unloading at the tissue level

This decreases O2 delivery to the tissues that have high oxygen demand

Infants & young children are prone to perioperative hypoxemia & tissue hypoxia

Renal Differences

Body Fluid Compartments

Full term infants have a large % of TBW & ECF

TBW decreases with age mainly as a result of loss of water in extracellular fluid

Renal Differences

Significance for Anesthesia Provider Higher dose of water soluble drug is needed

due to the greater volume of distribution However, due to the immaturity of clearance &

metabolism the dose given is equal to the dose used in adults

In the fetus the placenta is the excretory organ However, it still produces a large volume of

hypotonic urine & helps amniotic fluid volume It is only after birth that the kidney begins to

maintain metabolic function

Renal Differences

The healthy newborn has a complete set of nephrons at birth

The glomeruli are smaller than adults

The filtration surface related to body weight is similar

The tubules are not fully grown at birth & may not pass into the medulla

Renal Differences

Glomerular Filtration Rate (GFR)

At birth is ~30% of the adult

It increases quickly during the first two weeks, but then is relatively slow to approach the adult level by the end of the first year

Low GFR in the full term infant affects the baby’s ability to excrete saline & water loads as well as drugs

Full term infants can conserve Na+, as GFR increases so does the filtered load of Na+ increase & the ability of the proximal tubule to reabsorb the ion

In premature infants a glomerulotubular imbalance is present which may result in Na+ wastage & hyponatremia

Renal Differences

Factors that contribute to the increase in GFR

Increase in CO

Changes in renovascular resistance

Altered regional blood flow

Changes in the glomeruli

Maturation of the glomerular function is complete at 5-6 months of age

Renal Differences

Tubular Function & Permeability

Not fully mature in the term neonate & even less in the premature infant

The neonate can excrete dilute urine (50mOsm/L)

However, the rate of excretion of H2O is less & it cannot concentrate to more than 700mOsm/L (adult, 1200mOsm/L)

This is due, in part, to the lack of urea-forming solids in the diet, but mostly due to the hypotonicity of the renal medulla

Maturation of the tubules is behind that of the glomeruli

Peak renal capacity is reached at 2-3 years after which it decreases at a rate of 2.5% per year

Renal Differences

The kidney does show some response to antidiuretic hormone (ADH), but is less sensitive to ADH than the cells of mature nephrons

Diluting Capacity

Matures by 3-5 weeks postnatal age

The ability to handle a water load is reduced & the neonate may be unable to increase water excretion to compensate for excessive water intake

They are very sensitive to over hydration

In infants & children, hyponatremia occurs more frequently than hypernatremia

Renal Differences

• Creatinine– Normal value is lower in infants than in adults

• This is due to the anabolic state of the newborn & the small muscle mass relative to body weight (0.4mg/dl vs. 1mg/dl in the adult)

• Bicarbonate (NaHCO3)– Renal tubular threshold is also lower in the newborn

(20mmol/L vs. 25mmol/L in the adult)– Therefore, the infant has a lower pH, of about 7.34

• BUN– The infants urea production is reduced as a result of growth

& so the “immature” kidney is able to maintain a normal BUN

Hepatic Differences

• Glucose from the mother is the main source of energy for the fetus– Stored as fat & glycogen with storage occurring mostly in

last trimester• At 28 weeks gestation the fetus has practically no fat stored, but

by term 16% of the body is fat & 35gms of glycogen is stored

– In utero liver function is essential for fetal survival• Maintains glucose regulation, protein / lipid synthesis & drug

metabolism

• The excretory products go across the placenta & are excreted by the maternal liver

– Liver volume represents 4% of the total body weight in the neonate (2% in adult)• However, the enzyme concentration & activity are lower in the

neonatal liver

Hepatic Differences

• Glucose is the infants main source of energy

– In the 1st few hours following delivery there is a rapid drop in plasma glucose levels

• Hepatic & glycogen stores are rapidly depleted with fat becoming the principle source of energy

• The newborn should not be kept for a long period of time from enteral or IV nutrition

– The lower limit of normal for glucose is 30mg/dl in the term infant

– Infants do not usually show neurological signs & symptoms, but may develop sweating pallor or tachycardia

– A glucose level < 20mg/dl usually precipitates neurological signs such as apnea or convulsions

– Premature infants may have a tendency for hypoglycemia for weeks

Hepatic Differences

Increased hepatic metabolic activity

Occurs at about 3 months of age

Reaches a peak at 2-3 years by which time the enzymes are fully mature, then they start to decline reaching adult values at puberty

Renin, angiotensin, aldosterone, cortisol & thyroxine levels are high in the newborn & decrease in the first few weeks of life

Hepatic Differences

Physiologic Jaundice Increased concentrations of bilirubin occur in

the first few days of life This is excessive bilirubin from the breakdown of

red blood cells & deficient hepatic conjugation due to immature liver function

Treatment is phototherapy & occasionally exchange transfusions

If left untreated it can lead to encephalopathy (kernicterus)

Hepatic Differences

Coagulation At birth, Vit K dependent factors (II, VII, IX &

X) are at a level of 20-60% of the adult volume This results in prolonged prothrombin times

Synthesis of Vit K dependent factors occurs in the liver which being immature leads to relatively lower levels of these factors even with the administration of Vit K It takes several weeks for the levels of coagulation

factors to reach adult values Administration of Vit K immediately after birth is

important to prevent hemorrhagic disease

CNS Differences

The brain of the neonate is relatively large

1/10 of the weight as compared to 1/50 of adult

The brain grows rapidly

Doubles in weight by 6 months

Triples in weight by 1 year

At birth ~25% of the neonatal cells are present

By one year the development of cells in the cortex & brain stem is complete

CNS Differences

Myelination & Elaboration of Dendritic Processes Continue into the third year of life Incomplete myelinization is associated with

primitive reflexes such as motor and grasp Spinal Cord

At birth the spinal cord extends to L-3 By one year old the infant spinal cord has

assumed its permanent position at L-1

CNS Differences

Structure & Function of the Neuromuscular System Incomplete at birth

There are immature myoneural junctions & larger amount of extrajunctional receptors

Throughout Infancy: Contractile properties change The amount of muscle increases The neuromuscular junction &

acetylcholine receptors mature

CNS Differences

Junctions & Receptors

The presence of immature myoneural junctions might cause a predisposition to sensitivity

A large number of extrajunctional receptors might result in resistance

Within a short interval, (< 1 month) this variation diminishes & the myoneural junction of the infant behaves almost like that of an adult

Temperature Regulation

Body Temperature is a result of the balance between the factors leading to heat loss & gain and the distribution of heat within the body

The potential exists for unstable conditions to progress to a positive feedback cycle

The decrease in body temperature will lead to a decrease in the metabolic rate, leading to further heat loss & diminished metabolic rate

The body normally safeguards against this unstable state by increasing BMR during the initial exposure to cold or by reducing heat loss through vasoconstriction


Central Temperature Control Mechanism This is intact in the newborn

It is limited, however, by autonomic & physiologic factors Is only able to maintain a constant body temperature within

a narrow range of environmental conditions O2 consumption is at a minimum when the environmental

temp is within 3-5% (1-2°C) of body temp (an abdominal skin temp of 36°C)

This is known as the neutral thermal environment (NTE) A deviation in either direction from the NTE will increase O2

consumption An adult can sustain body temperature in an environment as cold as

0°C where as a full term infant starts developing hypothermia at about 22°C


Generation of Heat

Depends mostly on body mass

Heat loss to the environment is mainly due to surface area

Neonates have a ratio of surface area to mass about 3X’s higher than that of adults

Therefore they have difficulty regulating body temperature in a cold environment


Premature Infants & Temperature Control

Are more susceptible to environmental changes in temperature

The preemie has skin only 2-3 cells thick & has a lack of keratin

This allows for a marked increase in evaporative water loss (in extremes this can be in excess of heat production)


Important Mechanisms for Heat Production Metabolic activity Shivering Non-shivering thermogenesis

Newborns usually do not shiver Heat is produced primarily by non-shivering thermogenesis

Shivering does not occur until about 3 months of age


Non-shivering Thermogenesis Exposure to cold leads to production of Norepi

This in turn increases the metabolic activity of brown fat

Brown fat is highly specialized tissue with a great number of mitochondrial cytochromes (these are what provide the brown color)

The cells have small vacuoles of fat & are rich in sympathetic nerve endings

They are mostly in the nape & between the scapulae but some are found in the mediastinal (around the internal mammary arteries & the perirenal regions (around the kidneys & adrenals)


Once released Norepinephrine acts on the & β adrenergic receptors on the brown adipocytes This stimulates the release of lipase, which in turn splits

triglycerides into glycerol & fatty acids, thus increasing heat production

The increase in brown fat metabolism raises the proportion of CO diverted through the brown fat (sometimes as much as 25%), which in turn facilitates the direct warming of blood

The increased levels of Norepinephrine also causes peripheral vasoconstriction & mottling of the skin


Heat Loss

The major source of heat loss in the infant is through the respiratory system A 3kg infant with a Minute Volume (TV x RR) of

500ml spends 3.5cal/min to raise the temperature of inspired gases

To saturate the gases with water vapor takes an additional 12cal/min

The total represents about 10-20% of the total oxygen consumption of an infant


The sweating mechanism is present in the neonate, but is less effective than in adults

Possibly because of the immaturity of the cholinergic receptors in the sweat glands

Full term infants display structurally well developed sweat glands, but these do not function appropriately

Sweating during the first day of life is actually confined mostly to the head


Heat Exchange Review 1. Conduction:

The kinetic energy of the vibratory motion of the molecules at the surface of the skin or other exposed surfaces is transmitted to the molecules of the medium immediately adjacent to the skin Rate of transfer is related to temperature

difference between the skin & this medium

Use warm blankets, Bair huggers & warmed gel pads


2. Convection: Free movement of air over a surface

Air is warmed by exposure to the surface of the body then rises & is replaced by cooler air from the environment

Increase OR temp, radiant warmers, wrap in saran wrap, cover with blankets and/or OR drapes


3. Radiation:

Radiation emitted from the body is in the infrared region of the electromagnetic spectrum

The quantity radiated is related to the temperature of the surrounding objects

Radiation is the major mechanism of heat loss under normal conditions (same techniques to prevent as used in Convection)


4. Evaporation:

Under normal conditions ~20% of the total body heat loss is due to evaporation

This occurs both at the skin & lungs

Since the infant’s skin is thinner & more permeable than the older child’s or adult’s evaporative heat loss from the skin is greater

In the anesthetized infant the MV (relative to body weight) is high thus increasing evaporative heat loss through the respiratory system


Summary

Decreased body temperature is initially compensated for by increased metabolism

If this fails & temperature continues to decrease, regional blood flow shifts, causing a metabolic acidosis & eventually apnea

Pediatric Physiology All

Documents

Transcript of Pediatric Physiology All