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Pediatric Anatomy_ Physiology _ Pharmacology

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					Pediatric Anatomy, Physiology &
          Pharmacology
            848th FST
                 Introduction
 Of primary importance to the pediatric anesthesia
provider is the realization that infants and children
   are not simply a small adult. Their anesthetic
 management depends upon the appreciation of the
     physiologic, anatomic and pharmacologic
   differences between the varying ages and the
 variable rates of growth. Also of importance is a
      general knowledge of the psychological
development of children to enable the anesthetist to
 provide measures to reduce fear and apprehension
         related to anesthesia and surgery.
                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 Hgb (HgF) for 2,3-DPG as
    compared with adult Hgb (HgA)
  – Low concentration of 2,3-DPG in fetal blood
• O2 & 2,3-DPG compete with Hgb for binding, the
  reduced affinity of HgF for 2,3-DPG causes the
  Hgb to bind to O2 tighter
  – Higher fetal O2 saturation
               Fetal Circulation
• P50 is 27mmHg for adult Hgb, but only 20mmHg
  for fetal Hgb
   – 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, HgF
  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)
         Fetal Circulatory Flow
• 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
         Fetal Circulatory Flow
• 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
         Fetal Circulatory Flow
• 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”
Fetal Circulatory Flow
Fetal Circulatory Flow
       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
       Fetal Circulatory Flow
• 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
      Transitional & Neonatal
            Circulation
• 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
    Transitional & Neonatal
          Circulation
– 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
       Transitional & Neonatal
             Circulation
• 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
Transitional & Neonatal
      Circulation
Transitional & Neonatal
      Circulation
          Persistent Pulmonary
          Hypertension (PPHN)
• In 1969 a syndrome of central cyanosis was
  observed in neonates who had no:
   – Parenchymal pulmonary disease
   – Abnormal intracardiac relationships
   – Structural heart disease
• The syndrome was called persistent fetal
  circulation (PFC) & was identified by:
   – Increased PVR
   – Patent foramen ovale
   – Patent ductus arteriosus
         Persistent Pulmonary
         Hypertension (PPHN)
• A failure of the newborn’s circulation system to
  change from normal intrauterine to extrauterine
  patterns results in an abnormal shunting of blood
  from right to left via persistent fetal pathways
• However, because the placenta is no longer in
  continuity with the newborn’s cardiovascular
  system
   – The condition is not really persistence of the fetal
     circulation
   – Therefore, the syndrome is more accurately referred to
     as persistent pulmonary hypertension of the newborn
     (PPHN)
Persistent Pulmonary
Hypertension (PPHN)
Persistent Pulmonary
Hypertension (PPHN)
          Persistent Pulmonary
          Hypertension (PPHN)
• Treatment
  –   Optimal oxygenation
  –   Hyperventilation
  –   Sedation
  –   Paralysis
  –   Extracorporeal membrane oxygenation
      (ECMO)
       • Reserved for severe & persistent cases only
          Persistent Pulmonary
          Hypertension (PPHN)
• Implications for Anesthesia:
   – Pathophysiologic mechanisms that trigger this
     condition
      • Hypercarbia
      • Acidosis
   – Arterial Blood Sampling
      • Right radial artery or temporal arteries
          – More meaningful since these areas reflect the values in the blood
            reaching the brain & coronary arteries
      • Left radial artery
          – May be misleading because the left subclavian is very close to
            the ductus
   – Pulse Oximeter Probes
      • Should be placed on right upper limb or head
Closure of the Ductus Arteriosus,
   Foramen Ovale & Ductus
             Venosus
            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
   Persistent Ductus Arteriosus
• Also referred to as Pathologic PDA
  – Requires surgical closure & differs from the
    normal ductus in tissue structure
  – The PDA in the preterm infant is due to a weak
    vasoconstrictor response to O2 and should be
    considered a normal not pathologic response
     • This PDA may still need surgical correction
     • A left to right shunt through the ductus can flood the
       lungs of the premature infant prolonging mechanical
       ventilation, eventually leading to pulmonary edema
       & right sided heart failure
   Persistent Ductus Arteriosus
• Anesthetic Considerations
  – Excessive fluids may reopen a ductus or permit
    excessive left to right shunting through an
    already open ductus
  – Intraoperative short falls
     •   Strict fluid management
     •   Attention to acid base balance
     •   Oxygenation
     •   Ventilation
          – All are very important in premature infants to avoid
            reopening the ductus & causing CHF
   Persistent Ductus Arteriosus
• A PDA may also be beneficial
  – In cyanotic congenital heart malformations with right to
    left & decreased pulmonary blood flow
     • The PDA may be the major route by which the blood reaches
       the pulmonary arteries to receive O2
     • In this case closure of the DA causes severe cyanosis, tissue
       hypoxia & acidemia
     • To keep the ductus open prior to palliative or corrective
       surgery of the heart malformation, PGE 1 (0.05-
       0.1mcg/kg/min) can be administered IV
     • To help close the ductus prior to surgical intervention to ligate
       the PDA, Indomethacin (0.1-0.2mg/kg) can be administered
         – This is an inhibitor of PGE synthesis
                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
Cardiovascular Differences in the
             Infant
• 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
Cardiovascular Differences in the
             Infant
• 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
Cardiovascular Differences in the
             Infant
 – 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
Cardiovascular Differences in the
             Infant
• 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                       • Parasympathetic
  innervation of the                  innervation has been
  heart is incomplete at              shown to be complete
  birth with decreased                at birth therefore we
  cardiac catecholamine               see an increased
  stores & it has an                  sensitivity to vagal
  increased sensitivity to            stimulation
  exogenous
  norepinephrine
   – It does not mature until 4-6
     months of age
 Autonomic Control of the Heart
• The imbalance between sympathetic &
  parasympathetic tone predisposes the infant
  to bradycardia
  – Anything that activates the parasympathetic
    nervous system such as anesthetic overdose,
    hypoxia or administration of Anectine can lead
    to bradycardia
  – If bradycardia develops in neonates & infants
    always check oxygenation first
 Autonomic Control of the Heart
• Atropine may inhibit vagal stimulation
  – Is always given prior to, or at the same time,
    that Anectine is given or anytime that vagal
    stimulation will be present such as in an awake
    intubation
     • Dose of Atropine is 20mcg/kg where the minimum
       dose for children is 0.1mg
        – Anything less than 0.1mg can cause paradoxical
          bradycardia which may occur secondary to a dose
          dependent (low dose) central vagal stimulating effect of
          the drug
                 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
   Anatomic Differences in the
      Respiratory System
• 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
   Anatomic Differences in the
      Respiratory System
• 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
    Anatomic Differences in the
       Respiratory System
• 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
    Anatomic Differences in the
       Respiratory System
• 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
Anatomic Differences in the
   Respiratory System
Anatomic Differences in the
   Respiratory System
Anatomic Differences in the
   Respiratory System
    Anatomic Differences in the
       Respiratory System
• 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
Anatomic Differences in the
   Respiratory System
   Anatomic Differences in the
      Respiratory System
• 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
Anatomic Differences in the
   Respiratory System
Anatomic Differences in the
   Respiratory System
   Anatomic Differences in the
      Respiratory System
• 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
    Anatomic Differences in the
       Respiratory System
• 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
   Anatomic Differences in the
      Respiratory System
• 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
   Anatomic Differences in the
      Respiratory System
• 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)
   Anatomic Differences in the
      Respiratory System
• Ventilation/Perfusion Ratio (V/Q)
  – 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
   Anatomic Differences in the
      Respiratory System
• 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
   Anatomic 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
   Anatomic Differences in the
      Respiratory System
• 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
 Anatomic Differences in the
    Respiratory System
– 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
   Anatomic Differences in the
      Respiratory System
• 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 HgF
  – Hgb 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
  – HgF has a greater affinity for oxygen than HgA
  – After birth, the total Hgb level decreases rapidly as the
    proportion of HgF 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 HgF is
  replaced by HgA 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 Hgb
  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
• HgF 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
           Airway Management
• The technique of endotracheal intubation in the
  neonate & small infant differs from that in the
  adult because of the baby’s anatomical features
   – The large head & short neck may necessitate the need
     for a shoulder roll
   – The angle of the jaw is about 140° (adult is 120°)
   – The epiglottis is more “U” shaped, usually resembling
     the Greek letter omega
      • The epiglottis also protrudes over the larynx at a 45° angle
   – The larynx of an infant is high & has an anterior
     inclination
      • Straight (Miller or Phillips) blade is usually the best choice
      • The view can be markedly improved by applying cricoid
        pressure
           Airway Management
• Selection of Endotracheal Tube Size
  – Diameter
     • Greater than 2 years old
          – In millimeters=Age+16÷4
          – In french=Age+18
     •   12-24 months=4.0
     •   6-12 months=3.5-4.0
     •   Newborn-6 months=3.0-3.5
     •   Premie=2.0-3.0
  – Cuffed tubes
     • After 8 years old add 2 Fr. sizes to diameter
           Airway Management
• Distance or Depth to
  Tape Tube
   – If older than 2 years
      • Age÷2+12
   – If younger than 2 years
      • 1-2-3-4 kg then it is
        taped at 7-8-9-10cm
        respectively
      • Newborn to 6 months =
        10cm
      • 6 to 12 months = 11cm
      • 1 to 2 years = 12cm
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
Temperature Regulation
      Temperature Regulation
• 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
      Temperature Regulation
• 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
      Temperature Regulation
• 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)
      Temperature Regulation
• 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
      Temperature Regulation
• 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)
    Temperature Regulation
– Once released Norepi acts on the alpha & beta
  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 Norepi also causes
  peripheral vasoconstriction & mottling of the skin
Temperature Regulation
      Temperature Regulation
• Heat Loss
  – The major source of heat loss in the infant is
    through the respiratory system
     • A 3kg infant with a MV 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
    Temperature Regulation
– 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
      Temperature Regulation
• 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
    Temperature Regulation
– 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
      Temperature Regulation
• 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
  Pharmacological Differences
   with Inhalation Anesthetics
• Review
  – Factors that determine uptake & distribution of
    inhaled agents
     • Factors that determine the rate of delivery of gas to
       the lungs
        – Inspired concentration
        – Alveolar ventilation
        – FRC
     • Factors that determine the rate of uptake of the
       anesthetic from the lung
        – CO
        – Solubility of the agent
        – Alveolar-to-venous partial pressure gradient
   Pharmacological Differences
    with Inhalation Anesthetics
• In children there is a more rapid rise from
  inspired partial pressure to alveolar partial
  pressure than in adults
  – This is due to 4 differences between children &
    adults
     • 1. The ratio of alveolar ventilation to FRC
        – This a measure of the rate of “wash-in” of the anesthetic
          into the alveoli
        – In the neonate the ration is 5:1 compared to adults of 1.5:1
Pharmacological Differences
 with Inhalation Anesthetics
 • 2. There is a higher proportion of CO distributed to
   the VRG in the child
    – In adults an increase in CO slows the rate of rise in
      alveolar to inspired partial pressure, but in neonates it
      speeds the rate of induction because the CO is
      preferentially distributed to the VRG
    – The VRG constitutes 18% of the body weight of the
      neonate as opposed to only 6% in adults
    – Therefore, the partial pressure in the VRG (which includes
      the brain) equilibrates faster with the alveolar partial
      pressure
Pharmacological Differences
 with Inhalation Anesthetics
 • 3. Neonates have a lower blood/gas solubility of
   inhaled anesthetics (the less soluble the greater the
   amount that remains in the alveolus
    – This allows a more rapid rise in the alveolar to inspired
      partial pressure
 • 4. Neonates have a lower tissue/blood solubility of
   inhaled anesthetics
    – Less agent is removed from the blood therefore the partial
      pressure of the agent in the blood returning to the lungs
      increases
    Pharmacological Differences
     with Inhalation Anesthetics




•There are age related differences in MAC of inhalation
agents
Questions