PAEDIATRIC ANATOMY & PHYSIOLOGY:

ANAESTHETIC IMPLICATIONS

DR KANTA M RAHUL
SENIOR CONSULTANT & COORDINATOR
BLK MAX SUPERSPECIALITY HOSPITAL
NEW DELHI
 INTRODUCTION

CHILDREN ARE NOT MINI ADULTS

 Pediatric anatomy and physiology exhibit distinct characteristics compared to
adults,influencing drug metabolism, fluid dynamics, and response to
anesthesia.
 Developmental differences necessitate tailored approaches to anesthesia
management, including drug selection, dosing considerations, and monitoring
parameters
 Understanding these is key to the safe administration of anaesthesia care in
paediatric age group
 INTRAUTERINE DEVELOPMENT

 Intrauterine development starts from conception to birth

Divided into
 1) Germinal stage : conception to 2 weeks( embryo implantation )
Key feature → Formation of placenta
Genetic/ environmental factors may interfere with implantation → Loss of preg
 2) Embronic stage – 3’rd – 8’th weeks POG
Key feature → intense cell proliferation, migration & differentiation → formation of
major organs
↑ vulnerability to teratogens → Congenital defects ( May/may not be compatible with
life )
 Fetal stage : 9’th week- birth

Key feature : Growth & functional differentiation of the organs formed during the
embryonic stage.
Toxins, radiation, maternal infections, drugs- interfere with organ development →
Organ D/F of varying degree

Anaesthetic imp: - Congenital anamolies@ birth

Organ D/F of varies degrees ( Cong PUV- Hydronephrosis, deranged
kidney function )
Growth period
 Neonate - birth -28days of life
 Infant- birth-1 year of age
 Toddler-1-3 years of age
 Preschool-3- 5years of age
 Child: 1year - 12 years of age
 Adolescent: 13 -16 years
 Period of gestation Birth weight
Compatibility with life – 22-26’th week Normal – 2500-4200 gm
Full term- 37-42 week of gestation Low birth weight <2500 gm
Mild preterm- 32-37 weeks V low birth weight <1500 gm
Very preterm- 28-31 weeks Extremely low birth weight < 1000 gm
Extremely preterm- < 28 weeks Further divided into
Post term: born after 42 weeks of GA 1)AGA
2)SGA
3)LGA
 Cardiovascular System

 To understand the changes occurring in the cardiovascular

physiology of the newborn, one must first understand
intrauterine fetal circulation and the shunts involved, which
include the ductus venosus, foramen ovale, and ductus
arteriosus
 Fetal Circulation
SPO2 40-45%

SPO2- 55%
SPO2-65%
SPO2 40-45%

SPO2-70-80%
 FETAL CIRCULATION

 It is a parallel system in which both the ventricles pump most of their blood into systemic
circulation.
 Placenta (80% saturated) → ductus venosus → inferior vena cava (receives 25% saturated blood
from lower body) →right atrium(67% saturated)→FORAMEN OVALE →left atrium →left
ventricle →upper half of the body.
 Upper half of the body →superior vena cava → right atrium →right ventricle (due to its anatomy)
 Blood flows then into pulmonary artery. Because of high resistance, 95% of the ejected blood
from RV (60% saturated) is shunted across the ductus arteriosus, into the descending aorta, and
back to the placenta and lower body.
 The pulmonary vascular resistance is high in utero because of alveolar collapse. Other factors
responsible for high pulmonary vascular resistance include the relatively low PaO2 and pH of the
blood flowing through the vessels.
 PHYSIOLOGICAL TRANSITION OF THE FETUS AT BIRTH
↓ Pulmonary Vascular Resistance & ↑ Systemic Vascular Resistance

 Lung expansion increases both alveolar and arterial oxygen tensions and decreases pulmonary
vascular resistance.
 This acts as a potent stimulus for PA vasodilatation which augments the flow to the LA. THIS
INCREASED PRESSURE IN LA CLOSES THE FORAMEN OVALE.
 THE INCREASED ARTERIAL TENSION ALSO CAUSES THE DUCTUS ARTERIOSUS TO
CONTRACT AND FUCTIONALLY CLOSE.

 THUS ADULT CIRCUALRTION IS ESTABLISHED.

TRANSITIONAL CIRCULATION / FLIP-FLOP
CIRCULATION

3 connections between right and left side of circulation

Connection Functional closure Structural closure

Ductus venosus Soon after birth 3-7 days

Foramen ovale Soon after birth 3 months -1yr

Ductus arteriosus Soon after birth 2 months

 Transitional Circulation

 During this critical period, the infant can readily revert from the adult type of
circulation to a fetal type of circulation; this state is called transitional
circulation. When such a flip-flop occurs, pulmonary artery pressure increases to
systemic levels.

 Risk factors :prematurity, infection, acidosis, pulmonary disease resulting in

hypercapnia or hypoxemia (aspiration of meconium),
 hypothermia, and congenital heart disease.

 Care must be directed to keeping the infant warm, maintaining normal

arterial oxygen and carbon dioxide tensions, and minimizing the effects of
anesthetic induced myocardial depression for newborns requiring
anesthesia.
 Cardiovascular system

1) Myocardium:
 Neonatal myocardium1) more connective tissue
2)less contractile protein
3) ↓ intracellular calciul influx & sensitivity( Immature SR)

↓
limited cardiac contractility
2) Cardiac output = SV X HR ( High in neonates ⁓ 200 ml/kg/min)

Therefore , HR is the primary determinant of CO →bradycardia is poorly

tolerated
Excessive tachy is also detrimental by limiting diastolic filling & SV → ↓ CO &↑
Myocardial Oxygen demand
Therefore, both bradycardia & excessive tachy are detrimental for CO
(Normal HR in newborn – 120-180/min)
3)Vasomotor tone :

Autonomic innervation of heart & peripheral vasculature @ Birth is primarily

PARASYMPATHETIC with sparse innervation by symp sys → High vagal tone
INITIAL RESPONSE to any stress → BRADYCARDIA ( Parasympathetic )
Bradycardia M/c seen as a response to Laryngoscopy, Hypoxia, Hypotension, Hypovol
 Baroreceptor mech – weak
 Catecholamine stores – small & inadequate
 Stress response is blunted
Vasoconstrictive response to vol loss are weak- cannot tolerate blood loss
As the child matures sympathetic system takes over
Respiratory System
 EXTERNAL APPEARANCE:

 Large head and prominent occiput- Proper positioning:

place a pad under neck and shoulders and a large ring
under the occiput
 Short neck is more prone for airway obstruction during
sleep
Gentle mask holding with minimal pressure on soft tissue
 Small chin
 Small nostrils – airway resistance increases;
Get blocked easily by secretions
Gets injured easily ( avoid nasal instrumentation )
 Airway Anatomy

 Tongue is large for the oropharynx and visibility is reduced

during laryngoscopy
 Epiglottis – Large, floppy, omega shaped falls posteriorly
over the laryngeal inlet
 Larynx is funnel shaped with the narrowest part at the
cricoid cartilage
Located higher and anterior in the neck at the level of C 3-4
compared to C4-5 in adults
-External manipulation , BURP for L’scopy & intub
 Shorter & narrow hypopharynx – Supraglottic
AW placement,
pooling of secretions in retropharyngeal space
 Vocal cords are angled
 Trachea is short: 4-9 cm with 4-5mm diameter
in newborn.
 Rt & lt bronchus bifurcates @ same angle 45
deg till 3 yrs of age
 Small amount of narrowing subglottic region (due to edema, inflammation, etc.,) -
Sev consequences

Resistance to flow in airway – edema/stenosis

Poiseulle's law: R =8ƞL/πr4.

→ Selection of size/type of tube- ETT may pass the

VC but may get stuck @ cricoid

Cricoid ring is the ‘ACHILLES HEEL’ Of the

paediatric airway
 L’SCOPY & INTUBATION

 Straight blades are useful than curved blades- LIFTS UP THE EPIGOTTIS
 A blindly passed tube can get lodged into the anterior commissure
 A tracheal tube which easily crosses the vocal cords may be tight in the
subglottic region
 Uncuffed tubes preferred for children younger than 6 years age
 Newer Microcuff tubes – high vol, low pressure
 Leak should be maintained around the cuff to avoid injury to mucosa
 Endobronchial intubation and accidental extubation are more common
 The tube should sit 1cm above the carina and taped securely
 RESPIRATORY SYSTEM

 At term, complete development of surface active proteins help

maintain patency of airways
 Only 10% of the total number of alveoli found in adults present.
 Alveoli increase in number and size until the child is approximately 8
years old
 Both pulmonary airways and vascular system mature to allow gaseous
exchange
 The airway and chest wall are highly compliant. Horizontally placed,
soft , pliant ribs prevent the bucket handle action seen in adults.
 intercostal musc- poorly dev. Ventilation is primarily diaphragmatic,
 Fatigue resistant type 1 muscle fibres are deficient in infants- develop
only by 2 years of age
 Normal Pulmonary indices
Index Neonate Adult
O2 consumtion( ml/kg/min 6.4 3.5

CO2 prod (ml/kg/min) 6 3

Alv vent (ml/kg/min) 130 60
RR ( breaths/min) 35 15
MV (ml/kg/min) 200 90
TV (ml/kg) 6 7
VC (ml/kg) 35 70
CC( ml/kg) 35 23
FRC (ml/kg) 30 34
FRC/Alv vent Ratio 0.23 0.57
TLC ( ml/kg) 63 86
 Anaesthetic Implications

 Limited respiratory reserve

 Highly compliant airways and chest wall →poorly maintained negative intrathoracic pr.
 FRC is low. After anesthesia it falls below the closing capacity causing small airway closure,
atelectasis, and desaturation. CPAP or PEEP is required to prevent airway collapse
 Work of breathing is 3 times higher than adults. Oxygen consumption is higher
(7ml/kg/min). Minute ventilation also increases 200ml/kg/min for the demand
 Little scope ↑ tidal volume (constant 6 ml/kg). Compensated by ↑RR (20-60 breaths/min)
 Any ↑WOB →easy muscle fatigue → apnoea and rapid desaturation with airway obstruction
 Neonates, infants, and young children have relatively greater AV and ↓ FRC compared with
older children and adults. This greater minute ventilation-to-FRC ratio →rapid increase in
alveolar anesthetic concentration.
 RESPIRATORY CONTROL

 Hypoxic and hypercapneic drives are not well developed

 Apnoea can occur in all children who are predisposed to upper airway obstruction which
can be aggravated by anaesthetics, opioids, sedatives- Obstructive apnoea
 Periodic breathing ie. Rhythmic breathing interspersed with a series of short apneic
spells lasting less than 10 seconds without cyanosis or bradycardia can occur during sleep
and wakefulness.
 Central apnoea – cessation of breathing lasts longer than 15-20 seconds or shorter apnoea
with cyanosis/pallor/ bradycardia(HR<100) ( immature resp centre)
 Immature respiratory control, inc muscle fatigue →postoperative apnoea esp in
premature infants upto POG 56 weeks, <44 weeks gestational age with history of apnoea
 Other risk factors include extent of surgery, anesthetic techniques, postoperative
hypoxemia and anemia
 Central Nervous System

 New born brain weighs – 350-400 gm (1/4 of adult brain) – 90% of adult weight by 5
yrs
 Neonate – soft , pliable cranium ,
Non fused surtures ,
Two open fontanelle ( Anterior close by 18 mnths, posterior close by 6-9 mnths )
 Cerebral cortex- poorly developed BBB- immature @ birth but mature soon after
 BBB- immature Is permeable to large lipid sol molecules e.g volatile anaesthetics,
free bilirubin, barbiturates, opiods
 Rapid washin & washout of inhalational agents → clinical effect @ lower conc:
 Opioids appear to be more potent in neonates than in older children and adults
 Cereberovascular responsiveness to ↑ CO2 or ↓ O2 tension is attenuated in neonates.

 Cerebral autoregulation is present and functional from birth

 Cerebral vessels are thin walled and fragile - more prone for intraventricular hemorrhages

 Perception of pain/ noxious stimuli – Starts as early as 6 weeks of gest

Both premature & mature newborns show strong pain behaviour that is more diffuse & untuned
compared to older children .

Evidence →Early pain experience even if unconscious , might alter subsequent CNS func &
adequate pain relief can improve the out come
 Spinal cord

 Lower termination of spinal cord (L3-4)

 Lower projection of dural sac (S3-4)
 Delayed myelinization of nerve fibers
 Cartilaginous structure of bones and vertebrae
 Lack of fusion of sacral vertebrae
 Increased fluidity of epidural fat
 Loose attachment of sheaths and aponeuroses to underlying structures

Anaesthetic implications – SAB – lower space -L4-5

Dosage of drug
Caudal block
 Hepatic Anatomy & physiology

 Anatomy – Largest gland , 4% of BW in children compared to 2.5-3.5 % in adults

 Hepatic function is immature @ birth
 Carbohydrate reserves in liver, accumulate primarily in 3’rd trimester → Low
reserves esp in preterm – Gluconeogenesis mechanisms are immature → req 10%
dextrose infusion to prevent hypogycemia leading to neurological damage
Significant Hypogycemia –During first 3 days of life
Term Neonate < 30 mg/dL, Preterm Neonate < 20 mg/dL,
AFTER 3 DAYS – Hypoglycemia < 40 mg/dL
T/T- 0.5 -1 gm/kg bolus IV f/b infusion 5-6 mg/kg/min
Serial blood glucose monitoring
 Protein Metabolism – Protein production low, becomes normal by 1 yr of age
a)↓ drug binding to proteins( alb, α- glycoprotein) → High free fraction ( opiods, LA)
b) ↓drug metabolism → prolonged duration of drugs
Therefore, dosage of drugs to be ↓ed & interval b/w supplementation to be ↑ed
 Bilirubin Metabolism - @ birth S. Bil is high ( 17-20 gm%) → normalizes by 1 mnth
Liver is unable to conjugate bilirubin. Unconj fraction can cross BBB – kernicterus @
low levels of 12-13 %
 Synthethic Action: Deficiency of Vit K Dependent factors ( II/VII/IX/X)( full tern
neonate -20-60% of adult value ) → prolongation of PT → Parenteral Vit K reqd @
birth
 Hepatic metabolism of Drugs - Biotransformation of many drugs slower in neonates
 Enzyme systems for drug metabolism are developed but not yet stimulated
 As hepatic blood flow increases and enzyme systems are induced, drugs are rapidly
metabolized.
 Phase I reactions are relatively more developed than phase II
 Activity of Phase 1( Oxidation/reduction/hydrolysis) ,matures by 6 mnths of age
 Activity of Phase II ( Conjugation) ,mature by 1 yr
 ↑Elimination half life of drugs
 Slow drug metab → ↑Adverse effects of drugs + Risk of hepatotoxicity of immature
liver
 THE GASTROINTESTINAL SYSTEM

 At birth, gastric pH is alkalotic, by second day of life pH is in normal physiological

range.
 The ability to coordinate swallowing with respiration does not fully mature until infants
are 4 to 5 months of age.
 Thus there is high incidence of gastroesophageal reflux, particularly in preterm newborn.

 Bulky abdominal organs or a stomach filled with gases from poor Mask Vent
can impinge on the contents of the chest and splint the diaphragm, reducing the ability
to ventilate adequately.
Can regurgitate the gastric contents (Low GE junc tone )
 Renal System
Immature @ Birth- ↓ GFR ( 30% adult value )
↓ RBF( 5% of CO @ birth, adults- 25% of CO)
Poor tubular function ( Adult level by 1 yr )
 Neonate- Limited ability to concentrate urine (1/3rd of adult levels ) -Obligate Sodium losers
Cannot deal with solute loads, dehydration
 Limited ability to excrete large water load – matures by 6 wks – Cannot deal with vol overload
 Cannot conserve Bicarb- prone for acidosis
 ↓GFR, RBF, Tubular func→ ↑Elimination half life of drug with renal excretin- prolonged
action ( Musc relaxants , opiods antibiotics)
 Fluid administration should be carefully titrated and monitored
 Atrac preferred for musc relaxation
 INTRAVENOUS FLUID THERAPY

 Hypovolemia, often underestimated, is the most common cause of perioperative cardiac

arrest in children.
 The three major goals of perioperative fluid management are
(1)to meet maintenance requirements
(2)to replace preoperative deficits
(3)to compensate for ongoing losses occurring during the perioperative period.

 One of the simplest options to decrease preoperative fluid deficits is to minimize

preoperative fasting times for clear liquids.
 FASTING
 Infants and young children have a higher
metabolic rate and a larger body surface area-
to-weight ratio than adults and more easily
become dehydrated than adults.
 The major advantage of the liberalized fasting
guidelines may be a reduced incidence of
hypovolemia at the time of anesthesia
induction.
 Total Body Water, Blood Volume

 TBW- Higher in neonates comp to adults ( 80% of BW)

 Blood Vol- Also higher in neonates (85-100 ml/kg)

Category TBW& its distribution Blood Vol

(ICF:ECF)
Neonates 80-85%of BW 85-100 ml/kg
Full term 80 %(1:1) 85 ml/kg
Preterm 90 %( 1:3) 90-100 ml/kg
4 years 60% (2:1) 60-70 ml/kg
Adults 60% (2:1) 60 ml/kg
Anaesthetic implications:
 High TBW & proportion of ECF- Higher vol of distribution (Vd)of
drugs
 High Vd- Double edged sword
Greater dil of IV drugs ( Induction agents , opiods, musc relaxants )-
Lower serum conc → Higher doses needed for desired effect – prolonged
action & recovery time

 Immature hepatic & renal system further add to prolonged DOA

 Haematological system

 Hemoglobin- Term neonate - 16-20 gm ( 60 %

HbF)
 HbF- higher affinity for O2- Shifting of ODC to left
(P50-19 mm Hg)
 Low 2.3 DPG – Further shifts ODC to left( HbF less
affinity to 2,3 DPG
 Normal HbA conc by 6 mnths of age
Implications- PO2 ≤ 90 mmHg 3 ml of O2 released in
newborn Vs 4.6 ml in adults ( Offset by ↑Hb, Red cell
vol & CO)
 HCt- @ birth – 55% ,Falls to 40% by 2-4 mnths
 Transfusion recommended @ loss of 15% of circulatory vol
 Maintain the hematocrit values in the 20%-25% range
 High incidence of apnea in neonates and preterm infants d/t anaemia
 Allowable Blood Loss :
Estimated Blood Volume X ( Initial Hct- Acceptable Hct) / Initial Hct
For IVF Maintainanace- Holliday & Segar Formula
Losses -mild( 1-2 ml/kg) /mod ( 4-7 ml/kg ) /sev ( 8-10 ml/kg )
Fluid of choice: Ringer lactate
Adequacy: stable blood pressure, heart rate, adequate tissue perfusion, urine output of 1-2
ml/kg/hr
 Thermoregulation

Heat loss if profound in neonate d/t

1)Large ratio of body surface area to weight( 1400 cm/kg Vs 250 cm/kg in adults )
2) Thin skin, limited subcutaneous tissue
3) Minimal motor activity → Leads to inability to cope with cold stress
Heat loss occurs through 4 mechanisms
1) Conduction losses
2) Radiation
3) Convection
4) Evaporation
 WHY temp monitoring is a MUST in children?

 ↓ in temp below thermoneutrality level-→ ↑O2 & Glucose consumption , acidemia ,↓

cardiac output, ↑ risk of infection, ↓ enzymatic activity
 May ppt L→ R shunt
Thermoregulation
 Neonate preserve heat by peripheral vasoconstriction( similar to adults)
BUT THEY CANNOT SHIVER
 Depend Non shivering thermogenesis for 1st 3 months of life
Highly oxidative mech produces heat by burning of brown fat through nor epinephrine dep
pathway
 Brown fat – 5% of BW in newborns
Location of Brown fat- Around kidneys, interscapular region, nuchal area

Management of Hypothermia – Preventive & corrective

 Preventing heat loss by
Conduction: warm the surgical unit and place the baby on a warm mattress
Ambient temperature: 34°c for premature infant,
32°c for neonates,
28°c for adolescents
Convection: incubators and warm blankets
Radiation: using double shelled isolette during transport
Evaporation: humidification of inspired gases and using plastic wrap to decrease
water loss through skin
Temp monitoring is a must
 PSYCHOLOGY

• Infants less than 6 months of age are not usually upset by separation from their parents
and will more readily accept a stranger.
• Children up to 4 years of age are upset by the separation from their parents and the
unfamiliar people and surroundings. It is difficult to rationalise with a child of this age.
The behaviour of this group is more unpredictable.
• School age children are more upset by the surgical procedure, its mutilating effects and
the possibility of pain.
• Adolescents fear narcosis and pain, the loss of control and the possibility of not being
able to cope with the illness. This is worsened by long periods of hospitalisation.
• Parental anxiety is readily perceived and reacted on by the child.
 PRACTICALITIES FOR ANAESTHETISING CHILDREN

1. Pre-operative Visit
 Use this time to develop rapport and trust with the child and parent.
 It is important to take a medical and anaesthetic history.
• Any previous problems with anaesthetics
• Allergies
• Previous medical problems including congenital anomalies
• Recent respiratory illness
• Current medications
• Recent immunisations
• Fasting times
• Presence of loose teeth.
 Conduct a physical examination as appropriate , concentrating on the airway and
cardiorespiratory systems.
 Children must be weighed. All drug doses relate to body weight.
 Investigations

2. FASTING
3.PREMEDICATION
 Premedication is not normally necessary for the average 6-month-old infant
Seperation anxiety >8 mnths
 M/C Oral midazolam - 0.25 to 0.5 mg/kg( Max- 20 mg)
 Ketamine (2 to 4 mg/kg)I/M - children who refuse oral premedication
 Intranasal Dexmedetomidine – 1-2 mcg/kg
 Chloral hydrate 50 mg/kg orally to a maximum of 1g.
 Anticholinergic drugs are not routinely administered
 OT prep
 Warm the theatre and prepare any warming devices.
 Prepare emergency drugs
 Have your equipment ready and checked.
Induction of Anaesthesia
 An inhalational induction can be an excellent technique for the child that fears needles or has
difficult venous access.
 Halothane and sevoflurane are the agents of choice for gaseous induction.
 Intravenous induction can be undertaken with propofol, thiopentone or ketamine.
 Preoxygenation for a rapid sequence induction can be difficult in small children and should be
undertaken if able.
Intubation
• Straight Magill blades are useful in neonates and infants.
• A curved blade is usually easier once the child is 6-10 kg.
• Uncuffed tubes are used until 6 years of age.
• A small leak should be present. The leak is too large if it
compromises ventilation.
• Newer Microcuff tubes – High vol , low pressure cuffs
• Cuff pressure should be adjusted to ensure that a small leak
around the cuff at a peak inflation pressure of 20 to 30 cm
H2O.
• Tube size
 Supraglottic Airway

LMA SIZE WEIGHT

1 0-5 kg
1.5 5-10 kg
2 10-20 kg
2.5 20-30 kg
3 30-50 kg
4 50-70 kg
5 >70 kg
 Maintenance & recovery

• Add regional analgesia where necessary

• NDMR- Atrac preferred
• Intravenous narcotics – caution in especially ex-premature infants and neonates.
• Fluid Replacement – Fasting & losses . Transfusion if indicated
• Monitoring: HR, NIBP, SPO2, TEMP, ETCO2
• Extubation- Fully Awake ,
• Emergence delirium
• Monitoring in PACU
• Early feeds- better outcome
 Conclusion

Integration of knowledge about pediatric anatomy, physiology, and

anesthesia fundamentals forms the foundation for safe and effective
perioperative care in pediatric patients.

By recognizing the unique needs and characteristics of pediatric patients,

anesthesia providers can deliver tailored anesthesia management strategies
that prioritize patient safety, optimize outcomes, and enhance the overall
perioperative experience for pediatric patients and their families.
Thank You
 Muscle Relaxants

 Faster onset (up to 50% less delay) d/t shorter circulation times than in adults.
 DEPOLARISING MUSCLE RELAXANTS: ↑Vd -Dose higher in infants (2–3 mg/kg)
 Children are more susceptible than adults to cardiac arrhythmias, hyperkalemia, and malignant hyperthermia
 Succinylcholine has long been avoided for routine, elective paralysis for intubation in children and
adolescents.
 NDMR: The response of neonates to nondepolarizing muscle relaxants is variable
Immaturity of the neuromuscular junction tending to increase sensitivity (unproven)
Larger extracellular compartment, reducing drug concentrations (proven).
 Maturity of neonatal hepatic & renal sys :Atracurium and cisatracurium do not depend on hepatic
biotransformation and reliably behave as intermediate-acting muscle relaxants.
 Inhalational anesthetics

 Neonates, infants, and young children - ↑Minute ventilation-to-FRC ratio → rapid increase
in alveolar anesthetic concentration.
 MAC for volatile anesthetics is greater in infants than in neonates and adults.
 BP of neonates and infants appears to be esp sensitive to volatile anesthetics d/t less-well-
developed compensatory mechanisms (eg, vasoconstriction, tachycardia) and greater
sensitivity of the immature myocardium.
 Cardiovascular depression, bradycardia, and arrhythmias are less frequent with sevoflurane
than with halothane.
 Sevoflurane and halothane ↓ Airway irritation → inhalational induction .
 Desflurane or sevoflurane -Emergence fast BUT asso with emergence delirium.