Anesthesia for neurosurgery

Melaku B
Debre Berhan University
November 2016 EC
 Outline
 Introduction

 Neuroanatomy

 Cerebrospinal fluid

 Cerebral metabolic rate

 Cerebral blood flow

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 Objectives
After this lesson you will be able to:

 Describe the anatomy of central nervous system

 Explain secretion, absorption and function of CSF

 Clarify basic physiology of brain (CMRO2, CBF)

 Explain factors which affect CBF, CMRO2 and ICP

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 Introduction
 Brain is the basis of who we are as human being & also as a unique

individual.

 It weights 1.4 kg and accounts only 2% of the total body weight.

 The physiology of brain is mysterious and its anatomy is extraordinarily

confusing.

 Anesthetic agents may have profound effects on CMRO2, CBF, CSF

dynamics, CBV & CPP.

 So it is vital to understand the anatomy & physiology of brain and factors

which affect its physiology.

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 Peculiarities of brain
 Brain receives

 15% of cardiac output(50ml/100g/min or 750ml/min)

 20% of total O2 consumption(3-3.8ml/100g/min)

 25% of glucose consumption(5mg/100g/min)

 Brain

 Does not have oxygen store

 Does not undergo anaerobic metabolism

 Does not have pain sensation

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6 Neurophysiology and anesthesia 1/18/2024
 Neuro-anatomy
 CNS is composed of brain and spinal cord

 Brain: covered by cranium, bony compartment

 It is divided in to two:- supra and infratentorium

 Supratentorium composed of paired cerebral hemisphere & diencephalon

 Each hemisphere are divided into four lobes(frontal, parietal, occipital &
temporal)
 Cortical areas are responsible for motor and language(mostly in left
hemisphere)
 Primary somatosensory & motor cortex strips lie adjacent to the central
sulcus in the parietal and frontal lobes, respectively.
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  Language formation (broca area: located premotor frontal cortex)
and language acquisition(Wernike area: located posterior superior
temporal cortex)
 Extrapyramidal system: modify motor function but are not
components of corticospinal tract or primary motor cortex.
 Composed of basal ganglia, cerebellum and auditory & vestibular
pathways
 Dysfunction of this lead to difficulty in motor control without frank
weakness. PD, ataxia & tremor

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 Diencephalon(thalamus & hypothalmus) located cephalad to mid brain

 Thalamus: sensory and motor relay station, physically and functionally

connecting cortex to the rest of the body.

 The hypothalamus, has autonomic endocrine functions and is

connected to the pituitary gland via the infundibulum.

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  Limbic system: cognitive function, memory consolidation &

emotional response

 Composed of hippocampus, amygdala, part of hypothalamus

(modulation of behavior and sexual function) and part of cortex)

 Infratentorium composed of brainstem and cerebellum

 Brainstem(mid brain, pones and medulla: responsible for

consciousness and autonomic functions (resp & CVS control,

reflexes & cranial nerve 3-12)
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11 Neurophysiology and anesthesia 1/18/2024
 CNS structures and function

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 Blood supply
 Brain receives blood from each pair of

ICA(70%) & vertebral artery(VA)(30%)

 Circle of Willis, anastomotic ring at the

base of the skull, composed of each pair of

ICA & vertebral artery.
 ICA originate from CCA, and give rise to
PCOM, ACA, & MCA).

 VA originate from SA & form basilar artery

at the Ponto-medullary junction→PCA.

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14 Neurophysiology and anesthesia 1/18/2024
  Deep & superficial vein → dural

venous sinuses(valveless b/n

dura & skull periostyum) →
sigmoid sinus →IJV

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 Spinal cord anatomy
 Composed of 33 vertebras and ends at L2 & L3 in adults &
pediatrics respectively.
 Is composed of central gray matter & outer white matter with
different tracts
 Receives blood from single anterior(composed of 6-8 radicular
artery from aorta and supply anterior 2/3rd ) and paired
posterior spinal artery(originate from posterior cerebral
circulation and supply posterior 3rd ) of spinal cord.
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 The spinal cord blood supply
Note that the cervical spine
is served by the posterior
circulation emanating from
the circle of Willis.

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Neurophysiology and anesthesia
 Presentation out line
 Cerebrospinal fluid (CSF)

 Intracranial pressure (ICP)

 Cerebral metabolic rate(CMRO2)

 Cerebral blood flow (CBF)

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 Cerebrospinal fluid (CSF)
 Cerebrospinal fluid (CSF) is a specialized

extracellular fluid that surrounds the structures of

brain, spinal cord and fills the cerebral ventricles.

 CSF is clear, transparent fluid with normal pressure of

112 mmH2O.

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 CSF production
 Mainly by choroid plexus in(lateral, third and fourth

ventricles) by secretion and filtration of plasma.

 70% by choroid plexus and 30% ependymal cells lining

ventricles and brain capillaries (perivascular space).

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 Choroid plexus
 Highly vascular invagination of pia mater, covered by single-

layered ependymal epithelium.

 Produce CSF by modified ultrafiltration from the plexus

capillaries into the ventricles.

 The filtration barrier consists of capillary endothelium,

basement membrane and choroid epithelium, which

also actively modifies the composition of CSF produced.
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 Choroidal secretion of cerebrospinal fluid comprises two
steps
I. The first step: passive filtration of plasma from
choroidal capillaries to the choroidal interstitial
compartment according to a pressure gradient.
II. Second step: active transport from the interstitial
compartment to the ventricular lumen across the
choroidal epithelium involving carbonic anhydrase and
membrane ion carrier proteins.

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 Characteristics of CSF
 Osmotic pressure: approximately equal to that of plasma

 Sodium ion : Approximately equal to that of plasma

 Chloride ion : About 15 per cent greater than in plasma

 Potassium ion: approximately 40 % less

 Glucose: 30 % less than plasma

 Protein: very small than plasma

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 Characteristics of CSF

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  Rate of formation: About 20-25 ml/hour

 550 ml/day in adults. Turns over 3.7 times a day

 Total quantity: 150 ml:

 30-40 ml within the ventricles

 110-120 ml in the subarachnoid space [of which 75-80 ml in

spinal part and 25-30 ml in the cranial part].

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27 Neurophysiology and anesthesia 1/18/2024
 Absorption of CSF
 CSF is absorbed to venous sinus by arachnoid villi (90%)

and in others (10%) .

 Experimental data suggest that cranial and spinal

nerve sheaths, the cribriform plate and the adventitia of

cerebral arteries constitute substantial pathways of CSF
drainage into the lymphatic outflow system.

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 Absorption…
 The endothelial cells covering the villi have vesicular passages

directly through the bodies of the cells large enough to allow

relatively free flow of:

 Cerebrospinal fluid

 Dissolved protein molecules

 Particles as large as red and white blood cells into the

venous blood.

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  Arachnoid villi:

 Are fingerlike inward projections of the arachnoidal

membrane through the walls into venous sinuses.

 Has unidirectional valve

 Reabsorption ceases if CSF pressure is <70 mmH2O.

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  The brain tissue is separated from the plasma by three

main interfaces

 Blood–brain barrier (BBB)

 Blood–cerebral spinal fluid barrier (BCSFB)

 Arachnoid cells underlying the dura mater

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 BLOOD BRAIN BARRIER
 Structural and functional barrier which impedes and

regulates the influx of most compounds from blood to brain

Formed by:

 Endothelial cells (BMEC) of capillary

 Basement membrane

 Foot process of astrocytes

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 BLOOD CSF BARRIER
 Lumen of blood capillaries separated by ventricle

 Basement membrane

 Endothelial cell of capillaries

 Choroid epithelial cell with tight junction

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 CSF circulation
Lateral ventricle
Foramen of Monro
[Interventricular foramen]
Third ventricle
Cerebral aqueduct
[Sylvius]
Fourth ventricle:
Foramen of megendie
formen of luschka
Subarachnoid space of Brain and Spinal cord

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35 Neurophysiology and anesthesia 1/18/2024
 CSF function
I. Mechanical protection by buoyancy. The low
specific gravity of CSF (1.007) reduces the effective weight
of the brain from 1.4kg to 47g (Archimede’s principle).
This reduction in mass reduces brain inertia and thereby
protects it against deformation caused by acceleration or
deceleration forces.

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 Fun….
II. Protection: protects brain tissue from some forms of
mechanical injury. Shock absorber

III. CSF is important for acid-base regulation for control of

respiration.

IV. CSF provides a medium for nutrients after they are

transported actively across the blood-brain-barrier.

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 INTRACRANIAL PRESSURE
 ICP typically means the supratentorial CSF pressure
measured in the lateral ventricles or over the cerebral cortex.
 Normal ICP value is 10 mm Hg or 130 mm of H2O

 Intracranial hypertension is defined as a sustained increase above

37 mm Hg or 300mm of H2O.
 Intracranial elastance(determined by measuring change in ICP in
response to change in intracranial volume) plays major role in
determining ICP.

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  “ Any increase in one component must be offset by an equivalent

decrease in another to prevent rise in ICP”. MONRO-KELLIE

DOCTRINE.

 “Within the rigid skull the sum of volumes of brain, CSF & IC

blood is constant”.

 An increase in one should cause a decrease in one or both of the

remaining two if a rise in ICP is to be avoided

 Venous blood< CSF< art blood < then brain tissue.

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 Causes of raised ICP
 Increased extracellular fluid : Cerebral oedema.

 Increased blood volume

 Increased arterial flow: hypoxia, hypercapnea, acidosis

 Increased cerebral venous volume: JV obstruction,

 Increased CSF volume: subarachnoid hemorrhage,
obstructive hydrocephalus.
 Increased Brain Substance: Tumor, abscess, hematoma.

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  Cerebral edema: accumulation of extracellular water in the
cranium. Three types
 Cytotoxic edema:↑intracellular water(failed membrane ionic pump
due to cerebral ischemia)
 Vasogenic edema: ↑extracellular water due to disrupted BBB(
caused by tumors, abscess, contusions)
 Interstitial edema: permeation of CSF in to interstitial
space(hydrocephalus)
 Mostly cerebral edema is a combination of all three

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 Sign and symptoms of raised ICP
 Early : Headache , Nausea and Vomiting, seizure,

Papilledema and Focal neurological deficits .

 Late : Cushing’s triad ( increase BP, bradycardia, irregular

breathing) and herniation.

 Cheyne stokes breathing,apnea.

 Ipsilateral then bilateral pupillary dilatation.

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  Compensatory mechanisms that prevent the initial rise

in ICP include:

1) Displacement of CSF from the cranial to spinal

compartment

2) Decrease in production of CSF

3) Increase in absorption of CSF

4) Decrease in total cerebral blood volume

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 Potential cites of brain herniation
1. Cingulate gyrus under the falx
cerebri

2. Uncinate gyrus through the

tentorium cerebelli,

3. Cerebellar tonsils through the

foramen magnum

4. Any area beneath a defect in the

skull (transcalvarial)

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 Pathophysiology of intracranial
hypertension

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 Management goals
1. Avoiding increased cerebral blood flow
 Avoid hypercarbia ,hypoxia, hypertension and hyperthermia

 Use IPPV, control Paco2 and ensure good oxygenation, adequate

analgesia and anesthetic depth.
2. Avoid increasing venous pressure: Avoid coughing and straining
,head down position, obstructing neck veins with ET tube ties.
3. Prevent further cerebral edema: Generally fluid restricted, but
important to maintain intravascular volume and CPP.

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  Do not use hypotonic solutions: fluid flux across the BBB

is determined by plasma osmolality. Maintenance of a high

normal plasma osmolality is essential.

4. Maintain CPP: Avoid Hypotension(control blood pressure

using fluids and vasopressors) target to have above 70
mmhg.

5. Avoid anesthetic agents that increase ICP.

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 Specific measurements
I. Diuretics: Reduce cerebral edema

 Osmotic diuretics:mannitol 0.25 -1g/kg over 15 minutes

 Loop diuretics : Furosemide 0.25-1mg/kg

 Urinary catheterization is must.

II. Modest hyperventilation : has transient effects in reducing ICP

for 6-24 hours due to renormalization of CSF PH.

III. Corticosteroids : Reduce edema surrounding tumors and

abscess but has no role in head injury. Take several hours to act.
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  Dexamethasone 4mg 6 hourly is often given for elective

surgery preoperatively.

IV. Head –up tilt: to reduce central venous pressure,

always ensure that MAP is not significantly reduced as

the overall result could be a reduction in CPP.

V. Anticonvulsants: barbiturates, phenytoin, propofol,

benzodiazepines…

Surgicalanddecompression:
VI. Neurophysiology anesthesia
internal & external 1/18/2024
49
 Anesthetic agents that affect CSF volume
Agents CSF production CSF absorption

Halothane ↓ ↓
Isoflurane, Barbiturates , Little or no change ↑
Ethomidate , Benzodiazepines,
opioids
Disflurane ↑ ↓
Sevoflurane lidocaine Unknown Unknown
propofol
Nitrous oxide Little or no change Little or no
change
Ketamine Little or no change ↓

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 Bibliography
1. Fundamentals of anesthesia

2. Morgan , clinical anesthesia 5th edition

3. Up-to-date in anesthesia, 24, 2

4. Wikipedia ,free encyclopedia

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 Cerebral metabolism(CMRO2)
 Brain consumes 20% of total body O2(60% of it for electrical

activity & the rest for neuronal survival).

 The average CMRO2 is 3-3.8ml of O2/100g/min(50ml/min)

 CMRo2 parallels with electrical activity and glucose consumption

 Prone for irreversible cellular injury due to high O2 consumption

and negligible O2 reserve

 Higher brain regions(cortex, hippocampus…) are more sensitive

to hypoxic injury than brainstem.

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 CMRO2…
 Neuronal cells utilize glucose(5mg/100g/min) as a primary

energy source and >90% of it metabolize aerobically.

 Brain needs uninterrupted supply of glucose to maintain function

 Both hypoglycemia and hyperglycemia(acidosis) are hazardous to

brain.

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 Cerebral blood flow(CBF)
 The average CBF is 50ml/100g/min

 CBF is regulated by “flow metabolism coupling” (↑in regional

neuronal electrical activity →↑in regional blood flow)

 CBF=CPP/CVR(cerbrovascular resistance)

 CBF below 20ml/100g/min →isoelectric EEG and below

10ml/100g/min cause irreversible brain damage.

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 CBF regulation
I. Cerebral perfusion pressure

II. Auto-regulation

III. Extrinsic mechanisms

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 CBF regulation…
I. Cerebral perfusion pressure(CPP)

 Is the d/c b/n MAP & either ICP or CVP, depending on which is

higher.

 Normally CPP is 80-100mmhg

 CPP below 50mmhg →slow EEG

 CPP 25-40mmhg→ isoelectric EEG

 CPP below 25mmhg cause irreversible brain damage

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 CBF regulation…
II. Auto-regulation
 Is the ability of normal brain to maintain 50ml/100g/min of CBF
despite moderate changes in MAP or CPP.
 Cerebral auto-regulation is intact b/n Map of 60-160mmhg by
altering CVR (dynamic & static auto-regulation)
 Outside auto-regulation range CBF is pressure dependent

 Below LLA(maximum vasodilation & ischemia) and above

ULA(maximum vasoconstriction, disruption of BBB, cerebral
edema & hemorrhage)
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 CBF regulation…

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 CBF regulation…
 Both myogenic and metabolic mechanisms may explain

cerebral autoregulation.

 The cerebral autoregulation curve is shifted to the right in

patients with chronic arterial hypertension(both upper and

lower limits).

 Studies suggest that long-term antihypertensive therapy can

restore cerebral autoregulation limits toward normal.

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 CBF regulation…
III. Extrinsic mechanisms
1. PaCO2
2. PaO2
3. Temperature
4. Blood viscosity
5. Drugs

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 CBF regulation…
1. PaCO2 and PaO2
 The most important extrinsic influence on CBF is PaCO2.

 CBF is directly proportional to PaCO2 b/n 20-80mmhg

 CBF changes by 1-2ml/100g/min for each mmhg change in

PaCO2
 PaCO2 must be at lower normal(35-40mmhg) to prevent ↑ ICP

 Only marked changes in PaO2 alter CBF(PaO2>350mmhg

→↓CBF, but PaO2 <50 mm Hg → greatly ↑ CBF)

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62 Neurophysiology and anesthesia 1/18/2024
 2. Temperature
 CBF changes 5-7% for 1°C change in core temperature.

 Hypothermia decreases both CMRO2 & CBF

 It can reduce CBF & CMRO2 beyound isoelectric EEG.

 For every 10°c increase in temperature, CMRO2 doubles.

 For every 10°c decrease in temperature, CMRO2 halved.

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 3. Blood viscosity

 Blood viscosity is determined by HCT

 Decreased HCT decrease viscosity and improve CBF but it

reduces O2 carrying capacity.

 The optimum HCT for optimum cerebral O2 delivery is

30%.

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 4. Drugs

 Most anesthetic agents

 Reduce neuronal activity and so reduce CMR02, which

provide a protective mechanism when O2 demand is higher

than supply.

 Reduce MAP due to arterial vasodilatation which cause

adverse effect on CPP.

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 Volatile anesthetic agents
 Volatile anesthetics uncouple metabolism and CBF.

 Reduce CMRO2(iso,dis,sevo has 50% and halothane 25%

reduction)

 Cause a dose dependent ↑CBF & ICP due to vasodilation

(Halothane > Desflurane > Isoflurane > Sevoflurane).

 They abolish auto-regulation in sufficient doses(>1 mac).

 Response to CO2 is intact(timing of hyperventilation is varied)

 Has luxury perfusion and circulatory steal phenomena???

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67 Neurophysiology and anesthesia 1/18/2024
 Halothane Isoflurane
 Has greatest effect on CBF  Increase CBF

 Con.> 1% : abolishes auto  Auto regulation maintained up to 1

regulation MAC

 Generalized increase in CBF  CBF is > in sub cortical than

neocortical areas.
 At equivalent MAC with
isoflurane increase CBF up to  At equivalent MAC with halothane

200%. increase CBF up to 20%.

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  Sevoflurane:

 CBF effects similar to isoflurane.

 Produce slightly less vasodilation.

 Auto regulation maintained up to 1.5 MAC.

 Desflurane:

 CBF similar to isoflurane

 Autoregulation progressively abolished as dose increases .

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  Nitrous Oxide

 When administered on its own - increases both CBF and

metabolism.

 When added with another anesthetic, it increases CBF

without changing metabolism.

 It is a direct acting and potent cerebral vasodilator.

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 IV anesthesia agents
 IV anesthetic agents all decrease cerebral metabolism, CBF

and ICP with the exception of ketamine.

 All the reductions are in a dose dependent fashion.

 Once maximal suppression of metabolism occurs, no further

reduction in CBF occurs.

 CO2 reactivity and autoregulation of cerebral circulation

are well maintained during propofol/thiopental anesthesia.

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 Barbiturates /Thiopentone

 Barbiturates maximal 50% reduction in CBF and metabolism.

 CO2 reactivity is maintained but quantitatively reduced compared to the

awake response.

 Cerebral auto-regulation is intact.

 Suppression of seizures, membrane stabilizer & free radical

scavenger.

 Neuroprotection for focal (stroke, surgical retraction, temporary

clipping) but not for global (cardiac arrest) ischemia. Why???

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  Etomidate

 Decreases CMR(more in cortex than brainstem), CBF and

ICP the same way as barbiturates.

 Decreases production and enhances absorption of CSF.

 Cause myoclonic movements, but no seizure activity on the

EEG in normal individuals.

 Best avoided in patients with a history of epilepsy.

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  Propofol

 Propofol produces a coupled dose dependent reduction in

CMRO2 and CBF.
 High doses vasodilator effect overcomes the coupling & CBF
increases.
 Both CO2 responses and auto regulation are intact in the normal
brain.
 In head injured patients static auto regulation may be impaired by
high propofol infusion rates.
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  Ketamine

 Dilates the cerebral vasculature and increases CBF ( 50 – 60%)

 Increases in CBF, CBV, CSF volume can increase ICP markedly

in patients with decreased IC compliance.

 It is not routinely used for elective neurosurgical anesthesia at

present, but for emergency induction of anesthesia &

maintenance in head injured patients, particularly those
with hemodynamic compromise.
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 Benzosiazepins

 Reduce CBF & CMRO2 but less than barbiturates,

propofol & etomidate.

 Has anticonvulsant effect

 Have prolonged emergence time

 Not usually used as induction agent.

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  Opioids

 Opioids at low doses produce very little effect on CBF if an

increase in Paco2 is avoided .
 Auto regulation remains intact

 BP vasodilatation to maintain CBF .

 Fentanyl and morphine – these agents have little effect on

intracranial pressure or blood flow which makes them suitable
for titration to provide postoperative analgesia.

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  NMBD: No direct effect on CBF

 Histamine releasing agents can cause hypotension , reduce CPP.

 Suxamethonium:

 Causes a rise in ICP through muscle fasciculation increasing venous

pressure.

 This effect is moderate and of little clinical relevance.

 Should be used when rapid intubation is required in the presence

of full stomach.
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 Effects of anesthetic agents on cerebral
physiology

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 Bibliography
1. Morgan & Mickhail’s clinical anesthesiaology, 6th edition,2018

2. Clinical anesthesia, PG Barash, 8th edition, 2017

3. Textbook of anesthesia for postgraduates, Tk Agasti 1st edition, 2011

4. Miller’s anesthesia, Ronald Miller 8th edition, 2015

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