Anesthesia_Books Anesthesia 333 MCQs, Q _ A

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HELP LINE NO. 9391567707
1ANAESTHESIA
TOPIC 1: LOCAL ANESTHETIC
1. True about EMLA:
A. Can be used for intubation
B. Mixture of local anesthesia
C. Faster acting
D. Used in children
B & D
..........(PGI - DEC 2006)
• EMLA (Eutectic mixture of 2.5% Lidocaine base and 2.5%.
Prilocaine base) is a topial anaesthetic
formulation, widely used for cutaneous analgesia
through intact skin.
• The preparation should be applied under an occlusive
bandage for 45-60 minutes to obtain
effective cutaneous anaesthesia.
• Uses :
to decrease pain a/w percutaneous insertion of I:V. needles
and cannulas.
- Skin grafting procedures.
- in neonates or in needle phobics.
- Newborn circumcision.
2. Which of the following is not an amide:
A. Lidocaine
B. Procaine
C. Prilocaine
D. Etidocaine
B
..........(AIIMS PGMEE NOV - 2003)
Amide linked Local anaesthetics
Lidocaine
Bupivacaine
Dibucaine
Prilocaine
Ropivacaine
Ester linked local anaesthetics
Cocaine
Procaine
Chlorprocaine
Tetracaine
Benzocaine
3. Which one of the following local anesthetics belongs
to the ester group?
A. Procaine
B. Bupivacaine
C. Lignocaine
D. Mepivacaine
A
..........(AIPGMEE - 2006), AIPGMEE - 2007
5. Which of the following local anaesthetics causes
vasoconstriction:
A. Procaine
B. Lidocaine
C. Cocaine
D. Chlorprocaine
C
..........(AIPGMEE - 1999), AIPGMEE – 1998
PGI - 1997 – Dec, AIIMS PGMEE - DEC 1997
Cocaine
• Remember that while most local anaesthetics cause
vasdilatation,
Cocaine is one of the rare examples of local
anaesthetic which causes vasoconstriction’
• Pocaine, Chlorprocaine and Lidocaine all cause varodilation.Q
6. Longest acting L.A
A. Bupivacaine
B. Tetracaine
C. Xylocaine
D. Procaine
B
..........(AIPGMEE - 1994)
7. Nerve Fibre affected by local anesthesia first
A. Type A
B. TypeB
C. Type C
D. Type
C
.........(AIPGMEE - 1995)
ABCLocal 
Anesthetics
CBAPressure
CABHypoxia
Least 
susceptible
IntermediateMost 
susceptible
Susceptibility 
to
ABCLocal 
Anesthetics
CBAPressure
CABHypoxia
Least 
susceptible
IntermediateMost 
susceptible
Susceptibility 
to
8. Shortest acting local anaesthetic agent is:
A. Procaine
B. Leidocaine
C. Tetracaine
D. Bupivacaine
A
..........(AIPGMEE - 1997)
Procaine
Duration of action of various anaesthetic agents in
descending order are :
Dibucaine (Cinchocaine)>Tetracaine (amethocaine) >
Bupivacaine > Lidocaine > Procaine
Amongst the choices provided procaine is the shortest acting.
Other commonly asked questions on local anaesthesea :
• Safest LA agent – Prilocaine
• Longest acting LA – Dibucaine (Cinchocaine)
• Shortest acting LA – Chlorprocaine
• Best L.A. for Regional block – Bupivacaine
• Only naturally occurring LA-Cocaine
• Only LA agent which causes vasoconstriction – Cocaine
(Rest are vasodilators)
9. All of the following are example of amide linked local
anaesthetics except:
A. Lidocaine
B. Procaine
C. Bupivacaine
D. Mepivacaine
B
..........(AIPGMEE - 1998)
TOPIC 1: LOCAL ANESTHETIC
HELP LINE NO. 9391567707
2ANAESTHESIA
12. About lidocatne, all are true except:
A. LA effect
B. Cardiac arrhythmia
C. Ester
D. Acts on mucous membrances
C 
..........(PGI - 1998 - Dec)
• Lidocaine is AMIDE linked LA
good for both surface application and injections.
• Lidocaine has little effect on contractility and conductivity,
it abbreviates ERP, and is used as ANTI- ARRHYTHMIC.
Overdose of lidocaine can cause-cardiac arrhythmias, -
Decrased BP, convulsion, resp.arrest, coma etc.
13. True statements about local anaesthesia:
A. It inhibits the generation of action potential.
B. Unmyelinated thin fiber are most susceptible than
myelinated large fibers.
C. Toxicity is reduced by addition of vasoconstrictor.
D. Blocks all modalities of sensation at the same time
A
..........(.PGI - DEC 2003)
• Local anesthesia (LA) produce conduction blockade of
neural impulses by preventing passage of sodium ions
through ion selective sodium channels in nerve membranes
thus inhibiting generation of Action potential. It do not
alter the resting transmembrane potential or threshold
potential.
• Myelin increases conduction velocity and makes the nerve
membrane more susceptible to LA.
• Large myelinated fibers are more sensitive to LA than small
unmyelinated fibers.
• Preganglionic type ‘B’ fibers are more readily blocked by
LA than any fiber.
• In practice, the sequence of nerve block by LA are :
Autonomic -> Sensony -» Motor
• Addition of vasoconstrictors like adrenaline to LA
- Produces : decreased absorption and reduces toxicity
- Prolongs analgesic activity.
14. Local anaesthesia acts by
A. Na+ channel inhibition
B. Ca+ channel inhibition
C. Mg*4 channel inhibition
D. K+ channel inhibition
A
..........(PGI - JUNE 1997)
Local anaesthetic drugs exert their effect by binding to
the internal mouth of the sodium channel.
15. Drugs used in case of local anesthetic toxicity:
A. Antiarrhythmic
B. IV fluids
C. Anticonvulsant
D. O2
A
..........(PGI - JUNE 2006)
Emmergency treatment of local anaesthetic toxicities are:
- Facemask oxygenation.
- Restoration of haemodynamics with IVF & cardiac
massage if required.
- Prevention of metabolic acidosis with sodium bicarbonate.
- Prevention or early treatment of seizure a c t i v i t y
with Benzodiazepines.
- Inotropic support with Atropine, Epinephrine, Dopamine
& Calcium chloride.
Defibrillation, Antiarrythmic agents like Amiodarone.
16. True about local anaesthetic agents
A. Duration depends on protein binding
B. Potency depends upon lipid solubility
C. LA with low PK is more active
D. Higher dose produces more block
E. Signal transduction blockade
ALL 
..........(PGI - JUNE 2004)
• Local anaesthetics are chemical compounds which are
capable of reversibly inhibiting the propagation of
impulses in nerve cells.
• Three major factors determine the conduction-blocking
profile of a LA in an isolated nerve preparation :
 Lipid solubility, protein binding & PK.
LA agents which are highly lipid-soluble are able to penetrate
the neuronal membrane & gain access to their site of
action more readily than less lipid-soluble agents & is
reflected biologically in their increased potency.
Duration of action of LA appear to be influenced primarily by
their protein-binding capacity, agents with the longest
duration of action (Bupivacaine & Ropivacaine) are
highly protein bound.
• LA with PK closer to physiological PH will have more
rapid onset than those with higher PK.
• Onset of conduction block by LA depends on the dose or
concentration of LA.
• The physiological changes during laryngoscopy & intubation
are :
CVS :
Hypertension, Tachycardia & dysrhythemias & bradycardia
in children.
Respiratory :
Increased a irway reactivity & laryngospasm &
bronchospasm.
CNS : Stimulates CNS activity with Increased in EEG activity,
CMR (cerebral metabolic rate), cerebral blood flow, &
thus ICP & IOP.
Abdomen : Increased in intraabdominal pressure with
increased risk of aspiration in patients with full stomach.
17. Short acting L.A:
A. Procaine
B. Lignocaine
C. Bupivacaine
D. Tetracaine
A 
..........(PGI - June -2000)
Procaine, is a short acting local anaesthetic duration of nerve
block is 30-60 minutes
TOPIC 1: LOCAL ANESTHETIC
HELP LINE NO. 9391567707
3ANAESTHESIA
18. True about local anaesthetic:
A. Cocaine acts by decreasing norepinephrine
B. Act by decreasing sodium entry into the cell
C. Lignocaine is a amide
D. Dibucaine is drug of choice for epidural anaesthesia
B & C 
..........(PGI - June -2001)
19. Order of sensitivity of nerve fibres to Local
anaesthetic in decreasing order:
A. Pain (C and A-delta), Preganglionic sympathetic B., motor
B. Preganglionic sympathetic B., Pain (C and A- delta), sensory,
motor
C. Pain (C and A-delta), sensory, motor, Preganglionic
sympathetic B
D. Preganglionic sympathetic B. sensory, motor, Pain (C and
A-delta)
B
..........(AIIMS PGMEE - MAY 2008)
No++++07-2.30.3-1.3Postgan
glionic 
sympat
hetic 
fibers
C 
Sympat
hetic
No++++05-20.4-1-2Pain 
Warm 
and 
cold 
tempera
ture 
Touch
Type IVC 
Dorsal 
root
Some++++3-14<3Preganglionic
autono
mic 
fibers
B
Yes+++12-302-5Pain 
Cold 
tempera
ture 
Touch
Type-IIIA5
Yes++15-303-6Motor 
(muscle 
spindle)
Ay
Yes++30-705-12Touch 
pressur
e
Proprio
ception
Type IIAP
Yes++70-12012-30Proprio
ception
TypelbAa
Yes++70-12012-20Proprio
ception
Type laAa
Yes+70-12012-20MotorAa
Myelinat
ion
Local 
Anestheti
c 
Sensitivit
y
Condu
ction
{mis)
Diamete
r (mm)
Modality 
Served
Sensory 
Classifi
cation
Fiber 
Type
No++++07-2.30.3-1.3Postgan
glionic 
sympat
hetic 
fibers
C 
Sympat
hetic
No++++05-20.4-1-2Pain 
Warm 
and 
cold 
tempera
ture 
Touch
Type IVC 
Dorsal 
root
Some++++3-14<3Pregang
lionic
autono
mic 
fibers
B
Yes+++12-302-5Pain 
Cold 
tempera
ture 
Touch
Type-IIIA5
Yes++15-303-6Motor 
(muscle 
spindle)
Ay
Yes++30-705-12Touch 
pressur
e
Proprio
ception
Type IIAP
Yes++70-12012-30Proprio
ception
TypelbAa
Yes++70-12012-20Proprio
ception
Type laAa
Yes+70-12012-20MotorAa
Myelinat
ion
Local 
Anestheti
c 
Sensitivit
y
Condu
ction
{mis)
Diamete
r (mm)
Modality 
Served
Sensory 
Classifi
cation
Fiber 
Type
21. Which of the following local anesthetic is most likely
to produce an allergic reaction
A. Prilocaine
B. Ropivacaine
C. Etidocaine
D. Benzocaine
D
..........(AIIMS PGMEE - MAY 2004)
Ester linked local aneasthetics produce allergic reaction
because they are first metabolized to PABA derivative.
These metabolites are responsible for the allergic reaction
caused by ester linked local anaesthetics.
Out of the given options only Benzocaines is an ester
linked local anaesthetic,
22. L.A. causing Methaemoglobinemia
A. Procaine
B. Prilocaine
C. Bupivacaine
D. Cocaine
B
..........(AIPGMEE - 1994)
• Prilocaine is an amide linked local anaesthetic.
• Methamoglobinemia may be seen sometimes with use of
prilocaine.
• One of the degrading products of prilocaine has potential
of causing methamoglobirumia Congenital or acquired
methamoglobinumia are thus contraindications to the use
of Prilocaine
TOPIC 2: KETAMINE
23. Which of the following increases intracranial tension
A. Thiopentone
B. Ketamine
C. Halothane
D. Propofol
B 
..........(AIIMS PGMEE - SEP 1996)
24. Which of the following causes hallucination ;
A. Ether
B. Halothane,
C. Ketamine
D. Thiopentone
C 
......(AIIMS PGMEE - SEP 1996), AIIMS PGMEE - DEC 1997
25. Best anaesthesia for status Asthmaticus is
A. Thiopentone
B. Ether
C. Ketamine
D. N2O
C 
..........(AIIMS PGMEE - FEB - 1997)
Ketamine
• Ketamine causes Sympathetic stimulation which leads to
Bronchodilatation so it is the anaesthetic of choice
for Status Asthmaticus.
• It is more potent Bronchodilator than Halothane
• Muscle Relaxant of Choice in Asthma —Pancuronium
• Muscle Relaxant to be avoided in Asthma
• Metacurine & Succinyl choline (d/t secretion of histamine)
26. Anaesthetic agent causing raised intracranical tension
is:
A. Etoruidal
TOPIC 2: KETAMINE
HELP LINE NO. 9391567707
4ANAESTHESIA
B. Ketamine
C. Ether
D. Nitrous Oxide
B
..........(AIIMS PGMEE - JUNE - 1997)
Ketamine
• Ketamine is an analogue of phencyclidine and therefore it
causes hallucinations.
• Ketamine.
• It causes Dissociative Anaesthesia*.
It causes sympathetic stimulation which leads to
• Cardiac stimulation —increase O2 demand*
• Bronchodilation —
• it is anesthetic of choice for Bronchial Asthma
• Increase all pressure
• B.P.,I.C.T. ,I.O.P.
• It causes muscular rigidity*
• It increases salivation so Atropine is always given with
it*.
27. An unconscious pt. of head injury comes in casualty.
Examination shows raised intracranial pressure.
Which anesthetic agent is contra- indicated:
A. Propofol
B. Ketamine
C. Etomidate
D. Thiopentone sodium
B
..........(AIIMS PGMEE JUNE - 1999)
AIPGMEE - 2000 , AIPGMEE – 1998
PGI - JUNE 1997, PGI - June –1999
AIIMS PGMEE - MAY 2006, AIIMS PGMEE - DEC 1998
Ketamine
• Ketamine causes increase in all pressure of body fluids -
• Increased ICT
• Increased IOT
• Increased B.P.
• Therefore it is not used in raised ICT and IOT as it may
increase the pressure to morbid levels.
• Ketamine, like Phencyclidine, is primarily a non-
competitive antagonist of the NMDA receptor ,which
opens in response to binding of the neurotransmitter
glutamate. This NMDA receptor mediates the
analgesic (reduction of pain) effects of ketamine at
low doses
• Ketamine causes bronchodilation
• It is primarily used for the induction and maintenance of
general anesthesia, usually in combination with some
sedative drug.
• Other uses include sedation in intensive care, analgesia
(particularly in emergency medicine), and treatment of
bronchospasm.
• Ketamine
• The injection of a therapeutic dose of Ketamine produces
dissociative anaesthesia
• Ketamine is a phenycyclidine analogue, it produces
Hallucinations
• Ketamine is used as anaesthetic where maintenance
of blood pressure is important e.g. in states of shock
Ketamine produces profound analgesia
Ketamine
• Ketamine causes an increase in all pressure viz
intracranial pressure
Intraocular pressure
Blood pressure
It does not cause muscle Relaxation
Ketamine induces dissociative anaesthesia : profound
analgesia, immobility, amnesia with light sleep and
felling of dissociation Q from ones own body and the
surrounding.
It forms the answer to a set of questions. A quick revision
therefore :
• Anaeshesia of choice in shock/hypotension : Ketamine
• Anesthetic associated with increase in muscle tone :
ketamine
• Anaesthetic which does not abolish reflexes : Ketamine
• Profound analgesia is seen with : Ketamine
• Anaesthetic which increases cardiac oxygen demand :
Ketamine
• Anaesthetic of choice in Bronchial Asthma : Ketamine
• Anaesthetic which is associated with emergence delerium
and hallucinations : ketamine
Anaesthetic causing increased CT Anaesthetic which increase
IOT
• Ketamine • ketamine
• Halothane • Nitrous oxide
 • Scoline
 • Cyclopropane
Anaesthetics causing decreased ICT Anaesthetic which
decreased IOT
• Theopentone • Morphine
• Droperidol • Thiopentone
• Althesin • Halothane
29. Dissociative anesthesia is
A. Ketamine
B. Halothane
C. SCH
D. d-TC
A
..........(AIPGMEE - 1996)
AIIMS PGMEE - NOV 2006
TOPIC 2: KETAMINE
HELP LINE NO. 9391567707
5ANAESTHESIA
30. Maximum analgesic action is seen with:
A. Catecholamine
B. Propofol
C. Ketamine
D. Thiopentone
C 
..........(AIPGMEE - 1997) , PGI - 2001 - Dec
Ketamine
Ketamine is a rapidly acting parenteral anaesthetic, causing
Sedation and Profound analgesia besides other features.
Analgesia is a marked feature and extends into the
postoperative period.
32. Which drug of anaesthetics causes hallucination:
A. Ketamine
B. Trilene
C. Halothane
D. Trichloroethylene
A
..........(AIPGMEE - 1998)
“Dreaming, Hallucinations and delerium are seen with
ketamine” -
37. With regard to Ketamine, all of the following are
true except -
A. It is a direct myocardial depressant
B. Emergence phenomena are more likely if anticholinergic
premedication is used
C. It may induce cardiac dysarrythmias in patients receiving
tricyclic antidepressants
D. Has no effect on intracranial pressure
D
..........(AIIMS PGMEE - NOV 2005)
38. A 5 year old child is suffering from cyanotic heart
disease. He is planned for corrective surgery. The
induction agent of the choice would by -
A. Thiopentone
B. Ketamine
C. Halothane
D. Midazolam
B
..........(AIIMS PGMEE - NOV 2005)
• Cyanotic heart disease have predominantly Right to left
shunt i.e. blood flows directly from right ventricle to left
ventricle bypassing the pulmonary circulation.
• This produces cyanosis as the systemic blood coming to
the right ventricle cannot be oxygenated by the lung.
• Note that in right to left shunting , the fixed
component is determined by the severity of the right
ventricular obstruction while the variable component
depend upon difference between systemic vascular
resistance (SVR) and pulmonary vascular resistance (PVR)
• If the right ventricular obstruction remains same greater
the systemic vascular resistance the lesser the shunt,
• So in right to left shuntsa favourable ratio of systemic
vascular resistance to pulmonary resistance should be
maintained i.e. - Systemic vascular resistance should be
increased pulmonary vascular resistance should be
decreased.
• This will help to reduce the shunt in cyanotic heart
diseases.
• Therefore the goal of anaesthetic management in patients
with cyanotic heart disease is to maintain
intravascular volume or systemic vascular resistance.
• Anaesthetic drugs and procedures which increase
systemic vascular resistance and decrease pulmonary
vascular resistance should be preferred.
Ketamine (intramuscular or intravenous) is commonly used
as an induction agent in cyanotic heart disease because it
maintains or increases systemic vascular resistance and it
does not appear to increase pulmonary vascular resistance
(PVR) in children.
So the use of ketamine will decreased right to left shunting.
• Halothane’s safety in patients with cyanotic heart disease
and good cardiac reserve is well established
• Patients with milder degrees of Right to left shunting can
also tolerate inhalational induction with halothane
because Halothane tends to maintain systemic vascular
resistance (systemic arterial vasodilation is minimal
with halothane).
• But Remember, that halothane induction is not used in
very young patients (because it is pungent and it is slow
acting).
• Halothane is also not preferred for patients with low CO.
Important facts which should always be taken care of while
anaesthetizing a patient with right to left shunt.
• The right to left shunting tends to slow the uptake of
inhalational anaesthetics.
• In contrast it may accelarate the onset of intravenous
agents.
Nitrous oxide is usually used with inhalational induction (does
not increase PVR)
41. Which of the following increases cerebral oxygen
consumption
A. Propofol
B. Ketamine
C. Thiopentone
D. Alfentanyl
B
..........(AIIMS PGMEE - NOV 2007)
• This has been discussed so many times that ketamine
increases cerebral oxygen consumption. It increases
the intracranial tension too.
• Thiopentone and propofol decrease cerebral oxygen
consumption.
Alfentanyl is an opioid and opioids in general reduce cerebral
oxygen consumption, cerebral blood flow and
intracranial pressure.
TOPIC 2: KETAMINE
HELP LINE NO. 9391567707
6ANAESTHESIA
TOPIC 3: SUCCINYLCHOLINE
44. Malignant hyperthermia is seen with
A. Gallamine
B. Lignocaine
C. Succinylcholine (Sch)
D. Bupivacaine
C
..........(AIIMS PGMEE - MAY - 1993)
• Drug causing malignant hyperthermia
1) Sucinyl choline (Most common)
2) Halothane
3) Lidocaine
4) Mepivacaine
5) Methoxyflurane
6) Gallamine
7) Ethylene
8) Ethyl chloride
9) Trichlorethylene
45. Post anaesthetic muscle soreness is caused by
A. Gallamine
B. d-Tubocurarine
C. Suxamethonium
D. Xylocaine
C
..........(.AIIMS PGMEE - NOV - 1993)
• Suxamethonium causes muscle pain -
• This pain is influenced by age, sex and physical fitness.
i) Pain is more common in women
ii) More common in middle age than extreme age.
iii) Less common in muscularly fit
• The longer the interval b/w injection of barbiturate and
suxamethonium the more intense the pain.
Prevention of muscle pain caused by suxamethonium
1) Precurairzation - Nondepolarizing relaxants are given 3
minutes before suxamethonium injection
2) lignocaine injection before suxamethonium
Other adverse effects of Suxamethonium -
1) Hyperkalemia
2) Raised intraocular pressure
3) Malignant hyperpyrexia
4) Dystrophia myotonica
5) CVS - Bradycardia and cardiac arrest
46. Regarding myasthenia, what is true about sensitivity
to curare and succinylcboline Curare - Succinylcholine:
A. Decreased Increased
B. Decreased Normal
C. Increased Increased
D. Increased Decreased
D
..........(AIIMS PGMEE - NOV - 1993)
In myaesthenia gravis the muscles affected by myaesthenia
gravis are hypersensitive to non depolarizing relaxants
like curare but they are resistant to succinyl choline
and decamethonium (depolarizing blockers)
47. Administration of Scoline produces dangerous
hyperkalemia in:
A. Paraplegia
B. Fracture Femur
C. Raise intracranial pressure
D. Acute renal failure
A
..........(AIIMS PGMEE JUNE - 1999)
Paraplegia
• “Hyperkalemia caused by Scoline is insignificant except
after—>
• paraplegia
• burns &
• tetanus”
• Other adverse effect of Scoline:
1. Malignant Hyperthermia
2. Muscle Fasciculations
48. Hyperkalemia due to Scoline is seen in all except:
A. Muscular Dystrophy
B. Crush injury
C. Abdominal Sepsis
D. Burns
none
..........(AIIMS PGMEE JUNE - 2000)
None of the above
• Hyperkalemia d/f Scoline is seen in following
conditions:
• Trauma
• Burns
• Muscle disease such as myopathy
• Motor neuron disease
• Muscular Dystrophy
• denervation
• Spinal Cord transection
• Tetanus
• Congenital cerebral palsy
• Chronic Arterial insufficiency
• Severe Intra Abdominal infection
TOPIC 3: SUCCINYLCHOLINE
HELP LINE NO. 9391567707
7ANAESTHESIA
Suxamethonium –ADVERSE EFFECTS
• Side effects include fasciculations, muscle pains, acute
rhabdomyolysis with hyperkalemia, transient ocular
hypertension, and changes in cardiac rhythm
including bradycardia, cardiac arrest, and ventricular
dysrhythmias.
• In children with unrecognized neuromuscular diseases, a
single injection of suxamethonium can lead to massive
release of potassium from skeletal muscles with cardiac
arrest.
• Suxamethonium does not produce unconsciousness or
anesthesia, and its effects may cause considerable
psychological distress while simultaneously making it
impossible for a patient to communicate.
• For these reasons, administration of the drug to a
conscious patient is strongly contraindicated , except
in necessary emergency situations.
49. In a young patient who had extensive soft tissue
and muscle injury, which of these muscle relaxants
used for endotracheal intubation might lead to
cardiac arrest:
A. Atracurium.
B. Suxamethonium.
C. Vecuronium.
D. Pancuronium
B
..........(.AIIMS PGMEE MAY - 2003)
Hyperkalemia produced due to suxamethonium is
aggravated in muscular diseases. The hyperkalemia so
produced causes cardiac arrest.
50. Which muscle relaxant increases intra cranial
pressure?
A. Mivacurium
B. Atracurium
C. Suxamethonium
D. Vecuronium
C
..........(AIIMS PGMEE NOV - 2002)
Succinylcholine (or Suxamethonium) causes increase in -
(a) Intracranial pressure
(b) Intraocular pressure
(c) Intragastric pressure
51. The use of succinylcholine is not contraindicated in
A. tetanus
B. closed head injury
C. cerebral stroke
D. hepatic failure
D
..........(AIIMS PGMEE NOV - 2002)
Succinyl choline is short acting muscle relaxant as it is rapidly
metabolized by pseudocholinestrase secreted both by liver
and plasma.
 In liver failure ,this enzyme is reduced ,so succinylcholine
concentration is increase during liver failure and is also
maintained for greater periods.
The duration of paralysis produced by succinylcholine is
increased during liver failure but this does not require
Succinylcholine to be contraindicated in liver failure.
Conditions where succinyl choline use is contra
indicated due to hyperkalemia caused by succinyl choline
are-
(a) Tetanus (h) Massive trauma
(b) Stroke (i) Prolonged body immobilization
(c) Closed head injury (j) GB. syndrome
(d) Myopathy (k) Spinal cord injury
(e) Burn (L) Paraplegia
(f) Acidosis (M) Severe intraabdominal infection
52. A six-year old boy is scheduled for examination of
the eye under anaesthesia. The father informed that
for the past six months the child is developing
progressive weakness of both legs. His elder sibling
had died at age of 14 years. Which drug would you
definitely avoid during the anaesthetic management
?
A. succinylcholine
B. thiopentone
C. nitrous oxide
D. vecuronium
A
..........(AIIMS PGMEE NOV - 2002)
Weakness of the legs indicate that the boy is suffering from
myopathy {most probably Duchenes muscular dystrophy).
Succinyl choline use is contra indicted in myopathy due to
increased risk of hyperkalamia.
53. A young boy undergoes eye surgery under day caseanesthesia with succinyl choline and propofol and
after 8 hours he starts walking and develops muscle
pain. What is the likely cause?
A. Early mobilization
B. Due to the effects of eye surgery
C. Succinyl choline
D. Propofol
C
..........(AIPGMEE - 2007)
TOPIC 3: SUCCINYLCHOLINE
HELP LINE NO. 9391567707
8ANAESTHESIA
Muscle pain or Myalgia is a common adverse effect of succinyl
choline
It is common in women and young to middle aged adults and
in those who are ambulant shortly after surgery
The young adult in question has recieved succinylcholine and
is now ambulant after surgery.
He is classically presenting with myalgia secondary
to succinyl choline use.
Myalgia (Muscle Pain after succinyl chnline
• The incidence of muscle pain after administration of succinyl
choline varies from 0.2 % to 89%
It occurs more frequently in :
• Women /young to middle aged adults
• After minor surgery (day case)
In those who are ambulatory shortly after surgery
(rather than bedridden patients)
• Pain is believed to be secondary to damage produced in
muscle by unsynchronized contraction of adjacent muscle
fibres just prior to the onset of paralysis.
• Myalgia may be prevented (or attenuated) by a small dose
of non depolarizing neuro muscular block few minutes
before succinylcholine administration
54. Agent causing malignant hyperthermia
A. Succinyl Choline
B. Dantroline
C. gallamine
D. Ketamine
A 
..........(AIPGMEE - 1995)
Malignant hyperthermia is an autosomal dominant genetic
disorder of skeletal muscle that occurs in susceptible
individuals. It is precipitated by drug administeration,
particularly:
1. Succinyl choline
2. Halothane
3. Fluoranes : sevofluorane, isofluorane etc
4. Amide local analgesics eg lignocaine
5. Phenothiazines
6. Tricyclic antidepressant
7. Monoamine oxidase inhibitors
The drug of choice for treatment of malignant hyperthermia
is Dantrolene
55. Fasciculation are known to be caused by:
A. Suxamethonium
B. Vecuronium
C. Pancuronium
D. Atracumium
A
..........(AIPGMEE - 1997)
Suxamethonium
Suxamethanium or other depolarizing blockers depolarize
muscle end plates by opening Na+ channels and initially
produce twitching and fasciculations because in the
focally innervated mammalian muscle stimulation is
transient.
Neuro muscular blockage by depolarizing agents can be divided
into two phases:
Phase I block :• results from persistant depolarizatin of
muscle end plate.
• preceded by muscle fasciculation
• potentiated by isoflurane,
antichlinesterase, magnesium an lithium.
Phase IIblock:• results from desensitization of receptor
to Ach
• resemble block produced by TC and is
partially reversed by anticholinesterases.
56. Muscle pain after anaesthesia is caused by:
A. Vecuronium
B. D tubocurare
C. Suxamethonium
D. All
C
..........(PGI - 1999 - Dec)
• Muscle pain after anaesthesia is caused by
SUXAMETHONIUM- pain is influenced by age, sex and
physical fitness.
Important side effects of suxamethonium
- Prolonged Apnea
- Increased K+
- Increased IOP
- Muscle pain
- Malignant hyperpyrexia
- Dystrophia Myotonica
Bradycardia, cardiac arrest P-K reaction.
57. Drugs metabolized by cholinesterase:
A. Succinycholine
B. Mivacurium
C. Esmolol
D. Remifentanyl
E. Ketamine
A
..........(PGI - DEC 2004)
58. True about scoline are following except:
A. Fasciculations
B. ICT increases
C. Non Depolarising neuro muscular blocker
D. Short acting muscle relaxant
A & B
..........(PGI - JUNE 1997)
59. Myaesthenics are resistant to following muscle
relaxant:
A. Suxamethonium
B. Pancurium
C. Atracuronium
D. Vecuronium
A
..........(PGI - June -2000)
• Myasthenic patients are resistant to decamethonium and
suxamethonium.
Muscles affected by myasthenia gravis are hypersensitive to
non depolarizing muscle relaxants.
60. Which of the following is the neuromuscular blocking
agent with the shortest onset of action?
A. Mivocurium
B. Vecuronium
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9ANAESTHESIA
C. Rapacuronium
D. Succinylcholine
D
..........(AIIMS PGMEE - MAY 2006)
* Shortest acting muscle relaxant (both depolarizing and
non depolarizing) -
• Shortest acting non depolarizing muscle relaxant
Succinylcholine --> Mivacurium
60-1204-8Doxacurium
40-804-6Pancuronium
30-604-6d-Tubocurarine
50-1002-4Piperacuronium
20-403-6Cisatracurium
20-352-4Atracurium
30-602-4Vecuronium
25-401-2Rocuronium
12-202-4Mivacurium
3-61-1.5Succinyl choline
Duration (min.)Onset (min.)Muscle relaxants
60-1204-8Doxacurium
40-804-6Pancuronium
30-604-6d-Tubocurarine
50-1002-4Piperacuronium
20-403-6Cisatracurium
20-352-4Atracurium
30-602-4Vecuronium
25-401-2Rocuronium
12-202-4Mivacurium
3-61-1.5Succinyl choline
Duration (min.)Onset (min.)Muscle relaxants
61. All of the following statements are incorrect about
the treatment of prolonged suxamethonium apnoea
due to plasma cholinesterase deficiency (after a single
dose of suxamethonium) except-
A. Reversal with incremental doses of neostigmine
B. Continue anaesthesia and mechanical ventilation ti l l
recovery
C. Transfusion of fresh frozen plasma
D. Plasmapheresis
B
..........(AIIMS PGMEE - NOV 2004)
Suxamethonium is a very short acting muscle relaxant.
It has very rapid onset of action and very short duration of
action
Reason
Rapid onset of action
---> It is highly lipid soluble
Short duration of action
---> It is rapidly metabolized by pseudocholinesterase
But sometimes suxamethonium intake is associated with
prolonged apnoea. The reason are -
- Atypical serum cholinesterase
- Low level of serum cholinesterase
- Dehydration and electrolyte imabalance
An overdose of relaxant drug
Excessive formation of succinylcholine monocholine phase II
block
- Management of prolonged apnea after
suxamethonium.
- The best management in this case is to provide
mechanical ventilation, maintain anaesthesia and
continue monitoring till muscle function returns to normal.
- Transfusion of fresh frozen plasma is beneficial (It
will provide pseudocholinesterase)
62. Bradycardia is common after injection of -
A. Midazolam
B. Succinyl choline
C. Dopamine
D. Isoprenaline
B
..........(AIIMS PGMEE - NOV 2005)
• Succinylcholine releases a metabolite —>
Succinvlmonocholine
This metabolite causes excitation of the cholinergic
receptors in the sinoatrial node, resulting in bradycardia.
• Children are particularly susceptible to succinylcholine
induced bradycardia.
• In adults bradycardia is commonly seen when second dose
of succinylcholine is administered.
Prevention against succinvlcholine induced
bradvcardia.
“Intravenous atropine is often given prophylactically in
children and always before a second dose of
succinychotine”.
63. Phase II block is seen in
A. Halothane
B. Ether
C. D-tubocurare
D. Suxamethonium
D
..........(AIIMS PGMEE - DEC 1998)
Suxamethonium
• Suxamethonium causes Biphasic Block.
• With dose more than 500mg.
• Phase I block ---> Features of classical depolarization
 block
• Phase II block ---> Results from desensitization of
 receptor to actylcholine and
 resembles competitive block and
 partially antagonized by anticholinesterase.
There are two phases to the blocking effect of
suxamethonium
Phase 1 block
The first is due to the prolonged stimulation of the
acetylcholine receptor results first in disorganized muscle
contractions (fasciculations, considered to be a side
effect), as the acetylcholine receptors are stimulated .
On stimulation, the acetylcholine receptor becomes a
general ion channel, so there is a high flux of potassium
out of the cell, and of sodium into the cell, resulting
in an endplate potential less than the action potential.
So, after the initial firing, the cell remains refractory.
• Phase 1 blockade is potentiated by anticholinesterases
and antagonized by competitive blockers.
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10ANAESTHESIA
Phase 2 block
• If the duration of blockade is prolonged however, or if
the concentration of the blocker is excessive, then phase
two blockade occurs in which the pharmacological
characteristicis that of a competitive inhibition.
Phase 2 blockade is antagonized by anticholinesterases,
and potentiated by competitive blockers.
Why does Acetylcholine cause Hyperkalemia
• The side effect of hyperkalaemia is because the
acetylcholine receptor is propped open, allowing continued
flow of potassium ions into the extracellular fluid.
• A typical increase of potassium ion serum
concentration on administration of suxamethonium is 0.5
mmol per litre, whereas the normal range of potassium is
3.5 to 5 mmol per litre: a significant increase which results
in the other side-effects of ventricular fibrillation due to
reduced to action potential initiation in the heart.
• Phase 1 block potentiated by anticholinesterases and
antagonized by competitive blockers.
• Phase 2 block antagonized by anticholinesterases and
potentiated by competitive blockers.
Drug interactions
1. Potentiation of the neuromuscular blockade caused by
the aminoglycoside antibiotics , and tetracyclines.
2. Do not potentiate the effects of the halogenated
hydrocarbon anesthetics -halothane
3. Lithium in therapeutic concentrations used in the
treatment of manic disorders can slow the onset and
increase the duration of action of succinylcholine.
TOPIC 4: SPINAL ANAESTHESIA
64. A patient was administered epidural anaesthesia with
15ml of 1.5% lignocaine with adrenaline for hernia
surgery. He developed hypotension and respiratory
depression within 3 minutes after administration of
block. The commonest cause would be.
A. Allergy to drug administered.
B. Systemic toxicity to drug administered.
C. Patient got vasovagal shock.
D. Drug has entered the sub arachnoid space
D
..........(.AIIMS PGMEE MAY - 2003)
Sometimes during epidural analgesia, due to inadvertent
suparachnoid injection (i.e. the injection enters the
subarachnoid space) a condition termed ‘total spinal
analgesia” is produced. It is produced because large dose
of drug which is used in epidural anaesthesia enters the
subarachnoid space.
The manifestation of total spinal analgesia are-
1. Marked hypotension
2. Apnoea
3. Dilated pupils
Management
 Patient should be immediately intubated and 100% O2
should be given I.V. fluids and vasopressors should be given
65. In high spinal anaesthesia what is seen
A. Hypertension and Bradycardia
B. Hypertension and Tachycardia
C. Hypotension and Bradycardia
D. Hypotension and Tachycardia
C
..........(AIIMS PGMEE MAY - 2001)
Hypotension and Bradycardia
Effect of spinal block on cardiovascular system
Vessels 
Vasodilation of arterioles, resistance 
vessels and venous capacitance 
vessels (This causes Hypotension)
Heart
Decrease inotropic Action
Decrease chronotropic Action
Increase effective Refractory period
Decrease automaticity decrease 
level of catecholamine
(This causes Bradycardia)
66. Following spinal subarachnoid block a patient
develops hypotension. This can be managed by the
following means except.
A. Lowering the head end
B. Administration of 1000 ml of Ringers lacate before the
block
C. Vasopressor drug like methoxamine
D. Use of ionotrope like dopamine
A
..........(.AIIMS PGMEE MAY - 2003)
For spinal subarchnoid block, the anaesthetic agent is injected
into the subarchnoid space.
The subarchnoid space contains CSF.
If the head end is lowered, the anaesthetic drug will
move towards the cephalic direction (being heavier than
CSF). This will increase the level of spinal block and may
lead to cardiac & ventilatory failure.
(Sympathetic supply of heart comes from T3 to T4; phrenic
nerve supplying diaphragm arise from C3 to C5)
“Hyperbaric solution of bupivacaine are injected as a ‘single
shot’ into the cerebrospinal fluid, to produce rapidly an
intense blockade, usually within 5 minutes.
Autonomic sympathetic blockade results in hypotension,
necessitating prior intravenous fluid loading and titration
of vasoconstrictor drugs.
If the hyperbaric solution is allowed to ascend too
high, severe hypotension and ventilatory failure occur.
This factor limits the use of spinal anaesthesia to surgery
below the segmental level of T10.”
67. Centrineuraxial (spinal and epidural) anaesthesia is
not contraindicated in-
A. Platelets < 80,000
B. Patient on aspirin
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11ANAESTHESIA
C. Patient on oral anticoagulants
D. Raised intracranial pressure
B
..........(AIPGMEE - 2007)
Centrineuraxial anesthesia is not associated with increased
risk with most antiplatelet agents (eg. aspirin Q & NSAJDs).
Contraindications of Centrineuraxial (Spinal /Epidural)
Anesthesia
Absolute Contraindications
- Patient’s refusal
- Patient’s inability to maintain stillness during the needle
puncture (eg. dementia, psychosis)
- Raised intra cranial pressure
(papilledema, cerebral edema, tumors in posterior fossa,
suspected subarachnoid Hemorrhage)
- Severe hypovolemia
- Severe stenotic valvular heart disease, the patient may
be unable to compensate for vasodilation because of a
fixed cardiac output.
- Marked skin sepsis & marked spinal deformity
- Marked coagulopathy, blood dyscariasis or full anticoagulant
therapy
Relative contraindications
- Un coperative patient (may be performed in conjuction
with GA)
- Pre existing neurological deficit (eg demyelinating lesions).
- All severe & marked diseases in lesser degree i.e. spinal
deformity, sepsis etc.
- Pre eclamptic toxaemia - epidural block has been used
with great benefit in this condition, but a platelet count
of less than 100 xlO9 L”1 usually preclude epidural or
subarachnoid block.
- Mildly impaired coagulation
- Patients with platelet <80000 /ml
68. A Lower Segment Caesarean section (LSCS) can be
carried out under all the following techniques of
anaesthesia except:
A. General anaesthesia
B. Spinal anaesthesia
C. Caudal anaesthesia
D. Combined Spinal Epidural anaesthesia
C
..........(.AIPGMEE - 2005)
Caudal anaesthesia may be used for perenial operations.
It is not indicated in Lower segment caesarian section.
Further it is associated with potential risk of penetrating
the fetal head in obstetric practice.
69. A patient undergoing caesarean section following
prolonged labour under subarachnoid block
developed carpopedal spasm. Lignocaine was used
as anesthetic agent. The most likely diagnosis is:
A. Amniotic fluid embolism
B. Lignocaine toxicity
C. Hypocalcemia
D. Hypokalemia
C
..........(AIPGMEE - 2004)
During prolonged labour, pain from episodic uterine
contractions produces an increase in minute ventilation.
Hyperventilation thus produced results in development of
hypocarbia and respiratory alkalosis.
Resulting acute respiratory alkalosis causes intracellular shift
of K+, Na+ & PO4" and reduces free Ca
+2 by increasing
the protein bound fraction and precipitates
hypocalcemia.
Respiratory alkalosis secondary to hvperventilation following
prolonged labour may result in :
Lignocaine toxity is likely to cause hypercalcemia by 
releasing Ca into the blood and hence corpopedal
spasm as a manifestation is unlikely.
Symptoms 
secondary to 
hypophosphatemia
Muscle weakness
Symptoms 
secondary to 
hypocalcemia
Paraesthesias 
Carpopedal
spasm
Tetany
Neurological 
symptoms 
secondary to 
cerebral 
vasoconstriction
Dizziness Visual 
symptoms 
Syncope Seizure
Lignocaine toxity is likely to cause hypercalcemia by 
releasing Ca into the blood and hence corpopedal
spasm as a manifestation is unlikely.
Symptoms 
secondary to 
hypophosphatemia
Muscle weakness
Symptoms 
secondary to 
hypocalcemia
Paraesthesias 
Carpopedal
spasm
Tetany
Neurological 
symptoms 
secondary to 
cerebral 
vasoconstriction
Dizziness Visual 
symptoms 
Syncope Seizure
70. Concentration of Lidocaine used in spinal anaesthesia
A. 5%
B. 3%
C. 2%
D. 1%
A
..........(AIPGMEE - 1994)
Epidural 
Anesthesia
Topically in EyeSpinal 
Anesthesia
0.5%4%5%
Lignococine
Epidural 
Anesthesia
Topically in EyeSpinal 
Anesthesia
0.5%4%5%
Lignococine
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71. Post Spinal Headache canlast for
A. upto 10 min
B. upto 10 hours
C. 7-10 days
D. upto 10 months
C
..........(AIPGMEE - 1994)
Post spinal Headache starts in 1st 3 days and lasts for 1-
2 weeks
72. Best way to prevent hypotension during spinal
anesthesia
A. preloading with crystalloids
B. Mephentermine
C. Dopamine
D. Tredelenbug’s position
A
..........(AIPGMEE - 1995)
Hypotension following spinal anaesthesia is due to
blockage of sympathetic vasoconstrictor outflow
to blood vessels, venous pooling and decreased return
to heart. Prevention is by preloading with crystalloids.
73. Post sipnal headache is due to
A. Meningitis
B. Encephaletics
C. CSF leak
D. Increased ICT
C
..........(AIPGMEE - 1995)
‘Headache is due to seepage of CSF and can be minimized
by use of smaller bore needle’
74. In all of the following conditions neuraxial blockade
is absolutely contraindicated, except:
A. Patient refusal
B. Coagulopathy
C. Severe hypovolemia
D. Pre-existing neurological deficits
D
..........(AIPGMEE - 2003)
• Neuraxial block is combined name given to spinal, Epidural
and Caudal Blocks.
Principal site of action for neuroaxial block is Nerve root
Absolute contra indications are -
• Patient Refusal
• Bleeding Diathesis
• Severe Hypovolemia
• Raised ICT
• Infection at site of injection
Severe stenotic valvular Heart disease & fixed cardiac output
states
75. Spinal anaesthesea should be injected into the space
between:
A. T12 – L1
B. L1-L2
C. L3 – L4
D. L5 – S1
C
..........(AIPGMEE - 1997)
The LA is injected in the subarachnoid space between L 2_3orL
3_4, i.e. below the lower end of spinal cord.
• The primary site of action is the nerve root in the cauda
equina rather than the spinal cord.
• The level of anaesthesia depends on volume and speed
of injection, specific gravity of drug solution & posture of
the patient.
• Duration of spinal anaesthesia depends on drug used
and its concentration. e
• Autonomic pre-ganglionic fibres are more sensitive
and somatic motor fibres less sensitve than somatic sensory
fibres.
(Sympathetic block occurs before para-sympathetic and
somatic block).
76. Which is the true statement regarding post-dural
anesthetic headache:
A. Blood patch is the first line of treatment
B. Occurs due to low CSF pressrue
C. Increased incidence with early mobilization of patient.
D. Use of small guage needle prevents hea
A
..........(PGI - 2001 - Dec)
77. True about epidural anaesthesia in pregnancy:
A. Given through subarachnoid space.
B. Increases cardiac output.
C. Decreases venous return.
D. Venous pooling.
E. Decreased placental circulation
C
..........(PGI - DEC 2003)
• In epidural anesthesia, the anesthetic drug is injected in
a potential space within the bony cavity of the spinal canal
and outside the dural sac.
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In spinal anesthesia, only the drug is injected in the
subarachnoid space.
• CVS changes that occurs after epidural anaesthesia :
Epidural Anesthesia
• Loss of sympathetic vasomotor tone
• Vasodilatation
• Peripheral pooling of blood
• Reduced venous return
• Reduced cardiac output
Hypotension
• In the absence of hypotension, neither epidurals nor
spinal have any effect on the progress of labor nor
do they affect uterine blood flow.
Brief episode of hypotension do not appear to affect
the clinical condition of the neonates, the duration
seems more important than the degree.
Hypotension during epidural is usually said to occur if blood
pressure falls 20-30 mm Hg below the preepidural level or
systolic pressure drops below 100 Hg.
78. Vasopressor of choice in hypotension produced during
sub-arachroid block:
A. Ephedrine
B. Mephentermine
C. Adrenaline
D. Dopamine
E. Steroids
C & D
..........(PGI - DEC 2004)
79. Post dural puncture headache, true about
A. Common in elderly
B. Small bore needle prevents it
C. Early ambulation increases incidence
D. Occurs immediately after spinal anaesthesia
E. Blood patch is the first line of treatment
B
..........(PGI - JUNE 2004)
• Postdural puncture headache (PDPH) may occur after
deliberate or accidental dural puncture, or even after
uncomplicated block.
• Typically it comes on within an hour or two of the
anaesthesia & may be delayed for some days & may last
for weeks or even months.
• Pain usually occurs in the occipital region & a/w pain &
stiffness in neck.
It is worsened by sitting up & relived by lying down or by
abdominal compression.
Factors affecting PDPH :
• Increasing
- Younger age
- Females> male
• Larger needle
- Dural fibres cut transversely
- Pregnant females
- Multiple punctures
• Treatment:
PROPHYLACTIC
- Avoided in pts with h/o frequent severe headache
- Use of smaller sized needle
- Whitacre needle or sprotte needle should be used
- Prevention of dehydration,
DEFINITIVE
- Full hydration maintenance
- Simple analgesics
- Maintain supine position
- Continuous drip of Hartman’s solution in extradural space
with a catheter
Epidural blood patch with 10-20ml of venous blood.
80. Trendelenberg position produces decrease in all of
the following except-
A. Vital capacity
B. Functional residual capacity
C. Compliance
D. Respiratory rate
D
..........(AIIMS PGMEE - NOV 2004)
Trendelenburg position or head down position causes a
cephalad shift in the abdominal viscera and the
diaphragm.
This effects the lung volume in the following way
Functional residual capacity -----> Decreases
Total lung volume -----> Decreases
Vital capacity -----> Decreases
Lung compliance -----> Decreases
Although these changes are usually well tolerated by healthy
patients, it may cause hypoxemia in obese patients
and patients with preexisting lung disease.
The above mentioned changes also lead to increased
ventilation/perfusion mismatching and atelactasis.
There is also increased likelihood of regurgitation.
81. Site of action in epidural analgesia
A. Cortex
B. SubstantiaGelatinosa
C. Ventral horn
D. Sensory nerve ending
B
..........(AIIMS PGMEE - DEC 1998)
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• The epidural space is situated between the dura mater
and the vertebral canal . It extends from the cranium
to the sacrum and contains loose connective tissue, fat,
lymph vessels, blood vessels and nerves. Drugs can be
administered into the epidural space. 
• They diffuse across the dura and the subarachnoid
space and bind to receptors located in the
substantia gelatinosa in the dorsal horn of the spinal
cord. They also exert an effect on the nerve roots outside
the dura mater, are absorbed systemically from the epidural
blood vessels and may be distributed through the
subarachnoid space in the cerebrospinal fluid (CSF).
Substantia Gelatinosa
TOPIC 5: ANAESTHESIA COMPLICATIONS
82. Which does not cause bronchospasm after
anaesthesia
A. Regurgitation
B. Aspiration
C. Postintubation
D. Halothane
D
..........(AIIMS PGMEE - DEC 1994)
Halothane causes dilatation of Bronchi and is preferred in
Asthma
Causes of Bronchospam
The patients lower airways are excessively responsive to the
following –
1) Surgical stimulation
a) Intubation under light aneasthesia
b) Carinal stimulation by a tube that is too long
2) Respiratory infection
3) Pulmonary edema
4) Severe reduction in lung volume as in tension
pneumothorax, Drugs.
83. Mismatched blood transfusion manifests
intraoperatively as:
A. Rise in B. P.
B. Excessive bleeding
C. Dyspnoea
D. Hematuria
B
..........(PGI - 1999 - Dec)
Mismatched blood transfusion manifests intraoperatively as
EXCESSIVE BLEEDING.
84. Mendelson syndrome is due to:
A. Aspiration pneumonitis
B. Chemical pneumonitis
C. Oesophagitis
D. Oesophageal spasm
A
..........(PGI - 1998 - Dec)
• Mendelson’s syndrome is acid aspiration syndrome.
Aspiration of acid gastric contents cause a chemical trauma
to bronchial and alveolar epithelia i.e. acute exudative
pneumonitis
Mendelson’s syndrome usually occur with material (gastric
acid) at a PH of 2.5 or below, but known to occur with
fluid of a neutral PH as well.
85. Diffusionhypoxia is seen during:
A. Induction of anaesthesia
B. Recovering anaesthesia
C. Preoperatively
D. Postoperatively
B
..........(PGI - 1998 - Dec)
Diffusion hypoxia is seen during recovering anaesthesia. It is
seen with N2O.
Mechanism
After prolonged N2 O anaesthesia when discontinued N2O
having low Solubility rapidly diffuses to alveoli and dilutes
alveolar air PP of oxygen in alveoli is reduced: Resulting
hypoxia is called DIFFUSION HYPOXIA
86. Incubator heat is delivered by except:
A. Conduction
B. Convection
C. Radiation
D. Evaporation
D 
..........(PGI - 1998 - Dec)
• Incubator heat is delivered by radiation and convection.
Some incubators have humidifiers which will produce an
ambient relative humidity within the canopy of 90% or
more (compared with 30—40% hunidity without
humidifier).
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At such humidity infants evaporative heat loss is very low.
Also sometimes wall of the incubator is doubled which
also helps to prevent evaporative loss of heat from infant.
In infant heat loss through conduction is very small as infants
are not usually in direct contact with structure of
high thermal capacity.
87. During intra operative anesthesia mismatched blood
by transfusion is manifested by:
A. Hypotension
B. Increase Bleeding
C. Bonchospasm
D. Movement of limbs
E. Rash
A & B, C
..........(PGI - JUNE 2006)
* Mismatched blood transfusion in anaesthetic patient
present as :
Immediate rapid severe and progressive hypotension.
Tachycardia
General oozing from wound.
Urticarial rash.
Bronchospasm, raising airway pressures on intermittent positive
pressure ventilation. Later jaundice and oliguria in 5-10%
of these patient.
88. Cause of post-operative hypertension
A. Pre-operative hypertension
B. inadequate analgesia
C. Phaeochromocytoma
D. Hypoxaemia
E. Hypercarbia
All
..........(PGI - JUNE 2004)
89. True about aspiration pneumonia
A. Affected by volume of aspiration
B. Affected by PH of aspiration fluid
C. Increased incidence during induction
D. Inflammation
E. Infection
All
..........(PGI - JUNE 2004)
• Factors affecting Acid aspiration pneumonia:
- Aspirate volume > 25ml
- PH of aspirate <2.5
- Aspiration of partially digested food
• Conscious level of patients (e.g. alcoholics, drug
abusers, seizures, strokes or general anaesthesia)
- Mechanical impediments (e.g. nasogastric or
endotracheal tubes)
• Pure acid aspiration producing aspiration
pneumonitis or chemical pneumonitis (inflam­mation)
& aspiration of oropharyngeal secretion produces
severe bacterial pneumonitis.
91. Sodium nitroprusside infusion may result in:
A. Hypertension
B. Pulmonary oedema
C. Cyanide toxicity
D. Heart block
C
..........(AIIMS PGMEE - MAY 2005)
• Sodium Nitroprusside is an effective antihypertensive agent
(dilates both arteries and veins)
• Sodium Nitroprusside can sometimes cause toxicity due
to its conversion to cyanide and thiocyanate, when its
infused for longer duration.
• “Toxic accumulation of cyanide leading to severe lactic
acidosis, can occur usually if sodium nitroprusside is infused
at a rate greater than 5 microgm/kg.”
• Short-term side-effects of nitroprusside are d/t excessive
vasodilation with hypotension and its consequences
92. The most common cause of morbidity and mortality
in patients undergoing major vascular surgery is:
A. Renal complications
B. Thrombo embolic phenomenon
C. Coagulopathies
D. Cardiac complications
Ans d
..........(AIIMS PGMEE - MAY 2005)
93. The most common rhythm disturbance during early
postoperative period is:
A. Bradycarida
B. Ventricular fibrillation
C. Tachycardia
D. Complete heart block
Ans c
..........(AIIMS PGMEE - MAY 2005)
The most common acute post-operative arrhythmias
were junctional ectopic tachycardia
94. Most common cause of postoperative renal failure:
A. Decreased renal perfusion
B. Toxicity of anesthetic drugs
C. Toxicity of antibiotics
D. ——
A
..........(AIIMS PGMEE - MAY 2008)
• Most common cause of postoperative renal failure
is decreased renal perfusion due to hypovolemia.
Hypovolemia usually results from inadequate intraoperative
fluid replacement, continuing fluid sequestration by
tissues {third spacing) or wound drainage or postoperative
bleeding.
95. Which of the following does not represent a
significant anaesthetic problem in the morbidly obese
patient?
A. Difficulties in endotracheal intubation
B. Suboptimal arterial oxygen tension
C. Increased metabolism of volatile agents
D. Decreased cardiac output relative to total body mass
D
..........(AIIMS PGMEE - NOV 2004)
TOPIC 5: ANAESTHESIA COMPLICATIONS
HELP LINE NO. 9391567707
16ANAESTHESIA
Problems faced by obese patient during anaesthesia
Perioperative
These patients are often difficult to intubate as a result
of limited mobility of temperomandibular and atlantoccipital
joints, a narrowed airway and a shortened distance
between mandible and sternal fat pads.
Increased risk of developing aspiration pneumonia,
therefore routine t/t with H2 antagonists and
metoclopromide is given.
Intraoperative
Volatile anaesthetics are metabolized more rapidly while
the action of nonvolatile agents are prolonged.
Risk of aspiration
Difficulties in regional anaesthesia
Postoperative
Respiratory failure is the major problem
postoperatively
There is risk of postoperative hypoxia, so extubation should
be delayed until the effects of neuromuscular blocker is
completely reversed.
Cardiovascular changes in obesity
• High Blood volume
• High Cardiac output
• Hypertension (Systemic and pulmonary)
• High Workload on heart
• High Stroke volume
• Cardiomegaly
Respiratory changes in an obese patient
• Decrease in vital capacity and functional residual capacity
• Hypoxemia
• Decrease compliance
• Decrease respiratory drive
These patients require high FiO2 to achieve adequate
oxygenation, the ratio of Nitrous Oxide by O2 is kept at 2/
3
Gastrointestinal changes in obesity
Hiatal hernia
Gastroesophageal reflux
Poor gastric emptying
Hyper acidic gastric fluid
96. The most sensitive and practical technique for
detection of myocardial ischemia in the perioperative
period is -
A. Magnetic Resonance Spectroscopy
B. Radio labeled lactate determination
C. Direct measurement of end diastolic pressure
D. Regional wall motion abnormality detected with the help
of 2D transoesophagealechocardiography
D
..........(AIIMS PGMEE - NOV 2005)
Two dimensional transesophageal echocardiography is the
most sensitive method to detect myocardial ischemia in
the perioperative period.
• Hemodynamic monitoring - It is done by
Central venous or pulmonary artery pressure monitoring.
The most sensitive hemodynamic correlates are derived
from pulmonary artery pressure monitoring -
Ischemia is frequently but not always associated with an
abrupt increase in pulmonary capillary wedge pressure.
The most common hemodynamic abnormalities observed
during ischemic episodes are hypertension and
tachycardia.
97. Sallick’s manouvere is used
A. To reduce dead space
B. To prevent alveolar collapse
C. To prevent gastric aspiration
D. To facilitate assisted respiration
C
..........(AIIMS PGMEE - DEC 1997)
• Sallick’s manoeuvre is application of backward pressure
on Cricoid cartilage to prevent gastric aspiration.
TOPIC 6: HALOTHANE
98. Hepatoxic anaesthetic agent is:
A. Ketamine
B. Ether
C. Nitrous Oxide
D. Halothane
D
..........(AIIMS PGMEE - JUNE - 1997)
• Halothane is hepatoxic. It is “contraindicated” in liver
diseases.
• Other Important side effects of Halothane
• Arrythmia (Max Arrythmogenic)*
Malignant Hyperthermia*
99. Least analgesic gas used is
A. N20
B. Ether
C. Halothane
D. Cyclopropane
C
..........(AIIMS PGMEE - MAY - 1994)
• Halothane is a potent anaesthetic but poor analgesic
All the other agents mentioned in the question are good
analgesics
Nitrous Oxide - It is good analgesic but poor anaesthetic.
Ether - It is potent anaesthetic as well as good analgesic
Cyclopropane - It is a good anaesthetic and a good analgesic100. Which one of the following agents sensitizes the
myocardium to catecholamines?
A. Isoflurane
B. Ether
C. Halothane
D. Propofol
C
..........(AIPGMEE - 2006)
Halothane sensitize the heart to adrenaline (both
exogenous as well as endogenous, more prominently
exogenous) producing severe ventricular arrhythmias‘.
TOPIC 6: HALOTHANE
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17ANAESTHESIA
101. Repeated use of halothane causes:
A. Hepatitis
B. Encephalitis. .
C. Pancreatitis
D. Bronchitis
A
..........(AIPGMEE - 1999), PGI - JUNE 1997
Hepatitis
Massive hepatic necrosis has been seen following halothane
anesthesia.
Subclinical ‘Halothane Hepatitis1 with lesser degree of liver
impairment, and a hepatocellular pattern of elevated
transferases may also occur.
The most susceptible ones are middle-aged females and obese.
102. Anatomical dead space is increased by all of the
following except:
A. Atropine
B. Halothane
C. Massive pleural effusion
D. Inspiration
C
..........(AIPGMEE - 1999)
Anatomical dead space means those areas in the tracheo-
bronchial tree, where the gaseous exchange between
the lung and capillaries is not possible.
This area starts from the nasal cavity and includes,
larynx, trachea, bronchii and ends in the terminal
bronchiole.
Pleural effusion, normally tends to compress on the alveoli
and thus interferes with the physiological dead space
(space where gaseous exchange is occurring).
However, with a massive effusion, atleast some of the structure
comprising the anatomical dead space may be compressed
thereby decreasing the anatomical dead space.
103. All of the following are true except:
A. Halothane is good as an analgesic agent
B. Halothane sensitises the heart to action of catacholamines
C. Halothane relaxes brochi & is preferred in anaes thetics
D. Halothane may cause Liver cell necrosis
A
..........(AIPGMEE - 2001)
Halothane is good as an analgesic agent
• Halothane is a potent anaesthetic but not a good analgesic
or muscle relaxant.
• Halothane sensitizes the heart to arrythmogenic action of
Adrenaline
• Remember drugs which sensitizes the heat to
arrythmogenic action of adrenaline include
- Halothane
- Methoxyflurance
- Trichloroethylene
- Cyclopropane
- Chloroform
- Halothane causes bronchodilation. Thus it is preferred in
asthmatics (also Ketamine)
• Massive hepatic necrosis is following halothane
anaesthesia has been reported
104. Anesthesia agent with least analgesic property
A. N2O
B. Halothane
C. Ether
D. Propane
B
..........(AIPGMEE - 1994)
Halothane is a potent anaesthetic but provides poor analgesia.
Halothane Analgesic 
N2O Only analgesia 
Ketarnine Profound Analgesia 
TrileneBest/Maximum 
analgesia 
Halothane Analgesic 
N2O Only analgesia 
Ketarnine Profound Analgesia 
TrileneBest/Maximum 
analgesia 
105. Post operative jaundice is because of use of:
A. Isoflurane
B. NO
C. Melhoxyflurane
D. Halothane
D
..........(PGI - 1999 - Dec)
• Post operative jaundice can be cause by halothane. It
can cause massive hepatic necrosis, subclinical one is called
‘Halothane hepatitis.’
Note : Other causes of post. Operative jaundice
- Phenothiaziges
- MAO inhibitors
- Blood. Transfusion
- Sepsis
Coincidental viral infection.
106. True about halothane:
A. 1% Thymol is used as preservative.
B. It sensitizes heart to catecholamines at 1 MAC.
C. 20% metabolized.
D. It is not usually given in same patient within 3 months.
E. It forms compound-A with sodalime,
B
..........(PGI - DEC 2003)
• Halothane is a volatile, liquid with sweet odour, nonirritant
and noninflammable anaesthetic.
• It contains 0.01% thymol for stability and decomposed
by light, but is stable when stored in amber-lime and the
vapour is absorbed by rubber.
• An estimated 15-20% of absorbed halothane undergoes
metabolism.
• Sevoflurane reacts with soda-lime and thus produces
compound-i.e., pentafluoroisopropenyl fluromethyl ether.
• Pethidine is recommended in the management of
Halothane shakes.
• Halothane may persist in the liver for as long as 12 days
after administration.
107. True about halothane:
A. Causes bronchodilation
B. Anti-arrhythmic
C. Ted cardiac index
D. Uterine contraction occurs
E. Causes hepatitis
A & E
..........(PGI - DEC 2002)
TOPIC 6: HALOTHANE
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18ANAESTHESIA
108. True about Halothane:
A. Non-irritant
B. Antiarrhythmic
C. It antagonises bronchospasm
D. Vasodilator
A & C
..........(PGI - DEC 2006)
• Halothane is a colourless, relatively non-irritant vapour.
It is non-flammable non-explosive when mixed with O2 in
any concentrations used clinically.
Effects on organs :
CVS : - Myocardial depression, fall of arterial pressure.
- Vasodilatation, dilates coronary arteries
- Bradycardia.
- Increased myocardial excitability, ventricular extrasystoles.
Arrythmia after I.V. infusion of Adrenaline > 10 micro g/
min.
110. Which of the are the following contraindication for
halothane used:
A. Male sex
B. Middle age
C. Recent halothane use
D. Associated liver pathology
E. Obesity
C & D
..........(PGI - June -2001)
111. Which of the following fluorinated anaesthetics
corrodes metal in vaporizers and breathing systems?
A. Sevoflurane
B. Enflurane
C. Isoflurane
D. Halothane
D
..........(AIIMS PGMEE - MAY 2006)
• Halothane causes corrosion of metals in vaporizers and
breathing system
TOPIC 7: THIOPENTONE
112. Intra arterial injection of thiopentone causes:
A. Hypotension
B. Necrosis of vessel wall
C. Vasodilation
D. Vasospasm
D
..........(AIIMS PGMEE - Dec - 1995)
Vasospasm
When thiopentone is given intra arterial it results in ppt of
solid crystals of Thiopentone
↓
These solid crystal block small vascular channels at Arteriolar
and capillary levels
↓
Vasospasm
(d/t irritant properties of solid crystals)
• Morbidity due to Intra arterial injection of Thiopentone is
also d/t
– Thrombosis & Endothelial damage
While Intra arterial injection causes Vasospasm
intravenous injection causes Vasodilatation.
113. Thiopentone is contraindicated in:
A. Acute intermitent porphyria
B. Induction of GA
C. CHF
D. GI disease
A
..........(AIIMS PGMEE - FEB - 1997)
• Acute intermitent porphyria
• Barbiturates (Thiopentone) ppt acute intermitent
porphyria
Safe drugs in porphyria
Drugs used in anaesthesia
Adrenaline
Atropine 
Cyclopropane
Epinephrine
Ether
Isoflurane
Neostigmine
Nitrous oxide
Pancuronium
Phentolamine
Propofol
Suxamethonium
Local Anaesthesia
Amethocaine
Bupivacaine
Lignocaine 2
Prilocaine
Procaine
Tetracaine
Safe anticonvulsants in porphyria
Anticonvulsants
Clobazam
Clonazepam
Gabapentin
Sodium 
valporate
Valporate3
Vigabatrin
Safe drugs in porphyria
Analgesics
Alfentanil
Aspirin 
Buprenorphine
Codeine Phosphate
Dextromethorphan
Dextromoramide
Diamorphine
Dihydrocodeine
Fenbufen
Fentanyl
TOPIC 7: THIOPENTONE
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19ANAESTHESIA
Flurbiprofen
Ibuprofen
Indometacin
Ketoprofen
Meloxicam
Methadone
Morphine
Naproxen
Paracetamol
Pethidine
Piroxicam
Sulindac
Antidepressants
Fluoxetine
Mianserin
Antipsychotics
Chlorpromazine
Fluphenazine
Haloperidol
Olanzapine
Pipotiazine
Trifluoperazine
114. Intraarterial Thiopentone injection causes
A. Cardiac arrest
B. Respiratory arrest
C. Convulsion
D. Pain
D
..........(AIIMS PGMEE - NOV - 1993)
Signs and symptoms of intra arterial injection of
thiopentone
a) Immediate -
i) Pain
ii) White hand with cyanosed fingers
iii) Patches of skin discolouration
iv) Onset of unconsciousness is delayed beyond the usual
time
b) Late
i) Ulcers or blisters
ii) Edema of forearm and hand
iii) Gangrene - rare
115. A pt. Selected for surgery who was induced with
thiopentone i.v. through one of the antecubital veins
complains of severe pain of whole hand. The next
line of management is:
A. Give I.V. Ketamine through same needle
B. Give I.V. propofol through same needle
C. Leave it alone
D. Give I.V. lignocaine through same needle
D
..........(AIIMS PGMEE MAY - 2001), AIPGMEE - 1997
Give I.V. lignocaine through same needle
• Injection . has gone into the Artery which lies adjacent
to the antecubitalvein.
• Immediate symptoms and sign of intra arterial
thiopentone
1. Pain during injection
2. A white hand with cyanosed fingers d/t arterial spasm
which may be accompanied or followed by arterial
thrombosis
3. Patches of skin discoloration in the limb
4. Onset of unconsciousness may be delayed beyond the
usual, time.
Treatment
• Leave the canula in site
• Heparin 1000 units is given via cannula in the Artery
• Through Canula in the Artery inject
(a) Papavarine 40 -80 mg in 10- 20 ml of Saline
(b) Prostacycline
(c) Dexamethaethasone
(d) Tolazoline
(e) Phenoxybenzamine
(f) Urokinase
• Cancel the operation
• Possibly continue volatile anesthesia as an effective
method of securing vasodilatation
• Perform a Brachical plexus or stellae ganglion block to
remove all vasoconstrictor impulses
• I. V. lignocaine is a vasoditator
– (all local anesthetics are vasoditator except cocaine) and
can help overcome the vasoconstriction caused by
thiopentone.
116. During surgery for aortic arch aneurysm under deep
hypothermic circulatory arrest which of the following
anaesthetic agent administered prior to circulatory
arrest that also provides cerebral protection ?
A. Etomidate
B. Thiopental Sodium
C. Propofal
D. Ketamine
B
..........(AIIMS PGMEE NOV - 2002)
• During the surgery for aortic arch all the blood supply to
the brain has to be stopped so that proper arch
anastomosis can be performed. This carries great risk for
the brain. So the surgery for aortic arch aneurysm is
performed now days using deep hypothermia and
circulatory arrest method.
• It is based on the principle that brain can safely tolerate
circulatory arrest for periods of upto 45minutes, if the
temperature is carefully lowered to 15-17°C wide surgery.
So during surgery for aortic arch aneurysm temperature is
lowered till the temperature of the body is lowered up to
15-17°c and then surgery is performed.
• During this process we need an anaesthetic agent which
lowers the metabolic demands of the brain, so that the
brain can sustain longer periods of circulatory arrest.
Thiopentone sodium is one such drug, which lowers
the metabolic demands of brains and provides it
added protection, when its blood supply it reduced
during surgery.
117. Which of the following anesthetic agents does not
trigger malignant hyperthermia?
A Halothane
B. Isoflurane
C. Suxamethonium
D. Thiopentone
D
..........(AIPGMEE - 2006)
‘Muscle relaxant succinylcholine is the most commonly
implicated agent. Halothane and isoflurane have also been
implicated.
Barbiturates (thiopentone sodium) are safe drugs for
general anaesthesia in patients susceptible for
malignanthyperthermia
Malignant Hyperthermia
Malignant hyperthermia is a familial syndrome characterized
clinically by arise of temperature of at least 2DC/hour
Inheritance
TOPIC 7: THIOPENTONE
HELP LINE NO. 9391567707
20ANAESTHESIA
Autosomal dominant inheritance with incomplete
penetration .Defect in gene on chromosome
Pathology
Abnormality of Ryanodine Receptor: calcium releasing
channel of sarcoplasmic reticulum. Sudden rise in
intracellular calcium2 leads to hypermetabolic state.
118. Not intravenous Anasthetic agent
A. Ketamine
B. Thiopantone
C. Etomidate
D. Cyclopropane
D
..........(AIPGMEE - 1995)
Classification of Anaesthetic agents:
- Sevoflurane
- Desmoflurane
- Iso flurane
- Enflurane
Droperidol
(Neurolept
analgesia)
• Etomidate• Fluranes
• Fentanyl• Thiopentone• Cyclopropane
(dissociative
anesthesia)
•
Methohexitone
• Halothane
• Ketamine• Propofol• Ether• N2O
Slower ActingInducing agentLiquidGas
IntravenousInhalation
- Sevoflurane
- Desmoflurane
- Iso flurane
- Enflurane
Droperidol
(Neurolept
analgesia)
• Etomidate• Fluranes
• Fentanyl• Thiopentone• Cyclopropane
(dissociative
anesthesia)
•
Methohexitone
• Halothane
• Ketamine• Propofol• Ether• N2O
Slower ActingInducing agentLiquidGas
IntravenousInhalation
119. Sodium Thiopentone is ultra short acting d/t
A. Rapid absorption
B. Rapid metabolism
C. Rapid redistribution
D. Rapic excretion
C
..........(AIPGMEE - 1996)
121. Uses of thiopentone:
A. Seizure
B. Truth spell
C. Reduction of I.C.P.
D. Cerebral protection
E. Maintanance of Anesthesia
Ans a,b,c,d,e
..........(PGI - DEC 2004)
122. Which of the following is not analgesic
A. N2O
B. Thiopentone
C. Methohexitone
D. Ketamine
E. Fentanyl
B
..........(PGI - DEC 2005)
* N2O (nitrous oxide) is a weak anaesthetic agent having
potent analgesic property.
* Thiopentone & Methohexitone, both are barbiturate group
of induction agent without analgesic properties.
Thiopentone having ant-analgesic property only i.e.
it decreases the pain threshold.
* Ketamine is having profound analgesic property.
* Fentanyl is a synthetic opioid having intense analgesia.
123. Intravenous thiopentone, produces
A. Rash
B. Pain
C. Spasm
D. Hypotension
E. Muscular excitation (locally)
A & B & D
..........(PGI - JUNE 2003)
• Thiopentone is an ultra short acting barbiturate used for
induction of anaesthesia.
• The different effects produced by thiopentone are :
CNS & Respiratory system : Sedation, hypnosis, anaesthesia
& respiratory depression.
- Increased cerebral blood flow, decrease I C pressure,
Cerebral metabolism & O2 consumption leading to cerebral
protection..
- CVS : hypotension due to vasodilatation in skin & muscle.
Larynx : Increased sensitivity to stimuli producing laryngeal
spasm.
Eye : - pupils first dilate then constrict.
- Loss of eyelash reflex is an excellent sign of adequate
induction.
Allergic reaction : Rarely manifests as scarlantiniform rash,
angioneurotic edema & photosensitivity.
Injection effects : - The incidence of pain on injection is
1-2% when injected into small veins & essentially none
when injected into larger veins.
- Perivenous injection produces pain, redness & swelling,
haematoma formation, bruising, rarely ulceration.
- Accidental intraarterial injection produces intense arterial
spasm & excruciating pain that can be felt from the
injection site to the hand & fingers.
Musculo skeletal : Besides producing unconsciousness, it
can cause mild muscular excitatory movements such as
hypertonus, tremor or twitching & respiratory excitatory
effects including cough & hiccup. These are dose
dependent effects.
124. Regarding thiopentone all are true except
A. Sodium carbonate is added to improve its solubility
B. Cerebro protective
C. Contraindicated in porphyria
D. Induction agent of choice in shock
D
..........(AIIMS PGMEE - NOV 2007)
• Thiopentone is a short acting barbiturate used in the
induction of anaesthesia.
• Anaesthetic barbiturates are derivatives of Barbituric acid
with an oxygen or sulfur at 2 position.
• The three barbiturates commonly used for clinical
anaesthesia are :
• Sodium thiopental
• Thiamylal
• Methohexital
Barbiturates are formulated as the sodium salts with
6% sodium carbonate and reconstituted in water or
isotonic saline to produce alkaline solutions with pH of 10-
11.
• Once reconstituted these are stable in solutions for
upto 1 week.
TOPIC 7: THIOPENTONE
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21ANAESTHESIA
• Thiopentone is used for the induction of anaesthesia
because it has a very rapid onset of action.
• The typical induction dose (3-5 mg/kg) of thiopentone
produces unconsciousness in 10-30 seconds with a peak
effect in 1 minute and duration of anaesthesia of 5-8
minutes.
• Action of this drug terminates quickly because of rapid
redistribution.
• Thiopentone is highly lipid soluble, therefore its
redistribution is very rapid and this accounts for its short
duration of action.
• Sulphur is added to increase the lipid solubility of
thiopentone.
• Thiopentone is given intravenously.
• It produces little to no pain on injection.
• Venoirritation can be reduced by injection into larger non
hand veins and by prior intravenous injectionof lidocaine.
• If sometimes thiopentone inadvertently enter
intraarterial circulation it causes severe inflammatory
and potentially necrotic reaction.
Effects on system C.N.S.
• Besides producinga general anaesthesia, barbiturates
reduce the cerebral metabolic rate, as measured by
cerebral oxygen consumption (CMR0 2) in a dose
dependent manner.
• As a consequence of the decrease in (CMRO2) cerebral
blood flow and intracranial pressure are similarly reduced.
• Because it markedly lowers cerebral metabolism,
thiopentone has been used as a protectant against
cerebral ischemia.
• Thiopentone also reduces intraocular pressure.
• Presumbaly in part due to their CNS depressant activity
barbiturates are effective anticonvulsants.
• Thiopentone in particular is a proven medication in the t/
t of status epilepticus.
C.V.S
• Thiopentone produces dose dependent decrease in
blood pressure.
• The effect is primarily due to vasodilation particularly
venodilation.
Respiratory
• Theiopentone is respiratory depressants.
• It causes dose dependent decrease in minute ventilation
and tidal volume with a smaller and inconsistent decrease
in respiratory rate.
Other adverse effects
• Thiopentone has no clinically significant effect on hepatic,
renal or endocrine systems.
• Thiopentone (Barbiturates) can induce fatal attacks of
porphyria in patients with acute intermittent porphyria
and are contraindicated in such patients.
TOPIC 8: PAEDIATRIC ANESTHESIA
125. Method of anaesthetic induction in children is by
A. Intramuscular
B. Inhalation
C. Intravenous
D. Oxygen tent
C
..........(AIIMS PGMEE - NOV - 1993)
• In children intravenous induction of anaesthesia is the
most common method used for induction of anaesthesia.
• The drug most commonly used is thiopentone
Other drugs used are -
1) Methohexitone
2) Propofol
3) Etomidate
4) Ketamine
126. The ideal muscle relaxant used for a neonate
undergoing porto-enterostomy for biliary atresia is:
A. Atracurium.
B. Vecuronium
C. Pancuronium.
D. Rocuronium
A
..........(.AIIMS PGMEE MAY - 2003)
In this case a muscle relaxant is required whose metabolism
has nothing to do with liver (because liver is damaged in
biliary atresia)
• So Atracurium is the muscle relaxant of choice as it is
inactivated in plasma by spontaneous non enzymatic
degradation. (Hoffman elimination) so its duration of
action will not be affected in patients with hepatic
insufficiency.
127. In a 2 months old infant undergoing surgery for
biliary atresia, you would avoid one of the following
anaesthetic
A. Thiopentone
B. Halothane.
C. Propofol.
D. Sevoflurane
B
..........(.AIIMS PGMEE MAY - 2003)
halothane is known to cause liver toxicity. So Halothane
should be avoided in a patient undergoing surgery for
Biliary atresia (as the liver is already damaged)
128. Regarding neonatal circumcision, which one of the
following is true:
A. It should be done without anaesthesia, as it is hazardous
to give anaesthesia.
B. It should be done without anesthesia, as neonates do not
perceive pain as adults.
C. It should be done under local anaesthesia only.
D. General anaesthesia should be given to neonate for
circumcision as they also feel pain as adults
D
..........(.AIIMS PGMEE MAY - 2003)
Circumcision anaesthesia.
“A general anaesthetic is preferable in children, but in
adults local infiltrative anaesthesia, or regional anaesthesia
with a caudal or subpubic block is also satisfactory
TOPIC 8: PAEDIATRIC ANESTHESIA
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22ANAESTHESIA
129. Which of the following inhalational agents is the
induction agent of choice in children:
A. Methoxyflurane
B. Sevoflurane
C. Desflurane
D. Isoflurane
B
..........(AIPGMEE - 2006)
Faster, pleasant, and smooth in duction with no significant
systemic toxity makes sevoflurane the agent of choice
for induction, especially in children
130. A two-month-old infant has undergone a major
surgical procedure. Regarding postoperative pain
relief which one of the following is recommended:
A. No medication is needed as infant does not feel pain after
surgery due to immaturity of nervous system
B. Only paracetamol suppository is adequate
C. Spinal narcotics via intrathecal route
D. Intravenous narcotic infusion is lower dosage
Ans c
..........(AIPGMEE - 2006)
• Bupivacaine has, until recently, been the drug of choice
for postoperative epidural infusions in children. Despite a
reasonable safety profile, bupivacaine is currently being
replaced by many anesthesiologists with new local
anesthetics: levobupivacaine and ropivacaine. These
local anesthetics are associated with less risk for cardiac
and central nervous system toxicity and are also less likely
to result in unwanted postoperative motor blockade
131. A non ventilated preterm baby in incubator is under
observation. Which is the best way to monitor the
baby’s breathing and detect apnea?
A. Capnography
B. Impedence pulmonometry
C. Chest movement monitoring
D. Infrared End Tidal CO 2mesurement
A
..........(AIPGMEE - 2007)
• Capnography is the monitoring of the concentration or
partial pressure of carbon dioxide (CO2) in the
respiratory gases .
• Its main development has been as a monitoring tool
for use during anaesthesia and intensive care .
• It is usually presented as a graph of expiratory CO2
plotted against time , or, less commonly, but more
usefully, expired volume. The plot may also show the
inspired CO2, which is of interest when rebreathing
systems are being used.
• The capnogram is a direct monitor of the inhaled and
exhaled concentration or partial pressure of CO2,
and an indirect monitor of the CO2 partial pressure
in the arterial blood. In healthy individuals, the difference
between arterial blood and expired gas CO2 partial
pressures is very small, and is probably zero in children. In
the presence of most forms of lung disease, and some
forms of congenital heart disease (the cyanotic lesions)
the difference between arterial blood and expired gas
increases and can exceed 1 kPa.
• During anaesthesia, there is interplay between two
components: the patient and the anaesthesia
administration device (which is usually a breathing circuit
and a ventilator or respirator). The critical connection
between the two components is either an endotracheal
tube or a mask, and CO2 is typically monitored at this
junction. Capnography directly reflects the elimination of
CO2 by the lungs to the anaesthesia device. Indirectly, it
reflects the production of CO2 by tissues and the
circulatory transport of CO2 to the lungs.
132. All of the following agents can be given for
induction of anaesthesia in children except:
A. Halothane
B. Servoflurane
C. Morphine
D. Nitrous oxide
C
..........(AIPGMEE - 2001)
Morphine
Morphine should not be used in infants specially those
less than 6 months of age.
Morphine is also not commonly recommended in older children
(3-10 years) of age
Most commonly used method for inducing gaseous anaesthesia
is with O2, with or without N2O and either halothane
or sevoflurane.
TOPIC 8: PAEDIATRIC ANESTHESIA
HELP LINE NO. 9391567707
23ANAESTHESIA
• Halothane is well tolerated in children , in which the
risk of halothane induced hepatitis on repeated
administration is small.
• Enflurane and isoflurane are more pungent and not
recommended
• Sevoflurane, if available is the agent of choice
• Nitrous oxide is particularly useful because of the
speed of induction, absence of cardiovascular and
respiratory depression, its rapid onset and offset, and its
powerful analgesic action.
135. Upper respiratory tract infection is a common
problem in children. All the following anesthetic
complications can occur in children with respiratory
infections, except:
A. Bacteremia
B. Halothane granuloma
C. Increased mucosal bleeding
D. Laryngospasm
B
..........(AIPGMEE - 2002)
• Due to local infection there is hyperemia of the local area
& trauma can result in mucosal bleeding
• Due to local edema & inflammation laryngospasm can be a
complication
• Systemic infection can lead to Bacteremia
TOPIC 9: VENTILATOR
136. After Hyperventilating for some time holding the
breath is dangerous because:
A. Decrease CO2 shift the O2 dissociation curve to the left
B. Alkalosis