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Posted by Dr KAMAL DEEP on April 25, 2013

Guedels stages of anaesthesia is seen classically with
a) Ether b) Chloroform c) Morphine d) Nitrous oxide e) halothane

The term anasthesia was coined by
a) Guedel b) Morton c) Claude d) Oliver Wendel Holmes.

Intravenous Regional Anaesthesia was described by
a) Macintosh b) Magill c) Guedel d) Bains e) Bier

The first public demonstration of anesthesia was by
a) John snow b) 1. W magill c) Thomas morton d) H.G. Wells

First spinal anaesthesia was given by TN 2001
a) August Bier b) Sicard c) Morton d) Priestly

Ether was invented by
a) Morton b) Priestly c) Wells d) Simpson

Nitrous oxide was discovered by
a) J.B.Priestly b) Humphry Davy c) I4orace wells d) P.C.Barton e) G.Q. cotton


In 1937, Guedel published his classic description of the clinical signs of ether anesthesia. He used clear physical signs involving somatic muscle tone, respiratory patterns, and ocular signs to define four stages.

In the first stage, analgesia, characterized by slow, regular breathing with the diaphragm and intercostal muscles and the presence of the lid reflex, the subject experiences complete amnesia, analgesia, and sedation.

In the second stage (delirium), the subject experiences excitement, unconsciousness, and a dream state with uninhibited activity. Ventilation is irregular and unpredictable. Reflex dilatation of the pupils occurs, the lid reflex is intact, and the risk of clinically important reflex activity (e.g., vomiting, laryngospasm, or arrhythmias) increases.

The third stage (surgical anesthesia) consists of four progressive planes. Plane 1 is characterized by slight somatic relaxation, regular periodic breathing, and active ocular muscles. During plane 2, breathing changes, inhalation becomes briefer than exhalation, and a slight pause separates inhalation and exhalation. The eyes become immobile. In plane 3, the abdominal muscles are completely relaxed, and diaphragmatic breathing is very prominent. The eyelid reflex is absent. In plane 4, the intercostal muscles are completely paralyzed, and paradoxic rib cage movement occurs. Breathing is irregular, and pupils are dilated.

In Guedel’s fourth stage (respiratory paralysis), muscles become flaccid, and eyes widely dilate. Cardiovascular and respiratory arrest occurs, as does cardiovascular collapse.
In 1954, Artusio expanded Guedel’s description of ether analgesia (stage 1) into three planes. In plane 1, the patient has no amnesia or analgesia. In plane 2, the patient has total amnesia and partial analgesia. In plane 3, the patient has complete analgesia and amnesia, but is comfortable and responsive to verbal stimulation; there is little depression of reflexes. Artusio observed that once patients were anesthetized past stage II (delirium) to the deeper anesthesia of stage III, they could be brought back and forth between stage III and plane 3 of stage II without ever exhibiting stage II. The clinical signs of depth of anesthesia defined by Guedel and others had significant practical utility for the administration of ether, cyclopropane, and chloroform anesthesia.



Succinyl choline is a muscle relaxant which act by
a) persistent depolarisation b) competitive blockade c) mechanism of action uncertain d) a and b

Muscle relaxant contra indicated in CRF

a) Gallamine b) Succinylcholine c) Tubocurare d) Pancuronium


Muscle relaxant not to be used in liver failure is PGI 88
a) Pancuronium b) DTC c) Suxamethonium d) Decamethonium

Decamethonium (Syncurine) is a depolarizing muscle relaxant or neuromuscular blocking agent

Site of-action of anaesthetic muscle relaxants is PGI 88
a) Myoneural junction b) central c) ascending reticular activating system d) Red nucleus

Muscle relaxant most commonly implicated in malignant hyperpyrexia a) DTC b) Gallamine c) Succinylcholine d) Decamethanium

Decamethonium (Syncurine) is a depolarizing muscle relaxant or neuromuscular blocking agent

The muscle relaxant effect of succinylcholine last for
a) 1 minute b) 2 minutes c) 3 to 5 minutes d) 10 minutes

Shortest acting muscle relaxant is a) Curare b) Pancuronium c) Gallamine d) Succinylcholine

The most effective muscle relaxant is a) Ether b) N20 c) Halothane d) Trilene

Which of the following are antagonists of non depolarising muscle relaxants PG184
a) Neostigmine b) Edrophoium c) Pyridostigmine d) Cyclopyronium

To decrease awareness in general anaesthesia, the following is given PG! 89
a) increase depth of anesthesia b) more muscle relaxant used c) promedicate with morphine d) premedicate with diazepam

Which muscle relaxant does not cross the placental barrier in significant concentrations a) Succinyl choline b) D- tubocurare c) Gallamine d) all

The following are muscle relaxants except
a) Decamethonium b) Suxamethonium c) hexamethonium d) Pancuronium

Hexamethonium is a depolarising ganglionic blocker,[1] a nicotinic nACh (NN) receptor antagonist that acts in autonomic ganglia by binding mostly in or on the NN receptor, and not the acetylcholine binding site itself. It does not have any effect on the muscarinic acetylcholine receptors (mAChR) located on target organs of the parasympathetic nervous system but acts as antagonist at the nicotinic acetylcholine receptors located in sympathetic and parasympathetic ganglia (NN)

It was formerly used to treat disorders, such as chronic hypertension, of the peripheral nervous system, which is innervated only by the sympathetic nervous system. The non-specificity of this treatment led to discontinuing its use.[3]

The use of inhaled hexamethonium, an unapproved drug, in a normal volunteer during a medical study is believed to have caused or contributed to her death[4][5] in light of the presence of abnormal "ground glass opacities" on her chest X-ray

Which is not true of Non depolarising skeletal muscle relaxant
a) causes Histamine release b) Hypothermia
c) fasciculation of muscle d) ganglion blockade

In children, which of the following is preferred for intubation: AIIMS 84, 85, 86
a) Halothane b) Curare c) Muscle relaxant d) None of the above

Muscle relaxant action of scoline is not prolonged by
a) ethylene chloride b) chloroform c) enflurane d) halothane.

Non-depolarising relaxants may be reversed by
a) atropine b) succinyl choline c) neostigmine d) calcium chloride.

Shortest acting muscle relaxant
a) pancuronium b) Atracurium c) Mivacuriun d) Vecuronium

Muscle relaxant in kidney failure
a) atracurium b) pancuronium c) Gallamine d) all of the above

In the immediate post operative period the common cause of respiratory
insufficiency could be because of the following, EXCEPT AIIMS 2003
a) Residual effect of muscle relaxant b) Overdose of narcotic analgesic
c) Mild hypovalemia d) Myocardial infarction

21 years old lady with a history of hypersensitivity to neostigmine is posted for an elective casearean section under anesthesia. The best muscle relaxant of choice in this patient should be AIIMS 04
a) Pancuronium b) Atracurium c) Recuronium d) Vecuronium

Shortest acting on depolarizing muscle relaxant is: SGPGI – 05
a. Acetylcholine b. Succinylcholine c. Mivacurium d. Pancuronium

Muscle relaxant in hepatic failure Manipal 2006
a) Atracurium b) Gallium
c) Tubocurarine d) Scoline

Muscle relaxant in hepatic and renal failure Manipal 2006
a) Atracurium b) Gallium c) Tubocurarine d) Vecuronium

Which drug is contra indicated in myasthenia gravis Al 88
a) Succinyl choline b) Tubocurare c) Neostigmine d) Halothane e) Cyclopropane

Post operative aching of muscles occur with the use of a) succinyl choline b) panc’uronium c) Gallamine d) DTC

Succinylcholine causes all except a) Muscle pain b) Malignant hyperthermia c) Hyperkalemia d) Hypokalerriia

Which drug is totally excreted by the kidney a) Gallamine b) DTC c) Succinyl choline d) alcuronium

Succinylcholine causes intraocular tension TN 90
a) Decreased b) Normal c) Increased cl) Variable

Fasciculations with succinylcholine are first seen over PGI 80, Delhi 86, 93
a) Eyelids b) Limbs c) Neck d) Abdomen

Uterine tetanic contraction is most rapidly treated with: AIIMS 79, BHU 87
a) Spinal anesthesia b) Halothane c) D-tubocurarine d) Succinylcholine e) Surgical incision

Succinyl choline is short acting due to
a) rapid excretion b) poor absorption c) rapid hydrolysi- d) none.

A high potassium level with succinyl choline for intubation occurs with AIIMS 99
a) Renal failure b) Chronic paraplegia c) Fracture femur
d) Myocardial infarction

Psuedocholine esterase is acted upon by J&K 2001
a) Pancuronium b) Succinyl choline c) Choline d) Atracurium

The administration of succinylocholine to a paraplegic patient led to the
appearance of dysarrhythmias, conduction abnormalities and finally cardiac
arrest. The most likely cause is: AIIMS 2003
a) Hypercalcemia b) Hyperkalemia c) Anaphylaxis d) hypermagnesemia

Not used to the patient with penetrating eye injury Orissa 2004
a) Pancuronium b) Succinyl choline c) d IC A:racurium

Aggravation of myasthenia is a feature of all the
following drugs except – (MAHE 98)
a) Gentamic in b) Neomycin
c) Edrophonium d) Succinyl

Drug of choice for myaesthenia gravis – (PGI 99)
a) Gallamine b) Succinylocholine
c) D. tubocurare d) Pyridostigmine

Use of succinylcholine in ECT: PGI 78, AllMS 84
a) Safer than curare b) May cause prolongation of apnoea c) Reduces
possibility of fractures d) All are true

Injection of which is followed by pain Burdwan 2K
a) Succinyl choline b) Neostigmine c)Curare d) Morphine

A young boy undergoes eye surgery under day case
anesthesia 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

Hyperkalemia is a dangerous complication when
succinyl choline is given to patient with –
a) Spinal cord injury (PGMCET 07)
b) Head injury
c) Thoracic trauma
d) Abdominal trauma

True about Pseudocholineesterase
a) Present in neuromuscular junction
b) Level is increased in pregnancy
c) Succinylcholine is metabolized
d) Organophosphorus inhibit it

The enzyme pseudocholinesterase acts on
a) Decamethonium b) Tubocurarine c) Galiamine d) Suxamethonium

5 year old suffering from Duchenne muscular dystrophy has to undergo
tendon lengthening procedure. The most appropriate anaesthetic would be: Al 2003
a) Induction with intravenous thiopentone and N 20; and halothane for maintenance
b) Induction with intravenous suxamethonim and N 20; and oxygen for maintenance
c) Induction with intravenous suxamethonium and N 2 0; and halothane for maintenance
d) Inhalation induction with inhalation halothane and N 2 0; and oxygen for maintenance

During rapid sequence induction of anesthesia: Al 2003
a) Sellick’s maneuver is not required b) Pre — oxygenation is mandatory
c) Suxamethonium is contraindicated
d) Patient is mechanically ventilated before endotracheal intubation

Which of the following anesthetic agents doesn’t trigger malignant hyperthermia? All India 2006
a) Halothane. b) Isoflurane. c) Suxamethonium. d) Thiopentone.
( Ref. : Katzung 9th Edition Page 410)

Which of the following agents is used for the treatment of postoperative shivering? All India 2006
a) Thiopentone. b) Suxamethonium. c) Atropine. d) Pethidine.

Rapid termination of the action of Suxamethonium
is due to – (MAHE 98)
a) Rapid renal elimination
b) Enzymatic degradation by pseudocholinesterase
c) Metabolized by liver to acetyl CoA
d) Redistribution

Key Points for IV anesthetic agents:-


Barbiturates are almost water insoluble.

Dose:- 3-5 mg/kg

No analgesic action and may be antanalgesc at low doses.


Transient apnoea is common.Centrlly mediated respiratory depression.Laryngeal reflexes remain intact. Larngeal spasm can occur.

Slow recovery.

Enzyme inducers.

C/Ied in pophyria,status asthmaticus,severe shock,pericardial tamponade and uncompensated myocardial disease.


Two Isomers.

S-isomer is anesthetic.

Dose:- 0.3 mg/kg

Doesn’t release histamine.

CBF,CBM,CMRO2 and ICP fall.

Excitatory phenomenon may be seen with induction.Premedicate with Midazolam.

Induction agent of choice for poor risk patients with cardiorespiraory disease.

Etomidate doesn’t blunt the sympathetic response to laryngoscopy and inubation unless combined with a potent opioid analgesic.

The increased mortality in critically ill patients sedated with etomidate infusion due to inhibitory effect on cortisol synthesis even after a single induction dose of etomidate.

Inspite of its side effect profile,etomidate remains a valuable induction drug for specific indications such as patients with severe cardiovascular and cerebrovascular disease.

Etomidate is associated with high incidence of postoperative nausea and emesis when used in combination with opioids for short outpatient procedures.



Highly Lipid soluble.

1% or 2% emulsion in 10% soyabean oil with 1.2% egg phosphatide as the emulsifying agent.

Dose:- 1-2.5 mg/kg for induction.Lower dose should be used in elderly.

Sedation may be produced with 0.2 mg/kg bolus dose intravenously or infusion of 1 mg/kg/hr.

Co-induction with either an opioid(3ug/kg) or midazolam(1-3 mg) enables the induction dose to be reduced.

Rapidly and extensively metabolized.

Clearance rate exceeds hepatic blodd flow suggesting that an extrahepatic elimination route contributes to its clearance.

Decreases CBF,CM and CMRO2.

Analogous to the barbiturates,Children require higher induction and maintenance doses of propofol on a milligram-per kilogram basis as a result of their larger central distribution volume and higher clearance rate.

Elderly and patients with poor health require lower induction and maintenance doses of propofol.

Antioxidant Potential.Free radical scavenger.Its neuroprotective effect may be partially related to this antioxidant potential of propofol’s phenol ring structure,which may act as a free radical scavenger,decreasing free-radical induced lipid perodixation.

Propofol has been reported to inhibit phagocytosis and killing of bacteria in vitro and to reduce proliferative responses when added to lmphocytes from critically ill.

Anti-Emetic.Nausea and vomiting very uncommon.

Direct Myocardial Depressant.Arterial and Venodilatation without compensatory tachycardia.Arterial hypotension is more pronounced in the hypertensive patient.Alters the baroreflex resulting in smaller increase in heart rate for a given decrease in arterial pressure.? A central anticholinergic response may be responsible for bradycardia.

Green colour of urine due to oxidation to quinol derivative.

PROPOFOL INFUSION SYNDROME:-Identified in pediatric ICU.Metabolic acidosis,acute cardiomyopathy and skeletal myopathy associated with prolonged (>48 hrs) high dose (>5mg/kg/hr) infusion.It appears to be due to failure of FFA metabolism secondary to inhibition of both FFA entry into mitochondia and specific sites in the respiratory chain.




*Propofol Half Life in minutes

Dose:- 0.15 – 0.3 mg/kg for induction

Sedation:- Infusion 2-5 ug/kg/min in ICU.Higher maintenance infusion rates and prolonged administration will result in accumulation and prolonged recovery times. Lower infusion rates are sufficient to provide sedation and amnesia during local and regional anesthesia

Because of its high lipophilicity and short half-life, propofol has a rapid onset of action (1 to 2 minutes) and a short duration of action (10 to 15 minutes) compared with other sedative options. For patients receiving propofol infusions for longer than 72 hours, the wake-up time can extend to 30 to 60 minutes.

When infused over days for chronic sedation, the mean elimination half-life of 10 hours may increase to 30 hours as peripheral tissue stores release accumulated midazolam..

Inhibitors of CYP3A4, such as macrolide antibiotics, diltiazem, propofol, and fluconazole, reduce the metabolism of midazolam and prolong its seda-tive actions

Co-induction with a small IV dose (1-3 mg of midazolam) allows a reduction in the dose of propofol required for induction. and adds to the hypnotic and amnesic effects.

Two isomers-Open ring (water soluble)and closed ring(lipid-passage across BB barrier).

Midazolam is a water-soluble benzodiazepine that is available in an acidified (pH 3.5) aqueous formulation that produces minimal local irritation after iv or im injection.25 At physiologic pH, an intramolecular rearrangement changes the physicochemical properties of midazolam such that it becomes more lipid-soluble.

On IV injection a rise in PH changes it to closed ring form.

Amnesic effect greater than Diazepam.

Intranasal Midazolam more effective in terminating seizures than rectal diazepam.

Active Metabolites.

Low clearance.

Short terminal elimination half life.

Low steady state volume of distribution.

Confusional state after prolonged infusion in ICU-COMMON

CVS:- Stable when used in combination with opioid.


Dose:- 1-2 mg/kg IV for induction

25-100 ug/kg/min for maintenance of anesthesia.

Analgesic even at subanaesthetic doses.

Dissociative Anaesthesia:- Muscle tone maintained

Spontaneous respiration preserved

Pharyngeal reflexes preserved

Profound Analgesia and amnesia

Eyes open.

Involuntary movement is common



Increases ICP

Increases BP,HR,CO and myocardial oxygen demand.It also sensitizes the heart to small doses of epinephrine and can precipitate arrythmias.

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