ANAESTHESIA AND ANALGESIA

Dr. Hitesh Bayan, Ph.D

Associate Professor
Department of Veterinary Surgery & Radiology
College of Veterinary Sciences & Animal Husbandry
Central Agricultural University (I), Selesih, Aizawl, Mizoram.

William T.G. Morton

16th October, 1846
 “There are no safe anaesthetic agent;
there are no safe anaesthetic procedures;
there are only safe anaesthetists”

̶ Robert M. Smith

Mahabharata Nakula and Sahadeva, the two Pandava brothers were King Ashoka Erected the first known veterinary hospitals of the
period (1000 experts of horse and cattle husbandry, respectively. (273 – 237 BC) world
BC), Lord Krishna was an expert caretaker and conservator of Sukumar Wrote the book Hastividyarnava ,Commissioned
cow husbandry. Barkaith under the patronage of King Sivāsimha and his
Gokul and Mathura were famous for excellent breeds of (1713-1744 ) Queen consort Phuleswari .
cows, high milk production, quality curd, butter, and
Claude Bourgelat First veterinary college was founded in Lyon, France
other products 1762.
Shalihotra First known veterinarian of the world, was an expert in 1862 Establishment of an army veterinary school in Pune.
horse husbandry & medicine and composed a text
Gaja Ayurveda 1882 Veterinary college was established at Lahore.(then
undivided India under British rule)
Sushruta The Sushruta Samhita is an ancient Sanskrit text on
600 BC medicine and surgery and one of the most important such 1886, Bombay Veterinary College
treatises on this subject to survive from the ancient world.
1893 Bengal Veterinary College.
Atharvaveda provides interesting information about ailments of
animals, herbal medicines, and cure of diseases. 1989 The first veterinary university in India, (TANUVAS)
 1846 Oliver Wendell Used the word anesthesia
•The Sumerians are said to have cultivated and harvested Holmes
the opium poppy (Papaver somniferum) in Mesopotamia as early as
3400 BC 1846 W.T.G Morton The father of modern anaesthesia . Used
ether to a patient in Boston.
•Sushruta (600 BC) used cannabis vapour to sedate surgical patient.
1772 Joseph Priestley Nitrous oxide
•Valerius Cordus (1540), German physician and botanist synthesizes
diethyl ether by distilling ethanol and sulphuric acid into what he called 1844 Horace Wells Used Nitrous oxide (laughing gas)
"sweet oil of vitriol.”
1831 Liebig Discovered Chloroform*

1847 James Young Simpson Anaeshthetic property of Chloroform

1847 Flourens Used chloroform in animals

1853 John Snow Used chloroform to queen Victoria for

birth of prince Leopold

1803 Serturner isolated morphine

Anaesthesiology: The study of the whole art and
1884 Kohler Used cocaine in animal science relating to the production of insensibility..
1885 Corning Spinal analgesia
Anaesthetic: Drug or substanc which produce, in a
1901 Cathelin Epidural anaesthesia in dog
controllable and reversible manner, both loss of
1940 Farquharson Paravertebral block
consciousness and absence of response to noxious
1953 Larson Pudic nerve block stimuli.
Emmerson Cornual nerve block
Analgesia: It is the temporary loss of sensibility to
1930 E. H. Volwiler and Thiopentone sodium
Donalee L. pain.
1962 Farbenfabriken Xylazine was synthesized
Bayer (company) Analgesic: Drug or substance which temporarily
1963 Markel & Eger described the word MAC abolishes awareness of pain.
 • General anaesthesia: It is a state of unconsciousness • Sedative: Narcotic agent which is used to calm a nervous,
produced by a process of controlled, reversible intoxication vicious or excited subject by relieving anxiety and usually causes
of the central nervous system in which there is a lowered drowsiness.
sensitivity to the stimuli from the environment and a • Hypnosis - A state of artificially induced sleep, or a trance
diminished motor response to such stimuli. resembling sleep resulting from moderate depression of CNS
• Local analgesia: Loss of sensation in a circumscribed body from which the subject can be easily aroused by a wide variety
area. of stimuli.
• Hypnotic: Narcotic agents, used to induce sleep (a state of
• Regional anaesthesia: Loss of sensation in a larger but unconsciousness which may be regarded as physiological and
limited body area. from which the subject can easily be aroused by a minor stimuli
• Local analgesic: Drug or substance which when applied to such as noise).
nerve terminals or nerve fibers temporarily prevents the • Narcosis -A drug induced state of deep sleep due to deep CNS
conduction of impulses by the nerve tissue. depression from which the patient may or may not be
• Sedation: A mild degree of central nervous system arousable.
depression in which the patient is awake but calm. • Narcotic: Drug or Substance which can produce insensibility or a
stupor, from which only temporary arousal can be achieved by
simple stimuli.

• Tranquillizer or Ataractic: A drug with a predominant action in • Surgical anaesthesia: A stage of general anaesthesia that
relieving anxiety without producing undue sedation. provides unconsciousness, adequate muscular relaxation
and analgesia to enable surgery painlessly.
• Dissociative Anaesthesia: The state of anaesthesia produced by • Neuroleptanalgesia: A state of altered awareness, usually
drugs that disassociate the thalamocortic and limbic systems, sedation, accompanied by analgesia and produced by
resulting in a cataleptoid state, usually with muscle rigidity. combination of tranquillizer and narcotic analgesic.
• Catalepsy: A state of diminished responsiveness characterized by • Basal anaesthesia: A light level of anaesthesia usually
a trance-like state and constantly maintained immobility usually produced by pre anaesthetic drugs and serves as a basis
with rigidity. for general anaesthesia.
• Balanced anaesthesia: It is a state produced by a combination of • Induction: Refers to transition from conscious State to a
two or more drugs or anaesthetic techniques each contributing state of anaesthesia.
its own pharmacological effects to produce unconsciousness, • Pain: An unpleasant sensory or emotional experience
muscle relaxation, analgesia and attenuation of undesirable side associated with actual or potential tissue damage or
effects of a single drug. described in terms of such damage.
 Selection of anaesthetics

PRE-ANESTHETICS
➢ Drugs used to prepare the patient for induction and contribute to the
• Nature of the operation to be performed maintenance and smooth recovery from anaesthesia.

• Species ➢ Generally used 15-30 minutes prior to induction.

• Physical state or health of the animal ➢ This time may vary depending upon the drug, dose and route used.
• Availability of facilities and equipments
• Familiarity with the anaesthetic agent used
• Speed
• Cost

Indications: Factors for selection of pre-anaesthetic drugs:

• Reduces anxiety and improves induction quality
• Species, breed and age
• Decreases dose of induction agent and increases margin of
safety • Physical status of the animal
• Promotes smoother recovery • Nature of the surgical procedure and duration
• Decreases the minimum alveolar concentration (MAC) for
• Familiarity of the anaesthetist with the drugs
inhalation agents
• Decrease salivary and bronchial secretions
• Block vagal reflexes, which can cause brady-arrhythmias
• Provide sedation, analgesia and muscle relaxation.
PRE-MEDICANT DRUGS: Atropine:
• Competitive antagonist of ACH and blocks ACH at
A) Anticholinergic Agents:
preganglionic nerve terminals of cholinergic fibre.
Natural: atropine
• Derived from plant Atropa belladona and have
Synthetic: glycopyrrolate parasympatholytic activity.
B) Tranquilizers & Neuroleptics: • Stimulates the medulla and higher cerebral centres.
I) Phenothiazine derivatives: acepromazine ,triflupromazine • Paralyzes the ciliary body and causes mydriasis
II) Butyrophenones: droperidol, azaperone • Inhibits salivary and bronchial secretions
III) Benzodiazepines: diazepam, midazolam • Dilates bronchioles causing a decrease in airway resistance.
C) Sedatives
I) Alpha-2 agonists.e.g. xylazine, medetomidine
II) Chloral hydrate
D) Opioid & Analgesic Agents
Agonists: meperidine, morphine, oxymorphone
Agonist/Antagonists: pentazocine, butorphanol

Glycopyrrolate
• Increases heart rate by suppressing the vagal influence.
• Decrease gastric secretions, smooth muscle tone and
• Synthetic anticholinergic compound and more potent
peristalsis. than atropine.
• Does not penetrate blood brain barrier hence less
• Contraindicated for use in treatment of abdominal pain in central effect.
horse and most other animals because it can cause ileus. • Does not pass the placental barrier and no effect on
• Not very effective in reducing oral secretions in ruminants fetus.
Dose: • Rapid absorption following I/M administration, rapid
Equine: 0.0165-0.022 mg/kg I/V or I/M. clearance from the body
Bovine, ovine, caprine: 0.02-0.04 mg/kg I/V or I/M. • Decreases salivary and gastrointestinal secretions
Swine: 0.066-0.088 mg/kg I/M
• Increases heart rate
Small animals: 0.022-0.044 mg/kg I/V , I/M, S/C
• Dilates bronchioles, causing a decrease in airway
resistance.
 PHENOTHIAZINE DERIVATIVES
Dose: • Antipsychotic, neuroleptic (old)
• Dopamine antagonist – calming and antiemetic effect.
• 1. Equine, swine: 0.005 mg/kg, I/V, I/M or S/C. • Depresses brain stem – depresses alertness.
• 2. Bovine, caprine, ovine: 0.005-0.01 mg/kg, I/V, I/M or • No analgesic property but methotrimeprazine is powerful
S/C. analgesic in human
• Potentiate analgesic agents and GA agents.
• 3. Small animals: 0.01- 0.02 mg/kg, S/C • Moderate anti-acetylecholine, anti-histamine & anti-
cholinesterase effects.
• Alpha1 blockade - vasodilation & hypotension.
• Cause hypothermia
• Effect is less in excited animals.
• Increasing the dose will not improve sedation.
• Anti arrhythmic effect.
• Lower the seizure threshold.
• Anti-emetic

Chlorpromazine hydrochloride (Largactil)

Contra-indications • Limited use in large animal anesthesia-replaced by ACP.
• Organophosphate poisoning • Less potent than ACP
• Hypovolaemic or endotoxic shock. • Longer duration of action and less sedation.
• Do not use epinephrine to counteract hypotension due to • Not suitable for cattle as it leads to delayed recovery.
phenothiazine as it will potentiate hypotension by reversal effect. • Not reliable in horse – panic duce to muscle weakness.
• Alpha-receptor stimulation (vasoconstriction) provided by Dose:
epinephrine will be partially blocked by the tranquilizer, allowing • Equine – 1.1-2.2 mg/kg I/V or I/M
the beta effect (vasodilation) to prevail. • Cattle – 0.2-1.1 mg/kg I/V or 1.1-2.2 mg/kg I/M.
• It precipitate seizures and can cause death. • Swine – 1.1 mg/kg (0.5 mg/lb) I/M
• Do not use in diseases of the male external genitalia, especially in • Dog/Cat – 0.5-1.0 mg/kg I/M or I/V
horse.
• Causes permanent paraphimosis in stallions known as priapism.
Triflupromazine hydrochloride (Siquil) Acepromazine maleate (Acepril)
• 2-3 times as potent as chlorpromazine • Most potent phenothiazine derivative.
• May cause excitement of the animal
• Most of action occurs within 15-20 minutes following I/V
administration and last approximately 2 hours.
Dose: • Contraindicated for sedation during skin testing for allergy.
• Equine - 0.22-0.44 mg/kg I/V or I/M • May cause permanent penile paralysis.
• Cattle – 0.11 mg/kg I/V • May cause transitory stimulation of the animal.
• Sheep and goats – 1.0 mg/kg I/V • Poor analgesic.
• Dog - 1-2 mg/kg IV and 2-3 mg/kg IM Dose:
• Equine – 0.044-0.088 mg/kg I/V or I/M
• Bovine – 0.01-0.02 mg/kg I/V or 0.03-0.1 mg/kg I/M
• Caprine and ovine - <50kg- 0.1-0.2 mg/kg I/V,
>50kg – 0.05-0.1 mg/kg I/V
• Dogs – 0.03-0.05 mg/kg I/V or I/M.
• Cats – 0.03-0.05 I/V.

➢ GABA receptors contain ion channel that conducts chloride ions

BENZODIAZIPINE DERVATIVES across neuronal cell membranes and binding sites for
the neurotransmitter GABA.
➢ Increase chloride ion influx hyperpolarizes the neuron's membrane
• Anti-anxiety potential.
• Sedation and hypnosis- due to depression of limbic system ➢ This reduces the communication between neurons - calming effect
• Anticonvulsant
• Muscle relaxation – due to inhibition of internuncial
neurons at spinal level
Diazepam ( Calmpose / Lori 5mg/ml)
Midazolam (Mezolam 5 mg/ml)
• The effect is produced because of CNS depression.
• Can be given orally, IV • A water-soluble benzodiazepine, four times more
• IM injection is painful and absorption is unreliable. potent than diazepam with a shorter half-life.
• It is used primarily to treat seizures. • It may cause excitement if given alone in small animals,
• Diazepam is an effective appetite stimulant in cat when given particularly in cats.
orally.
• It potentiates the effect of barbiturates and narcotic
• It is absorbed well after intra muscular injection.
analgesics. • When used with an opioid analgesic to induce
• Produces muscle relaxation anesthesia in dogs the opioid is given first and followed
Dose: by midazolam.
• Dogs – 0.1-0.5 mg/kg I/V, p.3-0.5 mg/kg I/M Dose:
• Cats – 0.1-0.5 mg/kg I/V, 0.3-1.0 mg/kg I/M
• Horses – 0.02-0.1 mg/kg I/V • Lower range for diazepam.
• Bovine – 0.4 mg/kg I/V • Dog-0.06-0.3 mg/kg IV, IM, SC

Zolazepam BUTYROPHENONE DERIVATIVES

• Combined with tiletamine known as Telazol
• Blocks the central actions of dopamine and
• TELAZOL (tiletamine+zolazepam ) is mostly used in canine and norepinephrine.
feline species.
• Supplied sterile in vials – addition of 5 mL diluent produces a • Produces hallucinations, restlessness, mental agitation
solution containing the equivalent of 50 mg tiletamine, 50 mg and even feeling of aggression.
zolazepam per mL. • Produce hypotension due to alpha-adrenergic blockade.
• Deep intramuscular injection. • Potent anti-emetic
• Decrease motor activity
Flumazenil • Causes Behavioral changes.
 Droperidol Azaperone (Stresnil, Suicalm)
• Mostly use in combination with fentanyl known as • Used exclusively in pigs for sedation, as a premedication or to decrease
aggression.
Innovar-Vet (20 ml vial).
• Duration of action 2-3 hours.
• Contains fentanyl 0.4mg/ml + droperidol 20mg /ml • Causes vasodilatation and decrease blood pressure.
• When used alone decreases voluntary motor activity. • May cause transitory excitement after IM injection and should not be
given IV
• May cause behavioral changes especially in Doberman
Pinschers. Dose in Pigs:
• Potent anti emetic Low dose: 0.4-1.2 mg/kg IM. For transportation.
Medium dose: 2-4 mg/kg IM. Sedation and
• Dose: Dogs – 0.1-0.4 mg/kg I/V, I/M premedication.
Other drugs in this category are
➢ Haloperidol
➢ Lenperone
➢ Fluanisone

Alpha 2 adrenergic agonists: Xylazine Hcl:

• Alpha2 agonists directly stimulates central α2 receptors as well as • Thiazine derivative and often referred to as sedative analgesic.
peripheral α-adrenoceptors in a variety of tissues. • Very potent in ruminants than in other animals.
• Leads to a decrease in neurotransmission of NE and dopamine in the • Emetic action in carnivores
CNS by mimicking NE in binding to presynaptic surface auto- • Centrally acting muscle relaxant.
receptors, which leads to feedback inhibition of norepinephrine. • Provide Sedation and analgesia.
• Causes bradycardia, decrease in BP, cardiac output
 Detomidine (Dormosedan ,Norden)
• Depresses GI and ruminal motility and thermoregulation • Greater potency and longer duration than xylazine.
• Causes abortion in pregnant animals due to increase intrauterine • Primarily used as sedative in horses
pressure. • Ataxia in 80% cases and local muscle tremors possible with high doses.
• Acts as diuretic in cattle and should not be used in urethral • It has wide margin of safety , effective in all animals and used for
obstruction. chemical restraint
• Not suitable in debilitated and compromised cardiopulmonary, Dose:
hepatic or renal function patients. • Horse: 10-20 µg/kg IV
Dose: • Cattle: 15-30 µg/kg IM
• Dog: 20-40 µg/kg IM
Cattle: 0.02-0.1 mg/kg IV ; 0.1-0.2 mg/kg IM
Dog: 0.25-0.5 mg/kg IV ; 0.5-1 mg/kg IM
Pig: 1-2 mg/kg IV ; 2-4 mg/kg IM
Horse: 0.4-1.1 mg/kg IV ; 1-2 mg/kg IM

Medetomidine (Domitor) Dexmedetomidine (Dexdomitor)

It is one of newest alpha2 adrenoceptor agonist and more potent • Used in the intensive care setting for light to moderate sedation.
Provides good muscle relaxation, sedation and analgesia • It has analgesic properties in addition to its role as a hypnotic.
Used as preanaesthetic in animals and also for chemical immobilization • Not associated with significant respiratory depression.
of wild animals
Its specific antagonist is atipamezole (Antisedan)
Recently the dextro-rotatory form (Dexmedetomidine) is also available
which more potent.
Dose:
Dogs- 10-20 µg /kg IM
Cats - 80-150 µg /kg IM
Cattle-10-20 µg /kg IM
 Romifidine (Sedivet) OPIOID ANALGESICS:
• Pure opioid agonists: bind and stimulate receptors µ and κ eg
• Mainly used in horses. Morphine
• It is claimed to produce less ataxia than xylazine. • Antagonists: bind and block or inhibit activity at all receptors. eg.
• Romifidine's effects are longer lasting than xylazine. Naloxone
• Horse dose 20-80 µg /kg . • Partial agonists / antagonists:
➢ Act as agonist at one type of receptor and antagonist at another
type.
➢ Some have partial agonist actions at a single type of receptor, low
doses stimulating the receptor but higher doses antagonizing this
effect.
Alpha 2 Antagonists:
• Yohimbine (Pausinystalia yohimbe)/(Antagozil) Endogenous ligands: Encephalins, Endorphins and Dynorphin
• Atipamezole (Antisedan).
• Tolazolin Opioid receptors: μ, κ and σ.
• Idazoxan

• Produce their actions by activating opioid receptors. • Increasing the dose of pure agonist drugs increases analgesia but,
• Opioid receptors are G protein-coupled receptors (GPCRs). also increases respiratory depression.
• Activation has a number of actions including: • Partial agonists have a limit to the analgesia they can produce,
➢Closing of voltage sensitive calcium channels increasing doses sometimes antagonizes the analgesia of lower
➢Stimulation of potassium efflux leading to hyperpolarization doses .
➢Reduced cyclic adenosine monophosphate production.
• Overall, the effect is a reduction in neuronal cell excitability that in • Respiratory depression produced by the partial agonists is also
turn results in reduced transmission of nociceptive impulses. limited.
• Opioid drugs may be used to provide analgesia before, during and
after surgery as well as in combination with sedative drugs for
‘chemical control’.
Morphine: Oxymorphone:
• Morphine is the opioid agonist derived from opium poppy • Synthetic opioid and 10 times more potent to morphine and has
(Papaver somniferum). longer duration of action
• Produces some degree of sedation, analgesia • Produces less respiratory depression than morphine.
• It binds to µ and kappa receptor although it acts on other Dog and cat-0.05-0.2 mg/kg IV
receptors.
• Depresses respiratory center
• Rapid IV injection may cause hypotension
• Dog: 0.5-2 mg/kg IV , analgesia for 2-4 hours;
• Cat: 0.1 mg/kg SC analgesia for 4 hours

Fentanyl: Butorphanol:
• Synthetic opioid agonist, acts on µ opioid receptor and • A mixed agonist/antagonist with primary agonistic activity at the kappa
around 50 times more potent than morphine. receptor.
• Short duration (30-60 min) and given continuously for • Good all around analgesic for mild pain, free of any expected
long term pain management. undesirable effect
• Minimal effect on blood pressure and cardiac output. • Little, or no respiratory depression at clinical doses
• Also available as transdermal patch • Duration of effect is 30 minutes to 1 hour in dogs and 1 to 3 hours in
• Dog- 0.005-0.02 mg/kg IV cats
• Dog & Cats - 0.1 to 0.5 mg/kg IV, IM, SC duration - up to 4 hour
Buprenorphine:
• Partial µ agonist and 30 times more potent than
morphine.
• Slow onset (30-45 min) and longer duration (up to 6 hr)
• Little effect on cardiovascular and respiratory system.
• Dog- 6 to 10 µg/kg
 Pentazocine (Fortwin) Etorphine
• Agonist and antagonist properties and less potent than morphine
• Pentazocine has minimal effect on the cardiovascular system and is • Etorphine is a very potent derivative of morphine.
mild respiratory depressant. • Effective in a dose of about 0.5 mg per 500 kg.
• Effective analgesic.
• It has all the properties of morphine but equipotent doses cause
• Horse – 0.5-4.0 mg/kg I/V, 0.5-6.0 mg/kg I/M and Dogs 2.0
more respiratory depression.
mg/kg I/M
• High potency - small volume - suitable for dart gun projectiles for
immoblizing large wild animals.
• A difficult drug to handle and constitutes a hazard to the anaesthetist.
• Etorphine is an extremely long acting compound and recovery from
its effects is also delayed by enterohepatic recycling.
• Action is usually terminated by the use of diprenorphine.

• Etorphine is marketed in fixed ratio combinations with phenothizine Commercially available neuroleptanalgesic mixtures:
tranquillizers
Commercial Analgesic Neuroleptic/ tranquilizer
• Immobilon LA:
• Etorphine 2.45 mg/ml + Acepromazine 10mg/ml name
• ImmobilonSA: Thalamonal Fentanyl 0.05 mg/ml Droperidol 20 mg/ml
• Etorphine .074 mg/ml + Methotrimeprazine18mg/ml Hypnorm Fentanyl 0.315 mg/kg Fluanisone 10 mg/ml
• Accidental self-administration - death can result if the antidote is not Immobilon SA Etorphine 0.074 mg/ml Methotrimeprazine
readily available.
18 mg/ml
• Revivon LA: Diprenorphine 3.0 mg/ml
• Revivon SA: Diprenorphine 0.272 mg/ml Immobilon LA Etorphine 2.45 mg/ml Acepromazine 10 mg/ml

• M-99 – etorphine and M-50-50

• (diprenorphine)
Carfentanil NON-STEROIDAL ANTI-INFLAMMATORY DRUG: acts via inhibition of the
• One of the most potent opioids known. enzyme, cyclo-oxygenase (COX), also known as prostaglandin synthetase.
• It is said to be 3–8 times as potent as etorphine and has proved to be
cyclo-oxygenase is present in different forms :
useful in elephants.
• It is a dangerous drug to handle since it is rapidly absorbed across cyclo-oxygenase 1 (COX1)
mucous membranes. •COX-1 is essential for the maintenance of normal physiologic states in
• An antagonist drug suitable for use in humans should be readily tissues including the kidney, GIT and platelets.
available whenever carfentanil is used.
•COX-1 activation in the gastric mucosa leads to prostaglandin PGI2
(prostacyclin) production, which is cytoprotective.
•Thromboxane A2, primarily synthesized in platelets through COX-1
activity, causes platelet aggregation, vasoconstriction and smooth muscle
proliferation
•Inhibition of COX-1 cause gastrointestinal damage

NSAIDs
Cyclo-oxygenase 2 (COX2) is less widely expressed, but is
readily induced by pro-inflammatory stimuli and catalyses
production of prostaglandins that mediate inflammation.
• Anti-inflammatory efficacy results from inhibition of COX-
2.
• At therapeutic doses, COX-2 inhibitors inhibit COX-2 but
not COX-1 and they relieve inflammation with less
gastrointestinal toxicity than conventional NSAIDs.
• COX-2 has many other functions besides its role in
inflammation in vascular endothelium, it mediates
production of prostaglandin PGI2 (prostacyclin), a
vasodilator and inhibitor of both platelet aggregation and
proliferation of vascular smooth muscle cells.
Bone
morphogenetic
proteins
(TGF beta)

BAA
Butorphanol : 4ml of 10 mg/ml solution=40 mg
Acepromazine : 0.5ml of 10 mg/ml soution=5mg
Atropine : 8 ml of 0.5 mg/ml solution=4mg

BAG
Butorphanol : 4ml of 10 mg/ml solution=40 mg
Acepromazine : 0.5ml of 10 mg/ml soution=5mg
Glycopyrrolate : 8 ml of 0.2 mg/ml solution=1.6mg

Make the mixture up to 20 ml with sterile water

Preanesthetic dose:
Dog : 0.05 – 0.1ml/Kg IM or SC
Cat : 0.1 – 0.13 ml/Kg IM or SC
BAM kit: Each BAM Kit includes the following components:
➢ A patented, unique and safe anesthesia combination of 1. VIAL# 1 BAM [11ml]- :
Butorphanol tartrate, Azaperone tartrate and Butorphanol : 300mg (27.3 mg /ml)
Medetomidine hydrochloride that is used to immobilize a Azaperone : 100mg ( 9.1 mg / ml)
broad range of species. Medetomidine : 120 mg (10.9 mg /ml)
➢ All three of these pharmaceuticals seem to be “co-
synergistic” bringing the best attributes of each at the 2. VIAL # 2 [30 ml] :
lowest effective dose rate. Atipamezole : 750mg ( 25 mg/ml)

3. VIAL # 3[5.5 ml]- :

Naltrexone : 275mg (50 mg/ml)

Lytic cocktail Hellabrunn Mixture

• Lytic cocktail is a mixture of drugs used for women with Mixture of xylazine and ketamine
eclampsia.
Xylazine : Ketmine=1.25:1
• These are usually chlorpromazine, promethazine and
pethidine (meperidine).
• Injected intravenously to produce sedation, analgesia, (125 mg/ml xylazine and 100 mg/ml ketamine)
amnesia, hypotension, hypothermia and blockade of
functions of the sympathetic and parasympathetic nervous
systems during surgical anaesthesia.
 Skeletal Muscle Relaxant
General anaesthesia

GENERAL ANAESTHESIA Components of general anaesthesia:

“General anaesthesia is a state of unconsciousness, produced • Pre-anaesthesia
by a process of controlled, reversible intoxication of CNS, in • Induction
which there is a lowered response to the sensitivity to the • Maintenance
stimuli from the environment and a diminished motor response • Recovery
to such stimuli.” Properties of GA (anaesthetic triad) :
• Sedation
General anaesthetic: • Analgesia
A substance which produces, in a controllable manner, both • Muscle relaxation
loss of consciousness and absence of motor response to Types:
noxious stimuli • Injectable anaesthesia
• Inhalation anaesthesia
 Injectable anaesthesia
➢Single agent lacks qualities.
➢Depression of vital organ function.
➢Combination for balance anaesthesia and protect vital functions.
➢TOTAL INTRAVENOUS ANAESTHESIA (TIVA)
➢Additional analgesics and muscle relaxants required.
Advantage: ➢PARTIAL INTRAVENOUS ANAESTHESIA (PIVA)
• Easy to administer ➢CONTINUOUS (CONSTANT) RATE INFUSION (CRI)
• Speedy and pleasant ➢TARGET CONTROLLED INFUSTION (TCI)
• Minimum equipment ➢Cp
• Economical ➢Ce
Disadvantage
• Recovery depends on metabolism and redistribution
• Depth can not be controlled
• Longer procedure can lead to severe physiological changes
Factors affecting the effect of Intravenous anaesthesia
Ruminants are poor subject for G A
1. Blood flow to the brain and other tissues of the body.
1.Regurgitation
2. Amount of non-ionized drug: More the non- ionized form of
• Active regurgitation: during induction - uncontrollable
the drug, readily it crosses the cellular boundaries. contractions of oesophagus - reverse peristalsis.
3. Protein binding: Higher the protein binding lesser is the • Passive regurgitation: during maintenacr - animal in lateral
anaesthetic action.
recumbency - oesophagus & cardia relaxed - drainage of
4. Oil/water solubility: Lipid soluble drugs cross the cellular rumen contents into the oesophagus.
boundaries immediately and so less concentration in the • prevented by raising the head above the level of the cardia.
blood/brain.
2. Tympani
5. Rate of metabolism: Higher the rate, shorter/lesser is the
effect. 3. Respiratory depression
6. Excretion 4. Hypoxia with uneven ventilation
5. Radial paralysis

Stages of General Anaesthesia

Stage III (Stage of surgical anaesthesia):
Stage I (Stage of voluntary excitement):
➢Initial administration to loss of consciousness. ➢Unconsciousness with progressive depression of the reflexes.
➢Conscious but disoriented & all reflexes present. ➢Muscular relaxation.
➢Excited and apprehensive animals may struggle ➢Respiration slow and regular.
violently and voluntarily. ➢Loss of reflexes.
➢Hold their breath for short period.
Stage II (Stage of involuntary excitement):
➢Loss of consciousness to the onset of a regular pattern of
breathing.
➢All reflexes present.
➢Patient reacts to external stimuli by violent reflex -struggling,
breath holding, tachypnea, and hyperventilation.
➢Chew or swallow, yawning.
Stage-3 Surgical anaesthesia - divided into 3 planes Plane 3:
Plane 1: • Deep
• Light • Significant depression of circulation & respiration,
• HR reduced even in presence of surgical stimulus
• Regular respiration
• Reflexes totally absent
• Involuntary movement of limbs & eyeball ceases • Eye ball central with fully dilated pupil
• Corneal reflex
Plane 2: • Paralysis of intercostal muscle
• Medium depth • Spasmodic, jerky respiration
• Danger of respiratory and cardiac arrest
• Suitable for surgery
• Surgical stimulation increases HR& RR
• Respiration regular but shallow

Stage IV (Stage of medullary paralysis):

• CNS extremely depressed
• Respiration ceases
• Heart continues to beat only for a short time
• BP falls
• Total circulatory collapse and death

If the anaesthetic is withdrawn and artificial

respiration is initiated before heart action stops, the patient
may go through the stages in reverse order.
Bispectral index monitor (BIS monitor): EEG based
anaesthetic depth indicator.
 Barbiturates • Barbiturate slough:
➢ Causes CNS depression
• Glucose effect
➢ Produces mild sedation to total anesthesia
➢ Acts as anxiolytics, hypnotics, and anticonvulsants Duration and depth depends upon:
➢ Used in general anesthesia and in epilepsy.
➢ Addiction property -replaced by benzodiazepines
1.Amount of drug injected
2.Speed of injection
➢ Derivatives of barbituric acid
➢ Clinically used as sodium salts 3.Rate of distribution in non-fatty tissue/ vascularised tissue
➢ Available as powders to be dissolved in water or saline before use.
➢ Highly alkaline (pH 10) -only IV 4.Rate of uptake by body fat

Classification: onset & duration Pentobarbital sodium

1. Ultra-short-acting (5 to 15 minutes) : anesthetic Thiopentone
sodium, Thiomylal sodium ➢Depresses the CNS
2. Short –acting (45 minutes):anesthetic & anti anxiety or insomnia. ➢Available 60mg/ml and 65mg /ml solution
Pentobarbital sodium, Sacobarbital sodium. ➢Less lipid soluble - Slow in crossing BBB
3. Intermediate-acting (2-6 hours): Anti anxiety, replaced by ➢Excitement during induction and recovery
benzodiazipines, Amobarbital sodium ➢Rapidly crosses placental barrier; low neonatal survival
4. Long-acting (8-12 hours): convulsions, Phenobarbital sodium ➢Decreases arterial blood pressure
Chemically: ➢Primarily metabolized by hepatic microsomal enzyme
Oxybarbiturates : pentobarbital
Thiobarbiturates : thiopental Dog @ 20-30mg / kg, IV
Methylated oxybarbiturate : methohexital Horse: generally not used alone
Methylated thiobarbiturate : severe convulsion 1-2.5 gm or 15 to 20 ml of 6.5% IV
 Thiobarbiturates ➢Crosses BBB and placental barrier
➢Injection is followed by a brief period of apnoea
Thiopentone sodium ➢The degree of respiratory depression is parallel to the depth of
➢500mg and 1g Yellowish white crystalline powder narcosis
➢Recovery depends on redistribution
➢Unstable - air and aqueous solution
Dose:
➢Highly alkaline, pH 11-12
Dog: 20-25mg/kg, IV (2.5%) solution
➢2.5 -5% solutions used for induction
Usually 7 to 8 mg/kg is injected rapidly
➢Once prepared, should be stored in refrigerator (1 wks) Anaesthesia may further be prolonged by small doses
➢Depresses pulmonary and cardiovascular function Horse: 7 to 15mg/kg IV.
➢Used as a sole anaesthetic for brief procedures and for induction Anaesthetic effect within 25 to 30 secs
before inhalation anaesthesia

Factors governing duration & depth of narcosis due to an injection of

• A slow rate of injection of a larger quantity of the drug has the effect
thiopental:
of maintaining the plasma level as the drug is distributed to the body
1. The amount of the drug injected
tissues.
2. The speed of injection • Larger amount of thiopental will be necessary to obtain any given
3. The rate of distribution of the drug in the non-fatty tissues of the body.
depth of narcosis and recovery will depend more on the uptake of the
4. The rate of uptake of thiopental by the body fat.
drug by the body fat and detoxication, since the concentration of
thiopental in the non-fatty tissues will already be high at the end of
The speed of injection and the quantity injected are related. injection.
• A small amount injected rapidly produce a high plasma concentration
of undissociated drug & consequently a parallel high brain level - deep
narcosis induced rapidly.

• However, the drug soon becomes distributed throughout the non-

fatty tissues of the body - the plasma concentration and the brain
concentration are reduced and there is a rapid decrease in the depth
of narcosis.
Effect of hypoventilation or Carbon dioxide (CO2) retention –
Protein binding
• CO2 retention reduces plasma pH is • Thiopental bound to the plasma protein
• Undissociated fraction is increased and since only this fraction is fat • Degree of binding depends on - protein concentration & pH.
soluble - results in an increased uptake of the drug by fatty tissues. • Reduction in pH – reduced protein binding
• This lowers the plasma concentration and narcosis might be expected • Pharmacological activity resides in the unbound fraction, narcosis might
to lighten. be expected to deepen when the plasma pH is reduced by CO2.
• Higher dose required– increased duration

Thiamylal sodium Methohexital sodium

➢Rapid acting ultra short duration oxybarbiturate
➢2 to 3 times more potent than pentobarbital
➢ More potent and less cumulative effect than thiopental sodium
➢Primarily used for induction; also for maintenance
➢ Less excitement during induction & recovery
➢Quick recovery; animals are alert within 30 minutes
➢ Premedication with atropine sulphate - to check salivation ➢Excitement, muscle tremor & convulsions -during induction or recovery
➢Contraindicated in seizure patients
Dose: Dog @ 18-25mg/kg, IV
Dose: S A @ 10mg/kg (1%), IV till effect
L A @ 25mg/kg (2.5%) IV till effect
 Propofol Etomidate
➢Most popular IV agent
➢Imidazole derivative
➢1% milky white emulsion (10mg/ml)
➢2 mg/ml in 35% ethylene glycol
➢Ultra-short-acting ;Rapid onset, quick recovery
➢Stored at 2 to 8oC
➢Induction and maintenance (TIVA)
➢Rapidly hydrolyzed in liver & excreted in the urine
➢Induction and recovery smooth, excitement free
➢Remarkable stability of the cardio-respiratory system
➢Pain on injection
➢Excitement and seizure
➢Poor analgesic
Dog @ 1.5 and 3.0mg/kg IV
➢Microbial growth
Cat @ 3 mg/kg IV
Dog @ 5-6mg/kg, IV (Unpremedicated)
@4mg/kg, IV (Premedicated)

Saffan Chloral hydrate

➢Less rapidly acting agent
➢Steroid anaesthetic ➢White translucent crystal-sterilized by boiling
➢Alphaxalone (9mg/ml) and alphadolone(3mg/ml) ➢Hypnotic/narcotic- no analgesia
➢Used for induction ; also for maintenance ➢Surgical anaesthesia-slow recovery
➢Histamine release in cats and dogs ➢Reduces to trichloroethanol
➢Short duration with rapid and complete recovery ➢Horse and cattle- oral (less than 5%)or IV
➢Irritating
➢Little respiratory depression
Horse: 6-10g/ 50kg po
➢Adequate muscle relaxation 5 - 6.5g/50kg IV (6-8% solution)
Dog: anaphylactic reaction Cattle- 5g/ 50 kg, i/v.(6%)
Cat : 8 to 10 mg/kg IV (Unpremedicated) Calf -140mg/kg, i/v. (6%)
5mg/kg IV (premedicated). Cattle - 6-10 gm/50kg po
 Chloromag Equithesin
Chloral Hydrate + MgSO4 + Pentobarbitone Na
➢Chloral Hydrate + Magnesium sulphate Good for horse – low toxicity & excitement
➢2 parts of chloral hydrate and one part of MgSO4 Good muscle relaxation & rapid recovery
➢10 % solution Prepared within 1hr before administration
Composition:
➢Irritant effect of chloral hydrate is reduced
Chloral Hydrate 28 gm
➢Provides muscle relaxation Magnesium sulphate 14 gm
Pentobarbitone Na 6.5 gm
Distilled Water 1000ml
Horse and cattle ----- 5gm/50 kg, IV till effect
Dose in horse : 670ml/450 kg, IV

Chloralose Inhalation Anaesthesia

➢ Chloral hydrate and glucose 1:1- heated
➢ Two isomers produced: ✓Anaesthetic agents administered via lungs
➢ ά-chloralose: Narcotic property
➢ β chloralose: Muscular pain ✓Volatile agent is vaporized in a vaporizer by oxygen
➢ 1% solution is used ✓ Passed through a flow meter
➢ Prepared freshly by heating at 600C ✓Passed into the breathing
➢ Not used in vety. practice ✓Administered to the patient
 Advantages:
➢Fast recovery – primarily exhaled through lungs
and not dependent on the redistribution of the
anaesthetic.
➢Recovery not dependent upon the body
detoxification mechanisms.
➢Good control over the depth of anaesthesia.
➢Safe for longer duration surgical procedures.
➢Oxygen and assisted controlled ventilation is
available

Disadvantages:
➢ Not suitable for induction - slow speed.
➢ Requires constant surveillance by anaesthetist.
➢ Some agents are inflammable and explosive in nature.
➢ Some are irritant to the body tissue.
➢ Sophisticated instrument needed and can not be easily
transported.
➢ Trained personals are needed.
➢ Pollution of the work environment.
 Phases of inhalation anaesthesia Minimum alveolar concentration (MAC):
.
➢ Anaesthetic concentration required to prevent gross muscular
✓ Pulmonary phase: The inhalant gas or the vapor is movement in 50% of the patients in response to painful (surgical)
introduced into the lungs and transferred through the stimulus.
pulmonary epithelium to the capillary epithelium of the
➢ In order to achieve clinical anaesthesia the anaesthetic
blood. concentration in the inhalant mixture should be equal to or more
than MAC.
✓ Circulatory phase: The inhalant gas or the vapor is in the
➢ The clinical signs are due to the action of the inhalant
circulation and distributed to the body tissues especially anaesthetics on the CNS and depth of anaesthesia is related to
CNS. the amount of inhalant anaesthetic made available to the CNS.

✓ Tissue phase: The inhalant gas or the vapor enters the

tissues and produce the effect. Tissue with rich circulation
are the primarily involved tissues.

Volatile anaesthetic agents: Administration:

➢By all methods but closed system is preferred - explosive
Ether / diethyl ether :
nature.
➢Valerius Cordus in 1540 in Germany.
➢Mostly for maintenance since induction time is long (3-10)
➢Colorless / pungent smell / irritant in nature.
➢For induction 20% - fatal to the patient.
➢Inflammable and explosive in nature.
➢For maintenance 3.5 to 4.5% by volume in the inhalant
➢Oxidizes in the presence of air, oxygen or light –
mixture.
Produces toxic substances – peroxides and aldehydes.
➢Stored in sealed containers with copper or other ➢More than 6.7% may cause respiratory arrest.
metal from inside or dark amber colored bottles ➢MAC -1.92%.
➢Good CNS depressant and produces all stages of GA.
Clinical effects: Chloroform:
➢Clear with pleasant odor and noninflammable.
➢ Struggling for 3 min / Breath holding due to irritation of the ➢Non-irritant to skin and mucous membrane.
respiratory tract ➢When heated in air – highly toxic phosgene gas is produced.
➢ Good muscular relaxation ➢1% ethyl alcohol is added to prevent phosgene production.
➢Chloroform is the most powerful inhalant anaesthetic but has a low
➢ Causes excessive salivation and increase in respiratory tract safety margin.
mucous secretions - interfere with respiration- post ➢Cardiac arrest may coincide with respiratory failure.
operative pneumonia -can be minimized by atropine sulfate Administration: By open/closed systems.
premedication. Concentration:
➢ 1.35% for light anaesthesia and 1.65% for deep anaesthesia.
➢ Oliguria, post-anaesthetic nausea & cardiac arrhythmias. ➢ More than 2% concentration may cause death due to respiratory
arrest.
➢ The MAC value is 0.77%

Clinical effects: Halothane:

➢ Clear, colorless, non irritant, Noninflammable & non
➢ Deep and accelerated respiration during induction due to explosive.
struggling. ➢ Slight decomposition when exposed to light - stored in
➢ As anaesthesia deepens, respiration becomes slow and amber colored bottles and 0.01% thymol is added to it to
shallow. make it more stable.
➢ Dilatation of the left atrium when first exposed to high ➢ Not affected by warm soda lime.
concentration of the anaesthetic. - cardiac failure. ➢ Recovery is rapid and free from excitement.
➢ Anurea / polyurea and albuminurea are seen in the post ➢ Twenty-thirty percent of halothane is metabolized by the
anaesthetic period. liver
➢ Death during induction is common due to ventricular ➢ Metabolites –
fibrillation
Trifluoroacetic acid
➢ Not used nowadays.
Bromide ions - post-halothane sedation.
 Administration: Closed system with precision vaporizers - costly.
Concentration:
➢ Induction 2-4% for SA and 4-10% for LA
➢ Maintenance 0.8-2.3%
➢ MAC for dogs is 0.86% and for cats is 0.98%.
Clinical effects:
➢ Respiratory depression / decreased tidal volume/ apnea. respiratory
acidosis.
➢ Bradycardia / slow pulse / . Hypotension.
➢ Salivary, mucous and bronchial secretions are absent.
➢ Negligible direct effect on the liver and kidney functions.
➢ Halothane sensitizes heart to the action of epinephrine.
➢ Reasonable analgesia & muscle relaxation.

Methoxyflurane:
➢Clear colorless liquid / ‘fruity’ odor/ non explosive / non inflammable
➢Stable in air, moisture, alkali etc.
➢Reacts with metal (in anaesthetic circuits) & light.
➢Poor induction agent - slow inductions and recoveries.
Administration: Closed system - precision vaporizers - costly.
Concentration: 0.4 to 1% for maintenance.
Clinical effects:
➢Persists in the blood even 24 hr after anaesthesia.
➢Dose dependent depression of the cardiopulmonary system - heart rate and
BP remains stable - endogenous catecholamines.
➢Decrease tone and motility of GI tract but salivation is not observed.
➢Excellent muscular relaxation.
➢50-70% metabolized in the liver - renal toxic fluoride ions.
➢Should not be used with renally excreted drugs such as tetracyclines and
flunixin.
Enflurane:
➢Mildly pungent, potent, fairly insoluble and stable agent.
➢Rapid induction and recovery.
➢Analgesia is poor & muscle relaxation poor with increasing
concentrations.
➢Concentrations (>3.5%) - central stimulation and seizure -
Avoid use in seizure-prone patients.
➢Dose dependent depression of the cardiopulmonary system.
➢2% metabolized by the liver with some free fluoride ions
produced.
➢MAC - 2.1% in dogs,
➢More expensive than halothane with no real advantages.

Isoflurane:
➢Less potent than halothane or methoxyflurane
➢Relatively insoluble leading to fast inductions and recoveries.
➢Fairly pungent odour / non-flammable
➢Stable compound -does not break down on contact with soda-lime or in
presence of light.
➢Dose dependent cardiovascular depression
➢Better muscle relaxation than halothane and comparatively less
analgesia.
➢Does not promote seizure activity.
➢Due to its good cardiac stability – indicated in cardiac dysfunction.
➢0.2% metabolized by the liver - safe in serious liver dysfunction.
➢Isoflurane is more of a respiratory depressant than halothane,
➢MAC for dogs is 1.28% and for cats is 1.63%.
➢Induction dog 3-5%; maintenance 1.5-2.5 %
 Desflurane:
➢The one of the newest inhalant anaesthetic being popular in
dogs.
➢Less soluble, highly volatile with quicker induction, recovery
and rapid changes in anaesthetic depth.
➢Totally fluorinated ether.
➢Needs electronically controlled vaporizer technology- boils at
close to room teperature.
➢Cardiovascular and CNS effects are similar to isoflurane
➢Circulatory and respiratory effects are similar to isoflurane.
➢Costly
➢Induction 12-18% and maintenance 8-10%
➢MAC in dogs is 7-10

Sevoflurane:
➢Noninflamable, non explosive
➢MAC in cat is 2.58%; MAC in dog is 2.36
➢Rapid induction, recovery & change in depth due
to low blood solubility
➢Analgesia- poor
➢Cardiovascular and CNS effects simillar to
isoflurane
 ALVEOLAR TENSION CURVE OR SOLOUBILITY CURVE

➢ The rate with which the alveolar anesthetic concentration

increases relative to the inspired concentration is often
summarized as a plot of the ratio of FA / FI versus time.
➢ The position of individual curves representing different
anesthetics on a plot is related to the solubility
characteristics of the anesthetics.
The steep initial rise represents movement of anaesthetic into the lungs,
➢ A rapid initial rise results from the effect of alveolar i.e. the pulmonary wash-in phase.
ventilation bringing anesthetic into the lung. The slowly rising tail represents more gradual tissue saturation.
➢ The rate of rise of the curve then decreases as uptake by the ➢Solubility determines the height of the ‘knee’ in the alveolar uptake
blood occurs. curve.
➢With anaesthetics of low blood solubility the knee is high; with high
solubility the knee is low.

A totally insoluble gas would not diffuse into the pulmonary blood and Gaseous agents:
would not be carried in it away from the lungs.
The curve obtained would be all initial rise and there would be no tail. Nitrous oxide:
➢Colorless, sweet, inert and non irritant anaesthetic gas.
Such a gas could not ever be an anaesthetic, since none would ever reach ➢Non inflammable, Non explosive but supports combustion.
the brain.
➢Exhaled unaltered through lungs.
➢Very good analgesic but very poor anaesthetic.
➢MAC in dogs is 188% and in cats is 255% - impossible to achieve
clinically .
➢Used with oxygen and volatile anesthetics 40-70%
➢Minimum of 30% of oxygen should be there in the inhalant mixture.
➢May cause hypoxia and asphyxia - 100% oxygen after turning off the
nitrous oxide.
The second gas effect:
OOO OOO NNNNNN
➢ During the induction of anaesthesia, a large gradient exists between NNNN OOO
OOO OOO
the tension of N2O in the inspired gas and the arterial blood so that in IIIIIII OOO
the early moments of induction the blood takes up large volumes of OOO OOO 0000
gas. ALVIOLI CAPILALRY I

➢ Its rapid removal from the alveoli by the blood elevates the tension of
any remaining (second) gas or vapour such as oxygen or a volatile
anaesthetic agent and augments alveolar ventilation.
➢ Thus, during the first few minutes of N2O administration, anaesthetic N N
uptake is facilitated because, the enhanced tension of the second gas
I IIIIIII IIIIIII NNNN
ensures a steeper tension gradient for its passage into the blood.
O 0000 0000 NNNN

Diffusion hypoxia:
Cyclopropane (C3H6):
➢ Occurs immediately following anaesthesia when the gas is being ➢Potent and quick
rapidly eliminated from the lungs.
➢Nonirritating but highly explosive & inflammable
➢ N2O may form 10% or more of the volume of expired gas and the
➢Respiratory depressant
outward diffusion of N2O into the alveoli lowers the partial pressure
of O2 in the lungs (PaO2). ➢causes vasodilation –increased haemorrhage at the
operative site.
➢ This effect appears to have little clinical significance in healthy
animals but any hypoxia may be dangerous in elderly animals or in ➢Cause cardiac arrhythmias especially in the presence of
those suffering from cardiovascular or pulmonary disease and such hypercapnia.
animals should have an O2 enriched mixture to inhale for some 10 ➢15-20% concentration with oxygen.
minutes after the termination of N2O administration.
➢Highly explosive
➢Not used now a days
 Anesthetic Machines
1. Oxygen : Grey/black with white top. Delivers anesthetic gas mixture to the patient via an appropriate
2. CO2 : Grey/black breathing circuit.
3. N2O : Light or sky blue. Components of basic anesthetic machine -
4. Cyclopropane : Orange 1)The Fresh Gas Source:
Oxygen
➢Vital for the life of the patient
➢Vaporizes volatile agent and delivers to the patient
Nitrous oxide
➢Used in combination with liquid and gas
 2) Pressure Gauges:
➢Found on gas cylinders and on anesthetic machines
➢Shows the pressure within the cylinder
3) Pressure Regulators (Pressure Reducing Valves):
➢ Keeps the pressure constant in the line as pressure within a cylinder
may vary
4) Flow meters:
➢Gas from cylinder reducing valve (via high pressure tubing)
flow meter (via low pressure tubing)
➢Supply measured amount of gas to the breathing circuit & the patient.
➢Aluminum balls - read from the middle of the ball
➢Bobbin type - read from the top of the bobbin
➢Flow is measured in liters/minute.
➢Knobs colour code- White for oxygen and blue for nitrous oxide.

5) Flush Valves:
Precision vaporizers :
➢Delivers oxygen from reducing valve to the breathing circuit without
going through the vaporizer. ➢Compensate for ambient temperatures and the drop in temperature
➢Allows flushing of the circuit with 100% oxygen. seen during vaporization.
➢Used only with a circle system. ➢Highly conductive metal - heat from the surrounding is transferred
6) Vaporizers : to the volatile agent to supply the latent heat of vaporization.
Vaporizes the volatile agent used to anesthetize the patient. ➢Calibrated for one agent only
➢Deliver known concentration of anesthetic
Simple plenum vaporizers : 7) Reservoir (Rebreathing) Bag:
➢Allows accumulation of gas during exhalation and prevents dilution
➢Simple glass containers with room air in non-rebreathing systems.
➢Allow a certain amount of fresh gas (O2 +/- N2O) through the space above ➢Provides a means of assisting or controlling the ventilation of the
the liquid anesthetic agent. patient.
➢Allows visual observation of patient ventilation.
➢The gradations do not indicate the actual vapour concentration unlike ➢Acts as a safety factor, protecting the patient from excessive
precision vaporizers. pressure in the breathing system up to a point.
8) Breathing Tubes/Hoses: METHODS OF ADMINISTRATION OF INHALATION AGENTS
➢Corrugated plastic or rubber tube to avoid the risk of kinking 1. Open method
when bent
2. Semi-open method
➢Act as a reservoir in certain circuits.
➢Provide a flexible, low-resistance and lightweight connection 3.
from one part of the system to another.
9) Valves: (a) Closed method with CO2 absorption
➢Exhaust valves/ relief valves /`pop-off' valves (b) Semi closed method with CO2 absorption
➢Allow excess pressure to be vented to atmosphere,
4. Semi closed method with out CO2 absorption
➢Conduct away waste gases.
➢Not present in Ayre's T-piece

Commonly used non-rebreathing systems –

Non-rebreathing system:
Magill system:
➢Fresh gases flow from the anaesthetic machine into a ➢Reservoir bag, wide bore corrugated tubing and spring loaded
reservoir from which the patient inhales expiratory valve.
➢Exhaled gases are spilled, through an expiratory valve ➢Inhales from bag and wide bore tubing and the exhaled mixture
passes back up the tubing displacing the gas in it back into the bag
to the atmosphere. until it is full.
➢Expired gases are vented to the atmosphere and ➢The exhaled gas passes out of the valve into the atmosphere.
cannot be rebreathed
➢Carbon dioxide removal depends on the fresh gas
flow rate and tidal and minute volume of respiration of
the patient.
The T-piece system:
➢Ayre in 1937.
➢Suitable for small dogs and cats - low resistance and small dead space
➢An open tube acts as a reservoir and no valves
➢The exhaled gases swept out of the open end of the reservoir tube by
fresh gases flowing in from the anaesthetic apparatus during the
expiratory phase.

Coaxial circuits:
The waste gases ducted in the atmosphere by valves away
from the patient and there by prevents pollution of the
operating theatre.
There are two types of coaxial circuits –
•Bain system
•Lack system
Bain system:
➢Fresh gas passes through central tube and expired gas through the
outer sleeve.
➢A tube carrying fresh gas (F) travels inside an outer reservoir tube (R)
to the endotracheal tube connector (P).
➢Bain circuit functions in the same way as the T-piece, except that the
tube supplying fresh gas to the patient is located inside the reservoir
tube.

Lack system:
➢A co-axial modification of the Mapleson A system,
➢Facilitate scavenging of expired gas.
➢A four-way block is attached to the fresh gas outlet (F). This block is
connected to an outer reservoir tube (R) attached to the patient (P),
an inner exhaust tube (E), a breathing bag (B) and a spring-loaded
expiratory valve (V).
Rebreathing:
➢Exhaled gas is directed into a closed bag Disadvantages
➢Carbon dioxide is removed soda lime
➢Sufficient oxygen added ➢Poor control of the inspired anesthetic concentration- fresh gas
➢Rebreathed continuously from the bag delivered from the anesthetic machine is diluted by the gas already
Soda lime: contained within the circuit
Calcium hydroxide 90%
Sodium hydroxide 5% ➢High resistance due to soda lime, inhalation/exhalation valves, and
Silicate 5% pop-off valve.
Water to prevent powdering. ➢Less control of anesthetic depth than non-rebreathing circuit
Advantages
➢Economy of anesthetic consumption.
➢Warming and humidification of the inspired gases.
➢Reduced atmospheric pollution.

The ‘to –and-fro’ system:

➢Soda lime canister is interposed between animal and the
rebreathing bag
➢Fresh gases enters into the system as close to the animal as possible
to effect changes in the mixture rapidly.
➢Not really efficient in absorbing carbon dioxide.