This document discusses veterinary anesthesia. It begins by defining anesthesia and anesthesiology. It notes that anesthesia aims to minimize or eliminate pain, relax muscles, and facilitate patient restraint during procedures. Various types of anesthesia are discussed, including local, regional, and general anesthesia. Common drugs used in veterinary anesthesia are also outlined, including sedatives, analgesics, dissociatives, and neuromuscular blocking agents. The document also covers anesthesia administration techniques and important considerations for patient monitoring and recovery.

1. Presented by-
Sindhu K,
M. V. Sc. Scholar, Dept. of VPT, COVAS, Pookode.

2. Greek: an = without
aesthesia = sensation
Anesthesiology is defined as art & science of administration of
anesthesia.
Anesthesia term coined (1846) by an American physician Oliver
Wendell Holmes, Sr. (1809-1894)
In 1975, The American College of Veterinary Anesthesiologists
was officially recognized by the American Veterinary Medical
Association as the body to certify veterinarians as specialists in
veterinary anesthesia.

3. To apply methods to
minimize / eliminate pain,
relax muscles,
Facilitate patient restraint during surgical, obstetrical,
medical, diagnostic & therapeutic procedures.
To monitor & support
Life functions in patients during the operative as well as in
critically ill, injured, / seriously ill patients.

4. Elimination of sensibility to noxious stimuli.
Humane restraint (protect animal, facilitate
diagnostic/surgical procedure).
Technical efficiency (protect personnel, facilitate
diagnostic/surgical procedures).
Specific biomedical research tool (sleep time).
Control convulsions.
Euthanasia.

5. Prevention of the perception of noxious stimuli (pain) during
surgery is the primary justification for anesthesia.
A noxious stimulus = stimulus that potentially damages the
body tissue.
Nociception has no emotional/perceptional connotation.
Pain is an unpleasant sensory & emotional experience; it is a
perception, not a physical entity.
Perception of pain depends  functioning cerebral cortex.

6. • Sensory
• Discriminative
• Motivational
• Affective

7. Anesthesia is produced by
 Chemicals (drugs)
 Physical (sensory nerve destruction)

8. According to route of administration:
Topical.
Injection.
Gastrointestinal tact.
Respiratory system.

9. I. Cutaneous.
II. Mucous membrane.

10. I. Intravenous
II. Subcutaneous
III. Intramuscular
IV. Intraperitoneal
V. Intraosseous

11. Oral
Rectal

12. I. Inhalation

13. Based on extent of loss of sensation
1. Local/regional: drugs placed in close proximity to nerve
membranes, causing conduction block.
Eg: topical, area infiltration, perineural, peridural,
subarachnoid.
2. General anesthesia: state of controlled, reversible CNS
depression including unconsciousness produced by
one/multiple drugs.
Eg: injectable, inhalation, balanced.

14. Administered usually to
conscious or mildly sedated
animals, to desensitize a
localized or regional area of
the body.
It is deposited in close
proximity to nerve membrane
causing nerve conduction
blockade.

15.  GA is a condition induced by pharmacological or other means
that results in controlled, reversible CNS depression.
 Basic elements of GA:
I. Reversibility
II. Unconsciousness
III. Amnesia
IV. Analgesia
V. Muscle relaxation
VI. Immobility

16. A favorable anesthetic course begins with good plan – a
plan based on sound pharmacological & physiological
principles.
Anesthetic management = physiology of respiration +
circulatory + central + autonomic nervous system.
Pre-anesthetic period.
Anesthetic period/ peri-anesthetics period.
Post-anesthetic period.

17. Tranquilizer-sedative (Acepromazine, benzodiazepines).
Hypnotic sedatives (pentobarbital & chloral hydrate).
Opioid (agonist-morphine & meperidine, agonist-antagonist-
butorphanol).
Alpha-adrenergic agonist (xylazine, detomidine,
medetomidine).
Dissociative (ketamine)
Parasympatholytics (atropine & glycopyrrolate).
Sedative drugs (telozol = tiletamine + zolazepam).

18.  Administration of anesthesia requires a combination of
knowledge + skill+ ingenuity.
 Given by inhalation / injections.
 Classification
Hypnotic sedatives
Dissociative
Opioid
Tranquilizer-sedatives
Balanced anesthetics.

19.  Also known as anesthetic recovery period.
 Hazards of immediate postanesthetic period:
Circulatory system complication  arterial hypo- & hypertension,
cardiac dysrhythmias.
Respiratory system complications  hypoxemia, hypercapnia
Pain  nociception
Emergency excitement  physical trauma
Hyper-/hypothermia
Vomiting
Delayed awakening.

20. • Used clinically act by interfering with the effectiveness of the
endogenous neurotransmitter Ach to activate nicotinic
cholinergic receptors of skeletal muscle cells, thereby
inhibiting receptor-coupled transmembrane ion movements
necessary for muscle contraction. (Bouzat et al. 2004: Unwin
2005).
• End result = skeletal muscle paralysis + muscle relaxation.
• Most often used as adjuvants to anesthesia to facilitate
tracheal intubation, abdominal muscle relaxation, orthopedic
manipulations & as a part of balanced anesthesia procedure to
reduce the amount of GA required in high-risk patients.

21. A direct alteration of the effectiveness
of Ach to activate postjunctional
receptors.
According to the mechanisms of
postjunctional action, neuromuscular
blocking agents are classified as
I. competitive (nondepolarising)
agent.
II. depolarizing agent.

22.  Drugs compete with Ach for available cholinergic receptors at
postsynaptic membrane & by occupying these receptors, prevent the
transmitter function of Ach.
 Prototype: d-tubocurarine (Tubocurarine chloride, USP, Tubarine).
 Metocurine Iodide, USP (Metubine).
 Gallamine Triethiodide, USP, (Flaxedil) gallamine.
 Pancuronium Bromide, Pavulon, Pancuronium.
 Synthetic compound: alcuronium, atracurium.
 Vecuronium, a derivative of pancuronium.

23. Drugs exert their skeletal muscle paralyzing effects
by interfering with Ach-mediated depolarization of
the post synaptic membrane.
Prototype: Succinylcholine chloride USP (quelcin,
anectine, sucostrin, suxamethonium).
Decamethonium bromide, USP (syncurine, C-10)

24. Muscle paralysis head & neck muscles (head drop)  tail 
limb muscles deglutition & laryngeal muscles  abdominal
muscles  intercostal muscles  diaphragm.
Recovery usually proceeds in the reverse sequence (Hall, 1971).

25. Unique among anesthetic drugs
because of ease in administration & in large
part removed from the body, via the lungs.
Used widely for anesthetic management of
animals due to their pharmacokinetic
characteristics favors predictable & rapid
adjustment of anesthetic depth.
Specialized apparatus is used to deliver the
inhaled agents, helps minimize patient
morbidity/mortality  facilitates accurate &
controlled anesthetic delivery, lung
ventilation & improved arterial oxygenation.

26.  Group I : agents in current use for animals.
Volatile halothane, isoflurane, desflurane, sevoflurane.
Gas nitrous oxide (N2o)
 Group II : gaseous agent under investigation
Xenon
 Group III : volatile agents of immediate past use/ interest.
Enflurane
Methoxyflurane
Diethylether

27.  Provide rapid means of producing sedation/anesthesia in
veterinary patients.
 Advantage of injectable anesthetic over inhalation  the ability
to proceed more rapidly through stage II anesthesia (the
excitement stage).
 These agent allows a more rapid control of airway, smooth
induction of anesthesia, rapid control & reduction in CNS
activity, unobstructed visualization of URT for surgical
procedures.
 For large animal (horses), preventing the excitement stage is
paramount for the animal’s safety + medical personnel.

28. Physiological properties  unconsciousness, amnesia,
analgesia & skeletal muscle relaxant.
Pharmacological properties  margin of safety/
therapeutic index, short duration of action &
noncumulative, readily metabolized & excreted ideally by
> one route, a specific & complete reversal of anesthesia.
Ideal drug  chemically stable, long shelf life,
physiological pH, nontoxic vehicle & inexpensive.

29. I. Barbiturates.  (thiopental, pentobarbital, amobarbital &
phenobarbital.)
II. Non barbiturates – non dissociative anesthetics.
a. Phenol derivatives (propofol & fospropofol)
b. Imidazole derivatives (etomidate & metomidate)
c. Neurosteroids (alfaxalone-alfadolone & alfaxalone-CD)
d. Benzodiazepines (midazolam, diazepam & lorazepam)
e. Opiods, neuroleptanalgesics & neuroleptanalgesthics.
(fentanyl, fentanyl+droperidol, methadone+acepramazine+nitrous
oxide.)
f. Miscellaneous i/v anesthetics [chloralhydrate, Guaifenesin (triple
drip), chloralose, propranidid, tribromoethanol, urethane]
III. Dissociative anesthetics  (ketamine, phencyclidine &
tiletamine).

31. Classification Compounds Clinical
applications
Ultra short acting Thiopental, thiamylal,
thialbarbital, hexobarbital,
methohexital.
As general anesthetic
Short acting Pentobarbital, secobarbital. As hypnotic, pre-anesthetic &
emergency management of
seizures.
Intermediate acting Amobarbital, aprobarbital,
mephobarbital.
As hypnotic, pre-anesthetic &
emergency management of
seizures.
Long acting Barbital, phenobarbital. As anticonvulsant &
sedatives.

32. An anesthetic state caused from interruption of
ascending transmission from the unconscious to conscious part of
the brain.
Characterized by  catalepsy.
 somatic analgesia.
 intact ocular+laryngeal+pharengeal
reflexes.
 control of the airway may not be complete, intubation with a
cuffed endotracheal tube is recommended.
Commonly used  induction + maintenance of anesthesia in cats
& dogs.

33.  CNS acting drugs which decreases activity, moderate excitement,
produce drowsiness & calm the recipient.
 Drugs having capacity to decrease the CNS activity  calming &
drowsiness.
 Clinical indication  to produce restrain.
 to facilitate handling + transport.
 to modify behavior of animals.
 Sedative = non specific ~ general CNS depressants.
I. Hypnotic-sedatives/ Classical sedatives.
II. Tranquilliser-sedatives/Tranquillisers (ataractics, neuroleptics).

34. I. Benzodiazepines  diazepam, midazolam, lorazepam.
II. Alpha2 adrenoceptor agonists  xylazine, detomidine,
medetomidine, romifidine & clonidine.
III. Barbiturates  barbital, phenobarbital, amobarbital,
secobarbital, pentobarbital.
IV. Chloral derivatives  chloral hydrate.
V. Aldehydes  paraldehyde.
VI. Inorganic salts  sodium bromide, potassium bromide &
magnesium sulphate.
VII.Miscellaneous agents  ethyl alcohol, ethchlorvynol,
glutethimide, methyprylon, ethinamate & meprobamate.

35. I. Phenothiazines  chlorpromazine, acepromazine,
promazine, piperacetazine, triflupromazine.
II. Thioxanthenes  chlorprothixene, clopenthixol, thiothixene.
III. Butyrophenones  azaperone, droperidol, fluanisone.

36. Diverse group of drugs used primarily in the treatment of
epilepsy.
It is important to 1st approach epilepsy as a manifestation of an
underlying disease.
When the underlying cause of disease cannot be identified
(idiopathic epilepsy) or treated  management of epilepsy is
primarily based on control of seizures with anticonvulsant drugs.
Major molecular target of commercially available drugs
Voltage gated sodium channels.
GABA a receptors.
The GAT-1 GABA transporter.
GABA transaminase.

38. I. Barbiturates  phenobarbital, pentobarbital & mephobarbital.
II. Deoxybarbiturates  primidone
III. Hydantoins  phenytoin, mephenytoin, ethotoin, fosphenytion.
IV. Benzodiazepines  clonazepam, diazepam, lorazepam, oxazepam,
clorazepate.
V. Aliphatic carboxylic acids  valoproic acid & sodium valproate
VI. Bromides  potassium bromide & sodium bromide
VII.Succimides  ethosuximide, methsuximide, phensuximide &
mesuximide
VIII.GABA analogues  gabapentin, vigabatrin, pregabalin,
progabide

39. IX. Dicarbamates  felbamate & meprobamate
X. Sulphonamides  zonisamide, acetazolamide, methazolamide &
sultiame
XI. Pyrrolidines  levetiracetam, brivaracetam & seletracetam
XII. Carboxamides  carbamazepine, oxcarbazepine, eslicarbazepine
& rufinamide
XIII. Oxazolidinediones  trimethadione, paramethadione & etadione.
XIV. Miscellaneous agents  topiramate, lamotrigine, valpromide,
beclamide, lacosamide, paraldehyde, tiagabine, stiripentol &
valnoctamide.

40. Veterinary clinical ethology  A relatively new branch of vet. Medicine
dealing with study of customs & behaviour of animals in their natural
habitat.
Behaviour is a complex phenomenon.
It is not easy to define in terms of normal & abnormal behaviour.
Adverse behaviour in animals  disease condition (neural disorders).
 lack of socialization & training.
 genetically determined.
Classification of behaviour disorders on basis of their origin.
Genetic problems, developmental & age related problems, instinctive &
species related problems, socialization/ social behaviour related
problems, disease related problems & adaptation problems.

41. Sr. no. Behaviour disorder Etiology
1 Aggression Dominance, competition, fear, learned, idiopathic &
feeling of uncertainty.
2 Anxiety Separation, travelling, new place & unfriendly
environment.
3 Fear/phobia Thunderstorms, gunshots, fireworks, heavy vehicle’s
engine noise.
4 Destruction Fear anxiety, over activity & reaction to arousing
stimuli.
5 Excessive vocalization Frustrated social/sexual environment, aggression &
reaction to external stimuli.
6 Elimination behaviour
(urination/defecation)
Marking territory, urine spraying (cats), submission,
excitement, lack of training & separation.
7 Sexual behaviour Hyper-sexuality, lack of libido, false pregnancy.
8 Self mutilation Attention getting & stress response.
9 stereotypies Stress response & compulsive behaviour.

42. Abnormal behaviour in man/animal is closely related to
alterations in concentrations of various neurotransmitters
Biogenic amines
Acetylcholine
Excitatory AA
Inhibitory AA
A wide variety of drugs from different pharmacological classes
are employed to modify abnormal behaviour in animals 
Psychotropic drugs, anticonvulsants, hormonal preparations,
CNS stimulants, artificial pheromones & miscellaneous drugs.

43. Algesia = ill-defined, unpleasant sensation,
usually evoked by external / internal noxious stimulus.
Physiological pain  nociceptive pain.
Pathological pain  neurogenic & cancer pain.
Opioids  potent analgesic agents, which induces analgesia by
stimulation of central opioid receptors.
Classified into
I. Opioid agonists.
II. Opioid mixed agonist-antagonists & partial agonists.

44. I. Natural opium alkaloids  morphine & codeine.
II. Semi-synthetic opioids  diacetylmorphine, hydromorphine,
oxymorphone, hydrocodone, oxycodone, etorphine.
III. Synthetic opioids
1. Phenylpiperidines (pethidine, ketobemidone, prodine, allylprodine,
anileridine).
2. Anilidopiperidines (fentanyl, alfentanil, carfentanil, sufentanil).
3. Diphenylpropylamine derivatives (methadone, propoxyphene,
dextromoramide, dipipanone, loperamide & diphenoxylate).
4. Morphinans (levorphanol & levomethorphan).
5. Benzomorphans (phenazocine).
6. Miscellaneous drugs (tramadol, tapentadol & tilidine).

45. I. Semi-synthetic opioids (buprenorphine & nalbuphine).
II. Synthetic opioids
1. Morphinans (butorphanol).
2. Benzomorphans (pentazocine, dezocine & cyclazocine).
3. Miscellaneous agents (meptazinol).

47. Drugs which stimulate the CNS/improves specific brain
functions.
Classification  pyscostimulants / cerebral stimulants
 brain stem stimulants / analeptics
 convulsants
 psychotomimetics / hallucinogens

50.  Small animal clinical pharmacology: D. M. Boothe. (2nd ed.)
 Veterinary Pharmacology and Therapeutics: Jim E Riviere & Mark G Papich.
(9th ed.)
 Veterinary pharmacology and therapeutics: H. R. Adams. (8th ed.)
 Essentials of veterinary pharmacology & therapeutics: H. S. Sandhu. (2nd
ed.)
 Google images.