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I created this blog as an instrument of what I have encountered in the world of veterinary medicine as a proud vet student. Comments and suggestions are welcome here at;

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Aina Meducci 2012

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The following blog posts is not genuinely from my research but through readings and citation from trusted website. I do not own any of the copyright and therefore you may use it at your own risk

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Getting started-Anesthesia

Next semester (apparently my third year as veterinary student) we are introduce to this new subject-Anesthetic. Previously, we had only learn anesthetic drugs during pharmacology class but never go into details about it. Now it seems all those knowledge had been cross out from this brain. So, I decided to start it all over again; basic anesthesia.


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General Anesthesia

General anaesthesia (or general anesthesia) is a state of unconsciousness and loss of protective reflexes resulting from the administration of one or more anesthetic drugs. A variety of medications may be administered, with the overall aim of ensuring hypnosis, amnesia, analgesia, relaxation of skeletal muscles, and loss of control of reflexes of the autonomic nervous system.



Anesthesia performed in animal


Anesthetic drugs

An anesthetic is a drug that causes anesthesia reversible loss of sensation. They contrast with analgesics (painkillers), which relieve pain without eliminating sensation. These drugs are generally administered to facilitate surgery. A wide variety of drugs are used in modern anesthetic practice. Many are rarely used outside of anesthesia, although others are used commonly by all disciplines. Anesthetics are categorized in to two classes: general anesthetics, which cause a reversible loss of consciousness, and local anesthetics, which cause a reversible loss of sensation for a limited region of the body while maintaining consciousness. Combinations of anesthetics are sometimes used for their synergistic and additive therapeutic effects, however, adverse effects may also be increased.



Example of anesthetic


Mechanism of action

All local anesthetics are membrane stabilizing drugs; they reversibly decrease the rate of depolarization and repolarization of excitable membranes (like nociceptors). Though many other drugs also have membrane stabilizing properties, not all are used as local anesthetics (propranolol, for example).

Local anesthetic drugs act mainly by inhibiting sodium influx through sodium-specific ion channels in the neuronal cell membrane, in particular the so-called voltage-gated sodium channels. When the influx of sodium is interrupted, an action potential cannot arise and signal conduction is inhibited. The receptor site is thought to be located at the cytoplasmic (inner) portion of the sodium channel. Local anesthetic drugs bind more readily to sodium channels in activated state, thus onset of neuronal blockade is faster in neurons that are rapidly firing. This is referred to as state dependent blockade.

Local anesthetics are weak bases and are usually formulated as the hydrochloride salt to render them water-soluble. At the chemical's pKa the protonated (ionized) and unprotonated (unionized) forms of the molecule exist in an equilibrium but only the unprotonated molecule diffuses readily across cell membranes. Once inside the cell the local anesthetic will be in equilibrium, with the formation of the protonated (ionized form), which does not readily pass back out of the cell. This is referred to as "ion-trapping". In the protonated form, the molecule binds to the local anesthetic binding site on the inside of the ion channel near the cytoplasmic end.

Acidosis such as caused by inflammation at a wound partly reduces the action of local anesthetics. This is partly because most of the anesthetic is ionized and therefore unable to cross the cell membrane to reach its cytoplasmic-facing site of action on the sodium channel.All nerve fibers are sensitive to local anesthetics, but generally, those with a smaller diameter tend to be more sensitive than larger fibers.

Local anesthetics block conduction in the following order: small myelinated axons (e.g. those carrying nociceptive impulses), non-myelinated axons, then large myelinated axons. Thus, a differential block can be achieved (i.e. pain sensation is blocked more readily than other sensory modalities).

**ANESTHETIC DURATION: 3O Minutes of less upon administration.




Examples of anesthetic drugs

Local anesthetic-induce ansence of pain sensation in certain part of the body (suffix-caine). They do not produce unconsciousness.

  • Procaine
  • amethocaine
  • cocaine
  • lidocaine
  • prilocaine
  • bupivacaine
  • dibucaine
  • ropivacaine

Inhale anesthetic

  • Desflurane
  • Enflurane
  • Halothane
  • Isoflurane
  • Methoxyflurane
  • Nitrous oxide
  • Sevoflurane

Intravenous anesthetic-To produce sedation

  • Barbiturates (amobarbital, methohexital, thiamylal, thiopental)
  • Benzodiazepine (Diazepam, Lorazepam, Midazolam)
  • Ketamine
  • Propofol
  • Etomidate


Stages of anesthesia

Stage 1

Stage 1 anaesthesia, also known as the "induction", is the period between the initial administration of the induction agents and loss of consciousness. During this stage, the patient progresses from analgesia without amnesia to analgesia with amnesia. Patients can carry on a conversation at this time.

Stage 2

Stage 2 anaesthesia, also known as the "excitement stage", is the period following loss of consciousness and marked by excited and delirious activity. During this stage, respirations and heart rate may become irregular. In addition, there may be uncontrolled movements, vomiting, breath holding, and pupillary dilation. Since the combination of spastic movements, vomiting, and irregular respirations may lead to airway compromise, rapidly acting drugs are used to minimize time in this stage and reach stage 3 as fast as possible.

Stage 3

Stage 3, "surgical anaesthesia". During this stage, the skeletal muscles relax, and the patient's breathing becomes regular. Eye movements slow, then stop, and surgery can begin. It has been divided into 4 planes:eyes initially rolling, then becoming fixedloss of corneal and laryngeal reflexespupils dilate and loss of light reflexintercostal paralysis, shallow abdominal respiration, dilated pupils.

Stage 4

Stage 4 anaesthesia, also known as "overdose", is the stage where too much medication has been given relative to the amount of surgical stimulation and the patient has severe brain stem or medullary depression. This results in a cessation of respiration and potential cardiovascular collapse. This stage is lethal without cardiovascular and respiratory support.


Adverse effect of anesthesia (may varies from one to another)

  • Hyperkalemia
  • Muscle aches
  • Bradycardia
  • Suxamethonium
  • Anaphylaxis
  • Vomitting
  • Shaking and shivering uncontrollably
  • Toxicity (if given in access)
  • Methemoglobinemia



** I stop here. That's enough for basic

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