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Department of Pathophysiology Medical Faculty in Pilsen Charles University in Prague Principles of anaesthesia J. Voller Anaesthesia targeted ly induc ed loss of perception of all modalities (touch, heat, cold, pain) a) rever sible b) permanent ( tumour pain )

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Principles of anaesthesia

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principles of anaesthesia

Department of Pathophysiology

Medical Faculty in Pilsen

Charles University in Prague

Principles of anaesthesia

J. Voller

  • targetedly induced loss of perception of all modalities (touch, heat, cold, pain)
  • a) reversible
  • b)permanent (tumour pain)
  • options of anaesthesia induction :
      • farmacoanaesthesia
      • hypnoanaesthesia
      • audioanaesthesia
      • electroanaesthesia
      • acupuncture
      • cryoanaesthesia
  • division: general anaesthesia X localanaesthesia
general anaesthesia ga
General Anaesthesia (GA)
  • complete loss of perception & consciousness
  • fundamental attributes of GA
    • loss of consciousness – does not block autonomic reflexes to

painful stimuli (perspiration, arrhytmia, hypertension,

bronchoconstriction, bronchial hypersecretion)

    • vegetative stabilisation
    • analgesia – loss of pain sensation, supression of autonomic


    • muscle relaxation
  • induction of all the GA attributes facilitated by mosaic assembly

of partial effects of many substances such as anaesthetics,

analgetics, tranquillizers, myorelaxants

Types of GA according to the entry into organism
  • inhalational
  • intravenous
  • intramuscular
  • rectal – especially in children
  • intraperitoneal – in animals
Stages of GA (Guedel I-IV )
  • obviously present in ether monoanaesthesia (history)
  • nowadays shortcut stage I, supressed stage II

I. stage of analgesia (induction)

      • from the initial administration to the loss of consciousness
      • normally responsive pupils, later dilation
      • tachycardia
      • tachypnoea
      • unchanged skin reflexes
      • marked analgesia – minute operations (e.g: painfull re-bandage)
Stages of GA (Guedel I-IV )

II. stage of excitement

  • from the loss of consciousness to the beginning of the automatic respiration
  • extremely marked exciatation and motor agitation
  • hypersalivation, increased emetic reflex
  • arrhytmia, circulatory instability
  • irregular respiration
  • No action is allowed during this stage. Rapidly acting drugs are used to minimize time in this stage and reach stage 3 as fast as possible.
Stages of GA (Guedel I-IV )

III. stage of surgical anaesthesia

  • automatic respiration to respiration arrest
  • absent eye-lid and corneal reflex
  • absent reaction to pain
  • rhythmical eye-balls movements, sometimes nystagmus
  • In this stage operations including tracheal intubation are being done.
Stages of GA (Guedel I-IV )

IV. stage of paralysis (overdose)

  • after stage III if administration of medication continues
  • respiratory depression, first bronchial breathing, later abdominal breathing
  • cessation of respiration & circulatory collapse
  • lethal without cardiovascular and respiratory support
  • Warning signs: maximally dilated pupils, fading fotoreaction, irregular heart action, urinary & faecal incontinence
Monitoring depth of GA
  • concentration inhalational anaesthetics
  • bispectral index (computerized EEG analysis)
  • vegetative response (perspiration, pupils, blood

pressure, pulsation)

  • clinical status, esp. waning muscle tonus

(not available when muscle relaxants are used)

ga inhalational anaesthetics
GA – inhalational anaesthetics

According to physical properties:

  • anaesthetic gases
    • stored in pressure tanks
    • applied with anaesthetic machine
    • e.g.: nitrous oxide – laughing gas (formerly: cyclopropane)
  • volatile liquids
    • liquids with low boiling-point (about 40°C)
    • stored in dark flaskets (the light induces transformation in toxic aldehydes)
    • applied with vaporizers
    • e.g.: halotane, isoflurane, sevoflurane
Evaluation of inhalational anaesthetics efficiency

Minimum alveolar concentration (MAC)

  • Concentration of anaesthetic in alveolar space, that

prevents the reaction to a standard surgical stimulus

(skin incision) in 50% of subjects

  • the lower MAC, the more potent anaesthetic
  • imobility in 95% subjects: increasing concentration of

anaesthetic 30% over MAC

  • before inhalational induction 2-5 minutes 100% oxygen->

denitrogenation -> faster induction

  • at the end of anaesthesia again 100% oxygen -> faster

excretion of anaesthetic and waking up

ga intravenous anaesthetics
GA – intravenous anaesthetics
  • mostly used for induction (weak or no analgetic effects)
  • rarely for maintenance (TIVA)
  • combined with inhalational anaesthetics and some other medicaments (opioid analgetics, neuroleptics…..)
  • quick onset of the effect, quick arousal (redistribution)
  • MIR (minimal infusion rate) – rapidity of anaesthetics infusion,

thatprevents the reaction to a standard surgical stimulus

(skin incision) in 50% of subjects

Groups of intravenous anaesthics in use
  • barbiturates – thiopental
  • imidazoles – etomidat
  • alkyled phenols – propofol
  • steroids– althesin
  • eugenols – propanidid
  • phenylcyclidines – ketamine

7. benzodiazepines

ga praemedication
GA – praemedication

Purpose of praemedication

  • satisfactory rest at night before operation


  • calm down
  • basal analgesia
  • supression of readines to allergic reactions
  • supression of vegetative reflexes (bradycardia, hypersalivation, bronchial hypersecretion)

e.g: sedatives, hypnotics, anxiolytics, vagolytcs (atropin),


ga muscle relaxants
GA muscle relaxants

depolarising muscle relaxants

  • cholinergic receptor -> depolarisation -> generation AP
  • fasciculations
  • antagonisation is not possible
  • e.g.: Suxametonium (succinylcholine)

non-depolarising muscle relaxants

  • competetive block of cholinergic receptors without generation of AP
  • so called curariform medicaments, e.g.: Pancuronium, Atracurium
  • antagonist: neostigmin (decurarization)
local anaesthesia la
Local anaesthesia (LA)
  • contrary to general anaesthesia: consciousness is preserved
  • places of acting:
          • spinal roots
          • nerve plexi
          • peripheral nerves
  • types of local anaesthesia
          • topic (surface, mucosal)
          • infiltrative
          • conduct
          • spinal

- epidural

- subarachnoid

local anaesthesia
Local anaesthesia






scheme by J.Cendelín

Topic (surface, mucosal) anaesthesia
  • aerosol administration on the mucous sourface, liniments with LA (EMLA)
  •  ORL, ophtalmology, anaesthesia in oral or nasal cavity,

conjunctiva & cornea, in urology for anaesthesia of mucose of the urinary tract (urethral catheterization)

Infiltrative anaesthesia

  • infitration in zone of operation
  • reversibile block of terminal parts of nerve fibers
  • IVRA – intravenous regional anaesthesia (Bier´s block)
    • application into peripheral veins previously emptied of blood
    • diffusion and infiltration of surrounding tissue
    • danger of toxic effects of anaesthetic in the blood circulation

after the turnstile is released

Conductive anaesthesia
  • targeted application af anaesthetic near nerve or nerve plexus
  • anaesthesia of all parts controled by the particular nerve
  • usually also motor paralysis (dependent on dose of


  • examples of usage:
    • conductive LA of peripheral nerves (n. radialis, medianus,

ulnaris, femoralis, ischiadicus...)

    • anaesthesia of II. or III. branch of trigeminal nerve (stomatology)
    • in experiment: anaesthesia of rabbit auricle

Epidural anaesthesia

  • application of LA into the epidural space
  • block of impuls conduction in nerve exit from the dural sac
  • affected sensitive, sympatethic, motor nerves
Subarachnoid anaesthesia

(spinal, intrathecal)

  • LA administered subarachnoidally in CSF
  • izobaric LA - stays where applied + diffusion
  • hyperbaric LA – spread dependent on gravity -> range of anaesthetized zone can be influenced by positioning
  • risk of severe complications (respiration centre paralysis)
LA - farmakology

Division LA


  • less stable, shorter duration, hydrolyzed in liver and aslo in plasma by cholinesterases
  • more often allergic reactions
  • e.g.: Procaine, Tetracaine


  • more stable, longer lasting effect, hydrolyzed in liver only
  • allergic reactions uncommon
  • e.g.: Trimecaine (Mesokain), prilocaine
Mechanism of the effect of LA
  • blockade of the inner oriffice of sodium channel -> influenced depolarisation
  • non-ionized form – penetration throuhg connective tissue, myelin sheet and cell membrane, intracellularily ionization and attachment to the sodium channel (competetive antagonism)
  • ionizoed vs. non-ionized form ratio dependent on pH
    • healthy tissue: slightly alkaline pH -> more non-ionized form -> easy penetration of LA into cells -> quick effect onset
    • inflammatory focus: acid pH -> less non-ionized form ->

-> poor penetration intracellularily -> weak LA effect

  • Vasoconstrictive addition agents (adrenaline/epinephrine)
    • reduction of absorbtion ->longer lasting effect, lowered toxicity, less bleeding
Effects of LA on nerve fibers
  • block of sympathetic division (warming of skin)
  • loss of sensation of heat and pain
  • loss of sensation of touch and pressure
  • loss of motorics
  • Eduard Kasal a kolektiv: Základy anesteziologie, resuscitace, neodkladné medicíny a intenzivní péče pro lékařské fakulty, Univerzita Karlova v Praze, Praha 2006
  • Jan Pachl, Karel Roubík: Základy anesteziologie a resuscitační péče dospělých i dětí, Učební texty Univerzity Karlovy v Praze, Praha 2003
  • Pavel Sobotka a kolektiv: Patlogická fyziologie – Praktikum, Univerzita Karlova v Praze, Praha 2005
  • Sixtus Hynie: Farmakologie v kostce, druhé, přepracované vydání, Triton 2001