ANESTHESIA
History:-
• Egyptians gained knowledge of anatomy-making Mummies (removing
votting organs).
• 13th century (ibn e khalikan), 14th century (ibn e kathir) documented that
Irwa ibn Zubair(beginning of 8th century) developed gangrene and
Umayad’s Caliph Alwalid ibn abdul-Malik physicians team offered him Al-
murquid for induction of anesthesia.
• 12th century (sayed Alkhatir for ibn Aljawzi) has referred Anesthetic effect
of BHANJ.
• 14th century (Ibn al Quff) gave detail of the most advance techniques of
anesthesia in his book (Al Umda fi Aljiraha) in addition to advance
techniques in:
• Resuscitation
• Nutrition
• Upper airways obstruction management etc.
History of Local Anesthesia:-
• 1st Local anesthesia agent was cocaine- late 19th century from leaves
of coca- Erythroxylon coca
• Cocain 1st isolated – 1860- Albert Nieman – Nummed tongue when
extract tested.
• Physio active studied- 1884- Sigmund Freud.
• 1st introduced for chemical use 1884- Carl Koller
Opthalmic.
• Popularized its uses for infiltration and nerve block anesthesia-
Surgery Halstead.
• Many L.A.s now a days all stem from theses early observations.
DEFINITION:-
Local anesthetics are drugs which upon topical application or local injection cause
reversible loss of sensory perception ,especially pain in restricted area of the body
through blocking generation conduction of nerve impulses at all parts of nueron
where they come in contact without causing any structural damage.
DIFFERENCE B/W GENERAL ANESTHESIA(GA) AND LOCAL ANESTHESIA(LA):-
CLASSIFICATION OF LA:-
Local anesthetics are classified as:-
• Esters LA
• Amides LA
• Naturally derived LA
ESTERS LA:-
• Cocaine
• Procaine
• Tetracaine
• Chlorprocaine
• Benzocaine
• Cyclomethycaine
• Dimethocaine
• Larocaine
• Piperocaine
• Propoxycaine
• Proparocaine.
AMIDES LA:-
• Lignocaine
• Mepivacaine
• Prilocaine
• Bupivacaine-levo
• Etidocaine
• Ropivacaine
• Articaine
• Cinchocaine/dibucaine
• Trimecaine
• Ambucaine.
NATURALLY DERIVED LA:-
• Saxitixin
• Neo-saxitoxin
• Tetradotoxin
• Menthol
• Eugenol
• Cocaine.
CHEMISTRY:-
Weak bases –Amphipathic property
ADVANTAGES OF AMIDES:-
• More intense/tongue testing
• Not hydrolyzed in plasma.
• NO hypertensive reactions.
DISADVANTAGES OF ESTERS:-(RARELY USED)
• Short
• Less intense
• Risk of hypertensitivity.
MECHANISM OF ACTION:-
• Las lipophilicity PKa properties play an imp role in ionization/deionization
across cell membrane.
• LAs PKa (7.6-7.8) 30-40% unionized INC entering axonal membrane
at medium pH 7.4.
• Las gain protein (H+) and becomes ionized inside condition impart
bind with receptor of inactivated Na+ channel prolongation of
inactivated state NO response to voltage stimuli.
SITES OF ACTIONS:-
• Block sensory nerve ending
• Nerve trunks
• N-m junctions
• Ganglionic synapses through interaction
• Na+ channels inner receptor
• Dec. Ach release(Motor nerve ending).
SENSITIVITY:-
• Sensory and Motor fibers = sensitivity
• Myelinated blocked faster
• Smaller blocked faster than larger
• Autonomic more susceptible than somatic
• Somatic order of blockage
Pain Temp. Touch Deep pressure
• Order of taste blockade:
Bitter Sweet Sour Salty.
• The more susceptible fibers(1st to be blocked taste to be recovered )
• Outer layers fibers blocked faster than inner.
BENEFITS OF ADRENALINE ADDITION:-
• Inc. duration
• Inc. intensity
• Less systemic toxicity
• Inc. bloodless field for surgery.
DISADVANTAGES OF ADRENALINE ADDITION:-
• Inc. painfull injection tissue
• Inc. chance of local edemas, necrosis and DEC healing.
• Inc. B.P/ arrhythmia in some individuals.
SYSTEMIC ACTIONS:-
CNS:-
Stimulation Depression
• Cocaine: sequenced EUPHORIA-Excitement-m.Confusion-
Restlessness-Tremor and twitching-Convulsions-Unconcious-Resp.
dep.- DEATH.
• Procaine and others: Drowsiness and Lethargy – Stimulus-
Depression.
CVS:-
• Cardiac depressants, Quinidine like antiarrythmia.
• Inc. ERP, Dec. Conduction, Contraction, and Excitement.
GENERAL ANESTHESIA
DEFINITION:
Reversible medical state characterized by:
• Unconsciousness
• Analgesia
• Amnesia(forgetfulness)
• Skeletal muscle relaxation
• Loss of reflexes
PHARMACOKINETICS OF Inhaled Anesthetics:-
• Inc. pulmonary aveoli and tissue barriers
• Depth of anesthesia dep- potency(MAC)and (PP)
FACTORS INFLUENCING BRAIN ANESTHETICS (PP):-
• Partial pressure in inspired air mixture:
Inc. conc. Inc. PP blood brain
• Ventilation:
Inc. ventilation Inc. delivery of G.A.
• Exchange :
Diffuse freely-if ventilation and perfusion mismatch delay in
duration and recovery.
• Blood solubility:
Inc. solubility –Inc. busy (blood)- not free for brain-Dec. quality.
• Tissue solubility:
INC solubility- Inc. busy (tissues)- not free for brain- Dec. quality
• Cerebral blood flow:
INC CBF – deliberately:
1. Inc. CO2- vasodilation-Inc. brain-Inc. induction
2. Dec. O2-vasoconstriction-Dec. brain-redist-recovery.
ELIMINATION:-
Discontinued-gradient reverse-redistributed-blood tissue-alveoli
IDEAL PROPERTIES FOR G.A:-
1. Patient:
• Pleasant
• Non-irritant
• No nausea/vomiting
• INC induction and recovery.
2. Surgeon:
• Analgesia
• Immobility
• Muscle relaxation
• Non inflameable/explosive
3. Anesthetist:
• Administration should be easy,controllable and versatile
• INC margin of safety
• Potent
• INC. adjustment depth
• Cheap
• Stable
• Easy store.
