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Anesthesia

Anesthesia

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Published by: jgcriste on Jan 23, 2009
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History of Anesthesia
Nero(AD 37-65) – greek and roman surgeons gave the potion of condemned (Wine And Vinegar)
Ambroise Pare – compression of blood vessels and nerves near surgical site in 16
th
century
Also found out that half frozen soldiers have higher pain threshold
Refrigeration anesthesia was revived in 1941 for amputation in world war II.
Joseph Priestley (1733-1804) – Laughing gas - NO2 and O2 combination
Crawford Williamson Long – administered the 1
st
ether anesthetic
James Simpson – instituted the use of chloroform anesthesia in 1847
Friedrich Trendelenburg – ET Anesthesia
Chevalier Jackson – Laryngoscope
Harvey Cushing – founded the unconscious/unaware anesthesia
Ether synthesized in 1540 by Cordus
Ether used as anesthetic in 1842 by Dr. Crawford W. Long
Ether publicized as anesthetic in 1846 by Dr. William Morton
Chloroform used as anesthetic in 1853 by Dr. John Snow
Local anesthesia with cocaine in 1885
Thiopental first used in 1934
Curare ( a muscle paralyzing agent) first used in 1942 - opened the “Age of Anesthesia”
Basic Principles of Anesthesia
Anesthesia defined as the abolition of sensationAnalgesia defined as the abolition of pain
Triad of General Anesthesia
1.need for unconsciousness2.need for analgesia3.need for muscle relaxation
Factors that Determine the Choice of Anaesthesia
1.Patient physical condition2.Patients age3.Medication taken4.Type and probable duration of operation5.Laboratory findings6.Any known idiosyncracies7.Patient’s preference
Types of AnesthesiaGeneral Anesthesia
 Association pathway are broken in the cerebral cortex to produce more or less complete lack of sensory perceptionand motor dischargeUnconsciousness is produced when blood circulating to the brain contains an adequate amount of anesthetic agent.General anesthesia results in an immobile, quiet patient who does not recall the procedure.
 
Stages of General Anesthesia
FromTo Patients ReactionNursing ActionAnalgesiaInduction stageLoss of consciousness Drowsy, dizzy Close suites door, keeproom quiet stand by toassistExcitement/delirium, Lossof consciousnessRelaxation May be excited with irregular breathing and movements of theextremitiesSusceptible to external stimuli(e.g. noise, touch)Secure patient properly,remain at the side of thepatient quietly but readyto assist anesthesiologistas neededSurgicalAnesthesiaRelaxationLoss of reflexes;Depression of vitalfunctionRegular respirationContracted pupilsReflexes disappear Muscle relaxAuditory sensation lossPosition patient and prepskin only whenanesthesiologist indicatesthis stage in reachedDanger StageVital functionstoo depressedRespiratory failure;possible cardiac arrestNot breathingLittle or no pulse or heartbeatPrepare for cardiopulmonaryresuscitation
1.Inhalational Anesthetic Agents
Inhalational anesthesia refers to the delivery of gases or vapors from the respiratory system to produce anesthesiaPharmacokinetics--uptake, distribution, and elimination from the body
Two Methods of Administration
 
Inhalation
Gases and vapors can be delivered via face mask or endotracheal tube.
Mask Inhalation
Anesthetic gas or vapor of a volatile liquid is inhaled through a face mask attached to an anesthesia machineby breathing tubes.The mask must fit the face tightly to minimize escape of gases into environment.
Endotracheal Administration
Anesthetic vapor or gas is inhaled directly into trachea through a nasal or oral tube inserted between vocalcords by direct or blind laryngoscopy. The tube must be securely fixed in place to minimize tissue trauma. Thepatient is given oxygen before and after suctioning.
Intubation
, insertion of tube directly to the trachea and
extubation
removal of tube.
2.Intravenous
A drug that produce hypnosis, sedation, amnesia and or analgesia that is injected directly into the circulation, usuallyvia the peripheral vein.
Nitrous Oxide
Prepared by Priestley in 1776
Anesthetic properties described by Davy in 1799
Characterized by inert nature with minimal metabolism
Colorless, odorless, tasteless, and does not burn
Simple linear compound
Not metabolized
Only anesthetic agent that is inorganic
Major difference is low potency
Weak anesthetic, powerful analgesic
Needs other agents for surgical anesthesia
Low blood solubility (quick recovery)
 
Nitrous Oxide Systemic Effects
Minimal effects on heart rate and blood pressure
May cause myocardial depression in sick patients
Little effect on respiration
Safe, efficacious agent
Nitrous Oxide Side Effects
Manufacturing impurities toxic
Hypoxic mixtures can be used
Large volumes of gases can be used
Beginning of case: second gas effect
End of case: diffusion hypoxia
Diffusion into closed spaces
Inhibits methionine synthetase (precursor to DNA synthesis)
Inhibits vitamin B-12 metabolism
Dentists, OR personnel, abusers at risk
Halothane
Synthesized in 1956 by Suckling
Halogen substituted ethane
Volatile liquid easily vaporized, stable, and nonflammable
Most potent inhalational anesthetic
Efficacious in depressing consciousness
Very soluble in blood and adipose
Prolonged emergence
Halothane Systemic Effects
Inhibits sympathetic response to painful stimuli
Inhibits sympathetic driven baroreflex response (hypovolemia)
Sensitizes myocardium to effects of exogenous catecholamines-- ventricular arrhythmias
Johnson found median effective dose 2.1 ug/kg
Limit of 100 ug or 10 mL over 10 minutes
Limit dose to 300 ug over one hour 
Decreases respiratory drive-- central response to CO
2
and peripheral to O
2
Respirations shallow-- atelectasis
Depresses protective airway reflexes
Depresses myocardium-- lowers BP and slows conduction
Mild peripheral vasodilation
Halothane Side Effects“Halothane Hepatitis”
- 1/10,000 cases
fever, jaundice, hepatic necrosis, death
metabolic breakdown products are hapten-protein conjugates
immunologically mediated assault
exposure dependent
Malignant Hyperthermia
 1/60,000 with succinylcholine to 1/260,000 withouthalothane in 60%, succinylcholine in 77%Classic-- rapid rise in body temperature, muscle rigidity, tachycardia, rhabdomyolysis, acidosis, hyperkalemia, DICmost common masseter rigidityfamily historyhigh association with muscle disordersautosomal dominant inheritancediagnosis--previous symptoms, increase CO2, rise in CPK levels, myoglobinuria, muscle biopsy

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