General Anesthesia
2
GENERAL ANESTHETICS Anesthesia – denotes a lose ofsensibility Surgical Anesthesia – is a controlled degree of CNS depression w ith the follow ing com ponent • Analgesia – lack ofpain • Am nesia – lack ofm em ory •Inhibition from reflexes such as bradycardia and laryngospasm • Skeletal m uscle relaxation • (altered state consciousness)state ofunconsciousness. Two Kinds of General Anesthetics A. Inhalational B. Intravenous InhalationalG en A nesthetics 1.N 2O (N itrous oxide)– laughing gas 2.H alothane 3.Enflurane 4.Isoflurane 5.Methyoxyflurane 6.D iethyl ether Newer Inhalational General Anesthetics 1. Desflurane 2. Seroflurane M echanism ofA ction ofInhalationalG eneral Anesthetics These agents decrease the firing rate ofnerve cells by decreasing the rise of the action potential. They inhibit the rapid increase in m em brane prem eability to sodium ion. N o receptors have been found to interact w ith the anesthetic and no neurotransm itters are involve in theiraction. KINETICS OF ANESTHESIA 1. Induction 2. Maintenance 3. Recovery A Induction and R ecovery from Anesthesia Induction – is the period of time from onset of administration of the anesthetic to the development of effective surgical anesthesia in the patient.Itdepends on how fastthe anesthetic reaches the brain. R ecovery – is the time form discontinuation of adm. of anesthetic until consciousness is regained .It depends on how fast the anesthetic is rem oved from the brain. drugs administered by inhalation; the rate of onset & recovery are influenced by the follow ing factors: 1. Solubility ofanesthetic – this is expressed as the blood /gas concentration ofgas in the blood,relative to the gas equilibrium phase. The greaterthe blood /gas partition coefficientthe m ore soluble is the anesthetic agentin the blood. a. Ifa drug has a low solubility (low -blood /gas partition coefficient)little ofthe drug is dissolve in the blood. Therefore the equilibrium between inhaled anesthetic and arterialblood is rapidly achieve,and only a few additionalm olecules ofthe anesthetic is required to raise the arterial tension. This results to rapid induction and shortrecovery. Exam ple – N itrous O xide (N aO )= 0.47 B/G coefficient b.If the anesthetic has high solubility – it is more dissolve completely in the blood – so greater amounts of the anesthetic and longer periods of tim e are required to raise arterial tension. This results in increase tim es of induction and recovery also slower to changes in the cone of the inhaled drug .Ex.H alothane – 2.3 B/G coefficient 2.R ate ofventilation – an increase rate ofdelivery ofanesthetic gas to the lungs results in most anesthetic being delivered to the alveoli. This increases the rate at which the arterial blood approaches equilibrium. The effect of ventilation is most pronounced foranesthetics w ith high solubility in blood. 3.Increase alveolarblood flow – high blood flow causes m ore ofthe anesthetic agent to be removed from the alveoli hastening anesthesia. B.M aintenance ofAnesthesia – m aintenance is the tim e during w hich the patient is surgically anesthetized, anesthesia is usually maintained by the administration of gases or volatile anesthetics since these agents offergood m inute to m inute control overthe depth ofanesthesia. A nesthetic P otency ofInhaled G eneralA nesthetic: -is defined quantitatively as the m inim um alveolar concentration. (M AC) w hich is the concentration ofanesthetic gas needed to elim inate movement am ong 50% ofpatients challenge to a noxious stim ulus. The m orepotent an anesthetic,the low erits value forM AC. Properties ofM odern inhalationalA nesthetics Blood/gassolubility coefficient 0.43 – 0.47 2.3 – 2.4 1.9 1.4 12 M A C % atm 110 or 105 0.75 – 0.77 1.68 1.15 0.16 A .G A S Nitrous Oxide B.H alogenated gases (volatile) 1. Halothane 2.Enflurane 3.Isoflurane 4.M ethoxyflurane C om parison ofthe differentPharm acologic effects ofInhaled G eneral Anesthetics Respiration Rapid/shallow resp ventilatory depression D ose-dependent resp depression Causes bronchodilatation BP B.P D ose dependent B.P Sensitization of M yocardium to A ctions of Epinephrine Increases sensitization of m yocardium esp to adrenergic agonist,cardiac dis,hypoxia and electrolyte im balance –m ay Induce ventricular arrhythm ias Low erincidence ofarrhythmias and less sensitization to the m yocardium to catecholam ines Cardiac Effects slow s heart rate due to reduction of cardiac S ym pathetic activity cardiac output is N o Brady cardia,N o in C.O G eneral A nesthetic 1.H alothane 2.Enflurane -S ignificant resp D epression - due to the hypercapnia M inimaleffect B.P C.O BP and total Peripheral resistance w hen in Com bination of m ore Potent anesthetic does not cause sensitization of m yocardium rarely causes A rrhythm ias Little effect but com bination with a m ore potent anesthetic leads to sym pathetic stimulation Causes direct coronary vascular redistribution. Capable of w orsening ischemia M inimal C.O 3. Isoflurane 4.N itrous oxide 2% is m e tabolized to fluoride ion w hich is excreted by the kidney -contraindicated in pnts with RenalFailure.EEC pattern – char.of seizure activity – m ay lead to Frank S eizure G ood m uscle relaxation relaxes the uterus Less potent than halothane but it produces m ore rapid induction and recovery Enflurane Extensively m etabolize and Biotransform ation interm ediates m ay result to hepatotoxic m etabolites – “ H alothane H epatitis” -m alignant hypertherm ia G ood m uscle relaxation but lacks significant Analgesia Potent H alothane O rgan toxicity and other adverse effect M uscle relaxation – Analgesia Potency/induction recovery onset O ther D ifferences C om parison ofthe differentPharm acologic effects ofInhaled G eneral Anesthetics M ay diffuse into body cavities – the pressure or expand the volum e of gas in air pockets m ay lead to: a. D istention of the bow el b. Expansion or rupture of a pulm onary cyst c. Rupture of the tym panic m em brane in an occluded m iddle ear d. Pneum oce phalus -w hen it is dissolve in the blood m ay enlarge the volum e of air em boli Poor surgical anesthetic if use alone but good Analgesic N ot very potent w hen use alone but produce the fastest induction and recovery N itrous Oxide Low biotransform ation low organ toxicity G ood m uscle relaxation M ore potent than Enflurane Isoflurane
description
drugs for all sorts =)
Transcript of General Anesthesia
GENERAL ANESTHETICSGeneral Anesthetics
Anesthesia – denotes a lose of sensibility
Surgical Anesthesia – is a controlled degree of CNS depression with the following component
• Analgesia – lack of pain• Amnesia – lack of memory• Inhibition from reflexes such as bradycardia and
laryngospasm• Skeletal muscle relaxation• (altered state consciousness) state of unconsciousness.
Two Kinds of General AnestheticsA. Inhalational B. Intravenous
Two Kinds General Anesthetics
A. InhalationalB. Intravenous
Inhalational Gen Anesthetics
1. N2O (Nitrous oxide) – laughing gas2. Halothane3. Enflurane4. Isoflurane5. Methyoxyflurane6. Diethyl ether
Never Inhalational Gen Anesthetics
1. Desflurane2. Seroflurane
Newer Inhalational General Anesthetics1. Desflurane 2. Seroflurane
Mechanism of Action of Inhalational General AnestheticsThese agents decrease the firing rate of nerve cells by
decreasing the rise of the action potential. They inhibit the rapid increase in membrane premeability to sodium ion.
No receptors have been found to interact with the anesthetic and no neurotransmitters are involve in their action.
Kinetics of Anesthesia
Three stages of Anesthesia
1. Induction 2. Maintenance 3. Recovery
Mechanism of Action of Inhalational General AnestheticsThese agents decrease the firing rate of nerve cells by
decreasing the rise of the action potential. They inhibit the rapid increase in membrane premeability to sodium ion.
No receptors have been found to interact with the anesthetic and no neurotransmitters are involve in their action.
Kinetics of Anesthesia
Three stages of Anesthesia
1. Induction 2. Maintenance 3. Recovery
KINETICS OF ANESTHESIA1. Induction 2. Maintenance 3. Recovery
A Induction and Recovery from AnesthesiaInduction – is the period of time from onset of administration of the anesthetic to the development of effective surgical anesthesia in the patient. It depends on how fast the anesthetic reaches the brain.
Recovery – is the time form discontinuation of adm. of anesthetic until consciousness is regained .It depends on how fast the anesthetic is removed from the brain.drugs administered by inhalation; the rate of onset & recovery are
influenced by the following factors:
1. Solubility of anesthetic – this is expressed as the blood / gas concentration of gas in the blood, relative to the gas equilibrium phase. The greater the blood / gas partition coefficient the more soluble is the anesthetic agent in the blood.
a. If a drug has a low solubility (low-blood / gas partition coefficient) little of the drug is dissolve in the blood. Therefore the equilibrium between inhaled anesthetic and arterial blood is rapidly achieve, and only a few additional molecules of the anesthetic is required to raise the arterial tension. This results to rapid induction and short recovery.
Example – Nitrous Oxide (NaO) = 0.47 B/G coefficient
b. If the anesthetic has high solubility – it is more dissolve completely in the blood – so greater amounts of the anesthetic and longer periods of time are required to raise arterial tension. This results in increase times of induction and recovery also slower to changes in the cone of the inhaled drug. Ex. Halothane – 2.3 B/G coefficient
2. Rate of ventilation – an increase rate of delivery of anesthetic gas to the lungs results in most anesthetic being delivered to the alveoli. This increases the rate at which the arterial blood approaches equilibrium. The effect of ventilation is most pronounced for anesthetics with high solubility in blood.
3. Increase alveolar blood flow – high blood flow causes more of the anesthetic agent to be removed from the alveoli hastening anesthesia.
B. Maintenance of Anesthesia – maintenance is the time during which the patient is surgically anesthetized, anesthesia is usually maintained by the administration of gases or volatile anesthetics since these agents offer good minute to minute control over the depth of anesthesia.
Anesthetic Potency of Inhaled General Anesthetic:-is defined quantitatively as the minimum alveolar concentration. (MAC) which is the concentration of anesthetic gas needed to eliminate movement among 50% of patients challenge to a noxious stimulus. The more potent an anesthetic, the lower its value for MAC.
Properties of Modern inhalational Anesthetics
Blood/ gas solubility coeffi cient
0.43 – 0.47
2.3 – 2.4
1.9
1.4
12
MAC % atm
110 or 105
0.75 – 0.77
1.68
1.15
0.16
A. GAS Nitrous Oxide
B. Halogenated gases (volatile)
1. Halothane
2. Enflurane
3. I soflurane
4. Methoxyflurane
Comparison of the different Pharmacologic effects of Inhaled General Anesthetics
Respiration
Rapid/ shallowresp ventilatorydepression
Dose-dependentresp depressionCausesbronchodilatation
BP
B.PDosedependent
B.P
Sensitizationof Myocardium toActions ofEpinephrine
I ncreasessensitization ofmyocardium espto adrenergicagonist, cardiacdis, hypoxia andelectrolyteimbalance –mayI nduce ventriculararrhythmias
Lower incidenceof arrhythmiasand lesssensitization tothe myocardiumto catecholamines
CardiacEff ects
slows heartrate due toreduction ofcardiacSympatheticactivitycardiacoutput is
No Bradycardia, No in C.O
GeneralAnesthetic
1. Halothane
2. EnfluraneComparison of the different Pharmacologic effects of Inhaled
General Anesthetics
Respiration
- Signifi cant resp
Depression- due to thehypercapnia
Minimal eff ect
BP
B.P
C.O
BP and total Peripheralresistance when inCombinationof morePotentanesthetic
Sensitizationof Myocardium toActions ofEpinephrine
does not causesensitization ofmyocardium rarelycauses Arrhythmias
Little eff ect butcombination with a more potentanesthetic leads to sympatheticstimulation
CardiacEff ects
Causes direct coronaryvascularredistribution.Capable ofworseningischemia
Minimal C.O
GeneralAnesthetic
3. I sofl urane
4. Nitrous oxide
2% is me tabolized to fluoride ion which is excreted by thekidney-contraindicated in pnts withRenal Failure. EEC pattern –char. of seizure activity – maylead to Frank Seizure
Good musclerelaxation relaxesthe uterus
Less potent thanhalothane but itproduces morerapid inductionand recovery
Enfl urane
Extensively metabolize andBiotransformationintermediates may result tohepatotoxic metabolites – “Halothane Hepatitis”-malignant hyperthermia
Good musclerelaxation butlacks signifi cantAnalgesia
PotentHalothane
Organ toxicity and other adverse eff ect
Muscle relaxation – Analgesia
Potency/ induction recovery onset
Other Diff erences
Comparison of the different Pharmacologic effects of Inhaled General Anesthetics
Organ toxicity and otheradverse eff ect
Muscle relaxation– Analgesia
Potency/ inductionrecovery onset
May diff use into body cavities– the pressure or expandthe volume of gas in airpockets may lead to:a. Distention of the bowelb. Expansion or rupture of a
pulmonary cyst c. Rupture of the tympanic
membrane in an occluded middle ear
d. Pneumoce phalus-when it is dissolve in the blood
may enlarge the volume of air emboli
Poor surgicalanesthetic if usealone but goodAnalgesic
Not very potentwhen use alonebut produce thef astest inductionand recovery
Nitrous Oxide
Low biotransf ormation low organ toxicity
Good musclerelaxation
More potent than Enfl urane
I soflurane
Other Diff erences
Comparison of the different Pharmacologic effects of Inhaled General Anesthetics
0.0230.2220% Metabolized
LowLowLowModerateHighSensitization of myocardium
LowHighLow ModerateHighMyocardial depression
ModerateModerateModerateModerateLowMuscle relaxation
ModerateLowModerateLowLowIrritation of respiratory tract
0.40.71.41.82.3Induction speed ()
DesfluraneSevofluraneIsofluraneEnfluraneHalothane
Properties of Halogenated Inhalation Anesthetics
Diffusion hypoxia – can occur at the termination of nitrous oxide anesthesia if a patient abruptly breaths room air. (There is a rapid outward diffusion of nitrous oxide from tissues into the bloodstream and then into the alveoli where it decreases the alveolar tension – lowers arterial oxygen levels).
Treatment or Remedy – administration of 100% O2 for a short time at the termination of Nitrous Oxide Anesthesia.
N2O is also associated with high incidence of post-operative nausea & vomiting.
N2O – can cause leucopenia & Megaloblastic anemia due to in activation of Vit. B12
Methoxyflurane – fruity odor – most potent (MAC 0.16) but high blood – gas coeff about 12 results to prolonged induction and recovery. High renal toxicity –(High output Renal Failure) due to liberation of significant amount of Fluoride ion as Biotransformation product. Diethyl ether – highly flammable & explosive; sympathetic activity, bronchodilatation but may cause laryngospasm. It is a myocardial depressant –but C.O and B.P is due to the sympathetic activity.
Intravenous General Anesthetics : are often use for the rapid induction of anesthesia
A.Barbiturates – Ultra-short Acting:
1. Thiopental2. Thiamylal3. Methohexital
Acts less than one (1) minute, B.P due to myocardial depression.Depresses the resp center in a dose dependent manner may cause laryngospasm – not an analgesic.
B. Ketamine (Ketalar) – Dissociative anesthesia – a short – acting non barbiturate – induces a dissociative state in which the patient appears to be awake consist of Amnesia. Analgesia and often catatonia (rigidity). There is disorientation, hallucinations and changes in perception.
Combination Anesthetics – lighter stage of anesthesia is produce using 2 or more drugs.
A.Balanced Anesthesia : Full loss of consciousness and pain – induced reflexes with muscle relaxation using:
a. Ultra – short acting barbiturateb. Opioid analgesic (Meperidine, Morphine, Fentanyl or
Sufentamil)c. Muscle relaxationd. Nitrous Oxide + Oxygen
B. Neuroleptanesthesia – is induced by the combined actions of a narcotic analgesic (Fentanyl) and a neuroleptic agent (Droperidol), together with N2O & Oxygen. Consciousness is not lost, there is tranquility and reduce motor activity. Useful in pnt wherein cooperation is needed (diagnostic procedures) but may cause resp. depression.
Pre-Anesthetic Medications :
- Administered prior to anesthesia to reduce pain, relieve anxiety decrease excess salivation and to combat nausea.
A. Anxiolytic drugs – provides sedation, relieve anxiety-Benzodiazepam - diazepam, Lorazepam and Midazolam
B. Narcotic Analgesic - reduces pain – Morphine FentanylC.Neuroleptics - promethazine, trimeprazine or
chlorpromazine; use to sedate and for its anti-emetic properties.
D.Anticholinergic - Atropine and Scopolamine decreases bronchial and salivary secretions, and promote bronchodilatation.
Summary of Therapeutic Advantages and Disadvantages of Anesthetic Agents
Disadvantages
-Frank seizure-potential renal toxicity
-significant resp depression.
-no analgesia-little muscle relaxation-laryngospasm
-disorientation hallucinationchanges in perception
Advantages
Good muscle relaxation-prod. Bronchodilation rapidinduction/ recovery
-good muscle relaxation-rapid recovery-stability of cardiac output-does not raise intracranialpressure
-rapid onset
-potent analgesia
I nhalationAnesthetics
3. Enflurane
4. I soflurane
5.Thiopental
6. Ketamine
