inhaled anesthetics dr. abdul karim b othman clinical specialist anesthesiologist hsnz. 2013
TRANSCRIPT
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INHALED INHALED ANESTHETICSANESTHETICS
DR. ABDUL KARIM B DR. ABDUL KARIM B OTHMANOTHMAN
CLINICAL SPECIALISTCLINICAL SPECIALISTANESTHESIOLOGISTANESTHESIOLOGIST
HSNZ. 2013HSNZ. 2013
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HISTORY OF ANESTHETIC AGENTSHISTORY OF ANESTHETIC AGENTS
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Physical and chemical properties of inhaled anesthetic agents
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Pharmacokinetics of Inhaled Anesthetics
❖ absorption (uptake)
❖ distribution
❖ metabolism
❖ elimination
❖ How does aging influenced the pharmacokinetics of volatile anesthetics?
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Principle objective of inhalation Principle objective of inhalation anesthesia is anesthesia is to achieve a constant to achieve a constant and optimal brain partial pressure and optimal brain partial pressure
of the inhaled anesthetic.of the inhaled anesthetic.
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... THE DEPTH OF ANAESTHSIA VARIES ... THE DEPTH OF ANAESTHSIA VARIES DIRECTLY WITH THE TENSION OF THE AGENT DIRECTLY WITH THE TENSION OF THE AGENT
IN THE BRAIN, AND THEREFORE,IN THE BRAIN, AND THEREFORE,
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... THE RATES OF INDUCTION AND EMERGENCE ... THE RATES OF INDUCTION AND EMERGENCE DEPEND UPON THE RATE OF CHANGE OF GAS DEPEND UPON THE RATE OF CHANGE OF GAS
TENSION IN THE BLOOD AND TISSUES .....TENSION IN THE BLOOD AND TISSUES .....THUS, FACTORS WHICH DETERMINE THIS MAY THUS, FACTORS WHICH DETERMINE THIS MAY
BE CONSIDERED AS ACTING IN SEPARATE BE CONSIDERED AS ACTING IN SEPARATE STAGESSTAGES
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DETERMINED BY ..
❖ TRANSFER FROM INSPIRED AIR TO ALVEOLI
❖ TRANSFER FROM ALVEOLI TO ARTERIAL BLOOD
❖ TRANSFER FROM ARTERIAL BLOOD TO TISSUES
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TRANSFER FROM INSPIRED AIR TO ALVEOLI
❖ THE INSPIRED GAS CONCENTRATION
❖ ALVEOLAR VENTILATION
❖ CHARACTERISTIC OF THE ANAESTHETIC CIRCUIT
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TRANSFER FROM ALVEOLI TO ARTERIAL BLOOD
BLOOD : GAS PARTITION COEFFICIENT
CARDIAC OUTPUT
ALVEOLI TO VENOUS PRESSURE DIFFERENCE
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TRANSFER FROM ARTERIAL BLOOD TO TISSUES
TISSUE : BLOOD PARTITION COEFFICIENT
TISSUE BLOOD FLOW
ARTERIAL TO TISSUE PRESSURE DIFFERENCE
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PA is used as an index of
❖ depth of anesthesia
❖ recovery from anesthesia, and
❖ anesthetic equal potency (MAC
❖ equilibration between the two phases means same partial pressure NOT same concentrations
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Determinants of Alveolar Partial PressureDeterminants of Alveolar Partial Pressure(P(PA A <> Pa <>P<> Pa <>Pbr br ))
Determined by input (delivery) - uptake (loss) from alveoli into arterial Determined by input (delivery) - uptake (loss) from alveoli into arterial bloodblood
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Input depends on
❖ inhaled partial pressure (PI)
❖ alveolar ventilation
❖ characteristics of the anesthetic breathing (delivery) system
❖ Patient’s FRC influenced the PA that is achieved
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Uptake depends on
❖ solubility of the anesthetic in the body tissues
❖ cardiac output
❖ alveolar to venous partial pressure differences (A-VD)
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Inhaled Partial Pressure
❖ a high PI is required during initial administration
❖ to offsets the impact of uptake
❖ accelerating induction (PA <> Pbr)
❖ as uptake decreases, PI should be decreased
❖ to match the decreased in uptake and therefore maintain a constant and optimal Pbr
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Concentration effect( the impact of PI on the rate of rise of the PA )
❖ states that; the higher the PI, the more rapidly the PA
approaches the PI
❖ Results from
❖ a concentrating effect
❖ an augmentation of tracheal inflow
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Second-Gas effect
• ability of high-volume uptake of one gas (first gas) to accelerate the rate of increase of the PA of a concurrently administered “companion “ gas (second-gas)
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Second-Gas effect
• increased uptake of second gas reflects
• increased tracheal inflow of first and second gases
• concentrating effect of second gas
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SOLUBILITY IN BLOOD AND TISSUES IS DENOTED BY THE PARTITION COEFFICIENT
PARTITION COEFFICIENT IS A DISTRIBUTION RATIO DESCRIBING HOW THE INHALED ANESTHETIC DISTRIBUTES ITSELF BETWEEN TWO PHASES AT EQUILIBRIUM (PARTIAL PRESSURES EQUAL IN BOTH PHASES)
TEMPERATURE DEPENDENT
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SOLUBILITY
Q :
BLOOD : GAS PARTITION COEFFICIENT OF 0.5 ?
BRAIN : BLOOD PARTITION COEFFICIENT OF 2 ?
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REFLECTING THE RELATIVE CAPACITY OF EACH PHASE TO
ACCEPT ANESTHETIC
REFLECTING THE RELATIVE CAPACITY OF EACH PHASE TO
ACCEPT ANESTHETIC
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BLOOD : GAS PARTITION COEFFICIENT
RATE OF INCREASE OF THE PA TOWARD THE PI (MAINTAINED CONSTANT BY MECHANICAL VENTILATION OF THE LUNGS) IS INVERSELY RELATED TO THE SOLUBILITY OF THE ANESTHETIC IN BLOOD
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BLOOD : GASES PARTITION COEFFICiENT : ISSUES
HIGH BLOOD : GASS PARTITION
OVERPRESSURE : BY INCREASING THE PI ABOVE THAT REQUIRED FOR MAINTENANCE OF ANESTHESIA
LOW BLOOD : GAS PARTITION
IS ALTERED BY INDIVIDUAL VARIATIONS IN
WATER LIPID AND PROTEIN CONTENT
HEMATOCRIT OF WHOLE BLOOD
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PARTITION COEFFICIENT : ISSUES
TISSUE : BLOOD PARTITION COEFFICIENT
OIL : GAS PARTITION COEFFICIENT
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NITROUS OXIDE TRANSFER TO CLOSED GAS SPACES
BLOOD : GAS PARTITION COEFFICIENT OF
NITROUS OXIDE : 0.46
NITROGEN : 0.014
NITROUS OXIDE CAN LEAVE THE BLOOD TO ENTER AN AIR-FILLED CAVITY 34 TIMES MORE RAPIDLY THAN NITROGEN CAN LEAVE THE CAVITY TO ENTER BLOOD
INCREASES VOLUME OR PRESSURE OF AN AIR-FILLED CAVITY
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NITROUS OXIDE TRANSFER TO CLOSED GAS SPACES
AIR-FILLED SURROUNDED BY A COMPLIANT WALL :
GAS SPACE TO EXPAND
AIR-FILLED CAVITY SURROUNDED BY A NONCOMPLIANT WALL :
INCREASES IN INTRACAVITARY PRESSURE
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CARDIAC OUTPUT AND INHALED ANESTHETIC
CARDIAC OUTPUT (PULMONARY BLOOD FLOW) INFLUENCES UPTAKE AND THEREFORE PA BY CARRYING AWAY EITHER MORE OR LESS ANESTHETIC FROM THE ALVEOLI
ISSUES
HIGH CARDIAC OUTPUT
LOW CARDIAC OUTPUT
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CONCEPTUALLY, A CHANGE IN C.O IS ANALOGOUS TO THE EFFECT OF A CHANGE IN
SOLUBILITY
CONCEPTUALLY, A CHANGE IN C.O IS ANALOGOUS TO THE EFFECT OF A CHANGE IN
SOLUBILITY
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CARDIAC OUTPUT AND INHALED ANESTHETIC
CHANGES IN C.O MOST INFLUENCE THE RATE OF INCREASE OF PA OF A SOLUBLE ANESTHETIC
LOW CARDIAC OUTPUT VERSUS HIGH CARDIAC OUTPUT
SOLUBLE VERSUS POORLY SOLUBLE AGENTS
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IMPACT OF SHUNT AND INHALED ANESTHESTIC
PA IS IDENTICAL TO Pa ( IN THE ABSENCE OF INTRACARDIAC OR INTRAPULMONARY R - TO - L SHUNT )
R - TO - L SHUNT
DILUTING EFFECT OF SHUNTED BLOOD
DECREASE THE Pa
SLOWING THE INDUCTION
PA UNDERESTIMATE Pa
L - TO - R SHUNT
OFFSET THE DILUTIONAL EFFECT OF R - TO - L SHUNT
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DIFFUSION HYPOXIA OCCURS WHEN INHALATION OF NITROUS OXIDE IS DISCONTINUED ABRUPTLY
DIFFUSION HYPOXIA OCCURS WHEN INHALATION OF NITROUS OXIDE IS DISCONTINUED ABRUPTLY
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DIFFUSION HYPOXIA
REVERSAL OF PARTIAL PRESSURE GRADIENTS (NITROUS OXIDE LEAVES THE BLOOD TO ENTER ALVEOLI)
DILUTE THE PAO2 AND DECREASE PaO2
DILUTE THE PACO2 (DECREASE STIMULUS TO BREATHE)
GREATEST DURING THE 1ST TO 5 MINUTES AFTER ITS DISCONTINUATION
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PHARMACODYNAMICS OF INHALED PHARMACODYNAMICS OF INHALED ANESTHETICSANESTHETICS
MINIMUM ALVEOLAR CONCENTRATIONMINIMUM ALVEOLAR CONCENTRATION(MAC)(MAC)
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MAC
❖ CONCENTRATION AT 1 ATM THAT PREVENTS SKELETAL MUSCLE MOVEMENT IN RESPONSE TO SUPRA MAXIMAL PAINFUL STIMULUS (SURGICAL SKIN INCISION) IN 50 % OF PATIENTS (MARKEL AND EGER, 1963)
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MAC
❖ MAC IS AN ANESTHETIC 50 % EFFECTIVE DOSE (ED50)
❖ IMMOBILITY AS MEASURED BY MAC IS MEDIATED
❖ PRINCIPALLY BY EFFECTS ON SPINAL CORD
❖ MINOR COMPONENT FROM CEREBRAL EFFECTS
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MAC
❖ ESTABLISHES A COMMON MEASURE OF POTENCY
❖ PROVIDE UNIFORMITY IN DOSAGES
❖ ESTABLISH RELATIVE AMOUNTS OF INHALED ANESTHETICS TO REACH SPECIFIC END-POINTS (MACawake , MACBAR)
❖ VARYING ONLY 10 % TO 15 % AMONG INDIVIDUALS
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THE RATIONALE FOR THIS MEASURE OF ANAESTHETIC POTENCY IS ,
❖ ALVEOLAR CONCENTRATION CAN BE EASILY MEASURED
❖ NEAR EQUILIBRIUM , ALVEOLAR AND BRAIN TENSIONS ARE VIRTUALLY EQUAL
❖ THE HIGH CEREBRAL BLOOD FLOW PRODUCES RAPID EQUILIBRATION
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FACTORS WHICH SUPPORT THE USE OF THIS MEASURE ARE ,
❖ MAC IS INVARIANT WITH A VARIETY OF NOXIOUS STIMULI
❖ INDIVIDUAL VARIABILITY IS SMALL
❖ SEX, HEIGHT, WEIGHT & ANAESTHETIC DURATION DO NOT ALTER MAC
❖ DOSES OF ANAESTHETICS IN MAC’S ARE ADDITIVE
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MAC
• EXAMPLES OF MAC
• MAC awake : 0.3 MAC
• MAC BAR : 1.5 X MAC
• MAC intubation : 2 X MAC
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FACTORS WHICH AFFECT MAC
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INCREASE MAC
• HYPERTHERMIA
• HYPERNATRAEMIA
• DRUG INDUCED ELEVATION OF CNS CATECHOLAMINES STORES
• CHRONIC ALCOHOL ABUSE ? CHRONIC OPIOID ABUSE
• INCREASE IN AMBIENT PRESSURE
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DECREASE MAC
• HYPOTHERMIA HALOTHANE MAC27 IS ABOUT 50% MAC37C
• HYPONATRAEMIA
• INCREASE AGE MACHAL < 3 MTHS IS ABOUT 1.1% MACHAL > 60 YRS IS ABOUT 0.64%
• HYPOXAEMIA PAO2 < 40 mmHg
• HYPOTENSION
• ANAEMIA
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DECREASE MAC
• PREGNANCY ? PROGESTERONE
• CNS DEPRESSANT DRUGS BENZODIAZEPINES, OPIOIDS
• OTHER DRUGS LITHIUM, LIGNOCAINE, MAGNESIUM
• ACUTE ALCOHOL ABUSE
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NO CHANGE IN MAC
• SEX
• WEIGHT , BSA
• TYPE OF SUPRAMAXIMAL STIMULUS
• DURATION OF ANAESTHESIA
• HYPO / HYPERKALAEMIA
• HYPO / HYPERTHYROIDISM
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NO CHANGE IN MAC
• PaCO2 - 15 - 95 mmHg
• PO2 - 40 mmHg
• MAP > 40 mmHg
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THE IDEAL ANESTHETIC AGENT
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THE IDEAL ANESTHETIC AGENTS
PHYSICAL PROPERTIES
BIOLOGICAL PROPERTIES
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PHYSICAL PROPERTIES
NONFLAMMABLE, NON-EXPLOSIVE AT ROOM TEMPERATURES
STABLE IN LIGHT
LIQUID AND VAPORISABLE AT ROOM TEMPERATURE (I.E LOW LATENT HEAT OF VAPORISATION)
STABLE AT ROOM TEMPERATURE, WITH A LONG SHELF LIFE
STABLE WITH SODA LIME, AS WELL AS PLASTICS AND METALS
ENVIRONMENTALLY FRIENDLY, NO OZONE DEPLETION
CHEAP AND EASY TO MANUFACTURE
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BIOLOGICAL PROPERTIES
PLEASANT TO INHALE, NON-IRRITANT,INDUCE BRONCHODILATATION
LOW BLOOD : GAS SOLUBILITY, I.E FAST ONSET
HIGH OIL : WATER SOLUBILITY I.E HIGH POTENCY
MINIMAL EFFECTS ON OTHER SYSTEMS, I.E CVS, RESP, HEPATIC, RENAL OR ENDOCRINE
NO BIOTRANSFORMATION, SHOULD BE EXCRETED IDEALLY VIA THE LUNGS, UNCHANGED
NON-TOXIC TO OPERATING THEATRE PERSONNEL