anesthesia finalsurgical anestheisa
TRANSCRIPT
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ANESTHESIA
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ANESTHESIA SUPPRESSION OF
PAIN OF A SURGICAL PROCEDURE
ANALGESIA LOSS OF PAIN
SENSATION FROM OTHER CAUSES
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GENERAL ANESTHESIA
- W/ LOSS OF CONSCIOUSNESS
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LOCAL ANESTHESIA
- PATIENT IS AWAKE
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GENERAL ANESTHESIA
1. INHALATION ANESTH
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2. PARENTERAL ANESTHESIA
- IM- IV
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STAGES OF GEN ANESTH
1. ANALGESIA
2. DELIRIUM / EXCITEMENT
3. SURGICAL
4. MEDULLARY PARALYSIS
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PHARMACO KINETICS OF GEN
ANESTH1. FLOW ANESTHESIA MACHINE,
LUNGS, BLOOD, BRAIN, METABOLISM
ELIMINATION
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PHARMACO KINETICS
2. FACTOR
- TENSION DIFFERENCE OR
PARTIAL PRESSURE BETWEEN
ALVEOLI AND BLOOD
- FROM HIGHER TO LOWER CONC
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PHARMACO KINETICS
3. UPTAKE AND DISTRIBUTION
4. SOLUBILITY
5. CONC IN INSPIRED AIR
6. PULM VENTILATION
7. PULM BLOOD FLOW8. ARTERIOVENOUS CONC
9. ELIMINATION
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PHARMACO DYNAMICS
MECHANISM OF ACTION OF
GEN ANESTH
1. DEPRESSES THE ACTIVITY OF THE
NEURONS
2. INTERACTS W/ LIPID MATRIX OFNERVE MEMBRANE W/C LEADS TO
CHANGES IN ION FLUX
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- RESULTS TO MEMBRANE HYPER
POLARIZATION ( AN INHIBITORYACTION ), VIA ACTIVATION OF LIGAND
GATED K+ CHANNEL LINKED TO
NEUROTRANSMITTERS ( ACH,
DOPAMINE, NOREPINEPHRINE,
SEROTONIN
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- TARGET - TO ACTIVATE
GABA RECEPTOR CHLORIDECHANNEL (THE MEDIATOR OF
INHIBITORY SYNAPTIC TRANSMISSION)
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- RESULT
DECREASE ACTIVITY OF NEURONSDECREASE SENSORY TRANSMISSION
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Ideal Characteristics of InhalationalAnesthetics:
Rapid & pleasant induction & recovery
Rapid changes in depth of anesthesia
Adequate relaxation of smooth muscle Absence of toxic effect
Wide margin of safety
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ORGAN EFFECTS
CVS
ARTL PRESSURE
1. HALOTHANE
2. DESFLURANE
3. ENFLURANE
4. SEVOFLURANE5. ISOFLURANE
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BRADYCARDIA
1. HALOTHANE
TACHYCARDIA
1. ISOFLURANE
2. DESFLURANE
NO EFFECT ON RATE
1. METHOXYFLURANE
2. SEVOFLURANE
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MYOCARDIAL DEPRESSION
1. ALL INHALED ANESTH2. GREATEST DEPRESSION
a. ENFLURANE
b. HALOTHANE
3. LEAST DEPRESSION
a. NITROUS OXIDE ARRYTHMIA
1. HALOTHANE
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RESPIRATORY
MOST DEPRESSANT
ISOFLURANE ENFLURANE
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RESPIRATORY
DEPRESS MUCOCILIARY FXN
POOLING OF MUCUS
ATELECTASIS, PNEUMONIA BRONCHODILATATION
HALOTHANE, ENFLURANE
IRRITATION & COUGHING DESFLURANE
DIFFICULT INDUCTION
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BRAIN
CEREBRAL BLOOD FLOW
UNDESIRABLE IN ICP
ENFLURANE POTENTIAL SEIZURE NITROUS OXIDE
W/ LEAST IN CEREBRAL BLOOD FLOW
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TOXICITY
HEPATOTOXIC
HALOTHANE
FATAL HEPATITIS NEPHROTOXIC
METHOXYFLURANE
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MALIGNANT HYPERTHERMIA
HALOTHANE
SYNDROME
HYPERTHERMIA, TACHYCARDIA, RIGIDITY,HYPERTENSION, HYPERKALEMIA, ACIDOSIS
DUE TO FREE CALCIUM IN MUSCLE
TREATMENT DANTROLENE PREVENTS RELEASE OF Ca
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CHRONIC TOXICITY
MUTAGENECITY - NO EVIDENCE
FLUROXENE & ETHER NO LONGER USED
CARCINOGENECITY NO EVIDENCE
REPRODUCTIVE
MISCARRIAGE
TERATOGENIC
HEMATOTOXIC
NITROUS OXIDE MEGALOBLASTIC ANEMIA
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CLINICAL USE
RARELY USED ALONE
COMBINED W/ IV ANESTHETICS
COMMONLLY USED NITROUS OXIDE
DESFLURANE
SEVOFLURANE
ISOFLURANE
HALOTHANE
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NOT USED ANYMORE
METHOXYFLURANE
NEPHROTOXIC
CHLOROFORM
HEPATOTOXIC
CYCLOPROPANE & ETHER
EXPLOSIVE
FLAMMABLE
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CLASSIFICATION
GAS NITROUS OXIDE, CYCLOPROPANE
VOLATILE LIQUID
HALOGENATED HALOTHANE, ISOFLURANE, SEVOLURANE,
METHOXYFLURANE, ENFLURANE,
DESFLURANE
NON HALOGENATED
ETHER, CHLOROFORM
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HALOTHANE
CHOICE IN ASTHMA DUE TO
BRONCHODILATATION EFFECT
TOXICITY
ARRYTHMIA
HEPATITIS
MALIGNANT HYPERTHERMIA
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ENFLURANE
CNS IRRITABILITY SEIZURE
NEPHROTOXIC DUE TO FLUORIDE BY PRODUCT
CARDIAC DEPRESSION
SALIVATION & TRACHEOBRONCHIAL
SECRETION
NON HEPATOTOXIC
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ISOFLURANE
NON HEPATOTOXIC
NON NEPHROTOXIC
NON CARDIOTOXIC
CHOICE IN CARDIAC SURGERY
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METHOXYFLURANE
MOST TOXIC DESFLURANE
BP & CARDIAC OUTPUT
NO HEPATO RENAL TOXICITY
AIRWAY IRRITANT
SEVOFLURANE
NON IRRITANT TO AIRWAY33
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ETHER
FIRST ANESTHETICNO LONGER USED
EXPLOSIVE & FLAMMABLE
CHLOROFORM
NO LONGER USED
EXPLOSIVE & FLAMMABLE
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NITOUS OXIDE
THE ONLY INORGANIC GAS W/ ANESTHETICPROPERTY
NON EXPLOSIVE
POTENT ANALGESIC, BUT WEAK
ANESTHETIC NO MUSCLE RELAXATION, NO CVS EFFECT
ANESTH OF CHOICE, COMBINED W/HALOTHANE
CYCLOPROPANE
NO LONGER USED, EXPLOSIVE, FLAMMABLE
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INTRAVENOUS ANESTHETIC
BARBITURATE
BENZODIAZEPINE
KETAMINE
PROFOPOL
ETOMIDATE OPIATE
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IV ANESTH
USUALLY USED AS ADJUNCT TO
INHALED ANESTH
SOMETIMES USED ALONEDO NOT REQUIRE ANESTH
MACHINE
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SHORT ACTING IV ANESTH
RAPID ONSET
FOR OUT PATIENT USE
BARBITURATE THIOPENTAL
KETAMINE
PROFOPOL OPIATE
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LONG ACTING IV ANESTH SLOW ONSET
CANT BE USED FOR INDUCTION
FOR MAINTENANCE IF USED W/ INHALATION
ANESTH AS PRE OP MEDS TO RELAX PX & REDUCE
ANXIETY
BENZODIAZEPINE DIAZEPAM, MIDAZOLAM,LORAZEPAM
W/ RETROGRADE AMNESIA PX DO NOT
REMEMBER THE UNPLEASANT SURGERY39
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ULTRA SHORT ACTING BARBITURATES
THIOPENTAL
ONSET IN 10 -20 SEC
LAST FOR 20 30 MIN
FOR SHORT PROCEDURES
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LOCAL ANESTHETICS
BLOCKS NERVE CONDUCTION LOCALLY,THUS BLOCKS PAIN SENSATION THRU Na
CHANNEL BLOCKADE
HISTORYCOCAINE 1 ST AGENT USED 1860
PROCAINE 1905
LIDOCAINE 1943
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LOCAL ANESTH 2
CHEMISTRY
ESTER
COCAINE, PROCAINE, TETRACAINE,
BENZOCAINE
AMIDE
LIDOCAINE, MEPIVACAINE, BUPIVACAINE,ETIDOCAINE, PRILOCAINE, ROPIVACAINE
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PHARMACOKINETICS
ABSORPTION
LOCAL ANESTH HAS TO STAY WHEREINJECTED TO SUSTAIN ITS EFFECT
ONCE ABSORBED, IT LOSSES ITS EFFECT AS
A LOCAL ANESTH, AND SYSTEMIC EFFECTOR TOXICITY MAY POTENTIALLY HAPPEN
MORE VASCULAR TISSUE ABSORBS THE
DRUG FASTER, THUS DURATION IS SHORTER VASOCONSTRICTOR EPINEPHRINE DELAYS
ABSORPTION & PROLONGS LOCAL EFFECT
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PHARMACO DYNAMICS
MECHANISM OF ACTION
BINDING W/ SODIUM CHANNEL
RECEPTOR OF NERVE MEMBRANEBLOCKADE OF THE EXCITABLE
MEMBRANE OF AXON, THUS
BLOCKING THE NERVE IMPULSE
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ACTION OF LOCAL ANESTH ON NERVE
BOTH SENSORY & MOTOR BLOCKADE MOTOR PARALYSIS
MAYBE UNDESIRABLE IN NORMAL
DELIVERY W/C REQUIRE ABDOMINALMUSCLE CONTRACTION
BUT DESIRABLE IN ABDOMINAL
OPERATIONS LIKE CS, W/C REQUIRE
ABDOMINAL MUSCLE RELAXATION
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ACTIONS ON NERVE 2
AUTONOMIC PARASYMPATHETIC
BLOCKADE
VASODILATATION, HYPOTENSION SEQUENCE OF BLOCKADE
AUTONOMIC, TEMP, PAIN, TOUCH,DEEP PRESSURE, MOTOR
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ACTIONS ON NERVE 5
IN EXTREMITY
PROXIMAL SENSORY FIBERS ARE
LOCATED IN THE OUTER LAYER,THUS ARE BLOCKED FIRST, BEFORE
THE DISTAL FIBERS
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CARDIAC MUSCLE EFFECTS
ANTI ARRYTHMIC IN LOW CONC,
THUS IS USED AS TREATMENT
BUT CAN CAUSE ARRYTHMIA INHIGH DOSES, W/C IS THE TOXICITY
TO WATCH OUT FOR DURING
SURGERY UNDER LOCAL ANESTH
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CLINICAL PHARMA
SHORT ACTING - PROCAINE,CHLORPROCAINE
INTERMEDIATE ACTING LIDOCAINE,
MEPIVACAINE, PRILOCAINE
LONG ACTING TETRACAINE,
BUPIVACAINE, ETIDOCAINE,ROPIVACAINE
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ONSET
FASTER IF MIXED W/ Na
BICARBONATE SINCE THE CO2
PENETRATION OF ANESTH INTOMEMBRANE
SLOW IN INFECTION DUE TO ACIDIC
INFLAMMATION
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ROUTES
TOPICAL
LOCAL INFILTRATION
NERVE BLOCK
SPINAL INTRA THECAL
EPIDURAL CAUDAL
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TOPICAL
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LOCAL INFILTRATION
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NERVE BLOCK
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SPINAL
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EPIDURAL
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CAUDAL
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TOXICITY
TOXICITY OCCURS ONLY WHEN THE
ANESTH IS ABSORBED IN
CIRCULATION
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CNS TOXICITY
LOW DOSESLEEPINESS
LIGHTHEADEDNESS
VISUAL / AUDITORY DISTURBANCE
RESTLESSNESS
CIRCUMORAL / TONGUE
NUMBNESS
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CNS TOXICITY 2
HIGH DOSE
NYSTAGMUS, MUSCLE TWITCHING
CONVULSION, CNS DEPRESSION
DEATH
PREVENTION / TX DIAZEPAM,BARBITURATES, OXYGEN
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NERVE TOXICITY
PROLONGED MOTOR / SENSORY W/
CHLORPROCAINE OR LIDOCAINE IF
USED AS SPINAL ANESTH
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CVS TOXICITY
BLOCKS Na CHANNEL IN HEART -PACEMAKER, EXCITABILITY,
CONDUCTION
BLOCKS Ca CHANNEL DEPRESS
CONTRACTION - HYPOTENSION
(BUPIVACAINE)
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CVS TOXICITY 2
EXCEPT COCAINE W/C CAUSES
VASOCONSTRICTION &
HYPERTENSION DUE TO BLOCKADEOF NOREPINEPHRINE REUPTAKE
CAUSE ISCHEMIA & ULCERATION IF
USED IN NASOPHARYNGEAL
MUCOSA
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BLOOD TOXICITY
METHHEMOGLOBINEMIA DUE TOPRILOCAINE
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ALLERGY
COMMON W/ ESTERS W/C ARE
METABOLIZED TO P-AMINOBENZOIC
ACID W/C CAUSE THE ALLERGY