Transcript Anesthesia of the Surgical Patient

Anesthesia of the Surgical Patient
CA Blum, M.D.
•Pharmacology
•Local anesthetics
•Epidural / Spinal
•IV Agents
•Analgesics
•Paralytics
•Inhalational Agents
•Classifications
•Malignant
Hyperthermia
Anesthesia
 Embodies control of three great concerns of humankind:
 Consciousness
 Pain
 Movement.
Pharmacokinetics
 What the body does to the drug –describes
relationship bw DOSE and CONCENTRATION
 Involves: Absorption, Distribution, Elimination
 Route of Administration affects Absorption and
therefore pharmacokinetics
 different rates of drug entry into the circulation
based on admin route (IV, sublingual, IM, SubQ)
 Distribution – delivery from the circulation to the
tissues.
 Molecular size, capillary permeability, polarity, and
lipid solubility, protein and tissue binding.
 The fluid volume in which a drug distributes is termed
the volume of distribution (Vd).
 Elimination –Varies widely
 Some drugs:
 Excreted unchanged
 Decomposed by plasma enzymes
 Degrated by liver
Take home
 Response to drugs varies widely
 Age
 Weight
 Sex
 Pregnancy,
 Disease state,
 Drug interactions
 Genetic factors
 “The most important monitor in the operating room is the
anesthesiologist, who continously assesses the patient’s
response and adjusts the doses of anesthetic agents to match
the surgical stimulus”
ABSITE Pearls
 Sublingual and rectal drugs do not pass through liver first
 So no “first pass effect”
 First-pass effect concentration of a drug is greatly
reduced before it reaches the systemic circulation.
 Zero order kinetics – constant amount of drug elimated
regardless of dose
 1st order kinetics – constant amount of drug elimanted
regardless of dose
Pharmacodynamics
 What the drug does to the body
 How plasma concentration of drug translates
into effect on body
 Depends on biologic variability, receptor physiology,
and clinical evaluations of the actual drug.
Vocabulary
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Agonist: causes a response. (full/partial)
Antagonist: blocks an agonist
Additive effect: effect is sum of parts
Synergistic effect: effect greater than sum of parts
Potency: dose required for effect.
Efficacy: power to produce a desired effect.
Dose-response curves compare dose and pharmacologic effect
Effective dose (ED50) desired effect in 50% of the gen pop.
Lethal dose (LD50) death in 50% of animals to which it is given.
Ratio of the lethal dose and effective dose, LD50/ED50, is the
therapeutic index.
Anesthesia Written Boards
Local Anesthetics
 Local anesthetics block nerve conduction by
stabilizing sodium channels in their closed state,
preventing action potentials from propagating along
the nerve.
Amides and Esters.
 Amides: Lidocaine, bupivacaine, ropivacaine
 have in common an amide
 all have ‘I’ in first part of name
 Lidocaine has a more rapid onset and is shorter acting
than bupivacaine; however, both are widely used for
tissue infiltration, regional nerve blocks, and spinal
and epidural anesthesia.
 Esters: Cocaine, tetracaine, and benzocaine have an
ester linkage –
 Increased incidence of allergic reactions.
 Epinephrine is a vasoconstrictor, reduces local bleeding,
and keeps local anesthetic in the nerve proximity for a
longer period of time.
 Faster; Block Quality improved, longer duration
 Less local anesthetic absorbed in bloodstream –
reducing toxicity
 Avoid epi in nose – toes – fingers - hose
Local Anesthetic Toxicity
 CNS – tinnitus, slurred speech, seizures, and
unconsciousness
 CV - hypotension, increased P-R intervals, bradycardia,
and cardiac arrest
 NEURO FIRST!
 Toxic dose Lidocaine 5 mg/kg
 Infected tissue hard to anesthetize 2ndary to acidosis.
Calculations
 1 % = 10mg/ml
 1% lidocaine = 10mg/ml
 30ml = 300mg
 70kg person (toxic dose 5mg/kg)
 70 x 5 = 350 mg toxic dose
Anesthesia Sim Lab
 Table Up
 Table Down
 Head Up
 Head Down
Anatomy
Spinal Anesthesia
 Injected directly into the dural sac surrounding the
spinal cord (subarachnoid space, where CSF lives)
 Possible complications include hypotension, especially if the
patient is not adequately prehydrated
 High spinal block requires immediate airway management
 Spinal headache is related to the diameter and configuration
of the spinal needle, and can be reduced to approximately 1%
Epidural Anesthesia
 Local anesthetics are injected into the epidural space surrounding
the dural sac of the spinal cord
 Achieves analgesia from the sensory block, muscle relaxation from
blockade of the motor nerves, and hypotension from blockade of the
sympathetic nerves as they exit the spinal cord
 Provides only two of the three major components of anesthesia—
analgesia and muscle relaxation
 Anxiolysis, amnesia, or sedation must be attained by supplemental IV
administration of other drugs
 Complications are similar to those of spinal anesthesia
Epidural
 Bigger needle, accidental dural puncture often results in
severe headache
 Blood patch in epidural space
General Anesthesia
 A triad of three major and separate effects:
 unconsciousness (and amnesia)
 analgesia
 muscle relaxation
 A combination of IV and inhaled drugs
Intravenous agents
 Produces unconsciousness and amnesia - frequently used
for the induction of GA
 Barbiturates (sodium thopental),
 Benzodiazepines (versed),
 Propofol,
 Etomidate,
 Ketamine.
Barbiturates
 Fast acting
 Decreased cerebral blood flow and metabolic rate
 Hypotension
Propofol
 Very rapid on and off
 Amnesia and sedations NO ANALGESIA
 Profound hemodynamic effects – HYPOTENSION
 Respiratory Depression
 Decreased cerebral blood flow
Propofol
 GA 100 – 200 mcg/kg/min
 Icu 5-50 mcg/kg/min
 Comes 10mg/cc, 1mg = 1000mcg therefore 1ml
=10,000mcg
 5cc = 50,000mcg = 50mg
 Induction dose = 2mg/kg (70kg = 140mg)
Ketamine
 Dissociation (cataleptic state, amnesia and analgesia)
 NO RESPIRATORY DEPRESSION
 Hallucinations, increased secretions, increased cerebral blood
flow
 CONTRAINDICATED IN HEAD INJURY
 Good for Kids
Etomidate
 Fewer hemodynamic changes, fast acting
 Continuous infusion can lead to adrenal insufficiency
Benzodiazepines
 Hepatically metabolized
 Anticonvulsant
 Amnestic
 Anxiolytic
 Respiratory depression
 NOT analgesic
 Flumazenil – competitive inhibitor may cause seizures
and arrythmias, contraindicated in pts with elevated ICP
or status epilepticus
Analgesia
 Narcotic – morphine (histamine release, constipation),
demerol (seizures), codeine, fentanyl (80x stronger than
morphine)
 Act on mu receptors
 Profound anagesia, respiratory depression, no cardiac
effects, blunt sympathetic response
 Metabolized by liver, excreted by kidned
 NARCAN
 Non-narcotic
 Toradol
 Ketamine
Neuromuscular Blocking Agents
 Depolarizing – Succinylcholine – fast, short acting
 Rapid onset and offset
 Hyperkalemia ( not for burns, renal failure, SCI)
 Non-depolarizing – inhibit NMJ compete with ACH
 Pancuronium – long acting
 Rocuronium, vecuronium, – intermediate
 Reversed by neostigmine, edrophonium,
 Block ACETYLCHOLINESTERASE  Increase ACH
Paralytics
 Diaphragm – last muscle to go down, first to recover
 Neck and face muscles – first to go down, last to recover
Inhalational Agents
 Provides all three characteristics of GA: unconsciousness,
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analgesia, and muscle relaxation
A dose-dependent reduction in MAP (myocardial
depression)
Minimum alveolar concentration (MAC) measure of anesthetic potency = smallest conc of agent
at which 50% will not move w incision
Small MAC  MORE lipid soluble = MORE POTENT
Speed of induction INVERSELY PROPORTIONAL to
solubility
Nitrous FAST but HIGH MAC = LOW POTENCY
 Halothane – doesn’t smell bad, good for kids, HEPATITIS
 Enflurane - seizures
Mallampati Classification
ASA Class
 I – healthy
 II – mild disease without limitation (controlled HTN, DM,
obesity, older age)
 III – severe disease (angina, previous MI, moderate COPD)
 IV – severe constant threat to life (unstable angina, renal
failure, severe COPD)
 V- moribund (rutured AAA, saddle PE)
Malignant Hyperthermia
 MH is a life-threatening, acute disorder, developing
during or after general anesthesia
 Defect in calcium metabolism  muscle excitation
 1st sign = incrase in end tidal CO2, fever, tachcardia,
rigidity, acidosis, hyperkalemia, cardiac arrest, rise in
temperature is often a late sign of MH
 genetic predisposition
 Triggering agents include all volatile anesthetics and the
depolarizing muscle relaxant succinylcholine
 Treatment must be aggressive and begin as soon
as a case of MH is suspected
 Stop all volatile anesthetics and give 100% O2
 Hyperventilate the patient up to three times the
calculated minute volume
 Begin infusion of dantrolene sodium 2.5mg/kg IV
 Repeat as necessary to titrate for clinical signs
 Continue dantrolene for atleast 24 hours
 Give bicarbonate to treat acidosis if dantrolene
ineffective
 Treat hyperkalemia with insulin, glucose, and calcium
 Continue to monitor core temperature