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Anesthesiology

Glen T. Porter, MD

Faculty Advisor: Francis B. Quinn, MD, FACS

The University of Texas Medical Branch

Department of Otolaryngology

Galveston, Texas

June 2004

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History 1540 Valerius Cordus synthesizes ether

1842 Dr. Crawford Long (Georgia) first uses inhaled ether to anesthetize patient for surgery

1845 Dr. Horace Wells attempts to demonstrate use of Nitrous oxide in surgery

1846 William Morton (dentist) uses ether anesthesia at Massachusetts General Hospital (soon to become the ether dome). Dr. John Warren removes a neck mass.

1846 Nitrous oxide used for anesthesia

1847 Dr. James Simpson introduces Chloroform anesthesia

1853 Queen Victoria undergoes anesthesia performed by Dr. John Snow

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Crawford Long

Horace Wells W. Thomas Morton

History

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History

1878 Endotracheal tube invented

1885 Halstead introduces nerve block anesthesia with cocaine

1934 Sodium thiopentone (IV anesthesia)

1934 Curare

1940’s clinical use of muscle relaxants

1950s Introduction of flourinated inhalational anesthetic agents

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Anesthesia

Anesthesia=abolition of sensation

Analgesia=abolition of pain

General anesthesia renders the patient

unconscious and usually includes paralysis

Local anesthesia (analgesia) blocks

conduction of sensory nerves from the

operative site

“Triad of anesthesia”: asleep, pain-free, still

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Stages of Anesthesia

Stage I (analgesia stage) – Conscious and rational

– Perception of pain is diminished

Stage II (delirium stage) – Unconscious

– Body responds reflexively and irrationally

– Breath holding, pupils dilated

– Muscle tone intact

Stage III (surgical anesthesia) – Increasing degrees of muscular relaxation

– Unable to protect airway

Stage IV (medullary depression) – Depression of cardiovascular and respiratory

centers

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Inhalational Anesthesia

Effect is mediated by concentration of agent present in the nervous system

Each agent’s anesthesia effect mediated by solubility, metabolism, alveolar ventilation, cardiac output, potency

Minimum Alveolar Concentration (MAC) is a measure of relative potency

MAC=amount of an agent in which 50% of patients do not move with surgical stimulus.

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Nitrous Oxide

Discovered 1776 by David Priestly

Largely recreational use until mid 1800’s

Colorless, tasteless, odorless

Low potency (MAC=105%)

Usually used with additional agent to achieve surgical anesthesia

Weak anesthetic

Powerful analgesic

Poor solubility (rapid onset/offset time)

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Nitrous Oxide

Systemic effects

– Mild myocardial depression (usually innocuous)

– Severe cardiac depression with underlying

hemodynamic compromise

– No effect on respiration/neuromuscular junction

Side effects

– Blood:gas partition coefficient of nitrous oxide is 34

times greater than that of nitrogen.

Second gas effect

Pressure changes in air-filled spaces

– Prolonged exposure can result in megaloblastic or

aplastic anemia, B-12 deficiency (inhibits methionine

synthetase)

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Nitrous oxide

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Halothane

Synthesized by Suckling in 1956

First of the fluorinated anesthetics

Distinctive aroma, non-flammable, highly

potent (MAC=0.75%)

Poor analgesic properties

Very soluble in blood/fatty tissues with

potential for longer offset time

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Halothane

Systemic Effects – Reduces/eliminates sympathetic response (including

baroresponse)

– Depresses respiratory drive. Respiration is rapid, shallow, and unvaried predisposing to atelectasis

– Decreases airway reflexes

– Decreases myocardial contractility and heart rate resulting in decreased cardiac output and hypotension

– Myocardial sensitization to exogenous catecholemines

Side Effects – Hepatitis

Thought to be mediated by allergic response to byproducts

– Malignant hyperthermia

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Enflurane Introduced in 1972

Stable, nonflammable, pungent odor

MAC=1.68%

Systemic effects – Respiratory drive depressed (more than halothane), hypoxemia

response blunted

– Depresses cardiac contractility and heart rate more than Halothane

– Less sensitization of myocytes to exogenous catecholamines

– Metabolism 1/10th that of Halothane—less hepatotoxic

– Rare cases of fluoride toxicity (hyperthyroid, rifampin) Nephrogenic diabetes insipidus

Side effects – Similar to other fluorinated agents

– Epileptiform EEG at deep levels Avoid in patients with seizure d/o

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Isoflurane

Nonflammable

Properties similar to Halothane and

Enflurane

Pungent odor

Less soluble than Halothane/Enflurane,

more rapid induction/recovery

MAC=1.3%

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Sevoflurane

Fluorinated ether compound

Similar properties to other fluorinated agents

Mild respiratory/cardiac depression

Not bronchoirritant

Rapid onset/offset secondary to low lipid solubility

As enflurane, may cause renal and hepatic side effects

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Desflurane

Newer agent

Low blood and lipid solubility with rapid

onset/offset

High incidence of bronchoirritation with

cough, laryngeal spasm, breath holding

Minimal metabolism resulting in few side

effects

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Intravenous Anesthetic Agents

Barbiturates/other

– Thiopental

– Etomidate

– Ketamine

– Propofol

– Benzodiazepines

Narcotic agonists (opiods)/antagonists

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Thiopental

Barbiturate with alkaline formulation. May cause severe complications if extravasation or intraarterial injection occurs.

Unconsciousness within 10-15 seconds

Depresses neuronal activity—may decrease ICP

Poor analgesic

Varied effect on cardiovascular system

Decreased ventilatory drive, short period of apnea after bolus

Short duration secondary to rapid redistribution

Metabolized in liver

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Thiopental distribution

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Etomidate

Onset, elimination, ability to produce unconsciousness similar to Thiopental

Short duration of action secondary to rapid redistribution

Less cardiopulmonary depression

Can cause local pain and myoclonic movements with injection

Cortisol suppression and Addisonian crises reported in debilitation patients

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Ketamine

Similar in structure to PCP

Dissociative anesthesia, intense analgesia, amnesia

Slow nystagmus with eyes open

Systemic effects similar to sympathetic stimulation

Respiratory function not depressed, airway protection not effected

Rapid onset, lasts 10-15 minutes

Side effect is unpleasant dreams/hallucinations during emergence. Benzodiazepines shown to decrease this.

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Propofol

Substituted phenol

Rapid onset, short duration (metabolized)

Dilates peripheral vasculature leading to

decreased blood pressure—may be significant

in patients with blunted sympathetic response

Short period of apnea after administration

Venous irritation

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Benzodiazepines

Good for amnesia/sedation—via potentiation at GABA receptors

Diazepam onset 2-3 minutes (IV), Lorazepam (Ativan) onset 10-15 minutes, both have long half-life (Diazepam (Valium)<Lorazepam)

Pain with injection (except midazolam)

Midazolam (Versed) 2x more potent than diazepam

Can depress respiration when used with opiods

Flumazenil is antidote

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Narcotic agonists/antagonists

Analgesia, dpressed sensorium, respiratory depression

Effects are dose-related

Minimal cardiovascular effects, though vasodilatory effects can be serious in patients with hypovolemia

Side effects include bradycardia (doesn’t usually effect output), n/v, chest wall rigidity, seizure activity, decrease GI motility

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Narcotics

Several receptors – Mu: analgesia, respiratory depression, euphoria,

dependance

– Kappa: spinal analgesia, sedation, meiosis

– Omega: hallucinations, dysphoria, tachycardia

Meperidine, Morphine, Fentanyl, Sufentanil, Remifentanil

Nalorphine: agonist/antagonist—less analgesia, less respiratory depression

Naloxone: reverses analgesia/respiratory depression (30 minutes)

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Muscle Relaxants

Used clinically since 1940’s. 1960’s led to

the “balanced anesthesia” concept.

Important to provide motion-free surgical

field

Work at neuromuscular junction

Nondepolarizing vs. Depolarizing

– Competitive inhibition of endplate nicotinic

receptor vs. receptor binding with

depolarization

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Paralytic agents--Anatomy

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Neuromuscular junction

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Depolarization

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Nondepolarizing Agents

Bind to and competitively inhibit end-plate nicotinic receptors

Intermediate-acting (15-60 minutes) – Atracurium, vecuronium, mivacurium

– Relatively independent of renal function for clearance

– Less circulatory effect

Long-acting (>60 minutes) – Pancuronium, metocurine, d-tubocurarine, gallamine

– More hemodynamic effects

– Tubocurarine blocks autonomic ganglia, may cause mast cell degranulation

– Pancuronium inhibits vagal and muscarinic receptors and produces tachycardia

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Reversal of Muscle Relaxation

Effect is reversed when the ratio of ACh at the NMJ is increased

Neostigmine, edrophonium, acetylcholine (anticholinesterases)

Reversal agents can cause bradycardia by stimulation of heart muscarinic receptors

Preadministration of muscarinic blockers are effective in avoiding this side effect (atropine, glycopyrrolate)

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Depolarizing Muscle Relaxants

Bind to and depolarize end-plate ACh nicotinic receptors

The depolarization continues as long as receptor is occupied

Typically short duration of effect as drug is hydrolysed by plasma cholinesterases

Patients with abnormal cholinesterase are at risk for prolonged paralysis

Sustained depolarization produces transient fasiculations which can result in postoperative myalgias and extravasation of potassium in patients with damaged myocytes. Prior administration of low-dose non-depolarizing paralytic can attenuate incidence

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Succinylcholine

Only depolarizing paralytic used clinically

Sinus bradycardia, junctional arhythmias, even sinus arrest can follow administration—likely secondary to muscarinic receptors on heart (blocked with atropine)

Increased intraocular pressure, intragastric pressure, trismus reported.

Malignant hyperthermia

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Rapid-Sequence Induction

Preoxygenation

Anesthesia-inducing drugs (barbiturates,

benzodiazepines, opiods, etomidate,

ketamine, or propofol)

Succinylcholine

Intubation

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Local Anesthetics

Reversibly inhibit the generation and conduction of impulses from a particular area of the body

Effect is secondary to conduction blockade by decreasing permeability of nerve membranes to sodium

Binds to sodium channel and blocks it

All but cocaine are vasodilators and therefore usually are mixed with epinephrine

Ester/Amide family of drugs

Esters metabolized by plasma cholinesterase, amides metabolized by liver p-450 system

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Local Anesthetics

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Local Anesthetics

Lipophilic/hydrophilic ends

Non-ionized form crosses membranes

more readily

– Drugs have less effect in acidic environment

(infection)

– Addition of HCO3 to acidic preparations may

increase potency and decrease pain

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Local Anesthetics

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Local Anesthetic Injection –

The Target

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Local anesthetic injection - Otologic

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Local anesthetic - Intranasal

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Local Anesthesia - Maxilla

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Local Anesthesia -

Mandible

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Nontraditional Anesthesia Acupuncture – Acupuncture with electrical stimulation gave 50-65% decrease in

opiod use, decreased PCA use time, and decreased N/V after intraabdominal surgery (Wang, 1997, Hamza, 1999, Kotani, 2001)

– Decreased N/V after tonsillectomy in adults (NIH consensus, 1998)

– Pain control antagonized by naloxone (Sjolund, 1979)

– Thought to stimulate large nerve fibers which changes pain perception in the spinal cord transmitted by small fibers. Endorphins also increased.

Acupressure

TENS (transcutaneous electrical nerve stimulation) – 10-30% reduction in post-op pain and need

for analgesics (Tyler, 1982)

Capsiacin

Hypnosis

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Tidbits, odds

& ends

Malampatti

classification

Thyromental distance

Grading the intubation

view

SP system

Closed system

anesthesia

6.5cm

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Anesthesiology

Glen T. Porter, MD

Faculty Advisor: Francis B. Quinn, MD, FACS

The University of Texas Medical Branch

Department of Otolaryngology

Galveston, Texas

June 2004