Anesthesiology

Glen T. Porter, MD Francis B. Quinn, MD University of Texas Medical Branch 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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History

Crawford Long

Horace Wells W. Thomas Morton 3

History
1878 Endotracheal tube invented 1885 Halstead introduces nerve block anesthesia with cocaine 1934 Sodium thiopentone (IV anesthesia) 1934 Curare 1940s 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 agents 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.

Nitrous Oxide
Discovered 1776 by David Priestly Largely recreational use until mid 1800s 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 Halothaneless 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 13

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 activitymay 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 pressuremay be significant in patients with blunted sympathetic response Short period of apnea after administration Venous irritation

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Benzodiazepines
Good for amnesia/sedationvia 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 (doesnt 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/antagonistless analgesia, less respiratory depression Naloxone: reverses analgesia/respiratory depression (30 minutes)
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Muscle Relaxants
Used clinically since 1940s. 1960s 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 nondepolarizing paralytic can attenuate incidence
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Succinylcholine
Only depolarizing paralytic used clinically Sinus bradycardia, junctional arhythmias, even sinus arrest can follow administrationlikely 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 Francis B. Quinn, MD University of Texas Medical Branch Galveston, Texas

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