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Anesthetics Flashcards

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1
Q

types of general anasthesia

A

(a) monitored anesthesia care techniques = local anesthetic and sedatives, patient can still respond to verbal commands
(b) balanced anesthesia = iv anesthetic + inhaled anesthetic

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2
Q

intravenous anesthetics

A

(a) barbiturates (thiopental, methohexital)
(b) benzodiazepams (midazolam, diazepam)
(c) propofol
(d) ketamine
(e) opioid analgesics (morphine, fentanyl, sufentanil, alfentanil, remifentanil)
(f) misc sedative hypnotics (etomidate, dexmedetomidine)

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3
Q

inhaled anesthetics

A

(a) halothane, enflurane, isoflurane, desflurane, sevoflurane = volatile anesthetics, liquids at room temp
(b) nitrous oxide, xenon = gaseous anesthetics, gas at room temp

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4
Q

balanced anesthesia

A

(a) iv for induction

(b) inhaled for maintenance of anesthesia

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5
Q

**stages of anesthesia - inhaled anasthetics

A

(a) Stage I Analgesia, initially analgesia without amnesia
(b) Stage II Excitement, delirious and vocalizing but amnesic
**goal of all anesthesia is to get you through stage II as fast and safely as possible
(c) Stage III Surgical Anesthesia, pupil size used to determine plane of this stage
(d) Stage IV Medullary Depression, CNS depression, death ensues
(e) The most reliable indication of Stage III Surgical Anesthesia is loss of response to noxious stimuli (trapezius muscle squeeze) and reestablishment of regular respiratory pattern
GOAL IS TO GET TO 3 SAFELY AND STAY THERE! DONT GO TO 4 or you die

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6
Q

concentration of inhaled anesthetic gas is proportional to what?

A

the partial pressure (also called tension) of that gas

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7
Q

factors that control movement of gas into the CNS (time to induction) - inhaled anasthetics

A
  • solubility
  • concentration in inspired air
  • pulmonary ventilation
  • pulmonary blood flow
  • arteriovenous concentration gradient
  • if the gas is highly soluble, it will want to stay in the blood and enter the brain - slow induction - slow onset
  • if the gas is poorly soluble, it doesnt like the blood, prefers the fat of the brain - fast induction - fast onset - the higher the solubility, the less amount of gas is needed to induce anesthesia (this is good!) - eliminated from blood faster
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8
Q

movement of gas into CNS: solubility - inhaled anasthetics

A

(a) blood:gas partition coefficient
(b) solubility of gas in inspired gas vs blood
(c) nitrous oxide has low solubility in blood, has rapid onset of action (moves into the brain rapidly)
(d) Table 25-1 pg 425 for list of inhaled anesthetics and blood:gas partition ratio
(e) nitrous oxide 0.47 vs methoxyflurane 12 (rapid to slow induction) based on blood solubility

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9
Q

movement of gas into CNS: concentration in inspired air - inhaled anasthetics

A

(a) enflurane, isoflurane, halothane have moderate blood solubility
(b) increase the concentration in inspired air to 1.5% to increase blood levels and entry into brain, then reduce to 0.7% for maintenance

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10
Q

movement of gas into CNS: pulmonary ventilation - inhaled anasthetics

A

(a) minute ventilation = rate and depth of ventilation
(b) fourfold increase in ventilation rate almost doubles the arterial tension of halothane
(c) hyperventilation increases the speed of induction of anesthesia
(d) depression of respiration by opioid analgesics slows the
onset of anesthesia

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11
Q

movement of gas into CNS: pulmonary blood flow - inhaled anasthetics

A

(a) increased blood flow through the lung exposes the anesthetic to larger volumes of blood in the alveoli which reduces
(b) increased exposure to blood, increased solubility in blood, decreased transfer into the brain

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12
Q

movement of gas into CNS: arteriovenous concentration gradient - inhaled anasthetics

A

(a) arterial: venous blood gradient
(b) venous blood returning to the lung has less anesthetic due to drug taken up into tissues
(c) this will decrease drug entry into the brain

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13
Q

elimination of inhaled anasthetics

A
  • ***(a) most important factor is blood gas partition coefficient
  • poorly soluble, low gas partition, eliminated faster
    (b) gas has to leave the brain, enter the blood, then be exhaled
    (c) gas insoluble in blood (low blood:gas partition coefficient) is eliminated faster than more soluble gas anesthetics
    (d) halothane is twice as soluble in brain compared to nitrous oxide and takes longer to be eliminated compared to nitrous oxide
    (e) clearance of inhaled anesthetics via the lungs is the major route of elimination from the body
    (f) liver biotransformation may contribute to elimination for some inhaled anesthetics, halothane is 40% botransformed by liver, compared to < 10% for enflurane
    (g) liver biotranformation of fluoride containing inhaled anesthetics can lead to the production of chlorotrfluoroethyl free radicals which can produce an halothane hepatitis
    (h) liver biotransformation of enflurane and sevoflurane can produce fluoride ions which produce kidney dmage, more pronounced with methoxyflurane (rarely used for this reason)
    (j) sevoflurane is degraded by the carbon dioxide absorbent in anesthesia machines producing a vinyl ether which can cause kidney damage.
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14
Q

**MOA - inhaled anasthetics

A

(a) primary target is the GABA chloride channel
(b) inhaled anesthetics, barbiturates, benzodiazepines, etomidate, propofol all enhance GABA mediated inhibition
(c) ketamine, a dissociate anesthetic is an antagonist at NMDA glutamic acid excitatory channels.
(d) inhaled anesthetics may also act through hyperpolairzation of neurons through activation of potassium channels
(e) inhaled anesthetics may also block the excitatory actions of Ach at nicotinic receptors and their cation channel receptors

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15
Q

dose-response characteristics: Minimal Alveolar Anesthetic Concentration - inhaled anasthetics

A

MAC IS MEASURE OF POTENTCY

(a) dose-response relationships for the inhaled anesthetics are unique and have ethical considerations. Low doses allow pain, higher dose can allow pain and higher doses can induce death.
(b) at steady state the concentration (partial pressure) of the inhaled anesthetic in brain = concentration (partial pressure) in the lung
(c) anesthic can not be measured in the brain but can be measured in the alvelor air (lung air)
(d) concentration in the alvelor air is reported as the % of 760 mm Hg (atmospheric pressure at sea level)
(e) MAC = minimum alveolar anesthetic
(f) MAC = concentration that results in immobility in 50% of patients when exposed to noxius stimulus (surgical anesthesia)
(g) MAC = surrogate measure of the anesthetic requirement
(h) MAC = measure of anesthetic potency among the different gases
(i) MAC for nitrous oxide > 100%, the least potent
(j) MAC for enflurane is 1.7 %, more potent
(k) MAC dosing, a dose of 1 MAC will produce surgical anesthesia in 50% ofpatients
(l) MAC decreased with coadministered drugs, opioids, sympatholytics, sedative-hypnotics
* 0.5 MAC is mild amnesia, 99% pts immobilized at a 1.3 MAC

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16
Q

Effects on CV system - inhaled anasthetics

A

(a) decrease arterial bp in direct proportion to their alveolar concentration
(halothane, desflurane, enflurane, sevoflurane, isoflrane)
(b) mechanism varies, halothane and enflurane decrease cardiac output; iso-flurane, desflurane, sevoflurane decrease peripheral vascular resitance
(c) heart rate, halothane causes bradycardia through direct vagal stimulation, enflurane, sevoflurane no effect, desflurane and isoflurane increase heartrate.
(d) beta blockers used to treat increased catecholamine stimulated increase in blood pressure

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17
Q

effect on respiratory system - inhaled anasthetics

A

(a) all (except nitrous oxide) produce a decrease in tidal volume and an increase
in respiratory rate
(b) all volatile anesthetics are respiratory depressants
(c) all volatile anesthetics increase the pACO2
(d) all volatile anesthetics depress mucociliary function (mucous pooling,
atelectasis, postoperative lung infection)
(e) halothane and sevoflurane have bronchodilating actions which them drugs of choice in patients with asthma, bronchitis, COPD)

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18
Q

effect on brain - inhaled anasthetics

A

(a) all decrease the metabolic rate of the brain
(b) all increase cerebral blood flow, not desired in patients with increased
intracranial brain pressure due to tumor, or head injury
(c) nitrous oxide less likely to increase cerebral blood flow

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19
Q

effect on kidney - inhaled anasthetics

A

(a) decrease the glomerular filtration

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20
Q

effect on liver - inhaled anasthetics

A

(a) from 15-45% decrease hepatic blood flow

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21
Q

liver toxicity - inhaled anasthetics

A

(1) halothane hepatitis (prior exposure required)
(2) incidence 1 in 25 000 – 35 000
(3) halothane may induce immune mediate cause

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22
Q

kidney toxicity - inhaled anasthetics

A

(1) methoxyflurane, enflurane, sevoflurane are biotransformed and release fluoride ions that can lead to toxicity
(2) sevoflurane is degraded by carbon dioxide absorbents in anesthesia machines leads to a toxic compound which causes proximal tubular necrosis
(3) methoxyflurane no longer used due to potential for renal toxicity

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23
Q

malignant hyperthermia - inhaled anasthetics

A

(a) caused by a genetic disorder of skeletal muscle
(b) condition induced by general anesthetics and succinylcholine (skeletal muscle relanxant)
(c) condition presents with tachycardia, hypertension, muscle rigidity, hyperthermia, hyperkalemia, acidosis.
(d) triggering agents Table 16-4 pg 283
(e) cause is uncontrolled release of calcium from SR in muscle
(f) treat with dantrolene which blocks the release of Ca from SR
(g) skeletal muscle biopsy and caffeine-halothane contracture test required to screen for malignant hyperthermia

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24
Q

chronic toxicity - inhaled anesthetics

A

(a) Mutagenicity (1) no effect demonstrated
(b) Carcinogenicity (1) no effect demonstrated
(c) Reproductive Organs (1) higher incidence of miscarriages among OR personnel

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25
intravenous anesthetics
(a) used in addition to inhaled anesthetics and alone | (b) faster induction of anesthesia compared to inhaled agents
26
barbiturates
(a) thiopental, methohexital | (b) readily cross BBB (lipid soluble) and rapidly induce anesthesia
27
Benzodiazepines
(a) diazepam, lorazepam, midazolam used for preanesthesia medication (b) sedative, anxiolytic, amnestic inducing (c) medazolam drug of choice for iv administration
28
Opioids
(a) used with benzos to induce anesthesia | (b) fentanyl and sufentanil as adjuncts to general anesthetics
29
Propofol
(a) most popular iv anesthetic (think Michael Jackson) (b) reduced incidence of nausea and vomiting with rapid recovery at termination of iv infusion (c) used for both induction and maintenance of anesthesia (d) fospropofol, prodrug that reduces the incidence of injection site pain
30
Etomidate
(a) causes minimal cardiovascular and respiratory depression | (b) has no analgesic properties and opioids must be used
31
Ketamine
(a) sold on the streets by junkies as “Special K” (b) drug produces dissociative anesthetic state, which includes catatonia, amnesia, analgesia with or without loss of consciousness (hypnosis) . (c) drug blocks excitatory neurotransmitter glutamic acid at NMDA receptors (d) only iv anesthetic with both analgesic and anesthetic properties (e) drug often induces emergence phenomena following use as an anesthetic (perceptual illusions, vivid dreams) (f) diazepam or midazolam reduces incidence of emergence phenomena (g) useful in low dose because of lack of respiratory depression
32
how is pain transmitter from periphery
nerve ending receptors in peripheral tissues transmit impulse to CNS through primary afferent fibers and relayed by secondary afferent fibers to the brain
33
where can drugs block pain perception
(c) drugs can block pain perception in the periphery or in the CNS (d) drugs can block pain through inhibition of sodium channels in neurons in the spinal cord (e) local anesthetics block sodium channels in axons (f) cocaine was first local anesthetic introduced by Koller in 1884 as a topical ophthalmic anesthetic
34
chemistry of local anesthetics
(a) lipophilic group (aromatic ring) connected by an intermediate chain via an ester or amide to a ionizable group (tertiary amine) (b) ester linage drugs have shorter duration of action (c) pKa of most is between 8.0 – 9.0 (d) at physiological pH 7.4 most are charged and cationic (water soluble, not lipid soluble) (e) problem, charged form is most active at receptor but can not cross membranes to get to the receptor (f) infected sites have low pH (from bacterial growth), drugs are less effective because low pH promotes ionized form which is poorly lipid soluble (can not cross membranes) (g) Table 26-1 pg 442 for structures of local anesthetics
35
absorption of local anesthetics
(a) absorption from site of injection is controlled by (1) dosage (2) site of injection (3) drug-tissue binding (4) local tissue blood flow (5) use of vasoconstrictors (epinephrine) (6) physiochemical properties of the drug itself (b) vasoconstrictors (epinephrine) co-administered will reduce blood flow and prolong actions of the local anesthetic (c) epinephrine, clonidine and dexmedetomidine are agonists at alpha 2 receptors in the spinal cord, when co-administered with local anesthetics they prolong the actions by blocking the release of Substance P which reduces sensory neuron firing
36
distribution of local anesthetics
(a) amides widely distributed | (b) esters too rapidly biotransformed with very short half life
37
biotransformation of local anesthetics
(a) ester converted in the plasma by esterase enzymes (b) amides converted in the liver (takes longer compared to plasma bio-transformation) (c) procaine and chloroprociane half lives < 1 min (esters) (d) lidocaine (amide) takes 1.6 hours to be eliminated but this can increase to 6 hours with liver disease
38
mechanism of action of local anesthetics
(a) block voltage gated sodium channels (b) during action potential, (1) sodium channel opens, sodium flows in, (2) neuron depolarizes to + 40 mV (3) sodium channel closes (4) potassium channel opens (5) potassium flows out (6) neuron repolarizes (7) sodium channel returns to resting state (c) other ways to disrupt sodium channels (1) toxins block sodium channels (batrachotoxin, aconitine, veratridine, scorpion venoms) (2) these toxins bind to receptor and prolong inward flow of sodium (d) local anesthetic block of sodium channels is voltage and time-dependent
39
SAR studies
(a) structure activity relationships (SAR) | (b) potency correlated positively with lipid solubility
40
size and degree of myelination of target neurons in local anesthetics
(a) Size and degree of myelination contribute to the actions of local anesthetics (1) drugs preferentially block small fibers (2) small fibers transmit over shorter distance (3) for myelinated fibers 2-3 successive nodes of Ranvier must be blocked to stop conduction impulse (4) preganglionic B fibers are blocked before the smaller unmyelinated C fibers involved in pain transmission (b) Effect of Firing Frequency (1) drug blockade is more marked in high firing neurons (2) sensory (pain) fibers have high firing rates (c) Effect of Fiber Position in he Nerve Bundle (1) fibers located circumferentially are first exposed to local anesthetic (2) proximal sensory fibers are located in the outer portion of the nerve trunk
41
usual routes of administration of local anesthetics
(1) topical (nasal mucosa, wound [incision site] margins) (2) injection into vicinity of peripheral nerve endings (peri-neural infiltration) (3) injection into major nerve trunks (blocks) (4) injection into the epidural or subarachnoid spaces surrounding the spinal cord
42
Bier block
used iv for regional block in lower and upper extremities
43
local anesthetic + vasoconstrictors
vasoconstrictors (epinephrine) increases the duration of action by decreasing the blood flow at the site of injection
44
speed of onse tof action with sodium bicarb
- speed onset of action with sodium bicarbonate to the injection solution (1) this shifts the pH and converts more of the drug to the lipid-soluble (unionized) form
45
SE of repeated injection of local anesthetics
-can induce tachyphlaxis
46
effects of pH on drug actions
(1) injection drugs are in pH 4-6 (acidic) buffer to improve stability (2) after injection the drug is converted by body fluids to pH 7.4 (3) repeated injection depletes the buffering capacity of the tissues (4) tachyphylaxis
47
cocaine use as local anesthetic
cocaine used for ENT procedures because of excellent absorption from topical application and potent vasoconstrictor effects
48
Toxicity of local anesthetics
(a) systemic effects following absorption of the local anesthetic for the site of administration (injection) (b) direct neurotoxicity from the local effects of these drugs when high concentrations are administered in close proximity to the spinal cord and other major nerve trunks. (c) elevated blood levels can induce a variety of toxic actions
49
CNS toxicity of local anesthetics
(a) inadvertent intravascular administration induces local anesthetic toxicity (1) circumoral and tongue numbness (2) metallic taste (3) nystagmus and muscular twitiching (4) tonic-clonic convulsions (5) generalized CNS depression follows seizure activity (b) midazolam raises seizure threshold and prevents seizure activity from larger doses
50
neurotoxicity of local anesthetics
(a) pooling of excess drug in the cauda equina leads to toxicity not related to excess sodium channel blocking that results in neuropathic symptoms
51
cardiovascular effects of local anesthetics
(a) excess local anesthetics block cardiac sodium channels and thus depress abnormal cardiac pacemaker activity, excitability, and conduction (b) cocaine is an exception, it blocks NE uptake and cause blood pressure increase (vasoconstriction)
52
allergic reactions
(a) ester type local anesthetics are biotransformed to p-aminobenzoic acid (PABA) derivatives, responsible for allergic reactions (b) amide local anesthetics not biotransformed to PABA, allergic reactions extremely rare
53
drug groups that effect skeletal muscle function
1) neuromuscular blockers (used in surgery and ICU to induce muscle paralysis) (2) drugs to reduce spasticity (spasmolytics)
54
neuromuscular blocking drugs
interfere with transmission | (neurotransmitters) at the motor end plate and have no CNS actions
55
spasmolytics
thought to act centrally used to treat chronic back pain, painful fibromyalgic conditions
56
history of neuromuscular blocking drugs
(a) native South Americans used curare as an arrow poison to bring down small game (b) active agent in curare is d-tubocurarine
57
normal neuromuscular function
(1) arrival of electrical action potential at terminal of neuron causes Ca influx (2) Ach vesicles fuse with neuron membrane (3) Ach released from storage vesicles (4) Ach binds to muscle nicotinic receptor (5) Na flows into muscle (6) Na mobilizes intracellular Ca which activates muscle fibers (7) muscle fires (contracts) (8) Ach is hydrolyzed by AchE
58
two ways to block the motor end plate
(1) block Ach at the muscle receptor (a) nondepolarizing neuromuscular blocking drugs (b) d-tubocurarine is prototype example (2) excess Ach causes blockade (a) succinylcholine is prototype example (b) drugs and organophosphate pesticides that inhibit AchE and causes a rise in Ach, another example
59
chemistry of neuromuscular blocking drugs
(a) all neuromuscular blocking drugs resemble Ach in structure (b) succinylcholine is two Ach molecules linked together end-to-end (c) many have two quaternary nitrogens which make them poorly lipid soluble
60
Non-depolarizing neuromuscular blocking drugs
(1) isoquinolines (a) d-tubocurarine (b) atracurium (c) doxacurium (d) cisatracurium (e) mivacurium (2) steroids (a) pancuronium (b) vecuronium (c) pipecuronium (d) rocuronium
61
most common drug used in clinical practice
cisatracurium
62
mivacurium
shortest acting of all drugs
63
depolarizing relaxant drugs
(a) only succinylcholine in this class (b) succinylcholine removed by plasma cholinesterase with half life of 5-10 min compared to Ach which lasts seconds (c) plasma cholinesterase genetic polymorphisms have been identified which take longer than 10-15 min to hydrolyzed succinylcholine (1) molecular variants identified by the dibucaine number (2) 80% inhibition of plasma cholinesterase by dibucaine = normal (3) 20% inhibition of plasma cholinesterase by dibucaine = variant (d) molecular variant results in longer patient recovery time, prolonged apnea
64
MOA of nondepolarizing relaxant drugs
(a) d-tubocurarine prototype neuromuscular blocker (b) compete with Ach at nicotinic receptor at neuromuscular end plate (c) AchE inhibitors (neostigmine, edrophonium, pyridostigmine) increase Ach levels which competes off the blocker drug and recovery follows
65
depolarizing relaxant drugs: phase 1 blocking
(a) Phase I Blocking (depolarizing) (1) succinylcholine only drug in this class (2) succinylcholine binds to nicotinic receptor and opens the channel and motor end plate depolarizes (3) muscle contracts (4) succinylcholine not rapidly removed and channel remains open (depolarized) and can not respond to new impulses (5) flaccid paralysis results (6) AchE inhibitor drugs enhance this Phase I Blocking (good trivia question)
66
depolarizing relaxant drugs: phase II blocking
(b) Phase II Blocking (desensitizing) (1) membrane finally becomes repolarized (2) receptor can not be repolarized (made to fire) because it has become desensitized by the prolonged actions of succinylcholine which is sitting on the receptor
67
skeletal muscle paralysis
(a) skeletal muscle relaxant drugs produce deep muscle relaxation and prevent having to use higher doses of inhaled anesthetics to produce the same levels muscle relaxation
68
neuromuscular transmission
(a) peripheral nerve stimulation devices used during surgery to monitor neuromuscular blockade and recovery (pg 460)
69
2 most important properties of nondepolarizing drugs
(a) time to onset of action and duration of action are the two most important property of the nondepolarizing drugs
70
depolarizing drugs
(a) succinylcholine iv transient muscle fasciculations occur over chest and abdomen within 30 secs (b) paralysis develops in < 90 sec (c) AchE hydrolyzes the drug slowly and recovery occurs in about 10 min
71
CV effects of depolarizing drugs
(a) most have minimal cardiovascular effects (b) pancuronium, atracurium, mivacurium produce cardiovascular effects mediated by autonomic or histamine receptors (c) histamine release produces lowered BP (d) succinylcholine given with halothane can cause arrhythmias
72
other effects of depolarizing drugs
(a) Hyperkalemia: succinylcholine can cause release of K in certain conditions (b) Increased Intraocular Pressure: succinylcholine (c) Increased Intragastric Pressure: risk of regurgitation from succinycholine (d) Muscle Pain: succinycholine induced myalgias
73
inhaled anesthetics
(a) inhaled anesthetics potentiate the actions of nondepolarizing blockers (b) factors involved in this interaction (1) depression of CNS proximal to peripheral neuron blockade (2) increased muscle blood flow (gas cause peripheral dilation) (3) decreased sensitivity of the postjunctional membrane to depolarization
74
antibiotics
(a) aminoglycosides enhances neuromuscular blockade
75
use of AchE inhibitors to reverse drug actions
(a) neostigmine, pyridostigmine inhibit AchE and increase Ach at the motor end plate
76
uses of neuromuscular blocking drugs
(a) tracheal intubation (b) control of ventilation (c) treatment of convulsions
77
spasmolytic drugs
(a) often associated with spinal injury, cerebral palsy, multiple sclerosis, and stroke (b) mechanism involves stretch reflex arc and higher centers in the CNS
78
diazepam
(a) increases GABA activity but induces sedation at 60 mg/d doses required for muscle relaxation
79
Baclofen
(a) baclofen (p-chlorophenyl-GABA) (b) drug is agonist at GABAB receptors which are K conductance receptors, K outward flow blocks neuron firing (c) causes less sedation compared to diazepam (d) drug delivery through a catheter in the subarachnoid space also used (e) normal dosing is po
80
Tizanidine
(a) congener of clonidine an alpha 2 agonist (b) alpha 2 agonist inhibits the release of NE (c) reduces spasticity with fewer cardiovascular effects compared to clonidine
81
dantrolene
(a) derivative of phenytoin | (b) dantrolene blocks the release of Ca from the SR stores in skeletal muscle and inhibits muscle contraction
82
botulinum toxin
(a) treatment for spastic condition lasts from weeks to several months

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