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Anesthesia Review Questions > Chp 15 IV Anesthetics > Flashcards

Chp 15 IV Anesthetics Flashcards

1
Q

MOA etomidate?

A

Imidazole compound - appears to depress CNS function via GABA
- Appears to increase number of GABA receptors, possibly displacing endogenous inhibitors of GABA binding

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2
Q

MOA propofol?

A

CNS effects via modulation of GABA-activated Cl channel

Specific site of action appears to be distinct from those of barbiturates, steroids, benzos, and GABA

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3
Q

GABA

A

Most common inhibitory neurotransmitter in mammalian nervous system

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4
Q

GABA receptor

A

Oligomeric complex consisting of:

  • GABA R
  • Assoc chloride ion channel
  • Barbiturate receptor
  • Benzo receptor
  • picrotoxin binding site
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5
Q

Barbiturates

A
  • Modulate GABA transmission
  • Decreases rate of dissociation of GABA from R —> prolongs duration of GABA-induced opening of the chloride channel
  • Especially capable of depressing activity in the reticular formation whose activity is necessary to maintain wakefulness
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6
Q

GABA = ?

A

Gamma-aminobutyric acid

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7
Q

Other features of barbiturates

A
  • Selectively depress transmission at sympathetic ganglia —> may contribute to decreased BP following their administration
  • High doses reduce sensitivity of postsynaptic membranes of NMJ to Ach thereby interfering with transmission
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8
Q

MOA GABA

A

Activation of postsynaptic GABA R increases chloride conductance through Cl ion channel —> hyperpolarization —> inhibition of the postsynaptic neuron

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9
Q

How to reverse benzos?

A

Flumazenil - pure benzodiazepine R antagonist

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10
Q

Which drugs reduce ICP?

A

Etomidate, propofol, thiopental

- Reduce ICP secondary to decreased cerebral metabolic consumption of oxygen and decreased cerebral blood flow

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11
Q

Which drugs increase ICP?

A

Ketamine, tiletamine increase cerebral blood flow, ICP, and cerebral metabolism

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12
Q

Which benzodiazepines are used in veterinary medicine?

A

Diazepam
Midazolam
Zolazepam (only avail in combo with tiletamine ie Telazol)

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13
Q

Midazolam vs diazepam

A

Midazolam more potent, water soluble
Shorter half life
Similar in effects to diazepam

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14
Q

Zolazepam

A

Water-soluble benzo
Available only in combination with tiletamine
Pharmacokinetics similar to those of diazepam, midazolam
Produces less tranquilization than diazepam or midazolam
At higher doses, can induce dysphoria and excitement

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15
Q

Do barbiturates have adverse effects on other organ systems?

A
  • No direct effects on either liver or kidney function —> not nephrotoxic, hepatotoxic
  • Alterations in liver, kidney function associated with their use secondary to hemo dynamic effects of the drugs and altered perfusion
  • Placental transfer occurs rapidly —> when used at proper induction doses, excessive depression of the fetus does not occur
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16
Q

MOA ketamine

A

MOA not truly established

  • appears the cyclohexamines exert effects via antagonism of CNS muscarinic ACh receptors, agonism of opioid receptors
  • Specific NMDA ANTAGONIST
  • blockade of adrenergic, serotonergic receptors attenuate ketamine-induced analgesia
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17
Q

NMDA?

A

N-methyl-D-aspartate glutamate

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18
Q

Function of NMDA

A

Principle excitatory receptor system in the mammalian brain

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19
Q

How ketamine available

A

Racemic mixture

  • positive isomer: produces more intense analgesia, more rapid recovery, lower incidence of emergence reactions than the negative isomer
  • both isomers appear to have cocaine-like effect in that they inhibit catecholamines into postganglionic sympathetic nerves
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20
Q

Properties of an ideal anesthestic

A
  • Water soluble
  • Long shelf life (>1yr)
  • Stable on exposure to light
  • Require small volume for anesthetic induction
  • Safe/wide therapeutic index
  • Rapid onset of action (one circulation time)
  • Short duration of action
  • Inactivated by rapid metabolism to nontoxic metabolites
  • Not induce anaphylaxis or histamine release
  • Nontoxic, nonirritating, no SE (only producing primary CNS effects)
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21
Q

Properties of barbiturates

A
  • Dose-dependent state of sedation, hypnosis
  • Drug levels persist for several hours even with ultrashort-acting drugs administered to induce GA
  • Species differences in pharmacokinetics responsible for significant variation in duration of action among species
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22
Q

Which barbiturates are used in GA?

A
  • Thiopental
  • Methohexital
  • Pentobarbital
  • Thiobutabarbital (Inactin)
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23
Q

Recovery from barbiturates

A
  • Single dose of thiopental, methohexital - redistribution of the drug from brain to non-nervous tissue (viscera, skeletal m)
  • Methohexital: rapid hepatic metabolism as well
  • Redistribution of pentobarb occurs but recovery primary due to metabolism
  • Ultimate elimination of barbiturates by the body is by metabolsim: <1% recovered unchanged in the urine
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24
Q

Repeated exposure to barbiturates

A

-Results in tolerance due to induction of hepatic enzymes

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25
Q

Factors that affect barbiturate sleep time in mice and rats?

A 
Age
Sex
Strain
Nutritional status
Bedding material
Temperature
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26
Q

What other agents can cause renarconization during recovery from barbiturates?

A 
(Effect of little clinical significance)
Glucose
Fructose
Lactate 
Pyruvate
Glutamate 
Adrenergic agents 
Chloramphenicol
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27
Q

What other agents can cause increased sleep time from barbiturates?

A
  • Drugs that inhibit microsomal enzyme activity (ie chloramphenicol)
  • Drugs that highly protein bound (NSAIDS, sulfonamides) displace barbiturates from serum proteins
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28
Q

Hemodynamic effects of barbiturates?

A
  • Normal subjects: transient small decrease in arterial BP compensated for by increase in HR
  • Myocardial depression minimal –> far less than would occur with inhalant anesthetics
  • Compensatory tachycardia, unchanged myocardial contractility appear to be due to increased peripheral sympathetic activity mediated by the carotid sinus receptor
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29
Q

Effects of barbiturates on oxygenation

A

-Dose-dependent depression of medullary, pontine respiratory centers –> decreased hypercapnic, hypoxic drive of ventilation
+/- Apnea esp in presence of other depressant drugs
–When breathing resumes, at a reduced minute volume of ventilation

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30
Q

Effects of barbiturates on cerebral metabolic oxygen requirements

A
  • Decrease cerebral metabolic oxygen requirements by about 50% when electroencephalogram is isoelectric
  • Indicates reduction in neuronal but not metabolic oxygen needs
  • Barbiturate-induced decreases in cerebral metabolic oxygen requirements exceed decrease in cerebral blood flow
  • May account for protective effects against focal cerebral ischemia
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31
Q

Negative inotropic effects of barbiturates?

A
  • Direct negative inotropic effects occur in absence of compensatory increases in sympathetic activity
  • Initial decrease in arterial pressure due to peripheral vasodilation induced by depression of the medullary vasomotor center, decreased sympathetic outflow
  • In absence of carotid sinus baroreceptor activity, or in hypovolemic patients with less ability to compensate for vasodilation, VD results in pooling of blood on large capacitance vessels, decreased venous return, decreased arterial pressure/CO
  • Arrhythmias can occur on induction –> transient, well-tolerated
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32
Q

Pentobarbital and negative inotropic effects

A
  • Decreased contractility
  • Decreased ABP
  • Decreased SV
  • Decreased pulse pressure
  • Decreased CVP
  • Increased HR
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33
Q

Properties of propofol?

A
  • Isopropylphenyl compound

- Available as a 1% solution in soybean oil, glycerol, egg phosphatide

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34
Q

Propofol clearance

A
  • Plasma clearance exceeds hepatic blood flow –> tissue uptake also important
  • Less than 0.3% excreted unchanged in urine
  • No evidence of impaired elimination of propofol in either patients with cirrhosis or those with renal impairment
35
Q

Recovery with propofol?

A

More rapid, complete with minimal residual CNS effects following induction with thiopental or methohexital

36
Q

Propofol uses

A
  • Induction agent –> rapidly induces unconsciousness
  • Maintain unconsciousness for short procedures (eg bronchoscopy) or CRI
  • No analgesia
37
Q

Effects of propofol

A
  • Decreased cerebral blood flow, perfusion pressure, ICP
  • CV effects resemble those of thiopental but greater magnitude at comparable doses
  • HR less likely to increase than with thiopental
  • Potent resp depressant –> apnea common
38
Q

Properties of ketamine

A

-Most commonly used dissociative agent

39
Q

Dissociative anesthesia

A
  • State in which patient “dissociated” from the environment
  • Resembles catatonic state –> eyes open, patient not unconscious
  • Muscle relaxation not a feature
  • Varying degrees of hypertonus, purposeful movement occur independently of surgical stimulation
40
Q

What are DAs?

A

Cyclohexamines

41
Q

Electroencephalogram evidence of DAs?

A
  • Dissociation btw neothalamocortical and limbic systems

- differential depression and activation of various aspects of the brain

42
Q

Other features of DA

A
  • Amnesia present
  • Intense somatic analgesia
  • Variable visceral analgesia
  • Emergence excitement, delirium may occur
43
Q

Examples of other DAs

A

Tiletamine (available with zolazepam)
Ketamine
Phencyclidine - no longer available

44
Q

Ketamine’s pharmacokinetics

A
  • Resemble those of thiopental
  • Rapid in onset, short duration
  • 5-10x more lipid soluble than thiopental - ensures rapid transfer to the CNS and recovery through rapid redistribution
45
Q

Clearance of DAs

A

-Hepatic metabolism

46
Q

Norketamine

A
  • Intermediate metabolite
  • 1/5-1/3 potency of ketamine
  • May contribute to prolonged effects
47
Q

Ketamine excretion in the urine

A
  • Significant differences among species in the relative amount free ketamine excreted in the urine
  • People, dogs horses: metabolism extensive
  • Cats: most of drug excreted unchanged
48
Q

Ketamine induction of hepatic enzymes

A

Can happen with repeated exposure

49
Q

What is tiletamine?

A
  • DA with potency, duration of action intermediate btw ketamine, phencyclidine
  • Available 1:1 combo with zolazepam
50
Q

Goal of telazol?

A

-Longer acting DA for K9, Fl without negative side effects of rough recovery and muscle rigidity

51
Q

Effects of telazol?

A
  • Physiological SE similar to those of ket-benzo combos
  • HR, ABP increase
  • RR decreases transiently
  • Minute ventilation well maintained
52
Q

Resp effects of ketamine

A
  • Does not induce significant resp depression
  • Apneustic pattern of breathing commonly seen
  • Bronchodilation secondary to increased sympathetic tone occurs
  • Protective upper airway reflexes maintained
  • Airway, salivary secretions increased
53
Q

Hepatic, renal effects Ketamine

A

Does not significantly affect hepatic or renal function

54
Q

Ketamine CV effects

A
  • Sympathetic nervous system stimulation –> increased systemic and pulmonary ABP, HR, CO, cardiac work, myocardial oxygen consumption
  • Effects obtunded by prior administration of tranqs/sedatives
55
Q

In intact patients with functioning CNS…

A

…ketamine increases myocardial contractility

56
Q

What are ketamines CV effects primarily due to?

A

Direct stimulation of the CNS –> increased sympathetic outflow from the CNS

57
Q

What is the effect of ketamine on arrhythmias?

A

Controversial

58
Q

Ketamine in hypovolemic patients

A

Arterial BP better maintained bc of VC but tissue perfusion may be compromised

59
Q

Ketamine in critically ill patients

A
  • Depleted catecholamine stores, exhaustion of sympathetic compensating mechanisms
  • Ket can cause unexpected decreases in CO and ABP (not something appreciated clinically)
60
Q

What happens to plasma concentrations of norepinephrine and epinephrine following ketamine administration?

A

Increase transiently as a result of inhibition of their uptake at postganglionic sympathetic nerve endings

61
Q

Ketamine CNS effects

A
  • potent cerebral VD
  • Cerebral blood flow, ICP, brospinal pressure increase significantly
  • Mechanism (controversial) = increases arterial CO2 tension
  • Controlled ventilation to maintain normocapnea effectively prevents ketamine-induced increases in cerebral blood flow, ICP
62
Q

Other CNS effects of ketamine

A
  • Induces epileptiform bursts in thalamus, limbic system but without spread to cortical areas
  • Hallucinations, emergence delirium can occur
63
Q

Ketamine and seizures

A
  • Does not induce seizures in human epileptics
  • Increases seizure threshold in rats, mice
  • Reports of seizures in dogs and cats
64
Q

Other reported adverse effects of ketamine

A

Blindness

Hyperthermia

65
Q

Ketamine reactions in cats

A
  • Emergence reactions –> ataxia, increased motor activity, hyperreflexia, hypersensitivity to touch, inappropriate avoidance behavior, violent recovery
  • Responses usually cease within several hours
  • Minimized by concurrent treatment or pretreatment with tranquilizers or sedatives
66
Q

Etomidate properties

A
  • Duration of action intermediate btw thiopental, methohexital
  • Recovery from a single dose is rapid with little residual depression
  • Induces unconsciousness with one circulation time
67
Q

Does etomidate provide analgesia?

A

NO!

68
Q

Recovery from etomidate

A
  • Rapid as a result of extensive redistribution, rapid metabolism
  • Hydrolyzed by hepatic microsomal enzymes and plasma esterases
  • Less than 3% recovered unchanged in the urine
  • Overall clearance rate 3-5x that of thiopental
69
Q

Etomidate CNS effects

A
  • Potent direct cerebrovascular VC
  • Cerebral blood flow, oxygen requirements decrease 35-45% –> decreases ICP
  • May activate seizure foci in a manner similar to that of methohexital
70
Q

Etomidate CV effects

A
  • Relatively free of CV effects
  • HR, SV, CO minimally affected
  • BP may decrease may decrease slightly secondary to decreased vascular resistance
71
Q

Etomidate effects renal

A

No effect on renal blood flow

72
Q

Etomidine hepatic effects

A

Not altered

73
Q

Etomidate resp depression

A

Less than that induced by thiopental, of shorter duration

74
Q

Undesirable effects of etomidate

A
  • Pain on injection
  • Myoclonus
  • Adrenocortical suppression lasting 4-6 hours following an induction dose
75
Q

Properties of benzodiazepines

A
  • Lack antipsychotic effects in people –> classified as minor tranquilizers
  • Potent anxiolytic, anticonvulsant, muscle relaxant effects
  • Do not induce degree of tranquilization-sedation of the other tranquilizers
76
Q

Benzodiazepine use in veterinary medicine

A

-Anticonvulsants, coinduction agents with injectable anesthetics

77
Q

Benzodiazepine metabolism

A
  • Hepatic metabolism
  • Metabolites = active –> contribute to relatively long duration of action of these drugs
  • Metabolites excreted in the urine
  • Sensitivity, increased duration of action increases with age, not related to hepatic function
78
Q

Do benzos induce hepatic enzyme production?

A

No!

79
Q

Benzodiazepine elimination

A
  • Dog clears more rapidly than the cat
  • Elimination half-life increases up to 5 fold with liver disease
  • Sensitivity, increased duration of action increases with age - not related to hepatic function
80
Q

Electroencephalographic effects of benzos

A
  • Similar to those of barbiturates
  • decreased alpha, increased low beta activity
  • Tolerance to electroencephalographic effects of benzos does occur
81
Q

Benzos cardiopulmonary, renal, hepatic function

A

Minimal depressant effects

82
Q

Benzo respiratory effects

A
  • minimal depressant effects

- can enhance respiratory depression of other drugs such as opioids

83
Q

CV effects benzos

A
  • Induce minimal decreases in arterial blood pressure, CO, vascular resistance
  • Similar to those observed during natural sleep
84
Q

Benzos skeletal muscle effects

A

-relaxant effects caused by decreased transmission cat the internuncial neuron in the spinal cord, not at the myoneural junction

Anesthesia Review Questions (43 decks)

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