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Pharmacology > General Anaesthetics > Flashcards

General Anaesthetics Flashcards

1
Q

What are the five principles Anaesthesia Represent?

A

immobility, amnesia, and unconsciousness

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2
Q

Immobility?

A

Immobility- Immobility is the easiest anesthetic end point to measure. Edmond Eger and colleagues
introduced the concept of minimal alveolar concentration (MAC) to quantify the potency of an inhalational and Anesthetic

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3
Q

Amnesia?

A

Amnesia- The ablation of memory arises from several locations in the CNS, including the hippocampus,
amygdala, prefrontal cortex, and regions of the sensory and motor cortices. Memory researchers
differentiate two types of memory: (1) explicit memory, ie, specific awareness or consciousness under
anesthesia, and (2) im

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4
Q

Consciousness?

A

Consciousness- The ability of anesthetic drugs to abolish consciousness requires action at anatomic locations
responsible for the formation of human consciousness. Leading neuroscientists studying consciousness identify
three regions in the brain involved in generating personal awareness: the cerebral cortex, the thalamus, and the reticular activating system. These regions seem to interact as a cortical system via identified pathways,
producing a state in which humans are awake, aware, and perceiving. These neural pathways involved in
the development of consciousness are disrupted by anesthetics.

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5
Q

Stages of anaesthesia?

A

Induction, Maintanace

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6
Q

GA MAO?

A

No specific receptor has been identifieds the locus of GA action
o A variety of molecular mechanism may contribute to the activity of GA
o At [effective], GA increase the sensitivity of - GABAA receptors to the
inhibitory neurotransmitter GABA increase chloride (Cl ion) influx - hyper
polarization of neurons.
o Exception: ( Nitrous oxide and Ketamine; no action on GABAA receptors)
inhibition of the N-methyl-d- aspartate (NMDA) receptors

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7
Q

Volatile anesthetics?

A

halothane
enflurane
isoflurane
desflurane
sevoflurane

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8
Q

Gaseous anesthetics

A

nitrous oxide
xenon

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9
Q

GENERAL ANESTHETIC Factors Controlling Uptake?

A

Solubility - One of the most important factors influencing the transfer of an
anesthetic from the lungs to the arterial blood is its solubility characteristics.

Cardiac output - Changes in pulmonary blood flow have obvious effects on the
uptake of anesthetic gases from the alveolar space.

Anesthetic partial pressure difference between alveolar and mixed venous
blood is dependent - uptake of the anesthetic by the tissues, (incl) non- neural
tissues.

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10
Q

GENERAL ANESTHETIC Factors Controlling Uptake?

A

Solubility - One of the most important factors influencing the transfer of an
anesthetic from the lungs to the arterial blood is its solubility characteristics.

Cardiac output - Changes in pulmonary blood flow have obvious effects on the
uptake of anesthetic gases from the alveolar space.

Anesthetic partial pressure difference between alveolar and mixed venous
blood is dependent - uptake of the anesthetic by the tissues, (incl) non- neural
tissues

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11
Q

Nitric Oxide

A

Laughing gas is non-irrittaing potent analgesic but a weak general anaesthetic commonly combined with other more potent agents

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12
Q

Nitric Oxide solubility ?

A

Poorly soluble in blood and other tissue, allowing it to move very rapidly in and out of body

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13
Q

Nitric Oxide pneuomothorax?

A

It replaces nitrogen in various air spaces faster than nitrogen leaves

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14
Q

Nitric Oxide diffusion hypoxia?

A

Poorly soluble in blood and other tissues. Allowing it to move quickly and out of the body

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15
Q

Why induction of anesthesia is slower with more soluble anesthetic gases?

A

Solubility in blood is represented by the relative size of the blood compartment (the more soluble, the larger the
compartment).
Relative partial pressures (agents) in the compartments - indicated by the degree of filling - each compartment.
Given concentration or partial pressure of the two anesthetic gases (inspired air),
Take longer for the blood partial pressure of the more soluble gas (halothane) to rise - same partial pressure (alveoli).
[Anesthetic agent] in the brain can rise no faster than the the [blood]
Onset of anesthesia will thus be slower with halothane than with nitrous oxide.

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16
Q

The time to recovery from inhalation anesthesia depends?

A

The time to recovery from inhalation anesthesia depends on the rate of
elimination of the anesthetic from the brain.

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17
Q

Important factors governing rate of recovery?

A

The blood:gas
partition coefficient of the anesthetic agent.

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18
Q

Other factors controlling rate of recovery?

A

Other factors controlling rate of recovery include pulmonary blood flow,
magnitude of ventilation, and tissue solubility of the anesthetic.
Two features differentiate the recovery phase from the induction phase.

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19
Q

How can transfer of anaesthetic from lungs to blood be transferred and what for the reverse?

A

First, transfer of an anesthetic from the lungs to blood can be enhanced
by increasing its concentration in inspired air, but the reverse transfer process cannot be enhanced because the concentration in the lungs cannot be reduced
below zero.

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20
Q

Two parameters that can be manipulated by the anesthesiologist
are useful in controlling the speed of induction of and recovery
from inhaled anesthesia?

A

(1) Concentration of anesthetic in the inspired gas and
(2) Alveolar ventilation.

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21
Q

Metabolism of anesthetics?

A

Modern inhaled anesthetics are eliminated mainly by ventilation and are only metabolized to a
very small extent; thus, metabolism of these drugs does not play a significant role in the
termination of their effect.

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22
Q

What role does metabolism play?

A

However, metabolism may have important implications for their toxicity (see Toxicity of
Anesthetic Agents).

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23
Q

Hepatic metabolism contribution?

A

Hepatic metabolism may also contribute to the elimination of and recovery from some older
volatile anesthetics.

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24
Q

Nitrous oxide and human tissues?

A

Nitrous oxide is not metabolized by human tissues. However, bacteria in the gastrointestinal
tract may be able to break down the nitrous oxide molecule.

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25
Q

Nitrous oxide effect on brain?

A

Nitrous oxide can increase cerebral blood flow and cause increased intracranial
pressure.

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26
Q

Solution of nitrous oxide admin.?

A

Therefore, nitrous oxide may be combined with other agents (intravenous anesthetics) or techniques (hyperventilation) that reduce cerebral blood flow in patients with increased intracranial pressure.
o Potent inhaled anesthetics produce a basic pattern of change to brain electrical
activity as recorded by standard electroencephalography (EEG).

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27
Q

When is adminstration of high concentrations of volatile anesthetics undesirbale?

A

Therefore, administration of high concentrations of volatile anesthetics is
undesirable in patients with increased intracranial pressure

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28
Q

Drugs that depress normal
cardiac contractility

A

Halothane, enflurane, isoflurane, desflurane, and sevoflurane

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29
Q

Inhalation anaesthetics drugs?

A

SHINED

Sevoflurane
Halothane
Isoflurane
Nitrous Oxide
Enflurane
Desflurane

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30
Q

Halothan:
-Arrythmias
-Sensitivity to DA, NE
-Cardiac Output
-Blood Presssure
-respiratory reflex
-hepatix toxicity
-renal toxicty

A

-Arrythmias: Increased
-Sensitivity to DA, NE: Increased
-Cardiac Output: Decreased
-Blood Presssure: Dose-dependent
-respiratory reflex: inibited
-hepatix toxicity: high risk
-renal toxicty: Low risk

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31
Q

Isoflurane:
-Arrythmias
-Sensitivity to DA, NE
-Cardiac Output
-Blood Presssure
-respiratory reflex
-hepatix toxicity
-renal toxicty

A

-Arrythmias: No-effect
-Sensitivity to DA, NE: No-effect
-Cardiac Output: Minimum Effect
-Blood Presssure: Dose-dependent hypotension
-respiratory reflex: +++ irrittation
-hepatix toxicity: low risk
-renal toxicty: low risk

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32
Q

Desflurane?
-Arrythmias
-Sensitivity to DA, NE
-Cardiac Output
-Blood Presssure
-respiratory reflex
-hepatix toxicity
-renal toxicty

A

-Arrythmias: No-effect
-Sensitivity to DA, NE: No-effect
-Cardiac Output: Minimum Effect
-Blood Presssure: Dose-dependent hypotension
-respiratory reflex: stimulation
-hepatix toxicity: low risk
-renal toxicty: low risk

33
Q

Sevoflurane?
-Arrythmias
-Sensitivity to DA, NE
-Cardiac Output
-Blood Presssure
-respiratory reflex
-hepatix toxicity
-renal toxicty

A

-Arrythmias: No-effect
-Sensitivity to DA, NE: No-effect
-Cardiac Output: Minimum Effect
-Blood Presssure: Dose-dependent hypotension
-respiratory reflex: inhibited
-hepatix toxicity: low risk
-renal toxicty: high risk

34
Q

Haloothane therapeutic uses?

A

Usually co-administrated with nitrous oxide, opiods or local anaesthetics?

35
Q

Halothane P/K?

A

Metabolised in the body to tissue

36
Q

How to avoid a halothane toxic reaction?

A

Halothan must not be administered at intervals of less than 2-3 weeks

37
Q

Halothan hepatoxicity in children?

A

Not hepatoxic in children and combined with its pleasant odour, its suitable in paediatrics for inhlations induction

38
Q

Halothane adverse cardiac effects?

A

Bradycardia
Cardiac arrhythmias
Concentration-dependent hypotension

39
Q

Halothane and malignant hyperthermia?

A

in very small percentage of susceptible patients expouser to halogenated hydrocarbon anaesthetics or the NM, Succiny;choline may induce malignant hyperthermia

Uncontrolled in skeletal muscle oxidative metabolism, overwhelming the bodys capcity to supply oxygen, remove carbon dioxide and regulate temperature and causes circulatory collapse and death if not treated immediately

40
Q

Malignant hyperthermia susceptible patients?

A

Burn victims and individuals

41
Q

Halothane Rx?

A

Dantrolene(blocks release of Ca2+) from the sarcoplasmic reticulum of muscle cells, reducing. heat production and relaxing muscle tone

42
Q

Isoflurane metabolism?

A

Undergoes little metabolism and is therefore not toxic to the liver or kidney also, it does not induce cardiac arrhymias

43
Q

Isoflurane and hyotension?

A

Produce dose-dependent

44
Q

Isoflurane odour and respiratory effects?

A

Pungeny odur and stimulates respiratory effects(irritation, salivation, coughing, laryngospasm) therefore not used for inhalation induction in high risk patients

45
Q

Desflurane onset recoevry?

A

Provides very rapid onset and recovery due to low blood solubulity

46
Q

Desflurane use in outpatients?

A

Popular anaesthetics for outpatient procedures

47
Q

Desflurane volatility?

A

Low volatility , requiring admin. via special heated vaporizer

48
Q

Sevoflurane ability to allow rapid induction?

A

Has low pungency allowing rapid induction without irritating the airways

49
Q

What is sevoflurane suitable for?

A

Paediatric patients

50
Q

Sevoflurane onset?

A

Rapid onset and recovery due to low blood solubility?

51
Q

Sevoflurane metabolsim?

A

Metabolsied by the liver-metabolited can be nephrotic

52
Q

Propofol-1 replaced which drugs?

A

Propofol is the most frequently administered drug for
induction of anesthesia and has largely replaced barbiturates for this indication.

53
Q

What is the propofol-1 P/k profile?

A

pharmacokinetic profile allows for continuous infusions

54
Q

Propofol-1uses during anesthesia?

A

propofol is also used during maintenance of
anesthesia and is a common choice for sedation in the
setting of monitored anesthesia care.
o propofol is also used for sedation in the ICU as well as
conscious sedation and short-duration general anesthesia in locations outside the operating room

55
Q

Propofol-1 MOA?

A

The presumed mechanism of action of propofol is through potentiation of the
chloride current mediated through the GABA A receptor complex.

56
Q

Propofol-1 metabolism?

A

Propofol is rapidly metabolized in the liver; the resulting watersoluble
compounds are presumed to be inactive and are excreted through the kidneys.

57
Q

Propodol-1 clearance?

A

Plasma clearance is high and exceeds hepatic blood flow, indicating the
importance of extrahepatic metabolism, which is thought to occur to a significant extent in the lungs and may account for the elimination of up to 30% of a bolus dose of the drug

58
Q

clinical uses of propofol?

A

The most common use of propofol is to facilitate induction of general anesthesia by bolus injection

59
Q

Propofol pharmacological effects?

A

Depressese the CNS accompanied by excitatory phenomenal

Transient pain at the injection site is common

It decreases blood pressure without depressing the myocardium, also decreases intracranial pressure

It does not provide analgesia, has some antiemetic effects

Propopol is commonly infused in lower doses to provide sedation

60
Q

S/E of Propofol?

A

Tremorme
Urine Retension
Green urine
flushing
Infusion syndrome

61
Q

Clinical doses of fospropofol?

A

Fospropofol is approved for sedation during monitored anesthesia care.

o Supplemental oxygen must be administered to all
patients receiving the drug.
o Hence, it is recommended that fospropofol be
administered only by personnel trained in airway
management.
o The dose should be reduced by 25% in patients
older than 65 years and in those with an American
Society of Anesthesiologists
o Injection pain during administration of propofol is
often perceived as severe, and the lipid emulsion has
several disadvantages.

62
Q

Fosproprol?

A

o Fospropofol is a water-soluble prodrug of propofol

63
Q

Fospropofo organ system effects?

A

Because the active compound is propofol and fospropofol is a prodrug that
requires metabolism to form propofol, the pharmacokinetics are more
complex than for propofol itself.
o Multicompartment models with two compartments for fospropofol and
three for propofol have been used to describe the kinetics.
o The effect profile is similar to that of propofol, but onset and recovery are
prolonged compared with propofol because the prodrug must first be
converted into an active form.
o Although patients receiving fospropofol do not appear to experience the
injection pain typical of propofol, a common adverse effect is the
experience of paresthesia, often in the perianal region, which occurs in up
to 74% of patients. The mechanism for this effect is unknown.

64
Q

Thiopental?

A

An ultra-short acting barbiturate with high lipid solubility

65
Q

Thiopental anaesthetic and analgesic?

A

A potent anaesthetic but a weak analgesic

66
Q

Thiopental S/E?

A

Apnoea, coughing, chest well spasm, laryyngospasm and bronchospasm

67
Q

Clinical uses of barbiturates?

A

The principal clinical uses of thiopental or
methohexital is for induction of
anesthesia (unconsciousness) which
usually occurs in less than 30 seconds.
o Patients may experience a garlic or onion
taste after administration.
o Barbiturates such as methohexital
o (20–30 mg/kg) may be administered per
rectum;
o Facilitate induction of anesthesia in
mentally challenged and uncooperative
pediatric patients.

68
Q

Barbiturates?

A

Barbiturate hypnotics have been largely replaced as
induction agents by propofol.
o The anesthetic effect of barbiturates presumably
involves a combination of enhancement of inhibitory
and inhibition of excitatory neurotransmission.
o Although the effects on inhibitory transmission
probably result from activation of the GABA A receptor
complex, the effects on excitatory transmission are less
well understood.
63
o Barbiturates should not be administered to patients with
acute intermittent porphyria because they increase the
production of porphyrins through stimulation of amino
levulinic acid synthetase.

69
Q

Diazepam conjuction for sedation?

A

BDZs are used in conjunction with anaesthetics for sedation

70
Q

Diazepam metabolised?

A

Metabolised by liver, and erthromycin may prolong their effects

71
Q

BDz and amenesia?

A

BDZ can induce anterograde amnesia in which the patient retains memory of past events but new information is not transferred into long-term memory

72
Q

BDZ clinical uses and dosage?

A

Used-preoperative medication, intravenous sedation – suppression - seizure
activity -(desired effects anxiolysis/anterograde amnesia
o Midazolam and Diazepam (Less frequently) - also be used to induce general
anesthesia.
o Lorazepam- slow onset /prolonged duration of action – limit (usefulness);
for preoperative medication or induction of anesthesia;
o Rapid and sustained awakening at the end of surgery (desirable)
o Flumazenil (antagonist) (8–15 mcg/kg IV) useful for treating patients
experiencing delayed awakening;
o Duration of action is brief (about 20 minutes) and re-sedation may occur.
o Benzodiazepines -Delayed awakening (potential disadvantage);
o Limiting (usefulness) - induction of general anesthesia despite their
advantage of less pronounced circulatory effects.
o Benzodiazepines - unique among the group of intravenous anesthetics;
o Action can readily be terminated by administration of their (selective
antagonist)-Flumazenil.
o Benzodiazepines (highly lipid-soluble) - rapidly enter the CNS;
o Accounts - rapid onset of action,- redistribution to inactive tissue sites and
subsequent termination of the drug effect

73
Q

Etomidate?

A

Used-preoperative medication, intravenous sedation – suppression - seizure
activity -(desired effects anxiolysis/anterograde amnesia
o Midazolam and Diazepam (Less frequently) - also be used to induce general
anesthesia.
o Lorazepam- slow onset /prolonged duration of action – limit (usefulness);
for preoperative medication or induction of anesthesia;
o Rapid and sustained awakening at the end of surgery (desirable)
o Flumazenil (antagonist) (8–15 mcg/kg IV) useful for treating patients
experiencing delayed awakening;
o Duration of action is brief (about 20 minutes) and re-sedation may occur.
o Benzodiazepines -Delayed awakening (potential disadvantage);
o Limiting (usefulness) - induction of general anesthesia despite their
advantage of less pronounced circulatory effects.
o Benzodiazepines - unique among the group of intravenous anesthetics;
o Action can readily be terminated by administration of their (selective
antagonist)-Flumazenil.
o Benzodiazepines (highly lipid-soluble) - rapidly enter the CNS;
o Accounts - rapid onset of action,- redistribution to inactive tissue sites and
subsequent termination of the drug effect

74
Q

Clinical Uses and dosage of etomidate?

A

o Alternative to propofol and barbiturates for the rapid (IV)
induction of anesthesia- (patients with compromised
myocardial contractility).
o After a standard induction dose (0.2–0.3 mg/kg IV);
o Onset – unconsciousness- comparable - achieved by
thiopental and propofol.
o Injection (intravenous)- high incidence –pain - followed by
venous irritation-(Similar to propofol)
o Involuntary myoclonic movements are also common but
may be masked by the concomitant administration of
neuromuscular blocking drugs.
o Awakening rapid -single (IV) dose - little evidence- residual
depressant effects.
o No analgesia effect.
o Postoperative nausea and vomiting- more common-
thiopental or propofol

75
Q

Ketamine?

A

Partially water-soluble/ highly lipid soluble (phencyclidine
derivative) differing - most other (IV) anesthetics-
produces significant analgesia.
o The characteristic state observed after an induction dose
of ketamine is known as “dissociative anesthesia,”
wherein the patient’s eyes remain open with a slow
nystagmic gaze (cataleptic state).
o Of the two stereoisomers the S (+) form is more potent
than the R (–) isomer, but only the racemic mixture of
ketamine is available in the USA.
o Mechanism of action (complex) ; Major effect- produced
-inhibition - N-Methyl-D-aspartate receptor (NMDA)
complex.

76
Q

P/K Ketamine?

A

High lipid solubility - ensures a rapid onset of its effect.
o Effect of a single bolus injection- terminated by redistribution to inactive
tissue sites. As with other (IV) induction drugs,
o Metabolism- primarily (liver) – (N –demethylation) cytochrome P450 system.
o Nor-ketamine- primary active metabolite, less potent (one third to one fifth
the potency) ketamine;
o Subsequently hydroxylated and conjugated into water-soluble inactive
metabolites that are excreted in urine.
o Only (IV) anesthetic that has low protein binding (12%)

77
Q

Clinical Uses & Dosage-Ketamine?

A

o Unique properties- (incl) profound analgesia,
stimulation of the sympathetic nervous system,
bronchodilation- minimal respiratory depression,
o Important alternative to the other (IV)
anesthetics - desirable adjunct in - despite the
unpleasant psychotomimetic effects.
o Administered -multiple routes (intravenous,
intramuscular, oral, rectal, epidural) - useful
option for premedication in mentally challenged
and uncooperative pediatric patients.
o Popular as an adjunct administered at sub-
analgesic doses to limit or reverse opioid
tolerance.

78
Q

Dexmedetomidine?

A

o Highly selective α 2 -adrenergic agonist.
o Effects can be antagonized- α 2 -antagonist drugs.
o Active S –enantiomer - medetomidine
o Water soluble- available as a parenteral formulation.
o Rapid hepatic metabolism involving conjugation, N -
methylation, and hydroxylation, followed by
conjugation.
o Metabolites are excreted in the urine and bile.
o Clearance is high - elimination half-time is short.
78
Clinical Uses & Dosage - DEXMEDETOMIDINE
o Principally used -short-term sedation- intubated /ventilated patients ICU setting.
o Operating room - used as an adjunct

Pharmacology (44 decks)

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