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NS2 Test 3 > General Anesthetics DSA > Flashcards

General Anesthetics DSA Flashcards

1
Q

Anesthetic state produced by general anesthetics

A
  • unconsciousness
  • amnesia
  • analgesia
  • attenuation of autonomic reflexes to noxious stimulation
  • immobility in response to noxious stimulation (skeletal muscle relaxation)
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2
Q

monitored anesthesia care–what is it?

A
  • sedation-based anesthetic techniques
  • used for diagnostic and minor therapeutic surgical procedures
  • without general anesthesia
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3
Q

monitored anesthesia care–drugs used

A
  • midazolam (premedication–for anxiolysis, amnesia, mild sedation)
  • propofol infusion (deep sedation)
  • opioid analgesic or ketamine–added to minimize discomfort
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4
Q

conscious sedation–what is it?

A
  • used by nonanesthesiologists

- patient retains the ability to maintain a patient airway and is responsive to verbal commands

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5
Q

conscious sedation–drugs used/reversible by?

A

-benzodiazepines and opioid anelgesics (fentanyl)–reversible by specfic R antagonist drugs; glumazenil and naloxone, respectively

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6
Q

deep sedation–what is it?

A
  • transition from deep sedation to general anesthesia is fluid
  • loss of protective reflexes, inability to maintain a patent airway, lack of verbal responsiveness to surgical stimuli
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7
Q

deep sedation drugs used

A
  • IV –sedative hypnotics propofol and midazolam

- sometimes in combination with opioid analgesics or ketamine (depending on level of pain)

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8
Q

ICU-sedation–what is it? Drugs?

A
  • patients who require mechanical ventilation for long periods
  • sedative–hypnotic drugs and low doses of IV anesthetics
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9
Q

primary inhibitory ion channels for anesthetic action

A
  • Cl channels (GABAa, glycine receptor)

- K channels

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10
Q

excitatory ion channel targets

A
  • Ach (nAChR and mAChRs)
  • EAAs (AMPA, NMDA receptors)
  • serotonin (5HT2 and 3 Rs)
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11
Q

inhaled anesthetics types

A
  • volatile anesthetics

- gaseous anesthetics

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12
Q

volatile anesthetics

Gaseous anesthetics?

A

HEIDS

  • halothatne, enflurane, isoflurane, desflurane, sevoflurane
  • low vapor pressure so high boiling points–liquid at room temperature

Gaseous: Nitrous oxide; high vapor pressure so low boiling points–gas at room temp

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13
Q

driving force for uptake of an inhaled anesthetic

A

alveolar concentration

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14
Q

2 factors that determine how quickly the alveolar concentration changes

A
  • inspired concentration or partial pressure

- alveolar ventilation (increases in either direction will increase the rate of rise in alveoli–accelerate induction)

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15
Q

partial pressure in alveoli–expressed as

A

Fa (alveolar concentration)/Fi (inspired concentration)

-faster Fa/Fi approaches 1=faster anesthesia will occur

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16
Q

blood: gas partition coefficient–what is it? relationship?

A
  • affinity of an anesthetic for blood compared with that of inspired gas (ie blood solubility)
  • inverse relationship beteween blood:gas coefficient values and rate of anesthesia onset
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17
Q

agents with low blood solubility–onset of action

A
  • NO, desflurane
  • reach high arterial Pressure rapidly–results in rapid equilibration with brain
  • fast onset of action
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18
Q

Agents with high blood solubility–onest of action

A
  • halothane
  • reach high arterial Pressure slowly–results in slow equilibration with brain
  • slow onset of action
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19
Q

fastest onset of action (low blood solubility) to slowest onset o f action (high blood solubility)–drugs

A

-NO
-Desflurane
-Sevoflurane
-Isoflurane
-Enflurane
-Halothane
(NO, DSIEH)

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20
Q

increase in pulmonary blood flow (increase CO)- causes what?

A
  • increases uptake of anesthetic and decrease the rate by which Fa/Fi rises-decreases the rate of induction of anesthesia (Fa decreases bc of the increased pulmnonary blood flow–dilutes the drug in alveoli)
  • will increase uptake of anesthetic into blood–but will be distributed and diluted into all tissues (not just the CNS)
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21
Q

the slower the rate and extent of tissue uptake–does what to alveolar-venous partial pressure?

A

-greater the difference in anesthetic gas tensions bw arterial and venous blood–more time it will take to achieve equilibrium with brain tissue

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22
Q

larger alveolar-venous partial pressure differences means?

A

-less drugs are returning for elimination, which may increase the time for awakening

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23
Q

depression of respiration by opioid analgesics–does what to onset of anesthesia

A

-slows onset of anesthesia of inhaled anesthetics if ventilation is not assisted

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24
Q

increasing pulmonary blood flow (CO)–does what to rate of increase in arterial concentration

A

-slows rate of increase in arterial concentration of anesthetic because a larger volume of blood is exposed to anesthetic

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25
Q

what organs have higher immediate concentration of anesthetics

A
  • brain, heart, liver, kidneys, splanchnic bed

- highly perfused (receive 75% of resting CO)

26
Q

what tissues do anesthetics accumulate more slowly of anesthetics

A
  • muscle and skin

- only recieve 1/5 of resting CO

27
Q

major route of elimination from body of inhaled anesthetics

A

lungs

28
Q

insoluble in blood and brain–rate of elimination?

A

faster

29
Q

minimal alveolar concentration (MAC)–what is it?

A

-concentration of inhalation anesthetics that prevents movement in response to surgical stimulation in 50% of subjects (measures potency)

30
Q

a dose of 1 MAC does what?

A

-prevents movement in response to surgical incision in 50% of patients

31
Q

MAC values greater than 100%

A

-other agents must be supplemented to achieve surgical anesthesia (NO)

32
Q

4 stages of increasing depth of CNS depression

A
  • 1-stage of analgesia
  • 2-stage of excitement
  • 3-stage of surgical anesthesia
  • 4-stage of medullary depression
33
Q

stage 1

A

(analgesia)

  • analgesia without amnesia
  • with amnesia at end of stage
34
Q

stage 2

A

(excitement)

  • delirious
  • respiration is irregular
  • retching and vomiting may occur if patient is stimulated
  • regular breathing is established at end of stage
35
Q

stage 3

A

(surgical anesthesia)

-begins with regular breathing; extends to complete cessation of spontaneous respiration

36
Q

stage 4

A

(medullary depression)

-severe depression of vasomotor depression center in medulla and respiratory center

37
Q

inhaled volatile anesthetics–effects on CV system

A

-decrease mean arterial pressure in direct proportion to their alveolar concentration

38
Q

Heart rate effects?

A
  • Halothane–causes bradycardia

- Desflurane and isoflurane–increases HR

39
Q

Respiratory effects?

A
  • respiratory depressants

- depression of mucociliary function in airway–can result in pooling of mucus and postoperative respiratory infections

40
Q

May cause hepatitis

A

-halothane (2 days to 3 weeks after exposure)

41
Q

May cause renal toxicity

A
  • agents metabolized to products including fluoride ions

- enflurane, sevoflurane

42
Q

may cause malignant hyperthermia; antidote??

A
  • inhaled volatile anesthetics in combination with succinylcholine
  • antidote=dantrolene
43
Q

IV anesthetics are?

A
  • highly lipophilic
  • go into highly perfused lipophilic tissues (brain, spinal cord)
  • quick onset of action
44
Q

Most commonly used as parenteral anesthetic

A

propofol

45
Q

Propofol–MOA, characteristics, metabolized

A
  • rapid onset, recovery–able to ambulate quickly after use
  • time of onset–15-30 seconds
  • continuous infusions and maintenance of anesthesia, sedation in ICU, conscious sedation and short-duration general anesthesia outside operating room
  • agonist for GABA receptors–Cl current
  • metabolized in liver
  • low hangover effect–high plasma clearance
46
Q

context–sensitivity half life

contact sensitivity half life–drugs that increase dramatically and drugs that increase modestly

A

-describes the elimination half time after a continuous infusion; key factor of a drug to be used as a maintenance anesthetic; propofol–brief contact sensitivity half life–prompt recovery!

  • diazepam and thioental–half lives increase dramatically with prolonged infusions
  • Midazolam, ketamine, propofol, etomidate–half lives increase modestly (high to low half lives) MKPE
47
Q

propofol CNS effects

A
  • general suppression of CNS activity
  • no analgesic properties
  • decreases cerebral blood flow and cerebral metabolic rate for oxygen–which decreases intracranial pressure
  • burst suppression in EEG–neuroprotective effect during neurosurgical procedures
48
Q

Propofol CV effects

A
  • produces the decrease in systemic blood pressure due to vasodilation (most pronounced compared with other agents)
  • hypotensive effects–inhibits normal baroreflex response
49
Q

propofol respiratory effects

A
  • potent respiratory depressant
  • effects similar to propofol
  • onset and recovery prolonged
  • less pain on administration
  • adverse effects–paresthesias and pruritus–mostly limited to first 5 minutes of administration
50
Q

Fospropofol–what is it? Effects?

A
  • prodrug of propofol
  • effects similar to propofol
  • onset and recovery prolonged
  • less pain on administration
  • adverse effects–paresthsias and pruritus–mostly limited to first 5 minutes of administration
51
Q

Etomidate–effects? MOA?

A
  • hypnotic but not analgesic effects
  • MOA–enhances GABA on GABA receptors
  • minimal CV and respiratory depressions (useful in patients with impaired CV, resp systems)
  • rapid loss of consciousness and less rapid recovery rate
  • metabolized by liver and in plasma
52
Q

Etomidate–CNS, CV, Resp, endocrine effects?

A
  • CNS–potent cerebral vasoconstrictor, decreases cerebral blood flow and ICP
  • CV–stability is maintained–minimal change in HR and CO
  • endocrine–causes adrenocortical suppression by inhibiting 11B-hydroxylase (needed for cholestrol–>cortisol)
  • suppression lasts 4-8 hours after induction dose
53
Q

Ketamine–effects? MOA?

A
  • NMDA Receptor Antagonist
  • dissociative anesthetic state–catatonia, amnesia, analgesia, with or without loss of consciousness
  • lacrimation and salivation increase upon administration
54
Q

Ketamine–CNS, CV effects?

A
  • increases cerebral blood flow and CMRO2 (don’t use in patients with intracranial pathology)
  • unpleasant emergence reactions
  • may induce a euphoric state
  • increase systemic BP, HR, CO (stimulates Symp NS)
  • direct myocardial depressant (masked by stimulation of Sympathetic NS)
55
Q

Ketamine–only IV anesthetic to produce?

A

-analgesia, stimulation of SNS, bronchodilation, minimal respiratory depression

56
Q

Dexmedetomidine–MOA? effect? used for?

A
  • alpha-2 adrenergic agonist
  • hypnosis and analgesic effects
  • sedative effect–sleep state (act of endogenous sleep pathways)
  • moderate decreases in HR and systemic vascular resistance and systemic blood pressure
  • used for short term sedation of intubated and ventilated patients in an ICU setting or as an adjunct to general anesthesia
57
Q

Anesthetic Adjuncts–used to?

A

-augment components of anesthesia, permitting lower doses of general anesthetics with fewer side effects

58
Q

opioid analgesics–used with? MOA? common agents? Adjunct to?

A
  • -in combo with benzodiazepines to achieve a general anesthetic state
  • agonists and opiate receptors
  • fentanyl, sufentanil, remifentanil, morphone (FSRM)
  • adjunct to IV and inhaled anesthetics to provide perioperative analgesia
59
Q

Barbituates–common agents? MOA? effects? used for?

A
  • Thiopental, Metohexital
  • lipophilic, quick plasma:brain equilibrium
  • CNS depression
  • Respiratory depression
  • GABAa R agonist–increases the duration of channel opening
  • preferred for thiopental for short ambulatory procedures due to its rapid elimination
  • induces CYP450 enzymes
60
Q

Benzodiazepines–common agents? MOA? antagonist? Used for?

A
  • diazepam, lorazepam, midazolam
  • GABAa Rec agonist–increases R sensitivity to GABA
  • used in perioperative period–anxiolytic properties and produces anterograde amnesia
  • antagonist–flumazenil
  • Midazolam–drug of choice for parenteral administration–frequently administer IV before patients enter operating room because rapid onset, shorter elimination half life
  • potent anticonvulsant properties

NS2 Test 3 (14 decks)

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