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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
what organs have higher immediate concentration of anesthetics
- brain, heart, liver, kidneys, splanchnic bed | - highly perfused (receive 75% of resting CO)
26
what tissues do anesthetics accumulate more slowly of anesthetics
- muscle and skin | - only recieve 1/5 of resting CO
27
major route of elimination from body of inhaled anesthetics
lungs
28
insoluble in blood and brain--rate of elimination?
faster
29
minimal alveolar concentration (MAC)--what is it?
-concentration of inhalation anesthetics that prevents movement in response to surgical stimulation in 50% of subjects (measures potency)
30
a dose of 1 MAC does what?
-prevents movement in response to surgical incision in 50% of patients
31
MAC values greater than 100%
-other agents must be supplemented to achieve surgical anesthesia (NO)
32
4 stages of increasing depth of CNS depression
- 1-stage of analgesia - 2-stage of excitement - 3-stage of surgical anesthesia - 4-stage of medullary depression
33
stage 1
(analgesia) - analgesia without amnesia - with amnesia at end of stage
34
stage 2
(excitement) - delirious - respiration is irregular - retching and vomiting may occur if patient is stimulated - regular breathing is established at end of stage
35
stage 3
(surgical anesthesia) | -begins with regular breathing; extends to complete cessation of spontaneous respiration
36
stage 4
(medullary depression) | -severe depression of vasomotor depression center in medulla and respiratory center
37
inhaled volatile anesthetics--effects on CV system
-decrease mean arterial pressure in direct proportion to their alveolar concentration
38
Heart rate effects?
- Halothane--causes bradycardia | - Desflurane and isoflurane--increases HR
39
Respiratory effects?
- respiratory depressants | - depression of mucociliary function in airway--can result in pooling of mucus and postoperative respiratory infections
40
May cause hepatitis
-halothane (2 days to 3 weeks after exposure)
41
May cause renal toxicity
- agents metabolized to products including fluoride ions | - enflurane, sevoflurane
42
may cause malignant hyperthermia; antidote??
- inhaled volatile anesthetics in combination with succinylcholine - antidote=dantrolene
43
IV anesthetics are?
- highly lipophilic - go into highly perfused lipophilic tissues (brain, spinal cord) - quick onset of action
44
Most commonly used as parenteral anesthetic
propofol
45
Propofol--MOA, characteristics, metabolized
- 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
context--sensitivity half life | contact sensitivity half life--drugs that increase dramatically and drugs that increase modestly
-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
propofol CNS effects
- 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
Propofol CV effects
- produces the decrease in systemic blood pressure due to vasodilation (most pronounced compared with other agents) - hypotensive effects--inhibits normal baroreflex response
49
propofol respiratory effects
- 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
Fospropofol--what is it? Effects?
- 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
Etomidate--effects? MOA?
- 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
Etomidate--CNS, CV, Resp, endocrine effects?
- 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
Ketamine--effects? MOA?
- NMDA Receptor Antagonist - dissociative anesthetic state--catatonia, amnesia, analgesia, with or without loss of consciousness - lacrimation and salivation increase upon administration
54
Ketamine--CNS, CV effects?
- 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
Ketamine--only IV anesthetic to produce?
-analgesia, stimulation of SNS, bronchodilation, minimal respiratory depression
56
Dexmedetomidine--MOA? effect? used for?
- 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
Anesthetic Adjuncts--used to?
-augment components of anesthesia, permitting lower doses of general anesthetics with fewer side effects
58
opioid analgesics--used with? MOA? common agents? Adjunct to?
- -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
Barbituates--common agents? MOA? effects? used for?
- 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
Benzodiazepines--common agents? MOA? antagonist? Used for?
- 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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