Monday, 8-22-General Anesthetics-DSA-Kruse Flashcards

1
Q

__ and ___ in conscious sedation protocols have the advantage of being reversible by the specific receptor antagonist drugs (flumazenil and naloxone, respectively)

A

Benzodiazepines and opioid analgesics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

IV agents used in deep sedation protocols mainly include the sedative-hypnotics __ and __, sometimes in combo with potent __, depending on the level of pain associated with the surgery or procedure

A

Propofol and midazolam

Opioid analgesics or ketamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

These channels remain the primary inhibitory ion channels considered legitimate candidates of anesthetic action

A

Cl channels (GABAa and Glycine receptors) and K channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are some of the excitatory ion channel targets of general anesthetics?

A

Those activated by Ach (nAChRs and mAChRs), by EAAs (AMPA), kainite, and NMDA receptors, or by 5-HT receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Halothane, enflurane, isoflurane, desflurane, and sevoflurane are examples of these anesthetics

A

Volatile inhaled

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

NO is an example of this type of anesthetic

A

Gaseous inhaled

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

The driving force for uptake of an inhaled anesthetic is the __

A

Alveolar concentration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe the FA/F1 ratio and speed of inhaled anesthesia induction

A

The faster FA/F1 approaches 1, the faster anesthesia will occur during an inhaled induction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Agents with __ blood solubility (NO, desflurane), reach high arterial pressure rapidly, which in turn results in rapid equilibration with the brain and fast onset of action

A

Low

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Agents with __ blood solubility (halothane) reach high arterial pressures slowly, which in turn results in slow equilibration with the brain and a slow onset of action

A

High

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe the onset and recovery with inhaled NO

A

Rapid onset and recovery; incomplete anesthetic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe the volatility and recovery from inhaled desflurane

A

Low volatility; poor induction agent; rapid recovery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe the onset and recovery from inhaled sevoflurane

A

Rapid onset and recovery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe the onset and recovery with inhaled isoflurane, enflurane, and halothane

A

Medium rate of onset and recovery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

These tissues are highly perfused and receive over 75% of the resting CO, and as a result have higher immediate concentrations of anesthetic

A

Brain, heart, liver, kidneys, and splanchnic bed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Inhaled anesthetics that are relatively insoluble in the blood and brain are eliminated at __ rates compared to more soluble anesthetics

A

Faster

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Clearance of inhaled anesthetics via ___ is the major route of eliminate from the body

A

The lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Although recovery may be rapid with more soluble agents following a short period of exposure, recovery is slow after prolonged administration of ___

A

Halothane or isoflurane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

In regards to the stages of increasing depth of CNS depression, this stage is described by the pt experiencing analgesia without amnesia. Both analgesia and amnesia are produced at the end of this stage

A

Stage 1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

In regards to the stages of increasing depth of CNS depression, this stage is described by the pt appearing delirious. Respiration is irregular in both volume and rate, retching and vomiting may occur if pt is stimulated, and regular breathing is established at the end of this stage

A

Stage 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

In regards to the stages of increasing depth of CNS depression, this stage is described by beginning with regular breathing and extending to complete cessation of spontaneous respiration (apnea)

A

Stage 3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

In regards to the stages of increasing depth of CNS depression, this stage is described by including severe depression of the vasomotor center in the medulla as well as the resp center

A

Stage 4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

In regards to the effects of inhaled volatile liquid anesthetics on the CV system:

___ can cause bradycardia

___ increase heart rate

A

Halothane

Desflurane and isoflurane

24
Q

Depression of mucociliary function in the airway due to volatile anesthetics can result in ___

A

Pooling of mucus and post-op resp infx

25
Q

What are some common side effects of inhaled anesthetics?

A

Common-nausea and vomiting

26
Q

__ may cause hepatitis with or without previous exposure and develops 2-3 weeks after exposure

A

Halothane

Symptoms –> anorexia, nausea, myalgias, arthalgias, and rash, eosinophilia, hepatomegaly, and jaundice

27
Q

Agents metabolized to products including fluoride ions (enflurance and sevoflurane) may cause ___

A

Renal toxicity

28
Q

In combo with ___, inhaled volatile anesthetics may cause malignant hyperthermia, which consists of rapid onset tachycardia and HTN, severe muscle rigidity, rhabdomyolysis, hyperthermia, hyperK, and acid-base imbalance with acidosis. What is the antidote to this?

A

Succinylcholine

Dantrolene is the antidote

29
Q

__ are widely used to facilitate rapid induction of anesthesia and have replaced inhalation as the preferred method of anesthesia induction in most settings

A

Nonopioid IV anesthetics

30
Q

__ anesthetics are highly lipophilic and preferentially partition into highly perfused lipophilic tissues (brain and SC), which accounts for their quick onset of action

A

IV

31
Q

__ is the most commonly used parenteral anesthetic in the US. Its PK properties allow for continuous infusions and maintenance of anesthesia, sedation in the ICU, conscious sedation and short-duration general anesthesia in locations outside the OR

A

Propofol

32
Q

What is the MOA of Propofol?

A

Most likely targets GABAa receptors as an agonist and potentiates the Cl current

33
Q

Describe the pharmacokinetics of propofol:

A
  • Rapidly metabolized in the liver
  • Low hangover effect (high plasma clearance)
  • rapid rate of onset, rapid recovery, pts can ambulate quickly after use
  • time of onset is 15-30 secs
34
Q

Describe some CNS effects with propofol

A
  • no analgesic properties
  • decreases cerebral blood flow which decreases ICP and intraocular pressure
  • burst suppression in EEG when administered in large doses –> neuroprotective effect during neurosurg procedures
35
Q

Describe CV effects with propofol:

A

Pronounced decrease in systemic BP due to profound vasodilation

Hypotensive effects augmented by inhibition of normal baroreflex response

36
Q

List respiratory effects of propofol

A
  • potent resp depressant

- greater reduction in upper airway reflexes than thiopental does

37
Q

__ is a water-soluble prodrug of propofol that is rapidly metabolized by alkaline phosphatase. Its onset and recovery are prolonged (compared to propofol) because the prodrug must first be converted into an active form

A

Fospropofol

38
Q

What are some common adverse effects with administration of Fospropofol?

A

Common adverse effect is the experience of parasthesias and pruritis are mostly limited to the first 5 minutes of admin and usually described as mild-moderate in intensity (unknown mechanism)

39
Q

__ has hypnotic but no analgesic effects. Its MOA enhances the actions of GABA on GABAa receptors. It causes minimal CV and resp depression and useful in pts with impaired CV and pulm systems. It produces rapid loss of consciousness and less rapid recovery rate compared to propofol. It is extensively metabolized by the liver and in the plasma

A

Etomidate

40
Q

What are CNS effects of Etomidate?

A

Potent cerebral vasoconstrictor; decreases cerebral blood flow and ICP

41
Q

What are some CV effects of Etomidate?

A

CV stability is maintained even after bolus injection; minimal change in HR and CO

42
Q

What are endocrine effects with Etomidate?

A
  • causes adrenocortical suppression by producing a dose dependent inhibition of 11 B-hydroxylase
  • suppression lasts 4-8 hrs after induction dose
  • endocrine adverse effects limit use for continuous infusion
43
Q

___ is an NMDA receptor antagonist and produces a dissociative anesthetic state characterized by catatonia, amnesia, and analgesia with or without loss of consciousness (pts eyes remain open with a slow nystagmic gaze). Similar in structure to PCP

A

Ketamine

Lacrimation and salivation are increased upon administration and premedication with an anticholinergic may be indicated

44
Q

What is a CNS contraindication for ketamine?

A

Not recommended for use in pts with intracranial pathology, especially increased ICP

Ketamine increases cerebral blood flow as well as CMRO2

45
Q

___ is an a-2 adrenergic agonist that produces hypnosis presumably from stimulation of a-2 receptors in the locus ceruleus and analgesic effects at the level of the SC. Its sedative effect more completely resembles a physiologic sleep state through activation of endogenous sleep pathways

A

Dexmedetomidine

46
Q

___ is principally used for short-term sedation of intubated and ventilated pts in an ICU setting or as an adjunct to general anesthesia

A

Dexmedetomidine

47
Q

What are some common opioid analgesics? What are their MOA?

A

Fentanyl, sufentanil, remifentanil, and morphine

MOA: agonists at opioid receptors

48
Q

List some barbiturate anesthetic adjuncts:

A

Thiopental (prototype) and Methohexital

49
Q

__ are anesthetic adjuncts that are highly lipophilic and quick plasma:brain equilibrium. It causes dose-dependent CNS depression ranging from sedation to general anesthesia (no analgesia) and causes respiratory depression

A

Barbiturates

50
Q

What is the MOA of barbiturates?

A

Acts on the GABAa receptor to increase duration of channel opening (agonist) and enhances inhibitory neurotransmission

51
Q

This barbiturate may be preferred over thiopental for short ambulatory procedures due to is rapid elimination

A

Methohexital

52
Q

List some common benzodiazepine anesthetic adjuncts

A

Diazepam, lorazepam, and midazolam

53
Q

This anesthetic adjunct is commonly used in the perioperative period because of their anxiolytic properties and ability to produce anterograde amnesia; actions can be terminated by the antagonist flumazenil

A

Benzodiazepines

54
Q

This benzodiazepine anesthetic adjunct is frequently administered IV before pts enter the OR because it has a more rapid onset, shorter elimination 1/2 life (2-4 hrs), and steeper dose-response curve than other benzodiazepines

A

Midazolam

55
Q

This anesthetic adjunct has potent anticonvulsant properties; used in tx of status epilepticus, alcohol withdrawal, and local anesthetic-induced seizures

A

Benzodiazepines

56
Q

Monitored anesthesia care is performed without general anesthesia. It typically involves the use of __ for premedication (to provide anxiolysis, amnesia, and mild sedation), followed by a __ infusion (to provide moderate to deep levels of sedation). A potent ___ may be added to minimize the discomfort associated with the injection of local anesthesia and surgical manipulations

A

Midazolam

Titrated propofol

Opiod analgesic or ketamine