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Neuro 2 Exam 2 > Anesthetics (Waller) > Flashcards

Anesthetics (Waller) Flashcards

1
Q

Inhaled Anesthetics

drug list

A 
Volatile Anesthetics:
Desflurane
Enflurane
Halothane
Isoflurane
Sevoflurane

Gaseous Anesthetics:
Nitrous oxide

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2
Q

Intravenous Anesthetics drug list

A 
Propofol (Diprivan)
Fospropofol
Barbiturates (thiopental, methohexital)
Benzodiazepines (midazolam, lorazepam, diazepam)
Etomidate
Ketamine
Dexmedetomidine (Precedex)
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3
Q

Drug List – Local Anesthetics

A 
Esters
Benzocaine
Cocaine
Procaine (Novocain)
Tetracaine
Amides
Articaine
Bupivacaine
Lidocaine (Xylocaine)
Mepivacaine (Marcaine)
Ropivacaine
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4
Q

General Anesthesia

A

Anesthesia – loss of “awareness”
Goal – maintenance of physiologic homeostasis

Five Primary Effects:
Unconsciousness–> complete or partial unawareness
Amnesia
Analgesia
Inhibition of autonomic reflexes
Skeletal muscle relaxation–> neuromuscular blockade

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5
Q

Balanced Anesthesia

A

Minor Superficial Surgery or Invasive Diagnostic Procedures

  • Sedative (PO or IV) + local anesthetic
  • Profound analgesia with retention of patent airway

Extensive Surgical Procedures
- Preoperative sedative + anesthesia induction (IV) + maintenance with combination inhaled or intravenous drugs

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6
Q

General Anesthetic Action

A

Neuron Level:
Presynaptic- Alter release of neurotransmitters

Postsynaptic- Change frequency or amplitude of impulse exiting the synapse

Organ Level:
Strengthen inhibition or diminish excitation within the CNS

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7
Q

Inhaled Anesthetics

A

Agents:
Volatile – halothane, enflurane, isoflurane, desflurane, sevoflurane
Gaseous – nitrous oxide

Important PK Determinants:

  • Uptake – gas exchange in alveoli
  • Distribution/partitioning into effect compartment

Alveolar Concentration –> Solubility –> Cardiac Output –> Alveolar-Venous Partial Pressure –> Elimination

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8
Q

Alveolar Concentration

A

–> Solubility –> Cardiac Output –> Alveolar-Venous Partial Pressure –> Elimination

Factors Determining Change in Alveolar Concentration:

  1. Inspired concentration or partial pressure
    - Partial pressure expressed as ratio: FA/FI
    - – FA - alveolar concentration
    - – FI - inspired air concentration
    - The faster FA/FI approaches 1, faster anesthesia will occur
  2. Alveolar ventilation
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9
Q

Solubility

A

Blood:Gas Partition Coefficient
Describes relative affinity for blood compared to inspired gas
Inverse relationship between partition coefficient value & rate of anesthesia onset

Low blood solubility (nitrous oxide, desflurane) = fast onset of action. Blood:gas partition coefficient .47

High blood solubility (halothane) = slow onset of action- Blood: gas partition coefficient 2.3

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10
Q

Cardiac Output–> Alveolar-Venous partial Pressure

A 
Cardiac Output
↑ pulmonary blood flow
↑ uptake of anesthetic
↓ rate of FA/FI rise
↓ rate of induction

Alveolar-Venous Partial Pressure
Depends on tissue uptake
If venous blood contains significantly less anesthetic than arterial blood
Requires more time to equilibrium

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11
Q

Elimination

A

Recovery:

Follows same principles in reverse

If relatively insoluble in blood and brain –> eliminated faster

Time to recovery depends on elimination from brain

Remember factors controlling speed of induction?

  • Inspired concentration or partial pressure
  • Alveolar ventilation

Duration of exposure may also impact recovery

Lungs – major route of elimination
- Extent of hepatic metabolism: halothane > enflurane > sevoflurane > isoflurane > desflurane > nitrous oxide (none)

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12
Q

Inhaled anesthetics: Pharmacodynamics – Organ System Effects: CNS

A

Minimum alveolar concentration
Describes anesthetic potency
1.0 MAC = partial pressure of inhaled anesthetic, 50% of population remain immobile at skin incision
Value expressed as volume %
Successful anesthesia = 0.5 – 2 MAC
MAC is additive: 0.5 MAC of x + 0.5 MAC of y = 1 MAC

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13
Q

Nitrous oxide: MAC

A

> 100%

so even if 100% of the air were NO, would not immobilize half the population

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14
Q

Central Nervous System

Anesthesia Stages

A

Stage I Analgesia
- Analgesia without amnesia; later will experience both

Stage II Excitement
- Delirious, completely amnesic; rapid respirations; HR and BP increase

Stage III Surgical Anesthesia
- Slowing RR and HR, extends to apnea; four planes described

Stage IV Medullary Depression
- Requires circulatory and respiratory support

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15
Q

Toxicity of inhaled anesthetics

A

Nausea & vomiting
Halothane – hepatitis (1:20,000-35,000)
Renal toxicity – fluoride ions
Malignant hyperthermia

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16
Q

Propofol

A

MOA:
Potentiation of Cl- current mediated through GABAA receptor complex

PK:
Poorly soluble in water; formulated as a lipid emulsion
Rapidly metabolized (liver), excreted through kidneys
Fast onset, fast clearance
Brief context-sensitive half-time

Organ System Effects:
CNS – no analgesia; EEG burst suppression
CV – hypotension
Respiratory – depressant (apnea)

17
Q

Barbiturates

A

Agents: thiopental, methohexital

MOA:
Act on GABAA receptor to increase duration of channel opening

PK:
Highly lipophilic; hepatic metabolism

Organ System Effects:
- CNS – sedation; no analgesia
Decrease electrical activity on EEG (exception methohexital)
- Respiratory – depressant (apnea)

18
Q

Benzodiazepines

A

Agents: midazolam, lorazepam, diazepam

MOA:
- Act on the GABAA receptor, increase receptor sensitivity to GABA (agonist), enhance inhibitory neurotransmission

PK:

  • Highly lipid soluble; rapid onset of action
  • Midazolam shortest context-sensitive half-time

Organ System Effects:

  • CNS – potent anticonvulsants
  • Respiratory – depression may occur when given with opioids
19
Q

Etomidate

A

MOA:
GABA like effects, potentiation of GABAA mediated Cl- currents

PK:
Minimal effect on hemodynamics + short context-sensitive half-time = may give larger doses and repeat boluses

Organ System Effects:

  • CNS – cerebral vasoconstrictor
  • CV – minimal impact on hemodynamics
  • Endocrine – adrenocortical suppression
20
Q

Ketamine

A

MOA:
Inhibits NMDA receptor complex

PK:

  • High lipid solubility; fast onset of action
  • Similar in structure to phencyclidine (PCP)

Organ System Effects:
CNS – profound analgesia; cerebral vasodilator
** Emergence reactions; dissociative anesthesia
CV – *increase systemic BP, HR, CO; however, is a direct myocardial depressant

21
Q

Dexmedetomidine

A

MOA:
Highly selective α2-adrenergic agonist

PK:
Water soluble; rapid hepatic elimination; high clearance
Short half-time; however, significantly prolonged after longer infusion times

Organ System Effects:
CNS – hypnosis, analgesia, activates endogenous sleep pathways
CV – decrease in HR and SVR

good way to transition off of mechanical ventilation

22
Q

Local Anesthetics

A

Administration – drug is delivered directly to target organ
- Loss of sensation in limited region of the body

Disrupts afferent neural traffic
- May also cause muscle paralysis and suppression of somatic or visceral reflexes

23
Q

Local anesthetics - Basic Pharmacology

A 
Structure:
Lipophilic group (e.g., aromatic ring) + intermediate chain via an ester or amide + ionizable group (e.g., tertiary amine)

PK:
Those agents that are more lipid soluble = generally more potent, longer duration of action, take longer to achieve clinical effect
Metabolized in liver (amides) or plasma (esters)
Excreted in urine

24
Q

Neuronal Factors Affecting Anesthetic Block

A

Differential Block
- Block all nerve actions (not just loss of sensation)

Intrinsic Susceptibility of Nerve Fibers
Fiber diameter
-- Block smaller diameters first?
-- Variable portion of large fibers 
-- Myelinated fibers blocked faster than unmyelinated

Firing frequency
– More significant at high firing frequency

Anatomic arrangement
– Anesthetize from proximal to distal

25
Q

Routes of Administration

(anesthetics)

A

Topical: nasal mucosa, wound (incision site) margins
Injection:
Peripheral nerve endings (perineural infiltration) & major nerve trunks (blocks)
Epidural or subarachnoid spaces surrounding the spinal cord

26
Q

Orderly evolution of anesthetic block:

A 
Sympathetic transmission
Temperature
Pain
Light touch
Motor block
27
Q

anesthetic Toxicity

A

Systemic Effects
Inadvertent intravascular injection or absorption from site of administration
- CNS – sedation, light headedness, visual and auditory disturbances, restlessness
- CV – arrhythmia and cardiac arrest

Neurotoxicity
- Local effects by direct contact with neural elements

28
Q

A 21 y/o male is scheduled to undergo a laparoscopic hernia repair on an outpatient basis under general anesthesia. This is the first time he has undergone surgery and he is highly anxious in the preoperative area. Which benzodiazepine may be utilized in this situation to reduce his anxiety?

Benzocaine
Fentanyl
Midazolam
Propofol
Thiopental
A

Midazolam

29
Q

A 19 y/o female is admitted to the ambulatory surgery center for strabismus surgery to correct misalignment of her extraocular muscles. She is otherwise healthy and all laboratory values are within normal limits. Which intravenous induction agent may be used that is rapid in both onset and recovery and has antiemetic actions?

Halothane
Nitrous oxide
Procaine
Propofol
Sevoflurane
A

Propofol

30
Q

The chemical with which blood:gas partition coefficient will reach the highest concentration in the brain the fastest (assume brain:blood partition coefficients are equal)?

  1. 42
  2. 47
  3. 69
  4. 4
  5. 8
A

least soluble is best.

A: .42

31
Q

The anesthesiologist prepares to administer several drugs to a patient as part of normal perioperative care. Which drug lacks the ability to cause generalized CNS depression, lacks the ability to reduce or impair the patient’s level of consciousness, or lacks the ability to prevent or reduce pain?

Midazolam
Pancuronium
Propofol
Thiopental

A

Pancuronium

neuromuscular blockade

32
Q

Nitrous oxide is a common component in the technique of balanced anesthesia. It is used in conjunction with a volatile anesthetic. Which phrase best summarizes why nitrous oxide cannot be used alone for general anesthesia?

Almost total lack of analgesic activity, regardless of concentration
Great solubility in blood, effects take an extraordinarily long time to develop
Inspired conc. > 10% tend to have profound, negative cardiac inotropic effects
MAC (minimum alveolar concentration) is greater than 100%
Very high frequency of bronchospasm

A

MAC (minimum alveolar concentration) is greater than 100%

Neuro 2 Exam 2 (19 decks)

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