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Neuro exam 2 > Aesthetics 2 > Flashcards

Aesthetics 2 Flashcards

1
Q

Nitrous Oxide (N2O)

A 
• Potent analgesic
• Weak anesthetic
• “Balanced
Anesthesia”
• Rapid
induction/recovery
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2
Q

Nitrous Oxide: Cardiovascular

effects

A

Little effect on CV system
↓’s circulatory effects of halogenated anesthetics
Potentiates circulatory depression of narcotics/opioids

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3
Q

Nitrous Oxide: Respiratory

effects

A

Does not ↓ respiration alone
Enhances respiratory depression of other agents
At least 30% O2 should be used with N2O (limited to
70%; usually less due to other agents)
Can increase volume or pressure within closed body
compartments (N2O replaces N2; occluded middle ear,
pneumothorax, gut, lung)
Can ↓ O2 uptake during recovery → hypoxia

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4
Q

Nitrous Oxide: Other effects

A

Little hepatotoxicity; oxidizes cobalt of vitamin B12 → inhibits
methylation of macromolecules → chronic exposure can
cause megaloblastic anemia

“DOES NOT CAUSE MALIGNANT HYPERTHERMIA”

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5
Q

Second Gas Effect

A

• A rapidly absorbed gas INCREASES the
rate of uptake of a 2nd anesthetic gas
• Concentration of gas 1 is high
• As this volume of gas disappears from the
lung, fresh gases are literally sucked into
the lung from the breathing circuit to
replace the volume taken up.
• Rate of uptake of gas 2 is therefore higher

Nitric Oxide often used

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6
Q

Elimination of Inhalation

Anesthetics

A

• Major route: lungs
• Metabolism in liver → release of halide ions
• Halide ions can cause toxicity (hepatic/renal)
• Anesthetics with low blood solubility are
eliminated at a faster rate than those with high
blood solubilities

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7
Q

Intravenous Anesthetic Agents

A 
• Used for rapid induction of anesthesia which is then
maintained with inhalation agent
• Preanesthetic sedation
• Induction
• Perioperative analgesia
• Anesthesia for minor procedures
• Agents used include:
– Others
– Barbiturates
– Benzodiazepines
– Opioids
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8
Q

Propofol (Diprivan)

A 
– For induction and maintenance
• 2-8 min for distribution
• 30-60 min for elimination
– Less hangover, more rapid recovery
– Cardiovascular and respiratory depression
– Not analgesic
– Amnesia “milk of amnesia”
– Used for same day surgical procedures
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9
Q

Propofol: Mechanism

A

may potentiate GABA signaling

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10
Q

Propofol: effects

A 
Cardiovascular
effects
hypotension; approximately one-third of patients become
hypotensive following a bolus dose.
More pronounced in elderly
bradycardia, arrhythmias

Respiratory
effects
Respiratory depressant (can induce apnea)
respiratory acidosis

CNS effects
Decreases CBF and ICP
Minor neuroexcitatory effects

Other Antiemetic activity

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11
Q

Propofol: Other

A

• Propofol-related infusion syndrome (PRIS) is a serious side
effect with a high mortality rate characterized by
dysrhythmia (eg, bradycardia or tachycardia), heart failure,
hyperkalemia, lipemia, metabolic acidosis, and/or
rhabdomyolysis or myoglobinuria with subsequent renal
failure.
• Concomitant Opiate use may lead to increased sedative or
anesthetic effects of propofol, more pronounced decreases
in systolic, diastolic, and mean arterial pressures and
cardiac output. Lower doses of propofol may be needed. In
addition, fentanyl may cause serious bradycardia when
used with propofol in pediatric patients.
• Alfentanil use with propofol has precipitated seizure activity
in patients without any history of epilepsy.

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12
Q

• Etomidate

A

– Non-barbiturate for induction
– Minimal cardiovascular effects
– Decrease cerebrovascular blood flow to brain
– Advantage for brain/neural type surgeries
– Not analgesic
– Post-op nausea and vomiting

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13
Q

Barbiturates

A

• Examples: Thiopental, methohexital, thiamyl
• Ultra-short acting
• Used for induction
• Used for sedation
• Recovery from thiopental is due to redistribution
from the brain into less vascular regions (muscle,
skin)
• No antagonist in case of overdose

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14
Q

Barbiturates: SE and Contra

A 
• May cause a transient rise in BP
• Thiopental may result in hypotension, circulatory
collapse and cardiac arrest in cases of
hypovolemia, circulatory instability, sepsis,
toxemia or shock
• Barbiturates can depress respiration
• Contraindicated:
– Variegate porphyria
– Acute intermittent porphyria
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15
Q

Benzodiazepines (BDZs)

A 
• CNS depressants
• Examples: Diazepam,
lorazepam, midazolam
• Anxiolytic
• Amnesiac
• Sedative
• Antiepileptic
May depress respiration
Increase frequency of
channel opening
BDZ Antagonist: Flumazenil
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16
Q

Opioids

A

• Fentanyl, Morphine, Sulfentanil
• Used to induce analgesia
• Used in cardiac surgery as cardiac output and
myocardial contractility are preserved
• Can cause: Hypotension, respiratory depression,
muscle rigidity, postanesthetic nausea/vomiting
• Remember potential for interaction with propofol
or gaseous anesthetics mentioned earlier
• Opioid antagonist i.v. naloxone

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17
Q

Anticholinergics

A

• Used to combat secretions
• Used to prevent vagal effects
• Atropine, scopolamine, glycopyrrolate
• Scopolamine is more effective at preventing
salivation than atropine
• Scopolamine is less effective than atropine at
preventing reflex bradycardia

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18
Q

Anticholinergics: Glycopyrrolate

A 
Long acting
Less sedating than scopolamine
Better antisialogogue than atropine
Produces less tachycardia
More effective in preventing
bradycardia
Does not cross BBB
Causes peripheral effects
19
Q

Dissociative Anesthesia

A

• mental state where individual appears to be dissociated
from environment without complete loss of
consciousness

20
Q

Ketamine:

A

• chemically/pharmacologically related to phencyclidine
(PCP)
• Mechanism: Block NMDA receptor
• Induction agent / Dissociative anesthesia
• Profound Analgesia
• Recovery:
– delirium, hallucinations, irrational behaviour can
occur in adults; less likely to occur in children

21
Q

Stages of Anesthesia 1, 2

A

• Stage I: Analgesia
– Patient is conscious and conversational
• Stage II: Excitement
– Patient experiences delirium and violent,
combative behavior
– Increase in blood pressure
– Tachycardia
– Increase in respiration
– Mydriasis
– Increase in skeletal muscle tone; urinary and
or fecal incontinence

22
Q

Stage II: Excitement

A

NOTE: Goal of anesthesiologist is to keep the
duration and intensity of this stage to a minimum
Short acting barbiturate given IV before inhalation
anesthesia to avoid Stage II

23
Q

Stages of Anesthesia: 3, 4

A 
Stage III: Surgical anesthesia
– Regular respiration: Eye movements cease,
become fixed:
– Relaxation of skeletal muscle:
–Stage IV: Medullary paralysis
– Severe depression of respiratory and
vasomotor centers
– Death
24
Q

Local Anesthetics

A

Goal: To create loss of sensation without
loss of consciousness or impairment of
central control of vital functions

25
Q

Local Anesthetics: Ester type drugs

A

Benzocaine
Chloroprocaine
Cocaine
Procaine

26
Q

Local Anesthetics: Amide type drugs

A 
Bupivacaine
Etidocaine
Lidocaine
Mepivacaine
Prilocaine
Ropivacaine
27
Q

Local Anesthetic-Structure

A

Amine, weak base
Ionized form predominates at low pH
Inflammation/acidosis decrease tissue pH

28
Q

Local Anesthetic Mechanism of Action

A 
• Reversible inhibition of axonal
nerve conduction by binding to
Na+ channel
• Bind on internal site of Na+
channel
• Ionized anesthetic has more
affinity for channel
• Prolongs inactivation state of
channel
• Once bound, drugs greatly
restrict conformational
changes that underlie
activation
Small, unmyelinated fibers more easily
anesthetized: autonomic and sensory
nerves blocked easier than motor
neurons:
– Pain
– Temperature
– Touch
– Sympathetic vasomotor activity inhibited
before proprioception
– Muscle tone
– Somatic motor activity
– Nerves recover in reverse order
29
Q

Local Anesthetic: Chemistry/Pharmacokinetics

A 
• Duration of action
– Determined by rate of diffusion/absorption
(determined by chemical properties, local pH,
blood flow)
• Metabolism
– Ester type drugs: Esterases, plasma
cholinesterases
– Amide type drugs: Amidases, liver
– Urinary excretion of metabolites
30
Q

Local Anesthetic: AE

A

• If absorbed into systemic circulation, local
anesthetics can have:
– CNS effects
• CNS stimulation (restlessness, tremor, euphoria, clonic
convulsions) [inhibition of inhibitory neurons] followed by CNS
inhibition (sedation, drowsiness)
• Headache, paresthesias, nausea, seizures followed by coma
• Death occurs by respiratory failure
– CV effects
• Hypotension
• Cardiac depression
– Hypersensitivity reactions
• Allergic dermatitis or asthmatic attack
• Usually due to ester anesthetics due to metabolism to PABA
(allergic)

31
Q

Local Anesthetic: Vasoconstrictors

A

• Vasoconstrictors prolong effects of local anesthetics
• Epinephrine, phenylephrine
• Slows rate of absorption; decreases drug plasma concentration
• Less likelihood of side effects
• Should not be used in anesthetizing tissues with end arteries
(fingers, toes, ears, nose, penis). Sympathomimetic amines
increase oxygen consumption of tissue-coupled with
vasoconstriction-hypoxia results-potential tissue damage.
Gangrene could occur.
• Should not be used in patients in whom adrenergic stimulation may
have an adverse effect (hypertensive, ventricular arrhythmias)

32
Q

Local Anesthetic: Indications: Topical Anesthesia

A

Topical Anesthesia
– Skin (Benzocaine)
– Mucous membranes, cornea (Tetracaine,
lidocaine, cocaine)
– Epinephrine – no significant local effect; can’t
penetrate mucous membranes
Mixtures of Anesthetics:
– LET: Lidocaine, Epinephrine, Tetracaine
– EMLA: Eutectic mixture of lidocaine and others

33
Q

Local Anesthetic: Indications: Infiltration Anesthesia

A

– Anesthetic injected directly into tissues
– Dental procedures, minor surgical procedures
– Epinephrine doubles duration of anesthesia
– Disadvantage: Large amounts of drug used to
anesthetize small areas

34
Q

Local Anesthetic: Indications: • Iontophoresis

A

– Small electrical current forces anesthetic into a
tissue
– Used in dentistry

35
Q

Field Block Anesthesia

A 
• Administered in a series of injections to
form a wall of anesthesia encircling
operative field
• Advantage:
Less drug
for greater area of
anesthesia than
infiltration
36
Q

Nerve Block Anesthesia

A

• Injected into or adjacent to a nerve or nerve
plexus
• Example: (Brachial plexus – upper extremity;
Intercostals – anterior abdominal wall; Cervical
plexus – neck)
• Produces large area of anesthesia with small
amount of drug; even better than field block or
infiltration

37
Q

Spinal Anesthesia

A 
• Injection into lumbar
subarachnoid space below
the level at which the cord
terminates
• Spread of anesthetic in CSF
controlled by horizontal tilt of
patient and specific gravity of
anesthetic. Hyperbaric
solutions used (density >
CSF)
• Can be used for people
contraindicated for general,
for lower body (knee etc)
surgery
38
Q

Epidural Anesthesia

A 
• Injection into lumbar or
caudal epidural space
• Bupivacaine used for
labor/delivery
• Absorbed into systemic
circulation; has to be
monitored closely to
prevent cardiac depression
and neurotoxicity in
mother/neonate
39
Q

Cocaine

A

• Ester type local anesthetic
• Only local anesthetic that causes vasoconstriction
• Controlled substance; subject to abuse
• Used topically to anesthetize the internal structures of
the nose, ear, throat

40
Q

Procaine (Novacain)

A
  • 1st synthetic local anesthetic - Ester
  • Short duration (20-45 min)
  • Parenteral administration
  • Metabolized to PABA
41
Q

Benzocaine (Americaine)

A 
• Ester
• Pruritus
• Eardrops
• Teething/gum pain
• Supplied as lozenges for
pharyngitis
• Treatment of sunburn
42
Q

Lidocaine (Xylocaine)

A

• Amide
– Metabolized in liver
– Monoethylglycinexylidide & glycinexylidine
• Topical/parenteral administration
• Infiltration, nerve block, epidural, spinal
anesthesia
• Intermediate duration (60-120 min)

43
Q

Prilocaine (Citanest)

A 
• Lidocaine congener
• Metabolized to O-toluidine
Can cause methemoglobinemia
• Limited to topical/infiltration anesthesia
• Half life > Lidocaine
44
Q

Bupivacaine (Marcaine)

A

• Obstetrical anesthesia
• Cardiotoxic
– Decreases threshold for tachycardia
• Half life ~ 300 minutes

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