Anesthetics part1 Flashcards
1
Q
Anesthetic agent:
A
any drug used to induce a
loss of sensation with or without
unconsciousness
2
Q
Adjunct
A
a drug that is not a true anesthetic,
but that is used during anesthesia to produce
other desired effects such as sedation, muscle
relaxation, analgesia, reversal, neuromuscular
blockade, or parasympathetic blockade
3
Q
Four (4) Classifications of Anesthetic
Agents
and Adjuncts
A
route of admin. , time of admin, principal effect, chemistry
4
Q
route of admin. classification
A
Inhalant
Injectable
Oral
Topical
5
Q
time of admin classification
A
Preanesthetic
Induction
Maintenance
6
Q
principal effect classification
A
Local vs. general Sedatives and tranquilizers vs. analgesics Neuromuscular blockers Anticholinergic agents Reversal agents
7
Q
chemistry classification
A
(We won’t go into a lot of detail on
this)
*MANY anesthetic agents and adjuncts produce
more than one effec
8
Q
General Anesthesia
A
• Reversible • Produced by administration of one or more anesthetic drugs • Characteristics (4) 1) Unconsciousness (SPELL THIS CORRECTLY!) 2) Immobility 3) Muscle relaxation 4) Loss of sensation
9
Q
Surgical Anesthesia
A
• A stage of general anesthesia
• Analgesia and muscle relaxation
• Eliminate pain and patient movement
during the procedure
10
Q
sedation
A
– CNS depression – Drowsiness – Drug-induced – Various levels – Slightly aware or unaware of surroundings – Aroused by noxious stimulation – Uses: minor procedures
11
Q
tranquilization
A
– Calmness – Patient is reluctant to move – Aware of surroundings but doesn’t care
12
Q
hypnosis
A
– Drug-induced – Sleeplike state – Impairs patient’s ability to respond to stimuli – Patient can be aroused with sufficient stimulation
13
Q
narcosis
A
– Drug-induced sleep – Patient is not easily aroused – Associated with narcotic drugs
14
Q
Topical Anesthesia
A
Applied to body surfaces or a wound
Produces a superficial loss of sensation
15
Q
Regional Anesthesia
A
Loss of sensation to a limited area of the
body
Nerve blocks
epidural anesthesia
16
Q
Balanced Anesthesia
A
Using multiple drugs in smaller quantities
Maximizes benefits
Minimizes adverse effects
Gives anesthetist greater control
17
Q
Agonists
A
Bind to and stimulate target tissue
Most anesthetic agents and adjuncts
18
Q
Antagonists
A
Bind to target tissue but don’t stimulate
Reversal agents
19
Q
Partial Agonists and Agonist-Antagonists
A
Opioids
Partial agonists
Agonist-antagonists
Used to block pure agonists
20
Q
Analgesia
A
Most general anesthetics are not analgesics • Must provide analgesic pre- and postoperatively • No pain perception while anesthetized • True analgesics don’t provide general anesthesia!
21
Q
Drug Combinations
A
• Don’t mix drugs in a single syringe unless they are compatible • Don’t administer a drug combination if a precipitate (what’s this?) develops when the drugs are mixed • Most anesthetic agents and adjuncts are water soluble • Diazepam (Valium) is not water soluble!!
22
Q
opioids
A
Derivatives of opium
Produce analgesia and sedation
Anesthetic induction when combined with
other drugs
Classified as agonists, partial agonists,
agonist-antagonists, or antagonists
23
Q
opioids that are not controlled substances and how they are administered
A
antagonists and nalbuphine. Administered IV, IM, SC, oral, rectal,intranasal inhalant, transdermal,
subarachnoid, and epidural
Wide margin of safety
24
Q
Opioids—Pharmacodynamics
A
Mimic endogenous opioid peptides β-Endorphins, dynorphins, enkephalins (“Runner’s High”) Analgesia and sedative effects Result of action on the receptors in the brain and spinal cord
25
How opioids work:
```
They prevent nerves from
transmitting impulses.
They prevent presynaptic
release of neurotransmitters,
particularly excitatory afferent
neurotransmitters (?)
Decrease critter’s “perception”
of pain.
```
26
opioid agonist bind to and best for
mu and kappa receptors
| Best for moderate to severe pain
27
opioid agonist antagonist bind to and best for
delta, mu, and kappa receptors, but
typically stimulate only kappa receptors (Reversal
agent/mild pain)
28
opioid antagonist bind to
Bind to but don’t stimulate delta, mu and kappa
| receptors (reversal agents
29
Effects of Opioids
CNS
Effect depends on many factors
• Causes sedation
• Narcosis
• Euphoria .
Analgesia
30
•Pure opioid agonists are the
| BEST things
we have for
severe pain!
• Used as a premedication for painful surgery
31
Effects of Opioids on cardiovascular
Bradycardia except meperidine which has
| antimuscarinic effects that can produce tachycardia
32
effects of opioids on respiratory
Decreased rate and tidal volume (dose-related)
| Cough suppression (codeine {usually}, morphine)
33
opioids on eyes
miosis
34
Adverse Effects of Opioids GI system
Salivation and vomiting by stimulation of the
chemoreceptor trigger zone (CTZ)—(how could this
be beneficial?) it stimulates vomiting before intubation
Initial diarrhea, vomiting, and flatulence
GI stasis follows initial GI stimulation
35
opioids cause adverse urine
retention
36
affects of opioids on histamine
Histamine release
Allergic rxns are very common with morphine use.
Avoid in asthmatics.
*Increased intraocular and intracranial pressure
(so what?)
37
opioid cough suppresants
(codeine, dextromethorphan)
38
opioid pre anesthetics
Agonists, partial agonists, or agonist-antagonist
May be used alone or in combination with
• Tranquilizers
• Anticholinergics
39
opioid anlagesia
Prevent and treat postoperative pain
| Used with tranquilizer to produce neuroleptanalgesia
40
opioids used to induce Neuroleptanalgesia
– Morphine
– Buprenorphine
– Butorphanol
– Hydromorphone
41
tranquilizers used to induce Neuroleptanalgesia
– Diazepam
– Midazolam
– Thorazine
42
Neuroleptanalgesia definition
A profound state of sedation and analgesia
induced by simultaneous administration of
an opioid and a tranquilizer”
So it’s a state of “tranquil
dreaming”
43
Use of Opioids
Treatment of Acute Pulmonary Edema, as
in that seen with CHF. it does this by
Vasodilation
| Reduce anxiety of “drowning”
44
Opioid Antagonists
```
Reverse undesirable effects
– CNS and respiratory depression
• Wake up patient following sedation
• Emergencies
• Overdoses
• Naloxone (Narcan) hydrochloride
– IM or slow IV administration
• Naltrexone: Like Naloxone but longer-acting
and has the potential for liver toxicity
```
45
Naloxone Hydrochloride (Narcan). administration and doa
IM—5 minutes to reversal
IV (slowly)—2 minutes to reversal
Duration of action 30-60 minutes
46
naltrexone methylnaltrexone
revia, relistor. Longer duration of action than Narcan
Usually given orally (one dose of naltrexone lasts
24 hours)
Methylnaltrexone is a peripherally acting opioid
antagonist; theoretically shouldn’t reverse CNS pain
blockade…
…but recent evidence finds over half of opioid pain
relief is due to
PERIPHERAL
sensory neuron
blockade!
47
Effects of Opioid Antagonists
```
Reversal of effects of opioid
agonists, partial agonists, and
agonists-antagonists
Reversal can be complete in a
few minutes
Adverse effects are rare
Sudden analgesia loss can cause
excitement, anxiety, and
sympathetic nervous system
stimulation
Prevent by using an agonistantagonist
(why?)
```
48
tramadol
```
ultran. • Like an opiate
but not an opiate
-Usually given P.O.
-Like opioids it is a weak centrally-acting µ-
receptor agonist providing moderately
strong analgesia
```
49
Tramadol
| • Side effects similar to opioids (but generally milder EXCEPT for
“Serotonin Syndrome” which can be fatal.
| • Agitation • Muscular tremors • Sweating • Hyperthermia • Seizures
50
tramadol dependence can be reversed with
partially reversed with opioid antagonists
51
Injectable Anesthetics types and what they do and cant do
Can produce unconsciousness • Don’t provide analgesia or muscle
relaxation • Used with other agents • Administered “to effect” IV
• 1) Barbiturates, 2) propofol, and 3) etomidate
52
Barbiturates subclasses
– Ultrashort • Thiopental sodium & methohexital • Induce general anesthesia
– Short • Pentobarbital • Induce general anesthesia • Treat epilepsy
– Intermediate – Long-acting
53
Action of Barbiturates
Not fully understood Mimics the inhibitory neurotransmitter GABA
Causes CNS depression and loss of consciousness
54
termination of barbs
Agent leaves brain Is metabolized, excreted, or redistributed
55
```
Pharmacokinetics of Barbiturates
Protein binding (plasma proteins) Free (unbound) drug
```
enters the brain
56
hypoproteinemia affect in barbs
results in more
| free drug Increased drug amounts to brain
57
normal drug dose of barbs may
produce prolonged unconsciousness or death in
| hypoproteinemia
58
Thiopental
ultra–short-acting Redistributed to muscle and fat and slowly
released Continuous or repeated dosing may lead to “full”
muscle and fat and prolonged recovery, making it “seem” like a longer-acting drug (first order>> zero order kinetics)
59
Methohexital
ultra–short-acting Redistributed to muscle and fat but released
faster Muscle and fat don’t get “full” (saturated) so
there is no prolonged recovery with continuous or repeated doses (zero order kinetics avoided)`
60
Phenobarbital
long acting Sustained effect caused by slow uptake
and release from the brain, therefore
good for seizure disorders. Release is dependent on kidney
excretion, which is slowest
61
Pentobarbital
short acting
Brain levels decrease based on liver metabolism
Faster than kidney excretion
62
Use of Barbiturates
Rapid anesthetic induction To allow intubation (thiopental and
methohexital) Sustain with inhalation anesthetic (thiopental) Sustain with repeated doses or continuous
infusion (methohexital) Use alone for short procedures
Always
intubate!
63
Effects of Barbiturates
Dose-Dependent CV and Resp depression
| CNS Mild sedation to unconsciousness Possibly excitement at low dose
64
Other Adverse Effects of Barbiturates
Exaggerated potency in critically ill,
hypoproteinemic, or acidotic patients (why?)
Tissue irritation and sloughs Perivascular injection (lawsuit city) Treat with saline, with or without lidocaine Use dilute barbiturate solutions
65
Barbiturate-Drug Interactions
| Increase hepatic enzyme activity
Prolonged use (epileptics) Shorter duration of activity of drugs metabolized in
the liver
So long-term barbituate users (such as epileptics)
“chew up” drugs that are metabolized by the liver
MUCH faster.
66
propofol primary action of termination
Although it is both metabolized by the liver and excreted by the kidneys, the primary way Propofol’s action is terminated is by redistribution.
67
propofol half life (funtional and elimination)
This gives Propofol a very short functional half-life (a few minutes) although it’s elimination half-life is 2-4 hours
68
propofol onset/duration of action
Onset of action—30-60 seconds Duration of action—5-10 minutes
69
Effects of Propofol
| • CNS
– Dose-dependent depression from sedation to
| general anesthesia – No analgesia
70
Effects of Propofol cardio system
– Cardiac depressant – Transient hypotension
71
Effects of Propofol respiratory system
VERY potent respiratory depressant with
| possible (frequent) apnea upon induction – Administer slowly to effect – Monitor patient carefully
72
other effects of propofol
* Twitching during induction
* Muscle relaxation
* Safe to use in critters with liver disease or kidney disease.
* Antiemetic
* Decreases intraocular and intracranial pressure
73
Adverse Effects of Propofol
| • CNS
Transient excitement and muscle tremors
(induction)
– Thrashing, muscle twitching, nystagmus (what’s this?), opisthotonus (resembles seizures)
74
Adverse Effects of Propofol on cardiorespiratory system
– Hypotension—transient
• Respiratorysystem
– Apnea (rapid injection; high dose) • Intubation is usually necessary
75
other adverse effects of propofol
Seizure-like signs (induction) Treat with diazepam
Pain with IV injection Perivascular injection does not produce tissue
damage (hurts a lot!!)
76
Poor storage characteristics because of
Egg lecithin, glycerol, and soybean oil support
| bacterial growth – Use aseptic technique
77
In many ways, propofol is like a
better short acting barb
