Inhaled Anesthetics & Neuromuscular Blockers

Question 1

stages of general anesthesia

Answer 1

Induction -
General anesthesia in adults is normally induced with an IV agent likePropofol
Often, an IV neuromuscular blockeris administered to facilitate endotracheal intubation by eliciting muscle relaxation
For children without IV access, nonpungent volatile agents, such assevoflurane, are administered via inhalation to induce general anesthesia

Maintenance
Vital signs and response to stimuli are monitored to balance the amount of drug continuously inhaled or infused to maintain general anesthesia
Maintenance is commonly provided with volatile anesthetics, although total intravenous anesthesia with drugs likepropofolcan be used to maintain general anesthesia
Opioids such asfentanylare used for analgesia along with inhalation agents, because the latter alter consciousness but not perception of pain

Recovery
After cessation of the maintenance anesthetic drug, the patient is evaluated for return of consciousness.
For most anesthetic agents, redistribution from the site of action underlies recovery
Neuromuscular blocking drugs are typically reversed after completion of surgery, unless enough time has elapsed for their metabolism
The patient is monitored to assure full recovery of all normal physiologic functions (spontaneous respiration, blood pressure, heart rate, and all protective reflexes)

Question 2

inhalation anesthetics

Answer 2

used primarily for maintanece anesthesia

Steep dose - response curves with VERY NARROW THERAPEUTIC INDICES

NO antagonists exist -no antidote

decreases cerebrovascular resistance, resulting in increased BRAIN perfusions

decreased MAP (mean arterial blood pressure)) is related to a dec in systemic vascular resistance (SVR)
except HALOTHANE
-
Bronchodilation - increase in the diameter of the lower airways

Question 3

Steep dose

Answer 3

response curves with VERY NARROW THERAPEUTIC INDICES

Question 4

Halothane - says it wont be on test

Answer 4

Decreases the MAP by directly affecting the myocardium and thereby decreasing cardiac output (CO) with change in SVR

Question 5

factors impacting induction & recovery
factors to decreases MAC (minimum alveolar concentration):

Answer 5

Hypotension
Anemia
Hypothermia
Metabolic acidosis
Hypoxia
Pre-medications
Pregnancy
Aging
Hypothyroidism
Concurrent use of analgesics

Question 6

potency vs concentration

Answer 6

the more potent a drug is, the narrower the therapeutic indices

the higher the concentration, the less potent it is.

Question 7

Factors to increase MAC

Answer 7

Increased body temperature
Hyperthyroidism
Hypernatremia
Concurrent use of central nervous stimulants

Question 8

decreased uptake of anesthetics

Answer 8

drug will stay in body longer and will have a pronounced effect

Question 9

understand concept of changes in gases and how you can either increase the concentration vs. decreasing it

Question 10

isoflurane

Answer 10

good muscle relaxation
Rapid recovery
Stability of cardiac output
Does not raise intracranial pressure
No sensitization of heart to epinephrine

has no effect on brain pressure and doesn’t mess with cardiac output

used a lot in OR

Question 11

mechanism of action
of nitrous oxide

Answer 11

Works in GABA

slide 16

Question 12

nitric oxide

Answer 12

Avantages:
best way to administer it is if someone is intubated

rapid uptake and elimination

may speed up induction if mixed with other drugs/agents by the “second gas effect”

EX isoflurane

disadvantages:
- limited potency - does not work outside of the lung
danger of hypoxia -> occurs when you are weaning off pt from drug
-

Question 13

halothane

Answer 13

much more difficult to control - we don’t use halothane

Question 14

isoflurane

Answer 14

under goes little metabolism –> acts fast

still affects your MAP

but it does not induce cardiac arrythmias

use it more for maintenance than induction

more expensive

Question 15

desflurane

Answer 15

do not use in the OR

can be used for maintenance

Question 16

sevoflurance

Answer 16

rapid induction without irritiating airways
- rapid onset and recovery due to low blood solubility

metabolized by the liver
- compounds formed in the anesthesia circuit may be nephrotoxic if fresh gas flow is too low

don’t use in OR

Question 17

diff drugs reactions

Answer 17

Question 18

malignant hyperthermia (MH)

Answer 18

due to exposure to halogenated hydrocarbon anesthetics (or succinylcholine)

drastic and uncontrolled increase in skeletal muscle oxidative metabolism, overwhelming the body’s capacity to supply oxygen, remove carbon dioxide, and regulate temperature, eventually leading to circulatory collapse and death if not treated immediately

Strong evidence indicates that MH is due to an excitation–contraction coupling defect

Burn victims and individuals with muscular dystrophy, myopathy, myotonia and osteogenesis imperfecta are more susceptible

pt can have an allergy to it

Question 19

treatment of Malignany hyperthermia
(REMEMBER DRUG)

Answer 19

Dantrolene
- blocks release of Ca +2 from the sarcoplasmic reticulum of muscle cells, reducing heat production and relaxing muscle tone

rapidly cool the patient

Question 20

Neuromuscular blockers (NMBs) -

Answer 20

NMBAs exert their pharmacologic effect by modulating signal transmission in skeletal muscle

Action potential releases acetylcholine into mortor endplates

acetylcholine binds to nocotinic receptors ath te endplate and release of Na+ into muscle fibers, which triggers muscular action potential

Question 21

different categories of Neuromuscular Blockers (NMBs)

Answer 21

Non-Depolarizing
- Competitive antagonists at nicotinic receptors, blocking acetylcholine at the motor endplate. This prevents the action potential from spreading, thereby rendering muscle cells insensitive to motor nerve impulses. Muscle paralysis occurs sequentially, beginning with small, fast-twitch muscles in the eyes and larynx and progressing to the limbs, trunk, airway, intercostal muscles, and diaphragm. Recovery from neuromuscular blockage occurs in the reverse order

Depolarizing
- Act as agonists at nicotinic receptors. They hold open the ion-gated channels, leading to muscular fasciculation until the ion potential is depleted, and then to paralysis. Succinylcholine is the only depolarizing NMBA available

Question 22

Nondepolarizing NMBs

Answer 22

prevent depolarization of the muscle cell membrane and inhibit muscular contraction

low dose: muscle will respond to direct electrical stimulation to varying degrees allowing for monitoring of the extent of blockade

High doses: complete blockade, the muscle does not respond to direct electrical stimulation

Question 23

Nondepolarizing NMBs (cont’d) drugs

Answer 23

always use these

Vecuronium –>
Rocuronium–> COMPETITIVE INHIBITION
- both are deacetylated in the liver and excreted unchanged in bile

Cisatracurium –> degraded in plasma by esterases

Question 24

Depolarizing NMBs

Answer 24

Depolarizing the plasma membrane of the muscle fiber, similar to acetylcholine

More resistant to degradation by acetylcholinesterase (AChE)

Can more persistently depolarize the muscle fibers

Succinylcholine is the only depolarizing muscle relaxant used in practice

Question 25

succinylcholine

Answer 25

intubating quickly

Pharmaco kinetics:
Injected IV
Brief duration of action results from redistribution and rapid hydrolysis
Drug effects rapidly disappear upon discontinuation

Clinical Actions:
Respiratory muscles are paralyzed last
Duration of action extremely short, due to rapid hydrolysis
Therapeutic benefits last only for a few minutes

drug reactions -> Hyperkalemia

rapid endotracheal intubation during induction of anesthesia

Question 26

Atracurium

Answer 26

we dont use it at all bc it causes histamine release in the body

Question 27

rocuronium
vecuronium

Answer 27

metabolized by liver or kidney

does not affect blood pressure or heart rate or any cardiovascular system