Inhaled Anesthetics & Neuromuscular Blockers Flashcards
stages of general anesthesia
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)
inhalation anesthetics
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
Steep dose
response curves with VERY NARROW THERAPEUTIC INDICES
Halothane - says it wont be on test
Decreases the MAP by directly affecting the myocardium and thereby decreasing cardiac output (CO) with change in SVR
factors impacting induction & recovery
factors to decreases MAC (minimum alveolar concentration):
Hypotension
Anemia
Hypothermia
Metabolic acidosis
Hypoxia
Pre-medications
Pregnancy
Aging
Hypothyroidism
Concurrent use of analgesics
potency vs concentration
the more potent a drug is, the narrower the therapeutic indices
the higher the concentration, the less potent it is.
Factors to increase MAC
Increased body temperature
Hyperthyroidism
Hypernatremia
Concurrent use of central nervous stimulants
decreased uptake of anesthetics
drug will stay in body longer and will have a pronounced effect
understand concept of changes in gases and how you can either increase the concentration vs. decreasing it
isoflurane
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
mechanism of action
of nitrous oxide
Works in GABA
slide 16
nitric oxide
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
-
halothane
much more difficult to control - we don’t use halothane
isoflurane
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
desflurane
do not use in the OR
can be used for maintenance
sevoflurance
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
diff drugs reactions
malignant hyperthermia (MH)
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
treatment of Malignany hyperthermia
(REMEMBER DRUG)
Dantrolene
- blocks release of Ca +2 from the sarcoplasmic reticulum of muscle cells, reducing heat production and relaxing muscle tone
rapidly cool the patient
Neuromuscular blockers (NMBs) -
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
different categories of Neuromuscular Blockers (NMBs)
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
Nondepolarizing NMBs
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
Nondepolarizing NMBs (cont’d) drugs
always use these
Vecuronium –>
Rocuronium–> COMPETITIVE INHIBITION
- both are deacetylated in the liver and excreted unchanged in bile
Cisatracurium –> degraded in plasma by esterases
Depolarizing NMBs
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
succinylcholine
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
Atracurium
we dont use it at all bc it causes histamine release in the body
rocuronium
vecuronium
metabolized by liver or kidney
does not affect blood pressure or heart rate or any cardiovascular system
