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General: added Local: added Neuromuscular blockers: added
Terms in this set (54)
Anesthesia is defined as the lack of what?
Physiological response to noxious stimulus. (May also be defined as a state of loss of all sensation)
What are the qualities of an ideal anesthetic?
Amnesia, loss of consciousness, analgesia, muscle relaxation
What are the classic stages (depths) of anesthesia? Are these stages typically seen today?
Analgesia, delirium, surgical anesthesia, medullary depression. Modern anesthesia (comnbination anesthetics) often divided into awake and unconscious. Delirium occur during emergence.
What are the postoperative considerations for anesthetics?
Nausea and vomiting, pain, emergence excitement (transient confusional state that differs from delirium)
What is the mechanism of action of general anesthetics?
Thought to increase activity of GABA receptors and potassium channels and decrease the activity of acetylcholine and glutamate receptors
What general areas are responsible for the actions of anesthetics?
Amnesia and unconsciousness: brain
Immobilization and analgesia: spinal cord
What is balanced anesthesia?
Using multiple drugs/methods of anesthesia to maximize desired actions and minimize undesired actions
What are the general anesthetics that are administered intravenously?
Thiopental, propofol, etomidate, ketamine, (methohexital)
What are the general anesthetics that are inhaled ("volatile anesthetics")?
Isoflurane, sevoflurane, desflurane, nitrous oxide, (halothane, methoxyflurane, enflurane)
How is the half-life of thiopental influenced by infusion duration?
The longer the infusion, the longer the half-life due to the redistribution of thiopental
Describe the therapeutic window for inhalation anesthetics.
Generally fairly narrow
What form of an inhaled anesthetic distributes out of the lungs and into the blood and brain?
The insoluble gas contributes to the partial pressure and is distributed
What effect does solubility of an inhaled anesthetic have on recovery time?
The lower the blood solubility, the shorter the recovery time
What effect will a high blood/gas partition coefficient have on the action of an inhaled anesthetic?
The higher the blood/gas partition coefficient, the longer to reach equilibrium, the longer to induce anesthesia, and the longer the duration of action
What effect does ventilation have on time to reach anesthetic equilibrium?
An increased ventilator rate will decrease the time to reach anesthetic equilibrium
What effect will increased cardiac output have on the time to reach anesthetic equilibrium?
An increased cardiac output can delay the time to reach anesthetic equilibrium
How is potency of inhaled anesthetics compared?
What is a MAC?
The minimum alveolar concentration resulting in a lack of response to a noxious stimulus in 50% of subjects. (This can be used to compare potencies or to combine anesthetics: MACs can be added).
What drugs are associated with malignant hyperthermia?
Halogenated inhalation anesthetics and succinylcholine
What is the treatment for malignant hyperthermia?
How is local anesthesia defined?
The loss of sensation in a body part without the loss of consciousness or the impairment of central control of vital functions
By what mechanism do local anesthetics prevent (or relieve pain)?
Reversibly block nerve conduction via inhibition of voltage-gated sodium channel activity
What effect do local anesthetics have on the sodium channel?
Stabilize the inactive state of the channel
Where on the sodium channel do local anesthetics bind?
Within the channel - the local anesthetic must gain access through the open channel
What is meant by "use-dependence" of local anesthetics?
Local anesthetics are more effective when nerves are firing more frequently due to the necessity of an open channel in order to gain access to the local anesthetic binding site
What tissues can be blocked by local anesthetics?
Sensory nerves, motor nerves, central nervous system, cardiovascular system, other smooth muscle, skeletal muscle
What is the order of functional block by local anesthetics?
Pain, autonomic C fibers -> cold -> warmth -> touch -> deep pressure -> motor
In general, small fibers are more susceptible to blockade by local anesthetics than large fibers
What is the order of recovery from local anesthetic block?
Motor -> deep pressure -> touch -> warmth -> cold -> pain, autonomic C fibers
Which local anesthetics are amides?
Lidocaine, bupivacaine, ropivacaine, prilocaine (note the extra "i" before the "caine")
Which local anesthetics are esters?
Procaine, cocaine, benzocaine, tetracaine
The pKa of a local anesthetic influences what parameter?
Time of onset
What effect would a decrease in pH have on a local anesthetic?
Local anesthetics are weak bases so would be protonated and charged
Charged form crosses membranes poorly
Charged form binds sodium channel
The lipid solubility of a local anesthetic influences what parameter?
Potency (more hydrophobic = more potent but also more adverse)
Protein binding and hydrophobicity of a local anesthetic influence what parameter?
Duration of action
What is the difference in metabolism of local anesthetics that are amides versus those that are esters?
Amides undergo hepatic metabolism
Esters are hydrolyzed by cholinesterases in plasma (and lesser in CNS)
What effect would the addition of a vasoconstrictor have on the action of a local anesthetic?
Decrease systemic absorption/redistribution
Prolong duration of the anesthesia
Reduce risk of systemic toxicity
How do local anesthetics produce toxicity?
Generally systemic: may be CNS stimulation -> depression, CV depression (decreased inotropy, chronotropy, BP), decreased contraction of smooth muscle (e.g. bowel and uterus), hypersensitivity (dermatitis, asthma)
What drugs are associated with methemoglobinemia?
Prilocaine and benzocaine
What is an EMLA?
"Eutectic mixture (low melting point) of local anesthetics" containing lidocaine and prilocaine which allows anesthetic action to 5 mm depth after topical administration which bridges the gap between topical and infiltration anesthesia
What is the major indication of neuromuscular blockers?
To paralyze/relax skeletal muscle and prevent movement in patients under general anesthesia for surgical procedures
How does the use of a neuromuscular blocker affect the use of other anesthetics?
Allows for the use of less general anesthetic - "lighter" anesthesia
Do neuromuscular blockers have analgesic properties?
Do neuromuscular blockers produce sedation?
What is the sequence of paralysis when using neuromuscular blockers?
Muscles of fine movement (eyes, jaw, larynx, fingers) -> limbs -> trunk -> intercostals -> diaphragm
What is the sequence of recovery when using neuromuscular blockers?
Diaphragm -> intercostals -> trunk -> limbs -> muscles of fine movement (eyes, jaw, larynx, fingers)
Breathing recovers first
What is the difference between a non-depolarizing neuromuscular blocker and a depolarizing one?
Non-depolarizing neuromuscular blocker acts as a classical antagonist and just blocks access to the receptor
Depolarizing neuromuscular blocker first activates the receptor but because of continued activation (due to slow hydrolysis relative to ACh) the end-plate doesn't "reset" and further activation is prohibited
How are the non-depolarizing neuromuscular blockers eliminated?
Most are eliminated renal EXCEPT:
Rocuronium and vecuronium: hepatic metabolism
Atracurium: spontaneous breakdown (hofmann elimination) and plasma esterases
What drugs can be used to reverse the effects of non-depolarizing neuromuscular blockers?
Cholinesterase inhibitors such as neostigmine acting by increasing ACh in the synaptic cleft which can then out-compete the non-depolarizing neuromuscular blocker for binding to the nicotinic receptor.
What concerns are there regarding the administration of a cholinesterase inhibitor to hasten recovery from non-depolarizing neuromuscular blocker?
Muscarinic effects: bradycardia, bronchoconstriction, salivation, nausea, diarrhea, etc. so administer with muscarinic antagonist
Which neuromuscular blocker has the shortest time to onset?
Which neuromuscular blocker has the shortest duration of action?
What is the initial response with administration of succinylcholine?
Wave of fasciculation due to initial activation of the nicotinic receptor and subsequent depolarization of the membrane
What is the effect of cholinesterase inhibitors on succinylcholine effects?
During Phase 1 block (depolarization block) cholinesterase inhibitors can intensify the block
During Phase 2 block (receptor desensitization) cholinesterase inhibitors can reverse the block
What are examples of skeletal muscle relaxants?
Baclofen and dantrolene
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