The rate of onset of anesthesia from a drug like nitrous oxide or isoflurane is primarily determined by?
Degrees of solubility: the less soluble = the less potent (but gasses diffuse into the tissues quickly
Which one of the following inhalation anesthetics is most likely to produce hepatotoxicity?
What causes hepatotoxicity:
c. Halothane (even though its no longer used)
What are the 4 components of the anesthetic state?
Amnesia - partial or complete loss of memory
Sedation - decreased level of arousal
Hypnosis - unconsiousness
Immobility - lack of respone to noxious stimuli
Year for Ether Anesthesia?
What is an important preoperative consideration?
Taking a good history
Proposed mechanisms of action of general anesthesics:
It was hypothesized that volatile anesthetics and act nonspecifically on what component of cells?
Volatile anesthetics act on hydrophobic lipid components
Lipid solubility and relationship to potentcy?
More lipid soluble = more potent
Minimum Alveolar Concentration (MAC)
Concentration of gas in the ___ compartment that results in a ___ of response to a noxious stimulus in ___% of subjects.
Limitations: ___% of patients still respond
Absence of response to pain may ___ indicate ___ of consciousness
Concentration of gas in the alveolar compartment that results in a lack of response to a noxious stimulus in 50% of subjects.
50% of patients still respond
Absence of response to pain may NOT indicate LOSS of consciousness
Propsed mechanisms of action of general anesthetics:
General anesthetics increase the activity of ____ receptors and ___ channels and decrease the activity of ____ receptors and ____ receptors. Causes an increase in _____.
General anesthetics increase the activity of GABA receptors and potassium channels and decrease the activity of acetylcholine receptors and glutamate receptors. Causes and increase in inhibition
Pharmacology of general anesthetics:
What are the IV drugs?
What are the volatile drugs (inhaled)?
IV: thiopental, propofol, etomidate, ketamine
Volatile: halothane, isoflurane, sevoflurane, desflurane, and nitrous oxide
What drugs are IV?
What is thiopental used for?
What drug is not around anymore?
How many methohexital drugs are used?
Thiopental - executions
Thiamylal - not used anymore
Methohexital - only one used
Terminal ___ ___ longer with continued infuction but _____ has a relatively rapid clearance.
Contraindicated in patients with?
Terminal half lives longer with continued infusion but methohexital has relatively rapid clearance
Contraindicated in patients with porphyria
Clearance compared to barbiturates?
What is this drug for?
Rapid clearance compared to barbiturates
Drug is good for MS
1. Use in patients with risk for hypotension - why?
2. Suppression of?
2. Suppresion of adrenals!
1. Used in patients with risk for ___ or ___ since it increases ___ ___ and is a ____.
2. Toxicity causes increase in ____ blood flow or emergence ____.
3. Contraindicated in what patients?
1. Used in patients with risk for hypotension or bronchospasm since it increases blood pressure and is a bronchodilator.
2. Toxicity causes increase in cerebral blood flow or emergence delirium.
3. Contraindicated in patients with CLOSED HEAD INJURIES
Clinical problems of IV Anesthetics:
1. Depression of ____ and ____ drive.
2. What does Ketamine cause?
3. What does Etomidate cause?
Clinical problems of IV anesthetics:
1. Depression of respiratory and cardiovascular drive.
2. Ketamine - hallucinations and emergence delirium
3. Etomidate causes adrenal suppression
Which of the following can increase cerebral blood flow:
Cerebral blood flow can be increased by ketamine
Inhalation anesthetics are all part of what class?
NO: solubility? potentcy? speed of effects?
Halothane: solubility? potentcy? speed?
NO: very unsoluble, not very potent, but quick effects
Halothane: soluble, VERY potent, SLOW effects
Desflurane: why is it not used for induction?
Sevoflurane: used on who? Why?
Nitrous oxide: MAC=?
Desflurane: strong airway irritant
Sevoflurane: used on children bc it doesnt irritate the airway
Nitrous oxide: MAC=105%
Drugs to know?
Important to know about:
Methohexital - ECT and Barbs
Etomidate - cardiostable and adrenosuppression
Ketamine - cardiostable and increase cerebral BF
Isoflurane/Enflurane - inhalation agents
Sevoflurane - kids (doesnt irritate airway)
Desflurane - airway irritatne
Nitrous oxide - hallmark bc not very lipid soluble
Local anesthetics prevent/relieve pain by ___ blocking nerve ____.
Local anethetics block what channels? Can affect all ___ tissues.
Myelinated vs. Unmyelinated: A-delta and C fibers? Role of both?
Local anesthetics prevent/relieve pain by reversibly blocking nerve conduction
Local anesthetics block fast voltage-gated sodium channels and can affect all exciteable tissues
A-delta (small myelinated) C (unmyelinated) --> both are affected by anasthetics and transmit pain
What specific fibers are associated with pain?
What fibers are myelinated?
Put these in order in terms of fiber suceptibility to blockade by local anesthetics: pain fibers, motor fibers, autonomic fibers, sensory fibers
Pain: Adelta and C
Myelinated: A and B
Autonomic fibers> pain fibers > sensory > motor
Lidocane has an ____ link.
Procaine has an ____ link.
Where are amide type local anesthetics broken down?
What happens to ester type?
Lidocaine: amide link
Procaine: ester link
Amide: broken down in liver
Drugs with short duration vs. med vs. long?
Pro's are short: procaine
PriMeL is medium: PRIlocain, mepivocaine, lidocaine
BERT is long: Bupivicaine, Etidocaine, Ropivacaine, and Tetracaine
Metabolism of amides? Problem in who?
Metabolism of esters?
Addition of a vasoconstritor to local anesthetics will ___ systemic absorption, ___ duration of anesthesia, and ___ risk of systemic toxicity.
Amides - degraded by CYP450 (bad for severe hepatic disease)
Esters - degraded by plasma esterases
Addition of a vasoconstrictor to local anesthetics will decrease systemic absorption, prolong duration of anesthesia, and reduce risk of systemic toxicity
Infiltration Anesthesia has a ___ dose. To note: buvicaine has a ___ ___ dose and can cause __ ____.
Differences between epidural and spinal anesthetics?
Adverse effects when bupivacain exceeds max dose?
What can etidocain induce? what is this good for?
maximal; buvicaine has a small maximal dose and cause CV collapse
Epidural takes longer to work and requires more drug than spinal
Buvicaine - CARDIOTOXIC (can cause death)
Etidocaine induces motor block - good for muscle relaxation
What is the best topical anesthetic OTC?
Toxicity of local anesthetics:
1. What does it do to the CNS?
2. What does it do to the CV system?
Methemoglobinemia is a potential side effect of what drugs?
1. CNS stimulation (restlessness, tremor, convulsions) --> depression (drowsiness, sedation, respiratory failure)
2. Causes DECREASED conduction/force of contraction/excitability
Methemoglobinemia could be a side effect of prilocaine and benzocaine
BE ABLE TO RECOGNIZE THE STRUCTURE OF ACETYLCHOLINE
What is the sequence of paralysis? (5 things)
What is the sequence of recovery?
What does sugammadex do?
Example of a depolarizing neuromuscular blocker?
Paralysis: Muscles of fine movement --> limbs --> trunk --> intercostals --> diaphragm
Recovery: Diaphragm --> intercostals... (paralysis in reverse)
Sugammadex: inactivates local anesthetics
Succinylcholine is a depolarizing muscle _____.
With the use of succinylcholine: beware in patients with extensive ___ or ___ ___ damage and in ____.
Succinylcholine can cause?!
Succinylcholine is a depolarizing muscle relaxant
Bewar in patients with extensive burns or soft tissue damage and in paraplegics
Can cause malignant hyperthermia
How do you treat malignant hyperthermia?
Succinylcholine leads to ____. Reverse how?
Non-depolarizing neuromuscular blockade: give what?
Treat MH with dantrolene
Succinylcholine leads to fasciculations. Reverse by just letting the drug wear off
For non-depolarizing neuromuscular blockade: give anticholinesterase (kidney, blood, liver: competitive inhibitors)