Etomidate: 1. Use in patients with risk for hypotension - why? 2. Suppression of?

Etomidate: 1. _CARDIOSTABLE_ 2. Suppresion of adrenals!

Anesthesia Flashcards by Alyssa Shapiro

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

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Which one of the following inhalation anesthetics is most likely to produce hepatotoxicity?

a. Isoflurane
b. Enflurane
c. Halothane
d. Methoxyflurane

What causes hepatotoxicity:

c. Halothane (even though its no longer used)

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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

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Year for Ether Anesthesia?

1842

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What is an important preoperative consideration?

Taking a good history

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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

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Lipid solubility and relationship to potentcy?

More lipid soluble = more potent

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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.

Limitations:

50% of patients still respond

Absence of response to pain may NOT indicate LOSS of consciousness

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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

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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

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What drugs are IV?

Barbiturates

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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

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Barbiturates:

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

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Propofol:

Clearance compared to barbiturates?

What is this drug for?

Propofol:

Rapid clearance compared to barbiturates

Drug is good for MS

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Etomidate:

Use in patients with risk for hypotension - why?
Suppression of?

Etomidate:

CARDIOSTABLE
Suppresion of adrenals!

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Ketamine:

Used in patients with risk for ___ or ___ since it increases ___ ___ and is a ____.
Toxicity causes increase in ____ blood flow or emergence ____.
Contraindicated in what patients?

Ketamine:

Used in patients with risk for hypotension or bronchospasm since it increases blood pressure and is a bronchodilator.
Toxicity causes increase in cerebral blood flow or emergence delirium.
Contraindicated in patients with CLOSED HEAD INJURIES

Clinical problems of IV Anesthetics:

Depression of ____ and ____ drive.
What does Ketamine cause?
What does Etomidate cause?

Clinical problems of IV anesthetics:

Depression of respiratory and cardiovascular drive.
Ketamine - hallucinations and emergence delirium
Etomidate causes adrenal suppression

Which of the following can increase cerebral blood flow:

a. propofol
b. thiopental
c. ketamine
d. etomidate

Cerebral blood flow can be increased by ketamine

Inhalation anesthetics are all part of what class?

Halogenated hydrocarbons

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?

Methohexital

Propofol

Etomidate

Ketamine

Halothane

Isoflurane/Enflurane

Sevoflurane

Desflurane

Nitrous oxide

Important to know about:

Methohexital?

Etomidate?

Ketamine?

Isoflurane/Enflurane?

Sevoflurane?

Desflurane?

Nitrous oxide?

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 Ester: hydrolyzed

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?

Benzocaine 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

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)