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43 Cards in this Set

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Definition of anesthesia
drug-induced absence of perception of all sensations
Depth of anesthesia
a. stage I
b. II
c. III
d. IV
a. decreased perception, calm, some analgesia
b. excitement, delirium, irregular respiration, amnesia
c. surgical - regular breathing or no breathing, no perception
d. coma, no spontaneous breathing or movement, depressed/flat EEG (BAD)
What factor determines the speed at which an anesthtic reaches adequate blood levels to have effect
blood gas coefficient

if low, then gas has low solubility in blood --> high partial pressure --> high concentration --> rapidly reaches adequate blood level
5 factors that determine the concentration of anesthesia that gets to the alveoli
1. Amount of inspired gas (Fi)
2. Pulmonary ventilation
3. Gas solubility
4. Pulmonary blood flow
5. Arteriovenous concentration gradient
5. Movement from alveoli to arterial circulation
How does the concentration of given anesthetic lead to increased rate of induction of anesthesia
Higher partial pressure of anesthesia --> higher conentration gradient between alveoli and blood --> more gets to brain
How does pulmonary ventilation affect the amount of anesthetic
With continuous infusion, more gas is taken up by the blood as the rate or tidal volume of breathing increases
What is the relationship between the rate of induction/recovery and the solubility of a drug
Inverse - as solubility goes up, induction/recovery goes down
How does pulmonary blood flow affect the amount of anesthesia available
High blood flow --> less buildup of gas in the alveoli
What creates the AV gradient of anesthetic gas?

Why is this important?
Uptake in peripheral tissues creates AV gradient

Need gradient so that anesthetic gas will be taken up in the pulmonary circulation from the alveoli
Relationship between inhaled and alveolar gas conc.
FA/Fi < 1
Relationship between arterial and alveolar gas conc. on induction
Fa/FA < 1

arterial accumulation lags behind alveolar accumulation; made worse by ventilation-perfusion mismatches (pneumonia, atelectasis, PE)
Mechanism by which most inhaled anesthetics are eliminated

Factors that affect this process
Once conc. gradient is reversed, gas diffuses back into alveoli, expired

Rate of elimination increased by low blood solubility, low V/Q mismatch, increased ventilation
Which drug is extensively metabolized
halothane
Order of metabolism of inhaled anesthetics
halothane > sevoflurane > isoflurane > desflurane > nitrous oxide
What is the second gas effect
High volume uptake of one gas can increase the FA (alveolar conc) of a second gas, thereby increasing its uptake as well
2 drugs that exhibit the second gas effect

In what clinical circumstance is this used
Nitrous oxide and sevoflurane

Pediatric inhalations in which child has no IV access
What is the MAC

Sign of potency?
Minimal alveolar concentration = measure of anesthetic gas at which 50% of patients will not move in response to a noxious stimuli

Low MAC --> more potent
MAC of NO

How is it used normally
MAC > 100

Used to supplement other anesthesias via 2nd gas effect, given with IV opioids in minor surgeries (dental, etc)
What is the favorable pharmacokinetic property of NO
Low blood:gas coefficient --> rapid onset and recovery
Contraindications for NO

Why are these contras?
Pneumothorax, acute intestinal obstruction, suspected air embolus, intracranial air, tympanic membrane grafting

NO can fill any air filled cavity 3x faster than air can diffuse out of cavity into blood
Context of halothane use
pediatrics (becaue of its pleasant odor?)
How is halothane metabolized?

One potential side effect of use
hepatic

autoimmune hepatitis in adults
Halothan propoerties
a. speed
b. potency
a. soluble, so slow induction and emergence

b. low MAC --> potent
What has historically been the #1 inhalation anesthtic used in adults

What 2 drugs have since bypassed it
isoflurane

sevoflurane and desflurane
Drug with the lowest blood: gas partition coefficient

Benefits of this property
Desflurane

rapid control over depth of anesthesia (eliminated completely in lungs), rapid emergence
Contraindications for desflurane
Children (rapid emergence can lead to delirium), asthmatics or smokers (causes airway irritation)
Property of desflurante that precludes its use in inhalation inductions
highly pungent
How is sevoflurane different from desflurane
-more soluble (slower)
-less airway irritability
-more pleasant smell --> can use in pediatrics
Contraindications of sevoflurane
renal dysfunction
4 drugs that decrease mean arterial pressure
halothane
isoflurane
desflurane
sevoflurane
3 drugs that increase heart rate --> maintain cardiac output
isoflurane
desflurane
sevoflurane
drug with minimal CV effects
NO
What are the effects of general anesthetics effect on the respiratory system

exception
decrease minute ventilation, depress respiratory response to hypoxia and hypercarbia

Except NO
What is the effect of anesthetic gases on the CNS?
Luxury perfursion = decrease cerebral metabolic activity while increasing blood flow

--> raise ICP (bad in neursurgical patients)
Effect of anesthetic gases on kidneys
Decrease GFR and urine output (due to decrease in CO and BP)
What is the effect of anesthetics on the liver

One drug that is specifically worse than the others with the liver
decrease hepatic blood flow

Halothane is hepatotoxic, can have effects even after recovery from anesthesia
What is a potentially lethal toxic side effect of anesthetics

What is the exception drug that does not cause this
Malignant hyperthermia (also caused by succinylcholine)

NO does not cause this
Patient was given an inhalation anesthetic, now experiences:

Tachycardia, hypercarbia, hypertension, acidosis, hyperkalemia, increasing muscle rigidity, severe hyperthermia

Dx? How do you proceed?
Malignant hyperthermia = acute hypermetabolic state

1. stop anesthetic
2. cool patient
3. IV hydration
4. IV dantrolene (Ca channel antagonist)
Patient experiences severe hyperthermia and muscle rigidity after taking succinylcholine (depolarizing muscle relaxant)

What genetic mutation does the patient have that predisposes them to this reaction
Malignant hyperthermia

Mutation in the ryanodine receptor (Ca channel in SR), autosomal dominant inheritance
Patient has mutation in the ryanodine receptor

How should you proceed with general anesthesia?
What are you trying to avoid
Malignant hyperthermia

Give NO + IV anesthetic

Avoid succinylcholine
What is the mechanism of action of anesthetics

Meyer-Overtone principle -- status of theory
Decrease neuronal activity by raising the electrical threshold for firing

Theory debunked - people now think anesthetics bind to specific protein targets

More lipid soluble anesthetics are more potent
How do volatile anesthetics work
Depress excitatory glutamate receptors (NMDA) and enhance inhibitory NTs (GABA and glycine)
NO
Halothane
Desflurane
Isoflurane
Sevoflurane

Rate most potent to least potent (MAC)

Rate fastest to slowest
halo > iso > sevo > des > NO

des > NO > sevo > iso > halo