What was the first used inhaled anesthetic? Why is it no longer used?
diethyl ether
What were 3 desirable characteristics of diethyl ether?
What is the most common inhalant anesthesia in North America? What is it approved for use in?
isoflurane
dogs and horses - commonly used in other species
What allows for rapid induction and recovery associated with sevoflurane? What is it approved for use in?
low blood:gas partition coefficient —> highly controllable depth
dogs
What is the flammability of inhaled anestehtics like?
What are the odors of ether, isoflurane, and sevoflurane like?
irritant
pungent, animals resent mask induction
acceptable
What are the 3 major effects of inhalent anesthetics?
How do inhaled anesthetics affect blood pressure? What effects fo halothane, sevoflurane, desflurane, isoflurane, and nitrous oxide have?
reduce blood pressure (CO x SVR)
Which inhaled anesthetics have minimal effects on HR? Which ones increase it?
halothane and sevoflurane
isoflurane and desflurane cause sympathetic stimulation due to hypotension (can be confused with a too light plane)
How do inhaled anesthetics affect ventilation? What are 4 effects?
depressed TV and minute ventilation
What inhaled anesthetic attenuates ventilatory decrease?
nitrous oxide
What inhaled anesthetics are associated with airway irritation? What is typically added to decrease this? On what patients are these anesthetics avoided?
desflurane and isoflurane are pungent, making patients cough and bronchospasm
better tolerated with opioids and sedatives on board
avoided in “light patients” without other drugs due to potential for life-threatening bronchospasm
What inhaled anesthetics are not associated with airway irritation?
N2O, sevo, halo —> very little bronchospasm
How do inhaled anesthetics affect intracranial pressure? Which one has the most and least effect?
increase intracranial pressure by increasing cerebral blood flow (vasodilation)
What effect do inhaled anesthetics have on cerebral oxygen consumption? What is an exception?
decreases O2 consumption, but increases cerebral blood flow
N2O - increases cerebral O2 consumption and cerebral blood flow
What are the most common hepatic and renal effects of inhaled anesthetics?
HEPATIC = decrease portal vein flow and inhibit metabolism of other drugs
RENAL = dose-dependent reduction in blood flow, GFR, and urine output
How are inhaled anesthetics able to reach the brain?
gain entrance via the respiratory tract, where they maintain steady alveolar concentration and enter systemic circulation
What are 4 theories on molecular targets and anatomic sites of action of inhaled anesthetics?
What is anesthetic potency proportional to? What does it suggest?
solubility in olive oil
anesthesia is produced when a certain number of molecules occupy a region of nerve cell membranes, specifically ligand-gated GABA, NMDA, and nACh channels; voltage-gated Kv and BK channels; and background TREK, Kan, and S channels
How do anesthetic liquids travel to the brain and interact with lipid and proteins to induce anesthesia?
What affects the diffusion rate of inhaled anesthetics across alveoli walls? Distribution to tissues?
concentration gradient of alveoli and capillaries and lipid solubility of anesthetic gas
blood supply and lipid solubility (brain, heart, and kidney have greater blood flow = quickly saturated)
What is the maintenance of gas anesthesia dependent on?
sufficient quantities of anesthetic delivered to and maintained in the alveoli
What are gas and vapors? Whats the difference?
collections of molecules in constant state of motion and bombardment, attraction, and repulsion
What are quantities of inhaled anesthetics measured by?
partial pressure - force per unit area created by the constant state of motion