Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

27 Cards in this Set

  • Front
  • Back
MAC Value
measure of anesthetic potency

minimal alveolar anesthetic concentration (% of inspired air) at which 50% of patients do not respond to surgical stimulus

MAC values are additive, lower in elderly pt's and in precence of opioid analgesics and sedative hypnotics
Blood-gas solubility ratios
the more soluble the anesthetic in the blood, the longer it takes to achieve partial pressure that will permit movement to CNS and other tissues

high ratio--slow onset, longer recovery rate (e.g Halothane)

Desflurane and sevoflurane have low solubility ratios--rapid onset and recovery
Nitrous Oxide
lowest potency. often used in combination. rapid onset and recovery
Inhaled anesthetic

Desflurane--vasodilates, increases HR. Most rapid onset but airway irritation and coughing
low volatility---needs a special heated vaporizer
Inhaled anesthetic

decreased HR. Metabolized to F- ions--potential for renal damage. Rapid action
Inhaled anesthetic
decreased HR

SE: tonic clonic muscle spasms
Metabolized to F- ions--potential for renal damage.
Inhaled anesthetic
Vasodilation, increased HR.
SE: Brochiolar secretions and spasms
Inhaled anesthetic
Decreases HR directly, but sensitizes heart to catecholamines
SE: Hepatitis, malignant hyperthermia, cardiac arrhythmias
IV anesthetic

highly lipid soluble, rapid onset, short acting barbiturate
Effects of inhaled anesthetics on CNS
decrease the metabolic rate of the brain. Nevertheless, the more soluble volatile agents increase cerebral blood flow because they decrease cerebral vascular resistance. The increase in cerebral blood flow is clinically undesirable in patients who have increased intracranial pressure because of a brain tumor or head injury.

NO is least likely to cause increased blood flow
IV benzodiazepine, used for pre-op sedation & conscious sedation (anterograde amnesia). often used for colonoscopy

depresses respiratory function but can be reversed with BZ receptor antagonist--Flumazenil
IV Anesthetic
Very rapid onset and recovery + antiemetic effect

used for outpatient surgery
IV opioid analgesic used for anesthesia

chest wall rigidity with IV use

Neurolept anesthesia: Fentanyl, droperidol, NO
IV Anesthetic

rapid onset, short duration

causes dissociative anesthesia w/ amnesia, catatonia and analgesia

Only anesthetic that causes CV stimulation

SE: vivid dreams, hallusinations
Mode of action of local anesthetics
via infiltration near nerve bundles or by epidural/subarachnoid injection

bind to the inactivated Na+ channel in axonal membranes--block reactivation
2 Steps:
1.must cross lipid bilayer--non-ionized (if too acidic extracellularly, can decrease effect)
2. convert to ionized--binds Na+ channel
Ester vs Amide local anesthetics
Esters: have one "i" in their names (cocaine, procaine)

Amides: more than one "i" (lidocaine, bupivacaine)
The order of nerve fiber sensitivity to anesthetic blockage
small fibers more sensitive

type B & C> A delta> A beta/gamma> A alpha
skeletal muscle relaxants
interact with the nicotinic receptors at the skeletal muscle end plate

nicotinic receptors--comprised of five subunits--2 (alpha) bind ACh--open Na+ channels

most drugs bind to alpha subunits and prevent depolarization (competitive-nondepolarizing)
can be reversed w/ ACh inhibitors--neostigmine or pyridostigmine

Succinylcholine binds noncompetitively and opens Na+ channel causing excessive depolarization and desensitazion

cause progressive paralysis starting w/ muscles of eye and face--then limbs and resp. muscles.
No effect on cardiac or smooth muscle or consciousness
Malignant hyperthermia
life threatening syndrome associated with use of skeletal muscle relaxants (Succinylcholine, d-Tubocurarine)

symphtoms: Muscle rigidity, hyperthermia, HTN, acidosis, hyperkalemia

genotypic susceptibility:
ryonodine & L-Ca+ channels
blocks ANS ganglia and releases histamine--decreased BP, may cause bronchial secretion and bronchospasm, malignant hyperthermia
competitive (non-depolarizing muscle relaxant)
more rapid onset and recovery
increased BP (vagolytic and sympathomimetic)
competitive (non-depolarizing muscle relaxant)

More rapid recovery and safer in hepatic or renal dysfunction because spontaneously inactivated--forms laudanosine which enters CNS--seizures
competitive (non-depolarizing muscle relaxant)

very short duration--metabolized by plasma pseudocholinesterase, histamine release
Nicotinic receptor agonist muscle relaxant
Non-competitive (depolarizing)

Acts in two phases:
Phase I block (depolarizing)
following brief fasciculation--flaccid paralysis ensues, which is augmented, not reversed by ACh inhibitors

Phase II (desenziting)-- endplate repolarizes but the membrane is desensitized and remains unresponsive to ACh for some time before recovery

Short duration-- inactivated by plasma pseudocholinesterase

may cause hyperkalemia & hyperthermia
muscle relaxation caused by action of drug on CNS, spinal cord or muscle itself

used to reduce excessive muscle tone or spasm in acute muscle injury and CNS dysfunction (CP, MS, stroke)

usually no loss of muscle strength

facilitates GABA action by acting on direct agonist at GABA-b receptors in the spinal cord
*as effective as diazepam w/ much less sedation
Blocks Ca2+ release from SR

acts directly on skeletal muscle to decrease contractability
useful in tx of malignant hyperthermia muscle rigidity