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27 Cards in this Set
- Front
- Back
MAC Value
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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 |
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Blood-gas solubility ratios
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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 |
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Nitrous Oxide
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lowest potency. often used in combination. rapid onset and recovery
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Desfluranes
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Inhaled anesthetic
Desflurane--vasodilates, increases HR. Most rapid onset but airway irritation and coughing low volatility---needs a special heated vaporizer |
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Sevoflurane
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Inhaled anesthetic
decreased HR. Metabolized to F- ions--potential for renal damage. Rapid action |
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Enflurane
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Inhaled anesthetic
decreased HR SE: tonic clonic muscle spasms Metabolized to F- ions--potential for renal damage. |
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Isoflurane
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Inhaled anesthetic
Vasodilation, increased HR. SE: Brochiolar secretions and spasms |
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Halothane
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Inhaled anesthetic
Decreases HR directly, but sensitizes heart to catecholamines SE: Hepatitis, malignant hyperthermia, cardiac arrhythmias |
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Thiopental
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IV anesthetic
highly lipid soluble, rapid onset, short acting barbiturate |
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Effects of inhaled anesthetics on CNS
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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 |
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Midazolam
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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 |
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Propofol
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IV Anesthetic
Very rapid onset and recovery + antiemetic effect used for outpatient surgery |
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Fentanyl
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IV opioid analgesic used for anesthesia
chest wall rigidity with IV use Neurolept anesthesia: Fentanyl, droperidol, NO |
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Ketamine
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IV Anesthetic
rapid onset, short duration causes dissociative anesthesia w/ amnesia, catatonia and analgesia Only anesthetic that causes CV stimulation SE: vivid dreams, hallusinations |
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Mode of action of local anesthetics
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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 |
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Ester vs Amide local anesthetics
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Esters: have one "i" in their names (cocaine, procaine)
Amides: more than one "i" (lidocaine, bupivacaine) |
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The order of nerve fiber sensitivity to anesthetic blockage
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small fibers more sensitive
type B & C> A delta> A beta/gamma> A alpha |
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skeletal muscle relaxants
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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 |
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Malignant hyperthermia
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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 |
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d-Tubocurarine
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blocks ANS ganglia and releases histamine--decreased BP, may cause bronchial secretion and bronchospasm, malignant hyperthermia
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Pancuronium
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competitive (non-depolarizing muscle relaxant)
more rapid onset and recovery increased BP (vagolytic and sympathomimetic) |
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Atracurium
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competitive (non-depolarizing muscle relaxant)
More rapid recovery and safer in hepatic or renal dysfunction because spontaneously inactivated--forms laudanosine which enters CNS--seizures |
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Mivacurium
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competitive (non-depolarizing muscle relaxant)
very short duration--metabolized by plasma pseudocholinesterase, histamine release |
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Succinylcholine
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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 |
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Spasmolytics
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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 |
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Baclofen
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Spasmolytic
facilitates GABA action by acting on direct agonist at GABA-b receptors in the spinal cord *as effective as diazepam w/ much less sedation |
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Dantrolene
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Spasmolytic
Blocks Ca2+ release from SR acts directly on skeletal muscle to decrease contractability useful in tx of malignant hyperthermia muscle rigidity |