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88 Cards in this Set
- Front
- Back
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When are anesthetic agents used?
When are they not used? |
as an adjunct to a procedure
status epilepticus |
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What are the hydrocarbon IAs?
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Chloroform, cyclopropane, ethylene, halothane
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What are the ether IAs?
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Diethyl ether, enflurane, methoxyflurane, isoflurane, fluroxene, sevoflurane, desflurane
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What are the other IAs?
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NO, xenon
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What is true about xenon?
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favorable profile but limited supply and expensive to extract
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What is true about chloroform?
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toxic
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What reduces flammability?
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halogenation
hydrocarbons and ethers are explosive |
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Methoxyflurane AE
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nephrotoxicity
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What is MAC?
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minimum alveolar concentration
Scale to assess potency of IAs. End-tidal concentration at which 50% of people don't move on surigical incision. |
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What is MAC-BAR?
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conc. that blocks changes in blood pressure and heart rate to surgical incision
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What is LORR?
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loss of righting reflexes in animals, related to MAC-awake, can animal stand up?
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What is MAC-awake?
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conc that prevents response to spoken commands. Measures perceptive awareness rather than memory.
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What is implicit memory?
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unconsciously perceived and retained information. cannot be subsequently reported but effects performance thereafter.
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What is hypnosis?
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Drug induced impairment of cognitive functions needed to appropriately respond.
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What is sedation?
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hypnosis with anxiolysis, diminished motor activity, and decreased arousal.
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What is anesthesia?
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insensibility to surgical pain
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How do IAs work?
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Enhance inhibitory postsynaptic channel activity (GABA and glycine) and inhibit excitatory synaptic channel activity (nicotinic Ach, serotonin and glutamate).
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How does NO work?
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No effect on GABA. It inhibits NMDA-sensitive glutamate channels and neuronal nicotinic Ach receptors.
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How do IAs effect neurons and their behavior?
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Affect synaptic transmission more than axonal conduction.
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What does it mean that NO has a partition coefficient of 0.47?
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At equilibrium 1 mL of blood has 0.47 as much NO as does 1 mL of alveolar gas. Blood has 47% of the capacity for NO as gas.
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Does rate of ventilation alter ultimate depth of anesthesia?
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No, it influences rate of induction.
This means it influences elimination. |
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Halothane
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need for mechanical ventilation depends on situation. Tachypnea, dec BP, dec CO, dec HR
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Enflurane
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>resp depression compared to H. No tachypnea.
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Isoflurane
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progressive reduction in respiration and greater effect on ventilatory response to hypercarbia/hypoxia. Requires ventilation. Irritating to inhale.
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Desflurane
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similar to isoflurane
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Sevoflurane
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non-irritating inhalation. Respiratory effects similar to isoflurane.
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Why does shivering occur during recovery with AIs?
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Generally seen with all agents due to neurological recovery and heat loss from depressed thermoregulatory center.
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How does halothane effect ICP?
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increases, could aggravate situations of elevated ICP in CNS bleeds, aneurysm, tumor
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What are neurological effects of enflurane? When should it be avoided?
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less effect on ICP as H, can cause tonic-clonic movements and EEG changes at high conc so avoid in epilepsy
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What are the neurological effects of isoflurane?
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inc ICP except when combined with hypocarbia from changing vent settings it can be reduced, this is sometimes utilized during neurosurgery, EEG changes but no convulsions
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What are the neurological effects of desflurane and sevoflurane?
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insignificant inc ICP, EEG effects similar to I
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Are halogenated agent effects on skeletal muscle relaxation reveresed by neostigmine?
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No
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How does halothane effect muscle?
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some relaxation, uterine relaxation, increases blood loss if used during ceasarean section or abortion, malignant hyperthermia
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How does enflurane effect muscle?
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>H. dose related, sufficient for abd surgery, uterine relaxation, malignant hyperthermia?
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How do Isoflurane, Desflurane, and Sevoflurane effect muscle?
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similar to E, but D hasn't caused malignant hyperthermia, still don't use in those at risk
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How do halogenated agents effect kidneys?
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nephrotoxicity related to free F ions from metabolism, so depends on conc and % of dose metabolized
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Halothane: renal
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dose dep dec RBF and GFR, give fluids before, do F ion toxicity
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Enflurane: renal
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sim to H, more F ions but still not toxic
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Isoflurane: renal
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sim to H, less F ions
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Desflurane: renal
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minimal metabolism
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Sevoflurane: renal
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F ion toxicity, mild reversible effects, monitor
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What is halothane hepatitis?
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classic AD, 2-5 days post-op, liver failure and death as high as 50%
1:10,000 Enflurane 1:800,000 |
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What IAs are metabolized significantly?
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halothane 10-20%
enflurane 2-10% sevoflurane 3% |
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When is halothane used?
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pediatrics because of smooth induction properties
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When is enflurane used?
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adults as risk of arrhythmias, hepatitis, and postop shivering is less compared to H
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What are the advantages of isoflurane?
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rapid adjustment, safer CV, sustained CO, uncommon arrhythmias (epi), no observed renal or hepatic toxicities
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What are the advantages of desflurane?
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outpatient, rapid recovery, but more irritating to airways so not used for induction
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What are the advantages of sevoflurane?
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similar to D, but new agent so toxicities unknown
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Uses of N2O.
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combination with other agents, excellent analgesic even just alone, dentist, labor and delivery
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AEs of N2O
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few compared to other IAs. post op N/V 15%, pneumothoras or venous air embolism
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What is true of IV anesthetics?
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more rapid onset than IAs, highly potent, precise control, rapid recovery with traditional single bolus
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Describe IVAs plasma concentration levels.
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as plasma concentration falls drug exits highly perfused organs (CNS) to keep equilibrium resulting in termination of effect (not metabolism)
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Name the barbiturates.
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ultrashort acting: thiopental, methohexital, thiamylal
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MOA: barbiturates
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inhibits excitatory Ach neurtransmission and enhances GABA (duration), works at synapse not through axonal conduction
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Pharm effects: barbiturates
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dec cerebral BF and metabolism, dec ICP (neurosurgery), dec EEG activity, some excitatory movement with induction, no analgesia, resp depression but no effect on airway reflexes so cough, spasms, asthma, dec BP, induces aminolevulinic acid synthetase which stimulates porphyrin syn
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Name BZs
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diazepam, midazolam, lorazepam
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MOA; BZ
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inc frequency of GABA
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Pharm effects: BZs
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grand mal seizures, no analgesia, centrally mediated muscle relaxation
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MOA: Etomidate
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IV anes, binds GABA A
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Pharm effects: Etomidate
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quick onset and duration, involuntary muscle movements with induction so use BZ or NMJ blocker, dec cerebral BF and metabolism, dec ICP, enhance EEG so no epilepsy, no analgesia
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What is the preferred agent for patients with CV instability?
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Etomidate
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What is a unique AE of etomidate?
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inhibits adrenal steroidogenesis, interefering with response to stress so no go for long-term ICU
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MOA: Propofol
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GABA
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Pharm effects: Propofol
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depress laryngeal reflexes to promote intubation, antiemetic, short recovery, dec BP, CO, and preload. reduce SVR and neg inotrope, reflex tachycardia, small amount of muscle relaxation despite excitatory movements
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MOA: Ketamine
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noncompetitive antagonist of NMDA receptor (glutamate), does not depress RAS like others, instead dissociates thalamus and limbic system, inhibits some and excites other neurons, sim to PCP, norketamine is active metabolite
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Pharm effects: ketamine
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dissociative anesthesia where pt appears conscious but can't respond, analgesia, inc cerebral BF and metabolism and ICP, myoclonic movements but no EEG changes, full recovery may take hours and have bad dreams and hallucinations, unlike other agents it stimulates CV system, bronchodilates so good for induction, used in ER
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Name opioid analgesics
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morphine, alfentanil, fentanyl, sufentanil in increasing potency
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What has morphine been associated with?
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Intraoperative HTN thought to be due to insufficient anesthetic depth
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If opioids are used for anesthesia what must be done?
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must provide mechanical ventilation, can induce chest wall rigidity (tx with NMB)
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AE: opiods
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dec BP, bradycardia, resp depression, increased muscle rigidity, inc intestinal tone and dec propulsive peristalsis
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MOA: local anesthetics
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bind interior of Na channels in inactivated state without altering resting membrane potential or threshold level, but they slow the rate of depolarization, action potential not propagated b/c threshold is never attained, block K at high doses
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MOA: LA cont.
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effects stimulated>resting nerve, ionized to get to binding site when channel is open then channel inactivates, if pKa is close to physiologic pH more is nonionized to pass through nerve cell membrane so more rapid, lipophilicity enhances drugs action
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What is EMLA?
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eutectic mixture of local anesthetic for small skin procedures
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How are esters metabolized?
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hydrolyzed and inactivated primarily by plasma esterases, (spinal fluid does not contain plasma esterases), liver also
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How are amide linked agents metabolized?
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liver, highly bound to alpha 1 acid glycoprotein so higher toxicity in neonates
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AEs: LAs
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CNS first sign of systemic toxicity, restlessness, tremor, paresthesia, seizures, sedation, coma, can block Ach effects at NMJ, respiratory depression possible from CNS or spinal or epidurals effecting nerves, hypersensitivity more common with esters
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Cocaine
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LA, vasoconstrictor, shrinks mucous membranes in upper respiratory tract
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Procaine
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LA, low potency, slow onset, short DOA, infiltration anesthesia and diagnosis nerve block
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Lidocaine
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LA, faster, more intense, longer-lasting, and more extensive, good for those allergic to ester-type agents
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Bupivacaine
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LA, potent,prolonged, sensory>motor block, labor and delivery, continuous infusion, more cardiotoxic, severe arrhythmias and myocardial depression with inadvertent large doses
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Chlorprocaine
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rapid, short, reduced toxicity, no intrathecal use because high incidence of post-precedural muscular back pain
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Etidocaine
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faster than B, sim to L, but DOA longer, used for motor blockade (not for post-op analgesia or labor), potential cardiotoxicity
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Mepivacaine
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not effective topical, do not use in neonate or obstetrics b/c of inc toxicity
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Prilocaine
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sim to lidocaine except used without a vasoconstrictor as it causes little vasodilation, large Vd, methemoglobinemia(avoid in OB and neonates)
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Tetracaine
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more potent and longer than procaine, inc tox b/c of slower met, spinal anesthesia of long duration
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Benzocaine
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poorly soluble, slowly absorbed so can be applied to wounds and ulcerated surfaces
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LA ophthalmological agents
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proparacaine, tetracaine, one drop at time
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What is misopristol?
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A drug used to counteract GI AEs of NSAIDS. Prostagladin that protects GI mucosa. Category X.
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