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48 Cards in this Set
- Front
- Back
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regional anesthesia
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-effected by injection of drugs which block signal conduction near nerves
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ideal anesthetic
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cause loss of sensation esp. pain.
induce muscular relaxation. induce smooth onset and recovery induce anterograde amnesiatoxicity present no hazard to others cause no systemic amnesia cause no systemic toxicity |
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inhalation anesthetics
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-original agents were vapors from volatile liquids or gases: NO, ether, chloroform
-induction of anesthesia using older agents led to stages and planes of anesthesia -rarely seen today as induction is usually by injection -inhalation drugs used to maintain depth of anesthesia -only NO still in routine use esp in dentistry |
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intraoperative period of general anesthesia
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-3 phases
1. Induction: unconscious using inhaled or IV agents 2. Maintenance: mgmt of physiology and adjustments in anethetics (inhaled and IV) 3. Emergence: reduction of anesthetics to produce "awakening" form anesthesis |
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Stages of anesthesia
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I: analgesia
II: delirium or excitement with inc RR and BP (when pt waking up) III: surgical anesthesia: unconscious with muscle relaxation and dec response to painful stimuli IV: medullary paralysis |
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Anesthesia
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-only medical specialty brought into being by a class of drugs
-more hazardous than analgesia -2 classes: inhalational and IV mostly used in conjunction with each other |
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potency of anesthetics
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-potency measured:
-Minimum alveolar concentration (MAC) for inhaled agents (percentage of anesthetic agent in inhaled air that causes 50% of decreased response to surgical stimulus) -IV: free plasma concentration that produces loss of response to surgical incision in 50% of pts -1.2-1.3 MACs to maintain adequate general anesthesia state |
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IV agents
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-most commonly used for induction in adults
-act at GABA receptors: inhibitory NT --> depresses CNS function -Ketamine inhibits NMDA receptors -Lipophilic agents: Distributes into CNS --> redistributes in other tissues accounting for short duration of action -rapid onset and short-acting (may be long if infused over time) -thiopental and propofol are most commonly used IV agents |
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Barbituates
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-facilitate GABA binding
-Thiopental *, thiamylal and methohexital -rapid onset and short duration of action -for short term procedures -hepatic metabolism and renal excretion |
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barbituates AE
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1. Respiratory depression*
2. Hypotension 3. Anticonvulsant effects 4. C/I in porphyria (genetic defect in RBC synthesis) |
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Propofol IV
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-rapid onset and duration
-"milk of amnesia" -faster recovery than thiopental (10 min), less confusion -MOA: GABA receptor -induction and maintenance of anesthesia -day surgeries or short procedues -SE: 1. vasodilation (give in large vein and slowely) 2. hypotension 3. respiratory depression |
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Etomidate IV
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-rapid onset and lasts 4-8min
-hepatic metabolism -induction of anesthesia in hypotensive pts -AE: 1. minimal cardiovascular effects! 2. N/V 3. involuntary movements (give w/muscle relaxer) 4. suppresses adrenocortical hormones |
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Ketamine IV
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-lasts 10-15 min
-rapid clearance, continuous infusion ok -NMDA receptor antagonist (dec glutamate response (excitatory)) -used for pediatric pts -short procedures not requiring skeletal muscle relaxation (wound changes) -less respiratory depression and may inc BP and HR -good analgesia |
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AE of Ketamine
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1. CNS effects, analgesic effects, cataleptic state
2. pt may be awake in a trance like state 3. emergence delirium (hallucinations, vivid dreams) -4. inc BP and pluse 5. small respiratory depression |
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Ketamine pharmacodynamics
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-blocks thalamic-cortex tranmission
-increased CBF -hallucinations and confusions -may in muslce tone -increased secretions |
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Inhalation anesthetics
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-narrow TI
-low safety margin -potency expressed in MAC, % of inspired gas instead of blood concentration -With a MAC value of 105%, nitrous oxide, by itself is not suitable or safe as a sole anesthetic agent. -equilibrium = partial P in inspired gas = partial P in alveolar gas -When MAC is reached gas--> blood --> brain causing anesthetic effects |
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Halothane
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-1st of halogenated anesthetics
-used for maintenance of anesthesia -does not produce analgesia -AE: 1. dose-dependent BP reduction 2. affects heart rhythm--> arrhythmias 3. inhibits respiratory response to hypoxemia 4. inc CBF 5. fulminant hepatic necrosis 6. muscle- malignant hypothermia |
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Isoflurance
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-most commonly used
-induction and maintenance -skeletal muscle relaxation -AE: 1. hypotension but normal CO 2. ventilation depression, irritant 3. inc CBF 4. skeletal muscle relaxation -can relax uterine muscle os not used in preg |
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Desflurane
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-for outpt surgery
-rapid onset, rapid recovery -used for maintenance not induction -AE: 1. strong airway irritant so used after IV agent for maintenance 2. ventilation depressant 3. skeletal muscle relaxer 4. hypotension and inc HR |
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Sevoflurane
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-rapid induction and emergence from anesthesia
-used in outpt for induction -SE: 1. hypotension 2. hyperbarbia- bronchodilator 3. inc CBF 4. skeletal muscle relaxation 5. may produce renal injury |
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Nitrous Oxide
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-colorless, ordorless gas used in dental procedure
-weak so used in conjunction with other halogenated inhalation or IV agents -SE: 1. may reduce ventilatory response to hypoxemia 2. changes in BP and pulse 3. may enter air pockets and inc P |
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malignant hyperthemia
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-in a genetically predisposed pt after inhaled anesthesia and/or succinylcholine is given
-rise in temp, sometimes as high as 113 -muscle rigidity or pain, esp in the jaw, but possibly also in the arms, legs, abd and chest -inc CO2, rhabdomyolysis, hyperthermia, tachycardia, tachypnea, acidosis, hyperkalemia |
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what to do for malignant hyperthermia
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-stop admin of anesthetic
-administer the drug dantrolene which relaxes the muscles and stops the inc in muscle metabolism -initially given IV then in a pill |
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adjuncts to general-Analgesics
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-opiods are primary analgesics
-Sufentanil>remifentanil (very short acting) >fentanyl> alfentanil> morphine> meperidine (order of potency) AE: 1. respiratory depression 2. N/V and pruritis post-op |
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adjuncts to GA- Benzodiazepines
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-may be used for conscious sedation with opiates, or prior to induction
-preanesthesia -muscle relaxation -midazolam and lorazepam -IV onset 2-5 min and lasts 1-4 hrs |
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Neuromuscular blocker
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-presynaptic motor neurons, Ach and nicotinic receptors on skeletal muscle
-nondepolarizing agents--> block these N receptors --> nondepolaraztion of skeletal muscle -depolarizing blockade--> agonists bind to N receptors and last longer than Ach --> prolonged depolarization cannot be further deoplarized by Ach --> paralysis |
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neuromuscular blocker cont
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-admin during inhalation to facilitate ET
intubation and surgical procedures |
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depolarizing agent
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-Succinylcholine
-opens channels like Ach at the neuromuscular junction -initial depol which is prolonged so Ach cannot stimulate muscle and causes block and paralysis -onset in 30 sec-1.5 min and lasts 5-8 min -ideal for intubation -degraded by cholinesterases -releases K+ which may be a problem in CHF, burns, tissue trauma -AE: malignant hyperthermia , brief duration of action |
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nondepolarizing agents- ammonio steroids
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-Pancuronium (long duration)
-Vercuronium -Rapacuronium (intermediate duration 15-30 min) -MOA: competitive antagonists of Ach at nicotinic receptors -duration of action varies from 15-180 min -liver metabolism |
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therapeutic uses of NM blockers
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-adjuvant in surgical anesthesia to obtain muscle relaxation
-intubation, esophagoscopy, correct fxs and dislocations -IV admin |
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non depolarizing agents- Benzylisoquinolines
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-long duration- Doxacurium
-intermediate- Atracurium -short- Mivacurium -atracurium eleminated by esterases |
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effects and toxicity of neuromuscular agents
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-paralysis sequence in non-depolarizinf agents: Small muscles such as jaw, eyes, larynx then limbs and trunk then the intercostals and the diaphragm-> reverse recovery
-Toxicology: apnea, Cv collapse, malignant hyperthermia, resp, paralysis, histamine release, reversal of neuromuscular blockade |
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Spasmolytic drugs
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-Diazepam (valium): benzodiazepine that facilitates inhibitory GABA transmission reducing muscle spasms (sedating)
-Baclofen: acts as a GABA agonist in the brain (drowsiness, and inc seizure activity in epileptic pts) |
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drugs used for acute local muscle spasms
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-Carisoprodol
-Chlorphenesin -Chorzoxazone -cyclobenzaprine (anticholinergic, sedation) -metaxalone -used for acute muscle spamsms |
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local anesthetics used for
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1. Infiltration anesthesia (for cut or laceration)
2. Nerve blocks 3. Spinal anesthesia 4. Epidural anesthesia All end in …caine |
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local anesthetics- amides or esters
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Amides:
1. lidocaine 2. bupivacaine 3. mepivacaine 4. Dibucaine 5. Etidocaine Esters: 1. procaine 2. chloroprocaine 3. tetracaine 4. benzocaine |
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local anesthetics MOA
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-Inhibit nerve conduction by binding to inhibiting the voltage gated Na+ channels on neuronal membrane --> prevents generation and conduction of nerve impulses
-small unmyelinated fibers that conduct pain>temp>autonomic function and touch are affected first -pain fibers first and then sensory fibers with deep pressure later and last motor neurons with inc concentration |
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local anesthetics effects and pH
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-local anesthetics are weak bases
-bicarbonate added to increase percentage of unionized form-->lipophilic--> penetrate nerve sheath -once inside nerve sheath drug --> dissociates to cationic state to bind to Na+ channel -lower pH favor more ionized and less penetration into nerve sheath |
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local effects and addition of epinephrine to LA
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-Epinephrine is an alpha1 agonist --> vasoconstriction which inhibits distribution of LA away from site of injection =prolongs effects of local anesthesia
-allows for smaller doses -dec toxicity -DO NOT use epi in fingers, nose, penis or toes to avoid ischemia |
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Lidocaine and Bupivacaine
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-without epineph the max safe dose is approx 4mg/kg
-with epineph, the max safe dose is approx 7m/kg -without epi- 2.5mg/kg -with epi- 3mg/kg |
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Pharmacology of amides and esters
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-potencies and toxicities vary among local anesthetics
-Amides: metabolized by liver and have longer half lives -Esters: blood and tissue esterases which give them shorter half livesl higher incidence of allergenic rxns |
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onset, duration of action and select
local anesthetics |
1. Procaine and chloroprocaine are short acting (1hr)
2. Lidocaine, mepivacaine and prolocaine are intermediate action (few hrs) (2 min onset) 3. Tetracaine, bupivacaine, etidocaine and ropivacaine are long acting (several hrs) (10 min onset) |
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Routes of administration of local anesthetics
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1. Topical: on skin or mucous membranes
-EMLA cream (lidocaine + prilocaine) -Viscous lidocaine (good for oral lesions) -Lidocaine patch -Benzocaine (oragel) 2. Local infiltration: lidocaine, procaine (novacaine) 3. Local nerve blocks (brachial plexus, digital) 4. Epidural blocks 5. spinal blocks |
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local anesthetics adverse effect
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1. CNS stimulation (tremor)
2. Myocardial depressant 3. Arteriolar dilation and hypotension 4. Sympathetic nerve paralysis 5. allergic rxns |
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types of LA
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1. Tetracaine
2. Lidocaine 3. EMLA cream -superficial pain relief -rapid absorption from MM = potential for toxicity |
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Infiltration and nerve blocks
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Infiltration: injection into the tissue (skin procedures)
-lidocaine Nerve blocks: inject near peripheral nerves and plexuses -provide greater areas of anesthesia distal to site of injection -useful for orthopedic surgical procedures, finger injuries |
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Spinal anesthesia
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-LA injected into lumbar space into CSF
-effective for surgery of lower abdomen, C-section, perineum and lower extremities -often combined with opiate analgesic -causing ascending sympathetic nerve block and hypotension (give epinephrine and fluids) -complications: postdural HA |
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epidural anesthesia
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-injected into epidural space in various locations along the spine to affect spinal nerves
-used for obstetric during active labor -more absorption into blood then spinal anesthesia -may be used with opiate analgesic to minimize risk of AE -may be instilled via catheter for more control of pain |
