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109 Cards in this Set
- Front
- Back
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What is clonidine used for?
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htn, diagnose pheochromocytoma(decreases plasma catecholamines in normal patients but not those with pheo), suppresses signs of narcotic withdrawal, decreases MAC, can be used neuraxially
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Does epidural or intrathecal clonidine cause greater hypotension and bradycardia?
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intrathecal
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What is the mechanism of action of clonidine and methydopa?
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Both are alpha 2 agonists, methyldopa stimulates alpha 2 in the hypothalamus which inhibits SNS outflow from the vasomotor center, clonidine stimulates alpha 2 receptors in the vasomotor center
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What is the mechanism of action of reserpine?
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interferes with norepi reuptake in the nerve terminal storage vesicles leading to depletion of norepi
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What is the mechanism of guanethidine? What drugs decrease the effectiveness of guanethidine?
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enters storage granules and interferes with norepi release from storage vesicles; TCAs and ephedrine block this action and thus decrease the effectiveness of guanethidine
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What drug is 8 times more specific for alpha 2 receptors than clonidine?
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dexmedetomidine
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What patients should receive decreased doses of dexmedetomidine?
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Liver failure: dex undergoes almost complete biotransformation in the liver
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What is beneficial when using dexmedetomidine versus other sedatives?
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effective sedation and analgesia but patients are still arousable; postop provides substantial sympatholytic and analgesic effects without respiratory depression(does not have amnestic properties)
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What is the dosing of dexmedetomidine?
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1mcg/kg bolus and then 0.2-0.7mcg/kg/hr for no more than 24 hrs
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What is the molecular mechanism of alpha 2 agonists?
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decreased formation of cAMP via G protein activation
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What is the cause of the major sedative and analgesic effects associated with dexmedetomidine?
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stimulation of alpha-2 receptors in the locus coeruleus
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How does dexmedetomidine affect the cardiovascular system?
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loading dose is associated with transiet increase in BP and decrease in HR followed by 10-20% decrease in blood pressure and stabilization of HR below baseline values
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What is beneficial about alpha 2 agonists on the cardiovascular system during surgery?
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they appear to have anti-ischemic effects preoperatively, they blunt hemodynamic variability during surgery and recovery, high risk patients on dex experience significantly fewer ischemic episodes
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What is the effect of dexmedetomidine on the respiratory system?
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rightward shift of the CO2 response curve
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How does dexmedetomidine effect CBF and CMRO2?
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decreases CBF and CMRO2 is unaffected
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What patients should not receive dexmedetomidine?
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preexisting severe bradycardia or patients with preexisting severe ventricular dysfunction(EF<30%) including CHF and cardiac failure in whom sympathetic tone is critical for maintaining hemodynamic balance
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What drugs and other methods are used for the acute treatment of AF?
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digitalis, verapamil, propranolol, D/C countershock, pacing is effective for aflutter but not afib
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Why should lidocaine and pancuronium be avoided in patients with afib?
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lidocaine markedly increases A-V conductance and may lead to an accelerated ventricular response; pancuronium is antivagal and increases AV conductance
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What are the effects of digitalis?
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increases incracellular calcium and consequently prolongs A-V conductance, positive isotropy, and increases muscle automaticity
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How does renal or hepatic dysfunction affect the half life of digitoxin?
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it doesn't
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What are therapeutic levels of digoxin and digitoxin?
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digoxin: 0.5-2.0 ng/ml, children 2.5-3.5 ng/ml; digitoxin 10-35 ng/mL
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What has a longer half life digoxin or digitoxin?
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digitoxin
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What is the treatment of ventricular arrhythmias due to digitalis toxicity?
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treat ventricular arrhythmias with lidocaine, phenytoin, potassium
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What are causes of digitalis toxicity?
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renal failure, hypokalemia(<2.5mEq/L), hypothyroidism, hypomagnesemia, hypercalcemia
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Why should you avoid cardioversion in the setting of digitalis toxicity?
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may result in vfib
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What are signs of digitalis toxicity?
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ventricular arrhythmias, anorexia, nausea, vomitting
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Where is the action of thiazide diuretics?
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cortical portion of the ascending loop of henle and distal convoluted tubule inhibit Na and Cl reabsorption
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Why should you be careful about using loop diuretics in patients on digitalis?
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side effect of hypokalema increases the potential for dig toxicity
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How does lasix affect ICP?
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decreases ICP(alterations in BBB do not influence the ability of lasix to decrease ICP)
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How is mannitol filtered by the kidney?
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it is freely filtered at the glomerulus and not well reabsorbed
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Why should you avoid urea in increased ICP?
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crosses the BBB and is associated with rebound intracranial htn
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What are the potassium sparing diuretics?
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spironolacone(no effect in the absence of aldosterone), amiloride, triamterene
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What are the effects of acetazolamide on the blood gas?
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hypokalemic, hyperchloremic acidosis(dumps bicarb and prevents secretion of H)
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Is ephedrine direct or indirect acting?
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both, direct effect on adrenergic receptors and indirect effects upon catecholamine release
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What is the onset of action of ephedrine when given orally?
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>1hr also prolonged duration due to slow inactivation and slow excretion
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How does epinephrine and ephedrine affect glucose levels?
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epinephrine produces marked hyperglycemia, ephedrine does not
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What are the cardiovascular effects of ephedrine?
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increases MAP, HR, CO, coronary and skeletal muscle blood flow
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What are side effects of ephedrine?
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bronchodilation, increased uterine blood flow, tachyphylaxis
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How is norepinephrine inactivated?
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2/3s is removed from the synaptic cleft by reuptake into nerve terminals, the remainder is metabolized by monoamine oxidase in the cytoplasm
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What drugs block norepinephrine reuptake?
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cocaine, TCAs, amphetamines
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Where is norepineprine converted to epinephrine?
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adrenal medulla by the enzyme phenylethanolamine-n-methyltransferase
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What is the rate limiting step in the formation of catecholamines in the nerve terminals?
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tyrosine hydroxylated to form dopa by the enzyme tyrosine hydroxylase
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What drugs reduce the incidence of myoclonus associated with the administration of etomidate?
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fentanyl and benzos
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What percentage of patients have myoclonus during induction with etomidate?
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33%
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What induction agent should you avoid in the setting of a ruptured globe?
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etomidate(myoclonus may be hazardous)
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Toxicity of which opioid metabolite manifests as myoclonus and seizures?
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normeperidine
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What induction agents are associated with myoclonus?
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methohexital; propofol, and thiopental are also linked to myoclonus but much less than methohexital and etomidate
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What can you use to suppress myoclonus?
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valproate and clonazepam
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What is the usual dose of etomidate?
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0.1-0.4 mg/kg
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Does etomidate produce analgesia?
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no
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How is etomidate metabolized?
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hydrolyzed by liver plasma esterase's,
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What are the CNS effects of etomidate?
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potent cerebral vasoconstrictor, decreased CBF and CMRO2, activates epileptic seizure foci, increases amplitude of SSEPs, making monitoring more reliable
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What are the cardiovascular effects of etomidate?
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MAP is typically reduced 15% secondary to decreased SVR, minimal change in HR, SV, and CO, no detrimental effect when injected directly into an artery,
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How does etomidate affect ventilation?
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reduces tidal volume and increases RR
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Where is heparin produced and how is it prepared commercially?
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produced by mast cells and commercially prepared from cow lung and intestines
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What is the mechanism of action of heparin?
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acts indirectly by activating anti-thrombin III which neutralizes several coagulants(IX, X, XI) and inactivates thrombin-preventing its action on fibrinogen(prolongs both PT and PTT)
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What is the half-life of heparin?
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1-3 hrs
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When are heparin requirements increased or decreased?
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increased in pulmonary embolic disease and decreased in hypothermia, hepatorenal disease prolongs the half-life of heparin
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How is heparin given?
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loading dose of 5,000-10,000 u then 1000u/hr with dose adjusted to maintain PTT 2 x control
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How is heparin given intermittently for full treatment?
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loading dose 10,000 u IV followed by 5,000-10,000 Q4-6 hours
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What is the benefit of giving sub q heparin prior to surgery and how should it be given?
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significantly decreases the incidence of PE and DVT in patients over 40; 5000 u sub Q prior to surgery repeated Q 12 hours
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What are complications of heparin therapy?
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hemorrhage, alopecia, osteoporosis, thrombocytopenia
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How does protamine antagonize heparin?
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neutralizes it; hepain is an acid and protamine is a base
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Where is heparin inactivated?
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in both the liver and kidneys
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What are benefits of LMWH over heparin?
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administered subQ, no need for lab monitoring, more predictable anticoagulant response, better bioavailability, longer half-life, dose independent clearance, HIT occurs less frequently, more effective in trauma, venous thrombosis and orthopedics in preventing thrombus grotth
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What are the recommendations for the use of LMWH with neuraxial anesthesia?
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remove indwelling catheters 10-12 hrs following last dose of LMWH, LMWH therapy should be delayed as long as possible 12 hours minimum
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What are contraindications for the use of ketamine?
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heart: HTN, cardiac ischemia; brain: increased ICP, hx of CVA; Lungs: pulmonary htn, pulmonary emboli; endocrine: hyperthyroidism; eye: nystagmus might interfere with eye surgery; digitalis toxicity, severe pre-eclampsia
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What class of medication is ketamine?
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phencyclidine derivative
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What is the dose of ketamine?
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1-2 mg/kg IV or 5-10 mg/kg IM
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What are characteristics of ketamine administration?
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sympathetic stimulation, increased muscular tone, retention of pharyngeal and laryngeal reflexes, airway resistance decreases, myocardial depression with increased CO secondary to SNS simulation, increased CBF, CMRO2, ICP, IOP unchanged, profuse secretions
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What are indications for giving ketamine?
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burns, shock, COPD, asthma, CHF, cardiac tamponade, hypothyroidism, tetralogy of fallot
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How can you increase the ionized fraction of local anesthetics leading to a slower onset?
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decrease the pH of the local anesthetic
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How can you promote ionization and increase urine excretion of local anesthetics?
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acidification of urine
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What does the potency, onset, and duration of local anesthetics depend on?
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potency: lipid solubility, onset: pKa, Duration: protein binding
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What is responsible for the allergic reactions with local anesthetics?
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esters: para-aminobenzoic acid; amides: methylparaben
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If a patient has an allergy to an amide local anesthetic can you give an ester local anesthetic?
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yes, cross sensitivity does not occur
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What is the difference between pseudocholinesterase, plasma cholinesterase, butylcholinestease?
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they are the same thing
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How are amide local anesthetics metabolized?
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liver microsomal enzymes
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What local anesthetics should be used with caution in cirrhotics?
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amides
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What locations in the body absorb local anesthetics more readily?
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IV>intercostal>caudal>epidural=topical>brachial plexus
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How do local anesthetics affect vascular tone?
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all cause vasodilation except cocaine which causes vasoconstriction by limiting the reuptake of norepi from the synaptic terminal
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How does epinephrine affect peak levels of local anesthetics?
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reduces peak levels of local anesthetics
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What are CNS manifestations of local anesthetic toxicity?
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tinnitus, perioral paresthesias, dizziness, lightheadedness, grand mal seizure
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What drugs are useful in prevention and treatment of local anesthetic induced seizures?
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benzos and barbs
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What are the cardiovascular indications of local anesthetic toxicity?
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at 5-10ug/mL: EKG changes(prolonged PR interval and widened QRS), decreased CO and peripheral vasodilation; at >20 ug/mL asystole and circulatory collapse can be seen
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When does peak lidocaine concentration in the blood occur after initial infiltration?
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12 hours
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What is the maximum dose of lidocaine for liposuction using the tumescent technique?
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35-50mg/kg
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What are the benefits of ropivicaine over bupivicaine?
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less potential for cardiac and CNS toxicity and less associated with motor blockade
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Why does ropivicaine have a long duration of action?
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highly protein bound
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What are adverse effects of ropivicaine?
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hypotension, tachycardia, urinary retention, nausea, vomiting
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What is the typical epidural and spinal dose for ropivicaine?
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epidural: 20cc 0.5-0.75%; spinal: 3cc 0.5-0.75%
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What local anesthetics are used for EMLA cream?
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5% lidocaine and 5% prilocaine
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What surgeries can be performed with EMLA cream?
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laser removal of port-wine stains, lithotripsy, skin grafting, circumcision
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How much time is required for EMLA cream to be effective?
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1hr
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What are side effects of EMLA cream?
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skin blanching, edema, erythema, methemoglobinemia
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When and where should EMLA cream not be used?
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mucous membranes, broken skin, infants <1month old, patients with methemoglobinemia
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What neurotransmitters are broken down by MAOis?
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dopamine, norepinephrine, epinephrine, and serotonin
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What are the MAOis?
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nardil(phenylzine), marplan(isocarboxyazid), parnate(tranylcypromine), selegiline(eldepryl), pargyline(eutonyl)
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How are direct and indirect acting sympathomimetics affected by MAOis?
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indirect acting sympathmimetics can be greatly exaggerated by MAOIs, direct acting agents such as phenylephrine are recommended but the dose should be decreased
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What foods should be avoided in patients on MAOis?
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foods containing tyramine: cheese, chocolate, beer and wine can lead to hypertensive crisis
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What opioid should be avoided in patients on MAOis?
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meperidine when combined with MAOis can cause fatal excitatory reaction, other opioids when combined with MAOis cause sympathetic depression
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What is the mechanism of action of aminophylline?
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phosphodiesterase inhibitor which inhibits the breakdown of c-AMP by phosphodiesterase, the increase in cAMP leads to bronchodilation and increased diaphragmatic contractility
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What is the mechanism of action of metaproterenol?
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beta sympathomimetic agonist that activates adenyl cyclase which increases the concentration of c-AMP
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What is the mechanism of action of isordil?
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nitrate which causes the relaxation of vascular smooth muscle directly, this leads to improved blood flow and decreases ischemia
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What is the mechanism of dyazide?
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thiazide diuretic, which inhibits sodium reabsorption in the distal convoluted tubule, along with sodium free water is also lost in the urine
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When is nifedipine used?
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angina where beta blockers are contraindicated such as in heart failure, COPD, severe asthma
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What are signs of thyroid storm?
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hyperthermia, tachycardia, dysrhythmias, CHF, and shock
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When does thyroid storm typically occur in the perioperative setting?
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6-18 hours postop
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What precipitates thyroid storm?
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surgery, infection, trauma, toxemia, DKA
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