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187 Cards in this Set
- Front
- Back
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What is clonidine used for?
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1. htn,
2. diagnose pheochromocytoma (decreases plasma catecholamines in normal patients but not those with pheo), 3. suppresses signs of narcotic withdrawal, 4. decreases MAC, 5. 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 inhibitory alpha 2 in the hypothalamus which inhibits SNS outflow from the vasomotor center, -clonidine is a centrally acting alpha 2 agonist that stimulates inhibitory 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 of norepi and interferes with its 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 (glucuronidation and CYP 450 metabolism)
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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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1 mcg/kg bolus and then 0.2-0.7 mcg/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 which leads to the following:
1. inhibition of the release of norepi and termination of propagation of pain signals 2. inhibition of neuronal firing in the spinal cord and brain 3. reduction of Ca entry into cells, inhibiting NT release |
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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 (most important noradrenergic nucleus in the brain and an important modulator of vigilance and is also critical for nociceptive neurotransmission)
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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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-less resp depression than other sedatives
-coadministration with other anesthetics results in additive effects -some depression and rightward shift of the CO2 response curve (still maintains respiratory homeostasis better than other sedative-analgesics) |
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How does dexmedetomidine effect CBF and CMRO2?
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-decreases CBF without causing ischemia
-CMRO2 is unaffected |
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What patients should not receive dexmedetomidine?
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1. preexisting severe bradycardia
2. 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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1. digitalis,
2. verapamil, 3. propranolol, 4. D/C countershock, 5. 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 is the MOA of digitalis?
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It inhibits Na-K ATPase, resulting in increased intracellular 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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1. lidocaine - increases AV conductance
2. phenytoin 3. potassium - depending upon level; tx if it has potentiated toxicity 4. atropine for symptomatic bradycardia while digibind is prepared 5. tx hypothyroidism, hypomagnesemia, hypercalcemia |
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What are causes of digitalis toxicity?
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1. renal failure - most common
2. hypokalemia (<2.5 mEq/L) 3. hypothyroidism 4. hypomagnesemia 5. 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 is the MOA of thiazide diuretics?
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inhibit Na and Cl reabsorption in cortical portion of the ascending loop of henle and distal convoluted tubule
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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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What is the MOA of furosemide? What are its uses?
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Inhibit Na and Cl reabsorption (ie active Cl transport) in the medullary portion (thick) of the ascending Loop of Henle which disrupts the countercurrent multiplication mechanism so that both urinary concentration and dilution are impaired
-tx of acute pumonary edema and inc ICP (alterations in the BBB do not influence the ability of lasix to dec 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
-this creates increased osmolality in the renal tubules and free water follows mannitol |
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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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1. spironolacone (no effect in the absence of aldosterone) - an aldosterone antagonist
2. amiloride 3. triamterene |
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What are the effects of acetazolamide on the blood gas?
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it inhibits the reabsorption of bicarb which causes a hypokalemic, hyperchloremic acidosis (dumps bicarb and prevents secretion of H)
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Is ephedrine direct or indirect acting?
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It is a synthetic catecholamine-like drug with both a direct effect on adrenergic receptors (alpha and beta) and indirect effects upon catecholamine release (NE)
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What is the onset of action of ephedrine when given orally?
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>1 hr
-can be given orally bc it is resistant to metabolism by monoamine oxidase in the GI tract |
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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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1. bronchodilation,
2. increased uterine blood flow 3. 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,
- most is pumped back into vesicles with the remainder metabolized by monoamine oxidase in the cytoplasm |
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What drugs block norepinephrine reuptake?
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1. cocaine,
2. TCAs, 3. amphetamines |
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Where is norepineprine converted to epinephrine?
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adrenal medulla by the enzyme phenylethanolamine-n-methyltransferase (PNMT)
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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 from meperidine
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What induction agents are associated with myoclonus?
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1. etomidate
2. methohexital 3. propofol (less) 4. thiopental (less) |
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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? How do pts awaken?
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hydrolyzed by liver plasma esterase's
-redistribution |
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What are the CNS effects of etomidate?
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1. potent cerebral vasoconstrictor
2. decreased CBF and CMRO2 (35-45%) 3. activates epileptic seizure foci (use is caution in pts with focal epilepsy) 4. increases amplitude of SSEPs making monitoring more reliable |
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What are the cardiovascular effects of etomidate?
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1. MAP is typically reduced 15% secondary to decreased SVR,
2. minimal change in HR, SV, and CO, 3. no detrimental effect when injected directly into an artery, 4. decrease myocardial contractility less than thiopental 5. does not decrease renal blood flow |
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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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mucopolysaccharide 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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1. acts indirectly by activating anti-thrombin III which neutralizes several coagulants (IX, X, XI)
2. 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 (dose dependent)
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When are heparin requirements increased or decreased?
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-increased in pulmonary embolic disease
-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 1000 u/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 2 hrs prior to surgery repeated Q 12 hours |
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What are complications of heparin therapy?
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1. hemorrhage
2. alopecia 3. osteoporosis 4. thrombocytopenia |
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How does protamine antagonize heparin?
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neutralizes it;
heparin 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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1. administered subQ
2. no need for lab monitoring 3. more predictable anticoagulant response, 4. better bioavailability 5. longer half-life 6. dose independent clearance, 7. HIT occurs less frequently, 8. 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 and 24 hrs 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 -special: 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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1. sympathetic stimulation,
2. increased muscular tone, 3. retention of pharyngeal and laryngeal reflexes, 4. airway resistance decreases 5. myocardial depression with increased CO secondary to SNS simulation, 6. increased CBF, CMRO2, ICP, 7. IOP unchanged, 8. profuse secretions |
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What are indications for giving ketamine?
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1. burns,
2. shock, 3. COPD, 4. asthma, 5. CHF, 6. cardiac tamponade, 7. hypothyroidism, 8. tetralogy of fallot |
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How can you increase the ionized fraction of local anesthetics? What does this lead to?
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decrease the pH of the local anesthetic
-slower onset |
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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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"POD = LAP"
Potency = lipid solubility Onset = pKa (acid-base status) 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 (found in multidose vials) |
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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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How are ester local anesthetics metabolized?
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plasma cholinesterase
-AKA pseudocholinesterase, butylcholinesterase |
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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 > paracervical > epidural = topical > brachial plexus > sciatic/femoral
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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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1. tinnitus,
2. perioral paresthesias, 3. dizziness, 4. lightheadedness, 5. 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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- <5 ug/mL (of Lidocaine) - no symptoms
- 5-10 ug/mL (of Lidocaine) - 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 tumescent 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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35-50 mg/kg
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What are the benefits of ropivicaine over bupivicaine?
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1. less potential for cardiac and CNS toxicity
2. 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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1. hypotension,
2. tachycardia, 3. urinary retention 4. 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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1. laser removal of port-wine stains,
2. lithotripsy, 3. skin grafting, 4. circumcision |
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How much time is required for EMLA cream to be effective?
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1 hr
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What are side effects of EMLA cream?
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1. skin blanching,
2. edema, 3. erythema, 4. methemoglobinemia |
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When and where should EMLA cream not be used?
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1. mucous membranes,
2. broken skin, 3. infants <1month old, 4. patients with methemoglobinemia |
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What neurotransmitters are broken down by MAOis?
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1. dopamine,
2. norepinephrine, 3. epinephrine 4. serotonin |
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What are the MAOis?
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1. nardil (phenylzine),
2. marplan (isocarboxyazid), 3. parnate (tranylcypromine), 4. selegiline (eldepryl), 5. 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 can lead to hypertensive crisis: (MAOI's inhibit the inactivation of tyramine)
1. cheese, 2. chocolate, 3. beer 4. wine |
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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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1. hyperthermia,
2. tachycardia, 3. dysrhythmias, 4. CHF 5. 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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"SIT D"
surgery, infection, trauma, toxemia, DKA |
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Draw the chemotherapeutic man.
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'
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Explain the chemotherapeutic man.
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N = nitrosureas (lomustine, carmustine) = neurotoxic (xBBB)
C = cisplatin, carboplatin = oto/nephrotoxic B = bleomycin, busulfan = pulmonary fibrosis D = doxorubicin = cardiotoxic P = cycloPhosphamide = hemorrhagic cystitis MF = methotrexate and 5-FU = myelosuppresion V = vinca alkaloid (vincristine, vinblastine) = peripheral neuropathy |
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Which antihypertensive agent decreases both HR and BP?
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clonidine
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What is the mechanism in which clonidine works neuraxially?
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Receptors are located on dorssal horn neurons of the spinal cord, where they inhibit NTs such as substance P
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What is the MOA of clonidine?
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stimulates presynaptic alpha 2 receptors and inhibits NE release from both central and peripheral adrenergic terminals - results in marked reduction of sympathetic outflow
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What is the dose and effects of clonidine is a premediant?
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Dose - 5 mcg/kg PO
1. blunts tachycardia associated with laryngoscopy 2. reduces intraop lability of BP and HR 3. decreases plasma catecholamines 4. decreases MAC |
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When do withdrawal symptoms of clonidine occur? How long do they last? What are they?
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as early as 8 hrs or as late as 36 hrs after discontinuation, lasts 24-72 hrs
1. htn 2. tachycardia 3. insomnia 4. flushing 5. HA 6. apprehension 7. sweating 8. tremulousness |
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Which is more prominent with Clonidine use, declines in systolic or diastolic BP?
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systolic
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How is CO effected by clonidine use?
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Initially CO is reduced then with chronic use, CO returns to pretreatment levels
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What are the side effects of clonidine?
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1. sedation (MC)
2. xerostomia (MC) 3. skin rashes 4. constipation 5. impotence less of a problem 6. retention of Na and water 7. orthostatic hypotension (rare) |
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What type of rhythm is atrial flutter?
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A macro-reentrant arrhythmia that circulates in a counterclockwise manner in the right atrium
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Describe atrial flutter.
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-very fast HR with classic saw-tooth flutter waves on EKG best seen in leads II and V1
-generally accompanied by AV block |
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What are the causes of Aflutter?
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1. CAD
2. mitral valve disease 3. PE 4. hyperthyroidism 5. cardiac traume 6. myocarditis |
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Is the rhythm with aflutter regular or irregular?
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-the atrial rhythm is generally regular and the ventricular rhythm is regular if a fixed AV block is present or irregular in the setting of a variable block
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What is typically the AV block pattern seen in aflutter?
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2:1 which means an atrial rate about 300 beats/min and a ventricular rate about 150 beats/min
-Can vary from 2:1 to 8:1 |
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What is the pharmacologic tx of aflutter?
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-1st line - BBs such as esmolol (1 mg/kg IV) or propranolol to slow AV nodal conduction and control ventricular response
-2nd line - CCBs such as verapamil (5-10 mg IV) or diltiazem |
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What is the non-pharmacologic tx of aflutter?
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Indicated for excessively rapid V-rates or hemodynamic instability
-synchronized DC cardioversion starting at 100 J and increasing to 360 J |
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What are other pharmacologic txs that aren't as common for aflutter?
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1. Class III antiarrhythmic agents (Ibutilide 1mg) - good for new onset fllutter; must monitor for 12 hrs for torsades de pointes
2. amiodarone 150 mg over 10 min followed by 1 mg/min for 6 hrs 3. procainamide |
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Describe afib.
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An excessively rapid and irregular atrial focus with no P waves on EKG, but fine fibrillatory waves instead
-atrial rates 350-500 beats/min with irregularly irregular V-rates of 60-170 beats/min |
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What are the 2 important clinical considerations with Afib that aren't as valid with Aflutter?
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1. loss of atrial kick in afib can significantly impair CO
2. atrial thrombi are more likely to develop in afib |
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Which is more likely to be associated with significant cardiac disease, afib or aflutter?
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Afib
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What can be utilized to prevent postop Afib?
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1. periop amiodarone
2. sotalol 3. CCBs 4. Magnesium |
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What is pharmacologic tx for acute Afib?
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Acutely emphasis is upon ventricular response
1. BBs (esmolol) 2. CCBs (diltiazem) |
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What is the non-pharmacologic tx for acute afib?
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Indicated if pt unstable
-biphasic synchronized cardioversion -Bc of increased risk of thromboembolism, if present for longer than 48 hrs, pharmacologic attempts should be made and anticoagulation for 3-4 weeks considered before cardiovertin |
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What is the tx for chronic afib?
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1. anticoagulation with warfarin or dabigatran
2. when control of ventricular response is difficult with standard agents (BBs, CCBs, digitalis), electrode catheter ablation of the AV junction and permanent pacemaker 3. Those w/o significant CAD or LV dysunction, class Ic antiarrhythmic agents such as flecainide or propafenone have become agents of choice 4. antiarrhythmics that block repolarizing K currents (sotalol, amiodarone, and ibutilide) can be useful but have significant CV side effects |
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Why is digoxin preferred over digitoxin?
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Digoxin bc it can be brought to therapeutic levels faster than digitoxin and has a shorter elimination half time (important due to toxicity)
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When is digoxin indicated?
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1. tx of CHF
2. some SVTs such as afib to slow v response |
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Which drug is preferred, digoxin or digitoxin? Why?
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Digoxin bc it can be brought to therapeutic levels faster than digitoxin and has a shorter elimination half life
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What is the antidote to digoxin toxicity? How does it work?
|
Digibind - Fab antibodies capable of effectively achieving what even hemodialysis cannot
-antibody fragmentes bind free digoxin in both intravascular and interstitial spaces and facilitate renal clearance |
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What is the primary and most important manifestation of digoxin toxicity?
|
ventricular arrhythmias
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What is the earliest sign of digoxin toxicity?
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GI manifestations which include anorexia, nausea, and vomiting
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What are the CNS manifestations of digoxin toxicity?
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1. visual changes
2. HA 3. lethargy 4. confusion 5. hallucinations |
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How does digoxin toxicity relate to potassium levels?
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-hypokalemia is known to potentiate toxicity
-hyperkalemia is a marker of severe toxicity and a poor prognostic sign |
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How does hypokalemia potentiate digoxin toxicity?
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Bc it leads to greater myocardial tissue binding of drug
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How long does it take digibind to work?
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Effects usually begin withtin 1 hr of administration.
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What are the indications for digibind?
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1. digoxin related life-threatening dysrhythmias
2. K > 5 in the settin gof acute digoxin overdose 3. significantly altered mental status 4. renal failure 5. serum dig levels >6-10 ng/mL 6. ingestion of >4 mg in children or >10 mg in adults |
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What are the prototype osmotic diurectics?
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1. mannitol
2. urea |
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When should mannitol be avoided?
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If the BBB is disrupted bc it may enter the brain and bring fluid with it
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What are the effects of mannital on Na?
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-Initially - reduced Na reabsorption leading to hyponatremia
-Chronically - over time there is water loss which is greater than Na loss which leads to a relative hypovolemic hypernatremia |
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How does Lasix cause hypokalemia?
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The increased Na load reaching the distal tubule results in increased cation exchange and K loss?
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What are the clinical uses of Lasix?
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1. acute brain herniation - brain dehydration decreases CSF production
2. decreased preload through intravascular depletion 3. tx of ARF by converting oliguric renal failure to normal output renal failure |
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Why does ephedrine have a prolonged duration of action?
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secondary to slow inactivation and slow excretion
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How does propranolol effect glucose levels?
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It acts in concert with insulin to potentiate hypoglycemia
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Describe biosynthesis of catecholamines.
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Begins in the cytoplasm of he sympathetic nerve terminal
1. phenylalanine --> tyrosine 2. tyrosine --> dopa (via tyrosine hydroxylase) **rate limiting step 3. dopa --> dopamine (via dopa decarboxylase) 4. dopamine moved into storage vesicles and converted to norepinephrine 5. signals received which cause vesicle to fuse with cell membrane and release norepi into synaptic cleft |
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What happens to norepi not taken back up into the adrenergic terminal which enters the circulation?
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It is metabolized by:
1. MAO - monoamine oxidase 2. COMT - catechol-O-methyl-transferase |
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What is a concern when using etomidate?
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Adrenocortical suppression - may cause depression of adrenal steroidogenesis by inhibiting the conversion of cholesterol to cortisol
-can last 4-8 hrs after a dose |
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What type drug is etomidate? What are its properties at acidic and physiologic pH?
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carboxylated imidazole
-acidic pH - water soluble -physiologic pH - lipid soluble |
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Which induction agent has an increased incidence of PONV?
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etomidate
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Should etomidate dose be reduced in the elderly? Why?
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Yes due to age related decrease in the initial volume of distribution
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What causes the myoclonus associated with etomidate?
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It is probably secondary to disinhibition of subcortical structures that normally suppress extrapyramindal motor activity
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How does Ketamine act as an analgesic?
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It may act by suppressing spinal cord activity necessary for transmission of pain or bind opioid receptors
-also effect CNS neurotransmitters |
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When does the peak concentration of Ketamine occur? What is the elimination half life? How is it metabolized?
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-peak concentration - 1 min after IV and 5 min after IM
-half life - 1-2 hrs -metabolism - hepatic enzymes into norketamine |
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Is norketamine active?
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Yes - 1/5 -1/3 as potent as ketamine and can cause prolonged effects
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What drugs slow the metabolism of ketamine?
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halothane and diazepam
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What are the cardiovascular effects of Ketamine?
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Directly stimulates increase in sympathetic NS outflow --> inc BP, PAP, PVR, CO, MVO2
-also inhibits uptake of NE back into postganglionic nerve endings |
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How does ketamine effect the CO2 response?
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it is maintained
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What is a major side effect of ketamine?
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Emergence delirium - may be visual, auditory, proprioceptive illusion
-dreams and hallucinations can occur up to 24 hrs after dose, usually dissappear within a few hours |
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What factors increase risk of dreams and hallucinations following keatmine administration?
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1. age >16 y/o
2. female 3. dose > 2 mg/kg 4. personality problems |
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What drugs included in premeds can increase the incidence of emergence delirium with ketamine?
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1. atropine
2. droperidol |
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Repeated administration of which drugs metabolized by cyp 450 are capable of enzyme induction? What is the result?
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1. barbs
2. benzos 3. etomidate 4. alcohol 5. probably propofol -results in acceleration of metabolism resulting in a decrease in the intensity and duration of action of inducing agents and coadminstered drugs |
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Which form of local anesthetics crosses the cell membrane?
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only the non-ionized form
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Name the ester local anesthetics.
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1. procaine (Novacaine)
2. cocaine 3. tetracaine 4. benzocaine (Hurricaine) 5. chloroprocaine |
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Name the amide local anesthetics.
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All have 2 i's in the name
1. bupivacaine (Marcaine) 2. lidocaine 3. etidocaine 4. mepivacaine 5. ropivacaine 6. prilocaine 7. dibucaine |
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Are local anesthetics weak bases or weak acids?
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weak bases with a pKa > physiological pH
-less than 1/2 exists in lipid soluble nonionized form at pH 7.4 |
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Which local anesthetics is the lung capable of extracting following entry into venous circulation and limits the concentration reaching systemic circulation?
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1. lidocaine
2. bupivacaine 3. prilocaine |
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What enfluences placental transfer of local anesthetics?
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protein binding - the more highly protein bound, the lower the umbilical vein/maternal artery ratio
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Does CSF contain cholinesterase?
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No
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What is the placental transfer cutoff weight?
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1000 daltons
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Why is bupivacaine concentration less in fetal blood than maternal blood despite bupivacaine being < 1000 daltons in size?
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Maternal plasma proteins bind bupivacaine twice as avidly as fetal proteins and only the free-unbound drug is transferred
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Explain ion trapping.
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-LA are weak bases with low degrees of ionization and considerable lipid solubility
-At equilibrium of pH the concentrations of unionized drug in fetal and maternal plasma are equal -if the fetus becomes acidotic there is a tendency for more drug to exist in the ionized form, therby accumulating |
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What does an increase pKa mean?
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there is less nonionized forms at any pH
-with decreasing tissue pH there is less nonionized drug available |
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Why is bupivacaine more cardiotoxic than explained by its potency alone?
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-LA produce a dose-dependent delay in nerve impulse transmission in the cardiac conduction sytem by effects on Na channels
-Bupivacaine dissociates much more slowly from Na channel blockade therefore the blockade accumulates and greatly depresses cardiac conduction |
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What are signs and symptoms of cocaine toxicity?
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1. dysphoric agitation
2. hallucinations 3. seizures 4. mydriasis 5. diaphoresis 6. hyperthermia |
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What are the anesthetic considerations with cocaine intoxication?
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1. chronic abuse - if no acute intoxication, not associated with adverse interactions
2. acute cocaine intoxication potentiates d-tubocurare and pancuronium 3. MAC of halothan is increased with intoxication 4. exogenously administered epi in the presence of cocaine facilitates cardiac dysrhythmias |
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What paralytics should be used with caution in pts on MAOIs?
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1. suxx - may have decrease plasma cholinesterase
2. pancuronium - act synergistically as a sympathetic stimulant |
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Do MAOIs increase or decrease MAC?
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Increased
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When is surgery safe with MAOIs?
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Previously thought that they should be discontinued for 14-21 days
-current belief is that it is safer to continue and treat the symptoms |
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What is the MOA of MAOIs?
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Block the oxidative deamination of endogenous catecholamines into inactive vanillylmandelic acid with resultant accumulation of NE, Epi, and 5HT in post ganglionic nerve endings
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What are other drug effects in combination with MOAIs?
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1. guanadrel and levodopa - severe htn
2. insulin - increased hypoglycemic effect 3. methyldopa - hallucinations 4. meperidine - severe encephalopathy, htn, convulsions 5. reserpine - precipitation of mania by 5-hydroxytryptamine release |
