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Flashcards in Common Drugs Deck (71)
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1

Epinephrine

Class? MOA? Pharmacokinetics? SE? Contraindications? Doses?

CLASS= endogenous catecholamine & nonselective adrenergic agonist w/ a1=a2=ß1=ß2 affinity; MOST potent at alpha 1

MOA= . 

  • Low doses (B2) (1-2 mcg/minute) = vasodilation of skeletal muscle & decrease SVR, bronchodilation, & decrease histamine release;
    • MOA- B2 receptors coupled w/ G-alpha-s proteins which increase cAMP causing an influx intracellular Ca2+ causing agonist effects 
  • Moderate Doses (B1) (4-5mcg/min)= increase HR & contractility;
    • MOA B1- receptors coupled w/ G-alpha-s proteins which increase cAMP causing an influx intracellular Ca2+ causing agonist effects
  • High doses (A1&B) (10-20 mcg/min)= increase vasoconstriction= increase SBP, increase cardiac work; A2 = negative feedback & decrease BP
    • Binds to Alpha 1 (G=alpha-q) which increase PLC--> increase IP3/DAG--> increase PKC--> incrase Ca.
    • Binds to Alpha2 (G-alpha-i) inhibits adenylate cyclaSe--> decrease cAMP--> Increase K conductance causing hyperpolarization, relaxation,
      • Pre- Vascular- dilate, adrenergic- inhibit NT release, GI-relax
      • post- Cns- sedation, vascular- contraction, PLT- aggregation

Pharmacokinetics= poorly lipid soluble (little CNS effect);

  • onset- 1-2 min;
  • DOA- 5-10 min;
  • E1/2- 30 seconds;
  • metabolized & eliminated by MAO, COMT in the blood, liver & kidneys- reuptake & diffusion away

SE= tachycardia, HTN, angina, arrhythmias, hyperglycemia, decrease LA absorption, vasoconstriction of skin, GI tract, muscle, liver & kidneys; peripheral vascular insufficiency/gangrene in digits

CI= avoid in certain peripheral LA blocks, caution in DM, CAD, MI HTN, renal insufficiency, pheochromocytoma, hyperthyroidism, glaucoma, pregnancy

Dose= 1-2 mcg/min ß2; 4-5 mcg/min ß1; 10-20 mcg/min alpha & ß;

1 mg q 3-5 min for CV arrest ACLS;

2-8mcg/min infusion

2

Norepinephrine

Class? MOA? Pharmacokinetics? SE? CI? Dose?

CLASS= endogenous catecholamine & adrenergic agonist w/ potent alpha 1 & 2  minimal ß1 receptor affinity- lacks ß2 effects (a1=a2> B1>>>>>>>>>>>B2)

MOA= -alpha1= GalphaQ (Incrase Ca), Alpha 2=  Galphai (decrease cAMP) Beta 1= Galpha-s =binds to receptors coupled w/ G proteins which increase cAMP causing an influx of Ca2+ causing agonist effects  increases contractility, intense arterial & venous vasoconstriction (alpha1) of skin skeletal muscles, kidneys, & liver = increase BP, increase MAP, increase SVR; baroreceptor activation= decrease HR; decrease venous return- CO

 

Pharmacokinetics= onset- rapid; DOA- 5-10 min; E1/2- 2 min; metabolized & eliminated by MAO & COMT in blood, liver, kidneys, & lungs- reuptake or diffusion away

 

SE= increase SBP, DBP, MAP, SVR; decrease HR- d/t baroreceptors; decrease RBF, HBF & splanchnic BF; organ ischemia, metabolic acidosis & extravasation & necrosis of extremities & digits (do not administer in peripheral IV)

 

CI= thrombosis, cardiogenic & hypovolemic shock, MAOIs & TCAs (HTN crisis), caution in liver & renal disease (exacerbate damage d/t decrease BF) hyperthyroidism, pheochromocytoma

 

Dose= 4-16 mcg/min IV

3

Isoproterenol

Class? MOA? Pharmacokinetics? SE? CI? Dose?

CLASS = synthetic catecholamine & adrenergic agonist w/ ß1=ß2 affinity; minimal alpha (cardiac pacemaker)

 

MOA= binds to receptors coupled w/ G proteins to increase cAMP causing an influx of Ca2+ causing increase HR (greater) & contractility; increase SBP, decrease DBP; B2 = bronchodilation & peripheral vasodilation

 

Pharmacokinetics= onset- rapid; DOA- 5-10 min; E1/2- 3-5 min; rapidly metabolized & eliminated by COMT in the liver & pulmonary with 50% eliminated unchanged in the urine (need continuous infusion)

 

SE= tachycardia, angina, arrhythmias, increase SBP, decrease DBP, decrease CA BF ß1- increase contractility & increase O2 demand 

 

CI= HTN, CAD (increased O2 demand), MI, pheochromocytoma, hypertrophic cardiomyopathy, tachycardia, caution dig toxicity

 

Dose= 0.5-10 mcg/min

4

Dopamine

 

CLASS= endogenous catecholamine/precursor of NE & adrenergic agonist that stimulates all adrenergic receptors including DA receptors

 

MOA= Low doses (D1 1-3 mcg/kg/min)= vasodilates coronary, mesenteric, & renal vascular beds (ê afterload); Medium doses (B1 3-10mcg/kg/min)= é contractility, HR, & CO; High doses (A1 10mcg/kg/min)= vasoconstriction of all vascular beds including renal thereby increasing BP, SVR; also increase endogenous NE release

 

Pharmacokinetics= onset- rapid; DOA- 5-10 min; E1/2- 2 min; metabolized & eliminated by MAO & COMT in liver kidney, blood to 75% inactive & 25% NE

 

SE= tachycardia, arrhythmias, angina, extravasation, N/V, increase GFR, increase RBF, increase UOP; synergistic with Dobutamine to decrease SVR & increase CO (DA dilates renal & mesenteric vascular beds while Dobutamine dilates skin & skel muscle vascular beds)

 

CI= pheochromocytoma, hyperthyroidism, MAOIs, caution in HTN, CAD, sulfa allergy

 

Dose= DA1- low dose- 1-3 mcg/kg/min (ß1 medium dose- 3-10 mcg/kg/min; alpha- large dose- 10 mcg/kg/min

5

Dobutamine

CLASS= synthetic catecholamine & adrenergic agonist w/ ß1>B2 affinity & also weak alpha 1 stimulation; synthetic analog of isoproterenol 

MOA= B1 stimulation <5 mcg/kg/min, weak Alpha 1 stimulation at >5 mcg/kg/min; binds to receptors coupled w/ G proteins to increase cAMP causing an influx of Ca2+= B1 increases contractility & CO WITHOUT increase HR or BP too much; some ß2 bronchodilation & skin & skeletal muscle peripheral vasodilation= decrease SVR; minimal alpha 1 antagonism to further decrease afterload = good in CHF

 

Pharmacokinetics= onset- rapid; DOA- 5-10 min; E1/2- 2 min; metabolized & eliminated by MAO & COMT; reuptake or diffusion away from active site

 

SE= arrhythmias, SVT, angina, HTN, tachycardia; platelet inhibition, thrombocytopenia, coronary artery & pulmonary vasodilation, increase renal perfusion especially when used with DA (synergistic)

 

CI= avoid in hypertrophic cardiomyopathy, MAOIs, TCAs, caution in CAD & MI (ok for CHF)

 

Dose= 2-10 mcg/kg/min

6

Ephedrine

Class? MOA? Pharmacokinetcis? SE? CI? Dose?

CLASS= synthetic NON-catecholamine; direct & indirect (primarily) adrenergic agonist

MOA= indirectly activates alpha & ß receptors by stimulating NE release from post ganglionic SNS nerves; directly acts ß1 ---- increase contractility & increase HR, increase BP, increase CO; increase CA & skeletal muscle vasodilation (B2); decrease RBF & splanchnic BF

 

Pharmacokinetics= onset- rapid; DOA- 1 hr; E1/2- 3 hrs; slower MAO metabolism & excreted 40% unchanged in the urine

 

SE= arrhythmias, HTN, tachycardia, MI, CNS stimulation, can cause Tachyphylaxis, decrease uterine activity;

 

CI= HTN, CAD, MAOIs, TCAs, ephedra, caution in trauma (depleted stores)

 

Dose= 5-25mg IV

7

Phenyhlephrine?

Class? MOA? Pharmacokinetcis? SE? CI? Dose?

CLASS= synthetic NON-catecholamine; direct acting selective alpha 1 agonist

 

MOA= direct stimulation of alpha 1 receptors causing venous> arterial constriction; increase MAP, SBP, DBP, SVR; decrease HR & CO (strong activation of baroreceptors); can be used for hypotension & nasal decongestion

 

Pharmacokinetics= 90% PB; onset- rapid; DOA- 5-20 min; E1/2= 2-3 hrs; metabolized by MAO to phenolic conjugates & excreted in the urine 90%

 

SE= rebound nasal congestion, Bradycardia, HTN, arrhythmias, decrease RBF & splanchnic BF= decrease UOP; metabolic acidosis

 

CI= HTN, bradycardia, arrhythmias, CHF, glaucoma, cocaine, MAOI’s, TCA’s, renal impairment

 

Dose= 50-200 mcg IVP; 20-50 mcg/min gtt

8

Clonidine (unsure if for oral....)

CLASS= centrally acting alpha 2 adrenergic agonist

MOA= selectively activates alpha-2 adrenergic receptors in CNS, decreases sympathetic outflow from the medulla which decrease HR, contractility & decrease BP; has analgesia properties b/c alpha 2 receptors found in the dorsal horn of the SC inhibiting the release of substance P & decrease neuronal firing; used for HTN, induced sedation, analgesia

 

Pharmacokinetics= Vd 2.1 L/kg ; 20-40% PB; Onset 0.5-1 hour; DOA- 8 hrs; E1/2- 9-12 hrs; 50% metabolized in the liver & 50% excreted unchanged in the urine

 

SE= Bradycardia, hepatotoxicity, sedation, rebound HTN with abrupt w/d, Na+ & H2O retention, 

 

CI= hypersensitivity, pregnancy, clonidine potentiates the effects of VA or other anesthetics

 

Dose= 0.2-0.3 mg/day

 

9

Phentolamine

CLASS= nonselective competitive alpha adrenergic antagonist; a1=a2 affinity

MOA= binds to alpha-receptors to block the effects of catecholamines & inhibit G-protein coupled signaling cascade; peripheral vasodilation (arterial > venous) decrease BP;  may have some antihistamine and cholinomimetic activity

used to treat hypertensive emergencies especially those with pheochromocytoma, or as LA infiltration for tx. of sympathomimetic extravasation

Pharmacokinetics= onset- 2 min; DOA- 10-15 min; E1/2- 19 min; liver metabolism & excreted 10% unchanged in urine

SE= HA, arrhythmias, angina, MI, reflex tachy (baroreceptors activated from decrease BP), cramping, diarrhea (from cholinomimetic activity)

CI= CAD, MI, angina, PUD, treat hypotension after admin of phentolamine with NE over Epi

Dose= 1-5 mg IV bolus q 5 min, max 20 mg

for treatment of extravasation of norepinephrine- 5-10 mg in 10 mL of saline injected into affected area within 12 hours

10

Phenoxybenazmine

CLASS= nonselective covalent alpha adrenergic antagonist; a1>a2

MOA= covalently binds with alpha receptors to block the effects of catecholamines & inhibit G-protein coupled signaling cascade; peripheral vasodilation (arterial > venous) & decrease SVR & BP; given preop for patients with pheochromocytoma, or Raynaud’s disease>>- irreversible and long-acting

Pharmacokinetics= prodrug; onset- 1 hr; E1/2- 24 hrs; hepatic metabolism with renal/biliary excretion

SE= orthostatic hypotension, reflex tachy (baroreceptors- also increase HR/CO d/t NE having increaes effects at beta receptors), nasal congestion, impotence

CI= severe hypotension or hypovolemia; treat hypotension with NE over Epi

Dose= 10-120 mg/day PO

11

Prazosin

CLASS= alpha 1 adrenergic antagonist

MOA= blocks alpha 1 receptors antagonizing Epi & NE  vasodilation/ decrease SVR & minimal reflex tachycardia; used to treat HTN especially those with BPH (decrease  prostate size), used preop for pheochromocytoma, & decrease vasospasm in Raynaud’s disease

Pharmacokinetics= highly PB; onset- 1 hr; DOA- 6-10 hrs; E1/2- 4 hrs; metabolism & conjugation in the liver & excreted in the bile & feces

SE= dizziness, HA, orthostatic hypotension, edema, anticholinergic effects- dry mouth, urinary frequency; hepatotoxicity, SLE

CI= caution with regional- decrease BP exaggerated, caution with ßB & other drugs that decrease P, pregnancy

Dose= 1mg PO bedtime

12

Labetalol

CLASS= competitive  ß1, ß2 & alpha 1 antagonist 

MOA= blocks ß1, ß2 & alpha 1 receptors to block the effects of catecholamines & inhibit G-protein coupled signaling cascade (beta: alpha 7:1) thereby decrease BP, SVR, HR; CO unaffected (no alpha 2, so  negative feedback not blocked). Also, decreases stage 4 depolarization in SA & AV node

Pharmacokinetics= 50% PB; onset- 5 min; DOA- 4 hrs; E1/2- 5-8 hrs; conjugation to glucuronic acid & eliminated via liver by CYP2D6 & kidneys. LIpid soluble

SE= hypotension, bradycardia, angina, bronchospasm, mask hypoglycemia, exercise intolerance, exacerbate PVD

 

CI= hypotension, bradycardia, HB, caution: asthma, COPD, CHF, cardiogenic shock, DM; avoid concurrent use with CCBs; effect decreased by salicylates & NSAIDs (decreases antiHTN effect)

 

Dose= 5-20 mg IV q 5-10 min (max 300mg)

13

Esmolol

CLASS= ß1 selective adrenergic antagonist & class II anti-arrhythmic

MOA= selective blockade of ß1 receptors to block the effects of catecholamines & inhibit G-protein coupled signaling cascade to decrease HR without decrease BP significantly; class II antiarrhythmic- decrease rate of spontaneous phase 4 depolarization, decrease SA node discharge, decrease ANS activity and conduction velocity AV node. DECREASE automaticity

Pharmacokinetics= 55% PB; onset- 2min; DOA- 10-15 min; E1/2- 9 min; rapidly hydrolyzed by plasma esterases and excreted in urines

SE= CNS sedation (lipid soluble); hypotension, bradycardia, HB, bronchoconstriction, can mask hypoglycemia

CI= hypotension, bradycardia, HB, caution: asthma, CHF, DM; avoid concurrent use with CCBs; effect decreased by salicylates & NSAIDs. 2nd and 3rd trimester

Dose= 5-10 mg IV q 3 min max 80 mg; infusion- 50-300 mcg/kg/min

14

Propranolol

CLASS= nonselective beta antagonist; ß1=ß2

MOA= antagonizes the ß1 & ß2 receptors equally to block the effects of catecholamines & inhibit G-protein coupled signaling cascade; ß1- decrease contractility, HR, CO & O2 demands; ß2 blockade= increase PVR & increase CA vascular resistance (offset by decrease demand on the heart with the ß1)

Pharmacokinetics= 90% PB; high lipid solubility; large first pass effect; onset- 5 min; DOA- 4 hrs; E1/2- 2-3 hrs; extensive pulmonary uptake; liver metabolism by CYP450 which relies on HBF & excreted in the urine (can decrease clearance of other drugs metabolized by CYP 450- LA, benzos, warfarin, etc.)

SE= hypotension, bradycardia, bronchospasm, Na+ retention d/t renal response from decrease CO, mask hypoglycemia, exacerbate PVD

CI= HB, bradycardia, hypotension, asthma/bronchospasm, CHF, DM, decrease clearance of LA; decrease pulmonary 1st pass effect of fentanyl

Dose= 0.05 mg/kg IV or 1-10 mg (slowly 1mg q 5 min)

15

Metoprolol

CLASS= ß1 selective antagonist

MOA= selective blockade of ß1 receptors to block the effects of catecholamines & inhibit G-protein coupled signaling cascade causing decrease HR & BP

Pharmacokinetics= 10% PB; onset- 5 min; DOA- 3-4 hrs; E1/2- 7 hrs; liver metabolism by CYP2D6 & renal excretion; 50% first pass metabolism

SE= hypotension, bradycardia, angina, exercise intolerance; In high doses= bronchoconstriction, mask hypoglycemia, exacerbate PVD

CI= hypotension, bradycardia, HB, caution: asthma, CHF, DM; avoid concurrent use with CCBs; effect decreased by salicylates & NSAIDs

Dose= 1-5 mg IV q 2-5 min up to 15mg

16

Method of Action of all anti-cholinergics?

Competitively inhibit ACh at the muscarinic receptors & decrease PNS activity (preventing decrease cAMP & cGMP);

causes sedation by blocking Ach effects @ M1;

increase HR by blocking the ACh effects @ M2;

relaxes bronchial smooth muscle & decrease secretions by blocking Ach effects @ M2 & M3; also decrease GI secretions;

used to tx. Bradycardia, secretions, nausea, biliary spasm r/t opioids; bronchodilation, mydriasis for eye procedures; w/ anticholinesterases

17

Atropine

CLASS= tertiary amine anticholinergic- crosses BBB

(Most potent increase in HR)

MOA- Competitively inhibits muscariniac receptors at M1, M2, M3 with most predominant at M2, allowing SNS to dominate, raising the HR.

Pharmacokinetics= 40% PB; onset- 1 min; peak- 1-2 min; DOA- 30-60 min; E1/2- 2 hrs; hydrolyzed in the liver to tropine & tropic acid & excreted 18% unchanged in the urine. VD 1.6 L/kg

SE= increase IOP, sedation, post-op delerium- crosses BBB, increases HR, CO, arrhythmias, IOP, blurry vision; decreases secretions & GI motility, bronchodilation, urinary retention; inhibits diaphoresis; central anti-cholinergic syndrome

 

CI= glaucoma, renal disease, CAD, caution elderly

 

Dose= 0.01 mg/kg for reversal; 0.4-1 mg for brady; 1 mg q 3-5 min for asystole, PEA

18

Glycopyrrolate

CLASS= synthetic quaternary ammonia anticholinergic that does not cross the BBB; best for elderly

MOA: 

Competitively inhibit ACh at the muscarinic receptors & decrease PNS activity (preventing decrease cAMP & cGMP);

increase HR by blocking the ACh effects @ M2;

relaxes bronchial smooth muscle & decrease secretions by blocking Ach effects @ M2 & M3; also decrease GI secretions;

Pharmacokinetics= onset-2-3 min; DOA- 2-4 hrs; E1/2- 1 hr; liver metabolism & 85% excreted unchanged in the urine; poorly lipid soluble

SE= inrease HR (++), CO, IOP; arrhythmias; blurry vision; decrease secretions(++) & GI motility, bronchodilation (++)

CI= neonates, CAD, HTN, CHF, glaucoma, renal

Dose= 0.01-0.02 mg/kg IV reversal with neostigmine; 0.1-0.2 mg anti-sialagogue & bradycardia

 

19

Scopolamine

CLASS= tertiary amine anticholinergic that crosses BBB; used for motion sickness, PONV, sedation, bronchodilation; biliary & ureteral SM relaxation; NOT used for reversal of NMB

(Most potent anti-sialagogue (+++) & sedative anti-cholinergic) (+++)

MOA: 

Competitively inhibit ACh at the muscarinic receptors & decrease PNS activity (preventing decrease cAMP & cGMP);

causes sedation by blocking Ach effects @ M1;

increase HR by blocking the ACh effects @ M2;

relaxes bronchial smooth muscle & decrease secretions by blocking Ach effects @ M2 & M3; also decrease GI secretions;

Pharmacokinetics= lipid soluble; onset- 10 min; DOA- 2 hrs; E1/2- 4 hrs- may last 3-7 days; metabolized by the liver with <1% excreted unchanged in urine

SE= sedation, post-op delerium; increase HR (+), CO, IOP; OH; arrhythmias; blurry vision; decrease secretions (+++) & GI motility; urinary retention; central anti-cholinergic syndrome, bronchodilation (+)

CI= glaucoma, GI/GU obstruction; caution elderly

Dose= 0.3-0.6 mg IV q 4-6 hrs

20

MOA Benzodiazpines? 5 uses? Specific antagonist?

CLASS= benzodiazepine

 

MOA= potentiates binding of GABA to the GABA-A receptor facilitating the action of GABA- opens Cl- channels & increases Cl- conductance, hyperpolarizing the cell, decreasing neuronal transmission & making it more resistant to excitation

 

5 uses- anxiolysis, sedation, anterograde amnesia, muscle relaxation at the spinal level, anticonvulsants (no analgesia properties)

 

Specific antagonist- flumenazil

21

Midazolam

CLASS= benzodiazepine

MOA= potentiates binding of GABA to the GABA-A receptor facilitating the action of GABA- opens Cl- channels & increases Cl- conductance, hyperpolarizing the cell, decreasing neuronal transmission & making it more resistant to excitation

Pharmacokinetics= 94% (highly) PB, highly lipid soluble, large Vd (1-1.5L/kg); rapidly crosses BBB; comes as water soluble Imidazole ring- lipid soluble when injected; ONSET- 60-90 second, PEAK 3-5 min; DOA 15-80 min; hepatic metabolism by CYP450- excreted in urine; 1 active metabolite- 1-hydroxy-midazolam (1/2 as potent); E1/2= 1-4 hrs; redose in 5 min

 

SE= decrease CBF & CMRO2; does not produce isoelectric EEG; preserves cerebral response to CO2; CO2 response curve flattens; anticonvulsant and amnestic; decrease SVR & BP @ induction doses but no change in CO; CV stable; Depresses ventilation with induction dose or with opioids; depresses deglutition reflex; does not attenuate SNS response to DVL

 

CI= early pregnancy, glaucoma; decrease dose in hepatic impairment; increase sensitivity in old people; synergistic effect with opioids in respiratory depression; paradoxical excitement- rare

 

Dose= premed-1-2.5 mg IV (max 5mg); induction- 0.1-0.2mg/kg over 30-60 sec

22

Diazepam

CLASS= benzodiazepine

 

MOA= potentiates binding of GABA to the GABA-A receptor facilitating the action of GABA- opens Cl- channels & increases Cl- conductance, hyperpolarizing the cell, decreasing neuronal transmission & making it more resistant to excitation

Pharmacokinetics- highly PB, highly lipid soluble, large Vd; rapidly crosses BBB & placenta; hepatic conjugation by CYP450 & excreted in urine; rapidly absorbed in GI tract & rapid IV onset; 3 active metabolites- most active is desmethyldiazepam which lasts 48-96 hrs (hangover effect); E1/2= 21-37 hours; least potent of the benzos; pain on injection- propylene glycol

 

SE= DECREASE CBF, CMRO2, DOES NOT cause isoelectric EEG; preserves cerebral response to CO2; CO2 response curve flattens; DECREASE SVR, BP with induction dose but no change in CO; CV stable; Depresses ventilation with induction dose or with opioids; depresses deglutition reflex; does not attenuate SNS response to DVL

 

CI= pregnancy, glaucoma; decrease dose in renal/hepatic impairment; increase sensitivity in old people; synergistic effect with opioids in respiratory depression; paradoxical excitement-rare; Cimetidine prolongs clearance

 

Dose= premed- 0.2 mg/kg IV; 10-15 mg PO; induction- 0.5-1 mg/kg IV; anticonvulsant- 0.1mg/kg IV

 

23

Lorazepam

 

CLASS= benzodiazepine

MOA= potentiates binding of GABA to the GABA-A receptor facilitating the action of GABA- opens Cl- channels & increases Cl- conductance, hyperpolarizing the cell, decreasing neuronal transmission & making it more resistant to excitation

Pharmacokinetics= 80% (highly) PB, highly lipid soluble, large Vd; hepatic metabolism by CYP450 & 80% excreted unchanged in urine; 6 hours amnesia without sedation; most potent benzo; no active metabolites; lipid soluble- pain on injection- propylene glycol; does not alter NMB dose; SLOWER onset = 2 hours (limits usefulness); E1/2= 10-20 hours

 

SE= decrease CBF & CMRO2; DOES NOT produce isoelectric EEG; preserves cerebral response to CO2; does not flatten CO2 curve; decrease SVR, BP @ induction doses w/ no change in CO; Depresses ventilation with induction dose or with opioids; depresses deglutition reflex; does not attenuate SNS response to DVL

 

CI= glaucoma; increase sensitivity in old people; decrease dose in hepatic/renal impairment; synergistic effect with opioids in respiratory depression; paradoxical excitement- rare

 

Dose= premed- 1-4 mg IV; 50 mcg/kg PO

 

24

Propofol

Class? MOA? Pharmacokinetics? SE? CI? Dose?

CLASS= non-barbiturate induction agent; 2,6 di-isopropophenol

 

MOA= (1) discourages the dissociation of GABA from the GABA A receptor, prolonging the action- causing increase Cl- conductance- hyperpolarizing the cell & decreasing neuronal transmission; (2) ALSO inhibits glutamate at the NMDA receptor – both producing sedation & hypnosis

 

Pharmacokinetics= 90% PB; highly lipid soluble onset- rapid 30-60sec; DOA- short-2-8 min(terminated by rapid redistribution); Vd- 4L/kg; E1/2- 0.5-1.5 hrs; prepared with egg, soy & glycerol & has preservatives; conjugated in liver by CYP450 & excreted in the urine (<0.3% unchanged)- also extrahepatic metabolism (kidneys, lungs, intestinal mucosa); clearance exceeds HBF (not dependent on blood flow but enzymes); antiemetic & anti-pruritic @ low doses. Context sensitive 1/2 life infusion up to 8 hours is 40 minutes

 

SE= decreases CBF, CMRO2, ICP, & IOP- isoelectric EEG; myoclonus; Dose-dependent CV depression; decrease BP (25-40%), SVR, NO change in HR; apnea w/ induction dose- decrease RR & decrease ventilatory response to CO2; bronchodilation; pain on injection

 

CI= soy, egg allergy; decrease dose in elderly; caution in hypotension & hypovolemia (CV instability); caution in asthma & COPD w/ Na metabisulflate preservative (bronchoconstriction)

 

Dose= induction- 1-2.5 mg/kg IV; sedation- 25-100 mcg/kg/min IV; maintenance- 100-300 mcg/kg/min IV; (Anti-emetic-10-20mg IV)

25

Etomidate?

Class? MOA? Pharmacokinetics? SE? CI? Dose?

CLASS= carboxylated imidazole derivative

 

MOA= binds to GABA-A receptors & (1) increases affinity of GABA & also (2) mimics GABA at the GABA-A receptor site = increases Cl- conduction= hyperpolarizes cell= decreases neuronal transmission - producing sedation & hypnosis

 

Pharmacokinetics= 75% PB; lipid soluble; onset- rapid 30-60sec; DOA- short 5-15 min (terminated by rapid redistribution); Vd- 3L/kg; E1/2= 3-5 hrs; water soluble in solution & mixed w/ propylene glycol (burning on injection); liver hydrolysis & metabolism by plasmaesterases & excreted in urine (2%) & bile; clearance dependent on HBF (need HBF to clear drug, will be decreased clearance in time of decreased blood flow)

 

SE= decrease CBF, CMRO2, ICP, & CMRO2- can increase EEG- causing seizures;; NO change in BP, HR, SVR, CO- very cardiac stable; Potentiates NMB; 30-40% N/V; myoclonus; hiccups; adrenocorticoid suppression - may need cortisol replacement; pain on injection (reversible inhibition of 11- b-hydroxlyase and 11-a-hydroxylase)

 

CI= seizures, porphyria, Addison’s disease/adrenal insufficiency

 

Dose= induction- 0.3mg/kg; sedation- 5-8 mcg/kg/min; maintenance- 10 mcg/kg/min

26

Ketamine

Class? MOA? Pharmacokinetics? SE? CI? Dose?

CLASS= non-barbiturate induction agent; phencyclidine derivative

MOA= (1) blocks NMDA receptors to inhibit influx of Na+, Ca2+- inhibits the excitatory response of glutamate & produces a “dissociative state anesthesia” via depression of association areas of the brain (depresses cerebral cortex and thalamaus while increasing hippocampus); (1) analgesia effects by interacting with mu, kappa, delta & sigma receptors- (3) works on monoaminergic descending pain pathways & substance P in SC; (4) muscarinic (antagonist?) & (5) Ca++ channel antagonist

 

Pharmacokinetics= 12% (poor) PB; highly lipid soluble; onset- rapid 30-60sec; DOA= short 5-15min (short d/t redistribution); Vd- 3L/kg; E1/2- 2-3 hrs; acidic soluble & racemic mixture; metabolized by CYP450 to norketamine (active metabolite) then excreted in urine; clearance dependent on HBF

 

SE= increase CBF, ICP & CMRO2 & IOP; myoclonus, hallucinations & emergence delirium (can prevent with benzos); increase SNS stimulation = increase HR, SVR, BP; direct myocardial depressant (especially in critically ill patients that cannot surmount a SNS response); BRONCHODILATION (SNS); increase PVR; increase saliva production (laryngospasm risk), potentiates NMB’s

 

CI= psych disorders, head injury (increase ICP), eye injury, CAD, IHD, Systemic or pulmonary HTN

 

Dose= induction- 0.5-2 mg/kg IV; sedation 0.2-0.5 mg/kg IV; maintenance- 1-2 mg/kg/hr IV; 5-10 mg/kg IM/PR

27

Dexmedetomidine?

Class? MOA? Pharmacokinetics? SE? CI? Dose?

CLASS= highly selective central-acting alpha 2 adrenergic agonist; GA/TIVA adjunct (a2/a1 1620:1)

MOA= activates alpha 2 receptors- decrease SNS outflow & NE release causing sedation, anxiolysis, decrease neuroendocrine response; closely mimics sleep & causes analgesia by inhibiting substance P in SC (also locus ceruleus (hypnosis))

 

Pharmacokinetics= 90% PB; water soluble; Vd- 3L/kg; redistributes in 6 min; E1/2- 2-3 hrs- can build tolerance & dependence & has context sensitive ½ time- longer gtt on- longer it takes to metabolize; metabolized in the liver (rapid metabolism in liver by conjugaiton, n-methylation, hydroxylation) & excreted in urine & bile; antagonist- atipamezole

 

SE=  decrease CBF but no change in CMRO2 & ICP; decrease BP, HR (most significant), SVR; minimal change in RR & small decrease in TV; depresses thermoregulation; decreases MAC/doses of other anesthetic agents. Attenuates CV resposne to noxious stimuli, no change in CO2 response

 

CI= Afib, HB, severe bradycardia, pts that cannot tolerate lower BP or HR

 

Dose= 1 mcg/kg over 15 min bolus then 0.2-1 mcg/kg/hr

28

Succinylcholine

CLASS= Depolarizing NMB; benzylisoquinolone

MOA= PARTIAL AGONIST- Binds to alpha subunits of nicotinic Ach receptors mimicking the action of ACh at the NMJ opening Ca++ channels & depolarizing the motor endplate; fasciculations then flaccid paralysis occurs; Channels stay open & membrane cannot respond to subsequent ACh; effect terminated when SCh diffuses away from the NMJ

 

Pharmacokinetics= water soluble; small Vd (0.2L/kg) & PB; onset- 30-60 sec; DOA- 8-15 min; E1/2- 2-4 min; rapidly hydrolyzed by plasmaesterases when diffuses away from the NMJ & excreted in the urine

 

SE= increase ICP, IOP, IGP; histamine release - decrease HR & BP, HYPERK+ (increae 0.5-1 mEq/L) (dysrhythmias); masseter spasm, myalgias, fasciculations, rhabdomyolysis, myoglobinuria, MH

 

CI= MH, renal patient with high K+, high K, peds unless emergency, caution asthma & COPD; atypical plasma esterase deficiency; muscles weakness like muscular dystrophy; sepsis, burn patients

 

Dose= laryngospasm-10-20 mg IV; RSI/intubation- 1-1.5 mg/kg; infusion- 2-4mg/min

29

NDMR MOA?

COMPETITIVE ANTAGNOIST- Competitively inhibit ACh binding at the post-junctional nicotinic receptors thereby preventing Ca++ channels from opening, thus no depolarization of the muscle cell membrane & no contraction

 

30

Atracurium

CLASS= intermediate acting benzyllisoquinoline NDMR (-curium)

pre and post NMJ AcH inhibition

MOA: Competitively inhibit ACh binding at the post-junctional nicotinic receptors thereby preventing Ca++ channels from opening, thus no depolarization of the muscle cell membrane & no contraction

Pharmacokinetics= water soluble; 80% PB; Vd: 0.2L/kg; onset- 2-3 min; DOA- 30-60 min; E1/2- 20 min; metabolized by ester hydrolysis 2/3 & Hofmann elimination 1/3 (temp & pH dependent) & excreted in the urine; has metabolite Laudanosine (can accumulate in RF & cause CNS problems like seizures- is a tertiary amine and can cross BBB)

 

SE= Histamine release; decrease BP (minimal) & increase HR; skin flushing (all related to histamine release); muscle weakness; NMB can be potentiated with IA’s, ketamine, some abx, lithium, LA’s, antiarrhythmics, Mg++

CI= conscious patient, hypersensitivity; caution with asthma, COPD, CAD, seizure hx, muscle weakness, myasthenia gravis (increase sensitivity); metabolite can accumulate with renal problems; prolonged action in acidosis & hypothermia

Dose= initial- 0.5 mg/kg IV; maintenance- 0.08 - 0.1 mg/kg q 20-45 min