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b. pharm exam 2 (w13) > Pharm-cardiac-catecholamines > Flashcards

Pharm-cardiac-catecholamines Flashcards

1
Q

what are the physiological actions of sympathomiometic amines (7 things)?

A
  1. peripheral excitation-
  2. peripheral inhibitory action-
  3. cardiac excitation
  4. endocrine effects
  5. metabolic effects
  6. cns effects
  7. pre synaptic effects
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2
Q

what is periphreal excitation?

A

vasoconstriction of smooth muscles in blood vessels perfusing skin

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3
Q

what is peripheral inhibitory action?

A

relax smooth muscle in gut, broncioles, and blood vessels prerfusing skeletal muscles

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4
Q

what are sub types of adrenergic receptors & where are they found?

A

alpha 1- found in blood vessels, urinary sphincter
alpha 2- found in CNS & pre-synaptically
beta 1- found in heart
beta 2- found in lungs, pancreas, vessels, bladder, uterus, GI tract

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5
Q

what are the sympathomimetic amines actions on the heart?

A

chronotropic
dromotropic
inotropic

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6
Q

what are the 2 metabolic (energy) effects of sympathomimetic amines?

A

enhanced glycogenolysis and lipolysis

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7
Q

what are endocrine actions of sympathomimetic amines?

A

can modulate the secretion of insulin

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8
Q

action of sympathomimetic amines in the cns

A

released by neurons in the brain where they influence LOC and inhibit appetite

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9
Q

sympathomimetics on presynaptic terminals (what receptors, & what does their activation cause)?

A

alpha 2 receptors are pre synaptic on adrenergic terminals (activation inhibits the release of norepi).

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10
Q
  1. name an alpha 1 prototypical agonist?

2. prototypical antagonist?

A
  1. agonist=phenylephrine

2. antagonist=prazosin

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11
Q
  1. alpha 2 prototypical agonist?

2. antagonist?

A
  1. A2 agonist=clonidine

2. A2 antagonist=yohimbine

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12
Q
  1. beta one prototypical agonist?

2. antagonist?

A
  1. agonist: dobutamine

2. antagonist: metoprolol

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13
Q

beta two protatypical agonist?

A

terbutaline

dose .25 mg SQ

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14
Q
  1. epinephrine: the catecholamine ___?
  2. what receptors does it activate?
  3. what does it cause (BP)
  4. what is a side effect of this?
A
  1. the catecholamine PROTOTYPE (the big gun)
  2. activates both alpha and beta receptors
  3. causes increase in blood pressure
  4. there is some rebound hypotension before normalizing d/t initial stimulation of beta receptors (which cause vasodilation).
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15
Q
  1. what are effects of epi on heart? what does it increase overall? what receptors?
  2. blood vessels? what increases overall? what receptors?
A
    • inotrope, dromotrope, & chronotrope; increases cardiac output; B1.
  2. vasoconstriction of blood vessels servicing the skin; increases total periphreal resistance»TPR which increases BP; A1.
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16
Q
  1. what is the depressor effect?

2. why are there pressor and depressor effects?

A
  1. the depressor effect is vasodilation of blood vessels that supply skeletal muscles caused by epi (shunt blood to muscles during fght or flight)
  2. because you are shifting blood flow from organs of minor relevance (by “pressor”) vasoconstriction in an emergency to muscles by vasodilation (or “de-presor”) to facilitate survival (fight or flight)
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17
Q

what will any drug that infulences BP cause?

A

some sort of compensatory reflex and or baroreceptor response (as long as reflex is intact).
—–decrease pressure on baroreceptors, heart rate decreases; increase pressure baroreceptors, heart rate increases—-

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18
Q

drugs that influence cardiac functions can also cause what?

A 
cardic arrhythias (ex. high doses of epi cause arrhythmias)
this is a negative effect
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19
Q

what does epi do to these organs? what receptors for each?

  1. bladder (receptors) & sphincters (receptors)
  2. uterus (in 3rd trimester) (receptors)
  3. with that being said, what could you use epi for in pregnancy?
  4. what is this receptor action?
A
  1. bladder: relaxation of detrussor muscle of bladder (Beta 2); contraction of sphinctors (Alpha 1)- causing urinary retention
  2. uterus: variable response depening on phase of cycle, gestation etc. –during last trimester or so: inhibits tone and contractions (beta 2)
  3. epi can be used to prevent premature labor
  4. this is a Beta 2 agonist action because beta 2 activation relaxes the uterus.
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20
Q

epi effect on: (& what receptor is affected/ stimulated)?

  1. gi tract
  2. bronchiole smooth muscle
A
  1. the GI tract is relaxed by epi; peristalsis is slowed, tone reduced (gi motility not importain in fight or flight)-Beta 2 effect
  2. bronchioles relaxed by epi - Beta 2 effect
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21
Q

epi effect on metabolism:
1. effect on glycogen; what receptor; what does it cause?
2. effect on fat; what receptor; what does it cause?
3. effect on insulin; receptor; why?
4,. in a “nut shell”, epinephrine does what (as far as metabolism) for what?

A
  1. enhances glycogenolysis (??Alpha 1 or Beta 2??): results in increased glucose (energy source for fight of flight)
  2. increases lipolysis (Beta 3), allowing for more free fatty acids (for quick energy)
  3. insulin secretion inhibited by epi (Alpha 2 effect), prevents insulin from transporting glucose into cells right away.
  4. breaks glycogen into glucose and breaks fat into fatty acids; inhibits insulin all to increase available energy sources for immediate use.
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22
Q
  1. how effective is PO epi?
  2. how about SQ
  3. Inhaled?
A
  1. GI absorption is negligable (insignificant)
  2. SQ action is slowed d/t vasoconstricting properties (which makes it a good additive to LAs)
  3. inhalation effects are restricted to respiratory system, but it can cause arrhythmias (more selective drugs are better)
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23
Q

epi effects:

  1. what affect does 1-2 mcg/min have (on what receptors)?
  2. what does 4 mcg/min effect and what receptors?
A
  1. 1-2 mcg/min stimulate Beta 2 receptors in periphery; vasodilation of skeleta muscle vessels causes modest drop in BP
  2. 4 mcg/min stimulats Beta 1 receptors; this causes :
    • increased HR
    • increased CO (d/t increased HR, contractility & venous return)
    • increased systolic BP (d/t increased rate & c.o.)
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24
Q

what does 10-20 mcg/min of epi stimulate?

A
  1. alpha and beta (alpha more)
  2. alpha 1: cutaneous, mucosal, hepatorenal vasoconstriction
  3. beta 2: vasodilation and increased rennin secretion
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25
Q

epi dose for cardiac arrest:

  1. beginning?
  2. intermediate?
  3. escalating doses?
  4. high?
  5. ETT dose?
A
  1. beginning:1 mg IV q 3-5 min
  2. intermediate: 2-5 mg q 3-5 min
  3. escalating: 1mg, then 3mg, then 5 mg q 3 minutes
  4. high does: 0.1 mg/kg iv q 3-5 min
  5. ETT: 2-2.5 higher than IV dose and diluted with 10cc NS or distilled water
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26
Q

epinephrine for bronchodilator:

  1. IM or SQ dose
  2. onset
  3. nebulized dose
  4. onset
A
  1. epi (1:1,000) 0.1-0.5 mg IM or SQ q 15 min to 4 hrs
  2. onset: 5-10 min
  3. nebulized: 8-15 gtt: give 1 to 3 treatments q 4-6 hours
  4. onset: less than 1 minute
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27
Q

hypersensitivity epi dose;

  1. IM?
  2. IV (if hypotension)?
  3. folowed by Infusion of what rate?
A
  1. 0.3-0.5 mg IM or SQ; repeat PRN
  2. hypotension: 0.1 mg iv slow push over 5-10 min
  3. followed by gtt of 1-10 mcg/min
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28
Q

epi dose for: refractory hypotension (unresponsive to pressors) or bradycardia (unresponsive to atropine or pacing)

A

1-10 mcg/min iv gtt, titrate to effect

29
Q

epinephrine toxic effects:

  1. neurological
  2. cardiac rhythm
  3. blood pressure
A
  1. fear, anxiety, tenseness, restlessness
  2. atrioventricular arrhythmias (especially when combined with anesthetic drugs like Halothane
  3. pressor effect causing increased BP (which can lead to MI or CVI etc.).
30
Q

norepi:

  1. what is it/ what does it do in general (efffects/ receptors)?
  2. what does it do when given IV?
A
  1. a potent agonist at alpha1 and beta1 receptors causing intense vasoconstriction at all vascular beds, has little effect on beta2 (does not bronchodilate)
  2. when given IV it cause pronounced increase in SVR d/t vasoconstrictive effects
31
Q
  1. what un-desired side effect can come from the vasoconstrictive effects of norepi (levo)?
  2. what causes it?
A
  1. reflex bradycardia
  2. -intense vasoconstriction and increased SVR lead to
    - decreased venous return to the heart causing decreased C.O.
    - this stimulates baroreceptors to slow heart
32
Q

norepi toxic effects:

  1. how do they compare with epi’s tox effects?
  2. what are they (neuro, cardiac and with toxic doses of norepi)?
A
  1. much like epi but less pronounced and less frequent
  2. neuro: anxiety, headache;
    2b. cardiac: palpitations, dysrhythmia,
    2c. severe hypotension (with toxic doses)
33
Q

what does halothane do that epi and norepi are contraindicated while using it?

A

Halothane sensitizes the heart to arrhythmic effects of catacholamines

34
Q
  1. what can accidental extravisation of IV NE (levo) cause?

2. why shouldnt levo be given to pregnant women?

A
  1. extravisation causes anoxic tissue necrosis and impaired circulation to affected limb
  2. Norepi/ Levo stimulates alpha 1 receptors in uterus whicn could cause contractions
35
Q

Norepi dosing:

  1. initial dose (gtt)
  2. usual range for gtt
  3. ACLS dose range
  4. onset
  5. duration
  6. elimination
A
  1. initial: 0.5-1 mcg/min (titrate)
  2. gtt range: 8-30 mcg/min
  3. ACLS dose range: 0.5-30 mcg/min
  4. onset: 1-2 min
  5. duration: limitied
  6. elimination: 84-96% as INactive METABOLITE
36
Q

dopamine:

  1. acts on what receptor?
  2. receptors are found where?
  3. what is its action?
A
  1. acts on dopamine receptors (also beta and alpha at higher doses).
  2. receptors are found in renal, mesenteric and coronary vascular beds
  3. causes vasodilation when activated (ability to increase blood flow thru kidneys when blood pressure low)
37
Q

pharmodynamics of dopamine:

  1. what chemical class?
  2. what dose vasodilates renal vasculature?
  3. what other vessels does it dilate?
A
  1. direct acting natural catecholamine
  2. 1-3 mcg/kg/min
  3. increases blood flow to renal, mesenteric, coronary and cerebral areas via vasodilation
38
Q

dopamine pharmacodynamics:

  1. at medium doses stimulates what receptors ( located where)?
  2. what are the medium doses?
  3. at highest doses stimulates what receptors (located where)?
  4. what are high doses?
A
  1. stimulates beta 1 receptors in the heart at moderate doses
  2. moderate dose=2-10 mcg/kg/min
  3. stimulates alpha 1 receptors in peripheral vasculature at high dose
  4. high dose= greater than 10 mcg/kg/min
39
Q
  1. what does moderate dose dopamine cause?

2. what does high dose dopa cause?

A
  1. mod. dose dopa causes: increased myocardial contracility, stroke volume and cardiac output
  2. high dose dopa causes: increased PVR, decreased renal blood flow and increased potential for arrhythmias
40
Q
  1. toxic effects of dopa?
  2. how long does toxicity last?
  3. what is dopamine used for?
A
  1. similar to that of Ne (tachycardia, dysrhythmias, hypertension, MI).
  2. toxicity s/e dissapear shortly after discontinuation of drip (short half life)
  3. mainly used in treatment of shock especially in patients with reduced renal function
41
Q

dopamine administration:

  1. onset:
  2. peak effect
  3. DOA:
  4. dose (in general)
    a) renal dose
    b) beta dose
    c) alpha dose
A
  1. 2-4 min
  2. 2-10 min
  3. less than 10 min
  4. 1-20 mcg/kg/min
    a) renal: 1-3 mcg/kg/min
    b) beta: 2-10 mcg/kg/min
    c) alpha: 10-20 mcg/kg/min
42
Q

dobutamine

  1. action?
  2. effects?
  3. class?
A
  1. beta 1 agonist
  2. positive inotrope, dromotrope, minimal chronotrope (increases contractility, av conduction, with minimal to no increase in rate) (NO vasoconstrictor activity)
  3. direct acting synthetic catecholamine
43
Q

dobutamine effects:

  1. any other receptor agonism?
  2. effect on SVR?
  3. what changes in BP? what causes it?
  4. why not a good drug for pregnant women?
A
  1. minimal if any beta2 or alpha agonist effects
  2. decreases SVR (slight vasodilator due to minimal beta 2)
  3. increases BP (related to increased C.O.)
  4. increased uterine vascular resistance thereby decreasing uterine blood flow.
44
Q

dobutamine uses

  1. what patients?
  2. what does it do?
  3. what adjunct therapy is beneficial with this drug (under what circumstances)?
A
  1. CHF patients (especially those with high HR and high SVR)
  2. increases cardiac output and decreases atrial filling pressures without increasing SVR or heart rate (bp may increase d/t increased C.O.);
  3. –can be used with dopamine in renal patients
    • -can be used with vasodilators to decrease afterload (and help increase (C.O.) in patients with high SVR.
45
Q

dobutamine cautions:

  1. s/e at higher doses? (what are high doses?).
  2. use caution in what patients?
  3. increased risk of what? with what medications?
A
  1. at higher doses (>10 mcg/kg/min) predisposes patients to tachyarrhythmias and dysrhythmias
  2. use caution in patients with Afib related to increased conduction velocity through the AV node
  3. increased risk of SVT and ventricular arrhythmias with volatile agents.
46
Q

dobutamine administration

  1. dose:
  2. onset:
  3. peak:
  4. DOA:
A
  1. dose: 2-20 mcg/kg/min; >20mcg/kg/min increases HR by 10% and may lead to myocardial ischemia
  2. onset: 1-2 min
  3. peak: 1-20 min
  4. DOA: < 10 minutes
    4.
47
Q

isoproterenol:
1. trade name?
2. class
3. pharmicodynamics:
4. potency (relative to epi and NE):

A
  1. Isuprel
  2. synthetic sympathomimetic amine, structure similar to epi
  3. acts SELECTIVELY on beta receptors (no alpha agonist effect).
  4. MOST POTENT sympathomimetic on beta 1 and 2 (2-3 x more potent than epi and 100 x more potent than NE on beta receptors).
48
Q

isoproterenol effects

  1. what receptors are activated? where?
  2. what does it cause?
  3. what happens to SVR? why?
A
  1. activates B1 receptors in the heart and B2 receptors in vasculature of skeletal muscles and lungs
  2. increases HR, contractility and automaticity
  3. decreased SVR due to vasodilation of skeletal muscle vessels.
49
Q

isoproterenol effects

  1. on C.O.?
  2. what happens to MAP and coronary perfusion?
  3. whom does this affect? (good or bad)?
  4. what does it cause (side effects)?
A
  1. increased C.O. and MRo2 consumption
  2. MAP may drop due to vasodilation causing decreased coronary perfusion while requirements increase D/T increased HR
  3. bad for CAD patients (d/t decreased coronary perfusion)
  4. dyrrhythmias, hypotension, angina
50
Q

pharmicokinetics of isoproterenol

  1. metabolized by?
  2. at what rate?
  3. what must be done to maintain plasma levels?
A
  1. COMT in the liver
  2. rapidly metabolized
  3. a gtt must be infused to maintain theraputic plasma concentration
51
Q

uses for isoproterenol

A
  1. bronchodilator via nebulizer
  2. infusion to increase HR in presence of severe heart block or heart transplant
  3. decrease pulmonary vascular resistance in presence of pulmonary hypertension,
52
Q

why is isoproterenol use uncommon (2 reasons)

A
  1. presence of (better) specific beta 2 agonists

2. has a toxic profile

53
Q

I. for what conditions is isuprel (isoproterenol) contraindicated? (6 things)
II. why is it bad for these patients?

A 
I.  1. v tach
2. v fib
3. hypotension
4. idioventricular rhythm
5. ischemic heart disease
6. cardiac arrest
II.  because it increases o2 demand by speeding up rate- bad for all of these
54
Q

isoproterenol

  1. onset?
  2. duration?
A
  1. onset: 1-5 min

2. duration: 15-30 min

55
Q

isoproterenerol infusion:

  1. how to make an isoproterenol gtt:
  2. adult gtt rate
  3. child gtt rate
A
  1. dilute 1 mg in 500 ml of D5W (2 mcg/ml) or–
    - -dilute 1 mg in 250 ml D5W (4 mcg/ml)
  2. infuse 2-10 mcg/kg/min, titrate
  3. infuse 0.05-1.5 mcg/kg/min, titrate
56
Q

ephedrine:

  1. receptor action?
  2. what are the effects?
  3. what needs to be intact for ephedrine to work?
A
  1. works directly on beta 1 and 2 and indirecty on alpha 1 by causing NE release
  2. causes increased blood pressure, HR and some bronchodilation (causes smooth muscle (lung) relaxation at theraputic doses)
  3. norepi stores must be intact for increased BP
57
Q

ephedrine:

  1. why does blood pressure increase?
  2. what effect can it have on NE?
  3. what are CNS effects?
  4. what are other effects?
A
  1. blood pressure increase is more due to increase in C.O. and to a lesser extent- peripheral vasoconstriction
  2. may deplete NE stores at sympathetic nerve endings resulting in decreased cardiac and pressor effects to drug (tachyphylaxis).
  3. CNS effects are similar to amphetamines (but to a lesser extent)- patient may start to wake up earlier than usual.
  4. increases metabolic rate and oxygen comsumption possibly as a result of CNS stimulation
58
Q

ephedrine:

  1. who might have depleted norepi stores?
  2. what happens to effect on alpha and beta?
  3. what else can deplete patient norepi stores?
A
  1. persons under physiological stress (septic, trauma)
  2. you will only have beta effects
  3. by giving subsequent doses , this may use up patient’s norepi
59
Q 
ephedrine:
doses:
1. bolus dose:
2. max dose:
3. onset:
4. duration:
5. what can repeated doses cause?
A
  1. 5-15 mg
  2. 60 mg
  3. less than 60 seconds
  4. 5-15 minutes
  5. tachyphylaxis (subsequent doses are less effective).
60
Q
  1. where is ephedrine metabolized:
  2. excreted
  3. what is excretion rate dependent on?
  4. side effects?
A
  1. liver
  2. excreted in urine up to 40% unchanged
  3. pH affects urinary excretion rate
  4. may cause tachycardia, hypertension, possible cause arrhythmias with volatile agents
63
Q

ephedrine:
indications:
1. what is ephedrine for?
2. is it ok to use in pregnancy? if yes or no, why?

A
  1. used in low blood pressure d/t periphreal vasodilation following epidural anesthesia or drug overdoses (or effects).
  2. safe in pregnancy because it DOES NOT RECDUCE placental blood flow
64
Q

ephedrine/ phenylephrine:

  1. why would you choose ephedrine over phenylephrine or vice versa?
  2. what is direct vs. indirect action?
  3. does phenylephrine or ephedrine have indirect action?
A
  1. ephedrine is better with bradycardic hypotension (d/t B1,A1 stimulation)
    phynelephrine if better for tachycardic hypotension (d/t A1 stimulation)
  2. indirect is when another neurotransmitter (usually NE is stimulated).
  3. phenylephrine has an direct and some slight indirect alpha effect
    ephedrine has direct beta 1 and 2 but has indirect alpha 1
65
Q

phenylephrine aka…

  1. class
  2. action on what receptors
  3. how about beta?
  4. effect on vessels
  5. how does it compare to Norepi
A

neosynephrine

  1. synthetic non-catecholamine alpha agonist
  2. stimulates alpha 1 receptors directly with slight indirect effect (evokes release of NE)
  3. minimal beta effect (if any)
  4. venous constriction more than arterial
  5. less potent, longer acting version of norepi (good for patient’s with bad hearts)
66
Q

pheynlephrine:

  1. uses intra-op:
  2. who is this drug best for? why?
  3. what other uses (besides blood pressure)?
  4. how is it used for local anesthesia?
A
  1. used to treat hypotension due to anesthesia during surgery
  2. drug of choice in CAD patients (increases coronary perfusion —without increasing demand (rate))
  3. nasally for nasal intubations (shrinks nasal vessels)
  4. effective in prolonging LA in SAB
67
Q

phenylephrine:

  1. side effects
  2. what side effect can actually be good (not that neo is used to treat this)
  3. rapid administration can cause what?
  4. helpful when what hypotension therapy is restricted?
A
  1. decreased cardiac output d/t reflex bradycardia
  2. bradycardia can be useful in slowing rapid heart rates
  3. rapid administration can cause decreased left ventricular function
  4. useful when fluid boluses are restricted
68
Q

phenylephrine:

  1. supplied as:
  2. iv bolus
  3. infusion
A
  1. 1% solution (20 mg)
  2. iv bouls prepared as 0.01% solution (0.1 ml of 1% diluted in 10 ml NS)
  3. infusion: 30 mg in 500 ml (gives 60 mcg/ml)
  4. hypotension:
    • iv bolus of 50-100 mcg
    • infusion of 10-200 mcg
68
Q

phenylephrine:

  1. onset
  2. duration
A
  1. less than 1 minute
    10-15 min IM or sq
  2. duration: 15-20 min IV
    30-120 min sq/im
68
Q

autonomic receptors review:

  1. what NTs are the autonomic receptors activated by?
  2. activation of B1, A1 or dopa 1 results in formation of what secondary messenger?
  3. what does this secondary messenger do?
A
  1. dopa, epi, NE
  2. second messenger cyclic adenosine monophosphate (cAMP)
  3. cAMP initiates protein phosphorylation cascade in the cell stimulating the Na+/K+ pump causing cardiac effects.
69
Q

alpha and beta antagonists:

  1. what does it mean to antagonize?
  2. what does a beta antagonist do?
  3. what do alpha antagonists do?
  4. do any meds do both?
A
  1. to bind selectively to a receptor interfering with the ability to exibit a strong or completely inhibiting a response
  2. beta antagonists have affinity with no intrinsic action; completely inhibit beta stimulation by catecholamines or sympathiomimetics
  3. alpha antagonists block catecholamines and sypmathomimetic agents from eliciting an alpha response
  4. many drugs antagonize both

b. pharm exam 2 (w13) (8 decks)

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