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Cardio II Exam 3 > Adrenergic Agonists > Flashcards

Adrenergic Agonists Flashcards

1
Q

Epinephrine

A

Full adrenergic agonist: Alpha1, alpha2, beta 1 Agonist

B1: most important is B1 activation that increases inotropy and chonotropy of heart –> increased CO and O2 demand of heart

B2: see vasodilaton predominate at low levels (b/c epi has higher affinity for B2 than a1)

a1: see vasoconstriction dominate at high levels

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2
Q

NE

A

alpha 1,2 Beta1&raquo_space; B2

  • see dramatic increase in TPR due to affinity of alpha1, results in reflex bradycardia (elevation of MBP overall)
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3
Q

Isoproterenol

A

B1, B2, B3 nonselective agonist

may be used in emergencies to stimulate HR in pt. w/ bradycardia or heart blocks usually before placement of a pacemaker

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4
Q

Dobutamine

A

B1 selective agonist

  • see positive inotrpic and some increase in HR
  • increased CO, little vascular effect

Clinical use:

  • cardiogenic shock, MI, CHF
  • short term tx for cardiac decompensation

Adverse effects: may increase size in infarct due to increased O2 demand, can cause potential arrythmias

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5
Q

Dopamine

A

(Intropin)
D1>B1>a1

  • D1 receptors mediate vasodilation in renal, coronary, and mesenteric vascular beds –> increased blood flow to kidney
  • mild increase in HR and force (partial agonist of B1)
  • high doses cause vasoconstriction and increased BP due to alpha1 (which is not good in times of shock, causing decreased tissue perfusion)
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6
Q

Fenoldopam

A

D1 agonist

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7
Q

Clonidine

A

a2 agonist - used for tx of systemic HTN

** primarily used for off-label tx of withdrawal from narcotics, alcohol and tobacco

SE’s: dry mouth, sedation, impotence

** sudden w/drawal causes HTN crisis

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8
Q

methyldopa

A

a2 agonist - used for tx of systemic HTN

** preferred tx for HTN in pregnant women

  • False NT, converted to methyl-NE and stored in vesicle instead of NE. Released and acts centrally as alpha2 agonist. Decreases central sympathetic outflow and decreases blood pressure

side effects: sedation, dry mouth, sexual dysfunction

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9
Q

prazosin

A 
a1 antagonist ("minipress")
- third line agent for tx of HTN
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10
Q

phentolamine

A

a1, a2 antagonist

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11
Q

phenylephrine

A

alpha1 agonist prototype

  • Used as IV vasopressor agent: maintains BP in hypotensive state
  • over the counter nasal decongestant
  • tx of paroxysmal atrial tachycardia (due to baroreceptor slowing of HT)
  • results in increased peripheral resistance and bradycardia (reversed by atropine)
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12
Q

propanolol

A

prototype nonselective Betal blocker

  • blocks all beta receptors
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13
Q

nadolol

A

nonselective Beta blocker

- longer acting, once per day dosing

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14
Q

pindolol

A

nonselective Beta blocker

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15
Q

carteolol

A

nonselective Beta blocker

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16
Q

sotalol

A

nonselective Beta blocker

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17
Q

atenolol

A

cardioselective Beta blocker

18
Q

acebutolol

A

cardioselective Beta blocker

19
Q

metoprolol

A

cardioselective Beta blocker

20
Q

labetalol

A

beta blockade, along with alpha1 block (partial agonist of B2)

uses: HTN, pheochromocytoma

21
Q

carvedilol

A

beta blockade, along with alpha1 block

  • useful results in CHF clinical trials
  • has antioxidant and anti-inflamm. effects
  • improves ventricular function
22
Q

betaxolol

A

beta blocker, and blocks ca2+ entry

23
Q

carteolol

A

Beta1 blocker, agonist activity at Beta2

24
Q

what are roles of B1, B2, alpha1, muscarinic receptors?

A 
B1 = increased HR and force
muscarini = decrease HR
alpha1 = vasoconstriction
b2 = vasodilation
25
Q

NE vs. Epi vs. Iso

A

NE: alpha1 agonist: results in increase in peripheral resistance, and decrease in HR: overall increase in mean blood pressure

Epi: B2 agonist at low levels: results in drop in peripheral resistance due to B2, and a subsequent increase in HR due to B1/response. Overall MBP remains same.

Isoprotenerol: pure beta agonist: decrease in peripheral resistance and subsequent increase in HR - MBP slightly decreases

26
Q

clinical uses of epi?

A

During CPR for asystole: restoration of cardiac rhythm

Hemodynamic support after CABG surgery

Anaphylaxis (injectin of epi, decreases cutaneous blood flow through constricting precapillary vessels)

Local or topical hemostatic (causes vasoconstriction and stops bleeding)

27
Q

clinical uses of NE?

A

used as a vasoconstrictor to raise or to support BP in intensive care conditions

*NE is the pressor agent of choice for the treatment of septic shock and may be more appropriate than dopamine as first-line treatment for other types of shock as well, especially cardiogenic shock.

Unlike dopamine, NE decreases renal blood flow.

28
Q

clinical use of dopamine?

A

*** desirable effects in management of states of low CO assoc/ w/ compromised renal fn: shock, cardiogenic shock, unstable CHF (due to increased GFR and CO)

  • Cardiogenic shock: increased CO due to effect on B1
  • increases CO and enhances kidney perfusion
  • MUST monitor BP carefully b/c higher infusion rate or dose causes vasoconstriction and decreased tissue perfusion (at high concentrations, results in activation of alpha1 and vasoconstriction)
29
Q

alpha1 selective blockers?

A

prazosin, terazosin, doxazosin

  • effects: decrease in PVR, decrease in VR, decrease in preload
  • does not increase HR or CO
  • does not increaes NE release (no alpha2 block)

AEs: can cause postural Hypotension, syncope, hypotension - thus usually given at bedtime

30
Q

cardioselective beta antagonists?

A

acebutolol, atenolol, bisoprolol, esmolol, metoprolol

31
Q

third generation B1 selective antagonists?

A

betaxolol, celiprolol, nebivolol

32
Q

esmolol

A

B1 selective blocker, very short acting (used in times of surgery during acute procedure via IV)

33
Q

clinical uses for beta blockers?

A
  1. HTN: decreases CO and produces slow decrease in peripheral resistance (IHD, angina, MI, acute coronary syndrome)
  2. CHF: improves morbitiy and mortality
  3. arrhythmias: sinus tachy and supraventricular ectopic beat
  4. thyrotoxicosis: hyperthyroid pt. have increased B sensitivity: beta blockers reduce sensitivity- reducing peripheral symp signs and anxiety
34
Q

pharmacology of beta blockers?

A
  • decrease HR and CO
  • long term slight decrease in PVR
  • *decrease exercise tolerance
  • decrease O2 demand
  • decrease rate of pacemakers
  • decrease infarct size and re-infarction

NOTE: Beta blockers block an increase in renin

35
Q

when to use B-antagonists?

A

stable angina (CAD), Acute coronary syndromes

  • effective in reducing severity and frequency of attacks of exertional angina (though not vasospastic angina - may worsen)

****improve survivial in pt. who have had an MI!

  • beneficial effects are due to fall in myocardial O2 demand, decreased HR, decreased contractility and decreased arterial BP
36
Q

cotraindications of beta blockers?

A

block beta2 –> bronchospasm in pt. with asthma or COPD

diabetics: blocks beta receptor effects on lypolysis and glycoenolysis and masks signs of hypoglycemia (i.e. tachycardia, BP changes, tremor)
* sudden withdrawal: results in rebound HTN and anginal attacks/MI

other CIs: 2nd/3rd degree heart block, cardiogenic shock

37
Q

what to use for CHF?

A

beta blockers prevent HF in >50%, strokes are reduced and it improves ventricular remodeling

  • increased LVEF, causing beneficial remodeling of heart
  • only use in stable CHF (class II and III), gradually titrate the dose
38
Q

SE of beta antagonists?

A

dizziness, fatigue, diarrhea, constipation, nausea, depression, sexual dysfunction, bizarre dreams

less common: purpura, rash, fever

chronic use may increase VLDL and decease HDL

39
Q

timolol

A

nonselective beta blocker

40
Q

why use B1 selective blockers?

A
  • lessen risk of bronchospasm

- do not usually prolong hypoglycemia

Cardio II Exam 3 (15 decks)

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