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CV II Exam III > adrenergic agonists and antagonists (Martin) > Flashcards

adrenergic agonists and antagonists (Martin) Flashcards

1
Q

epinephrine

A

agonist at alpha 1 and 2, beta 1 and 2

increase inotropy (b1)
increase heart rate (b1)
work of heart and its O2 consumption are markedly increased

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2
Q

vascular effects of epi

A

vasoconstriction via alpha 1 at higher doses

lower doses b2 vasodilation

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3
Q

what type of receptor is on the juxtaglomerular apparatus

A

B1 receptors

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4
Q

what are the therapeutic uses of epinephrine

A

restoration of cardiac rhythm in patients with cardiac arrest

anaphylaxis

local or topical hemostat - mouth and bleeding peptic ulcers during endoscopy of the stomach and duodenum

hemodynamic support after CABG surgery

used in anesthetic to cause local vasoconstriction so the anesthetic lasts longer

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5
Q

NE

A

is a full agonist at all adrenergic receptors BUT has a very low affinity for B2’s

increases TPR by acting on alpha 1

reduces renal blood flow ***

constricts mesenteric and splanchnic and hepatic blood flow

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6
Q

what is the clinical use of NE ?

A

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.

NE can be used as a pressor agent to support blood pressure in surgical or intensive care settings.

Unlike dopamine, NE decreases renal blood flow.

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7
Q

dopamine

A

full agonist at all dopaminergic receptors (D1-D5)

at high concentrations it can activate B1 on the heart

even higher conc can activate alpha 1

***Mediate vasodilation in the renal and mesenteric vascular beds–> increases blood flow to the kidney

Vasodilates coronary beds (D1 receptors)

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8
Q

what is the effect of dopamine on the heart?

on blood vessels?

A

heart–> increase in rate and force (partial agonist at B1 and increases release of NE)
-improves cardiac output in the scenario of shock

blood vessels: high doses–> vasoconstrict and increase BP (in the situation of shock) which is undesirable cause for decreased tissue perfusion

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9
Q

what are the clinical uses of dopamine

A

shock, cardiogenic shock (B1 on heart), unstable CHF

increases CO and enhances tissue perfusion of kidney (increase GFR- natriuresis)

sometimes used in manage acute crisis in chronic CHF

TPR is usually unchanged when low or intermediate doses of DA are given probably b/c of the ability of DA to reduce regional arterial resistance in some vascular beds

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10
Q

Dobutamine

A

B1 -selective agonist

Clinically mostly Beta1-effects
positive inotropic & some increase in rate
Cardiac output increases
little vascular effect

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11
Q

what are the clinical uses of dobutamine?

A

Cardiogenic shock

MI

CHF

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12
Q

adverse effects of dobutamine

A

may increase the size of the infarct

potential arrhythmias

increase the work/O2 requirement

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13
Q

what are the centrally acting anti-hypertensive agents

A

Methyldopa
Clonidine

act as agonists at alpha 2

control (inhibit) sympathetic outflow to periphery

decrease sympathetic tone

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14
Q

clonidine

A

Clinical use –> Essential HTN
adjunct for narcotic, alcohol, and tobacco withdrawal

IV –> increase BP (peripheral alpha 2 receptors) followed by decreased BP (central alpha 2)

oral- decreased BP (decreased CO and preload)

patch- same as oral

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15
Q

what re the side effects of clonidine

A

dry mouth, sedation, impotence

sudden withdrawal causes hypertensive crisis

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16
Q

methyldopa

A

preferred drug to treat HTN in pregnancy- b/c of its safety

side effects - sedation, dry mouth, sexual dysfunction

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17
Q

phenylephrine

A

selective alpha 1 agonist–> vasoconstriction, increased TPR, increased BP–> causes reflex bradycardia (blocked by atropine)

IV vasopressor agent

OTC nasal decongestant

18
Q

what are the clinical uses of phenylephrine

A

to maintain BP in hypotensive states (spinal anesthesia)

paroxysmal atrial tachy –> give a pressor agent to elevated TPR which induces baroreceptor reflex slowing of rate

19
Q

what are the clinical uses of alpha 1 selective receptor blockers

A

2nd or 3rd line treatment of essential HTN

added to other agents from different class

EFFECTS:
↓PVR, ↓venous return, ↓ preload
Usually do not ↑ heart rate or cardiac output
Do not ↑ NE release (no a2 block)
Favorable effects on lipids
↓LDL & triglycerides; ↑HDL
20
Q

what are the adverse effects of alpha 1 selective receptor blockers

A

Can cause marked postural hypotension & syncope, orthostatic hypotension, especially with initial doses
Usually given at bedtime to minimize hypotensive effects

21
Q

phenoxybenzame

A

alpha 1 and 2 blocker

22
Q

phentolamine

A

alpha 1 and 2 blocker (reversible)

23
Q

propranolol

A

nonselective B blocker

high first pass metabolism

24
Q

Atenolol

A

b1 selective

used for HTN

25
Q

metoprolol

A

b1 selective

used for HTN, CHF

26
Q

esmolol

A

b1 selective

very short acting

used during surgery to control HR
1/2 life of min

used as IV infusion for peri-operative tachy, HTN and arrhythmias

27
Q

Labetolol

A

alpha 1 and nonselective beta blocker

partial agonist at B2

vasodilating

used in HTN, pheochromocytoma

28
Q

carvedilol

A

alpha and nonselective beta blocker
vasodilating

has antioxidant and anti-inflammatory effects

very lipid soluble

***improves ventricular function and reduces mortality and morbidity in patients with mild to severe CHF

29
Q

what are the adverse effects of b-blockers on the cardiovascular system?

A

blockade of beta receptors may cause or exacerbate heart failure in patients with compensated heart failure, acute MI, cardiomegaly

bradycardia

don’t use together with CCB’s b/c these can lead to heart block

decreased exercise tolerance

make sure to slowly come off chronic use of these b/c there is increased risk of sudden death or exacerbation of angina

exacerbation of asthma (b2)

masks hypoglycemia

30
Q

what are the benefits of b-blockers

A

effective in prolonging life in the therapy of heart failure in selected patient’s

31
Q

what are the clinical uses of B-blockers?

A

HTN- decreases CO and SLOW decrease in peripheral resistance

Ischemic heart disease (angina, MI, acute coronary syndrome) –> decreases work of heart by reduces cardiac work and O2 consumption

MI and post-MI prophylaxis- 5-12 days after –> reduces O2 demand and spread of infarct
Also by blocking B2 - there is less “negative” remodeling

COngestive heart failure

Arrhythmias - sinus tachy and supraventricular ectopic beat

32
Q

how are b-blockers used in thyrotoxicosis…..

A

hyperthyroid patients have increased beta receptor sensitivity

Beta blockers reduces sensitivity of myocardium to adrenergic stimulation in hyperthyroid patients.

33
Q

when are the effects of beta blockers greater?

A

if the sympathetic tone is high (during stress (MI) or exercise)

34
Q

what are the effects of beta blockers on the heart

A

decrease heart rate and cardiac output
decrease exercise tolerance
decrease rate of depolarization of ectopic pacemakers
decrease O2 demand
decrease AV nodal conduction (can produce AV block)
decrease infarct size & re-infarction- prevent sudden death

decrease phase 4 of the pacemaker AP

35
Q

what are the short term cardiovascular effects of b-blockers?
long term?

A

Short term - ↓CO, ↓HR
PVR ↑ to maintain BP as a result of blockade of b2 receptors & compensatory reflexes
Long term – PVR returns to initial values or ↓ in patients with hypertension (HTN)
a/b blockers – CO is maintained with greater ↓ in PVR

36
Q

beta blockers effects on rhythm and automaticity

A

decrease sinus rate
decrease spontaneous rate of depolarization of ectopic pacemakers

slow conduction velocity in the atria and AV node

increase functional refractory period of AV node

37
Q

betaxolol

A

b1 selective vasodilating beta blocker

38
Q

why are b-blockers beneficial in the treatment of ischemic heart disease, angina and MI

A

b blockers are effective in reducing the severity and frequency of attacks of exertional angina & in improving survival in patients who have had an MI.

Not useful for vasospastic angina –may worsen

Timolol, metoprolol, atenolol, and propranolol have been shown to exert cardioprotective effects

Beneficial effects due to:
Fall in myocardial oxygen demand & increased flow to ischemic areas
↓HR, ↓contractility, ↓arterial BP (especially during exercise or stress

Both acute and long-term treatment with b blockers has been repeatedly shown to decrease mortality from MI by as much as 25% or more.

39
Q

should you use b-blocker in CHF?

A

YES

prevent HF in >50%
improve ventricular remodeling and reduce mortality

increase LVEF

use only in stable CHF

40
Q

contraindications for beta blockers

A

Asthma/COPD

mask signs of hypoglycemia (tachy, BP changes, tremor, delays recovery from insulin-induced hypoglycemia)

acute treatment of decompensated heart failure

2nd and 3rd degree heart block

cardiogenic shock

41
Q

what are side effects of beta blockers

A 
Common: 
dizziness, fatigue, diarrhea, constipation, nausea, depression, sexual dysfunction, bizarre dreams
Severe but rare
purpura, rash, fever
May Interfere with SGOT and BUN tests
Chronic use VLDL & ↓HDL 
effects vary among agents

CV II Exam III (14 decks)

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