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General Pharm > Cardio Adrenergic Agents > Flashcards

Cardio Adrenergic Agents Flashcards

1
Q

Use during CPR for asystole
Hemodynamic support after CABG
Anaphylaxis
Local/topical hemostatic

A

Epinephrine

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2
Q

Pressor agent of choice in septic/cardiogenic shock

A

NE

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3
Q

NE does what to renal BF

A

Decreases it

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4
Q

Phenylephrine

A

IV vasopressor agent
Over the counter nasal decongestant
Increases TPR, BP with reflex brady

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5
Q

Maintains BP in hypotensive states

A

Phenylephrine

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6
Q

Tx for Paroxysmal atrial tachycardia

A

Baroreceptor reflex slowing

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7
Q

Vasodilates renal, coronary, and mesenteric vascular beds

A

Dopamine via D1 receptors

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8
Q

Dopamine

A

Acts at D1 receptors causes mild increase in rate and force
Enhances kidney perfusion
High doses cause vasoconstriction and increased BP –> not a good thing in shock

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9
Q

Tx for shock, cardiogenic shock and unstable CHF

A

Dopamine

Must monitor carefully because too high of doses causes vasoconstriction and decreased tissue perfusion

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10
Q

Dobutamine

A

B1 selective agonist
Positive inotropic, and some chronotropic effects
CO increases
Little vascular effect

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11
Q

Dobutamine is used to treat

A

Cardiogenic shock, MI and CHF

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12
Q

Adverse effects of Dobutamine

A

May increase size of infarct, cause arrhythmia and increase work/O2 requirement of the heart (b1)

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13
Q

Clinical Use of A1 blockers

A

2nd/3rd line treatment of essential HTN

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14
Q

A1 Antagonist Effects

A

Decrease PVR, VR and Preload
Do not increase HR or CO
Do not increase NE release (no A2 block)
Decrease LDL and trigly while increasing HDL

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15
Q

Adverse Effects of A1 Antagonists

A

Marked postural hypotension and syncope, orthostatic hypotenison
Admin at bedtime

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16
Q

Most popular A1 Antagonist

A

Prazosin

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17
Q

Very short acting B blocker

A

Esmolol

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18
Q

Partial agonist B blocker with ISA

A

Acebutolol

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19
Q

Both A and B blockers

A

Labetolol & Carvediol

20
Q

6 Clinical Uses of Cardioselective B Blockers

A

1) HTN: Decrease CO and TPR (SLOWLY OVER WEEKS)
2) Ischemic Heart Disease: Decreases cardiac work and O2 consumption
3) MI & Post MI Prophylaxis: protects against arrhythmias and limits infarct size (5-10days after)
4) CHF: Improves morbidity and mortality**
5) Arrhythmias: Sinus tachy and super ventricular beat suppressed
6) Thyrotoxicosis: block increased sensitivity of myocardium to betas

21
Q

What are B blockers role in treating CHF?

A

Improve morbidity and mortality **

22
Q

What are B blockers role in treating hyperthyroid pts?

A

Treats thyrotoxicosis
Hyperthyroid pt have increased B receptor sensitivity
Blockers reduce the sensitivity of myocardium to adrenergic stimulation

23
Q

Pharmacological Effects of B Blockers Depends on

A

Existing SNS tone

24
Q

B Blockers Effects on CO HR and PVR

A

Short term decrease in CO/HR
PVR increases to maintain BP as a result of B2 blocking/reflexes
Long term PVR returns to initial values or deceases in pt with HTN

25
Q

Long term effect so B/A blockers

A

CO maintained with greater decrease in PVR

26
Q

B blocker effects on rhythm and automaticity

A

Decrease sinus rate, decreases spontaneous depol of ectopic pacemakers, slow conduction velocity in atria/AV node
Increase function refractory period of AV node

27
Q

B Blocker Effects on Exercise

A

Blunt increase in HR and contractility, CO less affected
Decrease work capacity
DECREASE EXERCISE TOLERANCE

28
Q

B1 selective agent effect on exercise tolerance vs. nonselective agents

A

B1 have lesser effects on exercise tolerance vs nonselective agents

29
Q

B blockers do what to myocardial O2 demand?

A

They decrease it!

Net effect is improving relationship btw cardiac supply/demand

30
Q

B blockers increase exercise tolerance in which pt?

A

Pt with angina

31
Q

What blocks the reflex bradycardia of a A1 agonist?

A

Atropine

32
Q

High doses of Dopamine can cause

A

VC via A1 receptors and increased BP which would be undesirable in the treatment of shock as it would lead to decreased perfusion

33
Q

What receptors mediate catecholamine stimulation of renin release?

A

B1 receptors, increase in renin is blocked by B blockers

34
Q

B blockers also provide these effects which are helpful in chronic HTN or after stent placement

A

Antiproliferative effects and antioxidant activity

35
Q

B Blocker peripheral VD also results in decreased incidence of

A 
Bronchospasm 
Withdrawl Sx 
Insulin resistance 
DM 
Metabolic syndrome
36
Q

Contraindications for B Blockers

A

Asthma & COPD

Mask hypoglycemia in DM pt

37
Q

Sudden withdrawal of B blockers can cause

A

Rebound HTN, anginal attack and MI due to increased B receptor synthesis

38
Q

Atenolol and Metoprolol

A

B1 selective blockers

39
Q

Esmolol

A

B1 selective blocker with rapid onset and short duration of action

40
Q

Labetolol

A

A1 selective blocker
Nonselective B1/B2
Partial agonist B2

41
Q

Carvediol

A

Nonselective B/A blocker
Very lipid soluble (CNS permeable)
Antioxidant properties
Dramatic CHF clinical results (reduce mortality by 65%)

42
Q

A2 receptor agonist MOA

A

Centrally acting anti-HTN agents working on brain stem A2 receptors to inhibit SNS outflow to the periphery and decreases SNS tone

43
Q

Methyldopa

A

False NT concept (stored in vesicles instead of NE)
A2 agonist
Treat HTN in pregnancy
Side effects include sedation, dry mouth and sexual dysfunction

44
Q

Clonidine

A

A2 agonist

SUDDEN WITHDRAWAL CAUSES HYPERTENSIVE CRISIS

45
Q

When admin via IV Clonidine causes

A

An increase in BP from peripheral A2 stimulation and then a decrease in BP due to central A2 stimulation

General Pharm (5 decks)

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