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Pharm > Cardiac Drugs > Flashcards

Cardiac Drugs Flashcards

1
Q

Downward spiral of HF

A

Decrease in CO
Increase in NE, AII

-> vasoconstriction and increase in afterload, which decreases ejection fraction and CO, which increases AII and NE, increasing afterload

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2
Q

Iontropic Agents

A

Increase cardiac work for ventricular filling pressure

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3
Q

Vasodilator

A

Decrease preload

Decrease afterload = increase stroke volume

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4
Q

Diuretics

A

Improve symptoms of heart failure

  • decreases cardiac filling pressure
  • relieves congestion
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5
Q

ACE inhibitors

A

Number 1 drug for HF treatment

Captopril, enalopril, lisopril

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6
Q

Side effects of ACE inhibitors

A

Cough
Angioedema (swelling of the nose/throat) due to bradykinin secretion

Suppression of AII, decreases peripheral resistance, can cause risk of hypotension/hyperkalemia

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7
Q

ACE inhibitors

A

Decrease afterload by reducing peripheral resistance

Reduce preload by: reducing aldosterone secretion, thereby decreasing salt and water retention

Decreases conversion to AII (of which causes aldosterone secretion)
- this might increase risk of hyperkalemia

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8
Q

ACE inhibitors

A

Decreases sympathetic activity by decreasing NE release

Decreases remodeling of the heart and vessels - receptor for AII found in the heart

Increase in RENIN and AI (due to negative feedback)

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9
Q

ACE inhibitors (captopril, enalopril, lisinopril)

A

Decrease in degradation of bradykinin (this increases NO output and prostaglandin formation)

Side effect:

  • cough
  • angioneurotic edema
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10
Q

Angiotensin II Receptor Blocker (ARBs)

A

Losartan

Valsartan

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11
Q

ARBs Work By…

A

Decreasing afterload and preload

Blocks AT1 receptors (acts as competitive inhibitor)

Does not affect bradykinin (like ACE-i)

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12
Q

ARBs effect on AII

A

More selective than ACE bc there are other enzymes that generate AII, not just ACE

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13
Q

Side effects of ARBs

A

Hypotension

No cough and angioedema (like ACE-i)

Long-term ARB therapy: decreases risk of CV death in pts with HF

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14
Q

BiDil

A

hydralazine plus isosorbide dinitrate

  • less effective than ACE-i
  • might be more effective in black pts who are less responsive to ACE-i
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15
Q

Aliskiren

A

Renin blocker

Side effects similar to ACE inhibitors

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16
Q

Entresto

A

LCZ696

Better drug than enalopril

Dual inhibition of: COMBO drug

  • neprilysin (breaks down natruiretic peptide)
  • angiotensin receptors (valsartan)

Used in pts who on ACE-i or ARB still have reduced ejection fraction

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17
Q

Nitroprusside

A

nitrodilator
- used more in hospitals

Dilates artery/venous blood vessels to increase CO
Given by IV for acute HF
1/2 life = 2 minutes

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18
Q

Nitroglycerin

A

Topical nitrate
Decreases pulmonary and systemic venous pressures
Decreases left ventricular filling pressure

19
Q

Bisoprolol, Carvedilol, Metoprolol Succinate

A

Beta Blockers
Beta Adrenergic Antagonists

  • for patients with symptoms of HR
  • for patients asymptomatic with hx of MI
20
Q

Beta Blocker Drugs

A
  • oprolol

Bisoprolol
Carvedilol
Metoprolol Succinate (sustained release)

Lower sympathetic tone, which allows more dynamic its and increase in CO

21
Q

Benefits to Beta Blockers

A

Decrease sympathetic tone
Attenuation of adverse Effects of Cathecholamines
- reduced remodeling via inhibition of catecholamines

ST: vasodilator, slow HR

LT: reverses remodeling in dilated cardiomyopathy
- lowers cardiac B1 and B2 receptor activity

22
Q

Adverse Effects of Beta Blockers

A

Hypotension
Fatigue
Bradycardia/Heartblock

NOT used in pts with bradycardia or asthma

Start with low dose of the drug and then titration up acc. To tolerance

23
Q

Cardiac Glycosides

A

Digitalis
Digoxin
Digitoxin
Ouabain

Block the Na/K pump

24
Q

Cardiac Gylcosides: digitalis, digoxin, oubian

A

Block the Na/K pump, so that Na in cystosol raises

Action. Potential releases greater than normal Ca2+ to increase contraction
- build up of Ca2+

25
Q

Side Effects of Cardiac Glycosides

A

Causes arythmias
Holds narrow therapeutic index
K+ antagonizes action of digitalis

26
Q

Ouabain

A

Cardiac glycoside

Low lipid solubility and almost never used

27
Q

Digoxin

A 
Cardiac glycoside (iontropic agent)
T1/2 = 36-40 hours

Used almost exclusively in therapy

Increases cardiac output
Decreases heart size
Decreases venous pressure
Decreases EDV

28
Q

Digoxin

A

Freq prescribed

Produces diuresis
- inhibits Na/K ATPase, promoting diuresis
Decreases blood volume/ECF volume

At toxic levels = experience AV block

29
Q

DIG study for Digoxin

A

Reduces morbidity and hospitalizations in pts with CHF

Supports ACE inhibitors to retard progressive cardiac deterioration in CHF

30
Q

Digitalis = Digox

A

Cardiac Glycoside

Enhances vagal tone
Reduces sympathetic activity

31
Q

Digitalis/Digox at toxic levels:

A

AV block
Increases sympathetic outflow, sensitizing the myocardium
Extreme inhibition of NaK pump affects cells in the atria/ventricular purkinje fibers = promoting arrhythmia

32
Q

Digitalis side effects

A

Nausea
Vomiting
Visual disturbances

Tachycardia from digitalis

  • treated with K+
  • if hyperkalemia presents, then use lidocaine or digitalis antibody
33
Q

Milrione/Enoximone

A 
ST
Phosphodiesterase inhibitor 
Iontropic agent:
- increase Ca2+
- increase myocardial contractility
- increase in cAMP

In smooth muscle = increases deactivation of myosin light chain kinase

34
Q

Milrinone/Enoximone

A

Usually an IV drip

Less prone to arrhythmia than adrenergics/digitalis
Safe and effective for ST support of decompensated HF

Long term use is NOT recommended (fatal arrhythmia, bone marrow, liver toxicity)

35
Q

Increasing cAMP does what to Ca2+?

A

Increases Ca2+!

2 ways to increase cAMP:

  • increase activation of the receptor
  • inhibit destruction of AMP
36
Q

What to give first, beta agonist or milrinone/Enoximone?

A

B1 agonist = activate the receptor

Bipyridines = inhibit phosphodiesterase, which inhibits the destruction of AMP

37
Q

During acute HF, what drugs are used?

A

B-agonists

Bipyridines

38
Q

What is Milironone/Enoximone?

A

Bipyridimine

39
Q

What do Beta Adrenergic Agonists do?

A

Stimulate the B1 receptor
Activate adenylate cyclist
Produce cAMP
Ca2+ influx by calcium channel

Increase in Ca2+ in SR = increase in contraction

40
Q

Dobutamine

A

Beta Adrenergic agonist

Used for:
HF without hypotension
Insulates B1, B2 and alpha receptors

Exists as a racemic mixture (1/2 life = 2.5 min)
Does not increase the release of NE, does not stimulate DA receptors

41
Q

NE as a Beta Adrenergic Agonist

A

acts on B1, peripheral alpha-receptors

Stimulates heart when there is a drop in BP
Used for “warm” septic sock, or when the pt’s BP is low

42
Q

Epinephrine as a Beta-Adrenergic Agonist

A

Acts at B1, B2 and peripheral alpha receptors

Increases contraction, increases HR

Used for CARDIAC ARREST

Contraindicated by: pts who have Beta Blocker therapy (it would be a risk for severe hypertension)

43
Q

During acute HF, the goals are to:

A

Maintain blood pressure
Increase cardiac output

B-agonists (NE, E and Dobutamine)
Bipyridines (Milironone/Enoximone)

44
Q

During CHF, the goals are to:

A

Control ECF expansion
Increase CO
Decrease peripheral resistance

ACE-i
ARBs - Angiotensin II Receptor Blocker 
Digoxin. - cardiac glycoside
Beta Blocker
Aldosterone Antagonist

Pharm (6 decks)

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