Cardiac Drugs

Question 1

Downward spiral of HF

Answer 1

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

Question 2

Iontropic Agents

Answer 2

Increase cardiac work for ventricular filling pressure

Question 3

Vasodilator

Answer 3

Decrease preload

Decrease afterload = increase stroke volume

Question 4

Diuretics

Answer 4

Improve symptoms of heart failure

• decreases cardiac filling pressure
• relieves congestion

Question 5

ACE inhibitors

Answer 5

Number 1 drug for HF treatment

Captopril, enalopril, lisopril

Question 6

Side effects of ACE inhibitors

Answer 6

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

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

Question 7

ACE inhibitors

Answer 7

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

Question 8

ACE inhibitors

Answer 8

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)

Question 9

ACE inhibitors (captopril, enalopril, lisinopril)

Answer 9

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

Side effect:

• cough
• angioneurotic edema

Question 10

Angiotensin II Receptor Blocker (ARBs)

Answer 10

Losartan

Valsartan

Question 11

ARBs Work By…

Answer 11

Decreasing afterload and preload

Blocks AT1 receptors (acts as competitive inhibitor)

Does not affect bradykinin (like ACE-i)

Question 12

ARBs effect on AII

Answer 12

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

Question 13

Side effects of ARBs

Answer 13

Hypotension

No cough and angioedema (like ACE-i)

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

Question 14

BiDil

Answer 14

hydralazine plus isosorbide dinitrate

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

Question 15

Aliskiren

Answer 15

Renin blocker

Side effects similar to ACE inhibitors

Question 16

Entresto

Answer 16

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

Question 17

Nitroprusside

Answer 17

nitrodilator
- used more in hospitals

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

Question 18

Nitroglycerin

Answer 18

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

Question 19

Bisoprolol, Carvedilol, Metoprolol Succinate

Answer 19

Beta Blockers
Beta Adrenergic Antagonists

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

Question 20

Beta Blocker Drugs

Answer 20

• oprolol

Bisoprolol
Carvedilol
Metoprolol Succinate (sustained release)

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

Question 21

Benefits to Beta Blockers

Answer 21

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

Question 22

Adverse Effects of Beta Blockers

Answer 22

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

Question 23

Cardiac Glycosides

Answer 23

Digitalis
Digoxin
Digitoxin
Ouabain

Block the Na/K pump

Question 24

Cardiac Gylcosides: digitalis, digoxin, oubian

Answer 24

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+

Question 25

Side Effects of Cardiac Glycosides

Answer 25

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

Question 26

Ouabain

Answer 26

Cardiac glycoside Low lipid solubility and almost never used

Question 27

Digoxin

Answer 27

``` 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

Question 28

Digoxin

Answer 28

Freq prescribed Produces diuresis - inhibits Na/K ATPase, promoting diuresis Decreases blood volume/ECF volume At toxic levels = experience AV block

Question 29

DIG study for Digoxin

Answer 29

Reduces morbidity and hospitalizations in pts with CHF Supports ACE inhibitors to retard progressive cardiac deterioration in CHF

Question 30

Digitalis = Digox

Answer 30

Cardiac Glycoside Enhances vagal tone Reduces sympathetic activity

Question 31

Digitalis/Digox at toxic levels:

Answer 31

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

Question 32

Digitalis side effects

Answer 32

Nausea Vomiting Visual disturbances Tachycardia from digitalis - treated with K+ - if hyperkalemia presents, then use lidocaine or digitalis antibody

Question 33

Milrione/Enoximone

Answer 33

``` ST Phosphodiesterase inhibitor Iontropic agent: - increase Ca2+ - increase myocardial contractility - increase in cAMP ``` In smooth muscle = increases deactivation of myosin light chain kinase

Question 34

Milrinone/Enoximone

Answer 34

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)

Question 35

Increasing cAMP does what to Ca2+?

Answer 35

Increases Ca2+! 2 ways to increase cAMP: - increase activation of the receptor - inhibit destruction of AMP

Question 36

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

Answer 36

B1 agonist = activate the receptor Bipyridines = inhibit phosphodiesterase, which inhibits the destruction of AMP

Question 37

During acute HF, what drugs are used?

Answer 37

B-agonists | Bipyridines

Question 38

What is Milironone/Enoximone?

Answer 38

Bipyridimine

Question 39

What do Beta Adrenergic Agonists do?

Answer 39

Stimulate the B1 receptor Activate adenylate cyclist Produce cAMP Ca2+ influx by calcium channel Increase in Ca2+ in SR = increase in contraction

Question 40

Dobutamine

Answer 40

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

Question 41

NE as a Beta Adrenergic Agonist

Answer 41

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

Question 42

Epinephrine as a Beta-Adrenergic Agonist

Answer 42

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)

Question 43

During acute HF, the goals are to:

Answer 43

Maintain blood pressure Increase cardiac output B-agonists (NE, E and Dobutamine) Bipyridines (Milironone/Enoximone)

Question 44

During CHF, the goals are to:

Answer 44

Control ECF expansion Increase CO Decrease peripheral resistance ``` ACE-i ARBs - Angiotensin II Receptor Blocker Digoxin. - cardiac glycoside Beta Blocker Aldosterone Antagonist ```