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Cardiovascular 2 > Drugs for Heart Failure - Kruse > Flashcards

Drugs for Heart Failure - Kruse Flashcards

1
Q

Typical direct cause of heart failure

A

Decreased contractility of the myocardium –> insufficient oxygen supply to the body

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2
Q

Historically, drug therapy for heart failure has typically focused on what 2 end results?

But ____

A
  • Volume overload (diuretics)
  • Myocardial dysfunction/weakness (inotropic agents)

NOT ENOUGH to improve survival

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3
Q

Agents that act directly on _____ seem to be more valuable in the long run

A

Organs other than the heart that are involved in hemodynamic consequences of HF

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4
Q

Today, primary treatment for long term HF is aimed at doing what?

Mainly via altering what two compensatory systems?

A

Reducing preload and afterload

- RAAS
- Sympathetics
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5
Q

Common symptoms of all heart failure (5)

A
  • Tachycardia
  • Decreased exercise tolerance
  • Shortness of breath
  • Edema
  • Cardiomegaly
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6
Q

Digoxin

  • Drug class?
  • Things to be cautious of when administering? (3)
  • MoA?
  • Results? (2)
  • INDICATED WHEN?
  • Toxicity?
  • Cure?
A
  • Cardiac glycoside
  • Dose ∆ w/ renal problems, vasodilators, or sympathomimetics
  • Inhibits Na/K ATPase of sarcolemma –> increased calcium build-up
  • INCREASED CONTRACTILITY AND increased K+ efflux –> SHORTENED AP
  • INDICATED in HF w/ S3 or A. FIB.
  • Toxicity = ANY arrhythmia (next card)
  • Give K+ (decrease K+ outflow) and antidigoxin fab Ab
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7
Q

Describe how arrhythmias can develop with digitalis toxicity

A
  • Decreased atrial refractory period –> ectopic atrial contractions –> A. tach. –> A. fib
  • Increased ventricular refractory period –> AV dissociation –> ectopic ventricular contractions –> V tach. –> V fib.
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8
Q

Classic EKG finding for digitalis toxicity

A

Downward “U-shaped” ST segment

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9
Q

“-rinone” - drug class?

A

Bipyridines - PDE3 inhibitors

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10
Q

MoA of bipyridines (“-rinone”)

A

PDE3 inhibition –> increased cAMP –> increased Ca++ (contractility) and increased SM (vascular) dilation

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11
Q

End results of bipyridines (2)

A
  • Increased contractility

- Decreased preload and afterload

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12
Q

Use of bipyridines

A

SHORT-TERM relief in HF

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13
Q

Toxicities of each of the bipyridines

A

Inamrinone - GI, arrhythmias, thrombocytopenia, liver enzymes
Milrinone - arrhythmias ONLY

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14
Q

A patient is on Inamrinone for short-term HF but is having complications with bleeding. Replacement drug?

A

Milrinone

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15
Q

Dobutamine

  • MoA
  • Direct result
  • Overall result
  • DOC for what?
  • Side effects? (2)
A
  • Beta-1 agonist
  • AC –> cAMP –> PKA –> increased Ca++ (contractility)
  • Increased stroke volume (cardiac output)
  • DOC for SYSTOLIC DYSFUNCTION in HF
  • S.E. = tachycardia, arrhythmias
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16
Q

Dopamine

  • Used for what (in HF)?
  • How?
A
  • Raising BP in vasodilation circulatory collapse (sepsis, anaphylaxis)
  • HIGH DOSE –> alpha-1 and beta-1 agonist –> peripheral vascular constriction and increased contractility
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17
Q

When should dopamine use be avoided? Why?

A

CAD patients - tachycardia (increased O2 demand) may provoke ischemia

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18
Q

Diuretic class shown to improve survival in advanced HF? Why?

A

Aldosterone antagonists - aldosterone causes myocardial and vascular fibrosis and remodeling, and baroreceptor dysfunction

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19
Q

Main aldosterone antagonists used

A
  • Spironolactone

- Eplerenone

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20
Q

Antagonism of ____ from the RAAS system is a cornerstone for HF management

A

Angiotensin 2

21
Q

Negative effects of angiotensin 2 in HF (6)

A
  • Na/H20 retention
  • Increased catecholamines (sympathetics)
  • Arrhythmogenic
  • Vascular hyperplasia
  • Myocardial hypertrophy
  • Myocyte death
22
Q

Inhibiting Angiotensin 2 will do what? (multiple)

A
  • Reduce preload
  • Reduce afterload
  • Decrease sympathetics
  • Reduce aldosterone
  • Reduce myocardial/vascular remodeling
23
Q

Problem with loop diuretics in HF?

A

K+ wasting –> arrhythmias

24
Q

Why are ACE inhibitors maybe even better than aldosterone inhibitors?

A

ACE inhibitors ALSO inhibit aldosterone secretion

25
Q

Substance that directly slows myocardial and vascular remodeling by angiotensin 2

A

Bradykinin (increased w/ ACE inhibitors)

26
Q

Which is better 1st: ACEI or ARB? Why?

A

ACEI - increased bradykinin –> slowed tissue remodeling

27
Q

When to give an ARB?

A

Side effects from ACEI (cough, angioedema)

28
Q

2 functions of vasodilators in HF

A
  • Reduce preload (venous dilators)

- Reduce afterload (arteriolar dilators)

29
Q

MoA of vasodilators

A

N.O. –> G.C. –> cGMP –> relaxation

30
Q

Venodilator drugs

A
  • Isosorbide

- Nitroglycerin

31
Q

Adverse effects of venodilators

A
  • Postural hypotension
  • Tachycardia
  • Headache
32
Q

Arteriolar dilator drug

A

Hydralazine

33
Q

Use of Hydralazine in HF

A
  • Decrease afterload (BP), increased C.O.
34
Q

How are vasodilators really used?

A

Veno and arteriolar TOGETHER

35
Q

Hydralazine toxicity

A
  • Tachycardia
  • Fluid retention
  • Lupus-like symptoms
36
Q

Nitroprusside - MoA

A

Arteriolar AND venous dilator (via N.O.)

37
Q

Nitroprusside - clinical use

A
  • Acute cardiac decompensation

- HTN emergencies

38
Q

3 beta blockers that reduce mortality in HF

A
  • Bisoprolol (Beta-1)
  • Carvedilol (Beta-1, Beta-2, and alpha-1)
  • Metoprolol (Beta-1)
39
Q

Results of beta blockers in HF

A
  • Decreased myocardial remodeling
  • Slight EF rise over time
  • Decreased HR (oxygen demand, etc.)
40
Q

How to safely remove sodium in HF?

A
  • Loop diuretic + supplements

- K-sparing diuretics

41
Q

Potassium levels are especially important when giving which drug?

A

Digoxin (Digitalis)

42
Q

HF + edema…best first drug?

A

Diuretic

43
Q

HF w/o edema…best first drug?

A

ACEI (or ARB)

44
Q

How to know which vasodilator to use?

A

Based on patient symptoms

45
Q

Patient w/ dyspnea, pulmonary congestion, high atrial diastolic volume (filling pressure)…

Which vasodilator to give?

A

Venous dilators (nitro, isosorbide)

46
Q

How to administer beta blockers in HF?

A

LOW DOSES - prevent worsening of HF via too much sympathetic antagonism

47
Q

Are effects of beta blockers in HF immediate?

A

NO, may take months

48
Q

When is Digoxin given?

A

If ACEI and diuretics fail to control symptoms

49
Q

11 steps to treating chronic HF

A
  1. Control HTN, hyperlipidemia, DM, obesity
  2. Reduce heart workload (rest)
  3. Restrict Na, give diuretic
  4. Restrict water (rare)
  5. ACEI or ARB
  6. Digoxin (S3 or A fib.)
  7. Beta blocker (if stable; low dose)
  8. Aldosterone antagonist
  9. Vasodilator
  10. Cardiac resynchronization
  11. Cardiac transplant

Cardiovascular 2 (20 decks)

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