PMT, Kruse - Drugs for Heart Failure Flashcards

1
Q

What type of agent is best used in systolic failure? wHy?

A

Inotropic agents (digoxin) directly treat myocardial dysfunction by increasing cardiac contractility.

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2
Q

What agents DO NOT improve survival?

A

Diuretics (except aldosterone does) and inotropic agents.

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3
Q

What are the three types of inotropic agents?

A

1) Cardiac glycosides - digoxin
2) Bipyridines - inamrinon and milrinone
3) B-agonists - dobutamine and dopamine

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4
Q

Digoxin:

  • Agent and class
  • Used for
  • Pharmacokinetics
A
  • Agent and class - Inotropic, cardiac glycoside
  • Used for HF and afib
  • Pharmacokinetics - oral and 1/day dose
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5
Q

Digoxin:

  • MOA
  • Desired physiological effects
A
  • MOA - Inhibits membrane bound Na/K ATPase = increases Ca in SR
  • Desired physiological effects: 1) increase contractility; 2) prolong AVN refractory period in supraventricular arrhythmias
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6
Q

Digoxin:

  • Cardiac toxicity
  • Other toxicity
A
  • Cardiac - Arrhythmias and Tachycardia deteriorating into fibrillation is fatal.
  • GI - anorexia/N/V/D
  • CNS - hallucination, vision
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7
Q

Does SNS or PSN-mimetic effects dominate cardiac tissue at therapeutic levels of digoxin? What drug inhibits theses effects?

A

Parasympathomimetic effects.

Atropine inhibits

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8
Q

What electrolyte binds to the same sites as digoxin on Na/K ATPase? So, can use this electrolyte to do what?

A

Potassium. Use K to reduce digoxin toxic effects.

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9
Q

What increases risk of digoxin induced arrhythmias?

What do you give for a digoxin induced arrhythmia?

A

HyperCa and HypoMg

Mg

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10
Q

Inamrinone and milrinone

  • Agent and class
  • Used for
  • Pharmacokinetics
A
  • Agent and class - Cardiac glycoside, bipyridine
  • Used for SHORT TERM support of circulation in SEVERE HF
  • Pharmacokinetics - parenteral.
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11
Q

Inamrinone and milrinone

  • MOA
  • Desired physiological effects
A
  • MOA - inhibition of PDE3, which increases cAMP

- Desired physiological effects - stimulate myocardial contractility and decrease LV afterload, which INCREASES CO

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12
Q

What two things have the same MOA as bipyridines?

A

Caffeine and theophylline (asthma meds, bronchodilator).

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13
Q

Inamrinone and milrinone toxicity, respectively.

A

Inamrinone - N/V/D, thrombocytopenia, liver enzyme changes.

Milrinone - arrhythmias

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14
Q

Dobutamine

  • Agent and class
  • Used for
  • Pharmacokinetics
  • MOA
  • Desired physiological affects
  • Toxicity
A
  • Cardiac glycosides, B1-receptor AGONIST
  • Used for systolic dysfunction and HF
  • Pharmacokinetics - parenteral
  • MOA - B1 receptor selective stimulator
  • Desired physiological affects are increased SV and CO
  • Toxicity - tachycardia and arrhythmia
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15
Q

Dopamine

  • Agent and class
  • Used for
  • Pharmacokinetics
  • MOA
  • Desired physiological affects
  • Toxicity
A
  • Agent and class - cardiac glycoside, D1-receptor agonist
  • Used for raising BP (limited use in HF patients)&raquo_space; sepsis or anaphylaxis - in which circ failure dt vasodilation)
  • Pharmacokinetics - parenteral
  • MOA - D1 receptor selective stimulator
  • Desired physiological affects - 1) low doses vasodilate, 2) Intermediate doses stimulate B-receptors on heart 3) high doses cause peripheral vasoconstriction (stims alpha)
  • Toxicity - tachycardia, ischemia in CAD
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16
Q

What is the MOA of both stimulation of B1 and D1 receptors (dobutamine and dopamine)?

A

Stimulation of Gs-AC-cAMP-PKA pathway, which enhances Ca-dependent contraction and speeds relaxation.

17
Q

What are the four types of diuretics used in HF?

A

1) Loops - bumetamide, furosemide, torsemide
2) Thiazide - HCTZ
3) Aldosterone antagonists - eplerenone, spironolactone
4) ADH antagonists - Conivaptan, tolvaptan

18
Q

What is each type of diuretic used for most?

Which improves survival?

A

Tx congestive symptoms - dec. preload.

  • Loop - HF
  • Thiazide - systemic HTN
  • Aldosterone antagonists - advanced HF **improves survial
  • ADH antagonists - HF
19
Q

What is conivaptan toxicity.

MOA of this ADH antagonist.

A

Toxicity of conivaptan - hyperNa, nephrogenic DI.

V1a and V2 receptor antagonist in CCT.

20
Q

Other than Na and water retention, what else does Ald do that spironolactone and eplerenone inhibit?

A

Myocardial and vascular fibrosis/remodeling.

21
Q

MOA of ACEi (-ipril)

What does this result in?

A
  • Inhibit Ang2, which is a vasoconstrictor and increases Na/water retention.
  • Ang2 inhibition results in decreased preload (dec fluid) and afterload (vasodilates)
22
Q

ACEi does what three things?

A
  • Suppresses Ang2»ald
  • Dec. SNS activity
  • Reduces remodeling of heart and vessels
23
Q

MOA of ACEi reducing remodeling.

A

stops ACE degradation of bradykinin, which stimulates NO production. Increased bradykinin stops remodeling.

24
Q

MOA of ARBs (-sartan)

A

Antagonizes AT1

25
Q

Types of vasodilators and what vessels they affect.

A

1) Isosorbide dinitrate - venodilator (dec preload)
2) Hydralazine - arteriolar dilator (dec BP and afterload = inc CO)
3) Nitroprusside - veno and arteriolar dilator (inc. CO)

26
Q

Isosorbide dinitrate is used for what?

AE?

A
  • acute and chronic HR
  • Angina
  • AE - postural hypotension, tachy, HA
    Venodilator = use for dyspnea
27
Q

Hydralazine is used for what?

AE

A
  • Use with nitrates to reduce mortality in patients with HF.

- AE - tachycardia, fluid retention, Lupus-like syndrome

28
Q

Use nitroprusside for what?

A

Acute cardiac decompensation and HTN emergencies (malignant HTN).

29
Q

Nesiritide

  • Agent and class
  • Used for
  • Pharmacokinetics
  • MOA
  • Desired physiological affects
  • Toxicity
A
  • Agent and class - natriuretic peptide
  • Used in acutely decompensated HF with dyspnea at rest or minimal activity
  • Pharmacokinetics - given IV
  • MOA - type of BNP
  • Desired physiological affects - vasodilation, natriuresis, diuresis to counteract effects of angiotensin and NE
  • Toxicity - excessive hypotension, renal damage
30
Q

BBlockers

A

reduce mortality

  • Decrease SNS
  • Bisoprolol = B1antagonist
  • Carvedilil = NS B ant and A1 ant = mild to severe HF
  • Metoproplol = B1 sel antag - mild to severe HF
31
Q

First line of therapy for chronic HF.

A

ACEi and diuretics

32
Q

What do you initiate to antagonize cat effects?

A

BB

33
Q

What do you give if ACEi and diuretics fail to control symptoms?

A

digoxin

34
Q

Give what to:

1) Patient with dyspnea with high filling pressures

A

1) Venodilator - isosorbide

35
Q

Worsening HF due to cat effects, initiate what?

A

BB

36
Q

Do not combine what drug with a loop?

A

Digoxin - due to K loss with Loop.

37
Q

What four things reduce mortality?

A

1) Aldosterone antagonists
2) Hydralazine + nitrate
3) BB
4) ACEi