Drugs for Heart Failure Flashcards

1
Q

Symptoms of heart failure?

A

cardinal symptoms are dyspnea, fatigue, and fluid retention

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2
Q

Causes of HF are?

A
Atherosclerosis
Hypertensive heart disease
Valvular heart disease
Congenital heart disease
and many more
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3
Q

What benefits do pharmacological interventions give for heart failure?

A

reduced myocardial work load
decreased extracellular fluid volume
improved cardiac contractility
reduced rate of cardiac remodeling

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4
Q

The force of contraction of the cardiac muscle is directly related to the concentration of ___________

A

free (unbound) cytosolic calcium

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5
Q

What are the five phases of an action potential of myocyte?

A
Phase 0: Fast upstroke
Phase 1: Partial repolarization
Phase 2: Plateau
Phase 3: Repolarization
Phase 4: Forward current
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6
Q

What happens in phase 0?

A

Fast Upstroke: Na channels open resulting in fast inward current and ends as Na channels are rapidly inactivated

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7
Q

What happens in phase 1?

A

Partial Repolarization: The initial rapid phase of repolarization is due to

  1. Na channels are inactivated
  2. K channels open rapidly and close, causing a transient outward current
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8
Q

What happens in phase 2?

A

Plateau: Voltage sensitive Ca channels open, resulting in a slow inward depolarizing current that balances the slow outward (polarizing) leak of K+

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9
Q

What happens in phase 3?

A

Repolarization: Ca channels close.
1. K+ channels open, resulting in an outward current leading to membrane repolarization
2. Net result = Gain of Na & Loss of K
This imbalance is corrected by Na/K ATPase pump

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10
Q

What happens in phase 4?

A

Forward Current: Increasing depolarization results in sodium permeability
Spontaneous depolarization automatically brings the cell to the threshold of the next action potential (phase ) again)

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11
Q

Sodium current is blocked by antiarrhythmatic agents __________ (quinidine/amiodarone)

A

quinidine

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12
Q

What are the compensatory physiological responses in heart failure?

A

Increased sympathetic activity
Activation of RAAS
Activation of natriuretic peptides
Myocardial hypertrophy

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13
Q

____________(baroreceptors/chemoreceptors) sense a decrease in blood pressure and activate the sympathetic nervous system

A

Baroreceptors

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14
Q

What do stimulation of beta adrenergic receptors do?

A

Increased heart rate
Greater force of contraction of the heart muscle
Vasoconstriction enhances venous return

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15
Q

What are the effects of RAAS on the body?

A

Peripheral and pulmonary edema (water retention)

Remodeling, fibrosis, and inflammatory changes (due to angiotensin II)

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16
Q

Activation of the _____________ (angiotensin-aldosterone/natriuretic peptides) ultimately results in vasodilation, natriuresis, inhibition of renin and aldosterone release, and a reduction in myocardial fibrosis

A

natriuretic peptides

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17
Q

What is systolic failure?

A

When the ventricles are not able to pump the blood effectively (HFrEF)

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18
Q

What is diastolic failure?

A

When the ventricles are not able to relax properly due to structural changes like hypertrophy (HFpEF)

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19
Q

What are the symptoms of acute decompensated heart failure?

A
dyspnea on exertion
orthopnea
paroxysmal nocturnal dyspnea
fatigue
peripheral edema
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20
Q

How is Chronic HF typically managed?

A
  1. Fluid limitations (less than 1.5 to 2 L daily)
  2. Low dietary intake of sodium (less than 2000 mg/d); 3. Treatment of comorbid conditions
  3. Judicious use of diuretics
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21
Q

Name the drugs/food that can exacerbate heart failure?

A

Nonsteroidal anti-inflammatory drugs (NSAIDs)
Alcohol
Nondihydropyridine calcium channel blockers
Some antiarrhythmic drugs

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22
Q

____________ are reserved for acute signs and

symptoms of HF and are used mostly in the inpatient setting

A

Inotropic agents

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23
Q

What drugs can we use for HFrEF?

A

Inhibitors of the RAAS
Inhibitors of the sympathetic nervous system
Drugs that enhance activity of natriuretic peptides

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24
Q

What do ACE inhibitors do?

A

Decreased conversion of angiotensin I to AT II

Increased levels of bradykinin (dry cough and angioedema)

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25
Q

What is the effect of ACEIs on preload and afterload?

A

Decrease preload and afterload

26
Q

__________ is the initial stretching of the cardiac myocytes (muscle cells) prior to contraction. It is related to ventricular filling

A

Preload

27
Q

__________ is the force or load against which the heart has to contract to eject the blood.

A

Afterload

28
Q

What is the effect of ACEIs on

  1. preload
  2. afterload
  3. cardiac output
A

decreased preload
decreased afterload
increased cardiac output

29
Q

ACE inhibitors also blunt the usual angiotensin II–mediated increase in _________ and _________seen in HF (hormone names?)

A

epinephrine

aldosterone

30
Q

What are the therapeutic uses of ACEIs?

A

HFrEF (Systolic failure) (w/ or w/o symptoms)
Left ventricular failure (all stages)
HTN (w/ or w/o chronic kidney disease)
Recent MI (to reduce ventricular remodelling)
Patient at risk for cardiovascular events

31
Q

How should ACEIs be administered for HFrEF?

A

Started at low doses and titrated to target or maximally tolerated doses

32
Q

What is the ROA of ACEIs?

A

Oral and injectable (enalaprilat)

33
Q

Food may decrease the absorption of ___________ (ACEI), so it should be taken on an empty stomach

A

captopril

34
Q

All ACEIs except captopril and lisinopril are __________ (prodrug/drug)

A

prodrug

35
Q

___________ is the only ACE inhibitor that is not eliminated primarily by the kidneys

A

Fosinopril

36
Q

Plasma half-lives of active compounds (ACEIs) vary from _______ hours

A

2 to 12 hrs

37
Q

What are the adverse effects of ACEIs?

A
Postural hypotension
Renal insufficiency
Hyperkalemia
Persistent dry cough
Angioedema
Altered taste
Skin rash
38
Q

When on ACEIs, potassium supplements and potassium-sparing diuretics should be used with caution due to the risk of ______________

A

hyperkalemia

39
Q

What should we monitor if ACEIs are being given to a patient?

A

Serum potassium

Serum creatinine

40
Q

The potential for symptomatic hypotension with

ACE inhibitors is much more common if used concomitantly with a __________

A

diuretic

41
Q

An increase in serum creatinine of up to _____ above baseline is acceptable and by itself does not warrant discontinuation of ACEIs.

A

30%

42
Q

ACEIs _______ (can/cannot) be used in pregnant women.

A

cannot

43
Q

Vasotec is the brand name for ____________

it is injectable

A

enalapril

44
Q

What is the brand name of lisinopril?

A

Prinivil

Zestril

45
Q

What is the brand name of quinapril?

A

Accupril

46
Q

Altace is the brand name for __________

A

Ramipril

47
Q

Angiotensin receptor blockers (ARBs) are orally active compounds that are ____ (competitive/noncompetetive) antagonists of the angiotensin II type 1 receptor

A

competitive

48
Q

ARBs _______ (do/do not) affect bradykinin levels

A

do not

49
Q

ARBs block the ______ receptor

A

AT1

50
Q

What does ARB do to the following?

  1. preload
  2. afterload
  3. cardiac output
A

decrease preload
decrease afterload
increase cardiac output

51
Q

When are ARBs used?

A

ARBs are a substitute for patients who cannot tolerate ACE inhibitors due to cough or angioedema

52
Q

For what conditions, ARBs are used for?

A

Heart failure and HTN

53
Q

Can we give a diabetic patient an ARB if he/she was having dry cough on taking ACEIs?

A

yes

54
Q

ARBs are orally active and are dosed once daily, with the exception of __________, which is dosed twice daily

A

valsartan

55
Q

ARBs _________ (are/are not) highly plasma protein bound

A

are

56
Q

___________ differs in that it undergoes extensive first-pass hepatic metabolism, including conversion to an active metabolite

A

losartan

57
Q

ARBs are excreted in __________ (urine only/feces only/both urine and feces)

A

both urine and feces

58
Q

Can we give ARB to a pregnant woman?

A

No

59
Q

Aldosterone antagonists are indicated in patients with ___________ and ______________

A

HFrEF (w/ or w/o symptoms)

Recent myocardial infarction

60
Q

____________ (amiloride/spironolactone) also has affinity for androgen and progesterone receptors

A

spironolactone

61
Q

What are the endocrine related adverse effects of spironolactone?

A

gynecomastia

dysmenorrhea

62
Q

____________ (amiloride/spironolactone) has the additional benefit of diminishing the cardiac remodeling that occurs in heart failure

A

spironolactone