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Pharmacology - Winter > 5 - Heart Failure > Flashcards

5 - Heart Failure Flashcards

1
Q

What is heart failure?

A

Abnormality of cardiac structure or function leading to failure of heart to deliver oxygen at a rate that fulfills requirements of tissues in the body

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2
Q

Most px w/ heart failure have high ____

A

BP

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3
Q

Most px w/ heart failure have enlarged _____

A

Heart muscle and chamber

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4
Q

Most px w/ heart failure have low_____

A
  • Ejection fraction (percent of blood pumped from the heart)

- Heart failure = ejection fraction of 50% or less

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5
Q

What causes atrial systole?

A

Atrial contraction

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6
Q

What causes ventricular systole?

A
  • First phase = ventricular contraction

- Second phase = ventricular ejection

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7
Q

What causes ventricular diastole?

A
  • Early = isovolumic/isovolumetric relaxation

- Late = ventricular filling

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8
Q

When does atrial diastole occur?

A

Anytime that is not atrial systole (atrial contraction)

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9
Q

How do you calculate ejection fraction?

A

(amount of blood pumped out of ventricle) / (total amount of blood in ventricle)

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10
Q

Which ejection fraction is generally more important?

A

Left ventricular, b/c it pumps blood to the whole body

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11
Q

How do cardiomyocytes respond to an action potential?

A
  • By depolarization of the membrane

- Starts w/ shortening contractile proteins; ends w/ relaxation and return to resting state

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12
Q

How are cardiomyocytes connected and what do these connections do?

A

Connected by intercalated discs, which respond to stimuli as a unit

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13
Q

What is a echocardiograph and what does it tell us?

A
  • Sends soundwaves into body of heart, which are reflected at the interfaces btwn tissue
  • Return time tells us depth of reflecting surface
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14
Q

Force of muscle contraction is related to amount of _____

A

Cytosolic calcium

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15
Q

Where does calcium come from?

A

Sarcoplasmic reticulum and mitochondria stores outside of the cell

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16
Q

How is muscle relaxation achieved?

A

Through removal of free calcium by the Na/Ca exchangers, which then undergoes reuptake into SR and mitochondria

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17
Q

Why is heart failure not immediately perceived by the px?

A

Body compensates

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18
Q

Are compensatory mechanisms of the body for heart failure helpful?

A

Initially helpful b/c returns BP to normal, but ultimately become harmful

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19
Q

What are some risk factors for chronic heart failure?

A
  • Age
  • Smoking
  • Obesity
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20
Q

What are some co-morbidities that contribute to development of heart failure? Which is most common?

A
  • Hypertension
  • Coronary artery disease (most common)
  • Diabetes
  • Dyslipidemia
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21
Q

An MI can cause ___ dysfunction

A

Systolic

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22
Q

Left ventricular hypertrophy can cause ____ dysfunction

A

Diastolic

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23
Q

What does damage to cardiac myocytes and extracellular matrix lead to?

A

Changes in size, shape, and function of heart and cardiac wall stress

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24
Q

What can systemic neurohormonal imbalance lead to?

A
  • Fibrosis
  • Apoptosis
  • Hypertrophy
  • Cellular and molecular alterations
  • Myotoxicity
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25
Q

How does the body try to correct heart failure?

A

Slight decreases in BP by increased sodium retention, activation of RAAS, and symp. nerve activation

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26
Q

What affect does increased sodium retention have on BP? Is it a fast or slow process?

A
  • Causes increased water retention, which increases plasma volume
  • Slow process
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27
Q

What affect does activation of RAAS have on BP? Is it a fast or slow process?

A
  • Angiotensin constricts arteries/veins (fast)

- Aldosterone increases sodium retention (slow)

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28
Q

What affect does symp nerve activation have on BP? Is it a fast or slow process?

A
  • Increases heart rate and contractility

- Both are fast

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29
Q

What effect does increased plasma volume and constriction of veins have on early heart failure?

A

Increased venous return increases ventricular contraction

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30
Q

What effect does constriction of arteries have on early heart failure?

A

Increased peripheral resistance, but heart is still strong enough to pump against increased resistance

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31
Q

What effect does increased plasma volume and constriction of veins have on late heart failure?

A
  • Increased venous return stretches already overstretched ventricles, and heart no longer able to increase force of contraction
  • Heart size enlarges (dilates) and muscle thickens (hypertrophy)
  • Venous pressure increases => edema (peripheral and pulmonary)
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32
Q

What effect does constriction of arteries have on late heart failure?

A

Greatly increased peripheral resistance hard for heart to empty against

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33
Q

What effect does symp activation have on late heart failure?

A

Overstimulation of beta-adrenergic receptors causes down-regulation of these receptors, increased fibrosis, and increased apoptosis

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34
Q

What can left side heart failure cause?

A

Pulmonary edema

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35
Q

What can right side heart failure cause?

A

Peripheral edema

36
Q

What are the main sx of heart failure?

A
  • Shortness of breath (during day or at night); coughing*
  • Need to sit or stand to breathe easily
  • Reduced exercise tolerance
  • Fatigue*
  • Ankle swelling
  • Pulmonary/peripheral edema*
37
Q

What are the main signs of heart failure?

A
  • Sweating
  • Increased heart rate
  • Elevated jugular venous pressure
  • Rapid breathing
  • Cardiac murmur
38
Q

What does the severity of sx of heart failure depict and not depict?

A
  • Depicts likelihood of survival

- Doesn’t depict ventricular function

39
Q

Which drug is an ACE inhibitor?

A

Enalapril

40
Q

Which drugs are ARBs?

A

Losartan and valsartan

41
Q

Which drug is an ARNI?

A

Entresto (combo of sacubitril and valsartan 1:1)

42
Q

Which drugs are beta blockers?

A

Metoprolol and carvedilol

43
Q

Which drug is an inotrope?

A

Digoxin

44
Q

Which drugs are diuretics?

A

Furosemide and metolazone

45
Q

Which drug is a diuretic and an aldosterone antagonist?

A

Spironolactone

46
Q

What are some benefits of ACE inhibitors to heart failure?

A
  • Decreased constriction in arteries and veins = decreased preload and afterload
  • Decreased aldosterone by decreased angiotensin 2 = decreased blood volume
  • Decreased thickening of heart tissue
47
Q

What is the main function of ACE inhibitors and ARBs?

A

Decrease preload and afterload

48
Q

When are ACE inhibitors initiated for heart failure? Are they used as a monotherapy?

A
  • Soon after diagnosis

- Excellent monotherapy

49
Q

ACE inhibitors can reduce death caused by ____

A
  • Progressive heart failure
  • Cardiac arrhythmia
  • MI
  • Stroke
50
Q

What are the first line drugs for heart failure?

A
  • Should be ACE inhibitor (enalapril)

- Can be used w/ furosemide if edema present

51
Q

Can ACE inhibitors be used in pregnancy?

A

No

52
Q

What are some side effects of ACE inhibitors?

A
  • Hyperkalemia (b/c of aldosterone decrease)

- Dry cough

53
Q

Are ACE inhibitors metabolically neutral? What does this mean?

A
  • Yes, so they have no effect on lipids or blood glucose

- Ok to use in px on medications for diabetes or hyperlipidemia

54
Q

What are some drug interactions w/ ACE inhibitors and ARBs?

A
  • Spironolactone, valsartan, entresto, antacids, NSAIDs

- All can cause hyperkalemia when combined

55
Q

What is different about the side effects from ACE inhibitors and ARBs?

A

ARBs don’t cause cough

56
Q

Efficacy of ARBs are reduced by _____

A

Grapefruit juice

57
Q

What does ARNI stand for?

A

Angiotensin receptor blocker / neprilysin inhibitor

58
Q

What is the net effect of neprilysin?

A
  • Increased constriction in arteries and veins => increased preload and afterload
  • Increased aldosterone => increased blood volume
59
Q

Which drug inhibits neprilysin?

A

Sacubitril

60
Q

When are ARNIs used?

A
  • As a replacement for ACE inhibitors or ARB in px w/ heart failure w/ reduce ejection fraction
  • Currently used a second line drug in heart failure in px w/ heart failure stage B, C, D, or w/ high BP or reduced kidney function
61
Q

Can ARNIs be used in pregnancy?

A

No, valsartan can cause birth defects

62
Q

What are some side effects of ARNIs?

A
  • Hyperkalemia
  • Low BP
  • Kidney dysfunction
63
Q

How are beta blockers dosed for heart failure?

A

Low dose gradually increased over weeks

64
Q

When are beta blockers used?

A

Post myocardial infarction

65
Q

What are the benefits of beta blockers for heart failure?

A
  • Decrease adverse effects of high catecholamine levels on the heart
  • Decrease cardiomyocyte apoptosis (cell death)
  • Decrease cardiac remodeling
66
Q

What does carvedilol do? What is the benefit?

A
  • Blocks beta and alpha receptors
  • Alpha receptor blockade helps to dilate arteries, decreasing afterload
  • Beta receptor blockade slows the heart and decrease force of contraction
67
Q

What does metoprolol do?

A

Selectively blocks beta 1 receptors

68
Q

When should beta blockers not be used for heart failure?

A

When px also has asthma, COPD, peripheral vascular disease, insulin dependent diabetes, or is physically active

69
Q

Which co-morbidities w/ heart failure CAN beta blockers be used in?

A
  • Hypertension
  • Glaucoma
  • Certain arrhythmias
  • MI
  • Angina
70
Q

What some drug interactions w/ beta blockers?

A
  • Ventolin (carvedilol only)
  • Verapamil (carvedilol and metoprolol)
  • Anti-retroviral medications
  • Alcohol (has additive effects of lowering BP)
71
Q

What does dobutamine do?

A

Stimulate beta 1 receptors in the heart to increase heart rate and contractility

72
Q

When are inotropes used for heart failure?

A

In px experiencing end stages of heart failure

73
Q

How is dobutamine administered?

A

IV infusion

74
Q

What are disadvantages to dobutamine and digoxin?

A
  • May increase heart rate, myocardial oxygen consumption, and BP
  • May aggravate ischemia and provoke arrhythmias
75
Q

What does digoxin do?

A
  • Increases heart contractility (increases calcium in myocardial cells)
  • Blocks Na/K ATPase
76
Q

Does dobutamine improve mortality outcomes?

A

No, improves quality of life

77
Q

____ increases digoxin toxicity

A

Hypokalemia (can be caused by diuretics)

78
Q

What are some drug interactions w/ digoxin?

A
  • Antibiotics like amoxicillin, erythromycin

- Amiodarone (anti-arrhythmic)

79
Q

Why do px w/ heart failure and kidney failure need diuretics?

A

To help kidney deal w/ fluid overload from edema

80
Q

What is the major difference btwn thiazide diuretics and loop diuretics?

A

Loop diuretics increase calcium urinary excretion, while thiazide diuretics decrease urinary excretion

81
Q

Which diuretic is most commonly used for heart failure?

A

Loop diuretics, furosemide

82
Q

What is diuretic resistance?

A

Persistence of edema despite salt restriction and adequate diuretic therapy

83
Q

What causes diuretic resistance?

A

RAAS-induced adaptive responses by the kidney

84
Q

What is done to overcome diuretic resistance?

A
  • Increase dose or frequency of dose
  • Combo of loop and thiazide diuretics
  • *Both have associated risks of excessive depletion of water or electrolytes
85
Q

What is the sequence of medications for a typical px w/ heart failure?

A

1) Loop diuretic to control sx of edema
2) ACE inhibitor once diuretic therapy optimized; start at low dose
3) Beta blocker once px stable on ACE inhibitor; start at low dose
4) Inotropes if sx of heart failure persist in spite of above regimen

Pharmacology - Winter (18 decks)

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