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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
How does the body try to correct heart failure?
Slight decreases in BP by increased sodium retention, activation of RAAS, and symp. nerve activation
26
What affect does increased sodium retention have on BP? Is it a fast or slow process?
- Causes increased water retention, which increases plasma volume - Slow process
27
What affect does activation of RAAS have on BP? Is it a fast or slow process?
- Angiotensin constricts arteries/veins (fast) | - Aldosterone increases sodium retention (slow)
28
What affect does symp nerve activation have on BP? Is it a fast or slow process?
- Increases heart rate and contractility | - Both are fast
29
What effect does increased plasma volume and constriction of veins have on early heart failure?
Increased venous return increases ventricular contraction
30
What effect does constriction of arteries have on early heart failure?
Increased peripheral resistance, but heart is still strong enough to pump against increased resistance
31
What effect does increased plasma volume and constriction of veins have on late heart failure?
- 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)
32
What effect does constriction of arteries have on late heart failure?
Greatly increased peripheral resistance hard for heart to empty against
33
What effect does symp activation have on late heart failure?
Overstimulation of beta-adrenergic receptors causes down-regulation of these receptors, increased fibrosis, and increased apoptosis
34
What can left side heart failure cause?
Pulmonary edema
35
What can right side heart failure cause?
Peripheral edema
36
What are the main sx of heart failure?
- 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
What are the main signs of heart failure?
- Sweating - Increased heart rate - Elevated jugular venous pressure - Rapid breathing - Cardiac murmur
38
What does the severity of sx of heart failure depict and not depict?
- Depicts likelihood of survival | - Doesn't depict ventricular function
39
Which drug is an ACE inhibitor?
Enalapril
40
Which drugs are ARBs?
Losartan and valsartan
41
Which drug is an ARNI?
Entresto (combo of sacubitril and valsartan 1:1)
42
Which drugs are beta blockers?
Metoprolol and carvedilol
43
Which drug is an inotrope?
Digoxin
44
Which drugs are diuretics?
Furosemide and metolazone
45
Which drug is a diuretic and an aldosterone antagonist?
Spironolactone
46
What are some benefits of ACE inhibitors to heart failure?
- 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
What is the main function of ACE inhibitors and ARBs?
Decrease preload and afterload
48
When are ACE inhibitors initiated for heart failure? Are they used as a monotherapy?
- Soon after diagnosis | - Excellent monotherapy
49
ACE inhibitors can reduce death caused by ____
- Progressive heart failure - Cardiac arrhythmia - MI - Stroke
50
What are the first line drugs for heart failure?
- Should be ACE inhibitor (enalapril) | - Can be used w/ furosemide if edema present
51
Can ACE inhibitors be used in pregnancy?
No
52
What are some side effects of ACE inhibitors?
- Hyperkalemia (b/c of aldosterone decrease) | - Dry cough
53
Are ACE inhibitors metabolically neutral? What does this mean?
- Yes, so they have no effect on lipids or blood glucose | - Ok to use in px on medications for diabetes or hyperlipidemia
54
What are some drug interactions w/ ACE inhibitors and ARBs?
- Spironolactone, valsartan, entresto, antacids, NSAIDs | - All can cause hyperkalemia when combined
55
What is different about the side effects from ACE inhibitors and ARBs?
ARBs don't cause cough
56
Efficacy of ARBs are reduced by _____
Grapefruit juice
57
What does ARNI stand for?
Angiotensin receptor blocker / neprilysin inhibitor
58
What is the net effect of neprilysin?
- Increased constriction in arteries and veins => increased preload and afterload - Increased aldosterone => increased blood volume
59
Which drug inhibits neprilysin?
Sacubitril
60
When are ARNIs used?
- 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
Can ARNIs be used in pregnancy?
No, valsartan can cause birth defects
62
What are some side effects of ARNIs?
- Hyperkalemia - Low BP - Kidney dysfunction
63
How are beta blockers dosed for heart failure?
Low dose gradually increased over weeks
64
When are beta blockers used?
Post myocardial infarction
65
What are the benefits of beta blockers for heart failure?
- Decrease adverse effects of high catecholamine levels on the heart - Decrease cardiomyocyte apoptosis (cell death) - Decrease cardiac remodeling
66
What does carvedilol do? What is the benefit?
- 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
What does metoprolol do?
Selectively blocks beta 1 receptors
68
When should beta blockers not be used for heart failure?
When px also has asthma, COPD, peripheral vascular disease, insulin dependent diabetes, or is physically active
69
Which co-morbidities w/ heart failure CAN beta blockers be used in?
- Hypertension - Glaucoma - Certain arrhythmias - MI - Angina
70
What some drug interactions w/ beta blockers?
- Ventolin (carvedilol only) - Verapamil (carvedilol and metoprolol) - Anti-retroviral medications - Alcohol (has additive effects of lowering BP)
71
What does dobutamine do?
Stimulate beta 1 receptors in the heart to increase heart rate and contractility
72
When are inotropes used for heart failure?
In px experiencing end stages of heart failure
73
How is dobutamine administered?
IV infusion
74
What are disadvantages to dobutamine and digoxin?
- May increase heart rate, myocardial oxygen consumption, and BP - May aggravate ischemia and provoke arrhythmias
75
What does digoxin do?
- Increases heart contractility (increases calcium in myocardial cells) - Blocks Na/K ATPase
76
Does dobutamine improve mortality outcomes?
No, improves quality of life
77
____ increases digoxin toxicity
Hypokalemia (can be caused by diuretics)
78
What are some drug interactions w/ digoxin?
- Antibiotics like amoxicillin, erythromycin | - Amiodarone (anti-arrhythmic)
79
Why do px w/ heart failure and kidney failure need diuretics?
To help kidney deal w/ fluid overload from edema
80
What is the major difference btwn thiazide diuretics and loop diuretics?
Loop diuretics increase calcium urinary excretion, while thiazide diuretics decrease urinary excretion
81
Which diuretic is most commonly used for heart failure?
Loop diuretics, furosemide
82
What is diuretic resistance?
Persistence of edema despite salt restriction and adequate diuretic therapy
83
What causes diuretic resistance?
RAAS-induced adaptive responses by the kidney
84
What is done to overcome diuretic resistance?
- Increase dose or frequency of dose - Combo of loop and thiazide diuretics * *Both have associated risks of excessive depletion of water or electrolytes
85
What is the sequence of medications for a typical px w/ heart failure?
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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