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Pharmacology Test #3 > Drugs to Treat CHF > Flashcards

Drugs to Treat CHF Flashcards

1
Q

CHF occurs when

A

the heart is unable to pump enough oxygenated blood to meet the demands of the body

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2
Q

The heart is failing when

A

cardiac output is insufficient to meet the needs of the body

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3
Q

CO is mainly affected by which two factors:

A

stroke volume and heart rate, each of which are affected by different factors

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4
Q

Cardiovascular consequences of decreased CO

A

tachycardia; cardiomeglia; arrhythmias; fatigue/exercise intolerance

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5
Q

Respiratory consequences of decreased cardiac output (CO)

A

shortness of breath; pulmonary edema; cyanosis; orthopnea

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6
Q

Preload is the

A

left ventricular end diastolic pressure or volume, meaning the amount of stretch on the heart at the end of diastole before contraction

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7
Q

Afterload is the

A

force that the ventricle has to push against to eject blood during systole

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8
Q

Frank-Starling Relationship

A

input-output relationship of the heart

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9
Q

Why can the heart respond with greater stroke volume when it is stretched more?

A

Stretching the heart (sarcomeres in the myocytes) results in the myocyte responding with greater force of contraction

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10
Q

How does the heart contract more forcefully with more stretch?

A

actin and myosin become aligned better when the sarcomeres are stretched, with a maximum force being generated when sarcomeres are 2 to 2.2 microns in length

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11
Q

What happens when the sarcomeres are stretched ore tha 2 to 2.2 microns?

A

the actin and myosin are not aligned properly and force cannot be further increased

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12
Q

Contractility is

A

the force with which the heart contracts

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13
Q

What happens to stoke volume in conditions that increase inotropy (contractility)

A

stroke volume increases for a given LVEDV or preload

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14
Q

What do optimized hearts look like on the Frank-Starling relationship curve?

A

optimized hearts have a steeper curve, where small changes in preload (LV end diastolic volume) results in large increases in stroke volume

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15
Q

What do failing hearts look like on the Frank-Starling relationship curve?

A

Failing hearts do not respond well to increased preload, and a CHF patient will often exhibit a flatter curve resembling the red one

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16
Q

How are afterload and SV related?

A

inversely

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17
Q

Failing hearts start to show signs of being sensitive to what?

A

of being “sensitive” to afterload, with severe cases of heart failure being very sensitive to increases in afterload

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18
Q

What increases stroke volume for a given value of afterload?

A

preload and inotropy

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19
Q

Compensation in CHF

A

compensation is when heart function is stable, though there is an underlying disease, and the patient is able to participate in many or more normal activities (though symptoms of CHF are present)

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20
Q

Decompensation in CHF

A

Decompensation is a period of time when the heart/CV system cannot compensate adequately for the reduced effectiveness of the CHF heart, and the person often experiences symptoms sufficient enough to put them in the hospital

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21
Q

Systolic heart failure

A

primarily a deficit in contraction; the heart muscle itself is weak and often dilated, making it unable to contract with sufficient strength to meet the needs of the body

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22
Q

Diastolic heart failure

A

primarily a deficit in relaxation; it may be strong enough to contract, but it can’t expand enough to allow blood to enter during diastole, resulting in reduced cardiac output

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23
Q

Describe progression of CHF

A

increased vascular resistance -> heart works harder and requires more oxygen ->hypoxia -> decreased functioning of the heart ->increased pre-load, pulmonary edema -> hypertrophic response (eventually exacerbates the problem)

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24
Q

Compensatory mechanisms in early heart failure

A
  1. sympathetic discharge
  2. RAAS activity
  3. cardiac remodeling
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25
Q

Compensatory mechanisms in early heart failure results in

A

increased SV but at a cost

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26
Q

What is afterload, SV and preload like in early heart failure

A

afterload is potentially high (hypertention); SV is reduced; preload stands to increase

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27
Q

What happens to the Starling curve in early HF

A

the patient starts to drop off the normal healthy Starling curve and begins to have a lowered curve

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28
Q

Increased sympathetic discharge can lead to

A

arrhythmias and remodeling via activation of beta Ars

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29
Q

Angiotensin II causes

A

vasoconstriction, stimulates remodeling, and induces aldosterone (which causes salt and water retention, increasing preload)

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30
Q

What does a CHF heart look like compared to a normal heart

A

CHF heart will have thicker ventricular walls and increased deposition of connective tissue

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31
Q

Increased connective tissue in a CHF heart is due to

A

myocyte cell death and replacement of these dead myocytes with fibroblasts

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32
Q

Calcium signals in cardiac myocytes contributes to

A

changes in gene expression as part of the hypertrophic remodeling response

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33
Q

What contributes to the increased expression of genes that mediate the hypertrophic remodeling response

A

when the heart cell goes through more rounds of calcium entry/exit (calcium cycling)

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34
Q

Patients with congestive heart failure can have their CHF exacerbated by what disease?

A

hyperthyroidism

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35
Q

What does it mean to say that patients are “afterload sensitive”

A

increases in afterload (basically blood pressure) bring about sharp reductions in stroke volume

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36
Q

What happens in late stage congestive heart failure

A

compensatory mechanisms can no longer adequately compensate for the problems; preload continues to increase; afterload increases; SV decreases; preload values in the “congestive range” where pulmonary function is compromised

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37
Q

Two main categories of drugs to treat CHF

A
  1. Manipulate hemodynamics

2. Inhibit compensation

38
Q

Manipulate hemodynamics by

A

alleviating the extreme pressure problems of CHF and improve ability of the heart to function as a pump

39
Q

Inhibit compensation by

A

using agents that seek to reverse the cardiac remodeling that occurs during CHF

40
Q

ACE inhibitors address

A

both compensation as well as hemodynamics

41
Q

What do vasodilators do?

A

dilate veins, lower preload and congestive symptoms

42
Q

Vasodilators

A

organic nitrates, hydralazine

43
Q

Diuretics

A

furosemide, bumetamide, and torsemide

decreases blood volume

44
Q

Angiotensin inhibitors

A

ACE inhibitors, ATII rec. antagonists, renin inhibitors

decrease pressure and volume

45
Q

Inotropic agents

A

digoxin, PDE3 inhibitors, beta-AR agonists

stimulate cardiac contractility

46
Q

Inotropic agents for CHF

A
  1. Cardiac glycosides
  2. Phosphodiesterase inhibitors
  3. beta-adrenergic agonists
47
Q

Glycosides (digoxin) only used for

A

chronic therapy

48
Q

PDE inhibitors and beta agonists are only used for

A

acutely decompensated patients, typically in hospital/ER settings

49
Q

PDE inhibitors have a risk of inducing

A

arrhythmias long-term

50
Q

What can beta agonists cause long term

A

desensitization

51
Q

Role of calcium in cardiac myocyte contraction

A

Ca2+ enters through L-type channels and triggers further release of Ca2+ from internal stores via ryanodine receptors; Ca2+ must be removed from the myocyte before the next depolarization

52
Q

How is Ca2+ removed from the myocyte

A
  1. Ca2+ ATPase pumps Ca2+ out of the cell
  2. SERCA pumps Ca2+ into the SR
  3. NCX (Na+/Ca2+ exchange protein) extrudes Ca2+ in exchange for Na+
53
Q

Key to NCX function

A

maintaining the sodium gradient outside/inside the cell (high Na+ outside and low Na+ inside)

54
Q

partial blockade of the ATPase results in

A

increased release of Ca2+ into the cytoplasm during contraction and an increase in the strength of contraction

55
Q

Overall, what does mild to moderate blockage of the sodium potassium ATPase do?

A

increases cardiac contractility by enhancing Ca2+ release during contraction

56
Q

Specific effects of Na+/K+ ATPase blockade

A

increases [Na+]in which will decrease Ca2+ extrusion; more calcium is reloaded into intracellular stores; more Ca2+ is released in response to stimulation; muscle contracts with greater force

57
Q

What does digoxin do?

A 
increase cardiac contractility
increase AV node refractoriness
decrease heart rate
decrease vascular sympathetic tone in CHF secondary to resensitization of baroreceptors
vasodilation in CHF patients
58
Q

Digoxin blocks

A

the sodium potassium ATPase

59
Q

blocking the sodium potassium ATPase alters

A

the sodium gradient across the membrane, resulting in lower than normal sodium outside the cell and higher than normal sodium inside the cell

60
Q

If you don’t know the mechanism of action of digoxin go look at it

A

it’s on page 26 and it’s honestly really stupid; I don’t feel like writing it out

61
Q

Describe the structure of glycosides

A

all glycosides have a steroid nucleus; sugar moieties and lactone moieties define different classes of glycosides

62
Q

Problems with glycosides

A

glycosides have a narrow therapeutic window; loading doses must be monitored closely (serum levels, EKG)

63
Q

Common toxicities of glycosides

A

psychiatric: delirium, fatigue, malaise, confusion
G.I.: anorexia, N&V, abdominal pain
respiratory: increased response to hypoxia
CV: pro-arrhythmic (atrial tachy, AV block)

64
Q

Pharmacodynamics interactions of glycosides

A
  1. beta-blockers and Ca2+ channel blockers: depress the heart, oppose digoxin action
  2. Kaliuretic diuretics (increase K+ elimination): decrease K+, promoting digoxin action, raising risk for arrhythmias
65
Q

beta-AR agonists

A

dobutamine, dopamine

prone to densensitization; cause hypertension

66
Q

Phosphodiesterase 3 inhibitors

A

milrinone, amrinone

proarrhythmic; decreased survival

67
Q

Inotropic agents for acute failure

A

beta-AR agonists

phosphodiesterase 3 inhibitors

68
Q

CHF drugs: inhibiting compensation

A
  1. Renin/angiotensin system inhibition
  2. aldosterone antagonists
  3. beta-AR blockers
69
Q

Renin/angiotensin system inhibition

A

alleviates pressure and volume problems
some stop/reverse remodeling
first line treatment for CHF
ACEi; ATII receptor antagonist, aliskiren

70
Q

Aldosterone antagonists

A

decrease blood volume (diuretic-like)
reverse/arrest hypertrophy
spironolactone = aldosterone

71
Q

beta-AR blockers

A

inhibit sympathetic overactivity in CHF
decrease remodeling, reduce mortality
carvedilol, metoprolol, bisoprolol

72
Q

Spironolactone is used to block

A

the effects of aldosterone and inhibits angiotensin II’s ability to increase preload

73
Q

Pathophysiological effect of increased Na+ and water retention

A

edema, elevated cardiac filling pressures

74
Q

Pathophysiological effect of K+ and Mg2+ loss

A

arrhythmogenesis and risk of sudden cardiac death

75
Q

Pathophysiological effect of reduced myocardial NE uptake

A

potentiation of NE effects: myocardial remodeling and arrhythmogenesis

76
Q

Pathophysiological effect of reduced baroreceptor sensitivity

A

reduced parasympathetic activity and risk of sudden cardiac death

77
Q

Pathophysiological effect of myocardial fibrosis, fibroblast proliferation

A

remodeling and ventricular dysfunction

78
Q

Pathophysiological effect of alterations in Na+ channel expression

A

increased excitability and contractility of cardiac myocytes

79
Q

Beta blockers inhibit

A

the increased sympathetic drive in CHF, reducing the work of the heart, increasing time for filling in diastole, and prevention of remodeling

80
Q

Common beta blockers in CHF

A

metoprolol
bisoprolol
carvedilol

81
Q

afterload and preload with beta blockers

A

they decrease afterload though they might actually cause an increase in preload due to increased filling time during diastole

82
Q

Angiotensin II stimulates ADH (vasopressin) secretion, resulting in

A
  1. water retention
  2. vasoconstriction
  3. enhanced platelet aggregation
  4. VSM and myocyte proliferation
83
Q

Vasopressin receptor antagonists in CHF

A

Tolvaptan and Conivaptan

84
Q

Adverse reactions of tolvaptan and conivaptan

A

hypotension, osmotic demyelination, CYP3A substrate

85
Q

Tolvaptan and conivaptan used in

A

treatment of hyponatremia in HF and SIADH in acute care settings

86
Q

What does neprilysin inhibition do?

A

increases levels of vasoactive peptides
counters neurohumoral vasoconstriction, Na+ retention, and remodeling
is investigation for CHF

87
Q

What does neprilysin do?

A

neutral endopeptidase that degrades endogenous vasoactivate peptides (natriuretic peptides, bradykinin, adrenomedullin)

88
Q

When do ventricles secrete natriuretic peptides (vasodilators)

A

in response to increased blood volume and stretch

89
Q

Do inotropes improve preload problems?

A

No (only helps with the low output symptoms, not congestive symptoms)

90
Q

ACE inhibitors reduce

A

both preload (via blood volume reduction) and afterload (via blood pressure reduction)

91
Q

What would ACE inhibitors be expected to do with the Starling curve

A

might be expected to move a curve both upward out of the low-output range as well as leftward out of the congestive range

92
Q

What do diuretics do to the Starling curve

A

they improve pulmonary edema by reducing blood volume but don’t have much impact on stroke volume

Pharmacology Test #3 (13 decks)

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