Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharmacology > 12) Heart Failure > Flashcards

12) Heart Failure Flashcards

1
Q

Ejection fraction

A
  • Percentage of blood leaving your heart each time it contracts
  • Contraction = eject blood ventricles
  • Relaxation = ventricles refill with blood
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Stroke volume

A
  • Volume of blood pumped from the left ventricle per beat
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Cardiac output

A
  • Volume of blood being pumped by the heart (by L/R ventricle) per unit time
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Preload

A
  • What comes before/into the heart by veins

- Venous return to the heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Venodilator drugs effect on preload

A
  • Reduce preload
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Afterload

A
  • What comes after the heart

- Pressure and resistance for the outflow from heart via arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Arteriodilator drugs effect on afterload

A
  • Reduce afterload
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Drugs that serve as both venodilators and arteriodilators will reduce both

A
  • Preload

- Afterload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Systolic heart failure

A
  • Reduction of cardiac contractile force and ejection fraction
  • Heart failure with reduced ejection fraction (HFrEF)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Diastolic heart failure

A
  • Stiffening or other changes in the ventricles that prevent adequate filling during diastole
  • Ejection volume (stroke volume) is reduced but ejection fraction is normal
  • Heart failure with preserved ejection fraction (HFpEF)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Heart failure is a combination of

A
  • Systolic and diastolic dysfunction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

The severity of heart failure is traditionally indicated on the New York Heart Association (NYHA) scale…based on symptoms

A
  • Step I = symptoms occur only with maximal exercise
  • Steps II and III = symptoms that occur with marked (II) or mild (III) exercise
  • Step IV = symptoms are present at rest
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Heart failure results when

A
  • Cardiac output is inadequate for the needs of the body
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

A poorly understood defect in cardiac contractility is complicated by

A
  • Multiple compensatory processes that further weaken the failing heart
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Compensatory responses in heart failure

A
  • Baroreceptor response
  • RAAS activation, decreased GFR
  • Increased ventricular wall tension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Baroreceptor response in heart failure

A
  • SNS activation

- Increase in HR and contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

RAAS activation and decreased GFR in heart failure

A
  • Fluid retention

- Increased preload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Increased ventricular wall tension in heart failure

A
  • Myocyte growth

- Hypertrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

All bodily compensatory responses in heart failure lead to

A
  • Increased cardiac output
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

3 major groups of drugs utilized in congestive heart failure (CHF)

A
  • Positive inotropic drugs
  • Vasodilators
  • Miscellaneous drugs for chronic failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Positive inotropic drugs for CHF

A
  • Cardiac glycosides (digoxin)
  • Beta agonists (dobutamine)
  • PDE inhibitors (milrinone)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Vasodilators used for CHF

A
  • PDE inhibitors (milrinone)
  • Nitroprusside, nitrates, hydralazine
  • Loop diuretics, angiotensin inhibitors, nesiritide, sacubitril, SGLT2 inhibitors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Miscellaneous drugs used for CHF

A
  • Loop diuretics, angiotensin inhibitors, nesiritide, sacubitril, SGLT2 inhibitors
  • Beta blockers, spironolactone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Pharmacologic therapies for heart failure

A
  • Reduce Na/H2O retention (diuretics)
  • Reduce afterload/Na/H2Ocretention (ACEI)
  • Reduce sympathetic stimulation (β blockers)
  • Reduce of pre/afterload (vasodilators)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Pharmacologic therapy in systolic failure includes

A
  • Direct augmentation of depressed cardiac contractility with positive inotropic drugs (such as digitalis glycosides)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Prototypes and pharmacokinetics of cardiac glycosides (often called digitalis)

A
  • Several come from the digitalis (foxglove) plant
  • Prototype = Digoxin
  • Digoxin has an oral bioavailability of 60–75%, and a half-life of 36–40 h
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Cardiac glycoside mechanism of action

A
  • Inhibition of heart Na+/K+ ATPase
  • Small increase in intracellular sodium alters the driving force for Na/Ca exchange
  • Less calcium is removed from the cell
  • More Ca then stored in the sarcoplasmic reticulum and increases contractile force when released
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Cardiac glycoside effects/usage

A
  • Increase in contractility

- Used in heart failure and atrial fibrillation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Major signs of digitalis toxicity

A
  • Arrhythmias, nausea, vomiting, and diarrhea

- Rarely, confusion or hallucinations and visual or endocrine aberrations may occur

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Treatment for digitalis toxicity

A
  • Correction of potassium and magnesium deficiency
  • Anti-arrythmic
  • Digoxin antibodies (Digibind)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Digitalis drug interactions

A
  • Arrhythmogenesis is increased by hypokalemia, hypomagnesemia, and hypercalcemia
  • Loop diuretics and thiazides may significantly reduce serum potassium and thus precipitate digitalis toxicity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Hypokalemia, hypomagnesemia and hypercalcemia potentiate

A
  • Digitalis toxicity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Therapeutic index for digoxin

A
  • 0.5 to 0.8/0.9 ng/mL
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Rapid IV Ca2+ potentiates

A
  • Arrhythmias
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Digoxin metabolism

A
  • P-glycoprotein (Pgp)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Digoxin GI interactions

A
  • Antibiotics may wipe flora off (a route of digoxin metabolism)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Entresto is a combination of

A
  • ARB (valsartan) and NI (sacubitril)
38
Q

MOA of sacubitril

A
  • Inhibits the enzyme neprilysin that degrades natriuretic peptides (NP) and bradykinin
39
Q

Three molecules mediate the natriuretic peptide (NP) effects

A
  • Atrial natriuretic peptide (ANP) secreted from the cardiac atria
  • B-type natriuretic peptide (BNP) secreted from the cardiac
    ventricles
  • CNP activates natriuretic peptide receptor (BNP-receptor)
40
Q

All 3 NP effect mediators are broken down by

A
  • Neprilysin
41
Q

Natriuresis

A
  • Excretion of sodium in urine
42
Q

Diuresis

A
  • Increased production of urine
43
Q

Antifibrotic

A
  • Prevent formation of fibrous connective tissue as a response to injury
44
Q

Antiproliferative

A
  • Heart growth inhibition
45
Q

Antithrombotic

A
  • Blood clotting inhibition
46
Q

Entresto MOA/side effects

A
  • Hypotension
  • Hyperkalemia
  • Increase serum creatinine
  • Angioedema
  • Decrease hematocrit and hemoglobin
  • Cough (linked to increase bradykinin)
  • Renal failure
47
Q

Nesiritide (NP, vasodialator) mechanism of action

A
  • Recombinant human B-type natriuretic peptide (BNP)
  • Arterio- and veno-dilator by increasing cGMP in vascular smooth muscle
  • Net effect: decrease BP, increase diuresis
  • Promotes vasodilation, natriuresis, and diuresis
48
Q

Nesiritide B-type NP characteristic

A
  • Potent natriuretic peptide produced by ventricles
49
Q

Nesiritide advantage

A
  • Less arrhythmias (lack beta effects) vs. positive inotropes
  • No tolerance
50
Q

Nesiritide side effects

A
  • Hypotension
  • Azotemia
  • Increase serum creatinine
  • Headache
51
Q

Nesiritide DOA

A
  • 1 to several hours
52
Q

Milrinone MOA

A
  • Directly inhibits phosphodiesterase (PDE-3), increasing the effective concentration of cAMP
53
Q

Milrinone clinical effect

A
  • Positive inotropy (increase heart contractility)

- Decreased afterload

54
Q

Milrinone side effects

A
  • Thrombocytopenia
  • Hypotension
  • Arrhythmia
55
Q

Dobutamine and dopamine are used in

A
  • Systolic heart failure

- Some efficacy in acute HF (SE: arrhythmogenic)

56
Q

Beta blockers (carvedilol, labetalol, and metoprolol) have shown

A
  • Slower progression of chronic heart failure, especially in patients with hypertrophic cardiomyopathy
57
Q

Dobutamine characteristics

A
  • MOA = Beta 1 agonist

- Effect = increased contractility and cardiac output

58
Q

Dobutamine side effects

A
  • Hypertension
  • Angina
  • Tachycardia
  • Arythmias
59
Q

Low-dose dopamine

A
  • 0.5-2 micro g/kg/min

- Direct stimulation of peripheral DA1 and DA2 receptors

60
Q

Low-dose dopamine effects

A
  • Induces intrarenal vasodilatation, augmented renal blood flow
61
Q

Intermediate dose dopamine

A
  • 3-10 micro g/kg/min

- Beta(1)-adrenergic receptor stimulation

62
Q

Intermediate dose dopamine effects

A
  • Increase contractility
63
Q

High dose dopamine

A
  • > 10 micro g/kg/min

- Alpha-adrenergic receptor stimulation

64
Q

High dose dopamine effects

A
  • Peripheral vasoconstriction

- Systemic vascular resistance

65
Q

Loop diuretics and spironolactone effects

A
  • Reduces preload and edema

- Vasodilating effect on pulmonary vessels

66
Q

Loop diuretics action in HF

A
  • Acute and chronic HF
67
Q

Spironolactone action in HF

A
  • Chronic heart failure
68
Q

ACE inhibitor (anything ending in -il such as capropril) effects

A
  • Blocks ACE
  • Reduces Angiotensin II
  • Decreases vascular tone and aldosterone secretion
69
Q

Positive inotropes (names)

A
  • Cardiac glycosides (digoxin)

- Sympathomimetics (dopamine, dobutamine)

70
Q

Positive inotropes effects

A
  • Increase cardiac contractility
71
Q

Positive inotropes action in HF

A
  • Cardiac glycosides (digoxin) = chronic HF

- Sympathomimetics (dopamine, dobutamine) = acute HF

72
Q

Beta blockers (anything ending in -ol such as metoprolol) effects

A
  • Decrease heart remodeling
73
Q

Beta blockers action in HF

A
  • Chronic HF
74
Q

Vasodilators (names)

A
  • Nitroprusside
  • Hydralazine and isosorbide dinitrate
  • Nesiritide (natriuretic peptide)
  • Milrinone (phosphodiesterase inhibitors)
75
Q

Nitroprusside effects

A
  • Reduce preload and afterload
76
Q

Nitroprusside action in HF

A
  • Acute HF
77
Q

Hydralazine and isosorbide dinitrate effects

A
  • Poorly understood mechanism in HF
78
Q

Hydralazine and isosorbide dinitrate action in HF

A
  • Chronic HF in African Americans
79
Q

Nesiritide (natriuretic peptide) effects

A
  • Reduce preload and afterload
80
Q

Nesiritide (natriuretic peptide) action in HF

A
  • Acute HF
81
Q

Milrinone (phosphodiesterase inhibitors) effects

A
  • Increase contractility
82
Q

Milrinone (phosphodiesterase inhibitors) action in HF

A
  • Acute HF
83
Q

Neprilysin inhibitor (with ARB) names

A
  • Sacubitril/valsartan
84
Q

Neprilysin inhibitor (with ARB) effects

A
  • Increase BNP and ARB effects

- Reduce preload and afterload

85
Q

Neprilysin inhibitor (with ARB) action in HF

A
  • Chronic HF
86
Q

Adrenergic blockers site of action in HF

A
  • Decrease cardiac workload by slowing HR (b1) and decreasing BP (a1)
87
Q

Direct vasodilators site of action in HF

A
  • Decrease cardiac workload by dilating vessels and reducing preload
88
Q

Phosphodiesterase inhibitors site of action in HF

A
  • Increase cardiac output by increasing the force of myocardial contraction
89
Q

ACE inhibitors site of action in HF

A
  • Increase cardiac output by lowering BP and decreasing fluid volume
90
Q

Diuretics site of action in HF

A
  • Increase cardiac output by reducing fluid volume and decreasing BP
91
Q

Cardiac glycosides site of action in HF

A
  • Increase cardiac output by increasing the force of myocardial contraction

Pharmacology (27 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions