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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
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2
Q

Stroke volume

A
  • Volume of blood pumped from the left ventricle per beat
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3
Q

Cardiac output

A
  • Volume of blood being pumped by the heart (by L/R ventricle) per unit time
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4
Q

Preload

A
  • What comes before/into the heart by veins

- Venous return to the heart

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5
Q

Venodilator drugs effect on preload

A
  • Reduce preload
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6
Q

Afterload

A
  • What comes after the heart

- Pressure and resistance for the outflow from heart via arteries

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7
Q

Arteriodilator drugs effect on afterload

A
  • Reduce afterload
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8
Q

Drugs that serve as both venodilators and arteriodilators will reduce both

A
  • Preload

- Afterload

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9
Q

Systolic heart failure

A
  • Reduction of cardiac contractile force and ejection fraction
  • Heart failure with reduced ejection fraction (HFrEF)
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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)
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11
Q

Heart failure is a combination of

A
  • Systolic and diastolic dysfunction
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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
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13
Q

Heart failure results when

A
  • Cardiac output is inadequate for the needs of the body
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14
Q

A poorly understood defect in cardiac contractility is complicated by

A
  • Multiple compensatory processes that further weaken the failing heart
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15
Q

Compensatory responses in heart failure

A
  • Baroreceptor response
  • RAAS activation, decreased GFR
  • Increased ventricular wall tension
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16
Q

Baroreceptor response in heart failure

A
  • SNS activation

- Increase in HR and contractility

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17
Q

RAAS activation and decreased GFR in heart failure

A
  • Fluid retention

- Increased preload

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18
Q

Increased ventricular wall tension in heart failure

A
  • Myocyte growth

- Hypertrophy

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19
Q

All bodily compensatory responses in heart failure lead to

A
  • Increased cardiac output
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20
Q

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

A
  • Positive inotropic drugs
  • Vasodilators
  • Miscellaneous drugs for chronic failure
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21
Q

Positive inotropic drugs for CHF

A
  • Cardiac glycosides (digoxin)
  • Beta agonists (dobutamine)
  • PDE inhibitors (milrinone)
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22
Q

Vasodilators used for CHF

A
  • PDE inhibitors (milrinone)
  • Nitroprusside, nitrates, hydralazine
  • Loop diuretics, angiotensin inhibitors, nesiritide, sacubitril, SGLT2 inhibitors
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23
Q

Miscellaneous drugs used for CHF

A
  • Loop diuretics, angiotensin inhibitors, nesiritide, sacubitril, SGLT2 inhibitors
  • Beta blockers, spironolactone
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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)
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25
Pharmacologic therapy in systolic failure includes
- Direct augmentation of depressed cardiac contractility with positive inotropic drugs (such as digitalis glycosides)
26
Prototypes and pharmacokinetics of cardiac glycosides (often called digitalis)
- 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
27
Cardiac glycoside mechanism of action
- 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
28
Cardiac glycoside effects/usage
- Increase in contractility | - Used in heart failure and atrial fibrillation
29
Major signs of digitalis toxicity
- Arrhythmias, nausea, vomiting, and diarrhea | - Rarely, confusion or hallucinations and visual or endocrine aberrations may occur
30
Treatment for digitalis toxicity
- Correction of potassium and magnesium deficiency - Anti-arrythmic - Digoxin antibodies (Digibind)
31
Digitalis drug interactions
- Arrhythmogenesis is increased by hypokalemia, hypomagnesemia, and hypercalcemia - Loop diuretics and thiazides may significantly reduce serum potassium and thus precipitate digitalis toxicity
32
Hypokalemia, hypomagnesemia and hypercalcemia potentiate
- Digitalis toxicity
33
Therapeutic index for digoxin
- 0.5 to 0.8/0.9 ng/mL
34
Rapid IV Ca2+ potentiates
- Arrhythmias
35
Digoxin metabolism
- P-glycoprotein (Pgp)
36
Digoxin GI interactions
- Antibiotics may wipe flora off (a route of digoxin metabolism)
37
Entresto is a combination of
- ARB (valsartan) and NI (sacubitril)
38
MOA of sacubitril
- Inhibits the enzyme neprilysin that degrades natriuretic peptides (NP) and bradykinin
39
Three molecules mediate the natriuretic peptide (NP) effects
- 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
All 3 NP effect mediators are broken down by
- Neprilysin
41
Natriuresis
- Excretion of sodium in urine
42
Diuresis
- Increased production of urine
43
Antifibrotic
- Prevent formation of fibrous connective tissue as a response to injury
44
Antiproliferative
- Heart growth inhibition
45
Antithrombotic
- Blood clotting inhibition
46
Entresto MOA/side effects
- Hypotension - Hyperkalemia - Increase serum creatinine - Angioedema - Decrease hematocrit and hemoglobin - Cough (linked to increase bradykinin) - Renal failure
47
Nesiritide (NP, vasodialator) mechanism of action
- 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
Nesiritide B-type NP characteristic
- Potent natriuretic peptide produced by ventricles
49
Nesiritide advantage
- Less arrhythmias (lack beta effects) vs. positive inotropes - No tolerance
50
Nesiritide side effects
- Hypotension - Azotemia - Increase serum creatinine - Headache
51
Nesiritide DOA
- 1 to several hours
52
Milrinone MOA
- Directly inhibits phosphodiesterase (PDE-3), increasing the effective concentration of cAMP
53
Milrinone clinical effect
- Positive inotropy (increase heart contractility) | - Decreased afterload
54
Milrinone side effects
- Thrombocytopenia - Hypotension - Arrhythmia
55
Dobutamine and dopamine are used in
- Systolic heart failure | - Some efficacy in acute HF (SE: arrhythmogenic)
56
Beta blockers (carvedilol, labetalol, and metoprolol) have shown
- Slower progression of chronic heart failure, especially in patients with hypertrophic cardiomyopathy
57
Dobutamine characteristics
- MOA = Beta 1 agonist | - Effect = increased contractility and cardiac output
58
Dobutamine side effects
- Hypertension - Angina - Tachycardia - Arythmias
59
Low-dose dopamine
- 0.5-2 micro g/kg/min | - Direct stimulation of peripheral DA1 and DA2 receptors
60
Low-dose dopamine effects
- Induces intrarenal vasodilatation, augmented renal blood flow
61
Intermediate dose dopamine
- 3-10 micro g/kg/min | - Beta(1)-adrenergic receptor stimulation
62
Intermediate dose dopamine effects
- Increase contractility
63
High dose dopamine
- >10 micro g/kg/min | - Alpha-adrenergic receptor stimulation
64
High dose dopamine effects
- Peripheral vasoconstriction | - Systemic vascular resistance
65
Loop diuretics and spironolactone effects
- Reduces preload and edema | - Vasodilating effect on pulmonary vessels
66
Loop diuretics action in HF
- Acute and chronic HF
67
Spironolactone action in HF
- Chronic heart failure
68
ACE inhibitor (anything ending in -il such as capropril) effects
- Blocks ACE - Reduces Angiotensin II - Decreases vascular tone and aldosterone secretion
69
Positive inotropes (names)
- Cardiac glycosides (digoxin) | - Sympathomimetics (dopamine, dobutamine)
70
Positive inotropes effects
- Increase cardiac contractility
71
Positive inotropes action in HF
- Cardiac glycosides (digoxin) = chronic HF | - Sympathomimetics (dopamine, dobutamine) = acute HF
72
Beta blockers (anything ending in -ol such as metoprolol) effects
- Decrease heart remodeling
73
Beta blockers action in HF
- Chronic HF
74
Vasodilators (names)
- Nitroprusside - Hydralazine and isosorbide dinitrate - Nesiritide (natriuretic peptide) - Milrinone (phosphodiesterase inhibitors)
75
Nitroprusside effects
- Reduce preload and afterload
76
Nitroprusside action in HF
- Acute HF
77
Hydralazine and isosorbide dinitrate effects
- Poorly understood mechanism in HF
78
Hydralazine and isosorbide dinitrate action in HF
- Chronic HF in African Americans
79
Nesiritide (natriuretic peptide) effects
- Reduce preload and afterload
80
Nesiritide (natriuretic peptide) action in HF
- Acute HF
81
Milrinone (phosphodiesterase inhibitors) effects
- Increase contractility
82
Milrinone (phosphodiesterase inhibitors) action in HF
- Acute HF
83
Neprilysin inhibitor (with ARB) names
- Sacubitril/valsartan
84
Neprilysin inhibitor (with ARB) effects
- Increase BNP and ARB effects | - Reduce preload and afterload
85
Neprilysin inhibitor (with ARB) action in HF
- Chronic HF
86
Adrenergic blockers site of action in HF
- Decrease cardiac workload by slowing HR (b1) and decreasing BP (a1)
87
Direct vasodilators site of action in HF
- Decrease cardiac workload by dilating vessels and reducing preload
88
Phosphodiesterase inhibitors site of action in HF
- Increase cardiac output by increasing the force of myocardial contraction
89
ACE inhibitors site of action in HF
- Increase cardiac output by lowering BP and decreasing fluid volume
90
Diuretics site of action in HF
- Increase cardiac output by reducing fluid volume and decreasing BP
91
Cardiac glycosides site of action in HF
- Increase cardiac output by increasing the force of myocardial contraction

Pharmacology (27 decks)

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