Drugs for Heart Failure Flashcards
(105 cards)
1
Q
•impaired ability of the ventricle to fill with or eject blood
A
HEART FAILURE
2
Q
•inability of the heart to pump blood to meet the metabolic demands of the body
A
HEART FAILURE
3
Q
•formerly called CHF
A
HEART FAILURE
4
Q
HEART FAILURE
•common cause:
A
–Left systolic dysfunction secondary to CAD (~70%)
5
Q
•primary manifestations: HF
A
–dyspnea
–fatigue
–fluid retention
6
Q
–pulmonary congestion
A
•Left Ventricular Failure
7
Q
–pulmonary edema
A
•Left Ventricular Failure
8
Q
–dyspnea, orthopnea
A
•Left Ventricular Failure
9
Q
–systemic congestion
A
•Right Ventricular Failure
10
Q
–peripheral edema
A
•Right Ventricular Failure
11
Q
–jugular venous distention
A
•Right Ventricular Failure
12
Q
–due to NE → increased HR (can only increase O2 demand)
A
•tachycardia & increased contractility
13
Q
–increased preload → increased SV (leads to congestion)
A
•Frank-Starling mechanism
14
Q
–to redistribute blood flow (increases afterload)
A
•vasoconstriction
15
Q
–changes in cardiac muscle mass, size, shape, structure, function
A
•ventricular hypertrophy & remodelling
16
Q
GOALS OF PHARMACOLOGIC INTERVENTION
A
•To alleviate symptoms, slow disease progression, and improve survival
17
Q
•6 classes of drugs:
A
- 1) inhibitors of the renin-angiotensin system
- 2) ß-adrenoreceptor blockers
- 3) diuretics
- 4) direct vasodilators
- 5) inotropic agents
- 6) aldosterone antagonists
18
Q
BENEFICIAL EFFECTS OF DRUGS FOR HF
A
- Reduction of the load on the myocardium
- Decreased extracellular fluid volume
- Improved cardiac contractility
- Slowing the rate of cardiac remodeling
19
Q
•Agents of choice in HF
A
ACE INHIBITORS
20
Q
•Block ACE (conversion of angiotensin I to II)
A
ACE INHIBITORS
21
Q
•Diminish the rate of bradykinin inactivation
A
ACE INHIBITORS
22
Q
•Decrease vascular resistance, venous tone, BP
A
ACE INHIBITORS
23
Q
•Reduce preload and afterload -> increased cardiac output
A
ACE INHIBITORS
24
Q
•Indicated in patients with all stages of left ventricular failure
A
ACE INHIBITORS
25
•Should be taken on an empty stomach
ACE INHIBITORS
26
•Pro-drugs that require activation by hydrolysis via hepatic enzymes (except ______)
ACE INHIBITORS
| Captopril
27
• are adequately but incompletely absorbed following oral administration
ACE INHIBITORS
28
•Monopeptide, orally active compounds that are extremely potent competitive antagonists of the AT1 receptor
ARBs
29
•Advantage of more complete blockade of angiotensin action
ARBs
30
•Do not affect bradykinin levels
ARBs
31
•Similar actions with ACEIs but not therapeutically identical
ARBs
32
•Alternative to the ACEIs
ARBs
33
•All require only once-daily dosing
ARBs
34
only ARB that undergoes extensive first-pass effect, along with conversion to its active metabolite
Losartan:
35
•All are highly protein-bound
ARBs
36
•All have large Vd (except ______)
candesartan
37
•Ability to prevent the myocardial changes because of the chronic inactivation of the sympathetic nervous system –decreasing HR and inhibiting the release of renin
BETA-BLOCKERS
38
•Prevent direct deleterious effects of NE on the cardiac muscle fibers -> decreasing remodeling, hypertrophy, and cell death
BETA-BLOCKERS
39
is recommended for all patients with heart disease except those who are at high risk but have no symptoms and those who are in acute HF
BETA-BLOCKERS
40
nonselective ß-adrenoreceptor antagonist that also blocks alpha-adrenoreceptors
•Carvedilol:
41
long-acting ß1-selective antagonist
•Metoprolol:
42
•Reduce morbidity and mortality associated with HF
Carvedilol and Metoprolol
43
•Treatment should be started at low doses and gradually titrated to effective doses based on patient tolerance
Carvedilol and Metoprolol
44
•Additional benefit of antihypertensive action
Carvedilol and Metoprolol
45
•Relieve pulmonary congestion and peripheral edema
DIURETICS
46
•Useful in reducing the symptoms of volume overload (e.g., orthopnea, PND)
DIURETICS
47
•Decrease plasma volume -> decreased venous return to the heart (preload) -> decreased cardiac workload and oxygen demand
DIURETICS
48
•Decrease afterload by reducing plasma volume decreased BP
DIURETICS
49
relatively mild diuretics and lose efficacy if patient creatinine clearance is less than 50 mL/min
•Thiazide diuretics:
50
used for patients who require extensive diuresis and those with renal insufficiency; most commonly used diuretics in HF
•Loop diuretics:
51
–Overdoses can lead to profound hypovolemia
DIURETICS
52
•Dilation of venous blood vessels leads to a decrease in cardiac preload by increasing the venous capacitance
DIRECT VASODILATORS
53
reduce systemic arteriolar resistance and decrease afterload
•Arterial dilators
54
commonly used venous dilators for patients with congestive HF
•Nitrates:
55
if the patient is intolerant of ACEIs or ß-blockers, or if additional vasodilator response is required
•Hydralazine+ ISDN:
56
enhance cardiac muscle contractility -> increased cardiac output
INOTROPIC DRUGS
| •Positive inotropic agents
57
–Result of an increased cytoplasmic Ca concentration that enhances the contractility of cardiac muscle
INOTROPIC DRUGS
| •Positive inotropic agents
58
•Digitalis or digitalis glycosides (digitalis/foxglove plant)
I. DIGITALIS GLYCOSIDES
59
•Group of chemically similar compounds that can increase the contractility of the heart muscle
I. DIGITALIS GLYCOSIDES
60
•Influence Na and Ca ion flows in the cardiac muscle -> increased contraction of AV myocardium (positive inotropic action)
I. DIGITALIS GLYCOSIDES
61
•Narrow therapeutic index
I. DIGITALIS GLYCOSIDES
62
most widely used agent digitalis glycoside
•Digoxin:
63
•Digoxin (Lanoxin®)
DIGITALIS GLYCOSIDES
64
•Digitalis purpurea, Digitalis lanata
DIGITALIS GLYCOSIDES
65
•inhibit Na+/K+ - ATPase pump
DIGITALIS GLYCOSIDES
66
•Increases the force of cardiac contraction -> decreased EDV -> increased efficiency of contraction (EF) -> improved circulation -> reduced sympathetic activity -> reduced peripheral resistance -> decreased HR
Digoxin
67
•Increased vaga ltone -> decreased HR -> diminished myocardial oxygen demand
Digoxin
68
•Slows down AV conduction velocity (use in AF)
Digoxin
69
•Severe LVSD after initiation of ACEI and diuretic therapy
Digoxin
70
•HF with atrial fibrillation
Digoxin
71
•Only digitalis glycoside available in the US
Digoxin
72
•Very potent, with a narrow margin of safety
Digoxin
73
•Long half-life of ~36 hours
Digoxin
74
•Mainly eliminated intact by the kidney, requiring dose adjustment based on CrCl
Digoxin
75
•Large Vd: accumulates in muscle
Digoxin
76
•Dosage based on lean BW
Digoxin
77
•Loading dose regimen is used when acute digitalization is needed
Digoxin
78
•Cardiac: arrhythmia (slowing of AV conduction associated with atrial arrhythmias)
Digoxin
79
GI: anorexia, N/V
Digoxin
80
•CNS: headache, fatigue, confusion, blurred vision, alteration of color perception, halos on dark objects
Digoxin
81
PREDISPOSING FACTORS OF DIGOXIN TOXICITY
* Hypothyroidism
* Hypoxia
* Renal failure
* Myocarditis
82
MANAGEMENT OF DIGOXIN TOXICITY
* Discontinuation of cardiac glycoside therapy
* Determination of serum K levels
* Oral K supplementation (if indicated)
* Close monitoring of digoxin levels in renal insufficiency -> dose adjustments
* Administration of antiarrhythmic drugs
* Digoxin immune Fab
83
•Dobutamine and dopamine
II. BETA-ADRENERGIC AGONISTS
84
•Intravenous inotropic agent administered at the hospital
II. BETA-ADRENERGIC AGONISTS
–250 mg/20 mL vial
–250 mg/250 mL pre-mix (1:1)
–500 mg/250 mL pre-mix (2:1)
•Dobutamine and dopamine
85
•Positive inotropic effect and vasodilation
II. BETA-ADRENERGIC AGONISTS
| •Dobutamine and dopamine
86
•Treatment of acute HF
II. BETA-ADRENERGIC AGONISTS
| •Dobutamine and dopamine
87
III. PHOSPHODIESTERASE INHIBITORS
II. PHOSPHODIESTERASE INHIBITORS
•Inamrinone (formerly Amrinone)
•Milrinone
88
•Long-term treatment = higher risk of mortality
II. PHOSPHODIESTERASE INHIBITORS
•Inamrinone (formerly Amrinone)
•Milrinone
89
•Short-term IV milrinone: not associated with increased risk of mortality; symptomatic benefit in refractory HF
II. PHOSPHODIESTERASE INHIBITORS
•Inamrinone (formerly Amrinone)
•Milrinone
90
•Direct antagonist of aldosterone -> prevents salt retention, myocardial hypertrophy, hypokalemia
ALDOSTERONE ANTAGONISTS (Spironolactone)
91
•Reserved for the most advanced cases of HF
ALDOSTERONE ANTAGONISTS (Spironolactone)
92
•AEs: GI disturbances (e.g., gastritis, peptic ulcer); CNS effects (lethargy, confusion); endocrine abnormalities (e.g., gynecomastia, decreased libido, menstrual irregularities)
ALDOSTERONE ANTAGONISTS (Spironolactone)
93
•Competitive antagonist of aldosterone at mineralocorticoid receptors
ALDOSTERONE ANTAGONISTS (Eplerenone)
94
•Lower incidence of endocrine-related SE due to reduced affinity for glucocorticoid, androgen, and progesterone receptors
ALDOSTERONE ANTAGONISTS (Eplerenone)
95
•Reduces mortality in patients with LVSD and HF after acute MI
ALDOSTERONE ANTAGONISTS (Eplerenone)
96
At risk for developingHF. No identified structural or functional abnormality; no signs and symptoms.
Stage A
97
Developed structural heart diseasethat is strongly associated with the development of HF, but without signs and symptoms.
Stage B
98
SymptomaticHF associated with underlying structural heart disease
Stage C
99
Advanced structural heart disease and markedsymptoms of HF at rest despite maximal medical therapy
Stage D
100
No limitation of physical activity. Ordinary physicalactivity does not cause undue fatigue, palpitation, or dyspnea
Class I
101
Slight limitation of physical activity. Comfortableat rest, but ordinary physical activity results in fatigue, palpitation, or dyspnea
Class II
102
Marked limitation of physicalactivity. Comfortable at rest, but less than ordinary activity results in fatigue, palpitation, or dyspnea
Class III
103
Unable to carry on anyphysical activity without discomfort. Symptoms at rest. If any physical activity is undertaken, discomfort is increased.
Class IV
104
Stageof heart failurebased on structure and damage to heart muscle
ACC/AHAStages of Heart Failure
105
Severity based on symptoms and physical activity
NYHA Functional Classification
