Heart Failure Flashcards

1
Q

Symptoms of L-sided HF

A

dyspnea, fatigue, edema, and specifically for L: PULMONARY CONGESTION

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2
Q

Most common causes of L-sided HF

A

general: MI, atherosclerotic heart ds, hypertensive changes, valve ds, dilated cardiomyopathy, congenital heart ds. Most common: MYOCARDIAL ISCHEMIA due to coronary artery ds, followed by HTN

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3
Q

Symptoms of R-sided HF

A

dyspnea, fatigue, edema, and specifically for R: PERIPHERAL EDEMA

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4
Q

Most common causes of R-sided HF

A

general: MI, atherosclerotic heart ds, hypertensive changes, valve ds, dilated cardiomyopathy, congenital heart ds. Most common: MYOCARDIAL ISCHEMIA due to coronary artery ds, followed by HTN

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5
Q

Compensatory effects of HF

A

3 major responses: Increase sympathetic activity, activate RAS (renin-angiotensin system), myocardial hypertrophy

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6
Q

Two Pathways of SNS stimulation during HF

A

Stimulation of B-adrenergic receptors; alpha 1-adrenergic stimulation

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7
Q

Effects of alpha 1-adrenergic stimulation in HF

A

produces vasoconstriction that enhances venous return, Increase cardiac preload and afterload.

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8
Q

Effects of B-adrenergic stimulation in HF

A

Stimulation of B-adrenergic receptors in heart Increase HR, Increase force of contraction

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9
Q

Adverse Effects of SNS Stimulation as a Compensatory Measure in HF

A

Increase work-load of heart (which causes further decline in cardiac function)

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10
Q

Mechanism of Renin-Angiotensin System Activation due to HF

A

Decrease in CO leads to Decrease renal blood flow that triggers release of renin to both: Increase formation of angiotensin II (vasoconstrictor that Increase peripheral resistance); and release aldosterone

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11
Q

Effects of Renin-Angiotensin System Activation in HF

A

Release of aldosterone promotes retention of Na & water thus Increase blood vol and amount of blood returned to heart

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12
Q

Adverse Effects of Renin-Angiotensin System Activation in HF

A

edema because of Increase venous pressure due to inability of heart to pump extra vol

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13
Q

Effects of Myocardial Hypertrophy in HF

A

Myocardial Hypertrophy: heart Increase size via: chambers dilate; initial stretching leads to more forceful, stronger contraction, but excessive elongation of fibers and thus weaker contractions (ultimately Decrease ejection ability - systolic failure); a

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14
Q

Compensated HF

A

compensatory mechanisms (myocardial hypertrophy, RAS activation, SNS stimulation0 are restoring ADEQUATE CARDIAC OUTPUT

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15
Q

Decompensated HF

A

mechanisms eventually Increase overall workload on heart and lead to furhter decline in cardiac functio; compensatory mechanisms FAIL TO MAINTAIN ADEQUATE CO

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16
Q

Drug classes used to treat HF

A

Inhibitors of renin-angiotensin-aldosterone system (RAAS); β-blockers; diuretics; inotropic agents; direct vasodilators; aldosterone antagonists

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17
Q

Types of RAAS Inhibitors

A

ACE inhibitors; Angiotensin-Receptor Blockers (ARBs)

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18
Q

Indications for ACEIs

A

MONOTHERAPY (pts with mild DOE and no apparent signs of vol overload); ASYMPTOMATIC PTS WITH EJECTION FRACTION <35% (left ventricular dysfunction); PTS WITH RECENT MI; all stages LEFT VENTRICULAR FAILURE with or w/o symptoms

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19
Q

Indications for ARBs

A

Angiotensis-Receptor Blockers (ARBs): HTN, SUBSTITUTES FOR ACEI (esp. when ACEI associated with cough &/or angioedema)

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20
Q

Indications for B-Blockers

A

Unless BB therapy contraindicated, BB should be used in management of HF

21
Q

Indications for Loop Diuretics

A

provide relief of volume overload symptoms (dyspnea and peripheral edema)

22
Q

Primary Inotropic Drug

23
Q

Indications for Direct Vasodilators

A

Add on therapy

24
Q

Aldosterone Antagonists

A

Spironolactone; eplerenone

25
Indications for Aldosterone Antagonists
aldosterone antagonists: spironolactone: reserved for most severe HF cases; eplerenone: REDUCES MORTALITY in L VT SYSTOLIC DYSFUNCTION, HF AFTER ACUTE MI
26
Which B-blockers are indicated for HF
CARVEDILOL (COREG) - non-selective B-blockade, also alpha -blockade. METOPROLOL (LOPRESSOR); Long-Acting variant (Toprol)- B1 selective (cardioselective), immediate or extended release
27
When B-blockers are indicated for HF
used for structural heart ds, no symptoms in selected pts with ACEI; structural heart ds with previous or current symptoms in all pts with ACEI
28
3 Stages of HF
Stage A: High Risk, No Symptoms Stage B: Structure HD, No Symptoms Stage C: Structure HD, previous or current symptoms
29
Treatment Regimen for Stage A HF (Lowest Level)
Risk-factor reduction; patient education
30
Treatment Regimen for Stage A (2nd tier) HF
Treat HTN, DM, dyslipidemia; ACEIs or ARBs in SOME patients
31
Treatment Regimen for Stage B HF
ACEIs or ARBs in ALL patients; B-blocker in selected patients
32
Treatment Regimen for Stage C HF
ACEIs and B-Blockers in ALL patients
33
Treatment Regimen for Stage C HF (Highest Level)
ACEIs and B-Blockers in ALL patients; dietary Na+ restriction; diuretics & digoxin
34
Use of digoxin
1. increase cardiac contractility 2. improve ejection fraction 3. lower diastolic volume, 4. improved circulation
35
MoA of digoxin
promotes calcium entry into the cell and causees retention of calcium in the cell
36
Indication for digoxin
in severe left ventricular systolic dysfunction - after initiation of a ACE inhibitor and diuretic
37
Half-life of digoxin
36 hours (very long)
38
Side effects of digoxin
GI effects: anorexia (due to N/V), N/V; CNS effects: headache, fatigue, confusion, blurred vision, alteration of color perception and halos
39
Use of spironolactone
direct antagonist of aldosterone
40
MoA of spironolactone
prevents salt retention, myocardial hypertrophy and hypokalemia due to elevated aldosterone levels and angiotensin II stimulation and reduced hepatic clearence
41
Indication for for spironolactone
Reserved for the most severe heart failure cases
42
Half-life of spironolactone (active metabolites)
14-22 hr
43
Side effects of spironolactone
GI disturbances, lethargy and confusion, gynecomastia;progestational and antiandrogenic adverse effects due to its nonspecific binding to various steroid receptors
44
Use of eplerone
competitive antagonist of aldosterone
45
MoA of eplerone
lower incidence of endocrine related side effects because of reduced affinity for glucocorticoid, andogen and progesterone receptors
46
Indications for eplerone
left ventricular systolic dysfunction and heart failure after acute myocardial infarction
47
Half-life of eplerone
4-6 hr
48
Side effects of eplerone
Reduced compared to spironolactone
49
Treatment for overt HF
loop diuretics are initated first to provide relief of volume overload; then an ACE inhibitor or ARB is induced; third, beta blockers are started after the patient is stable on ACE and finally digoxin is added if needed (symptoms remain)