Medications for heart failure Flashcards

1
Q

Is the incidence of heart failure increasing or decreasing in the US?

A

increasing

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2
Q

What are large portions of the U.S. population at risk for?

A

HF or stage A

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3
Q

What are risk factors for heart failure? (10)

A
  • HTN
  • obesity
  • pre-diabetes
  • diabetes
  • cardiac disease (esp. MI)
  • familial or genetic cardiomyopathy
  • cardiotoxicity r/t cancer
  • substance abuse
  • autoimmune disease
  • iron overload
  • inflammatory disorders (covid)
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4
Q

What races/ethnicities have greater incidence of heart failure?

A
  • african americans
  • hispanics
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5
Q

What are the 4 etiologies of heart failure?

A
  • ischemic heart disease
  • chronic HTN
  • COPD
  • cardiomyopathies
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6
Q

How does ischemic heart disease cause heart failure?

A

r/t ischemic insults to myocardium, weakens the strength of ventricular contraction

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7
Q

How does COPD lead to heart failure?

A
  • leading cause of right ventricular failure
  • can cause RV changes & HF called cor pulmonale
  • development of pulmonary HTN due to constriction of arterial vessels & increased workload & exhaustion of RV
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8
Q

What kind of cardiomyopathies can lead to HF?

A
  • restrictive
  • hypertrophic
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9
Q

What are the underlying problems in HF related to muscle damage?

A

artherosclerosis or cardiomyopathy

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10
Q

What may cause the heart to increase workload to maintain an efficient output?

A
  • HTN
  • alcoholism
  • MI
  • A-fib
  • valvular disease
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11
Q

____________ ____________ are an underlying problem in HF resulting from congenital cardiac defects.

A

structural abnormalities

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12
Q

What is left-sided heart failure?

A

when lt ventricles are unable to pump re-oxygenated blood from the lungs to the heart’s left atrium; ventricles are too stiff and not contracting properly

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13
Q

What does left-sided heart failure lead to?

A
  • decreased cardiac output
  • pulmonary congestion
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14
Q

what is a common cause of right-sided heart failure?

A

left-sided heart failure

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15
Q

What are the two types of left-sided heart failure?

A

systolic heart failure
diastolic heart failure

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16
Q

What is happening in systolic HF?

A

LV cannot contract forcefully enough to keep blood circulating normally throughout the body

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17
Q

What is happening in diastolic HF?

A

LV has grown stiff or thick & is unable to fill the heart properly, which reduces the amount of blood pumped out of the body

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18
Q

Left-sided systolic HF deals with __________ of the heart

A

contraction

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19
Q

What is ejection fraction in left- sided systolic HF?

A

low (<40%)

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20
Q

What are the 9 symptoms of left-sided systolic heart failure?

A
  • fatigue
  • decreased urine production
  • increased HR; may be irregular
  • elevated BP
  • enlarged heart
  • pulmonary “congestion” - SOB
  • coughing (often worse at night)
  • weight gain
  • decreased blood flow to extremities
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21
Q

left-sided HF is an issue with ventricles being ____ _____ to properly _____ heart; able to contract (ventricular _____________)

A

too stiff; fill; hypertrophy

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22
Q

What is ejection fraction in left-sided diastolic HF?

A

typically normal (>50%)

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23
Q

What does lef-sided diastolic HF often result from?

A

HTN

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24
Q

Is there medication available to help with diastolic dysfunction?

A

no

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25
Q

What are sx of left-sided HF? (picture;10)

A
  • paroxymal nocturnal dyspnea
  • elevated pulmonary capillary wedge pressure
  • pulmonary congestion
  • restlessness
  • confusion
  • orthopnea
  • tachycardia
  • exertional dyspnea
  • fatigue
  • cyanosis
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26
Q

What are sx of pulmonary congestion?

A
  • cough
  • crackles
  • wheezes
  • blood-tinged frothy sputum
  • tachypnea
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27
Q

What is the vicious cycle of LV failure?

A

LVF leads to decreased renal perfusion which causes renin production and triggers persistent cycling RAAS which causes futher deterioration of heart function

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28
Q

Is left-sided or right-sided HF more common?

A

left-sided HF

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29
Q

What is the problem in right-sided Heart failure?

A

deoxygenated blood is coming from the body but the rt-side of the heart is not pumping as well as it should leading to “back-up of blood in the body

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30
Q

What are the 8 sx of right-sided HF? (on slide; 7)

A
  • fatigue
  • vein distension
  • weight gain
  • increased urination
  • hepatomegaly
  • increased abdominal girth
  • peripheral swelling
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31
Q

What are the 9 sx of right-sided HF? (picture)

A
  • fatigue
  • increased peripheral venous pressure
  • ascites
  • enlarged liver & spleen
  • may be secondary to chronic pulmonary problems
  • distended jugular veins
  • anorexia & complaints of GI distress
  • weight gain
  • dependent edema
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32
Q

What 7 things does activation of the sympathetic nervous system cause?

A
  • increased HR & contractility tachycardia
  • vasoconstriction
  • activates the renin-angiotensin system (RAS)
  • direct cardiotoxicity
  • increased myocardial O2 demand
  • increase wall stress
  • decreased preload & increases afterload
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33
Q

About ____ of pts with HF have three or more comorbidities

A

50%

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34
Q

The average HF pt is taking ___ medications

A

6

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35
Q

___ of HF pts had at least two admissions per year

A

78%

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36
Q

only ___ completed their annual prescription regimen

A

10%

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37
Q

____ of HF pt never refilled any HF prescriptions

A

1/3`

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38
Q

What should HF treatment address?

A

the effects of HF on airway, breathing & circulation

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39
Q

What are the 3 main goals of HF treatment?

A
  • treatment of the existing sx of the crisis situation
  • prevention of further or expanding complications
  • treatment of underlying cause
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40
Q

What are the 4 stages of HF?

A

stage A: at-risk for HF
stage B: pre-heart failure
Stage C: symptomatic HF
stage D: advanced HF

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41
Q

What is happening during stage A of HF?

A

pt is at risk for HF but w/o current of previous S/S of HF & w/o structural/ functional heart disease or abnormal biomarkers; pt has other disease process/ family hx related to HF

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42
Q

What are the risk factors for those in Stage A of HF?

A
  • HTN
  • CVD
  • diabetes
  • abesity
  • exposure to cardiotoxic agents
  • genetic variant doe cardiomyopathy
  • family hx of cardiomyopathy
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43
Q

What is happening in Stage B of HF?

A

pt w/o currect or previous S/S of HF but has evidence of:
- structural heart disease
-evidence of increased filling pressures
- increased natriuretic peptide levels
- persistently elevated cardiac troponin

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44
Q

What is happening in Stage C of HF?

A

pt with current or previous S/S of HF

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45
Q

What is happening in stage D of HF?

A

marked HF sx that interfere with daily life with recurrent hospitalizations despite attempts to optimize GDMT (treatment)

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46
Q

what are the 4 classifications of HF?

A

new onset/ de novo HF
resolution of sx
persistent HF
worsening HF

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47
Q

What is new onset/ de novo HF?

A
  • newly dx HF
  • no previous hx of HF
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48
Q

What is happening if Hf is classified as resolution of sx?

A

resolution of S/S of HF
- HF in remission w/ resolution of previous structural and/or functional heart disease

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49
Q

What is persistent HF?

A

persistent HF w/ ongoing S/S and/or limited functional capacity

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50
Q

What is worsening HF?

A

worsening S/S or functional capacity

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51
Q

What are the three classes of medication used to treat Hf?

A
  • vasodilators
  • loop diuretics
  • beta- adrenergic antagonists (beta blockers)
52
Q

What are the three types of vasodilators that can be used?

A
  • ACE inhbitors
  • nitrates
  • hydralazine
53
Q

How to vasodilators help with HF?

A

decrease the workload of overworked cardiac muscle

54
Q

How do loop diuretics help with HF?

A

decrease blood volume, which decreases venous return & BP

55
Q

How do beta blockers help with HF?

A

block the beta-receptors in the SNS, decreasingn calcum flow into the myocardial cells, & causing decreased contraction & workload

56
Q

How do ACE inhibitors work?

A

prevent the conversion of angiotensin I to angiotensin II; blocking RAAS & causing vasodilation

57
Q

What do ACE inhibitors help prevent?

A

cardiac remodeling

58
Q

ACE inhibitors allow for symptomatic improvement, reduced _______________ and _________ survival

A

hospitalization; improved

59
Q

if tolerated; all pts with _________ heart failure should be on an ACE inhibitor

60
Q

What affect do ACE inhibitors have on preload & afterload?

A

ACE inhibitors decrease preload & afterload

61
Q

In what ethnic groups do ACE inhibitors tend to not be as effective?

A

black & asian people

62
Q

What can be used as an alternative to ACE inhibitors for those ethnicities or in case of ACE intolerance?

A

angiotensin receptor blockers (ARBs)

63
Q

What is entresto?

A

sacubitril (neprilysin inhibitor) plus valsartan (ARB)

64
Q

What is entresto used for?

A

used for systolic heart failure to improve sx and reduce remodeling

65
Q

What does entresto do?

A
  • increases naturetic peptides (like BNP)
  • bradykinin (vasodilation)
  • increases other mediators which increase vasodilation
66
Q

What are the side effects of entresto?

A
  • angioedema
  • hypotension
  • hyperkalemia
  • renal failure
67
Q

What can entresto cause?

68
Q

is entresto safe for pregnancy?

A

no; contraindicated

69
Q

What type of medications cannot be taken with entresto?

70
Q

How do loop diuretics work?

A

inhibit reabsorption of sodium or chloride at the loop of henle

71
Q

How do look diuretics help the heart?

A
  • decrease workload on heart
  • decrease preload
  • decrease stroke volume
  • decrease cardiac output
72
Q

How are loop diuretics typically given?

A

initially given Iv then changed to oral

73
Q

What are three examples of loop diuretics?

A

bumetanide
furosemide
torsemide

74
Q

What are possible side effects of loop diuretics?

A
  • hyponatremia
  • hypokalemia
  • hypovolemia
  • hypomagnesemia
  • hyperglycemia
  • ototoxicity
75
Q

What should you monitor with pts on loop diuretics?

A
  • potassium
  • I & Os
76
Q

What are spironolactone & eplerenone considered to be?

A

mineralocorticoid receptor antagonists(AKA: aldosterone receptor blockers)

77
Q

What are spironolactone & eplerenone taken for?

A

hypertension & HF

78
Q

When are spironolactone & eplerenone taken as opposed to other medications?

A

used when one drug is not enough to treat sx

79
Q

How do spironolactone & eplerenone work?

A

block the exchange of sodium for potassium in the distal tubules

80
Q

Should spironolactone & eplerenone be taken with or without food?

A

should be taken with meals

81
Q

What should be monitored in pts taking spironolactone & eplerenone?

A
  • potassium
  • LFTs
  • BUN & creatinine
82
Q

When should a pt not recieve spironolactone or eplerenone?

A

when they have renal insufficiency

83
Q

What can spironolactone & eplerenone cause?

A

gynecomastia

84
Q

With what medications should spironolactone & eplerenone not be taken?

A

ACE inhibitors
ARBs
heparin
NSAIDS

85
Q

what do beta blockers help with?

A

help to improve sx, reduce hospitalization & enhance survival in pts with HF with reduced ejection fraction

86
Q

how do beta blockers help the heart?

A
  • decrease catecholamine stimulation
  • decrease myocardial energy demands
  • reduce remodeling due to cardiac myocyte hypertrophy & death
  • stimulation of other detrimental systems such as the renin-angiotensin-aldosterone syestem
  • anti-arrhythmia promotion
87
Q

What are the drugs in the beta blocker class?

A
  • carvedilol
  • metoprolol Succinate
  • bisprolol
88
Q

how should a beta blocker be started?

A

at a very low dose, as it can worsen HF

89
Q

What should you never do when taking a beta blocker?

A

never stop abruptly, need to taper off

90
Q

What are adverse effects of beta blockers?

A
  • worsening HF especially when first started
  • hypotension
  • bradycardia
  • bronchospasm (COPD,asthma)
  • exacerbation of peripheral vascular disease
91
Q

What should a nurse always do before giving a beta blocker?

A

take an apical HR, call MD if less than 60

92
Q

When are nitrates indicated?

A

prevention & treatment of attacks of angina pectoris & HF

93
Q

how do nitrates work on the body?

A
  • arterial & venous dilator
  • decrease preload & afterload
  • increase oxygen to the heart; decrease myocardial oxygen demands
94
Q

how quickly are nitrates absorbed?

A

very rapidly

95
Q

Can people develop tolerance to nitrates?

A

yes; tolerance develops easily, must have drug-free periods

96
Q

What drug-drug interaction with nitrates causes hypotension?

A

sildenafil (viagra)

97
Q

What are the routes of administration for nitroglycerin?

A
  • sublingual
  • translingual spray
  • transmucosal tablet
  • oral, SR tablet
  • intravenous
  • topical ointment
  • transdermal
98
Q

what should you do when administering any type of nitrate to a pt?

A

always wear gloves

99
Q

How long do nitroglycerin patches work?

A

patch is placed for 24 hrs but stops working before that to prevent tolerance

100
Q

how often can sublingual NTG be given?

A

every 5 minutes for a max 3 doses; if no relief, call 911

101
Q

How must a pt be positioned before taking NTG

A

sitting or laying

102
Q

where should NTG be stored?

A

in its original bottle & protected from sunlight

103
Q

What are some side effects that may be experienced with NTG?

A
  • tingles or burns under tongue
  • dizziness
  • headache
104
Q

What should the nurse do before and after giving NTG?

105
Q

What is the name for oral nitrate?

A

isosorbide

106
Q

What are the forms of oral isosorbide?

A

short acting or sustained release

107
Q

how long does isosorbide work?

A

works for about 18 hrs; has a drug free period in the delivery system

108
Q

What was the first drug regimen shown to improve the sx of HF?

A

hydralazine & nitrate (isosorbide)

109
Q

how does the combination of hydralazine & nitrate (isosorbide) affect the body?

A
  • decreases preload & aferload by achieving both venous & arterial vasodilation
  • decreases systemic & pulmonic vascular resistance
  • positive inotropic effect on heart
110
Q

With what pts is hydralazine & nitrate typically used?

A
  • pt who have sx despite ACE inhibitors, beta blockers, & diuretic therapy
  • those who cannot tolerate routine therapy
111
Q

When is digoxin indicated?

A

heart failure
atrial fibrilation

112
Q

is digoxin a first-line tx for HF?

113
Q

What does digoxin do?

A
  • increases intracellular calcium
  • allows more calcium to enter the myocardial cell during depolarization
  • positive inotropic effect (increase contraction)
  • increased renal perfusion w/ a diuretic effect ( decrease in renin release)
  • slowed conduction through the AV node (decrease HR)
114
Q

is the therapeutic margin for digoxin narrow or broad?

A

very narrow

115
Q

What is the normal and desired level for digoxin?

A

normal level: 0.5-2.0
desired level: 0.8

116
Q

What should be drawn when taking digoxin?

A

peak & troughs

117
Q

What are the risks with digoxin?

A

digoxin toxicity & increased risk of hypokalemia

118
Q

How is digoxin given?

A

orally or IV (not the same dosing)

119
Q

What is the onset & absorption of digoxin?

120
Q

How is digoxin excreted?

A

renal excretion

121
Q

What should be checked before giving digoxin?

A

always check apical HR, call MD if less than 60

122
Q

What labs should be monitored when taking digoxin?

A
  • BUN & creatinine
  • potassium
123
Q

What are sx of digoxin toxicity?

A
  • vision changes
  • N/V
  • dizziness
124
Q

What is the antidote to digoxin?

125
Q

With what pt populations should digoxin be used with caution?

A
  • pregnancy & lactation
  • children
  • geriatrics
  • renal insufficiency
126
Q

What are some nursing interventions for those with HF?

A
  • monitor lungs
  • monitor HR & BP
  • monitor BUN & creatinine
  • monitor potassium
  • monitor weight daily
  • question orders for IV fluids
  • pt education: no sodium, no OTC meds