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NAPLEX > Heart Failure > Flashcards

Heart Failure Flashcards

0
Q

What causes HF?

A

HF is most commonly caused Reduced ability of the heart to eject blood, known AD low-output heart failure

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1
Q

What’s heart failure (HF)?

A

HF is a syndrome where the heart is not able to supply sufficient blood flow (or cardiac output) to meet the metabolic needs of the body

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2
Q

Types of heart failure?

A

HF with Reduced ejection fraction (HFrEF)/Systolic dysfunction - impaired ability of LEFT ventricle to EJECT blood

HF with preserved ejection fraction (HFpEF)/ Diastolic dysfunction - impaired ability of LEFT ventricle to FILL with blood

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3
Q

What xterizes systolic dysfxn of HF?

A

Left ventricle ejection fraction < 40%

HFrEF

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4
Q

What xterizes diastolic dysfxn of HF?

A

Only mildly reduced (40-50%) or normal left ventricular ejection fraction

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5
Q

What sometimes xterizes low-output HF?

A

Both systolic and diastolic dysfunction

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6
Q

T/F? HF is one of the most important conditions to include lifestyle counseling and the requirements for strict medication adherence?

A

True

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7
Q

HF can be classified into 2 types based on underlying etiology. What are they?

A

Ischemic cardiomyopathy

Or

Non-ischemic cardiomyopathy

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8
Q

What does Ischemic cardiomyopathy result from?

A

From myocardial damage sustained during an acute myocardial infarction, resulting in loss of contractile function

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9
Q

What does Non-Ischemic cardiomyopathy encompass?

A

A variety of conditions that ultimately increase the workload of cardiomyocytes, accelerating cell death and lead to a thin-walled dilated left ventricle with reduced contractile function

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10
Q

What are the most common causes of HF in North America?

A

Ischemia heart dx (myocardial infarction)

And

HTN

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11
Q

List drugs that cause or worsen HF

A

Chemotherapeutic agents (Doxorubicin, (Adriamycin, Doxil))

Amphetamines and other sympathomimetics

Routine use of CCBs in systolic HF

Anti-arrhythmic drugs (lower risk with amiodarone and Dofetilide). Avoid class I drugs entirely

Avoid Itraconazole for non-life threatening inf such as Onychomycosis

Immunomodulators, including interferons, TNF inhibitors, rituximab etc

NSAIDs, including the selective COX-2 inhibitor Celecoxib (Celebrex)

Glucocorticoids can worsen HF

Triptan migraine drugs

Thiazolidinediones, esp, Rosiglitazone (Avandia) and Pioglitazone (Actos)

Excessive alcohol use

Heart valve dx can be cause by: fenfluramine (Pondimin), dexfenfluramine (Redux), ergot derivative including ergot (Ergostat), dihydroergotamine (Migranal), methysergide (Sansert) and others

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12
Q

What’s cardiac output? (CO)

A

Vol of blood (in L) pumped by the heat in 1 min

It’s a fxn of HR and stroke vol.

CO = HR x SV

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13
Q

What’s stroke vol?

A

Amt of blood ejected from the left ventricle during 1 cardiac cycle

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14
Q

What determines stroke volume?

A

SV is determined by vol of blood in ventricle (preload), the resistance to forward flow in arterial vessels (afterload), and how hard the ventricle squeezes during systole (contractility)

T4, SV is determine by preload, afterload and contractility

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15
Q

What’s preload?

A

Volume of blood in the ventricle

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16
Q

What’s afterload?

A

Resistance to forward flow in the arterial vessels

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17
Q

What’s contractility?

A

How hard the ventricle squeezes during systole

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18
Q

What’s cardiac index?

A

CO/BSA

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19
Q

HF is a progressive syndrome, what does that mean?

A

Regardless of the initial etiology of myocardial damage, over time left ventricular systolic fxn will continue to decline

T4 initial damage to heart => reduction in CO

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20
Q

One of the ways the heart tries to compensate during HF is by activating RAAS? Implication of this?

A

Results in vasoconstriction, which helps maintain BP and perfusion to vital organs

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21
Q

What other compensation by the heart increases HR and contractility? (T4 augmenting CO)

A

Sympathetic (adrenergic) activation

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22
Q

While the RAAS activation in HF is useful (maintains BP and adequate perfusion), what’s not so good abt it?

A

Na and water retention => edema

Excess fluid causes body to be congested and the classic sx of “congestive” HF is seen

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23
Q

Classic sx of “congestive” HF?

A

Dyspnea (SOB)

Fatigue

Peripheral edema

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24
Q

General s/sx of HF?

A

Dyspnea at rest or on exertion

Weakness/fatigue

Shortness of breath

Reduction in exercise capacity

LVH

Increased BNP (B-type Natriuretic Peptide): normal < 100 pg/ml

Increased NT-proBNP (N-terminal pro B-type Natriuretic Peptide) normal < 300 pg/ml

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25
Q

S/sx of left-sided HF?

A

SOB PE

S3 gallop

Orthoptera

Bibasilar rales

Paroxysmal nocturnal dyspnea (PND) or nocturnal cough

EF < 40%

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26
Q

S/sx of right-sided HF?

A

A JEHH

Ascites

Jugular venous distention (JVD)

Edema

Hepatojugular reflux (HJR)

Hepatomegaly

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27
Q

What’re gen the results of sx in HF?

A

Either congestion behind the failing ventricle

Or

Hypoperfusion due to reduced cardiac output

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28
Q

What’s the use of the staging system of HF?

A

Help practitioners optimize mgt of pts in order to slow the development of sx in asymptomatic pts (stages A and B) or slow the progression of syndrome (stages C and D)

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29
Q

Whats another type of classification system used in HF?

A

New York Heart Association functional class (NYHA)

Important prognostic indicator for HF pts

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30
Q

What’s the equivalent of ACC/AHA Staging System A to NYHA functional class?

A

No corresponding category

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31
Q

What’s the equivalent of ACC/AHA Staging System B to NYHA functional class?

A

NYHA functional class I

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32
Q

What’s the equivalent of ACC/AHA Staging System C to NYHA functional class?

A

NYHA functional class I, II, III

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33
Q

What’s the equivalent of ACC/AHA Staging System D to NYHA functional class?

A

NYHA functional class IV

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34
Q

Characteristics of ACC/AHA Staging System A?

A

At high risk for dev HF, but w/o structural HD or sx of HF (ie, pts with HTN, CHD, DM, obesity, metabolic syndrome

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35
Q

Characteristics of ACC/AHA Staging System B?

A

Structural heart dx present but w/o s/sx of HF (ie, LVH, low EF, valvular dx, previous MI)

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36
Q

Which stages of ACC/AHA Staging System is included in clinical diagnosis of HF?

A

C and D

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37
Q

Characteristics of ACC/AHA Staging System C?

A

Structural HD + prior/ current sx of HF (ie, pts with known structural HD, SOB and fatigue, reduced exercise tolerance

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38
Q

Characteristics of ACC/AHA Staging System D?

A

Advanced structural HD + sx of HF at rest despite maximal medical therapy (Refractory HF requiring specialized interventions)

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39
Q

Characteristics of NYHA Functional Class I?

A

No limitations of physical activity

Ordinary physician activity doesn’t cause sx of HF

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40
Q

Characteristics of NYHA Functional Class II?

A

Slight limitation of physical activity

Comfortable at rest, but ordinary physical activity results in sx of HF

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41
Q

Characteristics of NYHA Functional Class III?

A

Marked limitation of physical activity

Comfortable at rest, but minimal exertion (bathing, dressing) causes sx of HF

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42
Q

Characteristics of NYHA Functional Class IV?

A

Unable to carry on any physical w/o sx of HF

OR

HF at rest

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43
Q

Non-pharmacologic therapy for HF?

A

Monitor and document body weight DAILY

Notify provider of HF sx worsens or when weight increases (3 lbs in 1 day or >= 5 lbs in 1week)

Sodium restriction is reasonable for pts with symptomatic HF @
< 1500 mg/d

Daily MVTE

Fluid restrictions (1.5-2 L/D), esp stage D pts

BMI < 30 preferred

Exercise 30 mins/day, 3-5 days a wk as tolerated

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44
Q

What’s the appropriate sodium restriction for HF pts?

A

< 1500 mg/d

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45
Q

What OTC med is reasonable to be used as adjunctive therapy in pts with NYHA class II - IV to reduce mortality and CV hospitalizations?

A

Omega-3 polyunsaturated fatty acid (PUFA)

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46
Q

What meds should be avoided in HF?

A

Products contains ephedra (ma huang) or ephedrine

NSAIDs, including COX-2 inhibitors (due to risk of renal insufficiency and fluid retention)

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47
Q

What alt med has shown promise in HF?

A

Hawthorn and coenzyme Q10

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48
Q

What meds are the cornerstones of HF therapy?

A 
Diuretics to control fluid volume
\+
Angiotensin antagonist (ACE-I or ARBs)
\+
Beta blockers (to delay the progression of cardiac dysfunction and improve survival)

These combo should be used in everyone with HF, who doesn’t have a CI or intolerance to their use

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49
Q

Which of the cornerstones of HF therapy improves survival rate?

A

Beta blockers

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50
Q

What type of diuretic is more commonly used in HF?

A

Loop diuretics

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51
Q

MOA of loop diuretics?

A

They block Na and Cl reabsorption in the THICK ASCENDING LIMB OF LOOP OF HENLE =>

Increased excretion of water, Na, Cl, Mg and Ca

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52
Q

What’s excreted by loop diuretics in HF?

A

Water

Sodium

Chloride

Magnesium

Calcium

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53
Q

Whys the lowest effective dose of loop used in HF?

A

They haven’t been shown to alter the survival of HF pts

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54
Q

List loop diuretics used in HF?

A

Furosemide (Lasix)

Bumetanide

Torsemide (Demadex)

Ethacrynic Acid (Edecrin)

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55
Q

Whats the brand name of Furosemide (loop used in HF)?

A

Lasix

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56
Q

Whats the oral loop dose equivalency of Furosemide (Lasix)?

A

40mg

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57
Q

Whats the oral loop dose equivalency of Bumetanide?

A

1mg

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58
Q

Whats the oral loop dose equivalency of Torsemide (Dermadex)?

A

20mg

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59
Q

Whats the oral loop dose equivalency of Ethacrynic acid (Edecrin)?

A

50mg

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60
Q

What’s warning associated with loops use?

A

Sulfa allergy

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61
Q

Which loop is the sulfa allergy warning not applicable to?

A

Ethacrynic acid (Edecrin)

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62
Q

SEs of loop?

A

Hypokalemia

Orthostatic hypotension

Decreased Na, Mg, Cl, Ca (different than thiazides which increase Ca)

Metabolic alkalosis

Hyperuricemia (increased uric acid)

Hyperglycemia

Increased TGs, TC

Photosensitivity

Ototoxicity (more with Ethacrynic acid), including hearing loss, tinnitus and vertigo

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63
Q

Monitoring for loops?

A

BH REF

BP

Hearing with high doses of rapid IV admin

Renal fxn (SCr, BUN)

Electrolytes

Fluid status (in’s and out’s, weight)

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64
Q

Which loops are light-sensitive (stored in Amber bottles)?

A

IV furosemide and Bumetanide

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65
Q

What’s the furosemide IV to PO ratio?

A

1:2

Furosemide 20mg IV = Furosemide 40mg PO

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66
Q

Diuretics and lithium?

A

May decrease lithium renal clearance and increase risk of lithium toxicity

67
Q

MOA of ACE-I?

A

Block conversion of angiotensin I to angiotensin II by inhibiting the ACE

68
Q

MOA of ARBs?

A

They block angiotensin II receptor AT1, which is responsible for vasoconstriction, aldosterone stimulating and re-modeling effects of angiotensin II

69
Q

Is triple combo of ACE-I/ARB/aldosterone receptor antagonist recommended? Why/why not?

A

Not recommended due to elevated risk of hyperkalemia and increased incidence of renal insufficiency

70
Q

List ACE-I agents

A

Captopril (Capoten)

Enalapril (Vasotec)

Fosinopril

Lisinopril (Prinivil, Zestril)

Quinapril (Accupril)

Ramipril (Altace)

Trandolapril (Mavik)

71
Q

What’s the brand name of Enalapril (ACE-I)?

A

Vasotec

72
Q

What’s the brand name of Lisinopril (ACE-I)?

A

Prinivil

Zestril

73
Q

What’s the brand name of Quinapril (ACE-I)?

A

Accupril

74
Q

What’s the brand name of Ramipril (ACE-I)?

A

Altace

75
Q

Howz Captopril (Capoten) taken?

A

1 hr B4 meals

76
Q

Black box warning of ACE-I?

A

D/c as soon as pregnancy is detected

77
Q

CI to ACE-I use?

A

Angioedema

Bilateral renal artery stenosis

78
Q

SEs to ACE-I and ARBs use?

A

Cough (not for ARB, only ACE-I SE)

Hyperkalemia

Angioedema (d/c drug immediately and drug is then CI)

Hypotension

79
Q

Which ACE-I has more SEs? What are they?

A

Captopril (Capoten)

Taste perversion
Rash

80
Q

Monitoring parameters of ACE-I and ARBs?

A

BP

Potassium

Renal fxn

S/sx of HF

81
Q

List ARBs agents

A

Candesartan (Atacand)

Losartan (Cozaar)

Valsartan (Diovan)

82
Q

Which of the ARBs has shown benefit in clinical trials but no FDA indication for use in HF?

A

Lossrtan (Cozaar)

83
Q

What’s the brand name of Losartan (ARB)?

A

Cozaar

84
Q

What’s the brand name of Valsartan (ARB)?

A

Diovan

85
Q

Black box warning, CI, SEs, Monitoring Parameters same as ACE?

A

Same as ACE-I

86
Q

Which electrolyte is typically increased in ACE-I and ARBs use?

A

Potassium (Hyperkalemia)

87
Q

MOA of bb in HF?

A

Bb antagonize the effects of catecholamines, esp norepinephrine

88
Q

Both BB and ACE-I/ARBs reduce mortality and morbidity, but what’s the difference btw them?

A

BB don’t have a class effect, only Carvedilol, Metoprolol Succinate ext-release and Bisoprolol

ACE-I/ARBs have a class effect

89
Q

List BB used in HF?

A

Carvedilol

Metoprolol Succinate extended-release

Bisoprolol

90
Q

Which BB should be absolutely avoided?

A

BB with intrinsic sympathomimetic activity (ISA)

91
Q

List the selective BB used in HF

A

Bisoprolol (Zebeta)

Metoprolol Succinate ext-release (Toprol XL)

92
Q

What’s the brand name of Metoprolol Succinate ext-release (selective BB)?

A

Toprol XL

93
Q

List non-selective BB used in HF

A

Carvedilol (Coreg, Coreg CR)

94
Q

What’s the brand name of Carvedilol (non-selective BB)?

A

Coreg

95
Q

SE of selective BB (Bisoprolol and Toprol XL)?

A

Reduced HR

Hypotension

Fatigue

Dizziness

96
Q

Monitoring of selective BB (Bisoprolol and Toprol XL)?

A

HR

BP (titrate Q 2 wks, reduce dose if HR < 55 BPM)

S/Sx of HF

97
Q

How do u d/c BB?

A

Must taper

98
Q

Are IV doses of selective BB (Bisoprolol and Toprol XL) equivalent to oral doses?

A

IV doses are NOT equivalent to PO doses (IV is usually lower)

99
Q

How do u take Carvedilol (Coreg, Coreg CR) - no selective BB?

A

Take Carvedilol - all forms -‘with food

100
Q

Which DM sx are NOT masked by BB?

A

Sweating (Diaphoresis)

And

Hunger

101
Q

Which ARAs is non-selective?

A

Spironolactone

102
Q

Which ARAs is selective? Benefits?

A

Eplerenone

Doesn’t exhibit endocrine SE

103
Q

MOA of ARAs?

A

They compete with aldosterone at receptor sites in DISTAL CONVOLUTED TUBULE and COLLECTING DUCTS

104
Q

When ARAs used in pts with HF?

A

Standard therapy in pts who have progressed to NYHA class III or IV

105
Q

What’s the brand name of Spironolactone (ARAs)?

A

Aldactone

106
Q

CI of Aldosterone Receptor Antagonists (ARAs)?

A

Renal impairment (CrCl < 30mL/min)

Hyperkalemia

107
Q

SEs of ARAs?

A

Hyperkalemia

Increased SCr

Gynecomastia and breast tenderness (Spironolactone)

108
Q

Which SE is unique to Spironolactone?

A

Gynecomastia and breast tenderness

109
Q

Monitoring of ARAs?

A

Check K B4 starting and freq thereafter

BP

SCr/BUN

S/Sx of HF

110
Q

How do u minimize risk of hyperkalemia in pts treated with aldosterone blockers?

A

Higher risk if reduced renal fxn (CI if CrCl < 30ml/min)

Don’t start if K > 5 mEq/L

Use low doses, start low

Don’t use NSAIDs concurrently

Monitor freq

Counsel pt about increased risk of dehydration (due to vomiting, diarrhea or reduced fluid intake)

111
Q

What’s Hydralazine?

A

A direct vasodilator which reduces afterload

112
Q

What’s Nitrates?

A

Nitrates are venous vasodilators and reduce preload

113
Q

What’s the role of Hydralazine/Nitrate (combo) in HF?

A

Alternative therapy for pts who can’t tolerate ACE-I or ARBs

Standard therapy in black pts with class III or IV

114
Q

What’s the brand name of Hydralazine/Nitrate (combo) in HF?

A

BiDil

115
Q

What’s the brand name of Isosorbide mononitrate in HF?

A

Monoket

116
Q

CI to using BiDil (Isosorbide dinitrate/hydralazine), Hydralazine, Monoket (Isosorbide mononitrate)?

A

CI with PDE-5 inhibitors

117
Q

SE to using BiDil (Isosorbide dinitrate/hydralazine)?

A

Headache

Dizziness

Hypotension

Rare lupus-like syndrome

118
Q

Monitoring of BiDil (Isosorbide dinitrate/hydralazine), Hydralazine, Monoket (Isosorbide mononitrate)?

A

HR

BP

S/Sx of HF

119
Q

SE unique to Hydralazine? (Gen. SE include headache, rare lupus-like syndrome)

A

RAP

Reflux tachycardia

Anorexia

Palpitations

120
Q

SE of Monoket (Isosorbide mononitrate)?

A

Headache

Dizziness/ Lightheadedness

Flushing

Hypotension

Tachyphylaxis (need 10-12 hr nitrate free interval)

Syncope

121
Q

MOA of Digoxin?

A

Inhibits the Na/K ATPase pump => positive INOTROPIC effect (increased in CO)
+
Exerts a parasympathetic effect which provides a negative CHRONOTROPIC effect (decreased HR)

122
Q

Role of digoxin?

A

Added in pts who remain symptomatic despite receiving standard therapy, including ACE-I and BB.

123
Q

Effects of digoxin in HF?

A

Shown to improve sx, exercise tolerance and QOL

Shown to reduce hospitalizations for HF

But, doesn’t improve survival of HF pts

124
Q

What should be considered b4 dosing digoxin?

A

Pts renal fxn

Body size

Age

Gender

T4, lower dose for renal insufficiency, smaller, older, female

125
Q

What’s the brand name of Digoxin?

A

Lanoxin

126
Q

Usual dose of digoxin in HF?

A

0.125-0.25mg daily

LD not used in HF

127
Q

Therapeutic range for digoxin in HF?

A

0.5-0.9 ng/ml (higher range for A.Fib)

128
Q

What’s the antidote for Digoxin?

A

DigiFab

129
Q

What increases the risk of digoxin toxicity?

A

Hypokalemia (K < 3.5 mEq/L)

Hypomagnesemia

Hypercalcemia

130
Q

Why’s potassium oral supplementation necessary in HF?

A

Bcuz many HF drugs waste K

131
Q

What’s the most commonly used potassium oral supplementation in HF?

A

Potassium chloride (KCl)

132
Q

When should K levels be checked?

A

Baseline

Any change in diuretic, ACE-I, ARBs or ARAs dose

When a pt’s renal fxn changes

133
Q

What deficiency aggravates hypokalemia? What should be done?

A

Mg deficiency aggravates hypokalemia

Check Mg levels and correct prior to correcting K levels

134
Q

What’s the usual range of K? Exception?

A

3.5-5 mEq/L

In pts using Digoxin: 4-5 mEq/L

135
Q

Do all pts require K supplement?

A

No! Some, esp those in class I and II, are able to get their K from food e.g.

Banana, potatoes, orange juice, beans, dark leafy greens, apricots, peaches, avocados, white mushrooms and some varieties of fish

136
Q

What’s the brand name of Potassium chloride?

A

K-Tab, Klor-Com, Klor-Con M10; M15; M20, Micro-K; 10 etc

137
Q

How should Micro-K capsules be used?

A

Capsules may be opened and contents sprinkled on a spoonful of applesauce or pudding and immediately swallowed w/o chewing

138
Q

How should Klor-Con, K-Tab be used?

A

Swallow whole, don’t crush, cut, chew, or suck on tablet

139
Q

How should Kor-Con M be used?

A

Swallow whole, don’t crush, chew or suck on tablet

Tablet may be cut in half and swallowed separately or dissolve the whole tab in 4 oz of water - drink immediately

140
Q

What’s acute decompensated HF?

A

When pts experience episodes of worsening sx such as sudden wt gain, inability to lie flat w/o becoming SOB, decreasing functionality (eg, unable to perform their daily routine), increasing SOB and fatigue.

141
Q

What does most ADHF pts present with?

A

Worsening congestion

142
Q

When should BB be stopped in ADHF?

A

When hypotension or hypoperfusion is present

143
Q

Howz congestion treated in ADHF?

A

Diuretics and possibly IV vasodilators

144
Q

What’s the inotrope of choice in HF pts with SBP < 90 mmHg?

A

Dopamine

145
Q

How long should HF be on dopamine?

A

Inotropes (dopamine) are ass with worse outcomes and should be d/c once pt is stabilized

146
Q

List vasodilators used in ADHF?

A

Nitroglycerin

Nitroprusside

Nesiritide

147
Q

What must be monitored if ADHF pt is on vasodilators (NTG, nitroprusside and nesiritide)?

A

BP must be monitored closely

148
Q

Howz NTG effective in ADHF?

A

It’s more of a venous VD, esp at low doses; it’s effective as an arterial VD at higher doses (doses should be titrated up)

149
Q

In what cases is NTG preferred? Duration of tx?

A

In ADHF + active myocardial ischemia or uncontrolled HTN

Effectiveness may be limited after 2-3 days

150
Q

What’s Nitroprusside?

A

An equal arterial and venous VD at all doses

151
Q

Effect of Nitroprusside metabolism?

A

Results in the formation of Thiocyanate and Cyanide (both of which can cause toxicity)

152
Q

When’s Nitroprusside preferred in ADHF?

A

In pts with uncontrolled HTN, but renal and hepatic fxn must be monitored closely

153
Q

What’s Nesiritide?

A

Recombinant B-type natriuretic peptide

154
Q

Effect of Nesiritide (Natrecor)?

A

Both arterial and venous VD

155
Q

What’s the brand name of Nesiritide (VD used in ADHF)?

A

Natrecor

156
Q

What’s the brand name of Nitroprusside (VD used in ADHF)?

A

Nitropress

157
Q

SE of Nesiritide (Natrecor)?

A

Hypotension

SCr

158
Q

Monitoring of Nesiritide (Natrecor) and NTG?

A

BP

SCr

BUN

Urine output

159
Q

CI to NTG and Nitroprusside (Nitropress) use?

A

SBP < 90mmHg

CI with PDE-5 inh

Increased intracranial pressure

160
Q

Monitoring of Nitroprusside (Nitropress)?

A

BP

HR

BUN

Urine output

Thiocyanate/cyanide toxicity

Acid-base status

161
Q

SEs of Nitroprusside (Nitropress)?

A

Hypotension

Headache

Tachycardia

Thiocyanate/cyanide toxicity (esp, in renal and hepatic impairment)

162
Q

Storage of Nitroprusside (Nitropress)?

A

Need to protect infusion bag from light (cover with opaque material or aluminum foil)

163
Q

What’s indicates degradation of Nitroprusside (Nitropress) to cyanide?

A

A blue color solution

T4 don’t use

164
Q

What’s the target dose of Carvedilol (Coreg) in HF?

A

IR: 25 mg bid
Or
50 mg bid (if pt > 85kg)

CR: 80mg daily.

165
Q

What’s the brand name of Eplerenone?

A

Inspra

NAPLEX (73 decks)

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