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Cardio 1228 > Heart Failure (edited) > Flashcards

Heart Failure (edited) Flashcards

1
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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2
Q

Types of heart failure?

A

HF with Reduced ejection fraction (HFrEF)/Systolic dysfunction - impaired ability to eject blood during systole

HF with preserved ejection fraction (HFpEF)/ Diastolic dysfunction - impaired ventricular relaxation and filling during diastole

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3
Q

What characterizes systolic dysfxn of HF?

A

Left ventricle ejection fraction < 40%

HFrEF

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4
Q

What characterizes mixed dysfxn of HF?

A

mid-range reduction of EF (40-49%)

mixed diastolic and systolic dysfunction

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5
Q

What sometimes xterizes diastolic HF?

A

HF with preserved EF (HFpEF)
EF 50-54%

Normal EF is 55-70%

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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

What does Ischemic cardiomyopathy result from?

A

Ischemic=from decreased blood supply

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

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8
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

long standing HTN
valvular disease
excessive alcohol
illicit drugs
congenital heart defects
viral infections
diabetes
cardiotoxic drugs
chest radiation
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9
Q

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

A

myocardial infarction

And

HTN

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10
Q

List drugs that cause or worsen HF

A

DI NATION

Dipeptidyl peptidase 4 inhibitors (DPP-4 ———-inhibitors)
–alogliptin, sitagliptin
Immunosuppressants (TNF inhibitors)
–etanercept, rituximab and interferons
Nondihydropyridine CCBs
–diltiazem and verapamil (specifically in ————systolic HF)
Antiarrhythmics (avoid class I agents in HF)
–amiodarone and dofetilide have LESS risk of —worsening HF
Thiazolidinediones (increase risk of edema)
Itraconazole
Oncology Agents (anthracyclines-doxorubicin, —daunorubicin)
NSAIDs (all including celecoxib)

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11
Q

What’s cardiac output? (CO)

A

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

It’s a fxn of HR and stroke vol.

CO = HR x SV

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12
Q

What’s stroke vol?

A

Amt of blood ejected from the left ventricle during 1 cardiac cycle (one heartbeat)

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13
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)

So, SV is determine by preload, afterload and contractility

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14
Q

What’s preload?

A

Volume of blood in the ventricle

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15
Q

What’s afterload?

A

Resistance to forward flow in the arterial vessels

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16
Q

What’s contractility?

A

How hard the ventricle squeezes during systole

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17
Q

What’s cardiac index?

A

CO/BSA

It relates the CO to the size of the patient

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18
Q

HF is a progressive syndrome, what does that mean?

A

During low CO state (main problem in HFrEF), neurohormones try to compensate by increasing volume, or increasing force or speed of contractions

may temporarily increase CO

BUT chronic neurohormonal activation causes damage to myocytes and produces changes in size, composition and shape of heart CARDIAC REMODELING

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19
Q

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

A

In response to low CO, neurohormones are released to compensate by increasing volume of blood, or increasing force or speed of heart contraction

RAAS results in Ang II which causes VASOCONSTRICTION as well as Ang II stimulates the adrenal gland to release aldosterone which increases NA and H20 retention, K excretion. Ang II also stimulates adrenal release of vasopressin which cause vasoconstriction and water retention

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20
Q

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

A

Sympathetic (adrenergic) activation

SNS activation results in NE and EPI release which causes increased HR and contractility (+ inotrope) and vasoconstriction

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21
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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22
Q

General HF S/Sx

A

Dyspnea (SOB)
Cough
Fatigue, Weakness
Reduction of exercise capacity

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23
Q

Labs to distinguish between cardiac causes of SOB or other issues

A

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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24
Q

S/sx of left-sided HF?

A

Orthopnea-SOB when laying flat

S3 gallop-abnormal heart sound

hypo perfusion-renal impairment, cool extremities

Bibasilar rales-crackling lung sounds

Paroxysmal nocturnal dyspnea (PND) or nocturnal cough and SOB

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25
Q

S/sx of right-sided HF?

A

Peripheral edema

Ascites

Jugular venous distention (JVD)

Hepatojugular reflux (HJR)-neck vein distends when pressure put on abdomen

Hepatomegaly-enlarged liver due to fluid congestion

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26
Q

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

ACC/AHA

A

Help practitioners optimize mgt of pts in order to slow the development of sx
A-at risk for HF w/o structure disease or symptoms
B-structural disease w/o S/SX
C-structural disease w/ current or prior HF Sx
D-adv structural disease w/ Sx despite rest and maximal Tx

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27
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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28
Q

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

A

No corresponding category

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29
Q

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

A 
NYHA functional class I
(structure disease but no Sx)-no limitation
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30
Q

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

A

NYHA functional class I, II, III
I-no limitation
II-slight limitation
III-marked limitation

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31
Q

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

A 
NYHA functional class IV
IV-can't do physical activity w/o Sx OR Sx at rest
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32
Q

Non-pharmacologic therapy for HF?

A

Monitor and document body weight DAILY

Notify provider of HF sx worsens or when weight increases

  • –2-4 lbs in 1 day or
  • –3-5 lbs in 1week)

Sodium restriction in stage A & B
< 1500 mg/d

Daily MVTE

Fluid restrictions in stage D or hyponatremia
—1.5-2L/d

BMI < 30 preferred

Exercise recommended for pts who can

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33
Q

What’s the appropriate sodium restriction for HF pts?

A

< 1500 mg/d

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34
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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35
Q

What meds should be avoided in HF?

A

Products contains ephedra (ma huang) or ephedrine and stimulants such as decongests

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

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36
Q

What alt med has may improve HF symptoms

A

Hawthorn and coenzyme Q10

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37
Q

What meds are the cornerstones of HF therapy?

A

Diuretics to control fluid volume
+
Angiotensin antagonist (ACE-I or ARBs or ARNI)
+
Beta blockers (to delay the progression of cardiac dysfunction and improve survival)
+
Aldosterone Receptor Antagonists (ARA)

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

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38
Q

Which of the cornerstones of HF therapy improves survival rate?

A

Beta blockers, ACEi or ARB or ARA or ARNI

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39
Q

What type of diuretic is more commonly used in HF?

A

Loop diuretics

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40
Q

MOA of loop diuretics?

A

They increase excretion of NA, K, Cl, Mg, Ca, and H20
=Block NA and Cl reabsorption in THICK ASCENDING LIMB OF LOOP OF HENLE =>

Do not alter survival, but decrease fluid volume making it easier for heart to pump AND help control symptoms

lowest dose effective should be used w/ care not to over-diurese (=hypoTN or renal impair)

Can use in combo w/thiazide (metolazone, etc) if loop response is poor

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41
Q

What’s excreted by loop diuretics in HF?

A

Water

Sodium

Potassium

Chloride

Magnesium

Calcium

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42
Q

Whys the lowest effective dose of loop used in HF?

A

They haven’t been shown to alter the survival of HF pts, don’t want to over diurese and cause hypotension or renal failure

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43
Q

List loop diuretics used in HF?

A

Furosemide (Lasix)

Bumetanide (Bumex)

Torsemide (Demadex)

Ethacrynic Acid (Edecrin)

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44
Q

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

A

Lasix

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45
Q

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

A

40mg

Bum 1 torse 20 furo 40 etha 50

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46
Q

Whats the oral loop dose equivalency of Bumetanide?

A

1mg

Bum 1 torse 20 furo 40 etha 50

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47
Q

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

A

20mg

Bum 1 torse 20 furo 40 etha 50

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48
Q

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

A

50mg

Bum 1 torse 20 furo 40 etha 50

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49
Q

What’s warning associated with loops use?

A

Sulfa allergy

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50
Q

Which loop is the sulfa allergy warning not applicable to?

A

Ethacrynic acid (Edecrin)

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51
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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52
Q

Monitoring for loops?

A

BP

Hearing with high doses of rapid IV admin

Renal fxn (SCr, BUN)

Electrolytes

Fluid status (in’s and out’s, weight)

hearing w/ high doses or rapid IV admin

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53
Q

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

A

furosemide and Bumetanide

IV admixtures do not require light protection

STORE furosemide inj. at ROOM temp-crystallizes

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54
Q

What’s the furosemide IV to PO ratio?

A

1:2

Furosemide 20mg IV = Furosemide 40mg PO

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55
Q

Diuretics such as loops and lithium?

A

May decrease lithium renal clearance and increase risk of lithium toxicity

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56
Q

MOA of ACE-I?

A

Block conversion of angiotensin I to angiotensin II by inhibiting the ACE
=decrease vasoconstriction and decrease aldosterone secretion

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57
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

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58
Q

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

A

ACEi + ARB has been shown to decrease HF hospitalizations

BUT it is more common to combine ACEi+ARA OR ARB+ARA

ACEi+ARB+ARA is NOT recommended due to higher hyperkalemia or renal risks

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59
Q

List ACE-I agents in HF guidelines

A

Captopril (Capoten)

Enalapril (Vasotec)

Enalaprilat (vasotec IV)

Fosinopril

Lisinopril (Prinivil, Zestril)

Perindopril (Aceon)

Quinapril (Accupril)

Ramipril (Altace)

Trandolapril (Mavik)

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60
Q

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

A

Vasotec

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61
Q

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

A

Prinivil

Zestril

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62
Q

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

A

Accupril

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63
Q

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

A

Altace

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64
Q

Howz Captopril (Capoten) taken?

A

1 hr B4 meals

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65
Q

Black box warning of ACE-I?

A

D/c as soon as pregnancy is detected

66
Q

CI to ACE-I use?

A

Angioedema Hx

Bilateral renal artery stenosis

Use within 36 hr of neprilysin inhibitor (Entresto)

NOTE: ARBs do NOT have wash out warning for ENTRESTO

67
Q

SEs to ACE-I and ARBs use?

A

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

Hyperkalemia

Angioedema (less with ARB than ACEi)
–d/c drug immediately and drug is then CI

Hypotension

68
Q

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

A

Captopril (Capoten)

Taste perversion
Rash

69
Q

Monitoring parameters of ACE-I and ARBs?

A

BP

Potassium

Renal fxn

S/sx of HF

70
Q

List ARBs agents in HF guidelines

A

Candesartan (Atacand)

Losartan (Cozaar)

Valsartan (Diovan)

71
Q

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

A

Losartan (Cozaar)

72
Q

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

A

Cozaar

73
Q

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

A

Diovan

74
Q

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

A

Same as ACE-I

75
Q

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

A

Potassium (Hyperkalemia)

76
Q

MOA of bb in HF?

A

Bb antagonize the effects of catecholamines, esp norepinephrine

77
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

78
Q

List BB used in HF?

A

Carvedilol

Metoprolol Succinate extended-release

Bisoprolol

79
Q

Which BB should be absolutely avoided?

A

BB with intrinsic sympathomimetic activity (ISA)

80
Q

List the selective BB used in HF

A

Bisoprolol (Zebeta)

Metoprolol Succinate ext-release (Toprol XL)

81
Q

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

A

Toprol XL

82
Q

List non-selective BB used in HF

A

Carvedilol (Coreg, Coreg CR)

83
Q

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

A

Coreg

84
Q

SE of selective BB (Bisoprolol and Toprol XL)?

A

Reduced HR

Hypotension

Fatigue

Dizziness

Depression

increase TG

85
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

weight gain & edema (esp Carvedilol)

86
Q

How do u d/c BB?

A

Must taper

87
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)

88
Q

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

A

Take Carvedilol - all forms -‘with food

89
Q

Which DM sx are NOT masked by BB?

A

Sweating (Diaphoresis)

And

Hunger

90
Q

Which ARAs is non-selective?

A

Spironolactone-also blocks androgen (endocrine SE)

91
Q

Which ARAs is selective? Benefits?

A

Eplerenone (Inspra)

Doesn’t exhibit endocrine SE

92
Q

MOA of ARAs?

A

They compete with aldosterone (a mineralocorticoid) at receptor sites in DISTAL CONVOLUTED TUBULE and COLLECTING DUCTS

93
Q

When ARAs used in pts with HF?

A 
Decreases morbidity and mortality
should be added to Standard therapy NYHA class II-IV pts
94
Q

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

A

Aldactone

95
Q

CI of Aldosterone Receptor Antagonists (ARAs)?

A

Renal impairment (CrCl < 30mL/min)
Anuria
Hyperkalemia
Addison’s disease or other diseases that ———increase K

96
Q

SEs of ARAs?

A

Hyperkalemia

Increased SCr

Dizziness

Spironolactone: Gynecomastia and breast tenderness impotence, irregular menses, amenorrhea

Eplerenone: Increase TG

97
Q

Which SE is unique to Spironolactone?

A

Gynecomastia and breast tenderness impotence and menses irregularities

98
Q

Monitoring of ARAs?

A

Check K B4 starting and freq thereafter
—Do not start in HF if K>5 or eGFR<30

BP

SCr/BUN

S/Sx of HF

99
Q

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

A

Don’t start if K > 5 mEq/L
CrCl<30 or SCr >2 in women or >2.5 in men

Use low doses, start low

Don’t use w/NSAIDs-can cause increase K as well as decrease antihypertensive effect

Monitor freq

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

100
Q

What’s Hydralazine?

A

A direct arterial vasodilator which reduces afterload

101
Q

What’s Nitrates?

A

Nitrates are venous vasodilators and reduce preload by increasing nitric oxide availability

102
Q

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

A

Alternative therapy for pts who can’t tolerate ACE-I or ARBs due to poor renal function, angioedema, or hyperkalemia

Standard therapy in black pts with class III or IV who are symptomatic despite optimal treatment with ACEi and BB

Though individually beneficial for other indication alone, they do not affect HF outcomes if not both used

103
Q

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

A

BiDil

104
Q

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

A

Monoket- denitrate used in trial but mononitrate is used in practice

105
Q

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

A

mitral valve rheumatic heart disease, CAD

106
Q

SE to using BiDil (Isosorbide dinitrate/hydralazine)?

A

Headache

Hypotension

dizzy/lightheaed

flushing

DILE

107
Q

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

A

HR

BP

S/Sx of HF

ANA

108
Q

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

A

Headache

Hypotension

Reflux tachycardia

Palpitations

Fluid Retention

Peripheral Neuritis

DILE

109
Q

SE of Monoket (Isosorbide mononitrate)?

A

Headache

Dizziness/ Lightheadedness

Flushing

Hypotension

Tachyphylaxis (need 10-12 hr nitrate free interval)

Syncope

110
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)

111
Q

Role of digoxin?

A

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

112
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

113
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

114
Q

What’s the brand name of Digoxin?

A

Lanoxin DigiTek Digox

115
Q

Usual dose of digoxin in HF?

A

0.125-0.25mg daily

LD not used in HF

116
Q

Therapeutic range for digoxin in HF?

A

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

117
Q

What’s the antidote for Digoxin?

A

DigiFab

118
Q

What increases the risk of digoxin toxicity?

A

Hypokalemia (K < 3.5 mEq/L)

Hypomagnesemia

Hypercalcemia

119
Q

Why’s potassium oral supplementation necessary in HF?

A

Bcuz many HF drugs waste K

120
Q

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

A

Potassium chloride (KCl)

121
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

122
Q

What deficiency aggravates hypokalemia? What should be done?

A

Mg deficiency aggravates hypokalemia

Check Mg levels and correct prior to correcting K levels

123
Q

What’s the usual range of K? Exception?

A

3.5-5 mEq/L

In pts using Digoxin: 4-5 mEq/L

124
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

125
Q

What’s the brand name of Potassium chloride?

A

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

126
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

127
Q

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

A

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

128
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 -stir for 2 minutes- drink immediately

129
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.

130
Q

What does most ADHF pts present with?

A

Worsening congestion

131
Q

When should BB be stopped in ADHF?

A

When hypotension or hypoperfusion is present

132
Q

Howz congestion treated in ADHF?

A

Diuretics and possibly IV vasodilators

133
Q

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

A

Dopamine

134
Q

How long should HF be on dopamine?

A

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

135
Q

List vasodilators used in ADHF?

A

Nitroglycerin

Nitroprusside

Nesiritide

136
Q

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

A

BP must be monitored closely

137
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)

138
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

139
Q

What’s Nitroprusside?

A

An equal arterial and venous VD at all doses

140
Q

Effect of Nitroprusside metabolism?

A

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

141
Q

When’s Nitroprusside preferred in ADHF?

A

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

142
Q

What’s Nesiritide?

A

Recombinant B-type natriuretic peptide

143
Q

Effect of Nesiritide (Natrecor)?

A

Both arterial and venous VD

144
Q

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

A

Natrecor

145
Q

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

A

Nitropress

146
Q

SE of Nesiritide (Natrecor)?

A

Hypotension

SCr

147
Q

Monitoring of Nesiritide (Natrecor) and NTG?

A

BP

SCr

BUN

Urine output

148
Q

CI to NTG and Nitroprusside (Nitropress) use?

A

SBP < 90mmHg

CI with PDE-5 inh

Increased intracranial pressure

149
Q

Monitoring of Nitroprusside (Nitropress)?

A

BP

HR

BUN

Urine output

Thiocyanate/cyanide toxicity

Acid-base status

150
Q

SEs of Nitroprusside (Nitropress)?

A

Hypotension

Headache

Tachycardia

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

151
Q

Storage of Nitroprusside (Nitropress)?

A

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

152
Q

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

A

A blue color solution

T4 don’t use

153
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.

154
Q

What’s the brand name of Eplerenone?

A

Inspra

155
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

156
Q

Ivabradine

A

Corlander
Inhibits funny current (I f) in sinus node which reduces sinus rate and therefore HR reduction.

Reduces hospitalizations for HF but doesn’t affect mortality

For class II-III w EF=<35% on all appropriate 1st line meds and still have resting HR>= 70 BPM

Warning: decrease Hr, brady, increase QT

157
Q

ARNI

A

sacubitril/valsartan (Entresto

Box: Has ARB-D/C as soon as pregnancy detected
CI: Use w/ ACEi or ARB, angioedema hx
WARN: Angioedema, renal impair, hyperkalemia, hypotension
SE: Cough

MUST HAVE 36 HOUR WASHOUT of ACEi before starting ENTRESTO or WASHOUT entrust 36 HR before starting ACEi

158
Q

HF meds that decrease lithium clearance

A

ACEi, ARB, ARNI, Diuretics

159
Q

Cutting Toprol XL

A

Must use pill cutter and cut ONLY at score line
Swallow 1/2 tablet whole
Do NOT crush or chew

160
Q

Avoid with Ivrabradine

A

Grapefruit Juice, St Johns Wort

161
Q

Avoid with Bidil

A

PDE5 inhibitors DO NOT USE in these pts
as well as Riociguat

The combo can cause severe hypotension

Cardio 1228 (17 decks)

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