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PBL PY2 Fall > Heart Failure > Flashcards

Heart Failure Flashcards

1
Q

what is heart failure?

A

a complex clinical syndrome that results from any structural or functional cardiac impairment of ventricle filling or ejecting blood. The heart is unable to pump sufficiently to maintain the blood flow to meet the body’s needs

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2
Q

heart failure is most common in what patient populations?

A

males and the elderly

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3
Q

HF is responsible for more hospitalizations than all ____ combined

A

cancers

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4
Q

HF is the leading cause of hospitalization in patients older than _____

A

65

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5
Q

50% of patients diagnosed with HF will die within __ years

A

5

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6
Q

what are some conditions that increase risk for heart failure?

A

MI, HTN, myocarditis, anemia, COPD etc.

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7
Q

what are some drugs that increase risk for heart failure?

A

NSAIDs, corticosteroids, chemotherapies, biologic DMARDs

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8
Q

what are some social hx/diet factors that increase risk for HF?

A

excessive fluids, salt, alcohol intake, use of illicit drugs like cocaine, emthamphetamine, and ecstast (MDMA)

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9
Q

decreased CO caused by HF results in activation of which nervous system? what is the consequence of activating this nervous system?

A

sympathetic; causes the release of cathecholamines to increase HR, contractility and vasoconstriction

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10
Q

activation of the SNS by decreased CO causes what changes in pre-load and after load?

A

increases both (increasing preload is good, increasing after load is bad)

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11
Q

what is the eventual effect of SNS activation on CO?

A

will initially increase, but the cardiac O2 demand and work will also increase and eventually lead to decreased CO

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12
Q

what is teh effect of SNS activation on cell death?

A

increases

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13
Q

decreased cardiac output causes ____(activation or deactivation) of the RAAS system. What is the effect of this?

A

activation: decreased renal perfusion, renin release, increased angiotensin 2, increased aldosterone levels

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14
Q

how is activating the RAAS system crucial to CO?

A

maintains effective circulating volume (preload) mediated by aldosterone secretion and Na and water retention to increase CO

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15
Q

what is the “negative” of decreased CO causing activation of the RAAS system?

A

increased vasoconstriction leads to increased afterload, increased myocardial energy use, cell hypertrophy, fluid retention and edema

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16
Q

decreased CO causes a ______(increase or decrease) in ADH, what is the effect of this?

A

increase: increases the circulating volume which increases the preload but also may cause pulmonary edema

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17
Q

what 3 things affect stroke volume?

A

preload, afterload and contractility

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18
Q

what 2 things affect CO?

A

stroke volume and heart rate

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19
Q

what 2 (physiological) things affect BP?

A

cardiac output and systemic vascular output

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20
Q

describe NYHA class 1

A

physical activity not limited. Ordinary physical activity does not cause undue fatigue, heart palpatation, SOB or chest pain

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21
Q

describe NYHA class 2

A

some limitation on physical activity. comforatble at rest, but ordinary physical activity causes fatigue, heart palpatations, SOB, or chest pain

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22
Q

describe NYHA class 3

A

marked limitation on physical activity. Comfortable at rest, but less-than ordinary physical activity causes fatigue, heart palpitations, SOB or chest pain

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23
Q

describe NYHA class IV

A

Unable to carry on any physical activity w/o discomfort, may even have sx at rest and if any physcial activity is done, discomfort increses

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24
Q

what are the A-D classification of HF?

A

A: high risk (has HTN, CAD, diabtes, family hx etc.)
B: has asymptomatic LVD (past MI, systolic dx etc.)
C: symptomatic HF: known structural heart dx, has sx
D: refractory end-stage HF (marked sx at rest)

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25
Q

what is systolic dysfunction?

A

hypofunctioning ventricle (decreased contractility)

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26
Q

what is diastolic dysfunction?

A

stiff ventricle, imparied ventricle relaxation

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27
Q

what is the most common type of ventricular dysfunction?

A

left ventricular

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28
Q

when is right ventricular dysfunction typically seen?

A

in combo with LVD and can occur alone in pulmonary HTN

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29
Q

what is biventricular dysfunction?

A

combo of RV and LV dysfunction

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30
Q

what is ejection fraction?

A

amount of blood pumped out of the ventricle per heart beat

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31
Q

ejection fraction is typically referring to which ventricle?

A

left, as it is teh main pumping ventricle of teh heart

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32
Q

what is the normal EF%?

A

55-70%

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33
Q

explain in words what an EF% means

A

means that % of the total blood in the left ventricle is pumped out with each heart beat

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34
Q

in HFpEF, what is the LVEF?

A

50 or greater

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35
Q

in mid-range HF, what is the LVEF?

A

41-49%

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36
Q

in HFrEF, what is the LVEF?

A

40% or less

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37
Q

t/f patients can move back and forth between HFrEF and HFpEF depending on if they improve or worsen

A

true (if they improve goes to HFpEF and worsen goes to HFrEF)

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38
Q

what are the main sx of HF? what are the secondary sx?

A

Main: fatigue, SOB, peripheral edema
secondary: weakness, exercise intolerance, weight gain, paroxysmal nocturnal SOB, orthopnea, nocturia

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39
Q

what changes in vital signs would you expect in a HF patient?

A

BP may be up or down, increased HR and RR, decreased O2 sat

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40
Q

what respiratory findings would you expect in a HF patient?

A

normal or decreased air bilaterally, crackles (rales) at the base

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41
Q

what CV findings would you expect in a HF patient?

A

increased JVP, S3 sounds, hepatojugular reflux

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42
Q

what GI findigs might you see in HF?

A

abdominal distention, anorexia

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43
Q

what genito/urinary findings might you expect in a HF patient?

A

scrotal edema, may have decreased urine output

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44
Q

what MSK findings might you expect in a HF patient?

A

cool extremities, sacral edema, peripheral edema

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45
Q

what would expect the Na to be in a HF patient?

A

can be normal or low (due to high volume of fluid –> hypervolumic hyponaturemia)

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46
Q

what would expect of Scr and urea in a HF patient?

A

can be increased due to decreased renal perfusion

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47
Q

what would you expect of troponin in a HF patient?

A

can be slightly elevated from cardiac strian

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48
Q

what would you expect of BNP or NT-proBNP in HF patient?

A

often increased, there are cutoffs depending on age and clinical setting

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49
Q

what would you expect of chest XR in HF patient?

A

cardiomegaly, pulmonary edema, pleural effusions

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50
Q

what physical findings would you expect to find on ECG of HF patient?

A

LV hypertrophy

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51
Q

what is the gold standard for assessing teh function of teh heart in HF?

A

echo (gives us the most information about heart function)

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52
Q

volume or pressure overload causes the release of _____(natriuretic peptide) mainly from the ventricular myocardium

A

proBNP

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53
Q

proBNP is cleaved into ___ and ____

A

active BNP and inactive NT-proBNP

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54
Q

the action of BNP causes what effects?

A

natriuresis, vasodilation, decreased afterload, inhibits RAAS, reduces fibrosis

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55
Q

natriuretic peptides are used as diagnostic and prognostic tools (T/f)

A

true

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56
Q

HF is very likely of BNP is >___ and it is unlikely of BNP in

A

400pg/mL; 100pg/mL

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57
Q

for people aged less than 50, what NT-proBNP shows unlikely and very likely HF?

A

unlikely <300pg/mL, very likely>450pg/ML

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58
Q

for someone aged 50-75, what NTpronBNP is unlikley for HF and very likely for HF?

A

unlikely: <300pg/ml, very likely: >900pg/mL

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59
Q

for patients aged >75, what NT-proBNP is unlikely for HF and very likely for HF?

A

unlikely: <300pg/mL, very likely: >1800pg/mL

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60
Q

what are lifestyle modifications that can decrease risk and progression of HF?

A
  1. improving CV risk (managing lipids, BP, diabetes, alcohol and tobacco use)
  2. diet (lowering fluid and salt intake)
  3. moderate exercise
  4. keeping up to date on immuniazations (flu and pneumona0
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61
Q

what are the CCS recommendations around exercise in HF?

A

regular exercise to improve exercise capacity, sx, QOL and decrease hospital admissions in all HF patients

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62
Q

what should sodium be restricted to in HF patients?

A

2-3g/day

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63
Q

how should body fluid be managed?

A

diuretics, daily weights, limiting intake of liquid to 2L/day

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64
Q

what are the 4 classes of drugs in goal directed medical therapy (GDMT)?

A
  1. ACE/ARB/ARNI
  2. BB
  3. MRA
  4. SGLT2-i
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65
Q

GDMT is recommended in what HF population?

A

HfrEF (40% or less) and have symptoms

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66
Q

if a patient has been optimized on GDMT, and has HR >70bpm and sinus rhythm, what is an additional drug option?

A

ivabradine

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67
Q

if a patient has been optimized on GDMT, and has been hospitalized in the past 12 months, what is an additional drug option?

A

vericigaut

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68
Q

if a black patient has been optimized on GDMT or is unable to tolerate ACE/ARB/ARNI and requires additional therapy, what is an option?

A

combo hydralazine-nitrates

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69
Q

if a patient has AF and if having inadequate rate control or persistent symptoms despite optimized GDMT, what is a drug option?

A

digoxin

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70
Q

when starting new therapies, they should typically be titrated every ____weeks, and want to reach target doses by ___months

A

2-4 weeks; 3-6 months

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71
Q

what drugs are recommended in HFrEF patients who are asymptomatic?

A

beta blockers for all LVEF <40% and ACE for all with EF<35% (both)

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72
Q

what are the 2 ways to titrate medications? Is one way better than another?

A
  1. in-parallel: do all of them at once
  2. strict sequential: fully titrate 1, then start the next
    Neither has been proved to be better, but should consider pt factors like hemodynamics, renal fx, medication access, adherance, tolerability and preferences
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73
Q

what was found by the HOPE trial?

A

ramipril more effective than placebo in HF

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74
Q

what was found in the SOLVD trial?

A

enalapril decreased HF death compared to placebo

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75
Q

in the CONSENSUS and SOLVD trials, what other drugs were patients takign other than the ACE?

A

most were on diuretic and digoxin, <10% were on a BB

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76
Q

the SAVE, AIRE, and TRACE trials enrolled patients within a week of ___

A

acute MI

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77
Q

what was found by the SAVE, AIRE and TRACE trials?

A

ACE decreased mortalilty and readmission comaped to palcebo

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78
Q

what should be monitired in ACE use for HF?

A
  1. lying and standing BP

2. SCr and K at baseline, 3-7 days later, then 1 month, then q 3months

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79
Q

in ACE/ARB/ARNI use, it is not uncommon for the SCr to up by __%

A

30

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80
Q

all RAAS inhibitin agents should be held if serum K is above ___mmol/L

A

5.9

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81
Q

what can be done to manage sympotomatic hypotension while on ACE/ARB/ARNI?

A

seperate dose timings, lower the dose of diuretic if patient is stable, reassess their need for other vasodilators like nitrates and CCB for HTN

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82
Q

what was found by the CHARM study?

A

looked at pts who were taking candesartan bc they were intolerant to ACE and found that it decreased CV death and hospital admission for HF

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83
Q

what was found by the Val-HeFT trial?

A

increased survival with valsartan compared to placebo, also found that patients previously taking both ACE and BB had increased mortality

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84
Q

what was found in the CHARM-Added trial?

A

looked at combo candesartan with ptaients already on ACE and found that there was increased hypotension, hyperkalemia, and increased SCr

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85
Q

what does ARNI stand for?

A

angiotensin receptor neprilysisn inhibitor

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86
Q

what is the MOA of ARNI?

A

inhibit neprilysin which breaks down natriuretic peptides and other vasoactive peptides. By inhibiting this, those peptides like bradykinin and BNP can lower BP and promote Na excretion

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87
Q

inhibiting neprilysin causes an increase in ____, so a neprilysin inhibitor must be combined with a ___ drug

A

angiotensin 2; RAAS blocking

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88
Q

give an example of ARNI

A

entresto (sacubitril and valsartan)

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89
Q

what was found in the PARADIGM-HF trial?

A

sucubitril/valsartan had less cough, less increased Scr, less hyperkalemia and more symptomatic hypotension than enalapril 10mg BID and entresto showed lower death and hospitalization

90
Q

when does the CCS recommend ARNI?

A
  1. in place of ACE/ARB in HFrEF patients who remain symptomatic despite optimal GDMT to decrease hosptialization, death and symptoms
  2. for patients admitted for acute decompensated HFrEF switch to ARNI from ACE or ARB when stabilized and before discharge
91
Q

what is an ARNI suggestion from CCS?

A

suggest giving ARNI as first line as an alternative to ACE/ARB with new diagnosis for HFrEf and admitted to hospital

92
Q

when should ARNI use be avoided?

A

eGFR <30mL/min, K>5.2, symptomatic hypotension + SBP <100, hx of angioedema

93
Q

when switching from ACE to ARNI, you need a __hr washout period

A

36

94
Q

what should be monitored with ARNI?

A
  1. SCr and K at baseline, w/i 1 week, 1 month, q3 months (more frequent if dehydrating illness)
  2. lying and standing BP (llok out for orthostatic hypotension)
  3. can monitor NT-proBNP, but BNP will be elevated due to the MOA
95
Q

if the patient was on a low dose of ACE (<50% of target dose), what starting dose of entresto do you give?

A

50mg BID

96
Q

if patient had been on a high dose ACE/ARB (>50% of target), what starting dose of entresto should you give?

A

100mg BID

97
Q

entresto should be titrated every __weeks to a target dose of ___

A

3-6; 200mg BID

98
Q

50mg entresto contains __mg sacubitril and __mg valsartan

A

24.3, 25.7

99
Q

100mg entresto contains __mg sacubitril and __mg valsartan

A

48.6, 51.4

100
Q

200mg entresto contains __mg sacubitril and __mg valsartan

A

97.2, 102.8

101
Q

103 mg of valsartan in Entresto is equal to ___mg of valsartan in Diovan

A

160

102
Q

what are the exception status qualifications for entresto?

A

LVEF <40%, NYHA 2-3 despite 4 weeks of stable doses of: ACE/ARB, BB,and other recommended therapies like MRA

103
Q

patients should be ___ before starting BB if they are NYHA class IV

A

stable

104
Q

BB are clinically proven in patients with LVEF ___% or less

A

40

105
Q

which BB trials showed decreased HF hosptalizations?

A

CIBIS 2 (bisoprolol) and COPERNICUS (carvedilol)

106
Q

what was found in the COMET trial? why is it controversial?

A
  1. compared carvedilol and metoprolol tartrate and found carvedilol had lower deaths.
  2. controversial over whether tartrate was the best formulation compared to succinate
107
Q

significant improvement in LV function from BB may take ___months

A

6-12

108
Q

patients may notice that their HF symptoms may get worse for ___(length of time)while on BB before it gets better

A

days to weeks

109
Q

if reactive airways are present, what BB should be used?

A

bisoprolol

110
Q

if a patient is hypotensive while in a BB, what should be done?

A

consider decreasing the dose of other medications or change the timing and spacing of doses

111
Q

if a patients has bradycardia while on BB or AV block is present, decrease or stop what other medications?

A

digoxin or amiodarone if appropriate

112
Q

BB should not be abruptly stopped unless patient is experiencing ___

A

cardiogenic shock

113
Q

when a patient presents with new HF, should we start a BB or ACE first?

A

CIBIS 3 found that there is no significant difference in what one you start

114
Q

MRAs are recommended for HFrEF when symptoms are of what level?

A

moderate to severe

115
Q

what was found by the RALES trial?

A

spironolactone 25mg daily vs placebo (both also taking ACE and LVEF <35%) found increased survival and decreased HF hospitalization in spironolactone group

116
Q

a trend was seen where spironolactone Rx increased after the rales trials, but what also increased?

A

death from hyperkalemia

117
Q

what was found in the EMPHASIS-HF trial?

A

patients on ACE/ARB randomized to eplenerone 50mg vs placebo and found that drug decreased death and HF hospitalization, did find more K abnormalities

118
Q

when should MRA be avoided?

A

CrCl<30ml?min, K>5, on other K sparing diuretics

119
Q

what drugs should be avoided in MRA to avoid hyperkalemia?

A

NSAIDs and sulfamethoxazole/trimethoprim

120
Q

start spironolactone at ___ and titrate to ___

A

12.5mg, 25-50mg daily

121
Q

start eplenerone at ___mg and titrate to ___

A

25mg, 50mg daily

122
Q

what should be monitored on MRA?

A

K at baseline, 1 week, 1 month, every 3 months and increase frequency when acute dehydrating illness

123
Q

supplemental K is not recommended unless K is < ____

A

4 mmol/L

124
Q

why is eplenerone associated with less gynecomastia than spironolactone?

A

it has better affinity for teh mineralocorticoid receptors and less affinity for hormone receptors

125
Q

what were the findings of the DAPA-HF trial?

A

dapagliflozins 10mg UID vs palcebo (patients already on standard GDMT), found decreased hospitalizations and death and it did not matter if they had DM or not

126
Q

what was found in the EMPEROR-reduced trial?

A

emapgliflozin 10mg UID (basically the same as dapagliflozin)

127
Q

which NYHA classes were found to be most likely to benefit form SGLT2?

A

2 more than 3-4

128
Q

what is the CCS recommendation for SGLT2?

A

for those with mild to moderate HfrEF to improve symptoms, QOL, and reduce risk of HF hospitalizations and or CV death

129
Q

what is the coverage issue with SGLT2?

A

only covered if they have T2DM

130
Q

what is the most common ADR of SGLT2-i?

A

genital mycotic infections

131
Q

SGLT2-i may temporarily decrease eGFR by ___% and this typically takes how long to resolve?

A

15-20%, 1-3 months

132
Q

should SGLT2 be held on sick days

A

yes

133
Q

there is a rare risk of DKA with normal glucose levels in SGLT2, what can be monitored if it is suspected?

A

serum ketones

134
Q

SGLT2-i can contribute to diuresis, so you should keep an eye on volume status and possibly decrease loop diuretic dose by ___%

A

30-50

135
Q

what are the ionotropic effects of digoxin?

A

increased ventricular force of contraction, increased contractility

136
Q

what are the chronotropic effects of digoxin?

A

increased parasympathetic tone, lowered HR

137
Q

how does digoxin increase ionotropy?

A

inhibit Na/K exchange, which causes more Ca to be released, which increases contractility

138
Q

how does digoxin decrease chronotropy?

A

increase parasympathetic activity of AV node, slowing AV conduction to decrease HR

139
Q

of ionotropic and chronotropic activity, which does digoxin increase and which does it decrease?

A

increase ionotropic and decrease chronotropic

140
Q

what was found by the DIG trial?

A

digoxin reduced HF hospitalization compared to placebo

141
Q

what is the main goal with digoxin therapy?

A

improving symptoms, QOL and exercise tolerance

142
Q

what is the typical dose of digoxin? wha does it depend on?

A

0.0625mg - 0.25mg; depends on age and renal fx

143
Q

there is no reason to monitor digoxin levels unless toxicity is suspected, but if you are going to take it, you should draw when its at ___level or at least __hrs post dose. Why?

A

trough level or 6-8 hrs after dosing to allow for distribution

144
Q

what is teh target concentration for digoxin in HF?

A

<1.3nmol/L

145
Q

tell me everything you know about the Vd of digoxin

A

4-7L/kg due to extensive tissue binding and is not affected by obesity bc it is not very lipophillic and dosing should be based on ideal body weight

146
Q

tell me everything you know about the elimination of digoxin?

A

renal 60-80%, excreted unchanged in teh urine, teh otehr 1/3 is excreted by teh hepatobiliary route

147
Q

what is the T1/2 of digoxin?

A

30-40 hours

148
Q

how long does it take digoxin to reach steady state?

A

6-8 days

149
Q

digoxin is a substrate and inhibitor of ___ and this causes many drug interactions

A

PgP

150
Q

how should the interaction between digoxin nad amiodarone or verapamil be managed?

A

reduce digoxin by 50%

151
Q

aside from amiodarone and verapamil, what otehr drugs interact with digoxin? How should these interactions be managed?

A

clarithromycin, cyclosporine, diltiazem, erythromycin, itraconazole, ketoconazole, propafenone: adjust, monitor serum digoxin levels and adjust accordingly, consider empiric dose reduction

152
Q

drugs and diseases that alter electrolytes affect digoxin levels. What is the effect of hypokalemia on digoxin?

A

increased digoxin toxicity

153
Q

what is the effect of hypothyroidism, old age and renal dysfunction on digoxin levels?

A

increased digoxin levels and decreased Vd

154
Q

other than toxicity, when might you get a digoxin level?

A

when starting or stopping interacting drugs

155
Q

t/f the ADRs and toxicity of digoxin are dose-related

A

t

156
Q

what are the CNS ADRs / signs of toxicity of digoxin?

A

disorientation, confusion, depression

157
Q

what are the visual disturbances / signs of toxicity in digoxin?

A

blurriness, yellow/green vision, dark or movinf spots, photophobia, halos

158
Q

t/f digoxin can cause arrhythmias

A

t

159
Q

what are some of the GI ADRs / signs of toxicity of digoxin?

A

anorexia, nausea, vomiting, diarrhea

160
Q

what is the antidote for digoxin?

A

DigiFAB, an antibody fragment that binds to digoxin

161
Q

when is digiFAB indicated?

A

life-threatening toxicity

162
Q

According to teh IWK, when is digiFAB indicted?

A

when digoxin toxicity causes: tachy or brady-arrhythmias, hypotension, hyperkalemia (greater than 5 mEq/L) and/or a digoxin serum level of greater than 12.8 nmol/L (greater than 10 ng/mL).

163
Q

what are suggestions for digoxin use from teh CCS?

A
  1. if patients with HFrEF in sinus rhythm who continue to have moderate to severe symptoms despite optimal GDMT
  2. in patients with HFrEF and AF with poor rate control or persistent symptoms despite optimal BB or if BB not tolerated
164
Q

what is the MOA of nitrates in HF?

A

venous dilation, reduces preload

165
Q

what is the MOA of hydralazine in HF?

A

aterial dilation and reduces after load

166
Q

what is the combined role of nitrates/hydralazine for HF?

A

relive Sx of HF and increase exercise tolerance

167
Q

what are the ADR of nitrates/hydralazine?

A

hypotension, headache, dizziness

168
Q

what should be monitored when on nitrates/hydralazine?

A

BP and HR

169
Q

what were the findings of the V-HeFT trial?

A

looked at hydralazine/ISDN in patients already taking digoxin and loop diuretic and found that this combo had lower mortality and prazosin had no benefit

170
Q

what were the findings of the V-HeFT trial?

A

looked at hydralazine + ISDN vs enalapril and found that enalapril was superior

171
Q

what are the CCS recommendations for nitrate+hydralazine use?

A
  1. patients with HFrEF unable to tolerate ACE, ARB, or ARNI due to hyperkalemia or renal dysfunction
  2. in black patients in addition to regular GDMT with advanced sx
172
Q

what is the MOA of Ivabradine?

A

selectively inhibits the depolarizing If current in the SA node

173
Q

what were the findings of the SHIFT trial?

A

looked at NYHA 2-4 with normal sinus rhythm, resting HR >70, LVEF 35% and HF admission in past 12 months and found that ivabradine in addition to GDMT decreases CV death and HF admission

174
Q

Ivabradine can be considered for what patients?

A

symptomatic depsite adequeate GDMT, resting HR >70, sinus rhythm, hospitalization in past 12 months

175
Q

what is the dose and titration for ivabradine?

A

2.5-5mg PO BID with food; titrate q2-4 weeks to max of 7.5mg PO BID with food

176
Q

dose ivabradine to target a HR of ___

A

50-60 BPM

177
Q

t/f ivabradine is typically initiated by a specialist

A

t

178
Q

what are the drug interactions with ivabradine?

A

CYP3A4 inhibitors

179
Q

ivabradine is C/i when taking what other medications?

A

amiodarone, digoxin, simvastatin

180
Q

what are the ADRs of ivabradine?

A

bradycardia, AF, flashes of light

181
Q

will ivabradine lower BP?

A

it should not, as it is meant to be specific to the SA node

182
Q

drug coverage for ivabradine

A

exception status

183
Q

what is the role for diuretics in HF?

A

relieve signs/sx of Hf such as edema, congestion, SOB, weight gain

184
Q

what is the goal of diuretic therapy in HF?

A

achieve dry weight wile avoiding dehydration, hypotension, and renal dfx

185
Q

which type of diuretic is recommended for most patients with congestive symptoms (volume overload)?

A

loop diuretics like furosemide

186
Q

loop diuretics have more intense diuresis and natriuresis than ____ diuretic s

A

thiazide

187
Q

thiazides are not commonly used for HF with the exception of ___, which is ADDED to loop diuretics if there is diuretic resistance

A

metalozone

188
Q

t/f the lowest effective dose of loop diuretics should be used

A

t

189
Q

what should be monitored on furosemide??

A

electrolytes (Na, K, Ca), SCr, urea, lying and standing BP and daily weights

190
Q

what is the typical PO dosing for furosemide?

A

20-40mg PO BID with increased dose for renal impairment

191
Q

t/f some patients may take furosemide on a sliding scale based on weight gain

A

t

192
Q

what are the 3 loop diuretics?

A
  1. furosemide
  2. bumetanide
  3. ethracrynic acid
193
Q

tell me what you know about bumetanide

A

it is a daily loop diuretic and it is very rarely used

194
Q

if someone has a true allergy to furosemide, what drug are they given>

A

ethacrynic acid

195
Q

is ethacrynic acid daily or BID dosing?

A

BID

196
Q

HFpEF is also known as ____ heart failure

A

diastolic

197
Q

__% of patients with heart failure have HFpEF

A

50

198
Q

HFpEF is most common in what [atient population?

A

elderly women, longstanding HTN

199
Q

t/f the morbidity (i.e. hospitalizations) are similar in HFpEF to those of HFrEF

A

t

200
Q

explain the pathophysiololgy of HFpEF

A

there are abnormalities in diastolic function (relaxation and or stiffness), the ventricle cannot accept adequate blood volume during diastole and the volumes are not enough to maintain appropriate stroke volume

201
Q

what are the 4 principles of HFpEF?

A
  1. identify and treat underlying things that may have caused them to develop HFpEF
  2. identify and treat comorbid conditions that might worsen HF
  3. control their symptoms
  4. realization of clincally relavant CV end points like hospitalization and mortality
202
Q

the CCS suggests which ARB could be considered for patients with HFpEF?

A

candesartan

203
Q

for HFpEF, the CCS recommens that ____ be controlled

A

HTN (strong recommendation)

204
Q

for HFpEF, the CCS recommends the use of ____ to control symptoms of congestion and peripheral edema

A

loop diuretics

205
Q

for HFpEF patients with serum K <5.0mmol/L and eGFR >30mL/min, the CCS suggests the use of _______ with close SCr and K monitoring

A

MRA like spironolactone

206
Q

what were the findings of the CHARM-preserved trial?

A

looked at candesartan 32mg for EF>40% and found no difference in cardiac death or HF hospitalization unless it was their first HF hospitalization

207
Q

what was found in the i-preserved study?

A

looked at irbesartan 300mg daily vs placebo for EF>45% and found no difference

208
Q

what was found in the PEP-CHF trial?

A

looked at perindopril 4mg daily vs placebo for EF>40% and found no difference in death or unplanned hospitalization (but also may decrease hospitalization?)

209
Q

what was found about BB for use in HFpEF from observational studies?

A

BB statistically benefit all-cause mortality with no benefit in terms of HF hospitilization

210
Q

what was found about BB for use in HFpEF from 2 RCTs?

A

that BB had no significant decrease in all-cause mortality or HF hospitalization

211
Q

what was found from the TOPCAT trial?

A

spironolactone 15-45mg po daily NYHA EF>45% and found spironolactone vs placebo had no significant effect on death, but did decrease HF hospitalization (however, there was higher K and SCr )

212
Q

what was found from the PARAGON HF trial?

A

looked at ARNI (entresto 97/103mg BID) for HFpEF and found no significant difference in HF hospitalizations of death. They were more likely to have hypotension and angioedema but less likely to have hyperkalemia

213
Q

what is acute decompensated HF?

A

term used to describe worsening signs & symptoms of HF usually caused by volume overload or hypoperfusion that leadds to additional medical care like ER visits and hospitalizations

214
Q

what are 4 common etiologies of acute decompensated HF?

A
  1. diet, Rx and non-Rx medications
  2. non-adherence
  3. concurrent illness like infection
  4. cardiac event like MI, arrhythmia, HTN, valvular insufficiency
215
Q

what are the goals of therapy for acute decompensated HF?

A

reduce mortality, address underlying causes and triggers, get volume back to normal, treat congestive sx, treat sx of low CO, prevent readmissions, optimize QOL

216
Q

give a simple explanation of how acute decompensated HF is treated

A
  1. determine if its wet or dry (if wet, give IV diuretics like furosemide +/- nitrates like IV NTG or topical nitrates), if its dry, may require careful fluid resuscitation
  2. determine if cold or warm (cold means poor perfusion to the periphery due to low CO)
217
Q

what is the most common type of acute decompensated HF?

A

wet with cold

218
Q

what is cardiogenic shock?

A

acute decompensated HF with critically low optput resultsing in organ system dysfunction

219
Q

what is used to treat cardiogenic shock?

A

ionotropes and or vasopressors as IV infusions to increase CO and or maintain sufficient BP in acute care setting

220
Q

what are 2 ionotropes that are used for treatment of cardiogenic shock?

A

dobutamine and milronone

221
Q

give 2 examples of vasopressors used for the treatment of cardiogenic shock2

A

NE and epi

PBL PY2 Fall (21 decks)

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