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PHAR 253 > Heart Failure > Flashcards

Heart Failure Flashcards

1
Q

What is the definition for abnormal heart function?

A

Any cardiac structural or functional disorder leading to inadequate cardiac output &/or elevated ventricular filling pressures

Impairs the ability of the ventricle to fill (diastolic) or eject (systolic) blood

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2
Q

What is heart failure?

A

A complex clinical syndrome with signs and symptoms of:
- Reduced cardiac output (inability to meet metabolic demands of body or abnormally high cardiac pressures)
- Pulmonary or systemic congestion at rest or with stress

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3
Q

What are the mortality rates for heart failure?

A

10% will die after 30 days

20% will die after 1 year

50% will die after 5 years

Number of HF hospitalizations is a strong predictor of mortality

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4
Q

Is heart failure a stable condition?

A

No, it is a progressive condition
- Increasing frequency of decompensations punctuate gradual decline in function. Following each acute event, heart function does not return to previous level

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5
Q

What is the pathophysiology of heart failure?

A

Cardiac output (stroke volume x HR) is decreased in heart failure

Stroke volume is dependent on preload (muscle fiber stretching while filling), contracility (inherent ability of the myocardium to contract normally), afterload (muscle force required to overcome higher pressure in the aorta when pumping blood out)

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6
Q

What is the Frank-Starling Law?

A

It is the ability of the heart to alter contraction force based on changes in preload

Increased ventricle volume = Increased contactility = Increased stroke volume

Note: If the heart is overstretched (increased preload), it looses its ability to return equal force

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7
Q

What neurohormones do heart failure drugs target?

A

Norepinephrine
Angiotensin II
Aldosterone
Vasopressin
Pro-inflammatory cytokines

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8
Q

What are the four compensatory responses to reduced cardiac output?

A
  • Increased pre-load (via Na+ and water retention):
    a. Improves stroke volume
  • Vasoconstriction (maintains BP if CO is low)
  • Tachycardia (helps maintain CO if stroke volume is low)
  • Ventricular hypertrophy and remodelling (helps maintain CO)
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9
Q

What are the consequences of long-lasting increased pre-load?

A

Pulmonary and systemic congestion (blood is backing up)

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10
Q

What are the consequences of long-lasting vasoconstriction in response to reduced cardiac function?

A

Shunt blood from nonessential organs to brain and heart

Increased mycocardial oxygen demand

Increased afterload decreases stroke volume (activating further compensatory responses)

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11
Q

What are the consequences of ventricular hypertension and remodelling?

A

Increased risk of myocardial cell death, myocardial infarction, arrythmia, fibrosis

DIastolic and/or systolic dysfunction

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12
Q

What are some typical symptoms associated with heart failure?

A
  • Breathlessness
  • Orthopnea (dificulty breathing while lying down)
  • Paroxysmal nocturnal dyspnea (waking up with SOB)
  • Swelling of body
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13
Q

If a patient shows symptoms of heart failure, what else do they need to be diagnosed with heart failure?

A

Assess natriuretic peptides (gold standard biomarkers in HF)

Heart failure is present if patient has one of the following lab values:
- NT pro-BNP (greater than 125pg/mL)
- BNP (greater than 50pg/mL) (preferred in the SHA)

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14
Q

What are natriuretic peptides?

A

BNP
NT-proBNP (pro homone BNP)

They are synthesized and released by the ventricles in response to pressure or volume overload

BNPs promote natriuresis & diuresis, and attenute RAAS & SNS activation (opposes the action of heart failure compensatory actions, which is good)

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15
Q

What is neprilysin?

A

It is an enzyme that breaks down BNP

Neprilysin inhibitors like sacubitril are beneficial in reversing the negative heart failure compensatory actions

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16
Q

Can natriuretic peptide values alone be used to diagnose heart failure?

A

No, should be considered in relation to signs, symptoms, and information from diagnostic imaging

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17
Q

If BNP or NT-proBNP are elevated, what are the next steps?

A

Send for electrocardiogram & start or intensify neurohormonal blocking agents (ACEi, ARB, beta-blockers, MRAs)

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18
Q

What information can be gleaned from an ECG?

A

Size and shape of heart

Pumping capacity

Location and extent of damaged tissue (muscle, walls, valves)

Pressure estimates

Quality of ECG readings can vary by 10%

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19
Q

What are the three classifications of heart failure?

A

Chronic HF (persistent & progressive)

Acute/decompensated HF (gradual or rapid change in HF signs & symptoms, resulting in need for urgent therapy)

Advanced HF (frequent decompensations, mechanical devices, transplantation, palliative therapies)

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20
Q

Why is Left Ventricular Ejection Fraction significant?

A

Blood leaving left ventricle/blood entering left ventricle

Left ventricular ejection fraction can change depending on preload, contractility, and afterload. Therefore it is a good indicator for heart failure

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21
Q

What is HF-pEF?

A

Heart failure with preserved ejection fraction

In these HF patients, ejection fraction is above 50%. These patients may have problems with heart stiffness and ventricular relaxation (left ventricular hypertrophy)

Affects:
- Elderly
- Female
- DM, Atrial fibrillation, HTN

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22
Q

What is HF-mEF?

A

Heart failure with mid-range ejection fraction

In these HF patients, ejection fraction is between 41-49%

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23
Q

What is HF-rEF?

A

Heart failure with reduced ejection fraction

In these HF patients, ejection fraction is below 40%. These patients may experience systolic dysfunction, problems with the heart pump/contractility

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24
Q

Review slide 40 for the heart failure treatment algorithm?

A
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25
Q

What drugs are used in pharmacotherapeutic treatment of heart failure?

A

Initiate quadruple therapy

  1. ARNI (sacubitril/valsartan) or ACEi/ARB, then switch to ARNI
  2. Beta-blocker
  3. Mineralocorticoid receptor blocker
  4. SGLTi

Strive to initiate the above agents within 3 to 6 months after diagnosis, and titrate to target or maximally tolerated doses

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26
Q

What are the effects of ACEi drugs on CV health?

A

They prevent vasoconstriction (reduce BP) and especially post-glomerular (reduce GFR) and lower aldosterone associated sodium and H20 retention (reduced BP)

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27
Q

How are ACEi drugs titrated up?

A

Double dose every 1-3 weeks

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28
Q

What conditions are contraindicated for ACEi drugs?

A
  • Bilateral renal artery stenosis
  • History of angioedema
  • Pregnancy
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29
Q

What are some caution situations for ACEi use?

A
  • K+ greater than 5.2mmol/L, SCr greater than 220umol/L or eGFR under 30ml/min
  • SBP less than 90 mmHg or sympotmatic hypotension
  • Moderate to severe aortic stenosis
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30
Q

What are some drug interactions associated with ACEi drugs?

A

Increased risk of hyperkalemia associated with the following drugs:
- K+ supplements
- K+ sparing diuretics
- MRAs
- Renin inhibitors
- Trimethoprim (TMX)
- NSAIDs (should not be used in HF patients at all)
- Low salt substitutes (KCl)

Lithium (increased risk of lithium toxicity)

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31
Q

Is there a target for blood pressure in heart failure patients?

A

No fixed numbers (SBP around 90-100mmHg), but just before they start experiencing symptomatic hypotension

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32
Q

How do HCPs monitor K+ levels on patients on ACEis?

A

Lab work at baseline, & 1-2 weeks after initiating therapy and whenever increasing dose

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33
Q

How is renal function assessed in patients on an ACEi?

A

Lab work (SCr, BUN) at baseline, & 1-2 weeks after initiating therapy and whenver increasing dose

Increase in SCr or decrease in eGFR of up to 30% is acceptable

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34
Q

What is the use of ARBs over ACEi in heart failure treatment?

A

Use an ARB when patient has an ACEi intolerance
- Cough
- Angioedema

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35
Q

Why is ACEi first line for HF over ARBs?

A

ACEi simply have more evidence bc they have been out longer compared to ARBs

Do not combine ACEi and ARB, due to increased risk of hypotension, hyperkalemia, & renal dysfunction

Caution when starting patient on Entresto bc it contains valsartan and should not be used within 36 hours of ACEi dose

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36
Q

What ARBs are indicated for heart failure in Canada?

A

Candesartan:
- Start dose (4-8mg)
- Target dose (32mg daily)

Valsartan:
- Start dose (40mg BID)
- Target dose (160mg BID)

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37
Q

What drugs are found in Entresto?

A

Sacubitril/Valsartan

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38
Q

Review slide 57 for MOA for Entresto

A
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39
Q

What are some contraindications for Entresto?

A

Concurrent ACEi use (36 hour washout period ACEi <–> ARNI)

History of ACEi or ARB angioedema

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40
Q

What are the therapeutic doses of Entresto for heart failure?

A

Start dose (50-100mg BID)

Target dose (200mg BID)

Note dose values have been rounded

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41
Q

How is target dose for Entresto acheived?

A

Double dose in 3 to 6 weeks in patients on less than 50% of ACEi or ARB target dose

Double dose in 6 weeks for patients on more than 50% of ACEi or ARB target dose

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42
Q

What beta blockers are indicated for use in heart failure?

A

Bisoprolol
Carvedilol
Metoprolol

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43
Q

What is the mechanism of action for beta-blockers?

A

Block NE at the beta-adrenergic receptors (reduces heart hyperactivity, lowers HR)

Improves myocardial function by prolonging ventricular filling time (results in a more productive heartbeat)

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44
Q

What are the doses for the beta-blockers indicated for heart failure?

A

Carvedilol
- Starting (3.125mg BID)
- Target (25mg BID/50mg BID for patients over 85kg)

Bisoprolol
- Starting (1.25mg daily)
- Target (10mg daily)

Metoprolol
- Starting (12.5-25mg daily)
- Target (200mg daily)

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45
Q

How are beta-blockers titrated up to target dose?

A

Double dose every 2-4 weeks

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46
Q

What are some contraindications for beta-blockers in heart failure?

A
  • 2nd or 3rd degree AV block or HR under 50bpm (Does not apply if patient has pacemaker)
  • PR interval greater than 0.24 sec
  • Severe/uncontrolled asthma
  • Severe peripheral artery disease
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47
Q

What are some drug interactions associated with beta-blockers in heart failure?

A
  • Verapamil, diltiazem, amiodarone, digoxin (increased risk of bradycardia/AV block)
  • Clonidine (Increased risk of hypertensive crisis)
  • Phenobarbital (reduced beta-blocker efficacy)
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48
Q

What are some adverse effects associated with beta-blocker use in heart failure?

A
  • Hypotension
  • Bradycardia
  • Worsening HF symptoms
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49
Q

Can beta-blockers be stopped abruptly?

A

No, beta-blockers need to be tapered over 1 to 2 weeks

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50
Q

Which beta-blockers are cardioselective?

A

Bisoprolol and Metoprolol

Inhibit the beta-1 receptors in their heart (reduce HR)

Limited effect on BP

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51
Q

Which beta-blockers are non-cardioselective?

A

Carvedilol

Inhibits b-1 and b-2 receptors around the body (reduce HR, BP, airway obstruction)

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52
Q

What mineralocorticoid antagonists (MRAs) are indicated for heart failure in Canada?

A

Spironolactone
- Starting (12.5mg daily)
- Target (25-50mg daily)

Eplerenone
- Starting (25mg daily)
- Target (50mg daily)

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53
Q

What is the purpose of MRAs in heart failure treatment?

A

They are used to inhibit RAAS activation

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54
Q

How are MRAs titrated up to target dose?

A

Double dose every 4 to 8 weeks

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55
Q

What are some contraindications associated with MRAs?

A

Spironolactone and Eplerenon
- K+ is over 6mmol/L

Eplerenone:
- Severe hepatic impairment

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56
Q

What are some drug interactions associated with MRAs?

A

Both:
- Same as ACEi

Spironolactone:
- digoxin

Eplerenone:
- Caution for CYP3A4 inhibitors (only use 25mg max if concurrent therapy)

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57
Q

What are some adverse effects associated with MRAs?

A

Both:
- hyperkalemia

Spironolactone:
- Gynecomastia (dose-dependent), erectile dysfunction, menstrual irregularites

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58
Q

How are MRAs monitored once initiated?

A

Initial stage:
K+ and SCr baseline & test again 1 week after starting or increasing dose

Stable:
- Test monthly for 3 months in first year, then every 6 months after

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59
Q

At what CrCl is spironolactone use contraindicated?

A

When CrCl is below 30mL/min, spironolactone should not be used due to risk of hyperkalemia

Be more careful in monitoring to prevent kidney injury from hyperkalemia

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60
Q

Are spironolactone and eplerenone (both MRAs) similarly priced?

A

No, eplerenone ($80/month) is significantly more expensive vs spironolactone ($5-7/month)

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61
Q

Are MRAs effective in reducing BP in patients with heart failure?

A

No, MRAs do not reduce BP if it is normal

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62
Q

What SGLTis are indicated for heart failure in Canada?

A

Dapagliflozin
Empagliflozin

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63
Q

What is the mechanism of action for SGLTIs?

A

Multi-dimensional MOA

Review slide 103

64
Q

What is an adverse effect of SGLTis that is expected?

A

15-20% reduction in eGFR is expected, but SGLTi use will slow down eGFR reduction vs. placebo

65
Q

Will SGLTis cause hypoglycemia in patients without diabetes?

A

No

66
Q

How is diabetes therapy changed following starting a SGLTi for diabetes and heart failure?

A

A1C less than 8.0%:
- Reduce insulin secretagogues and insulin

A1C above 8.0%:
- No change to diabetes management

67
Q

What are some contraindications associated with SGLTi use?

A

Severe renal or hepatic dysfunction
- Dapagliflozin (CrCl less than 25mL/min)
- Empagliflozin (CrCL less than 20mL/min)

Caution is patients with hypovolemia or dehydrated

68
Q

What are some drug interations with SGLTis?

A

Diuretics (monitor for hypovolemia)

69
Q

What are some adverse effects associated with SGLTi use?

A
  • Genital mycotic infections
  • Euglycemic diabetic ketoacidosis in T2DM
70
Q

Is dapagliflozin indicated in HF-pEF?

A

No, despite evidence for its use in HF-pEF (due to patent shenanigans)

Only empagliflozin is indicated for heart failure regardless of ejection fraction

71
Q

What are some treatment options for heart failure beyond standard quadruple therapy?

A
  1. Ivabradine
  2. Vericiguat
  3. Hydralazine-Nitrates
  4. Digoxin
72
Q

What is the mechanism of action for ivabradine?

A

It is a sinus node inhibitor (cardiac pacemaker current)

Slows diastolic depolarization and extends time for blood to fill left ventricle before ejecting blood

73
Q

What patient profile benefits from ivabradine therapy?

A

Ivabradine can reduce hospitalization in patients with resting HR over 77bpm

74
Q

What is the role of ivabradine in heart failure therapy?

A

In symptomatic HF-rEF despite guideline directed therapy

The following must apply:
- Sinus rhythm
- Raised HR
- HF hospitalization within the last 12 months

75
Q

What is the benefit of ivabradine?

A

Ivabradine can reduce the risk of HF hospitalizations, but not mortality

76
Q

What is the doses for ivabradine?

A

Starting (in elderly): 2.5mg BID
Starting (adults under 65): 5mg BID

Target dose: 7.5mg BID

Titration instructions: double dose every 2-4 weeks if HR is above 60bpm

77
Q

What are some contraindications for ivabradine?

A
  • 3rd degree AV block
  • Sick sinus syndrome
  • Pacemaker dependence
78
Q

What are some drug interactions involving ivabradine?

A
  • CYP 3A4 inhibitors (ketoconazole, clarithromycin, ritonovir, dilitiazem)
  • Amiodarone (risk of QT prolongation)
  • Digoxin (excessive bradycardia)
  • Simvastatin (reduces simvastatin by 50%)
79
Q

What are some adverse events associated with ivabradine use?

A

Atrial fibrillation
Transient flashes of light (phosphenes)

80
Q

How is ivabradine monitored?

A

Dose increased up to 7.5mg if HR is above 60bpm

Reduce dose if HR is less than 50 or symptomatic bradycardia

81
Q

What is the mechanism of action for digoxin?

A
  • It has positive inotropic effect (strengthens myocardial contractions)
  • Offsets SNS activation (increases PNS
  • Reduces HR (negative chronotropic) which causes increased diastolic filling
82
Q

What are some contraindications for digoxin?

A

Ventricular fibrilation

83
Q

What is the role of digoxin in heart failure therapy?

A
  • Patients with HF-rEF in sinus rhythm who continue to have moderate to severe symptoms despite quadruple therapy
  • HF-rEF patients that also have chronic atrial fibrilation
84
Q

What is the benefit of digoxin in heart failure treatment?

A

Reduces the risk of HF hospitalizations, but not mortality

85
Q

What are some drug interactions associated with digoxin?

A
  • Amiodarone (reduce digoxin by 50%)
  • Dronedarone
  • Beta blockers
  • CCBs
  • Flecainide
  • Propafenone
86
Q

What are some adverse effects associated with digoxin use?

A

Toxicity (anorexia, nausea, vomiting, dizziness, visual changes)

87
Q

What are some lab values that should be monitored in digoxin therapy?

A
  • HR
  • SCr (caution if CrCl is below 30mL/min)
  • K+ (risk of arrhythmia in hypokalemia)
88
Q

How is digoxin dosed?

A

No HF target or loadind dose for digoxin in heart failure

Dose: 0.0625mg to 0.25mg PO once daily

Avoid digoxin serum concentrations above 1.2ng/mL

89
Q

Is digoxin relatively expensive?

A

No, it only costs $17/per month

90
Q

What other drug has similar benefit compared to digoxin?

A

Ivabradine

Compared to digoxin, ivabradine:
- Less drug interactions
- No renal dose adjustments
- Less real-world experience
- Cannot be used in atrial fibrilation
- More expensive
- Require EDS approval

91
Q

What is the mechanism of action for vericiguat?

A

It is a soluble guanylate cyclase (sGC) stimulator (increases cGMP, which reverses some of the compensatory HF actions)

92
Q

What is the role in therapy for vericiguat?

A

Considered for addition to optimize HF therapies for HF-rEF patients and patients who have had HF hospitalizations in the past 6 months

93
Q

What is the benefit of vericiguat in heart failure treatment?

A

Redices the risk of HF hospitalizations, but not mortality

94
Q

What are some contraindications for vericiguat?

A

Other sGC stimulators (not many available or used in Canada)

Pregnancy

95
Q

What are some drug interactions associated with Vericiguat?

A
  • PDE5 inhibitors (ex. sildenafil)
  • Long-acting nitrates
96
Q

What are some adverse effects associated with vericiguat use?

A

Anemia
Symptomatic hypotension
Syncope

97
Q

How is vericiguat dosed?

A

Initial (2.5mg PO daily x 2 weeks)

Titration (increase to 5mg x 2 weeks, then to 10mg based on BP and clinical symptoms)

98
Q

What is H-ISDN and its mechanism of action?

A

Hydralazine (direct acting arterial vasodilator)
- Reduces afterload on the left ventricle and enhances hearts ability to pump

Nitrates (venous dilators)
- Reduce preload and pulmonary/systemic edema formation

99
Q

What is the evidence for the use of H-ISDN in heart failure patients?

A

Patients with African descent and have HF-rEF with advanced symptoms may benefit from H-ISDN

Often used in patients that are not able to tolerate an ACEi, ARB, or ARNI due to hyperkalemia or renal dysfunction

100
Q

What are some contraindications for hydralazine alone?

A

Acute dissecting aortic aneurysm

Mitral valve rheumatic heart disease

101
Q

WHat are some drug interactions associated with hydralazine alone?

A

Can reduce digoxin levels and increase metoprolol

102
Q

What are some adverse effects associated with hydralazine?

A

Hypotension
Edema
Tachycardia

103
Q

What are some variables to monitor when patients are on hydralazine?

A

BP

HR

104
Q

Is hydralazine relatively expensive?

A

No, only $25-30/month

105
Q

What are some contraindications associated with ISDN use alone?

A
  • Cerebral hemorrhage
  • Severe anemia
  • Severe hypotension or bradycardia
  • Hypertrophic obstructive cardiomyopathy
106
Q

What are some drug interactions associated with ISDN use alone?

A

Do not take within 24-48 hours of a PDE5 inhibitor

Do not take with another sGC inhibitor

107
Q

What are some adverse effects associated with ISDN use alone?

A

Hypotension
Headache
Lightheadedness

108
Q

What should be monitored when on ISDN?

A

BP

HR

109
Q

Is ISDN relatively expensive?

A

No, only $26/month

110
Q

What is the dosing strategy for vericiguat?

A

Start (2.5mg daily)

Target dose (10mg daily)

111
Q

What is the dosing strategy for H-ISDN?

A

Starting dose (hydralazine 10-37.5mg TID/ISDN 10-20mg TID)

Target dose (hydralazine 75-100mg TID or QID/ISDN 40mg TID)

112
Q

What is the efficacy of using hydralazine (nitrate) alone in heart failure treatment?

A

Nitrates alone can releive orthopnea, paroxysmal nocturnal dyspnea, exercise-induced dyspnea or angina

Ensure 12-hour nitrate free interval to prevent tolerance to develop

113
Q

What is the definition of HF-pEF?

A

LVEF > 50%

  • Issues with heart stiffness/ventricular relaxation and filling
  • Affects elderly, females, DM, atrial fibrilation, and HTN
114
Q

Are there many treatment options for HF-pEF?

A

Not the same variety compared to HF-rEF

Empagliflozin (SGLT2i) is used in HF-pEF for symptomatic treatment

Consider Candesartan, Spironolactone, and diuretics for treatment of edema and HTN

115
Q

Can dapagliflozin be used for HF-pEF treatment?

A

No, Dapagliflozin is only officially indicated for use in HF-rEF, not HF-pEF

116
Q

Does the benefit of heart failure medications increase with ejection fraction?

A

No, efficacy declines with increased ejection fraction

117
Q

Can quadrule therapy for heart failure be stopped once reduced ejection fraction returns to normal values?

A

No, up to 44% of patients that d/c therapy after improved ejection fraction will see relapse into reduced ejection fraction

118
Q

What is the mechanism of action of diuretics in heart failure treatment?

A

Reduce preload by reducing Na+ and water retention, which inturn reduces pulmonary and peripheral edema

119
Q

What are the benefits of diuretic therapy in heart failure?

A
  • Most rapid agent in producing symptomatic relief due to fluid retention
  • Improve exercise tolerance and QOL
  • Reduce HF hospitalizations
120
Q

Do diuretics improve survival in heart failure patients?

A

No, they do not reduce mortality rates nor do they slow down disease progression

Diuretics are used for symptomatic treatment alone (reduce HF hospitalizations)

121
Q

What diuretic is used most commonly in heart failure patients?

A

Furosemide (Loop diuretics)

122
Q

How is diuretic use monitored in heart failure patients?

A

Changes in body weight is a sensitive marker of fluid retention or loss

Any rapid changes (gain or lose 2lb in 1-2 days OR gain or lose 5lbs over 1 week) are concerning and patient should seek HCP

123
Q

What is a commonly used diuretic combination therapy used in heart failure?

A

Furosemide (loop diuretics) and metolazone (TZD)

Less side effects vs. increasing loop diuretic dose

Combo therapy can also be beneficial to combat Na+ retention due to chronic loop diuretic use

124
Q

How is furosemide dosed for heart failure treatment?

A

Initial (20-40mg PO once daily to BID)

Max dose (200mg/day)

Usually max dose is avoided, and is combined with metolazone (TZD) to enhance diuretic therapy

125
Q

How is metolazone dosed in heart failure treatment?

A

Initial outpatient (2.5mg 2-3x/week)

Initial inpatient (5-10mg)

Reccomended to take metolazone 30 minutes before furosemide to align onset of action to occur at the same time

126
Q

What are the concerns with over-diuresis?

A

Reduced cardiac output, renal perfusion, and symptoms of volume depletion

Not ideal in heart failure

127
Q

What are some contraindications for diuretic use in heart failure treatment?

A

Anuria (kidneys are not producing urine)

Hepatic coma (liver damage causes toxins to build up which can cause coma)

pre-coma

128
Q

When should we use caution with diuretic use?

A

Hypokalemia and Hyponatremia (diuretics are known to reduce these ions)

eGFR below 30mL/min

SBP below 90mmHg

129
Q

What are some adverse events associated with diuretic use?

A
  • Hypotension
  • Volume depletion
  • Hyperuricemia (can cause gout)
  • Electrolyte disturbances
  • Ototoxicity in high doses
130
Q

What are some monitoring parameters for diuretics?

A

HF symptoms + daily morning weight

K+, Na+, and SCr levels at baseline and 5-7 days after diuretic adjustment

NT-proBNP or BNP levels (if decreased by more than 30%, then reduced diuretic dose)

131
Q

What are some dietary reccomendations for heart failure patients?

A
  • Restrict dietary salt intake between 2g/day and 3g/day (avoid added salt)
  • Restrict fluid intake to 2L/day for patients with fluid retention or congestion that is not easily controlled with diuretics
132
Q

What are some drugs that can aggravate heart failure symptoms?

A
  1. Drugs that can cause fluid retention
    a. Corticosteroids, NSAIDs, COX-2 inhibitors
  2. Drugs that decrease CO
    a. CCBs, Carbemazepine, TCAs
  3. Oral drugs with high Na+ content
    a. SPS, PEG
  4. Drugs with miscellaneous mechanism of cardiotoxicity
    a. Clozapine, Lithium, Saxagliptim
  5. Oncology drugs
133
Q

Can NSAIDs be used in heart failure patients?

A

No NSAIDs can cause prostaglandin-associated Na+ and H20 retention, which worsens the symptoms of heart failure

134
Q

Are there any natural medicines that are effective in heart failure patients?

A

Not really

evidence for omega-3 is limited (use less than 4g/day)

135
Q

Are most patients recieving the most effective doses for their heart failure drugs?

A

No, up to 80% of patients are using less than 50% of the target doses for the drugs they are using for heart failure

136
Q

What is the impact of pharmacist care in heart failure treatment?

A

Reduce all-cause and HF hospitalizations by 30% due to treatment optimization

NNT of 17 after 6-12 months

137
Q

What are the main categories of duties shared by hospital pharmacists?

A
  • Patient assessment
  • Medication management
  • Patient education
  • Operations and administration
138
Q

What are some common symptoms assoiated with heart failure?

A

Dyspnea
Orthopnea
Paroxysmal nocturnal dyspnea
Cough
Peripheral edema
Weight gain
Fatigue/exercise intolerance

139
Q

What are some considerations for assessing heart failure signs?

A
  • Identify recent baseline (do not rely on information from years ago)
  • Compared to baseline, what are their symptoms like
  • Ask the patient regarding usual and inital signs
  • BNP lvels, lifestyle changes, adherance
140
Q

How is dyspnea assessed in heart failure?

A
  • Is it with activity or at rest (what level of activity triggers SOB)
  • Medication profile
    a. drugs that cause fluid retention (NSAIDs)
    b. Non-adherance to heart failure therapy
    c. Uncontrolled comorbidities (COPD, asthma, anxiety, Afib)
141
Q

How is orthopnea assessed on heart failure?

A
  • Number of pillows, degree of head elevation
  • How does the individual wake up in the morning (is head still elevated, if so then patient probably has orthopnea)
142
Q

What is paroxysmal noctural dyspnea (PND)?

A

Waking up short of breath

143
Q

What are some characteristics of congestion/fluid retention-induced cough?

A

Productive cough

Noctural cough only, especially if they are experiencing orthopnea and PND

Increase diuretic dose and optimize HF therapy

144
Q

What are some characteristics of heart failure treatment drug-induced cough?

A

Usually a dry persistant cough
- More common in ACEi >ARNI>ARB
- If cough is bothersome and not associated with HF signs, then wither hold and rechallenge or switch

145
Q

How is severity of edema evaluated?

A

Pitting edema scale (if depression lasts longer to fill, it indicated more severe fluid retention)

146
Q

Is lower limb edema in heart failure bilateral?

A

Yes, this is a requirement for edema to be attributed to heart failure

Edema in one leg can be more severe than the other

147
Q

What patient group sees abdominal edema in heart failure?

A

Often seen in immobile and bed-ridden patients

148
Q

What does the New York Heart Association Classification assess?

A

Functional status is ranked on this scale (4 classes, with Class I being asymptomatic)

Majority of individuals enrolled in HF trails are NYHA class II to III (mild to moderate heart failure symptoms)

149
Q

What is a standard procedure to track volume change/fluid retention?

A

Patient should weigh themselves while naked and record these values to better see trends in weight

+2lbs in a few days or +5lbs in a week is largely due to fluid retention

150
Q

What are some consequences of diuretic-induced hypovolemia?

A
  • It can limit optimization of HF-rEF therapy
  • Weight is below dry weight
  • Reduce diuretics
151
Q

What are some consequences of hypervolemia for heart failure treatment?

A
  • New or worsening HF symptoms
  • Increase in weight
  • Increase diuretics dose
152
Q

Review slides 222 and 223 for assessing and managing hypo/hypervolemia in heart failure

A
153
Q

Review slides 224 and 225 for instructions on the order of initiation for quadruple therapy

A
154
Q

Why are mineralocorticoid antagonists included in quadruple therapy?

A

It is due to the neurohormonal benefit, not the the diuretic effect (MRAs are weak diuretics)

155
Q

Review last 20 slides for case studies for heart failure treeatment optimization

A

PHAR 253 (10 decks)

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