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Clinical 2 (Sam) > 6 - Chronic Heart Failure > Flashcards

6 - Chronic Heart Failure Flashcards

1
Q

When does HF occur?

A

When the heart is unable to deliver adequate supply of oxygenated blood to meet the metabolic demands of the organs

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2
Q

What causes decreased contractility?

A
  • Rheumatic heart disease
  • Cardiomyopathy
  • Coronary heart disease/MI
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3
Q

What causes increased afterload?

A
  • Hypertension

- Aortic stenosis

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4
Q

What causes increases preload?

A
  • Increased sodium/water retention
  • Malfunction of aortic valve
  • Drugs (steroid, NSAIDs)
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5
Q

What is a direct cardiotoxic drug?

A

ex. Adriamycin

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6
Q

What can cause high output failure?

A

anemia

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7
Q

What 2 factors affect Cardiac Output?

A
  • Heart Rate

- Stroke Volume

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8
Q

What 3 factors affect Stroke Volume?

A
  • Preload
  • Contractility
  • Afterload
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9
Q

What is the ejection fraction (EF)?

A

Fraction of blood ejected from left ventricle

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10
Q

What is the formula for EF?

A

EF = (EDV-ESV)/EDV

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11
Q

What is a normal EF for healthy patients?

A

50-70%

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12
Q

EF > ___% is considered normal

A

40

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13
Q

Preload

A

Degree of filling from left atrium (venous return, end-diastolic volume)

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14
Q

Afterload

A

Arteriolar resistance the heart must pump against to eject stroke volume

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15
Q

Contractility (inotropy)

A

Intrinsic ability of cardiac myocytes to contract

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16
Q

What is cardiac remodelling?

A

Usually begins as compensatory process that results in maladaptive complications:

  • Complex process that occurs at the structural, functional, cellular, molecular level
  • Systemic factors affecting remodelling can be attributed to changes in hemodynamic load, neurohormonal activation and metabolic status
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17
Q

What are the 3 general patters of remodelling?

A
  • concentric ventricular remodelling
  • eccentric left ventricular hypertrophy
  • mixed concentric/eccentric hypertrophy
  • concentric hypertrophy = adding of myocardium
  • eccentric hypertrophy = sarcomeres are being added, no change in wall thickness
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18
Q

Describe the compensatory mechanisms that the body tries to maintain CO & BP by?

A

1) Increase preload
- Increase venous return in an attempt to increase CO
- Sodium/water retention
- Activation of RAAS

2) Vasoconstriction
- Increases after load
- Increase systemic vascular resistance
- Sympathetic stimulation
- Activation of RAAS

3) Tachycardia and increased contractility
- Sympathetic stimulation

4) Neurohormonal Activation
- Compensatory release of hormones in response of hypovolemia - renin, NE, ADH
- In the long term, these contribute to progression of structural abnormalities (ex. Angiotensin 2: increase protein synthesis, cardiac myocyte hypertrophy)

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19
Q

HFrEF

A

Heart failure with reduced ejection fraction

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20
Q

Describe HFrEF

A
  • commonly referred to as systolic heart failure
  • low output (congestive) failure
  • hypofunctioning left ventricle; decreased contractility
  • EF < 40%
  • ventricles enlarge (dilate as retain blood)
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21
Q

HFpEF

A

Heart failure with preserved ejection fraction

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22
Q

Describe HFpEF

A
  • diastolic heart failure
  • normal contractility and heart size
  • impaired left ventricular filling during diastole
  • left ventricular stiffness and inability to relax during diastole
    • results in increased resting pressure within the ventricle
    • the increased pressure impedes ventricular filling, therefore reducing stroke volume (EF preserved)
  • can see with thickened left ventricle (hypertrophic cardiomyopathy) or stiff ventricle (restrict cardiomyopathy)
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23
Q

What are some signs and symptoms of compensatory mechanisms kicking in?

A

Vasoconstriction - leads to decreased CO

Increased HR - leads to increased oxygen utilization

Increased preload - leads to peripheral and pulmonary edema

Decreased exercise tolerance

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24
Q

Signs and symptoms of left-sided heart failure (pulmonary congestion)?

A
  • dyspnea on exertion
  • orthopnea (dyspnea that occurs when lying flat)
  • paroxysmal nocturnal dyspnea
  • pulmonary edema
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25
Q

Signs and symptoms of right-sided heart failure (systemic venous congestion)?

A
  • organomegaly (enlargement of organs) (ex. hepatomegaly)
  • jugular venous distension
  • hepatojugular reflex
  • lower extremity peripheral edema
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26
Q

What are some non-specific findings in patients with HF?

A
  • weakness
  • exercise intolerance
  • fatigue
  • CNS
  • cold, pale, clammy skin
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27
Q

Describe NYHA Class 1 HF

A
  • Uncompromised.

- Able to perform ordinary physical activity.

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28
Q

Describe NYHA Class 2 HF

A
  • Slightly compromised.

- Ordinary physical activity results in symptoms.

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29
Q

Describe NYHA Class 3 HF

A
  • Moderately compromised.

- Less than ordinary physical activity results in symptoms.

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30
Q

Describe NYHA Class 4 HF

A
  • Severely compromised.

- Symptoms may be present at rest.

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31
Q

Describe ACC/AHA Stage A

A

At high risk for HF but without structural heart disease or symptoms of HF.
(Risk factors: HTN, CAD, DM, obesity, metabolic syndrome)

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32
Q

Describe ACC/AHA Stage B

A

Structural heart disease but without signs or symptoms of HF

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33
Q

Describe ACC/AHA Stage C

A

Structural heart disease with prior or current symptoms of HF

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34
Q

Describe ACC/AHA Stage D

A

Refractory HF requiring specialized intervention

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35
Q

What tools can we use to diagnose HF?

A

1) Symptoms (weakness, fatigue, exercise tolerance)
2) Signs on clinical exams
- auscultation of heart and lung - S3 gallop, rales
- edema
- jugular vein distention
- hepatojugular reflux
- dyspnea
3) Echo - ejection fraction
4) Chest X-ray
5) Cardiac MRI
6) CV risk assessment

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36
Q

Goals of therapy for HF?

A
  • Minimize disabling symptoms
  • Decrease hospitalization
  • Improve quality of life
  • Minimize disease complications
  • Slow progression of disease
  • Improve survival
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37
Q

The drugs we have now are only for alleviating symptoms, but we cannot reverse the disease. The only way to have a healthy heart again = ________

A

transplant

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38
Q

What are some strategies for medical management of HF?

A
  • Eliminate exacerbating factors
  • Control associated diseases
  • Restrict activity when acute
  • Sodium restricted diet
  • Exercise conditioning when stabilized to strengthen heart
  • Drug therapy
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39
Q

What drug therapy options do we have for HF?

A

1) Diuretics - Excretion of excess water
2) Inotropic agents - Increase myocardial contractility
3) Vasodilators - Decrease cardiac work
4) ACEi - neurohormonal modulators

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40
Q

What do diuretics do?

A
  • Relieve breathlessness and deem in patients with symptoms and signs of congestion
  • Reduce intravascular volume, edema, preload and pulmonary congestion
  • Achieve diuresis through inhibiting reabsorption of sodium in thick ascending limb (loop diuretics), and distal convoluted tubule (thiazide diuretics)
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41
Q

What diuretics are more efficient: loop or thiazide?

A

LOOP

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42
Q

What is the dosing regimen for diuretics for HF?

A
  • Start with low dose and adjust to achieve positive diuresis with daily body weight reduction of 0.75 - 1 kg until euvolemia (normal body weight)
  • it is essential to know their dry weight
  • Aim to maintain patients on dry weight with lowest possible dose
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43
Q

Furosemide is a _____ diuretic

A

loop

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44
Q

Dose for furosemide

A

Initiate at 20-40mg daily, increase dose accordingly to achieve edema free state (dry weight); once symptoms relieved, use lowest possible maintenance dose

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45
Q

How do you treat diuretic resistance is severe, refractory HF with furosemide?

A
  • try furosemide IV

- add metolazone (usually given 30 mins prior to furosemide)

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46
Q

Thiazides are usually in combo with ??

A

loop diuretic

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47
Q

Thiazides are unlikely to be effective in patients with CrCl < ___

A

30

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48
Q

What is the dose of HCTZ (thiazide)?

A

-Starting dose of 25 mg, usual dose up to 100 mg/day

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49
Q

What is the dose of metolazone (thiazide)?

A

-Starting dose of 2.5mg, usual dose of 2.5-10 mg/day

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50
Q

What is the reasoning behind adding a thiazide diuretic to a loop diuretic?

A

You will achieve water loss in both the ascending limb and the distal tubule

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51
Q

What are some adverse effects/monitoring for diuretics?

A

1) Volume depletion - leads to dehydration and reduction in BP and CO (check for signs of hypovolemia and symptomatic hypotension)

2) Loss of K+ and Mg2+ (hypokalemia can induce digoxin toxicity)
* aim to keep K+ > 4 mmol/L

3) Renal impairment - want to monitor SCr

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52
Q

What things can we monitor to determine diuretic efficacy?

A
  • daily weight
  • input/output
  • jugular venous distention
  • peripheral edema
  • sitting/standing HR & BP
  • organ congestion (pulmonary rales and hepatomegaly)
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53
Q

When should renal function and electrolytes be checked when on diuretics?

A

1-2 weeks after initiation and after dose increase

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54
Q

Rationale of using BB in HF

A

Long term sympathetic activation may contribute to:

  • Disease progression
  • Augmented activation of RAAS
  • Peripheral vasoconstriction
  • Remodelling of cardiac myocytes (i.e. fibrosis, apoptosis)

**BB block sympathetic activation and all these things from occuring

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55
Q

Are BB considered useful in HF?

A

YES - 1ST LINE THERAPY (in addition to ACEi)

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56
Q

Beta blockers are indicated for all _____

A

HFrEF

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57
Q

Beta blockers are first line treatment along with ??

A

ACEi and MRA (mineralocorticoid receptor antagonist - ex. spironolactone) if NYHA 2 or above

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58
Q

Why are BB 1st line in HF?

A

proven to reduce mortality

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59
Q

Metoprolol SR:

Initial dose

A

12.5mg SR daily

or 12.5 mg BID

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60
Q

Metoprolol SR:

Target HF dose

A

200 mg SR daily

or 100 mg BID

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61
Q

Bisoprolol:

Initial dose

A

1.25 mg daily

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62
Q

Bisoprolol:

Target HF dose

A

10 mg daily

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63
Q

Carvedilol:

Initial dose

A

3.125 mg BID

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64
Q

Carvedilol:

Target HF dose

A

25 mg BID

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65
Q

Nebivolol:

Initial dose

A

1.25 mg daily

66
Q

Nebivolol:

Target HF dose

A

10 mg daily

67
Q

Why do we start BB at such low doses in HF?

A

Want to start with low dose bc they already have affected contractility, don’t want to push them into acute HF.
They are on BB to reduce oxygen demand.

68
Q

Describe the dosing approach of BB in HF

A
  • Used in all stages of NYHA 1 - 4
  • Initiate when patients are stable and not in acute decompensated heart failure
  • Start with very low dose
  • Increase dosage approximately every 2 weeks
  • Try to attain target doses (alternatively, aim for highest dose tolerated)
  • If hypotensive - consider decreasing dose of other meds or change timing of meds
  • Avoid large dose reduction or abrupt withdrawl
  • Decrease dose if on inotropes (in-hosp); discontinue if patient is in cariogenic shock
69
Q

What are some side effects of beta blockers?

A
  • postural hypotension
  • headache
  • dizziness
  • bradycardia
  • bronchospasm
  • fatigue
  • decreased exercise tolerance, fluid retention (on initiation)
  • insomnia, vivid dream
  • sexual dysfunction
  • PAD, cold extremity
  • caution in diabetic bc they mask the symptoms of hypoglycaemia
70
Q

What do we need to monitor for BB?

A
  • Clinical improvement
  • BP, HR (If symptomatic bradycardia, discontinue/adjust other HR reducing meds if possible. ex. amiodarone, CCBs, digoxin)
  • Worsening symptoms
71
Q

MOA of ACEi

A

1) Hemodynamic effects
- Increase CO
- Decrease preload
- Decrease systemic vascular resistance
- Decreased BP

2) Hormonal effects (Inhibit RAAS)
- Decrease angiotensin 2
- Decrease aldosterone
- Slow ventricular remodelling

72
Q

Who are ACEi indicated for?

A

all patients with HFrEF along with BB (regardless of what NYHA class)

73
Q

Benefit of using ACEi in HF patients?

A

reduces mortality, cardiac death and hospitalization

74
Q

Ramipril:

Initial dose

A

1.25-2.5 mg BID

75
Q

Ramipril:

Target HF dose

76
Q

Lisinopril:

Initial dose

A

2.5-5 mg daily

77
Q

Lisinopril:

Target HF dose

A

20-40 mg daily

78
Q

Perindopril:

Initial dose

A

2 mg daily

79
Q

Perindopril:

Target HF dose

A

4 mg daily

80
Q

Enalapril:

Initial dose

A

1.25 - 2.5 mg BID

81
Q

Enalapril:

Target HF dose

82
Q

Captopril:

Initial dose

A

6.25 - 12.5 mg TID

83
Q

Captopril:

Target HF dose

A

25 - 50 mg TID

84
Q

Trandolapril:

Initial dose

A

0.5 - 1 mg daily

85
Q

Trandolapril:

Target HF dose

A

4 mg daily

86
Q

Adverse effects of ACEi

A
  • Hypotension
  • Renal impairment
  • Hyperkalemia
  • Cough
  • Rash (more common with captopril)
  • Taste alterations
  • Angioedema (swelling of face, lips, tongue, larynx)
87
Q

Monitoring for ACEi efficacy?

A
  • Right and left sided symptoms
  • Exercise tolerance
  • Weight/fluid balance
88
Q

How do you monitor for adverse reactions of ACEi?

A
  • check renal fcn and electrolytes at baseline
  • monitor blood chemistry 1-2 weeks after dose initiation and 1-2 weeks after final dose citation, then monitor every 3-4 months thereafter
  • new cough
89
Q

Rationale for using MRAs (minteralcorticoid receptor antagonists) in HF ?

A

-Aldosterone contributes to sodium/water retention, sympathetic activation , myocardial and vascular fibrosis and other pathophysiologic effects seen in HF

90
Q

Who are MRAs indicated for?

A

All HF patients NYHA 2-4 in addition to ACEi and BB

91
Q

Evidence for using MRAs in HF?

A

yes - reduce mortality

92
Q

Examples of MRAs?

A
  • Spironolactone

- Eplerenone

93
Q

Spironolactone:

Initial dose

A

25 mg daily

94
Q

Spironolactone:

Target dose

A

50 mg daily

95
Q

Eplerenone:

Initial dose

A

25 mg daily

96
Q

Eplerenone:

Target dose

A

50 mg daily

97
Q

What types of patients would you caution use of MRAs in?

A
  • Hyperkalemic pts
  • Scr > 220 and K+ > 5
  • If on digoxin (hyperkalemia ay precipitate digoxin toxicity)
  • Male pts uncommonly develop breast discomfort of gynecomastia (spironolactone - 10%) - consider switching to eplorenone
98
Q

What does an ARB do?

A

blocks AT1 receptor

99
Q

______ shown to reduce CV mortality

A

candesartan

100
Q

______ shown to improve hospitalization rate due to HF

101
Q

When would you choose an ARB?

A

if someone got a cough using ACEi

102
Q

Valsartan:

Initial dose

103
Q

Valsartan:

Target HF dose

A

160 mg BID

104
Q

Candesartan:

Initial dose

A

4 mg daily

105
Q

Candesartan:

Target HF dose

A

32 mg daily

106
Q

Losartan:

Initial dose

A

25 mg daily

107
Q

Losartan:

Target HF dose

A

150 mg daily ???

**no clinical trials in HF

108
Q

What does Hydralazine/Nitrate Combo do?

A

significant reduction in mortality and improvement in exercise

109
Q

_____ is superior to Hyd/ISDN

110
Q

Is an ACEi with Hyd/ISDN better than ACEi alone?

111
Q

Hyd/ISDN:

Target dose

A

Hyd 75 mg/ISDN 40 mg TID-QID

112
Q

Rationale of using Hydralazine/Nitrate Combo?

A
  • Vasodilation decrease cardiac work by overcoming detrimental effects of compensatory mechanisms
  • Achieved through reduction of preload (nitrates) and after load (hydrazine)
113
Q

When is Hydralazine/Nitrate Combo recommended?

A

It is a standard add-on for individuals of African descent.

Can be given to all patients if:

  • Ongoing symptoms with ACEi and BB
  • Unable to tolerate neither ACEi or ARB
114
Q

What is an ARNI?

A

Angiotensin receptor neprilysin inhibitor:
sacubitril & ARB

*new class of combination agents (sacubitril/valsartan) that act on RAAS and natriuretic peptides

115
Q

Rationale of using an ARNI in HF?

A
  • Increase circulation of a-type natriuretic peptide (ANP) and BNP by inhibiting neprilysin
  • ANP and BNP enhances diuresis, natriuresis, myocardial relaxation, anti-remodelling
  • ANP and BNP also inhibit RAAS
  • AT1 receptor blockade by ARB reduces vasoconstriction, sodium/water retention and myocardial hypertrophy
116
Q

ARNI’s have a higher risk of what side effect than ACEi?

A

symptomatic hypotension

117
Q

Who are ARNIs recommended for?

A
  • May be considered as a replacement for ACEi in patients with HFrEF who remain symptomatic despite optimal treatment with an ACEi, a BB and an MRA
  • In patients with HFrEF NYHA class 2 or 3 who tolerate an ACEi or ARB, replacement by an ARNi is recommended to further reduce morbidity and mortality
118
Q

Sacubitril/valsartan:

Starting dose

A

49/51 mg BID

**valsartan 51 mg in Entresto is approx valsartan 80 mg.

119
Q

Sacubitril/valsartan:

Target dose for HF

A

97/103 mg BID

120
Q

If switching from ACEi to ARNI, how long should you space it out?

A

ARNI should not be given concomitantly with ACEi or within 36 hours of last dose of ACEi.

121
Q

What is Ivabradine and how does it work?

A

f-channel inhibitor

  • inhibit f-channels within SA node resulting in disruption of I(f) ion current flow, thereby prolonging diastolic depolarization and reducing heart rate
  • no effects on BP, myocardial contractility or AV conduction
122
Q

Who is Ivabradine recommended for?

A

Ivabradine can be beneficial to reduce HF hospitalization for patients with symptomatic (NYHA class 2-3) stable chronic HFrEF (LVEF < 35%) who are receiving guideline directed evaluation and management, including a BB at max tolerated dose and who are in sinus rhythm with a HR of 70 ppm or greater at rest.

123
Q

Ivabradine:

Starting dose

124
Q

Ivabradine:

Target dose

A

Up to 7.5 mg BID

125
Q

How does digoxin work?

A

Increases force and velocity of contraction through inhibition of Na-K-ATPase (positive ionotrope)

126
Q

Describe the clinical use of digoxin in HF

A
  • effective in heart failure associated with fast atrial rate, severe HF, S3 gallop, low EF and enlarged heart size
  • no mortality benefit
  • decrease rate of hospitalization
  • improves symptoms, expertise performance, decrease hospitalizations
  • improve QOL
127
Q

Describe the role of digoxin in HF

A

-use in patients with persistent symptoms despite maximized use of vasodilators and diuretics

128
Q

Elimination of digoxin is primarily ______

129
Q

Digoxin:

___% found in skeletal muscle

130
Q

Digoxin:

_____ distribution time

131
Q

Digoxin:

Normal half life

132
Q

Digoxin:

Half life for someone with kidney failure?

133
Q

Digoxin:

Therapeutic range?

A

Historically 0.5 - 2.0 mcg/L

*Current data supports targeting conc of < 1.0 mcg/L to gain neurohormonal modulating effects without enhancing adverse outcome

134
Q

Digoxin:

Dosing for CrCl > 20

A

0.125 mg/day

135
Q

Digoxin:

Dosing for CrCl < 20 or weight < 40 kg

A

0.0625 mg/day

136
Q

Digoxin:

What are some signs of toxicity?

A

Noncardiac: N/V, confusion, altered color vision, weakness, dizziness

Cardiac: AV conduction disturbances

137
Q

Digoxin:

What are some factors affecting digoxin activity or toxicity?

A
  • electrolyte disturbances (hypo and hyperkalemia)
  • renal function - renal impairment will cause decreased elimination
  • drug interactions
  • elderly
  • hypothyroidism
138
Q

What drugs increase bioavailability of digoxin?

A

tetracycline, erythromycin

139
Q

What drugs decrease bioavailability of digoxin?

A

antacids, cholestyramine, metoclopramide

140
Q

What drugs decrease elimination of digoxin?

A

quinidine, verapamil, spironolactone, amidoarone

141
Q

What drugs decrease K+ or Mg2+ leading to electrolyte disturbances?

142
Q

How do we treat digoxin toxicity?

A
  • withdrawal of digoxin
  • correction of electrolyte abnormalities
  • antiarrhythmic agents
  • pacemaker
  • digoxin specific antibodies
  • oral activated charcoal
143
Q

Hawthorn extract is a natural product for HF: describe it’s properties

A

inotropic, vasodilating, lipid-lowering, antioxidant, anti-inflammatory

144
Q

Evidence for hawthorn extract?

A
  • modest increase in exercise tolerance

- one randomized trial showed decrease in mortality

145
Q

L-carnitine is a natural product for HF: describe it’s properties

A
  • plays a role in myocardial energy production

- thought to increase exercise tolerance and decrease cardiac dimensions

146
Q

Are fish oils of benefit to HF patients?

A

small but significant mortality benefit

147
Q

Coenzyme Q10 is a natural product for HF: describe it’s properties

A
  • component of the electron transport chain in the mitochondria
  • micronutrient
  • there are decreases levels of coenzyme Q10 in patients with HF
148
Q

What drugs should be avoided in HF?

A
  • AAD (anti-arrthymic drugs)
  • non-DHP CCB
  • TCA’s
  • NSAIDs
  • corticosteroids
  • doxorubicin, trastuzamab
149
Q

Why should AAD (anti-arrthymic drugs) be avoided in HF?

A
  • proarrhythmia
  • negative inotropic effects
  • increased mortality
150
Q

Why should non-DHP CCB’s be avoided in HF?

A

-direct negative inotropic agents, CI in patients with systolic chronic heart failure

151
Q

Why should TCAs be avoided in HF?

A

-pro arrhythmic potential

152
Q

Why should NSAIDs be avoided in HF?

A

-inhibits effects of diuretics and ACEi, cause salt and water retention, can worsen both cardiac and renal fcn

153
Q

Why should corticosteroids be avoided in HF?

A

adverse effects on salt and water retention

154
Q

Why should doxorubicin and trastuzamab be avoided in HF?

A

dose-dependent cardiotoxicity

155
Q

Non-pharms for HF:

Exercise

A
  • recommended for all patients with stable HF symptoms & impaired LV systolic fcn
  • aerobic exercise 3-5x/week, 30-45 min per session for NYHA Class 1-3
156
Q

Non-pharms for HF:

Salt & Fluid restriction

A
  • No added salt diet (<2-3 grams of salt per day, equivalent of 1/4 tsp)
  • Limit fluid intake to 1.5-2L/day for patients with fluid retention or congestion that is not easily controlled with diuretics or in patients with significant renal dysfunction or hyponatremia
  • *All fluid counts (coffee, soup, jello)
157
Q

List some more non-pharos for HF

A
  • monitor daily weight (without clothes and after voiding)
  • no more than 1 alcoholic drink per day
  • smoking cessation
  • influenza and pneumococcal vaccination
  • aggressive risk reduction
  • patient education is key for drug adherence and fluid/salt restriction
158
Q

What is an ICD and who is it recommended for?

A 
Implantable Cardioverter Defibrillator:
-indicated for primary prevention of sudden cardiac death in selected patients with nonischemic dilated cardiomyopathy or ischemic heart disease > 40 days post MI with LVEF 35% or less and NYHA class 2 or 3
159
Q

What is CRT and who is it recommended for?

A

Cardiac Resynchronization Therapy:
-indicated for patients with LVEF < 35%, left bundle branch block with a QRS duration of 150 ms or greater, NYHA 2, 3, or 4 symptoms

160
Q

Who is a heart transplant indicated for?

A

end stage heart failure

161
Q

What is LVAD and who is it recommended for?

A

Left ventricular assist device:

-for end stage heart failure or as bridging to heart transplant

Clinical 2 (Sam) (18 decks)

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