Chronic Heart Failure Flashcards

1
Q

What is the mortality rate of heart failure?

A
  • up to 40-50% of patients with HF die within 5 years of diagnosis
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2
Q

What is heart failure?

A

a clinical syndrome with subsets of conditions due to cardiac dysfunction

  • this occurs when the heart is unable to deliver adequate supply of oxygenated blood to meet the metabolic demands of the organs
  • associated with the structural abnormality that develops over time secondary to a sudden or insidious injury
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3
Q

What kind of heart failure provides a reduced ejection fraction?

A
  • systolic failure
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4
Q

Is the ejection fraction compromised in diastolic failure?

A
  • it is
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5
Q

What conditions will decrease the contractility of the heart?

A
  • rheumatic heart disease
  • cardiomyopathy
  • coronary heart disease/MI
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6
Q

What conditions will increase the after load of the heart?

A
  • hypertension

- aortic stenosis

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7
Q

What conditions will increase the preload of the heart?

A
  • increased sodium and water retention
  • malfunction of the aortic valve
  • drugs (steroids, NSAIDs)
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8
Q

What causes a high output failure?

A

anemia

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9
Q

Cardiac output is the function of what?

A

CO= SV x HR

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10
Q

What factors influence stroke volume?

A
  • preload
  • contractility
  • after load
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11
Q

What is the definition of cardiac output?

A
  • volume of the blood pumped out of the heart per minute
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12
Q

What is the definition of heart failure?

A
  • those with an ejection fraction less than 40%
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13
Q

What is the definition of ejection fraction?

A
  • fraction of blood ejected form the left ventricle
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14
Q

What is the formula for ejection fraction?

A

EF = (EDV - ESV) / EDV

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15
Q

What is the definition of the preload?

A
  • degree of filling from the left atrium (venous return, end-diastolic volume)
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16
Q

What is the definition of the after load?

A
  • arteriolar resistance the heart must pump against to eject stroke volume
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17
Q

What is the definition of the end diastolic volume?

A
  • this is the volume that is filling the left ventricle at the end of the diastole
  • this is used as the concrete measure of the preload
  • need to have a normal functioning contractility in order to eject the normal stroke volume from the heart
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18
Q

What happens in the frank sterling relationship when a person has mild dysfunction?

A
  • when the preload increases, you require a higher amount of pressure or preload to maintain the same stroke volume - you need to increase the preload significantly to have the same output
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19
Q

What happens in the frank sterling relationship when someone has severe dysfunction?

A

when someone has severe heart failure, you will never be able to achieve the same pressure no matter how much you increase the preload

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20
Q

What are the three general patterns of remodelling?

A
  • concentric ventricular remodelling
  • eccentric left ventricular hypertrophy
  • mixed concentric/eccentric hypertrophy
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21
Q

Sarcomeres added in parallel adds to the ___________

A

thickness of the ventricular wall

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22
Q

What is eccentric hypertrophy?

A
  • the sarcomeres here are being stretched here, the ventricles are being stretched here, ventricles are being enlarged but the wall thickness here is still unchanged
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23
Q

What does the body do to increase the preload?

A
  • the body starts to retain water and salt, and the body activates the RAAS system
  • angiotensin 2 accomplishes vasoconstriction and leads to water retention
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24
Q

What body attempts to maintain CO and BP by doing what?

A

Increasing preload
- increasing the venous retire in an attempt to increase CO
- sodium and water retention
- activation of the renin angiotensin system
Vasoconstriction
- increase after load
- increase systemic vascular resistance (sympathetic stimulation, activation of renin angiotensin system)

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25
Q

What are some of the compensatory mechanisms associated with cardiac heart failure?

A
  1. tachycardia and increased contractility
    - sympathetic stimulation
  2. neurohormonal stimulation
    - compensatory release of hormones in response to hypovolemia - renin, NE, antidiuretic hormones
    - in the long term these contribute to the progression of structural abnormalities
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26
Q

What does angiotensin 2 do?

A
  • increase protein synthesis, cardiac myocytes hypertrophy
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27
Q

What causes a hypertrophied heart?

A
  • diastolic heart failure
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28
Q

What causes a dilated heart?

A
  • systolic heart failure
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29
Q

What is heart failure with reduced ejection fraction also known as?

A
  • also known as systolic heart failure
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30
Q

What structural abnormalities are involved in heart failure with reduced ejection fraction?

A
  • low output (congestive) heart failure
  • hypo-functioning left ventricle, decreased contractility
  • ventricles enlarge (dilate as retain blood)
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31
Q

What is heart failure with preserved ejection fraction known as?

A
  • diastolic heart failure
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32
Q

What are the structural issues involved in heart failure with preserved ejection fraction?

A
  • 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 or stiff ventricle (restrictive cardiomyopathy)
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33
Q

Compensatory mechanisms eventually induce symptoms of heart failure due to what?

A
  1. vasoconstriction: leads to decreased CO
  2. increased HR: leads to increased oxygen utilization
  3. increased preload: leads peripheral and pulmonary edema
  4. decreased exercise tolerance
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34
Q

What are the main signs and symptoms associated with left sided heart failure?

A

PULMONARY CONGESTION

  • dyspnea on exertion
  • orthopnea
  • paroxysmal nocturnal dyspnea
  • pulmonary edema
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35
Q

What are the main signs and symptoms associated with right sided heart failure?

A

SYSTEMIC VENOUS CONGESTION

  • organomegaly
  • jugular venous distention
  • hepatojugular reflex
  • lower extremity peripheral edema
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36
Q

What are other non-specific findings associated with heart failure?

A
  • weakness
  • exercise intolerance
  • fatigue
  • CNS
  • cold, pale, clammy skin
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37
Q

What is class 1 heart failure?

A
  • uncompromised cardiac function

- able to perform ordinary physical activity

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38
Q

What is class 2 heart failure?

A
  • slightly compromised

- ordinary physical activity results in symptoms

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39
Q

What is class 3 heart failure?

A
  • moderately compromised

- less than ordinary physical activity results in symptoms

40
Q

What is class 4 heart failure?

A
  • severely compromised function

- symptoms may be present at rest

41
Q

What are the signs on clinical exams of heart failure?

A
  • auscultation of heart and lungs (rales of the lungs)
  • edema
  • jugular vein distention
  • hepatojugular reflux
  • dyspnea
  • chest X ray
42
Q

What are the symptoms of heart failure?

A
  • weakness, fatigue

- exercise tolerance

43
Q

What are the medical management strategies associated with heart failure?

A
  • eliminate exacerbating factors
  • control associated diseases
  • restrict activity when acute
  • sodium restricted diet
  • exercise conditioning when stabilized
  • drug therapy
44
Q

What is the purpose of diuretics in CHF?

A
  • relieve breathlessness and edema in patients with symptoms of signs of congestion
    • reduce intravascular volume, deem, preload and pulmonary congestion
  • achieve diuresis through inhibiting reabsorption of sodium in thick ascending limb and distal convoluted tubule
45
Q

What diuretic works on the thick ascending limb?

A

loop diuretics

46
Q

What diuretic works on the distal convoluted tubule?

A
  • thiazide diuretics
47
Q

In what stage of heart failure are diuretics always used?

A
  • stage 3 and 4 heart failure
48
Q

What is the dose of furosemide that should be used in those with CHF?

A
  • initiate 20-40 mg daily
  • increase the dose accordingly achieve edema free state (dry weight); once symptoms are relieved, use the lowed possible maintenance dose
  • possible diuretic resistance is severe refractory HF - sodium/water reabsorption markedly increased
49
Q

_____ diuretics are unlikely to be effective with significant renal dysfunction (eGFR <30 ml/min)

A

thiazide

50
Q

Why are loop diuretics and thiazide diuretics usually used together?

A

– loop diuretics stop the adoption of Na in the ascending loop- by having both diuretics you are blocking the reabsorption in both the ascending and the distal loop

51
Q

What is the usual dose of HCTZ?

A
  • starting dose is 25 mg, usually dose up to 100 mg/day
52
Q

What is the usual dose of metolazone?

A
  • starting dose is 2.5 mg, usual dose is 2.5-10 mg/day
53
Q

What are the adverse events associated with diuretics?

A
  • volume depletion (leads to dehydration, and reduction in BP and CO)
  • loss of K and Mg (can induce or potentiate digoxin toxicity)
  • renal impairment
54
Q

What is the biggest risk associated with diuresing too aggressively?

A

renal failure- you need to make sure that you are monitoring the creatinine clearance

55
Q

What factors determine the efficacy of the diuretics?

A
  • daily weight
  • input/output
  • jugular venous distention
  • peripheral edema
  • sitting/standing HR and BP
  • organ congestion (pulmonary rales and hepatomegaly)
56
Q

Renal function and electrolytes should be checked ______ after initiation and after dose increase

A

1-2 weeks

57
Q

What is the rationale behind using beta blockers after HF?

A
  • decreases the disease progression and all-cause mortality
  • stops activation of RAAS
  • slows remodelling of cardiac myocytes
58
Q

What is the first line therapy after heart failure?

A
  • beta blockers

- ACE inhibitors

59
Q

What is the purpose of a positive ionotrope after an MI?

A
  • it helps with the contractility of the heart
60
Q

What is the choice of beta blockers by cardiologists?

A
  • bisoprolol

- carvedilol

61
Q

When should beta blockers be initiated those with heart failure?

A
  • initiate when patients are stable and not in acute decompensated heart failure
  • need to start with a very low dose
  • increase dosage approx every 2 weeks
  • aim for the highest dose tolerated
  • avoid large dose reduction or abrupt withdrawal
  • decrease dose if on ionotropes (d/c if patents are in cardiogenic shock)
62
Q

What are the main AE associated with beta blockers?

A
  • postural hypotension
  • headache
  • dizziness
  • bradycardia
  • bronchospasm
  • fatigue
  • decreased exercise tolerance and fluid retention
  • insomnia, vivid dreams
  • sexual dysfunction
  • PAD, cold extremity
  • caution in diabetic
63
Q

What are the hemodynamic effects of ACEI?

A
  • increase CO
  • decrease preload
  • decrease systemic vascular resistance
  • decrease blood pressure
64
Q

What are the hormonal effects of ACEI? (inhibit RAAS)

A
  • decrease angiotensin II
  • decrease aldosterone
  • slow ventricular remodelling
65
Q

What are the main adverse effects associated with ACEI?

A
  • hypotension
  • renal impairment
  • hyperkalemia (concurrent use with K sparing diuretics, MRAs or K supplements, low salt substitutes with high K content)
  • cough
  • rash
  • taste alterations
  • angioedema (swelling of face, lips, tongue and larynx)
66
Q

What ACE inhibitor is the most common to cause a rash as a side effect?

A
  • captopril
67
Q

What are the factors that will determines the efficacy of an ACEI?

A
  • right and left sided symptoms
  • exercise tolerance
  • weight/fluid balance
68
Q

How often should ACEI’s be monitored?

A
  • should be monitored 1-2 weeks after dose initiation and 1-2 weeks after dose titration, then monitor every 3-4 months thereafter
69
Q

What is the rationale for using mineralocorticoid/aldosterone receptor antagonists?

A
  • aldosterone contributes to the sodium/water retention, sympathetic activation, myocardial and vascular fibrosis and other pathophysiologic effects seen in heart failure
70
Q

When are mineralocorticoid/aldosterone receptor antagonists indicated?

A
  • indicated for heart failure state 2-4 in addition to ACEI and BB
71
Q

What are examples of MRAs?

A
  • spironolactone

- eplerenone

72
Q

What are the cautions behind using MRAs?

A
  • hyperkalemia (risk increases with concurrent ACEI, renal impairment)
  • exclude patients with SCr>220 mol/L
  • caution if on digoxin (hyperkalemia will precipitate digoxin toxicity)
  • male patients uncommonly develop breast discomfort or gynecomastia - consider switching to eplorenone
73
Q

____ is the ARB shown to reduce cardiovascular mortality

A

candesartan

74
Q

____ is the ARB shown to improve hospitalization rate due to HF

A

valsartan

75
Q

Hydralazine and nitrate combination has shown to show a significant reduction in ____ and improvement in _____

A

reduction in mortality

improvement in exercise

76
Q

What combination of antihypertensives should african americans be put on?

A
  • ACEIs

- hydralazine/ISN combination

77
Q

What is the rationale for using hydralazine/nitrate combination?

A
  • vasodilation decrease cardiac work by overcoming detrimental effects of compensatory mechanisms
  • achieved through reduction of preload (nitrates) and after load (hydralazine)
78
Q

Hydralazine/nitrate combinations are generally used when a patient is unable to tolerate either _______

A

ACEI or ARB

79
Q

What do angiotensin receptor neprilysin inhibitors (ARNI) act on?

A
  • they act on RAAS and natriuretic peptides
80
Q

What is the rationale for using ARNI?

A
  • increase circulation of a-type natriuretic peptide and BNP by inhibiting neprilysin
  • ANP and BNP enhances diuresis, natriuresis, myocardial relaxation and anti-modeling
  • ANP and BNP also inhibits RAAS
  • AT1 receptor blockage by ARB reduces vasoconstriction, sodium and water retention and myocardial hypertrophy
81
Q

What is neprilysin and what does it do?

A

it is an enzyme that breaks down ANP and BNP- we are inhibiting neprilysin in the body so that we have more ANP and BNP peptides in the body
- these peptides promote diuresis and excretion of sodium- also increase the preload and the after load

82
Q

What is the starting dose of sacubitril/valsartan?

A
  • starting dose of 49/51 mg bid, target dose of 97/103 mg bid
  • – should NOT be used at the same time as an ACEI, or within 36 hours of the last dose of ACEI
83
Q

What are the clinical criteria to use an ARNI?

A
  • NYHA class 2 and 3 HF
  • reduced LVEF <40%
  • patient has at least 4 weeks of treatment with a stable dose of an ACEI or an ARB
  • in combination with a beta blocker and other recommended therapies, including an aldosterone antagonist
  • initiation and up titration should be conducted by a physician experienced with the treatment of heart failure
84
Q

What is the action of If channel inhibitors?

A
  • inhibit f channels within SA node resulting in disruption of If ion current flow, thereby prolonging diastolic depolarization and reducing heart rate
  • no effect on BP, myocardial contractility or AV conduction
85
Q

What is the action of digoxin?

A
  • increase force and velocity pf contraction through inhibition of Na-K-ATPase
  • neurohormonal modulating effects through decreased sympathetic activity with digoxin concentration <1.0 mcg/L
  • decreased AV conduction, used in AF and other atrial arrhythmias
86
Q

Digoxin is a _____ ionotrope

A

positive

87
Q

Digoxin is effective in heart failure associated with what?

A
  • heart failure associated with fast atrial rate, severe HF, S3 gallop, low EF and enlarged heart size
  • no mortality benefit
  • decreases rate of hospitalization
88
Q

What are the benefits of digoxin?

A
  • improves symptoms, exercise performance, decrease hospitalizations
  • improves quality of life
89
Q

What is the role of digoxin in HF therapy?

A
  • use in patients with persistent symptoms despite maximized use of vasodilators and diuretics
90
Q

What are the toxicity symptoms of digoxin?

A
  • noncardiac: N/V, confusion, altered colour vision, weakness, dizziness
  • cardiac: AV conduction disturbances
  • can very easily push a person into a dysarrhythmia
91
Q

What are the factors that affect digoxin activity or toxicity?

A
  • electrolyte disturbances
  • renal function- decreased elimination
  • drug interactions
    (can increase bioavailability: tetracycline, erythromycin
    can decrease bioavailability: antacids, cholestyramine
    can decrease elimination: quinidine, verapamil, amiodarone
    drugs that decrease K or Mg: diuretics)
  • elderly
  • hypothyroidism
92
Q

What is the treatment of digoxin toxicity?

A
  • withdrawal of digoxin
  • correction of electrolyte abnormalities
  • anti-arrhythmic agents
  • pacemaker
  • digoxin specific antibodies
  • oral activated charcoal
93
Q

What are the properties of hawthorn extract?

A
  • inotropic, vasodilating, lipid-lowering, antioxidant, anti-inflammatory
94
Q

What is the evidence behind using hawthorn extract for HF?

A
  • modest increase in exercise tolerance - uncontrolled trials and case series
95
Q

What is the action of coenzyme Q10?

A
  • component of the electron transport chain in the mitochondria
  • micronutrient
  • decreased levels in HF
  • small studies- mixed results
96
Q

What are some common drugs to avoid in HF?

A
  • antiarrhythmic agents (pro arrhythmia, negative ionotropic effects, increased mortality)
  • non-dihydropyridine calcium antagonists (direct negaitve ionotropic effects, contraindicated in patients with systolic chronic heart failure)
  • TCAs (pro arrhythmic potential)
  • NSAIDS (inhibit effects of diuretics and ACEI, cause salt and water retention and can worsen both cardiac and real function)
  • corticosteroids (AE on salt and water retention)
  • doxorubicin, trastuzamab (dose dependent cardiotoxicity)
97
Q

What are some ways to non-pharmacologically manage HF?

A
  • exercise
  • salt and fluid restriction
  • monitor daily morning weight
  • no more than 1 alcoholic drink per day
  • smoking cessation
  • influenza and pneumonococcal vaccination
  • aggressive risk reduction
  • patient education is key (drug adherence, fluid and salt restriction)