Chronic Heart Failure Flashcards

1
Q

What is the definition of heart failure?

A

Cardiac output is inadequate for the body’s requirements.

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2
Q

Why is mild myocardial dysfunction not associated with decreased cardiac ouput?

A

CO is maintained by an increase in venous pressure (and hence diastolic volume)

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3
Q

What is systolic heart failure?

A

Inability of the ventricle to contract normally, resulting in decreased CO. The ejection fraction is < 40%

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4
Q

What is the ejection fraction in systolic HF?

A

<40%

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5
Q

What are causes of systolic HF?

A
  • IHD
  • MI
  • Cardiomyopathy
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6
Q

What is diastolic HF?

A

Inability of the ventricle to relax and fill normally, causing increased filling pressures. EF >50%

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7
Q

What can cause diastolic HF?

A
  • Constrictive pericarditis
  • Tamponade
  • Restrictive cardiomyopathy
  • HTN
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8
Q

What is important to note about systolic and diastolic HF?

A

They often co-exist

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9
Q

What is acute HF?

A

Term used to mean new onset acute or decompensation of chronic heart failure characterised by pulmonary oedema +/- peripheral oedema with or without signs of peripheral hypoperfusion

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10
Q

What is chronic HF?

A

HF that develops or progresses slowly. Venous congestion is common but arterial pressure is well maintained until late

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11
Q

What is low-output HF?

A

Cardiac output is decreased and fails to increase normally with exercise

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12
Q

What are causes of low-output HF?

A
  • Pump failure
  • Excessive preload
  • Chronic excessive afterload
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13
Q

What causes of pump failure can cause low-output HF?

A
  • Systolic +/- diastolic HF
  • Decreased HR - B-blockers, heart block, post MI
  • Negatively inotropic drugs
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14
Q

What are causes of excessive preload in low-output HF?

A
  • Mitral regurgitation
  • Fluid overload/retention
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15
Q

What are causes of chronic excessive afterload in low-output HF?

A
  • Aortic stenosis
  • Hypertension
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16
Q

What is high output HF?

A

Output is normal or increased in the face of greatly increased metabolic demand or shunting of blood which increases myocardial demand.

Cardiac failure occurs when CO fails to meet these increased needs. It will occur with a normal heart, but even earlier if there is heart disease

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17
Q

What are causes of high output cardiac failure?

A
  • Anaemia
  • Pregnancy
  • Hyperthyroidism
  • Paget’s disease
  • AV malformation
  • Beri Beri
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18
Q

What are features of RHF?

A
  • Peripheral oedema
  • Ascites
  • Nausea
  • Anorexia
  • Facial engorgement
  • Pulsation in the neck
  • Epistaxis
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19
Q

What are features of LHF?

A
  • Dyspnoea
  • Poor exercise tolerance
  • Fatigue
  • Orthopnoea
  • PND
  • Nocturnal cough +/- pink frothy sputum
  • Wheeze
  • Nocturia
  • Cold peripheries
  • Weight loss/Muscle wasting
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20
Q

How is CO maintained in mild/moderate myocardial dysfunction?

A

Increased venous return plus sinus tachycardia - this is in the context of decreased ejection fraction. In more severe cardiac dysfunction, CO is maintained by more marked venous return and tachycardia

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21
Q

What does increased venous pressure cause both at organ and system level?

A
  • Pulmonary oedema
  • Hepatic enlargement/congestion
  • Ascites
  • Peripheral oedema
  • Increased JVP
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22
Q

What pathophysiological changes occur in HF?

A
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23
Q

Why does salt and water retention occur in cardiac failure?

A

Increased venous pressure occurs when the ventricles fail. Reduced cardiac output also leads to diminished renal perfusion, activating RAAS, which promotes salt and water retention, which further increases venous pressure. Afterload is also increased by a combination of RAAS activity and Adrenergic activation

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24
Q

What is atrial natriuretic peptide released in response to?

A

Atrial stretching

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25
Q

What is the action of ANP?

A
  • Diuresis
  • Natriuresis
  • Vasodilatation
  • Suppression of RAAS
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26
Q

What is brain natriuretic peptide?

A

NP predominantly secreted by the ventricles, and has an action similar to that of ANP but greater diagnostic and prognostic value

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27
Q

What is the difference in ejection fraction between systolic and diastolic HF?

A
  • Systolic <40%
  • Diastolic >50%
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28
Q

What are the main symptoms of HF?

A
  • Exertional dyspnoea
  • Orthopnoea
  • Paroxysmal nocturnal dyspnoea
  • Fatigue
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29
Q

What are signs of heart failure?

A
  • Cardiomegaly
  • Third and fourth heart sounds
  • Elevated JVP/hepatojugular reflux
  • Tachycardia
  • Hypotension
  • Bi-basal crackles
  • Cool peripheries
  • Narrow pulse pressure
  • Pulsus alternans
  • Pleural effusion
  • Peripheral ankle oedema
  • Ascites
  • Tender hepatomegaly
  • Wheeze
  • Murmurs
  • Cyanosis
  • Weight loss
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30
Q

Why would you get cardiomegaly on CXR in heart failure?

A

Dilation of the heart atria and ventricles

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31
Q

Why would you get an S3 heart sound in HF?

A

In heart failure with systolic dysfunction there is elevated atrial pressure. When the mitral valve opens there is rapid filling down the pressure gradient into the stiffened dysfunctional ventricle.

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32
Q

Why would you get an S4 heart sound in HF?

A

Forceful contraction of the atrium pushes blood into a non-compliant left ventricle. The sudden deceleration of blood against the stiff ventricular wall produces a low-frequency vibration, recognised as the fourth heart sound.

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33
Q

Why would you get an elevated JVP in HF?

A

Peripheral veins are abnormally constricted - due to increased tissue oedema and sympathetic stimulation, which increases the blood volume in the central venous system

Volume overload – leads to increased ventricular end-systolic/diastolic volume and pressure, which in turn backs up into the jugular veins

Right ventricular systolic failure – leads to increased end-systolic pressure, which is transmitted back into the venous system

Right ventricular diastolic failure - increased stiffness causes pressure to ‘back-up’ into the venous system

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34
Q

What are causes of a raised JVP?

A
  • PE, Pericardial effusion, PS, PHT
  • Quantity overload - RVF
  • SVC obstruction
  • Tamponade, TR
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35
Q

Why would you get tachycardia in HF?

A

This is the body’s attempt at maintianing cardiac output as stroke volume decreases with progressively failing myocardium

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36
Q

What causes Bi-basal crackles in HF?

A

Pulmonary oedema - In left heart failure, raised left ventricular and atrial pressures back up into the lung vasculature. When pulmonary vasculature pressure increases above 19mm Hg, a transudate of fluid enters the lung interstitium and alveoli. The alveoli are filled with fluid and collapse. When the patient breathes in, the alveoli are filled with air and ‘pop’ open, causing inspiratory crackles.

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37
Q

Why would you get cool peripheries in HF?

A

Decreased cardiac output leads to vasoconstriction (to maintain blood pressure and venous return), which decreases blood flow to peripheral areas

38
Q

Why would you get narrow pulse pressures in HF?

A

Low SV leads to more sympathetic outflow and higher/maintained systemic vascular resistance in order to preserve blood pressure and assist venous return to the heart. Therefore, systolic blood pressure is lowered and diastolic blood pressure is maintained, creating a narrow pulse pressure.

39
Q

What is pulsus alternans?

A

A regular pulse that has alternating strong and weak beats. This can be identified at the bedside but can also be seen on arterial waveform at cardiac catheterisation as seen in

40
Q

Why would you get pleural effusions in HF?

A

Increased pulmonary capillary pressure - transudative

41
Q

What are signs of pleural effusion?

A
  • Asymmetrical chest expansion
  • Bronchial breathing above effusion level
  • Reduced/diminished breath sounds over effusion
  • Dull percussion
  • Decreased tactile vocal fremitus
  • Decreased vocal resonance
42
Q

Why can individuals with HF get peripheral oedema?

A

Increased venous hydrostatic pressure causes a transudative process in which fluid is ‘pushed out’ of vessels into the interstitium.

Factors contributing to this include:

  • Increased plasma volume
  • Raised venous pressure

It is normally seen in the context of right heart failure.

43
Q

What could the following be in the contrext of HF?

A

Peripheral oedema

44
Q

What does pitting oedema indicate?

A

Water retention

45
Q

What are causes of non-pitting oedema?

A
  • Lymphoedema
  • Myxoedema
46
Q

Why might you get hepatomegaly in HF?

A

In congestive heart failure pressure backs up into the venous system due to ineffective filling or forward outflow, leading to a congested and engorged liver.

47
Q

What is the mechanism behind ascites development in HF?

A

Reduced effective arterial volumes, leading to activation of the RAAS and salt and fluid retention (underfill theory)

48
Q

What could the following be in the context of HF?

A

Ascites

49
Q

Why might someone have hepatoguluar reflux in HF?

A

Putting pressure on the right upper quadrant assists in venous return to the right side of the heart via the inferior vena cava. This increased return cannot be dealt with by the dysfunctional right heart, so the force is the transmitted into the rest of the venous system, resulting in increaed JVP on pressure. This is exacerbated by raised venous tone.

50
Q

Why might you get wheezing in HF?

A

Oedema of the bronchial walls can lead to small airways obstruction and produce wheezing

51
Q

What is the mechanism behind peripheral cyanosis in HF?

A

Peripheral cyanosis is caused by the slowing of blood flow and increased oxygen extraction in the extremities.

When cold, peripheral vasoconstriction occurs to maintain warmth. This reduces blood flow to the periphery and effectively more time for oxygen to be taken out of the blood – hence more deoxygenated blood is present.

In CHF, decreased cardiac output leads to vasoconstriction (to maintain blood pressure and venous return), which decreases blood flow to peripheral areas.

52
Q

Why does malabsorption occur in CHF?

A

Gut wall oedema in CHF reduces absorption of nutrients and may alter permeability, allowing endotoxins to enter the circulation and further stimulate the immune system

53
Q

Why does weight loss occur in CHF?

A
  • Neuroendocrine abnormalities
  • Immune system activation
  • Malabsorption
  • Cellular hypoxia
54
Q

Why does orthopnoea occur in HF?

A

The current accepted hypothesis for the triggering of orthopnoea is the redistribution of fluid from the splanchnic circulation and lower extremities into the central circulation which occurs while lying flat

55
Q

What causes paroxysmal noctural dyspnoea in heart failure?

A

Occurs due to a combination of:

  • Increased venous return
  • Reduced adrenergic support of ventricular function – inability of the left ventricle to cope with the increased venous return. This leads to pulmonary congestion, oedema and increased airways resistance
  • Normal nocturnal depression of the respiratory centre
  • Increased pressure in the bronchial arteries - leading to airway compression

These factors cause decreased lung compliance, increased work of breathing and prompting of the pulmonary or chest wall receptors, which activate brainstem stimulation and arousal from sleep.

Alternatively, V/Q mismatch occurs causing a transient hypoxaemia that stimulates the brain to waken to correct the imbalance.

56
Q

If someone with heart failure had Kussmaul’s sign, what would this indicate?

A

Severe heart failure

57
Q

If you suspected heart failure, what investigations might you do?

A

Intial basic tests

  • Bedside - Urinalysis
  • Bloods - FBC, U+E’s, eGFR, TFTs, LFTs, fasting lipids, fasting glucose
  • CXR
  • ECG

Diagnosis

  • Bloods - BNP
  • ECHO - within 2 weeks with specialist review
  • Consider Peak Flow/spirometry - if HF not diagnosis

http://www.sign.ac.uk/assets/sign147.pdf

58
Q

Why would you look at BNP in someone with suspected HF?

A

Often elevated in heart failure, therefore low levels effectively excludes HF

59
Q

What might you see on CXR in someone with HF?

A
  • Alveolar oedema - Bat wings
  • Kerley B lines (interstitial oedema)
  • Cardiomegaly
  • Dilated upper lobe vessels
  • Pleural Effusion
60
Q

What is the classification system used for classifying heart failure?

A

New York Heart association Heart failure classification

61
Q

What is class I heart failure as per NYHA heart failure classification system?

A

No limitation - normal physical exercise that does not cause fatigue, dyspnoea or palpitations

62
Q

What is class II heart failure as per NYHA heart failure classification system?

A

Mild limitation - comfortable at rest, but normal physical exercise produces fatigue, dyspnoea or palpitations

63
Q

What is class III heart failure as per NYHA heart failure classification system?

A

Marked limitation - comfortable at rest, but mild physical produces signs of heart failure

64
Q

What is Class IV heart failure as per the NYHA heart failure classification system?

A

Symptoms occur at rest and exacerbated by any activity

65
Q

What are other causes of raised BNP, besides HF?

A
  • Left ventricular hypertrophy
  • Ischaemia
  • Tachycardia
  • Right ventricular overload
  • Hypoxaemia [including pulmonary embolism]
  • Renal dysfunction [GFR <60 ml/minute]
  • Sepsis
  • Chronic obstructive pulmonary disease
  • Diabetes
  • Age >70 years
  • Cirrhosis
66
Q

If ECG and BNP testing were normal, what would this indicate?

A

Heart failure unlikely

67
Q

If either ECG, BNP, or CXR were abnormal, what would this indicate?

A

Heart failure possible - Proceed to TTE

68
Q

What might ECG show when investigating heart failure?

A

A cause

  • MI
  • Ischaemia
  • Ventricular hypertrophy
69
Q

What things can you assess using echocardiography?

A
  • Cardiac chamber dimension
  • Systolic and diastolic function
  • Regional wall motion abnormalities
  • Valvular heart disease
  • Cardiomyopathies
70
Q

What are the different aspects to management of chronic HF?

A
  • Lifestyle advice
  • Medications
71
Q

What lifestyle advice would you give someone with Chronic HF?

A
  • Exercise
  • Education
  • Weight reduction/control
  • Smoking cessation
  • Vaccination
  • Driving
  • Reduce salt intake
72
Q

What vehicles does symptomatic HF disqualify drivers from driving?

A

Lorries and buses

73
Q

What medications are used in the treatment of Chronic HF?

A
  • Diuretics
  • ACE-i/ARBs
  • B-blockers
  • Spironolactone
  • Digoxin
  • Vasodilators
74
Q

What is the purpose of using diuretics in HF?

A

Used for the relief of congestive symptoms and fluid retention in patients with heart failure

75
Q

What are side effects of Diuretics?

A
  • Severe hypokalaemia/calcaemia/natraemia/magnesaemia
  • Dehydration
  • Hyperglycaemia
  • Deafness
  • Gout
  • Renal impairment
76
Q

What would you add to treatment if using diuretics was causing hypokalaemia?

A

Spironolactone

77
Q

How would you treat someone with chronic HF with preserved ejection fraction?

A

Low to medium dose of loop diuretics (for example, less than 80 mg furosemide per day).

Patients who do not respond to this treatment will require further specialist advice.

https://pathways.nice.org.uk/pathways/chronic-heart-failure#path=view%3A/pathways/chronic-heart-failure/managing-chronic-heart-failure.xml&content=view-node%3Anodes-heart-failure-with-preserved-ejection-fraction

79
Q

If someone with left ventricular systolic dysfunction was still symptomatic after initiation of ACE-i and beta blockers, what would be the second line treatment?

A

Refer to specialist, who will consider the following

  • Spironolactone
  • ARB licensed for heart failure
  • Hydralazine in combination with isosorbide dinitrate
80
Q

When is digoxin indicated for use in chronic left-ventricular systolic HF?

81
Q

What therapy should be added to standard therapy in black patients with chronic HF?

A

Hydralazine with isosorbide dinitrate?

82
Q

What would you start someone on if they had already been started on diuretics and ACE-i?

A

B-blockers

83
Q

How would you monitor heart failure treatment?

A
  • Symptomatic relief - SOB, Tiredness, Lethargy
  • Clinical relief - Peripheral Oedema, Ascites, Weight
  • Monitor Weight regularly
  • Increase medication according to symptoms or weight
  • Patient education
84
Q

What does the combination of hydralazine and nitrates do to preload and afterload?

A

Reduces both

85
Q

When are IV inotropes used?

A

Patients in extremis - with chronic heart failure who are not responding to oral medication

86
Q

What factors contribute to the sensation of dyspnoea in someone with heart failure?

A

Interstitial oedema stimulating pulmonary receptors (C-fibres), or hypoxaemia. The first cause (interstitial oedema) is the main mechanism. Interstitial fluid decreases lung compliance (which is picked up by pulmonary C-fibres) and increases the work of breathing.

87
Q

What is the mechanism behind pulsus alternans?

A

Frank–Starling theory – in left ventricular dysfunction there is a decrease in cardiac output that causes a raised end-diastolic volume. This raised volume allows for greater myocardial stretch and, via the Frank–Starling mechanism, causes the next contraction to be more forceful (the strong beat). After the strong beat, the end-diastolic volume is smaller and hence the next beat is weaker.

88
Q

What is pulsus alternans indicative of?

A

Advanced left ventricular failure

89
Q

What are causes of a fourth heart sound?

A
  • Heart Failure
  • Myocardial infarction
  • Cardiomyopathy
  • Hypertension (pressure overload)
90
Q

What are causes of a pathological third heart sound?

A
  • Heart failure
  • MI
  • Cardiomyopathy
  • Hypertension
  • Mitral + Aortic regurgitation (volume overload)
  • Constrictive pericarditis
91
Q

What is the difference between 3rd and 4th heart sounds in terms of sound?

A
  • 3rd heart sound - sound is lub…. de dub; extra sound immediately follows S2, like a horse galloping
  • 4th heart sound - sound is le lub… dub; extra sound immediately preceeds S1.
92
Q

When can a third heart sound be classed as physiologically normal?

A

In children and young adults up to the age of 30