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BS - Cardiovascular System > Muscle Pump Failure (Heart Failure) > Flashcards

Muscle Pump Failure (Heart Failure) Flashcards

1
Q

What is the equation for cardiac output?

A

CO = heart rate x stroke volume

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2
Q

What is the equation for cardiac reserve?

A

maximal cardiac output - cardiac output at rest

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3
Q

What is preload?

A

The level of stretch that a cardiomyocyte is exposed to before ventricular ejection

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4
Q

What is preload equivalent to?

A

left ventricular end-diastolic volume

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5
Q

What is left ventricular end-diastolic volume?

A

The volume within the ventricle at the end of diastole, just before it contracts

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6
Q

What is afterload?

A

The pressure against which the heart is contracting when it ejects blood

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7
Q

During which conditions is afterload increased?

A
  1. hypertension

2. increased peripheral vasoconstriction

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8
Q

In cardiac muscle, how does sarcomere length affect tension?

A

small increases in sarcomere length cause a rapid increase in tension

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9
Q

Using the Frank-Starling curve, what happens when a physiological limit is reached?

A

There is a decompensation which leads to a sudden and rapid decrease in tension

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10
Q

What is described by the Bowditch phenomenon?

A

As the heart rate increases, cardiac output increases

Increasing heart rate to an extreme can lead to a reduction in cardiac performance

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11
Q

What is on the x and y axis of the Bowditch curve?

A

Cardiac performance - y

Heart rate - x

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12
Q

What is described by the Anrep effect?

A

Increasing the afterload, through increasing systemic vascular resistance, increases cardiac performance up until a limit

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13
Q

What is on the x and y axis of the Anrep curve?

A

cardiac performance - y

afterload - x

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14
Q

what is the consequence of reducing cardiac output?

A

reduced organ perfusion

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15
Q

What is the role of the baroreceptor reflex?

A

It is an autonomic reflex that helps to detect changes in pressure of the blood

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16
Q

What do baroreceptors detect?

A

Arterial stretch

This determines whether the blood pressure is high or low

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17
Q

What does the afferent end of the baroreceptor end in?

A

The nucleus tractus solitarius and rostral ventrolateral medulla

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18
Q

How do the baroreceptors augment vagal tone?

What is the result of this?

A

They activate the vagus nerve which:

  1. reduces the heart rate
  2. reduces stroke volume
  3. causes vasodilation
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19
Q

What is the baroreceptor reflex pathway when blood pressure is too high?

A
  1. The parasympathetic NS innervates the SAN and AVN via the vagus nerve
  2. This decreases the heart rate
  3. This leads to reduced cardiac output
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20
Q

What is the baroreceptor reflex pathway when blood pressure is too low?

How does it affect the heart?

A
  1. The sympathetic NS innervated the SAN, AVN, conducting tissue and myocytes of the atria and ventricles
  2. This increases heart rate and contractility
  3. This increases cardiac output
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21
Q

How does the sympathetic nervous system in the baroreceptor reflex affect the blood vessels?

A

It causes constriction of blood vessels

This increases systemic vascular resistance

This acts to increase blood pressure

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22
Q

What happens when blood pressure is too high?

A
  1. baroreceptors detect increased arterial stretch

2. they activate the parasympathetic nervous system to increase vagal tone

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23
Q

What happens when vagal tone is increased?

A

The heart rate is lowered and cardiac output is reduced

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24
Q

What is the result of increasing systemic vascular resistance?

A

It leads to an increase in afterload

This causes a temporary increase in cardiac output

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25
Q

What does the juxtoglomerular apparatus detect?

A
  1. renal perfusion pressure at the glomerulus

2. sodium concentration in the fluid surrounding the distal convoluted tubule

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26
Q

What is the role of the juxtoglomerular apparatus?

A

If either renal perfusion or sodium concentration is reduced, it releases renin

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27
Q

What is the process in the kidney that occurs in order for renin to be produced?

A

Inactive prorenin is converted to renin and active prorenin

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28
Q

Where is angiotensinogen released from?

A

The liver

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29
Q

How does angiotensinogen interact with renin?

A

It is cleaved by renin to form angiotensin I

This is inactive

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30
Q

what is the main role of angiotensin converting enzyme (ACE)?

Where is it released from?

A

The lungs release ACE

It converts angiotensin I to active angiotensin II

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31
Q

What is the secondary role of angiotensin converting enzyme (ACE)?

A

It breaks down bradykinin (vasodilator)

This prevents vasodilation

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32
Q

What are the actions and effects of angiotensin II?

A
  1. increases water retention
  2. increases sodium reabsorption
  3. causes vasoconstriction

These act to increase systemic vascular resistance

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33
Q

What group of chemicals does angiotensin II cause the release of?

A

Catecholamines

These increase cardiac output and systemic vascular resistance

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34
Q

What main chemical does angiotensin II cause the release of, and what is the consequence?

A

Aldosterone release from adrenal glands

It increases plasma volume, which increases preload and consequently cardiac output

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35
Q

What is aldosterone and where is it released from?

A

A mineralocorticoid

It is released from the zona glomerulosa in the adrenal cortex

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36
Q

Where does aldosterone act on?

Why is it released?

A

Released in response to angiotensin II

It has effects on the distal convoluted tubule and collecting duct

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37
Q

What is meant by aldosterone being ‘internalised’?

A

It binds to an intracellular aldosterone receptor

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38
Q

What is the main consequence of aldosterone binding to an aldosterone receptor?

A

It increases transcription of the gene for epithelial sodium ion channels

This leads to increased sodium, and consequently water, reabsorption

39
Q

What are the other consequences of aldosterone binding to the aldosterone receptor?

A
  1. excretion of potassium ions

2. increases the amount of angiotensin II receptors

40
Q

What are the 2 types of myocardial dysfunction?

A

Systolic or diastolic

41
Q

What is systolic dysfunction (heart failure)

A

There is a reduction/dysfunction in how the heart contracts

42
Q

What is ejection fraction like in systolic heart failure?

A

There is a reduced ejection fraction of 25%

The amount of blood pumped around the body with each systolic impulse is reduced

43
Q

How is preload affected in systolic heart failure?

A

Over time, the preload increases

This increases the extent to which the left ventricle is stretched

44
Q

How is the left ventricle affected by systolic heart failure?

What is the long-term consequence of this?

A

The increased preload leads to thinning of the ventricle walls over time

The ventricle cannot pump blood with enough force to push it throughout the body

45
Q

What is involved in diastolic dysfunction (heart failure)?

A

There is a reduction/dysfunction in how the heart relaxes

This is due to the left ventricle being stiffer than normal

46
Q

What is ejection fraction like in diastolic dysfunction?

A

It is normal - over 55%

47
Q

What does a reduction in relaxation of the heart lead to?

A

Although ejection fraction is the same, there is less blood filling the LV

Less blood is being ejected

48
Q

What is the usual cause of diastolic dysfunction?

A

Left ventricular hypertrophy

49
Q

What are the 3 main consequences of a failed ejection fraction?

A
  1. reduced cardiac output leads to a reduction in systolic blood pressure
  2. reduced arterial stretch
    (activation of baroreceptors)
  3. reduced renal perfusion
    (activation of the RAAS)
50
Q

what is the consequence of myocardial infarction?

A

There is a reduction in systolic function as part of the heart dies and can no longer pump blood

51
Q

What happens in an anterolateral infarct?

A

The anterior wall of the LV is completely blocked off

This leads to death of heart muscle in the left ventricle

52
Q

What happens in a posteroinferior infarct?

A

There is death of a small portion of the right ventricle

53
Q

What are the 4 main risk factors for myocardial infarction?

A
  1. excessive alcohol consumption
  2. idiopathic cardiomyopathy due to genetic disorder
  3. viral cardiomyopathy
  4. tachycardic cardiomyopathy
54
Q

What is the initial reaction to a reduction in cardiac output?

A

Activation of the renin-angiotensin-aldosterone system and baroreceptors

55
Q

What is the response of the RAAS to a decreased cardiac output?

A

Increase in plasma volume

This increases preload, which lengthens the sarcomeres

56
Q

How does a raised preload affect the LV and stroke volume?

A

End-diastolic pressure is raised in the LV

This leads to an increase in cardiac output, which also augments stroke volume

57
Q

what is the name for the action of the RAAS increasing the cardiac output?

What is the problem with this?

A

This is compensation

It can work for a while, but is not maintained for very long

58
Q

What process happens as a result of the compensation effects not being able to be maintained?

A

Decompensation

59
Q

What process precedes decompensation?

A

The left ventricle stretch exceeds physiological levels

60
Q

What happens to sarcomere tension during decompensation?

A
  1. sarcomeres stretched beyond their physiological barrier
  2. this leads to movement to the descending limb of the sarcomere tension curve
  3. there is a sudden drop off in sarcomere tension
61
Q

How can small rises in preload affect sarcomere tension in decompensation?

A

Small rises in preload cause large drops in sarcomere tension

This affects LV contractility and stroke volume

62
Q

what is the result of large drops in sarcomere tension?

A

Reduced cardiac output

This has further effects on the autonomic nervous system and RAAS

63
Q

What curve can be used to describe how decompensation leads to reduced cardiac output?

A

Bowditch effect

cardiac output - y - heart rate - x

64
Q

In heart failure, what does back pressure in the left ventricle cause?

A

Raised pressure in the pulmonary circulation

65
Q

What is the consequence to the lungs of heart failure?

Why does it happen?

A

Increased hydrostatic pressure in PC forces fluid outside of the vascular compartment

The interstitial space in the lungs fills with fluid

This leads to pulmonary oedema and/or pleural effusion

66
Q

What signs of heart failure are exhibited by the patient?

A

They become breathless and their oxygen saturation drops

67
Q

What is meant by orthopnoea?

Why does it occur?

A

How lying flat worsens the symptoms in the patient

Lying flat causes fluid to enter a large proportion of the lungs

68
Q

What are the first steps leading to heart failure affecting the right ventricle?

A
  1. Back pressure in the lungs goes back on the RV
  2. The back pressure is transmitted to the venae cavae
  3. The pressure in the internal jugular vein rises
69
Q

what can usually be detected as a result of raised pressure in the internal jugular vein?

A

Jugular venous pulse is raised

Pulsing in the neck can often be detected

70
Q

What causes peripheral oedema in heart failure?

A

Gravity and raised orthostatic pressures will force fluid from vascular compartments to the peripheral tissues

71
Q

What does peripheral oedema in heart failure often occur alongside of?

A
  1. swelling of the ankles/sacrum

2. hepatomegaly/ascites

72
Q

What are the acute therapy options for heart failure?

A
  1. oxygen therapy
  2. non-invasive ventilation
  3. invasive ventilation
73
Q

Why is oxygen given to heart failure patients?

Why is it often not sufficient as a standalone treatment?

A

To optimise alveolar ventilation

Often there is a need to increase the pressure in the airways to oxygenate blood

74
Q

What is non-invasive ventilation?

What is the most common type of way to use this treatment?

A

Oxygen masks e.g. CPAP

This involves constant pressure through the mask that forces oxygen into the lungs and forces fluid out of the alveoli

75
Q

What does morphine do to help treat heart failure?

A

It causes pulmonary vasodilation

This relaxes the pulmonary vessels and reduces the pressure within them

It also helps with breathing and pain

76
Q

What is the consequence to the heart of taking morphine?

A

It helps to reduce the preload

It takes the strain off the left ventricle

77
Q

What are diuretics used for in treating heart failure?

A

They limit the reabsorption of fluid

78
Q

What is the consequence to the heart of taking diuretics?

A

Reduced plasma volume works to decrease the preload

This offloads the ventricles and maximises left ventricular contractility

79
Q

What are the side effects of taking diuretics?

A
  1. renal dysfunction
  2. reduction in Na+, K+ and Mg2+ levels
  3. Thiazides can induce diabetes
80
Q

what are beta receptors involved in?

A

Myocardial and renal responses to reduced cardiac output

81
Q

How do beta blockers affect the heart?

A

Blocking the beta receptors reduces heart rate

Reducing the heart rate gives more time for the LV to relax

This gives it more time to fill with blood, improving stroke volume

82
Q

How do beta blockers affect the kidneys?

A

They prevent RAAS overactivation which prevents fluid retention

It also causes bradykinin accumulation, which causes dry coughs

83
Q

Which types of patients should not receive beta blockers?

A
  1. asthma patients
  2. patients with heart blocks
  3. patients with low heart rate
84
Q

What is the role of spironolactone/eplerenone?

A

They block aldosterone as they are mineralocorticoid receptor antagonists

85
Q

Why are spironolactone/eplerenone known as ‘potassium sparing diuretics’?

A

Too much aldosterone causes excessive loss of potassium

86
Q

Why are potassium sparing diuretics often used alongside furosemide?

A

They prevent furosemide from getting rid of too much potassium

87
Q

what is the role of ACE inhibitors?

A

They block the conversion of angiotensin I to angiotensin II

This reduces the effects of angiotensin II on vasculature

88
Q

What are the effects of ACE inhibitors?

A
  1. diminish release of aldosterone

2. cause bradykinin accumulation (dry cough)

89
Q

What type of patients are given Ivabradine?

A

Asthma patients

90
Q

How does Ivabradine work?

A

It acts on funny ion channels in the SA node to reduce the heart rate

91
Q

When is Digoxin used to reduce the heart rate?

A

In elderly patients with low blood pressure

or

In patients with atrial fibrillation

92
Q

What is valsartan?

A

Angiotensin II receptor blocker

93
Q

What is sacubitril?

A

A neprilysin inhibitor

It enhances the action of natriuretic peptides, which promote sodium and water excretion

94
Q

What 2 drugs used in combination are more effective than ACEi/ARBs?

A

Sacubitril and valsartan

BS - Cardiovascular System (20 decks)

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