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ESA 2 - CVS > 28th March 2019 - Session Synopsis > Flashcards

28th March 2019 - Session Synopsis Flashcards

1
Q

What can chest pain be a result of?

A

Chest pain can be as a result of a number of cardiac and non-cardiac causes.

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2
Q

What may be required to determine the origin of chest pain?

A

Patient history, physical examination and investigations may be required to determine the origin of the pain.

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3
Q

What is crucial in ruling in or out certain causes of chest pain?

A

History-taking is crucial to ruling in or out certain causes.

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4
Q

What symptom do you need to investigate to make your differential diagnosis?

A

In this lecture you will look at the types of information regarding the pain that you need to find out to help you in narrowing down the causes.

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5
Q

What causes of chest pain will be considered?

A

The cardiac causes of chest pain that will be considered are pericarditis, myocardial ischaemia and myocardial infarction.

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6
Q

What is pericarditis, and what sort of pain is felt?

A

Pericarditis (inflammation of the pericardial sac) causes a pain that is usually sharp in nature, well-localised and worsens with movements such as coughing and lying flat.

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7
Q

What is the pericardium innervated by and what type of pain is experienced?

A

The pericardium is innervated by the phrenic nerve and the type of pain experienced is somatic pain.

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8
Q

How does pericarditis appear on an ECG?

A

In pericarditis there may be widespread ST elevation in all leads.

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9
Q

What pain is felt with ischaemia due to coronary artery disease?

A

Ischaemia due to coronary artery disease causes chest pain that is usually central but less well localised and may radiate to arms, neck or jaw.

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10
Q

What senses cardiac ischaemia?

A

Visceral afferent fibres of the heart respond to ischaemia.

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11
Q

Where do the visceral afferent fibres of the heart travel?

A

These fibres travel to the spinal cord with autonomic nerves.

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12
Q

What causes less well localised pain in cardiac ischaemia?

A

There is a mixing of visceral afferents in the spinal cord resulting in less well localised pain.

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13
Q

What causes coronary artery disease?

A

Coronary artery disease is due to the formation of atheromatous plaques in the coronary arteries.

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14
Q

What do atheromatous plaques in the coronary arteries do?

A

This causes narrowing of the arteries.

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15
Q

How are atheromatous plaques formed and what are the risk factors?

A

You should review the formation of atheromatous plaques and the risk factors in your Pathological Processes Unit (session 6).

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16
Q

What is stable angina?

A

Stable Angina is ischaemic pain which is experienced during exertion and resolves with rest.

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17
Q

What is the pathophysiology behind stable angina?

A

It occurs when the metabolic demands of the cardiac tissue exceeds the delivery of oxygen by the coronary arteries.

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18
Q

Explain what happens if a coronary artery is narrowed by 50%.

A

If stenosis narrows a coronary artery by 60% or less, this does not usually alter maximal blood flow to the region of heart supplied.

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19
Q

What happens if a coronary artery is narrowed by 70%?

A

With narrowing of around 70% blood flow at rest will be sufficient but maximal blood flow when demand is increased will be impaired.

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20
Q

What happens if a coronary artery is narrowed by 95%?

A

If narrowing exceeds around 90%, then blood flow at rest will be compromised.

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21
Q

What is ACS?

A

Acute coronary syndrome refers to a spectrum of acute ischaemic events from unstable angina through to non-ST elevated myocardial infarction and ST-elevated myocardial infarction.

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22
Q

What causes ACS?

A

In each case the acute event is caused by rupture of an atheromatous plaque and thrombus formation.

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23
Q

What pain is felt with unstable angina and does cell death occur?

A

In the case of unstable angina the pain occurs at rest, is of limited duration (but may last longer and be more intense than stable angina) and the duration of the ischaemia is not sufficient to cause cell death.

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24
Q

What causes both NSTEMI and STEMI?

A

Non ST-elevated myocardial infarction (NSTEMI) and ST-elevated myocardial infarction (STEMI) are again as a result of plaque rupture and thrombus formation.

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25
Q

What happens to the myocardium in both an NSTEMI and STEMI?

A

In these cases the blockage caused by the thrombus is sufficient to cause cell death in a region of myocardium.

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26
Q

How can myocardial cell death be detected?

A

Myocardial cell death can be detected from analysis of a blood sample for the cardiac isoforms of troponin-I (cTnI) or troponin -T (cTnT).

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27
Q

What do we measure cTnI or cTnT for?

A

These highly sensitive assays are useful diagnostic evidence of injury to cardiac myocytes.

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28
Q

What is a disadvantage to using troponin to measure myocardial infarction?

A

However you should be aware that troponins can be raised in conditions other than myocardial infarction.

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29
Q

How are both NSTEMI and STEMI distinguished?

A

NSTEMI and STEMI are distinguished by the ACUTE changes seen on the ECG recording.

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30
Q

How does an NSTEMI appear on an ECG?

A

NSTEMI is likely to show ST segment depression and / or T wave inversion in leads viewing that affected area.

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31
Q

How does a STEMI appear on an ECG?

A

STEMI shows elevation of the ST segment in leads viewing the affected area.

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32
Q

Why do NSTEMI and STEMI show different ECG changes?

A

ST elevation occurs when the full thickness of the myocardial wall is affected, whereas an NSTEMI is due to damage limited to the sub-endocardial tissue.

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33
Q

What are the ECG changes seen in

  • pericarditis
  • NSTEMI
  • STEMI
A

You should refer back to your lecture on the ECG in week 7.

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34
Q

Why is time important in a STEMI?

A

The ECG changes during a STEMI evolve with time.

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35
Q

What happens to the ECG of a STEMI with time?

A

It is important that you are aware of the acute changes and the development of Q waves over time.

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36
Q

Describe the ECG changes in a STEMI.

A

The diagram below is from your recommended text book, Pathophysiology of Heart Disease by Leonard S Lilly.

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37
Q

Draw a normal ECG trace.

A

Normal

38
Q

Draw an acute STEMI ECG trace.

A

Acute

- ST elevation

39
Q

Draw how a STEMI appears on an ECG trace hours after.

A

Hours

  • ST elevation
  • ↓ R wave
  • Q wave begins
40
Q

Draw how a STEMI appears 1 or 2 days after it occurs.

A

Day 1-2

  • T wave inversion
  • Q wave deeper
41
Q

Draw how a STEMI appears on an ECG trace days later.

A

Days later

  • ST normalises
  • T wave inverted
42
Q

Draw how a STEMI appears on an ECG trace weeks later.

A

Weeks later

  • ST & T normal
  • Q wave persists
43
Q

Define heart failure.

A

Heart failure can be defined as a state ‘in which the heart fails to maintain an adequate circulation for the needs of the body despite an adequate filling pressure’.

44
Q

What causes heart failure?

A

Heart failure can be due to an inability of the heart muscle to contract properly or due to an inability of the heart to fill properly.

45
Q

What must you understand to understand heart failure?

A

A term which you must understand to help you understand heart failure is the EJECTION FRACTION.

46
Q

How is ejection fraction measured?

A

Ejection fraction would normally be measured using echocardiography.

47
Q

What is the ejection fraction?

A

The ejection fraction is the fraction of the end diastolic volume which is pumped out with each heartbeat.

48
Q

What is ejection fraction normally expressed as?

A

It is usually expressed as a percentage.

49
Q

What is a normal ejection fraction?

A

An ejection fraction of 50 – 70% is normal.

50
Q

How do you work out the ejection fraction?

A

EF = (SV/EDV)x100

51
Q

What does an ejection fraction of less than 50% indicate?

A

An ejection fraction of less than this suggests the left ventricle is not pumping effectively.

52
Q

If a patient has a normal ejection fraction, do they have heart failure?

A

However if a patient has a normal ejection fraction that does not mean that they don’t have heart failure.

53
Q

How can heart failure cause a normal ejection fraction?

A

In some instances the left ventricle can contract adequately but it is unable to fill properly.

54
Q

Why might the left ventricle be able to contract adequately but be unable to fill properly?

A

This may be because it has become stiff.

55
Q

Explain why the ejection fraction can stay in the normal range in heart failure, relating to the equation.

A

In this case end diastolic volume will be reduced and although the stroke volume is reduced the ejection fraction remains in the normal range.

56
Q

Give 2 types of mechanisms of heart failure.

A

Therefore, as well as impaired ability of the heart to contract (heart failure with reduced ejection fraction HFrEF – formerly known as systolic dysfunction), there can be impairment of the filling of the heart (heart failure with preserved ejection fraction HFpEF – formerly known as diastolic dysfunction).

57
Q

What is similar about HFrEF and HFpEF?

A

Both types of heart failure trigger the same neurohumoral responses (see later).

58
Q

What needs to be understood to understand cardiac output in heart failure?

A

It is important to understand Starling’s law of the heart to appreciate what happens to cardiac output in heart failure.

59
Q

What is Starling’s law?

A

The force developed in the myocardium depends on the degree to which the fibres are stretched (or the heart is filled).

60
Q

How does Starling’s law affect HFrEF?

A

In heart failure with reduced ejection fraction (HFrEF) the heart can no longer produce the same amount of force (or cardiac output) for a given level of filling.

61
Q

How does Starling’s law affect HFpEF?

A

In heart failure with preserved ejection fraction (HFpEF) the heart cannot fill properly and so the heart operates at a lower point on the Starling curve reducing stroke volume and hence cardiac output.

62
Q

How many sides of the heart does heart failure affect?

A

Heart failure can affect one or both sides of the heart.

63
Q

Can right sided heart failure occur?

A

However right sided heart failure rarely occurs on its own (but can in the case of chronic lung disease).

64
Q

What is the most common cause of right-sided heart failure?

A

The most common scenario is one of left-sided heart failure which raises pulmonary arterial pressure leading to additional right-sided heart failure.

65
Q

What is congestive heart failure?

A

When both ventricles are affected this is often referred to as congestive heart failure.

66
Q

What can precipitate heart failure?

A

A variety of conditions can precipitate heart failure.

67
Q

In what condition can heart failure occur following another condition?

A

It can occur following a myocardial infarction if an area of the left ventricle is damaged.

68
Q

What conditions can heart failure be a sequelae of?

A

It can also occur as a consequence of conditions such as chronic hypertension or aortic stenosis which create additional afterload against which the heart must pump.

69
Q

What is activated in heart failure?

A

The sympathetic nervous system (SNS) and the Renin-Angiotensin-Aldosterone System (RAAS) are both activated in heart failure in an attempt to maintain cardiac output.

70
Q

The systems that are activated in heart failure - what effect does this have?

A

These have the effect of making an already struggling heart work harder.

71
Q

Systems are activated in heart failure. What damaging effect does one of the products have specifically?

A

In addition, angiotensin II can damage the heart and other organs.

72
Q

How is RAAS activated in heart failure?

A

A drop in blood pressure or a fall in tissue perfusion (as occurs in heart failure) stimulates renin release from the kidneys.

73
Q

What is renin?

A

Renin is an enzyme which catalyses the conversion of angiotensinogen to angiotensin I.

74
Q

What is ACE in RAAS?

A

Angiotensin I is converted to angiotensin II by the action of Angiotensin Converting Enzyme (ACE).

75
Q

What are ACE inhibitors used for?

A

ACE inhibitors are used in the treatment of heart failure to prevent the production of angiotensin II which is a powerful vasoconstrictor and promotes the release of aldosterone from the adrenal cortex.

76
Q

What does aldosterone do?

A

Aldosterone causes salt and water retention in the kidneys, increasing blood volume.

77
Q

What is the indirect effect of ACE inhibitors?

A

ACE inhibitors thus have an indirect vasodilatory and diuretic effect, both of which are beneficial in the treatment of heart failure.

78
Q

Other than ACE inhibitors, what other medication is indicated for heart failure?

A

Diuretics are also important in the treatment of heart failure to reduce blood volume and thus oedema.

79
Q

What other effects may occur in heart failure?

A

In the lecture other hormonal effects will also be considered.

80
Q

What is released in some heart failure patients?

A

In some heart failure patients secretion of antidiuretic hormone (ADH, or vasopressin) is increased.

81
Q

What does ADH do?

A

ADH promotes water retention by the kidney and, as its alternative name suggest, it also causes vasoconstriction.

82
Q

What physiological mechanisms occur in response to heart failure, and what are their effects?

A

Activation of the SNS, RAAS and ADH are all directed to increasing blood volume and perfusion, but ultimately their effects are deleterious, causing a failing heart to have to work harder and promoting venous congestion.

83
Q

What happens to the atria in HFrEF?

A

Impaired contractility of the ventricles leads to increased volume in the atria.

84
Q

What is released when the atria are stretched?

A

The natriuretic peptides, ANP and BNP are released as the atria are stretched.

85
Q

The effect of which molecules’ release is opposite in heart failure?

A

The effect of the natriuretic peptides is opposite to the other neurohormonal effects.

86
Q

What is the effect of natriuretic peptides?

A

They cause natriuresis (loss of sodium and water at the kidneys) as well as promoting vasodilation and inhibiting renin secretion.

87
Q

Why does the release of natriuretic peptides not counteract the SNS/RAAS/ADH systems?

A

Unfortunately the beneficial effects are not usually sufficient to overcome the deleterious effects of the other systems.

88
Q

What is a sign of right-sided heart failure?

A

The formation of peripheral oedema occurs due to right-sided heart failure.

89
Q

What is the effect of right-sided heart failure?

A

Failure of the right side of the heart to pump effectively raises venous pressure and therefore capillary pressure.

90
Q

What is the mechanism behind water movement in right-sided heart failure?

A

An increased capillary hydrostatic pressure favours the movement of water out of the capillaries.

91
Q

What sign occurs due to left-sided heart failure?

A

Pulmonary oedema occurs due to left sided heart failure which raises left atrial pressure and thus the pressure of vessels in the pulmonary system.

ESA 2 - CVS (4 decks)

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