Hypertension, Ischaemic Heart Disease and Cardiac Failure Flashcards

1
Q

Where does hypertension occur

A

It can occur in either the systemic or pulmonary circulation however is more difficult to diagnose in the pulmonary circulation.

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2
Q

What is the formula for blood pressure

A

Blood pressure (BP) = cardiac output (CO) X peripheral resistance (PR)

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3
Q

What is the difference between primary and secondary hypertension

A

Primary/essential hypertension occurs on its own. Secondary hypertension occurs due to an underlying cause.

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4
Q

What is malignant hypertension

A

Malignant hypertension is when there is acute end organ damage as a result of hypertension.

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5
Q

What is hypertension

A

Sustained resting blood pressure above a certain level.

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6
Q

Above what value is blood pressure considered to be high in most instances

A

140/90 mmHg

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7
Q

What determines the severity of hypertension

A

Diastolic pressure

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8
Q

What is more dangerous acutely - increased systolic or diastolic pressure?

A

Systolic as this can lead to haemorrhage.

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9
Q

What are some secondary causes of hypertension

A

Renal disease (which can also be caused by hypertension), endocrine disease, drug treatment, coarctation of the aorta

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10
Q

What are the risk factors for primary hypertension

A
  • Genetic Susceptibility
  • High salt intake
  • Chronic stress
  • Abnormalities in the renin-angiotensin system which controls blood volume and blood pressure
  • Obesity
  • Diabetes
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11
Q

What is benign hypertension

A

Where there are slow changes in the vessels and heart resulting in chronic end-organ dysfunction (as opposed to rapid changes and acute end-organ dysfunction).

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12
Q

Which organs are susceptible to the end-organ effects of hypertension

A

The heart, the kidney, the brain, the vessels.

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13
Q

Why is the retina important in hypertension

A

The retina acts like a window into the blood vessel system.

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14
Q

What technique can be used to see end-organ damage as a result of hypertension

A

Retinoscopy

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15
Q

What are the end organ effects on the heart due to hypertension

A

Left ventricular hypertrophy, coronary artery atheroma, ischaemic heart disease and cardiac failure.

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16
Q

What are the complications of left ventricular hypertrophy

A

Fibrosis and arrhythmias

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17
Q

What are the end organ effects on the kidney due to hypertension

A

Nephrosclerosis, “drop-out” of nephrons due to vascular narrowing, proteinuria, chronic renal failure

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18
Q

How do you assess renal dysfunction

A

Check the urine.

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19
Q

What are the end organ effects on the brain due to hypertension

A

Aneurysm resulting in intracerebral haemorrhage causing stroke.

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20
Q

What vascular changes other than atheroma result from hypertension

A

Hyaline change and fibrinoid necrosis.

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21
Q

What can be seen in retinoscopy if benign hypertension is present

A

Nipping of blood vessels and enlargement in other areas

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22
Q

What can be seen in retinoscopy if malignant hypertension is present

A

Rupturing blood vessels and evidence of end organ damage.

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23
Q

What is ischaemic heart disease

A

When the blood supply to the heart is insufficient for its metabolic demands. This can be deficient supply, excessive demand or both.

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24
Q

What factors cause deficient supply of blood resulting in ischaemic heart disease

A

Coronary artery disease or reduced coronary artery perfusion as a result of shock or severe aortic valve stenosis.

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25
Q

What factors cause excessive demand resulting in ischaemic heart disease

A
  • Pressure overload, e.g. hypertension or valve disease. Pressure overload occurs due to a tight valve.
  • Volume overload, e.g. valve disease. Volume overload occurs due to a leaky valve.
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26
Q

What level of occlusion leads to ischaemia in coronary heart disease

A

More than 75% occlusion.

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27
Q

What is myocardial infarction

A

An area of necrosis of heart muscle resulting from reduction (usually sudden) in coronary blood supply.

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28
Q

What are the causes of myocardial infarction

A

Coronary artery thrombosis, haemorrhage into a coronary plaque, increase in demand for oxygen in the presence of ischaemia.

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29
Q

What are the clinical features of MI

A

Central “crushing” chest pain

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30
Q

What can be used in the diagnosis of MI

A

ECG changes and blood markers

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31
Q

What blood markers are tested for in MI

A

Enzymes such as creatine kinase and other proteins such as troponin. Troponin is used most often now as it is more sensitive to heart muscle changes.

32
Q

How long after an MI are changes observable in the heart muscle

A

About 24 hours. Less than 18 hours after there will be no changes.

33
Q

What are the macroscopic changes that occur between 24 and 48 hours after an MI

A

Pale, oedematous muscle

34
Q

What are the microscopic changes that occur between 24 and 48 hours after an MI

A

Odema, neutrophil infiltration and necrosis of myocytes

35
Q

What are the macroscopic changes that occur between 3 and 7 days after an MI

A

A yellow, rubbery centre with a haemorrhagic border

36
Q

What are the microscopic changes that occur between 3 and 7 days after an MI

A

Obvious necrosis and inflammation. Early granulation tissue.

37
Q

What are the macroscopic changes that occur between 1 and 3 weeks after an MI

A

The infarcted area is paler and thinner than the unaffected ventricle.

38
Q

What are the microscopic changes that occur between 1 and 3 weeks after an MI

A

Granulation tissue then progressive fibrosis.

39
Q

What are the macroscopic changes that occur between 3 and 6 weeks after MI

A

Silvery scar becoming tough and white

40
Q

What are the microscopic changes that occur between 3 and 6 weeks after MI

A

Dense fibrosis

41
Q

How can you identify which artery the occlusion occurred in

A

By the location of the infarct

42
Q

Where will the infarct be situated if the right coronary artery is occluded

A

On the inferior surface. it can involve the posterior septum.

43
Q

Where will the infarct be situated if the left coronary artery is obstructed

A

This is the artery of “sudden death”. The infarct will be anterior.

44
Q

Where will the infarct be situated if the circumflex artery is obstructed

A

The infarct will be lateral.

45
Q

What are the complications of acute myocardial infarction

A

Sudden death, dysrhythmias, persistent pain, angina, cardiac failure, mitral incompetence, pericarditis, cardiac rupture, mural thrombosis, ventricular aneurysm.

46
Q

How does sudden death result from MI

A

The myocardial infarct can soften and rupture or ventricular fibrillation can occur.

47
Q

How do dysrhythmias result from MI

A

Due to abnormal electrical activity.

48
Q

How does persistent pain result from MI

A

Due to progressive necrosis

49
Q

How does angina result from MI

A

Ischaemia of non-infarcted cardiac muscle.

50
Q

How does cardiac failure result from MI

A

Due to ventricular dysfunction or dysrhythmias

51
Q

How does mitral incompetence result from MI

A

Due to papillary muscle dysfunction or necrosis

52
Q

How does pericarditis result from MI

A

The pericardium becomes inflamed which can cause sharp chest pain.

53
Q

How does cardiac rupture result from MI

A

Due to weakening of the cardiac wall by necrosis.

54
Q

How does mural thrombosis result from MI

A

Due to abnormal endothelial surface

55
Q

How does ventricular aneurysm result from MI

A

Due to the stretching of newly formed scar tissue.

56
Q

What is cardiac failure

A

Failure of the heart to pump sufficient blood to satisfy metabolic demands.

57
Q

What is the effect on the kidneys of heart failure

A

Under perfusion of the kidney leading to fluid retention and increased blood volume.

58
Q

What are the types of heart failure

A

Left heart failure, right heart failure, low output failure, high output failure, systolic failure, diastolic failure.

59
Q

What is cor pulmonale

A

This is right heart failure as a result of pulmonary hypertension

60
Q

What is acute heart failure

A

A rapid onset of symptoms often with a definable cause such as myocardial infarction.

61
Q

What is chronic heart failure

A

A slow onset of symptoms associated with ischaemic or valvular disease.

62
Q

What is congestive heart failure

A

Failure of both the right and left ventricles.

63
Q

What can cause high output heart failure

A

Thyroid disease.

64
Q

What can cause diastolic failure

A

The heart cannot relax properly. This can be due to TB.

65
Q

What is the most common cause of heart failure

A

A combination of hypertension and ischaemic heart disease.

66
Q

What are two examples of valvular heart disease

A

Bicuspid aortic valve and senile calcific stenosis.

67
Q

What is bicuspid aortic valve

A

Some people are born with a bicuspid as opposed to tricuspid aortic valve. This can lead to calcific stenosis at a younger age.

68
Q

What is senile calcific stenosis

A

Where there are lumps of calcification on the valve which stops it from opening or closing properly.

69
Q

What is the most common type of ventricular failure

A

Left ventricular failure

70
Q

What effect does left ventricular failure have on the pulmonary circulation

A

Pulmonary oedema and pulmonary hypertension

71
Q

How does right heart failure result from left heart failure

A

Left heart failure causes pulmonary hypertension which puts back pressure on the right ventricle and causes right ventricular failure.

72
Q

What are the clinical features of forward failure

A

Reduced perfusion of tissues. This is associated with advanced failure.

73
Q

What are the clinical features of backward failure

A

This results from increased venous pressure. For left ventricular failure backward failure results in pulmonary oedema. For right ventricular failure backward failure results in hepatic congestion and ankle oedema.

74
Q

What are the clinical features of left ventricular failure

A
  • hypotension
  • pulmonary oedema
  • paroxysmal nocturnal dyspnoea (accumulation of fluid in the lungs at night meaning they wake up breathless)
  • breathlessness of exertion
75
Q

What are the clinical features of right ventricular failure

A
  • ankle swelling

- hepatic congestion