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BRS YEAR 2 > Cardio - Structural Heart Disease > Flashcards

Cardio - Structural Heart Disease Flashcards

1
Q

What are the three layers of heart tissue?

A

Epicardium (layer of epithelial cells)
Myocardium (muscular layer)
Endocardium (layer of endothelial cells)

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2
Q

What are the 2 main phases of the cardiac cycle?

A

Systole - ventricles contract

Diastole - ventricles relaxed

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3
Q

What happens to the cardiac cycle in structural heart disease

A

In structural heart disease, there is a disruption of the cardiac cycle and thus less stroke volume possibly leading to heart failure.

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4
Q

What are the 3 main phases of systole?

A

Isovolumetric contraction, rapid ejection, reduced ejection

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5
Q

What are the 4 main stages of diastole?

A

Atrial systole
Isovolumetric relaxation
Rapid passive filling
Slow passive filling

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6
Q

What happens in atrial systole?

A

The atria contract to top up the blood filling the ventricles, which primarily occurred during the rapid and reduced passive filling.

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7
Q

How much does atrial systole contribute to ventricular filling?

A

10-40% - it is higher when there is a reduced diastolic window such as during exercise

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8
Q

What does atrial systole correlate with on the ECG?

A

P wave

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9
Q

What sound may be heard in atrial systole?

A

S4 sound

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10
Q

What does s4 sound represent?

A

Sometimes if the ventricles are already full, atria contracting to eject blood into them leads to back flow into the atria therefore an abnormal sound. This can occur in congestive heart failure, tricuspid incompetence or pulmonary embolism.

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11
Q

What happens in isovolumetric contraction?

A

The AV valves close when the ventricular pressure exceeds the atrial pressure, and the ventricles start contracting. The semilunar valves may not be open yet therefore volume in the ventricles is fixed.

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12
Q

What does isovolumetric contraction correlate with on ECG?

A

QRS complex

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13
Q

What sound do we hear in isovolumetric contraction?

A

S1 sound - lub - caused by mitral valve closing

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14
Q

What is rapid ejection?

A

When ventricular pressure exceeds the pressure in the aorta or pulmonary artery, then the semilunar valves open and blood is forced out into the ventricles at a rapid rate

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15
Q

What is reduced ejection?

A

This is ventricular repolarisation with a decline in ventricular active tension leading to a fall in the pressure gradient

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16
Q

What does reduced ejection correlate with on the ECG?

A

T wave

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17
Q

What is isovolumetric relaxation?

A

Semilunar valves shut but the AV valves remain open until ventricular pressure falls below atrial pressure

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18
Q

What sound do we hear in isovolumetric relaxation?

A

S2 - dub on semilunar valves closing

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19
Q

What is rapid passive filling?

A

As ventricles continue to relax, ventricular pressure eventually falls below atrial pressure causing the AV valves to open - meaning that blood can start filling the ventricles again

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20
Q

What heart sound may we hear during rapid passive filling?

A

S3

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21
Q

What does s3 represent?

A

Turbulent ventricular filling possibly due to severe hypertension or mitral incompetence. May be normal in athletes or pregnant women

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22
Q

What is another name for reduced passive filling?

A

Diastasis

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23
Q

What is reduced passive filling?

A

Ventricular volume rises more slowly without the help of the atria

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24
Q

What is ESV?

A

End systolic volume

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25
Q

What is EDV?

A

End diastolic volume

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26
Q

How do we calculate stroke volume?

A

EDV - ESV

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27
Q

When can we get structural heart defects?

A

They can be congenital or develop later in life

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28
Q

What are some examples of congenital heart diseases? (6)

A 
Atrial septal defect (ASD)
Ventricular septal defect (VSD)
Coarctation of the aorta 
Patent foramen ovale (PFO)
Patent Ductus Arteriosus (PDA)
Tetralogy of Fallot (TOF)
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29
Q

What are some examples of structural heart diseases developing later in life?

A

Cardiomyopathies

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30
Q

What happens in VSD?

A

Interventricular septum doesn’t develop properly and we may get mixing of oxygenated and deoxygenated blood

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31
Q

What are the clinical signs of VSD?

A

Poor weight gain
Poor feeding
Palpitations

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32
Q

How can VSD be cured/treated?

A

Hole may close up itself or open heart surgery or cardiac catheterisation

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33
Q

What does tetralogy of fallout include?

A

Widening of the aorta
Pulmonary stenosis
VSD
Right ventricular hypertrophy

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34
Q

What does widening of the aorta (TOF) cause?

A

Causes some mixing or diversion of the blood from the right ventricle into the aorta

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35
Q

Why and how do we correct right ventricular hypertrophy?

A

Critical defect - surgery is needed to correct abnormal breathing

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36
Q

What happens in ASD?

A

Atrial wall fails to develop properly

37
Q

What is coarctation of the aorta?

A

This is narrowing of the aorta e.g. in the descending aorta

38
Q

What may result from coarctation of the aorta?

A

Blood struggles to get through, therefore we may get LVH and eventually heart failure

39
Q

What is rheumatic heart disease?

A

Scarring or inflammation of the heart which results from rheumatic fever. It is the most common cause of problems leading to valvular heart disease in developing countries

40
Q

What is calcific aortic disease?

A

Aortic valve is calcified

41
Q

What is degenerative mitral valve disease?

A

Degeneration of the mitral valve due to age or other problems, more commonly affecting males

42
Q

Risk factors aortic stenosis?

A 
Old age
Hypertension
LDL
Increased CRP
Radiotherapy
Congenital Bicuspid Valves
Chronic Kidney Disease
43
Q

Causes of aortic stenosis?

A

Rheumatic heart disease
Congenital hearth disease
Calcium build up

44
Q

What precedes AS?

A

Aortic sclerosis - we don’t notice it

45
Q

How does AS develop?

A

Valvular endothelium is damaged due to abnormal blood flow across the valve, starting from an unknown trigger. This causes an inflammatory process and therefore fibrosis, calcium deposition and eventually low valve motility

46
Q

What is the consequence of AS?

A

Long standing pressure overload
LVH
Ventricles try to maintain wall stress despite pressure overload, however eventually the wall stress increases thus reducing systolic function and leading to systolic heart failure

47
Q

Presentation of AS?

A

Exertional dyspnoea
Fatigue
Chest pain
Ejection systolic murmur radiating to carotid

48
Q

AS Investigations?

A

Transthoracic echo
ECG
Cardiac catheterisation
Cardiac MRI

49
Q

AS Management?

A

Aortic Valve replacement
Antihypertensives
ACEis
Statins

50
Q

What is aortic regurgitation?

A

Diastolic leakage of the blood from the aorta into the left ventricle due to incompetence from valve leaflets, arising from valve disease or dilation of the aortic root

51
Q

What causes AR?

A 
Rheumatic heart disease
Infective endocarditis 
Aortic valve stenosis
Congenital heart defects
Congenital biscuspid valves
52
Q

What are causes of aortic root dilation in AR?

A

Marfan’s
Connective tissue diseases
Ankylosing spondylitis
Trauma

53
Q

What can acute AR lead to?

A

Cardiogenic shock

54
Q

What can chronic AR lead to?

A

Congestive heart failure

55
Q

What is the presentation of Acute AR?

A 
Cardiogenic shock 
Tachycardia
Cyanosis 
Pulmonary oedema 
Austin flint murmur
56
Q

What is the presentation of chronic AR?

A

Wide pulse pressure
Corrigan wate hammer poulse
Pistol shot pulse

57
Q

What investigations do we do for AR?

A

Echo
CXR
Cardiac catheterisation
Cardiac MRI

58
Q

How do we manage AR?

A

Aortic valve replacement or vasodilator therapy - prevention of rheumatic fever or infective endocarditis is key

59
Q

What is mitral stenosis?

A

Obstruction to left ventricular inflow at the level of the mitral valve to to sutrcutral abnormality of the mitral valve

60
Q

What are the causes of Mitral stenosis?

A 
Rheumatic fever
Carcinoid syndrome
SLE
Mitral annular calcification due to ageing 
Rheumatoid arthritis 
Congenital
61
Q

What can mitral stenosis lead to?

A

Pulmonary hypertension and right sided heart failure

62
Q

Mitral stenosis presentation?

A

Haemoptysis
Orthopnoea
Diastolic murmur
Neck vein distension

63
Q

Mitral stenosis management?

A

Adjuvant balloon valvotomomy, valve replacement and repair adjunct beta blockers if severe or symptomatic

64
Q

Mitral stenosis investigations?

A 
ECG
Echo
CXR
Cardiac catheterisation
Cardiac MRI/CT
65
Q

What is mitral regurgitation?

A

Abnormal several of blood from the left ventricle to the left atrium during systole due to damaged leaflets

66
Q

What causes acute MR?

A 
Mitral valve prolapse
Rheumatic heart disease
Infective endocarditis 
Post valvular surgery
Prosthetic mitral valve dysfunction
67
Q

What causes chronic MR?

A 
Rheumatic heart disease 
SLE
Scleroderma
Hypertrophic cardiomyopathy 
Drug related
68
Q

What happens in MR?

A

Progression of chronic MR cuases eccentric hypertrophy thus we get elongation of the myocardial fibres. This causes an increase in EDV and preload and a fall in after load. This leads to left ventricular overload this we get dysfunction and heart failure later on in life

69
Q

MR Presentation?

A 
Dyspnoea
Murmur high 
Fatigue
Orthopnoea
Chest pain
Atrial fibrillation 
Diminished S1
Pitched, blowing
70
Q

MR Investigations?

A 
ECG
Echo 
CXR
Cardiac MRI/CT
Cardiac catheterisation
71
Q

MR Management?

A

Emergency surgery if acute or chronic symptomatic along withe medical treatment, ACEis if chronic asymptomatic

72
Q

What are cardiomyopathies?

A

Disease of the heart muscle making it harder for the heart to pump blood to the rest of the body, thus potentially leading to heart failure

73
Q

Main types of cardiomyopathy?

A

Dilated
Hypertrophic
Restrictive

74
Q

What are the causes of dilated cardiomyopathy?

A 
Familial 
Heart valve disease
After child brith 
Thyroid disease 
Myocarditis 
Alcoholism 
Autoimmune
Ingestion of drugs
Mitochondrial disorders
75
Q

What happens in DCM?

A

Ventricular chamber enlargement and systolic dysfunction with normal left ventricular wall thickness - leads to lower EF and increase in ventricular wall stress and ESV. We get an increase in HR and TPR. Overconpensation leads to heart failure

76
Q

DCM Presentation?

A 
Dyspnoea
Murmur
Fatigue
Angina
Pulmonary congestion
Low cardiac output 
Displaced apex beat due to LVH
77
Q

DCM Investigations?

A 
Genetic testing
Viral serology
ECG
CXR
Cardiac catheterisation 
MRI/CT
Exercise stress test
Echo
78
Q

DCM Management?

A

Lifestyle modifications, medicine if ineffective

Treat underlying cause

79
Q

What is hypertrophic cardiomyopathy?

A

Genetic Cardiovascular disease defined by an increase in left ventricular wall thickness that is not solely explained by abnormal loading conditions

80
Q

What happens in HCM?

A

Abnormal diastolic function impairs ventricular filling and increases filling pressure, can lead to sudden death

81
Q

Presentation of HCM?

A 
Sudden cardiac death - common in children 
S3 gallop 
Congestive heart failures
Syncope 
Dizziness
Palpitations
Ejection systolic murmur
82
Q

Investigations for HCM?

A 
HB levels: anemia exacerbates chest pain and dyspnoea 
BNP
Trops
Echo
CXR
MRI
83
Q

Management of HCM?

A

Medications
Pacemaker
Surgery to increase ventricle size

84
Q

What is restrictive cardiomyopathy?

A

Diastolic dysfunction with restrictive ventricular physiology, whereas systolic function often remains normal

85
Q

What causes RCM?

A

Idiopathic
Familial
Systemic e.g. haemochromatosis

86
Q

What happens in RCM?

A

Increased stiffness of myocardium causes ventricular pressures to rise lots with small increases in volume, reduced cardiac output

87
Q

What is the presentation of RCM?

A 
Fluid or oedema 
Liver enlargement 
Weight loss 
Easy bruising 
Pulse volume decreased
88
Q

What is the investigations in RCM?

A 
CBC
Serology
Amyloidosis check 
CXR
ECG
Echo 
Catheterisation
MRI/Biopsy
89
Q

What is the management in RCM?

A 
Heart failure medications 
Antiarrhythmic therapy
Immunosuppression - steroids 
Pacemaker
Cardiac transplantation (last resort)

BRS YEAR 2 (37 decks)

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