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BRS YR2 > Structural Heart Disease > Flashcards

Structural Heart Disease Flashcards

1
Q

What are some examples of congenital heart defects?

A
  • atrial septal defect (ASD)
  • ventricular septal defect (VSD)
  • coarctation of aorta
  • tetralogy of Fallot (TOF)
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2
Q

What are some examples of developed heart defects?

A

valvular dysfunctions
- atrial stenosis/regurgitation
muscular
- cardiomyopathies

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3
Q

What are structural heart diseases?

A

defects that affect the valves and chambers of the heart and aorta

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4
Q

What is diastole?

A

relaxation of the heart

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5
Q

What happens in a ventricular septal defect?

A

wall between the 2 ventricles fails to develop - leading to a hole
- mixing of oxygenated and deoxygenated blood

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6
Q

How would a baby with a ventricular septal defect present?

A
  • poor weight gain
  • palpitations
  • poor eating
  • cyanosis
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7
Q

How can you treat a ventricular septal defect?

A
  • sometimes heals on its own
  • may require open heart surgery or a catheterisation
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8
Q

What happens in the tetralogy of Fallot?

A
  • ventricular septal defect
  • pulmonary stenosis
  • widening of the aortic valve
  • right ventricular hypertrophy
  • mixing of blood between ventricles and atria
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9
Q

What happens in pulmonary stenosis?

A

the pulmonary trunk is narrowed

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10
Q

What happens when the aortic valve widens in ToF?

A

the mixing of blood from both ventricles on entry to the aorta
(sits directly on ventricular septal defect)

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11
Q

What happens in right ventricular hypertrophy?

A

thickening of the right ventricle wall

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12
Q

What is the atrial septal defect?

A

hole in the wall between the 2 atria (can also be failure to develop)

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13
Q

What is coarctation of the aorta?

A

the narrowing of the descending aorta

  • thickening of the left ventricle
  • eventually heart failure
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14
Q

What is aortic/mitral stenosis?

A

narrowing of the aortic/mitral valve

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15
Q

What is aortic/mitral regurgitation?

A

incompetence of the aortic/mitral valve leading to back flow of blood

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16
Q

When is rheumatic heart disease most common?

A
  • 25-49 (more in female)
  • developing countries
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17
Q

When is calcific aortic valve disease most common?

A

> 80

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18
Q

When is degenerative mitral valve disease most common?

A

> 70 (more in female)

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19
Q

What are the causes of aortic stenosis?

A
  • rheumatic heart disease
  • congenital heart disease
  • calcium build up
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20
Q

What precedes aortic stenosis?

A

aortic sclerosis (aortic valve thickening without flow limitation)

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21
Q

What is the history and presentation of aortic stenosis?

A

Exertional dyspnoea and fatigue
Chest pain, Angina
Syncope
Heart failure
Ejection systolic murmur
H/O Rheumatic fever, High lipoprotein, high LDL, CKD, age >65
Doppler echo is essential to the diagnosis (for the pressure gradient)

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22
Q

What are the risk factors of aortic stenosis?

A
  • hypertension
  • LDL levels
  • smoking
  • elevated CRP
  • congenital bicuspid valves
  • Chronic kidney disease
  • Radiotherapy
  • Older age
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23
Q

How do valves change in aortic stenosis?

A
  • valvular endocardium is damaged due to turbulent blood flow
  • age related or congenital degeneration of the valves
  • Anti-strep B antibodies wrongly attack valves which initiates a inflammatory process
  • leaflet fibrosis and calcium deposition limits aortic leaflet mobility and eventually leads to stenosis
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24
Q

What happens in rheumatic disease?

A

autoimmune inflammatory reaction triggered by Streptococcus infection that targets the valvular endothelium, leading to inflammation and calcification

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25
Q

What is the pathophysiology of aortic stenosis?

A
  • Fibrosis and calcification of aortic valve
  • Disrupted blood flow through the aortic valve
  • LV contracts harder to pump blood through the stenotic valve
  • continuous forceful contraction of LV causes concentric LV hypertrophy
  • LV becomes stiff overtime and harder to fill leading to decreased cardiac output and diastolic dysfunction
  • LV can no longer maintain normal wall stress/afterload and it increases leading to systolic heart failure
  • Pressure overload in LV backs up in the left atrium causes it to dilate and ultimately leads to increase in pressure in lungs causing pulmonary congestion
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26
Q

How does aortic stenosis present?

A
  • exertional dysopnea and fatigue
  • chest pain
  • early ejection systolic murmur (crescendo-decrescendo pattern that peaks in mid-systole, radiates to carotid)
  • high lipoprotein
  • rheumatic fever
  • high LDL
  • CKD
  • age > 65
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27
Q

What investigations would be done for suspected aortic stenosis?

A
  • transthoracic doppler ECG
  • ECG
  • Chest xray
  • cardiac catheterisation
  • cardiac MRI
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28
Q

How do you manage aortic stenosis?

A

primary: aortic valve replacement
- transcatheter valve replacement
- surgical valve prosthesis
- balloon aortic valvuloplasty
- antihypertensive
- ACE inhibitors
- statins

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29
Q

When is aortic valve replacement considered for asymptomatic aortic stenosis?

A
  • severe AS, LV ejection fraction < 50% or undergoing another cardiac surgery
  • rapidly progressing AS
  • abnormal exercise test
  • elevated serum B-type
  • natriuretic peptide (BNP) levels
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30
Q

What are the congenital and acquired causes of aortic regurgitation?

A
  • rheumatic heart disease
  • infective endocarditis
  • aortic valve stenosis
  • congenital heart defects
  • congenital bicuspid valves
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31
Q

What is aortic regurgitation?

A

diastolic leakage of blood from the aorta into the left ventricle

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32
Q

Why does aortic regurgitation occur?

A

incompetence of valve leaflets resulting from either intrinsic valve disease or dilation of the aortic root

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33
Q

What are the 2 different onsets of aortic regurgitation

A
  • chronic: leading to congestive cardiac failure
  • acute: medical emergency, sudden onset of pulmonary oedema (left heart failure) and hypotension/cardiogenic shock
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34
Q

What are the causes of aortic root dilation leading to the development of aortic regurgitation?

A
  • Marfan’s syndrome
  • connective tissue disease/collagen vascular diseases
  • idiopathic
  • ankylosing spondilytis
  • trauma
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35
Q

How does acute aortic regurgitation occur?

A

infective endocarditis
- leads to rupture of leaflets or paravalvular leaks
- vegetations on the valvular cusps can cause inadequate closure of leaflets (blood leakage)
chest trauma - tear in the ascending aorta

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36
Q

How does acute aortic regurgitation present?

A
  • cardiogenic shock
  • tachycardia
  • cyanosis
  • pulmonary oedema
  • diastolic murmur
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37
Q

How does chronic aortic regurgitation present?

A
  • wide pulse pressure
  • pistol shot pulse (Traube sign)
  • water hammer pulse (Corrigan)
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38
Q

What investigations can be done for suspected aortic regurgitation

A
  • transthoracic ECG
  • chest x ray
  • cardiac catheterisation
  • cardiac MRI/CT scan
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39
Q

What is the management for acute aortic regurgitation?

A
  • ionotropes/vasodilators
  • valve replacement and repair
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40
Q

What is the management for chronic asymptomatic aortic regurgitation?

A

if LV function is normal manage by drugs or reassurance

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41
Q

What is the management for chronic symptomatic aortic regurgitation?

A
  • first line: valve replacement
  • adjunct vasodilator therapy
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42
Q

How can aortic regurgitation be prevented?

A

treat rheumatic fever and infective endocarditis

43
Q

What is mitral stenosis?

A

obstruction to left ventricular inflow at the level of mitral valve due to structural abnormality of the mitral valve.

44
Q

What does progression of mitral stenosis lead to?

A
  • pulmonary hypertension
  • right heart failure
45
Q

What are the causes of mitral stenosis?

A
  • rheumatic fever
  • carcinoid syndrome
  • SLE
  • mitral annular calcification (ageing)
  • use of ergot/serotonergic drugs
  • amyloidosis
  • rheumatoid arthritis
  • whipple disease
  • congenital valve deformity
46
Q

When does mitral stenosis tend to occur?

A

decades after the episode of acute rheumatic fever.

47
Q

What does the acute rheumatic fever do?

A
  • formation of multiple foci and infiltrates in the endocardium and myocardium and along the valves
  • thickens, calcified, and contracted resulting in stenosis
48
Q

What is the physiology of mitral valve stenosis?

A
  • moderate exercise or tachycardia leads to exertional dyspnoea due to increased left atrial pressure
  • severe stenosis leads to an increase in LA pressure, transduction of fluid into the lung interstitium leading to dyspnoea at rest or exertion
  • may lead to pulmonary hypertension
  • restriction leads to limited filling of the LV, limiting cardiac output
  • hemoptysis if bronchial vein rupture
49
Q

How does mitral stenosis present?

A
  • rheumatic fever
  • dyspnoea
  • orthopnea
  • diastolic murmur
  • loud S2
  • neck vein distension
  • hemoptysis
  • 40-50 yrs old
50
Q

What investigations should be done when mitral stenosis is suspected?

A
  • ECG
  • transthoracic ECG
  • chest x ray
  • cardiac catheterisation
  • cardiac MRI/CT scan
51
Q

What is the management for progressive asymptomatic mitral stenosis?

A

no management required

52
Q

What is the management for severe asymptomatic mitral stenosis?

A
  • no therapy generally needed
  • adjuvant balloon valvotomy
53
Q

What is the management for severe symptomatic mitral stenosis?

A
  • diuretic
  • balloon valvotomy
  • valve replacement
  • repair adjunct
  • beta blockers
54
Q

What is mitral regurgitation?

A
  • abnormal reversal of blood flow from the LV to the LA
  • most common valvular heart disease
55
Q

What causes mitral regurgitation?

A

disruption in any part of the mitral valve apparatus

56
Q

What factors can cause acute mitral regurgitation?

A
  • mitral valve prolapse
  • rheumatic heart disease
  • infective endocarditis
  • following valvular surgery
  • prosthetic mitral valve dysfunction
57
Q

What factors can cause chronic mitral regurgitation?

A
  • rheumatic heart disease
  • SLE
  • scleroderma
  • hypertrophic cardiomyopathy
  • drug related
58
Q

What is the pathophysiology of mitral regurgitation?

A
  • infective endocarditis
  • abscess formation
  • vegetations
  • rupture of chordae tendineae
  • leaflet perforation
59
Q

What is the physiology of chronic mitral regurgitation?

A
  • progression leads to eccentric hypertrophy leading to elongation of myocardial fibres
  • increased preload and decreased afterload
  • increased LV end diastolic volume and decreased end systolic volume
  • prolonged volume overload leads to LV dysfunction and increased LV end-systolic diameter
60
Q

How does mitral regurgitation present?

A
  • dyspnea
  • high pitched murmur
  • fatigue
  • orthopnea
  • chest pain
  • A fib
  • diminished S1
61
Q

What investigations would be done in suspected mitral regurgitation?

A
  • ECG
  • transthoracic ECG
  • chest xray
  • cardiac catheterisation
  • cardiac MRI/CT scan
62
Q

How is acute mitral regurgitation managed?

A
  • emergency surgery
  • adjunct preoperative diuretics
  • adjunct intra-aortic balloon counterpulsation
63
Q

How is chronic asymptomatic mitral regurgitation managed?

A
  • first line: ACE inhibitors and beta blockers
  • if LV ejection fraction <60%: first line - surgery
64
Q

How is chronic symptomatic mitral regurgitation managed?

A
  • first line: surgical and medical treatment
  • if LV ejection fraction if less than 30%: first line - intra-aortic balloon counterpulsation
65
Q

What is a cardiomyopathy?

A

disease of the heart muscle that makes it harder for the heart to pump blood to the rest of your body

66
Q

What are the main types of cardiomyopathies?

A
  • dilated
  • hypertrophic
  • restrictive
67
Q

When is dilated cardiomyopathy most common?

A

30-40yrs old

68
Q

What is the result of dilated cardiomyopathy?

A

progressive, irreversible, disease causing global systolic dysfunction with heart failure

69
Q

What are the primary causes of dilated cardiomyopathy?

A
  • family history
  • genetic
  • idiopathic
70
Q

What are the secondary causes of dilated cardiomyopathy?

A
  • heart valve disease
  • after child birth
  • thyroid disease
  • myocarditis
  • alcoholism
  • autoimmune disorders
  • drugs
  • mitochondrial disorders
71
Q

What is the pathophysiology of dilated cardiomyopathy?

A

ventricular chamber enlargement and systolic dysfunction with normal left ventricular wall thickness.

72
Q

What is the hallmark finding of dilated cardiomyopathy?

A

left ventricular dilation >4cm

73
Q

Is dilated cardiomyopathy genetic?

A
  • (rare) - autosomal dominant
  • first degree relatives have a 50% chance of inheritance
74
Q

What is the abnormal physiology involved in dilated cardiomyopathy and how does it cause heart failure?

A
  • LV enlargement
  • lower ejection fraction, increase in ventricular wall stress and end systolic volumes
  • early compensatory mechanisms include an increase in HR and tone of the peripheral vascular system
  • neurohumoral activation of the renin-angiotensin aldosterone system and an increase in circulating catecholamines
  • increased natriuretic peptides
  • compensatory mechanisms are overwhelmed and the heart fails.
75
Q

How does dilated cardiomyopathy present?

A
  • dyspnoea
  • murmur
  • fatigue
  • angina
  • pulmonary congestion
  • low cardiac output
    auscultation:
  • displaced apex beat
  • s3 on systole
76
Q

What investigations would be done if dilated cardiomyopathy is suspected?

A
  • genetic testing
  • viral serology
  • ECG
  • chest X ray
  • cardiac catheterisation
  • cardiac MRI/CT scan
  • exercise stress test
  • echocardiography
77
Q

What is the management available for dilated cardiomyopathy?

A 
first line:
- dietary changes
- fluid and sodium restrictions 
if heart failure:
- ACEi, beta blockers
- diuretics 
ultimately:
transplantation
78
Q

What is hypertrophic cardiomyopathy?

A

an increase in LV wall thickness that is not solely explained by abnormal loading conditions

79
Q

Is hypertrophic cardiomyopathies genetic?

A

autosomal dominant Mendelian-inherited disease in approximately 50% of patients.

80
Q

What tends to be the first clinical manifestation of hypertrophic cardiomyopathy?

A
  • sudden death
  • likely: ventricular tachycardia or fibrillation
81
Q

What is the hallmark of hypertrophic cardiomyopathy?

A

myocardial hypertrophy that is inappropriate, often asymmetrical and occurs in the absence of an obvious stimulus.

82
Q

Where does hypertrophic cardiomyopathy occur?

A
  • in any region of the LV
  • frequently involves interventricular septum - obstruction of flow from the LV outflow tract
83
Q

What abnormal physiology is seen in hypertrophic cardiomyopathy?

A
  • abnormal diastolic function
  • impaired ventricular filling and increased filling pressure, despite a normal/small ventricle
  • abnormal calcium kinetics and subendocardial ischemia
  • profound hypertrophy and myopathic process
84
Q

How does hypertrophic cardiomyopathy present?

A
  • sudden cardiac death
  • double carotid artery pulse
  • syncope
  • presyncope
  • congestive heart failure
  • dizziness
  • palpitations
  • angina
  • ejection systolic murmur
  • S3 gallop
85
Q

What investigations should be done when hypertrophic cardiomyopathy is suspected?

A
  • haemoglobin levels (check for anaemia)
  • BNP
  • Troponin T levels
  • ECG
  • Chest x ray
  • cardiac MRI
86
Q

Why is haemoglobin measured in suspected hypertrophic cardiomyopathy?

A

anaemia exacerbates chest pain and dyspnea

87
Q

Why are brain natriuretic peptide (BNP) and troponin T levels measured in suspected hypertrophic cardiomyopathy?

A

elevated BNP, NT-proBNP, troponin T levels are associated with a increased risk of CV events, heart failure and death

88
Q

How is hypertrophic cardiomyopathy treated?

A 
- beta blockers
if side effects
- verapramil 
- add disopyramide
- mechanical therapy (pace maker - short AV delay)
- surgery: septal myectomy or ablation
89
Q

What is restrictive cardiomyopathy?

A
  • less well-defined
  • based on estabilishing the presence of a restrictive ventricular filling pattern.
  • increased stiffness of the myocardium due to familial or secondary causes
90
Q

What characterises restrictive cardiomyopathy?

A
  • diastolic dysfunction with restrictive ventricular physiology
  • often normal systolic function
  • atrial enlargement due to impaired ventricular filling during diastole
  • volume and wall thickness of ventricles is normal
91
Q

What are the causes of restrictive cardiomyopathy?

A
  • idiopathic
  • familial (troponin 1 or desmin mutations)
  • haemochromatosis
  • amyloidosis
  • sarcoidosis
  • Fabry’s disease
  • carcinoid syndrome
  • scleroderma
  • anythracycline toxicity
  • previous radiation
92
Q

What are infiltrative cardiomyopathies?

A

deposition of abnormal substances (amyloid proteins, noncaseating granulomas, iron) in the heart tissue.

93
Q

What happens during infiltrative cardiomyopathies?

A
  • ventricular walls stiffen, leading to diastolic dysfunction
  • restrictive physiology predominates in the early stages, causing conductive abnormalities and diastolic heart failure
  • may lead to systolic dysfunction and ventricular arrhythmias
94
Q

What abnormal physiology of restrictive cardiomyopathy that leads to heart failure?

A
  • increased myocardium stiffness
  • increase in ventricular pressures with small increases in volume
  • accentuated filling occurs in early diastole and terminates at the end of the rapid filling phase
  • reduced compliance/increased diastolic stiffness
  • LV cannot fill enough at normal filling pressures
  • reduced LV filling leads to reduced cardiac output
95
Q

How do patients with restrictive cardiomyopathy present?

A
  • comfortable in sitting position but difficulty breathing when lying dowm
  • fluid in the abdomen (ascites)
  • pitting edema (lower extremities)
  • enlarged, sore liver
  • weight loss
  • cardiac cachexia
    amyloidosis:
  • easy bruising
  • periorbital purpura
  • macroglossia
  • carpal tunnel syndrome
  • increased jugular vein present
  • decreased pulse volume
96
Q

What investigations should be done if restrictive cardiomyopathy is suspected?

A
  • CBC
  • serology
  • amyloidosis check
  • chest xray
  • ECG
  • catheterisation
  • MRI/biopsy
97
Q

How is restrictive cardiomyopathy managed?

A 
- heart failure medication
(ACEi, ARB, diuretics and aldosterone inhibitors)
- antiarrhythmic therapy
- immunosuppression, steroids
- pacemaker
- cardiac transplant
98
Q

What are the clinical findings in aortic stenosis?

A
  • Ejection Systolic murmur (Crescendo- Decrescendo)
  • Syncope on exertion
  • Angina on exertion
  • Diffuse crackles on auscultation of lungs & Dyspnoea
99
Q

What are the congenital and acquired causes of aortic regurgitation?

A
  • Rheumatic heart disease
  • Infective endocarditis
  • Aortic valve stenosis
  • Congenital heart defects
  • Congenital bicuspid valve defects
100
Q

What is systole?

A

Contraction of the heart

101
Q

What causes chronic aortic regurgitation?

A
  • bicuspid aortic valve
  • rheumatic fever causing fibrotic changes leading to thickening and retraction of the valve leaflets
102
Q

What is the pathophysiology of acute aortic regurgitation?

A
  • increased blood volume left ventricle during systole
  • Left ventricle and diastolic pressure increases
  • Increase in pulmonary venous pressure
  • Dyspnoa and pulmonary oedema due to back flow into lungs
  • left sided heart failure
  • Cardiogenic shock
103
Q

What is the pathophysiology of chronic aortic regurgitation?

A
  • Gradual increase in the left ventricle volume
  • Left ventricle enlargement and eccentric hypertrophy
  • ejection fraction falls and left ventricle end systolic volume rises
  • left ventricle dyspnoea
  • Lower coronary perfusion
  • Ischaemia, necrosis and apoptosis

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