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Phase 1b - Cardiovascular & Respiratory Medicine > Structural Heart Disease > Flashcards

Structural Heart Disease Flashcards

1
Q

What is aortic stenosis?

A
  • Narrowing of the aortic valve that prevents it from completely opening and facilitating the flow of blood into the aorta
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2
Q

Outline the epidemiology of aortic stenosis (3).

A
  • AS is the most common valvular disease in the US and Europe requiring treatment
  • It is the second most frequent cause for cardiac surgery
  • It is largely a disease of older people (the seventh or eighth decade of life)
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3
Q

How would a patient with aortic stenosis present (4)?

A
  • Exertional dyspnoea and fatigue
  • Chest pain
  • Ejection systolic murmur (≥3/6 is present with a crescendo-decrescendo pattern that peaks in mid-systole and radiates to the carotid)
  • H/O Rheumatic fever, high lipoprotein, high LDL, CKD, age >65
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4
Q

Outline the aetiology of aortic stenosis?

A
  • It is preceded by aortic sclerosis (defined as aortic valve thickening without flow limitation)
  • It is often suspected by the presence of an early-peaking, systolic ejection murmur, and confirmed by echocardiography.

Aortic stenosis can be caused by:
* Rheumatic heart disease
* Congenital heart disease
* Calcium build up

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5
Q

What are the risk factors of aortic stenosis (8)?

A
  • Hypertension
  • High LDL (low density lipoprotein cholesterol) levels
  • Smoking
  • Elevated C-reactive protein
  • Congenital bicuspid valves
  • Chronic Kidney Disease (CKD)
  • Radiotherapy
  • Older age
  • H/O:
    • Rheumatic heart disease
    • Congenital heart disease
    • Calcium build up
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6
Q

Outline the pathophysiology of aortic stenosis (4 steps).

A
  1. Long-standing pressure overload
  2. Left ventricular hypertrophy (LVH)
  3. Ventricle to maintain a normal wall stress (afterload) despite the pressure overload produced by stenosis -> As the stenosis worsens, the adaptive mechanism fails and left ventricular wall stress increases
  4. Systolic function declines as wall stress increases, with resultant systolic heart failure
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7
Q

What investigations are recommended in a suspected aortic stenosis (4)?

A
  • Transthoracic echocardiography
  • ECG / Chest X ray (to identify LVH)
  • Cardiac catheterisation
  • Cardiac MRI
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8
Q

How is aortic stenosis managed (4)?

A

Surgical:
* Aortic Valve replacement (AVR) for:
* Symptomatic aortic sclerosis
* Asymptomatic patients with severe aortic sclerosis who have an LVEF < 50%
* Asymptomatic patients with severe aortic sclerosis who are undergoing other cardiac surgery
* Asymptomatic patients with severe AS with rapid progression
* Asymptomatic patients with an abnormal exercise test
* Asymptomatic patients with elevated serum B-type natriuretic peptide (BNP) levels
* Balloon aortic valvuloplasty (not the primary treatment)

Medical (for asymptomatic non-sever patients):
* Antihypertensive
* ACE inhibitors
* Statins

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9
Q

What is aortic regurgitation?

A
  • The diastolic leakage of blood from the aorta into the left ventricle
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10
Q

Outline the epidemiology of aortic regurgitation (3).

A
  • Aortic regurgitation is not as common as aortic stenosis or mitral regurgitation
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11
Q

How would a patient with acute aortic regurgitation present (5)?

A
  • Cardiogenic shock
  • Tachycardia
  • Cyanosis
  • Pulmonary oedema
  • Austin flint murmur
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12
Q

How would a patient with chronic aortic regurgitation present (3)?

A
  • Wide pulse pressure
  • Corrigan (water hammer pulse)
  • Pistol shot pulse (Traube sign)
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13
Q

Outline the aetiology of aortic regurgitation?

A
  • It occurs due to incompetence of valve leaflets resulting from either intrinsic valve disease or dilation of the aortic root
    • It can be chronic -> culminate into congestive cardiac failure
    • It can be acute -> medical emergency, presenting with sudden onset of pulmonary oedema and hypotension or cardiogenic shock

Congenital causes of aortic regurgitation:
* Rheumatic heart disease
* Infective endocarditis
* Aortic valve stenosis
* Congenital heart defects
* Congenital bicuspid valves

Causes of aortic root dilation:
* Marfan’s Syndrome
* Connective tissue disease / collagen vascular diseases
* Idiopathic
* Ankylosing spondilytis
* Traumatic

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14
Q

What are the risk factors of aortic regurgitation (8)?

A
  • H/O:
    • Rheumatic heart disease
    • Marfan’s Syndrome
    • Infective endocarditis
    • Connective tissue disease / collagen vascular diseases
    • Aortic valve stenosis
    • Congenital heart defects
    • Ankylosing spondilytis
    • Congenital bicuspid valves
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15
Q

Outline the pathophysiology of acute aortic regurgitation (7).

A
  1. Acute aortic regurgitation
  2. Increase blood volume in LV during systole
  3. LV end diastolic pressure increases
  4. Increase in pulmonary venous pressure
  5. Dyspnea and pulmonary oedema
  6. Heart failure
  7. Cardiogenic shock
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16
Q

Outline the pathophysiology of chronic aortic regurgitation (8).

A
  1. Chronic aortic regurgitation
  2. Gradually increase in LV volume
  3. LV enlargement and eccentric hypertrophy
  4. Early stages: Ejection fraction normal or slightly increase
  5. After some time: Ejection fraction falls and LV end systolic volume rises
  6. Eventually: LV dyspnoea
  7. Lower coronary perfusion
  8. Ischemia, necrosis and apoptosis
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17
Q

What investigations are recommended in a suspected aortic regurgitation (4)?

A
  • Transthoracic echocardiography
  • ECG / Chest X ray
  • Cardiac catheterisation
  • Cardiac MRI
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18
Q

How is acute aortic regurgitation managed (3)?

A
  • Ionotropes / vasodilators

AND

  • Valve replacememt & repair
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19
Q

How is chronic symptomatic aortic regurgitation managed (3)?

A
  • Ionotropes / vasodilators

AND

  • Valve replacememt & repair
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20
Q

How is chronic asymptomatic aortic regurgitation managed?

If LV function is normal

A

Drugs or reassurance

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21
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
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22
Q

Outline the epidemiology of mitral stenosis.

A
  • More common in developing countries (caused by rheumatoid fever).
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23
Q

How would a patient with mitral stenosis present (7)?

A
  • Dyspnoea
  • Orthopnoea
  • Diastolic murmur
  • Loud P2
  • Neck vein distention
  • Hemoptysis
  • 40-50 years age
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24
Q

Outline the aetiology of mitral stenosis?

A
  • Secondary to other diseases, mainly rheumatoid disease

Mitral stenosis can be caused by:
* Rheumatic fever
* Amyloidosis
* Carcinoid syndrome
* Rheumatoid arthritis
* Use of ergot/serotonergic drugs
* Whipple disease
* SLE
* Congenital deformity of the valve
* Mitral annular calcification due to aging

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25
Q

What are the risk factors of mitral stenosis (9)?

A

H/O:
* Rheumatic fever
* Amyloidosis
* Carcinoid syndrome
* Rheumatoid arthritis
* Use of ergot/serotonergic drugs
* Whipple disease
* SLE
* Congenital deformity of the valve
* Mitral annular calcification due to aging

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26
Q

Outline the pathophysiology of mitral stenosis (6 steps).

A
  1. Initially moderate exercise or tachycardia result in exertional dyspnoea due to increased left atrial pressure
  2. Severe mitral stenosis leads to increase in left atrial pressure
  3. Transudation of fluid into the lung interstitium leading to dyspnoea at rest or exertion
  4. Pulmonary hypertension may develop as the result of it
  5. The restricted orifice limits filling of left ventricle limiting cardiac output
  6. Hemoptysis if bronchial vein rupture
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27
Q

What investigations are recommended in a suspected mitral stenosis (5)?

A
  • Transthoracic echocardiography
  • ECG
  • Chest X ray
  • Cardiac catheterisation
  • Cardiac MRI
28
Q

How is progressive asymptomatic mitral stenosis managed?

A
  • No therapy required
29
Q

How is severe asymptomatic mitral stenosis managed?

A
  • No therapy generally required adjuvant balloon valvotomy
30
Q

How is severe symptomatic mitral stenosis managed (3)?

A
  • Diuretic

AND

  • Balloon valvotomy or valve replacement & repair

ADJUNCT

  • Beta-blockers
31
Q

What is mitral regurgitation?

A
  • Abnormal reversal of blood flow from the left ventricle to the left atrium
32
Q

Outline the epidemiology of mitral regurgitation.

A
  • It is the most frequent valvular heart disease
33
Q

How would a patient with mitral regurgitation present (10)?

A
  • Dyspnea
  • Diminished S1 sound
  • Murmur high
  • Fatigue
  • Pitched
  • Blowing
  • Orthopnea
  • Chest pain
  • Atrial fibrillation
34
Q

Outline the aetiology of mitral regurgitation?

A

It is caused by the disruption in any part of the mitral valve apparatus

Acute mitral regurgitation can be caused by:
* Mitral valve prolapse
* Rheumatic heart disease
* Infective endocarditis
* Following valvular surgery
* Prosthetic mitral valve dysfunction

Chronic mitral regurgitation can be caused by:
* Rheumatic heart disease
* SLE
* Scleroderma
* Hypertrophic cardiomyopathy
* Drug related

35
Q

What are the risk factors of mitral regurgitation (8)?

A
  • Hypertension
  • High LDL (low density lipoprotein cholesterol) levels
  • Smoking
  • Elevated C-reactive protein
  • Congenital bicuspid valves
  • Chronic Kidney Disease (CKD)
  • Radiotherapy
  • Older age
  • H/O:
    • Mitral valve prolapse
    • Rheumatic heart disease
    • Infective endocarditis
    • Following valvular surgery
    • Prosthetic mitral valve dysfunction
    • Rheumatic heart disease
    • SLE
    • Scleroderma
    • Hypertrophic cardiomyopathy
    • Drug related
36
Q

Outline the pathophysiology of acute mitral regurgitation (4 steps).

A
  1. Infectious endocarditis
  2. Abscess formation
  3. Vegetations
  4. Rupture of chordae tendineae and leaflet perforation
37
Q

Outline the pathophysiology of chronic mitral regurgitation (5 steps).

A
  1. Progression leads to eccentric hypertrophy
  2. Leads to elongation of myocardial fibres and increased left end diastolic volume
  3. Increase in preload & decrease in afterload
  4. Increase in end diastolic volume and a decrease in end systolic volume
  5. Left ventricular dysfunction and increased left ventricular end systolic diameter
38
Q

What investigations are recommended in a suspected mitral regurgitation (5)?

A
  • Transthoracic echocardiography
  • ECG
  • Chest X ray
  • Cardiac catheterisation
  • Cardiac MRI
39
Q

How is acute mitral regurgitation managed (3)?

A
  • Emergency surgery

ADJUNCT

  • Preoperative diuretics

ADJUNCT

  • Intra-aortic balloon counterpulsation
40
Q

How is chronic asymptomatic mitral regurgitation managed (3)?

A

Medical:
* 1st line: ACE inhibitors
* If left ventricular ejection fraction is less than 60%: Beta-blockers

OR

Surgery

41
Q

How is chronic symptomatic mitral regurgitation managed (3)?

A
  • 1st line: surgery plus medical treatment
  • If left ventricular ejection fraction is less than 30%: Intra-aortic balloon counterpulsation
42
Q

What is dilated cardiomyopathy?

A
  • A progressive, usually irreversible, disease causing global systolic (contractile) dysfunction with heart failure.
43
Q

Outline the epidemiology of dilated cardiomyopathy (3).

A
  • The estimated prevalence of dilated cardiomyopathy is 1:2500
  • This condition is among the most common causes of heart failure.
  • Dilated cardiomyopathy may manifest clinically at a wide range of ages, but this condition most commonly occurs in the third or fourth decade of life
44
Q

How would a patient with dilated cardiomyopathy present (7)?

A
  • Dyspnoea
  • Displaced apex beat
  • S3 or systolic murmur
  • Fatigue
  • Angina
  • Pulmonary congestion
  • Low cardiac output
45
Q

Outline the aetiology of dilated cardiomyopathy.

A
  • Could be familial (25%) or primary (idiopathic) or secondary to another disease

Dilated cardiomyopathy can be caused by:
* Myocarditis
* Alcoholism
* Autoimmune disorders
* Ingestion of drugs
* Mitochondrial disorders
* Heart valve disease
* After child birth
* Thyroid disease

46
Q

What are the risk factors of dilated cardiomyopathy (8)?

A

H/O:
* Myocarditis
* Alcoholism
* Autoimmune disorders
* Ingestion of drugs
* Mitochondrial disorders
* Heart valve disease
* After child birth
* Thyroid disease

47
Q

Outline the pathophysiology of dilated cardiomyopathy (6 steps).

A
  1. Enlargement of the left ventricle
  2. Lower ejection fraction and increase in the ventricular wall stress & end systolic volumes
  3. Early compensatory mechanisms include an increase in heart rate and tone of the peripheral vascular system
  4. Neurohumoral activation of the renin-angiotensin aldosterone system and an increase in circulating levels of catecholamines
  5. Levels of natriuretic peptides are also increased
  6. Eventually these compensatory mechanisms become overwhelmed and the heart fails
48
Q

What investigations are recommended in a suspected dilated cardiomyopathy (8)?

A
  • Genetic Testing
  • Viral serology
  • ECG
  • Chest X ray
  • Cardiac catheterisation
  • Cardiac MRI/CT Scan
  • Exercise stress test
  • Echocardiography
49
Q

How is dilated cardiomyopathy managed?

A
50
Q

What is hypertrophic cardiomyopathy?

A
  • It is defined by an increase in left ventricular wall thickness that is not solely explained by abnormal loading conditions
51
Q

Outline the epidemiology of hypertrophic cardiomyopathy (2).

A
  • Hypertrophic cardiomyopathy is the leading cause of sudden cardiac death in preadolescent and adolescent children
  • Familial hypertrophic cardiomyopathy occurs as an autosomal dominant mendelian-inherited disease in approximately 50% of cases
52
Q

How would a patient with hypertrophic cardiomyopathy present (10)?

A
  • Sudden cardiac death
  • Double carotid artery impulse
  • S3 gallop
  • Syncope
  • Ejection systolic murmur
  • Presyncope
  • Congestive heart failure
  • Dizziness
  • Palpitations
  • Angina
53
Q

Outline the aetiology of hypertrophic cardiomyopathy.

A
  • A genetic cardiovascular disease
54
Q

What is the major risk factor of hypertrophic cardiomyopathy?

A
  • Familial history
55
Q

Outline the pathophysiology of hypertrophic cardiomyopathy (5 steps).

A
  1. Most patients with hypertrophic cardiomyopathy have abnormal diastolic function
  2. Impairs ventricular filling and increases filling pressure, despite a normal or small ventricular cavity
  3. These patients have abnormal calcium kinetics and subendocardial ischemia
  4. Related to the profound hypertrophy and myopathic process
  5. Sudden cardiac death
56
Q

What investigations are recommended in a suspected hypertrophic cardiomyopathy (7)?

A
  • Hemoglobin level: Anemia exacerbates chest pain and dyspnea
  • Brain natriuretic peptide (BNP)
  • NT-proBNP
  • Troponin T levels
  • Echocardiography
  • Chest Xray
  • Cardiac MRI

Brain natriuretic peptide (BNP), troponin T levels: Elevated BNP, NT-proBNP, and troponin T levels are associated with a higher risk of cardiovascular events, heart failure, and death

57
Q

How is hypertrophic cardiomyopathy managed?

A
58
Q

What is restrictive cardiomyopathy?

A
  • It is a less well-defined cardiomyopathy as its diagnosis is based on establishing the presence of a restrictive ventricular filling pattern

It is characterized by diastolic dysfunction with restrictive ventricular physiology, whereas systolic function often remains normal. Atrial enlargement occurs due to impaired ventricular filling during diastole, but the volume and wall thickness of the ventricles are usually normal.

59
Q

Outline the epidemiology of restrictive cardiomyopathy (2).

A
  • RCM accounts for approximately 5% of all cases of diagnosed cardiomyopathies
60
Q

How would a patient with restrictive cardiomyopathy present (7)?

A
  • Comfortable in the sitting position because of fluid in the abdomen or lungs, and they frequently have ascites and pitting edema of the lower extremities
  • The liver is usually enlarged and full of fluid, which may be painful
  • Weight loss and cardiac cachexia are not uncommon
  • Easy bruising, periorbital purpura, macroglossia, and other systemic findings, such as carpal tunnel syndrome, should be an indication for the clinician to consider amyloidosis.
  • Increased jugular venous pressure is present
  • The pulse volume is decreased, consistent with decreased stroke volume and cardiac output
61
Q

Outline the aetiology of restrictive cardiomyopathy.

A

Idiopathic

Familial:
* Has been related to troponin I or desmin mutations, the latter often in association with a skeletal myopathy)

Secondary to systemic disorders:
* Haemochromatosis
* Amyloidosis
* Sarcoidosis
* Fabry’s disease
* Carcinoid syndrome
* Scleroderma
* Anthracycline toxicity
* Previous radiation

62
Q

What are the risk factors of restrictive cardiomyopathy (9)?

A
  • Familial history

H/O:
* Haemochromatosis
* Amyloidosis
* Sarcoidosis
* Fabry’s disease
* Carcinoid syndrome
* Scleroderma
* Anthracycline toxicity
* Previous radiation

63
Q

Outline the pathophysiology of restrictive cardiomyopathy (4 steps).

A
  1. Increased stiffness of the myocardium causes ventricular pressures to rise precipitously with small increases in volume
  2. Accentuated filling occurs in early diastole and terminates abruptly at the end of the rapid filling phase
  3. Patients typically have reduced compliance (increased diastolic stiffness), and the left ventricle cannot fill adequately at normal filling pressures
  4. Reduced left ventricular filling volume leads to a reduced cardiac output
64
Q

What investigations are recommended in a suspected restrictive cardiomyopathy (8)?

A
  • FBC
  • Serology
  • Amylodosis check
  • CXR
  • ECG
  • Echocardiography
  • Catheterisation
  • MRI/Biopsy
65
Q

How is restrictive cardiomyopathy managed (4 / 4)?

A

1st line:
* Heart failure medication
* Guideline-directed medical therapy for heart failure, including angiotensin-converting enzyme inhibitors or angiotensin receptor II blockers, diuretics and aldosterone inhibitors should be initiated in patients with reduced LV

2nd line:
* Antiarrhythmic Therapy
* Immunosuppression / Steroids
* Pacemaker
* Cardiac transplantation

Phase 1b - Cardiovascular & Respiratory Medicine (21 decks)

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