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1B structural heart disease Flashcards

1
Q

What is end systolic volume?

A

The volume of blood that stays behind in left ventricle after systole

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2
Q

What is end diastolic volume?

A

Amount of blood ventricle contains just before contraction

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3
Q

Define structural heart disease

A

Number of defects which affect the valves and chambers of the heart and the aorta

Can be congenital (present at birth) or develop later in life

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4
Q

Give 6 examples of congenital heart defects

A
  • Atrial septal defect (ASD)
  • Ventricular septal defect (VSD)
  • Tetralogy of Fallot (TOF)
  • Coarctation of the aorta
  • Patent foramen ovale (PFO)
  • Patent ductus arteriosus (PDA)
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5
Q

What is ASD?

A

Atrial septal defect: hole in the wall between the 2 atria

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6
Q

What is VSD?

A

Ventricular septal defect: when the wall between the two ventricles fails to develop in foetus leading to hole in wall.

This leads to mixing of oxygenated blood from left ventricle with deoxygenated blood in right ventricle.

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7
Q

What may a child with VSD present with?

A
  • Poor weight gain
  • Poor feeding
  • Palpitations
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8
Q

What are treatments for VSD?

A
  • Sometimes hole is small enough that it closes as child grows older
  • If hole is large, surgeon needs to do open heart surgery or cardiac catheterisation to manually close it with a badge
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9
Q

What is TOF?

A

Tetralogy of Fallot (4 things):

  • Ventricular septal defect- hole in wall between ventricles
  • Pulmonary stenosis- where pulmonary trunk is stenosed (narrowed down)
  • Widening of aortic valve so that it sits in both left and right ventricle and allows for mixing of blood between them and into aorta
  • Right ventricular hypertrophy- thickening of wall of right ventricle
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10
Q

What is the treatment of TOF?

A

Child needs multiple surgeries to fix all of this e.g. aorta takeover and VSD

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11
Q

What is coarctation of the aorta?

A
  • Narrowing of aorta
  • Blood has to force its way through the narrowing so ventricle has to work harder to push more blood through that narrowing
  • Leads to thickening of ventricles or heart failure
  • Serious condition and needs urgent repair
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12
Q

What are examples of structural heart disease that develop later in life?

A
  • Valvular dysfunctions (atrial stenosis/regurgitation)
  • Muscular dysfunctions (cardiomyopathies)
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13
Q

What is aortic stenosis?

A

Narrowing of aortic valve- same with mitral stenosis.

The valve doesn’t open fully, reducing or blocking blood flow into aorta.

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14
Q

What is aortic regurgitation?

A

Incompetence of aortic valve- same with mitral regurgitation.

It is the diastolic leakage of blood from the aorta into the left ventricle.

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15
Q

What is aortic stenosis preceded by?

A

Aortic sclerosis (aortic valve thickening without flow limitation so patients can’t tell they have it)

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16
Q

How is aortic stenosis suspected?

A

By presence of an early-peaking systolic ejection murmurs and confirmed by echocardiography (where you see heart walls and can see thickening)

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17
Q

At what age does aortic stenosis most likely happen?

A

Older people in 60s/70s

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18
Q

What are the risk factors of aortic stenosis?

A
  • HTN
  • high LDL
  • Smoking
  • Elevated CRP
  • Congenital bicuspid valves
  • CKD
  • Radiotherapy
  • Older age
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19
Q

What are the causes of aortic stenosis?

A
  • Rheumatic heart disease- commonest cause in developing countries
  • Congenital heart disease
  • Calcium build up
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20
Q

Describe the pathophysiology of aortic stenosis

A
  1. Wear and tear of valve/disruption of valve (degen/congenital) or Ab attack valves –> inflammation (Group A Strep URTI)
  2. Fibrosis and calcification of aortic valve
  3. Disrupted blood flow through the aortic valve
  4. LV has to contract harder to pump blood through
  5. LVH
  6. LV becomes stiff and harder to fill –> decreased CO and diastolic function
  7. Pressure overload in LV backs up in LA causing dilation therefore increase in lung pressure –> pulmonary congestion
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21
Q

What happens in rheumatic heart disease?

A

It’s an autoimmune inflammatory reaction triggered by prior Streptococcus infection that targets the valvular endothelium, leading to inflammation and eventually calcification of valve

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22
Q

How do aortic stenosis patients present and why?

A
  • Ejection Systolic murmur (Crescendo-Decrescendo)
    • Turbulent blood flow through valve during systole on auscultation
  • Syncope on exertion
    • LV has to contract harder so contraction less efficient during exercise, decrease in output to brain
  • Angina on exertion
    • Hypertrophied muscle-high oxygen demand
    • Increase in pressure in ventricles as compared to aorta resulting in less coronary perfusion
  • Diffuse crackles on auscultation of lungs and dyspnoea
    • Increase in back pressure in lungs –> pulmonary congestion
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23
Q

What do patients with aortic stenosis usually have a history of?

A
  • Rheumatic fever
  • High lipoprotein
  • High LDL
  • CKD
  • Age >65
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24
Q

What investigations are usually done for aortic stenosis?

A
  • Doppler echo is essential (for pressure gradient)
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25
Q

What is the primary treatment for symptomatic AS patients?

A

Aortic valve replacement (AVR)
- Transcatheter valve replacement
- Surgical valve prosthesis

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26
Q

When is AVR given to asymptomatic AS patients?

A
  • severe AS with LVEF <50%
  • severe AS with rapid progression
  • an abnormal exercise test
  • Elevated serum B-type natriuretic peptide (BNP) levels
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27
Q

What kind of murmur does aortic regurgitation create?

A

Early diastolic ejection murmur

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28
Q

Why does aortic regurgitation occur?

A

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

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29
Q

What does AS cause if it’s acute/chronic?

A

Acute: medical emergency, sudden onset of pulmonary oedema and HTN or cardiogenic shock

Chronic: it culminates into congestive cardiac failure

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30
Q

What are the congenital and acquired causes for AR?

A
  • Rheumatic heart disease
  • Infective endocarditis
  • Aortic valve stenosis
  • Congenital heart defects
  • Congenital bicuspid valves
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31
Q

What are the causes of AR through aortic root dilation?

A
  • Marfan’s syndrome
  • Connective tissue disease/collagen vascular diseases
  • Idiopathic
  • Ankylosing spondylitis
  • Traumatic
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32
Q

Describe the pathology of acute AR

A
  1. Aortic root dilation (Marfan’s, AS, syphilis, idiopathic) or inflammation of valvular endocardium –> abnormal valve leaflet (post infl, collagen vascular disease, congenital bicuspid valve)
  2. Valve leaflets close poorly when aortic pressure > LV pressure during diastole
  3. Blood flows back from aorta to LV
  4. Volume and pressure overload in LV: increase LV preload and afterload
  5. Dilatation: increase in SV due to Frank Starling Law
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33
Q

Describe the pathology of chronic AR

A
  1. Aortic root dilation (Marfan’s, AS, syphilis, idiopathic) or inflammation of valvular endocardium –> abnormal valve leaflet (post infl, collagen vascular disease, congenital bicuspid valve)
  2. Valve leaflets close poorly when aortic pressure > LV pressure during diastole
  3. Blood flows back from aorta to LV
  4. Volume and pressure overload in LV: increase LV preload and afterload
  5. LV dilates and eccentrically hypertrophies to accommodate increase in volume (LVH
  6. Weakens myocardium so impaired contraction –> systolic heart failure
  7. Back pressure in LV to atria therefore lung vasculature –> congestion
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33
Q

What are the clinical findings of AR and why?

A
  • Diastolic murmur
    • Blood flowing backwards through valve from aorta to LV
  • S3 gallop sound
    • Occurs in early diastole produced by early and rapid filling and expansion of ventricles
  • Angina on exertion/ fatigue
    • Hypertrophied muscle means high O2 demand
    • Pressure in aorta decreases so coronary circulation is compromised
    • Decrease in SV and less blood flow to body
  • Diffuse crackles on auscultation of lungs, Dyspnoea, Orthopnoea
    • Back pressure in lungs leading to pulmonary congestion
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34
Q

What is the history and presentation of AR?

A

Acute:
- Cardiogenic shock
- Tachycardia
- Cyanosis
- Pulmonary oedema
- Diastolic murmur

Chronic:
- Wide pulse pressure
- Corrigan (wate hammer pulse)

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35
Q

What investigations are done for aortic regurgitation?

A
  • Echocardiography is the best non-invasive test to diagnose and grade the severity of AR
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36
Q

What is the main way of managing AR?

A
  • AVR
  • Asymptomatic patients with chronic severe AR may use vasodilator therapy
    • improves haemodynamic and delays need for AVR
37
Q

What can we do to prevent chronic symptomatic AR?

A

Treat rheumatic fever and infective endocarditis

38
Q

What is mitral stenosis?

A

Obstruction to left ventricular inflow at level of mitral due to structural abnormality of mitral valve

39
Q

What does the progression of mitral stenosis lead to?

A

Pulmonary hypertension and therefore right heart failure

40
Q

What is the main cause of mitral stenosis in developing countries?

A

Rheumatic fever

41
Q

What are the other causes (other than Rheumatic fever) of mitral stenosis?

A
  • Carcinoid syndrome
  • Use of ergot/serotonergic drugs
  • SLE
  • Mitral annular calcification due to ageing
  • Amyloidosis
  • Rheumatoid arthritis
  • Whipple disease
  • Congenital deformity of the valve
42
Q

Describe the pathophysiology of mitral stenosis

A
  1. Recurrent inflammation (rhem fever, IE, calcific, congenital stenosis)
  2. Fibrous deposition and calcification of the MV leaflets & chordae tendineae leading to thickening and shortening of chordae tendineae
  3. Thick and stiff leaflets and fusion of junction between leaflets
  4. Decrease in area of the orifice leading to obstructed blood flow through MV
  5. Impaired emptying of the LA which leads to impaired filling of LV –> decreased SV and cardiac failure
  6. Impaired emptying of LA also leads to increase in LA pressure –> back pressure in LA –. lung vasculature –> congestion
43
Q

What are the clinical findings of MS?

A
  • Opening snap, Mid diastolic murmur
    • Turbulent blood flow across valve
  • A fib
    • LA enlargement –> stretch of conduction fibres
  • Dysphagia and hoarseness (rare)
    • LA enlargement –> compression of surrounding structures
  • Cardiogenic shock/congestive heart failure
    • Decrease in SV and CO
  • Right sided heart failure
    • RVH
  • Dyspnoea
    • Increase pulmonary vasculature pressure–> fluid in interstitium –> pulmonary oedema
44
Q

What investigations can we do for mitral stenosis?

A
  • ECG
  • CXR
  • Transthoracic echocardiography
45
Q

How do we manage progressive asymptomatic patients with mitral stenosis?

A

No therapy required

46
Q

How do we manage severe asymptomatic patients with mitral stenosis?

A
  • No therapy generally required
  • Can do adjuvant balloon valvotomy
47
Q

How do we manage severe symptomatic patients with mitral stenosis?

A
  • Diuretics
  • Balloon valvotomy
  • Valve replacement
  • Repair adjunct beta blockers
48
Q

What is mitral regurgitation?

A

Abnormal reversal of blood flow from left ventricle to left atrium

Most frequent valvular heart disease

49
Q

What are causes of acute mitral regurgitation?

A
  • Following valvular surgery
  • Infective endocarditis
  • Rheumatic heart disease
  • Mitral valve prolapse
  • Prosthetic mitral valve dysfunction

FIRMP

50
Q

What are causes of chronic mitral regurgitation?

A
  • Rheumatic heart disease
  • SLE
  • Scleroderma (autoimmune attack of connective tissue)
  • Hypertrophic cardiomyopathy
  • Drug related
51
Q

What triggers the pathophysiology of MR?

A
  • Coronary Artery Disease (IHD and MI/myocarditis)
    • Dilation of valve leaflets and tethering of chordae tendineae)
  • Papillary muscle rupture
    • Valve leaflets flail
  • Infective endocarditis
    • Vegetations on the leaflets
  • CTD
    • Weak valve leaflets
  • Rheumatic heart disease
    • Dilatation of the mitral valve annulus inflammation of the leaflets
  • Mitral valve prolapse
    • Structurally abnormal valve
52
Q

Describe the pathophysiology of MR?

A
  • MR: backflow of blood from LV to LA due to impaired closure
  • Increased volume and pressure in LA
  • Increased volume push back into LV in next diastole
  • LV dilation –> remodelling: decrease in LV systolic function
  • Leads to decrease SV and CO –> congestive heart failure
  • Also leads to back pressure in LA –> lung vasculature –> leading to congestion
53
Q

What are the clinical findings in MR?

A
  • Pansystolic murmur radiating to axilla
    • Blood flow consistently backwards in systole
  • S3 heart sound
    • Increase volume pushed back into LV
  • Increase in serum creatinine
    • Decrease O2 to kidneys (decreased organ perfusion –> parenchymal damage)
  • Cardiogenic shock/congestive heart failure
    • Decrease in stroke volume and cardiac output
  • Peripheral oedema
    • Congestive heart failure
  • Decrease in O2 sats, tachypnoea, wheeze crackles and frothy sputum
    • Fluid extravasates out of vessels and into the lungs
54
Q

What investigations do we do for MR?

A
  • ECG
  • Transthoracic echocardiography
  • CXR
  • Cardiac MRI/CT scan
55
Q

How do we manage acute severe MR?

A
  • Regurg can be corrected by repairing or replacing supporting valve structures
  • Prosthetic ring can be inserted to reshape the valve
56
Q

How do we manage severe chronic asymptomatic MR?

A
  • Watchful waiting or surgery
57
Q

How do we manage chronic symptomatic MR?

A
  • First line is surgery plus medical treatment
  • If LVEF <30% then 1st line is intra-aortic balloon counterpulsation
58
Q

What are cardiomyopathies?

A

Diseases of the heart muscle that make it harder for the heart to pump blood to the rest of the body

59
Q

What can cardiomyopathies lead to?

A

Heart failure

60
Q

What are the three main types of cardiomyopathies?

A
  • Dilated cardiomyopathy
  • Hypertrophic cardiomyopathy (HCM)
  • Restrictive cardiomyopathy
61
Q

How common is dilated cardiomyopathy?

A
  • Estimated prevalence of 1:2500
  • Among most common causes of heart failure
62
Q

When in life does dilated cardiomyopathy usually manifest?

A

Most commonly in 3rd or 4th decade of life

63
Q

What is dilated cardiomyopathy?

A

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

64
Q

What primary cause is there of dilated cardiomyopathy?

A

Primary without family history- idiopathic

65
Q

How common are familial causes of dilated cardiomyopathy?

A

25% of all cases

66
Q

What secondary causes of DCM are there?

A
  • MI/Heart valve disease
  • After child birth
  • Thyroid disease
  • Myocarditis
  • Alcoholism
  • Ingestion of drugs
  • Autoimmune disorders
  • Inherited disorders
67
Q

What is dilated cardiomyopathy characterised by?

A

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

68
Q

What is the hallmark at autopsy for dilated cardiomyopathy?

A

Left ventricular dilatation, usually more than 4 cm

69
Q

How is the heart’s physiology affected in DCM?

A
  1. Inflammatory damage and death of the myocytes (viral myocarditis, autoimmune, idiopathic, myocardial ischaemia) or age and death of myocytes (chronic alcoholism, inherited disorders, drugs)
  2. Eccentric fibrosis and increase in volume
  3. LV enlargement without corresponding increase in myocardial mass
  4. Frank starling law: contractility is ok
  5. Gradual over distention and systolic dysfunction
  6. Decreased CO and increased EDV/EDP
  7. Volume overload- Congestive heart failure
70
Q

What is the history and presentation of DCM?

A
  • Dyspnoea, cold clamming extremities
    • Low CO –> insufficient tissue oxygenation
  • Displaced apex beat
    • Enlarged LV
  • Fatigue
    • Low CO and decreased organ perfusion
  • Angina
    • Low coronary perfusion
  • Pulmonary congestion
    • Diffuse crackles
  • Peripheral oedema
    • Heart failure
  • Sudden cardiac death
71
Q

What investigations do we do for DCM?

A
  • Genetic testing
  • Viral serology
  • ECG
  • Echocardiography
  • CXR
  • Cardiac catheterisation
  • Cardiac MRI/CT Scan
72
Q

What is the management of DCM?

A
  • Fluids and Na restriction
  • Treatment of underlying disease
  • ACEi, b-blockers, diuretics, ARBs
  • Amiodarone
  • Anticoagulants
73
Q

What is HCM defined by?

A

A genetic cardiovascular disease defined by an increase in left ventricular wall thickness not solely explained by abnormal loading conditions

74
Q

What is HCM the leading cause of?

A

Sudden cardiac death in preadolescent and adolescent children

75
Q

What is the worrying thing about the symptoms for HCM?

A
  • Most patients are asymptomatic
  • The first clinical manifestation in these people may unfortunately be sudden death from ventricular tachycardia or fibrillation
76
Q

How commonly is HCM familial?

A

Familial HCM occurs as an autosomal dominant Mendelian-inherited disease in approx 50% of cases

77
Q

Describe the pathophysiology of HCM

A
  1. Thickening and disarray of LV myocardium; can occur in any region of the LV
  2. Frequently involves interventricular septum, results in obstruction of flow through LV outflow tract
  3. Disorganised myocytes disrupt signal conduction
  4. Ventricular arrythmias
  5. Sudden cardiac death
78
Q

How do patients with HCM present?

A
  • S4
    • Forceful atrial contraction into LVH
  • Syncope
    • Reduced CO to peripheries and head
  • Fatigue
    • Low CO and decrease organ perfusion
  • Angina
    • Low coronary perfusion
  • Ejection systolic murmur
    • Due to passage of blood through narrow outflow tract
  • Sudden cardiac death
79
Q

What investigations are done for HCM?

A
  • Echo
  • CXR
  • Cardiac MRI
80
Q

Describe the management of HCM

A

HCM with Symptoms:
Beta blockers

  • If contraindicated, Verapamil
  • If refractory and drugs fail, Mechanical Therapy with Pacemaker or Surgery (septal myectomy or ablation)
81
Q

What is restrictive cardiomyopathy characterised by?

A

Diastolic dysfunction with restrictive ventricular physiology but systolic function is normal

Atrial enlargement occurs due to impaired ventricular filling during diastole (due to stiffening of walls) but ventricular volume and wall thickness are normal

82
Q

What diseases is restrictive cardiomyopathy associated with?

A

CHAPFASS
- Carcinoid syndrome (rare cancerous neuroendocrine tumour secrets chemicals into blood)
- Haemochromatosis
- Amyloidosis (deposits of abnormal amyloid protein in heart)
- Previous radiation
- Fabry’s disease
- Anthracycline toxicity (Anthracycline is drug used in cancer chemo)
- Scleroderma
- Sarcoidosis (tiny collections of inflammatory cells forming granulomas in parts of body)

83
Q

Describe the pathophysiology of restrictive cardiomyopathy

A

Infiltrative cardiomyopathies are characterised by deposition of abnormal substances (i.e. amyloid proteins, noncaseating granulomas, iron) within heart tissue

  1. Infiltration causes ventricular walls to stiffen leading to diastolic dysfunction
  2. Atrial enlargement from impaired ventricular filling (but volume and thickness of ventricles normal)
  3. In early stages restrictive physiology predominates causing conduction abnormalities and diastolic heart failure
  4. Adverse remodelling may lead to systolic dysfunction and ventricular arrhythmias in advanced cases
  5. Reduced V filling leads to decreased CO
84
Q

How do patients present in restrictive cardiomyopathy?

A
  • Ascites and pitting oedema in peripheries
    • Increase VP –> right sided heart failure
  • Hepatomegaly
    • Hepatic congestion due to RHF
  • S4 heart sound
    • Atrium contracts into stiff ventricle
  • Increase in Jugular venous pressure
    • Due to RHF
  • Easy bruising, weight loss
    • Heart failure
85
Q

What investigations do we do for restrictive cardiomyopathy?

A
  • CBC- blood count
  • Serology
  • Amyloidosis check
  • ECG
  • Echocardiography
  • CXR
  • Catheterisation
  • MRI/Biopsy
86
Q

How do we manage restrictive cardiomyopathy?

A
  • Heart failure medication- including ACEi or Ang 2 receptor blockers, diuretics and aldosterone inhibitors for the reduced LV
  • Antiarrhythmic therapy
  • Immunosuppression- steroids
  • Pacemaker
  • Cardiac transplantation
87
Q

What is Patent foramen ovale (PFO)?

A

Where the naturally occurring opening hole between atria does not close after birth. PFOs can only occur after birth when the foramen ovale fails to close.

88
Q

What is Patent ductus arteriosus (PDA)?

A

An extra blood vessel found in babies before birth and just after birth. In most babies, the PDA will shrink and close on its own in the first few days of life. If it stays open longer, it may cause extra blood to flow to the lungs.

cardioresp (15 decks)

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