Valvular disease Flashcards

1
Q

What are the primary heart sounds?

A

S1 (atrioventricular valve closure) and S2 (semilunar valve closure)

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2
Q

What physiologically causes a heart sound?

A

As blood flows back towards the valve e.g., from ventricle back to atria, it pushes on the valve, causing it to snap shut = sound. In this case, it occurs because of the relative lower pressure in the atria compared to the ventricle.

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3
Q

What are heart murmurs?

A

Generated by turbulent flow of blood

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4
Q

What are the causes of heart murmurs? (x2)

A

Stenosis – restricting the opening of the heart valve; valvular insufficiency (regurgitation), which allows backflow of blood when the incompetent valve closes.

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5
Q

What is S1 split into?

A

T1 (tricuspid valve closure) and M1 (mitral valve closure)

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6
Q

What is S2 split into?

A

P2 (pulmonary valve closure) and A2 (aortic valve closure)

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7
Q

What is S3? Aetiology?

A

AKA ventricular gallop or Kentucky gallop because S1=Ken; S2=tuck; S3=y – it is a lower frequency sound. It indicates heart failure or volume overload: from oscillation of blood back and forth between the walls of the ventricles initiated by blood rushing from the atria. Benign in youth, some trained athletes and sometimes in pregnancy.

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8
Q

How can you differentiate between left and right-sided S3?

A

Right increased on inhalation, while left increased on exhalation.

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9
Q

What is S4? Aetiology?

A

AKA atrial gallop. Produced by the sound of blood being forced into a stiff or hypertrophic ventricle: TA-lub-dub or Tennessee (S4=Tenn; S1=ess; S2=ee). Stiff/hypertrophic ventricle can be caused by systemic hypertension, severe valvular aortic stenosis, and hypertrophic cardiomyopathy.

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10
Q

What is S7?

A

At rapid heart rates, the S3 and S4 merge to produce a summation gallop.

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11
Q

What do murmurs sound like?

A

Whooshing

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12
Q

How are heart murmurs categorised?

A

Systolic (heard during systole) and diastolic (heard during diastole)

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13
Q

What are the types of systolic heart murmur? (x3)

A
  • (Mid-)systolic ejection murmurs: due to turbulence through the semilunar valves at the start of ejection (between S1 and S2). The sound is crescendo-decrescendo.
  • Late-systolic murmurs: start AFTER S1 and, if left-sided, extend up to S2 in a crescendo manner
  • Holosystolic (pansystolic) murmurs: start AT S1 and extend up to S2.
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14
Q

What are the causes of mid-systolic ejection murmur? (x5)

A

Aortic stenosis, pulmonary stenosis, dilation of the aortic root/pulmonary artery, increased semilunar blood flow. Aortic regurgitation.

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15
Q

What are the causes of late systolic murmur? (x3)

A

Mitral valve prolapse, tricuspid valve prolapse, papillary muscle dysfunction (usually from STEMI)

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16
Q

What are the causes of holosystolic murmur? (x3)

A

Tricuspid regurgitation, mitral regurgitation, ventral septal defect.

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17
Q

What are the types of diastolic heart murmur? (x3)

A
  • Early diastolic: start AT the same time as S2 with the close of the SEMILUNAR valves and typically end before S1.
  • Mid-diastolic: start AFTER S2 and end before S1. They are due to turbulent flow across the ATRIOVENTRICULAR valves during the rapid filling phase.
  • Late diastolic (presystolic): start AFTER S2 and extend up to S1. They can be associated with ATRIOVENTRICULAR valve narrowing.
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18
Q

What are the causes of early diastolic murmur? (x3)

A

Aortic regurgitation, pulmonary regurgitation, late anterior descending artery stenosis.

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19
Q

What are the causes of mid-diastolic murmur? (x5)

A

Mitral stenosis, tricuspid stenosis, atrial myxoma (tumours), increased flow across the atrioventricular valve. Aortic regurgitation (see notes).

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20
Q

What are the causes of late diastolic murmur?

A

Complete heart block (third-degree block).

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21
Q

What is S1 splitting? Aetiology?

A

Delay of T1 leads to S1 splitting which is heard in right bundle branch block

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22
Q

What is S2 splitting? Aetiology – physiological and pathological?

A

Normally, A2 precedes P2 especially during inspiration where a split of S2 can be heard. Splitting of S2 is therefore also known as physiological splitting. A widely split S2 is associated with RBBB, pulmonary stenosis and atrial septal defect.

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23
Q

When is P2 louder?

A

P2 will be accentuated (louder) in pulmonary hypertension and pulmonary embolism, because the sound is the blood flowing back on the valve from pressure difference, and in these conditions, there is an abnormally high blood pressure in the pulmonary circuit.

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24
Q

What is aortic stenosis?

A

Obstruction of blood flow across the aortic valve due to pathological narrowing of the left ventricular outflow.

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25
Q

What is the aetiology of aortic stenosis? (x4)

A

(1) Stenosis secondary to rheumatic heart disease (where valves become damaged after rheumatic fever) – now uncommon in developed countries because of good treatment
(2) Calcification of a congenital bicuspid aortic valve
(3) Calcification or degeneration of tricuspid aortic valve in the elderly
(4) Congenital bicuspid valve (instead of normal tricuspid – results in abnormal shear and mechanical stresses on valve)

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26
Q

What are the risk factors of aortic stenosis? (x6)

A

Smoking, hypertension, diabetes, high cholesterol, high CRP, chronic kidney disease (associated with abnormal calcium homeostasis)

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27
Q

What is the pathophysiology of aortic stenosis?

A

Endocardium damage initiates inflammatory process that leads to calcium deposition on the valve.

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28
Q

What is the epidemiology of aortic stenosis: Prevalence? Gender?

A

3% of 75-year-olds. More common in men.

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29
Q

What are the symptoms of aortic stenosis? (x3)

A

Angina (because of increased oxygen demand of the hypertrophied ventricles to overcome obstructive valve), syncope/dizziness on exercise (unable to eject large volumes because of obstruction), and symptoms of heart failure e.g., dyspnoea (arising from left ventricular hypertrophy).

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30
Q

What are the signs of aortic stenosis on auscultation? (x2)

A

Harsh systolic ejection (or ejection systolic) murmur at aortic area radiating to carotid artery and apex. Second heart sound (A2 component) may be softened or absent because of calcification.

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31
Q

What are the other signs of aortic stenosis? (x4)

A
  • BP – narrow pulse pressure (since heart cannot pump much volume round systemic circuit, so pressure gradient between systole and diastole are less substantial)
  • Pulse – slow rising for the same reason
  • Pulsus parvus et tardus – in severe aortic stenosis; weak and delayed carotid upstroke. Felt by palpating carotid artery.
  • Palpation – thrill in the aortic area if severe, with no apex beat displacement
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32
Q

What are the two main differentials of aortic stenosis?

A

Aortic sclerosis and hypertrophic obstructive cardiomyopathy.

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33
Q

What are the investigations for aortic stenosis? (x5)

A
  • ECG: signs of left ventricular hypertrophy (deep S wave in V1 and 2, tall R wave in V5 and 6, inverted T waves in I, aVL, V5 and 6, and left-axis deviation), and LBBB
  • CXR: post-stenotic enlargement of the ascending aorta, calcification of the aortic valve
  • Echocardiogram (Doppler): visualises valve and level of stenosis (valvar, supravalvar, or subvalvar). You can also estimate aortic valve cross-sectional area and pressure gradients across the valve in systole (elevated in AS)
  • Cardiac angiography: allows differentiation from other causes of angina and to assess concomitant coronary artery disease (50% of severe aortic stenosis patients have significant coronary artery disease)
  • Catheterisation (only if diagnosis inconclusive) allows for direct measurement of pressure gradient across aortic valve – raised.
34
Q

What are the signs of left ventricular hypertrophy on ECG? (x4)

A

Deep S wave in V1 and 2, tall R wave in V5 and 6, inverted T waves in I, aVL, V5 and 6, and left-axis deviation

35
Q

What is aortic sclerosis?

A

Thickening and calcification of the aortic valve without an obstruction of the ventricular flow of blood. This condition affects the aortic valve and may lead to aortic stenosis.

36
Q

How does sclerosis and stenosis differ in signs and clinical significance?

A

Aortic sclerosis is physiological; Aortic stenosis is pathological. Stenosis can be differentiated on auscultation because although in both, you can hear systolic murmurs (from turbulent flow), in stenosis, you can hear in the carotids and across the whole heart. Sclerosis can be auscultated very locally.

37
Q

What is aortic regurgitation?

A

Reflux of blood from aorta into left ventricle during diastole. AKA Aortic insufficiency.

38
Q

What is the aetiology of aortic regurgitation? (x3)

A
  • Aortic valve leaflet abnormalities such as bicuspid aortic valve
  • Aortic valve leaflet damage such as infective endocarditis, rheumatic fever and trauma
  • Aortic root/ascending aorta dilation: systemic hypertension, aortic dissection, aortitis (e.g., syphilis), rheumatic heart disease, arthritides (rheumatoid arthritis, seronegative arthritides), Marfan’s syndrome, pseudoxanthoma elasticum, Ehlers-Danlos syndrome, osteogenesis imperfecta
39
Q

What is the pathophysiology of acute aortic regurgitation?

A

Reflux of blood into LV during diastole results in left ventricular dilation and increased end-diastolic volume (low end-diastolic pressure in the aorta). Heart tries to compensate by increasing HR and contractility (Starling’s law), but this is insufficient to maintain the normal stroke volume and the heart fails.

40
Q

What is the pathophysiology of chronic aortic regurgitation?

A

Increased left ventricular volume and pressure leads to increased wall tension, leading to compensatory hypertrophy. This results in systolic hypertension (secondary to increased stroke volume). There is also compensatory ventricular enlargement to balance out increased end-diastolic pressure.

41
Q

What is the epidemiology of aortic regurgitation: Age? Gender?

A

Chronic AR often begins in late 50s, documented most frequently in over 80s. More common in men.

42
Q

What are the symptoms of chronic aortic regurgitation? (x2)

A

Later, symptoms of heart failure such as exertional dyspnoea, orthopnoea and fatigue. Occasionally angina when heart tries to compensate.

43
Q

What are the symptoms of acute aortic regurgitation? Why?

A

Sudden cardiovascular collapse because left ventricle cannot adapt to the rapid increase in end-diastolic volume caused by regurgitant blood.

44
Q

What is cardiovascular collapse?

A

Severe hypotension from acute dysfunction of the heart.

45
Q

!!! What are the signs of aortic regurgitation on auscultation? (x3 murmurs, x2 sounds)

A

(1) Early diastolic murmur at lower left sternal edge, better heard with the patient sitting forward with the breath held in expiration.
(2) (Mid-)systolic ejection murmur (two names mean the same thing) is often heard because of increased flow across valve.
(3) Austin Flint mid-diastolic murmur (a type of mid-diastolic or early-diastolic murmur characterised by low-pitched rumbling sound) over the apex from turbulent reflux hitting anterior cusp of mitral valve and causing a physiological mitral stenosis.
(4) Soft S1 due to early adaptation of the mitral valve leaflets to increased end-diastolic pressure.
(5) Soft or absent A2 caused by inadequate closure of aortic valve in severe disease.

46
Q

What are the other signs of aortic regurgitation? (x2)

A
  • Collapsing ‘water-hammer’ pulse (forceful upstroke (because of high stroke volume) and descent (from regurgitation)) and wide pulse pressure (from the combination of increased stroke volume and low end-diastolic pressure in the aorta)
  • Rare signs associated with water-hammer pulse
47
Q

What are the rare signs associated with water-hammer pulse? (x10)

A
  • Quincke’s sign: visible pulsations on nailbed
  • de Musset’s sign: head nodding in time with pulse
  • Becker’s sign: visible pulsation of the pupils and retinal arteries
  • Muller’s sign: visible pulsations of the uvula
  • Corrigan’s sign: visible pulsations in neck
  • Traube’s sign: ‘pistol shot’ (systolic and diastolic sounds) heard on auscultation of the femoral arteries
  • Duroziez’s sign: systolic and diastolic bruit heard on partial compression of femoral artery with a stethoscope
  • Rosenbach’s sign: systolic pulsations of liver
  • Gerhard’s sign: systolic pulsations of spleen
  • Hill’s sign: popliteal cuff systolic pressure exceeding brachial pressure by 60 mmHg.
48
Q

What is another name for water-hammer pulse?

A

Hyperdynamic pulse.

49
Q

What are the investigations for aortic regurgitation? (x4 (x3, x1, x2, x1))

A
  • CXR: cardiomegaly, dilation of ascending aorta, signs of pulmonary oedema associated with left heart failure
  • ECG: left ventricular hypertrophy signs
  • Echocardiogram: 2D ECHO and M-MODE indicate cause e.g., aortic route dilation, bicuspid valve, OR the effects of the regurgitation e.g., left ventricular dilation and fluttering of the anterior mitral valve leaflet. DOPPLER detect the AR and assess severity by quantifying regurgitant flow
  • Cardiac catheterisation with angiography: if diagnostic uncertainty
50
Q

What is mitral stenosis?

A

Mitral valve narrowing causing obstruction to blood flow from the left atrium to ventricle.

51
Q

What is the aetiology of mitral stenosis? (x6)

A
  • Rheumatic heart disease
  • Congenital mitral stenosis
  • SLE
  • Rheumatoid arthritis
  • Endocarditis
  • Atrial myxoma (rare cardiac tumour)
52
Q

What is the epidemiology of mitral stenosis: Most common cause? Trend in incidence? Gender?

A

90% caused by rheumatic heart disease. Incidence declining in industrialised countries due to declining rheumatic fever. Higher incidence in females.

53
Q

What is the pathophysiology of mitral stenosis? (x2 points)

A

Mitral stenosis leads to increased left atrial pressure which is referred to the lungs resulting in congestion (oedema, right ventricular hypertrophy – hypertrophy leads to pulmonary hypertension). Mitral stenosis also limits filling of the left ventricle, thereby limiting CO.

54
Q

What are the symptoms of mitral stenosis?

A
  • Fatigue
  • SOB on exertion or orthopnoea
  • Palpitation (related to AF)
  • Rare symptoms: cough, haemoptysis, hoarseness caused by compression of the left laryngeal nerve by the enlarged left atrium
55
Q

What are the signs of mitral stenosis on auscultation? (x3)

A

Loud S1 with opening snap, mid-diastolic murmur, evidence of pulmonary oedema on lunch auscultation (if patient has decompensated)

56
Q

What are the other signs of mitral stenosis? (x3)

A
  • Pulse may be thready or irregularly irregular (AF)
  • Apex beat is not displaced and tapping. Parasternal heave (right ventricular hypertrophy and portal hypertension)
  • Peripheral or facial cyanosis (malar flush called mitral facies)
57
Q

What may an ECG show in mitral stenosis? (x3)

A

May be normal; broad bifid p-wave (p mitrale) caused by left atrial hypertrophy, AF, or evidence of right ventricular hypertrophy in cases of severe pulmonary hypertension.

58
Q

What are the other investigations for mitral stenosis? (x3)

A
  • CXR: left atrial enlargement, cardiac enlargement, pulmonary congestion, mitral valve may be calcified in rheumatic cases
  • Echocardiography: assess functional and structural impairments. Transoesophageal gives better valve visualisation
  • Cardiac catheterisation: measure severity of heart failure by calculating valve area and pressure gradient
59
Q

What is mitral regurgitation?

A

AKA Mitral insufficiency. Retrograde flow of blood from LV to left atrium during systole (unlike diastole in AR).

60
Q

What is the aetiology of mitral regurgitation? (x2 and x3)

A

Mitral valve damage: rheumatic heart disease, infective endocarditis; OR mitral valve dysfunction: prolapse (into left atrium during systole), papillary muscle rupture/dysfunction (secondary to IHD or cardiomyopathy), or chordal rupture and floppy mitral valve associated with connective tissue diseases.

61
Q

What connective tissue diseases are associated with mitral regurgitation? (x5)

A
  • Pseudoxanthoma elasticum (collagen/elastic tissue disorder characterised by yellow papules on the skin in flexures, ischaemic heart disease, GI bleeding and angioid streaks on fundoscopy)
  • Osteogenesis imperfecta (autosomal dominant mutation in Type I Collagen causing brittle, deformed bones, blue sclerae and hypermobile joints)
  • Ehlers-Danlos syndrome: genetic defects in Type III collagen resulting in joint hypermobility and skin hyper-elasticity and fragility. Can result in rupture of arteries.
  • Marfan Syndrome
  • SLE
62
Q

What is chordal rupture?

A

Chordae tendineae that hold mitral valve open become ruptured.

63
Q

What is the epidemiology of mitral regurgitation: Most common aetiology? Prevalence? Gender and age?

A

Most common cause is rheumatic heart disease. Affects 5% of adults. More common in young females.

64
Q

What is the pathophysiology of mitral regurgitation?

A
  • ACUTE PHASE: due to sudden rupture of a chorda tendinae or papillary muscle resulting in sudden volume overload of both the left atrium (from the regurgitation) and ventricle (from the excess that is pumped into the ventricle from the atrium overload). Overload leads to left ventricle failure, decreased ejection fraction and can lead to pulmonary congestion.
  • CHRONIC PHASE: left ventricle becomes hypertrophied and there is increased stroke volume. There is also LA enlargement. In a compensated state, patient is asymptomatic. In the long-term, patients become decompensated with left ventricular failure and ventricular dilatation. Pulmonary congestion also reappears.
65
Q

What are the symptoms of mitral regurgitation: Acute? Chronic?

A
  • ACUTE: symptoms of left ventricular failure, dilation
  • CHRONIC: exertional dyspnoea, palpitations if in AF and fatigue
66
Q

What are the symptoms of mitral valve prolapse? (x2)

A

Atypical chest pain or palpitations.

67
Q

What are the signs of mitral regurgitation on auscultation? (x3)

A

(1) Pansystolic murmur, loudest at apex, radiating to axilla (palpable as a thrill). (2) S1 is soft. (3) S3 may be heard from rapid ventricular filling in early diastole.

68
Q

What are the other signs of mitral regurgitation? (x3)

A
  • Pulse may be normal or irregularly irregular (AF)
  • Apex beat may be laterally displaced and thrusting from left ventricular dilation
  • Signs of left ventricular failure in acute mitral regurgitation
69
Q

What are the signs of mitral valve prolapse? (x2 on auscultation +1 change)

A

Mid-systolic click and late systolic murmur. The click moves towards S1 on standing and moves away on lying down.

70
Q

What may an ECG show with mitral regurgitation?

A

AF, AND broad, bifid p wave (p mitrale) indicating delayed activation of the left atrium due to left atrial enlargement

71
Q

What are the other investigations for mitral regurgitation? (x2) (CXR x1 and x3)

A
  • CXR: acute may produce signs of left ventricular failure. Chronic shows left atrial enlargement, cardiomegaly from left ventricular dilation, or mitral valve calcification in rheumatic cases.
  • Echocardiography: every 6-12 months for moderate-severe MR to assess the LV ejection fraction and end-systolic dimension
72
Q

What is tricuspid regurgitation?

A

Backflow of blood from right ventricle to the right atrium during systole.

73
Q

What is the aetiology of tricuspid regurgitation? (x8)

A
  • Congenital: Ebstein anomaly (malpositioned tricuspid valve), cleft valve in ostium primum defect.
  • Functional: consequence of right ventricular dilation e.g., in pulmonary hypertension, or valve prolapse
  • Rheumatic heart disease
  • Infective endocarditis: common in IV drug users
  • Carcinoid syndrome
  • Trauma
  • Long-standing cirrhosis
  • Iatrogenic: radiotherapy to the thorax, or pacemaker lead gets entrapped in valve
74
Q

What genus are most cases of endocarditis?

A

Staphylococcal.

75
Q

What is the pathophysiology of tricuspid regurgitation? (x4 processes leading to…x3 congestive consequences)

A

Dysfunction arises from a congenital abnormality in the valve, or from elevation of right ventricular pressure, ventricular enlargement or tricuspid annular dilation in a normal tricuspid. This results in elevated right atrial pressure, and atrial distension and hypertrophy leading to AF. This leads to congestion in the systemic system which can lead to cardiac cirrhosis (ascites from advanced liver disease), gut congestion (with symptoms of dyspepsia), and fluid retention with leg oedema.

76
Q

What is the epidemiology of tricuspid regurgitation: Most common cause?

A

Infective endocarditis most common cause.

77
Q

What are the symptoms of tricuspid regurgitation?

A

Fatigue, breathlessness, palpitations, headache, nausea, anorexia, epigastric pain made worse by exercise, jaundice, lower limb swelling, dyspepsia.

78
Q

What are the signs of tricuspid regurgitation on auscultation? (x2)

A

Pansystolic murmur heard best at lower left sternal edge, louder on inspiration (Carvallo sign). Loud P2 component of S2.

79
Q

What are the other signs of tricuspid regurgitation? (x6)

A
  • Pulse may be irregularly irregular with AF associated with atrial dilation
  • Increased JVP with giant v waves which may oscillate the earlobe. This is caused by transmission of right ventricular pressure to the great veins.
  • Parasternal heave
  • Pleural effusion from pulmonary hypertension (aetiology of TR)
  • Palpable liver (tender, smooth, pulsatile) and ascites
  • Pitting oedema
80
Q

What is AF associated with in tricuspid regurgitation?

A

Atrial dilation.

81
Q

How does tricuspid regurgitation present on an ECG? (x2)

A

Tall P wave (right atrial hypertrophy) in sinus rhythm, or AF.

82
Q

What are the other investigations for tricuspid regurgitation? (x4)

A
  • Bloods: LFTs, U&Es abnormal from congestion, and FBC shows anaemia from anaemia of chronic disease or renal failure. FBC may also show thrombocytopenia due to cardiac cirrhosis.
  • CXR: right-sided enlargement of cardiac shadow, and may show pleural effusion
  • Echocardiography: colour flow Doppler can estimate extent of regurgitation and may be able to detect abnormality and right ventricular dilation
  • Right heart catheterisation: may be considered to assess pulmonary artery pressure