Valvular Heart Disease Flashcards

1
Q

What are the four phases of the cardiac cycle?

A
  1. Ventricular filling (Diastole)
  2. Isovolumetric contraction (Systole)
  3. Ejection (Systole)
  4. Isovolumetric relaxation (Diastole)

Each phase has distinct physiological events that contribute to heart function.

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2
Q

What occurs during ventricular filling?

A

Passive filling of the atria from the vena cava and pulmonary veins into the left and right atria, flowing into ventricles; mitral and tricuspid valves open, semilunar valves closed

At the end of diastole, atrial contraction occurs, contributing to ventricular filling.

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3
Q

What happens during isovolumetric contraction?

A

Pressure builds in the ventricles, causing closure of the AV valves; all valves are closed and ventricular pressure rises without volume change.

This phase is critical for assessing cardiac contractility.

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4
Q

What happens during ejection?

A

SYSTOLE where ventricular pressure exceeds the aorta and this triggers the opening of the semi-lunar valves and blood passes through to the rest of the body, where the end systolic volume is created and can be used to determine ejection fraction. Eventually ventricular pressure is below arterial pressure, so the semilunar valves close, creating a rise in arterial pressure

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5
Q

What causes the diacrotic notch?

A

The closure of the semilunar valves, which indicates end of systole closure and successful prevention of backflow stream.

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6
Q

What triggers the ejection phase of the cardiac cycle?

A

Ventricular pressure exceeds aortic pressure, opening the semilunar valves and allowing blood to flow into the aorta.

This phase results in the creation of end-systolic volume.

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7
Q

What is the dicrotic notch?

A

A rise in arterial pressure created by the closure of the semilunar valves, indicating the end of systole.

It is an important feature in arterial pressure waveform analysis.

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8
Q

What is isovolumetric relaxation?

A

DIASTOLE where both sets of valves are now closed and ventricular pressure begins to reduce to below atrial pressure, which leads to opening of the atrioventricular valves and restarting of the cycle

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9
Q

What does the S1 heart sound indicate?

A

Closure of the atrioventricular valves during early systole.

It is one of the primary heart sounds used in auscultation.

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10
Q

What does the S2 heart sound indicate?

A

Closure of the semilunar valves during late systole, creating a dicrotic notch on a graph.

S2 is typically louder than S1 due to higher pressures on the left side of the heart.

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11
Q

What is a split S2 heart sound?

A

Occurs when the closure of the aortic and pulmonary valves is out of sync, often normal during inspiration.

Pathological causes can include conditions like pulmonary hypertension and right bundle branch block.

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12
Q

What is paradoxical split S2?

A

Delay in closure of the aortic valve, causing greater splitting during expiration and pulmonary valve to close first.

This can occur due t conditions affecting the aortic valve such as severe aortic stenosis, hypertrophic obstructive cardiomyopathy or left bundle branch block.

This can occur due to conditions such as severe aortic stenosis.

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13
Q

What is fixed split S2?

A

Fixed split S2 is where there is a delay in closure of the pulmonary valves with no effect from insipiration.

This can occur due to an atrial septal defect, where expiration causes presssure in the right atrium to decrease as normal but high pressure blood flows abnormally from the left to the right atria through the defect, which disrupts the pressure gradient and delays closure of the PV valve.

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14
Q

What are the features of the mitral valve?

A

Mitral valve is bicuspid, with the anterior leaflet longer than the posterior leaflet.

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15
Q

What is S3 heart sound?

A

S3 heart sound is a low pitched sound in the isovolumetric diastole phase after S2, indicating fast ventricular filling. It can indicate systolic heart failure, where the left ventircle is compliant due to dilation. This sound occurs with mitral and aortic regurgitation.
This can be normal finding in children, pregnant women and young athletes.

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16
Q

What is the S4 heart sound?

A

S4 heart sound occurs prior to S1 heart sound in the diastole ventricular filling phase due to reduced ventricualr compliance And slow filling, assoicated with left ventircular hypertrophy.

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17
Q

What are the atrioventricular valves?

A

Atrioventricular valves consist of
-> Tricuspid
-> Mitral which is bicuspid, between the left atrium and ventricle and anterior leaflet is longer than left.

They are attached by fibrous cords called the chordate tendinae to connect it to the valve cusps at the papillary muscles on the ventricles, which work simultaneously to promote valve closure. Papillary muscles contract during ventricular systole to prevent valve prolapse into atria.

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18
Q

What is the consequence of volume overload?

A

Volume overload of the heart chamber causes eccentric hypertrophy, where dilatation thins the chamber walls, resulting in S3 heart sound due to issue with systole causing backflow of blood.

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19
Q

What is the consequence of pressure overload?

A

Pressure overload of the heart chamber causes concentric hypertrophy to enlarge the myocardial cells hypertrophy to accomodate for increased force of contraction, resulting in S4 heart sounds due to issue with diastole filling.

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20
Q

What is acute rheumatic fever?

A

Acute rheumatic fever is an autoimmune condition that occurs 2-4 weeks following a Group A Strep with a throat infection such as streptococcus pyogenes. This has an M protein that is targeted by immune cells, however its similar structure to cardiomycin results in molecular mimicry and susceptibility to pericarditis, myocarditis, mitral regurgitation, heart failure and infective endocarditis.

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21
Q

What is the presentation of acute rheumatic fever?

A

Clinical presentation is with fever, abdominal pain and epistaxis
JONES
* Joint pain with asymmetrical poly arterial IgA
* Carditis, resulting in chest pain, dyspnoea and palpitations. Pericarditis may resolve in haemodynamic instability while the myocarditis may result in acute heart failure and arrythmia. Endocarditis commonly affects the mitral valve most, followed by the aortic valve and tricuspid valve, where regurgitation and heart failure occur.
* Nodules that are subcutaneous found on the extensor regions of the hands,s feet and knees lasting for 2 weeks, occurring after pericarditis
* Erythema marginatum, where a large red circle with a clear border forms on the centre of the chest. It begins
* Syndenham’s chorea: involuntary jerky movements due to inflammation of the caudate nucleus and putamen, involved in movement regulation

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22
Q

What is the pathophysiology of mitral stenosis?

A

There is limitations to the passive filling of the left atria and pressure in the left atria increases, creating an abnormal pressure gradient that causes backflow into the pulmonary vasculature and resulting in pulmonary hypertension and congestive heart failure. There is also left atrial diliatation which may result in atrial fibrillation and increases the risk of emboli formation . The pulmonary hypertension may result in pulmonary and tricuspid valve regurgitation, leading to right sided heart failure. Normal ventricular function maintains normal cardiac output initially, however reduced filling in diastole due to stenosis leads to loss of compensatory increase in CO during exertion.

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23
Q

What is the presentation of mitral stenosis?

A

Patients typically present with symtpoms of heart failure with
Shortness of breath, Paroxysmal nocturnal dyspnoea: SOB which worsens at night
Ascites , Oedema Hepatomegaly Fatigue and weakness on exertion ( reduced cardiac ouptut)
There is a risk of atrial fibrillation due to left atrial volume and pressure overload.

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24
Q

What are signs of mitral stenosis?

A

Tapping apex beat
Palpable and louder S1 sound due to stiff mitral valve
Opening snap sound due to stiff mitral valve
Mid-diastolic rumbling murmur at left heart apex due to reduced filling
S4 heart sound
Parasternal heave due to right ventricle hypertrophy
Prominent a waves in JVP
Malar flush

These signs reflect the hemodynamic changes due to the narrowed valve.

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25
Q

What is the clinical presentation of acute rheumatic fever?

A
  1. Fever
  2. Abdominal pain
  3. Epistaxis
  4. Joint pain (JONES criteria)
  5. Carditis
  6. Nodules
  7. Erythema marginatum
  8. Syndenham’s chorea

The JONES criteria help in diagnosing this autoimmune condition.

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26
Q

What is the treatment for rheumatic fever?

A
  1. Prophylactic antibiotics (e.g., erythromycin, benzylpenicillin)
  2. Aspirin for inflammation
  3. Management of heart failure with diuretics, ACE inhibitors, and digoxin

Early treatment is important to prevent long-term complications.

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27
Q

What is Malar flush?

A

Malar flush may occur, where there is reddening across the nose and cheeks due to CO2 retention from mitral valve stenosis, where back pressure into the right ventricle reduces gas exchange in the lungs.

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28
Q

What are the signs of right sided heart failure?

A

Raised JVP
Pedal oedema and ascites
Hepatomegaly
Early diastolic murmur due to pulmonary regurgitation from pulmonary hypertension
Signs of left sided heart failure:
Orthopnea
Exertional dyspnoea
Paroxysmal nocturnal dyspnoea
Fatigue

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29
Q

What are the ECG findings for mitral stenosis?

A

ECG which shows:
bifid (double peaked) P waves indicating left atrial enlargement
Atrial fibrillation
Right axis deviation when right ventricle hypertrophy occurs due to pulmonary hypertension

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30
Q

What does X-ray show for mitral stenosis?

A

Double border of right ventricle, indicating hypertrophy
Pulmonary congestion
Enlargement of all heart chambers (severe stage)
Prominent pulmonary arteries indicating hypertension
Mac-Callum’s patch
Kerley B lines indicating pulmonary oedema

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31
Q

What is Mac-Callum’s patch?

A

Irregular area of thickening in the left atrial wall due to previous severe rheumatic fever endocarditis

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32
Q

How is mitral stenosis managed?

A

Management is dependent on symptom severity
Mild/conservative management: salt restriction, diuretics,
Prophylactic antibiotic benzylpenicillin for those with rheumatic fever
Anti-arrythmia drugs, beta blocker or calcium channel blocker for rate control
Anti-coagulants due to risk of blood clots
Diuretics to manage heart failure

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33
Q

What is the pathophysiology of mitral valve regurgitation?

A

The backflow of blood into the left atrium causes the left atria to increase with pressure and volume overload. Due to the regurgitation back into the left atria, during the diastolic filling phase, there is more blood in the left atria and this passes to the left ventricle which undergoes hypertrophy. The anelargmeent of the left atria may compress the oesophagus and cause Chronic mitral regurgitation causes Fatigue, palpitations diaphoresis, exertional dyspnoea and pedal oedema.

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34
Q

What are the acute causes of mitral regurgitation?

A

Acute causes include infective endocarditis, acute myocardial infarction or trauma to the valve.

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35
Q

What are the chronic causes of mitral regurgitation?

A

Chronic damage to the valve, from mitral valve prolapse, dilatation cardiomyopathy, collagen vascular disease or hypertrophic cardiomyoapthy.

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36
Q

How does MI cause mitral regurgitation?

A

Myocardial infarction due to papillary muscle rupture or cardiac remodelling, where infarction induces myocyte necrosis and recruitment of immune cells such as neutrophils and macrophages which cause further damage and increase the ifnarcted area. This region is unable to withstand the blood pressure, and results in thinning and dilatation of the left ventricle chamber and cause thinning and dilatation of the left ventricle and the infarcted area stretches. The remaining healthy cardiomycytes undergo hypertrophy due to their compensatory effort to maintain ejection fraction, which dilates the chamber further making it prone to mitral valve regurgitation. The neurohormonal activation of the RAAS system and sympathetic system can further induce fibrosis.

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37
Q

How does dilated cardiomyopathy cause mitral regurgitation?

A

Dilated cardiomyopathy where the chambers become larger and the myocardium becomes thinner allows blood to leak more easily through the valves, that cannot of
Hypertrophic cardiomyopathy mitral valve does not adapt quickly enough and moves anteriorly during systole due to stenosis of septum pulling the anterior leaflet inwards and the annulus enlarges through dilatation, resulting in backflow of blood into left atrial

38
Q

What are common causes of mitral valve regurgitation?

A
  1. Acute infective endocarditis
  2. Acute myocardial infarction
  3. Mitral valve prolapse
  4. Dilated cardiomyopathy
  5. Papillary muscle rupture

Chronic causes can include degenerative changes or rheumatic heart disease.

39
Q

What is infective endocarditis?

A

Infective endocarditis, caused by endocardial insult followed by a period of bacteraemia that can arise from a contaminated prosthetic valve, chronic inflammation, devices-related trauma or turbulent blood flow around diseased valves which introduces infective pathogens and results in fibrin-platelet deposits. This eventually results in bacteria adhering onto the site and creating a film. Parts of this deposit can detach and form septic emboli distal to their site of origin. This typically affects highly vascularised organs like the heart affects the aortic and mitral valve, causing heart failure and increases the risk for stroke in the brain and glomerulonephritis, spleen infarction and abscess and pulmonary embolism.
Dental sepsis is a common risk.

40
Q

What are the investigations for infective endocarditis?

A

Investigations include:
Blood cultures, FBC for u&Es, LFTs, ESR
Urinalysis
ECG to assess for AV block or conduction defects
CXR for pulmonary oedema or infarction from septic embolism
ECHO for valve lesions

41
Q

How does infective endocarditis present?

A

There is varying onset presents with fever, rigours/chills, fatigue, dyspnoea, chest pain and haematuria with blackening of extremities due to emboli.
Cutaneous manifestations are Janeway lesions and Osler nodes

Investigations show raised CRP and ESR, leukocytosis. Management is typically antibiotics with fluid resuscitation and monitoring for sepsis

42
Q

What is myxomatous degeneration?

A

Myxomatosis degenration where mucopolysaccharides are deposited in the spongiest layer of the leaflets causes thickened leaflets that cauases chorae tendinae to elongate and eventually rupture, resulting in prolapse during ventricular systole.

This condition can predispose valves to further dysfunction.

43
Q

What are Janeway lesions and Osler nodes?

A
  1. Osler nodes are tender nodules found on the distal fingers and toes due to chronic endocarditis and are an immunological manifestation.

2.Janeway lesions are non-tender haemorrhagic plaques on the palms or soles and are a vascular manifestation

Both are cutaneous manifestations of infective endocarditis.

44
Q

What investigations are used for infective endocarditis?

A
  1. Blood cultures
  2. FBC for u&Es, LFTs, ESR
  3. Urinalysis
  4. ECG for AV block
  5. CXR for pulmonary complications
  6. ECHO for valve lesions

These investigations help confirm the diagnosis and assess the severity.

45
Q

What are the clinical signs of mitral regurgitation?

A

Pansystolic murmur radiating to axillary during systole due to backflow of blood into left atria during systole
Diminished S1 heart sound
Left ventricular heave which is Palpable apex thrill due to left ventricular hypertrophy

Splitting of S2 due to premature aortic valve closure because of early LV systole as a result of reduced resistance of blood from backflow into left atria affecting pressure gradient
S3 heart sound due to systolic heart failure indicating deceleration of blood from left atrial to left ventricle due to

46
Q

What are the investigations for mitral regurgitation?

A

Bifid P wave from left atria enlargement
Left axis deviation due to left ventricular hyertrophy
Atrial fibrillation

47
Q

What is acute mitral regurgitation?

A

normal compliance does not affect enlargement of left atria, however left atria rises in pressure and can lead to backflow, causing pulmonary oedema.the left ventricle remains abnormal size and no compensatory enlargement occurs, resulting in a reduced cardiac output.

48
Q

What is chronic mitral regurgitation?

A

Enlargement of LA occurs to accommodate volume overload and results in dilataiton and induces the left ventricle to dilate which eventually has volume overload, resulting in a large stroke volume to maintain ejection fraction.

49
Q

What does a Wilkins score assess?

A

The mitral valve to predict the success of balloon valvuloplasty based on leaflet thickness, calcification, fusion, and mobility.

This score helps in planning intervention strategies for mitral stenosis.

50
Q

What are the symptoms of embolism?

A

Fever, rigours/chills, fatigue, dyspnoea, chest pain, haematuria, blackening of extremities due to emboli

51
Q

What are Janeway lesions?

A

Non-tender haemorrhagic plaques on the palms or soles, a vascular manifestation

52
Q

What are Osler nodes?

A

Tender nodules found on the distal fingers and toes due to chronic endocarditis, an immunological manifestation

53
Q

What investigations show raised inflammatory markers in embolism?

A

CRP, ESR, leukocytosis

54
Q

What is the typical management for infective endocarditis?

A

Antibiotics, fluid resuscitation, monitoring for sepsis

55
Q

What is mitral valve prolapse?

A

Mitral valve prolapse is where the leaflets of the mitral valve billow during systole and collapse Ito the left atria, which are associated with connective tissue disorders like Ehers-Danlos syndrome and Marfan syndrome. Myxomatosis degenration where mucopolysaccharides are deposited in the spongiest layer of the leaflets causes thickened leaflets that cauases chorae tendinae to elongate and eventually rupture, resulting in prolapse during ventricular systole. Osteogenesis imperfecta can cause mitral valve.

56
Q

What is the presentation of mitral valve prolapse?

A

Presentiation is atypical chest pain and palpitations from ventricular arrythmias. There may be a mid or late systolic click due to tensing of chordae tendinae and leaflet prolapse. Activation of the sympathetic nervous system to compensate causes anxiety, syncope and panic attacks.

57
Q

What is the signs of mitral valve prolapse?

A

Irregularly irregular heart rate
Displaced apex beat due to hypertrophy of left ventricle from increased pressure from built up left atria
Mid-late systolic click murmur over mitral area due to regurgitation which is more easily heard with Valsalva manoeuvre which increases intrabdominal pressure and reduces preload and lengthen the murmur

ECG is typically normal or with atrial fibrillationand CXR unless mitral regurgitation occurs. Diagnosis is based on echocardiogram.

Management is mitral valve repair, anticoagulants for arrythmias and beta blockers for chest pain or palpitations

58
Q

What causes late prosthetic valve endocarditis?

A

Abnormal flow around prosthetic valve producing micro thrombi and non-bacterial thrombotic vegetations becoming infected

59
Q

What is the difference between early and late prosthetic valve endocarditis?

A

Early occurs due to staphylococci in the pre-operative period; late occurs due to abnormal flow around the valve

60
Q

What are the complications of prosthetic valve endocarditis?

A

High degree AV block, perforated IV septum

61
Q

Name the types of mitral regurgitation according to Carpentier’s classification.

A
  • Type 1: normal leaflet motion
  • Type 2: leaflet prolapse from myxomatous degeneration
  • Type 3a: restricted leaflet opening from rheumatic disease
  • Type 3b: restricted leaflet closing from ischaemic dilated cardiomyopathy
62
Q

What are the acute presentations of mitral regurgitation?

A

Cardiogenic shock, pulmonary oedema, hypotension

63
Q

What are the clinical signs of mitral regurgitation?

A
  • Pansystolic murmur radiating to axilla
  • Diminished S1 heart sound
  • Left ventricular heave
64
Q

What are the stages of mitral regurgitation?

A
  • Acute: normal compliance, left atrial pressure rises
  • Chronic: enlargement of left atrium and left ventricle dilation
65
Q

What does the auscultation of mitral regurgitation reveal?

A
  • Soft S1
  • Splitting of S2
  • Mid-diastolic flow murmur
  • S3 heart sound
  • Pansystolic murmur
66
Q

What are the key investigations for mitral regurgitation?

A
  • ECG: bifid P wave, left axis deviation, atrial fibrillation
  • CXR: cardiomegaly, left atrial and ventricular enlargement
  • Transoesophageal echocardiogram
67
Q

What is the prognosis for mitral regurgitation?

A

Poor with more symptoms, majority of deaths due to arrhythmia or heart failure

68
Q

What is the management for mitral regurgitation?

A
  • Salt restriction
  • Treatment of heart failure
  • Surgical repair if left ventricular ejection fraction below 60%
69
Q

What is mitral valve prolapse?

A

Condition where the leaflets of the mitral valve billow during systole and collapse into the left atrium

70
Q

What are the clinical signs of mitral valve prolapse?

A
  • Irregularly irregular heart rate
  • Displaced apex beat
  • Mid-late systolic click murmur
71
Q

What is the most common valvular diseases?

A

Aortic Stenosis.

72
Q

What is aortic stenosis commonly associated with?

A

Old age and aortic regurgitation

73
Q

What are the risk factors for aortic stenosis?

A
  • Hypertension
  • Obesity
  • Hyperlipidaemia
  • Smoking
  • Diabetes
74
Q

What are the symptoms of aortic stenosis?

A
  • Syncope
  • Angina
  • Dyspnoea
75
Q

What are the causes of aortic stenosis?

A

Congenital Heart disease With vicusppid valve
Rheumatic fever
Calcification

76
Q

What is the pathophysiology of aortic stenosis?

A

Decreased pumping capacity of the left ventircle results in increased after load and concentric hypertrophy. Pressure overload from failed ejection of blood results in a high end-systolic pressure and causes left ventricular hypertrophy that increases oxygen demand and systolic heart failure that progresses to congestive heart failure. The increased demand for oxygen results in angina. There is increased risk of ventricular arrythmias that can result in sudden cardiac death. The failure of the left ventricle when untreated leads to congestive heart failure. The narrowing of the valve decreases flow (volume) of blood but increases. There is dilatation of ascending aorta post-stenosis.

77
Q

What are the clinical signs of aortic stenosis?

A
  • Pulses parvus et tardus: slow rising low volume pulse at carotid due to reduced cardiac output
  • Mid-systolic crescendo-decrescendo ejection murmur with a click in the right upper sternum
  • Normal S1
  • Paradoxical splitting of S2
  • S4 gallop sound
78
Q

What is the diagnosis for aortic stenosis based on?

A
  • ECG: bifid P waves, left ventricular hypertrophy
  • Echocardiogram: calcified valve, hypertrophy
  • CXR: calcification in valve, aortic root dilatation
  • Cardiac catheterisation for coronary arteries
79
Q

What are the treatments for aortic stenosis?

A
  • Management of heart failure
  • Beta blockers
  • Transcatheter aortic valve implantation
  • Surgical aortic valve replacement
80
Q

What are the causes of aortic regurgitation?

A
  • Aortic root dilatation
  • Hypertension
  • Marfan syndrome
  • Rheumatic heart disease
  • Infective endocarditis
  • Congenital bicuspid aortic valve
  • Calcification of valve
81
Q

What is the pathophysiology of aortic regurgitation?

A

Backflow of blood returning from the aorta combined with blood entering the left ventircle during the filling diastolic phase due to volume overload and eccentric hypertrophy, causing dilatation of the heart chamber, overtime reducing LV function. There is a compensatory increase in left ventricle contraction, resulting in hypertrophy. This can lead to mitral valve stenosis over time.

82
Q

What is the presentation of aortic regurgitation?

A

It presents with exertional dyspnoea, chest pain and exertional psynpea due to reduced cardiac output and coronary blood flow. Patients can tolerate this for years and has a good prognosis if chronic, however acute regurgitation is associated with left ventricular fibrillation.

83
Q

What is a key clinical sign of aortic regurgitation?

A

High pulse pressure and collapsing pulse

84
Q

What are the signs of aortic regurgitation?

A
  • Apical systolic thrill
  • Displaced apex beat
  • Diastolic decrescendo murmur
  • Austin-Flint murmu, mimicking mitral stenosis that is a mid-diastolic murmur at apex due to mitral valve orifice over time narrowed from high left ventricular pressure resulting in anterograde blood flow
85
Q

What investigations are used for aortic regurgitation?

A
  • ECG: left ventricular hypertrophy
  • CXR: LVH, aortic dilation
  • Cardiac catheterisation
  • Doppler echocardiogram is best for assessing regurgitation
86
Q

What are the management strategies for aortic regurgitation?

A
  • Observation for asymptomatic patients
  • Non-pharmacological management
  • Surgical management for significant LV dysfunction
87
Q

How are heart murmurs graded?

A

Based on the Levine scale from 1 (very faint) to 6 (extremely loud without a stethoscope)

88
Q

What is a thrill in cardiology?

A

A palpable vibration caused by turbulent flow through a valve

89
Q

What are the risks associated with mechanical heart valves?

A
  • Valve thrombosis
  • Embolisation
  • Haemolysis
  • Endocarditis
  • Structural valve degeneration
  • Patient-prosthesis mismatch
90
Q

What are the characteristics of tissue valves compared to mechanical valves?

A

Do not require anticoagulation therapy but have lower durability