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Year 3 Academic Weeks > A7- Valvular Heart Disease > Flashcards

A7- Valvular Heart Disease Flashcards

1
Q

What are the 4 key parts of aortic valve?

A
  • aortic annulus
  • aortic root
  • cusps/leaflets
  • commissures
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2
Q

Aortic Valve Stenosis can be split into 3 types

and explain

A

-Degenerative- endothelial damage leading to inflammation, fibrosis and cacification. Happens faster in bicuspid valces due to difference in distribution of stress forces on the valves due to difference in distribution of stress forces on the valvulr cusps

-Rheumatic- aortic stenosis due to fusion of the valve commissures with scarring and calcification (Group A Streptococcal pharyngeal infection)

-Congenital- aortic stenosis- detected in young adults

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3
Q

WHat are the main symptoms of aortic stenosis?

A
  • some oatients are asymptomatic
  • breathlessness usually with activity
  • chest pain
  • fainting, weakness, dizzoness or even syncope, usually with activity
  • palpitations (AF, ventricular arrhythmias)
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4
Q

What is the average life expectancy of symptomatic aortic stenosis?

A

Life expectancy

  • 5 years after the onset of angia
  • 3 years after the onset of syncope
  • 1 year after the onset of congestive cardiac failure
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5
Q

What happens to preload in aortic stenosis?

A

Pre-load increases (elevated LVEDP)

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6
Q

What is the mechaism of Syncope seondary to aortic stenosis>

A
  • Severe aortic stenosis results in a nearly fixed cardiac output. During exercise there is a decrese in peripheral vascular resistance and BP falls secondary to fixed cardiac output
  • During exercise high pressures generated by the hypertrophied LV may cause a vasodepresso response, resulting in peripheral vasodilatation
  • Myocardial ischaemia occurs from the LV hypertrophy and inability of coronary arteries to adequately supply to the myocardium
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7
Q

What the physical signs of aortic stenosis

A

Narrow pulse pressure- check the BP and look at the BP chart

Carotid pulse is often anacrotic; low volume and slow rising

Sinus rhythm usually, but AF can develop as the left atrium enlarges

-Heart palpation- heaving apex, aterally displaced

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8
Q

On heart auscultation what do you hear for aortic stenosis?

A

A2 becomes quiet or absent with severe AS

S4 may be present S3 with LVF

ESM low pitched, aortic area, louder in expiration with patient leaning forwad

Muscial murmur can sometimes be best heard at cardiac apex (gallavardin) and confused with mitral regurg but does not radiate to the axilla

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9
Q

ECG in aortic Stenosis

A

The changes of LVH secondary to chronic pressure overload of the LV

the S wave in V1 is deep, the R wave in V4 is high

ST depression inV5-V6 (LVstrain pattern)

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10
Q

What does this aortic stenosis CXR suggest?

A

Marked Cardiomegally

LV prominence

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11
Q

WHat can you see Echocardiograph in aortic Stenosis

A
  • Calcification
  • restricted movement of cusps
  • Calculate the valve area by planimetry measurement
  • Measure the Doppler peak velocity (m/s) of forward flow through the AV
  • Calculate the peak and mena gradient across the valve from the peak velocity (bernoulli equation-pressure=4V2)
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12
Q

What are the types of heart valve preostheses

A
  • Mechanical and Biological valves
  • Mechanical heart valces all require patients to take warfarin
  • tilting Disc or Bi-leadlet (largest opening area and least thrombogenic)
  • Tissu heart valces (porcine or equine pweicardium (stented or not). Do not require wardarin. Last 15 years on average
  • Choice should be a shared decision making process taking in to account patient’s values and preferences indcluding discussion on need for reintervention and the risks of anticoagualtion. Patient’s age is relevant (<50, 50-70 and 70+ years)
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13
Q

Treatment Options for Aortic Stenosis

A
  • Aortic valve replacement for symptomatic patients imporves quality of life and life expectancy, provided the patient can tolerat the surgery and has no major co-morbidities
  • Many patients with aortic stensosi are elderly and have significant co-morbidities! TAVI should be considered in such patients. It is less invasive. Usually done via a femoral arterial approach and often under anaesthetic with short hospital stay
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14
Q

Patho of aortic Regurg

A

-Results in volume overload of the left ventricle

  • *chronic**: progressive LV dilatation an dhypertrophy, pressure overload LV
  • *acute:** sudden decrease in SC, increase in LV EDV, resulting in reduced CO, reflex tachycardia and profound hypotension. Rising LVEDP leads to pulmonary oedema
  • Percentage of blood that rgurgitates back through the AV is known as the regurgitant fraction. This causes a decrease in diastolic BP and a widening of pulse pressure, priducing an ‘bounding oulse’
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15
Q

WHat affect does Aortic Regurgutation have on Pre-load and After-Load?

A

Both Pre-load and After-load increase

  • the increased ventricular end-diastolic volume (preload) leads to an increase in the force of contraction through the frank-starling mechanism, which causes a greater than normal stroke volume into the aorta
  • WHen LV hypertrophy fails to keep up with chronic volume overload (elevated re-load), end-systolic wall stress rises, resulting CCF
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16
Q

Causes of aortic Regurgitation?

A

Aortic root diseasses are now the leading cause of AR, including aortic dissection, Marfan syndrome, arteriosclerosis, ankylosing spondylitis

Valve causes include degrenerative AV calcific disease, bicuspid valve, rheumatic and after aortic valvular surgery (prosthetic valvular or para-valvular regurgitation)

Aortic dissection and infective endocarditis are life-threatening

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17
Q

What are the red flags that poijnt you towards a diagnosis of infective endocarditis?

A

Persistent fever

postive blood cultures

High risk features

  • prosthetic valve
  • Recent surgical or medical procedures
  • IV drug abuse
  • Previous endocarditis
  • Pre-existing valvular disease
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18
Q

Signs and symptoms of AR

A
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19
Q

AR physical exam

A
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20
Q

What does ECG show in chronic AR?

A

The ECG in patients with aortic regurgitation is non-specific and may show LVH and left atrial enlargement. In acute aortic regurgitation, sinus tachycardia due to the increased sympathetic nervous tone may be the only abnormality on ECG. The chest radiograph is also non-specific in aortic regurgitation.

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21
Q

Echocardiography in aortic regurgitation

A

Subgle most useful imaging study in diagnosis and ongoing surveillance of severity of AR

Critical in determining the timing of aortic valve eplacement (AVR)

AVR should be performed if LVEF <55% or LV ESD is > 55mm

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22
Q

Chronic aortic regurgitation management

A
  • Medical therapy has a limited role as symptomatic cases should be treated ith valve replacement
  • Vasodilators are useful for those with hypertension. The goal is to reduce the afterload, thus reducing LVEDP, thus preserving LV function. This also benefits those patients with LV failure secondary to AR
  • AVR is indicated for symptomatic severe AR regradless of LV function and dimensions
  • the importance of the heart team and the MDT cannot be over emphasised
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23
Q

Mitral Valve Composition

A
  • Anterior and POsterior Leaflets
  • Annulus (forms a ring aound the leaflets and changes shape during the cardiac cycle, like a sphincter)
  • Papillary muscles (whihc tether the valve leaflets to the LV preventing prolapse in to LA)
  • Chordae tendinae (connect the valve leaflets to papillary muscles)
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24
Q

Classification Mitral Regurgutation

A
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25
Q

Patho Mitral Regurg

A
  • Decrease in coaptation between the valve leaflets
  • Acute MR: volume and ressure overload in tge left atrium occurs, transmitted in to the pulmonary vasculature, resulting in elevated pulmonary artery and capillary wedge pressure. SV is decreased

Chronic MR: develops slowly over months to years, which can decompensate id LV function worsens (LV EF<50%)

  • Mild MR has very few symptoms
  • Severe Mr leads to pulmonary hypertension and left/right sided cardiac failure
  • There is increase in pre-load, but afterload is reduced, in comparison to aortic regurg
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26
Q

Mitral Regurgitation: Symptoms and Signs

A
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27
Q

When should you assess asymptomatic patients with Mitral Regurg

A

Mild MR: Every 3-5 years

Moderated MR: Every 1-2 years

Severe MR; Every 6-12 Months (the frequency increases if the LV dilatation increases)

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28
Q

Mitral Regurgitation treatment Overview

A
  • Once symptomatic mitral valve surgery is the definitve therapy (repaur or replacement)
  • Afterload reduction with ACE inhibitors
  • Diuretics reduce LV volumes to imporve functional MR and imporve pulmonary oedema
  • B-Blockers only for functional MR. Regurgitant volume can increase with a slower heart rate
  • Anticoagulation for AF
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29
Q

Mitral Valve Surgery Choices

A
  • Choice between replacement or repair depends on the aetiology and extent of valvular damage
  • Repair should be performed over replacement whenever feasible (lower risk of subsequent endocarditis and better preservation of LV fucntion)

Surgery for acute MR should be performed BEFORE symptoms and deterioration of LV function (the afterload is no longer reduced after surgery and LV failure can then occur in such patients)

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30
Q

Mitral Stenosis Patho

A
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31
Q

Mitral stenosis clinical symptoms and signs

A
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32
Q

What is seen in Mitral stenosis?

A

Double right heart border (yellow) plus straight left heart border (red) due to large LA

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33
Q

Echocardiography for Mitral Stenosis?

A
  • Calcified stenotic valve
  • Massively enlarged LA
  • Doppler velocity shows prolonged presure half time- the time it takes for the pressure gradient across the MV to drop by half
  • Transoesophageal echocardiogram evaluates MV in more details and better looks for thrombus in left atrium
34
Q

What is the average life expectancy of a patient with severe symptomatic aortic stenosis?

A

-Average life span is 1.8 years

35
Q

Does surgical aortic valce replacement or TAVI aortic stenosis carry the same or different risks?

A

Potential complication from TAVI are similar to those of a conventional valve replacement, although the stroke risk is higher with TAVI. Shorter stay with TAVI (some as day cases). 5-10% risk of permanent pacemaker with TAVI

36
Q

When does mitral valve regurgitation require surgery?

A

When a patient with mitral regurgitation develops symptoms, a decrase in cardiac funtion or an increase in heart size, surgery is recommended. The onset of AF with mitral regurgutation also requires consideration of surgery

37
Q

Composition of Tricuspid Valve?

A
  • Usually has 3 leaflets and 3 papillary muscles (anterior>posterior>septal), plus chordae tendinae
  • Anterior leaflet attached to RVOT, posterior to muscular wall of RV and septal leaflet to septum
  • Commissures (*) separate the 3 leaflets
38
Q

Tricuspid Regurgitation - Pathogenesis

A
  • Involves backflow of blood into the right atrium during systole
  • Right atrium is relatively hemodynamically stable so there are no noticeable consequences with mild to moderate tricuspid regurgitation
  • When the regurgitation is severe there is noticeable increase in the venous pressure and raised right atrial pressure which can result in right-sided heart failure – • Ascites • Liver failure • Shortness of breath • Fatigue • Oedema in ankles, legs, feet and/or abdom
39
Q

What is primary and secondary TR

A
40
Q

WHich valve is commonly infected in IV drug users?

A

Tricuspid Valve

41
Q

Congenital abnormalities of TV can occur like…

A

like apical displacement is called EBstein;s anomaly, isially leading to signifcant tricuspid regurg

42
Q

Tricuspid Regurgitation Physical Examination

A
43
Q

What do you see in TR CXR

A

Enlarged pulmonary arteries

enlarged right ventricles

44
Q

What do you see Tricuspid Regurgitation Echocardiography

A
  • Structure of valve
  • Right ventricle structure/function
  • Right atrium structure/function
  • Severity of regurgitation
  • Left heart structure/function
  • Assess pulmonary artery pressure from the velocity of regurgitation jet (4V2) + JVP
45
Q

Complications of Tricuspid Regurgitation

A

Right heart failure

  • Atrial arrhythmias
  • Ventricular arrhythmias
  • Cirrhosis
  • Endocarditis
  • Weight loss
  • Anorexia
46
Q

Tricuspid Regurgitation Treatment

A
  • Medical to treat right and left heart failure (pulmonary hypertension)
  • Diuretics for volume overload/oedema (loop, aldosterone antagonists)
  • IV diuretics may be needed - monitor body weight, renal function, NOT THE JVP!!
  • ACE inhibitors and B-Blockers if associated left heart failure
  • Pulmonary vasodilators to be considered in presence of primary pulmonary arterial hypertension (sildenafil, bosentan, epoprostenol) – this needs supraspecialist referral to the ‘’pulmonary hypertension centre
47
Q

Tricuspid Regurgitation Surgical Treatment

A
  • The principal surgical repair for secondary TR is tricuspid annuloplasty. The aim is to improve leaflet coaptation by correcting annular dilatation and restoring annular geometry. The two principle surgical methods are Ring annuloplasty (implantation of an undersized ring) and Suture annuloplasty
  • Tricuspid valve surgery at time of left sided valve surgery decreases the rate of post-operative residual TR
  • Tricuspid valve replacement should be undertaken when valve repair is not technically feasible or predictably durable. Bioprosthetic valves are currently favoured.
  • The safety and feasibility of transcatheter therapies for treating severe tricuspid regurgitation are still being investigated
48
Q

Tricuspid Stenosis - causes

A
  • Rheumatic heart disease (in conjunction with mitral stenosis)
  • Large vegetations in infective endocarditis
  • Carcinoid syndrome
  • Permanent pacing or AICD leads
  • Benign tumours (myxoma)
  • Ebstein’s anomaly
49
Q

Tricuspid Stenosis – symptoms/signs

A
  • Right upper quadrant abdominal discomfort (due to an enlarged liver with systemic venous hypertension)
  • Jugular venous distention may occur, increasing with inspiration (Kussmaul’s sign). Large A wave.
  • Hepatic congestion and peripheral oedema may occur
  • S1 widely fixed; S2 single
  • Mid diastolic (rumbling) murmur increases in intensity with inspiration (Carvallo’s sign) and best heard over the left sternal border
  • Hepatomegally and ascites can occur
50
Q

A high haemoglobin can occur in Tricuspid Stenosis – why?

A

A disproportionately high haemoglobin (polycythaemia) level may be indicative of poor pulmonary blood flow associated with Tricuspid Stenosis

51
Q

• There may be hepatic congestion in Tricuspid Stenosis and/or Tricuspid Regurgitation, so what might the liver function tests show?

A

•Elevation in serum aminotransferase, alkaline phosphatase and serum bilirubin (most of which is unconjugated) can occur in patients with hepatic congestion. Their prevalence and severity are associated with the severity of Tricuspid valve disease.

52
Q

What can you is in ECG and Echocardiogram in Tricuspid Stenosis

A

Right atrial enlargement

  • Atrial arrhythmias
  • Thickening and calcification of leaflets with restricted opening
  • Increased forward flow Doppler velocity and a diastolic pressure gradient
53
Q

What does Cardiac CT and MRI show in Tricuspid Stenosis

A
  • CT provides greater detail with good spatial and temporal resolution – pre-surgical planning
  • MRI again good spatial and temporal resolution for right ventricular size and accurate functional quantification of both the valve and ventricle
54
Q

Tricuspid Stenosis: Treatment

Medical

A
  • Loop diuretics relieve hepatic congestion and peripheral oedema, decreasing pre-load
  • Can worsen a low-flow syndrome, however, and should be used with caution
  • Treatment of atrial arrhythmias
55
Q

Tricuspid Stenosis: Treatment

Surgical

A
  • Valve replacement – Open (bioprosthetic or mechanical)
  • Valvotomy - With valvotomy (balloon dilatation), there is significant decrease in transvalvular pressure gradient across tricuspid valve and a decrease in right atrial pressure.
56
Q

Can patients with severe tricuspid regurgitation remain asymptomatic?

A

•Patients with significant TR can remain asymptomatic despite impaired right ventricular function

57
Q

• What percentage of patients with severe mitral regurgitation have significant secondary tricuspid regurgitation?

A

• 30-50% of patients with severe MR have significant secondary TR

58
Q

•Is functional tricuspid regurgitation associated with persistent atrial fibrillation?

A

Functional TR with a structurally normal TV may occur secondary to chronic atrial fibrillation

59
Q

• What is the 5 year survival of patients with moderate to severe isolated tricuspid regurgitation treated medically?

A

• The 5 year survival is 75% for severe isolated TR

60
Q

Pulmonary Valve Composition

A
  • 3 equal sized, semilunar cusps or leaflets (right, left, anterior) - thinner when compared to the aortic valve (lower pressure system)
  • Cusps are joined by commissures
  • Opens in systole allowing the deoxygenated blood to be delivered to the lungs
61
Q

Which valve is Associated with other congenital heart diseases such as atrial septal defect or Ebstein’s anomaly

A

Pulmonary Valve Stenosis

62
Q

Pulmonary Valve Stenosis

A
  • Patients with mild stenosis are asymptomatic and are diagnosed by routine examination with an ejection systolic murmur
  • Moderate Pulmonic Stenosis: Patients present with exertional dyspnoea and fatigue
  • Severe Pulmonic Stenosis: Patients present with exertional dyspnoea, chest pain and syncope
  • Untreated patients develop features of right ventricular failure
63
Q

Pulmonary Stenosis: Clinical Examination

A
  • Mild stenosis - ejection mid-systolic murmur in the pulmonary area increasing in intensity during inspiration
  • In severe stenosis findings include –
  • Elevated JVP with prominent ‘’a’’ wave (atrial contraction)
  • Right ventricular heave
  • Split S2 with reduced or absent P2 component
64
Q

Pulmonary Stenosis: Investigations

A
  • ECG: features of right ventricular hypertrophy and right axis deviation
  • Echocardiography: show right ventricular hypertrophy and the site of obstruction.
  • Doppler studies can assess the degree of stenosis
65
Q

Pulmonary Stenosis: CT and MRI

A

(a) Axial CT angiogram of the chest shows post-stenotic dilatation of the main pulmonary artery (MPA) and left pulmonary artery (LPA); (b) Sagittal MRI image of the right ventricular outflow tract shows post-stenotic dilatation of the main pulmonary artery with incomplete opening of the pulmonic valve.

66
Q

Pulmonary Stenosis: Treatment

A
  • Medical – no specific treatment
  • Valvular PS, balloon valvulotomy should be the intervention of choice - considered in the presence of symptoms, decreased RV function or important arrhythmias
  • Surgery is recommended for subinfundibular or infundibular stenosis, hypoplastic pulmonary annulus and associated lesions such as severe PR or severe TR
67
Q

Pulmonary Stenosis: What Follow up is involved

A
  • Mild untreated or residual pulmonic stenosis: Follow up once every 5 years.
  • Moderate pulmonic stenosis: Annual visit with echocardiography every 2 years
  • Following valvuloplasty: regular echocardiography to evaluate the degree of pulmonary regurgitation, RV pressure, RV function and tricuspid regurgitation
68
Q

Pulmonary Regurgitation: Pathophysiology

A
  • Acquired alteration in valve morphology
  • Dilatation of pulmonary arteries or valve ring
  • Congenital abnormality or absence of valve •Associated with Tetralogy of Fallot repair (to relieve RVOT obstruction)
  • All conditions result in RV volume overload and progressive decline in function
  • Progressive dilation of the right ventricle also results in functional tricuspid regurgitation and increases the risk of developing atrial or ventricular arrhythmias and risk of sudden death
69
Q

Pulmonary Regurgitation: Clinical Examination

A
  • Pulmonary regurgitation is not a cyanotic heart disease
  • Elevated JVP if TR present
  • Right ventricular heave may be present
  • Pulmonic regurgitation is associated with wide splitting of S2
  • Classically a high-pitched early-diastolic murmur is heard at left upper sternal area, accentuated by squatting and on inspiration; made softer by Valsalva manoeuver or expiration
70
Q

Pulmonary Regurgitation: Investigations

A
  • ECG: non specific but can show signs of pulmonary hypertension and risk of AF or VT
  • Echocardiography: Transthoracic is first-line imaging modality
  • If non-diagnostic,Transoesophageal Echocardiography (TOE) should be considered
71
Q

Pulmonary Regurgitation: Cardiac MRI

A
  • Gold standard for assessment of the morphology of the pulmonary valve, for quantification of the severity of the regurgitation and the RV systolic function
  • quantification of the valve regurgitant volume
  • evaluating RV end-diastolic and end-systolic volumes, and RV ejection fraction
72
Q

Pulmonary Regurgitation: Surgical Therapy

A
  • Pulmonary valve replacement (PVR) is one of the most common procedures performed among adults with congenital heart disease. Patients may undergo reoperations during their lifetime
  • Indications include:
  • Patients with progressive right ventricular dysfunction/dilatation
  • The prime goals of pulmonary valve replacement include improved functional class and quality of life, maintenance of right (and left) ventricular function, risk modification of arrhythmia and sudden cardiac death.
  • Bioprosthetic valves usually preferred
  • The current transcatheter (Melody) valves are designed to treat conduit and bioprosthetic valve failure only
73
Q

• What is the most common cause of severe pulmonary regurgitation?

A

The most common cause of severe pulmonary regurgitation is iatrogenic due to surgical valvotomy or balloon pulmonary valvuloplasty for RVOT obstruction as a component of Tetralogy of Fallo

74
Q

• How is the morphology of the RVOT visualised when planning for transcatheter pulmonary valve replacement?

A

The morphology of the RVOT is best imaged by CT or MRI

75
Q

What type of valve conduits are placed to replace the pulmonary valve?

A

•Valve conduits used include homografts from cadavers, valved conduits, bovine jugular vein graft or a bioprosthetic valve implanted in to the RVOT

76
Q

• Describe 2 abnormalities of the raised JVP seen in severe tricuspid regurgitatio

A

• In severe TV regurgitation, there is a large V wave (venous filling of the right atrium when the tricuspid valve is closed). A rapid, deep y descent in early diastole also occurs (produced mainly by the tricuspid valve opening and the rapid inflow of blood into the right ventricle)

77
Q

What provocation manoeuvre accentuates the murmur of TR?

A

• Inspiration accentuates the TR murmur by increasing venous return to right side of the heart

78
Q

What are the auscultatory features of tricuspid stenosis?

A

• Mid-diastolic murmur at the left lower sternal border (tricuspid stenosis). The murmur can be louder with inspiration (venous return increases)

79
Q

What is the gold standard test to assess the severity of pulmonary regurgitation?

A

• Cardiac magnetic resonance imaging (CMR) is the gold standard to quantify pulmonary valve regurgitation

80
Q
A

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