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Year 2 > Valvular Heart Disease > Flashcards

Valvular Heart Disease Flashcards

1
Q

What is the most common cause of mitral stenosis

A

Rheumatic heart disease

Rheumatic fever due to infection by group A beta-haemolytic streptococcus

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2
Q

What gender does mitral stenosis commonly effect

A

Women

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3
Q

In what part of the world is mitral stenosis common in

A

Developing world

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4
Q

Pathophysiology of mitral stenosis

A
  1. Orifice area reduced from 4-6 cm^2 to less than 1cm^2
  2. To keep CO constant, left atrial pressure increases = left atrial hypertrophy and dilatation
  3. Pulmonary venous, pulmonary atrial and right heart pressure increases as a result
  4. Increase in pulmonary capillary pressure = pulmonary oedema
  5. Pulmonary hypertension
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5
Q

Consequence of mitral stenosis causing pulmonary hypertension

A
  1. Right Ventricular hypertrophy
  2. RV dilatation
  3. Failure of tricuspid regurgitation
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6
Q

How long is mitral stenosis asymptomatic for

A

Until orifice is less than 2cm^2 small

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7
Q

Symptoms of mitral stenosis

A
  1. Severe dyspnoea (due to LA pressure increase, vascular congestion)
  2. Bloody coughs (rupture of bronchial vessels)
  3. Pulmonary hypertension = R HF
  4. LA hypertrophy = AF
  5. AF = systemic emboli
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8
Q

Clinical signs of mitral stenosis

A
  1. Bilateral cyanosis in cheeks
  2. Prominent ‘a’ wave in jugular vein pulsations due to pulmonary hypertension + RV hypertrophy
  3. Right heart failure will cause distension of jugular veins
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9
Q

What is mitral stenosis

A

Obstruction of LV inflow that prevents proper filling during diastole

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10
Q

How does Mitral stenosis cause mortality

A

Progressive pulmonary congestion = infection and thromboembolism

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11
Q

How are heart sounds effected in Mitral Stenosis

A

Low-pitched diastolic rumble at apex

Loud opening S1 snap

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12
Q

When is diastolic murmur in Mitral Stenosis best heart

A

Patient lying on the left side in held expiration

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13
Q

Does intensity of the diastolic murmur in MS correlate wit the severity of the stenosis

A

No

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14
Q

Where is the loud opening S1 snap best heart at

A

Apex

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15
Q

Why is there a loud opening S1 snap

A

Due to the abrupt halt in leaflet motion in early diastole, after rapid initial opening + fusion at leaflet tips

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16
Q

What heart sound indicates a more severe MS

A

Shorter S2 opening snap interval

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17
Q

Three diagnostics used to evaluate MS

A

ECG
CXR
ECHO

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18
Q

How would an ECG help with MS

A

Shows Atrial fibrillation + LA enlargement

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19
Q

How would CXR help with MS

A

LA enlargement + pulmonary congestion - calcified MV

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20
Q

How would Echocardiography be used to DIAGNOSE MS

A

Mitral valve mobility, gradient and mitral valve area

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21
Q

How is MS managed

A

Serial echocardiography:
Mild (3-5 yrs)
Moderate (1-2 yrs)
Severe (yearly)

Medication: Beta-blockers, digoxin will control HR and prolong diastole to improve ventricular filling
Diuretics for fluid overload

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22
Q

What people should be given mitral valve replacement

A

Symptomatic patient with NYHA Class III or IV

Severe MS

Pliable valve suitable

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23
Q

Normal size of an aortic valve

A

3-4 cm^2

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24
Q

When do symptoms occur in aortic stenosis

A

1/4th of normal size

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25
Q

Three types of aortic stenosis

A
  1. Supravalvular
  2. Subvalvular
  3. Valvular
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26
Q

Pathophysiology caused by aortic stenosis

A
  1. Pressure gradient develops between LV and aorta (increased after load)
  2. LV function maintained by compensatory LV hypertrophy
  3. LV function eventually declines
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27
Q

Presentation of aortic stenosis

A
  1. Syncope
  2. Angina (increased myocardial oxygen demand)
  3. Dyspnoea (on exertion due to HF)
  4. Sudden Death
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28
Q

Physical signs of aortic stenosis

A
  1. Slow rising carotid pulse + decreased pulse amplitude
  2. Heart sounds - soft or absent second heart sound + S4 gallop due to LVH
  3. Ejection systolic murmur (crescendo-decrescendo character)
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29
Q

Does loudness of sounds caused in aortic stenosis tell you anything about severity

A

No

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30
Q

Can onset of symptoms in aortic Stenosis be a good prognostic indicator

A

No

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31
Q

Prognosis of Angina + AS

A

5 years survival

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32
Q

Prognosis of Syncope + AS

A

Survive 3 years

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33
Q

HF + AS

A

Survival is <2 years

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34
Q

How is AS investigated

A

Echocardiography :
LV size + function (LVH, dilatation and EF)
Doppler-derived gradients + valve area

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35
Q

How is AS managed generally

A
  1. Dental hygiene/ care

2. Consider IE prophylaxis in dental procedures

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36
Q

Medical management of AS

A

Surgical replacement

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37
Q

Problem with vasodilators in AS

A

Contraindicated in severe AS

38
Q

What surgical procedure is used to treat AS

A

TAVI (Transcatheter Aortic Valve implantation)

39
Q

When should patients be given surgical symptomatic

A
  1. Decreasing EF
  2. Patients undergoing CABG
  3. Symptomatic patients (asymptomatic can be used for medical management)
40
Q

Definition of Mitral Regurgitation

A

Back flow of blood from Lv to LA during systole

41
Q

4 Causes of Mitral Regurgitation

A
  1. MVP
  2. Ischaemic MR
  3. Rheumatic heart disease
  4. Infective Endocarditis
42
Q

Pathophysiology of Mitral Regurgitation

A
  1. Pure Volume Overload
  2. Compensatory mechanisms (LA enlargement, LVH and increased contractility

Pulmonary hypertension = left atrial dilatation continues and RVD

Progressive LV volume overload = dilatation and HF

43
Q

Auscultation of Mitral Regurgitation

A
  1. soft S1 + pan systolic murmur at apex radiating to axilla
    S3 (CHF/LA overload)
    Displaced hyper dynamic apex beat

Exertion Dyspnoea

Heart Failure: May coincide with increased haemodynamic burden

44
Q

Does intensity of murmur in Mitral regurgitation correlate with severity

A

Yes

45
Q

How long does the compensatory phase in MR last for

A

10-15 years

46
Q

How does mortality from MR occur

A

Progressive dyspnoea + HF

47
Q

Investigations for MR

A

ECG
CXR
ECHO

48
Q

ECG in MR diagnosis

A

LA enlargemet
Atrial Fibrillation
LV hypertrophy with severe MR

49
Q

CXR in MR diagnosis

A

LA enlargement

Central pulmonary artery enlargement

50
Q

ECHO in MR diagnosis

A

Estimation LA
LV size and function

Calve structure assessment

51
Q

How is MR medicated

A
  1. Vasodilators (ACEI, hydrazine)
  2. Rate control for AF with beta blockers, CCB and digoxin
  3. Anticoagulation for AF
  4. Diuretics for fluid overload
52
Q

Frequency of echocardiography in MR

A

Mild: 2-3 yrs
Moderate: 1-2 yrs
Severe: 6-12 mnths

53
Q

When is surgical intervention for MR given

A
  1. Any symptomatic patients at rest

Asymptomatic patients ONLY;

  1. EF<60%, LVESD> 45mm
  2. If onset AF is new
54
Q

What is aortic regurgitation

A

Leakage of blood into LV during diastole due to ineffective coaptation of the aortic cusps

55
Q

What causes AR

A
  1. Bicuspid aortic valve
  2. Rheumatic
  3. I. endocarditis
56
Q

Pathophysiology of AR

A

Combined pressure + volume overload

Compensatory mechanisms: Lv dilatation and LVH

Progressive dilatation = HF

57
Q

Physical exam findings of AR

A

Wide pulse pressure: most sensitive

Hyper dynamic + displaced apical impulse

Auscultations

58
Q

Auscultations for AR

A
  1. Diastolic blowing murmur at left sternal border
  2. Austin flint murmur at apex
  3. Systolic ejection murmur (due to increased blood flow across aortic valve)
59
Q

How long does AR remain asymptomatic for

A

Until 4th or 5th decade

60
Q

What are progressive symptoms of AR

A

Dyspnoea

Palpation’s (increased force of contraction and ectopics)

61
Q

How does CXR help with AR

A

Cardiomegaly

Aortic root enlgarment

62
Q

How does ECHO help with AR

A

Evaluation of AV and aortic root

Measurement of LV dimensions and function

63
Q

How is AR managed

A
  1. Vasodilators (ACEIs in symptomatic or HTN)
  2. Serial echocardiograms
  3. Surgical Treatment
64
Q

What patients should receive surgery for AR

A

EF drops below 50% or Lv becomes dilated

65
Q

What is the S1 sound

A

The ‘LUB’ sound caused by mitral and tricuspid valve closure - AV valves

66
Q

What causes the split S1 sound usually heard in a healthy adult

A

The mitral valve closes just before the tricuspid (more blood is usually flowing through the left side of the heart than the right)

67
Q

What is the S2 sound

A

The ‘DUB’ sound caused by closure of the semi-lunar valves - pulmonary and aortic valve

68
Q

What causes the normal S2 split in a healthy adult

A

Aortic valve closes before the pulmonary valve as blood flow is faster through the aortic valve (needs to close sooner)

69
Q

In what condition is an S1 split heard in

A

Right Bundle Branch Block or Ventricular Tachycardia

70
Q

Why can an S1 split be heard in RBBB

A

It is widened as more impulses are reaching the LV than the Rv so contracts more - delays closure of the tricuspid valve widening the split

71
Q

What happens to the S1 split in LBBB

A

Less impulses to LV than to RV causing mitral valve to delay closure, overlapping with tricuspid valve closure - split is lost

72
Q

When is an S2 split usually heard

A

During inspiration

73
Q

Where is S2 split best heard

A

At left upper sternal border

74
Q

Why is an S2 split usuallyheard during inspiration

A

Because there is increased venous return

Increased blood flow through the right side of the heart DELAYS closure of the pulmonary valve widening the split (aortic usually closes first anyways)

Aortic valve closes faster

75
Q

In what condition sis a pathological S2 split heard in

A

Aortic stenosis
Hypertrophic cardiomyopathy
LBBB

Anything that delays closure of the aortic valve

76
Q

What is a persistent WIDENED split

A

When A2 and P2 closure split can be heard throughout the process of respiration

77
Q

What conditions cause a persistent WIDENED S2 split

A

ANY DISEASE delaying pulmonary valve and faster aortic valve closure

RBBBB
Pulmonary stenosis
Pulmonary hypertension
Mitral regurgitation

78
Q

What condition is fixed split S2 an indication of

A

ASD

79
Q

What is fixed split S2

A

Inspiration causes S2 split as normal

Due to atrial septal defect, we get reduced pressure in right atrium = More blood flow from LA to RA

More blood flow = delayed closure of pulmonary valve

80
Q

What is the S3 sound known as

A

Ventricular gallop

81
Q

When does ventricular gallop occur during the cardiac cycle

A

By the large volume of blood striking the LV as it moves in (passive ventricular filling)

82
Q

When is S3 sound not normal

A

Over the age of 35

83
Q

What condition is associated with S3 ventricular gallop

A

Systolic heart failure - myocardium is overly compliant resulting in dilated LV

Mitral regurgitation: Mitral leaflets stop blood flowing from LA to LV resulting in LA overflow and rapid LV filling (gallop heard loudly)

Ventricular septal defect: Rapid filling due to high pressure in RV to LV filling)

Dilated cardiomyopathy (overly compliant ventricles)

84
Q

Where is S3 best heard

A

Apex of the heart

85
Q

What position does the patient have to be in to best hear S3 sound

A

Left lateral decubitus position

86
Q

S3 vs split S2 sound

A

S3 is low-pitched whilst S2 is high-pitched

87
Q

What is the S4 sound

A

Atrial gallop

88
Q

When does S4 sound occur in the cardiac cycle

A

JUST before S1 as atria contract blood into non-compliant ventricle (blood smashing against stiff ventricle)

89
Q

What conditions result in S4 sounds

A

ANY condition that results in a non-compliant ventricle:

Diastolic heart failure
Aortic regurgitation

90
Q

Why is S4 inaudible in AF

A

Because atria can’t contract properly (strongly enough) to force blood and make that smashing sound

91
Q

Why is S4 heard in AS

A

Because the ventricle may hypertrophy over time causing a stiff ventricle to occur

S3 heard when ventricle initially dilates

Year 2 (155 decks)

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