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Cardio > Valvular heart disease > Flashcards

Valvular heart disease Flashcards

1
Q

What are the causes of tricuspid regurgitation?

A

RV disease

  • Right ventricular dysplasia
  • Endomyocardial fibrosis

RV dilatation

  • Primary pulmonary hypertension
  • Secondary pulmonary hypertension (e.g. from lung disease, left sided heart disease)

Right ventricular volume overload

  • RA dilatation
  • Atrial fibrillation

All leads to tricuspid leaflet maladaptation –> functional tricuspid regurgitation

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2
Q

What are the PE findings in tricuspid regurgitation?

A
  • Pansystolic murmur at LLSE that is louder on inspiration

* SXS RV failure: Palpable (sometimes pulsatile) liver, Giant CV waves, Pitting edema, Ascites

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3
Q

What is the management of tricuspid regurgitation?

A

Medical therapy: Diuretics to relieve edema

Intervention
• Indications
- Severe symptomatic tricuspid regurgitation
- Asymptomatic + Significantly impaired RV function/ Significantly dilated RV/ Undergoing other cardiac surgery
• Valve repair
• Valve replacement

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4
Q

What are the causes of tricuspid stenosis?

A
  • rheumatic fever
  • rare isolated congenital malformations
  • carcinoid heart
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5
Q

What are the symptoms and signs in tricuspid stenosis

A

Symptoms

  • fatigue
  • leg swelling
  • abdominal distension

Signs

  • JVP raised with prominent a wave
  • split first heart sound
  • Mid diastolic murmur loudest at lowest left sternal edge
  • louder on inspiration and soften on expiration
  • ascites
  • pedal edema
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6
Q

What are the investigation findings in tricuspid stenosis?

A

Transthoracic echogram

  • valve thickening or calcification
  • restricted mobility with diastolic doming
  • right atrial enlargement
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7
Q

What is the cause of pulmonary stenosis?

A

Congenital

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8
Q

What are the symptoms and signs in pulmonary stenosis?

A

Symptoms
- fatigue

Signs

  • JVP raised with prominent a wave
  • widely split S2 (soft delayed P2)
  • precordial heave
  • ejection systolic murmur loudest at upper left sternal edge: softer on inspiration and louder on expiration (in congenital PS- pliable valves), louder on inspiration (non pliable valves- carcinoid/ rheumatic)
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9
Q

What are the investigation findings in pulmonary stenosis?

A

ECG
• RV hypertrophy with strain pattern (Tall R wave in V1 and V2)

Chest X-Ray Findings
• Prominent L pulmonary artery
• Lifted apex

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10
Q

How is pulmonary stenosis managed?

A

Indications for management

  • severe symptomatic PS
  • asymptomatic + very high pulmonary gradient

Management of Pulmonary Stenosis
• Balloon valvuloplasty
• Valve replacement (avoid as low flow system and easy to form clots)

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11
Q

What is the cause of pulmonary regurgitation?

A

Primary

  • Congenital heart disease (isolated- rare, more commonly including other defects)
  • following repair of TOF
  • infective endocarditis
  • rheumatic heart disease
  • carcinoid

Secondary: pulmonary hypertension

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12
Q

What are the signs and symptoms in pulmonary regurgitation?

A

Symptoms

  • fatigue
  • leg swelling
  • abdominal distension

Signs

  • JVP raised with prominent a wave
  • Decrescendo diastolic murmur at upper right sternal edge- louder on inspiration
  • ascites
  • pedal edema
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13
Q

What is the management of pulmonary regurgitation?

A

Medical therapy: diuretics to reduce fluid overload

Indications for surgery (valve replacement)
- severe symptomatic pulmonary regurgitation
- asymptomatic +
• significantly impaired RV function
• significantly dilated RV
• severe tricuspid regurgitation
• significant arrhythmia

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14
Q

What are the 2 kinds of valves used for valve replacement?

A

Mechanical Valve
• Need lifelong anticoagulation with warfarin
- If no risk factors: INR aim 2.5 – 3.5 (mitral), 2 – 3 (aortic)
• DOACs contraindicated for mechanical valves
- Not enough studies for FXa inhibitors
- Dabigatran associated with excess thromboembolic and bleeding risk (RE-ALIGN Trial)
• Recommended daily low dose aspirin (75-100mg) – 2014 AHA/ACC guidelines
• Longer durability (preferred for younger patients)

Bioprosthetic valve
• Only require first 3 months of anticoagulation (if no other thromboembolic risk factors e.g. AF)  DOACs not contraindicated but not much studies done
• Recommended daily low dose aspirin (75-100mg) – 2014 AHA/ACC guidelines
• Shorter durability (higher rate of deterioration in younger patients)

Bioprosthetic valve preferred if
• Patient’s life expectancy is shorter than lifespan of bioprosthetic valve (avoid reoperation)  reasonable if > 70 years old
• Contraindications to warfarin, or cannot be managed properly/not desired by patient

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15
Q

What are the causes of aortic stenosis?

A
  • Degenerative calcific aortic valve
  • Congenital bicuspid aortic valve (most common cause of AS in <65 year old)
  • Seen in 2% of population
  • Associated with coarctation (in 6%)
  • Fusion of 2 coronary cuffs (right, left, non-coronary)
  • Type 1: fusion of right and left
  • Type 2: fusion of left and non-coronary
  • Type 3: fusion of right and non-coronary
  • Manifests at 40 – 60 years
  • Rheumatic heart disease: GAS infection → develop anti-streptococcal antibodies → recognize tissues in the heart → inflammation and fibrosis of aortic valves → inflammation, fusion and fibrosis of commissures → aortic stenosis
  • Less common causes:
  • Subvalvular aortic stenosis
  • Supravalvular aortic stenosis: William’s syndrome
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16
Q

How does aortic stenosis results in CCF?

A

Outflow obstruction (pressure overload) → increased intraventricular pressure/ increased end diastolic pressure → LV concentric hypertrophy → decreased compliance → LA pressure increased to fill LV → increased post capillary venous pressure → pulmonary congestion → pulmonary edema

Over long time: decompensation from myocardial ischemia leading to dilated LV with poor EF

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17
Q

What is the natural progression of AS?

A

Angina (5 years median survival)

Syncope (3 years median survival)

Dyspnea (2 years median survival)

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18
Q

What are the PE findings in Aortic stenosis?

A

Murmur
• Crescendo-decrescendo ejection systolic murmur
• Best heart at aortic area, radiates to carotids
• Soft S2
• Systolic ejection click loudest at apex

Variants
• Gallavardin phenomenon (may radiate to apex)
• Aortic sclerosis (no radiation to carotids)

Other clinical features
• Slow rising pulse, small volume
• Heaving apex beat
• Narrow pulse pressure, low BP
• Complications: congestive cardiac failure, endocarditis
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19
Q

What are the differentials of ESM?

A
  • Aortic sclerosis
  • Pulmonary stenosis
  • Hypertrophic cardiomyopathy (HCM) –> louder with valsava
  • Atrial septal defect
  • Coarctation of aorta a/w bicuspid aortic valve
  • William’s syndrome
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20
Q

What are the indications of severity of aortic stenosis?

A
  • Early ejection click
  • Long systolic murmur & late peaking of murmur
  • Systolic thrill in aortic area
  • Paradoxical splitting of S2
  • S4 (atrial contraction into stiff ventricle)
  • Heaving, displaced apex beat
  • Narrow pulse pressure
  • Slow rising, slow volume pulse (pulsus parvus et tardus)
  • LVH leading to elevated end-diastolic pressure -> reduced coronary perfusion -> LHF
  • Signs of heart failure: JVP, pulmonary crepitations, pedal edema
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21
Q

What are the CXR findings in a patient with aortic stenosis?

A

• Post stenotic dilatation
–> ascending aorta projects to right side
• Valve calcification
• +/- Cardiomegaly (late severe aortic stenosis)  LV hypertrophy

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22
Q

What are the ECG findings in a patient with aortic stenosis?

A

Left ventricular hypertrophy (Sokolov lyon) WITH strain pattern (ST depression + T wave inversion in lateral leads)

23
Q

What are the echo findings in a patient with aortic stenosis?

A 
• Assess etiology
• Assess for associated regurgitation
• Assess severity
- Aortic valve gradient
- Aortic valve area
• Haemodynamic consequence
- Left ventricular hypertrophy
- Left ventricular EF
24
Q

What is the management of a patient with aortic stenosis?

A

Monitoring
• Mild: every 3-5 years
• Moderate: every 1-2 years
• Severe: 6 monthly to yearly

Intervention
• Indications
- Asymptomatic: LVEF <50%, Patient undergoing CABG
- Symptomatic: Severe AS, End organ damage
• Younger patients: metallic aortic valve replacement + conventional sternotomy
• Older patients: bioprosthetic valve (don’t need long term anticoagulation) + Transfemoral (TAVR) or conventional sternotomy

Medical therapy for those who refuse intervention
• Diuretics –> fluid overload
• ACE-I/ B-blockers –> LV dysfunction

Moderate AS does not cause symptoms

25
Q

What are the causes of aortic regurgitation?

A

Acute
• Aortic dissection -> tear progresses proximately to affect valve leaflets
• Infective endocarditis

Chronic
• Disease of Aortic Root
- 1. Genetics: CTD (Marfan’s, Ehler Danlos), bicuspid aortic valve
- 2. Inflammatory: Takayasu arteritis, Giant cell arteritis, Behcet’s
- 3.Increased aortic wall stress: hypertension, phaeochromocytoma, cocaine use, coarctation, trauma, smoking
• Disease of Leaflet
- 1. Bicuspid aortic valve
- 2. RHD
- 3. Chronic IE

26
Q

How does acute and chronic AR result in CCF?

A

Chronic AR:
• Volume overload → eccentric hypertrophy → decreased LV compliance →
fibrosis and dilatation of LV → LV failure (drop in EF)
• Decreased LV compliance → increased LA pressures to fill LV → increased post capillary venous pressure → pulmonary congestion

Acute AR
• increased LV blood volume → sudden increase in LV diastolic pressure (LV not dilated and non-compliant) → increased LA pressure → increased post capillary venous pressure → pulmonary edema
• Retrograde flow of stroke volume into LV → decreased forward ejection fraction → hypotension

27
Q

What are the physical examination findings in aortic regurgitation?

A

Murmur:
• Decrescendo early diastolic murmur heard best at LUSE with patient leaning forward, on expiration
• Soft S2, high-pitched murmur
• Austin flint murmur – low pitched MDM at apex (functional mitral stenosis)

Other clinical features 
• Bounding and collapsing pulse
• Wide pulse pressure
• Deviated, thrusting apex beat 
• Complications: congestive cardiac failure, acute APO, infective endocarditis,

Peripheral signs
• Corrigan: Visible carotid pulsation
• De Musset: Head nodding with each heart beat
• Quincke: Capillary pulsations in the fingernails
• Muller: Systolic pulsations on the uvula
• Duroziez: Compressing the femoral with a stethoscope produces to and fro systolic and diastolic murmurs
• Traube: Pistol shot sound over femoral arteries
• Hill: Higher systolic pressure in the leg than the arm

28
Q

What are the CXR findings in someone with aortic regurgitation?

A

Acute
• Pulmonary congestion
• Prominent aorta

Chronic
• Cardiomegaly
• Hypertrophy of LV

29
Q

What are the ECG findings in someone with aortic regurgitation?

A

Left ventricular hypertrophy WITHOUT strain pattern (c.f Aortic Stenosis)

30
Q

What are the echo findings in someone with aortic regurgitation?

A 
• Assess etiology
• Assess for associated stenosis
• Assess for severity of aortic regurgitation
- Regurgitant orifice area
- Regurgitant volume
• Haemodynamic consequence of aortic regurgitation
- Left ventricular EF
- Left ventricular size
31
Q

What is the management of Acute AR?

A

Medical therapy
• Normotensive /hypertensive: vasodilators e.g. nitroprusside
• Hypotensive: inotropes e.g. dopamine

Intervention: Emergency aortic valve replacement

32
Q

What is the management of Chronic AR?

A

Monitoring
• Mild: every 3 – 5 years
• Moderate: every 1 – 2 years
• Severe: 6 monthly to yearly

Intervention
• Indications
- Asymptomatic: EF <50%, Significant dilatation of LV
- Severe symptomatic
• Aortic valve replacement (mechanical vs bioprosthetic)

Medical therapy
• ACE and B blockers –> LV dysfunction
• Fluid overload –> diuretics

33
Q

What are the causes of MS?

A
  • Rheumatic Heart Disease***: Inflammation → fibrosis of mitral valve → commissural fusion +/- calcification
  • Infective Endocarditis
  • Calcific Degeneration of Mitral Valve
34
Q

What are the complications of MS?

A
  • Atrial fibrillation
  • Pulmonary hypertension
  • Congestive cardiac failure
35
Q

How does MS result in CCF?

A

Impairment of flow from LA to LV → increased LA blood volume → LA dilatation → increased precapillary venous pressure → pulmonary congestion → pulmonary edema

36
Q

How does mitral stenosis result in pulmonary hypertension?

A

LA dilatation → increased post capillary venous pressure → pulmonary hypertension → RV pressure overload → RV failure

37
Q

How does MS result in A fib?

A

LA dilatation → LA remodelling → Atrial fibrillation

38
Q

What are the physical examination findings in MS?

A

Murmur
• Mid-diastolic murmur heard best at apex (with bell)
• Loud S1, low-pitched murmur
• Opening snap (abrupt cessation of valve opening)

Other clinical features
• ‘Tapping’ apex beat (from accentuated 1st heart sound)
• Complications: AF, Pulmonary hypertension, Right heart failure
• Mitral facies/malar flush

39
Q

What are the indications of severity in MS?

A 
Indications of Severity
• Earlier opening snap to S2
• Long mid-diastolic murmur
• Mitral facies
• Pulsus parvus 
• Pulmonary hypertension, CCF
• Atrial Fibrillation
40
Q

What are the CXR findings in MS?

A

RV dilatation: Lifting of the apex

Pulmonary hypertension
• Prominent pulmonary vasculature
• Pruning of distal capillaries

LA dilatation
• Double density of right heart border - 1 line by LA and 1 line by RA
• Splaying of carina
• Left atrial appendage pushed out

41
Q

What is the ECG features in MS?

A
  • P mitrale
  • RV hypertrophy (dominant R waves in V1 and V2)
  • Atrial fibrillation
42
Q

What is the Echo features in MS?

A
  • Assess etiology
  • Assess for associated regurgitation
  • Assess for severity of mitral stenosis
  • Haemodynamic consequence of mitral stenosis
43
Q

What is the management of MS?

A

Monitoring
• Mild: every 3-5 years
• Moderate: every 1-2 years
• Severe: 6 monthly to yearly

Intervention
• Indications
- Asymptomatic: High thromboembolic risk (history of systemic embolism, new AF), High risk of haemodynamic decompensation (significant or new onset pulmonary HTN, desire for pregnancy, need for major non cardiac surgery)
- Symptomatic
• Percutaneous mitral valve commissurotomy (for pliable valve), mitral valve replacement (for calcified mitral valve)

Medical therapy
• Diuretics: fluid overload
• For AF
- Rate control: b-blockers, CCB, digoxin
- Anticoagulation for stroke prevention (use warfarin. No NOACS as this is valvular AF)
• Prolong diastole to ensure adequate LV filling: b-blockers, CCB, digoxin
• ACE-I not indicated as there is no LV failure

44
Q

What are the causes of MR?

A

Acute
• Myocardial infarction with papillary rupture
• Infective endocarditis

Chronic
• Degenerative (Mitral valve prolapse): Myxomatous valve can stretch and degenerate causing prolapse (doesn’t close well and leaks)
• Ischemic. Leaflet tethering: restricted leaflet closure because LV dilated → chordae tendinae doesn’t extend and pulls on leaflet so valves can’t close well
• Rheumatic Heart Disease
• Connective tissue disorder: Marfan’s, SLE, RA
• Functional Mitral Regurgitation
- Dilated left ventricle → leaflet tethering
- Dilated left atrium → annular dilatation

45
Q

How does acute MR result in complications?

A

Increased LA blood volume → LA not dilated (non-compliant LA) → Increased LA pressures → Increased post capillary venous pressure → pulmonary edema (backflow of blood into lungs)

Backflow of blood from LV to LA → decreased forward EF → hypotension

46
Q

How does chronic compensated MR result in complications?

A

Increased LA blood volume → LA dilatation → minimally increased LA pressures→ no significant pulmonary edema

LA dilatation → AF

47
Q

How does chronic decompensated MR result in complications?

A

Chronic volume overload → eccentric hypertrophy of LA → decreased LA compliance → increased LA pressure → increased post capillary venous pressure → APO

Increased post capillary venous pressure → increased pre capillary venous pressure → pulmonary HTN

LA dilatation → AF

LV volume → LVH and dilatation → decreased LVEF → hypotension

48
Q

What is the Physical Examination findings in Mitral Regurgitation?

A

Murmur
• Pansystolic murmur, best heard at apex, blowing sound
• Radiation to axilla (or carotids if posterior leaflet rupture)
• Soft S1, loud P2

Other clinical features
• Deviated, thrusting apex beat
• Pulse with sharp upstroke but small amplitude
• APO in acute MR due to non-compliant left atrium, AF in chronic MR
• Complications of AF, LVH, pulmonary hypertension, CCF, S3

49
Q

What are the DDx of PSM?

A
  • Tricuspid regurgitation (a/w large ‘v’ waves)

- Ventricular septal defect

50
Q

What are the CXR findings of MR?

A

LA dilatation
• Double density of right heart border
• Splaying of carina
• Left atrial appendage pushed out

LV dilatation
• Apex pushed laterally

Pulmonary hypertension
• Prominent pulmonary vasculature

Increased left atrial pressure
• Upper lobe diversion

51
Q

What are the ECG findings of MR?

A
  • P mitrale → left atrial dilatation

* Atrial fibrillation

52
Q

What are the echo findings of MR?

A

Severity of mitral regurgitation
• Regurgitant volume and fraction
• Regurgitant orifice area

Haemodynamic consequence of mitral regurgitation
• Left atrial size
• Left ventricular size
• Pulmonary artery systolic pressure
• RV size and function
53
Q

What is the management of MR?

A

Monitoring if asymptomatic
• Mild: every 3-5 years
• Moderate: every 1-2 years
• Severe: 6 monthly to yearly

Intervention
• Indications
- Symptomatic severe MR
- Asymptomatic: End organ damage (LV EF <60%), Significantly dilated left ventricle, New onset AF, new onset pulmonary HTN, Undergoing other cardiac surgery
• Mitral valve repair → first choice if valve suitable
• Mitral valve replacement (metallic, bioprosthetic)

Medical therapy:
• LV dysfunction : ACE-I, → blockers
• AF: anticoagulation (non-valvular so can use NOACs)
• Fluid overload: diuretics

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