Valve disease 1 Flashcards

1
Q

Normal aortic valve area?

A

3-4 cm2

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2
Q

What is aortic stenosis

A

obstruction of blood flow across the aortic valve due to pathological narrowing.

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3
Q

When do symptoms of aortic stenosis occur?

A

Symptoms occur when valve area is 1/4th of normal.

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4
Q

Symptoms of aortic stenosis

A
  • Fatigue
  • Shortness of breath
  • Angina
  • Dizziness
  • Fainting
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5
Q

Aortic valve normally

A

The aortic valve is normally made up of three leaflets: the left, the right, and the posterior leaflet. It opens during systole to allow blood to be ejected to the body. During diastole, it closes to allow the heart to fill with blood and get ready for another systole.

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6
Q

Types of aortic stenosis?

A

Supravalvular
Subvalvular
Valvular

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7
Q

What does aortic valve look like normally?

A

Closed - Mercedez logo
open - hole

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8
Q

RFs for aortic stenosis

A
  • Hypercholesterolaemia
  • Hypertension
  • Smoking
  • Diabetes
  • Rheumatic heart disease
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9
Q

Types of congenital aortic stenosis?

A

Congenital aortic stenosis
Congenital bicuspid valve

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10
Q

How does congenital aortic stenosis work?

A
  • Happen in unicuspid, bicuspid, tricuspid valve
  • Associated with aortic coarctation, dissection or aneurysm
  • Symptoms shown in 30s to 50s
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11
Q

How many valves does the normal aortic valve have?

A

Tricuspid

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12
Q

If theres fusion of the tricuspid valve what can you get?

A

BAV - bicuspid aortic valve

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13
Q

BAV symptoms:

A
  • 0.5-2% of general population
  • Up to 10% of first degree relatives will have BAV
  • Associated aortopathy and coarctation
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14
Q

What is the pathophysiology of aortic stenosis?

A
  • Smaller valve - dont open as easily - LV contracts creates high pressure pushing on valve until it snaps open - “ejection click”
  • Blood flows through narrower opening - creates murmur - louder as blood flows pas opening and quierer as it subsides - crescendo decrescendo
  • LV generates higher pressure - undergoes concenctric hypertrophy - still enough blood may not leave heart - lead to HF
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15
Q

What is the presentation of aortic stenosis?

A
  • Syncope: (exertional) 15%
  • Angina: (increased myocardial oxygen demand; demand/supply mismatch) 35%
  • Dyspnoea: on exertion due to heart failure (systolic and diastolic) 50%
  • Sudden death <2%
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16
Q

What are the physical signs of aortic stenosis?

A
  • Slow rising carotid pulse (pulsus tardus) & decreased pulse amplitude (pulsus parvus)
  • Ejection click
  • Heart sounds- soft or absent second heart sound, S4 gallop due to LVH - As valve becomes narrower second heart sound gets softer and softer and eventually goes away - murmur
  • Ejection systolic murmur- crescendo-decrescendo character.
  • “Loudness” does NOT tell you anything about severity
17
Q

Natural history of aortic stenosis:

A

Mild AS to Severe AS:
8% in 10 years
22% in 22 years
38% in 25 years

The onset of symptoms is an indication of poor prognosis if left untreated.

18
Q

What is the prognosis of AS?

A
  • Angina + AS: 50% survive for 5 years.
  • Syncope + AS: 50% survive for 3 years,
  • HF + AS mean survival is <2 years.
  • Risk of Sudden Cardiac Death in asymptomatic or minimally symptomatic patients is rare (<2%).
19
Q

How do we investigate aortic stenosis?

A

Echocardiography

Two measurements obtained are:
Left ventricular size and function: LVH, Dilation, and EF

Doppler derived gradient and valve area (AVA)

20
Q

Severity of AS:

A

mild: AVA >1.5cm2 Velocity 2.6-3m/s
moderate: 1-1.5cm2 3-4m/s
Severe: <1cm2 >4m/s

21
Q

What is the management for AS?

A

General:
Fastidious dental hygiene / care
Consider IE prophylaxis in dental procedures

Medical - limited role since AS is a mechanical problem. Vasodilators are relatively contraindicated in severe AS

Aortic Valve Replacement:
Surgical
TAVI – Transcatheter Aortic Valve Implantation

22
Q

What is TAVI?

A

TAVI – Transcatheter Aortic Valve Implantation

Pass balloon into damaged aortic valve – pass new valve through the aorta to sit above the old valve to put a new valve in – not an operation – is a PCI

23
Q

When do we intervene with AS?

A
  • Any SYMPTOMATIC patient with severe AS (includes symptoms with exercise)
  • Any patient with decreasing EF
  • Any patient undergoing CABG with moderate or severe AS
  • Consider intervention if adverse features on exercise testing in asymptomatic patients with severe AS
24
Q

What is chronic mitral regurgitation (CMR)?

A

Backflow of blood from the LV to the LA during systole
Mild (physiological) MR is seen in 80% of normal individuals.

25
Q

Causes of CMR:

A
  • MVP
  • Ischemic MR
  • Rheumatic heart disease
  • Infective Endocarditis
  • Damage post MI
  • Dilated + hypertrophic cardiomyopathies
  • Left sided HF
26
Q

What does CMR cause?

A

PURE VOLUME OVERLOAD

  • Compensatory Mechanisms: Left atrial enlargement, LVH and increased contractility
  • Progressive left atrial dilation and right ventricular dysfunction due to pulmonary hypertension.
  • Progressive left ventricular volume overload leads to dilatation and progressive heart failure.
27
Q

Physical signs of CMR?

A
  • Pansystolic murmur at the apex radiating to the axilla
  • Mid systolic click
  • Soft S1
  • Additional S3 sound
  • Tachycardia

Heart Failure: May coincide with increased hemodynamic burden e.g., pregnancy, infection or atrial fibrillation

28
Q

What is the natural history of CMR?

A
  • Compensatory phase: 10-15 years
  • Patients with asymptomatic severe MR have a 5%/year mortality rate
  • Once the patient’s EF becomes <60% and/or becomes symptomatic, mortality rises sharply
  • Mortality: From progressive dyspnoea and heart failure
29
Q

What are the investigations you take in CMR?

A
  • ECG: May show, LA enlargement, atrial fibrillation and LV hypertrophy with severe MR
  • Chest XRay: LA enlargement, central pulmonary artery enlargement.
  • ECHO: Estimation of LA, LV size and function. Valve structure assessment
  • TOE v helpful
30
Q

What medications do we use to manage CMR?

A
  • Rate control for atrial fibrillation with B-blockers, CCB, digoxin
  • Anticoagulation in atrial fibrillation and flutter
  • Nitrates / Diuretics in acute MR
31
Q

What do we use for the management of CMR other than medication?

A

Serial Echocardiography:
Mild: 2-3 years
Moderate: 1-2 years
Severe: 6-12 months

IE prophylaxis: Patients with prosthetic valves or a Hx of IE for dental procedures.

32
Q

When is it time for surgery with CMR?

A

ANY Symptoms at rest or exercise (repair if feasible)

Asymptomatic:
If EF <60%, LVESD >40mm
If new onset atrial fibrillation/raised PAP >50 mmHg

33
Q

RFs of CMR

A
  • Associated with females
  • Advanced age
  • Connective tissue disease e.g. Marfans syndrome or Ehlers-Danlos syndrome
  • Prior MI
  • Infective endocarditis
  • Rheumatic fever
34
Q

Mitral valve physiology

A

The mitral valve has two leaflets: the anterior leaflet and the posterior leaflet. Together, they separate the left atrium from the left ventricle. During systole the valve closes, which means blood is ejected out of the aortic valve and into circulation. During diastole, the mitral valve opens and lets blood fill into the ventricle.

The mitral valve is supported by papillary muscles and chordae tendinae.

35
Q

Pathophysiology of CMR

A

Mitral regurgitation refers to when the mitral valve doesn’t completely shut allowing blood to leak back into the left atria from the left ventricle.

36
Q

Symptoms of CMR

A
  • Dyspnoea and orthopnoea: due to pulmonary hypertension
  • Fatigue and malaise: due to reduced cardiac output
  • Palpitations: due to initial compensation and increased stroke volume
  • Peripheral oedema:
37
Q

Complications of CMR

A
  • Left sided heart failure
  • Pulmonary congestion, hypertension and right sided heart failure: in acute MR
  • Cardiogenic shock: as cardiac output isn’t maintained
  • Atrial fibrillation: