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Valvular diseases Flashcards

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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

RFs for aortic stenosis

A
  • Hypercholesterolaemia
  • Hypertension
  • Smoking
  • Diabetes
  • Rheumatic heart disease
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4
Q

How many valves does the normal aortic valve have?

A

Tricuspid

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5
Q

Types of congenital aortic stenosis?

A

Congenital aortic stenosis
Congenital bicuspid valve

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6
Q

Types of aortic stenosis?

A

Supravalvular
Subvalvular
Valvular

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7
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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8
Q

When do symptoms of aortic stenosis occur?

A

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

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9
Q

What does aortic valve look like normally?

A

Closed - Mercedez logo
open - hole

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10
Q

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

A

BAV - bicuspid aortic valve

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11
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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12
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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13
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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14
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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15
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

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16
Q

Symptoms of aortic stenosis

A
  • Fatigue
  • Shortness of breath
  • Angina
  • Dizziness
  • Fainting
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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.

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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%).

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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)

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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

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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

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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

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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

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24
Q

What is chronic mitral regurgitation (CMR)?

Study These Flashcards
A

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

25
RFs of CMR
- **Fatigue** - **Shortness of breath** - **Angina** - **Dizziness** - **Fainting**
26
Causes of CMR:
- MVP - Ischemic MR - Rheumatic heart disease - Infective Endocarditis - Damage post MI - Dilated + hypertrophic cardiomyopathies - Left sided HF
27
Mitral valve physiology
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.
28
Pathophysiology of CMR
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.
29
What does CMR cause?
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.
30
Physical signs of CMR?
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
31
Symptoms of CMR
- **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:**
32
What is the natural history of CMR?
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
33
What are the investigations you take in CMR?
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
34
What medications do we use to manage CMR?
Rate control for atrial fibrillation with B-blockers, CCB, digoxin Anticoagulation in atrial fibrillation and flutter Nitrates / Diuretics in acute MR Chronic HF Rx if chronic MR with CCF No indication for ‘prophylactic’ vasodilators such as ACEI, hydralazine
35
What do we use for the management of CMR other than medication?
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.
36
When is it time for surgery with CMR?
ANY Symptoms at rest or exercise (repair if feasible) Asymptomatic: If EF <60%, LVESD >40mm If new onset atrial fibrillation/raised PAP >50 mmHg
37
Complications of CMR
- **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:**
38
What is aortic regurgitation?
Leakage of blood into LV during diastole due to ineffective coaptation of the aortic cusps
39
What are the causes of chronic aortic regurgitation (CAR)?
Bicuspid aortic valve Rheumatic Infective endocarditis
40
What is the pathophysiology of AR?
Combined pressure AND volume overload Compensatory Mechanisms: LV dilation, Left ventricular hypertrophy. Progressive dilation leads to heart failure
41
What do you find on the physical exams for AR?
Wide pulse pressure: most sensitive Hyperdynamic and displaced apical impulse Auscultation- Diastolic blowing murmur at the left sternal border Austin flint murmur (apex): Regurgitant jet impinges on anterior MVL causing it to vibrate Systolic ejection murmur: due to increased flow across the aortic valve
42
What is the natural history of AR?
Asymptomatic until 4th or 5th decade Rate of Progression: 4-6% per year Progressive Symptoms include: Dyspnoea: exertional, orthopnea, and paroxsymal nocturnal dyspnea Palpitations: due to increased force of contraction and ectopics
43
How can we evaluate AR?
CXR: enlarged cardiac silhouette and aortic root enlargement ECHO: Allows evaluation of the AV and aortic root with measurements of LV dimensions and function (cornerstone for decision making and follow up evaluation)
44
How do we manage AR?
General: consider IE prophylaxis Medical: Vasodilators (ACEI’s potentially improve stroke volume and reduce regurgitation but indicated only in CCF or HTN Serial Echocardiograms: to monitor progression. Surgical Treatment: Definitive Tx
45
What are the indications of surgery in AR?
ANY Symptoms at rest or exercise Asymptomatic treatment if: EF drops below 50% or LV becomes dilated > 50mm at end systole
46
What is mitral stenosis (MS)?
Obstruction of LV inflow that prevents proper filling of ventricle during diastole due to thickness of mitral valve
47
What is the normal mitral valve area?
4-6 cm2
48
When do transmitral gradients and symptoms begin?
areas less than 2 cm2
49
What is the predominant cause of mitral stenosis?
Rheumatic carditis decreasing due to a reduction of rheumatic heart disease.
50
What are the causes of mitral stenosis?
Rheumatic heart disease: 77-99% of all cases Infective endocarditis: 3.3% Mitral annular calcification: 2.7% After this flashcard look at slide 59 onwards of the valvular heart disease powerpoint
51
What is the pathophysiolog of MS?
Progressive Dyspnea (70%): LA dilation > pulmonary congestion (reduced emptying) -worse with exercise, fever, tachycardia, and pregnancy Increased Transmitral Pressures: Leads to left atrial enlargement and atrial fibrillation. Right heart failure symptoms: due to Pulmonary venous HTN Hemoptysis: due to rupture of bronchial vessels due to elevated pulmonary pressure
52
What is the natural history of MS?
Mild MS: 10 years after initial RHD insult Moderate: 10 years later Severe: 10 years later
53
What is the mortality of MS due to?
Due to progressive pulmonary congestion, infection, and thromboembolism.
54
What are the physical signs of mitral stenosis?
prominent "a" wave in jugular venous pulsations: Due to pulmonary hypertension and right ventricular hypertrophy Signs of right-sided heart failure: in advanced disease Mitral facies: When MS is severe and the cardiac output is diminished, there is vasoconstriction, resulting in pinkish-purple patches on the cheeks
55
What are the heart sounds of ms?
Diastolic murmur: Low-pitched diastolic rumble most prominent at the apex. Heard best with the patient lying on the left side in held expiration Intensity of the diastolic murmur does not correlate with the severity of the stenosis
56
How do we evaluate MS?
ECG: may show atrial fibrillation and LA enlargement CXR: LA enlargement and pulmonary congestion. Occasionally calcified MV ECHO: The GOLD STANDARD for diagnosis. Asses mitral valve mobility, gradient and mitral valve area
57
What is the medical management of MS?
Medications: MS like AS is a mechanical problem and medical therapy does not prevent progression B-blockers, CCBs, Digoxin which control heart rate and hence prolong diastole for improved diastolic filling Duiretics for fluid overload
58
How else can you manage MS?
Serial echocardiography: Mild: 3-5 years Moderate:1-2 years Severe: yearly
59
What are the indications for mitral valve replacement?
ANY SYMPTOMATIC Patient with NYHA Class III or IV Symptoms Asymptomatic moderate or Severe MS with a pliable valve suitable for PMBV

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