Valvular Heart Disease Flashcards

1
Q

Symptoms of Heart Failure

A
  • Pitting oedema
  • Sacral oedema
  • Raised JVP
  • Ascites
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2
Q

What does N-terminal Brain Natriuretic Peptide measure?

A

Natruretic - reduction of salt and water
When cardiac myocytes are stressed they produce the above peptide reducing the blood pressure.
By measuring the peptide you can measure if the heart is under stress

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3
Q

What is the difference between aortic stenosis and aortic regurgitation?

A

Aortic stenosis: heard in systole - Narrowing of aortic valve, restricting blood flow from the left ventricle to the aorta
Aortic regurgitation: heard in diastolic, the aortic valve doesn’t shut properly so blood flows back from the aorta into the left ventricle during diastole

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4
Q

What are the causes of Aortic stenosis

A
  1. Degenerative - mechanical stress over time damages the endothelial cells causing fibrosis & calcification
  2. Bicuspid Valve (congenital)- more mechanical stress per leaflet
  3. Rheumatic Heart Disease - repeated inflammation leading to fibrosis, leaflets can fuse together
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5
Q

What are the causes of Aortic Regurgitation?

A

Acute
1. Idiopathic aortic root dilation
2. Aortic dissection
3. Aneurysms
4. Infective endocarditis

Chronic
1. Rheumatic fever
2. Bicuspid aortic valve
3. Degeneration
4. Connective tissue disorders e.g. Marfans

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6
Q

What are the symptoms & examination findings of aortic stenosis

A

Ejection-systolic murmur in a Crescendo-decrescendo pattern in the 2nd intercostal space.
Ejection Click
Radiates to the Carotids
Symptoms - Extertional syncope, Angina, Dyspnoea, Fatigue, Heart Failure symptoms

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7
Q

What are the symptoms & examination findings of aortic regurgitation

A

Diastolic murmur with an early decrescendo. Heard best at the left sternal edge (4th intercostal space), with the patient leaning forward.
Doesn’t radiate
Symptoms; Externtional dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea, pulmonary oedema

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8
Q

What is the Pathiohysiology of Aortic Stenosis

A
  • Narrowing of aortic valve means blood flow across the aortic valve is impeded during systole
  • Left ventricle has to generate higher pressure to push blood past hardened valve
  • This results in concentric left ventricle hypertrophy
  • Over time the left ventricle can no longer compensate and the left ventricle starts to enlarge so the ejection fraction will reduce and this will lead to reduced cardiac output
  • Eventually, leading to heart failure
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9
Q

What Investigations should you do to confirm a murmur?

A

Echo
CXR
ECG
Cardiac Catheterisation
Exercise Stress Test

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10
Q

How do you manage Aortic Stenosis?

A
  • The majority of patients with mild aortic stenosis will never progress to developing clinically significant aortic stenosis
  • Monitor with echocardiogram to assess valve; Severe AS monitored every 6 months
    Mild-to-moderate monitored yearly
    Younger patients monitored every 2 to 3 years
  • If patients develop symptoms of heart failure, may be given ACE inhibitors, diuretics, and beta-blockers
    Surgical and interventional indicated in:
  • All patients with symptomatic AS
  • Asymptomatic patients with a left ventricular ejection fraction (LVEF) <50%
  • Asymptomatic patients with an LVEF >50% who are physically active, and who have symptoms or a fall in blood pressure during exercise testing
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11
Q

What are the 2 main types of Valves for replacement?

A
  • Bioprosthetic: lasts 10 years so may require another replacement but no need for long term anticoagulant therapy
  • Metal: last a lifetime but require long-term anticoagulant therapy (warfarin)
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12
Q

What is the pathophysiology of Aortic Regurgitation?

A
  • Blood leaks from aorta into the left ventricle during diastole
  • Therefore, with each contraction, the LV must pump the regurgitant volume plus the normal quantity of blood from the left atrium
  • In acute AR the left ventricle is normal size, so the volume load of regurgitation causes the LV diastolic pressure to rise
  • In chronic AR, the LV undergoes compensatory adaptation through eccentric hypertrophy in response to excessive pressure load
  • The dilation increases the compliance of the left ventricle so it can accommodate a larger volume of blood
  • Compensatory left ventricular dilation and hypertrophy can meet the demands of chronic AR for many years meaning patients are asymptomatic
  • However, eventually as the LV increases in size, this leads to systolic dysfunction which leads to heart failure
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13
Q

What is the management of Aortic Regurgitation?

A
  • Asymptomatic patients are monitored year and echocardiography performed every 2 years
  • Asymptomatic patients but with severe AR may need vasodilators: calcium channel blocker, ACE inhibitor to treat accompanying hypertension
  • Symptomatic or asymptomatic with severe AR (LVEF <55%) offered surgery
    o Valve replacement
    o TAVI is not recommended unless patient has high surgical risk
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14
Q

What are the 2 types of heart murmur?

A
  • Innocent murmurs: These are typically soft, systolic murmurs without associated symptoms or abnormal physical findings. They are commonly heard in children and adolescents and do not require further evaluation or treatment.
  • Pathological murmurs: These can be further classified based on timing (systolic, diastolic,
    continuous), location (aortic, pulmonary, tricuspid, mitral), radiation, and associated
    symptoms
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15
Q

What is Infective Endocarditis?

A

Infective endocarditis is an infection of the inner surface of the heart, usually affecting the heart valves. It can be caused by a wide range of organisms that can cause high or low virulent infections.

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16
Q

Discuss the pathophysiology of Infective endocarditis

A
  1. endocardial surface injury
  2. platelet-fibrin-thrombus formation at the site of injury
  3. bacterial entry into circulation
  4. bacterial adherence to injured endocardial surface

The organisms are then free to multiply, which enlarges the infected vegetation. The latter provides a source for continuous bacteraemia and can lead to several complications.

17
Q

Discuss the presentation of infective endocarditis

A
  • Very variable & can be difficult to diagnose
  • Vague malaise to a ‘devastating’ acute presentation
  • Malaise, anorexia, weight loss, aches & pains
  • Vasculitic rashes
  • Splinter haemorrhages & petechial rash referred to as peripheral stigmata of endocarditis
  • Murmur – original lesion & valve erosion
  • Glomerulonephritis
  • Splenomegaly, clubbing, pigmentation – long term infection so rare
  • Osler’s nodes, Janeway lesions & Roth spots
18
Q

What are major complications of infective endocarditis?

A
  • Systemic embolism – from vegetation breaking off
  • Heart failure – damage to valve
  • Cerebrovascular;
    Embolism
    Infected aneurysm – mycotic aneurysms
19
Q

What different Bacteria cause Endocarditis

A

Viridans streptococci
Staph A
Staph Epidermidis
Coxiella burnetti
Candida albicans
HACEK organisms - gram negative bacteria from normal flora of mouth & throat
Haemophilus, Aggregatibacter, Cardiobacterium, Eikeneela, Kingella

20
Q

What microorganism is suspected in IE following dental work?

A

Viridans Streptococci
Attacks previously damaged valves
Found in mouth, low virulence

21
Q

What microorganism is suspected in IE following IV drug use?

A

Staph A
Infects damaged & healthy valves & can destroy valves
Found on skin, high virulence

Can also be fungal - Candida albicans

22
Q

What microorganism in IE is associated with severe colorectal disease?

A

Staph epidermidis
infects prosthetic material
Enters body during valve surgery or IV catheter

23
Q

What microorganism that causes IE is associated with infected animals

A

Coxiella burnetti
Normally only seen if immunocompromised

24
Q

Discuss investigations of Infective endocaridits

A

Bedside investigations:
ECG – prolonged PR interval. This suggests the development or worsening of aortic root abscess
Urine dip – looking for haematuria which could suggest glomerulonephritis

Bloods
Elevated inflammatory markers
If its subacute or chronic there may be normocytic anaemia present
Blood cultures – 3 different blood cultures much be taken at different times and sites

Imaging
Echocardiogram
CT
– can look for any septic emboli

25
Q

What is the Modified Duke’s Criteria

A

Major criteria: Blood culture positive for IE and endocardial involvement
Minor criteria: Fever, immunologic phenomena, vascular phenomena, echocardiography minor criteria, predisposition, and microbiologic evidence

26
Q

What is the management of infective endocarditis

A

When organisms are not known
- When patient has their own valve – amoxicillin (+/- gentamicin)
- When patient has a penicillin allergy or MRSA – vancomycin (+/-gentamicin)
- When the patient has a prosthetic valve – vancomycin + rifampicin + gentamicin

When the organism is S.aureus in a native valve:
- 1st line = flucloxacillin
- 2nd line = vancomycin + rifampicin

When the organism is S.aureus in a prosthetic valve:
- 1st line = flucloxacillin + rifampicin + gentamicin

When the organism is strep viridans
- 1st line = benzylpenicillin
- 2nd line = vancomycin + gentamicin

When the organism is one of the HACEK organisms (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella)
- 1st line = ceftriaxone

27
Q

What is the prevention of endocarditis?

A
  • Prophyalctic antibiotics are administered to individuals before invasive procedures who are more susceptible to bacterial infections
  • This includes some dental procedures upper respiratory tract procedures only if it involves incision or biopsy of the mucosa like a tonsillectomy. GI procedures if infection is present. Procedures on infected skin or musculoskeletal tissue.
  • Cardiac conditions which means you would need antibiotic prophylaxis: having a prosthetic heart valve, history of endocarditis, certain congenital heart diseases, cardiac transplant recipients who develop cardiac valve abnormalities.
28
Q

What is the prognosis of infective endocarditis

A

Without appropriate treatment infective endocarditis will lead to death The mortality rate within the first 30 days has been estimated at approximately 20%. Long-term survival for IE has been estimated at 50% at 10 years. The mortality in IE remains high.

29
Q

What are the prinicples & practice of Cardiac Rehab?

A
  • Health behaviour change & education
  • Lifestyle risk factor management - Physical activity, healthy eating & body composition, tobacco cessation
  • Psychosocial heath
  • Medical risk management - baseline assessment of potential comorbidities
  • Long term strategies
30
Q

What are the mitral valve murmurs

A
  1. Mitral valve prolapse - most common mitral
  2. Mitral regurgitation
  3. Mitral stenosis
31
Q

Describe the mitral valve

A

The Atrioventricular valve situated in the left side of the heart between the left atrium and the left ventricle
The mitral valve is made up of 2 anatomical leaflets, the anterior and posterior leaflets
During systole the valve closes, and blood is forced into the arterial circulation

32
Q

Discuss Mitral Valve prolapse

A

During ventricular contraction, there is a huge pressure generated in the left ventricle so a lot of pressure is exerted onto the mitral valve while its closed.
Normally, the papillary muscles and chordae tendineae prevent the valve from being forced back into the atrium and prolapsing.
However, when there is connective tissue degradation to the papillary muscles or chordae tendineae, called myxomatous degeneration, the structures can become weakened and stretch or rupture.
This leads to mitral valve prolapse, most commonly affecting the posterior leaflet of the valve.
There are strong links to connective tissue diseases such as Marfan Syndrome and Ehlers-Danlos Syndrome.
This prolapse then commonly leads to the two leaflets of the mitral valve not fully closing during systole, leading to blood leaking back into the left atrium causing mitral regurgitation.

33
Q

When is a collapsing pulse seen?

A

Aortic regurgitation

34
Q

When is a malar flush seen?

In valvular disease

A

Mitral stenosis