Cardiology Flashcards

1
Q

Summarise aortic stenosis.

A

Narrowed aortic valve.
Ejection systolic murmur, high-pittched crescendo-decrescendo murmur.
Radiates to carotids.
Other features: narrow pulse pressure, slow rising pulse, exertional syncope.
Most common cause is idiopathic age-related calcification and rheumatic heart disease.
Sound: BURR DUB

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2
Q

Summarise mitral regurgitation.

A

Incompetent mitral valve allowing blood to flow back during systolic contraction of the RV.
Pansystolic murmur. High-pitched whistling murmur.
Caused by idiopathic weakening of the valve with age, associated with IHD, IE, rheumatic HD, connective tissue disorders (Marfan’s, EDS).
Sound: BURR BURR

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3
Q

Summarise mitral stenosis.

A

Mitral valve becomes narrowed.
Mid-diastolic, low pitched, rumbling murmur. Loud S1 due to thick valves that require a lot of systolic force to shut.
Caused by rheumatic heart disease and IE.
Sound: LUB! DUB DURR

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4
Q

Summarise aortic regurgitation.

A

Aortic valve becomes incompetent.
Soft murmur, very subtle.
Associated with collapsing pulse, DeMusset’s sign, Quincke’s sign, Traube’s sign, Muller’s sign, heart failure, Austin-Flint murmur.
Caused by age-related weakness, connective tissue disorders (Marfan’s, EDS).
Sound: LUB TARRRR

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5
Q

What is an Austin-Flint murmur?

A

Heard at the apex, this is an early diastolic rumbling murmur caused by blood flowing back through the aortic valve and over the mitral valve, causing the mitral valve leaflets to vibrate. It is associated with severe aortic regurgitation.

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6
Q

Eponymous signs of aortic regurgitation?

A

DeMusset’s sign: head nodding with the heart beat.
Quincke’s sign: pulsation of nail beds.
Traube’s sign: pistol shot femorals.
Muller’s sign: pulsation of uvula.
Duroziez’s sign: to and fro murmur heard when stethoscope compresses femoral vessels.

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7
Q

Describe S1 and S2 heart sounds.

A

S1 (first heart sound) - ‘lub’
Closing of mitral and tricuspid valves.

S2 - ‘dub’
Closing of aortic and pulmonary valves.

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8
Q

Describe S3 and S4 heart sounds, if present.

A

S3 (third heart sound) - ‘lub de dub’
‘Ventricular gallop’ occurs just after S2 when the mitral valve opens. S3 is produced by a large amount of blood striking a very compliant LV.
Can be a sign of systolic heart failure, but can also be a normal finding.

S4 (fourth heart sound) - ‘le lub dub’
‘Atrial gallop’ occurs just before S1 when the atria contract to force blood into the LV. If the LV is noncompliant, and atrial contraction forces blood through the AV valves, an S4 is produced by blood striking the LV. Can be a sign of diastolic CCF.

Any condition producing an overly compliant LV produces S3, whereas any condition producing a noncompliant LV will produce S4.

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9
Q

Differential diagnosis for an ejection systolic murmur?

A

Aortic sclerosis
HCM
ASD
Pulmonary stenosis

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10
Q

What are the causes of aortic stenosis?

A

Common: calcific degeneration and bicuspid valve
Uncommon: rheumatic fever, HCM, congenital (other than bicuspid), supravalvular stenosis (Williams syndrome).

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11
Q

What are the indications for surgery in a patient with aortic stenosis?

A

Severe stenosis (mean AV gradient of 40mmHg)
Symptoms (angina / collapse / dyspnoea / heart failure) with moderate stenosis
Critical AS (valve area <0.8cm)

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12
Q

What differentiates severe aortic stenosis from aortic sclerosis?

A

It is difficult - they lie on a continuum.
In sclerosis, there is a normal pulse pressure and character, normal A2 component and little murmur radiation.

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13
Q

What happens to the loudness of the murmur with progressive aortic stenosis severity?

A

Murmur intensity is dependent on the flow turbulence through the valve, and cardiac output.
In critical AS with a failing ventricle, cardiac output will fall, and the murmur will be soft, but A2 will be absent.

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14
Q

Should exercise testing be performed in symptomatic patients with aortic stenosis?

A

Exercise testing should not be performed in symptomatic patients with AS, but is helpful for prognosis in ‘asymptomatic’ patients to unmask functional limitation.

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15
Q

Medical management of aortic stenosis?

A

Regular follow up and echocardiograms.

Diuretics, digoxin, ACE inhibitors or ARBs for heart failure.

Statins for prevention of atheroscelrotic events.

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16
Q

Surgical treatment of aortic stenosis?

A

Aortic valve replacement (+/- CABG) is the definitive treatment of symptomatic severe AS.

Balloon valvuloplasty has a limited role in adult AS, but is sometimes used as a bridge to surgery or TAVI if the patient is unstable.

TAVI considered if open aortic valve replacement is too high risk. Complications of TAVI include: stroke, pacemaker insertion and vascular complications. One year survival 60-80%.

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17
Q

What are the causes of aortic regurgitation?

A

Acute: infective endocarditis, aortic dissection.

Chronic: congenital aortic valve malformation, aortic root dilatation, prior endocarditis, rheumatic fever, post-TAVI.

CTDs: arthritis, SLE, ank spond, EDS, Marfan’s syndrome.

Seronegative arthritides: ank spond, reactive arthritis.

Syphilitic aortitis.

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18
Q

List the findings which would determine the need for surgery in aortic regurgitation.

A

Acute severe symptomatic AR.

Symptomatic patients with severe AR regardless of LV systolic function.

Patients with severe AR undergoing surgery for another reason (e.g., CABG, mitral or aortic surgery).

Asymptomatic patients with severe AR.

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19
Q

List some manifestations of Marfan’s syndrome.

A

Ectopia lentis (upwards lens dislocation)
Arm span > height
Dural ectasia
Pectus excavatum
Joint laxity
Scoliosis
Pes planus
High-arched palate

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20
Q

How often should asymptomatic patients with Marfan’s be screened?

A

Patients with Marfan’s with a dilated aorta should be screened with annual echocardiogram to monitor the proximal aorta / aortic root.

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21
Q

What is Eisenmenger’s syndrome?

A

Results from a left to right shunt causing increased pulmonary blood flow, increased pulmonary vascular resistance and pulmonary HTN as a result.

This leads to a reversal of the shunt.

This is clinically manifested as cyanotic heart disease.

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22
Q

What are the causes of Eisenmenger’s syndrome?

A

Large non-restrictive VSD
Non-restrictive PDA
AV septal defects
Large uncorrected or surgically created systemic-to-pulmonary shunts for treatment of congenital heart disease

23
Q

What are the potential complications of Eisenmenger’s syndrome?

A

Secondary polycythaemia and hyperviscosity
Heart failure
Arrhythmias
Stroke
CKD
Hyperuricaemia and gout
Sudden cardiac death

24
Q

What is the cause of the dynamic outflow gradient in HCM?

A

It is caused by systolic anterior motion of the mitral valve due to local under pressure (Venturi effect) exacerbated by the septal hypertrophy.

25
Q

What are the risk factors for sudden cardiac death in HCM?

A

Family history of SCD with HCM at a young age.
Unexplained syncope in young age.
Personal history of VF / VT.
Maximum LV wall thickness >30mm.
Hypotensive response to exercise.
Left ventricular outflow tract obstruction (LVOTO).

26
Q

What do you know about the genetics of HCM?

A

60% of HCM is inherited as autosomal dominant.
Most mutations occur in the cardiac sarcomere protein genes.
5-10% are due to other genetic disorders.
A detailed family history and first-degree relative screening is advised.

27
Q

When would an ICD be indicated in someone with HCM?

A

If the 5-year risk of sudden cardiac death is 4-6% and definitely indicated if the 5-year risk is >6% using the ESC HCM risk score calculator.

28
Q

What is a differential diagnosis for mitral stenosis (mid-diastolic murmur)?

A

Left atrial myxoma
Parachute mitral valve
Severe mitral annular calcification
Thrombosed mitral valve prosthesis

29
Q

What are the complications of mitral stenosis?

A

Pulmonary HTN and right-sided HF
Haemoptysis
Flash pulmonary oedema
Emboli
AF
IE

30
Q

What surgical procedures require antibiotic prophylaxis?

A

Prophylaxis is not generally recommended for surgical procedures.

Patients should be advised to maintain good oral health, and those at risk of IE should be treated and investigated promptly if show evidence of infection.

31
Q

What are the causes of mitral regurgitation?

A

Acute:
Chordae tendineae rupture due to degenerative valve disease, trauma, rheumatic HD, MVP.
Papillary muscle rupture post-MI.
IE.

Chronic:
MVP.
Functional MR secondary to LV dilatation.
Dilatation or calcification of the mitral valve annulus.
IE.
Connective tissue disease: SLE, RA, ank spond.
Inherited: Marfan’s, EDS, pseudoxanthoma elasticum.
HCM.

32
Q

What is the difference between primary and secondary mitral regurgitation?

A

Primary MR: includes all causes of MR in which intrinsic lesions affect one or more components of the mitral valve.

Secondary MR: usually functional, the valve is structurally normal.

33
Q

How does management differ between primary and secondary MR?

A

Primary MR: IE causing chordae tendineae rupture or muscle rupture - requires urgent surgical intervention.

Chronic primary: rheumatic heart disease, MVP, IE, CTD. Surgery is usually curative.

Chronic secondary: LV dilatation (ischaemic) or non-ischaemic heart disease. MV surgery is not usually curative, as it’s only one component of the disease.

34
Q

What are the associations of mitral valve prolapse (MVP)?

A

Congenital heart disease: ASD, AVSD, PDA.

Congenital disorders: Turner’s, Marfan’s, pseudoxanthoma elasticum.

Others: SLE.

35
Q

What are the clinical features of mitral regurgitation?

A

Atrial fibrillation.
Laterally displaced, heaving apex beat.
Pansystolic murmur.
Third heart sound.
Wide pulse pressure.

36
Q

What are the complications of mitral valve prolapse?

A

IE.
Atrial / ventricular arrhythmias.
Mitral regurgitation (MVP is the most common cause of chronic primary MR in developed countries).
Cerebral emboli.
Sudden cardiac death.

37
Q

What are the main causes of mixed aortic valve disease?

A

Bicuspid aortic valve.
Degenerative calcific aortic valve.
Radiotherapy.

38
Q

What are the complications of prosthetic valves?

A

Early: surgical complications, endocarditis.

Late: bleeding, IE, regurgitation, haemolysis, valvular stenosis, structure failure / embolisation.

The main risk with tissue valves is regurgitation with degeneration.

39
Q

What influences the type of valve a patient will receive?

A

Metallic valves: used in younger patients due to durability, unless female and planning to conceive in future (high VTE risk).

Tissue valves: useful in elderly (shorter life expectancy of valve), and those with increased risk of bleeding if anticoagulated.

40
Q

What types of metallic valve are available and what’s their thrombogenecity risk?

A

Disc valve (Tilting disc): high risk
Bileaflet valve (St Jude’s): low risk

Ball and cage (Starr-Edwards): rarely used anymore

41
Q

What happens to the intensity of the clicks from a metallic valve when failing?

A

Decreasing intensity of the closing metallic click.

42
Q

Is oral anticoagulation ever required after bioprosthetic valve surgery?

A

If there’s another indication for anticoagulation, i.e., AF.

Should be considered for 3 months following mitral or tricuspid tissue valve surgery.

Either low-dose aspirin or oral anticoag to be considered after aortic tissue valve replacement for 3 months.

43
Q

Causes of tricuspid regurgitation?

A

Primary: congenital, rheumatic heart disease, right-sided IE, carcinoid syndrome

Secondary: right sided HF (PE, MI), pulmonary HTN, Eisenmenger’s syndrome, biventricular failure

44
Q

What is carcinoid syndrome?

A

Rare neuroendocrine tumour of the enterochromaffin cells.

Products of the tumour are metabolised by the liver, resulting in a collection of symptoms including dyspnoea, wheeze, diarrhoea, flushing, tachycardia, dizziness.

Symptoms are caused by serotonin and vasoactive peptides release.

45
Q

How is a diagnosis of carcinoid syndrome established?

A

By urinary measurement of 24-hour urinary 5-HAA, a degradation component of serotonin.

Radiological methods to determine primary.

46
Q

How is carcinoid syndrome treated?

A

Medical: loperamide, octreotide, radiotherapy, chemo

Surgical: curative resection, tumour de-bulking

47
Q

What are the most common organisms in infective endocarditis?

A

Strep viridans, staph aureus (IVDU organism), staph epidermidis, enterococcus.

Staph endocarditis has the worst prognosis.

Others: strep bovis, HACEK group, pseudomonas.

48
Q

What are the diagnostic criteria for IE?

A

Modified Duke’s criteria - includes 2 major and 5 minor criteria.

49
Q

What are the causes of a VSD?

A

Congenital: ‘lone’ VSD, associated with other defects e.g. Tetralogy of Fallot, AVSD.

Acquired: post-MI, trauma

50
Q

What are the classifications of VSDs?

A

Membraneous septal defects (most common).

Muscular septal.

Atrioventricular canal.

Conal.

51
Q

What are the complications of a VSD?

A

IE, pulmonary HTN, Eisenmenger’s syndrome, aortic valve leaflet prolapse, AR.

52
Q

What diseases are associated with a VSD?

A

Aortic regurgitation
PDA
Coarctation of the aorta
Tetralogy of Fallot
Turner’s syndrome
Trisomies 13, 18, 21

53
Q

What are the risks associated with a transcatheter closure of a VSD?

A

Displacement, misplacement, cardiac tamponade, aortic regurgitation, haemorrhage, complete HB + pacemaker insertion, need for open heart surgery.