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AC1 > Heart Valves and Murmurs > Flashcards

Heart Valves and Murmurs Flashcards

1
Q

Define pericarditis

A

Inflammation of the visceral and/or parietal serous pericardium

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2
Q

What are the possible causes of pericarditis?

A
  • Idiopathic
  • Viral (e.g. Coxsackie)
  • Secondary to autoimmune
  • Malignancy
  • Post MI
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3
Q

Describe the clinical presentation of pericarditis

A
  • Retrosternal chest pain
    • Pleuritic and positional
  • Pericardial friction rub
  • Widespread concave ST elevation on ECG
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4
Q

Define pericardial effusion

Describe the pathology

What are the possible causes?

A

Accummulation of fluid within the pericardial space (blood, exudate, transudate)- inelastic pericardium limits how much fluid can accumulate.

Causes:

  • Secondary to pericarditis or systemic disease, e.g:
    • SLE
    • RA
    • Malignancy
    • Uraemia
    • Infection
  • Trauma
  • Idiopathic
  • Post cardiac surgery
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5
Q

Describe the clinical features of pericardial effusion

A
  • Features of underlying disease
  • Quiet, muffled heart sounds
  • Look for features of cardiac tamponade
  • Chronic effusions may give enlarged globular heart on CXR
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6
Q

Define cardiac tamponade and its pathology

A

Medical emergency where accumulation of fluid in the pericardial sac restricts cardiac filling and compromises cardiac output. Inelastic pericardium restricts how much fluid can accumulate- pericardial pressure rises and compromises cardiac filling.

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7
Q

What are some possible causes of cardiac tamponade?

A
  • Pericardial effusion causes:
    • SLE
    • RA
    • Malignancy
    • Uraemia
    • Infection
  • Trauma
  • Post MI (ventricular rupture)
  • Aortic dissection
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8
Q

Describe the clinical presentation of cardiac tamponade

A
  • Tachypnoea
  • Dyspnoea
  • Beck’s triad:
    • Hypotension (falling)
    • Muffled heart sounds
    • Jugular venous distension (rising)
  • Needs urgent decompression
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9
Q

Define myocarditis

Describe the pathology

What are the possible causes?

A

Group of conditions characterised by inflammation of the myocardium in the abscence of predominant ischaemia.

Causes:

  • Wide range of infectious causes (e.g Coxsackie virus)
  • Non infectious, immune and toxin/drug related causes

Inflammatory cell infiltrate with or without evidence of myocyte injury

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10
Q

Describe the clinical presentation of myocarditis

A
  • Acute or chronic presentations
  • Mainly clinical features of heart failure
  • Prognosis related to underlying cause
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11
Q

Define cardiomyopathies

A

Wide group of myocardial diseases (many have a strong genetic component) associated with mechanical and/or electrical dysfunction of the heart.

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12
Q

What should be excluded before diagnosing cardiomyopathies?

A

Ischaemic, hypertensive, valvular and congenital causes should be excluded.

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13
Q

What are the clinical features of cardiomyopathies?

A

Features of HF (systolic and/or diastolic dysfunction, arrhythmias, sudden death)

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14
Q

What are the main types of cardiomyopathies?

A
  • Dilated
  • Hypertrophic
  • Restrictive
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15
Q

Define hypertrophic cardiomyopathy

What are the causes?

Describe the clinical features

A

The most common cardiomyopathy. Hypertrophy of left ventricle and interventricular septum

Caused by genetic mutations in sarcomeric proteins.

Pathology:

  • Disorganised enlarged myofibres
  • Asymmetrical septal hypertrophy may obstruct LV outflow tract

Clinical presentation:

  • Manifests in adolescents/young adults
  • Complications include arrhythmias and sudden death
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16
Q

Define dilated cardiomyopathies

Describe the pathology

What are the clinical features?

A

Characterised by left ventricle dilation and often hypertrophy (after ischaemia/abnormal loading excluded)

Pathology:

  • Dilated left ventricle +/- hypertrophy and systolic dysfunction

Clinical notes:

  • Features of progressive cardiac failure
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17
Q

What are some of the causes of dilated cardiomyopathies?

A
  • 30% due to genetic mutations
  • Post myocarditis
  • Alcohol
  • Some chemotherapy agents
  • Storage disorders
  • Autoimmune
  • Idiopathic
18
Q

What is restricted cardiomyopathy?

What are the causes?

Describe the pathology and clinical features

A

Characterised by poorly compliant left ventricle with normal ventricular wall thickness.

Causes:

  • Idiopathic
  • Associated with infiltrative disease e.g. amyloidosis, haemochromatosis, sarcoidosis

Pathology:

  • Poor compliance leads to restrictive filling and diastolic dysfunction
19
Q

What is arrhythmogenic right ventricular cardiomyopathy?

A

Progressive replacement of ventricular myocardium with fibrous tissue leading to RV failure, arrhythmias and sudden death.

20
Q

What are the main causes of valve disease?

What causes the clinical manifestations?

A

Conditions that cause:

  • Degeneration, fibrosis or calcification of valve leaflets
  • Direct damage to endothelium/valve structure
  • Distortion/damage to supporting structures

Clinical manifestations are related to:

  • Valve stenosis (narrowing)
  • Valve regurgitatation (incompetence)
  • Valvular vegetations
21
Q

What is calcific valvular degeneration?

Describe the pathology

Which valve is most commonly affected?

A

Cumulative chronic injury from repetitive mechanical stress causes calcification (deposition of hydroxyapatite)

Results in valve dysfunction as the mounds of calcification impair the valves’ ability to open- usually results in a stenotic valve.

Obstructed outflow leads to increased pressure overload on the left ventricular myocardium.

Aortic valve most commonly and significantly affected.

22
Q

What is myxmatous degeneration?

Describe the pathology

Who is most at risk?

A

Deposition of mucoid (myxomatous) material within valve leaflets (usually mitral), often with associated thinning of other supporting tissues.

Results in floppy mitral valve leaflets that prolapse back into the left atrium during ventricular systole.

Affects mainly females, many asymptomatic.

23
Q

Who is most at risk from calcific valvular degeneration?

A

Older patients

Presents 1-2 decades earlier in patients with congenitally bicuspid valves

24
Q

What is rheumatic heart disease?

Describe causes and pathology

Who is most at risk?

What are the complications?

A

Acute, immune mediated multisystem inflammatory disease

Classically occurs after group A streptococcal pharyngitis. Thought to be due to a cross reaction of streptococcal antigens with host proteins.

Can lead to acute rheumatic carditis and may progress to chronic rheumatic heart disease due to repeat injury to the valves.

Characterised by fibrotic valvular disease that deforms valves (particularly mitral) due to thickened leaflets, fusing of commissures and short thick chordae tendinae.

Main cause of mitral stenosis.

25
Q

Define endocarditis

What are the types?

What usually results?

A

Inflammation of the endocardial surface of the heart, including valves, chordae tendinae, septal defects, as well as mural surfaces.

Types:

  • Infective (usually bacterial)
  • Non-infective (e.g. SLE associated)

Usually results in vegetations forming on endocardial surfaces which may be locally destructive or a source of emboli.

Can also affect prosthetic valves

26
Q

Describe the pathology of infective endocarditis

What are the clinical presentations?

A

Mainly bacterial:

  • Streptococcus viridans
  • Staphylococcus aureus

Pathology:

  • Bacteraemia due to infection, dental/surgical procedures, IVDU
  • Abnormal valve and/or virulent organism
  • Vegetations form from thrombus (fibrin/platelets/cells) and bacteria
  • May be locally destructive or a source of septic emboli
  • Mitral and aortic valve most commonly affected (N.B tricuspid valve in IVDU)

Clinical notes:

  • Often non-specific fever/malaise
  • New onset murmur +/- clinical effects of valve dysfunction
  • Embolic effects: many ‘classical’ clinical signs- most rare
  • Blood cultures and echocardiography
27
Q

What forms the normal heart sounds?

What can be palpated to allow for differentiated when heart rate is increased?

A

S1: closure of atrioventricular valves

S2: closure of the semilunar valves

Carotid artery can be palpated to allow for differentiated when heart rate is increased

28
Q

Describe the physiological splitting of the second heart sound

A

During inspiration, pulmonary valve may close later than aortic valve leading to ‘splitting’ of S2.

29
Q

Describe pathological ‘fixed’ splitting of the second heart sound

A

May be ‘fixed’ when the right side of the heart is chronically overloaded e.g. atrial-septal defect.

True fixed splitting is characteristic of this defect.

30
Q

Describe the pathological reverse splitting of the second heart sound

A

Reversed splitting e.g. during expiration, may occur, associated with delay of blood flow through aortic valve.

31
Q

What is a third heart sound

A

= dull, low frequency extra heart sound heard during early diastole.

  • Caused by rapid filling of left ventricle in early diastole
  • Can be pathological: large, poorly contracting LV or mitral regurgitation
  • Or physiological: healthy young adults, athletes, pregnancy, fever
32
Q

What are fourth heart sounds?

A

Low frequency extra heart sound that may be heard in late diastole (atrial contraction).

Caused as atrial contraction pushes blood into ‘stiff’ LV

Regarded generally as pathological and associated with conditions that reduce compliance of the left ventricle e.g. hypertrophy secondary to HTN, aortic stenosis.

33
Q

What are cardiac murmurs?

A

Produced by turbulent flow across abnormal valve, septal defect or obstructed outflow tract.

May also be generated by increased flow through normal valves (innocent/flow murmurs)

34
Q

When listening to a cardiac murmur, what should be recorded?

A
  • Location (where it is heard loudest)
  • Radiation
  • Timing- systolic or diastolic / early, mid or late (palpate carotid to establish this)
  • Intensity (grade)
  • Character and pitch e.g blowing, harsh, rumble, low or high
  • Accentuating manouevres e.g. posture, breathing, squatting, hand grip, valsalva
35
Q

Describe the grading of intensity of cardiac murmurs

A

Grade 1: Heard by an expert in optimum conditions

Grade 2: Heard by a non-expert in optimum conditions

Grade 3: Easily heard, no thrill

Grade 4: Loud murmur with a thrill

Grade 5: Loud murmur, heard over a wide area, with a thrill

Grade 6: Extremely loud, heard without a stethoscope

36
Q

What is aortic stenosis?

What are the causes?

Describe the clinical presentation

A

Narrowing of aortic valve

Prevalence increases with age.

Causes:

  • Calcific aortic valve disease most common (rheumatic heart disease)

Clinical notes:

  • LV hypertrophy (concentric) may develop (pressure overload)
  • Reduced exercise tolerance
  • Dyspnoea
  • Angina
  • Syncope
37
Q

What may be found on examination in a patient with aortic stenosis?

A
  • Mid (ejection) systolic murmur (may be ejection click at onset)
  • Crescendo-descrendo pattern
  • Radiates to carotids
  • May be associated thrill and S4
  • Narrow pulse pressure
38
Q

Describe the causes and clinical presentation of patients with aortic regurgitation

What may be found on examination?

A

Causes:

  • Dilation of aortic root (e.g. due to connective tissue disease, aortic root dissection, idiopathic)
  • Valve disease e.g. bicuspid valve, endocarditis

Clinical notes:

  • LV hypertrophy (eccentric) /dilation may develop (volume overload)
  • Features of acute or chronic HF

Examination:

  • Early diastolic high pitched decrescendo murmur
  • May be ejection systolic flow murmur & S3
  • Wide pulse presure
  • E.g. collapsing pulse; Corrigan’s; Quincke’s’ de Musset’s
  • Displaced apex beat
39
Q

Describe mitral regurgitation, its causes and clinical presentation

A

Incompetence of the mitral valve resulting from damage to any part of the mitral valve apparatus.

Causes:

  • Wide range of causes:
  • Post MI (papillary muscle damage)
  • Functional (due to dilation of LV)
  • Endocarditis (leaflets)
  • Myxomatous degeneration (leaflets/chordae)

Clinical notes:

  • LV hypertrophy (eccentric)/ dilation may develop (volume overload)
  • Features of acute or chronic heart failure
40
Q

What might be found on examination in a patient with mitral regurgitation?

A
  • Holo (pan) systolic blowing murmur
  • Radiates to axilla
  • S3 may be heard
  • Displaced apex beat
  • Thrill may be present
41
Q

What is a mitral valve prolapse?

List the causes, clinical manifestations and examination findings

A

Common valve disorder where one or both mitral valve leaflets billow back into the left atrium

Causes:

  • Mainly myxomatous degeneration of leaflets/chordae

Clinical notes:

  • Many asymptomatic
  • May be associated mitral regurgitation

Examination:

  • Mid-systolic click caused by tensing of the chordae tendinae as leaflet(s) prolapse
  • Timing shifts with manouevres, e.g valsalva, squatting
  • Classically associated with late systolic murmur
42
Q

What is mitral stenosis?

Describe the causes, clinical manifestations and examination findings

A

Narrowing of mitral valve opening due to thickening and fusion of leaflets

Causes:

  • Rheumatic heart disease (most common)

Clinical notes:

  • Features of pulmonary congestion and poor cardiac output +/- pulmonary HTN
  • Left atrial enlargement

Examination:

  • Low pitched rumbling mid-diastolic murmur
  • Often associated opening snap from stiffened valve leaflets
  • AF may be present
  • Malar flush/mitral fascies

AC1 (32 decks)

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