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BRS 1b > Structural Cardiac Disease > Flashcards

Structural Cardiac Disease Flashcards

1
Q

What is aortic stenosis?

A

There is a narrowing which prevents the valve from completely opening and facilitating the flow of blood into systemic circulation through the aorta.

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2
Q

At which diameter is aortic stenosis diagnosed?

A

less than 1cm

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3
Q

What is the pathophysiology of aortic valve stenosis?

A

Mechanical stress over time damages the endothelial cells –> Induces fibrosis and calcification besides the valve.
There is valvular endocardium damage which initiates an inflammatory process - calcium deposition which limits aortic leaflet mobility.

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4
Q

What are the main causes of aortic valve stenosis?

A

Biscuspid aortic valve - Greater risk predisposition to aortic valve stenosis given the mechanical stress is more significantly distributed between 2 aortic leaflets.

Rheumatic fever

Rare causes: Infective endocarditis and hypouricemia

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5
Q

What are the rare causes of aortic valve stenosis?

A

Infective endocarditis

Hypouricemia

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6
Q

What are the risk factors of aortic valve stenosis?

A 
Aortic sclerosis caused by smoking
Hypertension
Diabetes
LDL-cholesterol
Elevated CRP.
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7
Q

What investigations will be conducted in order to diagnose a patient with aortic valve stenosis?

A

Transthoracic echocardiogram (Elevation in aortic pressure gradient, calculate velocity of blood flow).

ECG (Abnormal enlarged QRS complex indicating left ventricular hypertrophy).

Turbulent flow - crescendo-decrescendo murmur during systole

Diminished S2

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8
Q

What will an ECG reveal in a patient with an aortic valve stenosis?

A

Abnormal enlarged QRS complex indicating left ventricular hypertrophy

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9
Q

Which murmur is detected in a patient with aortic valve stenosis?

A

Crescendo-decrescendo murmur during systole

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10
Q

What type of left ventricular hypertrophy occur in aortic valve stenosis?

A

Concentric left ventricular hypertrophy (Sarcomeres are added in parallel to existing ones)

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11
Q

Why is there left ventricular hypertrophy in aortic valve stenosis?

A

Hardening of the valve reduces the responsiveness to ventricular systolic pressure, thus during ventricular contraction a greater contractile force is required to force the valve to open.

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12
Q

What type of heart failure is associated with aortic valve stenosis?

A

Diastolic heart failure

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13
Q

Why is there diastolic heart failure with aortic valve stenosis?

A

Due to left ventricular hypertrophy, the radius of the chamber decreases, which reduces the end-diastolic volume capacity.
Patients report symptoms during exercise when there is an increased cardiac output - dyspnoea.

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14
Q

What are the complications with aortic valve stenosis?

A

Syncope
Dyspnoea
Angina

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15
Q

What type of anaemia is found in patients with aortic valve stenosis?

A

Macroangiopathic haemolytic anaemia - Damage to RBCs being forced through the narrowed aortic valve - fragmentation into schistocytes leading to haemoglobinuria

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16
Q

What type of treatment is available for aortic valve stenosis?

A

Metallic valve replacement

TAVR (Transcatheter aortic valve).

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17
Q

What is metallic valve replacement in aortic valve stenosis?

A

Requires long-term anticoagulation with Warfarin (Vitamin-K antagonist) in comparison to bioprosthetic valves

Metallic valves are recommended for younger patients

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18
Q

Why are metallic valves recommended for younger patients?

A

Since bioprosthetic valves have a short lifespan.

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19
Q

What is aortic regurgitation?

A

Aortic regurgitation is the diastolic leakage of blood from the aorta into the left ventricle due to inadequate coaptation of valve leaflets, during diastole (ventricular filling).

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20
Q

What are the main causes of aortic regurgitation?

A

Congenital bicuspid aortic valve and aortic root dilation

Connective tissue diseases (Marfan’s)

Rheumatic fever

Infective endocarditis –> Valvular damage

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21
Q

What type of hypertrophy occurs in aortic regurgitation?

A

Eccentric hypertrophy

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22
Q

What is the pathophysiology in aortic regurgitation?

A

There is pressure and volume overload in the left ventricle, this causes the ventricle to expand, increasing in diameter.
There is an increase in wall tension due to volume overload (greater myocardial oxygen consumption).

Eccentric hypertrophy occurs for increased wall tension.

SBP increases as there an increase in EDV - contracile force and pressure required to increase the stroke volume increases.

During diastole there is less blood flow into the aorta , since it returns to the ventricles - reduces DBP.

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23
Q

Why is there an increase in pulse pressure in patients with aortic regurgitation?

A

Since there is a significant reduction in DBP, yet a high SBP

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24
Q

What are the symptoms and signs with aortic regurgitation?

A

Diastolic murmur (Early decrescendo)
Dyspnoea due to pulmonary oedema in acute AR
Fatigue, and weakness due to left ventricular dysfunction
Orthopnoea

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25
Q

What treatment is available in aortic regurgitation?

A

Replace valve after symptoms of left ventricular hypertrophy develops

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26
Q

What is the structure of the mitral valve?

A

The mitral valve has two leaflets and consists of chordae tendinea and papillary muscles.

  1. Anterior leaflet
  2. Posterior leaflet.
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27
Q

What is mitral regurgitation?

A

During ventricular systole, blood reflows back through the left ventricle into the left atrium.

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28
Q

How does mitral valve prolapse occur?

A

During systolic ventricular contraction, there is an increase in pressure which is exerted onto the closed mitral valve, in prolapse there is myxomatous degeneration whereby the connective tissue is disrupted - causing a redundancy in chordal apparatus - can rupture.

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29
Q

What type of degeneration occurs in mitral valve prolapse?

A

Myxomatous degeneration

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30
Q

What forms of connective tissue disorders are associated with a mitral valve prolapse?

A

Marfan syndrome

Ehrler’s-Danlos syndrome

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31
Q

What are the causes of mitral regurgitation?

A

MI causing damage to the papillary muscles, thus the chordae tendinea cannot effective hold the valve closed.

Infective endocarditis

Rheumatic fever

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32
Q

What is mitral valve stenosis?

A

Mitral stenosis is a narrowing of the mitral valve orifice, the leaflets can fuse together (commissural fusion).

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33
Q

What is the pathophysiology of mitral valve stenosis?

A

Increase in left atrial pressure and volume - subsequent atrial dilation is referred to the lungs by the pulmonary veins leading to pulmonary congestion

Reduced diastolic filling of the left ventricle

Pulmonary hypertension increases afterload on right ventricle

Atrial dilation can lead to atrial fibrillation

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34
Q

What happens to the atria in mitral valve stenosis?

A

Increase in left atrial pressure and volume.

Atrial dilation

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35
Q

Why does atrial fibrillation occur in mitral valve stenosis?

A

Atrial dilation increases sensitivity of sinoatrial nodal cells

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36
Q

Why does pulmonary congestion occur in mitral valve stenosis?

A

Subsequent atrial dilation is referred to the lungs by the pulmonary veins.

37
Q

What is hypertrophic cardiomyopathy?

A

A disorder characterised by left ventricular hypertrophy, the myocardium becomes hypercontractile with assymmetrical hypertrophy of the interventricular septum.

The ventricular walls become stiffer and less compliant, therefore there is less stretch and diastolic filling - this reduces stroke volume.

38
Q

What type of heart failure is concerned with hypertrophic cardiomyopathy?

A

Diastolic heart failure

39
Q

What cardiac sound is heard in patients with hypertrophic cardiomyopathy?

A

S4.

40
Q

what are the implications of septal hypertrophy?

A

Obstructs the left ventricular outflow tract during systole, this increases blood velocity through the opening and causes the anterior leaflet to be pulled towards the septum.

41
Q

What does the ECG reveal on patients with hypertrophic cardiomyopathy?

A

There is an enlarged QRS complex.

42
Q

Which murmur is present in a patient with hypertrophic cardiomyopathy?

A

Crescendo-decrescendo murmur (systolic ejection).

43
Q

What is dilated cardiomyopathy?

A

This is a type of systolic heart failure given that the ventricles have poor contractility to effective pump blood into systemic circulation due to dilation of the cardiac chambers.

44
Q

What type of heart failure is concerned with dilated cardiomyopathy?

A

Systolic heart failure.

45
Q

What does an echocardiogram reveal in dilated cardiomyopathy?

A

Dilated left ventricle

46
Q

What are the causes of dilated cardiomyopathy?

A

1) Genetics (muscular dystrophies, and haemochromatosis)
2) Toxins (alcohols, cardiotoxic chemotherapy).
3) Peripartum cardiomyopathy
4) Viral infections (myocarditis)
5) Thyroid disease
6) Idiopathic

47
Q

Which genes are implicated in dilated cardiomyopathy?

A

Titin, lamin, phospholamban, cardiac myosin binding protein C, myosin heavy chain

48
Q

What is involved in the management of dilated cardiomyopathy?

A 
ACE inhibitors 
Beta-blockers
Mineralocorticoid receptor antagonists 
Anticoagulation for atrial fibrillation 
Digoxin
49
Q

Why are ace inhibitors prescribed in dilated cardiomyopathy?

A

Facilitates vasodilation to reduce after load onto the left ventricle, improving the cardiac contractile effectiveness.

50
Q

What does digoxin do?

A

Strengthens heart muscle contractions

51
Q

What cardiac devices are used for dilated cardiomyopathy?

A

Biventricular pacemakers
Implantable cardioverter-defibrillators (ICDs)
Left ventricular assist devices

52
Q

What is arrythmogenic right ventricular cardiomyopathy?

A

A disease of the cardiac muscle leading to abnormal cardiac contraction, there is a myocyte detachment which ultimately causes fibrofatty deposits.
• Dilated right ventricle  Reduces diastolic filling of the left ventricle and thus causes a reduced stroke volume.
• Patients are typically asymptomatic.

53
Q

What is cardiogenic shock?

A

Shock which describes a state whereby there is inadequate perfusion of tissues and blood oxygen saturation, or there being an increased oxygen demand from tissues - results in decreased end-organ oxygenation and dysfunction

54
Q

What is the end outcome for a patient with untreated cardiogenic shock?

A

End-organ failure

55
Q

What is a common cause of cardiogenic shock?

A

Myocardial infarction

56
Q

What are the effects implicated in cardiogenic shock?

A

There is a loss of cardiac output and an impairment in systolic function –> Leads to volume overload into the ventricles, reducing the efficacy of contractility.

57
Q

What treatment options are available for a patient with cardiogenic shock?

A

Percutaneous coronary intervention (PCI) - Stent to open the narrowing of the coronary arteries.

Inotropes

Early coronary angiography - visualise the blood flow within the coronary artery

58
Q

What are the two most common inotropes?

A

Dobutamine

Dopamine

59
Q

What effect is induced by inotropes?

A

These drugs potentiate catecholamine activity and induce potent inotropic activity by increasing the contractile strength of the myocardium –> Increases stroke volume

60
Q

What side effects are implicated in the use of inotropes?

A

Arrhythmias, tachycardia, hypertension, and anginal chest pain

61
Q

What is the Frank-Starling Relationship?

A

Increased diastolic fibre length increases ventricular contraction, attributed to an increased preload.

Increased stretching leads to greater increase in shortening and shortening velocity

62
Q

How does the Frank-Starling relationship apply to short diastolic fibre lengths?

A

At shorter lengths than optimal , the actin filaments overlap, reducing number of myosin cross bridges that can be made.
More stretch - the more optimum interdigitation of actin and myosin is achieved.

63
Q

What two factors affect ventricular contraction in regards to cardiac myofilaments?

A

Changes in the number of myofilament cross-bridges that interact.

Changes in calcium sensitivity of the myofilaments

64
Q

How does the change in the number of myofilament cross-bridges affect ventricular contraction?

A

Ventricular stretching subsequently increases the contact between myosin heads with the myosin binding sites presented by the thin actin filaments, this causes a decrease in lattice-spacing

Decreasing myofilament lattice spacing increases the probability of forming strong-binding cross bridges, providing more force for the same amount of activating calcium

65
Q

How does the chance in calcium sensitivity of the myofilaments affect ventricular contraction?

A

Calcium ions are required for myofilament activation, troponin C is a thin filament protein that binds to calcium, subsequently causing tropomyosin to exposure the myosin binding sites, regulating the formation of cross-bridges between actin and myosin.

At longer sarcomere lengths, the affinity of TnC for calcium is increased due to conformational change in protein, thereby less calcium is required for equivalent amount of force.

66
Q

What is stroke work?

A

The work done by the heart to eject blood under pressure into aorta and pulmonary artery

67
Q

What is the equation for stroke work?

A

Stroke work = stroke volume x pressure

68
Q

What are three factors that affect stroke work?

A

1) Preload
2) Contractility
3) Afterload

69
Q

What does the Law of Laplace state?

A

Assuming pressure within a cylinder is held constant, the tension exerted onto the walls increases with increasing radius.

70
Q

What is the equation for tension in a cylindrical vessel?

A

T =PR

71
Q

What is the equation for tension in a spherical vessel?

A 
T = PR/2
(P = internal pressure)
72
Q

What is afterload?

A

Refers to the tension/force that the ventricles must develop to pump blood effectively against the resistance in the vascular system.

The load against which the left ventricle ejects blood after opening the aortic valve.

73
Q

What is the equation for cardiac output?

A

Heart rate x stroke volume

74
Q

What are the units for cardiac output?

A

Litres/minute

75
Q

How do you calculate the ejection fraction?

A

Stroke volume/end-diastolic volume

76
Q

Which value of MAP is necessary to adequately perfuse the body organs?

A

> 65mmHg

77
Q

What is infective endocarditis?

A

An infection involving the endocardial surface of the heart, including the valvular structures, the chordae tendinea, sites of septal defects or the mural endocardium

78
Q

Which cardiac valves are commonly affected in infective endocarditis?

A

Mitral and aortic valve given that these areas are susceptible to sustained endothelial damage secondary to turbulent flow.

79
Q

What is the pathophysiology of infective endocarditis?

A

Endothelial damage secondary to turbulent flow to the cardiac valves cause platelets and fibrin to adhere to the underlying collagen surface to form a prothrombotic milleu.

Bacteriaemia leads to colonisation of the thrombus, perpetuating further fibrin deposition and platelet aggregation –> Infected vegetation

80
Q

Which bacteria is the mot common cause of infective endocarditis?

A

Streptococci (20-40% of cases)

81
Q

What are the symptoms associated with infective endocarditis?

A 
Fever
Malaise, night sweats, fatigue, anorexia, weight loss and mylagias
Weakness
Arthralgia
Headache
Shortness of breath
82
Q

What investigations are conducted to determine a patient with infective endocarditis?

A

Blood cultures –> To identify causative pathogen and confirm bacteriaemia

Blood tests –> FBC to identify anaemia or leukocytosis

Echocardiogram –> Reveals vegetation, abscess, valve perforation and/or new dehiscence of prosthetic valve.

There is often valve regurgitation and a new heart murmur

83
Q

What are the Duke’s criteria for determining a patient with infective endocarditis?

A

2 major clinical criteria
1 major and any 3 minor clinical criteria
5 minor criteria

84
Q

What are the major Duke’s criteria for infective endocarditis?

A

Positive blood culture for infective endocarditis (IE), 2 separate blood cultures.

Echocardiogram revealing: Vegetation, dehiscence of valve, abscess

New valvular regurgitation murmur

Coxiella Brunetti infection

85
Q

What are the minor Duke’s criteria for infective endocarditis?

A

Fever

Predisposing heart condition or intravenous drug use

Vascular: Major arterial emboli, septic pulmonary infarcts, intracranial haemorrhages and Janeway lesiond

Immunological: Glomerulonephritis, osler nodes, Roth spots, rheumatoid factor

Microbiological evidence: Positive blood cultures, however does not meet major criteria.

86
Q

What are the symptoms of cardiac decompensation?

A 
Shortness of breath
Frequent coughing
Peripheral oedema of the lower limb
Central oedema of the abdomen 
Fatigue

Raised JVP

87
Q

What are Osler’s nodes?

A

Tender, purple-pink nodules with a pale centre, generally found on the distal fingers and toes.

88
Q

What are Roth Spots?

A

A common manifestation in acute bacterial endocarditis, a red spot caused by a haemorrhaging with a characteristic pale white centre (represents fibrin-platelets plugs) within the retina.

BRS 1b (62 decks)

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