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Cardiovascular & Respiratory Medicine > Structural heart disease > Flashcards

Structural heart disease Flashcards

1
Q

What are structural heart diseases?

A

defects which affect the valves and chambers of the heart and the aorta.

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2
Q

Give some examples of congenital structural heart diseases?

A

Congenital include atrial septal defect (ASD), ventricular septal defect (VSD), coarctation of aorta, patent foramen ovale (PFO),Patent ductus arteriosus (PDA), Tetralogy of Fallot (TOF)

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3
Q

Give some examples of structural heart diseases that form later in life

A

(for due to damage caused by infections etc.)

Develop later in life: can be due to valvular dysfunctions (Atrial stenosis /regurgitation or muscular (cardiomyopathies)

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4
Q

What is “ventricular septal defect VSD”

A

“Hole between the left/right ventricles”- congenital
- Causes mixing of oxygenated and deoxygenated blood
- Blood goes left -> right
- Higher pressure to lower pressure
- Leads to right overload
= RIGHT HEART FAILURE

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5
Q

What is “Atrial Septal Defect ASD”

A

“hole in the wall (septum) that divides the upper chambers (atria) of the heart”- congenital
- A large atrial septal defect can cause extra blood to overfill the lungs
- & Overworks the right side of the heart
- If not treated, the right side of the heart eventually grows larger and becomes weak
- The blood pressure in the arteries in the lungs can also increase, leading to pulmonary hypertension

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6
Q

What is Tetralogy of Fallot (TOF)

A

TOF is a cardiac anomaly that refers to a combination of 4 heart defects (commonly occur together)

  1. Ventricle septal defect (hole in the wall of the septum)
  2. Over-riding Aorta (Aorta is in the wrong position- shifted more to the right and lies above the hole)
  3. Right ventricle hypertrophy/ ventricle septum hypertrophy
  4. Pulmonary valve stenosis (Constriction/ narrowing of pulmonary veins/ valves)
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7
Q

What are the consequences of an over-riding aorta in TOF?

A

Shifting of the body’s main artery (aorta):
- Normally the aorta branches off the left ventricle
- In TOF the aorta is in the wrong position- It’s shifted to the right and lies directly above the hole in the heart wall (ventricular septal defect)
- As a result, the aorta receives a mix of oxygen-rich and oxygen-poor blood from both the right and left ventricles.

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8
Q

What are the consequences of Ventricle Septal defect in TOF?

A

A hole between the bottom heart chambers (ventricular septal defect):
- A ventricular septal defect is a hole in the wall (septum) that separates the two lower chambers of the heart (left and right ventricles)
- The hole causes oxygen-poor blood in the right ventricle to mix with oxygen-rich blood in the left ventricle
- This causes inefficient blood flow and reduces the supply of oxygen-rich blood to the body
- The defect eventually can weaken the heart.

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9
Q

What are the consequences of Right Ventricle Hypertrophy in TOF?

A

Thickening of the right lower heart chamber (right ventricular hypertrophy):
- When the heart’s pumping action is overworked, the muscular wall of the right ventricle becomes thick.
- Over time this might cause the heart to stiffen, become weak and eventually fail.

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10
Q

What are the consequences of Pulmonary Valve Stenosis in TOF?

A

Narrowing of the lung valve (pulmonary valve stenosis):
- Narrowing of the valve that separates the lower right chamber of the heart (right ventricle) from the main blood vessel leading to the lungs (pulmonary artery) reduces blood flow to the lungs.
- The narrowing might also affect the muscle beneath the pulmonary valve.
- Sometimes, the pulmonary valve doesn’t form properly (pulmonary atresia).

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11
Q

What is Coarctation of the Aorta?

A

“narrowing of the aorta”
- Not enough blood from the left ventricle can get into the aorta
- decreases cardiac output
- Decreased stroke volume
= breathlessness
(requires emergency care)

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12
Q

What are examples of valvular defects?

A

Aortic stenosis
Aortic Regurgitation
Mitral stenosis
Mitral Regurgitation
(Stenosis and regurgitation does occur in tricuspid/ pulmonary calve- but mitral s/r is the most common)

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13
Q

What are the causes of aortic stenosis?

A

Rheumatic heart disease
Congenital heart disease (bicuspid valve)
Calcium build up

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14
Q

What are the risk factors of Aortic Stenosis?

A
  • Hypertension
  • LDL levels
  • Smoking
  • Elevated c- reactive protein
  • Congenital bicuspid valves
  • Chronic kidney disease
  • Radiotherapy
  • Older age
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15
Q

Describe the prevalence of Aortic stenosis

A
  • AS is the most common valvular disease in the US and Europe requiring treatment
  • It is the second most frequent cause for cardiac surgery.
  • It is largely a disease of older people (the seventh or eighth decade of life)
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16
Q

Aortic Stenosis is preceded by aortic sclerosis (defined as aortic valve thickening without flow limitation), true of false?

A

TRUE

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17
Q

What signs would make you suspect aortic stenosis?

A

It is often suspected by the presence of an early-peaking, systolic ejection murmur, and confirmed by echocardiography.

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18
Q

Describe the pathophysiology of Aortic Stenosis

A
  • The valvular endocardium is damaged as the result of abnormal blood flow across the valve (in the case of bicuspid valve) or by an unknown trigger
  • Endocardial injury initiates an inflammatory process similar to atherosclerosis and ultimately leads to leaflet (flaps of the valves) fibrosis and deposition of calcium on the valve
  • Progressive fibrosis and calcium deposition limit aortic leaflet mobility and eventually produce stenosis (narrowing)
  • In rheumatic disease, an autoimmune inflammatory reaction is triggered by prior Streptococcus infection that targets the valvular endothelium, leading to inflammation and eventually calcification
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19
Q

How can aortic stenosis lead to systolic heart failure?

A
  1. The calcified valve makes it hard for blood to be pushed out of the heart from the left ventricle
  2. This long-standing pressure overload leads to left ventricular hypertrophy
  3. Ventricle attempts to maintain a normal wall stress (afterload) despite the pressure overload produced by stenosis
  4. BUT as the stenosis worsens, the adaptive mechanism fails and left ventricular wall stress increases.
  5. Systolic function declines as wall stress increases, with resultant systolic heart failure.
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20
Q

describe the history and presentation of Aortic Stenosis

A

Exertional dyspnoea and fatigue
Chest pain
Ejection systolic murmur (≥3/6 is present with a crescendo-decrescendo pattern that peaks in mid-systole and radiates to the carotid)
H/O Rheumatic fever, high lipoprotein, high LDL, CKD, age >65

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21
Q

What investigations are used to monitor Aortic Stenosis?

A

Transthoracic echocardiography
ECG Chest X ray (LVH)
Cardiac catheterisation
Cardiac MRI

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22
Q

What is the management of aortic stenosis?

A
  1. Aortic Valve Replacement (AV):
    The primary treatment of symptomatic AS
    Asymptomatic patients with severe AS who have an LVEF <50% or who are undergoing other cardiac surgery.
    AVR may be considered in asymptomatic patients with very severe AS or severe AS with rapid progression, an abnormal exercise test, or elevated serum B-type natriuretic peptide (BNP) levels
  2. Balloon aortic valvuloplasty= a catheter is inserted in the heart and guided to the narrowed valve. The balloon is then inflated, which expands the opening of the valve
  3. Antihypertensive
  4. ACEi
  5. Statins
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23
Q

What is Aortic Regurgitation?

A

the diastolic leakage of blood from the aorta into the left ventricle.
- It occurs due to incompetence of valve leaflets resulting from either intrinsic valve disease or dilation of the aortic root

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24
Q

Describe the prevelance of aortic regurgitation

A

AR is not as common as aortic stenosis and mitral regurgitation

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25
Q

What are the 2 types of aortic regurgitation you can have?

A

It can be chronic: culminate into congestive cardiac failure

It can be acute: medical emergency, presenting with sudden onset of pulmonary oedema and hypotension or cardiogenic shock

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26
Q

What are the congenital or acquired causes of aortic regurgitation?

A

Rheumatic heart disease
Infective endocarditis
Aortic valve stenosis
Congenital heart defects
Congenital bicuspid valves

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27
Q

What are the “aortic root dilation” causes of aortic regurgitation?

A

Marfan’s syndrome
Connective tissue disease/ collagen vascular diseases
Idiopathic (cause unknown)
Ankylosing spondylytis
Trauma

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28
Q

How does acute aortic regurgitation lead to cardiogenic shock?

A

Acute AR:
- Increase blood volume in LV during systole
- LV end diastolic pressure increases
- increase in pulmonary venous pressure= dyspnea (shortness of breath) and pulmonary oedema
- leads to heart failure
- cardiogenic shock

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29
Q

How does chronic aortic regurgitation lead to cell death?

A

Chronic AR:
- gradually increase in LV volume
- LV enlargement and eccentric hypertrophy (volume overload- induced hypertrophy)
- Early stages: Ejection fraction normal or slightly increase
- after some time: Ejection fraction falls and LV end systolic volume rises
- Eventually LV dyspnoea (breathlessness)=
lower coronary perfusion=
ischemia, necrosis and apoptosis

30
Q

Describe the history & presentation of aortic regurgitation

A

Acute AR:
Cardiogenic shock
Tachycardia
Cyanosis
Pulmonary edema
Austin flint murmur

Chronic AR:
Wide pulse pressure
Corrigan (wate hammer pulse)
Pistol shot pulse (Traube sign)

31
Q

What are the investigations used to monitor Aortic Regurgitation?

A

Transthoracic echocardiography
Chest X ray
Cardiac catheterisation
Cardiac MRI/CT Scan

32
Q

How is Aortic Regurgitation managed?

A
  1. Acute AR: Ionotropes/vasodilators & valve replacememt & repair
  2. Chronic asymptomatic: If LV function is normal can be managed by drugs or reassurance
  3. Chronic symptomatic: First line is valve replacement with adjunct vasodilator therapy
  4. Prevention is key: Treat Rheumatic fever and infective endocarditis.
33
Q

What is Mitral Stenosis?

A

Obstruction to left ventricular inflow at the level of mitral valve due to structural abnormality of the mitral valve (narrowing of valve)
- As disease progresses it leads to pulmonary hypertension and right heart failure occurs

34
Q

What are the causes of Mitral Stenosis?

A

Rheumatic fever (this is the main cause)
Carcinoid syndrome
Use of ergot/serotonergic drugs
SLE
Mitral annular calcification due to aging
Amyloidosis
Rheumatoid arthritis
Whipple disease
Congenital deformity of the valve

35
Q

What are the consequences of mitral stenosis?

A
  1. Initially moderate exercise or tachycardia result in exertional dyspnoea (shortness of breath) due to increased left atrial pressure
  2. Severe mitral stenosis leads to increase in left atrial pressure , transudation of fluid into the lung interstitium (back pressure in the lungs) leading to dyspnoea at rest or exertion
  3. Pulmonary hypertension may develop as the result of it
  4. The restricted orifice limits filling of left ventricle limiting cardiac output
  5. Hemoptysis (coughing up blood) if bronchial vein rupture
36
Q

Describe the history and presentation of Mitral stenosis

A

H/0 of Rheumatic fever
Dyspnoea
orthopnoea
Diastolic murmur
Loud P2
Neck vein distention
Hemoptysis
40-50 years age

37
Q

What investigations are used to monitor Mitral stenosis?

A

ECG
Transthoracic echocardiography
Chest X ray
Cardiac catheterisation
Cardiac MRI/CT Scan

38
Q

How is mitral stenosis managed?

A

a) Progressive asymptomatic: No therapy required
b) Severe asymptomatic: no therapy generally required adjuvant (before any main treatment) balloon valvotomy (to open up the valve)
c) Severe symptomatic: diuretic, balloon valvotomy, valve replacement & repair adjunct b blockers

39
Q

What is mitral regurgitation?

A

Abnormal reversal of blood flow from the left ventricle to the left atrium.
- It is caused by the disruption in any part of the mitral valve apparatus

40
Q

What are the acute causes of mitral Regurgitation?

A

Mitral valve prolapse
Rheumatic heart disease
Infective endocarditis
Following valvular surgery
Prosthetic mitral valve dysfunction

41
Q

What are the chronic causes of mitral Regurgitation

A

Rheumatic heart disease
SLE
Scleroderma
Hypertrophic cardiomyopathy
Drug related

42
Q

Explain how infectious endocarditis can lead to mitral regurgitation

A

Infectious endocarditis:
- Abscess formation (collection of pus from bacterial infection),
- Irregular growths of germs form masses called “vegetations”,
- Rupture of chordae tendineae (fibrous connections between the valve leaflets and the papillary muscles. These are attached to the leaflets on to the ventricular side and prevent the cusps from swinging back into the atrial cavity) and leaflet perforation

43
Q

How can mitral regurgitation lead to left ventricular dysfunction?

A

Chronic MR:
- progression leads to eccentric hypertrophy (Volume overload-induced cardiac hypertrophy)
- Leading to elongation of myocardial fibres and increased left end diastolic volume
- Increase in preload & a decrease in afterload
- Increase in end- diastolic volume
- and a decrease in end-systolic volume

Eventually prolonged volume overload leads to left ventricular dysfunction and increased left ventricular
end-systolic diameter

44
Q

Describe the history and presentations seen with mitral regurgitation

A

Dyspnea (breathlessness)
Diminished intensity of S1 (closure of the atrioventricular (mitral and tricuspid) valves)
murmur high
Fatigue
“blowing” murmur (a sound caused by turbulent (rough) blood flow through the heart valves)
pitched diastolic sound
Orthopnea (breathlessness relived by sitting or standing)
Chest pain
Atrial fibrillation (calcifications/ emboli can detach; go into the heart circulation leading to AF)

45
Q

What investigations are used to monitor Mitral regurgitation

A

Investigations:
* ECG
* Transthoracic echocardiography
* Chest X ray
* Cardiac catheterisation
* Cardiac MRI/CT Scan

46
Q

How is mitral regurgitation managed?

A

Acute MR:
- Emergency Surgery adjunct preoperative diuretics adjunct intra-aortic balloon counterpulsation
- Chronic asymptomatic: 1st ACE inhibitors
- Beta blockers if left ventricular ejection fraction is less than 60% 1st line is surgery
- Chronic symptomatic: 1st surgery plus medical treatment
- If left ventricular ejection fraction is less than 30% 1st line is Intra-aortic balloon counterpulsation

47
Q

What is cardiomyopathy?

A

Cardiomyopathy is a disease of the heart muscle that makes it harder for heart to pump blood to the rest of your body (problems with heart tissue/ muscle)
- It can lead to heart failure

48
Q

What are the 3 main types of cardipmyopathies?

A
  1. Dilated
  2. Hypertrophic
  3. Restrictive
49
Q

What is dilated cardiomyopathy?

A

makes the muscle walls become stretched and thin (dilated). The thinner walls are weakened, this means the heart can’t squeeze (contract) properly to pump blood to the rest of the body.
- It is characterised by ventricular chamber enlargement and systolic dysfunction with normal left ventricular wall thickness

50
Q

What is a hallmark for dilated cardiomyopathy?

A

Left ventricular dilatation found at autopsy, usually more than 4 cm

51
Q

Familial DCM is a genetic condition, true or false?

A

TRUE

52
Q

Is dilated cardiomyopathy dominant or recessive?

A

familial dilated cardiomyopathy is inherited in an autosomal dominant pattern

53
Q

Describe how Dilated Cardiomyopathy can lead to heart failure?

A

Enlargement of the left ventricle=
- lower ejection fraction and increase in the ventricular wall stress and end systolic volumes.
- Early compensatory mechanisms include an increase in heart rate and tone of the peripheral vascular system.
- neurohumoral activation of the renin-angiotensin aldosterone system and an increase in circulating levels of catecholamines.
- levels of natriuretic peptides are also increased.
- Eventually these compensatory mechanisms become overwhelmed and the heart fails.`

54
Q

Describe the history and presentation of dilated cardiomyopathies

A

Dyspnoea (breathlessness)
murmur
fatigue,
angina,
pulmonary congestion
low cardiac output
displaced apex beat, S3 or systolic (due to enlargement, beat is misplaced- v. indicative of DCM)

55
Q

What investigations are used to monitor dilated cardiomyopathy?

A

Genetic Testing
Viral serology
ECG
Chest X ray
Cardiac catheterisation
Cardiac MRI/CT Scan
Exercise stress test
Echocardiography

56
Q

How is dilated cardiomyopathy managed?

A

1.Diet modifications: fluid and Na+ restriction
2. Immunosupressants for sarcoidosis and myocarditis phlebotomy for haemochromatosis
3. Symptoms of heart failure- ACEi, Beta blockers, diuretics, angiotensin II receptor antagonists
(if medical treatment ineffective: orthotopic heart transplantation)
4. Arrhythmias (AF, SVT, VT)
5. Thrombo-embolic events: anticoagulants (warfarin)

57
Q

What is Hypertrophic Cardiomyopathy?

A

Hypertrophic cardiomyopathy (HCM) is a genetic cardiovascular disease.

It is defined by an increase in left ventricular wall thickness that is not solely explained by abnormal loading conditions (left ventricle cavity v small)

58
Q

Describe the prevalence of hypertrophic cardiomyopathy

A

HCM is the leading cause of sudden cardiac death in preadolescent and adolescent children.

Familial HCM occurs as an autosomal dominant Mendelian-inherited disease in approximately 50% of cases.

Most patients with HCM are asymptomatic. Unfortunately, the first clinical manifestation of the disease in such individuals may be sudden death, likely from ventricular tachycardia or fibrillation.

59
Q

What is a hallmark for hypertrophic cardiomyopathy?

A

The hallmark of the disorder is myocardial hypertrophy that is inappropriate, often asymmetrical, and occurs in the absence of an obvious hypertrophy stimulus.

This hypertrophy can occur in any region of the left ventricle but frequently involves the interventricular septum, which results in an obstruction of flow through the left ventricular (LV) outflow tract.

60
Q

What consequences are seen from hypertrophic cardiomyopathy?

A

Most patients with HCM have abnormal diastolic function, which impairs ventricular filling and increases filling pressure, despite a normal or small ventricular cavity. (Decreased cardiac output)
These patients have abnormal calcium kinetics and subendocardial ischemia, which are related to the profound hypertrophy and myopathic process.

61
Q

Describe the history and presentations of hypertrophic cardiomyopathy

A

Sudden cardiac death
Double carotid artery impulse, S3 gallop,
Syncope (fainting)
ejection systolic murmur
Presyncope (the feeling you’re about to faint)
Congestive heart failure
Dizziness
Palpitations
Angina

62
Q

What investigations are used to monitor hypertrophic cardiomyopathy

A
  • Hemoglobin level: Anemia exacerbates chest pain and dyspnea
    Brain natriuretic peptide (BNP), troponin T levels:
  • Elevated BNP, NT-proBNP, and troponin T levels are associated with a higher risk of cardiovascular events, heart failure, and death
  • Echocardiography
  • Chest X ray
  • Cardiac MRI
63
Q

What is restrictive cardiomyopathy?

A

In restrictive cardiomyopathy (RCM), the muscles of your heart’s lower chambers (ventricles) stiffen and can’t fill with blood. This can cause heart failure, which increases pressure on your heart and may cause fluid buildup in your lungs.

It is characterized by diastolic dysfunction with restrictive ventricular physiology, whereas systolic function often remains normal. Atrial enlargement occurs due to impaired ventricular filling during diastole, but the volume and wall thickness of the ventricles are usually normal.

64
Q

Restrictive cardiomyopathy is a less well-defined cardiomyopathy, why?

A

its diagnosis is based on establishing the presence of a restrictive ventricular filling pattern.

65
Q

Describe the prevalence of restrictive cadiomyopathy

A

RCM accounts for approximately 5% of all cases of diagnosed cardiomyopathies

66
Q

Describe the pathophysiology of restrictive cardiomyopathy

A
  • Increased stiffness of the myocardium due to familial or other secondary causes e.g amyloidosis
  • Infiltrative cardiomyopathies are characterized by deposition of abnormal substances (ie, amyloid proteins, noncaseating granulomas, iron) within the heart tissue.
  • Infiltration causes the ventricular walls to stiffen, leading to diastolic dysfunction.
  • Restrictive physiology predominates in the early stages, causing conduction abnormalities and diastolic heart failure.
  • Adverse remodelling may lead to systolic dysfunction and ventricular arrhythmias in advanced cases.
67
Q

Explain how restrictive cardiomyopathy can lead to reduced cardiac output

A
  • Increased stiffness of the myocardium causes ventricular pressures to rise precipitously with small increases in volume.
  • Thus, accentuated filling occurs in early diastole and terminates abruptly at the end of the rapid filling phase.
  • Patients typically have reduced compliance (increased diastolic stiffness), and the left ventricle cannot fill adequately at normal filling pressures
  • Reduced left ventricular filling volume leads to a reduced cardiac output.
68
Q

Describe the history and presentation of restrictive cardiomyopathy

A
  • comfortable in the sitting position because of fluid in the abdomen or lungs, and they frequently have ascites and pitting edema of the lower extremities.
  • The liver is usually enlarged and full of fluid, which may be painful.
  • Weight loss and cardiac cachexia are not uncommon.
  • Easy bruising, periorbital purpura, macroglossia, and other systemic findings, such as carpal tunnel syndrome, should be an indication for the clinician to consider amyloidosis.
  • Increased jugular venous pressure is present.
  • The pulse volume is decreased, consistent with decreased stroke volume and cardiac output.
69
Q

What investigations are used to monitor restrictive cardiomyopathy?

A

CBC, Serology, Amylodosis check, Chest Xray ,ECG ,Echocardiography, Catheterisation, MRI/Biopsy

70
Q

How is restrictive cardiomyopathy managed?

A
  • Heart failure medication
    Guideline-directed medical therapy for heart failure, including angiotensin-converting enzyme inhibitors or angiotensin receptor II blockers, diuretics and aldosterone inhibitors should be initiated in patients with reduced LV
  • Antiarrhythmic Therapy
  • Immunosuppression- Steroids
  • Pacemaker
  • Cardiac transplantation

Cardiovascular & Respiratory Medicine (14 decks)

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