Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Cardio Resp > Structural Heart Disease > Flashcards

Structural Heart Disease Flashcards

1
Q

What is meant by the left ventricular end systolic volume?

A

Volume of blood remaining in the left ventricle after systole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is meant by the left ventricular end diastolic volume?

A

The volume of blood in heart’s left ventricle before contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How do you use Left Ventricular end systolic and LVE diastolic volume measurements to find stroke volume?

A

LVEDiastolicV - LVESystolicV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What briefly, is the pathophysiology in ventricular septal defect?

A

Wall between the ventricles fails to develop correctly in foetal development leading to a hole in the wall mixing deoxygenated and oxygenated blood
Right side failure as heart can’t cope with volume

Sometimes it will close as child grows older however if it does not then open heart surgery or cardiac catheterisation is required.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How would a baby with ventricular septal defect present?

A

Presents with poor weight gain, poor feeding, palpitations ect.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Explain briefly the pathophysiology of Tetralogy of Fallot?

A

4 different defects in foetal development within the heart

Hole in wall between ventricles - Ventricular septal defect

Pulmonary stenosis

Widening of aortic valve so that it goes between the ventricular wall

Right ventricular hypertrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the pathophysiology of Atrial Septal Defect?

A

Hole in wall between atria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the pathophysiology of Coarctation of the Aorta and how is afterload affected?

A

Narrowing of the wall of Aorta so more afterload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Is rheumatic heart disease more likely to occur in older or younger patients?

A

Younger - 25-49

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Is calcific aortic valve disease more likely to occur in older or younger patients?

A

Older -80+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Is aortic or mitral valve disease more common?

A

Mitral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are examples of conditions that involve valvular defects?

A

Aortic Stenosis - valve is narrowed

Aortic Regurgitation - aortic valve leaks

Mitral Stenosis - narrowing of mitral valve

Mitral Regurgitation - blood flows wrong way as the mitral valve does not close properly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What usually precedes aortic stenosis?

A

Aortic sclerosis - aortic valve thickening without flow limitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What would make you suspect the presence of aortic stenosis and how would you confirm it?

A

Early-peaking, systolic ejection murmur and confirmed by echocardiography

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are some of the risk factors for aortic stenosis?

A

Hypertension

LDL levels

Smoking

Elevated CRP - pro-inflammatory effects

Congenital bicuspid valves - aortic valve with 2 cusps so causes narrowing

Chronic Kidney Disease - through increased lipid concentrations

Radiotherapy

Older age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are 3 causes of aortic stenosis?

A

Rheumatic heart disease - an autoimmune inflammatory reaction triggered by prior streptococcus infection that targets valvular endothelium, leading to inflammation and eventually calcification

Congenital heart disease

Calcium build-up

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Explain the pathophysiology of Aortic Stenosis

A

Valvular endocardium is damaged as the result of abnormal blood flow across the valve (bicuspid valve) or by an unknown trigger.

Endocardial injury initiates an inflammatory process similar to atherosclerosis and ultimately leads to leaflet fibrosis and deposition of calcium on the valve.

Progressive fibrosis and calcium deposition limit aortic leaflet mobility and eventually produce stenosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What might the patient with aortic stenosis present with if they have 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)

History of Rheumatic fever, high lipoprotein, high LDL, CKD, age>65

-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What investigations would you do on a patient with aortic stenosis?

A

Transthoracic echocardiography - image of internal parts of heart using ultra-sound

Chest X-Ray (LV hypertrophy)

Cardiac catheterisation

Cardiac MRI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What management plan would you have for a patient with aortic stenosis?

A

Primary treatment of patients with symptomatic AS OR for asymptomatic patients with severe AS who have an LVEF <50% or who are undergoing other cardiac surgery is aortic valve replacement (AVR).

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

Balloon aortic valvuloplasty

Antihypertensive

ACE inhibitors

Statins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Is aortic regurgitation more common than aortic stenosis and mitral regurgitation?

A

No

22
Q

If AR is chronic, what can it become?

A

Congestive cardiac failure - heart unable to pump blood around the body

23
Q

If AR is acute, what does the patient present with?

A

Sudden onset of pulmonary oedema and hypotension or cardiogenic shock

24
Q

What are the causes of AR?

A

Congenital heart defects

Rheumatic heart disease

Aortic valve stenosis

Infective endocarditis

Congenital bicuspid valves - bicuspid aortic valve is leaky and lets blood flow into the heart when it relaxes

25
Q

What are the causes of AR associated with aortic root dilation?

A

Connective tissue disease/collagen vascular diseases - increased elasticity of artery walls

Marfan’s syndrome - increased elasticity of artery walls

Ideio

Ankylosing spondilytis - cellular inflammation → basal thickening of cusps leading to AR

Traumatic

26
Q

Explain the pathophysiology of acute AR?

A

Infective endocarditis can lead to rupture of leaflets or even paravalvular leaks

Vegetations on valvular cusps can also cause inadequate closure of leaflets resulting in leakage of blood

Chest trauma can cause tear in ascending aorta leading to AR

27
Q

Explain the pathophysiology of chronic AR?

A

Bicuspid aortic valve

Rheumatic fever → fibrotic changes causing thickening and retraction of leaflets

28
Q

n abnormal physiology where the aortic valve does not close, what is the pathophysiology of acute AR and how this leads to cardiogenic shock?

A

Increase in blood volume in LV during systole → LV end diastolic pressure increases → increase in pulmonary venous pressure → dyspnoea and pulmonary oedema → heart failure → cardiogenic shock

29
Q

In abnormal physiology where the aortic valve does not close, what is the pathophysiology of chronic AR and how does this lead to ischaemia, necrosis and apoptosis?

A

Gradually increase in LV volume → LV enlargement and eccentric hypertrophy

Early stages → ejection fraction normal or slightly increase → after some time Ejection fraction falls and LV end systolic volume rises

Eventually LV dyspnoea → Lower coronary perfusion → ischaemia, necrosis and apoptosis

30
Q

If a patient had acute AR, how would they present and how would this be different to how they would present with chronic AR?

A

Acute

Cardiogenic shock

Tachycardia

Cyanosis

Pulmonary oedema

Chronic

Wide pulse pressure

Pistol shot pulse (Traube sign)

31
Q

What investigations would you do on a patient to confirm AR?

A

Transthoracic echocardiography

Chest X ray

Cardiac catheterisation

Cardiac MRI/CT scan

32
Q

What would be the management plan of a patient with AR?

A

Acute → Inotropes/vasodilators and valve replacement and repair

Chronic asymptomatic → If LV function is normal can be managed by drugs or reassurance

Chronic symptomatic → First line is valve replacement with adjunct vasodilator therapy

Prevention: Treat rheumatic fever and infective endocarditis

33
Q

What is the main cause of Mitral Stenosis in developing countries?

A

Rheumatic fever

34
Q

As MS progresses, what can it lead to?

A

Pulmonary hypertension and right heart failure

35
Q

What are the causes of MS?

A

Rheumatic fever

Carcinoid syndrome - fibrous tissue in plaques → distortion of valves

Use of ergot/serotonergic drugs

SLE

Mitral annular calcification due to ageing

Amyloidosis

Rheumatoid arthritis

Whipple disease

Congenital deformity of the valve

36
Q

Explain the pathophysiology of MS

A

Stenosis of the valve typically occurs decades after the episode of acute rheumatic fever. Acute insult leads to formation of multiple foci and infiltrates in the endo and myocardium and along the walls of the valves.

With passage of time it gets thickened, calcified and contracts resulting in stenosis.

37
Q

In abnormal physiology, describe the consequences of mitral stenosis?

A

Moderate exercise or tachycardia result in exertional dysponoea due to increased left atrial pressure

Severe mitral stenosis leads to increase in left atrial pressure, transudation of fluid into the lung interstitium leading to dyspnoea at rest or exertion

Pulmonary hypertension may develop as the result of this

The restricted orifice limits filling of left ventricle limiting cardiac output

Hemoptysis if bronchial vein rupture

38
Q

What would a patient with MS present with?

A

H/O of Rheumatic fever

Dyspnoea - shortness of breath/ laboured breathing

Orthopnoea - breathlessness in recumbent position relieved by sitting or standing

Diastolic murmur

Loud P2

Neck vein distention

Hemoptysis

40-50 yrs old

39
Q

What investigations would you do on a patient with MS?

A

ECG

Transthoracic echocardiography

Chest X Ray

Cardiac catheterisation

Cardiac MRI/CT scan

40
Q

What would be the management plan of a patient with MS?

A

Progressive asymptomatic → No therapy required

Severe asymptomatic → No therapy generally required adjuvant balloon valvotomy

Severe symptomatic → diuretic, balloon valvotomy, valve replacement and repair, adjunct b blockers

41
Q

What is the most frequent valvular heart disease?

A

Mitral regurgitation (MR)

42
Q

What are the causes of acute MR?

A

Mitral valve prolapse

Rheumatic heart disease

Infective endocarditis

Following valvular surgery

Prosthetic mitral valve dysfunction

43
Q

What are the causes of chronic MR?

A
  • What are the causes of chronic MR?Rheumatic heart diseaseSLESclerodermaHypertrophic cardiomyopathyDrug related
44
Q

What is the pathophysiology of MR?

A

Infectious endocarditis → abscess formation → vegetation along walls → rupture of chordae tendinae and leaflet perforation

45
Q

What is the pathophysiology of Chronic MR after this abnormal physiology has developed?

A

Progression leads to eccentric hypertrophy leading to elongation of myocardial fibres and increased left end diastolic volume

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

46
Q

What would a patient with MR present with?

A

Dyspnoea

Diminished S1

Fatigue

Orthopnoea

Chest pain

47
Q

What investigations would you have with a patient with MR?

A

ECG

Transthoracic echocardiography

Chest X Ray

Cardiac catheterisation

Cardiac MRI/CT scan

48
Q

What would be the management plan of a patient with acute MR?

A

Emergency surgery adjunct preoperative diuretics adjunct intra-aortic balloon counterpulsation

49
Q

What management plan would you give a patient with chronic asymptomatic MR?

A

1st ACE inhibitors

Beta blockers if left ventricular ejection fraction is less than 60% 1st line surgery.

50
Q

What management plan would a patient with chronic symptomatic MR be on?

A

1st surgery plus medical treatment

If LV ejection fraction is less than 30% 1st line is intra-aortic balloon counterpulsation

Cardio Resp (1 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions