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Cardio > Structural Heart Disease > Flashcards

Structural Heart Disease Flashcards

1
Q

When does systole start

A

When mitral and tricuspid valves shut

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2
Q

What is the S1, lub sound

A

When mitral and tricuspid valves shut

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3
Q

What happens when the aortic pressure is higher than the ventricular pressure

A

Systole stops
Tricuspid and aortic valves closing *

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4
Q

What valves open at the start of diastole

A

Tricuspid and mitral

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5
Q

What happens in diastole

A

Volume increases but pressure stays the same

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6
Q

What are structural heart diseases

A

Cover a number of defects which affect the valves and chambers of the heart and aorta
Some congenital and some later

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7
Q

Congenital heart diseases?

A

Atrial septal defect
Ventricular septal defect
Coarctation of aorta
Patent foramen ovale
Patent ductus arteriosus
Tetralogy of fallot

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8
Q

Heart diseases that develop later in life?

A

Valvular dysfunctions (atrial stenosis / regurgitation or muscular (cardiomyopathies)

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9
Q

Ventricular septal defect?

A

Hole in septum
Mix of oxygenated and deoxygenated blood
More blood rushing from high pressure oxygenated left side to right
Leads to right side failure cause it’s overloaded

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10
Q

Tetralogy of fallot?

A

1, Ventricular septal defect
2. Overriding aorta - blood from both sides go to aorta
3. Leads to ventricular septal hypertrophy
4. Pulmonary atresia

Sinotic spell and can Therefore get breathless etc
Emergency surgery needed
Can be shown in scan before baby is born

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11
Q

Atrial septal defect?

A

Milder than VSD

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12
Q

Coarctation of the aorta?

A

Wall of the aorta is constricting
Less cardiac output–> reduced stroke volume
Emergency repair needed

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13
Q

What is the most common cause of regurgitation and stenosis?

A

Rheumatic heart disease (25-49)

Calcific aortic valve disease
Degenerative mitral valve disease (70+ most common)

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14
Q

Is aortic or mitral valve disease more prevalent?

A

Mitral ; esp 55 onwards

Mild mitral regurgitation most common

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14
Q

What is the most common valvular disease?

Does it affect older or younger people?

What is is preceded by?

A

Aortic stenosis

Older people

Aortic sclerosis- aortic valve thickening without flow limitation

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14
Q

How is aortic stenosis suspected?

How is it confirmed?

A

Presence of an early-peaking, systolic ejection murmur

Echocardiography

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14
Q

What are risk factors for aortic stenosis?

A

Hypertension
LDL
Smoking
Elevated C reactive protein
Congenital bicuspid valves
Chronic kidney disease
Radiotherapy
Old age

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14
Q

What are the causes of aortic stenosis?

A

Rheumatic heart disease
Congenial heart disease
Calcium build up

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15
Q

What happens during aortic stenosis?

A

The valvular endocardium is damaged as the result of abnormal blood flow across the valve (in the case of a 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.
In rheumatic disease, an autoimmune inflammatory reaction is triggered by prior Streptococcus infection that targets the valvular endothelium, leading to inflammation and eventually calcification.

Long-standing pressure overloadleft ventricular hypertrophy (LVH).

Ventricle to maintain a normal wall stress (afterload) despite the pressure overload produced by stenosis As the stenosis worsens, the adaptive mechanism fails and left ventricular wall stress increases.

Systolic function declines as wall stress increases, with resultant systolic heart failure.

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16
Q

What is 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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17
Q

What are the investigations for stenosis and regurgitation?

A

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

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18
Q

What is the management for aortic stenosis?

A

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
Balloon aortic valvuloplasty
Antihypertensive
ACE inhibitors
Statins

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19
Q

What is aortic regurgitation

A

Aortic regurgitation (AR) is 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

AR is not as common as aortic stenosis and mitral regurgitation

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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20
Q

What are the congenital and acquired causes for aortic regurgitation?

A

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

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21
Q

What are the causes for aortic regurgitation related to aortic root dilation?

A

Marfan’s Syndrome
Connective tissue disease/collagen vascular diseases
Idiopathic
Ankylosing spondilytis
Traumatic

22
Q

What is the pathophysiology of acute AR?

A

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

Vegetations on the 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

Acute AR Increase blood volume in LV during systoleLV end diastolic pressure increases increase in pulmonary venous pressure dyspnea and pulmonary oedemaheart failure cardiogenic shock

23
Q

What is the pathophysiology of chronic AR?

A

Bicuspid aortic valve
Rheumatic feverfibrotic changes causing thickening and retraction of leaflets

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  ischemia, necrosis and apoptosis

24
Q

What is the history and presentation of acute AR?

A

Cardiogenic shock
Tachycardia
Cyanosis
Pulmonary edema
Austin flint murmur

25
Q

What is the history and presentation of chronic AR?

A

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

26
Q

What is the management of acute AR?

A

Ionotropes/vasodilators & valve replacement & repair

27
Q

What is the management of chronic AR?

A

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

28
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

Rheumatic fever is the main cause ( in developing countries)

As disease progresses it leads to pulmonary hypertension and right heart failure occurs

29
Q

What are the causes for mitral stenosis?

A

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

30
Q

What is the pathophysiology for mitral stenosis?

A

Initially moderate exercise or tachycardia result in exertional dyspnoea 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 it

The restricted orifice limits filling of left ventricle limiting cardiac output

Hemoptysis if bronchial vein rupture

31
Q

What is 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

32
Q

What is the management of mitral stenosis?

A

Progressive asymptomatic No therapy required

Severe asymptomatic no therapy generally required adjuvant balloon valvotomy

Severe symptomatic diuretic, balloon valvotomy, valve replacement & repair adjunct b blockers

33
Q

What is mitral regurgitation?

A

Abnormal reversal of blood flow from the left ventricle to the left atrium.

It is the most frequent valvular heart disease

It is caused by the disruption in any part of the mitral valve apparatus

34
Q

What are the causes for acute mitral regurgitation

A

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

35
Q

What are the causes for chronic mitral regurgitation

A

Rheumatic heart disease
Drug related
SLE
Scleroderma
Hypertrophic cardiomyopathy

36
Q

What does infectious endocarditis lead to?

A

Abscess formation, vegetations, rupture of chordae tendineae and leaflet perforation

37
Q

What is the pathophysiology of chronic MR?

A

Progression leads to eccentric 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

38
Q

What is the history and presentation of MR?

A

Dyspnea diminished S1, murmur high
Fatigue pitched, blowing xx
Orthopnea
Chest pain
Atrial fibrillation

39
Q

What is the management of acute MR?

A

Emergency Surgery adjunct preoperative diuretics adjunct intra-aortic balloon counterpulsation

39
Q

What is the management of chronic MR?

A

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

40
Q

What is cardiomyopathy?

A

A disease of the heart muscle that makes it harder for heart to pump blood to rest of your body. Can lead to heart failure

The estimated prevalence of dilated cardiomyopathy is 1:2500.

This condition is among the most common causes of heart failure.

Dilated cardiomyopathy may manifest clinically at a wide range of ages, but this condition most commonly occurs in the third or fourth decade of life.

Dilated cardiomyopathy is a progressive, usually irreversible, disease causing global systolic (contractile) dysfunction with heart failure.

41
Q

What are the 3 main types of cardiomyopathy?

A

Dilated

Hypertrophic

Restrictive

42
Q

How much of the cardiomyopathies are caused without family history and are idiopathic?

A

25%

43
Q

What are secondary causes of cardiomyopathy?

A

Heart valve disease
After child birth
Thyroid disease
Myocarditis
Alcoholism
Autoimmune disorders
Ingestion of drugs
Mitochondrial disorders

44
Q

What is the pathophysiology of dilated cardiomyopathy?

A

Dilated cardiomyopathy is characterized by left ventricular chamber enlargement and systolic dysfunction with normal left ventricular wall thickness.

the hallmark gross finding at autopsy is left ventricular dilatation, usually more than 4 cm.

Familial DCM is a genetic condition.

In rare autosomal dominant inheritance patterns (at least two family member have idiopathic DCM), first degree relatives (parents, siblings, children) have a 50 percent chance of inheriting the condition

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.

45
Q

What is the history and presentation of dilated cardiomyopathy?

A

Dyspnoea, displaced apex beat, S3 or systolic murmur
fatigue,
angina,
pulmonary congestion
low cardiac output

46
Q

What are the investigations for dilated cardiomyopathy?

A

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

47
Q

What is the management for dilated cardiomyopathy?***

A

Refer to diagram

48
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.

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.

49
Q

What is the history and presentation of hypertrophic cardiomyopathy?

A

Sudden cardiac death
Double carotid artery impulse
S3 gallop,
Syncope
ejection systolic murmur
Presyncope
Congestive heart failure
Dizziness
Palpitations
Angina

50
Q

What are the investigations for 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 Xray
Cardiac MRI

51
Q

What is the management for hypertrophic cardiomyopathy?***

A

Refer to diagram

52
Q

What is restrictive cardiomyopathy?

A

It is a less well-defined cardiomyopathy as its diagnosis is based on establishing the presence of a restrictive ventricular filling pattern.

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.

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

It may be idiopathic, familial (has been related to troponin I or desmin mutations, the latter often in association with a skeletal myopathy), or associated with various systemic disorders, such as haemochromatosis, amyloidosis, sarcoidosis, Fabry’s disease, carcinoid syndrome, scleroderma, anthracycline toxicity, or previous radiation.

53
Q

What is the pathophysiology for 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.

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.
7

54
Q

What is 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.

55
Q

What are the investigations for restrictive cardiomyopathy?

A

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

56
Q

What is the management for restrictive cardiomyopathy?

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

Cardio (9 decks)

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