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cardio and resp yr 2 > STRUCTURAL heart disease and vascular disease > Flashcards

STRUCTURAL heart disease and vascular disease Flashcards

1
Q

what are the cusps of the aortic valve

A

left coronary cusp
right coronary cusp
non-coronary cusp

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2
Q

what sound does the aortic valve closure produce? and when does that happen?

A

Closure of the aortic valve during isovolumetric relaxation produces the “S2” heart sound.

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3
Q

what are the three main causes of aortic stenosis

A

1) calcification and fibrosis (Age)
2) congenital bicuspid valve (because more pressure on each cusp if only 2 instead of 3)
3) rheumatic heart disease

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4
Q

at what ages do calcification and fibrosis occur?

A

70s- 80s

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5
Q

describe ho calcification and fibrosis of the valves occurs and how it leads to aortic stenosis

A

repeated mechanical stress (hypertension) results in an atherosclerosis-LIKE fibrosis and calcification of the valve (the body’s way of trying to repair this mech damage done)

this makes the valve less compliant

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6
Q

risk factors for calcification and fibrosis of aortic valve?

A

Risk factors are therefore similar to those for atherosclerosis:​

high bp
smoking
genes?
kidney disease

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7
Q

describe how bicuspid aortic valve occurs and how it leads to aortic stenosis. what age does it present?

A

Mechanical stress of blood flow across the valve spread across two leaflets instead of the usual three, causing increased endothelial damage to each leaflet​

stenosis is caused because:
Ultimately causes calcification and fibrosis​

May present earlier in life​-
(its basically sam emech as the calcification and fibrosis but happens earlier because of the bicuspid valbe)

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8
Q

risk factors for congenital bicuspid valve?

A

same as for calcification and fibrosis

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9
Q

what causes rheumatic heart disease?

A

S. pyogenes infection​

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10
Q

when does rheumatic fever occur in the timeline of rheumatic heart disease?

A

may occur 1-5 weeks after s pyogenes infection

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11
Q

how does rheumatic heart disease lead to aortic stenosis

A

Antibodies targeting bacterial antigen at that time may cross-react with certain cardiac M- proteins

repeated damage to valvular endothelium results in scarring and fibrosis of aortic valve

fusion of valve leaflets (commissural fusion) occurs

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12
Q

what can aortic stenosis eventually lead to?

A

heart failure

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13
Q

describe the pathophysiology of aortic stenosis leading to heart failure

A

1) aortic stenosis reduces the surface area available for blood flow after the valve has opened

2) left ventricle must produce higher pressures to maintain the same force of ejection (stroke work= pressure* stroke volume)

3) heart undergoes conccentric hypertrophy. this compensates for the reduced valvular area for some time

4) eventually the compensation fails leading to heart failure

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14
Q

what is eccentric and conccentric heart failure

A

conccentric is when the volume of the right ventricle decreases vs eccentric its when it increases

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15
Q

what is preload

A

its the amount of stretch the heart muscle undergoes while its being filled by blood which determines the strength of the contraction

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16
Q

what does preload depend on?

A

venous return

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17
Q

what is afterload and what does it depend on

A

its the pressure in the aorta that the left ventricle has to overcome in order for the semilunar valves to open and blood to be ejected.
so it depends on diastolic bp

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18
Q

symptoms of aortic stenosis

A

(if that helps which it doesnt really in my case lol- think about symptoms of systolic HF)

-exertional dyspnea
-fatigue
-possible angina
-possible syncope/ presyncope on exertion

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19
Q

signs of aortic stenosis

A

-ejection systolic murmur over aortic valve
- with crescendo-decrescendo pattern (means the murmur increases in sound intensity and decreases )
- this may radiate to carotid arteries
- possible opening click and diminished S2 sound

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20
Q

what are the 2 first line diagnostic tools you use for all the structural heart diseases

A

transthoracic echocardiography
and
12-lead ECG

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21
Q

what other investigations can you do for structural heart diseases

A

CXR
cardiac catheterization
cardiac MRI scan

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22
Q

what can transphoracic echo tell you in aortic stenosis? is it diagnostic?

A

YES its diagnostic: confirms stenosis and can also
evaluate SEVERITY of stenosis

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23
Q

what can a 12-lead ECG tell you for aortic stenosis? is it diagnostic?

A

reveal LV hypertrophy or ischaemic changes
NO its not diagnostic bc its non specific meaning it doesnt show that these changes were caused by aortic stenosis.

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24
Q

what is the difference between managing non severe artic stenosis and severe/ symptomatic AS?

A

symptomatic/ severe need to do aortic valve replacement vs non severe only drugs

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25
Q

what is done for non severe AS

A

RISK FACTOR management
- ACE inhibitors (controlling hypertension reduces afterload)
- statins (lower cholesterol)

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26
Q

when is aortic valve replacement appropriate and what is an alternative? what do you also do in parallel with the procedures?

A

under65 yrs

transcatheter aortic valve implantation TAVI is an alternative

risk factor management in parallel

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27
Q

what are some factors that make AS severe?

A

-LV ejection fraction <50%
- abnormal exercise test
- elevated BNP (marker of HF)

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28
Q

What are the two physiological changes that lead to aortic regurgitation

A

1) aortic root dilation and
2) valve changes

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29
Q

causes of aortic root dilation

A

marfans syndrome
chest trauma (motor vehicle accidents)
ankylosing spondylitis
idiopathic

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30
Q

causes of valve changes

A

-infective endocarditis
-chronic rheumatic fever (fibrotic valves do not seal well)
-congenital bicuspid aortic valve

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31
Q

what are the two types of aortic regurgitation

A

acute and chronic

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32
Q

what happens in acute aortic regurgitation

A
  • sudden valve incompetence
  • sudden increase in left ventricule end-diastolic volume
  • diastolic blood backlogs to lungs
  • pulmonary hypertension causes pulmonary oedema. this causes dyspnoea
    = diastolic HF
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33
Q

explain what happens in chronic aortic regurgitation

A

1) gradual worsening of valve competence so
2) gradual increase in regurgitated volume leading to increase in left ventricle end-diastolic volume

but because this is gradual the heart has time to adapt

3) based on this: storke work = str vol* pressure, since the str volume increased the stroke work has to increase

4) this happens by eccentric hypertrophy

5) now the problem that eventually arises with the eccentric hypertrophy is shown by law of laplace: T= P*R since the R is radius, so has increased with the eccentric hypertrophy meaning the tension (T) also nicreased BEYOND WHAT THE heart is adapted for leading to

6) systolic heart failure

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34
Q

main symptom of acute and chronic AR

A

DYSPNOEA

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35
Q

signs of chronic AR

A

Wide pulse pressure (difference between systolic and diastolic BP)​

Water hammer pulse* (very bounding on palpation) ​

Traube’s sign*: like pistol shots when auscultating over femoral artery​

​

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36
Q

SIGNS od acute AR

A

UNIQUE:
Austin Flint murmur: mid-diastolic rumbling best heard at apex​

Cardiogenic shock (tachycardia, > capillary refill time)​

Cyanosis (sign of hypoxia due to pulmonary oedema)

+ the same ones as for chronic :
Wide pulse pressure (difference between systolic and diastolic BP)​

Water hammer pulse* (very bounding on palpation) ​

Traube’s sign*: like pistol shots when auscultating over femoral artery​

​

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37
Q

AR investigations

A

Transthoracic echocardiography ​

CXR (Cardiomegaly in chronic AR)​

Cardiac catheterisation (measure pressures in all chambers) ​

Cardiac MRI scan (when echo is suboptimal)

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38
Q

acute AR management

A

1) Inotropes (increase contractility): ​Adrenaline, dopamine, dobutamine etc. ​

2) Vasodilators (reduce afterload)​

… to stabilize the patient​

3) Valve replacement and repair​

​

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39
Q

asymptomatic chronic AR management

A

Asymptomatic: reassurance with regular echo monitoring or drugs (vasodilators such as calcium channel blockers, ACEI, ARBs)

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40
Q

symptomatic chronic AR management

A

Symptomatic: Vasodilators and valve replacement and repair​
​

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41
Q

what are the cusps of the mitral valve

A

2 cusps
anterior coronary cusp
posterior coronary cusp

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42
Q

what sound does the mitral valve closure produce? and when does that happen?

A

closeure of the mitral valve at end of atrial systole produces S1 heart sound

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43
Q

what is the main cause of mitral stenosis and what is the usual age of onset

A

rheumatic fever
40-50 yrs

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44
Q

other causes of mitral stenosis (not that important just have a look)

A

Carcinoid syndrome​

Congenital​

Rheumatoid Arthritis ​

Rheumatic Fever​

Amyloidosis​

Annular Calcification​

Whipple Disease​

SLE​

Serotonergic Drugs ​

45
Q

what pathologies can mitral stenosis eventually cause?

A

pulmonary oedema
systolic heart failure
and atrial fibrilation

46
Q

describe how mitral stenosis can lead to pulmonary oedema and systolic heart failure

A

1) mitral stenosis obstructs left ventricular inflow
2) blood backlogs to left atria and to pulmonary veins
3) as pulmonary hypertension worsens it causes pulmonary oedema which can cause dyspnea.

(NOTE: although this sounds like diastolic HF its not bc this backlog is NOT caused by too much filling of the left ventricle during diastole, that backlogs to left atrium. its direct overflow of atrium due to the mitral stenosis so not DIASTOLIC)

4) at the same time since LV filling is impaired. This can reduce cardiac output (systolic HF)

47
Q

what causes atrial fibrillation in mitral stenosis?

A

left atrial dilation can irritate pacemaker cells which can lead to AF

48
Q

what are the symptoms of mitral stenosis

A

exertional dyspnoea (can progress to dyspnoea at rest)
ppulmonary oedema
haemoptysis
orthopnoea (SOB when lying down)

49
Q

signs of mitral stenosis

A

mid diastolic murmur
loud p2 (s2= a2 and p2) due to severe pulmonary hypertension

50
Q

what could you see on an ECG for mitral stenosis?

A

signs of left atrial enlargement

51
Q

what could you see on CXR for mitral stenosis?

A

cardiomegaly

52
Q

what is the management of severe asymptomatic mitral stenosis

A

generally no therapy required
possibility of doing ballon valvotomy

53
Q

management of severe symptomatic mitral stenosis

A

1) DIURETIC (reducing BP reduces afterload and therefore stroke work)

2) valve replacement and repair with adjunct beta blockers (reduce HR)

54
Q

top 4 CAUSES of mitral regurgitation

A

mitral valve prolapse (Marfan’s Syndome causes looser chordae tendinae/ papillary muscle damage post-MI) ​

rheumatic heart disease

infective endocarditis (cause of acute MR if it causes leaflet rupture)

hypertrophic cardiomyopathy

55
Q

3 other causes of mitral regurg

A

autoimmune (SLE, scleroderma)
iatrogenic (surgery)
drugs

56
Q

what can Mitral regurgitation eventually lead to?

A

systolic heart failure

57
Q

describe how MR can lead to systolic HF/ the pathophysiology of MR

A

1) the regurgitated blood volume flows back into left ventricle form left atria during diastole

2) this increases the left ventricular end diastolic volume

3) so also increases stroke volume : stroke work= stroke vol* pressure
so stroke work has to increase

4)so LV undergoes eccentric hypertrophy to cope with volume overload

5) eventually the compensatory mech fails causing systolic heart failure

58
Q

MR symptoms

A

DA FOP

dyspnea
angina
fatigue
orthopnea
palpitations (from atrial fibrilations)

59
Q

signs of MR

A

MID-systolic click, followed by murmur (prolapse)

holosystolic murmr

diminished S1 (M+T)->mitral valve does not shut properly

60
Q

TWO Types of MR

A

ACUTE AND CHRONIC

61
Q

acute MR management

A

emergency surgery
pre op diuretics to reduce afterload and-> stroke work

62
Q

chronic asymptomatic MR management

A

if EF> 60% (further from heart failure) ACEi, beta blockers (reduce stroke work- slow HR)

IF EF<60% surgucal replacement and repair

63
Q

symptomatic CHRONIC MR management

A

EF >30%: surgical replacement and repair​

EF <30%: intra-aortic balloon counterpulsation*​

Intra-aortic balloon counterpulsation: therapeutic device that supports systolic heart function.

64
Q

which physics law explains how eccentric hypertrophy leads to systolic heart failure?

A

law of laplace stating that
“When the pressure within a cylinder or sphere is held constant, the tension on its walls increases with increasing radius.”
T= PxR
SO
1) eccentric hypertrophy
2. increased radius of left ventricle
3. increase wall tension on the heart
4. wall stress exceeds hearts ability to withstand pressure increases
5. systolic HF

65
Q

dilated cardiomyopathy causes

A

Idiopathic (most common)​

Following heart valve disease (volum overload) ​

Peripartum cardiomypathy (50% reversible) ​

Myocarditis (Coxsackievirus B)​

Alcohol abuse ​

Drugs (cocaine, chemotherapy drugs) ​

66
Q

dialted cardiomyopathy symtoms

A

Dyspnea ​

Angina ​

Fatigue

67
Q

dilated CMP signs

A

Displaced apex beat (cardiomegaly)​

S3 additional heart sound​

General signs of biventricular heart failure such as enlarged neck veins and leg swelling​

68
Q

age group common for dilated CMP

A

30-40

69
Q

INVESTGATIONS for cause identification in dilated CMP

A

Genetic testing ​

Viral Serology (myocarditis)​

70
Q

dilated cmp management

A

treat depending on symptoms

71
Q

management of someone with heart failure symptoms (dyspnoea, leg oedema) diagosed with dilated CMP

A

ACE inhibitors and beta blockers reduce stroke work (SW=V*P). If unresponsive you can consider LVAD (left ventricular assist device) ​

72
Q

management of someone with arrythmias diagosed with dilated CMP

A

antiarrhythmics (Amiodarone)

73
Q

management of someone with high risk of thromboembolic events diagosed with dilated CMP

A

anticoagulation

74
Q

what is hypertrophic CMP

A

Hypertrophy of myocardium, but occurs asymmetrically​

More pronounced on the side of the interventricular septum​

(INSTEAD OF THE myocardium in the outside side of the ventricles)

75
Q

causes of hypertrophic CMP

A

Most commonly autosomal dominant inheritance ​

Defect in certain sarcomere proteins​

76
Q

what is subendocardial ischaemia (just important for other understanding)

A

Subendocardial ischemia refers to a condition where there is inadequate blood supply to the innermost layer of the heart muscle, known as the subendocardium. This region is particularly vulnerable to ischemia because it is the farthest from the epicardial coronary arteries, which supply blood to the heart.

77
Q

pathophysiology of hypertrophic CMP

A

1) reduced LV volume due to hypertrophic growth impairs LV filling. This puts a limitation on the stroke volume, causing diastolic heart failure. ​

2) reduced stroke volume means the coronary circulation also gets less blood. ESPECIALLY since hypertrophied heart has an increased myocaridal oxygen demand, the demand outstrips the supply leading to subendocardial ischaemia

3) In situations of high cardiac demand, such as exercise, myocardial ischaemia can cause dangerously fast arrhythmias ​

​

78
Q

symptoms of hypertrophic CMP

A

Angina ​

Syncope/Presyncope

79
Q

signs of hypertrophic CMP

A

Ejection systolic murmur​

Bifid Pulse (double carotid artery pulse): Venturi effect ​

Arrhythmias​

80
Q

SOME unique investigs for hypertrophic CMP

A

FBC (anemia exacerbates cardiac ischemia) ​

  • Brain natriuretic peptide (BNP) levels, troponin T levels ​
81
Q

hypertrophic CMP management

A

​

  • Beta-blockers: reduce stroke work by reducing HR​
  • Alternatively, calcium channel blockers (reduce BP) ​

​

If still symptomatic, put in a pacemaker or do surgery to ablate myocardium.

82
Q

WHAT is restrictive CMP

A

myocardium stiffens and becomes less compliant but the heart remainssame size

83
Q

two types of restrictive CMP

A

infiltrative ( heart muscle is infiltrated or invaded by abnormal substances)

and non infiltrative (intrinsic abnormalities in the heart muscle)

84
Q

causes of infiltrative restrictive CMP

A

Amyloidosis (familial forms or as a consequence of ageing)
Sarcoidosis
Haemochromatosis

85
Q

causes of non infiltrative restrictive CMP

A

Radiation (produces reactive oxygen species which causes fibrosis)
Carcinoid syndrome
Scleroderma (fibrosis of heart)
Anthracycline (chemotherapy) toxicity

86
Q

restrictive cmp pathophysiology

A

1) Myocardium stiffens and becomes less compliant
2) This reduces the ventricular end-diastolic volumes. Therefore there is also a reduced stroke volume and cardiac output. This can lead to diastolic heart failure

Sequelae (consequences after smth. in this case disease)

1) Infiltration/remodelling of the myocardium can disrupt conduction, resulting in arrhythmias
2) Infiltration/remodelling of the myocardium can cause adverse remodelling, which can also cause systolic heart failure

87
Q

symtpoms of restricitve CMP

A

HEART FAILURE SYMP

88
Q

signs of restricitve CMP

A

Pitting oedema
Ascites
Increased jugular venous pressure (large neck veins)
Decreased pulse volume on palpation (brachial/carotids)
Signs of systemic disease ( coexisting carpal tunnel syndrome increases likelihood of amyloidosis)

89
Q

restricitve CMP investigations checking for causes

A

Checking for causes:
FBC
Serology (autoantibodies)

90
Q

restrictive CMP management

A

1) Manage symptoms.

Heart failure: ACE inhibitors, ARBs, diuretics, aldosterone inhibitors (spironolactone)
Arrhythmias: antiarrhythmics
Immunosuppression: Steroids

Pacemaker or Heart Transplant if all else fails

2) Treat underlying disease (Hereditary Haemochromatosis and venesection)

91
Q

what is infective endocarditis, where does it most commonly happen and why?

A

Infection of the endocardium, typically the heart valves as they are the location of turbulent blood flow.

92
Q

describe pathophysiology of infective endocard

A

1) Turbulent blood flow around valves damages endothelial lining
2) Non-bacterial thrombi form at locations of damage

Physiological Process but can happen more frequently if there is valvulopathy.

3) If patients acquire bacteraemia, bacteria can attach to thrombi and form a vegetation (adhesins)

4) This can cause valuvolpathies, e.g. aortic regurgitation, and rapid-onset heart failure and cardiogenic shock

93
Q

most common heart valves affected in infective endocarditis in averga person and IV drug users

A

Most commonly left-sided heart valves (aortic>mitral) du eto higher pressures
Tricuspid valve most common in IV drug users as bacteraemia most likely comes from venous system

94
Q

causes of infective endocarditis, in averge person and IV drug user

A

1) Streptococcus Viridans most common (e.g. dental procedures). Causes milder valve damage.
2) Staphylococcus aureus: most common in IV drug users. Causes more severe valve damage.

95
Q

signs of infective endocarditis

A
96
Q

what are 5 congenital heart diseases

A

ventricular septal defect

these two are mebryonic reminants:
atrial septal defect
ductus arteriosus

tetralogy of falot
aortic coarctation

97
Q

what does ventricular septal defect cause

A

Causes hypoxia and cyanosis as oxygenated and deoxygenated blood mixes.

98
Q

tetralogy of falot state the 4 pathologies

A

PROVe

pulmonary stenosis
right ventricular hypertrophy
aortic wall widening (Which is sitting right on top of:)
ventricular septal defect

99
Q

example of an atrial septal defect and explainwhat it is

A

An example is a patent (open) foramen ovale.

It is a fetal cardiac shunt, allowing blood to pass from the right atrium directly to the left atrium. The fetus receives oxygen from placenta so does not need to oxygenate lungs. Right atrial (deoxygenated) blood passes directly into the left atrium rather than passing through the pulmonary arteries to the lungs first.

100
Q

how common is patent foramen ovale

A

25% of people have it

101
Q

what can patent foramen ovale cause

A

It can cause paradoxical embolism (DVT clot can enter arterial circulation and cause a stroke.

102
Q

what is aortic coarctation and who commonly gets it

A

Aortic Coarctation is the severe narrowing of the aortic lumen.

It is more common in patients with Turner’s Syndrome.

103
Q

consequences of aortic coarctation

A

It can cause different BP measurements in the left and right arm depending on the location of the coarctation.

104
Q

what is patent ductus arteriosus

A

The ductus arteriosusis usually a connection between the aorta and pulmonary artery. In the embryo, it allows blood in the pulmonary artery to flow into the aorta, bypassing the pulmonary circulation (no need to perfuse lungs as oxygen is supplied by mother).

After birth, the ductus arteriosus usually obliterates to form the ligamentum arteriosum. If it the ductus remains open, this is patent ductus arteriosus.

105
Q

name of criteria used for infective endocarditis infection

A

duke criteria

106
Q

what duke criteria combo is needed for diagnosis of infective endocard?

A

There are major and minor criteria
2 major OR 1 major + 3 minor OR 5 minor are required to make the diagnosis

107
Q

what are the major duke criteria

A

Positive blood cultures (usually at least 2 separate positive cultures >12h apart)

Evidence of endicardial involvement (abscess, new valvular regurgitation, metallic valve dehiscence)

108
Q

what are the minor duke criteria

A

Fever

Predisposing cardiac conditions (e.g. mitral valve prolapse, bicuspid aortic valves)

Vascular phenomena

Immunological phenomena (Osler’s nodes, Roth spots, Janeway lesions, glomerulonephritis)

Microbiological and echocardiograohic evidence not fulfilling a major criterion

cardio and resp yr 2 (10 decks)

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