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BRS Cardio & Respiratory > 1b// Structural heart disease and Heart failure > Flashcards

1b// Structural heart disease and Heart failure Flashcards

1
Q

what is structural heart disease?

A

defects affecting the valves and chambers of the heart and aorta

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2
Q

What are 6 congenital structural heart diseases you need to know?

A
  • 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

Label.

A
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4
Q

What is the innermost, middle and outermost layer of the heart wall?

A

endocardium
it lines the cavities and valves of the heart
it regulates contractions of the heart

myocardium
composed of cardiac fibres
responsible for contraction of the heart

epicardium
aka visceral pericardium
thin layer of connective tissue and fat

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5
Q

What are pectinate muscles?

A
  • Pectinate muscles are muscular ridges located in the atria of the heart
    • Specifically in the right atrium and auricle
  • They help increase the SA in the right atrium
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6
Q

What are chordae tendinea?

A
  • Chordae tendinea are tendons that connect papillary muscles to tricuspid valve and mitral valve in the heart
    • They help prevent the valve from prolapsing during the ventricular systole
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7
Q

What are trabeculae carneae?

A

** - They are irregular muscular columns
- They project from the inner surface of the right and left ventricles of the heart
- The provide additional support to ventricular valves
- They help maintain stroke volume and cardiac output
**

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8
Q

What are papillary muscles?

A
  • Papillary muscles are small, cone-shaped muscles located in the ventricles of the heart
    • They attach to the cusps of the atrioventricular valves via chordae tendineae
    • They contract to prevent inversion or prolapse of these valves on systole (or ventricular contraction)
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9
Q

How do you calculate cardiac output?

A

heart rate (HR) x (stroke volume)

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10
Q

How do you calculate stroke volume?

A

end diastolic volume (EDV) - end systolic volume (ESV)

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11
Q

How do you calculate mean arteriole pressure?

A

(cardiac output(CO)) x Systemic vascular resistance (SVR))+ central venous pressure (CVP)
or
DP + 1/3(SP-DP)

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12
Q

How do you calculate ejection fraction?

A

SV/ EDV x100

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13
Q

How do you calculate ejection fraction?

A

SP-DP

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14
Q

What is mean arteriole pressure?

A

The mean arterial pressure is an average arterial blood pressure throughout a single cardiac cycle of systole and diastole. In health, a MAP >65 mmHg represents the pressure necessary to adequately perfuse the body organs. The estimation of MAP is useable at rest but during exertion (at high heart rate) MAP moves more closely toward an average of SP and DP.

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15
Q

What are the normal and abnormal heart sounds you can hear?

A

S1 and 2= normal

S3 and S4= abnormal

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16
Q

What is heart sound S1?

A
  • The first sound S1 is caused by the closure of the mitral and tricuspid valves, which occurs when the ventricles contract to pump blood into the pulmonary artery and aorta .
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17
Q

What is heart sound S2?

A

The second sound S2 is caused by the closure of the aortic and pulmonic valves, which occurs when the ventricles relax to receive blood from the atria after pumping blood.

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18
Q

What is heart sound S3?

A

The third sound (S3) is a low-frequency sound that occurs in early diastole, produced by rapid filling and expansion of ventricles. The most common cause of pathological S3 is congestive cardiac failure.

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19
Q

What is heart sound S4?

A
  • The fourth sound (S4) is a low-frequency sound that occurs in late diastole, produced by forceful atrial contractions forcing blood into stiff ventricles. Unlike S3, S4 is always pathological. It usually indicates atrial hypertrophy (seen in AS) or stiff ventricles ( systemic hypertension, hypertrophic cardiomyopathy, and ischemia)
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20
Q

What causes a heart murmur? And what are the types of murmurs?

A

A heart murmur is caused by the turbulent blood flow through the heart valves and is generally blowing, whooshing, or rasping sound heard during a heartbeat. There are 3 types of murmurs:
systolic, diastolic, continuous murmur

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21
Q

When does a systolic, diastolic and continuous murmur occur?

A

Systolic murmur: This type of murmur occurs when the heart is pumping blood to the rest of the body.
Diastolic murmur: This type of murmur occurs when the heart relaxes between beats to fill up with blood.
Continuous murmur: This type of murmur occurs throughout the heartbeat

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22
Q

What are the diseases that cause murmurs? (5)

A

aortic stenosis
mitral regurgitation
aortic regurgitation
mitral stenosis
patemnt ductus arteriosus

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23
Q

What is stenosis and what is aortic stenosis’ murmur?

A

stenosis means that valve is tight and not very flexible, and when the blood rushes through it during systole it has to gush through a tight opening

ejection systolic murmur

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24
Q

What is aortic regurgiation and what is its murmur?

A

valve leaflets are floppy they are not closed tightly when the valve is supposed to close after the systole is finished so there is a backflow of blood, simply can say leakage of blood back intop the ventricle from aorta.

diastolic murmur

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25
Q

What is patent ductus arteriosus and what is its murmur?

A

hole in the heart: PDA occurs when the opening between the aorta and the pulmonary artery does not close as it should. so there is mixing of blood and free flow of blood between lungs, aorta and pulmonary artery.

continuous murmur

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26
Q

What is mitral regurgitation and what its murmur?

A

floppy valves causing leaking of blood even when the valve is supposed to be closed i.e., during systole

holosystolic/ systolic murmur

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27
Q

What is mitral stenosis and what is its murmur?

A

stenosis means the valve is tight and whard for blood to flow through

mid-diastolic rumble

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28
Q

What is cardiac output?

A

the volume of blood the heart pumps in 1 minute. frequently given in L/min

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29
Q

What is VSD/ ASD?

A
  • Ventricular is when the wall between the 2 ventricles doesn’t fully develop
    Atrial is where there is a hole in the wall between the atria
    so there is mixing of oxygenated and deoxygenated blood

ventricular/ atrial septal defect

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30
Q

What happens to a baby with VSD/ ASD?

A

baby will turn blue due to mixing of blood
- as deoxygenated bloof is being pumped from the left ventricle to the body
- aka cyanosis (blue tinge of lips and nails)

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31
Q

what is the tetralogy of fallot?

A

combination of 4 congenital heart defects…
VSD, pulmonary stenosis, overriding aorta, hypertrophy of the right ventricle

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32
Q

What is meant by overriding aorta?

A

The aorta, which is the artery that carries oxygen-rich blood to the body, is out of place and rises above both ventricles. As a result, the body gets too much oxygen-poor blood.

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33
Q

What is meant by hypertrophy of the right ventricle?

A

The right lower chamber of the heart is bigger or thicker than normal, making it harder for blood to go through the pulmonary valve.

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34
Q

what is a coarctation of the aorta and what does it cause and increase the risk of?

A

narrowing of aorta at downward arc
causes hypertension
risk of heart attack and stroke

blood struggles to push through, may develop HF

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35
Q

what are the 4 valvular/ structural defects?

A

aortic and mitral stenosis

aortic and mitral regurgitation

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36
Q

what is the epidemiology of mitral valve disease? And the other valve diseases?

A

greatest rates in 70+ and females

major point is the prevalence increases dramatically from 60+
mild mitral regurgitation is the most common

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37
Q

what is aortic stenosis commonly preceded by?

A

aortic sclerosis (aka aortic valve thickening withoutr flow limitation)

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38
Q

when is aortic stenosis/ sclerosis often suspected? And how is it confirmed?

A

the presence of early peaking, systolic ejection murmur
- echocardiograph

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39
Q

how does aortic stenosis cause abnormal physiology?

A

long-standing pressure overload leads to left ventricular hypertrophy in order to maintain normal afterload
as stenosis worsens, adaptive mechanism fails and LV wall stress increases, declines systolic function
results in systolic heart failure

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40
Q

What are risk factors for aortic stenosis?

A
  • Hypertension
    • LDL levels
    • Smoking
    • Elevated C-reactive protein
    • Congenital bicuspid valves
    • Chronic kidney disease
    • Radiotherapy
      Older age **
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41
Q

What are pathologies that cause aortic stenosis?

A
  • Rheumatic heart disease
    • Congenital heart disease
      Calcium build up
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42
Q

what type of murmur is an S4 sound and what pathology?

A

ejection systolic

aortic stenosis

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43
Q

what does an aortic stenosis murmur sound like?

A

crescendo decrescendo
loudest over aortic area
radiates to carotid
ejection systolic (between lub and dub)

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44
Q

what does a mitral stenosis murmur sound like?

A

loudest over apex
and in expiration
lub-dub-whoooosh
mid diastolic murmur

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45
Q

what does an aortic regurgitation murmur sound like?

A

loudest at sternal edge
and when leaning forward
after dub
eARly diastolic murmur

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46
Q

what does a mitral regurgitation murmur sound like?

A

loudest over mitral area, radiates to axilla (left)
high pitched whistling
lub-whistle-dub
pansystolic murmur

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47
Q

what valve is open in systole?

A

aortic

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48
Q

what valve is open in diastole?

A

mitral

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49
Q

what are the investigations for valvular defects?

A

CXR
ECG
Transthoracic echocardiography
pos cardiac catheterisation, cardiac MRI/CT

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50
Q

basic pathophysiology of aortic stenosis

A

abnormal blood flow/trigger initiates inflammatory process similar to athersclerosis
damages valvular endocardium, leads to aortic sclerosis - leaflet fibrosis and calcium deposition
obstructs left ventricular emptying, increases pressure in left ventricle
compensatory left ventricular hypertrophy

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51
Q

How may someone present with aortic stenosis?

A
  • Presentation may look like…
    • Exertional dyspnoea and fatigue
    • Chest pain, angina
    • Syncope
    • Heart failure
    • Ejection systolic murmur
    • Rheumatic fever
      High lipoprotein and LDL and CKD
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52
Q

What is essential to diagnose aortic stenosis?

A

doppler echo

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53
Q

What is the management of aortic stenosis?

A

Aortic valve replacement (AVR):
* Treatment of severe aortic stenosis…
- Transcatheter valve replacement
- Surgical valve prosthesis

*choice of intervention should be a shared discussion making process, taking account of lifetime risks and benefits associated with the type of approach (transcatheter versus surgical) and type of valve (mechanical vs bioprosthetic)

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54
Q

what is aortic sclerosis

A

asymptomatic/pre-stenosis stage of aortic valve calcification

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55
Q

management of asmymptomatic aortic stenosis

A

observe only

56
Q

management of symptomatic aortic stenosis

A

valve replacement

57
Q

management of asymptomatic but less than 50% ejection fraction aortic stenosis

A

valve replacement

58
Q

what is the option of treatment for aortic stenosis when not fit for surgery?

A

TAVI - trans-catheter aortic valve replacement

59
Q

what is the trigger for aortic stenosis in rheumatic fever patients?

A

streptococcal infection triggering autoimmune reaction

60
Q

symptoms of coarctation of aorta?

A

pale skin
irritability
sweating
difficulty breathing

61
Q

management of coarctation of aorta?

A

surgery immediately

62
Q

pathophysiology of coarctation of aorta

A

wall narrowing blocks normal blood flow
backflow to left ventricle, it works harder
LV hypertrophy
eventual heart failure

63
Q

pathophysiology of atrial septal defect

A

hole between atria
blood flows from left-right
more blood goes to lungs, so lungs and heart work harder

64
Q

symptoms of atrial septal defect

A

asymptomatic

or signs of reduced HF - SOB, murmurs, palpitations, oedema

65
Q

symptoms of ventricular septal defect

A

murmurs
breathlessness
failure to thrive
or asymptomatic

66
Q

symptoms of tetralogy of fallot

A

cyanosis
SOB
systolic murmur

67
Q

pathophysiology of tetralogy of fallot

A

VSD
pulmonary stenosis
overriding aorta - enlarged, sits over VSD so blood from both ventricles enters
right ventricular hypertrophy as a result
lack of oxygenation as blood goes from right - systemic circulation, bypassing lungs

68
Q

pathophysiology of mitral stenosis

A

acute insult leads to formation of multiple foci and infiltrates in endo/myocardium, valve walls
thickens and calcifies leading to stenosis
blood struggles to pass from left atrium - ventricle
increased left atrial pressure, enlargement
increased LA pressure leads to pulmonary hypertension, congestion and right sided dysfunction

69
Q

common cause of mitral stenosis

A

rheumatic fever/ heart diseasew

70
Q

symptoms of mitral stenosis

A 
palpitations
angina
orthopnoea
exertional dyspnoea
paroxysmal nocturnal dyspnoea - wakes up short of breath
71
Q

What are causes of mitral stenosis?

A
  • Rheumatic fever
    • Carcinoid syndrome
    • Use of ergot/ serotonergic drugs
    • SLE
    • mitral annular calcification due to aging
    • Amyloidosis
    • Rheumatoid arthritis
    • Whipple disease
      Congenital deformity of the valve
72
Q

What is mitral stenosis?

A
  • Obstruction to the left ventricular inflow at the level of mitral valve due to structural abnormality of the mitral valve
  • As disease progresses it leads to pulmonary hypertension and right heart failure occur
73
Q

What are the clinical findings of mitral stenosis?

A
74
Q

management of mild mitral stenosis

A

observation

75
Q

management of severe asymptomatic mitral stenosis

A

balloon valvotomy

76
Q

management of severe symptomatic mitral stenosis

A

beta blockers
diuretics
balloon valvotomy
valve replacement

77
Q

What are investigations for mitral stenosis?

A
  • ECG
    • Chest x ray
      Transthoracic echocardiography
78
Q

What is the presentation of someone with mitral stenosis?

A
  • H/0 of rheumatic fever
    • Dyspnoea
    • Mid diastolic murmur
    • Opening snap/ loud S1 in early stages
    • Dysphagia
    • Atrial afibrillation
    • Haemoptysis
79
Q

pathophysiology of chronic aortic regurgitation

A

valvular incompetence leads to reflux from aorta into left ventricle
increased volume and pressure in left ventricle - LV hypertrophy
eventual reduced ejection fraction and end systolic volume increases
eventual dyspnoea and ischaemia

**aortic regurgiation is hte diastolic leakage of blood from the aorta into the left ventricle
- it occurs due top the imcompetence of valve leaflets resulting from ewither intrinsic valve disease or dilation of the aortic root

80
Q

Is acute or chronic aortic regurgirtation a medical emergency?

A
  • It can be acute–> medical emergency, presenting with sudden onset of pulmonary oedema and hypotension or cardiogenic shock
    It can be chronic–> culminate into congestive cardiac failure
81
Q

pathophysiology of acute aortic regurgitation

A 
inc end systolic LV volume
end diastolic pressure increases
increase in pulmonary venous pressure
dyspnoea and pulm oedema
heart failure and cardiogenic shock
82
Q

what are the main differences beyween acute and chronic aortic regurgitation

A

chronic allows for compensatory mechanisms - hypertrophy

83
Q

symptoms of acute aortic regurgitation

A 
cardiogenic shock
tachycardia
cyanosis
pulmonary oedema
austin flint murmur
84
Q

symptoms of chronic aortic regurgitation

A

wide pulse pressure

corrigan pulse/traube sign (booming pulse)

85
Q

management of acute aortic regurgitation

A

treat underlying cause
ionotropes
vasodilators
valve replacement

86
Q

management of mild chronic aortic regurgitation

A

reduction of afterload - diuretics, vasodilators

87
Q

management of severe aortic regurgitation

A

valve replacement

88
Q

What are the causes of congenital and acquired aortic regurgitation?

A
  • Rheumatic heart disease
    • Infective endocarditis
    • Aortic valve stenosis
    • Congenital heart defects
      Congenital bicuspid valves
89
Q

What are the causes of aortic root dilation aortic regurgitation?

A
  • Marfan’s syndrome
    • Connective tissue disease/ collagen vascular diseases
    • Idiopathic
    • Ankylosing spondylitis
      Traumatic
90
Q

Describe the pathyphysdiology of aortic regurgitation (IC).

A
91
Q

pathophysiology of mitral regurgitation following infective endocarditis

A

abcess formation, vegetations, rupture of chorade tendinae and valve perforations
leads to blood leakage LV-LA

*in general mitral regurg is the reversal of blood flow from the LV to the LA

92
Q

pathophysiology of chronic mitral regurgitation

A

reflux from LV to LA
increased LA pressure, inc pulmonary pressure
congestion by fluid buildup - congestive heart failure

93
Q

common cause of acute mitral regurgitation

A
  • Mitral valve prolapse ?**
    • Rheumatic heart disease
    • Infective endocarditis
    • Following valvular surgery
      Prosthetic mitral valve dysfunction

*it is caused by the disruption in any part of the mitral valve apparatu

94
Q

common causes of chornic mitral regurgitation.

A
  • Rheumatic heart disease
    • SLE
    • Scleroderma
    • Hypertrophic cardiomyopathy
      Drug related
95
Q

symptoms of mitral regurgitation

A

dyspnoea
orthopnoea
chest pain
fatigue

holosystolic murmur
S3 heart sounds
signs of congestive heart failure

96
Q

What are investigations for mitral regurg?

A
  • Transthoracic echocardiograph
    • ECG
    • Chest x ray
      Cardiac MRI/ CT scan
97
Q

management of acute mitral regurg

A

nitrates, diuretics, ionotropes,

intra-arotic balloon counterpulsation

98
Q

management of acute mitral regurg with severe regurg

A

surgery
- prosthetic ring can be inserted to reshape the valve

99
Q

management of severe chronic assymptomatic and chronic symptomatic mitral regurg

A

asymptomatic= watchful waiting or surgery

symptomatic= 1st surgery plus medical treatment

100
Q

What are cardiomyopathies and what are the main types?

A

disease of the heart muscle that makes it harder for the heart to pump blood to the rest of the body
- it can lead to heart failure

the main types are…
- dilated
- hypertrophic
- restrictive

101
Q

pathophysiology of dilated cardiomyopathy

A

ventricles stretch and thin
ventricular enlargement
ventricular systolic dysfunction
heart failure

progressdive, usually iireversible disease cuases systolic dysfunction with heart failure

102
Q

What is the hallmark gross finding at autopsy for dilated cardiomyopathy?

A

left ventricular dilation usually more than 4cm

103
Q

cause of dilated cardiomyopathy

A 
genetic 1/3 (25%, primary withouyt family history is idiopathic)
myocardial ischaemia/ heart valve disease
child birth
myocarditis
alcoholism
drug use
autoimmune
thyroid
hypertension/diabetes
104
Q

symptoms of dilated cardiomyopathy

A
    • Dyspnoea, cold clammy extremities
    • Low cardiac output leading to insufficient tissue oxygenation
    • Displaced apex beat
    • Enlarged left ventricle
    • Fatigue
    • Low cardiac output and decrease organ perfusion
    • Angina
    • Low coronary perfusion
    • Pulmonary congestion
    • Diffuse crackles
    • Peripheral oedema
    • Heart failure
  • Sudden cardiac death
105
Q

What are investigations for dilated cardiomyopathy?

A
  • ECG
    • Chest x ray
    • Cardiac catheterisation
    • Cardiac MRI/ CT scan
    • Echocardiography
    • Genetic testing
      Viral serology
106
Q

management of dilated cardiomyopathy

A

fluid and sodium restrictions
treat underlying cause
heart failure management - diuretics, beta blockers, ACEi

107
Q

What is hypertrophic cardiomyopathy?

A
  • Hypertrophic cardiomyopathy 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
    • Hypertrophic cardiomyopathy is the leading cause of sudden cardiac death on preadolescent and adolescent children
    • Familial hypertrophic cardiomyopathy occurs as an autosomal dominant 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
108
Q

pathophysiology of hypertrophic cardiomyopathy

A

genetic AD
abnormal increase of left ventricular wall
LV outflow obstruction, heart less able to fill, diastolic dysfunction

109
Q

cause of hypertrophic cardiomyopathy

A

familial or sporadic mutations

110
Q

symptoms of hypertrophic cardiomyopathy

A

S4
- Forceful atrial contraction into a hypertrophied left ventricle

Syncope
- Reduced cardiac output to the peripheries and head 

Fatigue
- Low cardiac output and decrease organ perfusion

Angina
- Low coronary perfusion 

Pulmonary congestion and oedema
- Diffuse crackles 

Systolic murmur
- Due to passage of blood through the narrow outflow 


Sudden cardiac death
111
Q

management of hypertrophic cardiomyopathy

A

HCM w symptoms–> beta blockers, if contraindicated B=Verapamil

If refractory and drugs fail–> mechanical therapy with pacemaker or surgery (septal myectomy or ablation)

112
Q

What are investigations for hypertrophic cardiomyopathy?

A
  • Echocardiography
    • Chest x ray
    • Cardiac MRI
113
Q

What is restruictive cardiomyopathy?

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

114
Q

pathophysiology of restrictive cardiomyopathy

A

ventricles become rigid, restricted from stretching/filling with blood
diastolic dysfunction
reduced cardiac output

115
Q

causes of restrictive cardiomyopathy

A

idiopathic
familial
assoc. with systemic disorders

116
Q

symptoms of restrictive cardiomyopathy

A

Ascites and pitting oedema in peripheries
- Increase venous pressure leads to right sided heart failure

Hepatomegaly 
- Hepatic congestion due to RHF 

S4 heart sound
- Atrium contracts into still ventricle 

Increase in jugular venous pressure
- Due to right heart failure 

Easy bruising, weight loss
- Heart failure
117
Q

management of restrictive cardiomyopathy

A

underlying cause

* 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
118
Q

What are investigatyions for restrictive cardiomyopathy?

A
  • CBC
    • Serology
    • Amyloidosis check
    • Chest x ray
    • ECG
    • Echocardiography
    • Catheterisation
      MRI/ Biopsy
119
Q

what is infective endocarditis

A

multisystem disease
infection of heart valves +/- adjacent endocardium
bacteria enters bloodstream, forms vegetations (bacteria, platelets, fibring)

an infection of the endocardium or vascular endothelium of the heart
- Typically affecting heart valves
- Result of bacteria entering blood stream forming a vegetation
- Causes fever, malaise, sweats and weight loss, heart murmur, blood tests= anaemia and raised markers of infection

120
Q

what are vegetations

A

bacteria
platelets
fibrin

121
Q

common cause of infective endocarditis

A

streptococci

122
Q

symptoms of infective endocarditis

A

Cardiac decompensation symptoms…
- Shortness of breath
- Frequent coughing
- Swelling of the legs and abdomen
- Fatigue
- Raised JVP (jugular venous pressure)
- Lung crackles
- Oedema

123
Q

who are at increased risk of infective endocaridtis?

A
  • Increased drug users are at increased risk of infective endocarditis due to repeated injection
    • Potentially exposing their bloodstream to bacteria on the surface of the skin or use of non-sterile needles
      It is also more common in people who are immunosuppressed or have congenital heart defects leading to damaged endocardium
124
Q

process of diagnosising of infective endocarditis

A

DUKES criteria

  • Fever, malaise, sweats and unexplained weight loss are common symptoms
  • There may be a new heart murmur on examination
  • Blood tests show anaemia and raised markers of infection
  • Blood cultures may isolate a microorganism
  • Echocardiogram can show a vegetation, abscess, valve perforation and/or new
    dehiscence of prosthetic valve. Often there is regurgitation of the affected valve
  • Transoesophageal echo has higher sensitivity compared with transthoracic
125
Q

most commonly affected valves of IE and why?

A

aortic then mitral then right sided

The formation of a vegetation at the valves of the heart either results in changes to their thickness or a failure in their ability open and close appropriates. It is more common for bacteria to attach to the endocardium if underlying damage is present, and this occurs more frequently at sites of turbulent blood flow such as the valves of the heart.

except IV drug users - tricuspid as infection enters intravenously usually

126
Q

symptoms of cardiac decompensation

A

SOB
frequent coughing
swelling of legs, abdomen
fatigue

clinically - raised JVP, lung crackles and oedema

127
Q

complications of IE

A

vascular/embolic phenomena - stroke, Janeway lesions, splinter/conjunctival haemorrhage
immunological phenomena - Oslers nodes, Roth spots

128
Q

what is cardiac decompensation

A

inability of heart to maintain adequate circulation (leading to end organ damage)

129
Q

What is dilated cardiomyopathy?

A

dilated cardiomyopathy is characterised by dilated and thin-walled cardiac chambers with reduced contractility

Dilation of the chambers leads to reduced contractility. Echo shows a dilated left ventricle with reduced systolic function (ejection fraction) and typically global hypokinesis

130
Q

What are the commonest causes of dilated cardiomyopathy?

A

Idiopathic, genetic, toxins (alcohol, cardiotoxic chemotherapy), pregnancy (peripartum cardiomyopathy), viral infections (myocarditis), tachycardia-related cardiomyopathy, thyroid disease, muscular dystrophies

131
Q

How is dilated cardiomyopathy managed?

A

Medical heart failure therapy - ACE inhibitors, beta-blockers, mineralocorticoid receptor antagonists Diuretics for fluid overload
Anticoagulation for atrial fibrillation
Cardiac devices – cardiac resynchronisation therapy and/or implantable cardioverter defibrillator Transplant

132
Q

What will be the implications on this gentleman in the future?

A

The gentleman is at risk of heart failure hospitalization, cardiac arrhythmias, sudden cardiac death due to ventricular arrhythmia, and reduced survival

133
Q

What is the difference between heart failure with preserved ejection fraction and heart failure with reduced ejection fraction?

A

HF with preserved ejection fraction: EF greater than 50%. Presence of diastolic or right heart dysfunction. Diastolic dysfunction leads to an increased reservoir of blood in the pulmonary veins, leading to increased pulmonary hypertension and pulmonary oedema.

HF with reduced ejection fraction: EF less than 50%. Impaired left ventricular systolic function leading to pulmonary oedema secondary to impaired systolic function and flow of blood via the aorta. This leads to the backflow of blood into the pulmonary veins and lungs (leading to pulmonary oedema).

134
Q

What are the clinical signs and symptoms of heart failure and how does it differ between left and right heart failure?

A

Right heart failure – peripheral oedema e.g. leg swelling, raised jugular venous pressure

Left heart failure – pulmonary oedema

135
Q

What medications are used to treat heart failure?

A

Heart failure with preserved ejection fraction: Diuretics and SGLT2 inhibitors.

Heart failure with reduced ejection fraction: ACE inhibitors (ACEi) and angiotensin II receptor blockers (ARBs) – e.g. preformulated in Entresto. Beta blockers. Mineralcorticoid receptor antagonists, SGLT2 inihbitors, diuretics.

136
Q

How is heart failure monitored?

A

Clinical signs and symptoms of fluid overload: E.g. shortness of breath, leg swelling, orthopnoea (needing an extra pillow at night), reduced exercise tolerance due to shortness of breath.

Observations: Low oxygen saturation

Biomarkers: NT-proBNP

Imaging: Echocardiogram

137
Q

Overview of both dialted cardiomyopathy and infective endocarditis.

A

BRS Cardio & Respiratory (28 decks)

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