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BRS2 - Cardiovascular & Respiratory Medicine > Structural Heart Disease & Case Studies > Flashcards

Structural Heart Disease & Case Studies Flashcards

1
Q

Which two layers of the heart protect the myocardium (muscle layer)?

A

Myocardium is protected on the outside by means of the EPICARDIUM and on the inside by means of the ENDOCARDIUM

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2
Q

What process is characteristic of:

a) systole?
b) diastole?

A

a) Contraction

b) Relaxation

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3
Q

What phase of the cardiac cycle is longer: systole or diastole?

A

Diastole is slightly longer than systole

Diastole ~2/3 of each heartbeat

Systole ~1/3 of each heartbeat

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4
Q

What two volumetric measurements are important for determining the stroke volume or cardiac output of the heart?

A

ESV and EDV

EDV - ESV = SV(mL)

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5
Q

What is LV end systolic volume (ESV)?

A

The volume of blood that stays behind in the heart in left ventricle following systole

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6
Q

What is LV end diastolic volume (EDV)?

A

The volume of blood in left ventricle just before systole

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7
Q

What are the 2 main phases of each heartbeat?

A
  1. Diastole

2. Systole

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8
Q

How many distinct phases can diastole be split into?

A

4

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9
Q

How many distinct phases can systole be split into?

A

3

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10
Q

How can you calculate the ejection fraction from stroke volume and end diastolic volume?

A

SV/EDV = EF(%)

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11
Q

What name can be used to refer to the aortic and pulmonary valves?

A

Semilunar valves

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12
Q

What are the 7 stages of the cardiac cycle?

A
  1. Atrial systole
  2. Isovolumetric contraction
  3. Rapid ejection
  4. Reduced ejection
  5. Isovolumetric relaxation
  6. Rapid passive filling
  7. Reduced passive filling
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13
Q

What are structural heart diseases?

A

SHD covers a number of defects which affect the valves and chambers of the heart and aorta

Some defects are present at birth (congenital) while others form later in life (adult; due to damage caused by infections etc.)

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14
Q

Name 3 examples of a congenital structural heart disease.

A

Congenital SHDs inc.

  • 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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15
Q

What are the two main types of defects that can cause structural heart diseases that form later on in life (i.e. not congenital)?

A
  • Valvular dysfunctions (stenosis/regurgitation)

- Muscular defects (cardiomyopathies)

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16
Q

Atrial septal defect (ASD) is an example of what type of heart disease?

A

Congenital structural heart disease

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17
Q

Ventricular septal defect (VSD) is an example of what type of heart disease?

A

Congenital structural heart disease

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18
Q

Coarctation of aorta is an example of what type of heart disease?

A

Congenital structural heart disease

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19
Q

Patent foramen ovale (PFO) is an example of what type of heart disease?

A

Congenital structural heart disease

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20
Q

Patent ductus arteriosus (PDA) is an example of what type of heart disease?

A

Congenital structural heart disease

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21
Q

Tetralogy of Fallot (TOF) is an example of what type of heart disease?

A

Congenital structural heart disease

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22
Q

What is ventricular septal defect (VSD)?

A

Congenital structural heart disease

When wall between 2 ventricles fails to develop normally —-> hole in the septal wall

This can cause mixing of oxygenated (oxygen-rich) blood from LV with deoxygenated (oxygen-poor) from RV

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23
Q

How might ventricular septal defect (VSD) present in a child?

A

In a child

  • Poor weight gain
  • Poor feeding, sweating while feeding
  • Palpitations
  • Shortness of breath
  • Fatigue or weakness
  • Fast breathing
  • Hard breathing
  • Pallor
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24
Q

What interventions might be needed to treat ventral septal defect (VSD)?

A

If the hole is very large, might require open heart surgery or cardiac catheterisation to manually close it

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25
Q

When might no interventions be needed for ventral septal defect (VSD)?

A

Sometimes the hole is small enough that it closes as the child grows older

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26
Q

What is tetralogy of fallot (TOF)?

A

Congenital structural heart disease

Composed of 4 different defects which occur together:

  1. Ventricular septal defect
  2. Pulmonary stenosis
  3. Widening of aortic valve
  4. Right ventricular hypertrophy
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27
Q

Explain the 4 defects that occur in tetralogy of fallot (TOF)?

A
  1. Ventricular septal defect
    - Hole in heart
  2. Pulmonary stenosis
    - Pulmonary trunk is narrowed down
  3. Widening of aortic valve
    - So wide that it can sit on both RV + LV directly allowing mixing of blood/diversion of blood from RV to aorta
    - Aortic valve also sits directly on top of this VSD
  4. Right ventricular hypertrophy
    - Thickening of RV wall
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28
Q

Tetralogy of fallot (TOF) is a very critical defect.

What intervention needed is needed and why?

A

Child must undergo different surgeries

Repair of VSD + repair of too wide aorta
- So child can breathe normally w/o mixing of oxygenated and deoxygenated blood

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29
Q

What is atrial septal defect (ASD)?

A

Congenital structural heart disease

~ to VSD (main difference is that problem is with atrial wall)

When wall between 2 atria fails to develop normally —-> hole in the septal wall

This can cause mixing of oxygenated (oxygen-rich) blood from LA with deoxygenated (oxygen-poor) from RA

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30
Q

What interventions might be needed to treat atrial septal defect (ASD)?

A

Medium to large atrial septal defect diagnosed during childhood or adulthood to prevent further complications

  • Cardiac catherisation
  • Open heart surgery
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31
Q

When might no interventions be needed for atrial septal defect (ASD)?

A

If hole is small enough that is closes on its own over time

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32
Q

When can atrial septal defect (ASD) develop?

A

In a baby, during pregnancy if the walls between the 2 atria fail to develop properly

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33
Q

When is surgery for atrial septal defect (ASD) not recommended?

A

If you have severe pulmonary hypertension, surgery might worsen condition

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34
Q

Why might someone with ASD be given medication?

What kind of medication might they be prescribed?

A

To help reduce some of the associated signs/symptoms of ASD (medication won’t repair the hole)

Medication e.g.
- Beta blockers —-> to keep heartbeat regular

  • Anticoagulants —-> to reduce risk of blood clots
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35
Q

What valves are most commonly affected in structural heart diseases?

A

Aortic valve

Mitral valve

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36
Q

What are the most common valvular defects?

A

Aortic stenosis - narrowing
Aortic regurgitation - incompetence leading to backflow of blood

Mitral stenosis - narrowing
Mitral regurgitation - incompetence of valve, leading to backflow of blood

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37
Q

What is coarctation of the aorta?

A

Congenital structural heart defect

Narrowing of the aortic wall - birth defect in which part of aorta is narrower than rest

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38
Q

What are some potential complications that can arise from coarctation of the aorta?

Why are they associated with this condition?

A

Ventricular hypertrophy
Heart failure

Birth defect - part of aorta narrower than rest

During ventricular systole, blood has to force through this narrow passage

Because of this, ventricle has to work harder to push more blood during each cycle

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39
Q

Coarctation of the aorta is very serious and needs urgent repair.

What intervention(s) might be needed to treat this condition?

A

Intervention depends on severity of condition and age at time of diagnosis

Interventions inc.

Surgery
Balloon angioplasty + stenting

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40
Q

Briefly describe the epidemiology of rheumatic heart disease, focusing on sex differences, age differences and overall prevalence.

A

Conclusions drawn from data (25yo to >=80)

  • More prevalent in women than across all age categories
  • More prevalent in younger age categories (most prevalent in 25 - 49 = youngest category included in data)

Mostly affects children + adolescents in low and middle income countries

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41
Q

Briefly describe the epidemiology of rheumatic heart disease, focusing on sex differences, age differences and overall prevalence.

A

Conclusions drawn from data in lectures (25yo to >=80)

  • More prevalent in women than across all age categories
  • More prevalent in younger age categories (most prevalent in 25 - 49 = youngest category included in data)

Mostly affects children + adolescents in low and middle income countries

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42
Q

Briefly describe the epidemiology of calcific aortic valve disease, focusing on sex differences, age differences and overall prevalence.

A

Conclusions drawn from data in lectures (25yo to >=80)

In general
- Increasing prevalence as age increased

  • More prevalent in men than women (more similar rates between M/W in older population)
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43
Q

Briefly describe the epidemiology of degenerative mitral valve disease, focusing on sex differences, age differences and overall prevalence.

A

Conclusions drawn from data in lectures (25yo to >=80)

In general
- Increasing prevalence as age increased

  • More prevalent in women than men (difference in prevalence increased as age increased)

BUT SOME STUDIES SUGGEST NO DIFFERENCE IN PREVALENCE BETWEEN MEN AND WOMEN

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44
Q

Of those that require treatment, what is the most common valvular disease in the US and Europe?

A

Aortic stenosis (AS)

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45
Q

What is the second most frequent cause for cardiac surgery?

A

Aortic stenosis

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46
Q

Aortic stenosis is largely a disease affecting what age group?

A

Older people - 7th/8th decade of life

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47
Q

What condition precedes aortic stenosis?

A

Aortic sclerosis - can be asymptomatic

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48
Q

What is aortic sclerosis?

A

Defined as aortic valve thickening w/o flow limitation

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49
Q

What signs detected in auscultation might suggest aortic stenosis?

A

Early-peaking, systolic ejection murmur - might hear shrill SEM

Confirmed by ECG

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50
Q

What are the risk factors associated with aortic stenosis?

A 
Hypertension
LDL levels
Smoking
Elevated C-reactive protein
Congenital bicuspid valves
Chronic kidney disease
Radiotherapy
Older age
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51
Q

Elevated C-reactive protein is a risk factor of aortic stenosis.

What does elevated CRP suggest?

Why is this significant?

A

Elevated CRP suggests presence of an active infection in the body

Infection can cause aortic stenosis and valvular damage

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52
Q

Congenital bicuspid valves are risk factors of aortic stenosis.

Why?

A

Valves more prone to wear and tear process and to infections that can cause aortic stenosis

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53
Q

Chronic kidney disease is a risk factor of aortic stenosis.

Why?

A

More exposed and prone to infection

Infections can cause aortic stenosis + valvular damage

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54
Q

What are the main causes of aortic stenosis?

A
  1. Rheumatic heart disease
  2. Congenital heart disease
  3. Calcium build up
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55
Q

What is the most common cause of aortic stenosis in developing countries?

A

Rheumatic heart disease

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56
Q

Calcium build up is a potential cause of aortic stenosis.

How?

A

Calcium build up can occur for various reasons (e.g. dietary reasons, homeostasis problems, etc.)

Can cause aortic sclerosis or calcified aortic walls leading to aortic stenosis in later life

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57
Q

Describe the pathophysiology of aortic stenosis.

A
  • Valvular endocardium = damaged due to abnormal blood flow across the valve (in the case of a bicuspid valve) or by an unknown trigger
  • Endochardial injury initiates an inflammatory process similar to atherosclerosis and ultimately leads to leaflet fibrosis + deposition of calcium on the valve
  • Progressive fibrosis + 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 valvular endothelium, leading to inflammation and eventually calcification
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58
Q

What initiates the inflammatory process leading to leaflet fibrosis and calcium deposition in the pathophysiology of aortic stenosis?

A

Endochardial injury

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59
Q

What does endocardial injury initiate in the pathophysiology of aortic stenosis?

A

An inflammatory process, leading to leaflet fibrosis and calcium deposition on the valve

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60
Q

What limits aortic leaflet mobility in the pathophysiology of aortic stenosis?

A

Progressive fibrosis and calcium deposition

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61
Q

What results from progressive fibrosis and calcium deposition in the pathophysiology of aortic stenosis?

A

Limited aortic leaflet mobility and, eventually, stenosis

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62
Q

How can aortic stenosis develop in rheumatic disease?

A

An autoimmune inflammatory reaction is triggered by prior Streptococcus infection that targets valvular endothelium, leading to inflammation and eventually calcification

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63
Q

How can aortic stenosis lead to left ventricular hypertrophy?

A

Stenosis leads to long-standing pressure overload

—–> LVH

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64
Q

How can aortic stenosis eventually cause systolic heart failure?

HINT - AS —-> LVH —-> HF

A

Aortic stenosis (AS) leads to long-standing pressure overload —–> LVH

Ventricle maintains a normal wall stress (afterload) despite the pressure overload produced by stenosis

—-> As stenosis worsens, adaptive mechanism fails + LV wall stress increases

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

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65
Q

Patient A has aortic stenosis and is found to have developed left ventricular hypertrophy.

How could this result in heart failure, if the stenosis worsens?

A

Previously, ventricle was maintaining a normal wall stress (afterload) despite the pressure overload produced by stenosis

However, as stenosis worsens, adaptive mechanism fails + LV wall stress increases

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66
Q

What might you expect to find in the history/presentation of a patient with aortic stenosis?

A
  • Exertional dyspnoea
  • Fatigue
  • Chest pain
  • Ejection systolic murmur (>=3/6 is present with a crescendo-decrescendo pattern that peaks in mid-systole + radiates to the carotid)
  • H/O Rheumatic fever, high lipoprotein, high LDL, CKD, age>65
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67
Q

What investigations would you carry out in a suspected case of aortic stenosis?

A
  • Transthoracic echocardiography
  • ECG Chest X-Ray (LVH)
  • Cardiac catheterisation
  • Cardiac MRI
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68
Q

For which patients might aortic valve replacement be considered?

A
  • With symptomatic AS
  • Asymptomatic patients with severe AS who have an LVEF <50%, or who are undergoing other cardiac surgery
  • AVR ? 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
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69
Q

What is the primary treatment for symptomatic aortic stenosis?

A

Aortic valve replacement, AVR

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70
Q

For which patients might aortic valve replacement be considered?

A
  • With symptomatic AS
  • Asymptomatic patients with severe AS who have an LVEF <50%, or who are undergoing other cardiac surgery
  • AVR ? 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
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71
Q

Aortic valve replacement might be recommended for patients with asymptomatic aortic stenosis.

What are the requirements for this?

A
  • Asymptomatic patients with severe AS who have an LVEF <50%, or who are undergoing other cardiac surgery
  • AVR ? 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
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72
Q

What are the options for management of aortic stenosis?

A

Aortic valve replacement, AVR

Balloon aortic valvuloplasty

Antihypertensive

ACE inhibitors

Statins

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73
Q

What types of valves are currently available to be used in aortic valve replacement in aortic stenosis?

A

Mechanical valves
- Surgical

Bioprosthetic

  • Surgical
  • Minimally invasive surgical (sutureless)
  • Transcatheter aortic valve implantation device
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74
Q

What types of valves are under development for use in aortic valve replacement in aortic stenosis?

A
  • Flexible polymeric valve

- Tissue-engineered heart valve

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75
Q

What is aortic regurgitation?

A

AR is the diastolic leakage of blood from the aorta into the left ventricle

  • Not as common as aortic stenosis + mitral regurgitation
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76
Q

Why does aortic regurgitation occur?

A

Occurs due to incompetence of valve leaflets resulting from either intrinsic valve disease or dilation of the aortic root

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77
Q

What are the two classifications of aortic regurgitation?

A

Chronic

Acute

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78
Q

What are the main congenital and acquired causes of aortic regurgitation?

A

Rheumatic heart disease

Infective endocarditis

Aortic valve stenosis

Congenital heart defects

Congenital bicuspid valves

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79
Q

What are the main causes (aortic root dilation) of aortic regurgitation?

A

Marfan’s Syndrome

Connective tissue disease/collagen vascular diseases

Idio

Ankylosing spondilytis

Traumatic

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80
Q

What can acute aortic regurgitation cause?

A

A medical emergency, presenting with sudden onset of pulmonary oedema and hypotension or cardiogenic shock

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81
Q

Acute aortic regurgitation is a medical emergency.

How does it present?

A

With sudden onset of pulmonary oedema and hypotension or cardiogenic shock

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82
Q

How can we categorise the causes of aortic regurgitation?

A
  1. Congenital & Acquired

2. Aortic root dilation

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83
Q

Describe the pathophysiology of acute aortic regurgitation.

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 aortic regurgitation
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84
Q

Describe the potential pathophysiology of acute aortic regurgitation.

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 aortic regurgitation
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85
Q

How can infective endocarditis result in acute aortic regurgitation (AR)?

A

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

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86
Q

How could vegetations on the valvular cusps lead to acute AR?

A

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

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87
Q

How could chest trauma result in acute AR?

A

Chest trauma can cause tear in ascending aorta, leading to aortic regurgitation

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88
Q

What pathophysiology can lead to chronic aortic regurgitation?

A
  • Bicuspid aortic valve

- Rheumatic fever —-> fibrotic changes causing thickening and retraction of leaflets

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Perfectly
89
Q

What pathophysiology can lead to chronic aortic regurgitation?

A
  • Bicuspid aortic valve

- Rheumatic fever —-> fibrotic changes causing thickening and retraction of leaflets

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90
Q

How could rheumatic fever result in chronic AR?

A

Rheumatic fever —-> fibrotic changes causing thickening and retraction of leaflets

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91
Q

Acute aortic regurgitation is a medical emergency and can eventually cause cardiogenic shock.

Describe the mechanism by which this can occur.

A
  1. Acute AR —-> increase blood volume in LV during systole

—–>

  1. LV end diastolic pressure increases

——>

  1. Increase in pulmonary venous pressure

——>

  1. Dyspnoea and pulmonary oedema

——->

  1. Heart failure

——->

  1. Cardiogenic shock
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92
Q

Chronic aortic regurgitaion can cause congestive heart failure.

In its later stages, chronic AR can result in ischaemia, necrosis and apoptosis.

Describe the mechanism by which this occurs.

A

Chronic AR —-> gradually increase in LV volume
—–> LV enlargement and eccentric hypertrophy

Early stages:
1. EF normal or slightly increased —–> after some time, EF falls + LV ESV rises

  1. Eventually, LV dyspnoea —-> lower coronary perfusion —–> ischaemia, necrosis + apoptosis
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93
Q

What is typical in a history/presentation of acute aortic regurgitation?

A
  • Cardiogenic shock
  • Tachycardia
  • Cyanosis
  • Pulmonary oedema
  • Austin glint murmur
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94
Q

What is typical in a history/presentation of chronic aortic regurgitation?

A
  • Wide pulse pressure
  • Corrigan’s pulse (water hammer pulse)
  • Pistol shut pulse (Traube sign)
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95
Q

What investigations might be carried out in a suspected case of aortic regurgitation?

A
  • Transthoracic echocardiography
  • Chest X-Ray
  • Cardiac catheterisation
  • Cardiac MRI/CT Scan
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96
Q

What is the main management option for aortic valve replacement?

A

Aortic valve replacement, AVR

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97
Q

How is acute aortic regurgitation managed?

A

Ionotropes/vasodilators and valve replacement & repair

98
Q

How is chronic asymptomatic aortic regurgitation managed?

A

If LV function = normal:

  • can be managed by drugs or reassurance
99
Q

How is chronic symptomatic aortic regurgitation managed?

A

First line - valve replacement with adjunct vasodilator therapy

100
Q

What is key in the management of aortic regurgitation?

A

Prevention is key

—–> treat rheumatic fever + infective endocarditis with proper protocols and appropriate antibiotics to prevent development of valve defects later on

101
Q

What is mitral stenosis?

A

Structural heart disease

  • Obstruction to left ventricular inflow at the level of mitral valve due to structural abnormality of the mitral valve

(Leading to reduced blood flow from atria to ventricles)

102
Q

What is the main cause of mitral stenosis in developing countries?

A

Rheumatic fever

103
Q

What can mitral stenosis lead to as the disease progresses?

A

Pulmonary hypertension —-> right heart failure

104
Q

Name at least 3 potential causes of mitral stenosis.

A

Causes inc.

  • 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
105
Q

Describe the pathophysiology of mitral stenosis.

A

Stenosis of valve typically occurs decades after the episode of acute rheumatic fever

Acute insult (or injury) leads to formation of multiple foci and infiltrates in the endocardium + myocardium and along the walls of the valves

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

106
Q

What causes exertional dyspnoea in the initial stages of mitral stenosis?

A

Initially, moderate exercise or tachycardia result in exertional dyspnoea due to increased left atrial pressure

107
Q

How can severe mitral stenosis lead to dyspnoea at rest or exertion?

A

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

108
Q

How does pulmonary hypertension develop in severe mitral stenosis?

A

Increased left atrial pressure —-> increased backflow pressure into pulmonary veins + ultimately leads to increased pressure in pulmonary vasculature

——> Transudation of fluid or increasing back pressure into pulmonary trunk:

109
Q

Why is cardiac output limited in mitral stenosis?

A

Narrowing of mitral valve

The restricted orifice limits filling of left ventricle, limiting cardiac output

110
Q

What could haemoptysis occur in severe mitral stenosis?

A

Haemoptysis could occur if bronchial vein ruptures due to increased pulmonary hypertension or increased back pressure into the pulmonary interstitium

111
Q

What is typical in a history/presentation of mitral stenosis?

A
  • H/O of rheumatic fever
  • Dyspnoea
  • Orthopnoea
  • Diastolic murmur
  • Loud P2
  • Neck vein distention
  • Haemoptysis
  • 40-50 yo
112
Q

What investigations might be carried out in a suspected case of mitral stenosis?

A
  • ECG
  • Transthoracic echocardiography
  • Chest X-Ray
  • Cardiac catheterisation
  • Cardiac MRI/CT Scan
113
Q

What is the typical management for progressive asymptomatic mitral stenosis?

A

No therapy required

114
Q

What is the typical management for severe asymptomatic mitral stenosis?

A

No therapy generally required

Adjuvant balloon valvotomy can be done

115
Q

What is the typical management for severe symptomatic mitral stenosis?

A

Diuretic

Balloon valvotomy

Valve replacement + repair adjunt

B-blockers

116
Q

What is mitral regurgitation?

A

= abnormal reversal of blood flow from the LV to the LA

= most frequent valvular heart disease

= caused by the disruption in any part of the mitral valve apparatus

117
Q

If the mitral valve is damaged, it won’t close properly/fully.

How will this affect blood flow during systole?

A

During systole, some of blood flows back into LA

—-> Increased LA pressure, etc.

118
Q

How can the causes of mitral regurgitation be categorised?

A

Acute

Chronic

119
Q

What are the main acute causes of mitral regurgitation?

A
  • Mitral valve prolapse
  • Rheumatic heart disease
  • Infective endocarditis
  • Following valvular surgery
  • Prosthetic mitral valve dysfunction
120
Q

What are the main chronic causes of mitral regurgitation?

A
  • Rheumatic heart disease
  • SLE
  • Scleroderma
  • Hypertrophic cardiomyopathy
  • Drug related
121
Q

What pathologies are associated with mitral regurgitation caused by infectious endocarditis?

A

Infectious endocarditis:

  • Abscess formation
  • Vegetations
  • Rupture of chordae tendineae
  • Leaflet perforation
122
Q

Chronic mitral regurgitation can lead to left ventricular dysfunction and increased left ventricular end-systolic diameter.

How does this happen?

A

Progression of CMR leads to eccentric hypertrophy

—-> Elongation of myocardial fibres, increased left end diastolic volume, increased preload & decreased afterload

—–> Increase in end-diastolic volume —–> and a decrease in end-systolic volume

Eventually, prolonged (V) overload leads to left ventricular dysfunction and increased left ventricular end-systolic diameter

123
Q

What is typical in a history/presentation of mitral regurgitation?

A
  • Dyspnoea
  • Murmur high
  • Fatigue
  • Orthopnoea
  • Chest pain
  • Atrial fibrillation
  • Diminished S1
  • High-pitched, blowing holosystolic murmur
124
Q

What investigations might be carried out in a suspected case of mitral regurgitation?

A
  • ECG
  • Transthoracic echocardiography
  • Chest X-Ray
  • Cardiac catheterisation
  • Cardiac MRI/CT Scan
125
Q

What is the typical management for acute mitral regurgitation?

A

Emergency surgery
Adjunct pre-operative
Diuretics
Adjunct intra-aortic balloon counterpulsation

126
Q

What is the typical management for chronic asymptomatic mitral regurgitation?

A

1st ACE inhibitors
Beta blockers

If LVEF<60% —-> 1st line = SURGERY

127
Q

What is the typical management for chronic symptomatic mitral regurgitation?

A

1st SURGERY + medical treatment

If LVEF<30% —-> 1st line = intra-aortic balloon counterpulsation

128
Q

What is cardiomyopathy?

A

Structural heart disease

A progressive disease of the heart muscle that makes it harder for heart to pump blood to rest of body

Usually irreversible, causes global systolic (contractile) dysfunction with heart failure

Among the most common causes of heart failure

129
Q

What are the 3 main types of cardiomyopathy?

A
  1. Dilated - very enlarged LV
  2. Hypertrophic - size of LV essentially reduces
  3. Restrictive - stiffness of ventricular wall
130
Q

What is the estimated prevalence of dilated cardiomyopathy?

A

1:2500

131
Q

What age groups are most commonly associated with dilated cardiomyopathy?

A

May manifest clinically at a wide range of ages

BUT most commonly occurs in the 3rd or 4th decade of life

132
Q

What can causes of dilated cardiomyopathy be categorised as?

A
  1. Familial - 25% (e.g. genetics, FHx)
  2. Primary without family history - idiopathic
  3. Secondary
133
Q

What are the main secondary causes of dilated cardiomyopathy?

A
  • Heart valve disease
  • After child birth
  • Thyroid disease
  • Myocarditis
  • Alcoholism
  • Autoimmune disorders
  • Ingestion of drugs
  • Mitochondrial disorders
134
Q

What characterises dilated cardiomyopathy?

A
  • Ventricular chamber enlargement
  • Systolic dysfunction
  • With normal left ventricular wall thickness
135
Q

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

A

Left ventricular dilatation, usually > 4cm

136
Q

Familial DCM is a genetic condition.

In rare autosomal dominant inheritance patterns (at least two family members have idiopathic DCM), what is the probability that first degree relatives will inherit the condition?

A

50% chance

137
Q

How is physiology affected in dilated cardiomyopathy?

A
  • Enlargement of LV
  • Lower EF + increase in the ventricular wall stress and ESVs

Early compensatory mechanisms inc.

  • An increase in heart rate + tone of the peripheral vascular system because of increased levels of neurohumoral activity
  • Neurohumoral activation of the RAAS + an increase in circulating levels of catecholamines
  • Levels of natriuretic peptides are also increased

Eventually, these compensatory mechanisms become overwhelmed and the heart fails

138
Q

What are the early compensatory mechanisms that occur in response to dilated cardiomyopathy?

A
  • An increase in heart rate + tone of the peripheral vascular system because of increased levels of neurohumoral activity
  • Neurohumoral activation of the RAAS + an increase in circulating levels of catecholamines
  • Levels of natriuretic peptides are also increased
139
Q

How are hormone levels affected by the compensatory mechanisms that occur in response to dilated cardiomyopathy?

A
  • Neurohumoral activation of the RAAS + an increase in circulating levels of catecholamines
  • Levels of natriuretic peptides are also increased
140
Q

As part of the early compensatory mechanisms that occur in response to DCM, levels of natriuretic peptides increase.

What is the purpose of this?

A

Helps heart contract more often to eject all blood that’s left in the ventricle because of its enlargement

141
Q

Early compensatory mechanisms occur in response to DCM. When these mechanisms get overwhelmed, heart failure can occur.

How might these mechanisms get overwhelmed?

A

Ventricles become so dilated that they can’t contract effectively (fully)

Therefore, can’t eject all blood from ventricles into aorta during each systole

Increased (v)-blood accumulated in LV over time —-> LV failure —-> overwhelming of early compensatory mechanisms

142
Q

What happens when the early compensatory mechanisms that occur in response to DCM become overwhelmed?

A

The heart fails

143
Q

What is typical in a history/presentation of dilated cardiomyopathy?

A
  • Dyspnoea
  • Murmur
  • Fatigue
  • Angina
  • Pulmonary congestion
  • Low cardiac output
  • Displaced apex beat, S3 or systolic
144
Q

What investigations might be carried out in a suspected case of dilated cardiomyopathy?

A
  • Genetic testing
  • Viral serology
  • ECG
  • Chest XR
  • Cardiac catheterisation
  • Cardiac MR/CT Scan
  • Exercise stress test
  • Echocardiography
145
Q

What are some of the main target areas for management of DCM?

A
  • Counselling
  • Diet modification
  • Treatment of underlying conditions
  • Treatment of heart failure symptoms
  • Treatment of arrhythmias (AF, SVT, VT)
  • Treatment of thromboembolic events
146
Q

Why is counselling recommended as part of DCM management?

A

Usually required because it’s a life-long condition

147
Q

What must you consider when deciding management plan for dilated cardiomyopathy?

A
  • Disease
  • Symptoms
  • Risk factors
  • Treatment + side effects
  • Exercise tolerance
  • Rehabilitation
148
Q

What is an example of diet modification for management of DCM?

A

Fluid and Na+ restriction

149
Q

What kind of options can be used to treat the underlying condition for management of DCM?

A

E.G. immunosuppressants for sarcoidosis + myocarditis

E.G. phlebotomy for haemochromatosis

150
Q

How might you treat symptoms of heart failure for management of DCM?

A
  1. ACEi, B-blockers
  2. Addition of +/- diuretics +/- angiotensin II receptor antagonists:
    - Lower dose of ACEi if patient develops cough, hypotension +/-renal dysfunction
  3. If medical treatment = ineffective:

Surgical candidate

  • LVAD*
  • Orthotopic heart transplantation

Non-surgical candidate

  • LVAD*
  • Optimise medical management
151
Q

A patient previously diagnosed with DCM has been prescribed ACEi to treat symptoms of heart failure.

Diuretics and ARBs have been added to their protocol.

If this patient develops a cough, hypotension +/ renal dysfunction, what should be done?

A

Lower dose of ACE inhibitor

152
Q

How might you treat arrhythmias for management of DCM?

A
  1. Amiodarone, Dofetilide

2. ICD or CRT

153
Q

How might you treat thrombo-embolic events in management of DCM?

A
  1. Hx previous TE, severe systolic dysfunction or ventricular dilatation
  2. Anticoagulants (warfarin)
154
Q

What is hypertrophic cardiomyopathy (HCM)?

A

Structural heart disease

HCM is a genetic cardiovascular disease

Defined by an increase in LV wall thickness that isn’t solely explained by abnormal loading conditions

155
Q

What is HCM defined by?

A

Defined by an increase in LV wall thickness that isn’t solely explained by abnormal loading conditions

156
Q

What is the leading cause of sudden cardiac death in preadolescent and adolescent children?

A

Hypertrophic cardiomyopathy (HCM)

157
Q

In what proportion of cases does familial HCM occur as an autosomal dominant Mendelian-inherited disease?

A

50%

158
Q

Most patients with HCM are asymptomatic.

Why is this an issue?

A

The first clinical manifestation of the disease in such individuals may be sudden death, likely from ventricular tachycardia or fibrillation

159
Q

What is the likely cause of sudden death in someone with HCM?

A

Likely from ventricular tachycardia or fibrillation

160
Q

What is the hallmark of HCM?

A

Inappropriate myocardial hypertrophy

  • Often asymmetrical
  • Occurs in absence of an obvious hypotrophy stimulus
161
Q

What characterises the myocardial hypertrophy that occurs in HCM?

A
  • = inappropriate
  • Often asymmetrical
  • Occurs in absence of an obvious hypotrophy stimulus
162
Q
  1. What region is frequently involved in the hypertrophy that occurs in HCM?
  2. How does hypertrophy of this region [1] affect blood flow?
A
  1. Can occur in any region BUT frequently involves interventricular septum
  2. Results in an obstruction of flow through LV outflow tract
163
Q

How is physiology abnormal in HCM?

A
  • Abnormal diastolic function
  • Abnormal calcium kinetics
  • Subendocardial ischaemia

Most patients have abnormal diastolic function
- Impairs ventricular filling & increases filling pressure, despite a normal or small ventricular cavity

These patients h/v abnormal calcium kinetics + subendocardial ischaemia
- Are related to the profound hypertrophy + myopathic process

164
Q

Most patients with HCM have abnormal diastolic function.

What is the impact of this?

A

Impairs ventricular filling & increases filling pressure, despite a normal or small ventricular cavity

165
Q

What is typical in a history/presentation of hypertrophic cardiomyopathy (HCM)?

A
  • Sudden cardiac death
  • Double carotid artery impulse, S3 gallop
  • Syncope
  • Presyncope
  • Congestive heart failure
  • Dizziness
  • Palpitations
  • Angina
  • Ejection systolic murmur
166
Q

What investigations might be carried out in a suspected case of hypertrophic cardiomyopathy (HCM)?

A

Haemoglobin level
- anaemia exacerbates chest pain + dyspnoea

Brain natriuretic peptide (BNP), troponin T levels
- elevated BNP, NT-proBNP, and troponin T levels = associated with a higher risk of cardiovascular events, heart failure + death

Echocardiography

Chest XR

Cardiac MRI

167
Q

What is associated with elevated BNP, NT-proBNP, and troponin T levels?

A

A higher risk of cardiovascular events, heart failure + death

168
Q

A patient is found to have symptomatic HCM.

What is the first line treatment?

A

Beta-blockers

169
Q

A patient is found to have symptomatic HCM.

What might prevent this patient from using B-blockers as treatment.

A
  1. Side effects with BBs

2. Non-cardiac contraindication to BBs

170
Q

A patient is found to have symptomatic HCM.

This patient was prescribe a beta-blocker but experienced unpleasant side effects and has requested a new drug.

What alternative drug choice can be prescribed in this case?

A

Verapamil

= calcium channel blocker

(also used instead of BB if patient has non-cardiac contraindication to BB)

171
Q

A patient has symptomatic HCM.

They have been prescribed a beta-blocker as there are no non-cardiac contraindications. They haven’t experienced any side effects to this dug.

(If contraindications/side effects, would have been prescribed verapamil)

However, overtime GP has become concerned with their LVOT gradient and persistent symptoms.

  1. What can be prescribed next to add to this beta-blocker (or verapamil)?
  2. What must be absent in order to prescribe this drug [1]?
A
  1. Add disopyramide

2. Must be absence of contraindication to disopyramide (this has to be true AND LVOT gradient AND persistent symptoms)

172
Q

A patient has symptomatic HCM.

They have been prescribed a beta-blocker as there are no non-cardiac contraindications. They haven’t experienced any side effects to this dug.

(If contraindications/side effects, would have been prescribed verapamil)

Their GP is now considering adding disopyramide to their prescription.

Why might this be so?

A

Because of LVOT gradient & persistent symptoms & absence of contraindication to disopyramide

173
Q

A patient has symptomatic HCM.

  1. Beta blocker or verapamil
  2. Add disopyramide

This patient is showing signs of refractory symptoms.

What is the next step in their management?

A

Next step = mechanical therapy

174
Q

A patient has symptomatic HCM.

Previous prescriptions:
1. Beta blocker (or verapamil)

  1. Add disopyramide

Next appointment:
- Dr suggests mechanical therapy.

Why might this be?

A

Patient showing refractory symptoms

175
Q

A patient with symptomatic HCM is being prescribed mechanical therapy.

  1. What are the two main options?
  2. What are the requirements for being eligible for these options?
A
  1. PM with short AV delay
    - Existing PM or contraindication to more invasive management
  2. Septal myectomy or ablation
    - Might change from [1] to [2] if refractory symptoms and NO contraindication to more invasive management
176
Q

What is the general order of the flow diagram for management of symptomatic HCM?

A
  1. B-blocker or verapmil
  2. Add disopyramide
  3. Mechanical therapy
    - PM with short AV delay, or
    - Septal myectomy or ablation
177
Q

What is restrictive cardiomyopathy characterised by?

A

Characterised by diastolic dysfunction with restrictive ventricular physiology

178
Q

Why is restrictive cardiomyopathy a less well-defined cardiomyopathy?

A

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

179
Q

What causes atrial enlargement in restrictive cardiomyopathy?

A

Atrial enlargement occurs due to impaired ventricular filling during diastole

180
Q

How are the ventricles typically affected in restrictive cardiomyopathy?

A

Volume and wall thickness of ventricles usually normal

—–> normal ventricle size/shape + normal contraction BUT stiff muscle

181
Q

What proportion of all cases of diagnosed cardiomyopathies are cases of RCM?

A

5%

182
Q

How can the causes of RCM be categorised?

A
  1. Idiopathic
  2. Familial, e.g.
    - has been related to troponin I or desmin mutations
    - desmin mutations often in associated with a skeletal myopathy
  3. Associated with various systemic disorders, e.g.
  • haemochromatosis
  • amyloidosis
  • Fabry’s disease
  • carcinoid syndrome
  • scleroderma
  • anthracycline toxicity
  1. Associated with previous radiation
183
Q

Describe the pathophysiology of RCM.

A

Increased stiffness of myocardium
- due to familial or other secondary causes, e.g. amyloidosis

Infiltrative cardiomyopathy
- characterised by deposition of abnormal substances w/in heart tissue

  • infiltration causes ventricular walls to stiffen —-> diastolic dysfunction

Restrictive physiology

  • predominated in ealy stages
  • causing conduction abnormalities + diastolic heart failure

Adverse remodelling
- may lead to systolic dysfunction + ventricular arrhythmias in advanced cases

184
Q

What are infiltrative cardiomyopathies characterised by?

A

Characterised by deposition of abnormal substances (i.e. amyloid proteins, non-caseating granulomas, iron) within the heart tissure

185
Q

How does infiltration of the heart tissue affect the ventricles in RCM?

A

Infiltration causes ventricular walls to stiffen —-> diastolic dysfunction

186
Q

In advanced cases of RCM, what can adverse remodelling lead to?

A

Systolic dysfunction + ventricular arrhythmias

187
Q

Give an example of a substance that could infiltrate the heart tissue in RCM.

A

E.G.

  • Amyloid proteins
  • Non-caseating granulomas
  • Iron
188
Q

How is physiology abnormal in RCM?

A

Increased myocardium stiffness

189
Q

How is physiology abnormal in RCM?

A

Increased myocardium stiffness
- causes ventricular pressures to rise precipitously w/ 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 LV cannot fill adequately at normal filling pressures

Reduced LV filling volume leads to reduced cardiac output

190
Q

How does increased myocardium stiffness affect ventricular pressure and volume in RCM?

What is the impact of this?

A

Causes ventricular pressures to rise precipitously w/ small increases in volume

Thus, accentuated filling occurs in early diastole and terminates abruptly at the end of the rapid filling phase

191
Q

How is compliance of heart typically affected in RCM?

What is the impact of this?

A

Patients typically have reduced compliance (increased diastolic stiffness)

LV cannot fill adequately at normal filling pressures

192
Q

What ultimately leads to a reduced cardiac output in RCM?

A

Reduced left ventricular filling volume

(Reduced volume occurs as LV cannot fill adequately at normal filling pressures due to reduced compliance (increased diastolic stiffness))

193
Q

What is typical in a history/presentation of restrictive cardiomyopathy (RCM)?

A

May be more comfortable in sitting position because of fluid in the abdomen or lungs

Frequently h/v ascites + pitting oedema of lower extremities

Liver usually enlarged + full of fluid - ?be painful

Weight loss + cardiac cachexia not uncommon

Easy bruising, Peri-orbital purpura, Macroglossia & Other systemic findings, e.g. carpal tunnel syndrome, should = indication for the clinician to consider amyloidosis

Increased JVP

Pulse volume is decreased - consistent with decreased SV and CO

194
Q

What investigations might be carried out in a suspected case of restrictive cardiomyopathy (RCM)?

A
  • CBC
  • Serology
  • Amyloidosis check
  • Chest XR
  • ECG
  • Echocardiography
  • Catheterisation
  • MRI/Biopsy
195
Q

What are the usual treatment options for management of restrictive cardiomyopathy (RCM)?

A
  1. Heart failure medication

Guideline-directed medical therapy for heart failure, inc.

  • ACE inhibitors
  • ARBs
  • Diuretics
  • Aldosterone inhibitors

Should be initiated in patients with reduced LV.

  1. Anti-arrhythmic therapy
  2. Immunosuppression - steroids
  3. Pacemaker ( - if heart is beginning to fail and there are multiple conduction abnormalities)
  4. Cardiac transplantation
196
Q

Why might a patient with RCM be more comfortable in the sitting position?

A

Because of fluid in the abdomen or lungs

197
Q

How is the liver usually affected in RCM?

A

Hepatomegaly, full of fluid

?be painful

198
Q

What should be an indication for the clinician to consider amyloidosis when examining a patient with suspected restrictive cardiomyopathy (RCM)?

A

Easy bruising
Peri-orbital purpura
Macroglossia
Other systemic findings, e.g. carpal tunnel syndrome

  • should = indication for clinician to consider amyloidosis
199
Q

A patient with suspected restrictive cardiomyopathy (RCM) has a decreased pulse volume.

What is this consistent with?

A

Consistent with decreased stroke volume + cardiac output

200
Q

A patient with RCM has a reduced LV.

What should be initiated in this patient?

A

Guideline-directed medical therapy for heart failure, inc.

  • ACE inhibitors
  • ARBs
  • Diuretics
  • Aldosterone inhibitors
201
Q

What type of medications are included in guideline-directed medical therapy?

A
  • ACE inhibitors
  • ARBs (angiotensin receptor II blockers)
  • Diuretics
  • Aldosterone inhibitors
202
Q

How do you calculate cardiac output?

A

CO = heart rate (HR) x stroke volume (SV)

SV = EDV - ESV

203
Q

What is cardiac output?

A

The volume of blood the heart pumps in 1 min

Frequently given in L/min (but can also be given as cm^3/min)

204
Q

What are the usual units given for cardiac output?

A

Frequently given in L/min (but can also be given as cm^3/min)

205
Q

How do you calculate the ejection fraction?

A

EF = (SV/EDV) x 100

206
Q

What is the ejection fraction?

A

The volumetric fraction of blood ejected by the ventricle with each contraction

207
Q

What units are commonly given for ejection fraction?

A

Commonly given as a % (hence multiplication by 100 in formula for EF)

208
Q

How do you calculate mean arterial pressure?

A

MAP = (Cardiac output x Systemic vascular resistance) + Central venous pressure

MAP = (CO X SVR) + CVP

OR

At normal resting heart rates:

MAP = Diastolic pressure + 1/3(Systolic pressure - Diastolic pressure)

MAP = DP + 1/3(SP - DP)

209
Q

How can you estimate mean arterial pressure (MAP) at normal resting heart rates?

A

At normal resting heart rates can estimate MAP using systolic and diastolic pressures:

MAP = DP + 1/3(SP - DP)

210
Q

What is the mean arterial pressure?

A

MAP is an average arterial blood pressure throughout a single cardiac cycle of systole and diastole

211
Q

What does a MAP >65 mmHg represent, in health?

A

Represents the pressure necessary to adequately perfuse the body organs

212
Q

How does the estimation of mean arterial pressure change with different levels of activity?

(i.e. at rest vs during exertion)

A

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

213
Q

Calculate MAP, SV, CO and EF for the following case:

60 yo man

Presented with shortness of breath to A+E

Idea/diagnosis:
- was in type 2 respiratory failure secondary to an infectious exacerbation of COPD

Plan/Actions:

  • Needed intensive care support
  • Had more invasive monitoring
  • A Swan-Ganz catheter was inserted, which measured end diastolic volume as 142ml and end systolic volume as 47 ml.

Observations
- patient was intubated and ventilated using BiPAP of 20/5 with saturations of 95 percent, heart rate 75 beats per minute, respiratory rate 12/minute, blood pressure 115/75mmHg and Temperature 36.5 degrees Celsius.

Work out the mean arterial blood pressure, stroke volume, cardiac output and ejection fraction.

A 
MAP = DP + 1/3(SP - DP)
MAP = 75 + 1/3(115 - 75)
MAP = 88.3 mmHg
SV = EDV - ESV
SV = 142 - 47
SV = 95 ml
CO = HR x SV
CP = 75 x 95
CO = 7125ml/min or 7.125 L/min
EF = (SV/EDV) x 100
EF = (95/142) x 100
EF = 66.9%
214
Q

21yo man presents to A&E with pyrexia of unknown origin

PMH - nothing of note
- apart from being a known intravenous heroin user

O/E

  • HR = 115bpm
  • BP = 90/60 mmHg
  • Temp = 39oC
  • RR = 17 per min
  • Sats = 99% on air
  • Ausc: early diastolic murmur in left sternal edge which is loudest with the patient sitting forward and at end expiration
  • Feet: cellulitis of his distal right leg w/ a deep penetrating ulcer

What is the most likely diagnosis?

A

Infective endocarditis

215
Q

What is infective endocarditis?

A

An infection of the endocardium or vascular endothelium of the heart

ENDO - inner lining
CARD - heart
ITIS - inflammation

216
Q

What type of pathogen is usually the cause of infective endocarditis?

A

Bacteria

IE is typically due to bacteria entering bloodstream + forming a “vegetation” in the endocardium

Streptococci (20-40% of cases) = most common infection

217
Q

How do you diagnose infective endocarditis?

A
  • Fever, malaise, sweats and unexplained weight loss are common symptoms
  • May be a new heart murmur o/e
  • Blood tests: anaemia, raised inflammatory markers
  • Blood cultures: may isolate a micro-organism
  • Echo: can show a vegetation, abscess, valve perforation +/ new dehiscence of prosthetic valve
  • Echo: often there is regurgitation of the affected valve
  • Trans-oesophageal echo: has higher sensitivity vs transthoracic
  • LOOK AT DUKE’S CRITERIA
218
Q

According to Duke’s criteria, what is the major criteria for diagnosing infective endocarditis?

A
  1. Persistently +ve blood culture for typical organisms
  2. ECHO: vegetation, dehiscence of prosthetic valve, abscess
  3. New valvular regurgitation murmur
  4. Coxiella burnetti infection
219
Q

According to Duke’s criteria, what is the minor criteria for diagnosing infective endocarditis?

A
  1. Predisposing heart condition or IV drug use
  2. Fever >38C
  3. Vascular: emboli to organs, brain
  4. Immunologic: glomerulonephritis, Oslers nodes, Roth spots
  5. +ve blood cultures that do not meet specific criteria
220
Q

According to Duke’s criteria, what is required for a definite diagnosis of endocarditis?

A
  • 2 major clinical criteria
  • 1 major + any 3 minor clinical criteria
  • 5 minor criteria
  • (+ve)gram stain or culture from surgery or autopsy
221
Q

According to Duke’s criteria, what is suggestive of possible endocarditis?

A
  • 1 major and >1 minor clinical criteria

- 3 minor criteria

222
Q

According to Duke’s criteria, what rejects a diagnosis of endocarditis?

A
  • Resolution after <4 days antibiotic treatment
  • No evidence of infection after surgery
  • Definite or possible criteria not met
223
Q

In a patient with infective endocarditis, what features of heart decompensation would you look for?

A

Symptoms inc.

  • shortness of breath
  • frequent coughing
  • swelling of legs + abdomen
  • fatigue

Clinical signs inc.

  • raised JVP
  • lung crackes
  • oedema
224
Q

What part of the heart does infective endocarditis affect?

Explain why.

A

IE affects endocardium, especially the valves of the heart

IE involves formation of a vegetation at the valves. Vegetation’s are bacterial infections surrounded by platelets and fibrin.

It’s 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

225
Q

What valve is affected most frequently in infective endocarditis?

A

Aortic valve is affected most frequently

Aortic > mitral > right-sided valves

226
Q

When is it more common for bacteria to attach to the endocardium?

A

When there is underlying damage present

227
Q

Why are intravenous drug users at increased risk of infective endocarditis?

A

Due to repeated injection - potentially exposing their bloodstream to bacteria on the surface of the skin or use of non-sterile needles

Entry of bacteria into bloodstream = first step of IE

228
Q

What is the first and critical step in infective endocarditis?

A

Entry of bacteria into bloodstream

229
Q

Infective endocarditis can be a complication of what kind of procedures?

A

Routine surgeries, e.g. dental surgery

230
Q

For which individuals is infective endocarditis more common?

A
  • IV drug users
  • Immunosuppressed individuals
  • Individuals with congenital heart defects (leading to damaged endocardium)
  • Those undergoing routine surgeries
231
Q

25yo man

Presentation

  • Palpitations
  • Syncope episodes

Investigations
- He has a 24gr Holter monitor: showed that patient was in fast atrial fibrillation for up to 6hrs in the 24hr recording

  • TT echo: showed hypokinesia in the inferolateral walls
  • Cardiac MRI: confirmed diagnosis of dilated cardiomyopathy (DCM)

What is the definition of dilated cardiomyopathy?

A

Structural heart disease

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

232
Q

In DCM, how does the dilation of the chambers of the heart affect contractility?

A

Leads to reduced contractility

233
Q

What are the typical Echo findings in DCM?

A
  • Dilated left ventricle
  • Reduced systolic function (ejection fraction)
  • Global hypokinesis (typically)
234
Q

25yo man

Presentation

  • Palpitations
  • Syncope episodes

Investigations
- He has a 24gr Holter monitor: showed that patient was in fast atrial fibrillation for up to 6hrs in the 24hr recording

  • TT echo: showed hypokinesia in the inferolateral walls
  • Cardiac MRI: confirmed diagnosis of dilated cardiomyopathy (DCM)

What is the definition of dilated cardiomyopathy?

A

Structural heart disease

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

235
Q

25yo man

Presentation

  • Palpitations
  • Syncope episodes

Investigations
- He has a 24gr Holter monitor: showed that patient was in fast atrial fibrillation for up to 6hrs in the 24hr recording

  • TT echo: showed hypokinesia in the inferolateral walls
  • Cardiac MRI: confirmed diagnosis of dilated cardiomyopathy (DCM)

What are the most common causes of dilated cardiomyopathy?

A

Idiopathic

Genetic

Toxins:

  • alcohol
  • cardiotoxic chemotherapy

Pregnancy
- peripartum cardiomyopathy

Viral infections
- myocarditis

Tachycardia-related cardiomyopathy

Thyroid disease

Muscular dystrophies

236
Q

25yo man

Presentation

  • Palpitations
  • Syncope episodes

Investigations
- He has a 24gr Holter monitor: showed that patient was in fast atrial fibrillation for up to 6hrs in the 24hr recording

  • TT echo: showed hypokinesia in the inferolateral walls
  • Cardiac MRI: confirmed diagnosis of dilated cardiomyopathy (DCM)

How is dilated cardiomyopathy managed?

A

Medical heart failure therapy:

  • ACE inhibitors
  • Beta-blockers
  • Mineralcorticoid receptor antagonists

Diuretics - for fluid overload

Anticoagulation - for atrial fibrillation

Cardiac devices:

  • cardiac resynchronisation therapy
  • and/or implantable cardioverter defribrillator (ICD) transplant
237
Q

25yo man

Presentation

  • Palpitations
  • Syncope episodes

Investigations
- He has a 24gr Holter monitor: showed that patient was in fast atrial fibrillation for up to 6hrs in the 24hr recording

  • TT echo: showed hypokinesia in the inferolateral walls
  • Cardiac MRI: confirmed diagnosis of dilated cardiomyopathy (DCM)

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

A

At risk of…

  • Heart failure
  • Hospitilisation
  • Cardiac arrhythmias
  • Sudden cardiac death due to ventricular arrhythmia
  • Reduced survival
238
Q

A number of genes have been associated with DCM.

  1. These associations have frequently been found in genes essential for what processes?
  2. These genes affect what 2 structures?
A

Frequently in genes essential for the formation or effective contraction of heart chambers

Thus either effect myofibril or cellular structure

239
Q

A number of genes have been associated with DCM.

  1. These associations have frequently been found in genes essential for what processes?
  2. These genes affect what 2 structures?
A

Frequently in genes essential for the formation or effective contraction of heart chambers

Thus either effect myofibril or cellular structure

240
Q

A number of genes have been associated with DCM, including mutations in genes encoding specific proteins.

What proteins do these genes encode?

A

Genes encoding cardiac cytoskeletal proteins

241
Q

A number of genes have been associated with DCM, including mutations in genes encoding specific proteins.

What proteins do these genes encode?

A

Genes encoding cardiac cytoskeletal proteins

242
Q

A number of genes have been associated with DCM, including mutations in genes encoding cardiac cytoskeletal proteins.

Name 2 cardiac cytoskeletal proteins.

A

E.G.

  • Titin
  • Lamin
  • Phospholamban
  • Cardiac myosin binding protein C
  • Myosin heavy chain

BRS2 - Cardiovascular & Respiratory Medicine (4 decks)

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