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Phase 2a > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

What can ECG’s identify?

A
  • Arrhythmias
  • Myocardial ischaemia & MI
  • Pericarditis
  • Chamber hypertrophy
  • Electrolyte disturbances (hyperkalemia/hypokalemia)
  • Drug toxicity
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2
Q

What is the intrinsic rate of the SA node? (main pacemaker)

A

60-100 bpm

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3
Q

What is the intrinsic rate of the AV node? (back up pacemaker)

A

40-60 bpm

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4
Q

What is the intrinsic rate of ventricular cells? (back up pacemaker)

A

20-45 bpm

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5
Q

P wave

A

Atrial depolarisation

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6
Q

What leads are the P wave seen in?

A

All leads except aVR

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7
Q

What does PR interval represent?

A
  • Time taken for atria to depolarise

- Time for electrical activation to get though AV node

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8
Q

QRS complex

A

Ventricular depolarisation

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9
Q

ST segment

A

Interval between depolarisation and repolarisation

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10
Q

T wave

A

Ventricular repolarisation

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11
Q

When does atrial repolarisation occur?

A

During the QRS

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12
Q

What is tachycardia?

A

Increased heart rate

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13
Q

What is bradycardia?

A

Decreased heart rate

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14
Q

What is dextrocardia?

A

Heart is on the right side of the chest

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15
Q

How long does atrial depolarisation last?

A

0.08-0.1s

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16
Q

How long does ventricular depolarisation last? (QRS)

A

0.06-0.1s

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17
Q

How long does one small box on the ECG represent?

A

40ms

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18
Q

How long does one large box on the ECG represent?

A

200ms

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19
Q

What does the first heart sound mean? (S1)

A

Mitral and tricuspid valve closing

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20
Q

What does the second heart sound mean? (S2)

A

Aortic and pulmonary valve closing

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21
Q

What does the third heart sound mean?

A
  • Early diastole

- rapid ventricular filling

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22
Q

What is the third heart sound associated with?

A

Mitral regurgitation / heart failure

normal in children/pregnant women

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23
Q

What does the fourth heart sound mean?

A

GALLOP

  • Late diastole
  • Blood is being forced into a stiff HYPERTROPHIC ventricle
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24
Q

What is the fourth heart sound associated with?

A

Left ventricular hypertrophy

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25
Q

Which arteries most commonly develop atherogenesis?

A

1) LAD
2) Right coronary arteries
3) Circumflex

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26
Q

Risk factors for atherosclerosis

A 
Age
Tobacco
High serum cholesterol
Obesity
Diabetes
Hypertension
Family history
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27
Q

Where are atherosclerosis plaques distributed?

A
  • Peripheral arteries
  • Coronary arteries
  • Focal distribution along artery length
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28
Q

The structure of an atherosclerotic plaque ?

A
  • Lipid
  • Necrotic Core
  • Connective tissue
  • Fibrous cap
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29
Q

What initiates atherosclerosis formation?

A

Injury to the endothelial cells

- leads to endothelial dysfunction

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30
Q

What happens after endothelial cells are injured?

A
  • Chemoattractants released
  • Attract leukocytes
  • Accumulate & migrate into vessel wall
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31
Q

Which inflammatory cytokines are found in plaques?

A

1) IL-1
2) IL-6
3) IFN (interferon)- gamma

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32
Q

Whats the earliest lesion of atherosclerosis?

A

Fatty streaks

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33
Q

When do fatty streaks present/

A

Less than 10 years old

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34
Q

What do fatty streaks consists of?

A
  • Aggregations of lipid-laden macrophages

- T lymphocytes - within intimal layer

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35
Q

What do intermediate lesions consist of?

A
  • Lipid laden macrophages (foam cells)
  • Vascular smooth cells
  • T lymphocytes
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36
Q

What are foam cells?

A

Macrophages that have taken up lots of lipids

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37
Q

What is happening in intermediate lesions?

A

Adhesion & aggregation of platelets to the vessel wall

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38
Q

Describe advanced lesions/fibrous plaques

A
  • Impeded blood flow
  • Prone to rupture
  • Covered by dense fibrous cap
  • May be calcified
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39
Q

What is a fibrous cap made up of?

A

Extracellular matrix proteins

e. g collagen & elastin
- laid down by smooth muscle cells (overlie lipid core & necrotic debris)

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40
Q

What do advanced lesions/fibrous plaques contains?

A
  • Smooth muscle cells
  • Macrophages & foam cells
  • T lymphocytes
  • Red cells
    (filled with fibrin)
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41
Q

Why does a plaque rupture?

A

If balance shifts - increased inflammatory conditions/enzyme activity
= cap becomes weak
= plaque ruptures

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42
Q

How is the fibrous cap maintained?

A

Needs to be resorbed and redeposited

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43
Q

What is angina?

A

Chest pain or discomfort as a result of reversible myocardial ischaemia

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44
Q

What are the types of angina?

A

1) Stable
2) Unstable (crescendo)
3) Prinzmetal’s angina

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45
Q

Describe stable angina

A
  • Induced by effort

- Relieved by stress

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46
Q

Describe unstable angina

A
  • Angina of recent onset (less than 24 hours)
  • Deterioration in previously stable angina
  • Symptoms frequently occur at rest
  • Increasing freq/severity
  • Occurs on minimal exertion/at rest
  • Form of acute coronary syndrome
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47
Q

What causes Prinzmetal’s angina?

A

Caused by coronary artery spasm

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48
Q

Why does myocardial ischaemia result in angina?

A

Mismatch between blood supply & metabolic demand

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49
Q

What can cause mismatch of blood supply & metabolic demand?

A
  • Atheroma/stenosis of coronary arteries
  • Valvular disease
  • Aortic stenosis
  • Arrhythmia
  • Anaemia (less O2 transported)
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50
Q

What are precipitants ?

A

Anything that increases metabolic demand & decreases blood supply

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51
Q

What can decrease blood supply?

A

1) Anaemia
2) Hypoxemia
3) Hypothermia
etc

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52
Q

What can increase metabolic demand?

A

1) Hyperparathyroidism
2) Cold weather
3) Hypertension
4) Emotional distress
5) Valvular disease

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53
Q

What are the 2 types of diagnostic tests that can determine angina?

A

1) Anatomical

2) Physiological

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54
Q

Examples of anatomical tests for angina

A

CT/invasive angiography

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55
Q

What info does CT angiography produce?

A
  • High negative predictive value (good for ruling out CAD)

- Low positive predictive value (difficult to interpret results)

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56
Q

What is CT angiography useful for?

A

Ruling out CAD in younger, lower risk patients

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57
Q

Examples of physiological tests for angina?

A

1) Treadmill test/ exercise
2) SPECT
3) Stress echo/cardiac MRI (same principle)

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58
Q

How does the treadmill test work?

A
  • ECG on patient
  • patient runs uphill on treadmill in increasing increments
  • tries to induce ischaemia
  • monitor length of time patient can exercise for
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59
Q

What do you look for in a treadmill test & what does it mean?

A

ST elevation = late stage ischaemia

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60
Q

Disadvantages of treadmill test

A

Most patients are unsuitable

E.G: can’t walk/exercise, are unfit, have bundle branch block

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61
Q

How does SPECT/myoview work?

A
  • radio-labelled tracer injected
  • taken up by coronary arteries (due to good blood supply)
  • lights up
    NO LIGHT AFTER EXERCISE = MYOCARDIAL ISCHAEMIA
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62
Q

How does CT scan calcium scoring work?

A

If there is atherosclerosis in arteries = calcium appears white
- significant calcium = angina

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63
Q

How to treat angina/CAD

A

1) Modify risk factors
- stop smoking
- encourage exercise
- weight loss
2) Treat underlying conditions
3) Pharmacological

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64
Q

What are the pharmacological treatments of CAD/angina?

A

1) Aspirin
2) Statins
3) Betablockers
4) GTN spray
5) Ca2+ channel antagonists/blockers
6) Revascularisation

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65
Q

What does aspirin do?

A
  • antiplatelet effect in coronary arteries - avoids platelet thrombosis
  • COX1 inhibitor - reduces prostaglandin synthesis & thromboxane A2 = reduced platelet aggregation
  • reduces events
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66
Q

What are the side effects of aspirin?

A
  • gastric ulcerations

- excessive bleeding

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67
Q

How do statins work?

A
  • HMG-CoA reductase inhibitors = reduces cholesterol produced by liver
  • reduce events
  • reduce LDL
  • anti-atherosclerotic
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68
Q

How do beta blockers work?

FIRST LINE ANTIANGINAL

A
  • reduce force of contraction of heart - contractility
  • reduces HR & CO
  • reduce work of heart & O2 demand
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69
Q

Examples of beta blockers

A

Bisoprolol

Atenolol

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70
Q

Side effects of beta blockers

A
  • tiredness
  • nightmares
  • bradycardia
  • erectile dysfunction
  • cold hands & feet
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71
Q

When should you not give beta blockers?

A
  • asthma
  • heart failure/block
  • hypotension
  • bradyarrhythmias
  • low heart rate
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72
Q

How does GTN spray work?

FIRST LINE ANTIANGINAL

A
  • nitrate is a primary venodilator
  • dilates systemic veins = reduces venous return to right heart
  • reduces preload
  • reduces work of heart & O2 demand
  • dilated coronary arteries
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73
Q

What is the side effect of GTN?

A

Headache immediately after use

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74
Q

How to Ca2+ channel antagonists/blockers?

A
  • primary arterodilators
  • dilates systemic arteries = BP drops
  • reduces afterload
  • less energy required to produce same CO
  • less work & O2 demand
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75
Q

Example of Ca2+ channel blocker

A

Verapamil

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76
Q

What is revascularisation?

A
  • restore patent coronary artery

- increase flow reserve

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77
Q

When is revascularisation done?

A
  • when medication fails

- when high risk disease is identified

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78
Q

What are the types of revascularisation?

A

1) PCI - Percutaneous Coronary Intervention

2) CABG - Coronary Artery Bypass Graft

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79
Q

What does PCI do?

A
  • dilates coronary atheromatous obstructions
  • stent - keps artery patent
  • expanding plaque - makes artery bigger
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80
Q

What are the pros of PCI?

A
  • less invasive
  • convenient
  • short recovery
  • repeatable
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81
Q

What are the cons of PCI?

A
  • risk of stent thrombosis

- not good for complex disease

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82
Q

What is CABG? (procedure)

A

LIMA (left internal mammary artery) used to bypass proximal stenosis in LAD

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83
Q

What are the pros of CABG?

A
  • good prognosis

- deals with complex disease

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84
Q

What are the cons of CABG?

A
  • invasive
  • risk of stroke/bleeding
  • one time treatment
  • long recovery
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85
Q

What is the clinical presentation of angina?

A
  • central chest tightness/heaviness
  • provoked by exertion - after a meal / cold weather / anger / excitement
  • relieved by rest/GTN
  • radiating pain (arm/s, jaw, neck, teeth)
  • dyspnoea, nausea, sweaty, faintness
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86
Q

What is the scoring criteria for angina?

A
  1. Central, tight, radiation
  2. Precipitated by exertion
  3. Relieved by rest/GTN
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87
Q

What does a 3/3 score for angina mean?

A

Typical angina

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88
Q

What does a 2/3 score for angina mean?

A

Atypical angina

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89
Q

What does a 1/3 score for angina mean?

A

Non-anginal pain

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90
Q

Differential diagnosis of angina

A
  • pericarditis/myocarditis
  • pulmonary embolism
  • chest infection
  • dissection of aorta
  • GORD
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91
Q

Acute Coronary Syndrome (ACS)

A

Umbrella term including STEMI, non-STEMI, unstable angina

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92
Q

What causes STEMI?

A
  • complete occlusion of MAJOR coronary artery

= full thickness damage of heart muscle

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93
Q

How can STEMI be diagnosed?

A
  • ECG
  • pathological Q wave some time after MI
  • ST elevation
  • Tall T waves / T wave inversion
  • LBBB
    A.K.A –> Q wave infarction
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94
Q

What causes non-STEMI

A
  • complete occlusion of MINOR coronary artery

- partial thickness damage of heart muscle

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95
Q

What kind of diagnosis is non-STEMI?

A

Retrospective (made after troponin level results)

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96
Q

How can non-STEMI be diagnosed?

A 
- troponin levels
ECG:
- ST depression
- T wave inversion 
A.K.A --> non-Q wave infarction
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97
Q

Difference between unstable angina (UA) and non-STEMI

A

IN NON-STEMI:
There is an occluding thrombus which leads to:
- rise in serum troponin
- rise in creatine kinase-MB

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98
Q

How many types of MI are there?

A

5

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99
Q

Type 1 MI

A
  • spontaneous with ischaemia

- due to primary coronary event

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100
Q

Examples of type 1 MI

A
  • plaque erosion/rupture
  • fissuring
  • dissection
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101
Q

Type 2 MI

A
  • secondary to ischaemia

- due to increased O2 demand/ decreased supply

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102
Q

Examples of type 2 MI

A
  • coronary spasm
  • coronary embolism
  • anaemia
  • arrhythmias
  • hypertension
  • hypotension
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103
Q

Type 3,4,5 MI

A
  • due to sudden cardiac arrest

- related to PCI & CABG

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104
Q

Risk factors for MI

A
  1. Age
  2. Male
  3. Family history of IHD - MI in first degree relative below 55
  4. Smoking
  5. Hypertension/ diabetes / hyperlipidaemia
  6. Obesity/sedentary lifestyle
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105
Q

What are the basic steps leading to an MI?

A

Fatty streak > fibrotic plaque > atherosclerotic plaque > plaque rupture/fissure & thrombosis > MI/ Ischaemic stroke/ Sudden CVS death

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106
Q

What is the triggering cause of MI?

A

Rupture or erosion of fibrous cap of coronary artery plaque

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107
Q

What does rupture/erosion of plaque lead to?

A
  • platelet aggregation
  • adhesion
  • localised thrombosis
  • vasoconstriction
  • distal thrombus embolisation
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108
Q

What is associated with a high risk of rupture?

A
  • presence of rich lipid pool within plaque

- thin, fibrous cap

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109
Q

What causes thrombus formation / vasoconstriction?

A

Release of serotonin & thromboxane A2

reduce coronary blood flow = so leads to MI

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110
Q

When does the thrombus result in partial occlusion?

A

In unstable angina

  • plaque has necrotic core
  • plaque has ulcerated cap
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111
Q

When does the thrombus result in total occlusion?

A

In MI

- plaque has necrotic core

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112
Q

Clinical presentation of MI

A
  • unstable angina
  • new onset angina
  • acute central chest pain >20 mins
  • may present without chest pain - SILENT INFARCT (elderly/diabetics)
  • distress/anxiety
  • pallor
  • increased pulse/ reduced BP
  • reduced 4th heart sound
  • tachy/bradycardia
  • peripheral oedema
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113
Q

What is unstable angina associated with?

A
  • breathlessness
  • pleuritic pain
  • indigestion
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114
Q

What is acute central chest pain associated with?

A
  • sweating/nausea/vomitting
  • dyspnoea
  • fatigue
  • palpitations
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115
Q

What are the differential diagnoses of MI?

A
  • angina
  • pericarditis
  • myocarditis
  • aortic dissection
  • pulmonary embolism
  • gastro-oesophageal reflux/spasm
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116
Q

What are the biochemical markers of MI?

A
  1. Troponin (T & I)
  2. CK-MB
  3. Myoglobin
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117
Q

What is the pattern of troponin (T & I) levels in MI?

A
  • serum levels increase 3-12 hours from onset of pain
  • levels peak at 24-48 hours
  • back to normal over 5-14 days
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118
Q

When do troponin levels peak?

A

24-48 hours after MI

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119
Q

When do troponin levels fall back to normal?

A

5-14 days

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120
Q

What is CK-MB a marker for? What does it determine?

A

Myocyte death

- determines re-infarction

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121
Q

When do levels of CK-MB drop back to normal?

A

After 36-72 hours

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122
Q

Why does CK-MB have low accuracy?

A
  • present in serum of normal patients/ patients with significant skeletal muscle damage
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123
Q

What happens to myoglobin levels during MI?

A

Becomes elevated very early in MI

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124
Q

What is the problem with myoglobin as a marker and why?

A
  • poor specificity

- present in skeletal muscle

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125
Q

What do you look for in a chest x-ray (CXR) when diagnosis MI?

A
  • cardiomegaly
  • pulmonary oedema
  • widened mediastinum (aortic rupture)
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126
Q

Treatment for MI?

A
  1. Pain relief
    - GTN
    - IV opioid
  2. Anti-emetic - stops nausea
  3. Oxygen
  4. Aspirin
  5. P2Y12 inhibitors
  6. Glycoprotein IIb/IIIa antagonists
  7. Beta blockers
  8. Statins
  9. ACE inhibitors
  10. Coronary revascularisation
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127
Q

What is the % O2 saturation we should aim for when treating MI?

A

94-98%

88-92& for COPD

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128
Q

Route of administration for aspirin?

A

Oral

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129
Q

Route of administration for P2Y12 inhibitors?

A

Oral

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130
Q

Examples of P2Y12 inhibitors?

A
  • Clopidogrel
  • Prasugrel
  • Ticagrelor
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131
Q

Side effects of P2Y12 inhibitors?

A
  • Neutropenia (low neutrophils)
  • Thrombocytopenia (low platelets)
  • Increased risk of bleeding
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132
Q

Route of administration for GP IIb/IIIa inhibitors?

A

ONLY IV

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133
Q

Examples of GP IIb/IIIa inhibitors?

A
  • Abciximab
  • Tirofiban
  • Eptifbatide
    RISK OF BLEEDING
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134
Q

Route of administration for beta blockers?

A

Oral and IV

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135
Q

What is the route of administration for statins?

A

Oral

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136
Q

Examples of statins?

A
  • Simvastatin
  • Pravastatin
  • Atorvastin
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137
Q

Route of administration for ACE inhibitors?

A

Oral

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138
Q

Examples of ACE inhibitors?

A
  • Ramipril

- Lisonopril

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139
Q

Define acute myocardial infarction

A

Necrosis of cardiac tissue due to prolonged myocardial ischaemia due to complete occlusion of artery by thrombus

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140
Q

ECG change if infarct site is on the anterior side?

A

ST elevation in V1-V3

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141
Q

ECG change if infarct site is on the inferior side?

A

ST elevation II, III, aVF

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142
Q

ECG change if infarct site is on the lateral side?

A
  • I
  • aVL
  • V5-V6
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143
Q

ECG change if infarct site is on the posterior side?

A
  • ST depression V1-V3
  • Dominant R wave
  • ST elevation V5-V6
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144
Q

ECG change if infarct site is on the subendocardial side?

A

Any

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145
Q

Pre-hospital treatment of MI?

A
  • 300mg chewable aspirin
  • morphine
  • GTN spray
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146
Q

Hospital treatment of MI?

A
  • IV morphine
  • oxygen if sats are <95%
  • beta blocker (atenolol)
  • P2Y12 inhibitor (clopidogrel)
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147
Q

What does fibrinolysis treatment of MI do?

A

Enhance breakdown of occlusive thromboses

- by activation of plasminogen - to form plasmin

148
Q

Define cardiac failure

A

The inability of the heart to deliver blood and thus O2 at a rate that is commensurate with the requirement of metabolising tissue of the body

149
Q

Main causes of cardiac failure?

A
  1. IHD
  2. Cardiomyopathy
  3. Valvular heart disease
  4. Cor pulmonale (enlarged R heart due to disease of lung/pulmonary vessels)
  5. Hypertension
  6. Alcohol excess
  7. Anaemia/ pregnancy/ hyperthyroidism/ obesity/ arrhythmias
150
Q

Risk factors for cardiac failure

A
  1. 65 or older
  2. African descent
  3. Men
  4. Obesity
  5. People who have had an MI
151
Q

Why are women more protected against cardiac failure?

A

Oestrogen is a protective agent

152
Q

How is venous return (preload) affected in cardiac failure?

A
  • reduced vol of blood ejection in systole
  • increased vol of blood remaining in ventricles
  • increased preload
  • myocardium doesn’t respond
  • contractions aren’t strong enough
  • cardiac output is NOT maintained - decreases
153
Q

How is outflow resistance (after load) affected in cardiac failure?

A
  • increased afterload
  • increase in end- diastolic volume
  • dilatation of ventricles = means ventricles have the work harder
  • decrease in cardiac output
154
Q

Systolic cardiac failure

A
  • inability of the ventricle to CONTRACT

- decreased cardiac output

155
Q

What causes systolic cardiac failure?

A
  • IHD
  • Myocardial infarction
  • Cardiomyopathy
156
Q

Diastolic cardiac failure

A
  • inability of the ventricles RELAX & fill fully

- decreased cardiac output

157
Q

What causes diastolic cardiac failure?

A
  • hypertrophy

- aortic stenosis

158
Q

What causes hypertrophy?

A
  • chronic hypertension
  • increases after load
  • heart pumps against more resistance
  • cardiac myocytes grow bigger to compensate
159
Q

How does hypertrophy cause diastolic heart failure?

A
  • less space for blood to fill in the ventricles

- decreased cardiac output

160
Q

How does aortic stenosis cause diastolic heart failure/

A
  • increases afterload

- decreases cardiac output

161
Q

Clinical presentation of cardiac failure?

A
  1. Breathlessness/fatigue/ankle swelling
  2. Dyspnoea (esp when lying flat)
  3. Cold peripheries - don’t have enough energy/metabolites or them
  4. Raised jugular venous pressure (JVP)
  5. Murmurs & displaced apex beat
  6. Cyanosis
  7. Hypotension
  8. Tachycardia
  9. Ascites
  10. Hepatomegaly
162
Q

What classification system is used to assess severity of cardiac failure symptoms?

A

New York Heart Association (NYHA)

163
Q

What is the NYHA classification?

A

Class I - IV

164
Q

What is Class I of the NYHA?

A

NO LIMITATION

  • Asymptomatic
  • no fatigue, dyspnoea or palpitations when exercising,
165
Q

What is Class II of the NYHA?

A

SLIGHT LIMITATION

  • Mild HF
  • comfortable at rest
  • normal activity = fatigue, dyspnoea & palpitations
166
Q

What is Class III of the NYHA?

A

MARKED LIMITATION

  • moderate HF
  • comfortable at rest
  • gentle activity = fatigue, dyspnoea & palpitations
167
Q

What is Class IV of NYHA?

A

INABILITY TO CARRY OUT ANY PHYSICAL ACTIVITY WITHOUT DISCOMFORT

  • severe HF
  • symptoms occur at rest
168
Q

Which methods can be used to diagnose cardiac failure?

A
  • Blood tests
  • CXR
  • ECG
  • Echocardiography
169
Q

What do you look for in a blood test for cardiac failure?

A
  • Brain natriuretic peptide (BNP)
  • Full blood count
  • U&Es (urea and electrolytes)
  • liver biochemistry
170
Q

How does BNP indicate cardiac failure?

A
  • BNP secreted by ventricles
  • in response to increased myocardial wall stress
  • high levels in heart failure patients
171
Q

What do BNP levels correlate with?

A
  • ventricular wall stress

- severity of heart failure

172
Q

Where is BNP secreted?

A

By the ventricles

173
Q

What will a CXR show if there is heart failure?

A
  • alveolar oedema
  • cardiomegaly
  • dilated upper lobe vessels of lungs
  • pleural effusions
174
Q

What does the ECG show if there is heart failure?

A

UNDERLYING CAUSES:

  • ischaemia
  • LV hypertrophy in hypertension/arrhythmia
175
Q

What would you do if ECG and BNP levels are abnormal?

A

Do an echocardiogram

176
Q

What would you look for in an echocardiogram? (heart failure)

A
  • cardiac chamber dimension
  • regional wall motion abnormalities
  • valvular disease
  • cardiomyopathies
  • sign of MI
177
Q

Treatment of cardiac failure

A
  1. Lifestyle changes
  2. Diuretics
  3. ACE inhibitors
  4. Beta blockers
  5. Digoxin
  6. Inotropes
  7. Revascularisation
  8. Surgery to repair valves
  9. Transplant
  10. Cardiac resynchronisation
178
Q

What do inotropes do?

A

Alter cardiac contractility

179
Q

Name the mitral valve diseases

A
  1. Mitral stenosis

2. Mitral regurgitation

180
Q

Define mitral stenosis

A

Obstruction of the LV inflow that prevents proper filling during diastole

181
Q

What is the most common cause of mitral stenosis?

A

Rheumatic heart disease

- secondary to rheumatic fever

182
Q

How does rheumatic fever cause mitral stenosis?

A
  • inflammation during fever = commissural fusion of valves
  • reduces mitral valve orifice area
  • causes doming seen on echocardiogram
183
Q

What else can cause mitral stenosis?

A
  • infective endocarditis

- mitral annular calcification

184
Q

What are the risk factors for mitral stenosis?

A
  • history of rheumatic fever

- untreated streptococcus infections

185
Q

Pathophysiology of mitral stenosis

A
  1. Progressive dyspnea (breathlessness)
  2. Increased transmitral pressures
  3. Right heart failure
  4. Hemoptysis (coughing up blood)
186
Q

How does mitral stenosis lead to dyspnea?

A
  • LA atrial pressure increases
  • LA hypertrophies
  • LA dilatation
    = pulmonary congestion - reduced emptying
187
Q

How does mitral stenosis lead to right heart failure?

A
  • pulmonary venous/arterial and RH pressures increase
  • pulmonary capillary pressure = pulmonary oedema
  • RV hypertrophy, dilatation, failure
188
Q

Why does the RV hypertrophy in mitral stenosis?

A

Due to pulmonary hypertension

189
Q

What does RV hypertrophy, dilatation and failure cause?

A

Tricuspid regurgitation

190
Q

What causes hemoptysis in mitral stenosis?

A

Rupture of bronchial blood vessels due to elevated pulmonary pressures

191
Q

Clinical presentations of mitral stenosis

A
  1. RH failure
  2. AF
  3. Systemic emboli
  4. Prominent ‘a’ wave in jugular venous pulsations
  5. Mitral facies
  6. Heart sounds
192
Q

Why does mitral stenosis cause AF?

A

Left atrium dilation gives rise to palpitations

193
Q

Why does mitral stenosis cause systemic emboli?

A

Due to AF - most common in cerebral vessels

194
Q

Why does mitral stenosis cause ‘a’ wave in JVP?

A

Pulmonary hypertension & RV hypertrophy

195
Q

Why does mitral stenosis cause mitral facies?

A

Vasoconstriction in response to diminished cardiac output

196
Q

What is mitral facies?

A

Pink/purple patches on the cheeks

197
Q

What heart sounds will you hear in mitral stenosis?

A
  1. Diastolic murmur

2. Loud opening S1 snap

198
Q

Where is diastolic murmur most prominent in mitral stenosis?

A

At the apex of the heart

best when the patient is lying flat in held expiration

199
Q

Does the intensity of diastolic murmur correlate with severity of mitral stenosis?

A

No

200
Q

Where is the loud opening S1 snap heard best in mitral stenosis?

A

At the apex when leaflets are mobile

201
Q

What indicates a more sever mitral stenosis?

A

Shorter interval between S1 and S2 sound

202
Q

Which methods are used to diagnose mitral stenosis?

A
  1. CXR
  2. ECG
  3. Echocardiogram
203
Q

What will CXR of mitral stenosis show?

A
  • LA enlargement
  • Pulmonary oedema/congestion
  • Occasionally calcified mitral valve
204
Q

What will ECG of mitral stenosis show?

A
  • AF

- LA enlargement

205
Q

What would you assess in an echocardiogram of mitral stenosis?

A
  • mitral valve mobility
  • mitral valve gradient
  • mitral valve area
206
Q

Why is medical therapy not very useful as a treatment for mitral stenosis?

A

MECHANICAL PROBLEM - MEDICAL THERAPY DOES NOT PREVENT PROGRESSION

207
Q

Which meds would you still give for mitral stenosis and why?

A

CONTROL HEART RATE - improve diastolic filling

  • B blockers
  • CCBs
  • Digoxin

CONTROL FLUID OVERLOAD
- Diuretics

208
Q

What are the surgical treatments for mitral stenosis?

A
  1. Percutaneous mitral balloon valvotomy (PMBV)

2. Mitral valve replacement

209
Q

How does PMBV work?

A
  • catheter inserted into RA (via femoral artery)
  • interatrial septum pierced - enters LA across mitral valve
  • balloon inflated = pressure on valve
  • increases mitral valve opening
  • more blood flows into LV
210
Q

Define mitral regurgitation

A

Backflow of blood from the LV to the LA during systole

211
Q

What are the causes of chronic mitral regurgitation?

A
  1. Myxomatous degeneration (most common)
  2. Ischaemic mitral valve
  3. Rheumatic heart disease
  4. Infective endocarditis
  5. Papillary muscle dysfunction/rupture
  6. Dilated cardiomyopathy
212
Q

What is myxomatous degeneration? (MVP)

A

Weakening of chordae tendinae

= floppy mitral valve that prolapses

213
Q

Risk factors for mitral regurgitation?

A
  • females
  • lower BMI
  • age
  • renal dysfunction
  • prior MI
214
Q

Pathophysiology of mitral regurgitation

A

Pure volume overload - due to leakage of blood into LA during systole

215
Q

What are the compensatory mechanisms for pure volume overload?

A
  • LA hypertrophy & increased contractility
  • LA dilation & RV dysfunction due to pulmonary hypertension
  • progressive LV overload = dilatation = heart failure
216
Q

What would you hear during auscultation of mitral regurgitation?

A
  • soft S1 sound
  • pan systolic murmur at apex radiating to axilla
  • displaced hypderdynamic apex beat
  • prominent extra 3rd heart sound (S3)
217
Q

Does the intensity of murmur correlate with severity in MR?

A

Yes - in chronic

218
Q

What are the clinical presentations of MR?

A
  • exertion dysponea
  • fatigue & lethargy (reduced CO)
  • ## increased stroke volume felt as a palpitation
219
Q

How long is the compensatory phase for MR?

A

10-15 years

220
Q

When does mortality for MR rise drastically?

A

If ejection fraction <60%

221
Q

What’s the mortality rate for severe MR?

A

5% / year

222
Q

What would an ECG of MR show?

A
  • LA enlargement
  • AF
  • LV hypertrophy (in severe)
223
Q

What would a CXR of MR show?

A
  • LA enlargement

- central pulmonary artery enlargement

224
Q

What would an echocardiogram of MR show?

A
  • estimation of LA & LV size & function
  • valve structure assessment
  • transoesophageal echo is v helpful
225
Q

What medication would you give for MR and why?

A
  1. ACEI & hydralazine - vasodilators
  2. B blockers, CCB, digoxin - control heart rate
  3. Anticoaggulants in AF
  4. Diuretics for fluid overload
226
Q

Name the types of aortic valve disease

A
  1. Aortic stenosis

2. Aortic regurgitation

227
Q

Define aortic stenosis

A

Narrowing of the aortic valve resulting in obstruction to the LV stroke volume

228
Q

What symptoms does aortic stenosis lead to?

A
  1. Breathlessness
  2. Chest pain
  3. Syncope
  4. Fatigue
229
Q

What is the normal aortic valve area?

A

3-4cm^2

230
Q

When do symptoms for aortic stenosis occur?

A

When the valve area is 1/4th of normal

231
Q

What are the 2 main causes of aortic stenosis?

A
  1. Ageing

2. Congenital

232
Q

Name the 3 types of aortic stenosis

A
  1. Valvular
  2. Subvalvular - fibrous ridge/diaphragm below valve
  3. Supravalvular - fibrous diaphragm above valve
233
Q

What’s the most common type of aortic stenosis?

A

Valvular

234
Q

What are the 3 main causes of aortic stenosis?

A
  1. Calcific aortic valvular disease (CAVD)
  2. Calcification of congenital bicuspid aortic valve (BAV)
  3. Rheumatic heart disease
235
Q

Describe a bicuspid aortic valve

A

Valve has 2 leaflets instead of 3

236
Q

Risk factors for aortic stenosis

A
  • BAV

- congenital BAV more common in MALES

237
Q

Pathophysiology of aortic stenosis

A
  • obstructed LV emptying = pressure gradient = increased afterload
  • LV pressure increase = LV hypertrophy
  • results in LV relative ischaemia due to inc. blood demand
    = angina, arrhythmia, LV failure
238
Q

When is LV obstruction more severe in aortic stenosis, and why?

A

During exercise BECAUSE:

  • increase CO
  • but due to narrowing CO can’t increase
  • BP falls
  • coronary ischaemia worsens
  • myocardium fails
  • results in arrhythmias
239
Q

What are the 4 main clinical presentations of aortic stenosis?

A
  • syncope
  • angina
  • heart failure
  • dyspnoea on exertion
240
Q

What heart sounds would you hear on a patient with aortic stenosis?

A
  • soft/absent 2nd heart sound
  • prominent 4th heart sound (bc of LV hypertrophy)
  • ejection systolic murmur (crescendo-decrescendo)

LOUDNESS DOES NOT EQUAL SEVERITY

241
Q

Name the differential diagnoses of aortic stenosis?

A
  • aortic regurgitation

- subacute bacterial endocarditis

242
Q

What info would an echocardiogram of aortic stenosis obtain?

A
  1. LV size/function
    - LVH / dilation / ejection fraction
  2. Doppler derived gradient / valve area
243
Q

What would an ECG of aortic stenosis show?

A
  • LVH
  • left atrial delay
  • LV ‘strain’ pattern
  • depressed ST segments
  • T wave inversion (in aVL, V5, V6, lead I)
244
Q

What would CXR of aortic stenosis show?

A
  • LVH

- calcified aortic valve

245
Q

How would you treat aortic stenosis?

A
  • rigorous dental hygiene (increased risk of IE)
  • mechanical problem = CAN’T RLY FIX
  • aortic valve replacement
  • transcutaneous aortic valve implantation (TAVI)
246
Q

Why would vasodilators be a bad treatment idea for aortic stenosis?

A
  • may trigger hypotension

= leads to syncope

247
Q

Describe the process of TAVI

A
  • catheter passed up aorta
  • inflate balloon across valve
  • cracks calcification
  • pass 2nd catheter
  • leaves stent with a valve
    = new aortic valve
248
Q

Describe aortic regurgitation

A

Leakage of blood into the LV from aorta during diastole

because of inactive coaptation of aortic cusps

249
Q

What are the main causes of aortic regurgitation and are the chronic or acute?

A
  1. Congenital BAV - chronic
  2. Rheumatic fever - chronic
  3. Infective endocarditis - acute
250
Q

What are the risk factors for aortic regurgitation?

A
  1. SLE
  2. Marfan’s & Ehlers-Danlos syndrome
  3. Aortic dilation
  4. Infective endocarditis / aortic dissection
251
Q

Pathophysiology of aortic regurgitation

A

If net CO has to be maintained:

  • LV size has to increase
  • to pump more blood into aorta
  • results in LV hypertrophy & dilation
  • progressive dilation = heart failure
252
Q

Why/how are the coronary arteries affected in aortic regurgitation?

A
  • coronary arteries filled during diastole BUT
  • regurgitation = diastolic BP falls
  • so coronary perfusion decreases
253
Q

Why does cardiac ischaemia develop in aortic regurgitation?

A
  • large LV size = less efficient
  • demand for O2 increases
  • ischaemia develops
254
Q

Clinical presentation of aortic regurgitation

A
  • exertion dyspnea
  • angina / palpitations / syncope
  • wide pulse pressure
  • apex beat displaced laterally
255
Q

What heart sounds can be heard in aortic regurgitation?

A
  • diastolic murmur at left sternal border

- systolic murmur bc of increased flow across aortic valve

256
Q

What are the differential diagnoses of aortic regurgitation?

A
  • heart failure
  • infective endocarditis
  • mitral regurgitation
257
Q

What info will an echocardiogram of aortic regurgitation show?

A
  • evaluation of aortic valve & root

- LV dimensions & function

258
Q

What will a CXR of aortic regurgitation show?

A
  • enlarged cardiac silhouette
  • aortic root enlargement
  • LV enlargement
259
Q

What will an ECG of aortic regurgitation show?

A
  • signs of LV hypertrophy (volume overload)
  • tall R waves
  • deeply inverted T waves in left chest leads
  • deep S waves in right chest leads
260
Q

How would you treat aortic regurgitation?

A
  • consider infective endocarditis prophylaxis
  • ACEI - improve stroke volume & reduce regurgitation
  • serial echos
  • valve replacement
261
Q

Under what conditions do ACEI work for aortic regurgitation?

A
  • only if patient is symptomatic

- or has hypertension

262
Q

Define infective endocarditic

A

Infection of the endocardium or vascular endothelium of the heart

263
Q

What is infective endocarditis also known as?

A

Subacute bacterial endocarditis

264
Q

What does infective endocarditis affect?

A
  • valves w/ congenital/acquire defects (usually on left side)
  • normal valves w virulent organisms (strep. pneumonia / staph. aureus)
  • prosthetic valves
  • pacecmakers
265
Q

Amongst whom is right sided IE more common?

A

IV drug addicts

266
Q

Who is most affected by IE?

A
  • common in developing countries
  • elderly people with prosthetic valves
  • young IV drug user
  • young with congenital heart disease
  • males
267
Q

What causes IE?

A
  • Staph. aureus (most common)
  • pseudomonas aeruginosa
  • Strep. viridian’s (dental) - gram +, alpha haemolytic & optochin resistant
268
Q

List the risk factors for IE?

A
  • IV drug use
  • poor dental hygiene
  • skin/soft tissue infection
  • IV cannula
  • cardia surgery
  • pacemaker
  • dental treatment
269
Q

Pathophysiology of IE

A
  • presence of organisms in blood + abnormal cardiac endothelium
  • damaged endothelium = inc. platelet growth & fibrin deposit
  • organisms adhere & grow
    = infected vegetation
270
Q

List the clinical presentations of IE

A
  • embolic events & sepsis of unknown origin
  • fever/sweats + any risk factor
  • ventricular arrhythmias / heart failure / conduction disturbances
  • kidney dysfunction / MI / bone infections
271
Q

Examples of clinical manifestations of IE?

A
  • splinter haemorrhages on nail beds
  • embolic skin lesions
    Osler nodes - tender nodules in digits
  • Janeway lesions (haemmorhages / nodules in fingers)
  • Roth spots (retinal spots)
  • Petechiae - red/purple spots caused by bleeds in the skin
272
Q

How to diagnose IE?

A
  • DUKES CRITERIA !!!
  • BLOOD CULTURES !!!!! (IMPORTANTTTTTTTTT)
  • Blood test
  • urine test
  • ECG
  • echo (transthoracic / transoesophageal)
  • CXR
273
Q

How many blood cultures should you take to identify IE?

A
  • 3 from different sites over 24 hours

- before antibiotics started

274
Q

What will a blood test show if a patient has IE?

A
  • raised ESR - measures inflammation rate in body
  • raised CRP
  • neutrophilic
  • normochromic, normocytic anaemia
275
Q

What will a CXR of IE show?

A

Cardiomegaly

276
Q

What ECG of IE show?

A
  • long PR interval at regular intervals
277
Q

What are the advantages of transthoracic echo?

A
  • non invasive
  • safe
  • no discomfort
  • can identify vegetations (if bigger than 2mm)
278
Q

What are the disadvantages of transthoracic echo?

A
  • low sensitivity

- negative TTE does NOT exclude IE

279
Q

What are the advantages of TOE?

A
  • more sensitive
  • can visualise mitral lesions / aortic root abscess
  • BETTER AT DIAGNOSING
280
Q

What are the disadvantages of TOE?

A
  • very invasive & uncomfortable
281
Q

How would you treat IE?

A
  • antibiotics for 4-6 weeks
  • treat complications (arrhythmias / heart block / failure / stroke etc)
  • surgery (to remove infected devices / large vegetations / if antibiotics won’t work)
282
Q

What antibiotics would you use to treat IE if it is caused by staphylococcus?

A
  • vancomycin

- rifampicin

283
Q

What antibiotics would you use to treat IE if it is NOT causes by staphylococcus?

A

Penicillin:
- benzylpenicillin
AND
- gentamycin

284
Q

How can patients prevent IE in general?

A
  • good oral hygiene
285
Q

Define cardiomyopathy

A

Group of diseases of the myocardium that affect the mechanical or electrical function of the heart

286
Q

Name the 4 types of cardiomyopathy

A
  1. Hypertrophy
  2. Dilated
  3. Restricted
  4. Arrhythmogenic right ventricle
287
Q

What are the risk factors for cardiomyopathy?

A
  • family history
  • high BP
  • obesity
  • diabetes
  • previous MI
288
Q

Describe hypertrophic cardiomyopathy (HCM)

A
  • ventricular hypertrophy
  • diastolic dysfunction
  • good systolic function - eject >90%
  • heart becomes ischaemic
  • arteries supplying heart can become hypertrophic too
  • lowers threshold for arrhythmias
  • most common cause for sudden cardiac death in young people
  • myofibrillar disarray - conduction affected
289
Q

What is the cause of HCM?

A

Sarcomeric protein gene mutations (Troponin T & B-myosin)

290
Q

Pathophysiology of HCM

A
  • hypertrophic, non-compliant ventricles
  • impairs diastolic filling
  • reduces stroke volume
  • reduces cardiac output
291
Q

Clinical presentation of HCM

A
  • myocardium hypotrophy (interventricular septum)
  • sudden death
  • chest pain/angina/dyspnea/ dizziness / syncope
  • LV outflow obstruction
  • cardiac arrhythmia
  • ejection systolic murmur
  • jerky carotid pulse
292
Q

What will an ECG of HCM show?

A

Will be normal

  • show LVH
  • progressive T wave inversion
  • deep Q waves
293
Q

What will an echo of HCM show?

A
  • ventricular hypertrophy

- small LV cavity

294
Q

What is the genetic cause of HCM?

A

Autosomal dominant

295
Q

How do you treat HCM?

A
  • anti-arrhythmatic meds ( amiodarone)
  • CCBs
  • B blocker
296
Q

Define dilated cardiomyopathy

A

Dilated LV which contracts poorly/ has thin muscle

297
Q

What is the genetic cause of dilated cardiomyopathy?

A

Autosomal dominant

298
Q

What are the other causes of dilated cardiomyopathy?

A
  • ischaemia
  • alcohol
  • thyroid disorder
  • CYTOSKELETAL GENE MUTATIONS
299
Q

Pathophysiology of dilated cardiomyopathy

A
  • LV / RV / all chambers dilatation = dysfunction

- poor contractile force = progressive dilatation

300
Q

Clinical presentation of dilated cardiomyopathy

A
  • shortness of breath
  • dyspnea
  • heart failure
  • arrhythmias
  • thromboembolism
  • sudden death
  • increased jugular venous pressure
301
Q

What would a CXR of dilated cardiomyopathy show?

A

Cardiac enlargement

302
Q

What could an ECG of dilated cardiomyopathy show?

A
  • tachycardia
  • arrhythmia
  • non specific T wave changes
303
Q

What would an echo of dilated cardiomyopathy show?

A

Dilated ventricles

304
Q

Treatment of dilated cardiomyopathy

A

Conventional treatment for heart failure and AF

305
Q

What are the causes of restricted cardiomyopathy?

A
  • amyloidosis
  • idiopathic
  • sarcoidosis
  • end-myocardial fibrosis
306
Q

Pathophysiology of restricted cardiomyopathy

A
  • normal/decreased vol. in both ventricles
  • bi-atrial enlargement
  • normal wall thickness
  • normal cardiac valves
  • impaired ventricular filling
307
Q

Clinical presentation of restricted cardiomyopathy

A
  • dyspnea, fatigue, embolic symptoms
  • elevated JVP
  • diastolic cllapse
  • elevated venous pressure in inspiration
  • 3rd & 4th heart sounds
  • hepatic enlargement
  • ascites
  • dependent oedema
308
Q

How to diagnose restricted cardiomyopathy?

A

CXR, echo and ECG are abnormal but non-specific

- cardiac catheterisation helps diagnose

309
Q

Treatment for restricted cardiomyopathy

A
  • no specific treatment
  • patients die within a year
  • cardiac transplantation
310
Q

What characterises arrhythmogenic RV cardiomyopathy? (ARVC)

A

Myocardium is replaced with progressive fatty & fibrous tissue

311
Q

What is the cause of ARVC

A

UNKNOWN

- familial form = autosomal dom. with incomplete penetrance

312
Q

Pathophysiology of ARVC

A
  • desmosome gene mutation
  • RV replaced by fat. fibrous tissue
  • muscle dies & replaced with fat (part of inflammatory process)
313
Q

Clinical presentation of ARVC

A
  • conduction issues (cardiac cells are less close together)
  • arrhythmia
  • syncope
  • right heart failure (in late stages)
314
Q

What might an ECG show for ARVC?

A

T wave inversion

315
Q

What may an echo show for ARVC?

A

Right ventricular dilation

316
Q

Treatment of ARVC

A
  • B blockers (atenolol)
  • Amiodarone (for symptomatic arrhythmias )
  • occasional transplant
317
Q

What are structural/congenital heart defects due to?

A
  • misplaced structures

- arrest of progression of normal structure development

318
Q

What are the causes of congenital heart disease?

A
  • maternal prenatal rubella
  • maternal alcohol misuse
  • singe genes (e.g Down’s)
  • drugs (thalidomide, lithium)
  • diabetes of the mother
  • genetic abnormalities
319
Q

What congenital heart disease can maternal prenatal rubella infection lead to?

A
  • persistent ductus arteriosus

- pulmonary valvular & arterial stenosis

320
Q

What congenital heart disease does maternal alcohol misuse lead to?

A

Septal defects

321
Q

What congenital heart diseases can genetic abnormalities lead to?

A
  • arterial spatial defect

- congenital heart block

322
Q

Why should pregnancy be avoided if the woman has a congenital heart disease?

A
  • pulmonary hypertension
  • severe left heart obstruction
  • systemic ventricular impairment (ejection fraction <30%)
  • Marfan’s syndrome (aortic root diameters = >47mm)
323
Q

What are the clinical presentations of congenital heart diseases?

A
  • central cyanosis
  • pulmonary hypertension
  • clubbing of fingers
  • syncope
  • growth retardation
324
Q

What specific problems do adolescents / adults with congenital heart disease present with?

A
  • endocarditis
  • calcification & stenosis of congenitally deformed valves
  • atrial & ventricular arrhythmias
  • sudden cardiac death
  • RH failure
  • end-stage heart failure
325
Q

What is central cyanosis?

A
  • patients’ skin will be blueish
326
Q

Why does central cyanosis occur?

A
  • R-L shunting / complete mixing of systemic & pulmonary blood
    = poorly oxygenated blood entering systemic circulation
327
Q

What leads to pulmonary hypertension in congenital heart disease?

A
  • large left to right shunting
328
Q

What does the high pressure from shunting lead to?

A
  • thickening of vascular walls of the pulmonary arteries
329
Q

What does the thickening of pulmonary artery walls cause?

A

Increased pulmonary artery vascular resistance

330
Q

What does increased pulmonary artery vascular resistance lead to?

A
  • increase in RV pressure
  • REVERSAL OF SHUNT TO R TO L
    = leads to cyanosis
  • EISENMENGER’S REACTION / COMPLEX
331
Q

Describe atrial septal defects

A
  • abnormal connection between atria
  • LA pressure > RA
  • shunts from L to R
  • acyanotic (NOT blue)
  • increased flow into RH & lungs
332
Q

What can happen if atrial septal defects go untreated?

A
  • RH overload & dilatation
  • RV also dilates to deal with inc. pulmonary flow
  • RVH
  • pulmonary hypertension
  • increased risk of IE
333
Q

Clinical presentations of atrial septal defects

A
  • dyspnea
  • exercise intolerance
  • may develop atrial arrhythmias from RA dilatation
  • pulmonary flow murmur
  • fixed split 2nd heart sound
334
Q

What will a CXR of atrial septal defects?

A
  • large pulmonary arteries

- large heart

335
Q

What will an ECG of atrial septal defects?

A
  • RBBB (due to RV dilatation)
336
Q

What will an echo of atrial septal defects?

A
  • RH hypertrophy & dilation

- pulmonary artery hypertrophy & dilation

337
Q

What are the treatments for atrial septal defects?

A
  • surgical closure

- percutaneous (key hole technique)

338
Q

Describe ventricular septal defects (VSD)

A
  • abnormal connection between 2 ventricles
  • LV pressure > RV pressure
  • L-R shunt
  • acyanotic
  • increased blood flow through lung
339
Q

What are the clinical presentations for LARGE VSD?

A
  • small breathless skinny baby
  • increased resp. rate
  • tachycardia
  • big heart on CXR
  • murmur varies in intensity
340
Q

What are the clinical presentations for SMALL VSD?

A
  • loud systolic murmur
  • buzzing sensation
  • well grown
  • normal HR & heart size
341
Q

Treatment for VSD

A
  • some will spontaneously close
  • surgical closure
  • prophylactic antibiotics
342
Q

What drug do you use to treat moderately VSD?

A
  • Furosemide

- ACE inhibitors (ramipril & digoxin)

343
Q

Describe atrio-ventricular septal defects (AVSD)

A
  • instead of 2 separate AV valves there is ONE
  • this valve leaks
  • can be complete / partial
344
Q

What genetic mutation is AVSD associated with?

A

Down’s syndrome

345
Q

What are the clinical presentations in patients with complete AVSD?

A
  • breathlessness as a neonate
  • poor weight gain / feeding
  • torrential pulmonary flow = Eisenmenger’s = cyanosis
346
Q

What are the clinical presentations in patients with partial AVSD?

A
  • dyspnea
  • tachycardia
  • exercise intolerance
  • can present in late adulthood
347
Q

What is the treatment for a large AVSD?

A
  • pulmonary artery banding

- surgical repair is challenging

348
Q

What is the treatment for partial AVSD?

A

May be left alone IF there is no right heart dilatation

349
Q

Describe patent ductus arteriosus (PDA)

A
  • persistent communication between proximal L pulmonary artery & descending aorta
  • abnormal L-R shunt
  • leads to pulmonary hypertension
  • increased after load = RVH
    = RH cardiac failure
350
Q

What does PDA increase the risk of?

A

Infective endocarditis

351
Q

What are the clinical presentations of PDA?

A
  • continuous machinery murmurs
  • bounding pulse
  • large heart & breathlessness
  • Eisenmenger’s w/ differential cyanosis
  • tachycardia
352
Q

What will a CXR of PDA show?

A
  • prominent aorta & pulmonary arterial system
353
Q

What will an ECG of PDA show?

A
  • LA abnormality

- LV hypertrophy

354
Q

What will an echo of PDA show?

A

Dilated LA & LV

355
Q

How would you treat PDA?

A
  • closed surgically / percutaneously
    (low risk complications)
  • indomethacin (prostaglandin inhibitor) given to stimulate duct closure
356
Q

Describe coarctation of the aorta

A
  • narrowing of the aorta at/distal to insertion of ductus arteriosus
357
Q

What does the narrowing of the aorta cause?

A

Excessive blood flow being diverted through carotid & subclavian vessels
- into systemic shunts
= causes stronger perfusion to upper body than lower

358
Q

What is coarctation of the aorta associated with?

A
  • Turner’s syndrome
  • Berry aneurysms
  • patent ductus arteriosus
359
Q

What are the clinical presentations of coarctation of the aorta?

A
  • right arm / upper limb hypertension
  • murmur
  • discrepant blood pressure between upper and lower limbs
360
Q

What are the long term problems of aortic coarctation?

A

HYPERTENSION - leads to:

  • early coronary artery disease
  • early strokes
  • sub-arachnoid haemorrhage
361
Q

What will a CXR of aortic coarctation show?

A
  • dilated aorta indented at site of coarctation
362
Q

What will an ECG of aortic coarctation show?

A

LVH

363
Q

What will a CT of aortic coarctation show?

A
  • demonstrates coarctation

- quantifies flow

364
Q

How would you treat aortic coarctation?

A
  • surgery
  • balloon dilation & stenting
    (risk of aneurysm formation at the site of repair)
365
Q

List the clinical presentations for tetralogy of Fallot

A
  • central cyanosis
  • dyspnea
  • low birthweight/ growth
  • delayed puberty
  • systolic ejection murmurs
366
Q

What will a CXR of tetralogy of Fallot show?

A

Boot shaped heart

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