Cardio Flashcards
1
Q
Define atherosclerosis
A
A degenerative condition of the arteries characterised by a fibrous and lipid rich plaque with variable inflammation, calcification and a tendency to thrombosis
2
Q
Risk factors for atherosclerosis
A
- Age
- Family history
- Smoking
- High LDL diet
- Obesity
- Sedentary lifestyle
- Diabetes
- Hypertension
3
Q
Which arteries is atherosclerosis most often found in`
A
Coronary and peripheral arteries (focal distribution along artery length)
4
Q
Virchow’s triad
A
Factors predisposing thrombosis:
- Change in blood constituents
- Change in flow (stasis)
- Change to vessel wall (endothelial injury)
5
Q
Structure of an atherosclerotic plaque
A
- Fibrous cap
- Necrotic core
- Connective tissue
- Lipid
6
Q
Major cell types involved in atherosclerosis
A
Endothelium, macrophages, lymphocytes, smooth muscle cells, platelets
7
Q
Basic mechanism of atherogenesis
A
- Fatty streak formation
- Intermediate lesions formed
- Fibrous plaques and advanced lesions
- Plaque rupture
8
Q
Describe formation of fatty streaks
A
Endothelial injury and build up of cholesterol within the intima. Monocytes migrate to site of injury and transform into macrophages. These ingest lipids and then die - foam cells.
9
Q
Components of intermediate lesions
A
Vascular smooth muscle cells, T lymphocytes, adhesion and aggregation of platelets to vessel wall
10
Q
Fibrous plaque formation
A
Smooth muscles have migrated into the plaque and start secreting elastin and collagen, forming a fibrous plaque round the periphery of the plaque.
11
Q
Plaque rupture
A
The plaque impedes blood flow causing more turbulence. Fibrous plaque constantly resorbed and redeposited - if balance shifts, cap weakens and may rupture. Thrombosis formation and vessel occlusion
12
Q
Define mural thrombi
A
Thrombi adhered to vessel wall
13
Q
Clinical stage of atherosclerosis
A
Plaque occludes vessel, increasing risk of haemorrhage. T cell accumulation stimulated. Inflammatory reaction against plaque contents - complications inc. ulceration, calcification and aneurysm.
14
Q
Clinical manifestations of atherosclerosis
A
Usually asymptomatic till artery narrowed enough to reduce blood flow to organs so its no longer adequate.
- Coronary arteries - chest pain/pressure (angina)
- Brain arteries - TIA, weak arms and legs, slurred speech, temporary vision loss, dropping face muscles
- Peripheral arteries - peripheral artery disease - leg pain when walking
- Renal arteries - HTN or kidney failure
15
Q
Examples of useful inflammation
A
- Pathogens
- Parasites
- Tumours
- Wound healing
16
Q
Examples of pathological inflammation
A
- Atherosclerosis
- Rheumatoid arthritis
- IHD
- Excessive wound healing
17
Q
Treatment of atherosclerosis
A
PCI (percutaneous coronary intervention)
18
Q
Biggest limitation of PCI
A
Restenosis
19
Q
What is done to prevent restenosis after PCI
A
Insertion of drug-eluting stents (anti-proliferative and inhibits healing) - stops the artery narrowing again
20
Q
Pharmacological interventions for atherosclerosis
A
Aspirin (low dose)
Clopidogrel/ticagrelor
Statins
21
Q
Drug action of aspirin
A
Irreversible inhibitor of COX1/2 - inhibits thromboxane A2
22
Q
Drug action of clopidogrel/ticagrelor
A
Inhibits P2Y12 ADP receptor on platelets - stops aggregation
23
Q
Drug action of statins
A
Inhibits HMG-CoA reductase - in pathway for cholesterol synthesis in the liver
24
Q
Investigations of heart disease: chest x-ray
A
Snapshot of heart with little detail.
- Enlarged heart suggests congestive heart failure
- Pulmonary oedema suggests decompensated HF
- Globular heart suggests pericardial effusion
- Shows previous surgeries (metal shows up)
25
Investigations of heart disease: Echocardiography
Ultrasound used to give real time images. Transthoracic (TTC) or Transoesophageal (TOE) at rest, during exercise or with infusion of a pharmacological stressor.
26
Investigations of heart disease: Cardiac CT
Detailed info about cardiac structure and function. CT angiography - contrast enhanced imaging of coronary arteries during single breath hold with low dose radiation.
- Can diagnose stenosis in coronary artery disease with 89% accuracy
27
CT coronary angiography NPV
>99% - means it's an effective non-invasive alternative to routine transcatheter coronary artery angiographpy to rule out CAD
28
Investigations of heart disease: CMR (cardiac magnetic resonance imaging)
Radiation free method - characterises cardiac structure and function including viability of myocardium
- First choice imaging method for diseases that directly affect the myocardium
- Safe with pacemakers
29
Investigations of heart disease: Nuclear imaging
Perfusion assessed at rest and with exercise/pharmacological stressor.
- Useful for assessing if myocardium distal to blockage is viable (will stenting or CABG be useful?)
- If hypoperfusion is fixed at rest, likely to be scar tissue (non-viable)
30
Define ECG
Electrocardiogram - a representation of electrical events of the cardiac cycle. Impulses travelling towards an electrode produce upright positive deflection
31
ECGs can identify:
- Arrhythmias
- Myocardial ischaemia and MI
- Pericarditis
- Electrolyte disturbances
32
Standard calibration of an ECG
25mm/s
| 0.1mV/mm
33
What are the 12 ECG leads
6 precordial (chest), 4 limbs (1 neutral)
34
Common ECG abnormalities: P wave
- Right atrial enlargement (>2.5mm) - P pulmonale
- Left atrial enlargement (notched M shaped) P mitrale
- Long PR interval - first degree heart block
35
Common ECG abnormalities: QRS
Generally QRS abnormalities hint at ventricular enlargement or conduction blocks.
- S wave depth shouldn't be >30mm
- Pathological Q wave = >2mm deep and >1mm wide. >25% amplitude of the subsequent R wave
36
Common ECG abnormalities: ST segment
Usually flat - elevation of >1mm pathological
37
Common ECG abnormalities: T wave
- Should be 1/8
38
Common ECG abnormalities: QT interval
Decreases when HR increases (0.35-0.45s)
| Shouldn't be more than half of the interval between adjacent R waves
39
Common ECG abnormalities: U waves
Small, round, symmetrical positive in lead II, amplitude <2mm. Same direction as T wave
40
Determining HR
- Regular = 300/number of boxes between adjacent QRS complexes
- Irregular = count number of beats on ECG and multiply by 6
41
Quadrant approach for QRS axis
lead I and AVF:
- both positive = normal
- aVF positive, I negative = RAD
- aVF negative, I positive = LAD
- both negative = indeterminate axis
42
Tachycardia
Fast heart rate (>100bpm)
43
Bradycardia
Slow heart rate (<60bpm)
44
Causes of sinus bradycardia
- Physical fitness
- Vasovagal attacks
- Sick sinus syndrome
- Drugs
- Hypothyroidism
- Hypothermia
- Raised intracranial pressure
- Cholestasis
45
Drugs causes bradycardia
B-blockers, digoxin, amiodarone
46
Common causes of AF
- IHD
- Thyrotoxicosis
- HTN
- Obesity
- HF
- Alcohol
47
ST elevation can be a sign of
- Acute MI
- Prinzmetal's angina
- Acute pericarditis
- Left ventricular aneurysm
48
ST depression can be a sign of
- Digitoxin toxicity
| - Ischaemic heart, angina, NSTEMI, acute posterior MI
49
T inversion in V1-3
- RBBB
| - RV strain
50
T inversion in V2-5
- Anterior ischaemia
- HCM (hypertrophic cardiomyopathy)
- Subarachnoid haemorrhage
- Lithium
51
T inversion in V4-6
- Lateral ischaemia
- LVH
- LBBB
52
ECG signs of an MI
- Within hours T wave is peaked and ST elevation
- Within 24h T wave inverts. ST elevation rarely persists unless left ventricular aneurysm. T wave inversion may or may not persist
53
ECG signs for PE
Sinus tachycardia, RBBB, right ventricular strain pattern
54
Types of echocardiography
```
M-mode
Two-dimensional (real time)
3D echocardiography
Doppler and colour-flow echocardiography
Tissue doppler imaging
Transoesophageal echocardiography
Stress echocardiography
```
55
M-mode (motion mode) echocardiography
A single-dimension image
56
Two-dimensional (real time) echocardiography
2D, fan-shaped image of segment of the heart. Visualising congenital heart disease, LV aneurysm, mural thrombus, LA myxoma, septal defects
57
Doppler and colour-flow echocardiography
Different coloured jets illustrate flow and gradients across valves and septal defects
58
Tissue doppler imaging
Uses Doppler ultrasound to measure velocity of myocardial segments over the cardiac cycle. Useful for assessing longitudinal motion - diagnosis of systolic and diastolic HF
59
Transoesophageal (TOE) echocardiography
More sensitive than transthoracic - transducer nearer the heart. Diagnose aortic dissection, assessing prosthetic valves and finding source of cardiac emboli
60
Stress echocardiography
Evaluates ventricular function, ejection fraction, myocardial thickening and characterises valvular lesions
61
Uses of echocardiography
1. Quantification of global LV function
2. Estimating right heart haemodynamics
3. Valve disease
4. Congenital heart disease
5. Endocarditis
6. Pericardial effusion
7. Hypertrophy cardiomyopathy
62
Echocardiography + quantification of global LV function
HF may be due to systolic/diastolic ventricular impairment. Echo measure EDV - large = systolic dysfunction small = diastolic dysfunction
63
Echocardiography + estimating right heart haemodynamics
Doppler studies of pulmonary artery flow and tricuspid regurgitation allow evaluation of RV function and pressure
64
Echocardiography + valve disease
Technique of choice for measuring pressure gradients and valve orifice areas in stenotic lesions
65
Echocardiography + congenital heart disease
Presence of lesions and their significance.
66
Echocardiography + pericardial effusion
Best diagnosed by echo - fluid accumulating between posterior pericardium and LV can be detected
67
Echocardiography + hypertrophic cardiomyopathy
Echo shows asymmetrical septal hypertrophy, small LV cavity, dilated left atrium and systolic anterior motion of the mitral valve
68
Define hypertension
Chronic elevation of blood pressure > 140/90 mmHg
69
Define malignant hypertension
Rapid rise in blood pressure leading to vascular damage >160/110 mmHg
70
Causes of HTN
Primary 90% - no known underlying cause
| Secondary - 10%
71
Secondary causes of HTN
Endocrine disease
Renal disease
Exogenous agents
Lifestyle
72
Endocrine disease causing HTN
- Overproduction of aldosterone (Conn's syndrome)
| - Chronic vascular disease - diabetes, Cushing's, hyperthyroidism
73
Renal disease causing HTN
- Intrinsic disease (glomerulonephritis, polycystic kidneys)
| - Renovascular disease
74
Exogenous agents causing HTN
NSAIDs, combined oral contraceptive, corticosteroids, ciclosporin, cold cures, antidepressants, recreational
75
Lifestyle factors causing HTN
Obesity, excessive salt and alcohol intake, stress, sedentary lifestyle, smoking
76
Signs and symptoms of HTN
Usually asymptomatic. Can sometimes cause headaches
| Look for end organ damage (e.g. retinopathy)
77
Signs and symptoms of malignant HTN
- Bilateral renal haemorrhages
- Papilloedema
- Headache and visual disturbance
78
Investigations for HTN
- 24hr ABPM
- Fasting glucose + cholesterol (quantify overall risk)
- ECG or echo (end organ damage)
- Renal ultrasound/arteriography
- 24h urinary meta-adrenaline
- Urinary free cortisol
79
Complications of HTN
- Cor pulmonale -> right ventricular hypertrophy and dilatation due to pulmonary HTN.
80
Management of HTN
- Lifestyle changes
- ACE-i/ARB or CCB
- ACE-i/ARB and CCB
- ACE-i/ARB and CCB and thiazide-like diuretic
- Add spironolactone, beta blockers or alpha blockers
81
Action and example of ACE-i
Inhibits ACE (angiotensin II not made, BP lowered). Ramipril
82
Action and example of ARB
Blocks angiotensin II at peripheral receptors. Candesartan
83
Action and example of CCB
Blocks VG calcium channels in vascular smooth muscle - reduced contraction. Amlodipine
84
Action and example of thiazide-like diuretic
Inhibit sodium reabsorption by DCT, reducing ECF volume. Bendroflumethazide
85
Define angina
Recurrent transient episode of chest pain due to myocardial ischaemia
86
Types of angina
1. Stable angina - induced by effort, relieved by rest.
2. Unstable angina (crescendo) - increasing frequency/severity - occurs on minimal exertion/rest. High risk of MI
3. Decubitis angina- precipitated by lying flat
4. Prinzmetal angina - causing by coronary artery spasm
87
Pathology of angina
- Stenosis causes increased resistance within a vessel.
- In exercise, microvascular resistance falls and increases flow
- With atherosclerosis, flow cannot meet metabolic demand
- Myocardial ischaemia
88
Causes of angina
ATHEROSCLEROSIS
- anaemia
- coronary artery spasm
- tachyarrhythmias
89
RF angina
```
Non-modifiable
- Gender
- FH
- PMH
- Age
Modifiable
- Smoking
- Diabetes
- HTN
- Hypercholesterolaemia
- Sedentary lifestyle
- Stress
```
90
Precipitants of angina
```
Affects supply
- Anaemia
- Hypoxaemia
- Hypothermia
- Hypovolaemia
- Hypervolaemia
Affects demand
- HTN
- Hyperthyroidism
- Valvular heart disease
- Tachyarrhythmia
- Cold weather
```
91
Clinical presentation of angina
1. Contricting/heavy discomfort to the chest, jaw, neck, shoulders, or arms
2. Symptoms brought on by exertion
3. Symptoms relieved by rest/GTN spray
92
Symptoms of angina
```
Dyspnoea
Nausea
Sweatiness
Faintness
Crushing chest pain (possibly radiating to the jaw)
```
93
Differential diagnoses of angina
- Pericarditis
- Pulmonary embolism
- Chest infection
- Dissection of the aorta
- Gastro-oesophageal reflux/spasm/ulceration
- Psychological
- Musculo-skeletal
94
Investigations for angina
- ECG (often normal)
- Blood tests (FBC, U%E, TFTs, lipids, HbA1C)
- Echocardiogram (normal)
- Chest x-ray
- Physiological - exercise stress treadmill, stress echo. perfusion MRI
95
Management of angina
Address exacerbating factors (anaemia, tachycardia, thyrotoxicosis) GTN
96
Primary prevention of angina
Reduce risk of CAD and complications
| Risk factor modification
97
Secondary prevention of angina
- Lifestyle changes
- 75mg daily aspirin
- ACE-i
- Address hyperlipidaemia
- Interventional (PCI and sometimes surgery)
98
Action and example of beta-blocker
Block beta receptors in the sympathetic NS - reduces CO and O2 demand. Bisoprolol
99
Action and example of nitrates
Dilate systemic veins to reduce heart preload on the heart. Isosorbide mononitrate
100
Action and example of statins
Block HMG-CoA reductase - enzyme in cholesterol production pathway. Reduces LDL- cholesterol. Atorvastatin
101
PCI (percutaneous coronary intervention) in angina
Balloon inflated inside a stenosed vessel, opening the lumen. Stent is inserted to reduce chance of restenosis
102
CABG (coronary artery bypass graft)
Internal mammary artery grafted to bypass stenosed vessel
103
Pros and cons of PCI
```
Pros
1. Less invasive
2. Convenient
3. Repeatable
4. Acceptable
Cons
1. Risk stent thrombosis
2. Restenosis
3. Can't deal with complex disease
4. Dual antiplatelet therapy
```
104
Pros and cons of CABG
```
Pros
1. Good prognosis
2. Deals with complex disease
Cons
1. Invasive
2. Risk of stroke, bleeding
3. Can't do if frail or co-morbid
4. One-time treatment
5. Increased length of stay and recovery time
```
105
Define acute coronary syndromes
Unstable angina and myocardial infarctions. Share common underlying pathology of plaque rupture, thrombosis, and inflammation
106
Rare causes of ACS
Coronary vasospasm without plaque rupture, drug abuse, dissection of the coronary artery, thoracic aortic depression
107
RF for ACS
```
Non-modifiable
- Gender
- FH of IHD
- Age
Modifiable
- Smoking
- Diabetes
- HTN
- Hyperlipidaemia
- Sedentary lifestyle
- Cocaine use
```
108
Diagnosis of ACS
- Increase in cardiac biomarkers (troponin)
- Symptoms of ischaemia
- ECG changes for new ischaemia
- Pathological Q waves
- New loss of myocardium
109
Symptoms of ACS
- Acute central crushing chest pain>20min
- Nausea
- Sweatiness
- Dyspnoea
- Palpitations
- ACS without chest pain = silent - seen in elderly and diabetics. Pulmonary oedema, syncope, epigastric pain, vomiting
110
Signs of ACS
- Distress
- Anxiety
- Pallor
- Sweatiness
- 4th heart sound
- Signs of HF
- Low grade fever
111
Differential diagnoses of ACS
- Stable angina
- Pericarditis
- Myocarditis
- Takotsubo cardiomyopathy
- Aortic dissection
112
Investigations for ACS
- ECG - STEMI (tall T waves, ST elevation, T wave inversion and pathological Q waves follow non-specific changes)
- CXR - cardiomegaly, pulmonary oedema, widened mediastinum
- Bloods (FBC, U&E, Glucose, lipids, cardiac enzymes - troponin + serial troponins required to differentiate NTEMI from unstable angina)
113
Troponin levels in NSTEMI vs unstable angina
Troponin levels raised in NSTEMI, the same in unstable angina
114
3 managements of ACS
1. Symptom control
2. Modify risk factors
3. Cardioprotective medications
115
Symptoms control of ACS
Relieve chest pain with PRN GTN and opiates
116
Modifying RF of ACS
- STOP SMOKING
- Treat diabetes, HTN and hyperlipidaemia
- Mediterranean diet
- Daily exercise encouraged
- Mental health flagged to GPs
117
Cardioprotective medications in ACS
1. Dual antiplatelet therapy - aspirin and clopidogrel
2. Anticoagulants - fondaparinux
3. Beta-blockers - propanolol (reduce myocardial o2 demand)
4. ACE-i - patients with LV dysfunction/HTN/diabetes
5. High dose statin
118
Action and example of anticoagulants
Inhibits both fibrin formation and platelet aggregation. Fondaparinux
119
NSTEMI presentation
Prolonged ischaemia chest pain on minimal or no exertion. Crescendo pattern. No significant rise in troponin and no ST elevation
120
Subendocardial/patchy infarction
Involves the innermost layer and some middle parts of the myocardium but not the epicardium (NSTEMI)
121
Transmural infarction
Full thickness of the myocardium
122
Initial management of STEMI
1. Attach ECG (12 lead)
2. IV access - bloods.
3. Hx of CVD, RF for IHD
4. Aspirin 300mg and ticagrelor 180mg
5. Morphine 5-10mg IV and anti-emetic
6. STEMI on ECG = primary PCI
123
Treatment of STEMI
1. Aspirin
2. LMW heparin
3. Thrombolytic therapy
124
Complications of MI (12)
1. Cardiac arrest
2. Cardiogenic shock
3. LV failure
4. Brady/tachyarrhythmia
5. RV failure (presents with low CO)
6. Pericarditis
7. Systemic embolism
8. Cardiac tamponade
9. Mitral regurgitation
10. Ventricular septal defect
11. Dressler's syndrome
12. LV aneurysm
125
MI related pericarditis
- Central chest pain relieved by sitting forwards
- ECG - saddle shaped ST elevation
- NSAIDs
126
MI related systemic embolism
- May arise from LV mural thrombus
| - Consider anticoagulation with warfarin for 3 months
127
MI related cardiac tamponade
- Low CO, pulsus paradoxus, muffled heart sounds
- Echocardiogram used to diagnose
- Treated by pericardial aspiration, surgery
128
MI related mitral regurgitation
- Presents with pulmonary oedema
| - Treated with valve replacement
129
MI related ventricular septal defect
- Presents with pansystolic murmur (extending through entire systolic interval), cardiac failure
- Diagnosed with echocardiogram
- Treated with surgery
130
MI related Dressler's syndrome
- Recurrent pericarditis, pleural effusions, fever, anaemia
| - Treatment - NSAIDs if severe
131
Define heart failure
Inability of the heart to keep up with demands - failure of the heart to pump blood with normal efficiency so CO is inadequate for body's requirements. Severe failure causes cardiogenic shock
132
Triggers for hypertrophic response
1. Angiotensin II
2. ET-1 and insulin-like growth factor 1
3. TGF-beta
133
Classifications of heart failure
Systolic, diastolic, LV, RV
134
Systolic heart failure
Inability of the ventricle to contract normally, resulting in low CO. Ejection fraction >40%
135
Causes of systolic HF
1. IHD
2. MI
3. Cardiomyopathy
136
Diastolic HF
Inability of the ventricles to relax and fill normally, causing increased filling pressures. Typically ejection fraction >50% (HF with preserved EF)
137
Causes of diastolic HF
1. Ventricular hypertrophy
2. Constrictive pericarditis
3. Tamponade
4. Restrictive cardiomyopathy
5. Obesity
138
LV failure
Pulmonary congestion (blood backs up in veins) pressure increases and fluid is pushed into the alveoli ->. overload of the right side
139
Symptoms of LV failure
- Dyspnoea
- Poor exercise tolerance
- Fatigue
- Orthopnoea (SOB lying flat)
- Paroxysmal nocturnal dyspnoea (SOB at night, awakening from sleep)
- Nocturnal cough
- Wheeze
- Cold peripheries
- Weight loss
140
RV failure
Venous HTN and congestion
141
Causes of RV failure
- LVF
- Pulmonary stenosis
- Lung disease
142
Symptoms of RV failure
- Peripheral oedema
- Ascites
- Nausea
- Anorexia
- Facial engorgement
- Epistaxis (nose bleed)
143
Define acute HF
New-onset acute or decompensation of chronic HF characterised by pulmonary and or peripheral oedema with/without signs of peripheral hypoperfusion
144
Define chronic HF
Develops slowly. Venous congestion common but arterial pressure is well maintained until very late
145
Define low-output HF
CO is low and fails to increase normally with exertion.
146
Causes of low-output HF
- Excessive pre-load: mitral regurgitation or fluid overload
- Pump failure - decreased heart rate, negatively inotropic drugs
- Chronic excessive afterload - aortic stenosis, HTN
147
Define high-output HF
Output is normally increased in the face of extremely increased needs. Failure occurs when CO fails to meet these needs
148
Causes of high output HF
- Anaemia
- Pregnancy
- Hyperthyroidism
- Paget's disease
149
Diagnosis of HF
- Symptoms of HF
- Objective evidence of cardiac dysfunction at rest
- Tests: FBC. CXR, ECG, echocardiography
150
Signs of HF
- Cyanosis
- Decreased BP
- Narrow pulse pressure
- Pulsus alternans
- Displaced apex (LV dilatation)
- Pulmonary HTN
- Pink frothy sputum
- Signs of valve diseases
151
Differential diagnoses of HF
- COPD
- Emphysema
- MI
- PE
- Pneumonia
152
Management of acute HF
1. Sit upright
2. High flow O2 if low peripheral capillary o2 saturation
3. Treat arrhythmias
4. Investigations while continuing treatment
5. Diamorphine 1.25-5mg IV slowly
6. Furosemide 40-80mg IV slowly
7. GTN spray 2SL puffs
8. If systolic Bp>100, start nitrate transfusion
9. If systolic <100 treat as cardiogenic shock and refer to ICU
153
Management of chronic HF
1. Stop smoking, alcohol, reduce salt, optimise weight and nutrition
2. Treat cause and exacerbating factors (e.g. anaemia)
3. Annual flu vaccine, one off pneumococcal vaccine
4. Drugs
154
Pharmacological management of chronic HF
1. Diuretics - furosemide
2. ACE-i treats LVSD
3. B-blockers decrease mortality
4. Mineralocorticoid receptor antagonists (spironolactone)
5. Digoxin
6. Vasodilators - hydralazine and isosorbide nitrate
155
Define intractable heart failure
Failure that is resistant to further treatment - transfer to palliative care
156
Define valvular heart disease
Any disease process involving one of more of the four valves of the heart
157
2 categories of valvular heart disease
Congenital and acquired
158
Examples of congenital valvular heart disease
Congenital aortic stenosis and congenital bicuspid valve
159
Examples of acquired valvular heart disease
Degenerative calcification, rheumatic heart disease, rare causes
160
Examples of mitral valve diseases
1. Mitral regurgitation
2. Mitral stenosis
3. Mitral valve prolapse
161
Define mitral regurgitation
Backflow through the mitral valve during systole
162
Difference between acute and chronic mitral valve regurgitation
Acute results in back up into the lungs, chronic results in dilation as it has had time for adjustment
163
Pathophysiology of mitral valve regurgitation
Volume overload. Compensatory mechanisms = left atrial enlargement, LVH and increased contractility.
- Progressive LA dilation and RV dysfunction due to pulmonary HTN
- Progressive LV volume overload leads to dilatation and progressive HF
164
Causes of mitral regurgitation
1. Rheumatic fever
2. Infective endocarditis
3. Mitral valve prolapse
4. Ruptured chordae tendinae
5. Papillary muscle dysfunction
6. Cardiomyopathy
165
Symptoms of mitral regurgitation
1. Dyspnoea (on exertion)
2. Pulmonary oedema
3. Fatigue
4. Palpitations
166
Signs of mitral regurgitation
1. AF - displaced, hyperdynamic apex
2. Pansystolic murmur at apex radiating to axilla
3. The more severe, the larger the LV
167
Investigations of mitral regurgitation
1. ECG - AF, p-mitrale if in sinus rhythm, LA enlargement, LV hypertrophy
2. CXR - enlarged LA and LV
3. Mitral valve calcification
4. Echo - assess LV size, function, MR severity. Cardiac catheterisation to confirm diagnosis
168
Management of mitral valve regurgitation
1. Control of HR if AF (b-blockers)
2. Anticoagulate with history of AF, embolism, prosthetic valve or additional mitral stenosis
3. Vasodilators (hydralazine)
4. Diuretics for fluid overload
5. Surgery - repair/replacement
169
Define mitral valve prolapse
The most common valvular abnormality. Condition in which 2 flaps of the mitral valve do not close smoothly or evenly, but instead bulge upwards into the left atrium
170
Symptoms of mitral prolapse
- Usually asymptomatic
| - May develop atypical chest pain, palpitations, autonomic dysfunction symptoms
171
Signs of mitral valve prolapse
Mid-systolic click and/or late systolic murmur
172
Complications of mitral valve prolapse
1. Mitral regurgitation
2. Cerebral emboli
3. Arrhythmias
4. Sudden death
173
Investigations for mitral prolapse
Echo is diagnostic. ECG may show inferior T wave inversion
174
Treatment of mitral prolapse
- B-blockers may help palpitations and chest pain. Surgery if severe
175
Define mitral stenosis
Obstruction of LV inflow that prevents proper filling during diastole due to stenosis of the mitral valave
176
Normal and pathological mitral valve area
Normal = 4-6cm2
| Pathological< 2cm2
177
Pathophysiology of mitral stenosis
1. Progressive dyspnoea - worse with exercise, fever, tachycardia, pregnancy
2. Increased trans-mitral pressure - LA enlargement and AF
3. Right HF symptoms - pulmonary venous HTN
4. Haemoptysis - due to rupture of bronchial vessels (elevated pulmonary pressure)
178
Causes of mitral stenosis
1. Rheumatic fever
2. Congenital
3. Infective endocarditis
4. Malignant carcinoid
179
Presentation of mitral stenosis
1. Pulmonary HTN - dyspnoea, haemoptysis
2. Pressure from large LA pressure on local structures - hoarse voice (recurrent laryngeal nerve)
3. Dysphagia
4. Bronchial obstruction
5. Fatigue
6. Palpitations
7. Chest pain
180
Signs of mitral valve stenosis
1. Prominent a wave in jugular venous pulsations (due to pulmonary HTN and RV hypertrophy)
2. Signs of right HF
3. Mitral facies - severe MS leads to vasoconstriction = pink patches on cheeks
4. Malar flush on cheeks
5. Low vol pulse
6. Low pitch rumbling at the apex
181
Investigation of mitral stenosis
1. ECG - AF and LA enlargement
2. CXR - LA enlargement and pulmonary congestion
3. Echo - assess mitral valve mobility, gradient and mitral valve areas
182
Management of mitral stenosis
1. Treat AF
2. Medication - warfarin, [b-blockers, CCB, digoxin - control HR and prolong diastole], Diuretics reduce fluid overload
3. Serial echocardiography
4. Mitral balloon valvotomy
5. Mitral valve replacement
183
Examples of aortic valve disease
1. Aortic stenosis
2. Aortic sclerosis
3. Aortic regurgitation
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Define aortic valve stenosis
Narrowing of the aortic valve opening that restricts blood flow from the left ventricle to the aorta
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Normal and pathological aortic valve size
Normal = 3-4cm2
| Pathological < 1/4 normal
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Types of aortic stenosis
- Supravalvular
- Subvalvular
- Valvular
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Pathophysiology of aortic stenosis
- Pressure gradient develops between LV and aorta
- LV function initially maintained by compensatory pressure hypertrophy
- LV function declines as compensation exhausted
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Causes of aortic stenosis
- Senile calcification (most common)
- Congenital (bicuspid valve, Williams syndrome)
- Rheumatic heart disease
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Presentation of aortic stenosis
- Classic triad of angina, syncope, SOB
- Extertional dyspnoea
- Dizziness, faints
- Systemic emboli (if infective endocarditis)
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Signs of aortic stenosis
- Slow rising carotid pulse with narrow pulse pressure
- Heaving, non-displaced apex beat
- Ejection systolic murmur - crescendo-decrescendo character
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Investigations of aortic stenosis
- Echo - LV size and function assessed (LVH, dilation, ejection fraction, doppler derived gradient and valve area)
- Cardiac catheter can access valve gradient, LV function, CAD
- Pulsus parvus et tardus - weak and late pulse
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Differential diagnosis of aortic stenosis
1. Hypertrophic cardiomyopathy
| 2. Aortic sclerosis
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Management of aortic stenosis
1. Poor prognosis without surgery for symptomatic patients
2. Valve replacement
3. Percutaneous valvuloplasty/replacement
4. TAVI - transcatheter aortic valve implantation
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Define aortic sclerosis
Senile degeneration of the valve. There is an ejection systolic murmur, but no carotid radiation and normal pulse and S2
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Define aortic regurgitation
Leakage of blood into LV during diastole due to ineffective coaptation of the aortic cusps
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Causes of acute aortic regurgitation
1. Infective endocarditis
2. Ascending aortic dissection
3. Chest trauma
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Causes of chronic aortic regurgitation
1. Congenital
2. Connective tissue disorders (e.g. Marfan's)
3. Rheumatic fever
4. Takayasu arteritis
5. Rheumatoid arthritis
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Pathophysiology of aortic regurgitation
Combined pressure and volume overload.
| - Compensatory mechanisms = LV dilation, LVH, progressive dilation leads to HF
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Presentation of aortic regurgitation
- Breathlessness
- Orthopnoea (breathless lying down)
- Palpitations
- Diastolic blowing murmur
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Investigations for aortic regurgitation
1. CXR - enlarged cardiac silhouette and aortic root enlargement
2. Echo - evaluation of the AV and aortic root with measurement of LV dimensions and function
3. Cardiac catheterisation to assess severity of lesion, anatomy of aortic root
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Management of aortic regurgitation
1. Medical - vasodilators
2. Serial echo to monitor progression
3. Surgical repair/replacement of valve
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Examples of tricuspid valve disease
1. Tricuspid regurgitation
| 2. Tricuspid stenosis
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Define tricuspid regurgitation
A disorder in which the tricuspid valve does not close tight enough. This problem causes blood to flow backward into the RA when the RV contracts
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Causes of tricuspid regurgitation
1. Rheumatic fever
2. Infective endocarditis
3. Carcinoid syndrome
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Symptoms of tricuspid regurgitation
1. Fatigue
2. Hepatic pain on exertion
3. Ascites
4. Oedema
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Signs of tricuspid regurgitation
1. Pansystolic murmur
2. Pulsatile hepatomegaly
3. Jaundice
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Management of tricuspid regurgitation
1. Drugs - diuretics for systemic congestion, treat underlying cause
2. Valve repair/replacement
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Define tricuspid stenosis
Narrowing of the tricuspid valve opening. It restricts blood flow between the upper and lower part of the right side of the heart
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Causes of tricuspid stenosis
1. Rheumatic fever
2. Congenital
3. Infective endocarditis
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Symptoms of tricuspid stenosis
1. Fatigue
2. Ascites
3. Oedema
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Signs of tricuspid stenosis
1. Opening snap, early diastolic murmur at left sternal edge in inspiration
2. AF
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Investigation for tricuspid stenosis
Echo
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Treatment of tricuspid stenosis
1. Diuretics
| 2. Surgical repair/replacement
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Define pulmonary stenosis
A condition characterised by obstruction to blood flow from the RV to the pulmonary artery. The pulmonary valve leaflets are thickened and fused together along their separation lines
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Causes of pulmonary stenosis
1. Congenital (e.g. Turner syndrome)
| 2. Acquired - rheumatic fever and carcinoid syndrome
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Symptoms of pulmonary stenosis
1. Dyspnoea
2. Fatigue
3. Oedema
4. Ascites
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Signs of pulmonary stenosis
1. Dysmorphic facies
2. Ejection click
3. Ejection systolic murmur
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Investigations for pulmonary stenosis
1. ECG - p pulmonale, RBBB
2. CXR - prominent pulmonary arteries (post-stenotic dilatation)
3. Cardiac catheterisation is diagnostic
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Treatment of pulmonary stenosis
Pulmonary valvuloplasty or valvotomy
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Define rheumatic fever
Pharyngeal infection with Lancefield AB-haemolytic streptococci triggers with rheumatic fever 2-4 weeks later
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Pathology of rheumatic fever
An antibody to the carbohydrate cell wall of the streptococcus cross-reacts with valve tissue and may cause permanent damage to the heart valves
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Diagnosis of rheumatic fever
Must be evidence of recent strep infection plus 2 major criteria or 1 major+2minor
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Evidence of group A b-haemolytic streptococcal infection
- Positive throat culture
- Rapid streptococcal antigen test +ve
- Elevated or rising streptococcal antibody titre
- Recent scarlet fever
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Major criteria diagnosis of rheumatic fever
- Carditis (tachycardia, murmurs)
- Arthritis
- Subcutaneous nodules
- Erythema marginatum 3
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Minor criteria diagnosis of rheumatic fever
- Fever
- Raised ESR/CRP
- Arthralgia
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Management of rheumatic fever
1. Bed rest until CRP normal for 2 weeks
2. Benzylpenicillin
3. Analgesia for carditis/arthritis
4. Immobilise joints in severe arthritis
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Define infective endocarditis
Infection of the heart valves or other endocardial lined structures within the heart (e.g septal defects). Bad infection that showers infectious material around the bloodstream
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Types of IE
1. Left side native (mitral or aortic)
2. Left side prosthetic IE
3. Right side IE
4. Device related IE (pacemaker/defibrillator)
5. Prosthetic
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Causes of IE
1. Have abnormal valve (regurgitant or prosthetic)
2. Introduce infectious material into the bloodstream or directly onto the heart during surgery
3. Previous IE
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Pathology of IE
1. S. aureus gains access in skin via indwelling vascular lines or IV drug abuse
2. S. viridans access via blood from oropharnyx following tooth brushing or dentistry
3. Enterococci access blood following instrumentation of bowel or bladder
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Clinical presentations of IE
1. Left side = fever, valve damage. Right side = fever, chills, pulmonary symptoms (septic emboli)
2. Systemic infection signs
3. Embolisation (stroke, pulmonary embolus, MI)
4. Valve dysfunction (HF arrthymias)
5. Petechiae (skin lesions)
6. Splinter haemorrhage
7. Osler's nodes (purple node on pulp of digits)
8. Janeway lesions
9. Roth spots on fundoscopy
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Diagnosis of IE
Modified Duke critieria (definitive IE = 2M/3m or 1M/5m) M=major m=minor
233
Major criteria of IE
1. Bugs grown from blood cultures
| 2. Evidence of endocarditis on echo or new valve leak
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Minor criteria of IE
1. Predisposing factor (e.g IV drug abuse)
2. Fever
3. Vascular phenomena (e.g Janeway lesions)
4. Immune phenomena (e.g Oslar nodes)
5. Equivocal blood cultures
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Investigations for IE
1. CXR - cardiomegaly, pulmonary oedema
2. Regular ECG (look for heart block)
3. CT (emboli)
4. Raised CRP
5. Echo - TOE (-ve result doesnt eliminate)
6. Blood tests - require long incubation so slow results
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Treatment of IE
1. Antimicrobials (IV for 6 weeks)
2. Treat complications
3. Surgery - indicated if not cured by antibiotics, severe valve damage, remove infected devices, replace valve, remove large vegetations before embolise
237
Complications of IE
HF, arrhythmias, heart block, embolisation, stroke
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Define congenital heart disease
General term for a range of birth defects that affect the normal way the heart works. Vary from minor to incompatible with left ex-utero
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Examples of structural heart defects
1. Ventricular septal
2. Atrio-ventricular septal
3. Patent ductus arteriosus
4. Coarctation of the aorta
5. Bicuspid aortic valve and aortopathy
6. Pulmonary stenosis
7. Eisenmenger syndrome
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Define Eisenmenger syndrome
Any untreated congenital cardiac defect with intracardiac communication that leads to pulmonary HTN, cyanosis, reversal flow
241
Investigations of structural heart defects
1. Echo first line
2. CT and MR used to provide precise anatomical and functional info
3. Exercise testing assesses functional capacity
242
What is a ventricular septal defect
Abnormal connection between the 2 ventricles
243
Physiology of VSD
- High pressure LV
- Low pressure RV
- Blood flows from high to low pressure
- Increased blood flow through the lungs
244
Causes of VSD
Congenital or acquired post-MI
245
Symptoms of VSD
1. Severe HF in infancy
2. High pulmonary blood flow in infancy
3. Breathless
4. Poor feeding
5. Failure to thrive
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Signs of VSD
1. Small, breathless, skinny baby
2. Increased RR
3. Tachycardia
4. Enlarged heart on CXR
5. Murmur varies in intensity
6. Harsh pansystolic murmur at left sternal edge
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Complications of VSD
- Pulmonary HTN
- Eisenmenger's complex
- HF from vol overload
248
Pathophysiology of Eisenmenger's
1. Pulmonary HTN from initial left to right shunt
2. Damage pulmonary structure
3. Resistance to blood flow through lungs increases
4. RV pressure increases
5. Shunt reverses
6. De-oxygenated blood enters systemic circulation
7. Cyanotic
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Investigations for Eisenmenger's
1. ECG = normal
2. CXR = normal heart size, large pulmonary arteries
3. Cardiac catheter = step up in O2 saturation in RV
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Treatment of VSD
- Many close spontaneously
| - Surgical closure - failed medical therapy, symptomatic, shunt>3:1
251
Physiology of ASD
- Higher pressure in LA
- Shunt left to right
- Increased blood flow to right heart and lungs
252
Symptoms of ASD
1. Significant increased blood flow through the right heart and lungs in childhood
2. Right heart dilatation
3. SOB on exertion
4. Increased chest infections
5. Chest pain
6. Palpitations
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Signs of ASD
1. Pulmonary flow murmur
2. Fixed split-second sound (delayed closure of PV because more blood needs to be let out)
3. Big pulmonary arteries and heart on CXR
254
Investigations of ASD
1. ECG - RBBB with LAD or RAD
| 2. CXR - small aortic knuckle, pulmonary plethora, atrial enlargement
255
Complications of ASD
1. Eisenmengers complex
| 2. Paradoxical emboli
256
Treatment of ASD
1. May close spontaneously
| 2. Transcatheter closure more common than surgical
