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
Which arteries most commonly develop atherogenesis?
1) LAD 2) Right coronary arteries 3) Circumflex
26
Risk factors for atherosclerosis
``` Age Tobacco High serum cholesterol Obesity Diabetes Hypertension Family history ```
27
Where are atherosclerosis plaques distributed?
- Peripheral arteries - Coronary arteries - Focal distribution along artery length
28
The structure of an atherosclerotic plaque ?
- Lipid - Necrotic Core - Connective tissue - Fibrous cap
29
What initiates atherosclerosis formation?
Injury to the endothelial cells | - leads to endothelial dysfunction
30
What happens after endothelial cells are injured?
- Chemoattractants released - Attract leukocytes - Accumulate & migrate into vessel wall
31
Which inflammatory cytokines are found in plaques?
1) IL-1 2) IL-6 3) IFN (interferon)- gamma
32
Whats the earliest lesion of atherosclerosis?
Fatty streaks
33
When do fatty streaks present/
Less than 10 years old
34
What do fatty streaks consists of?
- Aggregations of lipid-laden macrophages | - T lymphocytes - within intimal layer
35
What do intermediate lesions consist of?
- Lipid laden macrophages (foam cells) - Vascular smooth cells - T lymphocytes
36
What are foam cells?
Macrophages that have taken up lots of lipids
37
What is happening in intermediate lesions?
Adhesion & aggregation of platelets to the vessel wall
38
Describe advanced lesions/fibrous plaques
- Impeded blood flow - Prone to rupture - Covered by dense fibrous cap - May be calcified
39
What is a fibrous cap made up of?
Extracellular matrix proteins | e. g collagen & elastin - laid down by smooth muscle cells (overlie lipid core & necrotic debris)
40
What do advanced lesions/fibrous plaques contains?
- Smooth muscle cells - Macrophages & foam cells - T lymphocytes - Red cells (filled with fibrin)
41
Why does a plaque rupture?
If balance shifts - increased inflammatory conditions/enzyme activity = cap becomes weak = plaque ruptures
42
How is the fibrous cap maintained?
Needs to be resorbed and redeposited
43
What is angina?
Chest pain or discomfort as a result of reversible myocardial ischaemia
44
What are the types of angina?
1) Stable 2) Unstable (crescendo) 3) Prinzmetal's angina
45
Describe stable angina
- Induced by effort | - Relieved by stress
46
Describe unstable angina
- 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
47
What causes Prinzmetal's angina?
Caused by coronary artery spasm
48
Why does myocardial ischaemia result in angina?
Mismatch between blood supply & metabolic demand
49
What can cause mismatch of blood supply & metabolic demand?
- Atheroma/stenosis of coronary arteries - Valvular disease - Aortic stenosis - Arrhythmia - Anaemia (less O2 transported)
50
What are precipitants ?
Anything that increases metabolic demand & decreases blood supply
51
What can decrease blood supply?
1) Anaemia 2) Hypoxemia 3) Hypothermia etc
52
What can increase metabolic demand?
1) Hyperparathyroidism 2) Cold weather 3) Hypertension 4) Emotional distress 5) Valvular disease
53
What are the 2 types of diagnostic tests that can determine angina?
1) Anatomical | 2) Physiological
54
Examples of anatomical tests for angina
CT/invasive angiography
55
What info does CT angiography produce?
- High negative predictive value (good for ruling out CAD) | - Low positive predictive value (difficult to interpret results)
56
What is CT angiography useful for?
Ruling out CAD in younger, lower risk patients
57
Examples of physiological tests for angina?
1) Treadmill test/ exercise 2) SPECT 3) Stress echo/cardiac MRI (same principle)
58
How does the treadmill test work?
- ECG on patient - patient runs uphill on treadmill in increasing increments - tries to induce ischaemia - monitor length of time patient can exercise for
59
What do you look for in a treadmill test & what does it mean?
ST elevation = late stage ischaemia
60
Disadvantages of treadmill test
Most patients are unsuitable | E.G: can't walk/exercise, are unfit, have bundle branch block
61
How does SPECT/myoview work?
- radio-labelled tracer injected - taken up by coronary arteries (due to good blood supply) - lights up NO LIGHT AFTER EXERCISE = MYOCARDIAL ISCHAEMIA
62
How does CT scan calcium scoring work?
If there is atherosclerosis in arteries = calcium appears white - significant calcium = angina
63
How to treat angina/CAD
1) Modify risk factors - stop smoking - encourage exercise - weight loss 2) Treat underlying conditions 3) Pharmacological
64
What are the pharmacological treatments of CAD/angina?
1) Aspirin 2) Statins 3) Betablockers 4) GTN spray 5) Ca2+ channel antagonists/blockers 6) Revascularisation
65
What does aspirin do?
- antiplatelet effect in coronary arteries - avoids platelet thrombosis - COX1 inhibitor - reduces prostaglandin synthesis & thromboxane A2 = reduced platelet aggregation - reduces events
66
What are the side effects of aspirin?
- gastric ulcerations | - excessive bleeding
67
How do statins work?
- HMG-CoA reductase inhibitors = reduces cholesterol produced by liver - reduce events - reduce LDL - anti-atherosclerotic
68
How do beta blockers work? | FIRST LINE ANTIANGINAL
- reduce force of contraction of heart - contractility - reduces HR & CO - reduce work of heart & O2 demand
69
Examples of beta blockers
Bisoprolol | Atenolol
70
Side effects of beta blockers
- tiredness - nightmares - bradycardia - erectile dysfunction - cold hands & feet
71
When should you not give beta blockers?
- asthma - heart failure/block - hypotension - bradyarrhythmias - low heart rate
72
How does GTN spray work? | FIRST LINE ANTIANGINAL
- 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
73
What is the side effect of GTN?
Headache immediately after use
74
How to Ca2+ channel antagonists/blockers?
- primary arterodilators - dilates systemic arteries = BP drops - reduces afterload - less energy required to produce same CO - less work & O2 demand
75
Example of Ca2+ channel blocker
Verapamil
76
What is revascularisation?
- restore patent coronary artery | - increase flow reserve
77
When is revascularisation done?
- when medication fails | - when high risk disease is identified
78
What are the types of revascularisation?
1) PCI - Percutaneous Coronary Intervention | 2) CABG - Coronary Artery Bypass Graft
79
What does PCI do?
- dilates coronary atheromatous obstructions - stent - keps artery patent - expanding plaque - makes artery bigger
80
What are the pros of PCI?
- less invasive - convenient - short recovery - repeatable
81
What are the cons of PCI?
- risk of stent thrombosis | - not good for complex disease
82
What is CABG? (procedure)
LIMA (left internal mammary artery) used to bypass proximal stenosis in LAD
83
What are the pros of CABG?
- good prognosis | - deals with complex disease
84
What are the cons of CABG?
- invasive - risk of stroke/bleeding - one time treatment - long recovery
85
What is the clinical presentation of angina?
- 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
86
What is the scoring criteria for angina?
1. Central, tight, radiation 2. Precipitated by exertion 3. Relieved by rest/GTN
87
What does a 3/3 score for angina mean?
Typical angina
88
What does a 2/3 score for angina mean?
Atypical angina
89
What does a 1/3 score for angina mean?
Non-anginal pain
90
Differential diagnosis of angina
- pericarditis/myocarditis - pulmonary embolism - chest infection - dissection of aorta - GORD
91
Acute Coronary Syndrome (ACS)
Umbrella term including STEMI, non-STEMI, unstable angina
92
What causes STEMI?
- complete occlusion of MAJOR coronary artery | = full thickness damage of heart muscle
93
How can STEMI be diagnosed?
- ECG - pathological Q wave some time after MI - ST elevation - Tall T waves / T wave inversion - LBBB A.K.A --> Q wave infarction
94
What causes non-STEMI
- complete occlusion of MINOR coronary artery | - partial thickness damage of heart muscle
95
What kind of diagnosis is non-STEMI?
Retrospective (made after troponin level results)
96
How can non-STEMI be diagnosed?
``` - troponin levels ECG: - ST depression - T wave inversion A.K.A --> non-Q wave infarction ```
97
Difference between unstable angina (UA) and non-STEMI
IN NON-STEMI: There is an occluding thrombus which leads to: - rise in serum troponin - rise in creatine kinase-MB
98
How many types of MI are there?
5
99
Type 1 MI
- spontaneous with ischaemia | - due to primary coronary event
100
Examples of type 1 MI
- plaque erosion/rupture - fissuring - dissection
101
Type 2 MI
- secondary to ischaemia | - due to increased O2 demand/ decreased supply
102
Examples of type 2 MI
- coronary spasm - coronary embolism - anaemia - arrhythmias - hypertension - hypotension
103
Type 3,4,5 MI
- due to sudden cardiac arrest | - related to PCI & CABG
104
Risk factors for MI
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
105
What are the basic steps leading to an MI?
Fatty streak > fibrotic plaque > atherosclerotic plaque > plaque rupture/fissure & thrombosis > MI/ Ischaemic stroke/ Sudden CVS death
106
What is the triggering cause of MI?
Rupture or erosion of fibrous cap of coronary artery plaque
107
What does rupture/erosion of plaque lead to?
- platelet aggregation - adhesion - localised thrombosis - vasoconstriction - distal thrombus embolisation
108
What is associated with a high risk of rupture?
- presence of rich lipid pool within plaque | - thin, fibrous cap
109
What causes thrombus formation / vasoconstriction?
Release of serotonin & thromboxane A2 | reduce coronary blood flow = so leads to MI
110
When does the thrombus result in partial occlusion?
In unstable angina - plaque has necrotic core - plaque has ulcerated cap
111
When does the thrombus result in total occlusion?
In MI | - plaque has necrotic core
112
Clinical presentation of MI
- 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
113
What is unstable angina associated with?
- breathlessness - pleuritic pain - indigestion
114
What is acute central chest pain associated with?
- sweating/nausea/vomitting - dyspnoea - fatigue - palpitations
115
What are the differential diagnoses of MI?
- angina - pericarditis - myocarditis - aortic dissection - pulmonary embolism - gastro-oesophageal reflux/spasm
116
What are the biochemical markers of MI?
1. Troponin (T & I) 2. CK-MB 3. Myoglobin
117
What is the pattern of troponin (T & I) levels in MI?
- serum levels increase 3-12 hours from onset of pain - levels peak at 24-48 hours - back to normal over 5-14 days
118
When do troponin levels peak?
24-48 hours after MI
119
When do troponin levels fall back to normal?
5-14 days
120
What is CK-MB a marker for? What does it determine?
Myocyte death | - determines re-infarction
121
When do levels of CK-MB drop back to normal?
After 36-72 hours
122
Why does CK-MB have low accuracy?
- present in serum of normal patients/ patients with significant skeletal muscle damage
123
What happens to myoglobin levels during MI?
Becomes elevated very early in MI
124
What is the problem with myoglobin as a marker and why?
- poor specificity | - present in skeletal muscle
125
What do you look for in a chest x-ray (CXR) when diagnosis MI?
- cardiomegaly - pulmonary oedema - widened mediastinum (aortic rupture)
126
Treatment for MI?
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
127
What is the % O2 saturation we should aim for when treating MI?
94-98% | 88-92& for COPD
128
Route of administration for aspirin?
Oral
129
Route of administration for P2Y12 inhibitors?
Oral
130
Examples of P2Y12 inhibitors?
- Clopidogrel - Prasugrel - Ticagrelor
131
Side effects of P2Y12 inhibitors?
- Neutropenia (low neutrophils) - Thrombocytopenia (low platelets) - Increased risk of bleeding
132
Route of administration for GP IIb/IIIa inhibitors?
ONLY IV
133
Examples of GP IIb/IIIa inhibitors?
- Abciximab - Tirofiban - Eptifbatide RISK OF BLEEDING
134
Route of administration for beta blockers?
Oral and IV
135
What is the route of administration for statins?
Oral
136
Examples of statins?
- Simvastatin - Pravastatin - Atorvastin
137
Route of administration for ACE inhibitors?
Oral
138
Examples of ACE inhibitors?
- Ramipril | - Lisonopril
139
Define acute myocardial infarction
Necrosis of cardiac tissue due to prolonged myocardial ischaemia due to complete occlusion of artery by thrombus
140
ECG change if infarct site is on the anterior side?
ST elevation in V1-V3
141
ECG change if infarct site is on the inferior side?
ST elevation II, III, aVF
142
ECG change if infarct site is on the lateral side?
- I - aVL - V5-V6
143
ECG change if infarct site is on the posterior side?
- ST depression V1-V3 - Dominant R wave - ST elevation V5-V6
144
ECG change if infarct site is on the subendocardial side?
Any
145
Pre-hospital treatment of MI?
- 300mg chewable aspirin - morphine - GTN spray
146
Hospital treatment of MI?
- IV morphine - oxygen if sats are <95% - beta blocker (atenolol) - P2Y12 inhibitor (clopidogrel)
147
What does fibrinolysis treatment of MI do?
Enhance breakdown of occlusive thromboses | - by activation of plasminogen - to form plasmin
148
Define cardiac failure
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
Main causes of cardiac failure?
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
Risk factors for cardiac failure
1. 65 or older 2. African descent 3. Men 4. Obesity 5. People who have had an MI
151
Why are women more protected against cardiac failure?
Oestrogen is a protective agent
152
How is venous return (preload) affected in cardiac failure?
- 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
How is outflow resistance (after load) affected in cardiac failure?
- increased afterload - increase in end- diastolic volume - dilatation of ventricles = means ventricles have the work harder - decrease in cardiac output
154
Systolic cardiac failure
- inability of the ventricle to CONTRACT | - decreased cardiac output
155
What causes systolic cardiac failure?
- IHD - Myocardial infarction - Cardiomyopathy
156
Diastolic cardiac failure
- inability of the ventricles RELAX & fill fully | - decreased cardiac output
157
What causes diastolic cardiac failure?
- hypertrophy | - aortic stenosis
158
What causes hypertrophy?
- chronic hypertension - increases after load - heart pumps against more resistance - cardiac myocytes grow bigger to compensate
159
How does hypertrophy cause diastolic heart failure?
- less space for blood to fill in the ventricles | - decreased cardiac output
160
How does aortic stenosis cause diastolic heart failure/
- increases afterload | - decreases cardiac output
161
Clinical presentation of cardiac failure?
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
What classification system is used to assess severity of cardiac failure symptoms?
New York Heart Association (NYHA)
163
What is the NYHA classification?
Class I - IV
164
What is Class I of the NYHA?
NO LIMITATION - Asymptomatic - no fatigue, dyspnoea or palpitations when exercising,
165
What is Class II of the NYHA?
SLIGHT LIMITATION - Mild HF - comfortable at rest - normal activity = fatigue, dyspnoea & palpitations
166
What is Class III of the NYHA?
MARKED LIMITATION - moderate HF - comfortable at rest - gentle activity = fatigue, dyspnoea & palpitations
167
What is Class IV of NYHA?
INABILITY TO CARRY OUT ANY PHYSICAL ACTIVITY WITHOUT DISCOMFORT - severe HF - symptoms occur at rest
168
Which methods can be used to diagnose cardiac failure?
- Blood tests - CXR - ECG - Echocardiography
169
What do you look for in a blood test for cardiac failure?
- Brain natriuretic peptide (BNP) - Full blood count - U&Es (urea and electrolytes) - liver biochemistry
170
How does BNP indicate cardiac failure?
- BNP secreted by ventricles - in response to increased myocardial wall stress - high levels in heart failure patients
171
What do BNP levels correlate with?
- ventricular wall stress | - severity of heart failure
172
Where is BNP secreted?
By the ventricles
173
What will a CXR show if there is heart failure?
- alveolar oedema - cardiomegaly - dilated upper lobe vessels of lungs - pleural effusions
174
What does the ECG show if there is heart failure?
UNDERLYING CAUSES: - ischaemia - LV hypertrophy in hypertension/arrhythmia
175
What would you do if ECG and BNP levels are abnormal?
Do an echocardiogram
176
What would you look for in an echocardiogram? (heart failure)
- cardiac chamber dimension - regional wall motion abnormalities - valvular disease - cardiomyopathies - sign of MI
177
Treatment of cardiac failure
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
What do inotropes do?
Alter cardiac contractility
179
Name the mitral valve diseases
1. Mitral stenosis | 2. Mitral regurgitation
180
Define mitral stenosis
Obstruction of the LV inflow that prevents proper filling during diastole
181
What is the most common cause of mitral stenosis?
Rheumatic heart disease | - secondary to rheumatic fever
182
How does rheumatic fever cause mitral stenosis?
- inflammation during fever = commissural fusion of valves - reduces mitral valve orifice area - causes doming seen on echocardiogram
183
What else can cause mitral stenosis?
- infective endocarditis | - mitral annular calcification
184
What are the risk factors for mitral stenosis?
- history of rheumatic fever | - untreated streptococcus infections
185
Pathophysiology of mitral stenosis
1. Progressive dyspnea (breathlessness) 2. Increased transmitral pressures 3. Right heart failure 4. Hemoptysis (coughing up blood)
186
How does mitral stenosis lead to dyspnea?
- LA atrial pressure increases - LA hypertrophies - LA dilatation = pulmonary congestion - reduced emptying
187
How does mitral stenosis lead to right heart failure?
- pulmonary venous/arterial and RH pressures increase - pulmonary capillary pressure = pulmonary oedema - RV hypertrophy, dilatation, failure
188
Why does the RV hypertrophy in mitral stenosis?
Due to pulmonary hypertension
189
What does RV hypertrophy, dilatation and failure cause?
Tricuspid regurgitation
190
What causes hemoptysis in mitral stenosis?
Rupture of bronchial blood vessels due to elevated pulmonary pressures
191
Clinical presentations of mitral stenosis
1. RH failure 2. AF 3. Systemic emboli 4. Prominent 'a' wave in jugular venous pulsations 5. Mitral facies 6. Heart sounds
192
Why does mitral stenosis cause AF?
Left atrium dilation gives rise to palpitations
193
Why does mitral stenosis cause systemic emboli?
Due to AF - most common in cerebral vessels
194
Why does mitral stenosis cause 'a' wave in JVP?
Pulmonary hypertension & RV hypertrophy
195
Why does mitral stenosis cause mitral facies?
Vasoconstriction in response to diminished cardiac output
196
What is mitral facies?
Pink/purple patches on the cheeks
197
What heart sounds will you hear in mitral stenosis?
1. Diastolic murmur | 2. Loud opening S1 snap
198
Where is diastolic murmur most prominent in mitral stenosis?
At the apex of the heart | best when the patient is lying flat in held expiration
199
Does the intensity of diastolic murmur correlate with severity of mitral stenosis?
No
200
Where is the loud opening S1 snap heard best in mitral stenosis?
At the apex when leaflets are mobile
201
What indicates a more sever mitral stenosis?
Shorter interval between S1 and S2 sound
202
Which methods are used to diagnose mitral stenosis?
1. CXR 2. ECG 3. Echocardiogram
203
What will CXR of mitral stenosis show?
- LA enlargement - Pulmonary oedema/congestion - Occasionally calcified mitral valve
204
What will ECG of mitral stenosis show?
- AF | - LA enlargement
205
What would you assess in an echocardiogram of mitral stenosis?
- mitral valve mobility - mitral valve gradient - mitral valve area
206
Why is medical therapy not very useful as a treatment for mitral stenosis?
MECHANICAL PROBLEM - MEDICAL THERAPY DOES NOT PREVENT PROGRESSION
207
Which meds would you still give for mitral stenosis and why?
CONTROL HEART RATE - improve diastolic filling - B blockers - CCBs - Digoxin CONTROL FLUID OVERLOAD - Diuretics
208
What are the surgical treatments for mitral stenosis?
1. Percutaneous mitral balloon valvotomy (PMBV) | 2. Mitral valve replacement
209
How does PMBV work?
- 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
Define mitral regurgitation
Backflow of blood from the LV to the LA during systole
211
What are the causes of chronic mitral regurgitation?
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
What is myxomatous degeneration? (MVP)
Weakening of chordae tendinae | = floppy mitral valve that prolapses
213
Risk factors for mitral regurgitation?
- females - lower BMI - age - renal dysfunction - prior MI
214
Pathophysiology of mitral regurgitation
Pure volume overload - due to leakage of blood into LA during systole
215
What are the compensatory mechanisms for pure volume overload?
- LA hypertrophy & increased contractility - LA dilation & RV dysfunction due to pulmonary hypertension - progressive LV overload = dilatation = heart failure
216
What would you hear during auscultation of mitral regurgitation?
- soft S1 sound - pan systolic murmur at apex radiating to axilla - displaced hypderdynamic apex beat - prominent extra 3rd heart sound (S3)
217
Does the intensity of murmur correlate with severity in MR?
Yes - in chronic
218
What are the clinical presentations of MR?
- exertion dysponea - fatigue & lethargy (reduced CO) - increased stroke volume felt as a palpitation -
219
How long is the compensatory phase for MR?
10-15 years
220
When does mortality for MR rise drastically?
If ejection fraction <60%
221
What's the mortality rate for severe MR?
5% / year
222
What would an ECG of MR show?
- LA enlargement - AF - LV hypertrophy (in severe)
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What would a CXR of MR show?
- LA enlargement | - central pulmonary artery enlargement
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What would an echocardiogram of MR show?
- estimation of LA & LV size & function - valve structure assessment - transoesophageal echo is v helpful
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What medication would you give for MR and why?
1. ACEI & hydralazine - vasodilators 2. B blockers, CCB, digoxin - control heart rate 3. Anticoaggulants in AF 4. Diuretics for fluid overload
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Name the types of aortic valve disease
1. Aortic stenosis | 2. Aortic regurgitation
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Define aortic stenosis
Narrowing of the aortic valve resulting in obstruction to the LV stroke volume
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What symptoms does aortic stenosis lead to?
1. Breathlessness 2. Chest pain 3. Syncope 4. Fatigue
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What is the normal aortic valve area?
3-4cm^2
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When do symptoms for aortic stenosis occur?
When the valve area is 1/4th of normal
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What are the 2 main causes of aortic stenosis?
1. Ageing | 2. Congenital
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Name the 3 types of aortic stenosis
1. Valvular 2. Subvalvular - fibrous ridge/diaphragm below valve 3. Supravalvular - fibrous diaphragm above valve
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What's the most common type of aortic stenosis?
Valvular
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What are the 3 main causes of aortic stenosis?
1. Calcific aortic valvular disease (CAVD) 2. Calcification of congenital bicuspid aortic valve (BAV) 3. Rheumatic heart disease
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Describe a bicuspid aortic valve
Valve has 2 leaflets instead of 3
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Risk factors for aortic stenosis
- BAV | - congenital BAV more common in MALES
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Pathophysiology of aortic stenosis
- 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
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When is LV obstruction more severe in aortic stenosis, and why?
During exercise BECAUSE: - increase CO - but due to narrowing CO can't increase - BP falls - coronary ischaemia worsens - myocardium fails - results in arrhythmias
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What are the 4 main clinical presentations of aortic stenosis?
- syncope - angina - heart failure - dyspnoea on exertion
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What heart sounds would you hear on a patient with aortic stenosis?
- soft/absent 2nd heart sound - prominent 4th heart sound (bc of LV hypertrophy) - ejection systolic murmur (crescendo-decrescendo) LOUDNESS DOES NOT EQUAL SEVERITY
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Name the differential diagnoses of aortic stenosis?
- aortic regurgitation | - subacute bacterial endocarditis
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What info would an echocardiogram of aortic stenosis obtain?
1. LV size/function - LVH / dilation / ejection fraction 2. Doppler derived gradient / valve area
243
What would an ECG of aortic stenosis show?
- LVH - left atrial delay - LV 'strain' pattern - depressed ST segments - T wave inversion (in aVL, V5, V6, lead I)
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What would CXR of aortic stenosis show?
- LVH | - calcified aortic valve
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How would you treat aortic stenosis?
- rigorous dental hygiene (increased risk of IE) - mechanical problem = CAN'T RLY FIX - aortic valve replacement - transcutaneous aortic valve implantation (TAVI)
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Why would vasodilators be a bad treatment idea for aortic stenosis?
- may trigger hypotension | = leads to syncope
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Describe the process of TAVI
- catheter passed up aorta - inflate balloon across valve - cracks calcification - pass 2nd catheter - leaves stent with a valve = new aortic valve
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Describe aortic regurgitation
Leakage of blood into the LV from aorta during diastole | because of inactive coaptation of aortic cusps
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What are the main causes of aortic regurgitation and are the chronic or acute?
1. Congenital BAV - chronic 2. Rheumatic fever - chronic 3. Infective endocarditis - acute
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What are the risk factors for aortic regurgitation?
1. SLE 2. Marfan's & Ehlers-Danlos syndrome 3. Aortic dilation 4. Infective endocarditis / aortic dissection
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Pathophysiology of aortic regurgitation
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
Why/how are the coronary arteries affected in aortic regurgitation?
- coronary arteries filled during diastole BUT - regurgitation = diastolic BP falls - so coronary perfusion decreases
253
Why does cardiac ischaemia develop in aortic regurgitation?
- large LV size = less efficient - demand for O2 increases - ischaemia develops
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Clinical presentation of aortic regurgitation
- exertion dyspnea - angina / palpitations / syncope - wide pulse pressure - apex beat displaced laterally
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What heart sounds can be heard in aortic regurgitation?
- diastolic murmur at left sternal border | - systolic murmur bc of increased flow across aortic valve
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What are the differential diagnoses of aortic regurgitation?
- heart failure - infective endocarditis - mitral regurgitation
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What info will an echocardiogram of aortic regurgitation show?
- evaluation of aortic valve & root | - LV dimensions & function
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What will a CXR of aortic regurgitation show?
- enlarged cardiac silhouette - aortic root enlargement - LV enlargement
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What will an ECG of aortic regurgitation show?
- signs of LV hypertrophy (volume overload) - tall R waves - deeply inverted T waves in left chest leads - deep S waves in right chest leads
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How would you treat aortic regurgitation?
- consider infective endocarditis prophylaxis - ACEI - improve stroke volume & reduce regurgitation - serial echos - valve replacement
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Under what conditions do ACEI work for aortic regurgitation?
- only if patient is symptomatic | - or has hypertension
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Define infective endocarditic
Infection of the endocardium or vascular endothelium of the heart
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What is infective endocarditis also known as?
Subacute bacterial endocarditis
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What does infective endocarditis affect?
- valves w/ congenital/acquire defects (usually on left side) - normal valves w virulent organisms (strep. pneumonia / staph. aureus) - prosthetic valves - pacecmakers
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Amongst whom is right sided IE more common?
IV drug addicts
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Who is most affected by IE?
- common in developing countries - elderly people with prosthetic valves - young IV drug user - young with congenital heart disease - males
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What causes IE?
- Staph. aureus (most common) - pseudomonas aeruginosa - Strep. viridian's (dental) - gram +, alpha haemolytic & optochin resistant
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List the risk factors for IE?
- IV drug use - poor dental hygiene - skin/soft tissue infection - IV cannula - cardia surgery - pacemaker - dental treatment
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Pathophysiology of IE
- presence of organisms in blood + abnormal cardiac endothelium - damaged endothelium = inc. platelet growth & fibrin deposit - organisms adhere & grow = infected vegetation
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List the clinical presentations of IE
- embolic events & sepsis of unknown origin - fever/sweats + any risk factor - ventricular arrhythmias / heart failure / conduction disturbances - kidney dysfunction / MI / bone infections
271
Examples of clinical manifestations of IE?
- 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
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How to diagnose IE?
- DUKES CRITERIA !!! - BLOOD CULTURES !!!!! (IMPORTANTTTTTTTTT) - Blood test - urine test - ECG - echo (transthoracic / transoesophageal) - CXR
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How many blood cultures should you take to identify IE?
- 3 from different sites over 24 hours | - before antibiotics started
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What will a blood test show if a patient has IE?
- raised ESR - measures inflammation rate in body - raised CRP - neutrophilic - normochromic, normocytic anaemia
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What will a CXR of IE show?
Cardiomegaly
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What ECG of IE show?
- long PR interval at regular intervals
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What are the advantages of transthoracic echo?
- non invasive - safe - no discomfort - can identify vegetations (if bigger than 2mm)
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What are the disadvantages of transthoracic echo?
- low sensitivity | - negative TTE does NOT exclude IE
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What are the advantages of TOE?
- more sensitive - can visualise mitral lesions / aortic root abscess - BETTER AT DIAGNOSING
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What are the disadvantages of TOE?
- very invasive & uncomfortable
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How would you treat IE?
- 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)
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What antibiotics would you use to treat IE if it is caused by staphylococcus?
- vancomycin | - rifampicin
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What antibiotics would you use to treat IE if it is NOT causes by staphylococcus?
Penicillin: - benzylpenicillin AND - gentamycin
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How can patients prevent IE in general?
- good oral hygiene
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Define cardiomyopathy
Group of diseases of the myocardium that affect the mechanical or electrical function of the heart
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Name the 4 types of cardiomyopathy
1. Hypertrophy 2. Dilated 3. Restricted 4. Arrhythmogenic right ventricle
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What are the risk factors for cardiomyopathy?
- family history - high BP - obesity - diabetes - previous MI
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Describe hypertrophic cardiomyopathy (HCM)
- 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
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What is the cause of HCM?
Sarcomeric protein gene mutations (Troponin T & B-myosin)
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Pathophysiology of HCM
- hypertrophic, non-compliant ventricles - impairs diastolic filling - reduces stroke volume - reduces cardiac output
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Clinical presentation of HCM
- myocardium hypotrophy (interventricular septum) - sudden death - chest pain/angina/dyspnea/ dizziness / syncope - LV outflow obstruction - cardiac arrhythmia - ejection systolic murmur - jerky carotid pulse
292
What will an ECG of HCM show?
Will be normal - show LVH - progressive T wave inversion - deep Q waves
293
What will an echo of HCM show?
- ventricular hypertrophy | - small LV cavity
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What is the genetic cause of HCM?
Autosomal dominant
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How do you treat HCM?
- anti-arrhythmatic meds ( amiodarone) - CCBs - B blocker
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Define dilated cardiomyopathy
Dilated LV which contracts poorly/ has thin muscle
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What is the genetic cause of dilated cardiomyopathy?
Autosomal dominant
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What are the other causes of dilated cardiomyopathy?
- ischaemia - alcohol - thyroid disorder - CYTOSKELETAL GENE MUTATIONS
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Pathophysiology of dilated cardiomyopathy
- LV / RV / all chambers dilatation = dysfunction | - poor contractile force = progressive dilatation
300
Clinical presentation of dilated cardiomyopathy
- shortness of breath - dyspnea - heart failure - arrhythmias - thromboembolism - sudden death - increased jugular venous pressure
301
What would a CXR of dilated cardiomyopathy show?
Cardiac enlargement
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What could an ECG of dilated cardiomyopathy show?
- tachycardia - arrhythmia - non specific T wave changes
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What would an echo of dilated cardiomyopathy show?
Dilated ventricles
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Treatment of dilated cardiomyopathy
Conventional treatment for heart failure and AF
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What are the causes of restricted cardiomyopathy?
- amyloidosis - idiopathic - sarcoidosis - end-myocardial fibrosis
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Pathophysiology of restricted cardiomyopathy
- normal/decreased vol. in both ventricles - bi-atrial enlargement - normal wall thickness - normal cardiac valves - impaired ventricular filling
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Clinical presentation of restricted cardiomyopathy
- dyspnea, fatigue, embolic symptoms - elevated JVP - diastolic cllapse - elevated venous pressure in inspiration - 3rd & 4th heart sounds - hepatic enlargement - ascites - dependent oedema
308
How to diagnose restricted cardiomyopathy?
CXR, echo and ECG are abnormal but non-specific | - cardiac catheterisation helps diagnose
309
Treatment for restricted cardiomyopathy
- no specific treatment - patients die within a year - cardiac transplantation
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What characterises arrhythmogenic RV cardiomyopathy? (ARVC)
Myocardium is replaced with progressive fatty & fibrous tissue
311
What is the cause of ARVC
UNKNOWN | - familial form = autosomal dom. with incomplete penetrance
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Pathophysiology of ARVC
- desmosome gene mutation - RV replaced by fat. fibrous tissue - muscle dies & replaced with fat (part of inflammatory process)
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Clinical presentation of ARVC
- conduction issues (cardiac cells are less close together) - arrhythmia - syncope - right heart failure (in late stages)
314
What might an ECG show for ARVC?
T wave inversion
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What may an echo show for ARVC?
Right ventricular dilation
316
Treatment of ARVC
- B blockers (atenolol) - Amiodarone (for symptomatic arrhythmias ) - occasional transplant
317
What are structural/congenital heart defects due to?
- misplaced structures | - arrest of progression of normal structure development
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What are the causes of congenital heart disease?
- maternal prenatal rubella - maternal alcohol misuse - singe genes (e.g Down's) - drugs (thalidomide, lithium) - diabetes of the mother - genetic abnormalities
319
What congenital heart disease can maternal prenatal rubella infection lead to?
- persistent ductus arteriosus | - pulmonary valvular & arterial stenosis
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What congenital heart disease does maternal alcohol misuse lead to?
Septal defects
321
What congenital heart diseases can genetic abnormalities lead to?
- arterial spatial defect | - congenital heart block
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Why should pregnancy be avoided if the woman has a congenital heart disease?
- pulmonary hypertension - severe left heart obstruction - systemic ventricular impairment (ejection fraction <30%) - Marfan's syndrome (aortic root diameters = >47mm)
323
What are the clinical presentations of congenital heart diseases?
- central cyanosis - pulmonary hypertension - clubbing of fingers - syncope - growth retardation
324
What specific problems do adolescents / adults with congenital heart disease present with?
- endocarditis - calcification & stenosis of congenitally deformed valves - atrial & ventricular arrhythmias - sudden cardiac death - RH failure - end-stage heart failure
325
What is central cyanosis?
- patients' skin will be blueish
326
Why does central cyanosis occur?
- R-L shunting / complete mixing of systemic & pulmonary blood = poorly oxygenated blood entering systemic circulation
327
What leads to pulmonary hypertension in congenital heart disease?
- large left to right shunting
328
What does the high pressure from shunting lead to?
- thickening of vascular walls of the pulmonary arteries
329
What does the thickening of pulmonary artery walls cause?
Increased pulmonary artery vascular resistance
330
What does increased pulmonary artery vascular resistance lead to?
- increase in RV pressure - REVERSAL OF SHUNT TO R TO L = leads to cyanosis - EISENMENGER'S REACTION / COMPLEX
331
Describe atrial septal defects
- abnormal connection between atria - LA pressure > RA - shunts from L to R - acyanotic (NOT blue) - increased flow into RH & lungs
332
What can happen if atrial septal defects go untreated?
- RH overload & dilatation - RV also dilates to deal with inc. pulmonary flow - RVH - pulmonary hypertension - increased risk of IE
333
Clinical presentations of atrial septal defects
- dyspnea - exercise intolerance - may develop atrial arrhythmias from RA dilatation - pulmonary flow murmur - fixed split 2nd heart sound
334
What will a CXR of atrial septal defects?
- large pulmonary arteries | - large heart
335
What will an ECG of atrial septal defects?
- RBBB (due to RV dilatation)
336
What will an echo of atrial septal defects?
- RH hypertrophy & dilation | - pulmonary artery hypertrophy & dilation
337
What are the treatments for atrial septal defects?
- surgical closure | - percutaneous (key hole technique)
338
Describe ventricular septal defects (VSD)
- abnormal connection between 2 ventricles - LV pressure > RV pressure - L-R shunt - acyanotic - increased blood flow through lung
339
What are the clinical presentations for LARGE VSD?
- small breathless skinny baby - increased resp. rate - tachycardia - big heart on CXR - murmur varies in intensity
340
What are the clinical presentations for SMALL VSD?
- loud systolic murmur - buzzing sensation - well grown - normal HR & heart size
341
Treatment for VSD
- some will spontaneously close - surgical closure - prophylactic antibiotics
342
What drug do you use to treat moderately VSD?
- Furosemide | - ACE inhibitors (ramipril & digoxin)
343
Describe atrio-ventricular septal defects (AVSD)
- instead of 2 separate AV valves there is ONE - this valve leaks - can be complete / partial
344
What genetic mutation is AVSD associated with?
Down's syndrome
345
What are the clinical presentations in patients with complete AVSD?
- breathlessness as a neonate - poor weight gain / feeding - torrential pulmonary flow = Eisenmenger's = cyanosis
346
What are the clinical presentations in patients with partial AVSD?
- dyspnea - tachycardia - exercise intolerance - can present in late adulthood
347
What is the treatment for a large AVSD?
- pulmonary artery banding | - surgical repair is challenging
348
What is the treatment for partial AVSD?
May be left alone IF there is no right heart dilatation
349
Describe patent ductus arteriosus (PDA)
- 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
What does PDA increase the risk of?
Infective endocarditis
351
What are the clinical presentations of PDA?
- continuous machinery murmurs - bounding pulse - large heart & breathlessness - Eisenmenger's w/ differential cyanosis - tachycardia
352
What will a CXR of PDA show?
- prominent aorta & pulmonary arterial system
353
What will an ECG of PDA show?
- LA abnormality | - LV hypertrophy
354
What will an echo of PDA show?
Dilated LA & LV
355
How would you treat PDA?
- closed surgically / percutaneously (low risk complications) - indomethacin (prostaglandin inhibitor) given to stimulate duct closure
356
Describe coarctation of the aorta
- narrowing of the aorta at/distal to insertion of ductus arteriosus
357
What does the narrowing of the aorta cause?
Excessive blood flow being diverted through carotid & subclavian vessels - into systemic shunts = causes stronger perfusion to upper body than lower
358
What is coarctation of the aorta associated with?
- Turner's syndrome - Berry aneurysms - patent ductus arteriosus
359
What are the clinical presentations of coarctation of the aorta?
- right arm / upper limb hypertension - murmur - discrepant blood pressure between upper and lower limbs
360
What are the long term problems of aortic coarctation?
HYPERTENSION - leads to: - early coronary artery disease - early strokes - sub-arachnoid haemorrhage
361
What will a CXR of aortic coarctation show?
- dilated aorta indented at site of coarctation
362
What will an ECG of aortic coarctation show?
LVH
363
What will a CT of aortic coarctation show?
- demonstrates coarctation | - quantifies flow
364
How would you treat aortic coarctation?
- surgery - balloon dilation & stenting (risk of aneurysm formation at the site of repair)
365
List the clinical presentations for tetralogy of Fallot
- central cyanosis - dyspnea - low birthweight/ growth - delayed puberty - systolic ejection murmurs
366
What will a CXR of tetralogy of Fallot show?
Boot shaped heart