Cardiovascular Flashcards
(346 cards)
1
Q
Define atherosclerosis
A
A hardened plaque in the intima of an artery inflammatory process.
2
Q
Define Atherogenesis
A
development of an atherosclerotic plaque
3
Q
Where does plaque build up?
A
In the peripheral and coronary arteries
4
Q
What is seen as a precursor to atherosclerosis?
A
Fatty streaks
5
Q
What can Atherosclerotic plaque cause?
A
- Heart attack
- Gangrene
- Stroke
6
Q
What are the constituents of atherosclerotic plaque?
A
- Lipid core
- Necrotic debris
- Connective tissue
- Fibrous Cap
- Lymphocytes
7
Q
Give 5 risk factors for atherosclerosis
A
- Family history
- Age
- Smoking
- High LDLs
- Obesity
- Diabetes
- Hypertension
8
Q
Which layer is thinned by atheromatous plaque?
A
The media
9
Q
What is the role of a chemo-attractant?
A
Signal to leukocytes which accumulate and migrate into vessel walls -> Cytokine release
This causes inflammation
10
Q
What triggers chemoattractants?
A
A stimulus such as endothelial injury.
11
Q
What are the 5 steps of atherosclerotic progression?
A
- Fatty streaks
- Intermediate lesions
- Fibrous plaque
- Plaque rupture
- Plaque erosion
12
Q
What is the process of leukocyte recruitment?
A
- Capture
- Rolling
- Slow rolling
- Adhesion
- Trans migration
13
Q
What does the fatty streak consist of?
A
Foam cells and T lymphocytes
14
Q
What do intermediate lesions consist of?
A
Foam cells, T lymphocytes, smooth muscle, platelet adhesion and EC lipid pools
15
Q
What do fibrous plaque consist of?
A
Cap overlies lipid core and necrotic debris, macrophages, foam cells, T lymph
16
Q
Why are Fibrous plaque’s prone to rupture and what is the consequence?
A
The FP constantly grows and recedes, the Fibrous cap must be reabsorbed and redeposited
If balance is shifted in favour of inflammatory conditions, cap becomes weak and plaque ruptures
Consequence - thrombus and vessel occlusion = impeding blood flow.
17
Q
What is the treatment for atherosclerosis?
A
Percutaneous coronary intervention (PCI)
18
Q
What is a limitation of PCI?
A
The risk of restenosis.
19
Q
What is done to minimise the risk of restenosis post PCI?
A
Using Drug-eluting stents –> anti proliferative and drugs that inhibit healing to prevent restenosis
20
Q
What can be used to prevent atherosclerosis?
A
Aspirin as it is a platelet cyclooxygenase inhibitor
21
Q
What is Angina?
A
Mismatch of oxygen demand and supply experienced on exertion. A type of IHD.
22
Q
What is the main cause of Angina?
A
Most common cause is narrowing of the coronary arteries due to atherosclerosis
23
Q
Describe the pathophysiology of angina.
A
On exertion there’s an increased O2 demand, blood flow obstructed by plaque
This causes myocardial ischaemia –> angina.
Can be reversed by resting.
24
Q
List 5 causes of Angina
A
- Narrowed coronary artery
- Increased Distal resistance = LV hypertrophy
- Reduced O2 carrying capacity – anaemia
- Coronary artery spasm
- Thrombosis
25
List 5 modifiable risk factors for angina.
1. Smoking
2. Diabetes
3. High cholesterol
4. Obesity/sedentary lifestyle
5. Hypertension
26
List 3 non modifiable risk factors
1. Age
2. Male
3. Family history/genetics
27
What happens to microvascular resistance and flow when myocardial demand increases.
Microvasc resistance decreases
| flow increases
28
What happens to microvascular resistance in a patient with CV disease
Epicardial resistance is high so Microvasc resistance drops at rest to compensate.
When exerted it cannot drop any lower = angina
29
How might a patient present with Angina?
Centralised crushing pain, heavy and tight
May get worse with cold weather, stress and heavy meals.
Always gets worst post exertion.
30
Give 3 symptoms of Angina
1. Crushing central chest pain
2. Pain is relieved at rest or using a GTN spray
3. Pain is provoked by physical exertion
4. Pain may radiate to arms, neck or jaw
5. Breathlessness
31
What investigations could be considered for Angina?
1. ECG – usually normal
2. CT Angiography – has a high NPV and is good at excluding disease.
3. Exercise tolerance test – induce ischaemia
4. Invasive angiogram – tells you FFR – pressure gradient across stenosis
32
What test would you do to decide which investigation may be the best?
Pre test probability of CAD --> considers gender, age and typicality of pain.
33
What pharmacological therapies are used for Angina?
1. Beta blockers
2. Nitrates
3. Calcium channel blockers
34
How do beta blockers work?
Antagonise sympathetic action --> neg inotropic and chronotropic
Can cause bradycardia, tiredness and erectile dysfunction.
35
When shouldn't you give someone beta blockers?
If they have bradycardia or asthma
36
How do Nitrates work?
Venodilator --> decreased venous return --> decreased preload and less myocardial demand
37
How do calcium channel blockers work?
Arteriodilators --> reduced bp --> reduced afterload --> reduced myocardial demand
38
What primary prevention measure could be taken for Angina?
Risk factor modification and low dose aspirin
39
What secondary prevention measures could be taken for angina?
Risk factor modification, pharmacological therapies, interventional therapies e.g. PCI
40
What drugs can be used to improve the prognosis of someone at risk of angina?
Statins - Reduce amount of LDL in the blood.
Aspirin - COX inhibitors, prevents TXA2 Platelet aggregation (CAN CAUSE GASTRIC ULCERATION)
41
Define Revascularisation
Restores patent coronary artery and increases blood flow e.g. PCI and CABG
42
Two advantages of PCI and one disadvantage
Less invasive, convenient and acceptable
| Risk of restenosis
43
One advantage and two disadvtanges of CABG
Advantage - very effective
| Disadvantage - Very invasive, long recovery time
44
What is DVT?
A blood clot that develops within a deep vein in the body, usually the leg.
45
What are the symptoms of DVT?
```
Nonspecific symptoms
Pain and swelling
Tenderness
Warmth
Slight discolouration
```
46
What investigations would you order in DVT?
D-dimer – look for breakdown of fibrin products, if normal it excludes DVT
Ultrasound compression scan – if you can’t squash the vein it’s a clot.
47
What is the treatment of DVT?
1. LMWH
2. Oral Warfarin or DOAC (direct oral anti-coag)
3. Compression stockings
4. Treat underlying cause e.g. malignancy
48
What are the risk factors for DVT?
1. Surgery, immobility, leg fracture
2. OCP,HRT
3. Long Haul flights
4. Genetic predisposition
5. Pregnancy
49
How can you prevent DVT?
1. Hydration
2. Mobilisation
3. Compression stockings
4. Low dose LMWH (Low weight molecular heparin
50
What is the consequence of a dislodged DVT?
PE
51
How would you describe an Arterial thrombus?
platelet rich - white thrombosis
52
How would you describe a venous thrombus?
Fibrin rich - red thrombosis
53
Give 3 consequences of Arterial thrombosis
1. MI
2. Stroke
3. Peripheral vasc disease-e.g. gangrene
54
How would you treat an arterial thrombus?
Aspirin, LMWH, Thrombolytic therapy
55
What are the consequences of Venous Thrombosis?
PE
56
How does warfarin work?
It is an agonist of Vit K and produces non functional clotting factors 2,7,9,10
57
Why is warfarin difficult to use?
Constant monitoring
Lots of interactions
Teratogenic
58
What is a Pulmonary embolism?
A blood clot that has broken off and traveled to the lung.
59
What are the symptoms of PE?
Breathlessness
Pleuritic chest pain
SOB
60
What are the signs of PE?
Tachycardia, tachypnoea, pleural rub.
61
What can PE Cause?
Hypotension
Cyanosis
severe dyspnoea
Right sided heart failure/strain
62
What investigations would you order for a PE?
1. CXR normal, ECG Tachy
2. ABG – Type 1 resp failure, decreased O2 and CO2
3. Normal D-dimer excludes diagnosis
4. Ventilation perfusion scan – mismatch defects
63
What is the treatment for PE?
LMW Heparin, oral warfarin, DOAC, treat cause if possible.
64
How can you prevent a PE?
1. Hydration
2. Mobilisation
3. Compression stockings
4. Low dose LMWH (Low weight molecular heparin)
65
What is acute pericarditis?
inflammatory pericardial syndrome with or without effusion.
66
What is the major differential diagnosis?
Myocardial infarction
67
What are the symptoms of acute pericarditis?
1. Chest pain --> sharp, pleuritic, rapid onset pain radiates to the arm
2. Dyspnoea
3. Cough
4. Hiccups – caused by irritation of phrenic nerve
5. Skin rash
68
Why does cardiac tamponade sometimes occur in pericarditis?
The parietal pericardium can adapt when effusions accumulate
69
What are the causes of pericarditis?
1. Viral (Enteroviruses)
2. Bacterial e.g. Mycobacterium TB
3. Autoimmune e.g. RA
4. Neoplastic
5. Metabolic e.g. Uraemia
6. Traumatic and iatrogenic
7. Idiopathic
70
What investigation would you do for pericarditis?
1. ECG
2. CXR
3. Bloods
4. Echocardiogram
5. FBC, CRP, Cardiac enzymes
71
What would the ECG show?
ECG --> PR depression, saddle shaped ST elevation
72
What must a patient have to make a diagnosis of pericarditis?
Patient must have at least two of the following:
- Friction rub
- Chest pain
- ECG changes
- Pericardial effusion
73
How would you treat pericarditis?
1. Avoid strenuous activity until symptoms resolve
2. NSAID or aspirin – high doses
3. Colchicine – anti inflammatory
74
What is haemopericardium?
Direct bleeding from vasculature through ventricular wall post MI
75
What is dresslers syndrome?
A secondary form of pericarditis
- Myocardial injury stimulates auto-antibodies against the heart
- Causes fever, chest pain and a pericardial rub (Occurs 2-10 weeks after MI )
76
What is giant cell arteritis?
Vasculitis, localised, chronic and granulomatous inflammation of the temporal arteries.
77
Signs of Giant cell arteritis?
Thickened often palpable blood vessels
| Evidence of granulomatous inflammation
78
What is a consequence of giant cell arteritis?
Blindness if the occular artery is affected
79
What criteria is used to diagnose IE?
The duke criteria.
80
What is infective endocarditis?
Infection of the heart valves or other endocardial lined structure within the heart
81
Describe the pathogenesis of IE
Microbial adherence --> vegetation on valve --> cardiac valve distortion
Causes cardiac failure and septic problems
82
What is the hallmark of IE?
Vegetation - lumps of fibrin hanging off heart valves
83
What are the causes of IE?
1. Staph Aureus
2. Staph Epidermis (Coagulase neg staph)
3. Strep Viridians (alpha haemolytic)
84
Where are vegetations likely to grow?
Atrial surface of AV valves and ventricular surface of SL valves
85
Who is at risk of Infective endocarditis?
Elderly, IVDU, Those with rheumatic fever and Those with prosthetic valves
86
What are the risk factors for IE?
1. Having a regurgitant or prosthetic valve
| 2. If infectious material is introduced into the blood stream during surgery
87
What are the symptoms of IE?
1. Signs of systemic infection
2. Embolization e.g. stroke, pe, mi
3. Valve dysfunction e.g. HF or arrhythmia
88
What are the signs of IE?
splinter haemorrhages, oslers nodes, jaenway lesions, roth spots, heart murmurs
89
What investigations should be done if IE is suspected?
1. Blood culture
2. Echocardiogram shows endocardial involvement
3. Bloods – raised ESR/CRP
4. ECG
90
Give one disadvantage and two advantages of Transthoracic echo's
Poor images, but safe and nnon invasive
91
Give one advantage and two disadvtanges of transoesophageal echos
Good pictures, discomfort, perforation + aspiration possible
92
What criteria is used for diagnosing infective endocarditis?
Dukes criteria
93
How do you treat infective endocarditis?
1. Antibiotic based cultures
2. Treat any complications
3. Surgery
94
What are the different types of Infective endocarditis?
1. Left sided native IE
2. Left sided prosthetic IE
3. Right sided IE
4. Device related IE
95
True of false - Left sided IE is more likely to cause thrombo emboli.
True
96
True of false - Right sided IE is more likely to spread to the lungs.
True.
97
What are some indications for surgery in a patient with IE?
- AB not working
- Complications
- To remove infected devices
- To replace the valve
- To remove large vegetations before they embolise
98
What is the standard treatment of Myocardial infarction?
- MONA - Morphine,oxygen,nitrogen,aspirin
- PCI
- Aspirin and clopidogrel
- LMWH
- Anti-anginals --> Beta blockers, CCB, nitrates
- Prevent secondary event
99
What is the secondary prevention measures for NSTEMI?
1. Aspirin
2. Clopidogrel (P2Y12 Inhibitor)
3. Statins
4. Metoprolol (beta blocker)
5. ACE Inhibitor
6. Modification of risk factors
100
What is an acute coronary syndrome?
A spectrum of acute coronary conditions including unstable angina, NSTEMI and STEMI.
101
What is the commonest cause of ACS?
Rupture of atherosclerotic plaque and subsequent arterial thrombosis
102
What are uncommon causes of ACS?
Coronary Vasospasm
Drug abuse
Coronary artery dissection
103
What are the two types of Myocardial infarction?
M1 - Spontaneous MI with ischaemia due to plaque rupture
M2 - MI secondary to ischaemia due to increased O2 demand
104
What are the 3 cardiac enzymes?
Troponin
CK
Myoglobin
105
When are cardiac enzymes released?
During MI - during myocardial necrosis.
106
When is Troponin increased?
During MI - both NSTEMI and STEMI as a result of an occlusion causing ischaemia
Not significantly in angina
Can be in pericarditis but less so than an MI.
107
Other than an MI, when can Troponin be released?
- Gram negative sepsis
- Pulmonary embolism
- Myocarditis
- Heart failure
- Arrhythmia
108
What is a STEMI?
ST elevated myocardial infarction
Characteristed by ST elevation in anterolateral leads, Inverted T waves and Q waves become broad.
109
What is an NSTEMI?
Non ST elevated myocardial infarction
Can only be diagnosed after bloods (raised troponin)
ECG may be normal or show T wave inversion and ST depression.
110
What is unstable angina?
Type of IHD, Acute, poor blood flow to the heart characteristed by chest pain at rest.
111
What are the signs of unstable angina?
1. Cardiac chest pain at rest
2. Cardiac chest pain with crescendo patterns – pain more frequent and easily provoked
3. No significant rise in troponin.
112
What is the treatment for unstable angina?
Clopidogrel, aspirin, surgery, lifestyle changes
113
What is the ECG like in unstable angina?
Normal or T wave inversion and ST depression
114
What are the signs of a Myocardial infarction?
- Unremitting and severe cardiac chest pain
- Pain that radiates down the left arm
- Pain occurs at rest
- Sweating, breathlessness, nausea and or vomiting
- 1/3rd occur in bed at night.
115
What are the complications for Myocardial Infarction?
- Heart failure
- Rupture of infarcted ventricle
- Rupture of interventricular septum
- Mitral regurgitation
- Arrythmias
- Heart block
- Pericarditis
116
A patient presents with an ACS, what investigations should be ordered?
1. ECG
2. Blood tests – troponin
3. Coronary angiography
4. Cardiac monitoring for arrythmias
117
A patient is diagnosed with ACS, what management options should be explored?
1. Hospital
2. If STEMI – PCI centre for transfer
3. Aspirin 300mg, pain relief – morphine
4. Oxygen if hypoxic
5. Nitrates
118
What does P2Y12 do?
Amplifies platelet aggregation
119
What is a P2Y12 inhibitor?
Clopidogrel
120
What are some side effects of P2Y12 inhibitors?
Bleeding
Rashes
GI distrubances
121
What are the four types of valvular heart disease?
1. Aortic Stenosis
2. Mitral regurgitation
3. Mitral stenosis
4. Aortic regurgitation
122
What is aortic stenosis?
where the aortic orifice is restricted, and the LV can’t eject blood properly in systole --> pressure overload
123
What is the aetiology of aortic stenosis?
1. Congenital bicuspid valve
2. Acquired e.g. age-related degenerative calcification
3. Rheumatic heart disease
124
What is the pathophysiology of aortic stenosis?
1. Aortic orifice is restricted so there’s a pressure gradient between the aorta and LV
2. LV function is maintained due to compensatory hypertrophy
3. Overtime this leads to LV failure
125
What are the symptoms of aortic stenosis?
1. Exertional syncope
2. Angina
3. Exertional dyspnoea (difficult or laboured breathing)
126
What are the signs of aortic stenosis?
1. Slow rising carotid plus due to decreased pulse amplitude
2. Soft or absent heart sounds
3. Ejection systole murmur
127
What investigations would you order for aortic stenosis?
Echocardiography
128
What is the correct management for aortic stenosis?
1. Ensure good dental hygiene
2. Consider IE Prophylaxis
3. Aortic Valve replacement or TAVI
129
Who should be offered an aortic valve replacement in aortic stenosis?
1. Symptomatic patients with aortic stenosis
2. Any patient with decreasing ejection fraction
3. Any patient undergoing CABG with moderate aortic stenosis
130
Why does medication not work for mitral and aortic stenosis?
Medication doesn’t work for mitral and aortic stenosis as problem is mechanic so doesn’t prevent progression.
131
What is mitral regurgitation?
Back flow of the blood from LV to LA during systole – LV volume overload
132
What is the aetiology of mitral regurgitation?
1. Myxomatous degeneration
2. Ischaemic mitral regurgitation
3. Rheumatic heart disease
4. IE
133
What is the pathophysiology of mitral regurgitation?
1. LV volume overload
2. Compensatory mechanisms – LA enlargement and LVH and increased contractility
3. Progressive LV volume overload causes dilation and progressive heart failure
134
What are the symptoms of Mitral regurgitation?
1. Dyspnoea on exertion
| 2. Heart failure
135
What are the signs of mitral regurgitation?
1. Pansystolic murmur
2. Soft 1st heart sound
3. 3rd heart sound
136
What is a sign of MR getting worse?
The intensity of the murmur
137
What are the investigations in Mitral regurgitation?
1. CXR
2. ECG
3. Echocardiogram – estimate LA/LV size and function
138
What is the management of Mitral regurgitation?
1. Rate control for AF --> Beta blockers
2. Anticoagulation for AF
3. Diuretics for fluid overload
4. IE prophylaxis
5. If symptomatic --> Surgery
139
What is aortic regurgitation?
A regurgitation aortic valve means blood leaks back into the LV during systole due to ineffective aortic cusps.
140
What is the aetiology of Aortic regurgitation?
1. Bicuspid aortic valve
2. Rheumatic heart disease
3. IE
141
What is the pathophysiology of Aortic regurgitation?
1. Pressure and volume overload
2. Compensatory mechanisms -->LV dilation, LVH
3. Progressive dilation eventually leads to Heart failure
142
What are the symptoms of Aortic regurgitation?
1. Dyspnoea on exertion
2. Orthopnoea – breathlessness when lying down
3. Palpitations
4. Paroxysmal nocturnal dyspnea
143
What are the signs of aortic regurgitation?
1. Wide pulse pressure
2. Diastolic blowing murmur
3. Systolic ejection murmur
144
What investigations would you take in aortic regurgitation?
CXR
| Echocardiogram
145
What is the management of Aortic regurgitation?
1. IE prophylaxis
2. Vasodilators e.g. ACEi
3. Regular echocardiograms to monitor progression
4. Surgery if symptomatic
146
What is mitral stenosis?
Obstruction to LV inflow that prevents proper filling during diastole
147
What are the causes of mitral stenosis?
1. Rheumatic heart disease
2. IE
3. Calcification
148
What is the pathophysiology of Mitral stenosis?
1. LA dilation --> pulmonary congestion
2. Increased trans mitral pressures LA enlargement and AF
3. Pulmonary venous hypertensions cause RHF symptoms
149
What are the symptoms of mitral stenosis?
1. Dyspnea
2. Haemoptysis
3. RHF symptoms
150
What are signs of mitral stenosis?
1. A wave in jugular venous pulsations
2. Signs of RHF
3. Pink patches on cheeks due to vasoconstriction
4. Low pitched diastolic murmur
5. Loud opening 1st heart sound snap
151
What are the investigations for mitral stenosis?
1. ECG
2. CXR
3. Echocardiogram – gold standard
152
What is the management of mitral stenosis?
1. If in AF --> Beta blockers/CCB
2. If in AF --> anticoagulation
3. Balloon valvuloplasty or valve replacement
4. IE prophylaxis
153
What is a main symptom of hypertension?
Headaches
154
Does treatment improve symptoms of hypertension?
Not usually, but may help headaches.
155
What are the causes of hypertension?
1. Kidney disease
2. Genetics and family history
3. Lifestyle factors e.g. high salt, excess alcohol, obesity, stress and caffeine
4. Recreational drugs
5. Drugs such as OCP and NSAIDs
6. Hyperaldosteronism
156
What endocrine diseases can cause secondary hypertension?
1. Conn’s – hyperaldosteronism
2. Cushing’s syndrome – prolonged cortisol exposure --> raised bp
3. Pheochromocytoma --> adrenal gland tumour, excess NAd and Ad release
157
What could you examine in a patient with suspected Hypertension?
Eyes in hypertension – small exposed blood vessels due to high bp.
158
What investigations would you do in someone with suspected hypertension?
1. 24h ambulatory blood pressure monitoring to confirm diagnosis
2. ECG and blood tests may be done to identify secondary causes of hypertension
159
What is hypertension a risk factor to?
1. MI
2. Stroke
3. Heart failure
4. Chronic renal disease
5. Dementia
160
What is the target levels of treatment in hypertension?
Under 80s - 140/90
| Over 80s - 150/80
161
When would you start treating people with hypertension?
Low risk - 160/100
| High risk - 140/90
162
What is the ABCD Management for hypertension?
A – ACEi .g. Rampiril or ARB e.g. candesartan if ACEi Intolerant
B – beta blockers e.g. bisoprolol
C – Calcium CB e.g. amlodipine or verapamil
D – Diuretics – Bendroflumethiazide
163
What are the side effects of ramirpil?
1. Hypotension
2. Cough, rash due to increased kinin production
3. Hyperkalaemia
4. Teratogenic
5. Acute renal failure
164
What does Valsartan act on?
on AT-1 and prevents Ang 2 Binding
165
What are the side effects of valsartan?
hypotension, renal dysfunction, hyperkalaemia, rash and contraindicated in pregnancy
166
What are the side effects of bisoprolol
- Hypotension
- Fatigue
- Headaches
- Nightmares
- Bradycardia
- Hypotension
- Erectile dysfunction
- Cold peripheries
167
What are the side effects of amlodipine?
flushing,headache, oedema, palpitations
168
What are the side effects of Verapamil?
bradycardia, AV block (caused by neg chronotropic) and worsening cardiac failure caused by being negatively inotropic.
169
What are the side effects of Bendroflumethiazide?
- Hypovolaemia
- Hypotension
- Reduced --> K, Na, Mg, Ca
- Hyperuricaemia --> Gout
- Erectile dysfunction
170
What will 1 tablet of atenolol reduce your mmHg?
10mmHg
171
What is heart failure?
A complex clinical syndrome of signs and symptoms that imply that the hearts ability of acting as a pump is compromised.
172
What is the most common cause of HF?
IHD
173
What hormones do the heart produce?
The heart produces ANP and BNP
174
What are ANP and BNP metabolised by?
NEP
175
What are the functions of ANP and BNP?
1. Increased renal excretion of Na+ and therefore water
2. Vasodilators
3. Inhibit aldosterone release
176
How can NEP inhibitors work in heart failure?
1. NEP metabolises ANP and BNP
| 2. NEP inhibitors can increase the level of ANP +BNP in serum
177
What is the counter-regulatory system to RAAS?
ANP/BNP hormones
178
What nitrates are used in Heart failure?
Isosorbide mononitrate
| GTN spray
179
What are the side effects of nitrates?
Headaches, syncope and tolerance
180
Why are women less likely to develop heart failure?
Oestrogen is a protective hormone.
181
What is the different compensatory mechanisms in heart failure?
1. Sympathetic system
2. RAAS
3. Natriuretic peptides
4. Ventricular dilation and hypertrophy
182
How does the sympathetic system compensate for heart failure?
Improves ventricular function by increasing HR and contractility = CO maintained
Causes arteriolar constriction which increases after load and myocardial work
183
How does the RAAS system compensate for heart failure?
Reduced CO leads to reduced renal perfusion so it activates RAAS --> more fluid + preload
Causes arteriolar constriction which increases afterload and myocardial work
184
How do Natriuretic peptides compensate for heart failure?
- Diuretic
- Hypotensive
- Vasodilators
185
What are the signs of left side heart failure?
1. Pulmonary crackles
2. Added heart sounds (3rd and 4th) and murmurs
3. Displaced apex beat
4. Tachycardia
186
What are the causes of Heart failure?
- Ischaemic heart disease
- Hypertension
- Alcohol excess
- Cardiomyopathy
- Valvular
- Endocardial and pericardial causes
187
What is the pathophysiology of Heart failure?
When the HF, compensatory mechanisms attempt to maintain CO
As HF progresses, mechanisms are exhausted and become pathophysiological
188
What are the symptoms of Heart failure?
- Breathlessness and Tiredness/fatigue
| - Swelling in hands ankles and feet – peripheral oedema
189
What are the broad categories of Heart failure?
Systolic failure – ability of the heart to pump blood around the body is impaired
Diastolic failure – the heart is pumping blood effectively but relaxing and filling abnormally
190
What investigations would you do in someone with Heart failure?
1. ECG
2. CXR – cardiac enlargement
3. Natriuretic peptide levels – rise indicates HF
If suspected HF, patient should have an echocardiogram
191
What is the management of Heart failure?
First line – vasodilator therapy (ACEi, beta blockers) via the neurohumoral blockade (RAAS-SNS)
- Perindopril
Beta blockers in HF – Metoprolol, bisoprolol, carvedilol and Nebivolol
Drugs for symptom relief
Diuretics --> thiazides (Bendroflumethiazide) and loop diuretics --> Na loss + H20 loss
192
What are the two stages of hypertension?
Stage 1 – 140/90 and 135/85
| Stage 2 – 160/100 and 150/95
193
How would you diagnose hypertension?
Offered ambulatory blood pressure monitoring (ABPM) to confirm diagnosis)
Suspected hypertension – 140/90mmHg or higher
194
What is the equation for blood pressure?
CO X TPR
195
What are the functions of angiotensin 2?
1. Vasoconstrictor
2. Activates sympathetic nervous system Increased NAd
3. Activates aldosterone = Na+ retention
4. Vascular growth, hyperplasia and hypertrophy
196
How does the sympathetic nervous system increase BP?
- Noradrenaline is a vasoconstrictor increased TPR
- NAd has positive chronotropic + inotropic effects
- It causes increase renin release
197
What are 3 examples of ACEi?
1. Ramipril
2. Enalapril
3. Perindopril
198
Where are ACEi clinically indicated in?
Hypertension, heart failure and diabetic neuropathy
199
What are the side effects of ACEi?
- Hypotension
- Hyperkalaemia
- Acute renal failure
- Teratogenic
200
What can cause increased kinin production?
ACEi
201
How does ACE increase kinin production?
- ACE converts bradykinin into inactive peptides
| - Therefore ACE inhibitors lead to a build up of kinin
202
What is the side effect of increased kinin?
Dry chronic cough, Rash, anaphylactoid reaction
203
When are ARBs used?
When ACEi are contraindicated
204
What are ARBs?
Angiotensin 2 receptor blockers
205
What receptor does ARBs work at?
AT-1 receptors
206
What are 3 examples of ARBs?
Candesartan, valsartan, losartan
207
When are ARBs used?
Indicated in hypertension, heart failure and diabetic neuropathy
208
What are calcium channel blockers?
L type Ca2+ channels
209
Give 4 types of Calcium channel blockers
1. Amlodipine
2. Felodipine
3. Diltiazem – acts on heart and vasculature
4. Verapamil – acts primarily on the heart
210
What are dihydropyridines?
A class of CCB --> arterial vasodilators --> Amlodipine and felodipine
211
When are dihydropyridines indicated in?
Hypertension, IHD, Arrhythmia
212
What are the potential side effects of CCBs due to vasodilation?
- Flushing
- Headache
- Oedema
213
What is a potential side effect of CCBs due to their negatively inotropic nature?
Worsening heart failure
214
What is a potential side effect of CCBs due to their negatively chronotropic nature?
Bradycardia
| AV block
215
What are the side effects of verapamil?
- Worsening Cardiac failure
- Bradycardia
- Atrioventricular block
- Constipation
216
A patient on CCBs comes in with constipation, which CCB might they be on?
Verapamil
217
What are 3 examples of beta blockers?
1. Bisoprolol (Beta 1 selective)
2. Atenolol
3. Propanolol (Beta ½ non selective)
218
What conditions are beta blockers clinically indicated in?
1. IHD
2. Heart failure
3. Arrhythmia
4. Hypertension
219
What are the side effects of beta blockers?
1. Fatigue.
2. Headache.
3. Nightmares.
4. Bradycardia.
5. Hypotension.
6. Cold peripheries.
7. Erectile dysfunction.
8. Bronchospasm.
220
What is an example of a thiazide ?
thiazide Bendroflumethiazide
221
What do thiazides work on?
Distal tubule in the kidney
222
Give two examples of loop diuretics
1. Furosemide
| 2. Bumetanide
223
What is a K sparing diuretic?
Spironolactone
224
Why is spironolactone particularly effective?
Has anti-aldosterone effects too
225
When are diuretics clinically indicated?
HF and hypertension
226
What are the side effects of diuretics?
1. Hypovolaemia
2. Hypotension
3. Reduced Serum Na, K , Mg, Ca
4. Increased uric acid gout
5. ED
6. Impaired glucose tolerance
227
You see a 65 y/o patient who has recently been diagnosed with hypertension. What is the first line treatment?
Calcium channel blockers (as this patient is over 55) e.g. amlodipine.
228
You see a 45 y/o patient who has recently started taking ACE inhibitors for their hypertension. Unfortunately their hypertension still isn't controlled. What would you do next for this patient?
You would combine ACE inhibitors or ARB with calcium channel blockers.
229
You see a 45 y/o patient who has been taking ACE inhibitors and calcium channel blockers for their hypertension. Following several tests you notice that their blood pressure is still high. What would you do next for this patient?
You would combine the ACEi/ARB and calcium channel blockers with a thiazide diuretic e.g. bendroflumethiazide.
230
What is the vaughan williams classification?
Used to group anti-arrhythmic drugs
231
What are VW class 1 drugs?
Class 1 – Na channel blockers. 3 Sub divisions
1a. Disopyramide
1b. Lidocaine
1c. Flecainide
232
What are VW class 2 drugs?
Class 2 – Beta blockers
2a. propranolol
2b. atenolol
2c. bisoprolol
233
What are VW class 3 drugs?
prolong action potential e.g. amiodarone
234
What are VW class 4 drugs?
Class 4 drugs – CCB but not dihydropyridines as they don’t affect the heart
1. Verapamil
2. Diltiazem
235
What is Digoxin?
Inhibits Na/K pump therefore making AP more positive and ACh is released from PS nerves.
236
What are the main affects of Digoxin?
- Bradycardia
- Reduced atrioventricular contraction
- Increased force of contraction (positive inotrope)
237
Where is Digoxin clinically indicated?
AF and HF
238
What are the side effects of Digoxin?
Nausea, vomiting, diarrhoea, confusion
239
What are two drugs that increase the QT interval?
1. Sotalol
| 2. Amiodarone
240
What are the side effects of drugs that increase the QT intervals?
1. Pro-arrhythmic effects.
2. Interstitial pneumonitis.
3. Abnormal liver function.
4. Hyper/hypothyroidism.
5. Sun sensitivity.
6. Grey skin discolouration.
7. Corneal micro-deposits.
8. Optic neuropathy
241
What can you use Na channel blockers in and how do they work?
Ventricular tachycardia – block inactivation of Na Channel
242
What is the most useful beta blocker to control arrythmias?
Propranolol
243
What does Furosemide block?
Na/K/2Cl- transporter
244
How do beta blockers prevent symptom relief in angina?
- Reduce O2 demand – neg chronotropic (HR)
- Reduce O2 demand – neg inotropic (Contractility)
- Increase O2 distribution by slowing HR
245
Why can Doxazosin be used in hypertension?
Alpha 1 receptor antagonist.
246
ECG - What is the J joint?
Where the QRS complex becomes the ST segment
247
What is the normal axis of a QRS complex?
-30 degrees to 90 degrees
248
ECG - What does the P wave represent?
Atrial depolarisation
249
ECG - how long should a PR interval be?
120-200ms
250
What might a long PR interval indicate?
Heart block
251
How long should a QT interval be?
0.35-45s
252
ECG - what deos the QRS complex represent?
Ventricular depolarisation
253
ECG - what does the T wave represent?
Ventricular repolarisation
254
ECG - Where would you place lead 1?
Right arm to Left arm with positive electrode being at the left arm at 0 degrees.
255
ECG - Where would you place lead 2?
Right arm to left leg with positive electrode being at the left leg at 60 degrees.
256
ECG - Where would you place lead 3?
Left arm to left leg with positive electrode being at left leg at 120 degrees
257
Where would you place avF?
From halfway between left arm and right arm to the left leg with the positive at the left leg at 90 degrees
258
Where would you place avL?
From halfway between right arm and left leg to the positive electrode on the left arm at -30 degrees.
259
Where would you place avR?
From halfway between left arm and left leg to the right arm with positive electrode at the right arm at -150 degrees.
260
What is the dominant pacemaker of the heart?
SA node
261
How many seconds do the small and large squares represent on ECG paper?
```
Small = 0.04s
Large = 0.2s
```
262
How long should a QRS complex be?
Less than 110 ms
263
In which leads would you expect QRS to be upright in?
1 and 2
264
in which lead are all waves negative?
aVR
265
In which leads must the R wave grow?
Chest leads V1 to V4
266
In which leads must the S wave grow?
Chest leads V1 to V3 then dissapear in V6.
267
In which leads should T waves and P waves be upright?
Leasd 1,2 and V2-->V6
268
What may tall pointed P waves on an ecg suggest?
Right atrial enlargement
269
What may M shaped P waves on an ecg suggest?
Left atrial enlargement
270
What are 3 signs of abnormal T waves?
Symmetrical
Tall and peaked
Biphasic or inverted
271
What happens to the QT interval when the HR decreases?
QT interval decreases
272
Which part of the ecg does the plateau phase of the cardiac action potential coincide with?
QT interval
273
Define Shock
When the cardiovascular system is unable to provide adequate substrate for aerobic cellular respiration.
274
Give 3 signs and symptoms of shock?
```
Pale
Sweaty
Cold
Pulse is weak but rapid
Reduced urine output
Confusion
Weakness/collapse
```
275
What can cause hypovolaemic shock?
Loss of blood
Loss of fluid
276
Describe the vital signs in type 1 shock e.g. blood loss, bp, pulse presure , RR and urine output.
```
15% blood loss
100bpm +
normal pulse and bp
resp rate 14-20
Urine output 30ml/h
```
277
Describe the vital signs in type 2 shock e.g. e.g. blood loss, bp, pulse presure , RR and urine output.
```
15-30% blood loss
100bpm+
normal bp
decreased pulse
RR - 20-30
Urine output 20-30ml/h
```
278
Describe the vital signs in type 3 shock e.g. e.g. blood loss, bp, pulse presure , RR and urine output.
```
30-40% blood loss
120bpm
blood pressure and pulse down
RR - 30-40
Urine output 5-15ml/hr
```
279
What can cause cardiogenic shock?
Cardiac tamponade
PE
MI
Fluid overload
280
What is septic shock?
A systemic inflammatory response associated with an infection (Bacterial endotoxins)
281
What is anaphylactic shock?
An intense allergic reaction associated with massive histamine release and haemodynamic collapse.
282
What is the treatment for anaphylactic shock?
Adrenaline and supportive therapy
283
Give 2 signs of Acute resp distress syndrome?
Imapried oxygenation
No cardiac failure
Bilateral pulmonary infiltrates
284
Describe the pathophysiology of ARDS?
1. Exudative phase --> increased vasc permeability leads to platelet, fibrin and clotting factor exudate
2. Proliferative phase - fibroblast proliferation
3. Fibrotic phase
285
Give 4 extra-pulmonary causes of ARDS?
```
Sepsis
Trauma
Shock
Drug reaction
Pancreatitis
```
286
Give 3 pulmonary causes of ARDS?
Pneumonia
Near drowning
Smoke inhaling
287
How much serous fluid is there between the visceral and parietal pericardium?
50ml
288
What is the function of the serous fluid?
Acts as a lubricant so smooth movement of the heart inside the pericardium.
289
What is the function of the pericardium?
Restrains the filling volume of the heart
290
Name 3 Cardiomyopathies
1. Hypertrophic (HCM)
2. Dilated (DCM)
3. Arrhythmogenic R/L ventricular
291
What is the cause of HCM?
Sarcomeric gene mutations e.g. beta myosin and troponin T --> Affects 1 in 500
292
What is the cause of ARVC/ALVC?
Desmosome gene mutations
293
What is the inheritance pattern of CMs?
Cardiomyopathies tend to be AD --> offspring have a 50% chance of getting infected
294
What is the pathophysiology of HCM?
Systole is normal but diastole is affected
Heart is unable to relax due to the thickening of ventricular walls
295
What is the pathophysiology of DCM?
Ventricular dilation and dysfunction = poor contractility
296
What is the pathophysiology of ARVC/ALVC?
Desmosomes attach cells via intermediate filaments
Desmosome mutations lead to myocytes being pulled apart
Ventricles are replaced with fatty fibrous tissues
297
What is the symptoms of HCM?
Angina, Dyspnoea and syncope
298
What is the symptoms of DCM?
Similar to HF --> breathlessness, tiredness and oedema
299
What is a sign of ARVC/ALVC?
Ventricular tachycardia
300
What would an ECG look like in a patient with HCM?
Large QRS complex and large inverted T waves.
301
What might an ECG look like from a person with ARVC/ALVC?
Epsilon waves
302
What is restrictive cardiomyopathy?
Poor dilation of the heart restricts diastole
303
What is the cause of restrictive cardiomyopathy?
Amyloidosis --> deposition of amyloid.
304
What are channelopathies?
Mutations in genes coding for ion channels.
Common symptom is syncope
305
Give 3 examples of channelopathies
Long QT syndrome
Short QT syndrome
Brugada - Na defect with St elevation
CPVT
306
What are 4 main features of tetrology of fallot?
- Ventricular septal defect
- Overriding aorta
- RV hypertrophy
- Pulmonary stenosis
307
Is a baby cyanotic in TOF?
greater pressure in RV then LV so blood is shunted into LV
308
What is VSD?
Abnormal connection between 2 ventricles
309
Would a baby be cyanotic with VSD?
Would not be cyanotic --> higher pressure in the LV than RV so blood shunted to RV
310
What are the clinical science of VSD?
- High Pulmonary blood flow
- Breathless poor feeding and failure to thrive
- Tachycardia
- Increased RR
311
What is ASD?
Abnormal connection between the two atria
312
What is the signs of a large ASD?
1. Enlarged pulmonary arteries
2. Right heart dilation
3. SOBOE
4. Increased chest infection
5. Significant increase in blood flow through the right heart and lungs – pulmonary flow murmur
313
Would a baby be cyanotic with ASD?
Would not be cyanotic --> Higher pressure in LA than RA so blood is shunted L to R so more blood to the lungs --> No cyanosis
314
What is ASVD?
Atrioventricular septal defect (hole in centre of heart)
315
What are the signs of ASVD?
- Breathlessness
| - Poor feeding and poor weight gain
316
What is a PDA?
Patent ductus arteriosus
317
What are the signs of a PDA?
1. Torrential flow from aorta to the pulmonary arteries --> pulmonary hypertension
2. Breathlessness
3. Poor feeding, failure to thrive
4. Risk of endocarditis
318
What controls the sinus node discharge rate?
Autonomic nervous system
319
Define sinus rhythm
A p wave that precedes each QRS complex.
320
Give 3 consequences of arrhythmia
```
Sudden death
syncope
Dizziness
Palpitations
Asymptomatic
```
321
Give two categories of tachycardia
Supra-ventricular tachycardia
Ventricular tachycardia
322
Where does supra-ventricular tachycardia arise from?
From the atria or the atrio-ventricular junction.
323
Do supraventricular tachycardia's have narrow or broad QRS complexes?
Narrow.
324
Where does ventricular tachycardia arise from?
Ventricles
325
Do ventricular tachycardias have narrow or broad QRS complexes?
Broad
326
Name 3 Supra-ventricular tachycardias.
```
AF
Atrial flutter
Focal atrial tachycardia
AV node re-entry tachycardia
Accessory pathway
```
327
Give 4 causes of sinus tachycardia
```
Physiology response to excercise
Anaemia
Fever
HF
Hypovol
```
328
Describe 2 characteristics of an ECG with someone with Atrial fibrilation
1. Absent P waves
2. Fine oscillation of the baseline
This is because the aV node and ventricles can't keep up with the atria --> irregulary irregular pulse
329
Give 4 symptoms of AF
```
Palpitations
Sob
Fatigue
Chest pain
Increased risk of thromboembolism
```
330
What score can be used to calculate the risk of stroke in somone with AF?
CHADS2 VASc
331
What does the CHADS2 VASc score take into account?
```
Age
Hypertension
Previous stroke/TIA
Diabetes
Female
```
Over 2 = need for anti coag
332
What is the treatment for AF?
1. Rate control - BB, CCB an digoxin
2. pacemaker or flecainide
3. Long term catheter ablation and pacemaker
333
What would the ECG be like in a pt with atrial flutter?
Narrow QRS
| Sawtooth flutter waves
334
What pathophysiological mechanism can cause atrial flutter?
Re-entry mechanism - blockage of normal circuit --> another pathway forms and takes a different course and renters the circuit causing tachycardia.
335
What is the commonest type of supraventricular tachycardia?
AV node re-entry tachycardia.
P waves are seen within the QRS complex
336
Give 4 symptoms of AVNRT
```
Tachycardia
Sudden/onset palpitations
SOB
Chest pain
neck pulsation
```
337
Describe the acute treatment of AVNRT
Vagal manoeuvere and adenosine
BB,CCB and Flecainide will be given to prevent future episodes.
338
What is the pathophysiology of accessory pathway arrythmias?
Congenital muscle strands connect atria and ventricles --> causing pre excitation of the ventricles.
339
Describe 3 ECG features in someone with accessory pathway arrythmia
1. Delta wave
2. Short PR interval
3. Slurred QRS complex
340
Describe the pathophysiology of focal atrial tachycardia
Another area of the atrium becomes more autonomic than the sinus node so sinus node function is taken over
ECG --> Abnormal P waves before a normal QRS
341
What is the urgent treatment for Ventricular tachycardia?
DC cardioversion.
Long term an implantable defibrilator would be inserted
342
Give 3 causes of long QT syndrome?
Congenital
Electrolyte disturbances --> hypo cal and hypo kal
Drugs
343
Give 2 signs of long QT syndrome?
Palpitations
| Syncope
344
Give 4 causes of sinus bradycardia?
Ischaemia
Fibrosis of atrium
Inflammation
Drugs
345
Give 3 causes of Heart block?
CAD
Cardiomyopathy
Fibrosis
346
What heart block is assocated with wide QRS in an abnormal pattern?
RBBB or LBBB
