Cardiovascular Flashcards
(170 cards)
1
Q
Pathophysiology of IHD
A
- primarily caused by atherosclerosis
- when 70-80% sclerosed → exertional symptoms → angina
2
Q
What is the mechanism of atherosclerotic plaque formation?
A
- fatty streaks
- intermediate lesions
- fibrous plaques of advanced lesions
- plaque rupture → infarction
3
Q
What is an atherosclerotic plaque?
A
complex lesion consisting of:
- lipid
- necrotic core
- connective tissue
- fibrous cap
4
Q
What are the major cell types involved in atherogenesis?
A
- endothelium
- macrophages
- smooth muscle cells
- platelets
5
Q
What arteries does atherogenesis affect most commonly?
A
- LAD
- circumflex
- RCA
6
Q
Risk factors of IHD
A
- family history
- age
- South Asian
- smoking
- poor nutrition
- sedentary lifestyle
- alcohol
- stress
- HTN
- obesity
- DM
7
Q
Presentation of angina
A
- constricting discomfort in front of chest, neck, shoulders, jaw or arms
- precipitated by physical exertion
- relieved by rest/GTN spray (5 mins)
normal exam
- typical angina = all 3
- atypical angina = 2
- non anginal pain = 1/none
8
Q
Investigations for IHD
A
- ECG usually normal
- lipid profile → high LDL
- FBC
- HbA1c
GOLD STANDARD = CT coronary angiography
9
Q
Treatment of IHD
A
- antiplatelet therapy → aspirin/clopidogrel
- lipid lowering thearpy → statin
- good hypertensive/glycaemic control
10
Q
Treatment for angina
A
- symptomatic relief = GTN spray
- long term symptomatic relief = beta blocker/CCB
- secondary prevention = AAA
- PCI/CABG if extensive damage
11
Q
What is the secondary prevention for angina?
A
AAA
- aspirin
- atorvastatin
- ACEi
12
Q
What surgical interventions are available for angina?
A
- percutaneous coronary intervention
- coronary artery bypass graft → preferred in patients with diabetes, >65
13
Q
What is ACS?
A
Acute Coronary Syndrome
- thrombus from an atherosclerotic plaque blocking a coronary artery
- unstable angina = ischaemia
- STEMI = complete occlusion
- NSTEMI = partial occlusion → subendocardial infarction
14
Q
Presentation of ACS
A
- central constricting chest pain radiating to jaw/arms
- sweating
- SOB
- >20 mins
- unstable angina → pain not relieved by rest or GTN spray
- silent MI → in diabetics
15
Q
ECG changes in ACS
A
STEMI
- ST segment elevation
NSTEMI/unstable angina
- ST depression
- deep T wave inversion
16
Q
How do you differentiate between unstable angina and NSTEMI?
A
- unstable angina = troponin normal
- NSTEMI = troponin abnormal
17
Q
Immediate management of ACS
A
MONAC
- morphine
- oxygen
- nitrate
- aspirin
- clopidogrel
18
Q
Management of STEMI
A
PCI within 120mins
- clopidogrel/prasugrel and aspirin
Fibrinolysis if not PCI eg alteplase
- ticagrelor and aspirin
19
Q
Management of NSTEMI/unstable angina
A
- GRACE score
- fondaparinux
low risk
- ticagrelor
- aspirin
medium/high risk
- angiography and PCI
- prasugrel and aspirin
20
Q
What is the GRACE score?
A
- assess for PCI in NSTEMI
- gives 6 month risk of death and repeat MI after having a NSTEMI
21
Q
Secondary prevention of ACS
A
ACAB
- ACEi
- clopidogrel
- aspirin and atorvastatin
- beta blocker
22
Q
What are the post MI complications
A
DREAD
- death
- rupture of heart septum/papillary muscles
- edema (HF)
- arrhythmias and aneurysms
- Dressler’s syndrome
23
Q
Definition of HTN
A
- >140/90 in clinic (be aware of white coat HTN)
- >135/85 with ABPM/home readings
24
Q
Pathophysiology of HTN
A
95% idiopathic = essential HTN
rest = underlying cause → ROPE
- renal disease
- obesity
- pregnancy (pre-eclampsia)
- endocrine (Conns)
25
Risk factors for HTN
- \>65
- family history
- Afro-caribbean
- alcohol intake
- DM
- sedentary lifestyle
- sleep apnoea
- smoking
26
Investigations for HTN
1. clinic BP \>140/90
2. offer ABPM or home readings
3. ABPM \>135/95 = diagnosis confirmed
27
Stages of HTN
28
Further investigations for HTN
- urine ACR, dipstick, bloods
- ECG
- hypertensive retinopathy → fundus examination
- HbA1c
- lipids
29
What medications can be used to treat HTN?
ABCDA
- ACEi → ramipril
- beta blocker → bisoprolol
- CCB → amlodipine
- diuretic (thiazide like) → indapamide
- ARB → candesartan
ARB used instead of ACEi if
- not tolerated (dry cough)
- patient is black
30
When to offer medical management of HTN
- stage 2 HTN
- \<80, stage 1 HTN, QRISK score 10%+, complications
31
NICE guideline treatment for HTN
1. \<55 and non-black = ACEi, \>55 or black = CCB
2. ACEi and CCB, alternative ACEi and D, CCB and D, if black use ARB not ACEi
3. ACEi and CCB and D
4. ACEi and CCB and D and additional
32
Definition of HF
- CO is inadequate for body's requirement
- inability of heart to deliver blood and O2 at a rate the body needs to meet demand
- physiological changes occur to maintain CO
- eventually overwhelmed and become pathophysiological
33
Types of HF
- systolic = inability of ventricles to contract normally
- diastolic = inability of ventricles to relax and fill normally
- can be left or right ventricular failure
- acute or chronic HF
34
Causes of LHF
- coronary artery disease
- arrhythmias
- MI
- cardiomyopathy
- congenital heart defects
- valvular heart disease
35
Causes of RHF
- COPD
- pulmonary HTN
- right ventricular infarct
- cor pulmonale
- progression of LHF
- PE
36
Causes of systolic HF
- IHD
- MI
- cardiomyopathy
37
Causes of diastolic HF
- aortic stenosis
- chronic HTN
38
Pathophysiology of HF
1. myocardium fails
2. decreased volume of blood ejected, increased preload
3. increased ventricular load causes hypertrophy of myocardium
4. increase in muscle growth to compensate and pump more blood out
5. increased myocardial demand for oxygen
6. myocardium becomes ischaemic → patchy fibrosis → stiffness and reduced contractibility
7. decreased contractibility = increased workload and amount of blood remaining
8. more force needed to maintain cardiac output
9. cells become tired → pathological
39
How does HF activate RAAS
- increased afterload and preload
- increased cardiac work
- damage to myocytes
- decreased cardiac output
- activates RAAS and adrenergic pathway
- Na+ and water retention
- increased HR and contraction force
- cardiotoxicity
40
Common clinical presentation of HF
- SOB
- fatigue
- peripheral oedema
41
Symptoms of LHF
- exertional dyspnoea
- orthopnoea
- nocturnal cough
- wheeze
- nocturia
- cold peripheries
42
Symptoms of RHF
- peripheral oedema
- ascites
- facial engorgement
- epistaxis
43
Signs of HF
- tachycardia
- elevated JVP
- cardiomegaly
- 3rd/4th heart sounds
- displaced apex beat
- bi-basal crackles
- pleural/peripheral effusion
44
Investigations for HF
- ECG → may indicate cause
- BNP
- chest xray
45
What is BNP
- brain natriuretic peptide
- marker of HF
- released when myocardial walls are under stress
- levels correlated to ventricular wall stress and HF severity
46
Chest xray findings in HF
ABCDE
- alveolar oedema
- B Kerley lines
- cardiomegaly
- dilated upper lobe vessels of lungs
- effusions (pleural)
47
Treatment of HF
- lifestyle changes
- diuretics reduce preload and pressure on ventricles → loop/thiazide/aldosterone antagonist
- ACEi for LV systolic dysfunction
- beta blocker and spironolactone to decrease mortality
- digoxin for symptom relief
48
What is cor pulmonale?
right sided HF caused by chronic pulmonary arterial HTN
49
Causes of cor pulmonale
- chronic lung disease
- pulmonary vascular disorders
- neuromuscular and skeletal diseases
50
Signs and symptoms of cor pulmonale
- cyanosis
- tachycardia
- raised JVP
- RV heave
- pan systolic murmur
- hepatomegaly
- oedema
- dyspnoea
- fatigue
- syncope
51
Investigations for cor pulmonale
- ABG → hypoxia +/- hypercapnia
52
Management of cor pulmonale
- treat underlying cause
- oxygen
- same treatment as HF
53
Pathophysiology of PVD
- commonly atherosclerosis → claudication of vessels
- other causes of claudication = aortic coarctation, temporal arteritis, Burger's
- end stage PVD = critical limb ischaemia
54
Risk factors of PVD
- hyperlipidaemia
- history of CAD
- age \>40
55
What are the signs of critical limb ischaemia
6 Ps
- pain
- paresthesia
- pulselessness
- pallor
- paralysis
- poikilothermia = perishingly cold
56
Presentation of PVD
- pain in lower limbs on excercise, relieved on rest = intermittent claudication
- severe = unremitting pain in foot
- legs may be pale, bold, loss of hair, skin changes
57
Investigation for PVD
- ankle brachial pressure index ≤0.90
- ABPI = doppler ultrasonography
- should be 1
58
Treatment for PVD
control risk factors - lifestyle changes
antiplatelet therapy
59
Treatment for critical limb ischaemia
as stated plus:
- revascularisation eg stenting, angioplasty, bypassing
- amputation if unsuitable
60
What is pericarditis?
inflammation of the pericardium +/- effusion
2 types
- fibrinous = dry
- effusive → purulent serous/haemorrhagic
61
Causes of acute pericarditis
- infection
- autoimmune → RA, sjogren's, SLE
- secondary metastatic tumours
- traumatic and iatrogenic
- post cardiac injury
62
What infections can cause acute pericarditis?
- enteroviruses
- adenoviruses
- mycobacterium TB
63
Pathophysiology of pericarditis
1. inflammation
2. narrowing of pericardial space and scarring
3. if untreated, build up of exudate and adhesions in pericardial space → pericardial effusion
64
Symptoms of pericarditis
- severe chest pain
- dyspnoea
- cough
- hiccups
- fever
- myalgia
65
Signs of pericarditis
- pericardial rub on auscultation
- tachycardia
- peripheral oedema
- increased JVP
66
Investigations for pericarditis
ECG = DIAGNOSTIC
- saddle shaped ST elevation
- diffuse ST elevation in all leads
- PR depression
chest xray → effusion may cause cardiomegaly
67
What is chest pain like in pericarditis
- sharp, pleuritic, rapid onset
- worse when laying flat, relieved sitting forwards
- radiates to trapezius ridge
68
Treatment for pericarditis
- reduce physical activity until symptoms resole
- NSAIDs with gastric protection → ibuprofen/aspirin
- colchicine 3 months
- treat cause
69
What is infective endocarditis
- an infection of the endocardium or vascular endothelium of the heart
- fever and new murmur = infective endocarditis until proven otherwise
70
What microorganisms cause infective endocarditis
- staph aureus
- streptococcus viridans
- strep bovis
- enterococci
- coxiella burnetii
71
Risk factors for infective endocarditis
- IVDU
- immunocompromised
- people with prosthetic valves
- aortic/mitral valve disease
- poor dental hygiene
- pacemakers
- IV cannula
72
Pathophysiology of infective endocarditis
- abnormal cardiac endothelium and organisms in bloodstream
- adherence and growth of organisms
- infective endocarditis
- LHS of heart = most common side effected
- RHS affected in IVDU
73
Symptoms of endocarditis
- fever
- rigors
- night sweats
- malaise
- weight loss
74
Signs of endocarditis
- anaemia
- splenomegaly
- clubbing
- new murmurs
- sepsis
- embolic events
75
Typical presentation of endocarditis
- embolic skin lesions
- petechiae
- splinter haemorrhages
- osler nodes
- janeway lesions
- roth spots
76
Investigations for endocarditis
- Duke criteria
- echo
- ECG → long PR interval, regular
transoesophageal echo = more sensitive, uncomfortable, better at diagnosing
77
Treatment for endocarditis
- antibiotics
- treat any complications
- surgery
78
What surgery can be used to treat endocarditis?
- replace valve if infection cannot be treated with Abs
- remove/replace infected devices
- remove large vegetations at risk of embolising
79
Prevention of endocarditis
- good oral health
- no IV drug use
- educate surgery patients on symptoms
80
What is pericardial effusion
- occurs if pericarditis is untreated
- buildup of exudate in pericardial space
- puts pressure on cardiac myocytes → cardiac dysfunction
81
Signs of pericardial effusion
- bronchial breathing at left base
- muffled heart sounds
82
Treatment for pericardial effusion
- treat the cause
- pericardiocentesis
complication = cardiac tamponade
83
What is cardiac tamponade
- life threatening
- accumulation of fluid in pericardial space
- compression of heart chambers
- decreased venous return and filling of heart
- reduces cardiac output
84
Symptoms and signs of cardiac tamponade
- Beck's triad
- pulsus paradoxus = large decrease in stroke volume
85
What is Beck's triad?
- falling BP
- rising JVP
- muffled heart sounds
86
Investigations for cardiac tamponade
GOLD STANDARD = echo
87
Treatment for cardiac tamponade
pericardiocentesis
88
Murmur in mitral stenosis
- mid-diastolic murmur with opening snap
89
Symptoms of mitral stenosis
- haemoptysis due to pulmonary oedema
- palpitations AF
90
Signs of mitral stenosis
- malar flush
- tapping apex beat
- low volume pulse
- loud S1
91
Causes of mitral stenosis
- rheumatic heart disease
- IE
92
Murmur in mitral regurgitation
pansystolic high pitched whistling murmur
93
Symptoms of mitral regurgitation
- palpitations
- exertional dyspnoea
- fatigue
- weakness
94
Signs of mitral regurgitation
- AF
- displaced, thrusting apex
- soft/absent S1
95
Causes of mitral regurgitation
- idiopathic
- IHD
- rheumatic heart disease
- EDS, Marfans
96
Complication of mitral regurgitation
congestive HF
97
Murmur in aortic stenosis
ejection systolic murmur
98
Symptoms of aortic stenosis
triad of
- syncope
- angina
- dyspnoea
99
Signs of aortic stenosis
- sustained heaving apex
- slow rising pulse
- narrow pulse pressure
- soft S2 if severe
100
Causes of aortic stenosis
- idiopathic
- rheumatic heart disease
AS = most common valve defect
101
Murmur in aortic regurgitation
- early diastolic murmur
- Austin flint murmur at apex
102
Symptoms of aortic regurgitation
- palpitation
- angina
- dyspnoea
103
Signs of aortic regurgitation
- water hammer pulse
- wide pulse pressure
- displaced apex
- Corrigan's pulse → collapsing
104
Causes of aortic regurgitation
- idiopathic
- EDS, Marfans
105
Treatment for valve defects
- treat symptoms
- replace defective valve
106
What is VTE?
- venous thromboembolism
- blood clots develop in circulation
- due to stagnation of blood and hyper-cogulable states
107
What is a DVT?
- deep vein thrombosis
- thrombus that develops in the venous circulation
108
What is a PE?
- pulmonary embolism
- once thrombus develops, it can travel → embolise
- deep veins → through RHS of heart → lungs → PE
109
What is a complication of VTE?
- if patient has a hole in heart, clot can pass through LHS of heart into systemic circulation
- causes large stroke
110
Risk factors for VTE
- immobility, long haul travel
- recent surgery
- pregnancy
- hormone therapy with oestrogen → pill, HRT
- malignancy
- polycythaemia
- SLE
- thrombophilia → antiphospholipid syndrome
111
VTE prophylaxis
- hospital admission → risk assessment for VTE
- LMW heparin if high risk
contraindicated if active bleeding or existing coagulants
112
Presentation of DVT
- unilateral
- calf/leg swelling
- dilated superficial veins
- calf tenderness
- oedema
- colour changes in leg
113
What is a Wells score?
predicts risk of patients with symptoms having a DVT/PE
114
Diagnosis of VTE
D-dimer
DIAGNOSTIC FOR DVT = doppler US leg
GOLD STANDaRD FOR PE = CT pulmonary angiogram
- V/P scan if contraindicated
115
Initial management of VTE
- anticoagulation
- catheter directed thrombolysis
116
Long-term anticoagulation in VTE
DOAC, warfarin, LMW heparin
- 3 months if cause reversible
- 3-6 months if active cancer
117
What is an aneurysm?
weakening of vessel wall followed by dilation due to increased wall stress
118
What is the most common vessel aneurysm?
abdominal aortic aneurysm
119
Pathophysiology of aortic aneurysm
1. inflammation and degeneration of smooth muscle cells
2. loss of structural integrity of aortic wall
3. vessel widens
4. mechanical stress acts on weakened wall tissue
5. can lead to dilation or rupture
120
Complication of dilated aneurysm
peripheral thromboembolism
121
Risk factors of aortic aneurysm
- SMOKING
- family history
- connective tissue disorders
- age
- atherosclerosis
- male
122
Presentation of AAAs
- most are asymptomatic
- commonly found below renal arteries → infrarenal
- if big, pulsatile mass on palpation, bruit on auscultation
- lower back/abdominal pain if expanding rapidly
123
Diagnosis of aortic aneurysms
1. ultrasonography
124
Management of aortic aneurysms
symptomatic → repair
asymptomatic
- surveillance
- if diameter >5.5cm (m) or >5cm (f) → repair
125
Complications of aortic aneurysms
- rupture of AAA
- thromboembolism
- fistula formation
126
Presentation of ruptured AAA
- acute onset of severe, tearing abdominal pain with radiation back, flank, groin
- painful pulsatile mass
- hypovolaemic shock
- syncope
- nausea, vomiting
127
Diagnosis of ruptured AAA
clinical to save time
128
Treatment of ruptured AAA
- urgent surgery → endovascular aneurysmal repair
- maintain haemodynamic stability
129
What is an aortic dissection?
- tear in the intimal layer of aorta
- leads to collection of blood between intima and medial layers
- mainly in ascending aorta
130
Pathophysiology of aortic dissection
- tear in intimal layer
- blood passes through media propagating distally or proximally
- false lumen
- can occlude flow through branches of aorta
- ischaemia of affected regions
130
Pathophysiology of aortic dissection
- tear in intimal layer
- blood passes through media propagating distally or proximally
- false lumen
- can occlude flow through branches of aorta
- ischaemia of affected regions
131
Risk factors of aortic dissection
male
- 40-60
- HTN → most common
- trauma
- vasculitis
- cocaine use
- connective tissue disorders in younger adults
132
Clinical features of aortic dissection
- sudden and severe tearing pain in chest radiating to back
- hypotension
- asymmetrical BP
- syncope
133
Diagnosis of aortic dissection
- ECG
- chest xray
- CT
134
Management of aortic dissection
- maintain haemodynamic stability
- opioid analgesia
- endovascular stent-graft repair
- antihypertensives post surgery
135
How do you maintain haemodynamic stability?
- fluid resuscitation
- ionotropes
- noradrenaline
136
What is atrial fibrillation?
- chaotic irregular rhythm
- irregular ventricular rate
ECG
- no P waves
- irregularly irregular QRS
137
Causes of a fib
- idiopathic
- HTN
- HF
- coronary artery disease
- valvlular heart disease
- cardiac surgery
- cardiomyopathy
- rheumatic heat disease
138
Pathophysiology of a fib
- continuous rapid activation of atria
- no organised mechanical action
- 300-600bpm
139
Risk factors for a fib
- 60+
- diabetes
- high BP
- past MI
- structural heat disease
140
Presentation of a fib
- asymptomatic
- palpitations
- dyspnoea
- chest pain
- fatigue
- apical pulse>radial
141
Treatment of a fib
cardioversion
- LMW heparin
- shock with defib
142
What is atrial flutter?
- organised atrial rhythm
- rate of 250-250bpm
ECG → saw tooth pattern = DIAGNOSTIC
143
Causes of atrial flutter
- idiopathic
- coronary heart disease
- obesity
- HTN
- HF
- COPD
- pericarditis
144
Risk factors of atrial flutter
atrial fibrillation
145
Presentation of atrial flutter
- palpitations
- breathlessness
- chest pain
- dizziness
- syncope
- fatigue
146
Treatment of atrial flutter
- cardioversion
- catheter ablation → creates conduction block
- IV amiodarone → restore sinus rhythm
147
What is bundle branch block?
- block in conduction of one of the bundle branches
- ventricles don’t receive impulses at the same time
148
ECG changes in right BBB
- MaRRoW
- wide QRS
DIAGNOSTIC
149
Causes of right BBB
- PE
- IHD
- atrial ventricular septal defect
150
Causes of right BBB
- PE
- IHD
- atrial ventricular septal defect
151
Pathophysiology of right BBB
- right bundle doesn't conduct
- impulse spread from LV to RV
- late activation of RV
152
Presentation of right BBB
- asymptomatic
- syncope/presyncope
153
Treatment of right BBB
- pacemaker
- cardiac resynchronisation therapy
- reduce BP
154
ECG changes in left BBB
- WiLLiaM
- wide QTS and notched top
- T wave inversion in lateral leads
DIAGNOSTIC
155
Causes of left BBB
- IHD
- aortic valve disease
156
Pathophysiology of left BBB
- left bundle doesn't conduct
- impulse spreads from RV to LV
- late activation of LV
157
Presentation of left BBB
same as right BBB
158
Treatment of left BBB
same as right BBB
159
What is heart block?
a block at any level of the conduction system in which conduction seizes
160
What are the different types of heart block?
1st degree
2nd degree
- Mobitz I
- Mobitz II
3rd degree
161
1st degree heart block
- PR interval \>200ms
- asymptomatic
162
ECG changes 2nd degree Mobitz I
- progressive lengthening of PR interval
- one non-conducted P wave
- next PR interval is shorter
163
Presentation of 2nd degree Mobitz I
- light headedness
- dizziness
- syncope
164
ECG changes in 2nd degree Mobitz II
- SOB
- postural hypotension
- chest pain
165
ECG changes in 3rd degree heart block
- P waves and QRS at different rates → dissociation
- abnormally shaped QRS
166
Presentation of 3rd degree heart block
- dizziness
- blackouts
167
Treatment for 3rd degree heart block
- permanent pacemaker
- IV atropine
168
Causes of heart block
- athletes
- sick sinus rhythm
- MI
- drugs
- congenital
- aortic valve calcification
- cardiac surgery/trauma
169
Treatment for heart block
- cardioversion
- catheter ablation
- IV amiodarone
