1
Q
How do TAAs present?
A
- dilation of thoracic aorta = asymptomatic
- chest or back pain
- trachea/L bronchus compression > cough, SOB, stridor
- same nerve compressions as pericardial effusion
2
Q
Where is the abdominal aorta located?
A
- begins at T12
- ends at L4: divides into R and L common iliac
- supplies abdominal organs, pelvis, lower limbs, diaphragm, abdominal wall
3
Q
How do ruptured aortic aneurysms present?
A
- severe chest/back pain (TAA)
- abdo pain radiating to back/groin (AAA)
- shock (hypotension, tachy)
- collapse
4
Q
What is the aetiology of AAAs?
A
- coarctation of the aorta
- Marfan’s syndrome
- aortic surgery
- 3rd trimester pregnancy
5
Q
What is the screening programme for AAAs?
A
- single abdominal USS for males aged 65
6
Q
What are the AAA screening outcomes?
A
- <3cm: no further action
- 3-4.4cm: rescan every 12mo
- 4.5 - 5.4cm: rescan every 3mo
- ≥5.5cm: refer within 2 weeks to vascular surgery for intervention
7
Q
How are high rupture risk AAAs treated and what is one complication?
A
- treat with elective endovascular repair
- stent in abdominal aorta
- complication: endo-leak: stent fails to exclude blood from aneurysm
8
Q
How are ruptured aortic aneurysms treated?
A
- permissive hypotension to decrease blood loss
- immediate vascular review and emergency surgery
9
Q
How does a DVT present?
A
- unilateral calf pain and tenderness along deep vein line
- swelling >3cm
- erythema
- pitting oedema
- superficial veins distended
10
Q
What are risk factors for DVT?
A
- immobility
- recent surgery
- long haul travel
- pregnancy
- oestrogen (HRT and cocp)
11
Q
Well’s Score:
Active ____: 1
Paralysis or recent plaster immobilisation of the lower limbs: 1
Recently bedridden for 3+ days/ major surgery within 12 weeks: 1
Localised tenderness along the deep venous system: 1
Entire leg swollen: 1
Calf swelling > ?cm than asymptomatic side: 1
____ on symptomatic leg: 1
Collateral superficial veins (non-varicose): 1
Previously documented DVT: 1
An alternative diagnosis is at least as likely as DVT: _
A
**Well’s score
Active cancer: 1
Paralysis or recent plaster immobilisation of the lower limbs: 1
Recently bedridden for 3+ days or major surgery within 12 weeks requiring general or regional anaesthesia: 1
Localised tenderness along the deep venous system: 1
Entire leg swollen: 1
Calf swelling > 3 cm than asymptomatic side: 1
Pitting oedema on symptomatic leg: 1
Collateral superficial veins (non-varicose): 1
Previously documented DVT: 1
An alternative diagnosis is at least as likely as DVT: -2
12
Q
What is the first line investigation if DVT is ‘likely’? (>2 on Well’s)
What followup action is taken based on a positive or negative result?
A
- proximal leg USS within 4hrs
- Positive: Diagnose DVT and start anticoagulation
- Negative: D-dimer arranged. If -ve, DVT unlikely
13
Q
If the Well’s score is ≥2 but proximal leg USS cannot be carried out within 4hrs, what should be done instead?
A
- perform D-dimer
- give DOAC e.g. apixaban or rivaroxaban whilst waiting for USS
- perform USS within 24h
14
Q
Scenario:
- Well’s score ≥2
- proximal leg vein USS negative
- D-dimer positive
- Action?
A
- stop anticoagulation
- repeat USS 6-8 days later
15
Q
What should be done if a DVT is ‘unlikely’ (Well’s score ≤1)?
A
- D-dimer within 4h
- if not done within 4h, anticoagulate
- if negative, DVT unlikely
- positive: carry out USS within 4h
16
Q
Which anticoagulants are used in DVT?
A
- apixaban or rivaroxaban
- if unsuitable: use LmwH > dabigatran/edoxaban or LmwH > warfarin
17
Q
What drug should be used to treat DVT in:
- renal impairment (<15/min)
- antiphospholipid syndrome?
A
- renal: LmwH or unfractionated heparin
- antiphospholipid: LmwH > warfarin
18
Q
How long should a patient be anticoagulated for after VTE?
A
3 months
19
Q
How long after 3 months should treatment be continued for provoked VTE?
How does this differ in cancer?
A
- stop after inital 3 months
- if cancer, stop after 3-6 mo total
20
Q
How long is anticoagulation continued in unprovoked VTE?
A
- 3 further months after initial 3 mo
- 6 mo total
21
Q
What is syncope?
A
- transient loss of consciousness
- due to global cerebral hypoperfusion
- rapid onset, short duration, spontaneous complete recovery
22
Q
What are the causes of reflex syncope?
A
- vasovagal: triggered by emotion, pain, stress (fainting
- situational
- carotid sinus syncope
23
Q
What are the 4 categories of causes of orthostatic syncope?
A
- primary autonomic failure: Parkinson’s
- 2º autonomic failure: diabetic nephropathy
- drug-induced: diuretics, vasodilators
- volume depletion: haemorrhage, diarrhoea
24
Q
What are the causes of cardiac syncope?
A
- arrhythmia: brady or tachycardias
- structural: valvular, MI, HOCM
- PE
25
How is syncope investigated?
- CV exam
- postural BP readings
- ECG
26
What BP drop is significant for postural hypotension?
- lying to standing
- fall in systolic >20 or diastolic >10
- systolic falls below 90mmHg after standing
27
What are the 3 acute coronary syndromes?
- STEMI
- NSTEMI
- Unstable angina: prolonged, severe angina, usually at rest possibly with ECG changes
28
How does ACS develop?
- build up of fatty plaques in artery walls
- gradual narrowing > less blood and less oxygen reach heart leading to angina
- plaque rupture leading to occlusion
29
What are non modifiable risk factors for ACS?
- age
- male
- FHx
30
What are modifiable risk factors for ACS?
- smoking
- diabetes
- hypertension
- hypercholesterolaemia
- obesity
31
What are the causes and examination signs of cardiogenic shock?
- causes: heart failure, MI, cardiac tamponade, PE, IHD
- signs: heart failure signs, raised JVP, 4th heart sound
32
What are the causes and treatment of septic shock?
- uncontrolled bacterial infection
- ABCDE and broad spectrum antibiotics
33
What are the examination signs of septic shock? (temp and pulses)
- pyrexic and warm peripheries
- bounding pulse
- tachycardia
34
What are the causes of hypovolemic shock?
- blood loss: trauma, GI bleed
- fluid loss: dehydration
35
What are the symptoms of hypovolaemic shock?
- clammy, pale skin
- confusion
- hypotension
- tachycardia
36
What are the causes of neurogenic shock?
- spinal cord trauma e.g. RTA
- disrupted SNS, intact PSNS
37
What are the symptoms and treatment of neurogenic shock?
- hypotension, bradycardia, confusion, hypothermia
- ABCDE, IV atropine
38
What are the general signs of shock?
- confusion
- skin: pale, cold, sweaty, vasoconstriction
- prolonged hypotension
- inc capillary refill time
- reduced GCS
- weak, rapid pulse
39
In class I haemorrhagic shock, what is the:
- blood loss
- RR
- BP
- HR
- blood: <750ml
- RR: 14-20
- BP: normal
- HR: <100
40
In class II haemorrhagic shock, what is the:
- blood loss
- RR
- BP
- HR
- blood: 750-1500ml
- RR: 20-30
- BP: normal
- HR: >100
41
In class III haemorrhagic shock, what is the:
- blood loss
- RR
- BP
- HR
- blood: 1500-2000ml
- RR: 30-40
- BP: decreased
- HR: >120
42
In class IV haemorrhagic shock, what is the:
- blood loss
- RR
- BP
- HR
- blood: >2000ml
- RR: >35
- BP: decreased
- HR: >140
43
What causes anaphylactic shock and what are the symptoms?
- IgE mediated type 1 hypersensitivity
- hypotension, tachycardia, urticaria, puffy face
44
How is anaphylactic shock treated?
- ABCDE, IM adrenaline
- IM injection in anterolateral aspect of middle third of thigh
- repeat every 5 mins
45
What are the adrenaline doses for different ages in anaphylaxis?
- <6mo: 100-150mcg
- 6mo - 6y: 150mcg
- 6-12y: 300mcg
- >12y: 500mcg
46
If ECG changes are seen in leads II, III and aVF, which coronary artery may be affected by ACS, and which area of the heart is this?
- right coronary
- inferior leads
47
If ECG changes are seen in leads V1-V4, which coronary artery may be affected by ACS, and which area of the heart is this?
- left anterior descending
- anterior
48
If ECG changes are seen in leads I, V5 and V6, which coronary artery may be affected by ACS, and which area of the heart is this?
- left circumflex
- lateral
49
Where are ECG changes seen in a posterior MI and how is it confirmed? What coronary artery is affected?
- Changes in V1-3
- Posterior infarction is confirmed by ST elevation and Q waves in posterior leads (V7-9)
- L circumflex and R coronary
50
What are the reciprocal ECG changes seen in posterior MI?
- horizontal ST depression
- tall, broad R waves
- upright T waves
- dominant R wave in V2
51
What are the symptoms of unstable angina and how can it be diagnosed?
- cardiac chest pain at rest, with crescendo pattern
- new onset angina
- prolonged >20 mins
- diagnosed by history, ECG and troponin
52
How is unstable angina differentiated from NSTEMI?
- unstable angina if symptoms of ACS but no troponin elevation
- treat the same as NSTEMI until troponin is known
53
What are the symptoms of MI?
- unremitting cardiac chest pain radiating to left arm, neck, jaw (crushing/squeezing)
- usually severe but may be mild or absent
- sweating, breathlessness, nausea/vomiting
- dyspnoea
54
Describe unstable angina:
- occlusion
- infarction
- ECG
- troponin
1. partial occlusion of minor coronary artery
2. no infarction: ischaemia only
3. normal ECG, may show ST depression or T wave inversion
4. normal troponin
55
Describe NSTEMI:
- occlusion
- infarction
- ECG
- troponin
1. partial occlusion of major coronary artery/total occlusion of minor coronary artery
2. sub endothelial infarction so area distal to occlusion dies
3. ST depression, T wave inversion, new LBBB
4. elevated troponin
56
Describe STEMI:
- occlusion
- infarction
- ECG
- troponin
1. total occlusion of major c.a.
2. transmural infarction (full thickness of myocardium)
3. ST elevation in local leads,
4. elevated troponin
57
What is seen on an ECG after an MI?
- hyperactive T waves
- pathologically steep Q waves
- LBBB (left bundle branch block - electrical impulse disrupted) (prolonged QRS complex)
58
What is the gold standard investigation for stable angina?
CT coronary angiography to highlight any narrowing
59
What is the management strategy for immediate symptomatic relief of angina?
- GTN spray used PRN: vasodilation + ease symptoms
- 2nd dose after 5 mins if pain not relieved
- call ambulance after another 5 mins if pain hasn't gone
60
What medications are used for long term symptomatic relief of angina?
- β blockers (contraindicated by asthma)
- calcium channel blockers (CCB)
- lifestyle changes
61
What is a CABG?
- coronary artery bypass graft
- for multi vessel disease
- graft vein taken from leg (great saphenous vein/internal mammary artery) sewn on to bypass stenosis
62
What is PCI?
- Percutaneous coronary intervention with coronary angioplasty
- putting a catheter into the radial (ideal) or femoral artery
- contrast injected so stenosis is evident
- drug eluting stent can be inserted
63
What is the gold standard investigation for ACS?
CT coronary angiogram
64
What is the first line investigation for ACS?
12 lead ECG
65
What are ECG criteria for STEMI?
- clinical symptoms of ACS >20mins
- persistent ECG changes in 2 contiguous leads >20mins
- ST elevation in V2-V3
- new LBBB
66
What is the initial common management of patients with ACS?
- MONA
- morphine if severe pain
- oxygen if sats <94%
- nitrates: sublingual or IV if ongoing chest pain or htn (use w caution if hypotensive)
- aspirin 300mg
67
What are the 2 types of coronary reperfusion therapy?
- percutaneous coronary intervention
- fibrinolysis
68
How do you choose whether to offer PCI or fibrinolysis for STEMI?
- PCI should be offered if presenting within 12h of symptom onset and PCI can be delivered within 120 mins
- if presenting with ongoing ischaemia after 12h, can consider PCI
69
What antiplatelet therapy should be given prior to PCI in STEMI?
- dual antiplatelet therapy: aspirin + another drug
- if not taking oral anticoagulant: prasugrel
- if taking: clopidogrel
70
What drug should be given to patients undergoing PCI with radial access?
- radial: unfractionated heparin
- bailout glycoprotein IIb/IIIa if worsening thrombus
71
What drug should be given to patients undergoing PCI with femoral access?
- bivalirudin with bailout GPI
72
Describe fibrinolysis for STEMI?
- can use alteplase
- give antithrombin drug
- repeat ECG after 60-90 mins to see if resolved
- if persisting, consider PCI
73
How is NSTEMI managed?
- aspirin 300mg + fondaparinux if no immediate PCI
- calculate GRACE score
- if low: give ticagrelor
- if high: consider PCI
74
Describe PCI in NSTEMI
- offer immediately if unstable
- if stable, offer within 72h
- give prasugrel/ticagrelor
- give unfractionated heparin
- use drug eluting stent
75
What drug alternatives should be used in NSTEMI if the patient is a high bleeding risk?
- swap fondaparinux for antithrombin
- swap prasugrel for ticagrelor or ticagrelor for clopidogrel
76
What factors does the GRACE score take into account?
- age
- HR, BP
- cardiac and renal function (creatinine)
- cardiac arrest on presentation
- ECG findings
- troponin levels
77
What should patients be offered for secondary prevention of ACS/stable angina?
- lifestyle advice firstly
- aspirin
- second antiplatelet
- ACE inhibitor/ARB
- β blocker
- statin
78
What are the criteria for stable angina?
- central crushing chest pain radiating to neck/jaw, shoulders or arms
- brought on with exertion
- relieved with 5 mins rest/ GTN spray
- lasts <20 mins
79
What are the symptoms of stable angina?
- central crushing chest pain radiating to neck/jaw (worsens with time)
- nausea
- sweating
- fatigue
- dyspnoea
80
What investigations should be done in possible stable angina?
1. CT angiography
2. non-invasive functional imaging e.g. myocardial perfusion scintigraphy
3. invasive coronary angiography
81
How do calcium channel blockers work and in which disease are they contraindicated?
- reduce afterload
- relax smooth muscle cells in arterial walls
- contraindicated by heart failure
82
What is infective endocarditis?
- infection of heart valve(s) or other endocardial lined structures within the heart
- damages the valves + can cause heart failure
83
What are risk factors for infective endocarditis?
- previous endocarditis
- rheumatic heart disease
- valvular degeneration/prosthetic valve
- congenital heart defect
- IV drug use
84
Which bacteria cause infective endocarditis?
- MC: Staph aureus
- Strep viridans: poor dental hygiene/procedure
- Staph epidermidis: prosthetic valve
- Strep bovis: colorectal cancer
- SLE
85
What is the pathophysiology behind infective endocarditis?
- endocardial damage > thrombi formation made of platelets and fibrin
- valve cusps are avascular preventing normal immune response
- high pressure makes infection more likely
- thrombus is colonised by bacteria and these break off and travel round the bloodstream
- tricuspid most commonly affected due to first contact w blood from body
86
How does infective endocarditis present?
- fever and heart murmur
- haematuria (blood in urine)
- splinter haemorrhages
- Osler's nodes (nodules on digits)
- Janeway lesions (haemorrhages and nodules in fingers
- Petechiae (small purple spots)
- Roth spots (retinal haemorrhages)
- malaise
87
How many Duke criteria to diagnose infective endocarditis?
- positive pathological criteria
- 2 major
- 1 major and 3 minor
- 5 minor
88
What are the pathological Duke criteria?
- positive histology or microbiology obtained during autopsy or cardiac surgery
89
What are the major Duke criteria?
- 2 +ve blood cultures showing typical organisms
- persistent bacteraemia from 2 cultures 12h apart/3+ +ve cultures for less specific organisms
- positive echo
- new valvular regurg
90
What are the minor Duke criteria?
- predisposing heart condition or IVDU
- fever >38
- glomerulonephritis, Roth spots, Osler nodes
- emboli, splenomegaly
91
How is infective endocarditis investigated?
- Transthoracic echo for vegetations
- Raised CRP
- ECG: showing new heart block, ischaemia or infarction
- FBC, blood cultures, urinalysis
92
Which procedures do NOT require prophylaxis for infective endocarditis?
- dental
- upper and lower GI
- GU
- upper and lower resp
93
What are poor prognostic indicators for infective endocarditis?
- Staph aureus infection
- prosthetic valve
- culture negative
- low complement levels
94
What are indications for surgery in infective endocarditis?
- severe valvular incompetence
- aortic abscess
- infection resistant to Abx
- cardiac failure unresponsive to meds
- recurrent emboli after Abx
95
What are the INITIAL blind Abx therapy used in infective endocarditis?
- native valve: amoxicillin ± low dose gentamicin
- penicillin allergic/MRSA/septic: vancomycin + low dose gentamicin
- prosthetic valve: vancomycin, rifampicin, low-dose gentamicin
96
What Abx are used in native valve endocarditis caused by staphylococci?
- flucloxacillin
- penicillin allergic/MRSA: vancomycin + rifampicin
97
What Abx are used in prosthetic valve endocarditis caused by staphylococci?
- Flucloxacillin + rifampicin + low-dose gentamicin
- penicillin allergic or MRSA: vancomycin + rifampicin + low-dose gentamicin
98
What Abx are used in endocarditis caused by sensitive streptococci?
- Benzylpenicillin
- penicillin allergic: vancomycin + low-dose gentamicin
99
What Abx are used in endocarditis caused by less sensitive streptococci?
Benzylpenicillin + low-dose gentamicin
- penicillin allergic: vancomycin + low-dose gentamicin
100
What is Wolff-Parkinson White syndrome?
- congenital accessory conducting pathway between atria and ventricles
- leads to atrioventricular re-entry tachycardia
101
Explain the pathway of conduction in Wolff-Parkinson White
Normal heart: Atria → AV node → Ventricles → stops
WPW: Atria → AV node (down) → Ventricles → accessory pathway (back up) → Atria creating a loop
102
Describe the mechanism of double excitation in Wolff-Parkinson White (relate to ECG findings)
- accessory pathway allows AV node bypass (shortened PR interval)
- ventricles pre-excited (gradual depolarisation causes slurred delta upstroke)
- in addition to normal conduction: double excitation
- anterograde or retrograde
103
How does Wolff-Parkinson White present?
- teenagers/young adults
- palpitations: sudden onset
- lightheadedness
- presyncope
104
What is seen on ECG in Wolff-Parkinson White?
- short PR interval
- wide QRS with slurred upstroke (delta wave)
- R waves in V1-V3
- left axis deviation in R sided accessory pathway
105
What is the difference between type A Wolff-Parkinson White and type B on ECG?
- type A: left sided: positive delta wave in V1-V6
- type B: right sided: negative delta wave in V1-V2
106
How is Wolff-Parkinson White managed?
- radiofrequency ablation of accessory pathway
- sotalol, amiodarone, flecainide
107
What serious condition can develop in Wolff-Parkinson White and what drugs are CI?
- SVT
- atrial fibrillation/flutter can lead to SVT
- therefore anti-arrythmics (βblockers, CCB, digoxin, adenosine) are CI
108
What is 1st line conservative management of SVT?
- vagal manoeuvres
- Valsava manoeuvre: forced expiration against closed glottis
109
What are the two types of ventricular tachycardia and what commonly cause them?
- monomorphic: MI
- polymorphic: prolonged QT (could be Torsades de pointes)
110
In ventricular tachycardia, which 4 signs indicate immediate cardioversion is needed?
- systolic <90
- chest pain
- syncope
- heart failure
111
Which 3 drugs can be used as cardioversion in VT?
- amiodarone
- lidocaine
- procainamide
112
If cardioversion and antiarrythmics in VT fail, what should be the next line management?
- electrical cardioversion with DC shocks
113
What are the 3 severities of peripheral arterial disease?
1. intermittent claudication
2. critical limb ischaemia
3. acute limb-threatening ischaemia
114
What are the features of acute limb-threatening ischaemia? (6P's)
- pale
- pulseless
- painful
- paralysed
- paraesthetic
- perishing with cold
115
How is acute limb-threatening ischaemia investigated (peripheral arterial disease)?
- handheld arterial Doppler
- if signal present: ABPI
116
What features suggest acute limb-threatening ischaemia has been caused by thrombus?
- pre-existing claudication and sudden deterioration
- reduced/absent pulses in contralateral limb
- widespread vascular disease
117
What features suggest acute limb-threatening ischaemia has been caused by embolus?
- sudden onset of painful leg <24h
- no Hx of claudication
- obvious embolus source (AF, recent MI)
- no evidence of peripheral vascular disease
- proximal aneurysm evidence
118
How is acute limb-threatening ischaemia managed?
- ABC
- analgesia (IV opioid)
- IV unfractionated heparin
- vascular review
119
What is the definitive management of acute limb-threatening ischaemia?
- intra-arterial thrombolysis
- surgical embolectomy
- angioplasty
- bypass surgery
- amputation if irreversible
120
What is the presentation of critical limb ischaemia?
- resting pain in foot >2 weeks
- ulceration
- gangrene
- pt hanging legs out of bed at night to ease pain
121
How is critical limb ischaemia investigated and what value suggests a diagnosis?
- ABPI
- <0.5
122
What are features of intermittent claudication?
- intermittent claudication
- walk for predictable distance before symptom onset
- relieved within mins of stopping
- not present at rest
123
How do you assess + investigate intermittent claudication?
- check femoral, popliteal, posterior tibialis and dorsalis pedis pulses
- check ABPI
- 1st line: duplex USS
- magnetic resonance angiography before intervention
124
What is conservative management of peripheral arterial disease?
- quit smoking
- exercise training
125
What drugs are licensed for use in peripheral arterial disease?
- naftidrofuryl oxalate: vasodilator
- cilostazol: phosphodiesterase III inhibitor
126
How may severe PAD be treated?
- endovascular revascularization: percutaneous transluminal angioplasty ± stent placement
- surgical revascularization: surgical bypass with autologous vein or prosthetic, endarterectomy
127
What is aortic dissection and where does it most commonly occur?
- tear in tunica intima
- blood between intima and media creating false lumen
- MC in ascending aorta and aortic arch
128
How does aortic dissection present?
- ripping/tearing pain in chest/back
- hypertension > hypotension
- radial pulse deficit/difference in bp between arms
- aortic regurgitation (diastolic murmur)
- focal neurological deficit
129
Describe the pulse deficit in aortic dissection
- weak/absent carotid, brachial or femoral pulse
- variation >20mmHg between arms
130
What is the difference between type A and type B aortic dissection and what is the difference in presentation?
- type A: ascending aorta (chest pain)
- type B: descending aorta (upper back pain)
- overlap in symptoms
131
How is aortic dissection diagnosed?
- ECG and CXR exclude MI
- CXR: widened mediastinum
- 1st: CT/MRI angiogram: false lumen
- Gold: TOE shows intimal flap and false lumen
132
How is aortic dissection managed?
- analgesia for pain
- β blockers to control BP and HR and reduce stress on walls
- Type A: open surgery replaced with graft
- Type B: conservative, reduce BP with labetalol
if complicated type B: thoracic endovascular aortic repair (TEVAR) using catheterisation
133
What are the HR and BP targets in aortic dissection?
- HR: 60-80
- BP: systolic 100-120 mmHg
134
What are some common complications of aortic dissection?
- forward tear: stroke, renal failure
- backward tear: aortic regurg, inferior MI
- cardiac tamponade
135
How is aortic dissection classified?
- R lateral area is most common site
- Type A: affects ascending aorta, before brachiocephalic artery
- Type B: descending aorta after L subclavian artery
136
What are the risk factors for aortic dissection?
- hypertension
- age
- male
- smoking
- poor diet
- low physical activity
- raised cholesterol
137
What is a differential diagnosis for aortic dissection?
- MI
138
What are some causes of aortic dissection?
- hypertension
- bicuspid aortic valve
- coarctation of aorta
- CABG
- Ehlers-Danlos/Marfan's syndrome
139
What is aortic regurgitation?
- leakage of blood back from aorta into LV during diastole due to ineffective coming together of aortic cusps
140
What are causes of aortic regurgitation due to valve disease?
- infective endocarditis (acute)
- rheumatic fever
- calcified valve
- connective tissue (RA, SLE)
- bicuspid aortic valve
141
What are causes of aortic regurgitation due to aortic root disease?
- aortic dissection (acute)
- bicuspid aortic valve
- spondyloarthropathies
- hypertension
- syphilis
- Marfan's/Ehlers-Danlos
142
What is the pathophysiology of aortic regurgitation?
- combined pressure and volume overload due to backflow of blood in addition to circulating blood
- leads to LV hypertrophy and dilatation. Progressive dilation > heart failure
143
How does aortic regurgitation present?
- wide pulse pressure
- early diastolic blowing murmur at 2nd intercostal space on R sternal border
- collapsing pulse
- pulmonary oedema, pallor, sweating
144
What are the 3 other signs seen in aortic regurgitation? What is the unifying pathophysiology behind all 3 signs?
- Quincke's sign
- de Musset's sign
- Austin-Flint murmur (severe)
- wide pulse pressure (high systolic volume, low diastolic)
145
What is Quincke's sign in aortic regurgitation?
- capillary pulsation
- alternating blanching and flushing
146
What is de Musset's sign in aortic regurgitation? Why does this occur?
- head bobbing
- large SV
- carotid arteries transmit this pulsation leading to a nod during systole
147
What is the Austin-Flint murmur that can occur in severe aortic regurgitation?
- low-pitched, mid/late diastolic rumbling murmur heard at apex
- regurgitation jet from aorta strikes mitral valve leaflet
- partially closes valve
- causes turbulent flow from atrium > ventricle during diastole
148
How is aortic regurgitation investigated?
- GOLD: Echo: evaluate AV and aortic root, measure LV dimension and function
- CXR: enlarged cardiac silhouette
149
How is aortic regurgitation managed?
- IE prophylaxis as differential diagnosis
- ACEIs can improve SV and regurgitation
- surgical valve replacement if severe
150
What is aortic stenosis and what are the 3 types and causes?
- narrowing of the aortic valve area
- symptoms occur when valve area is 1/4 of normal
- types: supravalvular, subvalvular, valvular
151
What is the pathophysiology of aortic stenosis?
- pressure gradient develops between LV and aorta (inc after load)
- LV function initially maintained by compensatory hypertrophy
- LV function declines when compensatory mechanisms are exhausted
152
What are the signs of aortic stenosis?
- slow rising carotid pulse with decreased amplitude (little difference between systolic and diastolic)
- soft/absent 2nd heart sound, S4 aortic gallop
- thrill
- crescendo descendo ejection systolic murmur
153
What are the symptoms of aortic stenosis?
- syncope
- angina
- dyspnoea
- LVH or failure
154
How is aortic stenosis investigated?
- GOLD: Echocardiogram: LV size and function, Doppler derived area and gradient
155
How is aortic stenosis managed?
- vasodilators fairly contraindicated
- aortic valve replacement, prosthetic requires anticoagulants (healthy patient)
- TAVI: trans catheter aortic valve implantation (less invasive)
156
What is the target INR for aortic vs mitral valves?
- aortic: 3.0
- mitral: 3.5
157
Which anticoagulant is preferentially used in mechanical valve replacement?
- warfarin
- only give aspirin for additional indications
158
What is atrial fibrillation?
- cardiac arrhythmia
- disorganised electrical activity in atria overriding SAN
- leads to irregular ventricular contraction
159
What is the pathophysiology of AF?
- supraventricular cardiac arrythmia
- micro re-entry circuits cause chaotic activity
- intermittently conducted through AVN giving irregularly irregular ventricular rate
160
What are cardiac causes of AF?
- hypertension
- IHD
- HFrEF
- valve stenosis/regurg
- CHD
- dilation/hypertrophy
161
What are non-cardiac causes of AF?
- acute infection
- electrolyte imbalance
- PE
- thyrotoxicosis
- diabetes mellitus
162
What are the 4 types of AF?
- first episode
- paroxysmal: ≥2 episodes terminating spontaneously and lasting <7 days
- persistent: not self-terminating and lasts >7 days
- permanent: continuous AF, can't be cardioverted
163
How does atrial fibrillation present?
- palpitations
- tachycardia
- shortness of breath
- syncope
- chest pain
- symptoms of associated conditions e.g. stroke, sepsis
164
What are examination findings of AF?
- irregularly irregular pulse
- radial-apical deficit
- HF findings
165
How is AF investigated?
- 12 lead ECG
- paroxysmal (undetected on ECG): 24hr ambulatory ECG
- only do echo if result may alter management plan e.g. valve pathology
166
How is atrial fibrillation managed?
- treat underlying cause
- rate and rhythm control
- restore sinus rhythm: electrical/pharmacological cardioversion
167
What is rate control for atrial fibrillation?
- aims to extend diastole and coordinate filling
- β blocker (1st line), CCB, Digoxin
168
How is atrial fibrillation recognised on ECG?
- Absent P waves
- narrow QRS complex tachycardia
- irregularly irregular ventricular rhythm
169
What is paroxysmal AF and how is it treated?
- comes and goes in episodes <48 hrs
- anticoagulation based on CHADSVASc score
- pill in the pocket approach: flecanide
170
What are the components of the CHA2DS2VASc scoring system?
- calculates stroke risk for AF
- Congestive heart failure/left ventricular dysfunction
- Hypertension
- Age ≥75 (+2)
- Diabetes
- stroke/TIA (+2)
- Vascular disease
- Age 64-74 (+1)
- Sex category (female)
171
What scoring results of CHA2DS2-VASc mean anticoagulation should be given?
- 1: in males consider anticoagulation
- ≥2: give in both genders
172
What investigation should be done in AF if CHA2DS2-VASc is 0 and which disease does it exclude
- transthoracic echo
- exclude valvular heart disease
- AF + valvular heart disease = anticoagulation
173
Which score should be used to assess bleeding risk in AF if considering starting anticoagulation? What does this scoring system comprise?
- ORBIT
- Hb <130 g/L (male) and < 120 g/L for (female): 2
- Age > 74 years: 1
- Bleeding history (GI, intracranial or haemorrhagic stroke): 2
- Renal impairment (GFR < 60): 1
- Treatment with antiplatelets:1
174
Correlate the ORBIT scores with the risk level
- 0-2: Low
- 3: medium
- 4-7: high
175
Which drugs are recommended as anticoagulation in AF?
- DOACs: apixaban, dabigatran, edoxaban, rivaroxaban
- 2nd line: warfarin
- NOT aspirin
176
How can AF lead to stroke?
- uncontrolled, disorganised movement leads to stagnating blood
- this leads to a thrombus which becomes an embolus
- can lodge in brain
177
What are the 2 indications for cardioversion in AF?
- haemodynamically unstable pt
- cardioversion electively where rhythm control is preferred over rate control (if onset <48h)
178
What are the guidelines for cardioversion in AF if onset <48hrs?
- if not offering rate control, offer rhythm control
- electrical (synchronised DC shock) or pharmacological cardioversion
179
What rhythm control is offered in AF with onset >48hrs?
- give anticoagulation for at least 3wks
- OR TOE to exclude left atrial appendage thrombus
- if excluded: can heparinise and cardiovert immediately
- use electrical cardioversion
- anticoagulate for a further 4wks after
180
Which drugs can be used as pharmacological cardioversion in AF?
- amiodarone: blocks K channels to prolong refractory period
- flecainide: blocks Na channels to raise depolarisation threshold
181
Give one contraindication for each of flecainide and amiodarone related to the heart
- flecainide: structural/IHD
- amiodarone: QT prolongation
182
What drugs are used for long-term rhythm control in AF?
- β blockers
- other than sotalol
- dronedarone
- amiodarone
183
When is rate control NOT the first line strategy in AF?
- AF with reversible cause
- HF causing aF
- new onset AF <48h
- atrial flutter which can be treated with ablation
- rhythm control is more suitable
184
What medications classes may be used for rate control in AF?
- β blockers: CI in asthma
- CCB
- digoxin (consider 3rd line if little exercise)
185
Why and how may catheter ablation be done in AF?
- unresponsive to or wish to avoid antiarrhythmics
- ablates faulty electrical pathways
- performed percutaneously
- radiofrequency or cryotherapy ablation
186
What is atrial flutter?
- A re-entrant rhythm where the electrical signal recirculates in a self-perpetuating loop
- stimulates atrial contraction at 300bpm
- signal enters ventricles every 2nd lap due to long refractory period at AV node
- 150 bpm in ventricle
187
Describe anticoagulation relating to catheter ablation in AF
- anticoagulate for 4 weeks before and during procedure
- anticoagulate after as per CHA2DS2-VASc score
188
How is atrial flutter managed?
- more sensitive to cardioversion
- treat as AF
- radiofrequency ablation should be curative
189
What is 1st degree heart block and how does it present on ECG?
- delayed AV conduction through AV node
- PR interval greater than 0.20 seconds
190
What is 2nd degree heart block?
- some atrial impulses don't make it through the AV node > ventricles so some P waves aren't followed by QRS complexes
- Mobitz T1 and T2
191
What is Mobitz type 1?
- atrial impulses become weaker until they don't pass through AV node
- fails to stimulate ventricular contraction
- cycle repeats
- increasing PR interval until P wave no longer conducts to ventricles, QRS is missed then returns on next cycle
192
What is Mobitz type 2?
- failure or interruption of AV conduction
- leads to missing QRS complexes
- usually set ratio of P waves:QRS complexes
- e.g. 3:1 block
193
What is the presentation of Mobitz type II?
- palpitations
- pre-syncope and syncope
- regularly irregular pulse
194
How is Mobitz type II managed?
- cardiac monitor due to risk of progressing to complete heart block
- temporary pacing may be needed
- risk of asystole
195
What is 3rd degree heart block?
- complete heart block
- no observable relationship between P waves and QRS complexes
- ventricular rhythm too slow to maintain perfusion
- significant risk of asystole
196
Describe narrow vs broad complex in complete heart block and where they originate?
- narrow: QRS <0.12: originate above bundle of His
- broad: below bndle of His, slower Hr and worse presentation
197
How is heart block treated?
- atropine 500mcg IV up to 3mg
- transcutaneous pacing
- isoprenaline infusion
- permanent pacemaker
198
What is the presentation of 3rd degree heart block?
- syncope
- heart failure
- bradycardia (30-50bpm)
- wide pulse pressure
- haemodynamic compromise: prolonged CRT and hypotension
199
How is supraventricular tachycardia managed?
- continuous ECG monitoring
- Valsalva/carotid sinus massage
- IV adenosine: slows conduction through AV node (6mg> 12mg > 18mg)
- if asthmatic: verapamil
- if ineffective: verapamil, β blocker or cardioversion
200
What is supraventricular tachycardia?
- caused by electrical signal re-entering atria from ventricles causing self-perpetuating loop
- narrow complex tachycardia
- appears on ECG as QRS, T, QRS, T...
201
What is the presentation of haemodynamic compromise in bradycardia/tachycardia?
- shock symptoms (systolic <90)
- syncope
- MI
- HF
202
Give 4 risk factors for asystole?
- complete heart block with broad QRS
- recent asystole
- Mobitz type II
- ventricular pause >3s
203
In tachycardia, if there are signs of haemodynamic instability, what are the next steps according to ALS?
- synchronised DC shock (up to 3 attempts)
- unsuccessful:
204
What are the two shockable rhythms in cardiac arrest?
- pulseless ventricular tachycardia
- ventricular fibrillation
205
How does ventricular fibrillation appear on ECG?
- chaotic and disorganised electrical activity
- no identifiable QRS complexes
- progresses coarse > fine > asystole
206
What are the differentials for irregular broad complex tachycardia?
- AF with bundle branch block
- AF with ventricular pre-excitation
- torsades de pointes
207
What does a regular broad complex tachycardia suggest?
- assume VT (unless previously confirmed SVT with BBB)
208
What does an irregular narrow complex tachycardia suggest?
- probable AF
209
What does regular narrow complext tachycardia suggest?
- atrial flutter
210
What is ventricular tachycardia?
- broad complex tachycardia
- originates from ventricular ectopic focus
- potential to precipitate VF
211
What precipitates the two types of VT?
- monomorphic: post MI
- polymorphic: prolonged QT
212
What drugs cause a prolonged QT interval?
- amiodarone,
- sotalol
- tricyclic antidepressants,
- fluoxetine
- chloroquine
- erythromycin
213
What electrolyte abnormalities cause prolonged QT interval?
- hypocalcaemia
- hypokalaemia
- hypomagnesaemia
214
What conditions cause a prolonged QT interval?
-acute myocardial infarction
- myocarditis
- hypothermia
- subarachnoid haemorrhage
215
Which drugs can be used to manage VT? 3 drugs + 1 which should not be used
- amiodarone: ideally through a central line
- lidocaine: with caution in severe LV impairment
- procainamide
- do NOT use verapamil
216
How is Torsades de pointes managed?
- IV magnesium sulphate
217
What are the two non shockable rhythms?
- pulseless electrical activity (PEA)
- asystole
218
What are causes of PEA?
- severe fluid depletion/blood loss
- cardiac tamponade,
- massive PE
- tension pneumothorax.
219
What is PEA?
- absence of a pulse in a patient with electrical activity
220
What is asystole?
- absence of electrical activity on the rhythm strip
- slight undulations seen from ventilation and compressions
221
What are the reversible causes of cardiac arrest (H's)?
- Hypoxia
- Hypovolaemia
- Hyperkalaemia, hypokalaemia, hypoglycaemia, hypocalcaemia, acidaemia and other metabolic disorders
- hypothermia
222
What are the reversible causes of cardiac arrest (T's)?
- Thrombosis (coronary or pulmonary)
- Tension pneumothorax
- Tamponade - cardiac
- Toxins
223
When is adrenaline given in cardiac arrest ALS?
- non-shockable: 1mg ASAP
- shockable: 1mg after chest compressions restarted after 3rd shock then every 3-5mins
224
When is amiodarone given in cardiac arrest ALS?
- shockable: give 300mg after 3 shocks
- give a further 150 mg after 5 shocks
- lidocaine used as alternative
225
What is acute pericarditis? What is the duration?
- an inflammatory pericardial syndrome with or without effusion
- lasts less than 4-6 weeks
226
What is the epidemiology of pericarditis?
- 80-90% is idiopathic + seasonal with viral trends
- higher in young, previously healthy patients
227
What are the infectious causes of pericarditis?
- MAINLY viral: enteroviruses, herpesviruses (EBV, CMV, HHV-6), adenoviruses
- bacterial: tuberculosis
228
What are the non-infectious causes of pericarditis?
- autoimmune: Sjogren, RA, scleroderma
- post MI
- neoplastic (most common): lung/breast malignancy
- trauma (most common): PCI, pacemaker insertion
229
How does pericarditis present?
- severe chest pain, sharp and pleuritic
- KEY: **relieved by sitting forward and exacerbated by lying down**
- rapid onset
- left ant chest/epigastrium
- breathlessness, non-productive cough, hiccups
230
How can pericarditis be investigated?
- pericardial rub: heard around 2nd heart sound, sounds like crunching snow
- ECG, bloods, CXR, Echo
231
What is seen on the ECG in pericarditis?
- PR depression
- concave (saddle shaped) ST elevation
- similar ECG to acute STEMI
- global changes
232
Describe the management of pericarditis
- restricting physical activiity
- NSAIDs + PPIs for 1-2 weks
- colchicine
- 2nd line: corticosteroids if NSAIDs or colchicine fail
- avoid strenuous exercise for 3mo
233
What factors are used in diagnosis of acute pericarditis and how many factors are needed?
- diagnosis made with 2 of 4 factors:
- chest pain
- friction rub
- ECG changes
- pericardial effusion
234
What are the features of chronic pericarditis?
- dyspnoea
- RH failure
235
What is seen on examination of chronic pericarditis?
- prominent X and Y descent in JVP
- pericardial knock (loud S3)
- positive Kussmaul sign
236
What is pericardial effusion?
- collection of excess fluid in the pericardial sac
- acute or chronic
- transudates, exudates, blood, pus, gas
- creates inward pressure on heart making it more difficult to expand during diastole
237
What is cardiac tamponade?
- pericardial effusion is large enough to raise intra-cardiac pressure
- inc pressure leads to reduced filling during diastole and decreased CO during systole
238
What are the features of cardiac tamponade? Beck's triad
- hypotension
- raised JVP
- muffled heart sounds
239
What are some features of cardiac tamponade other than Beck's triad?
- dyspnoea
- tachycardia
- absent Y descent of JVP
- pulsus paradoxus
- electrical alternans on ECG (alternating QRS amplitude)
240
How is cardiac tamponade managed?
- urgent pericardiocentesis
241
How is pericardial effusion managed?
- treatment of underlying cause: aspirin, NSAIDs, colchicine, steroids
- drainage: needle pericardiocentesis or surgical drainage
242
How is pericardial effusion diagnosed?
- Echo: diagnose and assess size and effect on heart function
- fluid analysis: protein content, bacterial, viral, tumour markers
243
How does pericardial effusion present?
- chest pain
- SOB and orthopnoea
- fullness in chest
- quiet heart sounds
- pulsus paradoxus
244
What causes pericardial effusion?
- Transudative: congestive HF, pulmonary htn
- Exudative: infection, autoimmune, injury to pericardium
- rupture > tamponade: MI, trauma, aortic dissection
245
What nerve compressions cause which symptoms in pericardial effusion?
- phrenic nerve compression > hiccups
- oesophageal compression > dysphagia
- recurrent laryngeal > hoarse voice
246
What is the definition of hypertension (clinic and 24h BP)?
- clinic: ≥140/90mmHg
- 24h: ≥135/85mmHg
247
What symptoms may a very high (>200/120mmHg) BP cause?
- headaches
- visual disturbance
- seizures
248
What bedside investigations should be done for newly diagnosed hypertension and why?
- fundoscopy (retinopathy)
- urine dipstick (renal disease)
- ECG (LV hypertrophy or IHD)
249
Which bloods should be done following newly diagnosed hypertension?
- U&E
- HbA1c
- lipids
250
How is hypertension diagnosed?
- measure BP in both arms
- offer ABPM or home BPM if ≥140/90
251
What are the stages of hypertension? give clinic and home values
- stage 1: Clinic ≥140/90 or home ≥135/85
- stage 2: clinic ≥160/100 or home ≥150/95
- stage 3: clinic ≥180 or home ≥120
252
How is ambulatory BP monitoring conducted?
- at least 2 measurements per hour during waking hours
- use avg of >14 measurements
253
How is home BP monitoring conducted?
- 2 consecutive readings >1min apart each time
- BP recorded BD
- record for 7d
- avg values of all days except 1st day
254
If recorded BP is ≥180/120mmHg, what signs should be assessed for?
- signs of retinal haemorrhage or papilloedema
- new onset confusion, chest pain, signs of HF, AKI
255
in Stage 1 hypertension, patients should be treated if >80 AND any of the following apply:
- target organ damage
- established CVD
- renal disease
- diabetes
- QRISK ≥ 10%
256
What is the lifestyle advice given in hypertension?
- low salt diet (3g/day)
- reduce caffeine intake
- stop smoking, less alcohol, exercise
257
How is stage 2 hypertension treated?
- offer drug treatment regardless of age
258
What drugs should be used to treat hypertension if <55 y/o or T2DM?
- ACEi or ARB
- use ARB if ACEi not tolerated e.g. cough
259
What drugs should be used to treat hypertension if >55 y/o or black african/Afro-Caribbean?
- CCB
260
Which renal conditions cause secondary hypertension?
- glomerulonephritis
- pyelonephritis
- adult polycystic kidney disease
- renal artery stenosis
261
Which endocrine conditions cause secondary hypertension?
- phaeochromocytoma
- Cushing's syndrome
- congenital adrenal hyperplasia
- acromegaly
262
Which drugs can cause secondary hypertension?
- steroids
- monoamine oxidase inhibitors
- combined oral contraceptive pill
- NSAIDs
- leflunomide
263
What is pulmonary hypertension? What MAP defines it?
- increased resistance in pulmonary arteries
- strain on RH
- back pressure into venous system
- MAP >20mmHg
264
MLA
flashcards
Decks in class (28)
# Cards
-
Renal148
-
Respiratory161
-
CV264
-
Derm109
-
Endocrinology271
-
Oncology72
-
Rheumatology226
-
3a Neuro228
-
3a Obstetrics247
-
GI303
-
Ophthalmology250
-
ENT102
-
Gynaecology286
-
Paeds resp117
-
Paeds GI130
-
Sexual Health105
-
Paeds endo26
-
Paeds cardio59
-
Haematology158
-
Ortho90
-
Anaesthesia + surgery4
-
Paeds neuro52
-
Paeds derm41
-
Paeds infectious68
-
Psychiatry269
-
Paeds MSK69
-
Paeds renal5
-
Paeds Genetics38
