Cardiovascular - Level 2 Flashcards

1
Q

Description of pathology of stable angina?

A
  • Pain (discomfort) arising from the heart due to myocardial ischaemia
  • Coronary artery disease – atherosclerotic plaques cause progressive narrowing of the arteries (coronary), decreasing blood supply and thus oxygen/nutrients to myocardium
  • Symptoms occur when blood flow does not provide adequate oxygen in times of high demand (exercise)
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2
Q

Epidemiology of stable angina?

A
  • More than 1.5 million in UK

- CVD accounts for 25% of deaths – CHD 45% of CVD deaths

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3
Q

Risk factors of stable angina?

A
  • Older age, male gender, ethnicity
  • Hyperlipidaemia, hypertension, DM, obesity
  • Smoker, FHx, lack of exercise, high fat diet, stress, alcohol
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4
Q

Symptoms of stable angina?

A

Central, crushing, retrosternal chest pain
o Comes on exertion, relieved by rest, exacerbated by cold weather, anger and excitement
o Radiates to arms, shoulders, jaw and neck

Provoked by physical exertion, especially after meals, anger and in cold weather

Pain fades within minutes with rest

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5
Q

Symptoms of decubitus angina?

A

o Angina lying down, associated with LV dysfunction due to CAD

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6
Q

Symptoms of nocturnal angina?

A

o Occurs at night and may wake patient, provoked by vivid dreams
o Usually in critical CAD and may be vasospasm

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7
Q

Symptoms of variant (prinzmetal) angina?

A

o Without provocation, usually at rest due to coronary artery spasm
o Often women, ST elevation during pain/spasm

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8
Q

Symptoms of unstable angina?

A

o Classed as ACS

o Increasing rapidly in severity, occurs at rest with <1 month onset

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9
Q

Who to refer in stable angina?

A
  • Refer all people with typical or atypical angina to specialist chest pain clinic
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10
Q

Management of stable angina whilst awaiting diagnosis?

A

o Sublingual GTN spray used to relieve symptoms
 If they experience chest pain, stop and rest, use GTN as instructed
 Take 2nd dose after 5 mins, if pain still present call 999

o Aspirin (75mg) if likely to be stable angina

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11
Q

Initial tests in specialist chest pain service of stable angina??

A

 Bloods
• FBC (anaemia), TFTs, HbA1c, Lipids

 ECG
• May show ST depression, T wave flattening/inversion, pathological Q waves, LBBB

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12
Q

Diagnostic imaging in specialist chest pain service of stable angina??

A

 1st line - CT coronary angiography
 2nd line - Non-invasive functional imaging, offer when CT angiogram has shown CAD of uncertain functional significance or non-diagnostic
• Myocardial perfusion scintigraphy with SPECT
• Stress Echo
• Contrast MRI
 3rd line – Invasive coronary angiography, if results inconclusive

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13
Q

Investigations if known CAD in stable angina? Criteria for this?

A

o If known CAD (previous MI, revascularisation, previous angiograpy)
 Exercise testing ECG – ST depression <6 mins

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14
Q

Diagnosis of angina confirmed when?

A
  • Significant CAD during invasive or 64-slice CT angiography or,
  • Reversible myocardial ischaemia during non-invasive functional imaging
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15
Q

General advice given in management of stable angina?

A

o Lose weight, regular exercise, control DM
o Stop smoking, limit alcohol consumption
o Impact of stress on angina
o Take GTN before sex if needed
o Inform DVLA

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16
Q

Drug treatments given in stable angina?

A

o Sublingual GTN spray (sublingual tablets) used to relieve symptoms
 If they experience chest pain, stop and rest, use GTN as instructed
 Take 2nd dose after 5 mins, if pain still present call 999

o Beta-blocker/CCB (N-DHP) (1st line regular)
 Use both if symptoms persist (BB & DHP CCB)
 Alternatives if cannot tolerate BB/CCB or both CI: Isosorbide mononitrate, nicorandil, ivabradine, ranolazine

o Monitor 2-4 weeks after starting or changing dose

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17
Q

Secondary prevention of CVD in stable angina?

A

o Aspirin 75mg OD
o Atorvastatin 80mg OD
o ACEi (if hypertensive/diabetic)

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18
Q

Follow up in stable angina?

A

o Review every 6-12 months depending on severity

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19
Q

When to refer to cardiologist and for what in stable angina?

A
  • Referral to cardiologist for angiography (and possible revascularisation) if:
    o Extensive ischaemia on ECG
    o On optimal drug treatment given (2 drugs max doses)
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20
Q

Definitive management for patient of stable angina - for people adequately controlled on medical therapy?

A

 Consider further functional or anatomical testing (if not already available) to assess whether benefit from surgery

 Coronary angiogram – if functional testing indicates extensive ischaemia or likely left main stem or proximal three-vessel disease

 Coronary Artery Bypass Graft (CABG) if left main stem disease or proximal three-vessel disease

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21
Q

Definitive management for patient of stable angina - for people not adequately controlled on medical therapy?

A

 Revascularisation (CABG/PCI)

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22
Q

Management if remain symptomatic despite reperfusion interventions?

A

o Offer Myocardial perfusion scintigraphy using SPECT

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23
Q

Complications of stable angina?

A
  • Stroke, MI, Unstable angina
  • Sudden Cardiac death
  • Reduced QoL and anxiety
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24
Q

Prognosis of stable angina?

A
  • Indicators of prognosis – extent and severity of CAD, LV function, exercise tolerance and comorbidities
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25
Description of AF?
- Atrial activity chaotic and ineffective, rapidly firing cells cause conduction through atria but only proportion activate AV node - Irregular ventricular RR intervals and often >160bpm – atrial rhythm 300-600bpm
26
Definition of paroxysmal AF?
2 or more episodes >30 seconds but <7days and self-terminating/recur rent
27
Definition of persistent AF?
o Episodes >7 days
28
Definition of permanent AF?
o AF fails to terminate using cardioversion or > 1 year where cardioversion is not indicated
29
Definition of atrial flutter?
o Abnormal, rapid heart rhythm | o Macro-reentrant tachycardia
30
Types of atrial flutter?
 Typical – origin in right atrium at level of tricuspid valve  Atypical – Origin elsewhere in right or left atrium
31
How common is AF?
- Most common sustained arrhythmia – 10% of patients >65 years
32
Causes of AF?
- IHD - Hypertension - Valvular heart disease - Hyperthyroidism - Rheumatic heart disease - Sick sinus syndrome - Heart failure - Cardiomyopathy - Thyroxine, bronchodilators - Acute infection - PE
33
Risk Factors for AF?
- Caffeine - Alcohol intake - Obesity
34
Symptoms of AF?
``` o Asymptomatic o Chest pain o Palpitations o SOB o Syncope o Reduced exercise tolerance ```
35
Signs of AF?
o Irregularly irregular pulse o Tachycardia o 1st HS variable intensity o Signs of reduced LVF
36
Investigations to perform if suspected AF?
- Pulse – irregularly irregular - ECG o No P waves, chaotic baseline, irregularly irregular rate o Tachycardia o Atrial flutter- sawtooth baseline prominent in AVF, II, III and V1 - Bloods o FBC, Ca, Mg, glucose, TFTs, U&Es, Cardiac enzymes
37
Investigations to perform if paroxysmal AF suspected?
o 24-hour ambulatory ECG monitor/7-day Holter monitor
38
Management of acute AF (<48 hours) - investigations?
Investigations o Bloods – FBC, VBG, TFT, LFT, U&E o CXR Are there signs of haemodynamic instability? o BP<100 o Tachycardia o LoC or dizziness
39
Management of acute AF (<48 hours) - if no life-threatening signs of haemodynamic instability?
Offer rate or rhythm control if <48 hours  BB or CCB – target HR<110bpm Consider cardioversion  Electrical DC cardioversion  Pharmacological • IV amiodarone (preferred in structural heart disease) or IV flecainide Offer rate control if >48 hours
40
Management of acute AF (<48 hours) - if haemodynamically unstable?
``` o O2 o Emergency electrical DC cardioversion o Treat cause o Verapamil/Bisoprolol o LMWH ```
41
Management of chronic AF - rate control?
 Monotherapy Beta-blocker/CCB (bisoprolol/diltiazem)  Add on other drug if not controlled with monotherapy  Digoxin if needed/sedentary
42
Management of chronic AF - rhythm control?
o Refer to cardiologist for consideration of rhythm-control o Rhythm Control (if symptoms continue after HR control or not successful)  DC cardioversion • DC if <48 hours • If >48 hours, need 3 weeks anticoagulation and 4 weeks after • Amiodarone for >4 weeks before and 12 months after  Pharmacological cardioversion • Flecainide • Amiodarone (if structural heart disease)
43
Management of chronic AF - rhythm control if drug measures fail?
* Catheter ablation of left atrium or AV node or pulmonary veins * Pacing?
44
Management of chronic AF - paroxysmal specifically?
 PRN flecainide – Pill in the pocket | • If no LVHF, valvular disease, IHD, have BP >100 and HR >70
45
Management of chronic AF - anticoagulation?
o Use CHA2DS2-VASc stroke-risk score and HASBLED major-bleed score to assess risk – IN NON-VALVULAR DISEASE (valvular disease ALWAYS ANTICOAGULATE – mitral regurgitation or prosthetic valve) o Offer anticoagulation when CHADVASc score of 2 or above/1 or above in men  DOACs (Apixaban/dabigatran) or warfarin (if DOACs not tolerated)  Calculate TTR at each visit (Rosendaal method)  Review annually
46
When to review anticoagulation in AF?
o Review at aged 65 if not taking anticoagulant or when they develop diabetes, HF, PAD, CHD, CVA
47
Management of chronic AF - general advice?
o Harmful alcohol consumption o Inform DVLA o Flying OK
48
Management of chronic AF - Follow up?
o 1 week of starting rate-control treatment o After starting anticoagulation treatment  Warfarin • Calculate time in therapeutic range (TTR) and INR • Poor control need correction of compliance, medications, lifestyle factors such as diet and alcohol  Dabigatran/Apixaban • Calculate time in therapeutic range (TTR) • At least annually
49
Complications of AF?
- Stroke and thromboembolism - Heart Failure - Tachycardia-induced cardiomyopathy - Reduced QoL
50
Prognosis of AF?
- 2x more likely to die prematurely - Associated with CVD - 5x more likely for stroke
51
Description of SVT?
- Supraventricular tachycardia is narrow complex tachycardia | - Rate>100bpm, QRS<120ms
52
Pathology of SVT?
o Reentry circuit forming next to, or within, the AV node | o The circuit most often involves two tiny pathways one faster than the other
53
Types of narrow complex tachycardias?
``` o Sinus tachycardia o SVT o AF o Atrial flutter o Atrial tachycardia o Junctional tachycardia o WPW ```
54
Symptoms and signs of SVT?
- Palpitations - Chest pain - Presyncope/Syncope - Hypotension or pulmonary oedema - SOB
55
ECG findings in SVT?
o Regular rhythm o High HR o P waves absent or inverted after QRS (merged in T wave) o Normal QRS
56
Initial management of tachyarrhythmias?
o Monitor O2, give oxygen if hypoxic o Monitor ECG and BP and record 12-lead ECG o Obtain IV Access o Identify and treat any electrolyte abnormalities (K, Mg, Ca)  Bloods – U&Es, cardiac enzymes, Ca, Mg, K  VBG  ABG (if pulmonary oedema, sepsis)
57
Management of tachyarrhythmias - assessing for adverse features? What are they? Management of yes or no?
``` o Shock (sBP<90, pallor, sweating, cold, clammy, confusion) o Syncope (transient LoC) o Myocardial ischaemia (typical chest pain and/or MI on ECG) o Heart failure (pulmonary oedema and/or raised JVP) ```  If yes, Synchronised DC cardioversion – up to 3 attempts • Then Amiodarone 300mg IV over 10-20 mins and repeat shock then 900mg over 24 hours • Correct K and Mg • Further cardioversion if needed • Consider flecainide, lidocaine  If no, move down • Correct K and Mg
58
Management of tachyarrhythmias - assessing QRS complexes?
o If >0.12s – broad complex tachycardia treatment | o If <0.12s – narrow complex tachycardia – move below
59
Management of tachyarrhythmias - assessing rhythm - if irregular narrow complex?
o Irregular – Treat as AF  Rate control with B-Blockers or digoxin  If <48h – cardioversion with either amiodarone 300mg IVI over 20-60 mins then 900mg over 24h or DC shock  Anticoagulation
60
Management of tachyarrhythmias - assessing rhythm - if regular narrow complex tachycardia?
o Regular Narrow complex tachycardia  Vagal manoeuvres (carotid sinus massage, Valsalva manoeuvre)  Adenosine 6mg IV bolus • 2nd 12 mg and then 3rd 12mg if needed • CI in 2o and 3o heart block, WPW and asthmatics  Continuous ECG trace  If adenosine fails, Verapamil 5mg IV over 2-3 mins (not if on BB) • 2nd 5mg if <60
61
What happens if management of regular narrow complex tachycardia does not resolve with initial management?
 If resolves, probable re-entrant paroxysmal SVT |  If still not resolved – expert help
62
Description of VT?
``` - Broad complex tachycardias o ECG shows rate >100bpm with QRS >120ms - Ventricular tachycardia defined as >3 ventricular complexes at rate of >100 - If >30s – sustained - Can be monomorphic or polymorphic ```
63
Pathology of VT?
o The electrical signals causing this rapid beating originate in the ventricles o May lead to life threatening conditions such as ventricular fibrillation, asystole and sudden death
64
Predisposing condition to VT?
``` o Brugada syndrome o WPW o Prolonged QT (Macrolides, metoclopramide, TCA, haloperidol, methadone) o Abnormal K, low Mg, low Ca o Structural heart disease ```
65
Symptoms and signs of VT?
- Palpitations - Chest pain - Presyncope/Syncope - Hypotension or pulmonary oedema - SOB
66
What is Torsades de pointes?
o Polymorphic VT associated with low Mg, K, long QT) o QRS undulate in amplitude and may degenerate VF o Rx with magnesium sulphate
67
ECG findings in VT?
o Regular, tachycardia o Broad QRS, often bizarre o Positive QRS concordance in chest leads o Marked left axis deviation o AV dissociation or AV block o Fusion beats (normal beat fuses with VT complex) o Capture beats (normal QRS between abnormal beats
68
Initial management of tachyarrhythmias?
o ABCDE Approach o Monitor O2, give oxygen if hypoxic o Monitor ECG and BP and record 12-lead ECG o Obtain IV Access o Identify and treat any electrolyte abnormalities (K, Mg, Ca)  Bloods – U&Es, cardiac enzymes, Ca, Mg, K  VBG  ABG (if pulmonary oedema, sepsis)
69
Management of tachyarrhythmias - adverse features?
``` o Shock (sBP<90, pallor, sweating, cold, clammy, confusion) o Syncope (transient LoC) o Myocardial ischaemia (typical chest pain and/or MI on ECG) o Heart failure (pulmonary oedema and/or raised JVP) ```  If yes, Synchronised DC cardioversion – up to 3 attempts • Then Amiodarone 300mg IV over 10-20 mins and repeat shock then 900mg over 24 hours • Correct K and Mg • Further cardioversion if needed • Consider flecainide, lidocaine  If no, move down • Correct K and Mg
70
Management of tachyarrhythmias - assessing QRS complex and assessing rhythm?
- Assess QRS complex o If >0.12s – broad complex tachycardia – see below - Assess rhythm o Irregular – Seek expert help  Possible AF with BBB, pre-excited AF or polymorphic VT o Regular – move on
71
Management of regular broad complex tachycardias?
o Amiodarone 300mg IV over 20-60 mins via central line o Then Amiodarone 900mg over 24 hours o May need cardioversion
72
Description of mitral stenosis?
- Fusion, thickening and immobility of valves leaflets reduces orifice area and leads to obstruction from LA to LV - Atrial pressure elevates and leads to pulmonary hypertension and RVF - Normal mitral valve orifice area is 4-6cm2 but severe stenosis is <1cm2
73
Epidemiology of mitral stenosis?
- 50% had rheumatic fever and 90% had rheumatic heart disease - Women > Men - Usually in 4th and 5th decades
74
Causes of mitral stenosis?
``` o Rheumatic heart disease following rheumatic fever  Group A beta-haemolytic streptococci  RF: overcrowding, poor hygiene  Symptoms: sore throat (3 weeks prior), arthritis, carditis, chorea, subcutaneous nodules, fever, ESR/CRP raised  Ix: antibody titres, throat swab, ECG  Rx: Penicillin, aspirin o Congenital o Carcinoid tumours ```
75
Symptoms of mitral stenosis?
``` o Exertional dyspnoea (worsening) o Orthopnoea o Productive blood-tinged cough o Palpitations (AF) o Chest pain o Fatigue ```
76
Signs of mitral stenosis?
``` o Malar flush o Low volume pulse o AF o Tapping apex beat o Loud S1 o Rumbling mid-diastolic murmur (worse on expiration, left side) ```
77
Investigations of mitral stenosis?
- ECG o Progressive RAD, AF, LA hypertrophy (bifid P wave), RVH - CXR o Left atrial enlargement, pulmonary oedema, calcifications - Transthoracic Echo o Diagnostic – hockey stick-shaped mitral deformity o Used to measure mitral orifice area and assess pulmonary artery pressure - Cardiac Catheterisation o If surgical correction planned, severe
78
Management of mitral stenosis - if asymptomatic?
o No treatment
79
Management of mitral stenosis - if symptomatic?
o Diuretics (furosemide 40mg) o Surgery  Percutaneous balloon valvotomy  Mitral valve repair/replacement - Follow Up o Annual
80
Complications of mitral stenosis?
``` o AF o Pulmonary hypertension o Emboli o Hoarseness o Dysphagia o Infective endocarditis (rare) ```
81
Description of mitral regurgitation?
- Mitral valve consists of anterior and posterior leaflets, chordae tendineae, anterolateral and posteromedial papillary muscles and mitral annulus - Mitral valve regurgitation may result from defects in any part of valve
82
Pathology of mitral regurgitation?
o Longstanding regurgitation produces increase in atrial pressure and dilatation o Increase can cause pulmonary hypertension and oedema – LV dilatation
83
How common is mitral regurgitation?
- 2nd most prevalent valve disease after aortic stenosis
84
Aetiology of mitral regurgitation?
``` o Functional (LV dilatation) o Annular calcification o Rheumatic heart disease o Mitral valve prolapse o Infective Endocarditis o Ruptured chordae tendineae o Papillary muscle rupture o Hypertrophic Cardiomyopathy o Ehlers Danlos Syndrome ```
85
Symptoms of mitral regurgitation?
``` o SOB (exertional) o Fatigue o Lethargy o Palpitations o Oedema ```
86
Signs of mitral regurgitation?
``` o Heart failure o Apex beat laterally displaced o RV heave o Soft S1 o S3 in early diastole o Pansysytolic murmur  Loudest at apex, radiates axilla ```
87
Investigations of mitral regurgitation?
- ECG o AF, P-mitrale, LVH - CXR o Dilated LA/LV, calcification, pulmonary oedema - Transthoracic or oesophageal Echo o Assess severity and function - Doppler o Assess severity of regurgitation, LV dimensions and size and function of RV - Catheterisation o Exclude other valve disease, assess CAD
88
Management of severe, acute mitral regurgitation?
``` o Annuloplasty or mechanical valve o Diuretics (furosemide) ```
89
Management of chronic mitral regurgitation - asymptomatic?
 If LVEF >60% • ACE inhibitors (captopril/enalapril/lisinopril) • Beta-blockers (metaprolol/atenolol)  If LVEF <60% • Valvuloplasty/annuloplasty/mechanical/prosthetic valve replacement
90
Management of chronic mitral regurgitation - symptomatic?
 LVEF >30% • Valvuloplasty/ annuloplasty/ mechanical/ prosthetic valve replacement • ACE inhibitor (captopril/enalapril/lisinopril) • Beta-blocker (metaprolol/atenolol) • Diuretic (furosemide)  LVEF <30% • ACE inhibitor (captopril/enalapril/lisinopril) • Beta-blocker (metaprolol/atenolol) • Diuretic (furosemide) • Intra-aortic balloon counterpulsation (reduces afterload)
91
Follow up of chronic mitral regurgitation?
o Regular follow up and echocardiogram
92
Complications of chronic mitral regurgitation?
``` o Prosthesis stenosis o AF o Pulmonary Hypertension o Post-operative stroke o Heart Failure ```
93
Prognosis of chronic mitral regurgitation?
o Progression variable | o May remain asymptomatic for many years
94
Description of aortic stenosis?
- Degeneration and calcification of aortic valve o Endocardium of valve damaged and inflamed, leading to deposition of calcium on valve – limits aortic leaflet mobility and stenosis o Occurs slowly and pressure overload leads to LVH (increased afterload) o Increased myocardial oxygen demand, relative ischaemia
95
Epidemiology of aortic stenosis?
- Most common valvular disease - 2nd most common cause for cardiac surgery - Incidence highest in over 70s - Bicuspid valve and William’s syndrome present earlier
96
Risk factors of aortic stenosis?
o Advanced age o Congenital bicuspid valve o Rheumatic fever o CKD
97
Aetiology of aortic stenosis?
o Senile degeneration o Congenital (bicuspid valve, Turner’s syndrome, William’s syndrome) o Rheumatic heart disease
98
Symptoms of aortic stenosis?
- Usually asymptomatic until <1/3 normal size ``` - Symptoms o Exertional SOB o Angina o Exertional syncope o Dizziness ```
99
Signs of aortic stenosis?
``` o Congestive heart failure o Slow rising pulse o Narrow pulse pressure o Heaving, non-displaced apex o LV heave, aortic thrill o Ejection systolic murmur  Heard best at right sternal edge, radiates to carotid o Ejection click (or S4) ```
100
Investigations and their findings in aortic stenosis?
- ECG o P-mitrale o LVH with strain pattern (T-wave inversion, ST depression) o LBBB or complete block - Transthoracic Echo & doppler o Diagnostic – elevated aortic pressure gradient, measures valve area and LVEF - CXR o LVH, calcified aortic valve, post-stenotic dilatation of ascending aorta - Cardiac Catheterisation o Used if echo inconclusive o Assess function and CAD but risks emboli
101
Management of aortic stenosis - asymptomatic?
follow up and echo
102
Management of aortic stenosis - symptomatic?
o Surgery  Aortic valve replacement  TAVI o Anticoagulation  Vitamin K antagonist (warfarin) • If prosthetic mechanical valve
103
Management of aortic stenosis - general management?
o Good oral hygiene
104
Complications of aortic stenosis?
o Congestive heart failure o Infective endocarditis o Systemic emboli
105
Definition of aortic regurgitation?
- Diastolic leakage of blood from aorta into left ventricle - Due to inadequate coaptation of valve leaflets - Leads to LV hypertrophy and dilatation - Stroke volume increases and pulse pressure rises
106
Acute risk factors of aortic regurgitation?
 Infective Endocarditis  Ascending aortic dissection  Chest trauma
107
Chronic risk factors of aortic regurgitation?
```  Congenital – bicuspid aortic valve  Connective tissue disorders (Marfans, Ehlers-Danlos)  Rheumatic fever  Takayasu arteritis  RA  SLE  Hypertension  Syphilis ```
108
Symptoms of aortic regurgitation?
``` o Exertional SOB, orthopnoea, PND o Palpitations (pounding) o Angina o Syncope o Congestive heart failure ```
109
Signs of aortic regurgitation?
o Collapsing (Waterhammer pulse) o Wide pulse pressure o Displaced laterally-thrusting apex beat o High-pitched early diastolic murmur  Heard best in aortic area on expiration, with patient sitting forwards
110
Investigations of aortic regurgitation?
``` Investigations - ECG o LVH (strain pattern - T-wave inversion, ST depression) ``` - Echocardiogram & Doppler o Diagnostic - CXR o Cardiomegaly, dilatation of ascending aorta, pulmonary oedema - Cardiac Catheterisation
111
Management of aortic regurgitation - asymptomatic?
Asymptomatic patients (LVEF>50%): o Regular 6-12 month follow up and echo o ACE inhibitors – if hypertensive
112
Management of aortic regurgitation - symptomatic?
- Symptomatic patients, enlarging heart, ECG changes, LVEF <50%: o Aortic valve replacement o TAVI
113
Management of acute, severe aortic regurgitation?
o Inotropes and vasopressors | o Urgent aortic valve replacement
114
Definition of infective endocarditis?
- Infection of endocardium of heart valve - Mass of fibrin, platelets and infectious organisms form vegetations along edges of valves - Virulent organisms destroy valve and produce regurgitation
115
Risk factors of infective endocarditis?
``` Cardiac disease  Valvular heart disease (stenosis or regurgitation)  Hypertrophic cardiomyopathy  Previous IE  Structural congenital heart disease  Valve replacement Dermatitis IVDU Renal failure Organ transplant DM ```
116
Organisms of infective endocarditis?
o Staph Aureus (indwelling catheters, IVDU, DM, cellulitis) o Streptococcal viridans (oral disease/procedures) o Enterococci (GU disease, hospitalisation) o Streptococcal bovis (bowel malignancy) o HACEK organisms  Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella corrodens, Kingella kingae o Culture negative (prior Abx, Coxiella, chlamydia, legionella) o SLE o Malignancy
117
Most common valves of infective endocarditis?
o Mitral valve o Aortic valve o Combined aortic and mitral o Tricuspid valve
118
Symptoms of infective endocarditis?
o Fever + new murmur (endocarditis until proven otherwise) | o Fatigue, flu-like illness, arthralgia, weight loss
119
Signs of infective endocarditis - systemic?
 Fever, Rigors, night sweats, malaise, weight loss, anaemia, splenomegaly, clubbing
120
Signs of infective endocarditis - cardiac?
 New murmur  Regurgitation  Aortic root vegetation may prolong PR interval – heart block
121
Signs of infective endocarditis - immune complex?
 Vasculitis  Microscopic haematuria  Acute glomerulonephritis
122
Signs of infective endocarditis - FROMJASE?
 Fever  Roth spots (boat-shaped retinal haemorrhage with pale centre)  Oslers nodes (painful pulp infarcts in fingers and toes)  Murmur  Janeway Lesions (painless, red haemorrhagic spots on palms/soles)  Anaemia  Splinter Haemorrhages  Emboli
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Investigations performed in infective endocarditis?
Blood Cultures o Before antibiotics, 3 sets over 24 hours from different peripheral sites ``` Bloods o FBC (normochromic normocytic anaemia, neutrophilia), CRP (raised), ESR (raised), LFT, U&Es ``` Urinalysis o Microscopic haematuria CXR ECG Echocardiogram <24 hours (TTE then TOE) Cardiac CT scan can be used
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Diagnostic criteria of infective endocarditis?
o Duke Criteria for IE
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What are major diagnostic criteria in infective endocarditis?
* Positive blood culture (typical organism in 2 separate cultures or persistently positive in 3) * Endocardium involved (positive echo or new valvular regurgitation)
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What are minor diagnostic criteria in infective endocarditis?
* Predisposition (heart problems, IVDU) * Fever >38 * Vascular signs (arterial emboli, septic pulmonary infarcts, infectious aneurysms, intracranial haemorrhage, conjunctival haemorrhage, Janeway lesions) * Immunological phenomenon (glomerulonephritis, Oslers nodes, Roths spots, RF) * Positive blood culture or positive echo that does not meet criteria
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Criteria for diagnosis of infective endocarditis?
2 major or 1 major and 3 minor or all 5 minor
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Management of infective endocarditis - empirical?
o 4-6-week IV course of antibiotics  Native – Amoxicillin +/- gentamicin • Pen allergic: use vancomycin +/- gentamicin  Prosthetic – Vancomycin + Gentamicin + Rifampicin
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Specific management of infective endocarditis - staphylococcus? Native and prosthetic?
 Native – Flucloxacillin (4 weeks, at least 6 weeks if secondary lung abscess or osteomyelitis) • If pen allergic or MRSA – vancomycin + rifampicin  Prosthetic – Flucloxacillin + rifampicin + gentamicin (6 weeks, review need for gentamicin at 2 weeks) • If pen allergic – vancomycin + rifampicin + gentamicin
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Specific management of infective endocarditis - streptococcus?
 Benzylpenicillin +/- gentamicin (4-6 weeks, 6 weeks prosthetic valve) • If pen allergic – vancomycin + gentamicin
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Specific management of infective endocarditis - enterococci?
 Amoxicillin + gentamicin (4-6 weeks, 6 weeks for prosthetic valve, after 2 weeks review need for gentamicin) • If pen allergic – vancomycin + gentamicin • If gentamicin resistant – Amoxicillin + streptomycin
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Specific management of infective endocarditis - HACEK microorganisms?
 Amoxicillin + gentamicin (4 weeks, 6 weeks for prosthetic valve, stop gentamicin after 2 weeks) • If amoxicillin resistant – ceftriaxone + gentamicin
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Surgical management of infective endocarditis? When is it indicated?
o Total removal of infected tissues and reconstruction of cardiac morphology or valve replacement Indications: o severe valvular incompetence o aortic abscess (often indicated by a lengthening PR interval) o infections resistant to antibiotics/fungal infections o cardiac failure refractory to standard medical treatment o recurrent emboli after antibiotic therapy
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Complications of infective endocarditis?
``` o MI, pericarditis, arrhythmias o CHF o Valvular insufficiency o Aortic root or myocardial abscesses o Emboli o Glomerulonephritis ```
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Prognosis of infective endocarditis?
o 1-year mortality at 30%
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Definition of PE?
- DVT embolised into pulmonary circulation
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Pathology of PE?
o Embolism obstructs outflow tract and causes acute right sided failure o Lung tissue ventilated but not perfused so no gas exchange
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Risk factors of PE?
``` o Surgery (pelvic/abdominal) o Thrombophilia o Leg fracture o Bed rest/Reduced mobility o Malignancy o Pregnancy o OCP/HRT ```
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Causes of PE?
``` o Embolism of DVT o RV thrombosis (post-MI) o Right endocarditis o Fat, air or amniotic fluid o Neoplastic cells ```
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Symptoms of PE?
``` o Acute dyspnoea o Pleuritic chest pain o Cough and Haemoptysis o Syncope o Symptoms of DVT ```
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Signs of PE?
``` o Tachycardia o Tachypnoea o Hypotension o Pyrexia with lung infarction o Pleural rub o Cyanosis o Gallop rhythm o Increased JVP o RV heave ```
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Assessment of patient with suspected PE? What is PE rule out criteria?
``` o ECG o CXR o Pulmonary Embolism Rule-Out Criteria  Rule out PE if none of 8 criteria are present with low Wells Score (<2) • age < 50 years • pulse < 100 beats min • SaO2 ≥ 95% • No haemoptysis • No oestrogen use • No surgery/trauma requiring hospitalization within 4 weeks • No prior VTE • No unilateral leg swelling ```
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Initial management of PE?
o Full history and examination of respiratory and CV systems o Examine legs for signs of DVT o CXR  Often normal – wedge shaped area of infarction, decreased vascular markings, small pleural effusion  Excludes pneumonia and pneumothorax o PE Wells Score
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What is the PE Well's score?
Clinical signs and symptoms of DVT (minimum of leg swelling and pain with palpation of the deep veins) 3 An alternative diagnosis is less likely than PE 3 Heart rate > 100 beats per minute 1.5 Immobilisation for more than 3 days or surgery in the previous 4 weeks 1.5 Previous DVT/PE 1.5 Haemoptysis 1 Malignancy (on treatment, treated in the last 6 months, or palliative) 1
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Interpretation of PE Well's Score?
 Score of more than 4 – PE likely |  Score of 4 or less – PE unlikely
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Management of PE Well's score more than 4? When is PE diagnosed?
• Immediate CTPA o If CTPA cannot be carried out immediately – interim LMWH anticoagulation and hospital admission o IF CTPA negative and DVT suspected – proximal leg US o V/Q Scan  If allergy to contrast or renal impairment (eGFR<30) or pregnant or woman <40 * Diagnosed PE with positive CTPA or V/Q scan * Consider alternative diagnosis if negative CTPA and no suspected DVT
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Management of PE Well's score 4 or less? When is PE excluded?
• D-Dimer o If positive, then CTPA  If CTPA cannot be carried out immediately – interim LMWH anticoagulation and hospital admission  V/Q Scan • If allergy to contrast or renal impairment (eGFR<30) or pregnant or woman <40 o If negative D-dimer or positive D-dimer and negative CTPA, then excluded
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What other tests are performed upon initial assessment of someone suspected of PE?
 Bloods • FBC, U&Es, baseline clotting, D-Dimer (if Wells of <4 to exclude PE)  ABG (if hypoxic, SOB) • Low PaO2, Low PaCO2, pH often raised  ECG (if tachycardic or chest pain) • Commonly normal – can have sinus tachycardia, RBBB, RV strain pattern (S1Q3T3), RAD, AF • S1Q3T3 – in up to 50% (sign of Cor Pumonale)
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when to perform diagnostic imaging in PE?
CTPA  First-line  When Wells >4 or, elevated D-Dimer V/Q Scanning  Used in pregnancy or young people (women<40)  Usually need CTPA afterwards to confirm
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Management of PE - initial management?
o If hypoxic – 15L/min Oxygen o Analgesia (Morphine) + Antiemetic – if in pain or very distressed o If massive PE/haemodynamically unstable (BP <90mmHg, hypoxic, tachycardia, tachypnoea):  Urgent ICU help  Rapid colloid infusion  If BP still <90mmHg – consider dobutamine then IV noradrenaline infusion  Alteplase 100mg over 2 hour or 0.6mg/kg over 15 mins
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Management of PE - pharmacological interventions?
 LMWH (175U/kg Tinzaparin SC/24h) as soon as possible for at least 5 days or until INR >2 for at least 24 hours, whichever is longer • For severe renal impairment (eGFR <30) – Unfractionated heparin (UFH) • If PE and haemodynamically unstable – offer UFH and thrombolytic therapy  Warfarin offered within 24 hours of diagnosis and continue for 3 months with unprovoked PE • Alternatives: NOACs (Apixaban, dabigatran, rivaroxaban)  If cannot have anticoagulation therapy: • Temporary inferior vena cava filter  If recurrent DVT: • Inferior vena cava filter after alternatives (raise INR 3-4, switching to LMWH)
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Follow up advice for diagnosed PE?
 Follow-up appointment to anticoagulation services and medical outpatient  Advise to return immediately if become breathless or chest pain
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Management of PE - thrombolytic therapy?
* Consider systemic thrombolytic therapy for patient with haemodynamic instability * Alteplase 100mg over 2 hour or 0.6mg/kg over 15 mins
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Investigations to perform following management of patient with PE? When to perform thrombophilia testing?
 Cancer investigations for unprovoked DVT: • Examination • CXR • Bloods (FBC, serum Ca, LFTs) • Urinalysis • Consider abdomino-pelvic CT scan if >40 with 1st unprovoked DVT  Thrombophilia testing • Antiphospholipid antibodies in patients with unprovoked DVT if it is planned to stop anticoagulation therapy • Hereditary thrombophilia testing – unprovoked DVT with 1st degree relative with DVT/PE if planned to stop anticoagulation
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Definition of varicose veins?
- Dilated, tortuous, superficial veins | - Most commonly found in legs, visible and palpable
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Causes of varicose veins?
o Indication of superficial lower extremity venous insufficiency  Incompetent valves in vein lead to reflux of blood and increased pressure in vein distally  Weakness or degeneration of vein wall may contribute o Unknown, congenital
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Risk factors of varicose veins?
``` o Increasing age o FHx of varicose veins o Females o Pregnancy o Obesity o Prolonged standing/sitting o Hx of DVT ```
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Symptoms of varicose veins?
o Dilated veins on leg o Pain, itching, swelling  Especially after prolonged standing o Restless legs and leg cramps
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Signs of varicose veins?
o Irregular bulges consistent with varicose veins o Telangiectasias o Skin changes – hyperpigmented, venous eczema, lipodermatosclerosis o Ulcers or thrombophlebitis
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Examination of varicose veins?
o Inspect patient standing o Feel for cough impulse at saphenofemoral junction o Trendelenberg test – assess SFJ incompetence – patient lying down, elevate leg and empty vein by massaging distal to proximal – occlude superficial veins using tourniquet – patient stands  If veins do not re-fill – incompetent valve above this level  If veins re-fill – incompetent valve lower down  Test then above knee, below knee
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Management of varicose veins - bleeding varicose veins?
o First aid and admit to vascular service
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Management of varicose veins - non-bleeding varicose veins - general advice?
```  Reassure complications uncommon  Lose weight  Light-to-moderate physical activity  Avoid standing for too long  Elevate legs where possible ```
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Management of varicose veins - non-bleeding varicose veins - when to refer to vascular surgeons?
 Symptomatic varicose veins  Skin changes (pigmentation or eczema)  Superficial vein thrombosis (hard painful veins)  Leg ulcer – active or healed
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Management of varicose veins - non-bleeding varicose veins - secondary care investigations?
• Duplex US
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Management of varicose veins - non-bleeding varicose veins - secondary care treatment?
* Endothermal ablation – seal affected veins * US-guided Foam Sclerotherapy – injection of irritant foam, inflammation closes vein * Surgery – Ligation and stripping of affected vein
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Management of varicose veins - non-bleeding varicose veins - primary care treatment?
 Compression stockings following Doppler • If compression stockings considered: o Doppler to assess ABPI to exclude arterial insufficiency  <0.5 – severe PAD and stocking contraindicated  0.8-0.5 – avoid stockings – refer  0.8-1.3 – safe to wear  >1.3 – refer as incompressible arteries
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Management of varicose veins - non-bleeding varicose veins - safety net?
 Seek medical advice if hard and painful, skin changes, venous ulcer, bleeding
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Complications of varicose veins?
``` o Bleeding (after trauma) o Thrombophlebitis (hard, painful veins) o DVT o Skin changes (pigmentation caused by hemosiderin, venous eczema, lipodermatosclerosis) o Skin Ulceration o Decreased QoL ```
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Definition of peripheral artery disease?
- Peripheral artery disease describes narrowing or occlusion of peripheral arteries, affecting blood supply to lower limbs - Chronic limb ischaemia can present as: o Intermittent claudication (most common) o Critical limb ischaemia/Rest Pain
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Causes of peripheral artery disease?
o Atherosclerosis o Vasculitis o Embolism o Buerger’s disease
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Risk factors of peripheral artery disease?
``` o Smoking o DM o Age o Hypertension o Hypercholesterolaemia o Atherosclerosis elsewhere (coronary, carotid) ```
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When to suspect peripheral artery disease?
o Progressive cramping pain in calf, thigh or buttock on walking which is relieved by rest o Non-healing wounds
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What is the Fontaine Classification of peripheral artery disease?
o Asymptomatic  ABPI <0.9 ``` o Intermittent Claudication  Felt in calfs, thighs, buttocks  Tightness/cramping pain developing after certain distance  Worse on uphill  Pain disappears when resting ``` ``` o Ischaemic Rest Pain  Woken up by pain  Occurs due to gravitational effect lost when lying flat  Relief by swinging legs over bed  Dependent oedema ``` o Ulceration/Gangrene
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Signs of peripheral artery disease?
``` o Absent pulses o Cold, hairless, dry, white legs o Atrophic skin o Punched out ulcers (painful) o CRT prolonged o Buerger’s angle <20o ```
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Assessment of peripheral artery disease?
o Examine ulcers, temperatures, skin changes, pulses, CRT o ABPI  <0.9 means peripheral artery disease  <0.5 critical limb ischaemia  >1.2 means vessels not compressible – calcifications - DM likely
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Management of intermittent claudication - primary care?
 Smoking cessation  Diet and weight modification  Clopidogrel 75mg OD (aspirin 75mg OD if clopidogrel CI or not tolerated)  Supervised exercise programme – 3 months twice a week  Refer for vascular surgery  If not for surgery – Praxaline (naftidrofuryl oxalate)
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Management of intermittent claudication - secondary care?
 Supervised exercise programme – 3 months, 2hours, twice a week  Duplex US if revascularisation considered • +/- contrast-enhanced MR angiography  Angioplasty and stenting  Bypass Surgery and grafts
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Management of critical limb ischaemia - primary care?
 Refer to vascular MDT  PRN paracetamol + weak/strong opioids (+/- antiemetic) • Refer to pain management services if pain not controlled and revascularisation inappropriate  Manage cardiovascular risk • Smoking cessation • Diet and weight modification • Clopidogrel 75mg OD (aspirin 75mg OD if clopidogrel CI or not tolerated)
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Management of critical limb ischaemia - secondary care?
 Duplex US if revascularisation considered • +/- contrast-enhanced MR angiography (CT if CI)  Angioplasty and stenting  Bypass Surgery and grafts  Amputation if ALL options have been considered by MDT
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Prognosis of peripheral artery disease?
o Amputation required in 1-2% of intermittent claudication patients o Critical limb ischaemia risk of amputation and premature death o 3x more likely to die from CVD
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Complications of peripheral artery disease?
o Impaired QoL o Ulceration and gangrene o Amputation o CVD, CVA
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Definition of AAA?
- Artery with dilatation >50% of its original diameter o True aneurysms – abnormal dilatations that involve all layers of arterial walls o False aneurysm – Collection of blood in outer layer only (adventitia) - May be fusiform (most AAA) or sac-like (Berry aneurysms)
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Definition of unruptured AAA?
- Unruptured AAA definition >3cm o 3% of those >50 years o Males 3:1 Females o Majority infrarenal
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Definition of ruptured AAA?
o Majority found infrarenal and haemorrhage into retroperitoneum o Mortality 41% and untreated 100%
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Risk factors of AAA?
``` o Hypertension o Smoker o Male o Increasing age o COPD o Hyperlipidaemia o Family history ```
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Causes of AAA?
o Degeneration of elastic lamellae and smooth muscle loss
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Symptoms and signs of unruptured AAA?
- Unruptured often have no symptoms – incidental finding o Pulsatile mass in abdomen o May have pain in back, abdomen or groin - Unruptured Signs o Expansile abdominal mass o Abdominal bruit
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Symptoms and signs of ruptured AAA?
``` - Ruptured Symptoms o Classical central abdominal and lower back pain in patient with known aneurysm o Sudden onset and severe pain o PEA cardiac arrest o Sudden painless collapse ``` ``` - Ruptured Signs o Pale, sweating, tachycardia, hypotensive o Mottled skin of lower body o Tender pulsatile abdominal mass o Pulses in femoral region may be absent ```
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Investigations in AAA?
- Low clinical suspicion - USS - CT Scan o Used if evaluated for surgery
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Screening in AAA?
o All men aged 65 years screened USS of abdomen
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When to refer unruptured AAA to vascular surgeons?
 AAA 5.5cm or larger to vascular surgeon within 2 weeks |  AAA 3-5.4cm to vascular surgeon within 12 weeks
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General management of unruptured AAA?
 Stop smoking service |  Treat hypertension
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Surveillance of unruptured AAA?
 Asymptomatic AAA • Every 3 months if AAA 4.5-5.4cm • Every 2 years if AAA 3.0-4.4cm
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Surgical management of unruptured AAA - when and what?
 When? • Aneurysms >5.5cm, larger than 4cm and expanding at >1cm/year or symptomatic  What? • Open Repair • Stenting (EVAR)
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Management of ruptured AAA?
o Get vascular surgeon and anaesthetist, warn theatre o High flow Oxygen o 2 large bore cannulas, Bloods (FBC, LFTs, U&Es, amylase, glucose, coagulation screen, Crossmatching (Emergency – 10U Red cells, 8U platelets, 8U FFP) o IV morphine & 50mg Cyclizine o IV Fluids (aim BP >90mmHg but <100mmHg due to risk of rupture) o Portable USS, CXR, Urinary catheter and radial artery line, ECG o Prophylactic Abx – Cefuroxime + Metronidazole IV o Vascular surgeon - Aortic cross clamping  Endovascular repair or open surgery
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Prognosis of AAA?
- No more than 1 in 3 patients with ruptured AAA will reach hospital alive and 20% of those who do, fail to reach theatre