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vessels Flashcards

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1
Q

Define abdominal aortic aneurysm? (AAA)

A

Permanent aortic dilation exceeding 50% where diameter >3cm Typically infrarenal (below renal arteries), in elderly men

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2
Q

Prevalence of AAA?

A

1.3 to 12.7% in the uk, most commonly affecting elderly men Often inherited

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3
Q

A negative risk factor for AAA?

A

Diabetes but unknown reason

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4
Q

Risk factors for AAAs?

A

Smoking = biggest risk factor Increasing age Make Hypertension Connective tissue disorders - Ehlers Danos and Marfan syndrome (changes in balance of collagen and elastic fibres) Family history

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5
Q

Pathophysiology for AAA?

A

Smooth muscle, elastic + structural degredation in all 3 layers of vasuclar tunic (intima, media, adventitia) All 3 layers = true aneurysm Not all 3 = pseudoaneurysm (usually due to trauma ) Dilation in AAA typically 3cm+ A dilation that is 5.5cm+ has an increased rupture risk Rupture = surgical emergency

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6
Q

Inflammatory AAA?

A

Type that usually affects younger patients and is associated with smoking, atherosclerosis and vasculitis 5-10% of AAAs Same symptoms + pyrexia (fever)

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7
Q

Symptoms of AAA?

A

Mostly asymptomatic and discovered incidentally Symptoms generally when ruptured/impending rupture -sudden epigastric pain radiating to flank -pulsatile abdominal mass - tachycardia and hypertension

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8
Q

Surface potential signs of AAA?

A

Grey-Turner’s sign = flank bruising secondary to retroperitneal haemorrhage (also potentially haemorrhagic pancreatitis) Cullen’a sign = pre-umbilical bruising more associated with acute pancreatitis and ectopic pregnancy but also linked with AAA

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9
Q

Primary diagnosis tool for AAA?

A

Abdominal ultrasound -fast, cheap, reliable -highly sensitive and specific (Axial plane at level of the navel)

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10
Q

Treatment for an asymptomatic aneurysm <5.5cm?

A

Surveillance + offer advice to manage risk factors (decrease smoking, BMI, BP and satins)

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11
Q

Treatment for asymptomatic AAA and >= 5.5cm or >4.0cm and expanded more than 1cm per year?

A

Elective surgery Either: 1) EVAR (Endovascular aortic repair) - stent inserted through femoral/iliac artery -Less invasive but more post op complications 2) open surgery (favoured by nice unless sig comorbidities) -more invasive but fewer complications Survival for both=equivalent (EVAR)

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12
Q

Treatment for symptomatic AAA?

A

Urgent surgical repair (EVAR or open surgery)

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13
Q

Treatment for a ruptured AAA?

A

Stabilise ABCDE, fluids then urgent surgical repair -Nice says EVAR preferred in all women, and men over 70 otherwise open surgery preferred -Do not offer complex EVAR (eg BEVAR) if open surgery is suitable 20% of AAAs rupture anteriorly into peritoneal cavity= poor prognosis 80% rupture posteriorly = better prognosis 100% mortality for ruptured AAA if not treated immediately

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14
Q

Cause and treatment for rare AAA in thoracic aorta?

A
  • main cause = marfans/ehlers danos +atherogenesis - treatment = monitor with CT/MRI or if symptomatic‚Äî> surgery immediately
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15
Q

Pathophysiology of aortic dissection?

A

Surgical emergency!! Tear in intima resulting in blood dissecting through media and separating layers apart -due to mechanical wall stress Creates a false lumen (can propagate forwards and backwards) Abnormal flow can occlude flow through branches of aorta Decreased perfusion to end organs = shock/failure

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16
Q

Risk factors for aortic dissection(AD)

A

Hypertension = most key Connective tissue disorders (ED,Marafan) Family history of AAA/AD Truma Smoking

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17
Q

Most common location for aortic dissection

A

Sinotubular junction = where aortic root becomes tubular aorta, near aortic valve (Stanford A)

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18
Q

Stanford classification for aortic dissection

A

A = proximal to left subclavian artery (ascending + arch) (2/3=most common) B = distal to left subclavian artery (descending thoracic) (1/3=less common)

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19
Q

Debakey classification of aortic dissection

A

Type I = originates in ascending aorta and involves at least the aortic arch, but can extend distally Type II = originates and confined to the ascending aorta Type III = originates in the descending aorta and extends distally, but can extend proximally

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20
Q

Signs and symptoms of aortic dissection

A

Symptoms: -Sudden onset ripping/tearing chest pain that may radiate to the back -Syncope (fainting) red flag Signs: -Radio-radial and/or radio-femoral delay -Diastolic murmer due to aortic regurgitation -diff in blood pressure between two arms >10mmHg -hypertension -tachycardia and hypotension (commonly type A)

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21
Q

Differential diagnosis for AAA?

A

Acute pancreatitis Typically non pulsatile + more associated with grey-turner/Cullen signs

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22
Q

Investigations for diagnosing aortic dissection?

A

ECG Chest X-ray -may show widened mediastinum >8cm is suspicious (1= widened mediastinum and 2= enlarged aortic knuckle) Contrast-enhanced CT angiogram (gold standard) -v specific and sensitive and used if patient is hemodynamically stable -shows intima flap, false lumen, dilation of aorta and rupture (Type a aortic dissection)

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23
Q

Investigation in an unstable patient?

A

Transthoracic (TTE) or transoesphageal (TOE) echo TOE is more invasive but more specific for AD and v sensitive -shows intima flap and false lumen -Allows classification of AD as type A or B

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24
Q

Treatment for type A aortic dissection

A
  • Blood transfusion - IV labetol (aim for systolic bp 100-120) - Urgent open surgical repair to replace ascending aorta
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25
Treatment for type B aortic dissection
- conservative management: analgesia and bed rest - IV lavetol (aim for 100-120 systolic bp) - thoracic endovascular aortic repair (TEVAR) may be performed to reduce risk of further dissection yet not standard practice
26
Complications of aortic dissections?
-cardio tampenade -aortic insufficiency (regurgitation) -pre renal AKI -stroke (ischemic)
27
Mortality rate for untreated aortic dissection?
Will result in a false channel rupture and fatal haemorrhage in 50-60% if patients within 24hrs Estimated 20% of patients die before reaching hospital and 30% die before reaching theatre 5 yr survival rate after surgery is 80%
28
Pathophysiology of types of deep vain thrombosis (DVT)?
Formation of thrombus in a deep leg vein -around\below calf = minor veins (eg. Anterior and posterior tibial) => less concerning and more common -above calf (in thigh) = major veins (eg. Superficial femoral) occlusion may impede distal flow => life threatening and less common
29
Risk factors for DVT?
Dependant on Virchow’s triad: 1. Hypercoagulability 2. Venous stasis 3. Endothelial damage (abnormality in any component can result in thrombus)
30
Hypercoagulabilty and causes? (Virchow’s triad)
= increased platelet adhesion and clotting tendency Hereditary: - Factor V Leiden - protein C and S deficiency - antiphospholipid syndrome Acquired: - malignancy - chemotherapy - COCP/HRT - Pregnancy - Obesity
31
Venous stasis and cause? (Virchow’s triad)
=blood flow is normally laminar to spread out platelets and clotting factors without activation Stasis —> aggregation of clotting factors = thrombus formation Cause = immobility (long flights, after surgery)
32
Endothelial damage and causes? (virchow’s triad)
=endothelial cells normally prevent thrombosis by secreting anticoagulants, as well as blocking exposure to pro-thrombotic collagen - damaged endothelial cells cannot!! Causes: — endothelial dysfunction: - smoking — endothelial damage:
33
Symptom and signs of DVT?
Symptom: Unliateral calf pain, redness and swelling Signs: -unliateral swelling -oedema -tender and erythematous -distension of superficial veins Right leg = swollen and erythematous
34
What is phlegmasia cerulea dolens?
Occurs in a massive DVT, resulting in obstruction of venous and arterial outflow (rare). => ischemia and a blue, painful leg
35
What is a Wells score?
Calculates the risk of DVT and determines investigations + management >= 2 DVT likely =< 1 DVT unlikely (Don’t learn all but know a few)
36
Gold standard for diagnosis of DVT
Duplex ultrasound of leg (Duplex USS) -if unavailable, alternative is D-dimer
37
Positive d-dimer and negative duplex USS? (In patient with suspect DVT)
-stop interim anticoagulation -offer repeat ultrasound 6 to 8 days later +ve= restart anticoagulation -ve= alternative diagnosis
38
Treatment for DVT?
Offer DOACs: apixaban or rivaroxaban If there’s a CI eg patient is renally impaired offer one of: -LMWH -Unfractionated heparin Treatment for at least 3 months or 3 to 6 months if they’re a cancer patient +mobilisation and compression stockings
39
Complications of DVT
Pulmonary embolism Post thrombotic syndrome Increased risk of bleeding (as on anticoagulants)
40
Risk of recurrence with DVT?
30% in the next five years
41
Differential diagnosis to DVT?
Cellulitis Skin infection-typically staph aureus + strep pyogenes -tender, inflamed swollen calf with pronounced demarcation *will show leukocytosis on FBC while DVT will have normal levels*
42
Pathophysiology of pulmonary embolism (PE)
Most commonly DVT embolises and lodges in oil on art after circulation (Could be any embolus) Can cause strain on right ventricle due to increased pulmonary vascular resistance
43
Risk factors for PE?
Virchow’s triad (Mentioned in detail in DVT)
44
Symptoms of PE
Pleuritic chest pain (present in only 10% of patients) Dyspnoea Cough or haemoptysis Fever Syncope üö©
45
Signs of PE?
Tachypnoea and tachycardia Hypoxia DVT (swollen tender calf) Pyrexia Hypotension (SBP <90 mmHg suggests massive PE) Elevated JVP (suggest cod Pulmonale)
46
Wells two level score?
Used to determine probability of PE >4: high probability =<4: low probability (Don’t learn all just a few examples)
47
Process for investigating PE?
D-dimer is NOT diagnostic but CTPA is -CXR should be normal -ECG: Often find sinus tachycardia S1Q3T3 (classic finding but only in 20% px) RBBB and right axis deviation suggest right heart strain
48
Why is D-dimer not diagnostic?
Measure of clot burden; a small protein relaxers into blood when blood clot fibronlysed Is sensitive (rules PE in) Not specific (doesn’t rule out other conditions)
49
What’s massive PE?
Hypotensive patient with <90 systolic bp Less common that non massive
50
Treatment for massive PE?
Thrombolysis => alteplase (“clot buster”)
51
Treatment for non massive PE?
Anticoagulation (DOAC) 3 to 6 month treatment 1st line = apixaban\riveroxaban *If there’s a CI due to renal impairment offer LMWH or UFH
52
Another name for peripheral vascular disease? (PVD)
Peripheral arterial disease (PAD)
53
What is PVD?
Peripheral vascular disease is essentially reduced blood supply and ischaemia in the lower limbs due to atherosclerosis and thrombosis in the arteries
54
Risk factors for PVD?
Smoking = singke greatest risk factor T2DM Ageing Males affected at younger age Obesity Hypertension CKD
55
Three main patterns of presentation of PVD?
1. Intermittent claudication (least severe) 2. Critical limb ischaemia 3. Acute limb-threatening ischaemia (most severe)
56
Intermittent claudication?
Reflects an inadequate increase in skeletal muscle perfusion during exercise - atherosclerotic partial lumen occlusion - pain on exertion
57
Critical limb ischaemia?
Advanced form of chronic limb ischaemia - big occlusion and blood supply barely adequate to meet metabolic demand - pain at rest - risk of gangrene/infection
58
Acute limb-threatening ischeamia?
Most commonly caused by emboli, usually cardiac origin, resulting in sudden decrease in limb perfusion - total vessel occlusion - emboli tend to lodge at bifurcations or sudden narrowing
59
Symptoms of acute limb-threatening ischeamia
6Ps Pulselessness Pallor Pain Perishingly cold Paralysis Paresthesia - present in chronic limb ischemia too but more you have=more limb threatening - all 6 = deadly!!
60
What happens when BV supplying region is occluded?
1) irreversible nerve damage (within 6h) 2) irreversible muscle damage (6-10h) 3) skin changes are last to appear =>likely gangrenous
61
Fontaine classifications of PVD
I) asymptomatic II) intermittent claudication- aching or burning of leg muscles -stage IIa = after 200m walking -stage IIb = after less than 200m walking Relieved within minutes of rest III) critical limb ischaemia - pain at rest + night IV) tissue loss: ulceration or gangrene
62
Why might symptoms be masked in PVD?
Inability to walk (eg severe heart failure) Pain insensitivity (eg diabetic neuropathy)
63
Signs to look for in PVD?
-Low ABPI (<0.9) or lack of lower leg pulse -Skin changes on leg (ulceration, thin, shiny, discolouration -Buerger’s test +ve -Bruits: pulsatile regions due to turbulent blood flow (aortic, femoral, carotid) -Some of 6Ps
64
Buerger’s test?
1) lie patient flat 2) elevate leg to 45° for 1 min 3) positive = pallor then reactive hyperaemia
65
Primary investigations for PVD?
1) ABPI (ankle-brachial blood pressure index) 0.8-1.3 normal 0.5-0.8 intermediate claudication <0.5 critical limb ischaemia Pulse absent = acute limb-threatening ischaemia 2) duplex ultrasound imaging- assess location and severity of stenosis 3) ECG, U+E, FBC, HbA1c - assess cardiovascular risk *Ct angiography if surgery considered, not routine as more invasive*
66
Treatment of intermittent claudication
RF management: -Supervised exercise programme if available (2 hrs per week for three months) -or if not then unsupervised exercise training -smoking cessation -bp control -diet and weight management -statins -HbA1c control -antilplatelets If 3 months exercise doesn’t improve quality of life then consider Revascularisation surgery
67
Treatment of chronic limb ischaemia
Revascularisation surgery (PCI if small, bypass if larger) Amputation if severe
68
Treatment for acute limb threatening ischeamia
Surgical emergency Revascularisation within 4-6hrs otherwise increased amputation risk
69
Complications of PVD
Amputation Ulceration + gangrene Permanent limb weakness Infection and poor tissue healing Increased risk of cerebrovascular accidents + CVD
70
Treatment for cardiac tamponade
Urgent therapeutic pericardiocentesis - needle inserted between xiphisternum and left costal margin and directed towards left shoulder -sometimes done under ultrasound guidance -pericardial fluid aspirated to relieve intrapericardial presure
71
What is cardiac tamponade
Accumulation of a large vol of fluid in the pericardial space (pericardial effusion) that begins to impair ventricle filling
72
Cause of Cardiac tamponade
Typically pericarditis Hence risk factors are all pericarditis related
73
Symptoms of cardiac tamponade
Related to pericarditis
74
Signs of cardiac tamponade
Beck’s triad: - hypotension (reduced cardiac output) - raised JVP (heart failure) - muffled heart sounds Pulses paradoxes: systolic bp reduction of >10mmHg on inspiration
75
Primary investigations to diagnose cardiac tamponade
ECG: may show electrical alternations - varying QRS amplitudes due to heart bouncing back and forth in pericardial fluid CXR: big globular heart ECHO: diagnostic tool
76
What does regurgitation cause?
Insufficiency + proximal chamber dilation -loss of structural chamber integrity and strength
77
What does stenosis cause?
Increase in upstream pressure + proximal chamber dilation+hypertrophy - heart becomes huge and rigid; poorly compliant
78
Main valve disorders?
Aortic regurgitation and stenosis Mitral regurgitation and stenosis
79
What do the main valve disorders cause?
Murmers
80
How are murmers best heard?
Using RILE Right side defects (tricuspid /pulmonary) heard on Inspiration Left sided defects (mitral\aortic) heard on Expiration
81
Normal size of mitral bicuspid lumen and after undergoing stenosis?
Mitral bicuspid lumen = 4-6cm2 Symptoms of stenosis start at <2cm
82
Causes of mitral stenosis
Most common = rheumatic fever (Post strep pyogenes infection) Also valve calcification in older patients + infective endocarditis
83
Pathophysiology of mitral stenosis
RHD causes mitral reactive inflammation, after years exacerbated with calcification => LA hypertrophy and chamber dilation
84
Symptoms and signs of mitral stenosis
-malar cheek flush (due to CO2 retention) - association with Atrial Fibrillation (due to Stasis in LA and hypertrophy of LA) -dyspnoea - A wave on JVP
85
Mitral stenosis murmur?
Low pitched Mid diastolic murmer Loudest at apex Best heard on expiration with patient lying on left hand side
86
Investigations to diagnose mitral stenosis
CXR (LA enlarged) EVG (AFib, P mitrale= bifid “m” shale P waves when LA enlarged) ECHO -assess valve area, gradient, mobility (gold standard)
87
Treatment for mitral stenosis
Surgical Percutaneous balloon valvotomy (stent open mitral valve opening) Mitral valve replacement
88
Why is mitral stenosis more atrial fibrillation associated?
Mitral stenosis causes left atrium hypertrophy - more chances of embolisation as blood actively pumped harder
89
Causes of mitral regurgitation
Myxomatous mitral valve (most common valve disease) = mass of cells in valve connective tissue makes leaflets heavier + prolapse
90
What is mitral regurgitation
Heart valve disease in which the valve between the left heart chambers doesn't close completely, allowing blood to leak backward across the valve
91
Risk factors for mitral regurgitation
Females Older Decreased BMI Prior MI Connective tissue disorder (marfan, ehlers danos)
92
Symptoms of mitral regurgitation
Exertion dyspnoea (due to pulmonary hypertension from back logging of blood)
93
Mitral regurgitation murmer?
Pan systolic blowing murmur radiating to axila (at apex) *soft S1, prominent S3 in heart failure (severe cases)*
94
Investigations for diagnosing mitral regurgitation
ECG CXR ECHO (gold standard) - check left atrium size and left ventricle function analysis Also assess valve structure to decide treatment
95
Treatment for mitral regurgitation
ACEi, Bb + serial ECHO monitoring If severe - (symptoms at rest) = valve repair\replacement
96
What is aortic stenosis
Pathological narrowing or aortic valve -decrease in flow Normal area 3-4cm Symptoms at 1/4 lumen size Most common valve disorder- results in LV dilation + hypertrophy
97
Symptoms of aortic stenosis
SAD Syncope (exertional) Angina Dyspnoea (relates to heart failure)
98
Aortic stenosis murmur
Ejection systolic crescendo decrescendo, radiating to carotids heard at right sternal border, second IC space -prominent S4 seen in LVH - narrow pulse pressure + slow rising pulse (not collapsing corrigan’s pulse)
99
Investigations to diagnose aortic stenosis
ECG CXR ECHO = gold standard for LV size and function + aortic valve area
100
Treatment for Aortic stenosis
General: Fastidious dental care to prevent IE As it is a mechanical problem-drugs are not effective Surgical if symptomatic: - in a healthy patient -> open repair\valve replaced (definitive) - more at risk (eg 75+) ->TAVI (transcutaneous aortic valve implant) less invasive and stents valve open
101
Differential diagnosis for aortic stenosis
Hypertrophic cardiomyopathy may also cause S4 - associated with sudden death in young men
102
What is aortic regurgitation
Leaky aortic valve which makes it insufficient
103
Causes of aortic regurgitation
Congenital bicuspid valve RHD Connective tissue disorders (Marfan/ehlers danos) Infective endocarditis
104
Symptoms and signs of aortic regurgitation
-Collapsing carrigon’s pulse with wide pulse pressure -Quincke’s sign (nailed pulses when pressed) -De Musset sign (head bobbing in time with arterial pulsation)
105
Aortic regurgitation murmur
Early diastolic blowing murmer at right sternal border 2nd intercostal space - Austin fling murmer (severe) - mid diastolic low pitched rumble - heard when regurgitation is so severe blood bounces if mitral valve cusps and makes sound
106
Investigations to diagnose aortic regurgitation
ECG CXR ECHO gold standard, evaluates aortic valve, root, dimensions
107
Treatment for aortic regurgitation
Consider IE prophylaxysis (consider as differential diagnosis) Surgical valve replacement if symptoms
108
Pathophysiology of aortic stenosis
- A pressure gradient develops between left ventricle and aorta - LV function initially maintained by compensatory pressure hypertrophy - When compensatory mechanism exhausted, LV function declines
109
Systolic murmurs?
ASMR Aortic Stenosis Mitral Regurgitation
110
Diastolic Murmer?
ARMS Aortic regurgitation Mitral stenosis

2a cardio (6 decks)

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