Vascular Flashcards
Where are baroreceptors?
Carotid sinuses (glossopharyngeal) and aortic arch (vagus)
What is the average pulse pressure?
40 mm Hg
Why does the pulse pressure increase in ageing?
SBP increases due to less elastic aorta
DBP decreases due to lack of elastic recoil
When does the pulse pressure decrease?
haemorrhage
How often should BP be measured?
Every 5 years in adults
Annually over 80
How to investigate hypertension?
ECG - LVH
Fundoscopy - hypertensive retinopathy
Urinalysis
Cardiovascular risk assessment
Bloods: U&Es, glucose, lipids
NICE hypertension criteria
Stage 1: 140/90 clinic, 135/85 ABPM/ HBPM
Stage 2:160/100, 150/95
Stage 3: 180/110
If BP elevated in clinic, how is hypertension confirmed?
ABPM (2 readings every hour)
HBPM (2 readings daily)
What are the hypertensive crises?
MALIGNANT (ACCELERATED) HTN: stage 3 + accompanied with end-organ damage - refer hospital same day
SUSPECTED PHAECHROMOCYTOMA: refer same day
HYPERTENSIVE URGENCY: stage 3 without impending organ damage - refer within few days
Secondary causes of hypertension
Renal: intrinsic or renovascular
Endocrine: Cushing’s - Conn’s - thyroid - phaechromocytoma - acromegaly - hyperparathyroidism
Coarctation of the aorta
Obstructive sleep apnoea
Pre-eclampsia and HTN in pregnancy
Drugs: alcohol, cocaine, amphetamines, antidepressants, COCP, etc.
Management of hypertension
Young + non-black // Black or over 55
STEP 1: A (or B if contra-indicated) // C (or D if contra-indicated)
STEP 2: A + C (AIIRA in black)
B + C if initially started on B
A + D (if C contraindicated)
STEP 3: A + C + D
STEP 4: Consider fourth agent/ specialist
Mx HTN: HF
Normally already on A + B
Add D - refer to specialist for spiro
Mx HTN: DM
A is first-line, regardless of age/ race
Then add D
Then add C
Mx HTN: AF
If rate control needed, add B or CCB (diltiazem better than amlodipine)
MoA beta-blockers
B1 mainly in heart
B2 mainly smooth muscle of vessels and airway
Blockade reduces speed of contraction and speed of conduction
Five 5 indications for beta-blockers
IHD (symptoms + prognosis) HF (prognosis) AF (reduce ventricular rate) SVT (restores sinus rhythm) HTN
Who requires a low dose of beta-blockers?
Hepatic failure
In whom should beta-blockers be avoided?
Asthma (in COPD use B1-selective, not propranolol)
Heart block
Avoid in haemodynamically unstable
Which medication should not be given with beta-blockers?
Non-dihydropyridine CCB (eg verapamil, diltiazem) –> HF, bradycardia, asystole
Needs specialist supervision
What are the classes of CCBs?
Dihydropyridines (more vasc-selective): nifedipine, amlodipine
Non-dihydropyridines (more heart-selective): diltiazem, verapamil
3 indications for CCBs
HTN (amlodipine, nifedipine less oftten)
Stable angina (beta-blockers main alternative)
Rate control in SVT arrhythmias (diltiazem and verapamil)
MoA CCBs
reduced calcium entry into vascular and cardiac muscle –> less contraction
ADRs of CCBs
Dihydropyridines: ankle swelling, flushing, headaches, palpitations (vasodilataion + compensatory tachycardia)
Verapamil: constipation - bradycardia, heart block, cardiac failure
Diltiazem has both as less selective
When should dihydropyridines not be given?
Unstable angina (don't want to increase O2 demand of heart) Severe AS (provokes collapse)
When should non-dihydropyridines not be given?
Avoid in AV nodal conduction delay
Caution in poor LV function
Total cholesterol healthy limit
< 4 mmol/L
How long after an acute cardiac event should cholesterol be measured?
8 weeks
What should raise suspicion of an inherited hyperlipidaemia?
Consider if values v high
FHx first-degree premature CHD
Premature corneal arcus, tendon xanthomata, xantholasma
Where are tendon xanthamata often found?
Knuckles and achilles tendon
Before starting a statin, what should be checked?
Thyroid levels: hypothyroidism causes hyperlipidaemmia
Causes of secondary hyperlipidaemia
Pregnancy
Obesity
Alcohol excess
Medical: hypothyroid, obstructive jaundice, Cushing’s, anorexia nervosa, nephrotic syndrome, DM, CKD
Drugs: thiazides, glucocorticoids, beta-blockers, ciclosporin, antiretrovirals, atypical antipsychotics
4 indications for statin therapy
Primary hyperlipidaemia
Familiar hypercholesterolaemia
Established atherosclerotc disease
Everyone over 40 with T1DM and T2DM
Diabetic 18-39 with: poor glycaemic control retinopathy, nephropathy HTN evidence of metabolic sx FHx CVD (first-degree, premature)
NICE recommends everyone over 85
When should statins be taken?
Evening - greatest effect when diet reduced
MoA statins
Inhibit HMG CoA reductase (makes cholesterol) - also indirectly reduces TGs and increases HDLs
In whom should statins be avoided?
Pregnant/ BF (need cholesterol)
Caution in hepatic impairment
Who needs lower doses of statins?
Renal disease
How to manage interactions with statins?
Metabolism REDUCED by cytochrome P450 inhibitors –> accumulation of statins –> side effects
Reduce statin dose, or withhold if other drug only needed for short time
ADRs of statins?
Rare but: headache, GI disturbance, muscles (from aches to serious myopathy), drug-induced hepatitis
What are the 3 stages of peripheral vascular disease and their equivalents?
Intermittent claudication (stable angina)
Critical limb ischaemia (unsuable angina)
Acute limmb ichaemia (MI)
Pain in buttock is usually claudication where?
Iliac artery
Pain in calf is usually claudication where?
Femoral or popliteal artery
Mx intermittent claudication
Encourage aerobic exercise –> angiogenesis
Lifestyle advice
Monitor DM/ HTN
Statins
ACEi (though 25% will have renal artery stenosis)
Antiplatelets if symptomatic
Peripheral vasodilator therapy
Angioplasty to dilate stenosed vessel
Defining criteria for critical limb ischaemia
Pain at rest
Gangrene
ABPI <0.3
Mx critical limb ischaemia
Usually bypass (greater saphenous), can be helped by angioplasty Or amputation
6Ps of acute limb ischaemia
Pallor Pulselessness Perishingly cold Pain Paraesthesia Pulselessness
Causes of acute limb ischaemia
Thrombus (ruptured plaque)
Embolism (esp from AF, vegetations from infective endocarditis, thrombus within sac of aneurysm)
Raynaud’s syndrome (if excessive vasoconstriction)
Trauma
Compartment syndrome
Ix acute limb ischaemia
Hand-held Doppler ultrasound scan may help demonstrate any residual arterial flow
Bloods:
FBC (ischaemia is aggravated by anaemia).
ESR (inflammatory disease - eg, giant cell arteritis, other connective tissue disorders).
Glucose (diabetes).
Lipids.
Thrombophilia screen.
If diagnosis is in doubt, perform urgent arteriography.
Investigations to identify the source of embolus: ECG. Echocardiogram. Aortic ultrasound. Popliteal and femoral artery ultrasound.
Mx acute ischaemic limb
Hospital admission
Immediate heparinisation
Pain relief
Causes of claudication with normal pulses
Neurogenic claudication (spinal stenosis)
Anaemia
Beta-blockers
What is Leriche syndrome?
Common iliac disease
Bilateral buttock pain and impotence
Buerger’s disease
Thromboangiitis obliterans
Vessels become blocked and inflamed by thrombi
Associated with smoking
Why are lower doses ACEi given in diabetic nephropathy and CKD?
Risk of hyperkalaemia
MoA of ACEi
Prevents conversion of angiotensin I to angiotension II (potent vasoconstrictor that stimulates aldosterone)
ACEi promotes Na+/H2O excretion - reduces preload
ADRs of ACEi
Hypotension (esp after first dose)
Persistent dry cough (increased bradykinin - usually inactivated by ACE)
Hyperkalaemia (reduced aldosterone)
Rare: angioedema (anaphylactoid)
When should ACEi not be given?
Pregnant/ BF
Renal artery stenosis
AKI
Caution interactions with ACEi
NSAID + ACEi –> predisposes to renal failure
potassium-sparing drugs + ACEi –> only under specialist advice, HF
Name some ACEi and ARBs
Ramipril, lisinopril
Losartan, candesartan
4 indications of aspirin
Treatment of ACS + acute ischaemic stroke (rapid inhibition of platelets aggregation)
Secondary prevention of thrombotic arterial events
Reduce thrombus formation in AF (where warfarin/ oral anticoags contra-indicated)
Pain (though not best NSA/iD)
MoA aspirin
Irreversibly inhibits cyclooxygenase –> reduces production of thromboxane
How long do the effects of aspirin last?
7-10 days (lifetime of plts)
ADRs of aspirin
GI ulceration/ haemorrhage (co-prescribe omeprazole if has risk factors + on other damaging drugs, eg NSAIDs/ pred)
Hypersensitivity (inc bronchospasm)
Tinnitus if reg high doses
Why should under 16s not be given aspirin?
Reye’s syndrome: liver + brain effects
When should pregnant women not take aspirin?
3rd trimester: premature closure of ductus arteriosus
Who should not be given aspirin?
Peptic ulceration
Gout (precipitates attack)
Indications for clopidogrel
Usually with aspirin
Prevents occlusion of coronary stents
What is the MoA of clopidogrel?
Binds irreversibly to ADP receptors on platelets
When should clopidogrel be stopped before surgery?
7 days
if emergency, may need platelet transfusion
Which gastro-protection should be avoided with clopidogrel?
Omeprazole can inhibit clopi
TRUE ANEURYSM
All 3 layers involved
2 types of aneurysm
Fusiform, saccular
FALSE ANEURYSM (PSEUDO-)
contained by outer layers of vessel or surrounding connective tissue
DISSECTING ANEURYSM
False lumen between intima and media due to tear
Risk factors for aneurysmal disease
HTN- hyperlipidaemia - old - smoker - COPD
[NOT DM]
Family hx
Atherosclerosis
Connective tissue disorders
Congenital: Berry aneurysms in circle of Willis (rupture = subarachnoid)
Vasculitis predisposes
Infection: tertiary syphilis –> saccular aortic aneurysm
The following vasculitides predispose to aneurysms where:
Kawasaki’s
GCA
Takayasu’s
K: coronary artery aneurysm
GCA: ascending aorta
T: all
Complications of aneurysmal disease
Can be asymptomatic:
Rupture
Thrombus (turbulent flow)
Emboli (sent anywhere!)
Pressure on adjacent structures
Investigations for aneurysmal disease
Bloods: FBC, U&Es, LFTs, clotting, group & save if needs surgery, ESR/ CRP if suspect inflammatory cause
ECG, CXR
USS
CT/ IV Contrast
How is a ruptured thoracic aortic aneurysm usually diagnosed?
Usually leads to MI and/ or death - a post-mortem diagnosis
Definition of AAA
More than 3 cm
normal is 2 cm
Clinical features of unruptured AAA
Asymptomatic
Or
pressure symptoms
uterohydronephrosis
microembolic lower limb infarcts (+ good pulses should raise suspicion)
inflammation and retroperitoneal fibrosis may cause symptoms due to entrapment-related structures (eg back pain, weight loss)
Monitoring AAA diameters
- 0 - 4.4 cm: annual US
- 5 - 5.4 cm: 3- monthly US
- 5+: SURGERY
Management of AAA
Monitoring
Smoking cessation
Strict BP
Statins, anti-platelets
Surgery, if indicated: open-repair or EVAR (stent-graft via femoral)
Presentation of ruptured AAA
Triad: back pain - hypotension - pulsatile mass
likely to look unwell, be cold + sweaty
rapid, weak + thready pulse
peritoneal bleeding –> acute abdomen
Types of aortic dissection
Type A: ascending aorta
Type B: descending aorta (not immediately life-threatening)
How does aortic dissection present?
Severe chest pain, ‘ripping’
Pain might be worse on onset and then improve (cf MI) - and may then rupture > tamponade
Radiates to the back
Difference in BP in both arms
May be other symptoms due to occlusion by dissecting arteries: angina (coronary arteries) limb ischaemia (distal aorta) paraplegia (spinal arteries) neurological deficit (carotid arteries)
How is aortic dissection best visualised?
MRI or TOE
Mx of aortic dissection
HDU/ ITU > surgery
How is dissection prevented in those with connective tissue disorders?
Periodic aortic diameter screening
Lifelong beta-blockade
Moderate restriction of physical activity
What is carotid artery disease?
Atherosclerosis at bifurcation of carotid artery
How might carotid artery disease present?
If bilateral: cerebral hypoperfusion
Can throw off emboli –> TIA
How is carotid artery disease managed?
Doppler for degree of stenosis
If symptomatic: carotid endarterectomy (scrape out atheroma) or stenting
Causes of varicose veins
Caused by valvular incompetence or compression of deep veins causing stasis
Risk factors for varicose veins
pregnancy, obesity, prolonged standing, previous DVT, pelvic mass pressing on deep veins
Complications of varicose veins
Poor circulation can cause….
Bleeding: mild trauma causes profuse bleeding (pressure is high but walls are thin)
Phlebitis: can be complicated by bacterial infection
Venous eczema: haemosiderin released as cells pushed into tissue by increased presure
Venous ulcers
Oedema
Management of varicose veins
lifestyle
compression stockings
refer:
urgently if active bleeding
routine if complications
imaged via duplex
Endothermal ablation
Ultrasound-guided foam sclerotherapy (if ablation unsuitable)
others
Where do DVTs tend to occur?
Usually lower limb but can be pelvic veins
Clinical features of DVT
Can be hard to diagnose, esp if complicated by cellulitis
Limb pain + tenderness along line of deep vein
Swelling of calf or thigh (usually unilateral but if high up may cause bilateral leg oedema)
Pitting oedema
Distension of superficial veins
Hot, erythematous (sometimes cyanosed)
Risk factors for DVT
Previous DVT - family hx - thrombophilia - immobility - dehydration - cancer - smoking - COCP/ HRT - antiphospholipid sx - HF - varicose veins
DDx for soft and tender leg
Superficial thrombophlebitis Peripheral oedema Venous/ lymphatic obstruction Vasculitis Ruptured baker's cyst cellulitis septic arthritis compartment syndrome
Investigations for DVT
Wells’ score gives likelihood + leg USS
D-dimer
If positive:
gold-standard is contrast venography (rarely used)
Full examination/ look for cancers, esp if under 40
Management of DVT
LMWH or fondaparinux
UFH if GFR <30 or increased risk of bleeding
oral anticoags for 3 months
POST-THROMBOTIC SYNDROME
Due to damage to deep veins and their valves
Chronic venous hypertension can cause pain, swelling, hyperpigmentation, ulcers, gangrene etc
2 indications for heparins and fondaparinux
prophylaxis and initial DVT treatment
ACS: first-line to improve revascularisation
What is used to reverse heparins?
Protamine
3 indications for warfarin
Prevents clot extension + recurrence of VTE
Prevent embolic complications in AF
“ after heart valve replacement
Why is warfarin not used in arterial thrombosis?
These are driven by platelets: need anti-platelets
MoA of warfarin
Inhibits hepatic production of vit K-dependent coag factors
ADRs or warfarin
Bleeding! Including spontaneous (eg epistaxis) and peptic ulcers
What can increase/ decrease effects of warfarin?
cytochrome P450 inhibitors: inhibit warfarin
inducers: stimulate warfarin
many abx increase anticoag as kill the gut flora synthesising vit K
How much INR to prescribe?
Initially 5-10 mg, then guided by yellow book
Changes in INR lag behind dose changes
Describe typical appearance and location of ulcers
Venous: shallow, throbbing pain, exudate, skin changes - GAITOR REGION
Arterial: punched out, painful ++, associated with gangrene - FEET, TOES, MEDIAL MALLEOLUS
Neuropathic: painless - BOTTOM OF FEET + GOOD PULSES
Management of ulcers
Venous: compression bandages to reduce venous hypertension + abx
arterial: not compression!, address risk factors, consider surgery
Neuropathic: foot care to remove callous + orthowedge
Describe types of gangrene
Wet: death + infection
Dry: just death
Gas: bacterial infection causing gas in tissues
What is Fournier’s gangrene?
Multiorganism infection of scrotum
Pts usually DM + catheterised
Sudden pain in scrotum - needs urgent abx and debridement
Secondary prevention of PAD
75 mg clopidogrel
Who should be offered ABPM?
More than 140/90
If severe: 180/110, no need to confirm with ABPM. Consider starting Mx. Check no red flags
Who should be treated for HTN?
All stage 2+
For stage 1, if under 80 and: target organ damage CVD DM renal disease 10 year CVD risk >20%
Which thiazide used in BP management?
Chlortalidone or indapamide, rather than bendroflumethazide or hydrochlorothiazide (but if already on, don’t need to change)
Target BP in over 80s
<150/90 (ABP/HBPM <145/85)
Red flags for hypercholesterolaemia
Chest pain
Leg pain
Red flags for hypertension
Diastolic BP >120
Microscopic haematuria
Encephalopathy
Pregnant
Impending complications, eg TIA, LVF
Severe HTN: look for papilloedema, retinal haemorrhage
Phaechromocytoma: headache, palpitations, pallor, excessive sweating, fever, abdo pains
What tests after initiating statins?
LFTs at 3 months and 12 months
Statin first-line doses
Primary prevention: atorvastatin 20 mg
Secondary prevention: atorvastatin 80 mg (20 mg if CKD)
Aiming for 40% reduction in non-HDL cholesterol after 3 months
?familial hypercholesterolaemia
Cholesterol over 7.5
Tendon xanthamata
FHx premature CHD (under 60)
Red flags for intermittent claudication
Critical limb ischaemia (Ps)
Red flags for varicose veins
DVT
Abdominal mass
Definition postural hypotension
Drop in >20 systolic or >10 diastolic within 3 mins of standing
