Cardiology - Blood vessels, aneurysms, veins, lymphatics, tumours Flashcards
What is an aneurysm?
Aneurysms are defined as a weakening of the vessel wall, followed by dilation due to increased wall stress. Aneurysm affecting the abdominal aortia (AAA) is the most common type?
What patients are most commonly affected by abdominal aortic aneurysm?
AAA is the most common vessel aneurysm.
Usually occurs in men >60 years old (4:1 M:F).
They are usually located BELOW the renal artery orifices.
What is the pathogenesis of AAA?
Atherosclerosis weakens the arterial wall
- vessel wall stress increases with diameter (law of Laplace)
- vessel lumen fills with atheromatous debris and blood clots
Other factors play a role: familial, structural defects in connective tissue, absence of vasa vasorum in abdominal aorta (vessel that supplies the blood vessel)
What are the clinical findings associated with AAA?
Usually asymptomatic!
Can present as a pulsatile epigastric mass that may or may not be tender.
Bruit (harsh sounds) is heard if renal artery stenosis or visceral arterial stenosis is present.
Atherosclerotic plaques can chip off and embolize to distal extremities. Rupture is the most common complication.
What are the clinical findings of a ruptured AAA?
There is a triad of:
1) Sudden onset of severe left flank pain (bleed is initially retroperitoneal)
2) Hypotension from blood loss into the retroperitoneum
3) Presence of pulsatile mass on physical examination
What is the greatest predictor of rupture in AAA?
Diameter.
Surgical repair is beneficial if the diameter of the aneurysm is >5.0-5.4 cm.
How are AAA diagnosed?
Ultrasound is 100% accurate (excellent initial screen)
CT scan can be used preoperatively to localise extent into renal vessels and evaluate the integrity of the vessel wall to exclude rupture.
Angiography gives detailed arterial anatomy.
Large diameter asymptomatic aneurysms (i.e. >5cm) are usually referred for repair, as diameter predicts rupture. Distal embolisation is also a factor.
What is the most common peripheral aneurysm?
Popliteal artery aneurysm:
- predominantly seen in males (>95%)
- pulsatile mass behind the knee
- treated surgically
What is a mycotic aneurysm?
This is a weakening of the vessel wall due to infection. It does NOT have to be fungal, but fungi are most common.
Fungi that commonly invade the arterial wall and weaken them include Candida, Aspergillus, and Mucor.
Bacteria that invade the vessel wall and weaken them include Bacteroides, Pseudomonas, and Salmonella.
Clinical findings include thrombosis with or without infarction and in some cases rupture. They are treated surgically.
What is a Berry aneurysm?
This is a saccular dilatation typically found around the circle of Willis and base of the brain.
What risk factors are associated with Berry aneurysms?
Normal haemodynamic stress HTN of any cause Coarctation of the aorta Atherosclerosis Polycystic kidney disease
What artery is most commonly affected in Berry aneurysms?
Most common site is at the junction of the communicating branches with the anterior cerebral artery (ACA).
What is the pathogenesis of Berry aneurysms?
At the junction of the communicating branches with the main cerebral vessels, the vessels normally lacks an internal elastic lamina and smooth muscle. Rupture of the aneurysm releases blood into the subarachnoid space or into the brain parenchyma. Classic CT features are blood filled ventricles.
What are the clinical findings of a subarachnoid haemorrhage?
Sudden onset of severe occipital headache - described as the “worst I’ve ever had!”.
Nuchal rigidity from irritation of the meninges.
How common are syphilitic aneurysms?
These occur as a complication of tertiary syphilis due to infection by Treponema pallidum (spirochete).
Aneurysms usually occur in men aged between 40 to 55 years of age.
What is the pathogenesis of syphilitic aneurysm?
T.pallidum infects the vasa vasorum of the ascending and transverse portions of the aortic arch:
- vasculitis is called endarteritis obliterans
- characteristic plasma cell infiltrate is present in the vessel wall
- inflammation is intense and often occludes the lumen of the vessel
Vessel ischaemia of the medial tissue leads to weakness and subsequent dilatation of the aorta and aortic valve ring.
What are the clinical findings of syphilitic aneurysm?
Aortic regurgitation
Brassy cough
- left recurrent laryngeal nerve is stretched by the aneurysm
How is syphilitic aneurysm diagnosed?
There are linear calcifications seen in the aortic wall on a plain radiograph, but the definitive diagnosis is with aortography.
Treatment is with antibiotics for syphilis and surgery, if warranted.
Why is the pulse pressure increased in aortic regurgitation?
This is a problem in closing the AV valve. Because the AV valve closes in diastole, the murmur occurs in early diastole as blood leaks back into the ventricle. The increase in left ventricular end diastolic volume results in an increase in stroke volume (increased systolic pressure - due to Starlings Law). Blood rapidly draining back into the left ventricle decreases the diastolic pressure. The wide pulse pressure is manifested by a hyperdynamic circulation (e.g. pulsating uvula, bounding pulses).
What is an Ausin-Flint murmur?
Excessive blood dripping back onto the anterior mitral valve leaflet produces another diastolic mumur called the Austin-Flint murmur. This finding indicates the need for aortic valve replacement.
In what group of patients does aortic dissection occur most commonly?
This most often occurs in men (3:1 male/female ratio) with a mean age of 40-60 years and a history of antecedent HTN.
It can also occur in young people with connective tissue disorders, usually Marfan’s syndrome or Ehlers-Danlos syndrome type 1.
What is Marfan’s syndrome? What clinical features are often seen?
This is an autosomal dominant disorder resulting in the production of weak elastic tissue due to a defect in synthesizing fibrillin (missense mutation). Cardiovascular abnormalities dominate. Dilation of the ascending aorta may progress to aortic dissection and/ or AV regurgitation. Mitral valve prolapse (MVP) is the most common valvular defect and is often associated with conduction defects causing sudden death. Skeletal defects include hypermobile joints, eunuchoid proportions (lower body length > upper body length, arm span > height), and arachnodactyly (spider hands). Dislocation of the lens is another finding, because the suspensory ligament holding the lens is composed of elastic tissue.
What is the pathogenesis of aortic dissection?
Cystic medial degeneration (CMD)
- elastic tissue fragmentation in the media weakens the elastic artery
- degraded matrix material collects in areas of fragmentation in the media
Risk factors for CMD:
- Increased wall stress: HTN, pregnancy (increased plasma volume) and coarctation of the aorta
- Defects in connective tissue: Marfans syndrome (defects in elastin), EDS (defects in collagen)
Intimal tear in the aorta:
- tear is due to HTN or underlying structural weakness in the media
- usually occurs within 10cm of the aortic valve
- blood dissects under arterial pressure through areas of weakness
- blood dissects proximally and/or distally
What is aortic dissection classified?
There are 2 classification systems used to aortic dissection:
1) Stanford classification
- Type A = ascending aorta/ aortic root; treatment is with surgery - aortic root replacement
- Type B = descending aorta; medical therapy with anti-hypertensives
2) DeBakey classification
- Type I = ascending aorta, aortic arch, descending aorta
- Type II = ascending aorta only
- Type III = descending aorta distal to the left subclavian artery
What are the clinical features of aortic dissection?
Tearing, sudden onset chest pain (painless 10%)
Hypertension or Hypotension
A blood pressure difference (in each arm) greater than 20 mm Hg
Neurologic deficits (20%)
There is quite often loss of upper extremity pulses due to compression of the subclavian artery by blood in the false lumen.
Rupture is also a danger - sites include pericardium, pleural cavity and peritoneal cavity.
How is aortic dissection investigated?
CXR: widened mediastinum, abnormal aortic knob, ring sign, deviation of the trachea/oesophagus
CT angiography of the thoracic aorta
MRI angiography
Conventional angiography (now rarely used diagnostically)
How is aortic dissection treated?
Beta-blockers: aim HR 60-80 bpm and systolic BP 100-120 mm Hg
For type A dissections the standard of care is aortic root replacement
What is peripheral arterial disease? What is meant by the term chronic lower limb ischaemia?
Almost all peripheral arterial disease (PAD) is due to atherosclerosis and it shares the same risk factors as CAD. Around 20% of UK adults aged 55–75 yrs have PAD, but only one-quarter have symptoms. PAD affects the leg eight times more often than the arm. The pres- ence and severity of lower limb ischaemia can be determined by clinical examination and measurement of the ankle:brachial pressure index, the ratio between systolic ankle and brachial BPs (ABPI, normal >1.0). Chronic lower limb ischaemia presents as two distinct clinical entities: intermittent claudication (IC; ABPI 0.5–0.9) and critical limb ischaemia (CLI; ABPI <0.5).
What are the clinical features of chronic lower limb ischaemia?
Pulses - diminished or absent
Bruits - denote turbulent blood flow but bear no relationship to severity of the underlying disease
Reduced skin temperature
Pallor on elevation and rubor on dependency (Buerger’s sign)
Superficial veins that fill sluggishly and empty (“gutter”) upon minimal elevation
Muscle wasting
Loss of hair
What is intermittent claudication?
IC refers to ischaemic pain of the leg muscles precipitated by walking and relieved by rest. It is usually felt in the calf muscles (superficial femoral artery disease) but may occur in the thigh or buttock (iliac artery disease). Typically, the pain comes on after a reasonably constant ‘claudication distance’ and rapidly resolves on stopping.
How is intermittent claudication managed?
All patients with PAD should receive ‘best medical therapy’ (BMT), which comprises standard secondary prevention measures for atherosclerosis (smoking cessation, regular exercise, low-dose aspirin, reduction of cholesterol, diagnosis and treatment of hyper- tension and diabetes) and optimisation of exacerbating conditions (e.g. heart failure, anaemia). Peripheral vasodilators such as cilostazol can improve walking distance. Intervention (angioplasty, stent- ing, endarterectomy or bypass) is usually only considered after 6 mths of BMT, and then only in patients whose disability is severe or threatens their livelihood. Provided patients comply with BMT, only 1–2%/yr will require amputation and/or revascularisation, but the annual mortality rate exceeds 5%, reflecting a high incidence of MI and stroke.
What is the definition of critical limb ischaemia?
CLI is defined as rest (night) pain, requiring opiate analgesia, and/or tissue loss (ulceration or gangrene), present for >2 wks, in the presence of an ankle BP <50 mmHg. Whereas IC is usually due to single-segment plaque, CLI is always due to multi-level disease. Patients are at risk of losing their limb (or life) in a matter of weeks or months without surgical bypass or endovascular revascularisa- tion, but treatment is difficult because they are often elderly with significant multisystem comorbidity and have severe multi-level disease.
How is critical limb ischaemia investigated?
Imaging is performed using duplex ultrasonography. More detailed non-invasive imaging can be provided by contrast MRI or CT. Intra-arterial digital subtraction angiography is indicated for patients suitable for endovascular revascularisation.
How is diabetic vascular disease managed?
Diabetes is present in 30–40% of those with severe limb ischaemia. It does not cause obstructive capillary microangiopathy; revascularisation is therefore effective when used together with control of infection and protection from pressure.
What is buerger’s disease?
This inflammatory obliterative arterial disease usually affects male smokers aged 20–30 yrs, causing claudication and finger pain, with absent wrist and ankle pulses. Smoking cessation is essential, and sympathectomy and prostaglandin infusions may help.
What is acute limb ischaemia?
Acute limb ischaemia (ALI) is most frequently caused by acute thrombotic occlusion of a pre-existing arterial stenosis or throm- boembolism (often secondary to AF). All suspected acutely ischaemic limbs must be discussed immediately with a vascular surgeon. If there are no contraindications, an IV bolus of heparin (3000–5000 U) should be given to limit thrombus propagation and protect the collateral circulation. Distinguishing thrombosis from embolism is frequently difficult.
Evidence of chronic lower limb ischaemia (e.g. previous IC symptoms, bruits, diminished contralat- eral pulses) favours thrombosis, while the absence of such features and the presence of AF favour embolism.
How is acute limb ischaemia treated?
This depends on whether the occlusion is caused by thrombosis or embolism. ALI due to thrombosis can often be treated medically with IV heparin (target APTT 2.0–3.0), antiplatelet agents, high-dose statins, IV fluids and oxygen. ALI due to embolus (no collateral circulation) normally results in extensive tissue necrosis within 6 hrs unless the limb is revascularised. Irreversible ischaemia mandates early ampu- tation or palliative therapy.
What features may suggest acute limb ischaemia?
Pain
Pallor
Pulseless
Perishingly cold
Paraesthesia*
Paralysis*
- More reliable signs of ALL and suggest irreversible ischaemia
How is the saphenous venous system organised?
Superficial saphenous veins drain blood into the deep veins via perforating branches.
Valves in the posterior branches prevent reversal of blood flow into the superficial system.
Deeps veins direct blood back to the heart.
What are varicose veins?
These are veins that are abnormally distended (>3 mm) and often tortuous underneath the skin surface.
Most commonly located:
- superficial saphenous venous system
- distal oesophagus (due to portal hypertension)
- anorectal region (due to portal hypertension)
- left scrotal sac (varicocele)
What risk factors are associated with superficial varicosities in the lower extremities?
Most common clinical manifestation of chronic venous insufficiency.
Risk factors:
- famale gender
- family history of varicose veins
- multiple pregnancies, jobs with prolonged standing, obesity, advanced age
What is the pathogenesis of lower leg varicosities?
Valve incompetence of the perforator branches leads to reversal of blood flow from the high pressure deep venous system into the superficial system.
They may be secondary to DVT. Retrograde blood flow through the perforating branches into the superficial system causes increased pressure and dilatation of vessels.
