Peripheral Arterial and Venous Disease

Question 1

Flow = vol/time and lower limb veins are superficial draining into deep (perforating veins go between), where do they lie?

Answer 1

Superficial veins are in the subcutaneous fat and deep veins are in the calf muscles; they are separated by the deep fascia.

Question 2

What is the purpose of the deep fascia?

Answer 2

It encloses internal compartments containing muscles and deep veins. Contraction within a compartment raises pressure, pushing blood towards the heart and on relaxation, drawing more blood in, from superficial veins.

Question 3

Give examples of superficial veins (plus their locations) and deep veins of the lower limb.

Answer 3

Deep veins: external iliac, femoral and popliteal veins.
Superficial: short saphenous (midline of back of calf, drains to popliteal) and long saphenous veins (medial side behind knee and invariably anterior to medial malleolus, drains into femoral).

Question 4

The arterial system has the heart as its pump and the venous system has calf muscles. The flow is superficial to deep, what are the valves for?

Answer 4

To stop the backflow of blood.

Question 5

Ultrasound can be used to assess peripheral vessels: a stenosis ___________ velocity and ___________ flow. You can’t __________ the flow, but it may be inferred from velocity. There is lower velocity in the ____________ and more reflection in diastole. Exercise leads to dilatation and so ______ backflow.

Answer 5

Increases
Decreases
Measure
Peripheries
Less

Question 6

What is the effect on velocity and flow when the abdominal aorta bifurcates into the common iliac arteries and why?

Answer 6

The total surface area reduces, so velocity increases and flow decreases, before the common iliac arteries branch.

Question 7

What’s the Doppler effect?

Answer 7

Increased frequency of waves as the source and observer move towards each other and vice versa.

Question 8

What is a varicose vein and what causes it?

Answer 8

Varicose veins are tortuous, twisted or lengthened veins (perhaps saphenous). The vein wall inherently weak in varicose veins, which leads to dilatation and separation of the valve cusps, so that they become incompetent.

Question 9

What are the symptoms of varicose veins?

Answer 9

Heaviness, tension, aching and itching (histamine mediated) along the vein.

Question 10

Complications of varicose veins are either from the vein itself or from the resultant venous hypertension, describe some of either.

Answer 10

From vein: haemorrhage (standing in shower-vasodilate), thrombophlebitis (wall inflamed with thrombosis). From venous hypertension: oedema, skin pigmentation, varicose eczema, lipodermatosclerosis (fat in skin hardening) and venous ulceration.

Question 11

Explain thrombophlebitis as a result of varicose veins.

Answer 11

As a result of venous hypertension, venous thrombosis produces an inflammatory response, including pain - haemosiderin staining as oxidising enzymes in macrophages Fe2+ –> Fe3+.

Question 12

How does venous hypertension (the cause of some varicose vein complications), come about?

Answer 12

A result of calf muscle pump failure: failure of contraction (immobile, obese, hip/knee/ankle movement restricted), deep vein incompetence, volume overload (superficial vein incompetence).

Question 13

Superficial vein incompetence can cause venous hypertension by producing a retrograde circuit, explain.

Answer 13

Blood flows deep to superficial and back through the perforating veins, because the valves in the superficial veins don’t prevent backflow.

Question 14

The pathophysiology of thrombosis can be explain by Virchow’s triad, describe it and state which are particularly responsible for arterial and venous thrombi.

Answer 14

Changes in the lining of the vessel wall (arterial, as in atherosclerosis with an atheroma).
Changes in blood flow (venous).
Changes in the blood constituents.

Question 15

What leads to venous thrombosis?

Answer 15

Stasis plus another provocateur e.g. Oral contraceptive pill, trauma, dehydration, cancer.

Question 16

In terms of the pathways and the main constituents of the thrombi, how do arterial and venous thrombosis differ?

Answer 16

Arterial thrombosis responding to bleeding triggers extrinsic then intrinsic pathways and involves platelets - the thrombi is platelet rich (become activated).
Different to arterial, intrinsic then extrinsic pathways are involved in making venous thrombi, which are fibrin rich.

Question 17

Deep vein thrombosis mostly begins in the deep calf veins and produces an inflammatory response, what are the signs?

Answer 17

Rubor, calor, dolor, tumor and loss of function.

Question 18

What are the symptoms of DVT?

Answer 18

Pain, swelling, blue-red skin discolouration or there may be none.

Question 19

What are the signs of DVT?

Answer 19

Calf tenderness, muscle induration (hardening), skin warmth and discolouration, distended and warm superficial veins, oedema and pyrexia.

Question 20

The dreaded and often fatal complication of deep vein thrombosis is pulmonary embolism. What is its association with surgery?

Answer 20

Immobilisation prior to and after, no action of the calf pump during and surgery is trauma -> ‘prothrombotic state’.

Question 21

What are the 2 types of peripheral artery disease?

Answer 21

Acute and chronic.

Question 22

There is natural collateral circulation in the cardiovascular system, where in particular?

Answer 22

Collateral circulation is particularly common across joint like the elbow and the knee and may develop further (weeks/months) in response to stenosis, eventually bypassing the occlusion.

Question 23

What is Acute limb ischaemia and what can it lead to?

Answer 23

Normal to greatly impaired blood supply over minutes (no time for collateral development), caused by an embolism or trauma, sudden onset. If not reversed within 6 hours, necrosis can lead to hyperkalaemia and so requires amputation.

Question 24

The symptoms/signs of acute ischaemia can be remembered using the 6 Ps of acute ischaemia, what are they?

Answer 24

Pain, parasthesia, pallor, paralysis, perishing cold and pulseless.
Over the next hour, patchy cyanosis results, which initially blanches when presses, then there’s fixed mottling which needs amputation ASAP.

Question 25

What are the 3 types of chronic peripheral arterial disease (and how do they relate to coronary syndromes)?

Answer 25

Intermittent claudication (stable angina) or Critical ischaemia: rest pain (unstable angina) or ulceration/gangrene (MI).

Question 26

What is claudication?

Answer 26

Pain in the muscles of the lower limb elicited by walking/exercise.
The pain can be relieved by stopping the exercise for a matter of minutes.

Question 27

The calf muscles are most commonly affected by intermittent claudication, why?

Answer 27

The superficial femoral artery, which supplies its blood is the most frequently diseased.

Question 28

The femoral artery is felt at the ____________ point (ASIS-pubic symphysis), while the popliteal artery is very ___________ to feel. The anterior tibial artery becomes the ________ ________ (________ to extensor hallicus longus) and the posterior tibial becomes continues into the foot (felt posterior to the _________ __________).

Answer 28

Mid-inguinal
Difficult
Dorsalis pedis
Lateral
Medial malleolus

Question 29

You can work out the site of stenosis by using the site of claudication and feeling the lower limb pulses, what is the buttock region supplied by?

Answer 29

The internal iliac artery.

Common iliac, internal and external - common moral, deep and superficial, arteries of the leg

Question 30

Superficial femoral artery occlusion is the most common type to present, what would you be told and notice on examination?

Answer 30

Right (eg) calf claudication, femoral pulse present, absent popliteal and dorsal pulses.

Question 31

Rest pain is a type of critical ischaemia, what is it?

Answer 31

Pain in the foot that comes on when the patient goes to bed - relieved by hanging the fort out of the bed. The ischaemia is very severe; there is not enough oxygen to provide for the cell’s (skin, muscle, bone) basic metabolic requirements.

Question 32

Name a common site of ischaemic ulceration.

Answer 32

The anterior shin.

Question 33

Why does hypertension not (generally) lead to oedema?

Answer 33

The arterioles are constricted, so the capillary hydrostatic pressure falls. The pressure drop across the system is greater as the resistance is increased (pressure on the arterial side rises and that on the venous side falls).

Question 34

Right-sided heart failure can lead to peripheral oedema, but how can left-sided heart failure lead to pulmonary oedema and why is this bad?

Answer 34

The left ventricle can’t empty, increasing the left atrial pressure, which means it’s also high in the pulmonary veins and capillaries. High hydrostatic pressure in the capillaries leads to oedema, impairing gas exchange.

Question 35

The pulmonary circulation usually has a low pressure and a low __________?

Answer 35

Resistance.

Question 36

What are the pressures in the RA, RV, PA, LA, LV and aorta (they overlap)?

Answer 36

Right atrium: 0-8mmHg,
Right ventricle: 0-8 / 15-30mmHg,
Pulmonary artery: 15-30 / 4-12mmHg.

Left atrium: 1-10mmHg,
Left ventricle: 1-10 / 100-140mmHg,
Aorta: 100-140 / 60-90mmHg.

Question 37

The most common cause of right sided heart failure is left sided heart failure (bilateral/congestive), but what can cause it on its own and how?

Answer 37

Chronic lung disease.
Hypoxic pulmonary vasoconstriction (opposite to systemic circulation) ensures an optimal ventilation to perfusion ratio (don’t want deoxygenated blood leaving lungs). Chronic hypoxia due to lung disease can increase the vascular resistance in the lungs (Cor pulmonale), leading to right-sided heart failure.

Question 38

ACE inhibitors stop the conversion of Angiotensin I to Angiotensin II and are used to treat both hypertension and heart failure, how are they useful in hypertension?

Answer 38

Decrease the circulating blood volume (so stroke volume) which decreases the pressure (Ang II directly and through aldosterone, makes kidney reabsorb sodium and water. It also stops the vasodilators effects of Angiotensin II and so lowers total peripheral resistance.

Question 39

ACE inhibitors stop the conversion of Angiotensin I to Angiotensin II and are used to treat both hypertension and heart failure, how are they useful in heart failure?

Answer 39

Reduces total peripheral resistance and so afterload (Ang II vasoconstricts), meaning the heart has to work less hard to pump the blood.
Decreases blood volume (Ang II directly and via aldosterone stimulates kidney to retain sodium and water) - venous pressure is reduced so there’s less oedema and preload is reduced, so the heart can move on Starling’s curve. Stop the negative effect that Angiotensin II has on AT1 receptors in the heart in HF.