CVS Session 11 - Venous System Flashcards Preview

Cardiovascular System > CVS Session 11 - Venous System > Flashcards

Flashcards in CVS Session 11 - Venous System Deck (25):

Outline the role of the calf muscles in blood circulation in the limbs

- The venous return from the lower limb is dependent upon a pumping mechanism within the deep fascia of the leg.  

- The veins in the lower limb have valves which permit the flow of blood only towards the heart.  

- When the calf muscles contract, the deep veins are compressed and blood flows upwards.  

- When the muscles relax, blood is “sucked” into the deep veins via the communicating (perforating) veins from the superficial veins, the valves in the perforating veins allowing blood flow only in this direction; when the valves in the perforating veins become incompetent or diseased, varicosities in superficial veins result


Outline the pathophysiology of varicose veins.

Varicose veins are tortuous, twisted, or lengthened veins 

- The vein wall is inherently weak in varicose veins, which leads to dilatation and separation of valve cusps so that they become incompetent 

- Symptoms: heaviness, tension, aching and itching (must occur along the vein itself)

- The above symptoms are significantly associated with trunk varices



What are the complications of varicose veins?

- Resulting from the vein itself: 

I. Haemorrhage

II. Thrombophlebitis


- Resulting from venous hypertension (resulting from calf failure): 

I. Oedema

II. Skin pigmentation

III. Varicose eczema

IV. Lipodermatosclerosis

V. Venous ulceration 


What are the causes of calf muscle pump failure?

- Failure’ of calf muscle contraction - immobility, obesity, reduced hip, knee and/or ankle movement

- Deep vein incompetence

- Volume overload - superficial vein incompetence 


What is the pathophysiology of thrombosis?


What is the pathophysiology of arterial thrombosis?


What is the pathophysiology of venous thrombosis?


Why does stasis lead to thrombosis?


Describe venous bleeding and distinguish it from arterial bleeding.

- Venous thrombosis does not involve platelets in a major way, initially the intrinsic pathway is involved and then the extrinsic. Venous thrombi are fibrin rich.

- In evolutionary survival terms we need a mechanism for stopping bleeding from high pressure arterial bleeding and a mechanism for dealing with abnormally low flow (no flow) around a venous bleed.

- Both involve blood vessel constriction (vasoconstriction and venoconstriction) initially.

- Arterial bleeding cessation needs platelets and both pathways, venous bleeding particularly needs the intrinsic pathway initially then both pathways 


Outline the pathophysiology of DVT

- Most commonly begins in the deep calf veins

- Produces an inflammatory response: calor, dolor, rubor, tumor, functio laesa

- Symptoms:

I. Pain, cannot walk

II. Swelling

IV. Blue-red skin discolouration

- Signs:

I. Calf tenderness

II. Muscle induration

III. Skin warmth

IV. Skin discolouration

V. Distended, warm superficial veins

VI. Oedema

VII. Pyrexia 



What is the association between surgery and DVT?


Outline the pathophysiology of acute limb ischaemia (peripheral arterial disease)

- The limb goes from a normal blood supply to greatly impaired blood supply over a period of minutes. No chance for collateral vessel development (which takes weeks/months)

- Commonest causes are embolism (from heart or abdominal aortic aneurysm) and trauma

- Sudden onset

- If not reversed within 6 hours the limb cannot be recovered and if not amputated the patient will die (hyperkalemia due to dead tissue releasing intracellular potassium) 

- Signs/symptoms: pain, paralysis, paraesthesia, pallor, pulselessness, perishing cold



Outline the pathophysiology of chronic peripheral arterial disease

- Intermittent claudication (equivalent to stable angina)

- Critical ischaemia

I. Rest pain (equivalent to unstable angina)

II. Ulceration/gangrene (equivalent to myocardial infarction)

- Clinical features: 

I. The calf muscles are most frequently affected, although more proximal muscles may be affected

II. Pain relieved rapidly by stopping exercise for a few minutes, even whilst standing up 



Where can you feel the femoral pulse?


Where can you feel the popliteal pulse?


Where can you feel the pedal pulse: dorsalis pedis artery?


Where can you feel the pedal pulse: posterior tibial artery?


Outline critical ischaemia

- Rest pain (equivalent to unstable angina)

- Ulceration/gangrene (equivalent to myocardial infarction) 


What is rest pain?

- Pain in the FOOT that comes on when the patient goes to bed and is relieved by hanging the foot out of the bed

- The ischaemia is so severe that at rest the foot skin, muscles, bones are ischaemic at rest. This means that there is not enough oxygen to provide for the cells basic metabolic requirements

- If left untreated then will progress to: 


Outline normal lower limb circulation


Outline aortoiliac occlusion


Outline common iliac occlusion


Outline common femoral occlusion


Outline superficial femoral artery occlusion


What is ischaemic muscle pain?

- When muscle is ischaemic the pH drops and this is thought to be a key factor in stimulating pain afferents (nociceptors) in muscle. Substance P, a neuropeptide is released locally which then increases the sensitvity of pain afferents in muscle

- Ischaemia means insufficient blood supply to a cell, tissue or organ. It is the lack of oxygen that is particularly damaging