Circulation in lower extremities

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					Patophysiology of blood and lymph
  circulation in lower extremities

   Assoc. prof. Jana Plevkova MD, PhD
     Department of Pathophysiology
  Jessenius Faculty of Medicine in Martin
Blood circulation is sophisticated system which conduct
  the blood from the heart and lungs into the tissues
  - it's main function is to provide suitable metabolic
supply to the cells /oxygen, substrates/, aw well as the
     cleavage of metabolic products from the tissue

   vessels – resistance, capacity, capillary network,
    other specific vascular structures
   high pressure / low pressure part of circulation
   regional specific circulations
Arterial system of lower extremities

   source :
            Principles of blood flow

science discipline analyzing the flow of the blood
  within the circulation

             P. .r4
                                  Q – blood flow
                                  P – pressure gradient
                                  between two different points
                                  of the tube /vessel/
                                  r – vessel diameter
                                  l – vessel length
                                   - blood viscosity
        Arterial system of lower extremities

-a part of high pressure circulation

Energy of the heart ejection /systolic effort/ continues into
1) frontal pressure, responsible for the forward movement
    of the blood within the vessel
2) lateral pressure affecting the wall of the artery causing
    it's distension, giving the base for the pulse wave

laminar flow (flow within individual layers smoothly gliding
    one on another )
- This mutual gliding is responsible for the tangential
    tension among the layers and most external layer and
    endothelium, as well (shear stress)
shear stress – this mechanism is able to influence
   some of the regulatory and secretory functions of
   the endothelium

Turbulent flow within the blood stream could be
    physiological only at the sites of wide vessels
-   aortal arc, pulmonary artery, site of the vessel
    branching, sudden bending of the vessel

Predisposition for turbulent blood flow
- wide vessel
- sudden change of the diameter
- high blood flow velocity
- low blood viscosity
- uneven endothelial surface
The blood flow in the arteries has three phases, due to
    elastic properties of the vessel wall

1st phase – forward movement of the blood caused by
    ventricular contraction – systolic ejection. Vessel wall
    is distended during this phase, because of lateral
    pressure applied onto the vessel wall

2nd phase is characterized by return of the distended
    vessel diameter into the former size – elastic recoil
    the flow is directed to the beds with low resistance

3rd phase of the diastolic period – the flow is directed
    forward again
Regulation of the blood flow in lower extremities

Relative constant pressure gradient – diving pressure is
  constant, so regulation is secured predominantly by the
  change of vessel resistance – change of vessel diameter

1.   myogenic (Bayliss regulation)
2.   metabolic (autoregulation) lactic acid, CO2, H+, K+, adenosin
3.   other humoral factors (catecholamine, histamine, acetylcholine,
4.   nerve regulation - sympathetic fibers
Endothelium – is not only a mechanical barrier

It has high metabolic activity, participates in vessel
reactivity, regulation of thrombogenesis, influences the
functions of circulating cells

Endothelial surface – 500 - 1000 m2 – contact surface for
the mediation of „signals“ between circulating cells and
intimal surface

It seems to be the largest endocrine organ /1500g/

Metabolic and secretoric systems influence mainly vessel
tone therefore resistance and blood flow

Physiological tendency to vasodilatation
                        Endothelial vasodilators

   production of NO – from L arginine by NO synthasis – enzymatic process,
    new molecule of NO is released into the smooth muscle cells layer
    beneath the endothelium – activation of guanylatcyclase -  production of
    cGMP leads to relaxation of muscle cells and thus to vasodilatation

   production of NO is responsible for permanent „natural“ tendency to
    vasodilatation in arterial system

   production of NO is stimulated by – shear stress, platelets derived
    molecules like (ATP, ADP, serotonin), vessel distention – flow dependent

   NO is dominant vasodilator in basal conditions
   endothelium produce also other vasoactive substances like - PGI2
    (prostacyclin) PGE2, PGD2
               Endothelial vasoconstrictors

   endothelins, tromboxan A2, nonstable endoperoxides, and
    molecules of local RAA system

   Endothelins (1, 2, 3) – group of peptides containing 21
    AA, derived from molecule of proendothelin, which is
    fragmented to active molecules

   ETA a ETB receptors – vasoconstricting response, long
    lasting effects involve proliferative effects on smooth
    muscle cells within the vessel wall
                Endothelial dysfunction

Functional changes of the endothelial cells

   predominance for production of vasoconstricting
   increased production of cytokines
   increased permeability for plasmatic proteins and
   predominance of procoagulating processes
   increased production of CAM molecules
      Pathogenesis of diseases of arterial system of lower

Diseases with different ethiology may have the same, or
  very similar signs and symptoms
- So it is not correct to talk about „arterial occlusion“ only

Ischemia of lower extremities
- acute – sudden onset of ischemic attac /dangerous, bc
   of the risk of the lost of the extremity/
- chronic – long lasting ischemization, trophic changes...

-   Degenerative processes - atherosclerosis /ATS/
-   Aneurysmal arterial disease
-   Inflammation and thrombosis
-   Vasospastic disease
             Atherosclerosis obliterans
                   Risk factors
fatty and cholesterol containing diet
less fruits/vegetable/fiber diet
low concetration of HDL
+ family history for CVS diseases
increased fibrinogene level
male sex
 (Atherosclerosis obliterans - ASO)
 patogenesis of ATS – response of the vessel wall to injury

1.   functional changes of endothelial cells
2.   deposition of lipid particles into the vessel wall with subsequent
     reaction – creation of fibromuscular plaque
3.   chemotactic activity of monocytes – fagocythosis of lipid particles of
     macrophages (foam cells)  lipid plaque

Formation of ATS plaques of different size and position in the
    arterial system of lower extremities

   turbulent flow at the site of the plaque location
   presence of the plaque may lead to „serious“ stenosis limiting the
    blood flow
   damage of the vessel wall due to plaque may lead to weakening of
    media and formation of aneurysma
   bleeding into the plaque with possibility for formation of false
   dysrupture of the plaque with subsequent thrombosis of the artery
   abruption of the plaque and embolization of those fragments into
    more peripheral circulation
    acute or chronic ischemization of extremity
                                         Arterial aneurysms

Arterial aneurysms – localized dilatation of the vessel wall

1)   True aneurysms – consist of all three layers of arterial wall, usually
     has fusiform or circumferential shape, the underlying condition for
     such a dilatation is weakening of the vessel wall due to some
     pathological process – mainly ATS

The damage of the vessel wall with weakening of media could be
    acquired (atherosclerosis, inflammation, toxic ifl.) or inherited
    (syndroms with weak connective tissue like sy. Marfan)

2)   False aneurysms – extra vascular accumulation of blood with
     disruption, two or all three vascular layers  the wall of the
     aneurysms is formed by thrombus and adjacent tissues, or
False aneurysms is usually consequence of trauma, or complication of ATS
Whatever the cause, the aneurysm becomes progressively
 larger !

   tension within the vessel wall is directly influenced by the diameter
    and the lateral blood pressure
   localized dilatation of the vessel at the site of aneurysms leads to
    increase of diameter and therefore enhance the tension within the
    vessel wall, what again may enhance it´s enlargement

 Ischemia below the location of aneurysma
 Acute thrombosis at the site of aneurysma
 Dysrupture of aneurysma
 Embolization of the thrombus into the more peripheral circulation
Inflamatory diseases – Thrombangitis obliterans
Burger´s disease

Inflammatory disease of small peripheral arteries

   chronic inflammatory process
   inflammation is localized at the intima of affected vessels,
    and thrombosis is just a secondary consequence of it
   affected vessels are prone to vasospasm
   affected are mainly tibial and plantar arteries
Etiopathogenesis of the disease is unknown
 affected population - men 20 – 40 yrs, smokers,

Disease has three stages
1)    inflammatory and spastic phase (phlebitis saltans,
2)    obliterative phase with symptoms and signs of
3)    gangrene
Vasospastic diseases

Attacks of sudden constrictions of small diameter arteries and
   arterioles of upper and also lower extremities, commonly
   fingers, sometimes toes

Raynaud disease – primary vasospastic without   any obvious or
  clear cause, most affected are young ladies

Raynaud phenomenon – syndrome, secondary problem usually
  linked with systemic collagen diseases, autoimmune diseases,
  toxic influences, long lasting vibration exposition, ...
Raynaud disease

In spite the cause is unknown, there was identified hypetrophy of
   myoepithelial cells, which participate in regulation of blood supply to
   the capillary bed and hyperplastic changes of a-v- anastomoses

   cold or emotional stimulus is usually the provoking factor, leading to
    severe vasoconstriction, blood is redirected through a-v anastomoses
    into the venous system, while the capillaries are compromised

Typical three phasic color changes of the skin, changes are
   always symetric
a) sudden pallor (dogiti mortui)
b) followed by cyanosis
c)    finally redness caused by reactive hyperaemia
Raynaud phenomenon

   It is only a sign (manifestation/ of other primarily well
    defined disease
   Example: systemic lupus erythematodes, primary
    pulmonary hypertension, some endocrine disorders –
    myxedema-, exposition to vibrations, intoxication with
    ergot (claviceps purpurea)

Symptoms are asymetric, affected persons are both men
  and women
All mentioned diseases may lead to acute or chronic
   progressive obliteration of the vessel lumen.

Obliteration of the lumen increases the vessel resistance.

Increased resistance means - decreased blood supply to the
  affected region with a possibility of ischemia.
Occlusive arterial disease

Chronic occlusive arterial disease  ischemia as a result of
 arterial obstruction

Obstructive arterial lesions occur more frequently in the lower
 extremities than in the upper extremities.Obstruction
 influencing the blood flow to lower extremities is usually
 localised. at:
                   - aortoiliac level

                   - femoropopliteal level

                    - popliteo-tibial level

- arterial lumen is progressively narrowed  resistance
  to blood flowblood flow to the tissue below the lesion
  is reduced  tendency to tissue ischemia

- vessel lumen must be reduced by approximately 50% in
  diameter or 75% in crossectional area to produce clinically
  significant interference with blood flow

- in combination (stenosis occurring in sequence), less
  significant lesions can seriously impair blood flow
  Stenosis less than 75% of crossectional area is not
  compromising blood flow during the rest condition, but
  during the physical exercise – it could interfere with the
  blood supply leading to ischemia

At the site of stenosis and below the stenosis we can see changes of
   the blood flow like
- acceleration of the blood flow at the site of stenosis
- turbulent blood flow below the stenosis with recirculation of the
   blood, whirls (murmors present above the affected vessel
- poststenotic dilatation with possibility for thrombogenesis
Example for stenosis occurring in sequence, less significant
  lesions can seriously impair blood flow

When small nonsignificant stenosis may lead to ischemia?
 During physical exercise (O2 requirements,
  vasodilatation in working muscle, decrease of driving
 During elevation of the extremity (no hydrostatic effect
  supporting the blood supply)
Intensity of ischemic damage depends on –

   the site /level/ of the vessel occlusion – aortoilic,
    femoropopliteal, popliteotibial level
   extent and seriousness of stenosis
   time course of occlusion development /acute vs. chronic/
   presence and quality of collateral circulation

Collateral circulation is unique and important compensatory
  mechanism of long lasting, progressively worsening
  ischemia. Increased resistance of affected arteries is
  responsible for „opening“ of collateral circulation. Mainly
  muscular arterial branches could be base for collateral
Symptoms and signs of occlusive arterial disease

chronic course - usually ATS

 claudicatio intermittens
 pain at rest
 no pulse
 postural changes of the skin color
 temperature gradient bellow and above stanosis
 neurologic symptoms – paresthesis
 trophic changes of the skin, hair, nails
 atrophic muscles and soft tissues
 ulceration and gangrene – (dry, wet)
Symptoms and signs of occlusive arterial disease

acute course – thrombosis, embolisation, trauma

 dominant severe ischemic pain
 no pulse
 distal part below the stenosis is pale
 temperature gradient
 decreased filling of superficial venous system
 no trophic changes – there is no time for their
Occlusive arterial disease in patients with DM

macroangiopathy – ATS (in DM patients is accelerated)
-    hypertension
-    hyperlipidaemia and dyslipidaemia
-    impaired nutrition of vessel wall because of dysfunction of vasa vasorum

Damage of small diameter arteries and capillaries by
  generaliezed chronic complication of DM

    endothelial damage        (diffusion of glucose into the cells, change into sorbitol,
     endothelial swelling – endothelial dysfunction....)

In this group of patients – ischemic problems with lower
   extremities are very common, shifted to „younger“ age,
   and are usually complicated by immunodeficiency and
   metabolic disorder /worse healing of wounds/
Venous system of lower extremities

Blood flow in veins – lower extremities

   vis a tergo – rest of left ventricle ejection energy
   vis a fronte – suction of right atrium caused by up and down
    movement of AV junction
   negative thoracic pressure during inspiration
   craniocaudal movement of diaphragm
   corresponding changes of abdominal pressure
   horizontal body position
   rhythmic compression and decompression of deep venous
    system by muscles /walking/
   valves
   plantar venous mechanism
   pulsation of commitant arteries
Venous system of lover extremities

 superficial venous system
 (10% of venous returs)
 deep venous system (90% of
 venous return)
 system of perforating veins

 Physiological pattern of
 venous return from lower
Function of the valves

If the valves are working properly:
 they completely prevent pervasion of the blood from deep into
    superficial system
 they redirect central blood flow within the deep system
 they prevent retrograde blood flow from the upper level, if once the
    blood was ejected by muscle pump to upper level. During the muscle
    relaxation they completely prevent backward blood flow to more
    distal levels.

Pathological process affecting mainly superficial venous system.
   Primary affection is inflammation of spa. vein by the process
   spreading from the surrounding tissue

Creation of thrombus is usually secondary phenomenon superimposed
   to inflammation.

Thrombus is fixed to the vein wall by fibrin connections between the
   thrombus and inflamed vessel wall. The process is usually localized
   to the site of inflammation, no or minimal systemic symptoms, only
   local signs of inflammation.
No risk of emboli, b/c the thrombus if fixed onto the vein wall, and as
   well is localized within the superficial system.
Deep venous thrombosis DVT

 - intravital coagulation of the blood inside the vessels
 - physiological mechanisms against thrombosis
 continual blood flow
 intact endothelium
 balance in production of pro and anti coagulating

Impairment of those three mechanisms , known as
  Virchow´s trias has crucial role in pathogenesis of DVT.
Predisposing factors for DVT

 history of DVT
  immobilization (slowness of venous return from LE DK)
 senior age (polymorbidity, dehydration, change of
  rheologic properties of the blood)
 obesity, malignity (production of procoagulating factors)
 heart failure, decompensation (venous congestion in
  backward failure)
 surgical procedures, trauma (release of tissue
 pregnancy, puerperium, abortion (occlusion of pelvic
  veins by pregnant uterus, enhanced coagulation, tissue
  of trophoblast)

Slowing of the blood flow during immobilization, or in case
   of procoagulative status the blood there is a possibility of
   deposition of small amounts of fibrin at the site of vein

The fibrin deposition is growing progressively by apposition
  of „new“ fibrin fibers and platelets trapped into the fibrin
  matrix – formation of thrombus

The thrombus is a serious occlusion, which impairs or
  completely blocks the venous return through the
  affected deep vein

disease/article/136677   /
Venous return from affected extremity
• the blood flow in central direction
through affected vein is blocked by the
•muscle contraction eject the blood into
the surrounding deep vein /deep veins are
usually doubled/ via anastomosis
• this deep vein provide central flow of the
blood, which is of course limited – so
venous return as a complex process is

 In this phase of DVT the blood
does not flow into the spf. System,
b/c perforators and their valves are
not affected/destroyed, YET.
Venous return in a stage of recanalisation

Muscle contraction ejects the blood into
three directions
•through partially recanalized vein upwards
• through anastomosis into surrounding
deep vein
•through perforating veins /which valves
are destroyed/not working / into the spf.

During muscle relaxation – spf. veins are
emptying only partially into the deep veins,
with sudden balancing of the pressure in
both systems.
Blood is cumulating in spf. veins – leading
to permanent hypertension in spf. system
and recanalized part of deep venous
Venous return after total recanalisation

Total recanalisation means healing of the vein, desobliteration,
   consequence of this process unfortunately is fibrotisation, or
   destruction of the valves.

During muscle contraction the blood from deep vein is ejected into
   three directions
-to SPF veins b/c of insufficient valves of perforating veins
-to central direction through recanalised vein upwards
-to central direction through surrounding deep vein

Muscle relaxation: tendency for downward blood flow with rise of
  pressure in deep system, therefore emptying of spf. veins which had
  to be enhanced by the „suction“ of negative pressure is limited

   physiological pattern of venous return is affected
   onset of hypertension in spf. system and retrograde

Venous congestion – consequence for the capillary
Congestion leads to
- rise of hydrostatic pressure at the venous end of the
- hypoxic damage to the endothelial cells
- increase of capillary permeabilityh and therefore
  transudation of fluids into the pericapillary space
          Symptoms and signs of DVT
-   Depends on the level of deep system which is altered by
    thrombosis, crural thrombosis – pain, asymetric edema,
    fever – not so severe symptoms

Ileofemoral level
- severe pain
- edema, feeling of „heavy“ leg,
- dilatation of superficial veins
- skin is stretched, pale or cyanotic /according the
   progress of disease/
- phlegmasia alba/coerulea dolens
- always fever, shivering, general symptoms, restlessness,
 Cyllindric or saccular dilatation of spf. veins usually linked with relative
   valve insufficiency
Primary varices
Secondary varices

Primary varices
 genetic predisposition, inherited insufficiency of connective tissue,
   abnormal collagen moleculle,
The vein´s wall is weakened because of abnormal connective tissue, less
   tonus of muscular layer  passive dilatation of the vein

Supporting risk factors
 repeated increases of the pressure in spf. veins
 long lasting sitting, or standing without muscle contractions, obesity,
Secondary varices

Always as a consequence of DVT, and valve damage

– dilatation of vein enhances more and more relative
  insufficiency of the valves in perforating and spf. Veins

Muscle contraction ejects the blood upwards, but also into
  the spf. system, what is not physiological - spf. venous
Chronic venous insufficiency

CHVI – due to inappropriate venous return form the lover extremity as
  a consequence of severe impairment of hemodynamic mechanisms
  of venous return itself, is always linked with hypertension in spf.

Venous hypertension in lover extremities
Retrograde venostasis with simultaneous imbalance of hydrostatic
   pressures within the capillary – Starling mechanism
 transudation of fluids into IST space  edema
 endothelial hypoxic damage
 increase of capillary permeability
 transudation of proteins, RBC into he IST space
 fibrotic processes within IST space
Symptoms and signs of CHVI

 pain – venous claudication, improves during elevation
  of extremity
 edema
 induration and thickness of subcutaneous tissue
 hyperpigmentation    of the skin – caused by
  hemosiderine from RBC trapped and destroyed within
  the tissue
 trophic changes (sclerosis of the skin, ulcerations, scars
  after ulcers healing) – edema and fibrotisation limit
  transport of oxygen and substrates to the tissues,
  that´s why we have trophic changes
 ulcus cruris


Lymphatic system provide filtration of the
blood, participates in immune reaction
and production and outflow of lymph is a
part of Starling balance.

Lymphedema – edema of the tissue due to
impaired production and/or outflow of the

 - no pain
 - in this case the fluid contains considerable amount of

Dysfunction of lymphatic system could be:

inherited (inherited hypoplasia of lymphatic capillaries and vessels –
  Sy. Nonne – Milroy) , lymphedema is usually symmetric, affecting
  both extremities, in kids

acquired (obstruction of lymphatic vessels or nodes by tumor, scar
  tissue, parasites, external compression, etc), lymphedema is usually
  asymmetric, mainly adults
Mechanisms involved

1)   static insufficiency of lymph. system – decrease of the
     transport capacity of the normal ly. system, volume of
     produced lymph within the tissue is normal /block of ly.

2)   dynamic insufficiency of lymph. system – ly. system is
     intact, but is not able to drain lymph from the tissue,
     because of overproduction of the lymph
     - localized regional inflammation
     - venous congestion
Lymphedema is chronic progressive pathological
- accumulation of the protein molecules within the tissue
- edema (osmotic action of proteins)
- chronic inflammation
- fibrosis

Consequence: fibrotic obliteration of ly. Vessels and/or
  nodes  decreased transport capacity leading to total
  block of lymphatic flow
– onset of blisters in affected area
– repeated inflammations of the skin and subcutaneous
– hyperkeratosis and papilomatosis of the skin
Signs and symptoms

   soft edema of the extremity, dough like consistence
   touching or pressing with the finger can make several hollows, with
    slow alignment
   edema progressively gets more solid, creates folding
   typically it is not painful
   pallor, cold extremity, because of compromising of „normal“ blood
   lymph edema could crate bizarre shapes, leading to deformation of
    affected part of the body
   Long lasting lymphedema could lead to secondary skin affection like
    repeated inflammations caused by spteptococcus sp., or trophic

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