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a;lskdjf > 10 and 11 - Peripheral Vascular Disease > Flashcards

10 and 11 - Peripheral Vascular Disease Flashcards

1
Q

What is peripheral vascular disease?

A
  • Any compromise of the circulation outside of the heart

Arterial

  • Occlusive vs. Functional
  • Peripheral Arterial Occlusive Disease (PAOD) = most common vascular disease

Venous

  • Varicose veins
  • Valve disease
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2
Q

Etiology of arterial vascular disease

A
  • Atherosclerosis (narrowing of the artery) = most common etiology
  • Mechanical occlusive disorders
    o Thrombi (clot)
    o Emboli
    o Hematological disorders
  • Vasculitis and arteritis = acute problem of inflammation
  • Buerger’s Disease (thromboangiitis obliterans) = related to smoking, very severe arteritis
  • Vasospastic disorders = Raynaud’s is the most common (functional problem)
  • Combination of factors listed above
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3
Q

Arterial atherosclerosis

A
  • Intimal and smooth muscle proliferation
  • Accumulation of matrix & lipids
  • Results in narrowing, hardening or weakening
  • Provides nidus for thrombus
  • Provides source of emboli
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4
Q

Atherosclerosis risk factors

A
  • Hypertension, hyperlipidemia
  • Diabetes
    o Most common occlusion is under popliteal at the “trifurcation”
    o Diabetics tend to develop more severe peripheral arterial disease at a younger age
  • Advanced age, male Gender
  • Family History
  • Stress
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5
Q

Clinical manifestations of PVD

A
  • Diminished or absent pulses due to arterial occlusion
  • Pain
    o 1st = Leg pain with walking (claudication)
    Claudication is a problem with exercise, but they may never have an ulcer form
    o 2nd = Ischemic rest pain
    A progression from claudication – more severe, critical ischemia***
  • Slow healing wounds and tissue damage (ulcer or gangrene)
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6
Q

Clinical indicators of the quality of distal perfusion

A
  • Pulses and capillary refill time
  • Skin color and temperature
    o Rubor on dependency (purple legs when they are hanging down)
    – Due to ischemia and toxic byproducts in the skin
    – When you elevate this foot, it will rapidly become very white (pallor)
    o Pallor on elevation (Buerger’s sign)
    – When the elevated foot is white (pallor)
    o Acrocyanosis (bluish or purple coloring of the hands and feet caused by slow circulation)
  • Skin tone and turgor (hydration)
  • Hair growth on toes (hair needs oxygen to grow) and status of nails
  • Presence of tissue injury (gangrene, ulcers)
    o Gangrene  a type of necrosis caused by a critically insufficient blood supply
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7
Q

Ischemic ulcers

A
  • Dry, distal ulcers that cause severe pain (unless neuropathy is present in the limb)
    o Ischemia is typically painful (same as a heart attack)
  • Ulcers have irregular edges, poor granulation (new tissue formation) and exhibit little bleeding with manipulation (by definition, little blood is present)
    o Other signs of arterial insufficiency present as well
  • Generally you do NOT debride the tissue right away – priority infection/circulation assessment
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8
Q

Clinical features of ischemic ulceration

A

o Distal extremities (as we get more distal, the arterial system is smaller, more vulnerable)
o Full thickness (through all layers of skin)
o Dry necrosis (unless infected) with poor granulation
o Variable locations and spontaneous expansion of affected areas
o Poor pedal pulses and Doppler signal

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9
Q

Associated findings with ischemic ulceration ***

A

o Pain (claudication, night pain, rest pain)
o Dependent rubor, elevation -pallor
o Skin atrophy and nail dystrophy
o Decreased skin temperature

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10
Q

REVIEW - arterial ulcers

A
  • Distal extremities, full thickness ulceration
  • Dry necrosis with poor granulation
  • Spontaneous expansion
  • Pain, atrophy, pallor and rubor
  • Poor pulses and Doppler
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11
Q

Arterial thrombus

A
  • In situ (local) clotting occluding the vessel
  • Gradual onset of worsening ischemia
  • Signs of arterial disease
  • Atheroma already present
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12
Q

Arterial embolus

A
  • When a portion of a proximal plaque breaks off and continues to flow until it reaches an artery that it can’t fit through
  • Sudden and severe ischemic symptoms
  • No preexisting arterial symptoms
  • Identifiable source of free body (atrial fib)
  • Signs of PAOD not necessarily present
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13
Q

Embolus pathology

A
  • Proximal atheroma or clot (thrombus) breaks off and floats distally, causing an acute onset
  • Ischemic damage is based on the distribution of the occlusion
  • Pulses may be normal and 85% of emboli are cardiac in origin (A-fib)
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14
Q

What to focus on so far

A

NEED TO KNOW THE CLINICAL SIGNS AND SYMPTOMS OF THE OCCLUSIVE PHENOMENONS

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15
Q

Raynau’d phenomenon

A
  • FUNCTIONAL arterial problem
  • Epidemiology
    o 2% of the population experiences Raynaud’s phenomenon
  • Pathophysiology
    o Episodic reduction in peripheral blood flow in response to cold exposure or stress
    o This is NOT an occlusive (atherosclerotic) disorder, but rather a vascular malfunction
  • Skin color changes
    o White – ischemia from vasoconstriction
    o Blue – venous stasis
    o Red – hyperemia
  • Sensory changes
    o Pain and paresthesias (“pins and needles”)
  • Treatment
    o Nifedipine
    o V Prostacyclin or prostaglandin E1 for severe cases
    o Evening primrose oil
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16
Q

Venous ulceration anatomy

A
  • Arterial system
    o High pressure system of blood “in flow”
  • Venous system
    o Low pressure system of blood “out flow”
    o Includes superficial veins, deep veins, perforating veins, all with one way valves
  • Valves
    o Veins have one-way bicuspid valves opening to the deep system
    o The valves close when pressure rises in the deep system preventing retrograde flow
    o Transmission of elevated pressure to the superficial veins
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17
Q

Venous pressure

A
  • Normal Resting Venous Pressures at ankle in standing position is 60-90mmHg
  • Venous insufficiency increases the pressure and amount of blood in the venous system (pooling)
  • High pressure induces mechanical and physiologic effects in the vein w/ secondary skin changes
18
Q

Venous pump in foot and calf

A

o This is the primary mechanism to return venous blood to the heart
o “Calf pump” muscle contraction can increases venous pressure, to force blood to the heart, but more and more research is pointing to a greater role of the “foot pump”
o Emptying the deep system decreases venous pressure, opening the valve and forcing blood from the superficial to the deep system

19
Q

Foot pump history and anatomy

A

o Le Dentu 1869
– Recognized venous foot pump, hypothesized muscular activity powers pump
o Gardner 1989
– Venous emptying occurs prior to muscular contraction in gait
– Clarified the motor of the pump to be direct compression and/or stretching of the veins in the sole of the foot
– Correlates with clinical observations of improved post-traumatic and surgical swelling with early ambulation

20
Q

Hemodynamics of foot pump

A

o Impulse pumping causes a sudden rise in venous pressure which causes a greater percentage of the venous capillary loops to open causing proximal drainage
o Direct stretching and compression of the plantar foot veins is the mechanism (NOT Muscular)
– This is a DIRECT mechanical function  NO muscular function
– ***This means that it is very important for your venous patients to be walking
o Powerful enough to displace a column of blood from the LE to the heart
o Venous pump is powerful enough to move blood past a 100mm/hg cuff
o Venous priming opens closed arterial capillaries and reduces tissue pressure
– Hyperemic flow lasts 20 seconds after each impulse and increases popliteal artery flow by 93% in normal arteries and 84% in PAOD
– Local release of endothelium derived relaxing factor dilates vessels and increases capillary flow

21
Q

Pressure-induced vein pathology

A
  • Dilation of venous system (varicose veins) and increased venous permeability lead to fluid retention (pooling of blood)
  • There will be bi-directional flow (valve failure) and shunting of blood from deep to superficial
22
Q

Venous insufficiency physiology

A
  • Varicose veins = genetics, standing, high abdominal pressure
  • Incompetence of valves = aging, genetic defects, DVT
    o DVT: the clot forms around the valve, so even after the DVT is resolved, the valve is ruined and no longer prevents blood from pooling in the lower extremity, leads to residual edema in the leg and foot
  • Pump failure = age, arthritis, immobility
23
Q

Venous ulcer pathophysiology

A
  • Arterial-venous shunting
  • Fibrin cuff theory
  • White blood cell trapping theory
24
Q

Arterial-venous shunting

A

o Fistulae divert blood away from dermis = Ischemia
o If you have higher pressure in the venous system, there is less flow in the arterial system, meaning you will have ischemia

25
Q

Fibrin cuff theory

A

o Fibrin “leaks” out and is transformed to fibrinogen, damaging the vessels themselves
o Cuff surrounding capillaries impedes oxygen - tissue exchange leading to tissue death

26
Q

White blood cell trapping theory

A

o Distended veins lead to decreased velocity of blood flow
o White blood cells allowed to separate from plasma and migrate from vessel into tissue
o Release of proteolytic enzymes contributes to endothelial and tissue damage
o These enzymes are very irritating and damaging to the tissues, causing derm problems

27
Q

Symptoms of venous stasis

A
  • General
    o Pain, burning, heavy feeling
  • Skin manifestations of stasis
    o Edema (chronic, distal, pitting)
    o Induration (hardening/change in turgor)
    o Varicose vein formation (could also be deep venous system with no varicose)
    o Erythema (redness)
    o Hyperpigmentation (hemosiderin – iron byproduct buildup in the skin)
    o Dermatitis (irritation/infection of the skin) and ulceration (end stage dermatitis)
28
Q

Lipodermatosclerosis

A
  • End stage severe scaring (intradermal scaring of the skin)
    o If this ulcerates, it is extremely difficult to get it to heal because this skin is so unhealthy
  • Severe induration (hardening) and tight bound skin
    o Swelling and venous pressure/fluid leaking and damage from enzymatic products cause chronic scarring of the skin, meaning that the skin never recovers, it is just replaced by scar tissue

Notes
o Chronic scarring in the skin
o Swelling, venous pressure, fluid leaking, damage from enzymatic products
o Skin does not recover, it is replaced with scar tissue

29
Q

Venous ulcer characteristics

A
  • Large, superficial ulcers with irregular borders and fibrous, granular tissue with high drainage
  • Most common on the hind foot and ankles, less common on the forefoot
30
Q

Treatment

A
  • TREAT THE CAUSE, NOT THE SYMPTOMS
  • Rule out PAOD and other causes of ulceration
  • Systemic treatment of edema (edema is causing the ulcer)
  • Identify and treat infection, local reduction of edema***
31
Q

Edema reduction

A
  • Sustained compression is the cornerstone
    o Increased volume flow
    o Activation of calf pump
    o Decreased venous blood volume
  • Elevation above heart level (is this realistic?), pneumatic pumps (ICD leg pumps)
  • Walking rather than static dependency (foot pump is activated)
32
Q

Compression therapy

A
  • Circumferential compression in acute phase to effect rapid reduction in the edema
  • Multi-layer better than single layer
  • 40 mm/hg pressure at the ankle graduated to 17 mm/hg at the knee is the goal
    o Graduated means the pressure increases as you move up the leg
  • Maintenance with short stretch elastics or non-elastic bandages
  • Maintain activity to maintain foot pump
33
Q

Level of compression

A 
Low = 20-30 mmHg
Moderate = 30-40 mmHg
High = 40-55 mmHg 
TEDs = 18 mmHg (NOT GRADUATED)
34
Q

TEDS

A
  • Does NOTHING for an ambulatory patient – not enough compression to get the edema out
  • Need graduated (elastic) bandages if you want the swelling to get better
  • TEDS are for hospital patients lying in bed, they are NOT graduated
35
Q

Elastic compression

A

Reduce swelling
o Long stretch (ACE, multi-layer systems)
o Short stretch (stockings)

36
Q

Non-elastic compression

A

Maintain swelling
o Unna’s Boot
o CircAid Boots

37
Q

How can you consistently graduate compression?

A
  • Law of Laplace  Pressure = 2x tension / radius of leg
38
Q

NEED TO KNOW

A
  • Circumferential elastic bandaging OBTAINS the result

- Inelastic wraps or socks MAINTAIN the result

39
Q

What does compression do?

A
  • Reduces venous hypertension
  • Increases venous return velocity
  • Reduces exudation from the veins into the tissue
    o By reducing transmural pressure gradients, thereby reducing skin irritant factors
  • Improves arterial flow
40
Q

Multilayer compression

A
  • Double cast padding layer from toes to tibial tuberosity
  • Two six inch ACE bandages with 50% overlap from toes to knee
  • Even graduated compression
    o Law of Laplace
41
Q

Compression stocking

A
  • 40 mmHg = required to reverse chronic venous hypertension
    o Very difficult to achieve with stockings
    o TEDS stockings = 18mmHg, non-graduated
    o Stockings do not provide adequate compression at the ankle in most cases
  • Effective for long term maintenance in selected patients
42
Q

Unna boot

A
  • Rigid bandage with no active compression, so not used for ACUTE venous stasis edema
  • Can produce tourniquet if improperly applied – devastating effects
  • Zinc oxide is a good wound interface

a;lskdjf (11 decks)

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