PVD Flashcards

1
Q

2 types of PVD

A
  • Arterial (PAD)
  • Venous (PVD)
  • Physiologically both present as insufficient tissue perfusion
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2
Q

PAD: Facts (Bloods)

A
  • atherosclerosis can affect any arteries in the body
  • in the neck or brain = risk for stroke
  • In the arteries of the legs = pain, tissue damage, and gangrene
  • most commonly: claudication
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3
Q

PVD: Facts (Crips)

A
  • Phlebitis
  • DVT
  • PE
  • Chronic venous insufficiency
  • Varicose veins
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4
Q

PAD: Guidelines

A
  • Emphasizes use of ankle-brachial index (ABI) measurements for earlier diagnosis
  • Increased attention on smoking cessation
  • Better use of antiplatelet and other antithrombotic medications
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5
Q

PAD: Causes

A
  • Atheroscleriosis (plaques of cholesterol forms on arterial wall) vs. arteriosclerosis (hardening of arteries)
  • Lower extremity PAD may be atherosclerotic, thromboembolic, inflammatory, or traumatic
  • Common Causes: *Atherosclerosis, blood clots, trauma, spasms, congenital structural defects, and venous incompetence 2/t valve obstruction
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6
Q

PAD: Risk factors

A
  • Smoking
  • Age
  • Gender
  • HTN
  • HLD
  • DM
  • Hyperhomocysteinemia
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7
Q

PAD in lower extremities

A
  • Asymptomatic LE PAD
  • Intermittent claudication
  • Chronic ischemic limb pain
  • Acute ischemic limb pain
  • Lower extremity limb pain
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8
Q

Leg Pain: Causes

A
  • Problems with blocked blood vessels and poor circulation
  • Problems with bones and joints: Arthritis of knees, ankles, and hips
  • Nerve problems: Sciatica, diabetic neuropathy
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9
Q

Focus on PAD

A
  • 50% of pt’s with PAD are asymptomatic
  • The most common symptoms are intermittent claudication and rest pain
  • Intermittent claudication is pain or cramping in arms or legs that occurs with exercise and subsides with rest
  • Severity and location of the pain depends on location and extent of blockage of involved artery
  • Most common location is calves
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10
Q

Atherosclerosis: Target organs

A
  • Carotid-> Brain-> TIA/stroke
  • Aortic/Iliac-> Legs-> Intermittent claudication/impotence
  • Renal-> Kidneys-> HTN/ESRD
  • Mesenteric-> Intestines-> Ischemic bowel
  • Femoral, popliteal, tibial-> Legs-> Intermittent claudication, rest pain, amputation
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11
Q

Rest Pain

A
  • Occurs when artery occlusion is so critical there is an O2 deficit in lower extremities at rest
  • Typically affects feet, is usually severe, and occurs at night when patient is supine
  • This is critical limb ischemia (CLI)
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12
Q

PAD: Other symptoms

A
  • Numbness of extremities
  • Weakness and atrophy of calf muscle
  • A feeling of coldness in the legs or feet
  • Changes in color of feet: Pallor when elevated/rubor in dependent position
  • Hair loss over dorsum of feet
  • Thickening of toenails
  • Painful ulcers and/or gangrene in tissue with CLI; typically in toes
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13
Q

Claudication

A
  • Symptoms of leg fatigue and cramps that patients with PAD describe when they exert the muscles of the legs
  • Severity of ichemia can be classified according to either the Fontaine or Rutherford categories
  • Iliac arteries -> pain high in thigh and buttocks while walking
  • Femoral/popliteal arteries -> pain in calves
  • Tibial -> pain in feet
  • Leriche syndrome: intermittent claudication and impotence with clinical significant decreased or absent femoral pulses = narrowing of aorta
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14
Q

Goals for Treatment of PAD

A
  • Limb outcomes: Improved ability to walk, increase in peak walking distance, improvement of QoL, prevent progression to CLI and amputation
  • Cardiovascular morbidity and mortality outcomes: Decrease in morbidity from non-fatal MI and CVA; Decreases in cardiovascular mortality from fatal MI and CVA
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15
Q

Management of PAD: Cardiovascular risk reduction

A
  • Antihypertensives
  • Diabetes therapy
  • Statins
  • Homocysteine lowering therapy
  • Lifestyle modifications
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16
Q

Management of PAD: Pharmacologic treatment

A
  • Cilostazol (Pletal)
  • Pentoxifylline (Trental)
  • ASA
  • Clopidogrel (Plavix)
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17
Q

PAD: Exercise

A
  • 3-5x/week
  • 35-50min
  • Treadmill or track walking to near-maximal claudication pain
  • > =6 months
  • 100-150% improvement in maximal walking distance and associated improvement in QoL
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18
Q

Lipid goals for PAD

A
  • Treatment with statin for LDL <70
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19
Q

Inflammation and Omega-3s

A

AHA Recommendations

  • Eat fish 2x/wk
  • Forms: fish, tofu, soybeans, walnut, flaxseed
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20
Q

Antiplatelet therapy: PAD

A
  • ASA: 75-325mg/day (early)

- Plavix 75mg/day (severe)

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21
Q

Vitamins to decrease homocysteine levels

A

B complex:

  • Folic acid
  • Cobalamin (B12)
  • Pyridoxine (B6)
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22
Q

Pharmacotherapy for claudication

A
  • Cilostazol (Pletal) 100mg PO BID (start at 50mg BID)
  • Platelet aggregation inhibitor; vasodilator; increases HDL; lowers TG; inhibits smooth muscle proliferation
  • Pentoxifylline (Trental): 400mg TID
  • Mild vasodilation; weak antiplatelet activity
23
Q

Cilostazol (Pletal): Black box warning

A
  • CI in HF of any severity

- Causes decreased survival in patients with class III & IV HF

24
Q

PAD: Lifestyle modifications

A
  • low-fat diet
  • regular exercise
  • tobacco cessation
  • foot care
25
Q

PAD: When to refer

A
  • Lower extremity pain with rest
  • severe claudication
  • prolonged pain
  • sudden color change or numbness in extremity
  • s/s of gangrene
26
Q

Critical limb ischemia (CLI)

A
  • limb pain that occurs at rest or impending limb loss that is caused by severe compromise of blood flow to the affected extremity
  • CLI should be used for all patients with all patients with chronic ischemic rest pain, ulcers, or gangrene attributable to proven PAD
27
Q

Treatment of CLI

A
  • Objective: increase blood flow to the affected extremity to relive pain, heal ischemic ulcerations, and avoid limb loss
  • Medical Mgmt.: antiplatelet agents, anticoagulants, maintenance of limb in dependent position
  • Treatment of infection
  • Use of non-weight bearing orthotics
  • Chronic CLI is associated with 1yr mortality >20%
28
Q

Acute Limb Ischemia

A
  • Rapid or sudden decrease in limb perfusion threatens tissue viability
  • “Blue toe syndrome”: shower of atherosclerotic plaque occludes previously healthy microarterial vessels in feet and toes
  • Aneurysm: typically popliteal artery; less commonly in femoral artery
  • 5 P’s: pain, pallor, paresthesia, pulselessness, paralysis + polar (cold extremity)
29
Q

Acute Limb Ischemia: Treatment

A
  • Hospitalization

- Heparin

30
Q

Upper extermity PAD

A
  • Same mgmt.

- Raynaud’s phenomenon: Unsure of cause; may or may not have vascular origin

31
Q

Occlusion of the peripheral veins

A
  • Varicose veins
  • Venous stasis/Chronic venous insufficiency
  • DVT
  • Stasis dermatitis
  • Ulceration of lower extremities
32
Q

Varicose Veins

A
  • Engorged superficial veins in the lower extremities
  • Treatment:
  • Exercise
  • Elevation of legs
  • Compression stockings
  • Sclerotherapy
  • Ablation
  • Laser therapy
  • Vein stripping
33
Q

Preventing varicose veins

A
  • Cross legs at ankles instead of knees when sitting
  • Avoid high heels, which limit the use of calf muscles
  • Avoid restrictive clothing which limit blood flow in groin and calf
  • Avoid prolonged sitting or standing
  • Take breaks to elevate legs or walk around to help move blood along and prevent valve failure
34
Q

Chronic venous insufficiency

A
  • Same causes as varicose veins
  • S/S: Swelling ankles; tightness in calves; legs feel heavy, tired, restless orachy
  • Sometimes feel pain while walking or shortly after stopping
  • Early treatment same as varicose veins
  • Later: Surgical bypass and repair
35
Q

Thrombophlebitis

A
  • Superficial Tx: Rest, pain relief, antibiotic, warm compresses, compression stockings
  • Deep vein thrombophlebitis: tx is anticoagulants and thrombolysis, same as DVT
36
Q

DVT: Facts

A
  • Formation of blood clots in veins depp in legs -> becomes life threatening when/if the clot breaks free
  • Anticoagulant therapy often doesn’t completely remove clots -> 33% develop post-thrombotic syndrome
  • Post-thrombotic syndrome: causes leg pain, difficulty walking, skin changes, and venous ulcers
37
Q

DVT and PE: Facts

A
  • Leading causes of preventable in-hospital mortality in US
  • PE is most common complication of DVT
  • Physiologically, occurs secondary to activation of coagulation in areas of reduced blood flow
  • Most successful prophylactic regulation are anticoagulation and preventing venous stasis
38
Q

Virchow’s Triad

A
  • Venous stasis + Vessel wall injury + Hypercoagulable state
39
Q

DVT: Causes

A
  • General: Age, immobilzation, pregnancy, major surgery, long plane or car trips
  • Medical: Cancer patients, CVA, MI, sepsis, ulcerative colitis
  • trauma: multiple fractures, lower extremity fractures, burns, CNS injury
  • Vasculitis: Lupus
  • Hematologic: Factor V leiden, etc.
  • Meds: chemo, IV drugs, OC’s (estrogen), menopause with estrogen replacement
40
Q

DVT: Diagnosis

A
  • Wells clinical prediction guide
  • Labs:
  • D-Dimer: Negative r/o; positive requires further testing
  • Venous duplex US
41
Q

DVT: Treatment

A
  • Bedrest
  • elevation of limb
  • Compression stockings
  • Pharmacotherapy w/anticoagulants or thrombolytics (prevent extension, stabilize, dissolve)
42
Q

Mgmt. of DVT: Anticoagulants

A
  • Heparin: Does not actively dissolve clots but inhibits further thrombogenesis and prevents reaccumulation of a clot after a spontaneous fibrinolysis
  • Lovenox: LMWH
  • Used in treatment of DVT and PE; used for prophylaxis; enhances inhibition of clotting factors and thrombin by increasing antithrombin III activity
  • Average duration of treatment is 7-14d
  • Generic equivalent just approved
43
Q

Fondaparinux Na (Arixtra)

A
  • For prevention of DVT/PE in at-risk patients undergoing ortho surgery
  • Synthetic anticoagulant; works by inhibiting a specific clotting factor; highly predictable response
  • T1/2=14-16hr
  • Does not affect Pt or PTT; does not affect platelet function or aggregation
  • initiate warfarin within 72hr; continue arixtra for 5d until warfarin effect established
44
Q

Dalteparin (Fragmin)

A
  • LMWH used as prophylaxis in ABD surgery and arthroplasty
45
Q

Tanzaparin (Innohep)

A
  • LMWH that inhibits clotting factors and thrombin bu increasing antithrombin
  • Increases inhibition of factor Xa
  • Average duration of Tx = 7-14d
46
Q

Outpatient care of DVT

A
  • Most patients w/confirmed proximal DVT may be safely treated as outpatient
  • Exclusion criteria for outpatient mgmt.
  • Treatment of 1st DVT is individualized
  • Discharge meds
  • Follow-up care and repeat Dx studies in 7d
47
Q

Length of treatment: Warfarin

A
  • PLT should be monitored and therapy d/c’d if PLT 3-6mo

- 2+ DVT -> 1yr

48
Q

Treatment for PE

A
  • Anticoagulation
  • Vena cava filter
  • Thrombolytic therapy
  • Percutaneous thrombectomy
49
Q

Complications of DVT

A
  • PE

- Hemorrhagic complications: d/c dug, FFP or platelets, Protamine or Vk

50
Q

DVT: Prognosis

A
  • Long-term risk of chronic venous insufficiency
  • ~20% of untreated (above calf) DVTs progress to PE -> 10-20% fatal -> w/anticoagulants, mortality 5-10%
  • Patients w/calf DVt should be reassessed in 7 days w/US
51
Q

Ankle-Brachial Index (ABI)

A
  • Noninvasive method of diagnosing PAD
  • High specificity and sensitivity
  • Ratio of highest ankle SBP (measured at DP or PT with doppler on BOTH legs)
  • Divided by the highest brachial SBP (must check both arms)
  • NL >1 (ankle SBP>Brachial SBP in healthy pt’s)
  • Resting ABI PAD
  • If you calculate >1 then use lower ABI
52
Q

ABI: procedure

A
  • Patient in supine pos.
  • Arms and legs at same level as heart
  • Must remain lying for 10min
  • Measure both side of each extremity
  • Measure both DP and PT and use higher
  • Divide ankle pressure by brachial pressure
53
Q

ABI: Results

A
  • 0-0.4 = severe PAD (REFER)
  • 0.41-0.9 = PAD sufficient to cause claudication (refer to vascular surgery)
  • 0.91-1.3 = NL (0.91-0.99: borderline -> refer for stress test)
  • > 1.3 = noncompressible, severe calcification