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PVD

Cardiology

QuestionAnswer
LE pain after long periods of standing. Dilated, tortuous, veins Varicose veins. Tx w/ compression stockings
Trendelenberg test of extremities Tests for venous insufficiency.
Blue extremities worse w/ cold exposure, improves w/ warming Acrocyanosis
PAD location: Buttock/Hip: Aortoiliac disease
PAD location: Thigh: Common femoral artery
PAD location: Upper calf: superficial femoral artery
PAD location: Lower calf: popliteal artery
PAD location: Foot: tibial/peroneal artery
PAD symptoms Intermittent Claudication (pain w/activity, often in calf); ischemic rest pain in severe disease; foot ulcers; ED
PAD Clinical Findings Diminished peripheral pulses, femoral bruits, cool skin temp, abnormal skin color, poor hair growth, ulceration, tissue necrosis; LE rubor (pallor with elevation)
Intermittent Claudication: contrasts with: pseudoclaudication of spinal stenosis (normal pulses/color)
PAD: Diff dx Baker Cyst; Chronic compartment syn; Arthritis; Nerve root compression; Spinal stenosis; Venous claudication
PAD Screen: ABI: Normal 1.0+ (blood pressure augments distally)
PAD Screen: ABI: < 0.9 dx of peripheral vascular dz
PAD Screen: ABI: < 0.7 intermittent claudication
PAD Screen: ABI: < 0.4 rest pain
PAD Screen: ABI: < 0.1 impending tissue necrosis
PAD Mgmt: Risk factor mod; SMK cessation; Walking program; antiplt tx (aspirin & clopidogrel); Pletal Trental; revascularization (Surgery vs Stenting)
ABIs helpful to predict: CLI (Critical Limb Ischemia) & amputation; wound healing; or to screen/ monitor
Acute arterial occlusion: Etiologies: EMBOLISM (valvular dz/prosthesis, AF, IE, MI, DM, myxoma, myocardial or proximal arterial aneurysm). Thrombus in situ (atherosclerotic plaque, trauma, hypercoagulable dz)
Acute arterial occlusion: Clinical Findings (5 P's): Pain, pallor, paresthesia, pulselessness, paralysis/weakness; Poikilothermia; possibly livedo reticularis (w/arterial occlusions) and cyanosis
Acute arterial occlusion: 80-90% of arterial emboli arise from: the heart
Acute arterial occlusion: A-fib prevalence present in 60-70% (thrombus forms in left atrial appendage)
Venous Dz Varicose V; Chronic Venous Insuff; Superficial Thrombophlebitis; DVT
Dilated, tortuous alterations of the saphenous v. & tributaries (lie immediately under skin in the LE) Varicose Veins
Varicose veins pathology related to: venous valve incompetence & subsequent venous reflux from increased pressure
Varicose veins Clinical Findings Asymptomatic to dull, aching pain or discomfort of legs usu worse after prolonged standing
Varicose veins - increased frequency after: pregnancy
Varicose Veins: DDx Secondary VV d/t: chronic venous insufficiency of deep vein; Retroperitoneal venous obstruction; Arteriovenous fistula; congenital venous malformation
Varicose: complications Thrombophlebitis
Sluggish blood flow in varicose v. => local thrombosis = Thrombophlebitis
Chronic V. Insuff: Pathophys: Functionally inadequate v. valves in LEs d/t bad leaflets (do not coapt) (poss 2/2 post-thrombotic syndrome or vein dilatation
Chronic V. Insuff: Tx Grad compression stockings; avoid long stand/ sit; elevate legs; last: pneumatic leg compressions
Inflammation, induration, erythema & tenderness along a superficial vein = Superficial Thrombophlebitis (usually long saphenous v.)
Superficial Thrombophlebitis: Clinical Findings fever, local pain, edema, linear erythema, warmth, & dull tenderness along affected vein; induration (palpable cord)
Superficial Thrombophlebitis: Tx: if progressive recurrence = Ligation surgery (if septic: PCN +/- aminoglycoside)
Superficial Thrombophlebitis: Tx if extension into deep venous system = Anticoagulation
Paroxysmal digital ischemia from exag response of digital arterioles to cold or emotional stress (fingers, toes, ears & nose) = Raynaud Phenomenon (may be 2/2 other dz state: scleroderma/SLE)
Raynaud: Excessive vasoconstriction causes: pallor
Raynaud: subsequent vasodilation (after vasoconstriction) causes: cyanosis then rubor (white to blue to red)
Raynaud Tx Lifestyle changes (gloves), CCB/ nitrates for chronic vasodilation; tx underlying condition
Fontaine and Rutherford systems are used to classify: severity of arterial occlusive disease
Thromboangiitis obliterans AKA: Buerger dz; M SMK 20-40 yo
LE rubor, pallor on elevation, no hair, brittle nails, calf or LE pain w/walking short distances, relieved w/rest; claudication with rest pain (ABI < 0.4) = Arterial insufficiency/PAD, intermittent claudication
Giant Cell Arteritis: clinical findings: Unilateral temporal HA; tender scalp; jaw claudication; visual (amaurosis fugax, scotoma, diplopia), pale fundi; aortic regurg murmur
Giant Cell Arteritis: 50% of patients also have: polymyalgia rheumatica
Sequela of Giant Cell Arteritis: Blindness due to ophthalmic artery occlusion
Giant Cell Arteritis pts: higher risk of: Thoracic aortic aneurysms (17X more frequent)
Most common cause of chronic lower limb occlusive disease Atherosclerosis
PAD hx Hx of intermittent claudication or rest pain
PAD S/S Diminished peripheral pulses, femoral bruits, cool skin temp, abnormal skin color, poor hair growth
PAD Clinical Findings Intermittent Claudication; ischemic rest pain; ulceration; tTissue necrosis
Intermittent Claudication: mx pain in LE induced by exercise and relieved with rest; highly reproducible
Intermittent Claudication: contrasts with: pseudoclaudication of spinal stenosis (normal pulses/color)
PAD Mgmt: Risk factor mod; SMK cessation; Walking program; antiplt tx (aspirin & clopidogrel); Pletal Trental; revascularization (Surgery vs Stenting)
ABIs performed to assess: Asx PAD or mild to mod claudication
Acute arterial occlusion: some due to embolism from: heart, aorta, large arteries
Acute arterial occlusion: Thrombus in situ due to: atherosclerotic plaque, trauma, hypercoagulable dz
Acute Arterial Occlusion Tx Revascularization; IV heparin; Intra-arterial thrombolytic therapy; Surgical thromboembolectomy; Surgical bypass
Dilated, tortuous alterations of the saphenous v. & tributaries (lie immed under skin in the Les) Varicose Veins
Varicose V. pathology related to: venous valve incompetence & subsequent venous reflux from increased pressure
Varicose V. Clinical Findings Asymptomatic to dull, aching pain or discomfort of legs usu worse after prolonged standing
Varicose v: Increased frequency after: pregnancy
Varicose: complications Thrombophlebitis
Sluggish blood flow in varicose v. => local thrombosis = Thrombophlebitis
Thrombophlebitis: predisposing conditions = pregnancy, local trauma, long periods sitting
Thrombophlebitis rarely: ascends in trunk of Gr saphenous v. & leads to thrombosis of femoral vein
Varicose V. Tx: Graduated compression stockings (TED); Elevate legs; endovenous ablation (radiofrequency vs laser); sclerotherapy; greater saphenous vein stripping (older)
Chronic V. Insuff: Pathophys: Functionally inadequate v. valves in LEs d/t bad leaflets (do not coapt)
Chronic V. Insuff: valve damage poss d/t: post-thrombotic syndrome (scarred/thick) or dilatation of vein & unable to coapt
Chronic V. Insuff: Clinical Findings Hx DVT/ leg trauma; EDEMA (below knees); brawney skin pigmentation & venostasis ulcer (above ankles); pruritic, dull discomfort(esp w/ long standing)
Chronic V. Insuff: DDx LE edema d/t: CHF; chronic renal dz; decomp liver dz; Lymphedema (usually unilateral); Autoimmune; PAD
Chronic V. Insuff: Tx Grad compression stockings; avoid long stand/ sit; elevate legs; last: pneumatic leg compressions
Superficial Thrombophlebitis usu involves what vein: long saphenous v.
Superficial Thrombophlebitis: spont occur in pt with: PG, blunt trauma, IV infusion, thromboangitis obliterans, abd ca;
Superficial Thrombophlebitis : assoc with DVT how often: 20% of cases
Superficial Thrombophlebitis: Clinical Findings linear erythema, induration, & dull tenderness along affected vein
Superficial Thrombophlebitis: Fever & chills suggest: septic phlebitis (IV line)
Superficial Thrombophlebitis: Circular lesion more consistent with: cellulitis
Superficial Thrombophlebitis: prevention: Avoid prolonged standing
Superficial Thrombophlebitis: Tx local heat & elevation, bed rest, NSAIDs; Sx usually resolve in 7- 10 days
Superficial Thrombophlebitis: Tx: if progressive recurrence = Ligation surgery
Superficial Thrombophlebitis: Tx if extension into deep venous system = Anticoagulation
Superficial Thrombophlebitis: Prognosis usually benign & brief (Varicose v. etiology: recurrent)
Septic thrombophebitis mortality = 20% (usu Staph (Antibx & vein excision)
Phlebitis of saphenous vein rarely: extends to deep veins (potential for PE)
HA, scalp tenderness, visual sx, jaw claudication/ throat pain = Giant Cell Arteritis
Giant Cell Arteritis labs High ESR, CRP & Interleukin-6 ; mild norm/norm anemia w/ thrombocytosis; temporal art bx is diagnostic
Giant Cell Arteritis Tx prevention of blindness, Prednisone 60 mg ASAP & continue for 1-2 months before taper dosage
Paroxysmal digital ischemia from exagd response of digital arterioles to cold or emotional stress (fingers, toes, ears & nose) = Raynaud Phenomenon
Raynaud prevalence Primarily affects young women
Raynaud: Excessive vasoconstriction = pallor
Raynaud: Subsequent vasodilation = cyanosis then rubor (white to blue to red)
Raynaud can be: primary or secondary to other disease states (scleroderma/SLE)
Giant cell arteritis DDx PMR, Takayasu, RA, amyloid, SLE, polymyositis
Giant cell arteritis physiology Immune-mediated, large arteries (MOST COMMONLY temporal arteries; also subclavian, axillary, Ao); M>F; w/polymyalgia rheum
Arterial occlusive dz RF M>F; 20-30% of >70 yo; Smoking, dyslipidemia, HTN, homocysteinemia, DM, metabolic syndrome; <50 yo w/DM + 1 other RF; 50 - 69 yo with h/o smoking or DM; ≥70 yo
Arterial occlusive dz Pathophysiology flow limiting stenoses occur segmentally
Arterial occlusive dz Sx/Sx exertional intermittent claudication; dec periph pulses, bruits, hair loss, thin shiny skin, mx atrophy
Arterial occlusive dz 2 systems of classification Fontaine and Rutherford: based on sx severity and presence of ulcer or gangrene
Leriche syndrome = aortoiliac disease (arterial occlusive dz of buttock and hip)
Buerger test foot pallor with elevation of leg and, in the dependent position, a dusky red flush spreading proximally from the toes
Arterial occlusive dz DDx DVT, musculoskeletal d/o, peripheral neuropathy, lumbar degenerative spinal canal stenosis (not relieved w/rest) (pseudoclaudication)
Arterial occlusive dz: Dx studies ABI <0.9 (nl = 0.9-1.3); duplex u/s & waveform studies (esp if false normal d/t DM or renal calcification); CTA or MRA; gold std: cath angio (only for pts getting revascularization)
Arterial occlusive dz Tx RF mods: smoking, DM, HTN, HLD; surg (aorto-fem, fem-fem, fem-pop), angioplasty & stenting; cilostazol (PDE5 inhib)
Venous insufficiency RFs: age, FH, ligamentous laxity (eg, hernia, flat feet), prolonged standing, inc BMI, SMK, sedentary, LE trauma, prior DVT, AV shunt, PG, high estrogen
Venous insufficiency Patho reflux (incompetent venous valves), obstruction, venous pump dysfn
Venous insufficiency Dx studies venous u/s; ABI; venography
Venous insufficiency Tx Conservative: leg elevation, exercise, and compression therapy; derm agents; ulcer mgmt. If refractory >6 mos: ablation tx (chem, thermal, mechanical)
Venous insufficiency Mgmt guided by CEAP (clinical, etiologic, anatomic, pathophysiologic) categories
PAD etiology: Atherosclerosis (arteriosclerosis obliterans; most common); thromboangiitis obliterans (Buerger); trauma, arteritis; extrinsic compression
PAD pathophysiology: obstruction / narrowing of lumen of peripheral arteries (most commonly in LE) -> interruption of blood flow -> high risk for CAD
PAD risk factors Old age, smoking, DM, HTN, HLD, obesity; M>F
PAD dx studies Arteriography (gold standard); U/S; ABIs; MRA
PAD mgmt: Stop smoking; diet (low fat/chol/calorie); exercise; foot care; FD ASA; Pletal vs Trental vs Plavix; consider propionyl-L-carnitin; surgery
PAD: surgery angioplasty, bypass graft, arthrectomy, stents
Acute arterial occlusion mgmt: Dx (Doppler extremity; TTE; angiography). Embolism: heparin; thrombosis: antiplatelet meds (alteplase); embolectomy; tx underlying cause
Superficial Thrombophlebitis etiology: Septic (SA, Klebs, Candida, CMV in HIV); malignancy; OCP & PG: hypercoag dz; Behcet dz; Buerger dz
Superficial Thrombophlebitis pathophysiology: inflammation of superficial veins with thrombosus
Superficial Thrombophlebitis risk factors: Immobility, obesity, older age, IV >2 days, burns, steroids, AIDS, varicose veins, post-op, PG
Systemic granulomatous inflammation of medium & large arteries (CRANIAL, subclavian, axillary, aorta); >60 yo, M>F; pale fundi; aortic regurg murmur ) = giant cell arteritis
Giant cell arteritis has been associated with: severe infections, high doses of Abx, chronic autoimmune disorders (RA, SLE)
Cold induced pain at extremities with color change as they warm up Raynaud phenomenon
Volkmann contracture of forearm, peroneal nerve injury, foot drop, pain with passive flexion, all suggest: compartment syndrome
Created by: Abarnard