NSG210 Week 08 Lecture: Alterations in Perfusion - Peripheral Vascular Diseases

Course: NSG210 Medical-Surgical Nursing, Fall 2026 Week: 08 (Oct 12-16), “Alterations in Perfusion / PVD” Exam: Exam 3

Source: lecture deck raw/nsg210_PeripheralVascularDiseases2026.ppt (65 slides; text extract raw/nsg210_PeripheralVascularDiseases2026.md). This page summarizes the slides in lecture order. Slides 9, 12, and 36 are image-only (rubor of dependency and gangrene, an untitled image, Buerger disease photo). Matching textbook chapters: Hinkle Ch. 26 (vascular) and Ch. 37 (amputation). Where the slides and textbook differ, the slide value is given and the textbook value is noted.

Textbook detail: nsg210-hinkle-ch26-vascular-disorders and nsg210-hinkle-ch37-musculoskeletal-trauma. Slide-vs-textbook differences for all of Exam 3: nsg210-exam-3-lecture-vs-textbook. (This file absorbed the earlier standalone PAD notes on Oct 14.)

Learning Objectives (slide 2)

1. Identify anatomic and physiologic factors that affect peripheral blood flow and tissue oxygenation.
2. Apply assessment parameters for determining the status of peripheral circulation.
3. Use the nursing process for the patient with arterial and venous disorders.
4. Compare pathophysiology, manifestations, management, and prevention of arterial diseases.
5. Describe pathophysiology, manifestations, management, and prevention of VTE, venous insufficiency, leg ulcers, and varicose veins.

Part 1: Arterial Disorders

I. Vascular disorders overview (slide 3)

• Vascular = related to blood vessels; the vascular system delivers oxygen and nutrients to tissues
• Arteries carry oxygenated blood AWAY from the heart (exception: pulmonary artery)
• Veins return deoxygenated blood TO the heart (exception: pulmonary vein)
• Peripheral vascular disorder (PVD): arterial or venous insufficiency leading to ischemia
• Common symptoms: pain, skin changes, diminished pulse, possible edema

II. Peripheral arterial disease (PAD) (slides 4-6)

• Disruption of arterial flow from narrowing or complete blockage of the vessel
• 8-12 million Americans; 75% are asymptomatic; prevalence rises sharply with age
• Risk factors are the same as cardiovascular disease (nicotine, diabetes, HTN, lipids, age)
• Gerontologic: most common arterial condition in older adults; present in 80% of people over 65 (slide figure); aging thickens and stiffens vessel walls
• Arteriosclerosis: “hardening of the arteries”; small arteries and arterioles lose elasticity; the most common arterial disease
• Atherosclerosis: fatty deposits, cholesterol, cellular waste, calcium build up in the INTIMA of large and medium arteries

III. Nursing assessment (slides 7-10)

• Intermittent claudication: muscular, cramp-type pain consistently reproduced by exercise and relieved by rest; occurs with 50-70% vessel occlusion; felt about one joint level BELOW the disease (textbook: about 50% lumen / 75% cross-sectional area)
• Rest pain: persistent forefoot pain at rest, worse at night = severe arterial insufficiency
• Skin and temperature:
  • Cool, pale extremities
  • Pallor (white, blanched), especially with elevation
  • Rubor (reddish-blue) within 20 seconds to 2 minutes of dependency
  • Cyanosis (less oxygenated hemoglobin)
  • Hair loss, brittle nails, dry skin, ulcers
  • Edema, unilateral or bilateral
  • Gangrene with severe ischemia and necrosis (slide 9 photo)
• Pulses: an absent pulse means the stenosis is PROXIMAL to that point; palpate both sides for symmetry, rate, rhythm, quality
• Older adults: symptoms more pronounced because of long duration and coexisting chronic disease

IV. Diagnostic evaluation (slides 11-18)

• Doppler ultrasound: reflected sound waves evaluate flow; gel and probe over vessel; a signal means blood flow is present
• Duplex ultrasonography: Doppler plus ultrasound - shows vessel structure, flow, and speed
• Ankle-brachial index (ABI): ratio of ankle to arm systolic pressure; objective, quantifies stenosis
• ABI technique (slide 14):
  • Highest systolic in BOTH arms (first Doppler sound as cuff deflates at the radial pulse); use the higher arm
  • Cuff on the calf; Doppler at dorsalis pedis (DP) and posterior tibial (PT); use the higher ankle pressure for each leg
  • ABI = highest ankle / highest arm

(Textbook: normal 1.00-1.40, PAD under 0.90, severe under 0.40, over 1.40 noncompressible; cuff above the malleolus.)

• ABI technique tips (textbook): supine, rest 5 minutes; correctly sized cuffs; inflate 20-30 mm Hg past the last signal, deflate 2-4 mm Hg/second; check both arms because a silent subclavian stenosis can make one arm read 15-20 mm Hg low; no nicotine or caffeine for 2 hours before
• Errors: ABI 1.20 or more or ankle pressure over 250 mm Hg suggests calcified vessels (diabetes, CKD) and a falsely high reading; a pressure under 40 mm Hg may be the venous signal - recheck
• Worked example (textbook):

• Right ABI = 80 / 160 = 0.50 (the low end of the claudication range on both scales; below 0.50 is rest pain)

• Left ABI = 120 / 160 = 0.75 (claudication range)

• Exercise tolerance testing: evaluates claudication; with or without treadmill; dipyridamole (Persantine) or adenosine can mimic exercise; pulse volumes and pressures before and after symptoms or 5 minutes of exercise; DELAYED return to normal pressures = arterial disease; normal = little or no drop in ankle pressure
• Angiography: invasive x-ray of vessels by interventional radiology; confirms blockage or stenosis; contrast through catheter shows obstruction and collaterals; allergic reaction signs: dyspnea, nausea and vomiting, sweating, tachycardia, numbness; arteriogram = arteries, venogram = veins
• Arteriogram nursing care (slide 17):
  • Before: informed consent; check iodine allergy; confirm meds held; NPO after midnight, clear fluids up to 2 hours before; takes about 1-2 hours; catheter in groin or arm
  • After: bed rest 6 hours; monitor puncture site, foot pulses, BP; encourage fluids unless contraindicated
• CT: cross-sectional images; x-ray and contrast exposure
• MR angiography: MRI with software that isolates vessels; 3-D images; slide says no contrast needed (textbook says IV contrast is used)

V. Planning and implementation (slides 19-22)

• Goals: improve circulation, promote vasodilation, prevent vascular compression, relieve pain, maintain tissue integrity, promote home and community care
• Health teaching:
  • Lower extremities BELOW heart level
  • Moderate exercise as prescribed
  • Keep warm, avoid chilling; direct heat must not exceed body temperature
  • Stop nicotine
  • No leg crossing
• Nutrition: balanced diet with protein and vitamins for healing; weight reduction; lower lipids
• Pharmacology:
  • Antiplatelets: aspirin, clopidogrel (Plavix), pentoxifylline (Trental)
  • Vasodilators (relax vascular smooth muscle, lower BP)
  • Cilostazol (Pletal) for intermittent claudication (starred on slide) - contraindicated in heart failure
  • Antihypertensives: ACE inhibitors, ARBs
  • Cholesterol: statins, niacin
  • Analgesics: oxycodone, Percodan, Percocet

VI. Vascular bypass surgery (slides 23-28)

• Reroutes blood around stenosis or occlusion; for disabling claudication or limb at risk of amputation
• Surgeon picks the distal anastomosis site; distal outflow vessel must be at least 50% patent; grafts synthetic or autologous (patient’s own vein)
• Types: femoral-popliteal (fem-pop), femoral-tibial (fem-tib), aortobifemoral
• Nursing goal: maintain circulation through the repair
  • Assess pulses, Doppler, color, temperature, capillary refill, sensation and movement, vital signs, ABI
  • DISAPPEARANCE OF A PULSE may mean graft occlusion - notify the surgeon IMMEDIATELY (bolded on slide)
  • Prevent respiratory complications, support fluid balance, promote wound healing
• Complications: continuous VS, urine output, bleeding; avoid leg crossing and prolonged dependency; elevate to reduce edema; watch for compartment syndrome (severe edema, unrelenting pain, decreased sensation)
• Self-concept and role (slide 27): assess independence and support; motivation for lifestyle change in chronic disease; stress management; let patient discuss feelings; coordinate care team
• Discharge (slide 28): include family; written instructions; foot and leg care; rehab, home care, outpatient therapy; self-help groups (smoking cessation, stress, weight, exercise); when to seek care

VII. Amputation (slides 29-34)

• Surgical removal of a limb to relieve symptoms, improve function, save or improve quality of life; PVD causes most lower-extremity amputations
• Needs rehab, lifestyle changes, assistive devices; goal is the most functional length that removes all infected or ischemic tissue
• Complications: hemorrhage, infection, skin breakdown, phantom limb pain, neuroma, joint contracture
• Post-op physiologic stability: monitor for hemorrhage; VS and dressing/drainage at least every 2 hours; TOURNIQUET at the bedside; deep breathing, turning, coughing; effective pain control
• Positioning:
  • Residual limb elevated on a pillow for the FIRST 24 HOURS ONLY
  • No flexion at hip or knee (prevents contractures)
  • Encourage PRONE position to stretch hip flexors
  • PT for strengthening
• Conditioning the residual limb:
  • Watch incision for infection
  • Compression bandage at ALL times (venous return, less edema)
  • Figure-eight wrap with pressure at the distal end to shape a cone for the prosthesis
  • After healing: daily care with mild soap and water; NO oils or creams; desensitization
• Coping and self-care: accepting atmosphere to express feelings and grieve; acknowledge the loss; PT for ROM, ambulation, conditioning, upper-body strength for crutches, safe transfers; OT for self-care; patient is an active participant; allow time
• Home care: patient and family active in care; rehab, social services, home care; assess home; support group; health promotion

VIII. Other arterial disorders (slides 35-37)

A. Raynaud phenomenon (slide 37; textbook Ch. 26)

What it is:

• Intermittent episodes of vasoconstriction (vasospasm) of the small arteries and arterioles of the fingers and toes, causing color and temperature changes (slide)
• Cause unknown (slide); textbook suggests a defect in basal heat production that reduces the ability of skin vessels to dilate
• Two forms (textbook):
  • Primary (Raynaud disease): no underlying disease; usually mild
  • Secondary (Raynaud syndrome): with an underlying disease - connective tissue disorders (SLE, RA, scleroderma), trauma, or arterial obstruction; can have fixed blockages leading to ischemia, ulcers, gangrene
• Five times more common in women; onset usually before age 30 (textbook)
• Also appears as a systemic feature of RA and SLE in the rheumatic lecture

Triggers:

• COLD (including air conditioning, cold drinks, freezer, steering wheel)
• Emotional STRESS
• NICOTINE in any form - including nicotine gum and patches (textbook)
• Decongestants and other OTC sympathomimetics (vasoconstrictors) (textbook)

Manifestations - the color sequence WHITE, BLUE, RED:

• WHITE (pallor): sudden vasoconstriction
• BLUE (cyanosis): deoxygenated blood pools during the spasm
• RED (rubor): reactive hyperemia as blood returns when the spasm ends
• Numbness, tingling, burning pain with the color changes
• Usually bilateral and symmetric; fingers and toes
• Prognosis varies; gangrene and amputation are uncommon unless another disease is causing arterial blockage

Management:

• Avoid triggers - the primary treatment (slide)
• Calcium channel blockers (nifedipine, amlodipine) to relax vessels (slide; textbook names them) - teach about ORTHOSTATIC HYPOTENSION
• Sympathectomy for some severe cases (textbook)

Nursing teaching (textbook):

• Dress in layers; hat and gloves or mittens whenever outdoors in cold weather; insulated fabrics
• Wear gloves when reaching into the freezer
• Warm up the car before getting in (avoid touching a cold steering wheel or door handle)
• Carry a sweater for air-conditioned rooms in summer
• Stop all nicotine products
• Stress management
• Handle sharp objects carefully (reduced sensation in fingers)
• Reassure that gangrene and amputation are rare

Acrocyanosis (textbook, related condition): persistent, symmetric blue color of hands and feet with cold, clammy, sweaty skin (not episodic like Raynaud, no white phase); usually benign; protect from cold and trauma; calcium channel blockers do NOT help

B. Buerger disease - thromboangiitis obliterans (slides 35-36)

Note: Buerger disease is on the lecture slides but is NOT in Hinkle 15e Ch. 26. Points marked “general reference” come from standard med-surg knowledge, not from the course textbook - check against the instructor’s emphasis.

What it is (slides):

• Recurring INFLAMMATION of the intermediate and small ARTERIES AND VEINS
• Leads to THROMBUS formation and OCCLUSION of distal vessels
• Microscopic appearance: generally bilateral and symmetric with focal (patchy) lesions
• Strong evidence that heavy SMOKING or CHEWING TOBACCO causes or aggravates it
• Slide 36 is a photo (typically shows ischemic, ulcerated, or gangrenous fingertips/toes)

Who gets it (general reference): young adults, classically men under 45 who are heavy tobacco users

Manifestations (general reference):

• Claudication in the arch of the foot or the calf (distal claudication), and in the hands and forearms
• Rest pain in fingers and toes
• Cold sensitivity and Raynaud-like color changes
• Superficial migratory thrombophlebitis (because veins are involved)
• Diminished or absent distal pulses (radial, ulnar, dorsalis pedis, posterior tibial)
• Painful ulcers and gangrene of the fingertips and toes

Management (general reference):

• COMPLETE and PERMANENT tobacco cessation is the only treatment that stops progression - including smokeless tobacco and nicotine replacement products
• Continued tobacco use often leads to amputation of fingers, toes, or limbs
• Wound care, pain control, protection from cold and injury, the same foot and hand care as PAD
• Avoid vasoconstrictors; keep extremities warm

C. Raynaud vs Buerger vs PAD

Part 2: Venous Disorders

IX. Peripheral venous disorders (slide 38)

• Problems with veins that interfere with blood return from the extremities
• Superficial veins thick-walled; deep veins thin-walled; valves keep flow one way toward the heart
• Valve obstruction or reflux causes prolonged high venous pressure (venous hypertension); walls distend, valves stretch and cannot close, blood refluxes

X. Deep vein thrombosis (slides 39-46)

• Terms: thrombo = clot; thrombosis = clot formation; phlebitis = vein inflammation
• Thrombophlebitis: clot causes vein inflammation (superficial or deep)
• DVT: clot in a deep vein, mostly the lower leg; life-threatening when it breaks loose and travels to the lung (PE); over 500,000 hospitalized patients a year, 50,000 deaths from PE (slide figures)
• Pathophysiology: platelets attach to vein wall with a tail of fibrin, WBCs, RBCs; inflammation thickens vein wall leading to embolization
• Risk factors: the exact cause is unclear; risk factors drive development (slide 42). DVT and PE are one process (VTE), so they share these factors.
  • Virchow triad (slide 42 for DVT; repeated on slide 61 for PE): stasis of blood, vessel wall injury, altered coagulation (hypercoagulability)
  • Named list (slide 61): prolonged immobility or bed rest, recent surgery or hospitalization, major trauma, prior DVT or PE, cancer, pregnancy and the postpartum period, estrogen-containing medications, obesity, smoking, inherited or acquired thrombophilia, increasing age
  • History to ask (slide 45): varicose veins, hypercoagulation, cardiovascular disease, recent surgery
  • Textbook Chart 26-8 sorts examples under each arm of the triad (age over 65, where the slide says increasing age; heart failure, where the slide says cardiovascular disease). That table is in the VTE note below.
• Manifestations: warmth, swelling, redness, tenderness, pain in the affected limb; only HALF of patients have symptoms and they are nonspecific; Homans sign NOT reliable
• PE warning: sudden tachycardia, shortness of breath, tachypnea, chest pain, anxiety, hypoxia
• Assessment: history of risk factors (varicose veins, hypercoagulability, CV disease, recent surgery); limb pain, heaviness, functional impairment, ankle engorgement, edema; compare leg circumference thigh to ankle; increased surface warmth; tenderness
• Diagnostics: duplex venous ultrasound; D-dimer (fibrin degradation fragments; elevated = active clotting process)

XI. DVT prevention and management (slides 47-56)

• Prevention: elastic compression stockings (TEDs), intermittent pneumatic compression devices, positioning and exercise, anticoagulation for surgical patients
• Anticoagulation:
  • Unfractionated heparin: subcut or IV for 5-7 days; prevents extension and new clots
  • Warfarin (Coumadin): oral; started WITH heparin; takes about 1 week to inhibit clotting factors
  • LMWH (enoxaparin/Lovenox): subcut; self-administered; longer half-life; fewer bleeding complications
  • Thrombolytics: dissolve clot in about 50%; give within 3 days of acute thrombosis; less valve damage and chronic venous insufficiency; higher bleeding risk
• Surgery when anticoagulants and thrombolytics contraindicated, PE danger extreme, or drainage so poor the limb will be damaged: thrombectomy; vena cava filter (traps large emboli)
• Nursing - monitoring therapy:
  • Labs: PTT, PT, INR, H&H, platelets, fibrinogen
  • Weight-based dosing per protocol
  • Heparin therapeutic: PTT 1.5 times control (textbook: 1.5-2 times)
  • Warfarin therapeutic: PT 1.5-2 times normal or INR 2.0-3.0
• Bleeding: watch LOC changes; minor bleeding in urine, stool, skin, nose
  • Heparin reversal: protamine sulfate
  • Warfarin reversal: vitamin K and fresh-frozen plasma
• Heparin-induced thrombocytopenia: platelets under 100,000/mL or a 25% drop (see note below)

Note: Thrombocytopenia

Definition and thresholds (textbook Ch. 12; normal platelets about 150,000-400,000/mm3):

Causes relevant to Exam 3:

• HEPARIN (heparin-induced thrombocytopenia, HIT) - the lecture focus (slide 51)
• Chemotherapy and radiation (marrow suppression), leukemia, MDS, tumor infiltration of marrow (Ch. 12, 30)
• Enlarged spleen sequestering platelets (hypersplenism), infections, some drugs (heparin, vancomycin), DIC, autoimmune (ITP, CLL, SLE) (Ch. 12, 30, 34)

Heparin-induced thrombocytopenia (HIT):

• Slide 51: monitor and manage thrombocytopenia due to heparin; monitor platelet counts - concern when under 100,000/mL or a 25% decrease
• Textbook Table 26-2: heparin requires monitoring of aPTT AND platelet count for HIT; LMWH (enoxaparin) has a LOWER HIT risk; argatroban (IV direct thrombin inhibitor) is used to prevent and treat thrombosis in patients with or at risk for HIT
• General reference (not in slides or textbook, check with instructor):
  • HIT is an immune (antibody) reaction to heparin, typically 5-10 days after starting heparin (sooner with recent prior exposure)
  • Paradox: despite low platelets, the main danger is new CLOTTING (arterial or venous thrombosis), not bleeding
  • Management: STOP ALL heparin, including heparin flushes and heparin-coated lines; LMWH is also avoided once HIT is diagnosed; switch to a non-heparin anticoagulant (argatroban); document heparin allergy; warfarin is not started until platelets recover

Signs of thrombocytopenia (Ch. 12):

• Early: PETECHIAE and ECCHYMOSES (bruising) - often the first signs
• Bleeding gums, nosebleeds, prolonged bleeding from venipuncture or minor cuts
• Blood in urine, stool (red or black/tarry), or emesis
• Altered mental status (possible intracranial bleed); hypotension and tachycardia (blood loss)
• Falling hemoglobin and hematocrit

Bleeding precautions (Ch. 12, Chart 12-6; slides 51 - watch LOC, urine, stool, skin, nose):

• Soft toothbrush; no commercial (alcohol) mouthwash; water-based lip lubricant
• Electric razor only; emery board for nails
• No rectal temperatures, suppositories, or enemas; avoid IM injections (smallest needle if unavoidable)
• Apply pressure to puncture sites at least 5 minutes; bundle labs into one daily venipuncture
• Avoid aspirin, NSAIDs, and other drugs that affect platelets
• Stool softeners and fluids (3 L/day unless contraindicated) to prevent straining; avoid hard-to-chew foods
• No forceful nose blowing; supervise ambulation and clear hazards (fall prevention)
• Water-based lubricant before intercourse
• Platelet transfusion as prescribed (premedicate with diphenhydramine or hydrocortisone if ordered)

Exam pointers:

• On heparin, watch PLATELETS as well as aPTT; a drop under 100,000 or by 25% = suspect HIT and notify the provider
• LMWH has lower HIT risk; argatroban is used for HIT
• First visible sign of low platelets: petechiae and bruising
• Thrombocytopenia patient: no IM injections, no rectal temps, no aspirin/NSAIDs, electric razor, soft toothbrush
• Drug interactions: review the full medication schedule
• Comfort: bed rest, elevate the extremity, compression stockings when walking, analgesics, warm moist packs, bed exercises (foot dorsiflexion)
• Compression stockings: correct fit for even pressure over the calves (narrows superficial veins, increases deep flow); for ambulatory patients remove at night and reapply BEFORE legs are lowered in the morning; remove to inspect skin
• Intermittent pneumatic compression: with or without stockings; 3-compartment sleeves inflate sequentially ankle, calf, thigh at 35-55 mm Hg; check fit and comfort
• Positioning and exercise: on bed rest elevate feet and lower legs ABOVE the heart; active and passive leg exercises (calf); early ambulation; avoid long sitting; deep breathing (negative thoracic pressure helps empty large veins)
• Home care: teach stocking application; leg elevation and exercise; medication purposes and interactions; outpatient blood tests; PE symptoms needing emergency care

XII. Other venous disorders (slides 57-58)

• Superficial thrombophlebitis: serious complications rare (no surrounding muscle to squeeze and dislodge the clot); self-care with warm cloth, elevation, NSAIDs
• Varicose veins: abnormally dilated, tortuous superficial veins from incompetent valves; usually legs; up to 60% of people; mostly women and people who stand for long periods; hereditary or from pregnancy

Note: VTE vs DVT vs Thrombophlebitis

Terms (slides 39-40 plus textbook Ch. 26):

(“VT” in this context means venous thrombosis/VTE. On a cardiac strip, VT means ventricular tachycardia - different topic.)

Why it matters which vein:

• Superficial veins are thick-walled and lie just under the skin, with NO surrounding muscle to squeeze the clot loose - so they rarely embolize and most dissolve on their own
• Deep veins are thin-walled, run beside the arteries inside the muscle, and the calf muscle pump can dislodge a clot - so DVT can become a PE
• A clot “tail” of fibrin, WBCs, and RBCs grows in the direction of blood flow; pieces can break off with sudden standing or muscle activity after inactivity (textbook)

Virchow triad with examples (slides; examples from textbook Chart 26-8):

Superficial thrombophlebitis vs DVT:

Special forms (textbook):

• Upper-extremity DVT: 5-10% of DVTs (much higher with central lines); subclavian vein most common; effort thrombosis (Paget-Schroetter) from repetitive overhead motion in athletes and laborers
• Phlegmasia cerulea dolens: massive iliofemoral DVT - whole leg massively swollen, tense, painful, COOL, bluish; can cause venous gangrene - emergency
• Postthrombotic syndrome: chronic swelling, brown pigmentation, pain, and ulcers after 20-50% of DVTs (damaged valves); compression stockings 30-40 mm Hg for 6 months after DVT help prevent it

DVT diagnostic tests (slide 46 lists duplex ultrasound and D-dimer; the rest are from textbook Ch. 26):

If PE is suspected (slide 63 plus textbook): D-dimer, CBC, coagulation studies, cardiac biomarkers, ABG, ECG, V/Q scan, lower-extremity venous ultrasound; CT pulmonary angiography is the standard imaging test (textbook). The slides list the ECG and do not describe the tracing. Textbook ECG findings are in the PE note below.

Exam pointers:

• First-line imaging for DVT = DUPLEX ultrasound
• Elevated D-dimer = active clotting process (slide); a negative D-dimer helps rule out, a positive one does not confirm (general reference)
• Get baseline CBC/platelets and PT/INR/aPTT BEFORE starting anticoagulants
• Homans sign is not a diagnostic test

Assessment pitfalls:

• Homans sign (calf pain on dorsiflexion) is NOT reliable - do not use it to rule DVT in or out
• Measure and compare leg circumference at the same levels (thigh to ankle) on both legs
• In a patient with DVT, sudden dyspnea, tachycardia, chest pain, or anxiety = suspect PE

Safety points:

• Do not massage a leg with a suspected DVT (general nursing practice - risk of dislodging the clot; not stated in the slides)
• Stockings and compression devices are for PREVENTION; in active DVT follow the provider’s orders before applying compression
• Bed rest patients: elevate feet and lower legs above heart, active and passive calf exercises, deep breathing; ambulatory patients: walk at least 10 minutes every 1-2 hours, avoid sitting over 1 hour (textbook)

XIII. Pulmonary embolism (slides 59-65)

• Blockage of one or more pulmonary arteries, usually by a DVT that traveled through the venous system to the lungs; potentially life-threatening emergency
• Path: risk factors, DVT, clot breaks loose, vena cava, right atrium, right ventricle, pulmonary artery, obstruction, impaired pulmonary blood flow
• Risk factors: same list as DVT (section X). Slide 61: prolonged immobility or bed rest, recent surgery or hospitalization, major trauma, prior DVT or PE, cancer, pregnancy and the postpartum period, estrogen-containing medications, obesity, smoking, inherited or acquired thrombophilia, increasing age. Virchow triad: venous stasis, vessel wall injury, hypercoagulability
• Signs and symptoms: dyspnea, tachypnea, tachycardia, pleuritic chest pain, anxiety or feeling of impending doom, cough, hemoptysis, lightheadedness or syncope, sweating, low SpO2, hypotension in severe PE
• Diagnostic tests: D-dimer, CBC, coagulation studies, cardiac biomarkers, ABG, V/Q scan, ECG, lower-extremity venous ultrasound (textbook adds CT pulmonary angiography as the standard)
• ECG: see the note below. Slides name the test only. Textbook: sinus tachycardia plus nonspecific ST-T wave abnormalities. Those findings do not diagnose PE.
• Medical management: oxygen and respiratory support; anticoagulation
• Nursing assessment priorities: airway and breathing, respiratory rate and pattern, SpO2, heart rate and rhythm, BP, LOC, chest pain, anxiety, skin color, signs of DVT, VTE risk factors, response to treatment

Note: ECG changes in PE

• Slide 63 lists an ECG among the diagnostic tests and does not describe the tracing.
• Textbook (Hinkle Ch. 26): “In addition to sinus tachycardia, the most frequent ECG abnormality is nonspecific ST-T wave abnormalities.” The same paragraph says the chest x-ray is usually normal and that the workup is used to rule out other diseases. MDCTA (CT pulmonary angiography) is the criterion standard for diagnosing PE. The ECG findings do not diagnose PE.
• Sinus tachycardia (same definition as the dysrhythmia notes, Hinkle Ch. 22): rate over 100 from the sinus node, with a P wave before every QRS. At a fast rate the P wave may be buried in the preceding T wave.
• Nonspecific ST-T wave abnormalities (explanation of the textbook phrase, not a separate quoted pattern): the ST segment or the T wave looks abnormal, but the pattern does not name one diagnosis. It is not, for example, an ST-elevation myocardial infarction.
• Not in the slides or in Ch. 26: the classic right-heart strain pattern (an S wave in lead I, a Q wave in lead III, and an inverted T wave in lead III, sometimes with a new right bundle branch block). Do not treat that pattern as course content.

Arterial vs Venous at a Glance (from the lecture content)

PVD vs PAD

On slide 3, PVD means either arterial or venous insufficiency. When a question says “PVD vs PAD,” it means venous disease versus arterial disease. This chart uses that exam meaning. PAD column: slides 7-10. Venous column: DVT slides 43-45, plus textbook Table 26-1 and the chronic venous section for color, skin changes, and ulcer sites.

Note: Assessment Findings - PAD vs Peripheral Venous Disease

Terms: on the slides, PVD (peripheral vascular disorder) is the umbrella term for BOTH arterial and venous insufficiency (slide 3). PAD is the arterial type; the venous type (peripheral venous disease) covers DVT, chronic venous insufficiency, and varicose veins. When a question says “PVD vs PAD,” it usually means venous vs arterial. The comparison chart is in the section above.

Memory hook: arterial = blood can’t get IN (tissue starved: pale, cold, painful with use, no pulse). Venous = blood can’t get OUT (tissue congested: swollen, warm or discolored, aching, pulses still there).

Likely Exam Points From This Lecture

• ABI calculation and slide ranges (1.0 normal; 0.95-0.50 claudication; under 0.50 rest pain; under 0.25 severe)
• Absent pulse = blockage proximal to that site
• Claudication at 50-70% occlusion, one joint below the lesion
• Arterial: legs below heart, warm, no nicotine, no leg crossing
• Arteriogram: iodine allergy, NPO, bed rest 6 hours, check puncture site and pedal pulses, fluids
• Cilostazol for claudication
• After bypass, a disappearing pulse = call the surgeon now
• Amputation: tourniquet at bedside; pillow first 24 hours only; prone positioning; figure-eight wrap to a cone; no oils or creams
• DVT/PE risk factors: Virchow triad (stasis, vessel injury, altered coagulation) plus immobility or bed rest, recent surgery or hospitalization, major trauma, prior DVT or PE, cancer, pregnancy and postpartum, estrogen, obesity, smoking, thrombophilia, increasing age
• Homans sign unreliable; D-dimer and duplex ultrasound for DVT
• Heparin PTT 1.5 times control; warfarin INR 2-3; reversal protamine vs vitamin K/FFP; HIT at platelets under 100,000 or 25% drop
• Stockings: reapply before legs are lowered in the morning
• DVT on bed rest: legs elevated above heart, calf exercises
• PE: sudden dyspnea, tachycardia, pleuritic chest pain, anxiety, low SpO2 - oxygen and anticoagulation
• PE ECG (textbook; slides list the test and do not describe it): sinus tachycardia (rate over 100, P before every QRS) and nonspecific ST-T changes (abnormal ST or T that does not name one diagnosis, and is not an ST-elevation MI). These do not diagnose PE; CT pulmonary angiography is the standard. The classic right-heart strain pattern (S in I, Q and inverted T in III, sometimes a new right bundle branch block) is not in the slides or Ch. 26

Practice Questions (self-check)

1. Calf cramping after walking two blocks, gone after a few minutes of rest. Which artery is most likely narrowed? (Superficial femoral or popliteal - pain is distal to the lesion.)
2. Brachial 140 (R) and 130 (L); right ankle 70 (PT) and 84 (DP). Right ABI? (84 / 140 = 0.60 - claudication range.)
3. A patient with PAD wants the legs on pillows at night for foot pain. Best response? (Keep legs dependent or level; elevation reduces arterial flow and worsens rest pain.)
4. Which home-care statement needs correction: “I’ll put lotion between my toes so they don’t crack.” (Lotion between toes causes maceration.)
5. Six hours after a fem-pop bypass, a dorsalis pedis Doppler signal that was present is now absent. First action? (Notify the surgeon immediately - possible graft occlusion.)
6. A patient with heart failure and claudication is prescribed cilostazol. Nurse action? (Question the order - cilostazol is contraindicated in heart failure.)
7. A patient on a heparin drip has platelets drop from 240,000 to 150,000. Concern? (Heparin-induced thrombocytopenia - more than 25% drop; notify provider.)
8. After an above-knee amputation, on day 2 the patient asks for a pillow under the residual limb. Response? (No - a pillow after the first 24 hours causes hip flexion contracture; encourage prone positioning.)

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• INDEX