Peripheral Vascular Disease II · why it happens and what goes wrong
NG-127CARDIOADHD-friendly visual edition
Think of anything that SCARS the lining of a blood vessel. Every arterial risk factor on this page does exactly one thing — it injures the endothelium. Fat, calcium and clot then settle into those tiny tears and become plaque. Veins fail a different way: pressure and stasis blow out the valves. Different insult, different complication list.
Split them the way the exam splits them: what the client can change, and what they can't.
🔥 MODIFIABLE — anything that scars the lining of the blood vessels
Risk factor
How it damages the vessel
The number
🚬 Smoking
Chemicals directly scar the lining; nicotine also causes vasoconstriction, so a narrowed vessel gets squeezed narrower.
The #1 modifiable risk factor for PAD. Quitting is the single highest-yield teaching point.
🍬 Diabetes (uncontrolled)
High sugar turns the blood to mud / syrup — thick, sticky blood scrapes and scars the vessel wall. Also causes neuropathy, so injuries go unfelt.
A1C ≥6.5% diagnoses DM; a common general adult target is <7%. Fasting glucose 70–99 mg/dL normal.
🧈 High cholesterol
Fatty deposits stick to the vessel walls, making them narrow & hard (plaque).
Total <200, LDL <100, HDL >40 (higher is better), Trigs <150 mg/dL.
💥 Hypertension
Uncontrolled over a long period damages & stretches out the vessels — high-pressure flow shears the endothelium.
Normal <120/80; Stage 1 130–139/80–89; Stage 2 ≥140/90(ACC/AHA).
⚖️ Obesity
Puts pressure on the blood vessels, worsens lipids, BP and insulin resistance all at once.
BMI 25–29.9 = overweight · ≥30 = obese.
🪑 Sedentary “sitting” lifestyle
Makes the vessels stiff and stops the calf muscle pump from moving venous blood.
Hits both the arterial and the venous side.
😖 High stress
Drives up blood pressure and heart rate — chronic catecholamine load on an already-injured wall.
Leads back into HTN.
🧠 “SCARS” — Smoking · Cholesterol · Age-old high BP (hypertension) · Restless-free sitting (sedentary) · Sugar (diabetes). Every one of them literally scars the endothelium, and the word is the mechanism.
🧬 NON-MODIFIABLE — the three you can't teach away
🎂AGEvessels stiffen with time
⚧️GENDER
🧬GENETICSfamily history
These still matter on the exam — they tell you who to screen. They just aren't where the teaching plan goes.
🧠 “The three G's you can't fix: Getting older, Gender, Genes.” If a question asks which risk factor the nurse should focus teaching on, the answer is never one of these three — pick smoking, diet, activity or glucose control.
🧪 The lipid panel, on one bar scale
🧠 LDL = “Lousy, Lodges in the wall.” HDL = “Healthy, Hauls it away.” So for LDL you want the number LOW; for HDL you want it HIGH. Triglycerides flip high over 150.
⚖️ Same leg, two different risk lists — arterial vs venous
The exam loves to hand you a risk history and ask which kind of vascular disease to expect. They do not share a cause.
🩸 ARTERIAL (PAD) risk = plaque risk
🚬 Smoking (strongest)
🍬 Diabetes
🧈 High LDL / low HDL
💥 Hypertension
🎂 Age, male sex, family history
💔 Known CAD, prior MI or stroke
⬇️ Still DANGLE the leg
🫙 VENOUS (CVI) risk = stasis & pressure risk
🧍 Prolonged standing or sitting (nurses, teachers, cashiers)
🤰 Pregnancy · 💊 estrogen
⚖️ Obesity
🩸 Previous DVT — scarred valves
🎂 Age · family history of varicose veins
🏋️ Heavy lifting, chronic straining
⬆️ Still ELEVATE the leg
🧠 “Arteries get CLOGGED, veins get CLOGGED-UP-TRAFFIC.” Arterial risk is anything that builds plaque. Venous risk is anything that makes blood sit still or push back down — standing, pregnancy, obesity, an old clot.
⚙️
WHAT GOES WRONG
STEP 2 · THE MECHANISM
From a scratch in the lining to a hard, narrow, rupture-ready artery — and the parallel story in the veins.
🧱 ATHEROSCLEROSIS in five frames — hardening & narrowing that limits O₂ perfusion
🧠 “Scratch → Snack → Scab → Stone → Snap.” Risk factors scratch the lining, lipids & macrophages snack in the tear, the body throws a fibrous scab (cap) over it, calcium turns it to stone, and one day the cap snaps and a clot forms. Five words, whole disease.
📍 MAIN SITES — where plaque parks
🧠 “CAIF” — Carotid, Aorta (abdominal), Iliac, Femoral. Say it like “safe” with a C. Top to bottom: neck → belly → hip → thigh. The pain lands one level below the block, so hip pain = iliac, calf pain = femoral.
🌊 The venous mechanism: pressure, not plaque
Notice what is not in this chain: no plaque, no lipids, no ischemia. That's why statins and antiplatelets don't fix a venous leg — compression and elevation do.
🧠 “Pool → Pressure → Puddle → Pigment → Punch-through.” Five P's for the venous side, so you don't mix them up with the arterial 6 P's of emergency.
💥
COMPLICATIONS
STEP 3 · WHAT IT COSTS
Plaque doesn't just narrow — it can burst, leading to a blood clot that can kill the client. And a starving foot eventually dies.
🚨 The rupture tree — one burst plaque, four ways to die or lose a limb
🧠 “Legs today, heart tomorrow.” If a question gives you a PAD client and asks what else to assess, the answer lives in the chest or the neck — not the leg you're looking at.
🖤 Arterial endgame: ulcer → gangrene → amputation
1
Non-healing wound — a tiny toe injury that will not close, because healing needs oxygen the artery can't deliver.
2
Arterial ulcer — round, punched-out, on a toe, heel, or lateral ankle. Very painful.
GANGRENE — black, dry, mummified toes. Tissue is dead.
5
AMPUTATION — the reason foot inspection and smoking cessation are the two biggest teaching points in this whole topic.
Diabetes doubles this pathway: ischemia stops healing, and neuropathy means the client never felt the injury that started it.
🧠 “The pebble in the shoe.” Picture a diabetic client walking all day on a pebble they can't feel, in a foot that can't heal. That's the whole amputation story in one image — and it's why you inspect between the toes daily.
🪱 Varicose veins — dilated, twisted, rope-like superficial veins. Cosmetic first, painful and heavy later.
🟤 Venous stasis dermatitis — itchy, weepy, brown, scaly skin at the ankle. Scratching becomes the wound.
🧱 Lipodermatosclerosis — the calf hardens and tapers, giving the classic “inverted champagne bottle” leg.
🕳️ Venous stasis ulcer — the medial-malleolus ulcer from page 1. Slow, weepy, recurrent, notoriously hard to heal.
🦠 Cellulitis — broken, boggy skin is an open door for infection.
🩸 DVT — stagnant blood clots. And a clot that breaks free becomes a pulmonary embolism. SEE NG-223
🧠 “Rope → Rash → Rock-hard → Raw → Red-hot → Runaway clot.” Six R's, in the order the venous leg falls apart. The last R is the one that kills.
⭐ Complication cheat-sheet — which side did the damage?
Finding on the exam question
🩸 Arterial
🫙 Venous
Ulcer that will not heal
Toe / heel / lateral ankle, dry, punched out
Medial ankle, weepy, irregular
Black, dry, mummified tissue
Gangrene — yes, this is the arterial ending
Not typical
Brown discoloration around the ankle
No
Hemosiderin staining — yes
Sudden cold pulseless painful limb
Acute arterial occlusion — 6 P's, emergency
No
Sudden unilateral warm swollen calf
No
DVT — emergency because of PE
Life-threatening downstream event
MI · stroke · limb loss
Pulmonary embolism
Position that makes it better
DANGLE ⬇️ lower the legs
ELEVATE ⬆️ above the heart
🧠 Two killers, two directions. The arterial clot travels toward the brain and heart (MI, stroke). The venous clot travels toward the lungs (PE). Knowing which pipe it started in tells you which organ to worry about.
➡️ You know the damage — now the fixes
🩸 Arterial fixes ahead
ABI & Doppler, antiplatelets, statins, angioplasty/stent, bypass, endarterectomy — plus the C-words to avoid.
⬇️ DANGLE / hang the legs down
🫙 Venous fixes ahead
Compression stockings, limit standing, elevation, calf pumping, vein ablation/ligation — plus anticoagulation if a clot forms.
💥 Rupture= clot = limb ischemia · MI · stroke. Venous clot instead goes to the lungs (PE).
🎯 Cover & check — 6 rapid-fire questions
Q1: In one sentence, what do ALL the modifiable arterial risk factors have in common?
They all scar/injure the lining (endothelium) of the blood vessel — and plaque settles into those tears.
Q2: What three things make up an atheroma?
Lipids, calcium and possible clots — sitting in large arteries under a fibrous connective-tissue cap.
Q3: Arteriosclerosis vs atherosclerosis?
Arteriosclerosis = hardening/stiffening of the artery wall (general term). Atherosclerosis = fatty plaque inside the lumen; it is one TYPE of arteriosclerosis and is the driver of PAD.
Q4: Name the four main sites of atherosclerosis and one consequence of each.
Carotids → TIA/stroke. Abdominal aorta → AAA. Iliac → hip/buttock claudication. Femoral → calf claudication and a cold, pulseless foot.
Q5: Which lipid do you want LOW and which do you want HIGH?
LDL LOW (optimal <100 mg/dL) — it Lodges in the wall. HDL HIGH (≥60 mg/dL is protective) — it Hauls cholesterol away. Total <200, triglycerides <150.
Q6: A client with a chronically swollen, brown-stained, weepy ankle now has a hard, tapered calf. What is happening, and what is the risk?
Chronic venous insufficiency progressing — stasis dermatitis plus lipodermatosclerosis (the “inverted champagne bottle” leg). Risk is a venous stasis ulcer at the medial malleolus, cellulitis, and DVT with possible PE.