JC

Peripheral Vascular System: Comprehensive Study Notes

Anatomy of the Arterial Wall

  • Three concentric layers

    • Intima
    • Single layer of endothelial cells with extensive metabolic activity
    • Internal elastic membrane forms its outer border
    • Site where atherosclerosis begins
    • Media
    • Smooth-muscle layer with elastic properties (internal & external elastic laminae)
    • Receives blood via the vasa vasorum
    • Adventitia
    • Outer connective-tissue layer containing nerve fibers & vasa vasorum
  • Atherosclerosis (Box 17-1, Fig 17-2)

    • Endothelial injury (e.g.
    • Smoking, hypertension) → LDLs enter intima → oxidation → inflammatory response
    • Monocytes → macrophages → foam cells → fatty streaks → fibrous cap over necrotic lipid core
    • Plaque rupture/erosion exposes thrombogenic core → thrombus →
    • Coronary arteries → acute MI
    • Carotids → embolic stroke
    • Key concept: plaque activation (not just luminal stenosis) precipitates ischemia/infarction

Arterial Tree, Diameters & Functional Sub-classes

  • Elastic (conducting) arteries: aorta, common carotid, iliac
  • Muscular (distributing) arteries: coronary, renal
  • Small arteries: <2\,\text{mm}
  • Arterioles: 20\text{–}100\,\mu\text{m} – principal “resistance vessels” (major determinant of systemic vascular resistance & BP)
  • Capillaries: 7\text{–}8\,\mu\text{m} (≈1 RBC width); endothelium only → rapid gas exchange
  • Collateral circulation: chronic obstruction → enlargement of anastomoses

Major Palpable Arterial Pulses

  • Upper limb (Fig 17-3)
    • Brachial: medial to biceps tendon in antecubital fossa
    • Radial: lateral flexor wrist
    • Ulnar: medial flexor wrist (often obscured)
    • Two palmar arches protect hand/finger perfusion
  • Abdomen (Fig 17-4)
    • Aortic pulsation in epigastrium
    • Branches (non-palpable):
    • Celiac trunk → foregut organs
    • Superior mesenteric → midgut
    • Inferior mesenteric → hindgut
  • Lower limb (Fig 17-5)
    • Femoral: below inguinal ligament (midway ASIS ↔︎ symphysis)
    • Popliteal: deep behind knee
    • Posterior tibial (PT): behind medial malleolus
    • Dorsalis pedis (DP): dorsum foot, lateral to extensor tendon of great toe

Venous System

  • Thin-walled, highly distensible; accommodate ≈\tfrac23 circulating blood
  • Intima: non-thrombogenic endothelium; valves ensure unidirectional flow
  • Media: elastic tissue + smooth muscle; caliber changes with small pressure variations
  • Deep vs Superficial leg veins (Fig 17-6 & 17-7)
    • Deep: ≈90\% of venous return, well supported
    • Superficial: subcutaneous, poor support
    • Great saphenous → femoral vein
    • Small saphenous → popliteal vein
    • Perforators bridge systems; calf-muscle pump propels blood ↑
  • Leg veins prone to dilatation, compression, ulceration, tumor invasion

Lymphatic System

  • Capillaries → thin channels → collecting ducts → venous angles
    • Right lymphatic duct: right head/neck, thorax, upper limb
    • Thoracic duct: remainder of body
  • Lymph nodes: filter lymph & mount immune response
    • Palpable superficial groups: cervical, axillary, epitrochlear (≈3\,\text{cm} above medial epicondyle), inguinal
    • Inguinal nodes (Fig 17-9)
    • Horizontal chain: drains lower abdomen, buttock, external genitalia (not testes), anal canal, lower vagina
    • Vertical group: along upper great saphenous; drains leg
  • Clinical terms
    • Lymphedema: obstructed lymph drainage → non-pitting, brawny swelling
    • Lymphadenopathy: enlarged nodes (>1\text{–}2\,\text{cm} inguinal; smaller elsewhere)

Trans-Capillary Fluid Exchange & Edema Pathogenesis

  • Forces: venous hydrostatic pressure, plasma oncotic pressure, capillary permeability, lymphatic clearance
  • Mechanisms → edema
    • \uparrow Plasma volume (Na⁺ retention)
    • Altered Starling forces with net filtration
    • Lymphatic or venous obstruction
    • \uparrow Capillary permeability (e.g.
      sepsis)
  • Pitting vs non-pitting
    • Pitting → low protein fluid (HF, nephrotic syndrome, cirrhosis, dependency)
    • Non-pitting → lymphatic etiology or myxedema

Health History & Symptom Assessment

  • Key aims: differentiate vascular vs neuro/musculoskeletal causes; assess perfusion
  • Common/Concerning Sx
    • Pain, cramping, throbbing, coldness, numbness, pallor, hair loss, ulcers, swelling
    • Intermittent claudication (relieved within \le10 min rest)
    • Rest pain (critical limb ischemia)
    • Abdominal/flank/back pain (consider AAA, mesenteric ischemia)
  • Peripheral Arterial Disease (PAD)
    • Atherosclerotic dz distal to aortic bifurcation
    • Triples risk of MI & stroke
    • Classic claudication in only \approx10\%; many have atypical leg pain or are asymptomatic
    • Risk factors = CAD risks: age ≥50, smoking, diabetes, HTN, hyperlipidemia, African American ethnicity, family Hx AAA
    • PAD warning signs (Box 17-2)
    • Fatigue, aching, numbness, pain limiting walking/exertion
    • Erectile dysfunction (aorto-iliac)
    • Non-healing wounds
    • Rest pain changing with position
    • Post-prandial abd pain + weight loss (mesenteric ischemia)
  • Symptom location → likely arterial level
    • Buttock/hip → aorto-iliac
    • Thigh → common femoral
    • Upper calf → superficial femoral
    • Lower calf → popliteal
    • Foot → tibial/peroneal
  • AAA clues: sudden flank/back pain, pulsatile abd mass; food fear, early satiety, urinary sx
  • Venous thromboembolism (VTE)
    • DVT ~2,000,000 cases/yr US; \approx20\% → PE
    • Upper-extremity DVT \approx10\% (catheters, pacers)
    • Unilateral swelling, pain, discoloration
    • Use Wells or Geneva scores; individual findings unreliable

Physical Examination Strategy (Top ↘ Bottom)

  1. Carotids → Upper extremities → Abdomen → Lower extremities
  2. Compare bilaterally:
    • Pulse quality & amplitude
    • Vessel size
    • Skin temp & color
    • Hair distribution
    • Edema presence
  3. Palpate abdominal aorta for width & pulsatile mass (AAA)

Pulse Grading (ACC/AHA 0–3 scale, Box 17-3)

  • 3+ = bounding
  • 2+ = brisk/normal
  • 1+ = diminished
  • 0 = absent

Upper Extremity Exam

  • Inspection: size, symmetry, color, venous pattern
  • Palpation
    • Radial pulse (Fig 17-11)
    • Brachial pulse (Fig 17-13)
    • Epitrochlear nodes (Fig 17-14)
  • Raynaud disease: normal wrist pulses but episodic digital pallor (Fig 17-12)

Abdominal Exam Highlights

  • Auscultate: aortic, renal, femoral bruits
  • Palpate: aortic diameter (<3\,\text{cm} normal); detect pulsatile masses
  • Palpate superficial inguinal nodes (Fig 17-15) – normal ≤2\,\text{cm}, nontender

Lower Extremity Exam

  • Inspection (supine & standing)
    • Size (measure calf ≈10\,\text{cm} below tibial tuberosity; ⊿>3\,\text{cm} → LR>2 for DVT)
    • Edema pattern (uni vs bilateral)
    • Venous pattern/varicosities (Fig 17-16) – fill when standing
    • Skin: color, texture, ulceration (Tables 17-3 & 17-4)
    • Hair loss, nail dystrophy
  • Palpation – Arteries
    • Femoral (Fig 17-19) – absent pulse LR >6 for PAD; widened → aneurysm
    • Popliteal (Fig 17-20 & 17-21) – deeper, diffuse; widened → aneurysm (men ≥50)
    • DP (Fig 17-22) – congenitally absent ≈8\%; absent with preserved proximal pulses LR >14 for PAD
    • PT (Fig 17-23) – behind medial malleolus
    • Temperature: asymmetric coolness LR >6 for PAD (poikilothermia)
  • Palpation – Veins & Edema
    • Pitting: press dorsum foot, behind medial malleolus, shin (Fig 17-24)
    • Grading 1+ to 4+ (Fig 17-25 shows 3+)
    • Tenderness/cords: calf & groin (iliofemoral DVT → painful, pale, swollen leg)
    • Homan sign is obsolete

Special Tests

  • Ankle–Brachial Index (ABI)
    • Procedure (Fig 17-26 & 17-27)
    1. Supine ≥10 min
    2. Measure bilateral brachial systolic BP with Doppler (avg of 2)
    3. Measure ankle systolic BP (DP & PT both legs)
    • Calculation
      {\displaystyle \text{ABI} = \frac{\text{higher ankle SBP}}{\text{higher brachial SBP}}}
    • Interpretation
    • Normal 0.90\text{–}1.40
    • >1.40 → non-compressible (calcified) artery
    • <0.90 → PAD; <0.50 → severe PAD
    • Caveat: diabetes/elderly calcification → falsely high readings
  • Allen Test (Fig 17-29 – 31)
    • Occlude radial & ulnar; patient opens hand → release one artery
    • Flush in 3\text{–}5\,\text{s} = patent
    • Persisting pallor (Fig 17-32) → occlusion
    • Barbeau test: oximeter-based alternative

Documentation Example

"Extremities warm, no edema or varicosities. Calves supple, nontender. No bruits. Brachial, radial, femoral, popliteal, DP, PT pulses 2+ & symmetric."

Health Promotion & Screening

  • PAD Screening
    • Prevalence: 200\,\text{M} worldwide; 8\% (65-75 y) → 18\% (>75 y)
    • ABI
    • USPSTF: evidence insufficient (I); ACC/AHA: reasonable in high-risk patients
  • AAA Screening
    • Definition: infrarenal aorta ≥3\,\text{cm}; rupture risk ↑ markedly >5.5\,\text{cm}
    • Prevalence: 3.9-7.2 % men, 1.0-1.3 % women >50 y
    • Strongest risks: male, age, smoking, family Hx (15-28 %)
    • Modality: abdominal US (Sn 94\text{–}100\%, Sp 98\text{–}100\%)
    • USPSTF: one-time US men 65-75 y with ≥100 lifetime cigarettes (grade B); selective for nonsmokers (C); against routine in women nonsmokers (D)

Edema Types (Table 17-1)

  • Pitting (low protein): HF, nephrotic, cirrhosis, dependency, meds
  • Chronic Venous Insufficiency: soft pitting ± brawny skin, pigmentation, ulceration
  • Lymphedema: initially pitting → indurated, non-pitting; thick skin; usually bilateral; no pigmentation

Chronic Insufficiency of Arteries vs Veins (Table 17-3)

FeatureArterialVenous
PainIntermittent claudication → rest painOften painful
Pulses↓/absentNormal
ColorPale on elevation; dusky red dependentCyanotic/brown; petechiae
TempCoolNormal
EdemaNone/mildMarked
SkinThin, shiny, hairless, ridged nailsBrown pigmentation, stasis dermatitis
UlcerToes, trauma pointsMedial ankle
GangreneMay occurRare

Common Ulcers (Table 17-4)

  • Venous: medial/lateral malleolus; irregular shallow; edema + pigmentation; pain in 75 %
  • Arterial: toes/feet; punched-out; severe pain unless neuropathic; gangrene common
  • Neuropathic: pressure points in insensate foot; surrounding callus; painless; no gangrene unless infected

Practical/Philosophical Points

  • Vascular assessment integrates anatomy (palpable pulses), physiology (ABI), & pathology (plaque biology)
  • Atherosclerosis is systemic—finding PAD should prompt CV risk reduction (statins, antiplatelets, lifestyle)
  • Venous & lymphatic disorders impact quality of life (pain, ulceration, disfigurement); early recognition prevents morbidity
  • Ethical duty: screen those who benefit (AAA in male smokers) but avoid over-screening low-yield populations
  • Remember “diligent comparison” – asymmetry is a powerful diagnostic clue

Key Numbers & Formulas

  • Arteriole diameter: 20\text{–}100\,\mu\text{m}
  • Capillary diameter: 7\text{–}8\,\mu\text{m}
  • ABI formula: \text{ABI}=\dfrac{\text{ankle SBP}}{\text{brachial SBP}}
  • ABI normals: 0.90\text{–}1.40; severe PAD <0.50
  • AAA: diameter \ge3\,\text{cm}; rupture risk high >5.5\,\text{cm}
  • Calf ⊿ >3\,\text{cm} → consider DVT
  • Leg veins carry \approx90\% of return via deep system
  • Portal vein supplies \approx75\% of hepatic blood flow