CHAPTER 26-

LEARNING OUTCOMES (LO1–LO6)

LO1. Identify anatomic and physiologic factors that affect peripheral blood flow and tissue oxygenation

⭐ Key Components

• Structure of peripheral arteries & veins

• Vessel wall integrity

• Pressure gradients

• Blood viscosity

• Autoregulation mechanisms

• Capillary exchange

• Lymphatic drainage

Normal vs. Abnormal

Nursing Response

• Assess pulses, color, temp, cap refill.

• Use ABI for arterial disease.

• Evaluate for cyanosis, rubor, edema.

• Promote circulation (positioning, warming, activity).

LO2. Apply assessment parameters appropriate for determining the status of peripheral circulation

Key Components

• Pulse quality (0–3+)

• Skin color (pallor, cyanosis, rubor)

• Temperature (cool = arterial; warm = venous)

• Capillary refill

• Presence of edema

• ABI

• Bruits

• Pain patterns (intermittent claudication, rest pain)

Normal vs. Abnormal Findings

🔴 Red-Flag Signs

• Absent pulses

• Severe pain unrelieved by rest

• Blue, cold limb

• Ulcers with gangrene

• Sudden swelling → possible DVT

Nursing Response

• Elevate venous issues; do NOT elevate arterial ischemia.

• Notify provider immediately for acute limb ischemia signs.

LO3. Use the nursing process as a framework for care of the patient with arterial and venous disorders

Assessment Priorities

• Pulses, temperature, color

• Presence of edema or varicosities

• Pain pattern

• Tissue integrity

• Mobility limitations

Nursing Diagnoses

• Ineffective peripheral tissue perfusion

• Impaired skin integrity

• Chronic pain

• Activity intolerance

Interventions

• Promote circulation based on disorder (arterial vs venous)

• Administer anticoagulants for VTE as ordered

• Compression for venous disease (never for acute arterial ischemia)

• Smoking cessation education

Evaluation

• Improved perfusion, pain decreased, increased activity tolerance

LO4. Compare pathophysiology, clinical manifestations, management, and prevention of diseases of the arteries

Include:

• Atherosclerosis

• Arterial stenosis

• Aneurysms

• Dissections

• Peripheral arterial disease (PAD)

Comparison Focus

LO5. Describe pathophysiology, clinical manifestations, management, and prevention of venous thromboembolism, venous insufficiency, leg ulcers, and varicose veins

Key Areas

• VTE/DVT

• Venous insufficiency

• Chronic venous stasis ulcers

• Varicose veins

Clinical Focus

LO6. Describe the pathophysiology, clinical manifestations, and management of lymphatic disorders and cellulitis

Key Areas

• Lymphedema

• Cellulitis

Clinical Focus

NURSING CONCEPTS TABLE

GLOSSARY WITH CONTEXT

⭐ = MUST-KNOW FOR EXAMS

Anatomic and Physiologic Overview

🌡 Big Picture: Vascular Conditions

• The chapter starts by grouping vascular conditions into:

  • Arterial disorders

  • Venous disorders

  • Lymphatic disorders

  • Cellulitis (acute infection of skin/subQ tissue)

• These can appear in inpatient and outpatient settings.

• Key idea: 🧠 Good nursing care absolutely depends on understanding how the vascular system works—anatomy + physiology → assessment → management.

How Perfusion Works (Core Concept)

• Adequate perfusion = tissues get:

  • Enough oxygen

  • Enough nutrients

• Perfusion depends on:

  • 🫀 Heart as a pump → must contract effectively.

  • 🩸 Patency & responsiveness of vessels → open, able to constrict/dilate.

  • 🩻 Adequate blood volume → not too low (hypovolemia), not too high.

• Other influences:

  • Nervous system activity (especially sympathetic system).

  • Blood viscosity (thicker blood ⇒ more resistance).

  • Metabolic needs of tissues (high-demand tissues need more flow).

🔗 Cause → Effect

• ↑ metabolic demand ➡ vessels should dilate ➡ ↑ blood flow ➡ adequate perfusion

• If any component fails (pump, pipes, volume) ➡ ↓ perfusion ➡ ischemia.

Systemic vs Pulmonary Circulation (Fig. 26-1)

• There are two interdependent vascular systems:

  • Right heart → pulmonary circulation

    • Pumps blood to the lungs to be oxygenated.

  • Left heart → systemic circulation

    • Pumps oxygenated blood to all body tissues.

• Blood vessels:

  • Carry blood from heart → tissues → back to heart in a loop.

• Contraction of the ventricles = main driving force that propels blood through both systems.

🫀 Figure 26-1 key points:

• Oxygen-rich blood:

  • Lungs → left heart → aorta → systemic arteries → capillaries

  • Exchange of nutrients & waste occurs at capillaries.

• Deoxygenated blood:

  • Capillaries → systemic veins → right heart → pulmonary circulation again.

💡 Memory cue:
Right = Respiratory (lungs), Left = “Leave” to the body.

Arteries, Veins, and Microcirculation

• Arteries

  • Carry oxygenated blood from the left heart → tissues.

• Veins

  • Carry deoxygenated blood from the tissues → right heart.

• Capillaries

  • Tiny vessels that connect arteries to veins within tissues.

  • Site of nutrient and waste exchange.

• Microcirculation = arterioles + capillaries + venules

  • Arterioles & venules right next to capillaries + the capillaries themselves.

  • This is where small vessel problems → big tissue problems (ischemia, ulcers).

Lymphatic System – Complement to Circulation

• Lymphatic system supports the circulatory system by:

  • Transporting lymph and tissue fluid (proteins, cells, debris) from interstitial space → venous system.

• Lymph fluid empties into:

  • Subclavian veins and internal jugular veins.

• Key idea: If lymphatic drainage is blocked ➡ protein-rich fluid and debris stay in tissues ➡ lymphedema.

Anatomy of the Vascular System

• This line is just telling you the “cast of characters”:

  • Arteries & arterioles

  • Capillaries

  • Veins & venules

  • Lymphatic vessels

Arteries and Arterioles

Structure & Size

• Arteries are thick-walled vessels that carry blood from heart → tissues.

• Aorta:

  • Diameter ≈ 2.5 cm (1 inch).

  • Branches into progressively smaller arteries (~4 mm).

  • Eventually → arterioles (~30 micrometers), embedded in tissues.

• Arterioles = smallest arteries.

Three Layers of Arterial Wall

1. Intima

   • Inner layer, made of endothelial cells.

   • Smooth surface ➡ reduces friction ➡ prevents clotting.

2. Media

   • Middle layer: smooth muscle + elastic tissue.

   • Thickest layer in aorta and large arteries.

   • Provides:

     • Strength (resists pressure).

     • Elasticity (stretch and recoil with each beat).

     • Constriction/dilation to buffer stroke volume and maintain steady flow.

3. Adventitia

   • Outer layer of connective tissue.

   • Anchors vessel to surrounding structures.

Size & Composition Differences

• Larger arteries:

  • Media has lots of elastic fibers ➡ good stretch/recoil.

• Smaller arteries & arterioles:

  • Much less elastic tissue.

  • Media is mostly smooth muscle.

  • Smooth muscle responds to:

    • Chemical factors

    • Hormones

    • Nervous system (autonomic)

Functional Role of Arterioles

• Arterioles are “resistance vessels”:

  • Adjust their diameter to regulate:

    • Arterial volume

    • Arterial pressure

    • Blood flow to capillaries

  • Small changes in diameter ➡ big changes in resistance and blood flow.

• Arterial walls are relatively thick:

  • Wall thickness ≈ 25% of total diameter.

Blood Supply to Arterial Walls

• Intima + inner third of media:

  • Close enough to blood inside vessel to be nourished by direct diffusion.

• Adventitia + outer media:

  • Need their own blood supply → vasa vasorum (“vessels of the vessels”).

  • These tiny vessels supply nutrients to the walls of larger arteries.

💡 Memory cue:
ArteriOles = Opposition (resistance) vessels.

Capillaries

Structure & Size

• Capillary walls:

  • Made of a single layer of endothelial cells.

  • No smooth muscle or adventitia.

• Diameter: 5–10 micrometers

  • RBCs must change shape to squeeze through.

Function

• Thin walls allow rapid exchange:

  • Nutrients → tissues

  • Wastes → blood

• Capillary diameter changes passively due to:

  • Changes in upstream/downstream vessel tone (arterioles/venules).

  • Chemical stimuli.

Precapillary Sphincters

• Some capillary beds have precapillary sphincters:

  • Cuffs of smooth muscle at arteriolar end.

  • Help control capillary blood flow along with arterioles.

Arteriovenous Anastomoses

• In some beds (e.g., fingertips):

  • There are direct artery → vein connections = arteriovenous anastomoses.

  • They help regulate heat exchange between body and environment.

Distribution by Tissue Type

• Tissues with high metabolic needs:

  • e.g., skeletal muscle → dense capillary networks.

• Tissues with low metabolic needs:

  • e.g., cartilage → fewer capillaries.

🔗 Concept link:
↑ metabolism ➡ ↑ capillary density ➡ better oxygen delivery.

Veins and Venules

Structural Analogy

• Capillaries → venules → veins.

• Venous system mirrors arterial system:

  • Venules ↔ arterioles

  • Veins ↔ arteries

  • Vena cava ↔ aorta

• They often have similar diameters, but very different walls.

Vein Wall Structure

• Veins are thinner and less muscular than arteries.

  • Wall ≈ 10% of diameter (vs ≈ 25% in arteries).

• Also have three layers (intima, media, adventitia) but:

  • Layers are less well-defined.

  • Less smooth muscle and elastic tissue.

Functional Role – Capacitance Vessels

• Thin, less muscular walls = veins can distend easily:

  • They can hold large volumes of blood at low pressure.

  • → “Capacitance vessels”.

• About 75% of total blood volume is in veins.
  🧪 Important number.

Sympathetic Control & Muscle Pump

• Sympathetic nervous system innervates vein musculature:

  • Can cause venoconstriction ➡

    • ↓ venous volume

    • ↑ blood volume in general circulation.

• Skeletal muscle contraction (especially in legs):

  • Major “pump” pushing venous blood back to the heart.

Valves in Veins

• Veins, especially those working against gravity (legs), have:

  • One-way bicuspid valves that:

    • Prevent retrograde (backward) flow.

• Valves are made of endothelial leaflets.

  • Competency depends on integrity of the vein wall.

• When valves fail ➡ venous reflux, varicose veins, chronic venous insufficiency.

🔴 Clinical danger:
Valve failure + poor muscle pump ➡ stasis ➡ VTE/DVT risk ↑.

Lymphatic Vessels

Structure & Pathway

• Lymphatic vessels:

  • Thin-walled, capillary-like network.

  • Collect lymph from tissues and organs → return it to venous circulation.

• They converge into two main ducts:

  • Right lymphatic duct:

    • Drains right side of head, neck, thorax, and right upper arm.

  • Thoracic duct:

    • Drains the rest of the body.

• Both ducts empty into:

  • Junction of subclavian and internal jugular veins.

Lymph Nodes

• Lymph passes through regional lymph nodes:

  • Nodes filter foreign particles and immune-related debris.

Permeability & Movement

• Lymphatic vessels are highly permeable to large molecules:

  • Provide only route for interstitial proteins to return to venous system.

• With muscle contraction:

  • Lymph vessels deform → spaces open between endothelial cells → proteins & particles enter.

• Lymph propulsion:

  • Combination of lymphatic wall contraction + surrounding muscle movement.

🔴 If lymph flow is obstructed → protein-rich edema (lymphedema) that is hard to mobilize.

Function of the Vascular System

Main functions:

• Supply circulatory needs of tissues.

• Maintain:

  • Blood flow

  • Blood pressure

• Provide:

  • Capillary filtration & reabsorption

  • Hemodynamic resistance regulation

  • Peripheral vascular regulatory mechanisms

Circulatory Needs of Tissues

Matching Blood Flow to Metabolism

• Blood flow needs are constantly changing.

• Distribution of flow to organs depends on:

  • Tissue metabolism rate

  • Oxygen availability

  • Tissue function

• When metabolic requirements increase:

  • Vessels dilate → ↑ flow of O₂ and nutrients.

• When metabolic needs decrease:

  • Vessels constrict → ↓ blood flow.

📈 Metabolic ↑ with:

• Exercise/physical activity

• Local heat

• Fever

• Infection

📉 Metabolic ↓ with:

• Rest

• Decreased physical activity

• Local cold

• Cooling of body

🔴 If vessels fail to dilate when needs ↑ → tissue ischemia.

• Mechanism of dilation/constriction aims to:

  • Keep blood pressure normal while still meeting metabolic needs.

Oxygen Extraction Example

• As blood passes through capillaries:

  • O₂ removed, CO₂ added.

• Different tissues extract different amounts of oxygen:

  • 🫀 Myocardium: ~50% of O₂ in one pass.

  • 🩺 Kidneys: ~7%.

  • Average for all tissues: ~25%.

• So: vena cava blood has ~25% less O₂ than aortic blood.

  • This is called systemic arteriovenous oxygen difference.

• When less O₂ is delivered than needed:

  • This AV difference increases (tissues pull more O₂ out of each mL of blood).

🧪 Numbers to remember:

• Heart O₂ extraction ≈ 50%

• Kidney O₂ extraction ≈ 7%

• Average tissue extraction ≈ 25%

Blood Flow

Direction & Pressure Gradient

• Blood always flows:

  • Left heart → aorta → arteries → arterioles → capillaries → venules → veins → vena cava → right heart.

• This is unidirectional due to pressure gradient:

  • Arterial pressure ~100 mm Hg

  • Venous pressure ~40 mm Hg

• Fluid moves from high → low pressure, so:

  • Blood flows arterial → venous side.

Flow Equation

• ΔP = pressure difference between two ends of a vessel.

• R = resistance.

• If resistance increases, need more pressure to maintain same flow.

  • Body does this by ↑ force of heart contraction.

• If arterial resistance is chronically high:

  • Myocardium hypertrophies to generate more force.

🔴 Chronic ↑ resistance → LV hypertrophy → HF risk.

Laminar vs Turbulent Flow

• Laminar flow (normal):

  • Blood in center flows faster than blood near the wall.

• Turbulent flow occurs when:

  • Flow rate is high,

  • Viscosity increased,

  • Vessel diameter abnormally large,

  • Vessel segment narrowed or constricted.

• Turbulent flow produces abnormal sound = bruit.

🔴 Bruit = warning of stenosis, aneurysm, or other pathology.

Blood Pressure

• The text notes that Chapter 27 covers BP physiology and measurement in more detail.

• Here, BP is referenced mainly as:

  • The driving force for blood flow.

  • The creator of hydrostatic pressure in capillaries.

Capillary Filtration and Reabsorption

Fluid Exchange Basics

• Fluid is constantly moving across capillary walls, forming interstitial fluid.

  • Composition: like plasma minus proteins.

• Movement is governed by:

  • Hydrostatic pressure (pushing force)

  • Osmotic pressure (pulling force from plasma proteins)

  • Capillary permeability

Arterial vs Venous End of Capillary

• Arterial end:

  • Hydrostatic pressure high.

  • Drives fluid out of capillary → tissue space.

  • Osmotic pressure pulling fluid back in is not enough to overcome high hydrostatic.

• Venous end:

  • Hydrostatic pressure low.

  • Osmotic pressure (from plasma proteins) predominates.

  • Net movement of fluid back into capillary (reabsorption).

Lymphatic Role

• Almost all fluid filtered out at arterial end is reabsorbed at venous end.

• Excess filtered fluid → enters lymphatic circulation.

• Filtration + reabsorption + lymph formation:

  • Help maintain tissue fluid volume.

  • Remove waste and debris.

Causes of Edema

Abnormal conditions where filtered fluid > reabsorbed + drained:

• Damage to capillary walls → ↑ permeability.

• Obstructed lymphatic drainage.

• Elevated venous pressure.

• Low plasma protein osmotic pressure (e.g., low albumin).

➡ These all lead to excess interstitial fluid = edema.

🔴 Edema = key sign of venous or lymphatic problems, low protein, or high venous pressure.

Hemodynamic Resistance

Main Determinant: Radius

• Vessel radius is the most important factor for resistance.

  • Small radius change → huge resistance change.

• Main sites of resistance:

  • Arterioles

  • Precapillary sphincters

Other Factors

• Resistance is proportional to:

  • Blood viscosity (thickness)

  • Vessel length

  • Inversely to vessel diameter.

• Under normal conditions:

  • Viscosity and vessel length don’t change much.

• But:

  • Large ↑ hematocrit → ↑ viscosity → ↓ capillary flow.

💡 Clinical thought:
High Hct = “sludgy” blood → ↑ risk for tissue ischemia.

Peripheral Vascular Regulating Mechanisms

Need for Constant Regulation

• Even at rest, tissue metabolic needs change.

• The body uses a coordinated system:

  • CNS influences

  • Hormones & circulating chemicals

  • Local vessel wall activity

Sympathetic (Adrenergic) Control

• Sympathetic NS, via the hypothalamus, is main regulator of peripheral vessel caliber.

• All vessels except:

  • Capillaries

  • Precapillary sphincters
    are innervated by the sympathetic system.

• Stimulation → vasoconstriction.

  • Neurotransmitter: norepinephrine.

• Sympathetic activation occurs with:

  • Physiologic stress (e.g., hypovolemia).

  • Psychological stress (anxiety, fear).

• Reduced sympathetic activity or sympathectomy → vasodilation.

Hormonal Influences

• Epinephrine (from adrenal medulla):

  • In most tissue beds → acts like norepi → vasoconstriction.

  • In low concentrations → vasodilation in:

    • Skeletal muscles

    • Heart

    • Brain

• Renin–angiotensin system:

  • Kidney releases renin.

  • Renin + angiotensinogen → angiotensin I.

  • In lungs, ACE converts angiotensin I → angiotensin II.

  • Angiotensin II = potent arteriolar vasoconstrictor.

  • Important in abnormal states:

    • Heart failure

    • Hypovolemia

Local Vasoactive Substances

• Potent vasodilators:

  • Nitric oxide

  • Prostacyclin

  • Histamine

  • Bradykinin

  • Prostaglandins

  • Certain muscle metabolites

• Local environment changes:

  • ↓ O₂, ↓ nutrients, ↓ pH → alter local blood flow (usually ↑ flow).

• Proinflammatory cytokines:

  • Released from platelets at site of vascular injury.

  • Cause arteriolar vasoconstriction.

  • Promote continued platelet aggregation.

🔴 These mechanisms are key in inflammation, thrombosis, HF, shock.

Pathophysiology of the Vascular System

Core Pathologic Theme

• All peripheral vascular diseases share:

  • Reduced blood flow through peripheral vessels.

• Severity of consequences depends on:

  • How much tissue demand exceeds supply.

  • If demands are high, even modest flow reduction can be enough to cause damage.

• Progression:

  • ↓ flow ➡ tissues become ischemic ➡ malnourished ➡ ultimately die if blood flow not restored.

🔴 Tissue death (necrosis) = critical endpoint of untreated ischemia.

Pump Failure

• Inadequate peripheral flow also occurs when:

  • Heart fails as a pump.

Two HF Types Mentioned

1. HFrEF (heart failure with reduced ejection fraction / systolic HF):

   • Blood backs up in lungs.

   • Forward flow (cardiac output) ↓.

   • Result: Inadequate arterial blood flow to tissues.

2. HFpEF (heart failure with preserved EF / diastolic HF):

   • Causes systemic venous congestion.

   • Also leads to reduced forward flow.

🔗 Connection:
Pump failure = both arterial insufficiency (poor output) and venous congestion (backward flow).

Alterations in Blood and Lymphatic Vessels

Arterial Problems

• Arteries can be damaged or blocked by:

  • Atherosclerotic plaque

  • Thromboembolus

  • Chemical/mechanical trauma

  • Infections or inflammatory processes

  • Vasospastic disorders

  • Congenital malformations

• Sudden arterial occlusion:

  • Causes profound, often irreversible ischemia and tissue death.

  • 🔴 This is limb- or life-threatening.

• Gradual occlusion:

  • Less sudden death risk because:

    • Collateral circulation develops over time.

    • Tissues adapt to gradually reduced flow.

Venous Problems

• Venous blood flow ↓ due to:

  • Thromboembolus obstructing a vein

  • Incompetent venous valves

  • Reduced effectiveness of surrounding muscle pump

• ↓ venous outflow leads to:

  • ↑ venous pressure ➡

  • ↑ capillary hydrostatic pressure ➡

  • ↑ net filtration into interstitial space ➡

  • Edema

• Edematous tissues:

  • Get poor nutrition.

  • More prone to breakdown, injury, infection.

Lymphatic Problems

• Lymphatic obstruction (tumor, trauma, inflammation) also:

  • Causes edema (lymphedema).

  • Especially problematic because fluid is protein-rich and harder to mobilize.

Circulatory Insufficiency of the Extremities

• Many peripheral vascular diseases lead to ischemia in limbs.

• Common symptoms:

  • Pain

  • Skin changes

  • Diminished pulses

  • Possible edema

• Symptom type and severity depend on:

  • Type of disease

  • Stage

  • Extent of disease

  • Speed of development

• For this chapter:

  • Peripheral vascular disease is categorized as:

    • Arterial

    • Venous

    • Lymphatic

Gerontologic Considerations

Vascular Changes with Aging

• Intima:

  • Thickens due to cell proliferation and fibrosis.

• Media:

  • Elastin fibers become:

    • Calcified

    • Thin

    • Fragmented

  • Collagen accumulates in both intima and media.

• Result:

  • Vessels become stiffer.

Consequences

• ↑ stiffness ➡ ↑ peripheral resistance.

• ➡ Impaired blood flow.

• ➡ ↑ left ventricular workload:

  • Can cause:

    • LV hypertrophy

    • Ischemia

    • HFrEF

• In microvessels (brain, kidney):

  • Stiffness and damage can lead to:

    • Thrombosis

    • Hemorrhage

🔴 Elderly patient with sudden neuro change or kidney issues + vascular disease = high suspicion for microvascular damage.

TABLE 26-1 – Characteristics of Arterial vs Venous Insufficiency and Resulting Ulcers

General Characteristics

Pain

• Arterial:

  • Intermittent claudication → sharp, unrelenting, constant.

  • Often worse with activity & elevation, relieved by rest (early) and can become rest pain (late).

• Venous:

  • Aching, throbbing, cramping.

  • Often worse with standing; improves with elevation.

Pulses

• Arterial:

  • Diminished or absent.

• Venous:

  • Pulses present, but can be hard to feel under edema.

🔴 Absent distal pulses + pain + coolness = arterial emergency.

Skin Characteristics

• Arterial:

  • Dependent rubor (red when dangling).

  • Elevation pallor (pale when elevated).

  • Dry, shiny skin.

  • Cool–cold temperature.

  • Loss of hair over toes and foot dorsum.

  • Thickened, ridged nails.

• Venous:

  • Pigmentation in gaiter area (around medial & lateral malleolus).

  • Skin thickened, tough.

  • May appear reddish-blue.

  • Often dermatitis present.

Ulcer Characteristics

Location

• Arterial:

  • Tips of toes

  • Web spaces

  • Heel

  • Other pressure points if immobile.

• Venous:

  • Medial malleolus

  • Lateral malleolus

  • Anterior tibial area

Pain

• Arterial:

  • Very painful.

• Venous:

  • Minimal to severe pain, but often less intense than arterial.

Depth

• Arterial:

  • Deep, may involve joint space.

• Venous:

  • Superficial.

Shape

• Arterial:

  • Typically circular.

• Venous:

  • Irregular borders.

Ulcer Base

• Arterial:

  • Pale to black

  • May show wet or dry gangrene.

• Venous:

  • Granulation tissue:

    • Beefy red

    • May have yellow fibrin in chronic ulcers.

Leg Edema

• Arterial:

  • Minimal edema unless the limb is kept dependent to relieve pain.

• Venous:

  • Moderate to severe edema.

💡 Fast distinction:

• Arterial =

  • Airless skin (pale, shiny, cool),

  • Absent pulses,

  • Aching sharp pain,

  • At toes & pressure points.

• Venous =

  • Varicose-looking edema,

  • Velvety brown skin in gaiter area,

  • Very swollen legs,

  • Venous ulcers near malleoli.

🧠💥 KEY TAKEAWAYS (HIGH-YIELD)

• Perfusion basics:

  • Depends on heart pump, open responsive vessels, adequate volume, and proper neural/hormonal regulation.

• Arterioles = resistance vessels; main control of systemic vascular resistance.

• Veins = capacitance vessels; hold ~75% of blood volume and are key in venous return.

• Lymphatics:

  • Only route for large proteins to return to venous system.

  • Blockage → protein-rich edema (lymphedema).

• Capillary Starling forces:

  • Arterial end: filtration (hydrostatic > oncotic).

  • Venous end: reabsorption (oncotic > hydrostatic).

  • Disruption → edema.

• Flow equation:

  • Flow = ΔP / R.

  • ↑ resistance → heart must work harder → LV hypertrophy.

• Laminar vs turbulent flow:

  • Turbulence → bruit → think stenosis/aneurysm.

• Sympathetic & hormones:

  • Norepi/epi/angiotensin II = vasoconstrictors; key in HF/hypovolemia.

  • Local vasodilators (NO, prostacyclin, histamine, etc.) regulate regional flow.

• Ischemia progression:

  • Reduced flow → ischemia → malnutrition of tissues → death if not corrected.

• HF and vascular flow:

  • HFrEF → pulmonary congestion + ↓ forward flow.

  • HFpEF → systemic venous congestion + ↓ forward flow.

• Venous vs arterial insufficiency:

  • Arterial: pain with activity, cool, pale, no pulses, ulcers on toes/pressure points, little edema.

  • Venous: aching, edema, brown pigmentation at ankles, ulcers at malleoli, irregular & shallow, pulses intact.

• Older adults:

  • Vessel stiffening → ↑ peripheral resistance, ↑ LV workload → LV hypertrophy, ischemia, HFrEF, microvascular brain/kidney damage.

Assessment of the Vascular System

Health History 🩺

• The nurse must do a focused health history + physical exam to:

  • Establish the patient’s baseline.

  • Find alterations in the vascular system (arterial, venous, lymphatic).

• For patients with peripheral vascular disorders, the nurse needs an in-depth description of:

  • Pain (or discomfort/fatigue).

  • What brings it on (precipitating factors).

  • What relieves it.

  • Pattern (how far they can walk, when it starts, what it feels like).

Intermittent Claudication (Arterial Insufficiency Pain) 🦵

• Patients with peripheral arterial insufficiency experience:

  • Muscular, cramp-type pain, discomfort, or fatigue in extremities.

  • Pain is:

    • Consistently reproduced with the same degree of activity or exercise.

    • Relieved by rest.

• This classic pattern is called intermittent claudication:

  • Happens because the arterial system cannot deliver enough blood to meet the increased demand for oxygen/nutrients during exercise.

  • Tissues must complete their energy cycle without enough O₂ and nutrients, so:

    • Muscle metabolites + lactic acid are produced.

    • These metabolites irritate nearby nerve endings → the patient feels pain.

• Degree of obstruction required before symptoms appear:

  • About 50% of the arterial lumen
    OR

  • About 75% of the cross-sectional area must be obstructed before intermittent claudication is felt.

• When the patient rests:

  • Muscle O₂ demand drops.

  • Metabolic needs ↓.

  • Pain subsides.

• The progression of arterial disease can be monitored by:

  • Documenting:

    • The amount of exercise.

    • The distance walked before onset of pain.

  • Distance is measured in:

    • Blocks, feet, or meters.

💡 Clinical pattern:
“Every time I walk 2 blocks my calves cramp, when I stop and rest, it goes away” → classic intermittent claudication.

Rest Pain (Severe Arterial Insufficiency) 🔴

• Rest pain:

  • Persistent pain in the forefoot (anterior part of the foot) when the patient is resting.

  • Indicates a severe degree of arterial insufficiency and a critical state of ischemia.

• Characteristics:

  • Often worse at night.

  • May interfere with sleep.

  • Frequently, the patient has to lower the extremity into a dependent position (hanging off the bed) to:

    • Improve perfusion to distal tissues.

    • Temporarily relieve the pain.

🔴 Red-flag:

• Rest pain = critical ischemia, much more serious than intermittent claudication.

Using Pain Location to Deduce the Site of Disease 🧠

• The site of arterial disease can often be inferred from where the claudication occurs because:

  • Pain is felt in muscle groups distal to the diseased vessel.

• Examples:

  • Calf pain:

    • Suggests reduced blood flow in:

      • Superficial femoral artery

      • Popliteal artery.

  • Hip or buttock pain:

    • Suggests reduced blood flow in:

      • Abdominal aorta

      • Common iliac artery

      • Hypogastric (internal iliac) artery.

💡 Clinical mapping:
Higher up the blockage ➡ pain higher up the leg (buttocks/hip).
More distal blockage ➡ pain lower (calf).

Physical Assessment

• Physical exam should focus on:

  • Skin color

  • Skin temperature

  • Peripheral pulses (presence, strength, symmetry).

Inspection of the Skin 👀

• With adequate blood flow:

  • Extremities are warm.

  • In lighter skin tones → rosy coloring.

• With inadequate blood flow:

  • Extremities become cool.

  • Skin appears pale.

• In people with pigmented (darker) skin:

  • Color changes are harder to detect.

  • Nurse must look more carefully.

Effects of Elevation and Dependency

• When blood flow is further reduced:

  • Elevation of the extremity can lead to:

    • Pallor → a whiter or more blanched appearance.

• When the extremity is placed in a dependent position:

  • Within 20 seconds to 2 minutes, rubor may appear:

    • Reddish-blue discoloration of the extremities.

    • Rubor suggests severe peripheral arterial damage.

    • It indicates vessels that cannot constrict and remain dilated.

  • Even with rubor, the extremity becomes pale again when elevated.

• Cyanosis:

  • Bluish tint of the skin.

  • Occurs when the amount of oxygenated hemoglobin in the blood is reduced.

Chronic Nutrient Deficiency Changes

Chronic reduction in nutrient supply to tissues leads to:

• Loss of hair on the extremity.

• Brittle nails.

• Dry or scaling skin.

• Atrophy (tissue wasting).

• Ulcerations.

• Edema:

  • May be bilateral or unilateral.

  • Often related to:

    • Keeping the affected extremity in a dependent position because of rest pain.

• Gangrenous changes:

  • Occur after prolonged, severe ischemia.

  • Represent tissue necrosis (death).

🔴 Red-flag signs:

• Elevation pallor + dependent rubor

• Hair loss, shiny skin

• Ulcers, especially with gangrene
  → Strong indicators of advanced arterial disease.

Palpation of Pulses ✋

• Assessing the presence/absence and quality of peripheral pulses is essential in evaluating peripheral arterial circulation.

• This is visually referenced by Fig. 26-2 (pulse sites), but your text gives the key principles.

Technique Considerations

• In an edematous extremity, pulse assessment must be done carefully.

  • Palpation is subjective, and there’s a risk:

    • The nurse can accidentally feel their own pulse instead of the patient’s.

To avoid this error:

• Use light touch.

• Use more than just the index finger:

  • The index finger has the strongest arterial pulsation of all the fingers.

• Do NOT use the thumb:

  • The thumb has a strong arterial pulse of its own.

Interpretation of Pulses

• Absence of a pulse may indicate:

  • The site of stenosis or occlusion is proximal (above) that level.

• Occlusive arterial disease:

  • Impairs blood flow.

  • Can reduce or obliterate palpable pulses in the extremities.

Comparing Pulses

• Pulses should be palpated:

  • Bilaterally

  • Simultaneously (same level on both sides).

• Compare for:

  • Symmetry in:

    • Rate

    • Rhythm

    • Quality (strength)

🔴 Key clinical principle:

• A missing or much weaker pulse on one side compared to the other suggests arterial disease at or above that level.

🧠💥 KEY TAKEAWAYS FROM THIS SECTION

• History matters:

  • Ask detailed questions about pain location, pattern, triggers, and relief.

• Intermittent claudication:

  • Cramping/fatigue in muscles with the same level of exercise, relieved by rest.

  • Occurs when ≥50% lumen or 75% cross-sectional area obstructed.

• Rest pain:

  • Forefoot pain at rest, worse at night.

  • Patient often dangles leg to relieve pain.

  • 🔴 Indicates critical ischemia and severe arterial insufficiency.

• Pain location tells you blockage level:

  • Calf pain → femoral/popliteal disease.

  • Hip/buttock pain → aorta/iliac/internal iliac disease.

• Skin inspection clues:

  • Elevation pallor + dependent rubor → severe arterial disease.

  • Cyanosis → reduced oxygenated hemoglobin.

  • Chronic signs: hair loss, brittle nails, dry/scaly skin, atrophy, ulcers, gangrene.

• Edema in arterial disease:

  • Can occur when limb is kept dependent to relieve rest pain.

• Pulse assessment:

  • Use light touch, not thumb, and not only index finger.

  • Compare bilaterally & simultaneously.

  • Absent or diminished pulses → possible proximal stenosis or occlusion.

• Advanced arterial disease:

  • Pain (claudication → rest pain), color changes, trophic skin changes, ulcers, gangrene, and pulse changes all fit together.

Diagnostic Evaluation

The nurse’s role here is education + trend-watching:

• Explain to the patient:

  • Why each test is being done.

  • What to expect.

  • Possible side effects.

• Look at trends (not just single values):

  • Trends tell you about disease progression and response to therapy.

• These tests target arteries, veins, and lymphatics to identify structural or flow abnormalities.

Doppler Ultrasound Flow Studies

Purpose

• Used when pulses cannot be reliably palpated.

• A handheld continuous wave (CW) Doppler detects blood flow.

How It Works

• Device emits a continuous ultrasound signal into tissues.

• Moving blood cells reflect the signal back.

• The device filters and outputs the signal to:

  • Speaker or headphones, where the clinician hears:

    • Arterial vs venous flow patterns.

Frequency & Depth

• Depth of detection depends on the Doppler frequency (MHz):

  • Lower frequency → deeper penetration.

  • A 5–10 MHz probe is used to evaluate peripheral arteries.

Technique (Lower Extremity)

• Patient position:

  • Supine, head of bed elevated 20–30°.

  • Legs externally rotated, if possible → better access to medial malleolus.

• Steps:

  • Apply acoustic water-soluble gel to skin → uniform ultrasound transmission.

  • Place Doppler transducer at 45–60° angle over expected artery location.

  • Angle slowly to find arterial blood flow.

  • Avoid excessive pressure:

    • Severely diseased arteries may collapse even with minimal pressure.

Interpretation

• The transducer can detect blood flow even in advanced arterial disease, especially if collaterals exist.

• Important nuance:

  • Detecting a signal only tells you there is some blood flow, not whether it’s adequate.

• Critical nursing point:

  • If a signal was present before and is now absent, the provider must be notified immediately. 🔴

Link to ABI

• CW Doppler is most useful when combined with:

  • Ankle pressures → to calculate Ankle-Brachial Index (ABI) (Fig. 26-3).

• ABI:

  • Ratio: systolic pressure at ankle ÷ systolic pressure at arm.

  • Used to quantify degree of arterial stenosis:

    • As arterial narrowing increases, systolic pressure distal to narrowing decreases.

Ankle-Brachial Index (ABI)

Step-by-Step Procedure

1. Patient Rest

   • Rest supine (not seated) for ~5 minutes.

2. Cuff Placement at Ankles

   • Use appropriate cuff (e.g., 10-cm cuff for average adult).

   • Place cuff above malleolus.

3. Identify Ankle Arterial Signals

   • Use Doppler to locate:

     • Posterior tibial artery

     • Dorsalis pedis artery

   • Obtain systolic pressures in both ankles, listening via Doppler.

   • Diastolic pressures cannot be measured with Doppler at the ankle.

   • If you cannot obtain pressures from posterior tibial or dorsalis pedis:

     • Measure in peroneal artery at ankle.

4. Measure Brachial Pressures

   • Use Doppler to measure brachial systolic pressures in both arms.

   • Why both?

     • There may be asymptomatic stenosis in the subclavian artery, causing:

       • One brachial pressure to be 15–20 mm Hg or more lower than systemic.

     • That abnormally low pressure must NOT be used in ABI calculation.

5. Calculate ABI

   • For each ankle:

     • Take the highest ankle systolic (posterior tibial or dorsalis pedis).

     • Divide it by the higher of the two brachial systolic pressures.

   • Example from the text:

   Given:

   • Right brachial: 160

   • Left brachial: 120 → use 160 (higher)

   • Right posterior tibial: 80

   • Right dorsalis pedis: 60 → use 80

   • Left posterior tibial: 100

   • Left dorsalis pedis: 120 → use 120

   Right ABI = 80 / 160 = 0.50
   Left ABI = 120 / 160 = 0.75

Normal ABI

• In a healthy person:

  • Systolic ankle pressure is the same or slightly higher than brachial.

  • ABI ≈ 1.0 → indicates no arterial insufficiency.

Nursing Implications for ABI

• Nurses should perform a baseline ABI on:

  • Any patient with decreased pulses.

  • Any patient ≥65 years, especially with:

    • Diabetes

    • Nicotine use (smoking or other forms).

• ABIs should also be done:

  • After arterial interventions or surgery, per protocol.

  • When there is a change in clinical status, such as:

    • Sudden cold limb

    • Sudden painful limb 🔴

Patient Teaching Before ABI

• Explain:

  • Indications: why the ABI is needed.

  • What to expect: cuffs on arms/ankles, Doppler probe, lying flat.

• In nonurgent testing:

  • Instruct to avoid nicotine and caffeinated beverages for at least 2 hours before.

• Warn:

  • There may be some discomfort when cuffs are inflated.

Chart 26-1 – Avoiding Common ABI Errors (What It Really Means)

This chart is about getting accurate ABI measurements.

Cuff Size

• Use correctly sized BP cuffs:

  • Bladder width ≥ 40% of limb circumference.

  • Bladder length ≥ 80% of limb circumference.

• Document cuff size in the nursing plan of care:

  • Example: “12-cm adult cuff for brachial; 10-cm pediatric cuff for ankle.”

  • This prevents shift-to-shift discrepancies.

Cuff Inflation & Deflation

• Inflation:

  • Inflate cuff 20–30 mm Hg above the point where the last arterial signal is heard.

  • Ensures complete artery closure for accurate systolic measurement.

• Deflation:

  • Deflate at:

    • 2–4 mm Hg per second for patients without arrhythmias.

    • 2 mm Hg per second or slower for patients with arrhythmias.

  • Deflating too fast:

    • May miss the true highest pressure → falsely low BP.

Medial Calcific Sclerosis

• Suspect medial calcific sclerosis if:

  • ABI ≥1.20

  • or Ankle pressure >250 mm Hg.

• It is associated with:

  • Diabetes

  • Chronic kidney disease

  • Hyperparathyroidism

• These conditions harden the media of arteries → noncompressible vessels → falsely elevated ankle pressures.

Pressures That Are Suspiciously Low

• Be cautious if arterial pressure recorded is <40 mm Hg.

  • May mean the nurse is actually hearing a venous signal, not arterial.

• If arterial pressure (normally ~120 mm Hg) is measured <40 mm Hg:

  • Ask a colleague to double-check before accepting it.

Chart 26-2 – ABI Ranges & Ischemic Manifestations

These ranges classify disease severity.

• ABI > 1.40

  • Abnormal

  • Indicates noncompressible arteries

  • Requires further testing with Toe-Brachial Index (TBI).

• ABI 1.00–1.40

  • Normal

• ABI 0.91–0.99

  • Borderline

• ABI ≤ 0.90

  • Abnormal

• ABI 0.50–0.90

  • Mild to moderate arterial insufficiency

  • Usually seen in patients with claudication.

• ABI < 0.50

  • Seen in patients with ischemic rest pain.

• ABI ≤ 0.40

  • Indicates severe ischemia or tissue loss (e.g., ulcers, gangrene).

🔴 Key thresholds:

• ≤0.90 → PAD present.

• <0.50 → rest pain.

• ≤0.40 → severe ischemia/tissue loss.

Exercise Testing

Purpose

• Determines:

  • How long a patient can walk.

  • How their ankle systolic pressure responds to walking.

Method

• Before exercise:

  • Obtain brachial systolic BP in each arm.

• Standard treadmill protocol:

  • Walk at 1.5 mph.

  • 12% incline.

  • Maximum of 5 minutes or until claudication occurs.

• Variations:

  • Gradual rise in speed and incline to the point of claudication.

  • Modified test:

    • Walking a set distance in a hallway.

    • Cycling may be used to approximate walking capacity.

Who Can Do It?

• Most patients can complete it unless they have:

  • Significant arterial insufficiency.

  • Severe cardiac disease.

  • Severe pulmonary disease.

  • Orthopedic problems.

  • Physical disability.

Normal vs Abnormal Response

• Normal:

  • Little or no drop in ankle systolic pressure after exercise.

• True vascular claudication:

  • Ankle pressure drops after exercise.

• Results:

  • Walking time + hemodynamic changes help determine whether intervention is needed.

Nursing Role

• Reassure patient:

  • They won’t be required to run.

  • It usually involves walking on a slight incline.

• If cycling is used:

  • It is to estimate walking ability without requiring actual walking.

Duplex Ultrasonography

What It Is

• Combines:

  • B-mode grayscale imaging of tissues, organs, and blood vessels.

  • Pulsed Doppler to estimate velocity changes.

• Color flow techniques:

  • Help identify vessels and shorten exam time (Fig. 26-5).

Uses

• Evaluate:

  • Level and extent of venous disease.

  • Chronicity (how long it’s been there).

• Using B-mode and Doppler, it can:

  • Image and assess blood flow.

  • Evaluate distal vessel flow.

  • Locate stenosis vs occlusion.

  • Determine anatomic morphology and hemodynamic significance of plaque.

Role in Care

• Helps:

  • Plan treatment.

  • Monitor outcomes of treatment.

• Advantages:

  • Noninvasive.

  • Usually needs no prep.

  • Portable → can be used anywhere:

    • Initial diagnosis.

    • Screening.

    • Follow-up.

Special Prep (Abdominal Vascular Duplex)

• For abdominal vascular studies:

  • Patient should be NPO at least 6 hours before.

  • Reason: reduce bowel gas that can interfere with imaging.

Computed Tomography (CT) Scanning

What CT Shows

• Provides cross-sectional images of soft tissue.

• Visualizes:

  • Areas of volume change in an extremity.

  • Which compartment those changes occur in.

• Abdominal CT:

  • Useful to monitor aorta, such as:

    • Increasing aortic diameter → suggests aneurysm formation.

• CT of lymphedematous limb:

  • Shows characteristic honeycomb pattern in subcutaneous tissue.

Multidetector CT (MDCT)

• Uses:

  • Spiral CT scanner.

  • Rapid IV infusion of contrast.

• Produces:

  • Very thin sections.

  • 3D reconstructions that can be rotated and viewed from multiple angles.

• Technique:

  • Scanner head moves circumferentially around the patient.

  • Patient is moved through scanner.

  • Creates overlapping images in a continuous spiral.

• Pros:

  • Short scan times.

• Cons:

  • Exposure to x-rays.

  • Requires contrast injection.

  • High-volume contrast via peripheral vein may contraindicate MDCT in:

    • Children

    • Patients with significantly impaired renal function.

Nursing Implications for MDCT

• Patients with impaired renal function:

  • May need preprocedural treatment to prevent contrast-induced nephropathy:

    • Oral or IV hydration 6–12 hours before.

    • Sodium bicarbonate:

      • Alkalinizes urine.

      • Protects against free radical damage.

  • Studies do NOT support using:

    • Oral or IV N-acetylcysteine for protection.

• Postprocedure:

  • Encourage fluids.

  • Monitor urine output:

    • Should be at least 0.5 mL/kg/hour.

  • Watch for contrast-induced acute kidney injury:

    • Can occur within 48–96 hours postprocedure.

    • If it occurs, the nurse should notify the primary provider.

• Patients with iodine or shellfish allergies:

  • May need premedication with:

    • Steroids

    • Histamine blockers

Angiography

Purpose

• Angiography produces an arteriogram.

• Used to:

  • Confirm occlusive arterial disease, especially when surgery or intervention is considered.

• How:

  • Inject radiopaque contrast agent directly into the arterial system.

  • Visualize:

    • Obstructions

    • Aneurysms

    • Collateral circulation

Patient Experience

• May feel a temporary warmth as contrast is injected.

• Local irritation can occur at injection site.

Allergic Reactions (Iodine Contrast) 🔴

• Rare but serious immediate or delayed reactions:

  • Dyspnea

  • Nausea & vomiting

  • Sweating

  • Tachycardia

  • Numbness of extremities

• These must be reported immediately.

• Possible treatments:

  • Epinephrine

  • Antihistamines

  • Corticosteroids

Other Risks

• Vessel injury

• Acute arterial occlusion

• Bleeding

• Contrast nephropathy

Magnetic Resonance Angiography (MRA)

What It Is

• Uses a standard MRI scanner with special software:

  • Isolates blood vessels from surrounding tissues.

• Produces images that can be:

  • Rotated and viewed from multiple angles.

Nursing Implications

• Contraindicated in patients with certain metal implants.

Pre-Scan Assessment

Check for:

• Aneurysm clips

• Old tattoos:

  • May contain trace elements (newer materials like nitinol and titanium are MRI-compatible).

• Some medication patches

• Any cardiac implantable electronic device (CIED):

  • These patients must be screened to see if MRI is safe.

Patient Teaching (What It Feels Like)

• The patient will lie on a cold, hard table.

• Table slides into a small enclosed tube.

• They will hear:

  • Noises, including banging and popping.

• For claustrophobia:

  • May receive a sedative beforehand.

  • Instruct to close eyes before entering and keep them closed.

  • Reassure:

    • A panic button is provided.

    • They can press it if they need to stop.

Post-Procedure Care

• MRA uses IV contrast dye.

• Nursing implications afterward are the same as MDCT:

  • Hydration

  • Monitoring kidney function/urine output

  • Watching for contrast-induced nephropathy.

Contrast Phlebography (Venography)

What It Is

• Involves injecting a radiopaque contrast agent into the venous system.

• If a thrombus is present:

  • The x-ray shows an unfilled segment in an otherwise filled vein.

Patient Experience

• Injection may cause brief but painful inflammation of the vein.

Current Role

• Rarely performed now.

• Duplex ultrasonography is the standard for diagnosing lower extremity venous thrombosis.

Nursing Responsibilities

• Instruct patient:

  • They will receive contrast dye through a peripheral vein.

  • They will be monitored 2 hours post-venogram for:

    • Access site oozing

    • Hematoma

• Post care:

  • Follows same guidelines as MDCT (monitoring, fluids, kidney function).

Lymphoscintigraphy

What It Is

• Involves injection of radioactively labeled colloid:

  • Injected subcutaneously in the second interdigital space (between toes or fingers).

• The extremity is then exercised:

  • Helps uptake of the colloid by lymphatic system.

• Serial images are taken at preset intervals to:

  • Visualize lymphatic flow and obstruction.

Nursing Implications

• Educate patient about expectations:

  • Blue dye used may stain the injection site.

  • If the patient has a lymphatic leak (e.g., from groin incision):

    • There may be blue drainage from the incision.

    • This can persist for several days until the dye clears.

🧠💥 Key Takeaways

• Doppler + ABI are frontline tools for PAD assessment:

  • ABI = ankle systolic / highest brachial systolic.

  • Normal ≈ 1.0.

  • ≤0.90 = PAD;
    <0.50 = rest pain;
    ≤0.40 = severe ischemia/tissue loss.

• Always:

  • Use correct cuff size, adequate inflation, and slow deflation for ABI.

  • Watch for falsely high ABIs with noncompressible arteries (>1.20, ankle >250 mm Hg).

• Exercise testing:

  • True vascular claudication → drop in ankle pressure after walking.

• Duplex ultrasound:

  • Noninvasive, portable; evaluates venous and arterial disease, stenosis vs occlusion, chronicity.

• CT/MDCT:

  • Great for aneurysms, lymphedema patterns, 3D vascular imaging.

  • Contrast risk: contrast-induced nephropathy, especially in kidney disease.

• Angiography:

  • Direct arterial imaging for surgical planning.

  • Watch for allergic reactions, bleeding, acute occlusion, nephropathy.

• MRA:

  • Requires strict metal implant and device screening.

  • Claustrophobia and noise → prepare and premedicate if needed.

• Venography:

  • Now rarely used; replaced by duplex ultrasound for DVT.

• Lymphoscintigraphy:

  • Visualizes lymph flow; blue dye can stain skin and leak through incisions.

ARTERIAL DISORDERS

Arterial disorders → ischemia ➡ tissue necrosis.
They can result from:

• Chronic, progressive changes (e.g., atherosclerosis).

• Acute loss of blood flow (e.g., aneurysm rupture).

When arteries fail, the downstream tissues starve and die unless perfusion is restored.

Arteriosclerosis and Atherosclerosis

• Arteriosclerosis = “hardening of the arteries”

  • Most common arterial disease.

  • Diffuse process:

    • Muscle fibers + endothelial lining of small arteries and arterioles become thickened.

• Atherosclerosis = intimal disease of large and medium-sized arteries.

  • Characterized by accumulation of:

    • Lipids

    • Calcium

    • Blood components

    • Carbohydrates

    • Fibrous tissue

  • On the intimal layer → form atheromas / plaques.

• In reality:

  • These processes usually coexist.

  • Terms are often used interchangeably.

  • Atherosclerosis is generalized:

    • If it’s in the legs, it’s usually elsewhere too (coronaries, carotids, etc.).

Pathophysiology

Direct & Indirect Results

Direct results of atherosclerosis in arteries:

• Stenosis (narrowing of lumen)

• Thrombosis (clot forming on plaque)

• Aneurysm

• Ulceration

• Rupture

Indirect results:

• Malnutrition of organs served by affected arteries.

• Over time → fibrosis of those organs.

🧬 Tissue response:

• All active tissues need abundant O₂ + nutrients.

• If reduction in supply is severe & permanent:

  • Cells → ischemic necrosis (death from low blood flow).

  • Replaced by fibrous tissue:

    • Needs much less blood.

    • But doesn’t function like original tissue.

Common Sites

Atherosclerosis can appear anywhere, but is more common:

• At bifurcation points or branch sites → turbulent flow.

• In proximal lower extremity:

  • Distal abdominal aorta

  • Common iliac arteries

  • Orifice of:

    • Superficial femoral

    • Profunda femoris arteries

  • Superficial femoral artery in the adductor canal (a narrow segment).

• Below the knee:

  • Can occur anywhere along arterial course.

• Males → more below-the-knee pathology than females.

Reaction-to-Injury Theory

No single theory explains atherosclerosis fully, but the reaction-to-injury theory is key:

• Endothelial cell injury is the trigger:

  • Causes:

    • Prolonged hemodynamic forces (shear stress, turbulent flow)

    • Irradiation

    • Chemical exposure

    • Chronic hyperlipidemia

• Injury leads to:

  • ↑ platelet aggregation and monocyte adherence at the injury site.

  • Smooth muscle cells migrate + proliferate into intima.

  • Formation of collagen + elastic fiber matrix.

  • ➡ Progressive plaque formation.

Types of Atherosclerotic Lesions

1. Fatty Streaks

   • Yellow, smooth, slightly protrude into lumen.

   • Composed of:

     • Lipids

     • Elongated smooth muscle cells.

   • Found in arteries of all ages, even infants.

   • Clinical:

     • Unclear if they lead to plaques or are reversible.

     • Generally do not cause symptoms.

2. Fibrous Plaques

   • Composed of:

     • Smooth muscle cells

     • Collagen fibers

     • Plasma components

     • Lipids

   • White to white-yellow, protrude variably into lumen.

   • Can partially or completely obstruct.

   • Frequently found in:

     • Abdominal aorta

     • Coronary arteries

     • Popliteal arteries

     • Internal carotid arteries

   • Believed to be progressive lesions.

Collateral Circulation

• Gradual narrowing of arterial lumen:

  • Stimulates collateral circulation (Fig. 26-7).

  • Collaterals:

    • Preexisting tiny vessels that enlarge to bypass stenosis/occlusion.

    • Help maintain perfusion.

• But:

  • Often insufficient when metabolic demand ↑.

  • ➡ Ischemia still occurs with activity.

Figure 26-6 (Progression Overview)

• Shows progression:

  • Fatty streak → fibrous plaque → atheroma.

  • Atheromatous plaque may be complicated by:

    • Hemorrhage

    • Ulceration

    • Calcification

    • Thrombosis

  • Complications lead to:

    • MI

    • Stroke

    • Claudication

    • Rest pain

    • Gangrene

🔴 Once plaques become complicated (ulcerated, thrombosed), risk for acute events skyrockets.

Risk Factors

Chart 26-3 + text = risk profile for atherosclerosis & PAD.

Nicotine (Tobacco, ENDS, Chew) 🚭

• One of the most important risk factors.

• Nicotine:

  • Decreases blood flow to extremities.

  • Increases HR & BP via sympathetic stimulation → vasoconstriction.

  • ↑ Platelet aggregation → ↑ clot risk.

• Carbon monoxide (from smoking):

  • Binds hemoglobin more readily than oxygen.

  • ➡ Tissues deprived of O₂.

• Smoking also:

  • ↓ HDL (good cholesterol).

  • Alters ratios:

    • HDL:LDL

    • HDL:triglycerides

    • HDL:total cholesterol.

• Amount of tobacco (cigarettes, e-cigs, chew) is directly related to disease extent.

• Cessation of any nicotine product → reduced risk.

Chart 26-3 – Risk Factors for Atherosclerosis & PAD

Modifiable:

• Nicotine use (cigs, e-cigs, chewing tobacco)

• Diabetes:

  • Thickens basement membranes in large + small vessels.

  • Speeds atherosclerosis.

• Hypertension

• Hyperlipidemia

• Diet that promotes hyperlipidemia.

• Stress

• Sedentary lifestyle

• Elevated C-reactive protein (CRP)

• Hyperhomocysteinemia

Nonmodifiable:

• Increasing age

• Familial predisposition / genetics

Diabetes & PAD

• Diabetes:

  • 2–4× increased risk of PAD.

  • Amputation rates 5–10× higher than non-diabetics.

  • Earlier onset + more rapid progression.

  • Different distribution:

    • More severe disease in:

      • Profunda femoris

      • All segments below the knee.

• Mechanisms (multifactorial):

  • Inflammatory activation

  • Cellular derangement in vessel walls

  • Pro-coagulant state

  • Impaired fibrinolysis
    ➡ More plaque, more clots, more obstruction.

• Other contributors:

  • Obesity

  • Stress

  • Lack of exercise

C-Reactive Protein (CRP)

• CRP = sensitive marker of cardiovascular inflammation:

  • At systemic and local levels.

• Slight CRP elevation + other risk factors (age, HTN, high cholesterol, obesity, ↑ glucose, nicotine, family history) → ↑ vascular damage risk.

Hyperhomocysteinemia

• Linked to increased risk of:

  • Peripheral artery disease

  • Cerebrovascular disease

  • Coronary artery disease

  • Venous thromboembolism (VTE)

• Homocysteine:

  • Promotes coagulation:

    • ↑ Factor V and XI activity.

    • ↓ Protein C activation.

    • ↑ binding of lipoprotein(a) to fibrin.

  • ➡ ↑ thrombin formation → ↑ thrombosis risk.

• Folic acid & vitamin B12:

  • Lower serum homocysteine.

  • BUT: No data show they reduce cardiovascular events.

  • ➡ B-complex vitamins are NOT recommended solely to reduce cardiovascular disease in PAD.

Prevention

• Intermittent claudication = symptom of generalized atherosclerosis.

  • May indicate plaques in:

    • Coronary arteries

    • Carotids

    • Other vascular beds.

• Because high-fat diets are suspected contributors:

  • Reasonable to:

    • Measure serum cholesterol.

    • Start diet modification for prevention.

Dietary Measures (AHA)

• Reduce total fat intake.

• Substitute unsaturated fats for saturated fats.

• Decrease cholesterol intake.

• Goal: Reduce cardiovascular disease risk.

Medications to Lower Lipids

• First-line (ACC/AHA) for PAD, secondary prevention & CV risk reduction:

  • HMG-CoA reductase inhibitors (statins):

    • Atorvastatin

    • Lovastatin

    • Pitavastatin

    • Pravastatin

    • Simvastatin

    • Fluvastatin

    • Rosuvastatin

• Other lipid-lowering classes:

  • Bile acid sequestrants:

    • Cholestyramine

    • Colesevelam

    • Colestipol

  • Nicotinic acid (niacin)

  • Fibric acid derivatives:

    • Gemfibrozil

    • Fenofibrate

  • Cholesterol absorption inhibitor:

    • Ezetimibe

• Patients on long-term therapy:

  • Need close monitoring.

Hypertension & Atherosclerosis

• HTN:

  • Accelerates atherosclerotic lesion formation, especially in high-pressure vessels.

  • Complications:

    • Stroke

    • Ischemic renal disease

    • Severe PAD

    • Coronary artery disease

• HTN is a major PAD risk factor:

  • May be more significant for women.

• Most patients:

  • Need >2 antihypertensive agents to reach target BP.

  • ≥⅓ need >3 agents.

• Bottom line:

  • The more risk factors present, the higher the risk.

  • Eliminating controllable risk factors, especially nicotine, is strongly recommended.

Clinical Manifestations

• Depends on which organ is affected:

  • Coronary atherosclerosis: angina, MI (Chapter 23).

  • Cerebrovascular disease: TIA, stroke (Chapter 62).

  • Aorta & extremities: covered later in this chapter.

  • Renal (renovascular disease): RAS, end-stage kidney disease (Chapter 48).

Medical Management

Management of atherosclerosis includes:

• Risk factor modification

• Controlled exercise program:

  • Improves circulation.

  • Improves functional capacity.

• Medication therapy

• Interventional/surgical procedures

Surgical Management

• Vascular surgery divided into:

1. Inflow procedures:

   • Improve blood supply from aorta → femoral artery.

2. Outflow procedures:

   • Improve blood supply to vessels below the femoral artery.

• Inflow procedures discussed with aorta diseases.

• Outflow procedures discussed with PAD.

Endovascular Therapy

Endovascular = catheter-based interventions via puncture/small incision.

• Replaced many open surgical approaches.

Indications

• When imaging shows isolated lesion(s):

  • Options:

    • Angioplasty / PTA (percutaneous transluminal angioplasty)

    • Atherectomy

Angioplasty (PTA)

• After local anesthetic:

  • Balloon-tipped catheter is guided across stenosis.

• Mechanism:

  • Likely cracks and flattens plaque against vessel wall.

  • Some theorize over-stretching of elastic fibers in nondiseased segments → dilation.

Atherectomy

• Reduces plaque using:

  • Cutting device or

  • Laser.

Complications (PTA/Atherectomy)

• Hematoma

• Embolus (plaque or clot debris traveling distally)

• Dissection (intimal separation)

• Acute arterial occlusion

• Bleeding

Stents & Stent Grafts

• Used to decrease restenosis risk:

  • Small mesh tubes:

    • Nitinol

    • Titanium

    • Stainless steel

• Placed after balloon deflation to support arterial walls and prevent collapse.

• Best for short-segment stenoses.

Complications:

• Distal embolization

• Dissection

• Dislodgment

Advantages:

• Shorter hospital stay.

• Many procedures are now outpatient.

Nursing Management

Chart 26-4 gives an overview (not reproduced), but key nursing focuses:

• Improve peripheral arterial circulation

• Promote vasodilation & prevent vascular compression

• Relieve pain

• Maintain tissue integrity

• Address special considerations in older adults

• Support home & community-based care

Improving Peripheral Arterial Circulation

• Arterial blood flow can be improved by:

  • Positioning the limb below heart level.

For lower extremities:

• Elevate head of bed.

• Use recliner.

• Have patient sit with feet on the floor (not elevated).

Concept Mastery Alert

• PAD:

  • Problem: arterial inflow.

  • Goal: enhance blood flow down to legs.

  • Position: neutral or dependent legs.

• Venous insufficiency:

  • Problem: venous return.

  • Goal: enhance return to heart.

  • Position: elevate legs.

• Exercise:

  • PAD: promotes collateral circulation (arterial).

  • Venous disease: enhances musculovenous pump.

Walking / Exercise Program

• Nurse can:

  • Assist with walking or moderate / graded isometric exercises.

  • Purpose:

    • Promote blood flow.

    • Encourage collateral development.

• Determine:

  • Baseline exercise tolerance before pain occurs.

• Teach:

  • Walk to point of pain.

  • Rest until pain subsides.

  • Resume walking.

  • Pain = signal of inadequate O₂ → time to rest.

• A Supervised Exercise Therapy (SET) program:

  • Should be prescribed for claudication.

  • Can increase walking distance before pain.

• Always consult primary provider before starting exercise/SET.

Contraindications to exercise:

• Leg ulcers

• Cellulitis

• Gangrene

• Acute thrombotic occlusions

Promoting Vasodilation & Preventing Vascular Compression

• Goal: Arterial dilation → ↑ blood flow.

• But:

  • Severely sclerosed, inelastic, damaged arteries may not dilate well.

  • Meds/endovascular procedures may have limited effect.

Nursing Interventions

• Apply warmth (within safe limits) to promote arterial flow.

• Teach to avoid cold exposure:

  • Cold → vasoconstriction.

• Recommend adequate clothing and warm environments.

Quality and Safety Nursing Alert – Heat Use

• Patients should:

  • Test bath water temperature first.

  • Avoid hot-water bottles & heating pads directly on extremities.

• Safer:

  • Apply heat (bottle/pad) to abdomen:

    • Causes reflex vasodilation in extremities.

Vasospastic Disorders (e.g., Raynaud’s)

• Heat may be applied directly to ischemic extremities using:

  • Warmed or electric blanket.

• BUT:

  • Temperature must not exceed body temperature.

  • Even low temps can cause tissue trauma in ischemic limbs.

Quality and Safety Nursing Alert – Excess Heat

• Too much heat:

  • ↑ Metabolic rate in extremity.

  • ↑ O₂ demand beyond what diseased artery can deliver.

• 🔴 Result: worsened ischemia, potential tissue damage.

• Therefore:

  • Heat must be used with great caution.

Nicotine & Emotional Stress

• Nicotine:

  • Causes vasospasm, markedly reduces circulation.

  • Impairs O₂ transport and use.

  • Increases blood viscosity.

• Patients with arterial insufficiency who:

  • Smoke

  • Chew tobacco

  • Use ENDS (e-cigs, e-pens, e-pipes, e-hookahs, e-cigars)
    → Must be fully educated on these effects and strongly encouraged to quit.

• Emotional stress:

  • Activates sympathetic NS → peripheral vasoconstriction.

• Stress management:

  • Avoid stressors where possible.

  • Use structured stress management.

  • Consider:

    • Counseling

    • Relaxation

    • Yoga

    • Aromatherapy

    • Mindfulness

Avoiding Compression

• Constrictive clothing/accessories:

  • Tight socks

  • Tight shoelaces
    → Can impede arterial flow and ↑ venous stasis → avoid.

• Leg crossing:

  • Crossing legs for >15 minutes compresses leg vessels.

  • Should be discouraged.

Relieving Pain

• PAD pain:

  • Often chronic, continuous, disabling.

  • Impacts:

    • Activity

    • Work

    • Sleep

    • Overall well-being

• Patients may:

  • Be depressed, irritable.

  • Lack energy to adhere to therapy.

• Analgesics that may help:

  • Hydrocodone + acetaminophen

  • Oxycodone

  • Oxycodone + acetylsalicylic acid (ASA)

  • Oxycodone + acetaminophen

• Pain control:

  • Helps patients participate in circulation-improving therapies.

• Caution:

  • Especially in older adults:

    • These meds ↑ risk of:

      • Delirium

      • Falls

  • For all:

    • Must consider dependence issues.

Maintaining Tissue Integrity

• Poor perfusion = high risk for damage + infection.

• PAD + diabetes → very high risk.

• Once lesions occur:

  • Healing is delayed because of poor blood supply.

  • Nonhealing ulcers:

    • Can be debilitating.

    • Expensive to treat.

    • May lead to amputation (toe, forefoot, or limb).

• Prevention:

  • High priority, must be aggressively implemented.

  • Multidisciplinary amputation-prevention centers are increasingly used.

Foot & Skin Care

• Avoid trauma:

  • Wear sturdy, well-fitting shoes or slippers.

  • Use neutral soaps and body lotions to prevent drying/cracking.

  • Do NOT apply lotion between the toes:

    • Moisture → maceration, infection risk.

• Hygiene:

  • Pat feet dry, don’t rub vigorously.

  • Stockings: clean and dry.

• Nail care:

  • Trim nails straight across.

  • File sharp corners to match nail contour.

  • If unsafe to trim (vision, reach, disease):

    • Refer to podiatrist.

    • Podiatry can also remove corns/calluses.

    • Special shoe inserts may prevent recurrence.

• Prompt reporting:

  • Blisters

  • Ingrown toenails

  • Infections

  • Any foot problem → must be evaluated.

• Patients with:

  • Diminished vision or

  • Limited arm/leg mobility
    → May require help inspecting their feet and legs.

Nutrition & Weight

• Good nutrition:

  • Promotes healing.

  • Prevents breakdown.

• Diet:

  • Adequate protein.

  • Adequate vitamins:

    • Especially vitamin C and zinc for wound healing.

• A meta-analysis:

  • No evidence that vitamin/antioxidant supplements prevent vascular disease.

• Obesity:

  • Strains the heart.

  • ↑ venous congestion.

  • ↓ circulation.

  • Weight reduction plan may be needed.

• A low-fat, low-lipid diet is indicated in atherosclerosis.

Gerontologic Considerations

• In older adults, PAD symptoms may be more pronounced.

• In inactive older adults:

  • First sign may be limb ischemia or gangrene.

• Many older patients:

  • Adjust lifestyle to avoid walking far.

  • Have comorbidities (COPD, HF) that limit activity.

  • So they may never walk enough to report classic claudication.

• Circulation is already reduced but not obvious until:

  • Trauma occurs.

  • Trauma → edema formation.

  • Edema further impairs already minimal arterial flow.

  • ➡ Gangrene.

• Intermittent claudication in older adults:

  • May appear after walking only:

    • ½–1 block or

    • Slight incline.

• Any prolonged pressure on foot:

  • Can cause pressure injury → ulcer, infection, gangrene.

• Outcomes:

  • Reduced mobility and activity.

  • Loss of independence.

  • Less likely to stay in community setting.

  • ↑ hospitalizations.

  • ↓ quality of life.

• Those with cognitive impairment:

  • May not be able to verbalize pain or symptoms.

Nursing Research Profile – PAD Symptoms & Ischemia (Chart 26-5)

Problem:

• PAD affects >8 million Americans.

• Associated with ↑ cardiovascular risk & mortality.

• Typically identified by claudication:

  • Aching, cramping, fatigue in calves with activity.

• BUT:

  • <33% of patients with PAD report classic claudication → underdiagnosis risk.

Purpose:

• Explore:

  • Range of symptoms (typical vs atypical, location, description).

  • Relationship between symptom variation and calf muscle ischemia.

• Goal:

  • Improve early detection and treatment.

Design:

• Descriptive study of patients with diagnosed PAD.

• Inclusion:

  • ≥21 years

  • English-speaking

  • Met specific criteria.

• Exclusion:

  • Uncontrolled HTN

  • Angina or dyspnea during exercise testing

  • Recent vascular procedures (<3 months).

• Data:

  • Demographics, clinical data, ABI.

  • Treadmill exercise with near-infrared spectroscopy:

    • Measured tissue saturation index (TSI) in calf.

  • Patients rated symptom intensity with NRS.

  • Self-report of symptom location & descriptors.

• Data collected:

  • At rest, during exercise, and during recovery.

  • Across three treadmill tests.

• Analysis:

  • Descriptive stats.

  • Multilevel modeling of:

    • Symptom variables

    • Demographics

    • ABI

    • TSI changes.

Findings:

• 40 participants → 120 exercise tests.

• Majority: Caucasian males, average age 68.

• 69.2% of tests:

  • Stopped due to calf discomfort.

• Only 55%:

  • Used classic claudication descriptors.

• TSI:

  • Declined rapidly from start of exercise to symptom onset.

  • Lowest TSI often occurred before max discomfort reported.

• TSI changes related to:

  • Exercise time (p < 0.001)

  • Baseline TSI (p < 0.001)

  • Exercise rating (p < 0.001)

  • ABI (p < 0.5).

• During recovery:

  • TSI increased as pain decreased.

  • TSI related to:

    • Recovery rating (p < 0.001)

    • ABI (p < 0.03).

Nursing Implications:

• Symptom presentation in PAD is variable:

  • Patients may say:

    • “Burn”

    • “Pressure”

    • “Tightness”

  • Symptoms may occur in atypical locations:

    • e.g., foot instead of calf.

• Nurses:

  • Should recognize this range to avoid missing PAD.

• Pain in PAD:

  • Unlike many conditions, pain onset:

    • Is used to adjust exercise, not stop all activity.

    • Exercise prescription can extend walking distance.

    • Can slow progression of atherosclerosis not only in legs but also coronary + cerebral circulation.

• Nurses should:

  • Use these findings to guide:

    • Patient education

    • Safe exercise regimens

    • Encourage risk factor modification.

Promoting Home, Community-Based, and Transitional Care

• Self-care plan is made with the patient, not just for them:

  • Includes:

    • Activities that:

      • Promote arterial & venous circulation

      • Relieve pain

      • Promote tissue integrity

• Patient & family must:

  • Understand:

    • Why each part of the plan matters.

    • Consequences of nonadherence.

    • Importance of follow-up visits.

• Long-term foot & leg care:

  • Critical for preventing:

    • Trauma

    • Ulceration

    • Gangrene

  • Chart 26-6 gives detailed patient instructions (foot & leg care).

🧠💥 Key Takeaways

• Atherosclerosis:

  • Intimal plaque disease of large/medium arteries; leads to stenosis, thrombosis, aneurysm, ulceration, rupture.

• Fatty streaks vs fibrous plaques:

  • Streaks = early, may or may not progress, asymptomatic.

  • Fibrous plaques = obstructive, progressive, high-risk.

• Collateral circulation:

  • Develops with gradual narrowing, but often insufficient with increased demand.

• Major risk factors:

  • Nicotine, diabetes, HTN, hyperlipidemia, sedentary lifestyle, stress, CRP, hyperhomocysteinemia, age, genetics.

• Diabetes:

  • PAD risk ↑ 2–4×, amputations ↑ 5–10×, more below-knee disease.

• ABI thresholds (from earlier section, but critical here for PAD):

  • ≤0.90 → PAD present.

  • 0.50–0.90 → claudication.

  • <0.50 → rest pain.

  • ≤0.40 → severe ischemia/tissue loss.

• Prevention:

  • Diet (low saturated fat, low cholesterol).

  • Statins as first-line for PAD risk reduction.

  • Multiple meds usually required for HTN control.

  • Stopping all nicotine is non-negotiable.

• Endovascular therapy:

  • PTA, atherectomy, stents: less invasive, shorter stay, but risk of dissection, embolization, acute occlusion, bleeding.

• Nursing care in PAD:

  • Position legs dependent, not elevated (opposite of venous disease).

  • Supervised walking: walk → pain → rest → walk.

  • Use heat cautiously; avoid direct hot sources on ischemic limbs.

  • No tight socks, leg crossing, or nicotine.

• Tissue integrity:

  • Foot care, trauma prevention, proper shoes, careful nail care, early reporting of problems.

  • Nutrition with adequate protein, vitamins; manage weight.

• Older adults:

  • May not report classic claudication.

  • First sign may be trauma → edema → gangrene.

  • PAD → reduced mobility, independence, and QoL.

• PAD symptoms are variable:

  • Not always “cramping calves” – can be burn, tightness, pressure, foot pain.

  • Nurses must actively assess, not assume.

Peripheral Artery Disease

Overview

• PAD = chronic arterial insufficiency of the extremities from atherosclerotic obstruction.

• More common in men and a major cause of disability.

• Most often affects the legs, but upper extremities can be involved.

• Age of onset & severity depend on:

  • Type and number of atherosclerotic risk factors (Chart 26-3: nicotine, diabetes, HTN, hyperlipidemia, etc.).

• In PAD:

  • Obstructive lesions usually run from:

    • Aorta below renal arteries → popliteal artery (see Fig. 26-9).

  • Distal occlusive disease (below knee, foot):

    • Seen more in diabetes and older adults.

🔗 So: Proximal PAD = classic claudication; distal PAD (esp. diabetics/elderly) = more ulcers, gangrene, toe/foot ischemia.

Chart 26-6 — Home Care Checklist: Foot and Leg Care in Peripheral Vascular Disease

This is what the patient and/or caregiver must be able to do and explain at discharge.

1. Understand why foot and leg care matters

• They should be able to state the rationale:

  • Poor blood flow = slow healing, high risk of ulcers, infection, gangrene, amputation.

  • Care = prevention of trauma/infection and protection of tissue.

💡 Memory cue: “Bad blood flow = fragile feet.”

2. Daily Foot Hygiene

• Wash feet daily, including between toes:

  • Use mild soap + lukewarm water.

  • Rinse thoroughly.

  • Pat dry, don’t rub (rubbing can cause micro-injury).

• Recognize thermal injury risk:

  • PAD feet can’t detect heat well → high burn risk.

🚨 PAD patients can burn themselves with “normal” hot water because nerve + blood flow are impaired.

3. Socks & Shoes

• Wear clean, loose, soft cotton socks:

  • Cotton = comfy, lets air circulate, absorbs moisture.

• In cold weather:

  • Wear extra socks in extra-large shoes (so there’s no constriction).

• Always wear soft shoes/slippers when out of bed:

  • No barefoot walking → prevents trauma.

🚨 Avoid thong sandals:

• They rub between toes → friction, breakdown, infection.

4. Avoid Heat & Sun Injury

• Avoid:

  • Heating pads

  • Whirlpools

  • Hot tubs

  • Sunburn

• Reason:

  • Poor sensation + poor blood flow = burns that don’t heal.

🔴 PAD feet should never be exposed to direct heat sources.

5. Safety Around the Home

• Inspect feet daily using a mirror:

  • Look for redness, dryness, cuts, blisters, cracks, fungal changes, etc.

• Clear pathways in the house:

  • Remove clutter to prevent stubbing toes / falls / skin tears.

• Use lamb’s wool or foam:

  • Between toes that overlap or rub → reduces friction, prevents wounds.

6. Nail & Skin Care

• Trim toenails:

  • Straight across, after a shower (nails are softer).

• If vision is poor or patient is unable to safely trim:

  • See a podiatrist:

    • For nail trimming

    • For corns, blisters, ingrown nails

• For dry, scaly feet:

  • Use a cream/lotion with emollient.

  • Never put lotion between toes unless prescribed:

    • Moisture between toes = maceration + fungal infection.

• Avoid:

  • Scratching

  • Vigorous rubbing
    ➡ These cause abrasions and open the door to infection.

If feet sweat a lot, especially between toes:

• Use lamb’s wool between toes to promote drying.

7. Avoid Constricting Blood Vessels

• Do not use:

  • Tight knee-high stockings

  • Tight socks

  • Constricting bandages around legs/feet

• Do not cross legs at the knees.

  • This compresses vessels → worse perfusion.

🚨 Any circumferential compression around the leg/foot is dangerous in PAD.

8. Nicotine & Exercise

• Stop all nicotine:

  • Smoking

  • Chewing

  • ENDS (e-cigarettes, vapes, etc.)

  • Nicotine = vasoconstriction + vasospasm → worsens ischemia.

• Participate in regular walking or SET:

  • Walking stimulates circulation and collateral formation.

🔗 Exercise = “natural bypass building” for PAD.

9. When to Seek Medical Attention

• Call provider at first sign of:

  • Skin breakdown (abrasions, blisters)

  • Fungal infection (athlete’s foot)

  • New or worsening pain

• Do not:

  • Use any medication on feet/legs unless prescribed.

  • Use:

    • Iodine

    • Alcohol

    • Corn/wart removers

    • Adhesive products
      without checking with provider.

10. Community Resources

• Patient should be able to state:

  • Which community resources or referrals are available:

    • Podiatry

    • Wound clinic

    • Diabetes educator

    • Vascular clinic

    • Smoking cessation programs

Figure 26-9 – Common Sites of Atherosclerotic Obstruction

• Shows typical PAD locations:

  • Aorta below renal arteries

  • Common iliac

  • Femoral (esp. superficial femoral)

  • Popliteal

  • Distal tibial and foot arteries in advanced disease.

• Clinically:

  • Location of pain (buttock, thigh, calf, foot) helps localize which artery is involved.

💡 Memory cue:

• Buttock/hip pain → aortoiliac

• Thigh → iliac/femoral

• Calf → femoral/popliteal

• Foot → tibial/pedal.

Clinical Manifestations

Hallmark symptom: intermittent claudication

• Described as:

  • Aching, cramping, fatigue, or weakness in muscles.

  • Occurs with activity/exercise.

  • Relieved by rest.

• Pain occurs in muscles distal to the stenosis/occlusion:

  • Ex: superficial femoral stenosis → calf pain.

As PAD progresses:

• Patient notices:

  • Shorter walking distance before pain.

  • Pain is more frequent, more intense.

Rest Pain (Critical Limb Ischemia)

• Occurs when arterial insufficiency is severe.

• Pain is:

  • Persistent

  • Aching or boring

  • Can be excruciating

  • Frequently not relieved by opioids

  • May be disabling

• Worse at night, often wakes patient.

• Elevation/horizontal position:

  • Increases pain (less arterial perfusion).

• Dependent position:

  • Reduces pain (gravity helps perfusion).

• Patients may sleep:

  • With leg hanging off bed, or

  • In a recliner with legs dependent.

🔴 Rest pain = critical ischemia and is a red-flag for limb-threatening disease.

Assessment and Diagnostic Findings

• Coldness or numbness in extremities:

  • From reduced arterial flow.

• Extremity findings:

  • Cool and pale when elevated.

  • Ruddy/cyanotic when dependent (reactive hyperemia + chronic changes).

• Other signs:

  • Skin and nail changes:

    • Thick, opaque nails

    • Shiny, atrophic, dry skin

    • Sparse/absent hair

  • Ulceration

  • Gangrene

  • Muscle atrophy

• Bruits may be heard over affected arteries.

Peripheral Pulses

• May be diminished or absent.

• Exam:

  • Compare right vs left.

  • Unequal pulses or absent normally palpable pulse = strong sign of PAD.

Diagnosis

• Based on:

  • Careful symptom history

  • Physical exam:

    • Color

    • Temperature

    • Pulses

    • Skin, nails, hair, ulceration.

• Confirmed by:

  • CW Doppler & ABI

  • Treadmill testing for claudication

  • Duplex ultrasonography

  • Other imaging (CT, MRA, angiography) as earlier in chapter.

Medical Management

Exercise Therapy

• Most patients have less claudication after SET (Supervised Exercise Therapy).

• SET programs:

  • Covered by insurance for a fixed number of sessions.

  • Must be:

    • Under direct provider supervision:

      • Provider must be immediately and physically available (not necessarily in room).

    • Supervised by someone trained in:

      • SET delivery

      • Basic Life Support

      • Advanced Cardiac Life Support.

• Unsupervised home walking programs:

  • Attractive for patients without access to SET.

  • Recent trials:

    • Show similar benefit between supervised and unsupervised programs → home-based can be effective.

• Best results:

  • Walking program + weight reduction + nicotine cessation.

Important counseling point:

• Do NOT promise claudication will fully resolve with nicotine cessation:

  • Symptoms may persist despite quitting.

  • Over-promising → loss of motivation if symptoms don’t fully go away.

Additional exercise option:

• Arm-ergometer training:

  • Improves:

    • Overall fitness

    • Cardiorespiratory function

    • Walking capacity in claudication patients.

🔗 Even upper body training can improve peripheral circulation and overall PAD tolerance.

Pharmacologic Therapy

Cilostazol

• FDA-approved for claudication.

• Class: Phosphodiesterase III inhibitor.

• Actions:

  • Direct vasodilator

  • Inhibits platelet aggregation

  • Decreases intimal hyperplasia after angioplasty/stenting.

• Clinical benefit:

  • ↑ max walking distance

  • ↑ pain-free walking distance

  • Benefits seen within 4–6 weeks.

• 🔴 Contraindicated in patients with a history of heart failure.

💡 NCLEX memory cue:
“Cilostazol = Claudication, but Contraindicated in CHF.”

Antiplatelet Therapy

• Aspirin or clopidogrel:

  • Prevent thromboemboli → ↓ risk of MI, stroke.

  • Recommended for symptomatic PAD.

• Aspirin:

  • Proven to ↓ CV events (MI, stroke, CV death).

  • Adverse effects:

    • GI upset

    • GI bleeding

Dual Antiplatelet Therapy (DAPT)

• Aspirin + clopidogrel:

  • Not well established for routine symptomatic PAD.

  • May be reasonable to ↓ limb-threatening events after revascularization.

Statins

• Improve endothelial function in PAD.

• Studies show:

  • ↓ severity of intermittent claudication.

  • ↑ walking distance before onset of pain.

• Additional benefits:

  • ↓ vascular inflammation

  • Plaque stabilization

  • Improve endothelial dysfunction

  • ↓ thrombosis

  • Linked to:

    • ↓ repeat peripheral interventions

    • ↓ amputations

    • ↓ major adverse cardiovascular events for up to 3 years post-procedure.

🔗 In PAD, statins are not just for cholesterol → they’re vascular protectors.

Endovascular Management

Endovascular options:

• Balloon angioplasty

• Stent

• Stent graft

• Atherectomy

Key points:

• Less invasive than open surgery.

• Objective: establish adequate inflow to distal vessels.

• Meta-analysis:

  • Efficacy & safety comparable to surgery.

Some stents are drug-eluting:

• More expensive but particularly useful in recurrent disease.

• Release antiproliferative drugs:

  • ↓ restenosis risk.

• Drug-eluting balloons & stents:

  • Proven to ↓ restenosis.

Eligibility requirement:

• Candidate must be able to take antiplatelet medications for at least 6 months post-procedure.

Surgical Management

Surgery is reserved for:

• Rest pain (critical ischemia)

• Severe, disabling claudication

• Limb at risk of amputation from tissue necrosis

Choice of procedure depends on:

• Degree, length, and location of stenosis/occlusion.

• Single vs multiple lesions.

• Patient’s overall health, procedure length, anesthesia tolerance.

Endarterectomy

• Surgeon:

  • Makes an arteriotomy (incision into artery).

  • Removes atheromatous obstruction directly (see Fig. 26-10).

  • Then suturing the vessel closed.

• Goal: restore lumen and blood flow.

Bypass Grafts

• Purpose: reroute blood flow around stenosis/occlusion.

• First, surgeon decides where to place distal anastomosis:

  • Distal outflow vessel must be ≥50% patent for graft to stay open.

Example:

• Occlusion below inguinal ligament in superficial femoral artery:

  • Preferred surgery: femoral-to-popliteal graft.

  • Classified:

    • Above-knee

    • Below-knee, based on distal anastomosis location.

Graft materials:

• Synthetic:

  • Woven/knitted Dacron

  • PTFE (expanded polytetrafluoroethylene)

• Biologic:

  • Cryopreserved saphenous veins

  • Umbilical veins

• Autologous vein (patient’s own vein):

  • In situ:

    • Vein stays in place, valves are stripped.

    • Vein ends are anastomosed to proximal and distal arteries.

  • Reversed vein:

    • Vein is harvested, reversed, and anastomosed proximal & distal.

Distal (Lower Leg / Ankle) Grafts

• If lower leg or ankle vessels have occlusions:

  • May need grafts.

• If popliteal artery is completely occluded, perfusion may depend only on collaterals.

• Distal anastomosis sites:

  • Tibial arteries (posterior tibial, anterior tibial, peroneal)

  • Dorsalis pedis

  • Plantar artery

• Site selection depends on:

  • Ease of surgical exposure

  • Which vessel gives best distal flow.

• These distal grafts:

  • Require autologous vein for best patency:

    • Greater or lesser saphenous

    • Or combination with upper extremity vein (e.g., cephalic).

Graft Patency

Patency depends on:

• Graft size

• Location

• Degree of intimal hyperplasia at anastomoses.

Complication:

• Infection of synthetic grafts:

  • May cause sepsis.

  • Usually requires graft removal.

Handling Vein Grafts

• In OR:

  • Careful handling to avoid damage.

  • Vein is:

    • Occluded at one end.

    • Inflated with heparinized solution to:

      • Check for leaks.

      • Check valve competency.

    • Then stored in heparinized solution to prevent drying/brittleness before placement.

Palliative Option

• For patients too high-risk for major vascular surgery:

  • Primary amputation may be chosen instead of bypass/endarterectomy.

🔴 This is a palliative, limb-sacrificing strategy when limb salvage surgery is not feasible/safe.

Nursing Management

(Nursing care for PAD overall is in Chart 26-4; here we focus on postop care.)

Postoperative goals:

• Maintain circulation

• Identify/manage complications early

• Plan for discharge + long-term care

Maintaining Circulation Postop

Primary objective: keep arterial repair patent.

• Assess:

  • Pulses (palpation + Doppler)

  • Color

  • Temperature

  • Capillary refill

  • Sensory & motor function

• Compare with other extremity.

• Frequency:

  • Initially: every 15 minutes.

  • If stable: gradually increase interval.

• Use Doppler distal to bypass graft:

  • More sensitive than palpation.

• ABI monitoring:

  • At least once every 8 hours for first 24 hours, then daily until discharge.

  • Not usually done with pedal artery bypass → risk of compressing anastomosis with cuff.

Ensure adequate circulating blood volume.

🔴 Disappearance of a previously present pulse = possible thrombotic graft occlusion → notify surgeon immediately.

Monitoring & Managing Potential Complications

Monitor:

• Urine output

• Central venous pressure

• Mental status

• Pulse rate and volume

To detect fluid imbalance early.

Bleeding risks:

• From intra-op heparin or anastomotic leak.

• Possible hematoma formation.

Nurse should:

• Review operative note:

  • Check if heparin was reversed with protamine.

Positioning:

• Avoid leg crossing.

• Avoid prolonged dependency (too long hanging down) → ↑ risk thrombosis.

Edema:

• Some postop edema is normal from increased arterial flow.

• Manage by:

  • Elevating extremities.

  • Encouraging leg exercises in bed.

Stockings:

• Graduated compression / anti-embolism stockings may be prescribed.

• Caution:

  • Don’t compress distal bypass grafts.

  • Avoid pressure injuries.

  • Don’t obscure visualization of limb.

🚨 Severe edema, pain, ↓ sensation of toes/fingers → could indicate compartment syndrome (see Chapter 37) → emergency.

Promoting Home, Community-Based, and Transitional Care

Discharge planning:

• Assess ability to manage ADLs independently.

• Determine support system (family/friends for ADLs, transport, wound care).

Teach and reinforce:

• Lifestyle changes:

  • Pain management

  • Diet modifications

  • Activity progression

  • Skin/hygiene care

• Teach patient to monitor for complications:

  • Infection (redness, drainage, fever)

  • Graft/artery occlusion (sudden pain, pallor, pulselessness, coldness)

  • Decreased blood flow signs.

Tobacco cessation:

• Help patient develop and implement a smoking cessation plan.

• This is central to protecting graft and preventing progression.

🧠💥 Key Takeaways

• PAD = chronic arterial insufficiency usually from atherosclerosis, mostly in legs, especially in men, diabetics, and older adults.

• Hallmark symptom: intermittent claudication → activity-induced leg pain relieved by rest.

• Rest pain at night in feet/toes, relieved by dependency = critical ischemia → limb-threatening.

• Assessment:

  • Cool, pale with elevation; ruddy/cyanotic dependent.

  • Shiny skin, thick nails, hair loss, ulcers, gangrene, muscle atrophy.

  • Diminished/absent pulses; bruits.

• Diagnosis:

  • ABI, Doppler, duplex, treadmill test, imaging.

• Home care:

  • Meticulous foot care, safe shoes, daily inspection, no barefoot walking, no heat pads, no tight socks or leg crossing, no OTC foot chemicals.

• Exercise:

  • SET or home walking improves claudication.

  • Walk to pain → rest → walk again.

• Drugs:

  • Cilostazol (claudication, but contraindicated in HF).

  • Aspirin/clopidogrel for CV event prevention.

  • Statins = vascular protection + ↑ walking distance.

• Endovascular:

  • Balloon, stent, atherectomy; drug-eluting stents require ≥6 months antiplatelet therapy.

• Surgery:

  • Reserved for rest pain, disabling claudication, tissue loss.

  • Options: endarterectomy, bypass grafts with synthetic or vein conduits.

  • Graft infection → sepsis → possible graft removal.

• Postop nursing:

  • Q15min extremity checks initially (pulses, temp, color, cap refill, motor/sensory).

  • Loss of pulse = emergency.

  • Watch for bleeding, hematoma, edema, compartment syndrome, and fluid problems.

  • Plan for long-term lifestyle changes and tobacco cessation.

Upper Extremity Arterial Disease

Overview

• Upper extremity (arm) arterial stenosis/occlusion is less common than in the legs.

• Symptoms are usually less severe because:

  • Arms have better collateral circulation.

  • Arms have less muscle mass and lower workload compared with legs.

🔗 Translation: arms are “easier to perfuse,” so the same degree of narrowing causes fewer symptoms than in the legs.

Clinical Manifestations

• Causes:

  • Atherosclerosis

  • Trauma

• Typical lesion:

  • Stenosis usually at the origin of the vessel proximal to the vertebral artery.

  • Because of that, the vertebral artery becomes the dominant pathway for blood flow to the arm.

• Symptoms from arm ischemia:

  • Arm fatigue and pain with exercise → “forearm claudication.”

  • Inability to hold or grasp objects, especially:

    • Combing hair

    • Reaching overhead (placing objects on high shelves)

    • Driving
      ➡ These all increase arm demand and uncover ischemia.

Subclavian Steal Syndrome

• Patho:

  • The subclavian stenosis causes blood to be “stolen” from the vertebral/basilar circulation.

  • There is reverse flow in vertebral and basilar arteries → blood is diverted away from the brain to supply the arm.

• Resulting vertebrobasilar (cerebral) symptoms:

  • Vertigo

  • Ataxia

  • Syncope

  • Bilateral visual changes