CHAPTER 44. Peripheral Vascular Care
Maureen E. Lisberger
OBJECTIVES
At the conclusion of this chapter, the reader will be able to:
1. Explain three factors that affect peripheral circulation.
2. Describe three causes of arteriosclerosis.
3. Compare the signs and symptoms of arterial and venous vascular disease.
4. Identify the risk factors that contribute to the development of peripheral vascular disease.
5. List three postarteriography assessment criteria.
6. Identify the most common sites of occurrence of peripheral vascular disease.
7. Describe operative and interventional radiology procedures performed on patients with peripheral vascular disease.
8. Describe the immediate postoperative nursing considerations for each operative procedure.
9. List postoperative complications of vascular surgery.
10. Describe complications of endovascular repair.
11. Describe the preoperative assessment, intraoperative, and postoperative care of the vascular patient.
I. ANATOMY AND PHYSIOLOGY
A. Peripheral vascular anatomy
1. Includes:
a. Peripheral arterial
b. Venous systems
2. Excludes:
a. Cardiac
b. Pulmonary
c. Cerebral systems
B. Arterial and venous wall structure contains three layers (Figure 44-1).
1. Adventitia—thin outer layer containing:
a. Collagen
b. Lymphatics
2. Media: thick middle layer containing smooth muscle cells arranged into strong, intertwining sheets of elastin that constrict or dilate. Medial layer is thinner in veins.
3. Intima: thin, inner, single endothelial layer; easily traumatized
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| FIGURE 44-1 ▪
A, Layers of artery and vein. B, Microcirculation. C, Cross section of an artery and vein showing the three layers: tunica intima, tunica media, and tunica adventia. Note the difference in wall thickness between the artery and the vein and the lack of valves within the artery.
( A and B from Thibodeau GA, Patton KT: Anatomy and physiology, ed 5, St Louis, 2003, Mosby; C from Thompson JM, McFarland GK, Hirsh JE, et al: Mosby’s clinical nursing, ed 5, St Louis, 2002, Mosby.)
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C. Circulatory path (Figure 44-2)
1. Artery → Arteriole → Precapillary sphincter → Capillary (Figure 44-3)
a. Artery: high pressure, low volume
b. Arteriole (diameter <0.5 mm)
(1) Offers resistance to blood flow
(2) Regulates blood flow into capillary bed
c. Precapillary sphincters
(1) Rings of smooth muscle located at proximal end of a true capillary
(2) Regulates flow of blood and oxygen (see Figure 44-1)
d. Capillary: site of gas and nutrient exchange
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| FIGURE 44-2 ▪
Systemic circulation.
(From Price SA, Wilson LM: Pathophysiology: Clinical concepts of disease processes, ed 6, St Louis, 2003, Mosby.)
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2. Capillary → Venule → Vein (see Figure 44-3)
a. Venule: as venules merge, rate of blood flow increases.
b. Vein
(1) Low pressure
(2) High volume
(3) Veins are capacitance vessels because they accommodate large volumes of blood.
(4) Unidirectional valves direct venous flow from feet toward heart and prevent reflux.
(5) Approximately 70% of blood volume contained in venous circulation (Figure 44-4)
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| FIGURE 44-3 ▪
Internal diameter, wall thickness, and relative amounts of the principal components of the vessel circulatory system. Cross sections of the vessels are not drawn to scale because of the huge range from aorta to vena cava to capillaries.
(From Berne RM, Levy MN: Cardiovascular physiology, ed 8, St Louis, 2001, Mosby.)
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| FIGURE 44-4 ▪
Percentage of the total blood volume in each portion of the circulation system.
(From Urden LD, Stacy KM, Lough ME: Thelan’s critical care nursing diagnosis and management, ed 5, Philadelphia, 2006, Mosby.)
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D. Arterial circulation (Figure 44-5)
1. Aorta: largest peripheral vessel, which includes four sections (Figure 44-6)
a. Ascending aorta: from aortic valve to arch
b. Arch: where brachiocephalic and carotid vessels originate
c. Descending thoracic aorta: from aortic arch to level of diaphragm
d. Abdominal aorta: from thoracic to aortic bifurcation
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| FIGURE 44-6 ▪
The aorta.
(From Rothrock J: Alexander’s care of the patient in surgery, ed 12, St Louis, 2003, Mosby.)
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| FIGURE 44-5 ▪
Principal arteries of the body.
(From Thibodeau GA, Patton KT: Anatomy and physiology, ed 6, St Louis, 2007, Mosby.)
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2. Aortic bifurcation: where aorta divides into common right and left iliac arteries
a. Common iliac divides into:
(1) Internal iliac (hypogastric)
(2) External iliac: continuation of common iliac artery that becomes common femoral artery in thigh
b. Common femoral (thigh) (Figure 44-7)
(1) Lateral and medial femoral circumflex
(2) Profunda (deep) femoral
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| FIGURE 44-7 ▪
Major arteries of the lower extremity.
(From Rothrock J: Alexander’s care of the patient in surgery, ed 12, St Louis, 2003, Mosby.)
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c. Popliteal: continuation of common femoral located posterior to knee surface divides into:
(1) Anterior tibial
(a) Dorsalis pedis
(b) Posterior tibial
(i) Medial and lateral plantar
(ii) Peroneal
E. Venous circulation (Figure 44-8)
1. Superficial system: in subcutaneous tissue
a. Greater saphenous: longest vein in body extending from malleolus of ankle to femoral vein (saphenous junction)
b. Lesser saphenous: extends from ankle to popliteal vein in knee (saphenopopliteal junction)
2. Deep veins: in muscular layers
a. Anterior and posterior tibial
b. Peroneal
c. Popliteal
d. Femoral, profunda femoris
e. Iliac
3. Perforating (communicating): vascular channels (Figure 44-9)
a. Communicate between deep and superficial veins
b. Flow shunted from superficial to deep system with help of unidirectional valves and finally to inferior vena cava
c. Muscle contraction promotes forward flow; valves prevent backflow during muscular relaxation.
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| FIGURE 44-9 ▪
Anatomy of the venous system of the leg.
(From Price SA, Wilson LM: Pathophysiology: Clinical concepts of disease processes, ed 6, St Louis, 2003, Mosby.)
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| FIGURE 44-8 ▪
Principal veins of the body.
(From Thibodeau GA, Patton KT: Anatomy and physiology, ed 6, St Louis, 2007, Mosby.)
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F. Factors affecting circulation
1. Cardiac output (Cardiac output = Stroke volume × Heart rate): venous capacity will determine venous return that will affect stroke volume of heart.
2. Arteriolar resistance: systemic vascular resistance (SVR) depends on:
a. Degree of arteriolar constriction
b. Resistance
(1) Increases as vessels constrict
(2) Decreases as vessels dilate
c. High SVR will:
(1) Decrease blood flow
(2) Increase myocardial workload
3. Vessel wall elasticity
a. With low compliance, pressure is greater.
b. Increased pressure will increase myocardial oxygen consumption.
4. Fluid volume status: low fluid volume will reduce peripheral resistance.
5. Diameter of vessel (arteriole diameter <0.5 mm)
a. Vasoconstriction: exposure to cold, vasoconstrictive agents
b. Vasodilation: exposure to heat, vasodilator agents
6. Sympathetic nervous system: regulates amount of vasoconstriction
G. Common sites of vascular disease (Figure 44-10)
1. Internal carotid arteries
2. Aorta above inguinal ligament inflow disease
3. Aortoiliac: bifurcation of aorta and iliac arteries inflow disease
4. Superficial femoral: middle to distal thigh below inguinal ligament outflow disease
5. Popliteal artery outflow disease
6. Tibial arteries: common in patients with diabetes outflow disease
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| FIGURE 44-10 ▪
Sites of arterial obstruction and corresponding levels of claudication.
(From Fahey VA: Vascular nursing, ed 4, St Louis, 2004, Saunders.)
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H. Incidence and risk factors associated with peripheral vascular disease
1. Highest incidence among elderly, men, persons with diabetes, smokers
2. Gender
a. More common in men
b. Earlier onset in men
c. Postmenopausal women susceptible
3. Age
a. Occurs beyond 30 years of age
b. Symptoms worsen after 65 years of age.
I. Risk factors of atherosclerosis
1. Lifestyle habits
a. Psychophysiologic stress triggers vasoconstriction.
b. Sedentary; lack of exercise
c. Smoking (major risk factor) for smokers and passive smoking (environmental tobacco smoke exposure)
(1) Vasoconstrictive effect of nicotine
(2) Inhalation of carbon monoxide in cigarette smoke
(a) Increases carboxyhemoglobin levels (carbon monoxide binds with hemoglobin)
(b) Impaired oxygen transport
(c) Hypoxic injury to intimal lining of artery
(d) Increased platelet aggregation caused by enhanced platelet adhesiveness
d. Diet
(1) Hyperlipidemia (hyperlipoproteinemia): accumulation of lipids in arterial wall
(a) Elevated cholesterol: total serum levels
(b) Elevated triglycerides
(i) Low-density lipoproteins (LDL): high serum levels related to premature development of atherosclerotic process
(ii) High-density lipoproteins (HDL): high serum levels demonstrate protective effect against atherosclerosis.
(iii) Homocysteine: high serum levels block production of nitric oxide on vascular endothelium, making cell walls less elastic and permitting plaque to build up.
(2) Obesity
2. Positive family history
3. Disease processes
a. Diabetes mellitus
b. Hypertension (major risk factor)
J. Indications for surgical intervention
1. Ischemic pain at rest
2. Significant limb ischemia
3. Limiting claudication
II. PATHOPHYSIOLOGY
A. Arterial occlusive disease
1. Classified as inflow or outflow above or below inguinal ligament (Figure 44-11)
a. Inflow obstruction involves distal end of aorta.
(1) Common iliac arteries
(2) Internal iliac arteries
(3) External iliac arteries
b. Outflow obstruction involves infrainguinal arteries below superficial femoral artery (SFA).
(1) Femoral arteries
(2) Popliteal arteries
(3) Tibial arteries
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| FIGURE 44-11 ▪
Common locations of inflow and outflow lesions.
(From Ignatavicius DD, Workman L: Medical-surgical nursing: Critical thinking for collaborative care, Philadelphia, 2006, Saunders.)
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2. Obstruction or stenosis of vessel
a. Decreased peripheral vessel blood flow
b. Decreased vessel diameter
c. Increased peripheral vascular resistance
d. Decreased blood flow velocity
3. Degenerative changes
a. Reduced tissue oxygen and nutrient supply
(1) Inadequate tissue integrity
(2) Ischemic tissue
(3) Destruction of muscle and elastic fibers
b. Formation of calcium and/or cholesterol deposits
(1) Thickening of arterioles
(2) Loss of elasticity
B. Venous disease
1. Deep vein thrombosis (DVT): disease of deep veins of lower extremity, often accompanied by intraluminal clot
2. Superficial thrombophlebitis: inflammation and clot in superficial veins
3. Virchow’s triad: three factors that increase incidence of venous thrombosis
a. Hypercoagulability caused by alteration of platelet and clotting factors
b. Venous stasis caused by incompetent venous valves
c. Intimal damage caused by trauma, intravenous infusions, ischemia
4. Pulmonary embolism: dislodged DVT with migration to pulmonary vasculature
5. Varicose veins
a. Structural weakness
b. Vessel tortuosity
c. Dilation
(1) Incompetent venous valves
(2) Reflux of blood results in venous pooling.
6. Venous hypertension: hereditary
a. Incompetent valves result in reduced blood return to heart.
b. Venous stasis and pooling of blood results in venous hypertension.
C. Arterial insufficiency: arterial occlusive disease
1. Arteriosclerosis obliterans
a. Atherosclerosis: most common form of arteriosclerosis obliterans
(1) Accumulation of lipids and connective tissue
(2) Intraluminal plaque formation
(3) Platelet aggregation
(4) Thrombus formation
(5) Loss of elasticity
b. Mönckeberg’s arteriosclerosis: arteriosclerosis of peripheral arteries
(1) Characterized by calcium deposits within medial layer
c. Arteriolosclerosis: sclerosis of arterioles
2. Aneurysm: abnormal dilation of vessel wall with high incidence of rupture and mortality when greater than 6 cm in diameter (Figures 44-12, 44-13 and 44-14)
a. Fusiform: diffuse circumferential dilation of artery
b. Saccular: area of pouching; affects localized part of arterial wall
c. Dissecting: intimal layer torn; blood accumulates between layers.
d. False aneurysm—when palpable hematoma often present, a complete tear of all three layers of arterial wall occurs caused by:
(1) Trauma
(2) Needle puncture
(3) Suture failure at anastomosis site of prosthetic graft
e. Pseudoaneurysm: dilated or tortuous segment of arterial wall without interruption of layers
f. Theories of aneurysm pathogenesis (Table 44-1)
| Etiology | Clinical Evidence | Theory |
|---|---|---|
| Genetic |
Genetically linked enzyme deficiencies are associated with aneurysms.
Familial clustering is observed.
Male siblings have up to 25% lifetime risk of aneurysm.
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X chromosome linked and autosomal dominant inheritance pattern
Specific deficits in collagen
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| Atherosclerotic |
Risk factors are similar to occlusive disease including smoking, hypertension, and aging.
Aneurysm wall contains calcium and atherosclerotic lesions.
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Compensatory dilation of the artery becomes uncontrolled. |
| Immunologic | A variant called inflammatory aneurysm is characterized by gross inflammation and microscopic leukocyte infiltrates. | Antigen, possibly through molecular mimicry, precipitates autoimmune response. |
| Degenerative |
Disruption of normal aortic wall architecture
Decreased amounts of elastin and collagen are found in aneurysms.
Hernias are common in patients with aneurysms.
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Elastin and collagen are aberrantly formed or digested. |
| Hemodynamic | Aneurysms typically occur proximal to bifurcations or distal to stenoses. | Wall tension, turbulence, vibration, and shear stress are increased dramatically in these areas. |
| Iatrogenic | Occur at graft anastomosis, after endarterectomy, angioplasty, or full-thickness traumatic disruption | Structural injury, end-to-side anastomosis |
| Infectious | Salmonella, Chlamydia pneumoniae, Streptococcus species, Staphylococcus species, Treponema pallidum are associated with aneurysms. | Microorganisms by direct extension, emboli, or infection from unknown primary may stimulate inflammation or degradation. |
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| FIGURE 44-12 ▪
Aneurysm types.
(From Smeltzer SC, Bare BG: Brunner and Suddarth’s textbook of medical-surgical nursing, ed 10, Philadelphia, 2004, Lippincott Williams & Wilkins.)
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| FIGURE 44-13 ▪
Two popular classification schemes for aortic dissections. Diagnosis of involvement of ascending aorta has important prognostic and therapeutic implications. DeBakey types I and II are called type A in the Stanford classifications; DeBakey type III is equal to Stanford type B.
(From Hamilton IN, Hollier LH: Thoracoabdominal aortic aneurysms. In Moore W, ed: Vascular surgery: A comprehensive review, ed 5, Philadelphia, 1998, W.B. Saunders.)
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| FIGURE 44-14 ▪
Aortic dissection. A, Separation of vascular layers. B, Classification of aortic dissection.
(From Price SA, Wilson LM: Pathophysiology: Clinical concepts of disease processes, ed 6, St Louis, 2003, Mosby.)
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D. Vascular diseases and conditions
1. Acute
a. Arterial embolism: sudden onset of symptoms of acute arterial insufficiency
(1) Originates in myocardium or arterial aneurysm
(2) May be secondary to external or iatrogenic trauma (catheter placement)
b. Trauma: arterial wall tear or dissection
2. Chronic
a. Diabetes mellitus: medial layer calcification; arteries become noncompressible.
b. Hypertension: increases permeability of intimal endothelium
c. Polycythemia: increased blood viscosity caused by increase in red blood cell count
d. Inflammatory processes: may cause occlusive lesions
(1) Arteritis: inflammation of arterial wall
(a) Polyarteritis nodosa (PAN): systemic disease causing arterial inflammation and aneurysm rupture in adults
(b) Kawasaki: similar to PAN; occurs in children
(c) Cogan’s: (rare condition) similar to PAN; inflammatory infiltration of large veins and muscular arteries
(d) Behcet’s: similar to PAN; affects both arteries and veins
(e) Drug abusers: similar to PAN; necrotizing arteritis (intra-arterial injection of drugs)
(2) Fibromuscular dysplasia: multiple areas of arterial stenosis and dilation
(3) Buerger’s disease: thromboangiitis obliterans, autoimmune disease
(a) Inflammation of arterial walls
(b) Thrombus formation caused by intimal thickening
(c) Affects plantar and digital vessels
(d) Pain at rest, extremity cold, cyanotic
(4) Granulomatous/giant cell arteritis
(a) Takayasu’s arteritis: transmural inflammatory process
(i) Type I aortic arch and vessels originating from arch
(ii) Type II abdominal aorta and visceral vessels
(iii) Type III both the arch and abdominal aorta
(iv) Type IV pulmonary arteries
(b) Temporal arteritis: thickening of intima, necrosis of media
(5) Hypersensitivity angiitis: arterial damage from antigen-antibody complexes
e. Raynaud’s phenomenon and Raynaud’s disease: vasospastic diseases that are related
(1) Intense vasospasm of arteries and arterioles of extremities
(2) Precipitated by exposure to cold
(3) Ischemic changes: cyanosis, numbness, tingling
(4) Occurs in 40% of patients with systemic lupus erythematosus, and 90% of patients with scleroderma
(5) Raynaud’s phenomenon occurs unilaterally in both men and women older than 30 years.
(6) Raynaud’s disease occurs bilaterally, mostly in females, between 17 and 50 years of age.
f. Compartment syndrome: swelling within osteofascial compartments of leg or arm
(1) Intracompartmental pressure increases from bleeding within the compartment, or external compression from dressings, cast, traumatic crush injury.
(2) Vascular perfusion decreases, compromising tissue.
(3) Ischemia affects nerves and muscles.
(a) Pain
(b) Tenseness of compartment
(c) Paresthesia
(d) Pulselessness
(e) Paralysis
(f) Pallor
III. CLINICAL SIGNS AND SYMPTOMS
A. Arterial insufficiency
1. Decreased blood flow may cause inadequate tissue oxygenation distal to lesion.
2. A 70% to 90% occlusion of a large artery usually must occur before a decrease in blood flow or pressure causes symptoms at rest.
3. A 60% obstruction may be sufficient to precipitate signs and symptoms during exercise.
4. Acute
a. Peripheral pulses diminished, weak, or absent
b. Cold and pale extremity (sudden onset)
c. Sudden, severe pain may occur during exercise or at rest: moderate to severe inflow disease.
(1) Lower back and buttock pain: common iliac or abdominal aorta inflow disease (Figure 44-11)
(2) Thigh pain at or above profunda femoris artery
d. Limited sensory and motor function
(1) Possible paresthesia
(2) Atrophied skeletal muscle: restricted limb movement
e. Minimal edema: usually unilateral
f. Bruit present with partial occlusion; no bruit with total occlusion
5. Chronic
a. Diminished or weak distal pulses outflow disease (see Figure 44-11)
(1) Below SFA
(2) Popliteal artery
b. Pain at rest related to severe ischemia: burning or cramping in calves, ankles, feet, toes
c. Tissue necrosis: gangrene
d. Intermittent claudication
e. Skin
(1) Skin ulceration
(2) Delayed healing of skin lesions
(3) Skin texture: thin, shiny, dry
(4) Cool skin: poikilothermic
f. Color: pale extremity
(1) Increased pallor when elevated
(2) Rubor or cyanosis or both when dependent
g. Possible paresthesia of limb
h. Edema: none or mild
(1) Hair loss distal to occlusion
i. Nails: thick, brittle
j. Impotence: associated with aortoiliac disease
B. Venous insufficiency
1. Acute
a. Moderate pain localized to area of inflammation
b. Pulses present or diminished (absent in presence of concomitant disease)
c. Skin warm, cyanotic, mottled, or pale
d. Engorged veins when legs slightly dependent
e. Moderate to severe peripheral edema
2. Chronic
a. Minimal to moderate pain
b. Moderate to severe edema, unilateral or bilateral
c. Sensation of heaviness at site of occlusion
d. Muscle cramps, aching
e. Ulceration of ankle area
f. Superficial veins may be prominent.
g. Skin
(1) Warm
(2) Brawny (reddish brown) color
(3) Pronounced lower leg pigmentation
(4) Texture: thickening, scaling, and/or scarring
IV. DIAGNOSTIC ASSESSMENT
A. Arterial tests
1. Noninvasive laboratory studies
a. Segmental pressure measurement: measurement of systolic blood pressure along selected segments of each extremity
(1) Gradient >20 mm Hg: evidence of arterial stenosis in lower extremity
(2) Gradient >10 mm Hg: evidence of arterial stenosis in upper extremity
b. Ankle/brachial index (ABI): ratio of ankle to brachial pressure (normal ABI, ≥1.0)
(1) One limitation is calcified vessels as in renal failure or diabetes.
c. Toe pressure measurements: assess distal arterial flow.
(1) Useful in diabetics with calcification of larger vessels
d. Pulse volume recording: quantifies arterial flow to determine location of lesion and severity.
e. Doppler ultrasound: determines blood flow and velocity
f. B-mode ultrasonography: projects two-dimensional image in real time
g. Duplex ultrasound imaging: assesses both anatomic characteristics and stenosis of peripheral arteries; combination of Doppler and B-mode ultrasonogram
h. Air plethysmography (APG) and photoplethysmography: record volume changes in limb
i. Treadmill exercise testing: objective evidence of walking capacity and evaluation of peripheral stenosis
j. Computed tomography (CT): a tomograph is an image of a cross-sectional slice of a body part.
(1) CT image is three dimensional: a camera rotates around selected body part taking two-dimensional images at multiple angles, which are converted to a composite three-dimensional image by a computer.
(2) Contrast material (usually iodine) injected to heighten contrast between vessel wall and blood
(3) Used for diagnosis of aortic aneurysms and aortic dissection
(4) Able to detect hematomas or thrombi better with CT than with arteriography
k. Magnetic resonance imaging: detailed and three-dimensional imaging of vessel lumen where contrast not needed; contraindicated in patients with pacemakers and cerebral aneurysm clips
l. Magnetic resonance angiography: has replaced angiography for severe carotid stenosis and the lower extremities; uses intravenous gadolinium; no arterial puncture required
2. Invasive laboratory studies
a. Arteriography: invasive radiographic procedure in which radiopaque contrast injected into artery
b. Transcatheter therapy: percutaneous transluminal angioplasty, stenting, lyse clot, therapeutic embolization
(1) Purposes
(a) Depict location of stenosis, occlusion, or view aneurysm
(b) Visualize collateral, proximal, and distal arterial circulation to determine surgical treatment options
(2) Complications
(a) Intimal disruption
(i) Hematoma formation at puncture site
(ii) Plaque dislodgement
(iii) Arterial occlusion: thrombosis
(iv) Distal embolization
(v) Arteriovenous (AV) fistula
(vi) Arterial dissection
(vii) Renal failure
(b) Transient ischemic attack (TIA) or cerebrovascular accident (CVA)
(c) Toxic reaction to contrast media: renal or cardiac
(d) Allergic reaction
(i) Rash
(ii) Bronchospasm
(iii) Altered consciousness
(iv) Convulsions
(v) Anaphylaxis
(vi) Cardiac arrest
(3) Postarteriography assessment and intervention
(a) Assessment
(i) Vital signs
(ii) Hematoma and/or bleeding at puncture site
(iii) Signs and symptoms of acute arterial insufficiency
[a] Skin: color, temperature
[b] Pulses distal to puncture site
[c] Pain
[d] Urinary output
[e] Neurologic status
[f] Signs of heart failure or respiratory distress
(b) Intervention
(i) Observe for rash.
(ii) Maintain adequate hydration to flush contrast.
(iii) Head of bed at 30° or less
(iv) Keep affected extremity straight for 4 to 6 hours after procedure.
(v) Wait a minimum of 4 hours to resume heparin if previously receiving heparin.
B. Venous tests
1. Noninvasive laboratory studies
a. Venous Doppler ultrasonography examinations: used to determine blood flow patterns and velocity
(1) During inspiration, intrathoracic pressure decreases and venous return to heart increases.
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