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Vascular disorders have become major health concerns
among people in this present generation. These are primarily
lifestyle diseases, therefore greatly preventable.

Hypertension and other vascular disorders potentially pose

life-threatening complications. Hypertension affects vital organs
leading to cerebro- vascular accident (stoke),myocardial infarction
(heart attack), renal failure, retinopathy, cataract and many other
pathophysiologic alterations.

Peripheral vascular disorders deplete the blood flow to

tissues in the extremities. This results to tissue ischemia, excessive
accumulation of waste and fluids. In more advanced state of
disorders, necrosis of tissue and finally gangrene develops.
Gangrene necessitates amputation of the affected limb
In the light of the issues cited, prevention and
adequate control of hypertension and the other vascular
disorders become essential nursing responsibility.

Lifestyle modification will greatly reduce the risk

and control of the disorders. Therefore, client teaching
could not be overemphasized as the primary aspect of
nursing interventions.

This chapter intends to assists student nurses gain

essential knowledge, skills and attitudes in the
management of clients with peripheral vascular disorders,
and ultimately contribute in the prevention of morbidity
and reduction of mortality related to these disorders.
Learning outcomes
At the end of this chapter, the learner should be able to:
1. Assess the client for clinical manifestations associated
with peripheral vascular disorders.
2. Discuss the etiology, risk factors, basic pathophysiology
and clinical manifestations of peripheral vascular
3. Develop plan of care for the prevention, collaborative
management and rehabilitation of clients with peripheral
vascular disorders.
4. Implement nursing interventions that optimize the quality
of life for clients with peripheral vascular disorders.
5. Evaluate planned client outcomes, using outcome criteria
developed in the planning phase of care.
Assessment of the Peripheral Vascular Disorders
o Health History
 Risk factors for cardiovascular disease.
 Use of medication that increase risk of vascular disease
(e.g. birth control pills)
o Chief Complaint ( Effects of PVD’s in extremities
 Pain, burning and stinging
 Cramping and numbness
 Intolerance to local heat and cold
 Inability to sense temperature changes
 Decreased touch sensations
 Edema
 Color changes (rubor/redness, pallor, cyanosis)
 Lesion and Poor healing
o History
 Medical history
 Hypertension
 Phlebitis
 DM
 Edema
 Varicose veins

 Dietary intake (Na, Fats, Cholesterol)

 Use of tobacco, alcohol, drugs
 Occupational History ( number of hours of standing,
 Activity, rest, sleep habits
 Degree to which symptoms interfere with ADL
 Stress level and emotional state
 Physical Examination
 Inspection
 Skin color, hair distribution, venous pattern, swelling,
atrophy, lack of hair growth petechiae, capillary refill,
 Skin temperature
 Pulses
• 0 absent
• +1 weak, thready
• +2 normal
• +3 full, bounding
 Allen’s Test
 Homan’s sign
 Auscultation
 BP of both arms
 Pulse points(assess presence of bruit)

Anatomy and Physiology of the Vascular System

• The vascular system is closed transport system where blood
• The main components of the vascular system are: arteries,
veins and capillaries
• Arteries carry blood away from the hearth while the veins
return the blood to the heart
• Arteries are thick-walled vessels which transport oxygen
and blood via the aorta from the heart to the tissues. They
branch into arterioles.
 The three layer of the arteries are as follows:
1. Tunica Intima. The inner layer of endothelium
2. Tunica Media. The middle layer of the connective tissue,
smooth muscle, or elastic fibers.
3. Tunica Adventitia. The outer layer of connective tissue

• The capillaries are thin- walled vessels located in the

• The capillaries connect the arterioles with the venules,
where exchanges of gases, nutrients and metabolic waste
products occur.
• The veins are thin-walled vessels which transport
deoxygenated blood from the capillaries back to the
right heart.
• The veins are composed of three layers: intima, media
and adventitia.
• The veins are distensible, allowing accumulation of large
volume of blood. This is because of lesser connective tissues
and smooth muscles than in the arterial walls
• Veins have one-way valves, directed upward which allow
blood flow against the gravity.

Diagnostic Tests
• Limb Blood Pressure
 Acute and chronic arterial occlusion produces regional
• Doppler Ultrasonography.
 Use high-frequency sound waves.
 Permits assessment of arterial and venous flow in the limbs with
the use of a probe moved over a skin surface.
• Ultrasonic Duplex Scanning
 Provides ultrasonographic image of the vessel and doppler
 Localizes the site of vascular obstruction and evaluates the
degree of narrowing and the amount of vascular reflux.
 Detects deep vein thrombosis
• Computed Tomography
 Allows visualizations of the arterial wall and its structures.
 May detect AAA( Abdominal Aortic Anuerysm)
 Nursing Interventions
 Explain the procedure. That the client will be placed in a tunnel-like
 NPO, if with contrast medium
 Ascertain history of allergy to iodine and seafoods
 Assess for claustrophobia.
 Advise client to remain still during the entire procedure.
 Sedation is done if client is unable to remain still.
 Magnetic Resonance Imaging
 Use magnetic fields to obtain sectional images of the body
 Used to detect aneurysms and DVT from pelvic iliac veins and leg
 Nursing Intervention
 Assess for implanted metal devices in the body, including artificial
cardiac pacemakers. These make the client ineligible to undergo MRI
 Assess for claustrophobia. The client will be placed in tunnel-like
 Instruct client to remain still during the procedure. To have accurate
 Sedation may be done if the client is a child or is restless
• Plethysmography
 Measures venous blood volume changes in the extremities
 Pressure cuff is applied
 Last 30-60 minutes
 Placed in supine position with the involved extremity elevated
above the level of the heart.
 Venography
 Involves injection of contrast medium into the veins via catheter,
followed by radiographic studies
• Vascular Endoscopy (Angioscopy)
 Permits imaging of intra- arterial disease in color and in three
dimensions through the use of fiberoptic endoscope
• Angiograpgy
 Involves injection of iodinated contrast medium into the arteries
via a catheter followed by radiographic studies
 Nursing Intervention
• Before the procedure
o NPO for 2 to 6 hours
o Assess for allergy to seafoods and iodine
o Mild sedative is administered
o Local anesthesia at the injection site
o Procedure last 30-90 minutes.
• After the procedure
o Monitor VS, LOC (Level of Consciousness), peripheral pulses
o Assess puncture site for hematoma
o Bed rest for 6 to 8 hours with the punctured extremity extended.
o Apply pressure dressing and small ice pack at the puncture site. To
prevent bleeding.
o IV fluids foe 6 to 8 hours to excrete contrast medium
Pathophysiology: Peripheral Vascular Disorders
Hypercoagulability of Blood
Inflammatory processes
Mechanical/Chemical Trauma

Decreased Blood Flow

Tissue Ischemia

Tissue Hypoxia


Ulceration/ Gangrene
Hypertension (HPN)
• Is an abnormal elevation of BP; systolic pressure above 140 mmHg
and or diastolic pressure above 90mmHg for at least two readings.
• Positive family history strongly supports the diagnostic of HPN
• Classification of Hypertension
 Essential/ Idiopathic/Primary of HPN
 Accounts for 90% to 95% of all cases HPN
 Cause is unknown
 Secondary HPN
 Due to known causes, e.g. Renal failure, Hyperthyroidism,
pheochromocytoma, Crushing’s disease, etc.
 Malignant Hypertension
 Is severe, rapidly progressive elevation in BP that causes rapid onset 0f the
end target organ complications
 Labile HPN
 Is intermittently elevated BP
 Resistant HPN
 Is HPN that does not respond to usual treatment
 White Coat HPN
 Is elevated of BP only during clinic visit
 Hypertensive Crisis
 Situation that requires immediate blood pressure lowering (within 1 hour,
systolic pressure above 240mmHg; Diastolic pressure above 120mmHg)

• Accelerates atherosclerosis
• In hypertension, vasoconstriction-> vasospasm-> increased Peripheral Vascular
Resistance-> decreased blood flow to organs (brain, heart, kidneys, eyes-the
end target organs)
• Hypertensive effects on target organs are as follows
 Heart- Myocardial ischemia and infarction, congestive heart failure,
myocardial hypertrophy, dysrhythmias
 Eyes- blurred/ impaired vision, retinopathy, cataract

 Brain- cerebrovascular accident, encephalopathy

 Kidneys- renal insufficiency, renal failure

 Peripheral Blood Vessels- dissecting aneurysm, gangrene.

Risk Factors
Family History
High Salt Intake
Low Potassium intake
Excess Alcohol Consumption

Changes in Arteriolar Bed

Systemic Vascular Resistance


Blood Flow to Organs

Blood Pressure
Renal Perfusion Beta-receptor

Juxtaglomerular cells Hypovolemia


Angiotensinogen Renin Angiotensin I

Angiostiensin- Converting Enzyme (ACE)

Arterial Vasoconstriction Angiotensin II

Adrenal Cortex Stimulation II

Peripheral resistance
Na Reabsorption
Blood pressure
H2O Reabsorption

plasma Volume (ECF)

Summary 0f Clinical Manifestation of Hypertension
• Headache (especially upon waking). This is the most characteristics
manifestation of hypertension
• Epistaxis
• Dizziness
• Tinnitus
• Unsteadiness
• Blurred vision Depression
• Nocturia
• Retinopathy, papilledema (on fundoscopy) * ( may be asymptomatic)

Collaborative Management for Hypertension

1. Prevention
 Primary prevention – aimed at reducing the risk factors associated
with HPN.
• Moderation in sodium intake
• Decrease saturated fats in diet
• maintenance of Ideal Body Weight (IBW
• maintenance of regular pattern of exercise
• cessation of cigarette smoking
• moderation in consumption of alcohol
• stress reduction through effective coping strategies
 Secondary prevention. Focus on identification and control of HPN in
high risk group
2. Pharmacology control of hypertension

Stepped- Care Approach

Step I. Diuretics, beta blocker, calcium blocker , ACE inhibitor
Step II. Diuretics with beta blocker, Sympatholytic
Step III. Direct acting vasodilator, Sympatholytic with diuretic
Step IV. Adrenergic neuron blocker, combinations from step I,II, III
Diuretic are the first line of drugs for treating mild hypertension
Hydrodiuli (hydrochlorothiazide) is the most frequently prescribed
diuretic to control mild hypertension.
Diuretics promote sodium and water excretion, which decrease
extracellular fluid volume. This in turn, lowers BP.
A. Potassium-wasting diuretics
Diuril (Chloroyhiazide)
HydroDIURIL (Hydrochlorothiazide)
Naturetin (Bendroflumethiazide)
Exna (Benzthiazide)
Saluron, Diucardin (hydroflumenthiazide)
Aquatensen, Enduron (methylChlorthiazide)
Renese- R (Polythiazide)
Diurese, Metahydin, Naqua (Trichlomenthiazide)
 Thiazide-like
Hygroton (Chlorthalidone)
Lozol (Indapamide)
Zoroxoly (Metolazone)
Hydromox (Quinethazone)
Bumex (Bumetamide)
Edecine (Ethacrynic acid)
Lasix (Furosemide)
Demadex (Torsemide)
B. Potassium-Sparing
Midamor (Amioride)
Aldactone (Spironolactone)
Dyrenium (Triamterene)
C. Thiazide With Potassium-Sparing Diuretics-(Combination Diuretics)
Moduretic (Amiloride and Hydrochlorothiazide)
Aldactazide (Spironolactone and Hydrochlorothiazide)
Thiazide and Thiazide- like diuretics
 Promote sodium, chloride, potassium and water excretion.
Hypokalemia may occur.
 Cause vasodilation which lowers BP.
 Promote calcium absorption. Hyperglycemia may result
 Hypoglycemia can also occur, and should be used cautiously in clients with DM.
 Side effects and adverse reaction (thiazide)
 Electrolyte imbalance ( hypokalemia, hyperkalemia, hypomagnesium, and
bicarbonate loss
Increased serum cholesterol, LDL, triglycerides
Dizziness, headache, nausea and vomiting, constipation
 Thiazides are contraindicated in renal failure (oliguria, elevated BUN, elevated
serum creatinine)
Loop (High-ceiling) diuretics
 Act on the ascending loop of Henle
 Inhibit reabsorption of sodium, water, potassium, calcium, and magnesium.
 Loop diuretics are more potent than thiazides as diuretics but they are less effective
as antihypertensive agents.
Side effects and adverse reaction (loop diuretics)
 Electrolyte imbalances (hypokalemia, hyponatremia, hypokalemia,
hypomagnesemia, and hypochlremia)
 Orthostatic hypotension
 Thiamine deficiency on prolonged use of loop diuretics
 Ototoxity (rare)
 Rash
 Photosensitivity
 Hyperuricemia
 Thrombocytopenia, leukopenia
 Elevated lipids
o Furosemide is contraindicated if the client has hypersensitivity to
o Potassium-sparing diuretics
o Promote sodium and water excretion and potassium retention.
o The main side effect of these drug is hyperkalemia.
o Other side effect are: GI disturbances (anorexia, nausea, vomiting,
Loop Diuretics
• Assess VS, serum electrolytes, weight and urine output for baseline
• If furosemide is given IV, the urine output should increase in 5 to 20
minutes. If urine output does not increase, notify physician. Severe
renal disorders may be present.
• Monitor urinary output.
• Check client’s weight to determine body fluid gain or loss.
• Instruct client to arise slowly to prevent or with food to avoid nausea.
Potassium Diuretics-sparing Diuretics
• Assess VS, serum electrolytes, weight and urinary output for baseline
• Administer medication in the morning to avoid nocturia
• Take medication with or after meals to prevent nausea.
• Instruct client to avoid exposure to direct sunlight because the drug can
cause photosensitivity.
Nursing Intervention in Diuretic Therapy
Thiazide diuretics
• Monitor VS and serum electrolytes especially potassium,
uric acid, and cholesterol levels. Report to , physician:
hypotension, hypokalemia, hyperglycemia, hyperirucemia,
and increased serum cholesterol, LDL, triglycerides levels
• Sign and symptoms of hypokalemia include muscle
weakness, leg cramps, and cardiac dysrhythmias.
• Check the client daily weights a weight gain of 2.2 to 2.5
lbs. is equivalent to an excess liter of body fluids.
• Monitor urine output to determine fluid loss or retention
• Administer medication in early morning to avoid sleep
disturbance resulting from nocturia.
 Sympatholytics (Sympathetic Depressants)
1. Beta- adrenergic blockers
2. Centrally- acting sympatholytics (Adrenergic blockers)
3. Alpha- adrenergic blocker
4. Adrenergic neuron blockers (periphically acting sympatholytics)
5. Alpha- 1 beta – 1 adrenergic blockers

1. Beta-adrenergic blockers (beta-blockers)

 Beta- blockers reduce cardiac output by diminishing SNS respose;
lower blood pressure by diminishing vascular resistance.
 Beta- blockers reduce heart rate, contractility, and renin release.
 African- American hypertensive clients do not respond well to
beta-blockers, unless they take them with diuretics.
 Nonselective beta- blockers inhibit beta 1 (heart) and beta 2
bronchial receptor). Bronchoconstriction may occur
 Beta- blockers are contraindicated in second and third degree heart
block, cardiogenic shock, CHF, sinus bradycardia
Examples of Beta-adrenergic blockers: ‘old drug’
• Cardioselective Beta- 1
• Spectral (acebulolol
• Tenormin (atenolol)
• Kerlone (betaolol HCI)
• Zebeta (bisoprolol)
• Lopressor (metoprolol)
• Blocadren (timolol maleate)
Nursing Intervention in Beta- Blockers Therapy
• Monitor VS, especially BP and pulse; hypotension and
bradycardia may occur.
• Monitor BUN, serum creatinine, AST and LDH. Metoprolol may
affect renal and liver function
• Instruct client to change prevent postural hypotension
• Instruct client to report dizziness =, slow pulse rate, changes in
BP, palpations, confusion or GI upset to the health care
2. Centrally –acting sympatholytics (adrenergic blockers)
 Decrease CNS response from the brainstem to the
peripheral vessels. Stimulate alpha-2 receptors; increase
vagus activity; and decrease serum epinephrine,
norepeniphrine, and release.
 Methyldopa and clonidine can cause sodium and water
retention. These medications should be administered with
 Side effects and adverse reactions (cebtrally acting
Dry mouth
Peripheral edema
Examples of centrally acting sympatholytics:
 Catapress (clonidine HCL)
 Wytensin (guanabenz Acetate)
 Tenex (guanfacine HCI)
 Aldomet (methyldopa)

3. Alpha-adrenergic blockers
 Block alpha-adrenergic receptors, resulting in vasodilation and decreased
blood pressure
 Alpha blockers do not affect glucose metabolism and they do not affect
respiratory function. They are safe for patients with diabetes and COPD
 These drugs cause sodium and water retention with edema. Diuretics are
frequently given with alpha-adrenergic blockers to decrease fluid
accumulation in the extremities
Examples of alpha-adrenergic blockers
Selective alpha- adrenergic blockers
 Cardura (doxazosin mesylate)
 Minipress (prozosin HCI)
 Hytrin (terazosins HCI)
Nonselective alpha-adrenergic blockers
 Dibenzyline (phonexybenzamine HCl)
 Regitine (phentolamine)
 Priscoline HCI (tolazoline HCI)
 Side effects and adverse reactions (alpha-adrenergic blockers)
 Dizziness
 Faintness
 Lighteadedness due to postural
 Increased heart failure
 Nausea
 Drowsiness
 Nasal congestion caused by vasodilation
 Edema
 Weight gain
Side effects of phentolamine
 Hypotension
 Reflex tachycardia
 Nasal congestion
 GI disturbances
 Examples of centrally acting sympatholytics:
• Catapress (clonidine HCL)
• Wytensin (guanabenz Acetate)
• Tenex (guanfacine HCI)
• Aldomet (methyldopa)

4. Adrenergic neuron blockers (peripherally acting

• Block norepinephrine release from the SNS, that results in
lowering of BP. There is decrease both cardiac output and
peripheral vascular resistance
• Orthostatic hypotension is a common side effect; advise client
to rise slowly from reclining or sitting position
Examples of adrenergic neuron blockers
o Hylorel (guanadrel sulfate)
o Ismelin (guanethidine monosulfate)
5. Alpha-1 and beta-1 adrenergic blockers
 By blocking the alpha-1 receptor, dilatation of the
arterioles and viens occurs, therefore blood pressure is
 Clients witth severe asthma should not take large doses
because these medications cause bronchoconstriction
 Side effects include orthostatic hypotension, GI
disturbances, nervousness, dry mouth, fatigue. Large
doses may cause AV heart block
 Cartrol, Ocupress (carteolol HCI)
 Trandate, Normodyne (Labetalol HCI)
Direct- Acting Arteriolar Vasodilators
• Relax smooth muscles of the blood vessels, mainly the arteries,
causing vasodilation
• Promote an increase in blood flow to the brain and the kidneys.
• With vasodilation, the BP decreases and sodium and water are
retained resulting in peripheral edema. Diuretics can be given to
decrease edema

Examples of direct- acting anteriolar vasodilators

hyperstat, progylcem (diazoxide
loniten, rogaine (minoxidil)
Side effects and adverse reaction (Direct-Acting Anteriolar Vasodilators)
 Hydralazine and Minoxodil
 Tachycardia
 Palpitations
 Edema
 Nasal Congestion
 Headache
 Dizziness
 GI bleeding
 Lupus-like symptom
 Neurologic symptoms (tingling, numbness)

 Angiotensin Antagonist (Angiotensin-Converting Enzymes Inhibitor)

• Inhibit angiotensin-converting enzyme (ACE), which in tum inhibits the
formation of angiotensin II (vasoconstrictor) and blocks the release of
 Aldosterone promotes sodium and water retention and potassium
 When aldosterone is blocked, sodium and water are excreted and
potassium is retained.
 ACE inhibitors should not be given during pregnancy because they
reduce placental blood flow
Side effects and adverse reaction (ACE inhibitor)
• Cough , Nausea
• Diarrhea, Dizziness
• Fatigue, Insomnia
• Hyperkalemia, Tachycardia
• Hypotension, oliguria, urticarial, (adverse reaction)
• Bruising, petechiae, and/or bleeding (adverse reaction to capoten)
Examples of ACE (“pril drugs”)
Lotensin (benazepril HCL)
 Capoten (captopril)
 Vasotec (enalapril maleate)
 Monopril (fosinopril)
 Prinivil ,Zestri (lisonopril)
 Aceon (perindopril)
 Altace (ramipiril)
 Mavik (trandolapril)
Note: Ace inhibitor should generally not be taken with potassium-sparing
diuretics or salt substitutes that contain potassium because of risk,

It is necessary to reduce the drug dose, except for Fosinopril

(Monopril), for clients with renal insufficiency.
Captopril may cause life-threatening effects: acute renal
faire, broncospasm, angioedema, agranulocytosis.
 Angiotesion II Receptor Antagonists/Blokers (ARBs)
• Angiotensin II blockers block the angiosin II absorption by the receptor
found in many tissues, while ACE inhibitors inhibit the angiotensin-
converting enzymes in the formation of angiosin II.
• A-II blockers prevent the release of aldosterone; cause vasodilation; and
decrease peripheral resistance.
• A-II blockers are less effective treating hypertension in African-Americans.
• A-II blockers may cause angioedema; should be used with great caution, it
at all, with clients who have diabetes mellitus, heart failure or renal
dysfunction. Cough a common side effect of ACE inhibitors is not a
problem in ARBs therapy.
Examples of ARBs
• Atacanda (Candersartan)
• Teveten(Eprosarta)
• Avapro (irebesartan)
• Cozaar (losartan)
• Micardist (Telmisartan)
• Diovan (Valsartan)
 Calcium Channel Blockers (CCB’s Calcium Antagonist/ Calcium Blockers)
• Calcium increase muscle contrability, peripheral resistance, and blood
• Calcium channel blockers decrease calcium levels and promote
• Calcium blockers lower BP better in African-American than drugs in
either categaories.
Side effects and adverse reactions (CCB’s)
• Flushing
• Headache
• Dizziness
• Ankle edema
• Bradycardia
• AV block
 Examples of CCB’s
• Calan SR, Isoptin SR (Verapamil)
• Cardizem, CardizemCD or SR (diltiazem HCL)
• Norvasc (Amlodipine)
• Plendil (Felodipine)
• Dyna Circ (Isradipine)
• Sular, Nisocar (Nisoldipine)
Note: Normally, beta-blockers are not prescribed with calcium-blockers
because both drugs decreases myocardium contractility.
Nursing Intervention
 Patient Teaching/Counseling
• Teaching about HPN
• Teaching about risk factors
• Stress therapy
• Low sodium, low saturated fat diet
• Avoid stimulants, e.g. caffeine, alcohol, cigarette smoking
• Regular pattern of exercise
• Weight reduction if obese
 Teaching about medication
• The most common side effects of diuretics are potassium depletion
and orthostatic hypotension
• The most common side effect of the different antihypertensive drug is
orthostatic hypotension.
• Take anti-hypertensive medications at regular basis
• Assume sitting or lying position for few minutes
• Change position gradually
• Avoid very warm bath
• Avoid prolonged sitting or standing
• Avoid alcoholic beverages
• Avoid tyramine- rich foods (protiens) as follows.
Aged cheese, Liver
Beer , Wine
Chocolates, Yogurt
Herring pickle, Sausage, Soy sauce
*these foods may cause hypertensive crisis.
Preventing Vascular Disorders
• The causes of peripheral vascular disorders are atherosclerosis, thrombosis,
embolization, hypercoagulability of blood, hypertension, and
inflammatory processes mechanical or chemical trauma.
• These factors cause decreased blood flow, tissue ischemia, tissue hypoxia,
necrosis, ulceration and gangrene. The most distal parts of the body are
commonly affected, especially the lower extremities
• The disorders affecting the arteries are arteriosclerosis obliterans,
aneurysm, and Reynaud’s disease
• The disorders affecting the veins are thrombophlebitis (superficial vein
thrombosis and deep vein thrombosis), and varicosities.
• The disorders affecting the arteries and veins is Buerger’s disease
(thromboangitis obliterans)

Arterial Disorders
Arteriosclerosis is hardening of arteries. It affects the tunica media.
Atherosclerosis is narrowing /occlusion of lumen of arteries due to
accumulation off fatty plaques in the tunica intima
The Clinical Manifestation of arterial disorders are as follows.
1. Pain. Intermittent claudication. This is leg pain on activity
and exercise , relieved by rest. Rest improves blood flow and
oxygen supply to the legs, thus pain is relieved.
2. Coldness or cold sensitivity. This is because of tissue
ischemia. 3.
3. Impaired arterial pulsations. Indicates decreased blood
flow due to arterial spasm.
4. Color changes. Cyanosis on dependency of legs.
5. Ulceration and gangrene. Due to tissue ischemia, hypoxia or
6. Sexual dysfunction. Decreased penile circulation due to
occlusion of terminal aorta. This may be experienced as
unsustained erection.
 Collaborative Management for Arterial Disorders:
1. Medication
Peripheral Vasodilators
=Increased blood flow to the extremities, by promoting
Alpha – Adrenergic antagonists
Vasodilation (isoxsuprine HCL)
Priscoline HCl (totazoline)
Direct Acting Peripheral Vasodilators
Hydergine (Ergoloid mesylate)
Pavabid (papaverine
Trental (pentoxifylline)
Side effects and adverse reaction (Peripheral vasodilators)
Orthostatic hypotension
GI distress

Note: trental improves microcirculation and tissue perfusion by

decreasing blood viscosity and improving the flexibility of erythrocytes
thus increasing tissue oxygenation. It alleviates intermittent
claudication and improves cerebral function for those with
cerebrovascular ansufficiency and may be decrease stroke incidence for
those having recurrent TIA ( Transient Ischemic Attack.
 Lower abnormal blood lipid levels, especially for ‘bad’ lipoproteins
(chylomicrons, very low- density lipoproteins/VLDL, low- density
lipoproteins/LDL). These lipoproteins are composed mainly of cholesterol
and triglycerides and contribute to atherosclerosclerotic plaque in the blood
 The high-density lipoproteins (HDL), the ‘friendly ‘ or ‘good’ lipoproteins
have a higher percentage of protein and less lipids. Their function is to
remove cholesterol from the bloodstream and deliver it to the liver.
Questran (cholestyramine resin)
Atromid- S (clofibrate)
Colestid (colestipol HCL)
Lopid (gemfibrozil)
Lorelco (probucol)
Vastatins/Statins (HMGCoA Reductase Inhibitors)
Lipitor (atorvastatin calcium)
Lescol (fluvastatin)
Mevacor (lovastatin)
Pravachol (pravastatin sodium)
Zocor (simvastatin)
Side effects and adverse reaction (antilipemics)
 Cholestyramine: constipation, peptic ulcer
 Clofibrate and probucol: decreased libido impotence
 Gemfibrozil: hyperglycemia
 Nicotinic acid: dizziness, faintness due to vasodilation
 GI disturbances
 Flushing of the skin
 Hyperglycemia
 Hyperuricemia

Statins: increased in liver enzyme levels (hepatotoxicity)

Rhabdomyolysis (skeletal muscle adverse effect)

Note: Gemfibrozil should not be used in combination with Lovastatin

because increase in CPK. Gallstones may occur with long term use.
1. Treatment for arterial disorders
 Quit smoking. Nicotine causes vasoconstriction
 Skin and foot care. To prevent ulceration and gangrene
 Diet: Low-fat, low-cholesterol
 Activity: Daily walking program

2. Surgical management
 Balloon angioplasty
 Laser angioplasty
 Stents: It involves use of rigid but flexible structure that maintains the
integrity of the vascular wall and patency of the artery.
 Amputation. It is performed in clients with gangrene. Gangrene is a wound
composed of necrotic tissues that is usually infected and does not heal.
3. Nursing Intervention
 Promotion tissue perfusion.

• Maintain warm environmental temperature

• Place legs in slight dependency (lower than level of heart) to promote
arterial flow.
• Avoid pressure on affected extremity; use padding or support.
• Avoid vigorous massage of extremities, to prevent release of
thrombus, if present
• Patient teaching includes the following:
Avoid chilling and exposure to cold; use several layers of
clothing and socks during cold weather.
Avoid constricting clothes
Avoid crossing the legs
Quit smoking

(Exposure to cold and smoking cause vasoconstriction; and

infection clothings and crossing the legs inhibit arterial flow).
Maintaining skin integrity and preventing infection. Skin breakdown
and infection may lead to gangrene formation.
 Patient teaching include the ff.
• Examine the skin for signs of breakdown and infection
• Take daily bath and dry the skin gently
• Apply moisturizing cream or lotion on the skin
• Avoid using alcohol. Alcohol causes dryness of the skin
• Wear comfortable, well-fitted pair of shoes
• Consult physician for any signs of skin breakdown
Promoting activity. To promote circulation, maintain vascular tone, and
enhance production of chemical activators (tissue type plasminogen
activator) that prevent platelet aggregation.
• General exercises: aerobic such as walking, swimming, jogging, bicycling.
Do exercise 30 to 45 minutes, 3 to 4 times a week.
• Special exercises: ankle rotations. Ankle pumps, knee extension, Buerger-
Allen’s exercise

Note: Buerger- Allen’s exercise primarily promotes arterial circulation.

Aneurysm. Is localized, irreversible dilatation of an artery due to an
alteration in the integrity of its wall.
 The differenet types of aneurysm are as follows
 Fusiform aneurysm. Both sides of the arterial wall are dilated
 Saccular aneurysm. One side of the arterial wall is dilated.
 Dissecting aneurysm. There is separation between the tunica media
and tunica intima.
 Abdominal aortic aneurysm (AAA). This is the most common type
of aneurysm
 The clinical manifestation of AAA are as follows:
Pulsatile mass over the abdomen
Low back pain, lower abdominal pain, and flank pain. This is
due to compression of structures and nerve ending in the area
by the dilated artery.
 Collapse and shock due to hemorrhage.
 The most common cause of aneurysm is hypotension
 The most dangerous complication of aneurysm is rupture
 Collaborative management for aneurysm include the ff.
 Antihypertensive drugs
 Surgery, if aneurysm is greater than 4cm. Teflon, Dacron or Gortex graft
may be used in surgical repair of aneurysm. Aneurysm clip may also be
Raynaud’s Disease. Is intermittent vasospasm of arteries in the digit as a
result of exposure to cold and emotional stress. It is aggravated by cigarette
• Women, ages 15 to 40 years are most commonly affected
• Collaborative management for Raynaud’s disease include the ff.
 Medical Management
Calcium- channel blockers
 Surgery
• Sympathectomy to relieve vasospastic
• Amputations for severely infected or non-healing ulcerations and gangrene
Nursing intervention
 Patient teaching include the ff.
• Avoid exposure to cold
Wear gloves when handling frozen foods
Practice caution when cleaning refrigerator
Wear socks during cold climate
• Smoking causes vasoconstriction
• Reduce emotional stress
• Avoid drugs that cause vasoconstriction, like contraceptive pills and
Venous Disorders
 Superficial Thrombophlebitis (SVT). It is venous thrombosis and
inflammation in a superficial vein
• The greater or lesser saphenous veins in the legs are most commonly affected
• The clinical manifestation of SVT are as follows
 Pain in the calf of the leg (positive Homan”s sign is assessed by flexing
the knee and asking the client to dorsiflex the foot.
 Tenderness
 Palpable induration (redness) along the course of the vein.
Note: There is no leg edema in SVT

 Collaborative Management for SVT

• Bed rest with leg elevation. To prevent dislodgement of thrombus and to
promote venous return.
• Local moist heat application on the leg, to relieve pain and reduce blood
viscosity, thus preventing thrombus formation
• Non-narcotic analgesics
• Nonsteroidal anti-inflammatory agents: (NSAIDs)
• Patient teaching include the ff.
 Prevention of venous stasis:
 Avoid prolonged sitting or standing
 Elevate legs when sitting
 Avoid crossing the legs at the knee
 Wear compression support stocking.
 Avoid constriction on legs by tight bonds such as garters.
 Daily exercise and activity
 Prevention of recurrence of SVT
 Maintain ideal body weight (IBW). Obesity causes venous stasis.
 Alternate standing with sitting at work or at home
 Regular patter of exercise.

Deep Vein Thrombosis (DVT). It is venous thrombosis and inflammation in

a deep vein.
It is caused by Vircho’s triad:
 Vessel wall injury (e.g. cigarette smoking)
 Venous stasis (e.g. prolonged bedrest)
 Hypercoagulability of the blood (e.g. use of contraceptive pills, dehydration,
• DVT is potentially life- threatening because it may lead to pulmonary
• The clinical manifestation of DVT are as follows.
Calf-pain (+Homan’s sign
Palpable induration (redness) along the course of the vein.
Collaborative management for DVT
1.Medical management
• Thrombolytics
• Anticoagulants: Heparin, Courmadin
• Thrombolytics: Disintegrate blood clot (thrombus)
1. Streptokinase (streptase, kabikinase
2. Urokinase (abbokinase)
3. Tissue plasminogen activator (t-PA, alteplase, activase)
4. Anisolyted plasminogen streptokinase activator complex (APSAC
5. Retaplase (retavase)
6. Tenecteplase (TNKase)
 Side effects and adverse reaction (thrombolytics)
• Allergic reactions (anaphylaxis may occur with streptokinase)
• Hemorrhagic (antidote is Amicar/Aminocaproic acid)
Anticoagulants. Inhibit clot formation
• Used in clients with venous and arterial disorders that put them at high risk
for clot formation
• Oral and parental anticoagulants (Warfarin and Heparin) primarily by
preventing venous thrombosis. Whereas antiplatelet drugs act primarily by
preventing arterial thrombosis. However, both groups of drugs suppress
thrombosis in general.
Heparin. Inhibits the action of thrombin; conversion of fibrinogen to fibrin
does not occur and the formation of a fibrin clot is prevented.
• It is given subcutaneous or IV
• It can decrease the platelet count, causing thrombocytopenia.
• It prolongs clotting time. PPT and APTT are monitored during therapy
Side effects and adverse reaction include: hemorrhage, itching and
Coumadin (Warfarin). Inhibits hepatic synthesis of Vitamin K, thus
affecting the clothing factors II,VII, IX and X.
 Monitor PT and INR
 Side effect and adverse reaction include:
 Internal bleeding (petechiea, ecchymosis, tarry stools, hematemesis)
 Anorexia
 Nausea and Vomiting
 Diarrhea
 Abdominal cramps
 Rash fever
 Stomatitis

Surgical management
 Thromboembolectomy. Surgical removal of blood clotwith the use of
balloon-tipped catheter.
 Greenfield vena cave filter and umbrella filter. These are inserted in the
inferior vena cava to prevent pulmonary embolism in clients with
Nursing Intervention
 Maintaining tissue perfusion
 Bed rest for 5 to 7 days. To prevent dislodgement of blood clots.
 Evaluate legs to promote venous retum and to prevent edema
 Apply compression support stocking to promote venous retum. It is
inverted (turned inside out) to facilitate application.
 Check pulse distal to the site of thrombosis, to asses for circulatory
 Monitor calf-pain. Presence of calf pain indicates thromphlebitis.
 Promoting comfort
 Analgesics to relieve pain
 NSAIDs to reduce edema.
Varicose Vein. Dilated veins, usually in the lower extremities
 The most common cause of varicose veins is hereditary weakness of the
valves of the veins.
 Other causes are congenital absence of valves of the veins, prolonged sitting
or standing, wearing of constricting clothings, obesity, thrombophlebitis,
pregnancy, disease condition, e.g. right –sided CHF, liver cirrhosis
 The clinical manifestation of varicose veins are as follows.
 Dilated, purplish, tortuous veins
 Leg edema
 Heaviness in the legs
 Collaborative management of varicose veins
 Evaluation of the legs for 15 to 30 minutes at a time, average of 20 minutes
 Use of compression or support stocking
 Sclerotherapy. Injection of sclerosing agent into the varicose veins
 Surgery vein ligation and stripping
 The priority consideration after vein surgery is prevention of the
thrombophlebitis. Early ambulation prevents thrombophlebitis.
 Monitor for bleeding postop.
Arterial and Venous Disoders.
Buerger’s Disease. (Thromboangitis Obliterans). It is diffuse inflammation of
the small and medium arteries, followed by the veins. It involves inflammation
and fibrosis of nerves
 Males, 30 to 50 years of age are most commonly affected
 Most common ethiologic factors is cigarette smoking.
 Other causes are genetic factors and coagulation abnormalities.
 Most characteristics clinical manifestation is intermittent claudication
 Collaborative management for Buerger’s Disease.
1. Eliminate cigarette smoking
2. Medication: Calcium- channel blockers, anti-platelet agents
3. Surgery
 Sympathectomy (to eliminate vasospasm)
 amputation of ulcerated finger and toes.