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Among the different vascular diseases, hypertension is the most commonly known.

Hypertension is known to be the major risk


factor for global CVD morbidity and mortality, with an estimated half of the CVD events attributed to it. Thus, it is important to
prevent, treat and control hypertension to reduce the risk of CVD events and related healthcare burden

Case analysis

A 59-year-old man with type 2 diabetes presents with concerns about high blood pressure (BP). At a recent visit to his doctor, he
was told his BP was high. However, he doesn't remember the exact reading. He has no symptoms. He has never taken
medications for high BP. He takes metformin for type 2 diabetes. What action should be done to diagnose the hypertension on
this patient? What management strategies must be done for the patient considering the type of hypertension the patient may
have?

THE VASCULAR SYSTEM

Functions of the vascular system

1. Circulatory needs of tissues

o Factors affecting blood supply

 Rate of tissue metabolism- Factors the increase metabolic demands include physical activity or exercise, local heat
application, fever, and infection. Factors that decrease metabolic demands include rest or decreased physical
activity, local cold application, and cooling of the body

 The availability of oxygen

 Function of the tissues

o Ischemia

 Deficient blood supply to tissues

 Results from blood vessels failure of blood vessels to dilate in response to the need for increased blood flow

o Systemic arteriovenous oxygen difference

 Difference in the concentration of oxygen between venous and arterial blood

 Blood in vena cava contains 25% less oxygen than aortic blood

2. Blood flow

 Unidirectional flow of blood follows: left side of the heart to the aorta, arteries, arterioles, capillaries, venules, veins,
vena cavae, and right side of the heart.

 Factors affecting rate of blood flow

 Pressure Difference (∆P)- Responsible for unidirectional flow of blood. Difference in pressure between arterial
(approximately 100mmHg) and venous (approximately 4mmHg) system

 Resistance (R)- Impediments to blood flow which offer the opposing force

 Laminar (streamlined) flow of blood0 Blood in the center of the vessel moving slightly faster than the blood near the
vessel walls. Blood flows in a linear, smooth manner

 Turbulent flow- Alteration to normal laminar flow of blood characterized by chaotic flow. Occurs when, The blood flow
rate increases, When blood viscosity increase, When the diameter of the vessel becomes greater than normal, When
segments of the vessel are narrowed or constricted.
 Bruit- An audible vascular sound associated with turbulent blood flow. May occasionally also be palpated as a thrill.

3. Blood pressure

 Systolic Blood Pressure - Pressure exerted when blood is ejected into arteries. Normal systolic blood pressure is 120
mmHg or below
 Diastolic Blood Pressure- Pressure blood exerts within arteries between heartbeats. Normal diastolic blood pressure is
80 mmHg or below

4. Capillary filtration and reabsorption


o Factors affecting fluid movement across capillaries
 Affects the amount and direction of movement
 The equilibrium between hydrostatic and osmotic forces of the blood and interstitium
o Hydrostatic pressure- pushing force generated by blood pressure.
o Osmotic pressure- pulling force created by plasma proteins
 Capillary permeability

Edema occurs as a result of the imbalance in fluid filtered and reabsorbed causing accumulation of fluid in the interstitial space.
The amount of fluid that is filtered in the arterial end greatly exceeds the amount of fluid that is reabsorbed in the venous end.

5. Hemodynamic resistance

o Most important determining factor is vascular radius

o Peripheral vascular resistance- The opposition to blood flow provided by the blood vessels.

o Factors that determine PVR:

 Viscosity or thickness of the blood (directly proportional)


 Length of the vessel (directly proportional)
 Vessel radius (inversely proportional to the fourth power)

Vessel radius greatly affects PVR such that any change in vessel radius affects PVR four times as much as blood viscosity or vessel
length.

6. Peripheral vascular regulating mechanism

o Complex and consists of central nervous system influences, circulating hormones and chemicals, and independent
activity of the arterial wall itself.

o Regulatory mechanisms include:

 SNS (Adrenergic) activity- Norepinephrine and epinephrine

 Most important factor in regulating the caliber and therefore the blood flow of peripheral blood vessels.
 All vessels are innervated by the sympathetic nervous system except the capillary and precapillary sphincters.
 Stimulation causes vasoconstriction

 Hormonal regulators

 Epinephrine- Same effect as norepinephrine, however mat cause vasodilation in skeletal muscles, heart and
brain in low concentrations

 Angiotensin- A potent substance formed from the interaction of renin (synthesized by the kidney) and a
circulating serum protein, stimulates arterial constriction

 Serotonin- Causes vasoconstriction of arterioles

 Vasoactive substances- Vasodilators such as histamine, bradykinin, prostaglandin, and certain muscle
metabolites.

 Reduction in oxygen, nutrients and pH changes

 Heat and cold application

Pathophysiology of Vascular System

The major mechanism involved in all peripheral vascular diseases is reduced blood flow. Many underlying mechanisms can cause
this which is discussed in the following section of the module. Physiologic effects of altered blood flow depend on the extent to
which tissue demands exceed the supply of oxygen and nutrients available. This means that in organs that require greater blood
flow due to oxygen and nutrient demands (such as the brain), even a minimal decrease in blood flow can cause manifestations of
ischemia as compared to other organs.

Pump failure

o Inefficient pumping action of the heart

o Left ventricular failure- Causes an accumulation of blood in the lungs and a reduction in forward flow or cardiac output,
which results in inadequate arterial blood flow to the tissues.

o Right ventricular failure causes systemic venous congestion and a reduction in forward flow
Alterations in blood and lymphatic vessels

o Intact, patent, and responsive blood vessels are necessary to deliver adequate amounts of oxygen to tissues and to
remove metabolic wastes

o Causes of changes in blood and lymphatic vessels are summarized below

  Obstruction Damage

Arteries ·         Atherosclerotic plaque, ·         Chemical or mechanical trauma

·         Thrombus ·         Infections or inflammatory processes

·          Embolus ·         Vasospastic disorders

·         Congenital malformations

Veins ·         Thrombus ·         Incompetent venous valves

  ·         Reduction in the effectiveness of the


pumping action of surrounding muscles

Lymphatic vessels ·         Tumor ·         Mechanical trauma

·         Inflammatory processes.

Although many types of peripheral vascular diseases exist, most result in ischemia and produce some of the same symptoms:
pain, skin changes, diminished pulse, and possible edema. The type and severity of symptoms depend in part on the type, stage,
and extent of the disease process and on the speed with which the disorder

Circulatory insufficiency of extremities

Characteristics of Arterial and Venous Insufficiency


CHARACTERISTIC ARTERIAL VENOUS
Pain Intermittent claudication to sharp, unrelenting, Aching, cramping
constant
Pulses Diminished or absent Present, but may be difficult to palpate through
edema
Skin characteristics Dependent rubor-elevation pallor of foot, dry, Pigmentation in gaitor area (area of medial and
shiny skin, cool-to-cold temperature, loss of lateral malleolus), skin thickened and tough, may
hair over toes and dorsum of foot, nails be reddish blue, frequently with associated
thickened and ridged dermatitis
Ulcer characteristics

Location Tip of toes, toe webs, heel or other pressure Medial malleolus; infrequently lateral malleolus
areas if confined to bed or anterior tibial area

Pain Very painful Minimal pain if superficial or may be very painful

Depth of ulcer Deep, often involving joint space Superficial

Shape Circular Irregular border

Ulcer base Pale to black and dry gangrene Granulation tissue—beefy red to yellow fibrinous
in chronic long-term ulcer

Leg edema Minimal unless extremity kept in dependent Moderate to severe


position constantly to relieve pain
Assessment of Vascular Function

Health history and Clinical Manifestations

o A description of the pain and any precipitating factors, the skin color and temperature, and the peripheral pulses are
important for the diagnosis of arterial disorders.

o Intermittent claudication

 A muscular, cramp-type pain in the extremities consistently reproduced with the same degree of exercise or activity
and relieved by rest is experienced by patients with peripheral arterial insufficiency.

 Caused by the inability of the arterial system to provide adequate blood flow to the tissues in the face of increased
demands for nutrients during exercise

 About 50% of the arterial lumen or 75% of the cross-sectional area must be obstructed before intermittent
claudication is experienced

What to assess

 Amount of exercise or the distance a patient can walk before pain is produced

 Presence of rest pain- Persistent pain in the forefoot when the patient is resting. Indicates a severe degree of arterial
insufficiency and a critical state of ischemia. May be worse at night and may interfere with sleep. Relieved by lowering
extremity to a dependent position

 Location of claudication to assess site of arterial disease- Pain of intermittent claudication occurs one joint level below the
disease process

 Changes in skin appearance and temperature- Inadequate blood flow results in cool and pale extremities. Skin changes
observed due to further reduction of blood flow: Pallor. Rubor (suggests severe peripheral arterial damage in which
vessels that cannot constrict remain dilated). Cyanosis

 Changes resulting from chronic reduction in nutrients and oxygen supply: Loss of hair. Brittle nails. Dry or scaling skin.
Atrophy. Ulcerations. Edema related to extremities’ dependent position. Gangrenous skin changes results from chronic
ischemia and represent tissue necrosis

 Pulse- To assess the status of peripheral arterial circulation. Assess for presence or absence, rate, rhythm and quality.
Pulses should be palpated bilaterally and simultaneously, comparing both sides for symmetry. Absence of pulse may
indicate stenosis proximal to the location of the pulse

Diagnostic Evaluation

 Doppler Ultrasound Flow Studies- Use of a microphone-like, hand-held Doppler ultrasound device (transducer or
probe). May be helpful in detecting and assessing peripheral flow
 Continuous-wave (CW) Doppler ultrasound device may be used to hear (insonate) the blood flow in vessels when pulses
cannot be palpated. The depth at which blood flow is determined by the frequency (in megahertz [MHz]) it generated;
The lower the frequency, the deeper the tissue penetration. A 5- to 10-MHz probe may be used to evaluate the
peripheral arteries.
 Limitations: Differentiating arterial from venous flow. Detecting the site of a stenosis
 Used to determine Ankle-Brachial Index (ABI) or ankle-arm index (AAI)- Ratio of the ankle systolic blood pressure to the
arm systolic blood pressure. Objective indicator of arterial disease that allows the examiner to quantify the degree of
stenosis. Higher peripheral BP is observed distal to the site of narrowing/ stenosis

Right ABI = Highest Pressure in Right Foot / Highest Pressure in Both Arms
Left AB = Highest Pressure in Left Foot / Highest Pressure in Both Arms

ABI Value Interpretation Recommendation


Greater than 1.4 Calcification/Vessel Hardening Refer to vascular specialist
1.0-1.4 Normal None
0.9 - 1.0 Acceptable None
0.8 -0.9 Some Arterial Disease Treat risk factors
0.5-0.8 Moderate Arterial Disease Refer to vascular specialist
Less than 0.5 Severe Arterial Disease Refer to vascular specialist

Exercise testing

 To determine how long a patient can walk


 To measure the ankle systolic blood pressure in response to walking
 Patient walks on a treadmill at 1.5 mph with a 10% incline for a maximum of 5 minutes
 A normal response to the test is little or no drop in ankle systolic pressure after exercise.
 In a patient with true claudication, however, ankle pressure drops

Duplex ultrasonography

 Involves B-mode gray-scale imaging of the tissue, organs, and blood vessels (arterial and venous)
 Permits estimation of velocity changes by use of a pulsed Doppler
 Color flow techniques, which can identify vessels, may be used to shorten the examination time.
 Determine the level and extent of disease
 Universally employed to evaluate the venous system
 Image and assess blood flow
 Evaluate the runoff status of the distal vessels
 Locate the disease (stenosis versus occlusion)
 Determine anatomic morphology and the hemodynamic significance of plaque causing stenosis
 Help in planning therapy and monitoring its outcomes

Computed Tomography

 Provides cross-sectional images of soft tissue


 Identify the area of volume changes to an extremity
 Identify compartment where changes take place

Computed tomographic angiography (CTA)

 Spiral CT scanner and rapid intravenous infusion of contrast agent are used to image very thin (1-mm) sections of the
target area
 The results are configured in three dimensions so that the image closely resembles a regular angiogram
 Shows the aorta and main visceral arteries better than it shows smaller branch vessels.
 Limitations: Large volume of contrast medium used. Risk for allergic response. Cannot be used in patients with renal
disease or dysfunction

Magnetic resonance angiography

 Performed with a standard MRI scanner but with image-processing software specifically programmed to isolate the
blood vessels.
 Produces 3D images
 Useful in patients with poor renal function or allergy to contrast agent.

Angiography

 Involves injecting a radiopaque contrast agent directly into the vascular system to visualize the vessels.
 To confirm the diagnosis of occlusive arterial disease to determine management
 Demonstrates location of a vascular obstruction or an aneurysm (abnormal dilation of a blood vessel) and the collateral
circulation

Complications

 Allergic reaction to contrast agent


 Vessel injury
 Bleeding
 CVA (brain attack, stroke)
Arterial Disorders

Arteriosclerosis

Most common disease of the arteries. Hardening of the arteries. Diffuse process
whereby the muscle fibers and the endothelial lining of the walls of small arteries and
arterioles become thickened

Atherosclerosis

Affects the intima of the large and medium-sized arteries. Characterized by atheroma/
plaque formation. Involves the accumulation of lipids, calcium,
blood components, carbohydrates, and fibrous tissue on the
intimal layer of the artery. Most common cause of heart attack,
stroke and peripheral artery disease

Two types of lesions:

Fatty streaks

Yellow and smooth, protrude slightly into the lumen of the


artery, and are composed of lipids and elongated smooth
muscle cells. May predispose the person to the formation of
fibrous plaques or May be reversible. Do not usually cause
clinical symptoms

Fibrous plaques

Composed of smooth muscle cells, collagen fibers, plasma


components, and lipids. White to whitish yellow. Protrudes in
various degrees into the arterial lumen, sometimes completely
obstructing it. Found predominantly in the abdominal aorta and
the coronary, popliteal, and internal carotid arteries. This plaque
is believed to be an irreversible lesion

Characteristics Arteriosclerosis Atherosclerosis

Hardening or stiffness of vessel Present Present

Narrowing of arterial lumen May or may not be present Present

Vessels involved Small arteries and arterioles Medium-sized and large arteries

Layer/s of arterial wall involved Intima and/or media Intima or inner

Plaque formation May or not be present Present

Thickening of arterial walls Present Absent

Onset May begin in childhood or fetal Later in life


stage

Location   At any point of the body; but


more commonly in bifurcated
areas

Acute events Absent Present

Complete blockage of vessel Absent Present


   

Risk factors

Modifiable

 Nicotine use (i.e., tobacco smoking, chewing)


 Diet (contributing to hyperlipidemia)
 Hypertension Diabetes (which speeds the atherosclerotic process by thickening the basement membranes of both large
and small vessels)
 Stress
 Sedentary lifestyle

Non-modifiable

 Age
 Gender

Prevention

 Reduce the amount of fat ingested in a healthy diet


 Substitute unsaturated fats for saturated fats
 Decrease cholesterol intake to no more than 300 mg daily to reduce the risk of cardiovascular disease
 Monitor serum cholesterol
 Exercise
 Lipid lowering medications:
o Bile acid sequestrants (cholestyramine [Questran, Prevalite] or colestipol [Colestid])
o Nicotinic acid (niacin, B3, Niacor; Niaspan)
o Statins (atorvastatin [Lipitor], lovastatin [Mevacor], pravastatin [Pravachol], simvastatin [Zocor])
o Fibric acids (gemfibrozil [Lopid])
o Lipophilic substances (probucol)

Clinical manifestation

 Depend on the organ or tissue affected


 Coronary atherosclerosis (heart disease)- angina, and acute myocardial infarction
 Cerebrovascular diseases, including transient cerebral ischemic attacks
 Atherosclerosis of the aorta, including aneurysm, and atherosclerotic lesions
 Renovascular disease (renal artery stenosis and end-stage renal disease), including hypertension

Management

Medical management

 Modification of risk factors


 Controlled exercise program to improve circulation and increase the functioning capacity of the circulation
 Medication
 Interventional or surgical graft procedures

Surgical management

 Inflow procedures which provide blood supply from the aorta into the femoral artery, and
 Outflow procedures which provide blood supply to vessels below the femoral artery

Radiologic interventions
 Angioplasty or percutaneous transluminal angioplasty (PTA)
 For isolated lesion or lesions are identified during the arteriogram

Complications include: hematoma formation, embolus, dissection (separation of the intima) of the vessel, and bleeding

Stents

Small, mesh tubes made of nitinol, titanium, or stainless steel. May be inserted to support the walls of blood vessels and prevent
collapse immediately after balloon inflation

Nursing management

Nursing diagnosis

 Ineffective peripheral tissue perfusion related to compromised circulation


 Chronic pain related to impaired ability of peripheral vessels to supply tissues with oxygen
 Risk for impaired skin integrity related to compromised circulation
 Deficient knowledge regarding self-care activities

Patient goals

 Increased arterial blood supply to the extremities


 Promotion of vasodilation
 Prevention of vascular compression
 Relief of pain
 Attainment or maintenance of tissue integrity
 Adherence to the self-care program

Nursing interventions

Improving peripheral arterial circulation

 Positioning the part below the level of the heart


 Elevating HOB to improve circulation to lower extremity
 Assist the patient with walking or other moderate or graded isometric exercises that may be prescribed to promote
blood flow and encourage the development of collateral circulation
 Instruct client to walk until pain is felt, rest until pain fades then may continue the exercise to increase endurance and
promote collateral circulation
 Maintain a regular exercise program
 Assess the amount of exercise that patient can tolerate before pain is felt to provide baseline
 Exercise is contraindicated for patients with leg ulcers, cellulitis, gangrene, or acute thrombotic occlusions.

Promoting vasodilation and preventing vascular compression

 Application of warmth to promote arterial flow (temperature of heat source must not exceed body temperature)
 Instruct the patient to avoid exposure to cold temperatures, which causes vasoconstriction
 Ensure adequate clothing and warm temperatures protect the patient from chilling
 Avoid or halt smoking
 Avoid emotional upsets which stimulate the sympathetic nervous system, resulting in peripheral vasoconstriction
 Avoid constrictive clothing
 Discourage crossing of legs

Relieving pain

 Pain is chronic and continuous


 Administer analgesics as prescribed
Maintaining tissue integrity

 Avoid trauma to extremities


 Advise the patient to wear sturdy, well-fitting shoes or slippers to prevent foot injury and blisters
 Recommend neutral soaps and body lotions to prevent drying and cracking of skin
 Pat dry to prevent scratching and vigorous rubbing which can abrade skin and create a site for bacterial invasion
 Fingernails and toenails should be carefully trimmed straight across and sharp corners filed to follow the contour of the
nail.
 All signs of blisters, ingrown toenails, infection, or other problems should be reported to the physician
 Recommend good nutrition to promote healing and prevent tissue breakdown

Peripheral arterial occlusive disease

Occlusive peripheral arterial disease is blockage or narrowing of an artery in the legs (or rarely the arms), usually due to
atherosclerosis and resulting in decreased blood flow. Most commonly develops in the arteries of the legs, including the two
branches of the aorta (iliac arteries) and the main arteries of the thighs (femoral arteries), of the knees (popliteal arteries), and
of the calves (tibial and peroneal arteries)

Risk factors

o Older people
o Males
o People who have ever smoked regularly
o People with diabetes, high blood pressure, abnormal cholesterol levels, or high blood homocysteine (a component of
protein) levels
o People who have a family history of atherosclerosis
o People who are obese
o People who are physically inactive

Etiology

o Gradual narrowing due to atherosclerosis


o Sudden blockage due to thrombus formation or embolus

Clinical manifestation

o Symptoms of occlusive peripheral arterial disease vary depending on Which artery is affected, How completely the artery
is blocked, Whether the artery is gradually narrowed or suddenly blocked

o Intermittent claudication
o Loss of sensation in or paralysis of a limb
o Necrosis and gangrene formation

Diagnostic evaluation

o Physical examination and symptoms


o Measurement of blood pressure and blood flow

Prevention

o Quitting smoking
o Controlling diabetes
o Lowering high blood pressure and high cholesterol levels
o Losing weight
o Engaging in regular physical activity
o Sometimes drugs to prevent complications such as coronary artery disease

Management

The aims of treatment are the following:

 To prevent the disease from progressing


 To reduce the risk of heart attack, stroke, and death due to widespread atherosclerosis
 To prevent amputation
 To improve the quality of life by relieving symptoms (such as intermittent claudication)

Treatment depends on:

 Whether the blockage developed suddenly or gradually


 The severity of the symptoms
 The severity of the blockage
 The location of the blockage
 The risks related to the treatment (particularly for surgery)
 The person's overall health

Control risk factors

Exercise

Drugs

 Drugs for underlying disorders like DM, MI or stroke


 Drugs for hypertension
 Aspirin or clopidogrel is usually given because these drugs help prevent clot formation and reduce the risk of heart
attack or stroke.
 Thrombolytics, fibrinolytics to dissolve clot

Angioplasty

Surgery to relieve or bypass the blockage- Bypass grafts are performed to reroute the blood flow around the stenosis or
occlusion.

Amputation of a limb if tissue dies

Nursing management

Maintaining circulation

 Post-operative nursing management of patient who has undergone surgical intervention

 Monitoring of pulses, Doppler assessment, color and temperature of the extremity, capillary refill, and sensory and
motor function of the affected extremities

 Maintain adequate circulating blood volume

Monitoring for potential complications

 Fluid imbalances: Continuous monitoring of urine output (more than 30 mL/hour), central venous pressure, mental
status, and pulse rate and volume

 Assess for bleeding and hematoma formation

 Leg crossing and prolonged extremity dependency are avoided to prevent thrombosis

 Elevating the extremities and encouraging the patient to exercise the extremities while in bed to reduce edema
 Elastic compression stockings as prescribed.

Aneurysm

A distention of an artery brought by a weakening/ destruction of the arterial wall. A balloon-like bulge in an artery

Types of Aneurysms

Abdominal aortic aneurysm- Aneurysm in the abdominal portion of the aorta. Most common type

Thoracic aortic aneurysm- Aneurysm in the chest portion of the aorta (above the diaphragm)

Cerebral aneurysm- Occurs in an artery in the brain. Also called berry aneurysms because they're often the size of a small berry

Peripheral Aneurysm- Aneurysms in arteries other than the aorta and the brain arteries. Common locations for peripheral
aneurysms include the popliteal, femoral and carotid arteries.

Risk factors

o Male gender - Men are more likely than women to have aortic aneurysms.

o Age - Abdominal aortic aneurysms are more likely to occur in people who are aged 65 or older

o Smoking - Smoking can damage and weaken the walls of the aorta

o Family history - People who have family histories of aortic aneurysms are at higher risk for the condition, and they may
have aneurysms before the age of 65.

o History of aneurysms in the arteries of the legs

o Diseases and conditions that weaken the walls of the aorta (hypertension, atherosclerosis)

o Bicuspid aortic valve - has two leaflets instead of the typical three

o Car accidents or trauma - also can injure the arteries and increase the risk for aneurysms.

Etiology
Abdominal aortic aneurysm
 Atherosclerosis
 Smoking
 Hypertension
 Vasculitis (infection in the aorta)
 Cocaine use
 Genetic factors
Thoracic aortic aneurysm
 Same as with aortic aneurysms
 Marfan Syndrome - this is a genetic disorder of the connective tissue; it is a much less common cause of aortic aneurysm.
 Previous aorta injury
 Traumatic injury - cause by a vehicle accident or a bad fall.
Brain (cerebral) aneurysm
 Weakness in the artery wall (usually present since birth)
 Hypertension
 Arteriosclerosis (plaques of cholestrol, platelets, fibrin, and other substance form on the arterial wall)
 Most cerebral aneurysms develop at the forks or branches in arteries because the walls in these sections are weaker.
They most commonly form at the base of the brain - but can form anywhere in the brain.

A saccular aneurysm is a rounded sac containing blood that is attached to a main


artery or one of its branches. A fusiform aneurysm balloons or bulges out on all
sides of the artery. A mycotic aneurysm occurs as the result of an infection that
can sometimes affect the arteries in the brain. The infection weakens the artery
wall, causing a bulging aneurysm to form.

Clinical manifestation

Abdominal Aortic Aneurysms- A throbbing feeling in the abdomen. Deep pain in


back or the side of the abdomen. Steady, gnawing pain in the abdomen that
lasts for hours or days. If an AAA ruptures, symptoms may include:

 Sudden, severe pain in lower abdomen and back;


 Nausea and vomiting;
 Constipation
 Problems with urination
 Clammy, sweaty skin
 Light-headedness
 Rapid heart rate when standing up
 Shock

Thoracic Aortic Aneurysms

 Pain in jaw, neck, back, or chest


 Coughing and/or hoarseness
 Shortness of breath and/or trouble breathing or swallowing
 Loss of voice If a TAA ruptures or dissects
 Sudden, severe, sharp or stabbing pain starting in the upper back and moving down into the abdomen.
 Pain in chest and arms, and pt. can quickly go into shock.

Cerebral (brain) aneurysm symptoms

 Very severe headache that occurs suddenly


 Nausea
 Vomiting
 Eyesight problems
 Seizures (fits)
 Loss of consciousness
 Confusion
 A drooping eyelid
 Stiff neck
 Light sensitivity
 If the cerebral aneurism bursts it will cause bleeding in the brain and a hemorrhagic stroke - it can also cause intracranial
hematoma

Diagnostic evaluation

 Abdominal or chest X-ray may show calcification that outline aneurysm

 Ultrasound and Echocardiography: These tests can show the size of an aortic aneurysm

 CT scan: can show the size and shape of an aneurysm

 Magnetic Resonance Imaging: detect aneurysms and pinpointing their size and exact location
 Angiography: This test shows the amount of damage and blockage in blood vessels.

Management

Goals of management

 Preventing the aneurysm from growing


 Preventing or reversing damage to other body structures
 Preventing or treating a rupture or dissection
 Allowing the patient to continue doing their normal daily activities

Aortic aneurysm

 Medicines are used to lower blood pressure, relax blood vessels, and lower the risk that the aneurysm will rupture (burst)

 Beta blockers, calcium channel blockers

Cerebral Aneurysm

 To relieve symptoms and manage complications

 Painkillers - usually for headaches.

 Calcium channel blockers: reduce the amount of widening and narrowing of blood vessels; often a complication of a
ruptured aneurysm.

 Vasopressor: raises blood pressure; widens blood vessels which have remained stubbornly narrowed; to prevent stroke

 Anti-seizure drugs - seizures may occur after an aneurysm has ruptures. Examples include levetiracetam (Keppra),
phenytoin (Dilantin, Phenytek, others) and valproic acid

 Ventricular catheter- To reduce the pressure on the brain caused by hydrocephalus (excess cerebrospinal fluid). Drains
the excess liquid into an external bag. Connected to a shunt system that drains fluid from the brain

 Rehabilitation therapy: for cognitive impairments due to complications like stroke

Surgical management

Aortic aneurysms

Open Abdominal or Open Chest Repair- Aneurysm is removed and the section of aorta is replaced with a graft made of material
such as Dacronor Teflon 2. Endovascular Repair

Endovascular repair- Aneurysm isn't removed. Instead, a graft is inserted into the aorta to strengthen it. Insertion of graft (also
called a stent graft) into the aorta to the aneurysm. Prevents rupture of aneurysm

Brain aneurysms- Surgical clipping - the aneurysm is closed off by placing a tiny metal clip on the neck of the aneurysm to block
off the blood flow. Endovascular Repair

Prevention of atherosclerosis- Brain aneurysm clipping

Complications

 Hemorrhage leading to shock and even death


 Myocardial ischemia
 Stroke
 Paraplegia due to interruption of anterior spinal artery
 Abdominal ischemia
 Graft occlusion
 Graft infection
 Acute renal failure
 Lower extremity ischemia

Nursing management

Nursing assessment

 Thoracoabdominal aortic aneurysm: be alert for sudden onset of sharp, ripping or tearing pain located in anterior chest,
epigastric area, shoulders or back, indicating acute dissection or rupture.
 Abdominal aortic aneurysm: assess for abdominal (particular left lower quadrant) pain and intense lower back pain
caused by rapid expansion. Ne alert for syncope, tachycardia, and hypotension which may be followed by fatal
hemorrhage due to rupture

Nursing diagnosis

 Ineffective tissue perfusion (Vital organs) r/t aneurysm or aneurysm rupture


 Risk for infection r/t surgery
 Acute pain r/t pressure of aneurysm on nerves and postoperatively

Maintaining perfusion of vital organs

Preoperatively

 Assess for chest pain and abdominal pain


 Prepare patient for diagnostic studies or surgery as indicated
 Monitor for s/s of hypovolemic shock
 Examine neurovascular distal extremities

Postoperatively

 Monitor vital signs frequently


 Assess for s/s of bleeding - Hypotension, tachycardia, tachypnea, diaphoresis
 Monitor laboratory values as ordered
 Monitor urine output hourly
 If thoracoabdominal aneurysm repair has been performed, monitor for s/s of spinal cord ischemia: - pain, numbness,
paresthesia, weakness

Preventing infection

 Monitor temperature
 Monitor changes in WBC count
 Monitor incision for signs of infection
 Administer antibiotics as ordered

Relieving pain

 Provide diversional therapy like listening music, reading newspaper etc.


 Place the patient in comfortable position
 Administer pain medication as ordered
 Keep head of bed elevated no more than 45 degrees for the first 3 days postoperatively to prevent pressure on incision
site
 Assess abdomen for bowel sounds and distention.

Patient education

 Instruct pt. about medications to control BP and the importance of taking them
 Discuss disease process and s/s of expanding aneurysm or impending rupture, or rupture to be reported
 For postsurgical pt. discuss warning signs of postoperative complications (fever, inflammation of operative site, bleeding
and swelling)
 Encourage adequate balanced intake for wound healing
 Encourage patient to maintain an exercise schedule postoperatively

Peripheral Venous Disorders

Venous Thrombosis

DVT, Thrombophlebitis, Phlebothrombosis Thrombophlebitis, for clinical purposes often used interchangeably. However, it
should be noted that they do not reflect identical disease processes.

Venous thrombosis- A blood clot (thrombus) that forms within a vein can occur in any vein; commonly in the lower extremities,
superficial and deep veins of the extremities may be affected

Thrombophlebitis- Thrombus that is associated with inflammation most frequently occurs in deep veins of lower extremities.

Deep vein thrombophlebitis- Deep vein thrombosis (DVT). More serious than superficial thrombophlebitis because it presents a
greater risk for pulmonary embolism

Phlebothrombosis (PE)- Thrombus without inflammation. Thrombus develops


initially in veins as result of stasis or hypercoagulability but without
inflammation

Phlebitis vein inflammation associated with invasive procedures (IV therapy)

Venous thrombi- Aggregates of platelets attached to the vein wall, along with a
tail-like appendage containing fibrin, WBCs, and RBCs. The “tail” can grow or
can propagate in direction of blood flow as successive layers of thrombus form.
A propagating venous thrombosis is dangerous because parts of thrombus can
break off and produce an embolic occlusion of the pulmonary blood vessels.

Etiology

 Exact cause unclear


 Thrombus formation has been associated with Virchow’s triad
 Stasis of blood (venous stasis)
 Endothelial injury / vessel wall injury
 Hypercoagulability / altered blood coagulation
 At least two of the factors seem to be necessary for thrombosis to occur.
 Recent major surgery or injury (mostcommon: hip surgery or open prostatesurgery)
 Ulcerative colitis
 Heart failure
 Cardiovascular disease
 Immobility: prolonged bedrest (ex: duringperiop period)
 Hypercoagulation

Clinical Manifestations

 May have symptoms or may be asymptomatic.


 Classic s/s of DVT
 Calf or groin tenderness and pain
 Sudden onset of unilateral swelling of the leg.
 Phlegmasia cerulea dolens (“painful blue inflammation)
 An uncommon severe form of deep venous thrombosis which results from extensive thrombotic occlusion
(blockage by a thrombus) of the major and the collateral veins of an extremity.
 Massive iliofemoral venous thrombosis entire extremity becomes massively swollen, tense, painful, and cool to
the touch.
 Limb pain
 A feeling of heaviness
 Functional impairment
 Ankle engorgement
 Edema
 Differences in leg circumference bilaterally from thigh to ankle
 Increase in surface temperature of leg, particularly the calf or ankle areas of tenderness or superficial thrombosis (ie,
cordlike venous segment)
 Positive Homans sign
o Pain in calf on dorsiflexion of the foot
o Appears in only 10% of clients with DVT and false-positive findings are common
o Therefore, checking a Homan s sign is not advised
The area described as painful, must be examined and compared with the contralateral limb. Observe for warmth, edema, and
swelling of the extremity. Determine amount of swelling by measuring circumference of affected extremity at various levels with
a tape measure and comparing one extremity with the other at the same level to determine size differences (+) tenderness
usually occurs later

Diagnostic tests
 Contrast venography
 Duplex ultrasonography
 Doppler flow studies
 Impedance plethysmography
 PE findings are often adequate for diagnosis.

Management
 Focus prevents complications, such as pulmonary emboli
 Prevent increase in size of thrombus.
 Bedrest and elevation of the extremity
 Intermittent or continuous warm, moist soaks to the affected area as prescribed
 Evaluate for signs and symptoms of pulmonary embolism (PE) SOB and chest pain
 Emboli may also travel to the brain or heart, but these complications are not as common as PE.

Medical Management
Drug therapy
 Prevent the thrombus from growing and fragmenting (risking pulmonary embolism)
 Prevent recurrent thromboemboli
Anticoagulant therapy
 Prevent the formation of a thrombus in postop patients
 Forestall extension of a thrombus after it has formed
 IV unfractionated heparin (low-molecular weight heparin) followed by oral anticoagulation with warfarin (Coumadin)
 Unfractionated Heparin (UFH; Hepalean)
 Prevent formation of other clots, which often develop in the presence of an existing clot
 Prevent enlargement of the existing clot.
 Initially given in bolus IV dose (100 units/kg of body weight) followed by constant infusion.

Nursing responsibilities
 Check labs b4 administration baseline prothrombin time (PT), activated partial thromboplastin time (aPTT),
International Normalized Ratio (INR), complete blood count (CBC) with platelet count, urinalysis, stool for occult blood,
and creatinine level.
 Use electronic infusion device.
 aPTTs are obtained daily (therapeutic levels 1-2 times the normal control levels.
 Assess s/s of bleeding (hematuria, frank or occult blood in the stool, ecchymosis (bruising), petechiae, an altered level of
consciousness, or pain)
 The nurse ensures that protamine sulfate, the antidote for heparin, is available, if needed, for excessive bleeding

Low-Molecular-Weight Heparin enoxaparin (Lovenox) dalteparin (Fragmin) ardeparin (Normiflo)


 Route: Subcutaneous
 Dose: given in 1 or 2 subq /day; Doses are adjusted according to weight.
 Prevention and treatment of DVT
 Prevents extension of thrombus and development of new thrombi
 Has longer half-life than unfractionated heparin
 Monitor INR and stools daily for occult blood
 Associated with fewer bleeding complications than unfractionated heparin.
 May be used safely in pregnant women patients may be more mobile and have an improved quality of life.
 Disadvantage cost is higher than for unfractionated heparin

Nursing responsibilities
 Dosing schedule must be based on product used and protocol at each institution: coz there are several preparations
 Frequently monitor PTT, PT, Hb, Hct , platelet count, and fibrinogen level.
 Monitor bleeding episodes if bleeding occurs, report STAT and DC anticoagulant therapy
 Administer through continuous IV infusion by electronic infusion device
 Coagulation tests and Hct level
 Therapeutic range: PTT 1.5 times the control intermittent
Warfarin
 Route: PO works in liver to inhibit synthesis of 4 vitamin K-dependent clotting factors and takes 3 to 4 days before it can
exert therapeutic anticoagulation.
 Monitor PT or INR.
 Clients usually receive warfarin for 3 to 6 months after an episode of DVT. Ensure that vitamin K, the antidote for
warfarin, is available in case of excessive bleeding
 Foods that have high levels of vitamin K (eg, green leafy vegetables, broccoli, liver, certain vegetable oils) may change
the effect of Warfarin.
Thrombolytic Therapy
 Effective in dissolving thrombi quickly and completely
 Prevent new clots during 1st 24 hrs
 Platelet inhibitors such as abciximab (ReoPro) given within first 3 days
after acute thrombosis
 Tissue plasminogen activator [t-PA, alteplase, Activase], reteplase [r-
PA, Retavase], tenecteplase [TNKase], staphylokinase, urokinase,
streptokinase monitor closely for signs and symptoms of bleeding
 Advantages: Less long-term damage to venous valves. Reduced
incidence of postthrombotic syndrome and chronic venous
insufficiency
 Disadvantages: Greater incidence of bleeding than heparin. If bleeding
occurs and cannot be stopped, the thrombolytic agent is discontinued.
 Contraindications: Postoperatively during pregnancy after childbirth,
trauma, brain attacks, or spinal injuries.

Surgical Management
Thrombectomy- removal of thrombus

Inferior vena caval interruption may be placed at the time of the thrombectomy this filter traps large emboli and prevents
pulmonary emboli
Chronic Venous Insufficiency

Results from obstruction of venous valves in legs or a reflux of blood back through valves. Can involve superficial and deep leg
veins. The disorder is long-standing, difficult to treat, and often disabling.

Diagnostic evaluation

Duplex ultrasonography: Confirms obstruction and identifies the level of valvular


incompetence.

Clinical Manifestations

 Skin Discoloration
 Eczema
 Venous Ulcers
 Varicose vein rupture
 Leg swelling

Complications

 Venous ulceration is the most serious complication of chronic venous insufficiency and can be associated with other
conditions affecting the circulation of the lower extremities.

Management

 Goal: reducing venous stasis and preventing ulcerations.


 Antigravity activities
 Measures that increase venous blood flow
 Elevate leg
 Compression of superficial veins with elastic compression stockings.

Nursing management

Elevating the legs

 Decreases edema, promotes venous return, and provides symptomatic relief.


 Legs elevated frequently throughout the day (at least 15 to 30 minutes every 2 hours).
 At night, patient should sleep with the foot of bed elevated about 15 cm (6 inches).

Avoid prolonged sitting or standing

 Encourage walking
 When sitting: avoid placing pressure on popliteal spaces Ex: avoid crossing legs or sitting with legs dangling over side of
bed.
 Avoid constricting garments (ex: panty girdles or tight socks)

Compression of the legs with elastic

 Compression stockings
 Reduces pooling of venous blood and enhances venous return to heart.
 Stocking should fit so that pressure is greater at foot and ankle and then gradually declines to a lesser pressure at
the knee or groin.
 If the top of the stocking is too tight or becomes twisted, a tourniquet effect is created, which worsens venous
pooling.
 Applied before standing or in the morning
 Stockings should be applied after legs have been elevated for a period, when amount of blood in the leg veins is at
its lowest.
 Protect extremities from trauma skin is kept clean, dry, and soft
 Signs of ulceration are immediately reported to the health care provider

Leg Ulcers

An excavation of skin surface that occurs when inflamed necrotic tissue sloughs off.

Etiology

 75% result from chronic venous insufficiency.


 20% - due to arterial insufficiency
 5% - burns, sickle cell anemia, and other factors

Etiology Arterial Ulcers Venous Ulcers


Wound Depth • Partial-thickness • Partial-thickness
• Full-thickness • Full-thickness
Location • Between toes, over phalangeal heads, tips • Gaiter area
of toes, lateral malleolus
Characteristics • Punched-out appearance • Irregular shape
• Pale or necrotic wound tissue • Granular wound
• Minimally exudating wound • Moderate to highly exudating wound
• Pale skin, shiny, taut, thin • Hemosiderin staining
• Absence of hair • Lipodermatosclerosis
• Firm edema
Risk Factors • Diabetes, uncontrolled • Diabetes
• Inadequate footwear • Pregnancy
• Foot deformities Advanced age • Advanced age
• Secondary to peripheral arterial disease • Deep vein thrombosis, varicose veins
• Peripheral vascular disease • Congestive heart failure
• Malnutrition
• Obesity
• Immobility

Clinical manifestations

Characteristic Arterial Ulcer Venous Ulcer


Location Toes or foot Malleolus or metatarsal
Appearance Irregular margin cool cyanotic Typically, sloped edges: may have exudate, irregular shape
Foot temperature Cold Warm
Pain Usually, severe Mild
Sensation Variable, often decreased Present, variable (pain, temperature)
Arterial Pulses Absent Present, variable (pain, temperature)
Veins Collapsed Dilated, varicosities, edema

Management

Pharmacologic therapy

 Antibiotic therapy
 Oral antibiotics usually are prescribed
 Topical antibiotics have not proven to be effective for leg ulcers.

Debridement

 Removal of nonviable tissue from wounds.


 Removing the dead tissue is important, particularly in instances of infection.
Types of debridement

Sharp surgical debridement

 Fastest method can be performed by a physician, skilled advanced practice nurse, or certified wound care nurse in
collaboration with the physician.

o Nonselective debridement

 Apply isotonic saline dressings of fine-mesh gauze to the ulcer.

 When the dressing dries, it is removed (dry), along with the debris adhering to the gauze.

 Need pain management

o Enzymatic debridement

 Application of enzyme ointments

 Ointment is applied to lesion but not to normal surrounding skin.

 Use of Debriding agents Dextranomer (Debrisan) beads: small, highly porous, spherical beads ; can
absorb wound secretions.

 Calcium alginate dressings used when absorption of exudate is needed. Should not be used on dry or
nonexudative wounds.

o Topical Therapy

 Remove devitalized tissue

 Keep ulcer clean and moist while healing takes place.

 Treatment should not destroy developing tissue.

o Wound Dressing

 After the circulatory status has been assessed and determined to be adequate for healing (ABI of
more than 0.5) surgical dressings can be used to promote a moist environment.

Varicose Veins/ Varicosities

Abnormally dilated, tortuous, superficial veins caused by incompetent venous valves. Most commonly occurs in lower
extremities, saphenous veins, or lower trunk; can occur elsewhere in body (ex: esophageal varices). Occur in up to 60% of adult
population; increased incidence correlated with increased age

Risk factors

 Women
 People whose occupations require prolonged standing (ex: salespeople, hair stylists, teachers, nurses, ancillary medical
personnel, and construction workers)
 Hereditary weakness of vein wall not uncommon to occur in several members of same family.
 Pregnancy may cause varicosities-Leg veins dilate during pregnancy because of hormonal effects related to
distensibility. Increased pressure by the gravid uterus
 Leg trauma

Etiology
Primary- Result from hereditary weakness of vein wall and valves. Without involvement of deep veins

Secondary- A sequel to DVT as a result of Dilation of collateral veins. Damage to valves of deep veins. Resulting from obstruction
of deep veins

Clinical Manifestations

 Distended protruding veins that appear darkened and tortuous. Symptoms, if present: Dull aches, muscle cramps, and
increased muscle fatigue in the lower legs. Heaviness or fullness in legs. Ankle edema and a feeling of heaviness of the
legs may occur. Nocturnal cramps are common (leg cramping that intensifies at night) (+) Trendelenburg test
 Brown discoloration of affected extremity
 Stasis ulcer
 When deep venous obstruction results in varicose veins, patients may develop s/s of chronic venous insufficiency:
edema, pain, pigmentation, and ulcerations. Susceptibility to injury and infection is increased

Diagnostic evaluation

 Duplex scan Documents anatomic site of reflux and provides a quantitative measure of the severity of valvular reflux.
 Air plethysmography Measures changes in venous blood volume.
 Venography- Not routinely performed to evaluate for valvular reflux. When used, involves injecting x-ray contrast
agent into leg veins so that vein anatomy can be visualized by x-ray studies during various leg movements.

Prevention

 Avoid activities that cause venous stasis


 Avoid wearing tight socks or a constricting panty girdle
 Avoid Crossing legs at thigh
 Avoid sitting or standing for long periods. promote leg circulation
 Change position frequently Elevate legs as much as possible (20 mins) get up to walk for several minutes of every
hour.
 Encourage to walk 1 or 2 miles each day if there are no contraindications.
 Walking up the stairs rather than using the elevator or escalator is helpful in promoting circulation.
 Swimming: good exercise for the legs.
 Elastic compression stocking or antiembolic stockings, especially knee-high stocking.
 Weight-reduction plan for overweight
 Avoid constrictive clothing

Management

Ligation and stripping- Ligation and stripping of the great and the small saphenous veins. Veins are removed if they are larger
than 4 mm in diameter or if they are in clusters requires that the deep veins be patent and functional . Saphenous vein - ligated
and divided. Postop care:

 Evaluate pulses
 Elastic bandages
 Elevate legs
 Monitor extremities for edema, warmth, color, bleeding
 Analgesics

Endovenous Laser Treatment- Thin fiber is inserted into damaged vein via a very small skin nick. Laser light energy is delivered to
the targeted tissue, which reacts with the light, causing the vein to close and seal shut.

Radiofrequency Ablation- Endovenous radiofrequency (RF) ablation. Insertion of a catheter with electrodes into the target vein
and passage of RF energy (electricity) through the vein tissue.
Sclerotherapy (Sodium murrhuate)- Chemical is injected into vein, irritating venous endothelium and producing localized
phlebitis and fibrosis, thereby obliterating the lumen of vein. May be performed alone for small varicosities or may follow vein
ligation or stripping. Sclerosing is palliative rather than curative. Post procedure:
 Elastic compression bandages are applied to the leg; worn approx 5
 Patients are encouraged to perform walking activities as prescribed to maintain blood flow in the leg.
 Walking enhances dilution of the sclerosing agent.
 Incision and drainage of trapped blood are performed after 14-21days
Hypertension

A systolic blood pressure greater than 140 mm Hg and a diastolic pressure greater than 90 mm Hg based on the average of two
or more accurate blood pressure measurements taken during two or more contacts with a health care provider.

Classification

Blood Pressure Categories SYSTOLIC mm Hg (upper number) DIASTOLIC mm Hg (lower number)


NORMAL LESS THAN 120 LESS THAN 80
ELEVATED 120 - 129 LESS THAN 80
HIGH BLOOD PRESSURE (HYPERTENSION) 130 - 139 80 - 89
STAGE 1
HIGH BLOOD PRESSURE (HYPERTENSION) 140 OR HIGHER 90 OR HIGHER
STAGE 2
HYPERTENSIVE CRISIS (consult your doctor HIGHER THAN 180 HIGHER THAN 120
immediately),

Types/

Primary (essential) hypertension

Most common form of hypertension, accounting for 90–95% of all cases of hypertension. Cause is unknown. Insulin resistance,
which is common in obesity and is a component of syndrome X (or the metabolic syndrome), is also thought to contribute to
hypertension

Risk factors
 Age: SBP increase progressively with increasing age. After 50, an SBP>140 mmHg is a more important risk factor for CAD
than DBP.
 Alcohol
 Cigarette smoking: increase the risk of CVD.
 Diabetes mellitus: hypertension is more common in diabetes mellitus.
 Elevated serum lipids: primary risk factor for atherosclerosis
 Excess dietary sodium: contribute to hypertension.
 Gender: Hypertension more prevalent in young adulthood. After55yr, more prevalent in women.  .
 Family history
 Obesity
 Ethnicity: Twice as high in African Americans than that of whites.
 Sedentary life style: Regular physical activity reduce obesity and decrease BP.
 Socio economic status: more prevalent in people with low socio-economic status.
 Stress: Increase the incidence of hypertension

Secondary hypertension

Results from an identifiable cause. Renal disease is the most common secondary cause of hypertension. Hypertension can also
be caused by endocrine conditions, such as Cushing's syndrome, hyperthyroidism, hypothyroidism, acromegaly, Conn's
syndrome or hyperaldosteronism, hyperparathyroidism and pheochromocytoma.

Hypertensive crisis

Hypertensive crisis broadly covers both hypertensive urgency and emergency.

Hypertensive emergency

 Formerly malignant hypertension


 Severe elevation in BP (>180/120 mmHg) complicated by evidence of impending or progressive target organ dysfunction
and damage.

Hypertensive urgency

 When severe elevation in BP occurs without acute target organ dysfunction or damage

Resistant hypertension

 Hypertension that remains above goal blood pressure in spite of concurrent use of three antihypertensive agents
belonging to different antihypertensive drug classes

Clinical manifestations

 Headaches - Headaches may be experienced due to elevation in blood pressure. Sometimes morning headaches can
also be due to hypertension.
 Dizziness - Dizziness is often experience by people with high blood pressure. However dizziness cannot always be
treated as a symptom of hypertension. If dizziness is experienced it is always wise to consult a medical practitioner.
Heart pain
 Palpitations
 Nosebleeds - Nosebleeds without particular reason might be a symptom of high blood pressure. It is better to check the
blood pressure in such cases.
 Difficulty in breathing
 Tinnitus (ringing or buzzing in the ears) Blurred Vision, Frequent urination

Diagnostic evaluation
 History and physical examination
 24-hour ambulatory blood pressure monitors and home blood pressure monitoring
 Patterns of Blood Pressure
 Based on 24-hour ambulatory BP monitoring and office BP readings, 4 patterns of BP have been described

 Sustained hypertension

 Masked hypertension- Normal blood pressure (BP) in the clinic or office (<140/90 mmHg), but an elevated BP out
of the clinic (ambulatory daytime BP or home BP>135/85 mmHg)

 White coat hypertension- Occurs when the blood pressure readings at doctor's office are higher than they are in
other settings

 Normal dipping pattern

 Renal- Microscopic urinalysis, proteinuria, BUN and/or creatinine

 Endocrine- Serum sodium, potassium, calcium, TSH

 Metabolic- Fasting blood glucose, HDL, LDL, and total cholesterol, triglycerides

 Electrocardiogram

 Echo cardiography

Prevention

 Maintain normal body weight for adults (e.g., body mass index 20–25 kg/m2)

 Reduce dietary sodium intake to <100 mmol/ day (<6 g of sodium chloride or <2.4 g of sodium per day)

 Engage in regular aerobic physical activity such as brisk walking (≥30 min per day, most days of the week)

 Limit alcohol consumption to no more than 3 units/day in men and no more than 2 units/day in women

 Consume a diet rich in fruit and vegetables (e.g., at least five portions per day);

 Effective lifestyle modification may lower blood pressure

Management

Goals of Therapy

 The primary goal of therapy of hypertension should be effective control of BP in order to prevent, reverse or delay the
progression of complications and thus reduce the overall risk of an individual without adversely affecting the quality of
life.
 Patients should be explained that the lifestyle modifications and drug treatment is generally lifelong and regular drug
compliance is important

Lifestyle Modification

Weight reduction

 Maintain normal body weight (body mass index, 18.4–24.9 kg/m2)


 Adopt DASH eating plan
 Consume diet rich in fruits, vegetables, low- fat dairy products, with reduced content of saturated and total fats
 Reduce dietary sodium intake should be reduced to no more than 100 mmol/day (2.4g sodium or 6g sodium chloride)
 Physical activity Engage in regular aerobic physical activity (e.g., brisk walking) at least 30 min/day, most days of the week
 Moderation of alcohol consumption
 Most men: limit consumption to no more than two drinks/day
 Most women and those who weigh less than normal: no more than one drink/day
 Adopt DASH (Dietary Approaches to Stop Hypertension)
 Eating more fruits, vegetables, and low-fat dairy foods
 Cutting back on foods that are high in saturated fat, cholesterol, and trans fats
 Eating more whole grain products, fish, poultry, and nuts
 Eating less red meat (especially processed meats) and sweets
 Eating foods that are rich in magnesium, potassium, and calcium
 Different programs aimed to reduce psychological stress such a biofeedback, relaxation or meditation are advertised to
reduce hypertension

Pharmacologic therapy

 Goals of treatment
 Patient’s overall well being
 Control of associated risk factors
 Protection from future target organ damage
 Achieve gradual reduction of blood pressure.
 Use low doses of antihypertensive drugs to initiate therapy.
 Choice of an antihypertensive agent is influenced by
 Age
 Concomitant risk factors
 Presence of target organ damage
 Other co-existing diseases
 Socioeconomic considerations
 Availability of the drug
 Past experience of the physician.

Combining low doses of two or more drugs having synergistic effect is likely to produce lesser side effects. In 60-70 % of patients,
goal blood pressure will be achieved with two or more agents only. Use of fixed dose formulations should be considered to
improve compliance

Centrally acting alpha agonists- Stimulate a2 receptors in brainstem, reducing sympathetic outflow

Beta adrenergic blocking agents- Block cardiac B1 adrenergic receptors, reducing heart rate and cardiac contractility

Angiotensin converting enzyme inhibitors- Block conversion of angiotensin I to angiotensin II, a potent vasoconstrictor

Angiotensin II receptor blockers- Competitively block angiotensin Il receptors

Dihydropyridine calcium channel blockers- Bind a1 subunit of L-type calcium channel in muscle cell membrane, reducing
vascular smooth muscle contractility

Director vasodilators- Hydralazine reduces intracellular calcium in vascular smooth muscle cells and minoxidil causes potassium
efflux with smooth muscle relaxation; both drugs cause arteriolar dilation

Thiazide diuretics- Inhibit Na-Cl cotransporter in distal convoluted tubule of nephron, causing natriuresis

Loop diuretics- Inhibit Na-K-Cl cotransporter in loop of Henle of nephron, causing natriuresis

Mineralocorticoid receptor blockers- Competitively inhibit aldosterone binding to the mineralocorticoid receptor, ultimately
reducing sodium reabsorption in collecting duct of nephron

Complications of hypertension
 Hypertension is the most important preventable risk factor for premature death.
 Ischemic heart disease
 Strokes
 Peripheral vascular disease,
 Other cardiovascular diseases: heart failure, aortic aneurysms, diffuse atherosclerosis, and pulmonary embolism
 Hypertension is also a risk factor for cognitive impairment and dementia, and chronic kidney disease.
 Hypertensive retinopathy
 Hypertensive nephropathy.
 Hypertensive encephalopathy

Nursing management

 Maintain or enhance cardiovascular functioning.


 Prevent complications.
 Provide information about disease process, prognosis, and therapy.
 Support active client control of condition
 Prevention of hypertension
 Health Promotion
 Hypertension’s pathology
 Correct blood pressure measurement
 Therapy Adherence
 Drug therapy
 Inform about support groups and Community support
 Home Blood Pressure Monitoring

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