SEPTEMBER 2020 NURSING CLASS

CARDIOVASCULAR DISORDERS

Module objectives

By the end of the module the student should be able to:

1. Manage patients suffering from cardiac disorders using nursing process approach
2. Manage patients suffering from vascular disorders using nursing process approach

CARDIAC HEMODYNAMICS

The basic function of the heart is to pump blood.

Ability of the heart to pump is measured by cardiac output (CO)
• CO is determined by the heart rate (HR) and stroke volume (SV),
• Stroke volume is the amount of blood pumped out of the ventricle with each contraction
while heart rate is the number of beats per minute
• CO = HR × SV.
• The HR is primarily controlled by the autonomic nervous system.
• When SV decreases, the nervous system is stimulated to increase HR and thereby
maintain adequate CO.
• SV depends on: preload, afterload, and contractility
A. Preload: is the amount of blood in the ventricle just before systole (contraction).
Preload is determined by:
1. Venous return - volume of blood that enters the ventricle during diastole (relaxation).
2. Ventricular compliance- elasticity when blood enters the ventricle will determine the volume
of blood the ventricles will accommodate.
Preload increases with:
 Fluid volume increases
 Vasoconstriction (squeezes blood from vascular system into heart)
Preload decreases with:
 Fluid volume losses
 Vasodilation ( blood vessels are able to hold more blood, therefore less is returning to
heart)

• Decreased elasticity leads to a higher pressure within the ventricles which then increases
the workload of the heart and can lead to heart failure (HF).

B. Afterload refers to the amount of resistance the ventricle must overcome to pump blood. It is
the resistance caused by tension in the aorta and systemic vessmels.

Afterload is determined by:

 • the diameter and distensibility of the great vessels (aorta and pulmonary artery)
• The opening and competence of the semilunar valves (pulmonic and aortic valves).
Afterload increases with:
 Hypertension
 Vasoconstriction
Afterload decreases with:
 Vasodilation

C. Contractility: this is the force of contraction of the myocardium.

• Contractility is increased by catecholamines released by sympathetic stimulation or

positive inotropic medications(medications that enhance contractions e.g. digoxin)
• Contractility decreases with:
• infarcted tissue – dead tissue lacks ability to contract
• Ischemic tissue – reduced contractile strength.
• Electrolyte/acid-base imbalance
• Negative inotropes (medications that decrease contractility, such as beta blockers
Starling’s Law states that; the greater the heart muscle fibers are stretched (due to increases in
volume), the greater their subsequent force of contraction – but only up to a point. Beyond that
point, fibers get over-stretched and the force of contraction is reduced
GENERAL CARDIAC ASSESSMENT
In all cardiac conditions, the assessment includes the following:
• Health history
• Demographic information
• Family/genetic history
• Cultural/social factors
• Risk factors
Modifiable: High blood cholesterol, obesity, smoking, stress, hypertension, diabetes
mellitus.
Nonmodifiable: Family history, increasing age, gender, race

CARDIAC DISORDERS

Congestive cardiac failure

Description

Heart failure is the inability of the heart to pump sufficient blood to meet the needs of the tissues
for oxygen and nutrients.
It is referred to as congestive cardiac failure due to congestion that occurs in upper and lower
body tissues and organs.

Etiology
Caused by disorders of heart muscle resulting in decreased contractile properties of the heart;
• valvular heart disease-reduced cardiac output
• congenital heart disease-ineffective pumping/also mixing of oxygenated and
deoxygenated blood
• cardiomyopathies-reduced contraction of myocardium
• Coronary artery disease- reduced perfusion of myocardium
• Hypertension- narrowed blood vessels increase the afterload
• Pulmonary embolism/chronic lung disease-impaired oxygenation of myocardium
• Hemorrhage and anemia- heart compensates to maintain adequate output hence
hypertrophy
• Anesthesia and surgery-may cause reduced cardiac functions
• Transfusions or infusions- increase the preload
• Increased body demands (fever, infection, pregnancy).
• Drug-induced- e.g. cocaine increases heart rate hence increased myocardial oxygen
demand), can also cause dysrhythmias,
• Physical and emotional stress-release of catecolamines
• Excessive sodium intake-increases preload
Risk factors
• Hyperlipidemia causes atherosclerosis
• Age-becomes more prevalent in older age groups
• Obesity: increased cardiac work load
• Cigarette smoking is the major risk factor in atherosclerosis
• Diabetes mellitus: common cause of atherosclerosis through triglycerides
• African descent
• Family history
• Alcohol consumption; alcohol is cardio toxic
• Use of cardio toxic drugs.
Pathophysiology of Heart failure
Heart which is a pump fails leading to decreased stroke volume /Cardiac output. This is followed
by compensatory mechanisms;
a. Sympathetic nervous stimulation causes release of epinephrine/nor-epinephrine hence
Increase heart rate, Increase contractility, Peripheral vasoconstriction (increases
afterload)
b. Reduced kidney perfusion leads to release of renin, which stimulates conversion of
angiotensin I to angiotensin II, which causes vasoconstriction of peripheral blood vessels.
 c. Aldosterone is also released leading to sodium and water retention (via antidiuretic
hormone secretion).
NB Compensatory mechanisms may restore CO to near-normal, but in excess they can
worsen heart failure because vasoconstriction increases the resistance against which heart has
to pump.
Effects of Compensatory mechanisms
 Sodium and water retention leads to too much stretch in the ventricles which will reduce
the strength of contraction hence reduced Cardiac Output (starling law).
 Increased heart rate leads to reduced ventricular filling hence reduced stroke volume and
cardiac output
 The reduced cardiac output results in myocardial hypertrophy as a long term
compensatory mechanism.
 Although hypertrophy increases the systolic function of the heart initially, it eventually
leads to diastolic dysfunction and myocardial ischemia.
 The increased muscle mass of the hypertrophied heart increases the need for oxygen
delivery which may exceed the ability of the coronary vessels causing ischemia.
 Hypertrophy of cardiac muscle cells may be accompanied by the growth of fibrous tissue
that produces stiffness of the ventricle.

Classification of heart failure

High-output failure

• In high-output failure, the function of the heart is normal but there is excessive metabolic
needs for example in cases of severe anemia, thyrotoxicosis, infections, excessive
exercise

Low-output failure

• Low-output failure is caused by disorders that impair the pumping ability of the heart,
such as ischemic heart disease and cardiomyopathy

Right-sided heart failure (backward failure)

Inability of the right side of the heart to effectively pump deoxygenated blood from the systemic
venous circulation into the pulmonary circulation causing accumulation of blood in the systemic
venous circulation.
Clinical manifestations
• The external jugular veins become distended and can be visualized when the person is
sitting up or standing.
• Peripheral edema particularly in the dependent parts of the body; lower limbs and the
sacrum
 • Liver congestion may produce upper abdominal pain. In severe cases liver function is
impaired and hepatic cells may die. Congestion of the portal circulation also may lead to
engorgement of the spleen and the development of ascites.
• Anorexia and nausea and vomiting from hepatic and visceral engorgement
• Nocturia diuresis occurs at night with rest and improved Cardiac Output
• Weakness
Left-Sided Heart Failure (forward failure).

Inability of the left side of the heart to effectively pump oxygenated blood from the lungs to the
rest of the body causing congestion in the lungs from blood backing up into pulmonary veins and
capillaries.

Clinical manifestations

• Exertional dyspnea- shortness of breath on increased physical activity

• Orthopnea: shortness of breath that occurs when a person is supine; fluid from the legs
and dependent parts of the body is mobilized and redistributed to an already distended
pulmonary circulation, causing the person to sleep propped up in bed or sitting in a chair
• Paroxysmal nocturnal dyspnea during sleep; It disrupts sleep, and the person awakens
with a feeling of extreme suffocation that resolves when he or she sits up. Initially, the
experience may be interpreted as awakening from a bad dream.
• Nonproductive cough, which becomes worse when the person is lying down
• Bronchospasm
• Cheyne-Stokes respiration/ periodic breathing; the person breathes deeply for a period
when the arterial carbon dioxide pressure is high and then slightly or not at all when it
falls.
• Pulmonary edema
• Cough may be dry, unproductive; usually occurs at night
• Fatigability from low CO,
• In a supine position at night edema fluids from the dependent parts of the body e.g
sacrum and lower limbs returns back to the circulation, as a result, the cardiac output,
renal blood flow, glomerular filtration, and urine output increase leading to nocturia.
• Tachycardia, restlessness
Other Clinical manifestations of congestive cardiac heart failure
Cardiac cachexia

Refers to malnutrition and loss of weight that occurs in persons with end-stage heart failure due
to fatigue and depression that interfere with food intake

It is caused by congestion of the liver and gastrointestinal structures; this impairs digestion and
absorption and produces feelings of fullness. The circulating toxins and mediators released from
poorly perfused tissues impair appetite and contribute to tissue wasting.
Neurological symptoms: Reduced oxygen supply to the brain due to respiratory insufficiency
causes confusion and mental clouding

NOTE: Both sides of the heart may fail at the same time so that the patient will present with
features of left and right side heart failure for example jugular vein distension, pulmonary edema,
ascites lower limb edema.

Cardiac failure patients can be categorized based on tolerance to physical activity

• Class 1: No limitation of physical activity

• Class 2: Slight limitation

• Class 3: Marked limitation

• Class 4: Inability to carry on any physical activity without discomfort

Diagnostic studies

• Echocardiography-two-dimensional with Doppler flow studies may show ventricular

hypertrophy, dilation of chambers, and abnormal wall motion.
• ECG (resting and exercise) may show ventricular hypertrophy and ischemia.
• Chest X-ray may show cardiomegaly, pleural effusion, and vascular congestion.
• Cardiac catheterization to rule out CAD
• Arterial Blood Gasses (ABG) studies may show hypoxemia due to pulmonary vascular
congestion.
• Liver function studies may be altered because of hepatic congestion.
• Blood chemistry; raised sodium levels, raised Levels of urea. These levels may be
elevated due to renal insufficiency,

Medical management

• Diuretics: Eliminate excess body water and decrease ventricular pressures.

• Positive inotropic agents increase the heart's ability to pump more effectively by
improving the contractile force of the muscle e.g Digoxin, Dopamine, Dobutamine

• Vasodilator therapy decreases the workload of the heart by dilating peripheral vessels e.g

Nitrates, such as nitroglycerin, isosorbide, Hydralazine, Prazosin Sodium nitroprusside

• Morphine decreases venous return, decreases pain and anxiety and thus cardiac work
 • Angiotensin-converting enzyme (ACE) inhibitors inhibit the adverse effects of
angiotensin II (potent vasoconstriction/sodium retention).Captopril and enalapril

• Beta-adrenergic blockers decrease myocardial workload and protect against fatal

dysrhythmias by blocking norepinephrine effects of the sympathetic nervous system.
Metoprolol or metoprolol are commonly used.

• Angiotensin II-receptor blockers (ARBs). Used in patients who cannot tolerate ACE
inhibitors due to cough or angioedema.

• Aldosterone antagonist decrease sodium retention, e. g Spironolactone (Aldactone) .

• Human B-type natriuretic peptide produces smooth muscle cell relaxation, diuresis, and
a reduction in afterload.

Nursing Management

Nursing Assessment

• Obtain history of symptoms, limits of activity, response to rest, and history of response to
drug therapy.
• Assess peripheral arterial pulses; note quality, character; assess heart rhythm and rate and
BP; assess edema.
• Inspect and palpate precordium for lateral displacement of PMI.
• Obtain hemodynamic measurements as indicated and note change from baseline.
• Assess weight and ask about baseline weight.
• Note results of serum electrolyte levels and other laboratory tests.
• Identify sleep patterns and sleep aids commonly used by patient.
Nursing Diagnoses

• Decreased Cardiac Output related to impaired contractility and increased preload and
afterload

• Impaired Gas Exchange related to alveolar edema due to elevated ventricular pressures

• Excess Fluid Volume related to sodium and water retention

• Activity Intolerance related to oxygen supply and demand imbalance

Planning

Overall goals:

a. reduce Peripheral edema

 b. manage Shortness of breath
c. increase Exercise tolerance
d. Drug compliance
e. No complications

Nursing Interventions

1. Maintaining Adequate Cardiac Output

 semi-recumbent position to promote breathing and diuresis

 Provide bedside commode to reduce work of getting to bathroom and for defecation.
 Provide for psychological rest
 Auscultate heart sounds frequently and monitor cardiac rhythm or, poor capillary
refill of nail beds.
 Administer pharmacotherapy as directed.
 Monitor clinical response of patient (lessening dyspnea and orthopnea, decrease in
crackles, relief of peripheral edema).

2. Improving Oxygenation

 Raise head of bed 20 to 30 cm to reduce venous return to heart and lungs;

alleviates pulmonary congestion.
 Auscultate lung fields at least every 4 hours for crackles and wheezes in
dependent lung fields (fluid accumulates in areas affected by gravity).
 Observe for increased rate of respirations (could be indicative of falling arterial
pH).
 Observe for Cheyne-Stokes respirations (may occur in elderly patients because of
a decrease in cerebral perfusion stimulating a neurogenic response).
 Position the patient every 2 hours (or encourage the patient to change position
frequently) to help prevent atelectasis and pneumonia.
 Encourage deep-breathing exercises every 1 to 2 hours to avoid atelectasis.
 Offer small, frequent feedings to avoid excessive gastric filling and abdominal
distention with subsequent elevation of diaphragm that causes decrease in lung
capacity.
 Administer oxygen as required to enhance tissue oxygenation

3. Restoring Fluid Balance

 Give diuretic early in the morning nighttime diuresis disturbs sleep, keep input
and output record.
 Weigh patient daily to monitor edema: weight loss should not exceed 0.5 to 1
kg/day.
  Assess for hypovolemia caused by diuretic therapy such as thirst, decreased urine
output, orthostatic hypotension, weak, thready pulse, increased serum osmolality,
and increased urine specific gravity.
 Be alert for signs of hypokalemia, which may cause weakening of cardiac
contractions and may precipitate digoxin toxicity in the form of dysrhythmias,
anorexia, nausea, vomiting, abdominal distention, paralytic ileus, paresthesias,
muscle weakness and cramps, confusion.
 Monitor for pitting edema of lower extremities and sacral area. Use convoluted
foam mattress and sheepskin to prevent pressure ulcers (bed sores).
 Observe for the complications of bed rest pressure ulcers (especially in edematous
patients), phlebothrombosis and pulmonary embolism.
 Be alert to complaints of right upper quadrant abdominal pain, poor appetite,
nausea, and abdominal distention (may indicate hepatic and visceral
engorgement).
 Monitor patient's diet. Diet may be limited in sodium to prevent, control, or
eliminate edema; may also be limited in calories.
Improving Activity Tolerance

 Increase patient's activities gradually. Alter or modify patient's activities to keep

within the limits of his cardiac reserve.
 Observe the pulse, symptoms, and behavioral response to increased activity.
 Relieve nighttime anxiety and provide for rest and sleep. Patients with heart
failure have a tendency to be restless at night because of cerebral hypoxia. Give
appropriate sedation to relieve insomnia and restlessness.

Patient Education and Health Maintenance

 Explain the disease process to the patient; the term failure may have terrifying
implications.
 Teach the signs and symptoms of recurrence.
 Review medication regimen..
 Review activity program.
 Restrict sodium as directed.

Evaluation: Expected Outcomes

 Normal BP and heart rate

 Respiratory rate 16 to 20, ABG levels within normal limits, no signs of crackles
or wheezes in lung fields
 Weight decrease of 2.2 lb (1 kg) daily, no pitting edema of lower extremities and
sacral area
 Heart rate within normal limits, rests between activities
CARDIOMYOPATHIES
Cardiomyopathy is a heart muscle disease leading to cardiac dysfunction.
Classified according to the structural and functional abnormalities of the heart muscle;
 Dilated cardiomyopathy
 Hypertrophic cardiomyopathy
 Restrictive or constrictive cardiomyopathy
 Arrhythmogenic right ventricular cardiomyopathy
 Unclassified cardiomyopathy
A patient may have pathology representing more than one of these classifications
Pathophysiology
All types of cardiomyopathies lead to reduced cardiac output. Decreased stroke volume
stimulates the sympathetic nervous system and the renin–angiotensin–aldosterone response,
resulting in increased systemic vasoconstriction and increased sodium and fluid retention, thus
increased workload to the heart. These alterations can lead to heart failure

Dilated Cardiomyopathy
 The most common form of cardiomyopathy
 The ventricles are dilated but cardiac muscles are not enlarged
 Reduced contractile proteins cause poor contraction and decreased blood ejection -
increased blood remaining in the ventricle causes ventricular stretching and dilatation.
 Systolic and diastolic volumes are high
 pulmonary and systemic venous pressures are increased
 Regurgitation results from an enlarged stretched ventricle
 Thrombi may form and embolize to other locations in the body.
Causes:
 Pregnancy,
 Heavy alcohol intake,
 Viral infection (eg, influenza),
 Anti-cancer medications (eg, daunorubicin, doxorubicin,
 Chagas disease
 Genetic factors
 Idiopathic

Hypertrophic Cardiomyopathy
Increase in size of heart muscles and subsequent reduced size of ventricular cavities; less blood
enters the ventricules.
Ineffective contractions cause dysrhythmias such as ventricular tachycardia and ventricular
fibrillation.
Thickened Coronary arteriole walls restrict blood supply to the myocardium, causing ischemia,
necrosis fibrosis and scar, further hindering ventricular contraction.
Cause: 1. Genetic2. Idiopathic

Restrictive Cardiomyopathy
Stiffness of the ventricle, endocardial fibrosis and thickening; ventricle does not relax during
diastole leading to reduced ventricular filling. The myocardium also fails to completely contract
during systole; end-result is decreased cardiac output
Cause:
1. Amyloidosis (amyloid, a protein substance, is deposited within cells) and other such
infiltrative diseases.
2. Idiopathic in most cases
Signs and symptoms
Dyspnea, nonproductive cough, and chest pain

Arrhythmogenic Right Ventricular Cardiomyopathy

Myocardium of the right ventricle is progressively infiltrated and replaced by fibrous scar and
adipose tissue.
The right ventricle dilates and develops poor contractility, wall abnormalities and dysrhythmias.
Palpitations or syncope may develop between 15 and 40 years of age.
Cause is genetical
Unclassified Cardiomyopathies
Unclassified cardiomyopathies are different or may have characteristics of more than one of the
previously described types.

Clinical Manifestations of cardiomyopathies

Patients may remain stable without symptoms for many years
Dilated or restrictive cardiomyopathy cause signs and symptoms of heart failure (e.g. dyspnea on
exertion, fatigue) Paroxysmal Nocturnal Dyspnea, cough (especially with exertion), and
orthopnea, which may lead to a misdiagnosis of bronchitis or pneumonia.
Other symptoms:
Fluid retention, peripheral edema, and nausea, caused by poor perfusion of the gastrointestinal
system, chest pain, palpitations, dizziness and syncope with exertion
With hypertrophic cardiomyopathy, cardiac arrest (i.e. sudden cardiac death) may be the initial
manifestation in young people, including athletes

Cardiomyopathy may lead to severe heart failure, lethal dysrhythmias, and death.

Assessment and Diagnostic Findings

 History
 Physical examination may reveal tachycardia and extra heart sounds (eg, S3, S4) and
diastolic/systolic murmurs
  Heart failure (eg, crackles on pulmonary auscultation, jugular vein distention, pitting
edema of dependent body parts, and enlarged liver)
 Echocardiogram to observe the structure and function of the ventricles
 Cardiac MRI
 ECG demonstrates dysrhythmias (atrial fibrillation, ventricular dysrhythmias)
 Chest x-ray reveals heart enlargement and possibly pulmonary congestion.
 Cardiac catheterization to rule out coronary artery disease
 Endomyocardial biopsy to analyze myocardial cells
Medical Management
Aim: managing possible underlying or precipitating causes; correcting heart failure
 Low-sodium diet and an exercise/rest regimen
 Antiarrhythmic medications or implanted electronic device, such as cardioverter
defibrillator to control dysrhythmias
 Anticoagulation to prevent thromboembolic events
 In case of congestion, fluid intake may be limited to 2 L each day
 Hypertrophic Cardiomyopathy should avoid dehydration and may need beta-blockers
(atenolol, metoprolol, propranolol) to maintain cardiac output
 Hypertrophic Cardiomyopathy or Restrictive Cardiomyopathy need to limit physical
activity to avoid a life-threatening dysrhythmia.
 A pacemaker to alter the electrical stimulation of the muscle and prevent the forceful
contractions that occur with hypertrophy
 biventricular pacing increases the ejection fraction and reverses some of the structural
changes in the myocardium in hypertrophic and dilated cardiomyopathy
 Septal reduction, also called alcohol septal ablation,to treat obstructive hypertrophy; 96%
to 98% ethanol (ethyl alcohol) is injected through a cardiac catheter to destroy the
myocardial cells hence the obstruction is decreased.
Surgical Management
Heart transplant; organ donors are limited, many patients die waiting for transplantation
Left ventricular assist device is implanted to support the failing heart until a donor is available

Nursing Management
Assessment
History of the presenting signs and symptoms
Identification of etiologic factors; heavy alcohol intake, recent illness or pregnancy,
History of the disease in immediate family members
Chest pain and its precipitating factors
Orthopnea, paroxysmal nocturnal dyspnea, syncope or dyspnea with exertion
Number of pillows needed to sleep,
Usual weight, any weight change, and limitations on activities of daily living
Evaluated diet to determine the need to reduce sodium intake,
Psychosocial history to assess the impact of the disease on the patient’s roles
Identify stressors
Identify patient’s support systems
Depression is common in a patient with cardiomyopathy who has developed heart failure.
Physical examination:
Vital signs
Calculation of pulse pressure and identification of pulsus paradoxus
Current weight; any weight gain or loss
Palpate the point of maximal impulse, often shifted to the left
Auscultate for a systolic murmur and S3 and S4 heart sounds
Pulmonary auscultation for crackles
Measurement of jugular vein distention
Assess edema and its severity

Nursing Diagnoses
Based on the assessment data, major nursing diagnoses may include:
1. Decreased cardiac output related to structural disorders caused by cardiomyopathy or to
dysrhythmia from the disease process and medical treatments
2. Ineffective cardiopulmonary, cerebral, peripheral, and renal tissue perfusion related to
decreased peripheral blood flow (resulting from decreased cardiac output)
3. Impaired gas exchange related to pulmonary congestion caused by myocardial failure
(resulting from decreased cardiac output)
4. Activity intolerance related to decreased cardiac output or excessive fluid volume, or
both
5. Anxiety related to the change in health status and in role functioning
6. Powerlessness related to disease process
7. Noncompliance with medication and diet therapies

Collaborative Problems/Potential Complications

Based on the assessment data, potential complications include:
Heart failure
Ventricular dysrhythmias
Atrial dysrhythmias
Cardiac conduction defects
Pulmonary or cerebral embolism
Valvular dysfunction

Planning and Goals

 Improvement or maintenance of cardiac output,
 Increased activity tolerance,
 Reduction of anxiety,
  Adherence to the self-care program,
 Increased sense of power with decision making,
 Absence of complications
Nursing Interventions
Improving Cardiac Output
 Encourage rest to conserve energy
 Patient to sit up with legs down, blood pools in the veins in the periphery reducing
preload
 Assessing oxygen saturation at rest and during activity
 Oxygen is administered through a nasal cannula when indicated
 Ensuring medications as prescribed to preserve adequate cardiac output
 Patients with dilatation avoid verapamil, hypertrophy to avoid diuretics, restrictive to
avoid nifedipine to maintain contractility.
 Inotropic medication (digoxin) may create or worsen left ventricular outflow track
obstruction in hypertrophy.
 Restrictive disorders have increased sensitivity to digoxin, low doses will be prescribed,
assess for digoxin toxicity.
 Low sodium diet to reduce fluid retention
 Weigh every day note any significant change
 Assess shortness of breath after activity and compare to before treatment
 keep warm and change position frequently to stimulate circulation and reduce the
possibility of skin breakdown
 Patients with hypertrophy to avoid dehydration, they should anticipate the urge to void at
least every 4 hours while awake; if the urge to void is not present or the urine is a deep
yellow color, more fluid intake is necessary.
Increasing Activity Tolerance
 The nurse plans so that rest alternates with activity to improve physiologic status
 Ensure that the patient recognizes the symptoms indicating the need for rest and actions
to take when the symptoms occur.
 Patients with hypertrophy or constrictive disorder must avoid strenuous activity and
competitive sports.
Reducing Anxiety
 Spiritual, psychological, and emotional support for patients, families, and significant
others
 Eradicate perceived stressors by providing appropriate information about cardiomyopathy
and self-management activities.
 Provide an atmosphere in which patients feel free to verbalize concerns and receive
assurance that their concerns are legitimate.
 If the patient is awaiting transplantation or facing death, allow time to discuss these
issues. Providing realistic hope helps reduce anxiety while he or she awaits a donor heart.
 Help the patient, family and significant others with anticipatory grieving.
Decreasing the Sense of Powerlessness
 assist in identifying the things in life that he or she has lost (eg, foods that the patient
enjoyed eating but are high in sodium, the ability to engage in an active lifestyle, the
ability to play sports, the ability to lift grandchildren) and his or her emotional responses
to the loss (eg, anger, depression).
 Assist in identifying the amount of control that he or she still has over life, such as
making food choices, managing medications, and working with health care providers to
achieve the best possible outcomes.
Promoting Home and Community-Based Care
TEACHING PATIENTS SELF-CARE
Teach the patients about the medication regimen, symptom monitoring, and symptom
management.
CONTINUING CARE
 Reinforce previous teaching and perform ongoing assessment of the patient’s symptoms
and progress.
 Assist the patient and family to adjust to lifestyle changes. Teach the patient on
appropriate nutrition, daily weights and symptoms, and to organize daily activities to
increase activity tolerance.
 Assess response to recommendations about diet and fluid intake and to the medication
regimen and stress the signs and symptoms that should be reported to the physician.
 Because of the risk of dysrhythmia, it may be necessary to teach the patient’s family
cardiopulmonary resuscitation.
 Women are advised to avoid pregnancy, but each case is assessed individually.
 Assess the psychosocial needs of the patient and family on an ongoing basis, fears about
the prognosis, changes in lifestyle, effects of medications, and the possibility of others in
the family having the same condition; these often increase the patient’s anxiety and
interfere with effective coping strategies.
 Establish trust to enhance relationship with the chronically ill patients and their families.
 This is particularly significant when involved with a patient and family in discussions
about end-of-life decisions.
Evaluation
Expected Patient Outcomes
1. Maintains or improves cardiac function
a. Exhibits heart and respiratory rates within normal limits
b. Reports decreased dyspnea and increased comfort; maintains or improves gas exchange
c. Reports no weight gain; appropriate weight for height
d. Maintains or improves peripheral blood flow
2. Maintains or increases activity tolerance
a. Carries out activities of daily living (eg, brushes teeth, feeds self)
b. Reports increased tolerance to activity
3. is less anxious
a. Discusses prognosis freely
b. Verbalizes fears and concerns
c. Participates in support groups if appropriate
4. Decreases sense of powerlessness
a. Identifies emotional response to diagnosis
b. Discusses control that he or she has
5. Adheres to self-care program
a. Takes medications according to prescribed schedule
b. Modifies diet to accommodate sodium and fluid recommendations
c. Modifies lifestyle to accommodate activity and rest behavior recommendations
d. Identifies signs and symptoms to be reported to health care professionals

CORONARY ARTERY DISEASE (CAD)

The arteries that supply blood to heart muscle become hardened and narrowed due to the build-
up of cholesterol and other material, called plaque, on their inner walls in a process referred to as
atherosclerosis. As the plague grows, there is reduced supply of oxygen and nutrients to the heart
cells leading to myocardial ischemia. This can lead to chest pain (angina) or a myocardial
infarction (heart attack).
Heart attacks happen when a blood clot suddenly cuts off the hearts' blood supply, causing
permanent heart damage. Over time, CAD can also weaken the heart muscle and contribute to
heart failure and arrhythmias.
Pathophysiology
The plaques protrude into the lumen of the artery, leading to narrowing and obstruction of the
blood flow. Blood supply through arteries gets disrupted, or the oxygen content of the blood is
not adequate to meet the demands of the body. The vascular endothelium in the involved areas
becomes necrotic, narrow and rough, making them prone to clot formation.
Thrombi forms on the surface of the plaque, further bleeding causes the thrombus to enlarge
occluding the coronary artery. The myocardial cells become ischemic within ten seconds of
coronary occlusion resulting in chest pain.
Phases of plague development
Plague deposition which normally starts in childhood progresses through phases
Phase 1: Fatty streaks- injury to intimal endothelium, lipid deposits, do not obstruct flow
Phase II: fibrous plaques – plaque and thrombus formation, protrusion into arterial lumen,
proliferation of smooth muscle cells, irreversible progression; elevated lesion protruding into
lumen obstructs flow to varying degrees
Phase III: complicated lesions- partially or totally occlude lumen, plaque calcification, plaque
rupture and thrombus formation

Progression of plague

Major effects of myocardial ischemia include:

 Decreased contractility-leading to heart failure and cardiogenic shock
 Electrical instability causing arrhythmias

Angina pectoris is chest pain caused by the buildup of lactic acid and irritation to the myocardial
nerve fibers triggered by the 4 E’s (Exertion, Emotion, Exposure to Cold, Eating), usually
relieved with rest, pain medications and nitrates
Types of Angina
Chronic Stable Angina: Is the most common angina type caused by physical exertion,
emotional stress, cold weather, and large meal. With rest, the angina attack symptoms generally
improve.
Unstable Angina: Is the second most common angina type. This is a dangerous condition that
requires emergency treatment. Can occur without physical exertion and is not relieved by rest or
medicine. The condition is caused by blood clots that partially or totally block a coronary artery.
It is a major predictor of an impending myocardial infarction.
Prinzmetal’s Angina also called Variant angina: Is a rare angina type caused by a spasm in a
coronary artery

Risk factors for coronary artery disease

Are classified into non-modifiable and modifiable
Non modifiable risk factors
 Age: Increasing age increases the chances of developing arteriosclerosis &
atherosclerosis. Death from CAD increases with age
 Gender: Males are more prone to develop atherosclerosis than females due to protective
effect of estrogen, after menopause, the risk is equal
 Family history: history of premature CAD in siblings or parents increases incidence
 Race/ethnic background: Afro Americans have approximately 45% chance of
hypertension than Caucasians (Hypertension is a major cause of CAD and Stroke)
Modifiable risk factors
Cigarette smoking: Nicotine, tar and carbon monoxide damage the blood vessel/ increases the
risk of CAD X 2
 Hypertension : Damages blood vessels leading to plaque formation and Atherosclerosis
 Hyperlipidemia: causes build up in artery walls increasing the risk of CAD and
atherosclerosis
 Physical inactivity: increased levels of fat deposition
 Diabetes mellitus: Mobilization of fats increases lipid levels, diabetes causes multitude
of small and large vascular problems leading to increased risk, twice in men and thrice in
women
 Obesity: Associated with higher levels of cholesterol
 Stress in daily living: Increased catecholamine release leads to increased sympathetic
response increasing myocardial oxygen demand and workload/ Mobilization of fat from
fat stores to provide energy in response to stress may contribute to developing the disease
 Diet high in calorie contributes to high blood lipid levels

Nursing and Collaborative Management

Assessment
Subjective data
 Angina pectoris- A substernal pain that radiates to the left arm, jaw, neck, back or
epigastrium region
 The patient will describe the pain as follows: Chest pain or discomfort, a strange feeling,
pressure, or ache in the chest, constrictive, squeezing, choking, or suffocating sensation,
indigestion, burning, heavy (like an elephant sitting on my chest)
 Assess for frequency, duration, location, character, aggravating & relieving factors.
 Associating factors such as dyspnea on exertion, pallor, diaphoresis, dizziness, nausea &
vomiting
 Psychosocial information, e.g. Age & gender lifestyle & habits: smoking, alcohol intake
exercise, stress, occupation, medication history: prescribed and over the counter
medication, contraceptives, hormone therapy
 Past medical history,
 Family history of cardiovascular disease, diabetes mellitus, hypertension, hyperlipidemia
etc.
Objective data-
Physical examination with the following signs: Chest pain, pallor or cyanosis, distended neck
veins, abnormal heart sounds.
Baseline: pulse rate and rhythm, peripheral pulses, respiration rate, rhythm and depth, blood
pressure, level of consciousness, urinary output
Diagnostic tests
 ECG
 Exercise stress test
 Coronary angiography
 Echocardiogram
Blood chemistry
 Creatine phosphokinase (CPK): raised levels indicate that muscles have been damaged.
 Lactic dehydrogenase (LDH): muscle protein
 Creatine kinase - MB (CKMB): type of creatine that is specific to myocardium and raised
levels indicate damage to the myocardium
  Troponin (Trop T): protein found in muscle, raised levels indicate myocardial damage
General management
 Health Promotion
 Identification of high-risk persons
 Management of high-risk person’s
 Risk factor modification
 Physical fitness
 Health education in schools
 Nutrition (weight control, fat, cholesterol intake)
 Cholesterol-lowering medications

Treatment for stable angina

 Bypass Surgery-a piece of saphenous vein is grafted in the heart muscles to bypass the
blocked coronary artery
 Coronary Angioplasty is a procedure used to open blocked or narrowed coronary arteries

 Vascular stent to prevent the artery from closing and prevent restenosis
 Medical therapies: Nitrates Beta blockers Calcium channel blockers
 Control of risk factors
 Dietary & lifestyle changes
 Follow-ups

 Educate patient: e.g. inform about triggers such as eating a heavy meal, Valsalva
maneuver- bearing down during passage of hard stool

ACUTE CORONARY SYNDROME/MYOCARDIAL INFARCTION

Acute coronary syndrome/myocardial infarction (MI) otherwise known as heart attack occurs
when there is blockage of the coronary vessels as a result of a thrombus (clot).
The thrombus is formed on top of an ulcerated or unstable atherosclerotic plaque in the coronary
artery.
The blockage which leads to myocardial cell damage and ischemia, contractile function stops in
the necrotic areas of the heart.
Myocardial infarction is described by the area of the myocardium where it occurs-Anterior,
Inferior, Lateral or Posterior.

Pathophysiology
Once the coronary artery is blocked, myocardial cell death begins at the endocardium, the area
most distal to the arterial blood supply. As vessel occlusion continues cell death spreads to the
myocardium and eventually to the epicardium.
Ischemia develops when there is an increased demand for oxygen or a decreased supply of
oxygen. Ischemia can develop within 10 seconds and if it lasts longer than 20 minutes,
irreversible cell and tissue death occurs.
Severity of the MI depends on three factors.
1. Level of occlusion
2. Length of time of occlusion
3. Presence or absence of collateral circulation

Areas of Injury
1. Zone of ischemia- Outer most area, source of arrhythmias, viable if no further infarction
occurs, this zone is salvageable with quick intervention otherwise it progresses to injury
2. Zone of injury – severe cellular injury: may be viable. Without intervention may progress
to necrosis
3. Zone of necrosis- electrically and mechanically dead tissue that turns into scar

Classifications
1. MI’s can be subcategorized by anatomy and clinical diagnostic information; Transmural
and Subendocardial
 2. ST elevations MI (STEMI) and non ST elevations MI (NSTEMI)
Risk Factors
1. Non Modifiable • Age • Gender • Family history
2. Modifiable
 Smoking tobacco increases the risk of coronary artery disease two to six times more than
non-smokers. Nicotine increases platelet thrombus adhesion and vessel inflammation
 Diabetes increases the rate of atherosclerotic formation in vessels at an earlier age
 Hypertension - The constant stress of high blood pressure increases rate of plaque
formation through shearing stress and inflammation of endothelial lining
 Hyperlipidemia: Elevated levels of cholesterol, LDL’s or triglycerides lead to risk of
coronary plaque formation and MI
 Obesity: central obesity has a higher incidence of coronary artery disease
 Physical Inactivity: physically inactive people have lower HDL levels with higher LDL
levels and an increase in clot formation.

Signs and Symptoms

Signs and symptoms are unique to each individual patient, ranging from no symptoms (in
diabetic neuropathy) to sudden cardiac arrest.
 Chest Pain is the most common initial manifestation not relieved by rest, position change
or nitrate administration. Pain is described as heaviness, pressure, fullness and crushing
sensation.
Pain location: A substernal pain that radiates to the left arm, jaw, neck, back or
epigastrium region
Assessment for chest pain • P- Precipitating events • Q- Quality of pain • R- Radiation of
pain • S- Severity of pain • T- Timing
 Nausea and Vomiting - a reflex from severe pain
 Diaphoresis and vasoconstriction of peripheral blood vessels, “Cool Sweat” with a
temperature increase during the first 24 hours.
 Dyspnea
 Shock due to drop in cardiac output- clammy, cold skin, dizziness, tachycardia
 Fear and anxiety
  Initially the BP and pulse may be elevated later; BP will drop due to decreased cardiac
output. Urine output will decrease
 Lung sounds will change to crackles
 Jugular veins may become distended and have obvious pulsations.

Serum Cardiac Markers

Myocardial cells produce certain proteins and enzymes for cellular functions. When cell death
occurs, these cellular enzymes are released into the blood stream.
 Creatine phosphokinase (CPK) are in 3 types: MB (found in Heart) MM (found in
skeletal muscles) BB (found in brain)
 In Myocardial infarction CPKMB rises in 3-6 hours post MI, peaks at 24 hours, returns to
normal in 3-4 days
 LDH lactic dehydrogenase is most specific for myocardial damage; Increased LDH
occurs after CPK elevation: helpful in making diagnosis in patients who delay seeking
medication attention
 Myoglobin- found in both heart and skeletal muscles; rises within 2 hours but not specific
to exclude skeletal damage.
 Troponin T and I a structural protein found only in cardiac muscles, more specific than
CK MB rises within 24 hours stay elevated for 5- 10 days, released due to myocardial
injury (unstable angina, MI, blunt trauma)

Management of Myocardial Infarction (MI)

The immediate goal for any acute MI is to restore normal coronary blood flow and to salvage
myocardium.
Aims of treatment
 Reestablish supply and demand balance
 Limit infarction size (salvaging ischemic cells)
 Relieve pain
 Prevent / treat complications
 Identify and manage risk factors
Immediate acute interventions recommended in the first 10 minutes of AMI)
Within the first 10 minutes upon arrival to the hospital:
 Take a brief focused history and perform a physical exam
 Check vital signs and evaluate oxygen saturation
 Establish IV access
 Obtain and review 12-lead ECG
 Obtain blood samples to evaluate initial cardiac markers, electrolytes and coagulation
 Immediately begin MONA
• Morphine • Oxygen • Nitroglycerin • Aspirin
1) Morphine dilates arteries, (coronary and systemic) hence decreases afterload and increases
supply. Analgesic that relieves chest pain, decreases anxiety-contraindicated if Systolic BP is
less than 90mmHg or in hypovolemia
2. Oxygen therapy
4-6 liters/hr. via nasal cannula to maintain oxygen saturation of > 90%; reduces ischemia
3. Nitroglycerine dilates coronary arteries, especially collaterals (increases supply, decreases
preload and afterload), decreases pain of ischemia
4. Acetyl Salicylic Acid (aspirin) Inhibits platelet aggregation hence prevents further clot
formation, 160-325 mg/day (chewable/rectal)

Interventions to limit infarct size

I. Thrombolytic/Fibrinolytic therapy should be given within 12 hours of onset of symptom.

Example: heparin will break down clots found within the vessels
Contraindications: post-operative surgical patients, history of hemorrhagic stroke, ulcer disease,
pregnancy
II. Cardiac Catheterization- Passage of a catheter through the femoral or brachial artery into the
coronary arteries to help in dilatation and introduction of a stent.
III. Coronary artery bypass graft (CABG); surgical treatment where saphenous vein is harvested
from the lower limb and used to bypass the occluded coronary artery

Other therapies to prevent ventricular remodeling

1) Beta blockers
Reduce myocardial demand by:
Decreases arrhythmias, tachycardia
Decreases Hypertension
Decreases contractility

2) Angiotensin Converting Enzyme inhibitors (ACEI)

Reduces preload and afterload
Reduces infarct expansion
Inhibits remodeling process
Monitor closely for hypotension
Monitor increase in creatinine levels

3. Lipid lowering drugs “Statins” e.g. atorvastatin are recommended for all patients with LDL
(low density lipoproteins) >100

4. Health education on risk factor modification

Key messages: Stop smoking/alcohol intake, Low fat diet, Low sodium diet, management of
preexisting conditions; diabetes, hypertension, hyperlipidemia, physical exercise

Nursing Management

Nursing Assessment
 A careful history (history of presenting illness, past med-surg history, socio-economic
history, family history, medication history)
 Assess immediately any complaints of chest pain using a pain scale of 0 – 10 and its
characteristics (chest pain, palpitation, dyspnea, syncope or sweating), each symptom
must be evaluated with regard to time, duration, precipitating & relieving factors.
 Complete physical assessment for: Vital signs, level of consciousness, Heart sounds,
Peripheral pulses, skin color, Lung sound
  Evaluation of ECG
 Evaluation of cardiac enzymes; CKMB, Troponin, Myoglobin, LDH
Nursing diagnosis
1. Acute pain related to myocardial ischemia, radiation of pain to the neck and arms.
2. Ineffective tissue perfusion (cardiac muscles) related to coronary blockage.
3. Anxiety related to perceived threat of death, pain, possible lifestyle changes as evidenced
by restlessness.
4. Risk-prone health behavior related to unhealthy lifestyle choices (e.g., tobacco use, high
calorie/high sodium intake, overweight)
5. Health maintenance alteration related to non-adherence to therapeutic regimen
Planning
Goals
1. Relief of chest pain
2. Preservation of myocardium
3. Effective coping with illness associated anxiety
4. Reduction of risk factors
5. Help the patient to adhere to the self-care program

Implementation
To relieve chest pain
 Administer PO morphine, an opioid analgesic
 Administer oxygen to prevent tissue hypoxia
 Administer coronary artery vasodilators (nitroglycerin) to improve blood supply to the
myocardium
 Use a cardiac monitor, this will provide information on cardiac condition continuously
 The patient is in semi fowlers position for comfort and rest, this reduces cardiac work
load
 Provide quiet and calm environment to promote rest
To preserve myocardium
 Administer oxygen at 4-6L/hr. to prevent further ischemia of the myocardium
 Administer nitroglycerine to dilate coronary arteries for improved myocardial perfusion
  Administer aspirin to prevent further clot formation in the coronary arteries
 Use pulse oximetry to guide therapy and maintain oxygen saturation above 90%
To ensure effective coping with illness associated anxiety
 Explain in simple terms the pathophysiology of acute MI, description of signs and
symptoms such as pain, pressure, or heaviness in chest.
 Provide information about medications; indications and side effects.
 Administer anxiolytic medication to ensure enough rest and to alley anxiety
 Provide an enabling environment for patient and family to freely express their fears and
concerns,
 Engage services of a counselor to help patient with handling of emotional stress and
anger.
To reduce risk factors
 Teach the patient about risk factor modifications such as decreasing fat intake, stopping
smoking, reducing salt intake, controlling hypertension and diabetes, increasing physical
activity as tolerated, and achieving normal body weight.
 Administer statins to reduce cholesterol levels
 Effectively manage comorbidities such as diabetes, hypertension
 Teach the patient about the importance of avoiding the Valsalva maneuver (bearing down
when going to bath room). This maneuver increases intrathoracic pressure that decreases
venous return to the right side of the heart leading to hypotension and bradycardia.
 Administer laxatives (stool softeners) to avoid constipation and therefore avoid Valsalva
maneuver
To help the patient to adhere to self-care program
 Teach on importance of adherence to medication
 Health Promotion: Risk factor modification such as control of hypertension, blood
cholesterol levels, diabetes, stoppage of tobacco use ensuring physical activity, managing
stress, acquiring required body weight
 Should be empowered to be able to recognize angina, precipitation factors in order to
seek for help promptly
 Involve the family to facilitate social and emotional support and to assist with care
Evaluation
Reports pain relief
Effective myocardial function
Effective coping with illness associated anxiety
Patient verbalizes willingness to reduce risk factors
Adheres to self-care program
Complications
 Dysthymias
 Cardiogenic shock
 Cardiac failure-Left sided heart failure occurs more often than right sided heart failure
 Necrotic tissue (myocardium)
 Rupture of intra cardiac structures
 Left ventricular aneurysm
 Deep vein thrombosis and embolisms
 Sudden death
Rheumatic heart disease
Rheumatic Heart Disease is a chronic condition which is as a result of rheumatic fever.
Rheumatic fever on the other hand is an acute multisystem inflammatory disease that follows a
group A beta-hemolytic streptococci (GAS) throat infection.
Immune reaction to the bacteria causes lesions in the connective tissues known as Aschoff
bodies. Aschoff bodies are localized areas of tissue necrosis surrounded by immune cells. The
lesions affect the connective tissues of heart, blood vessels, joints, central nervous system, skin
and subcutaneous tissues.
All the layers of the heart i.e. endocardium, myocardium and pericardium are affected. The heart
valves are also involved leading to leakage and narrowing. As the heart compensates changes in
the chamber sizes and thickness of chamber walls occur. This involvement of the heart is what is
termed as Rheumatic Heart Disease.
INCIDENCE
 Rheumatic fever is mostly a disease of childhood, with a median age of 10 years, although it
also occurs in adults (20% of cases).
 Rheumatic fever occurs in equal numbers in males and females, but the prognosis is worse for
females than for males.
 The disease is seen more commonly in poor socio-economic strata of the society living in
damp and overcrowded place.
ETIOLOGY
  Group A beta-hemolytic streptococcus
 Rheumatic fever
RISK FACTORS
 Poor socio-economic status
 Over-crowding: People who are living in a slum or damp area are more prone to get
Rheumatic
 Age: It appears most commonly in children between the age of 5 to 15 years.
 Climate and season: It occurs more in the rainy season and in the cold climate.
 Upper respiratory tract infection: Rheumatic fever is an outcome of upper respiratory
tract infection with group A beta- hemolytic streptococcus.
 Previous history of Rheumatic fever
 Genetic predisposition: Rheumatic heart disease shows familial tendency
Diagnosis
A diagnosis of rheumatic heart disease is made after confirming rheumatic fever.
Rheumatic fever is diagnosed by use of Jones Criteria; evidence of a previous streptococcal
throat infection and 2 major Jones criteria or 1 major plus 2 minor Jones criteria.

Major manifestations
 Carditis Cardiomegaly, new murmur, congestive heart failure, pericarditis
 Migratory polyarthritis, shifting tenderness of the large joints, warm and swollen
 Subcutaneous nodules (Aschoff bodies) Firm, painless fibrous nodules on the extensor
surfaces of the wrists, elbows, and knees
 Erythema marginatum: Long lasting rash on trunk or extremities
 Sydenham's Chorea (St. Vitus’ dance) bizarre movement rapid and purposeless
involving face and arms; generally, movements cease during sleep

Minor manifestations

Arthralgia (Joint pain), fever, together with Clinical findings and Laboratory findings

Clinical findings
 Previous rheumatic fever or rheumatic heart disease
 Arthralgia
 Sudden onset of sore throat; throat reddened with exudate
 Swollen, tender lymph nodes at angle of jaw
 Headache and fever >38 degrees celsius associated with weakness, malaise, weight loss
and anorexia
 Abdominal pain (children)
 Some cases of streptococcal throat infection are relatively asymptomatic
Imaging studies
Chest X-ray: enlarged heart. pulmonary congestion, and other findings consistent with heart
failure
Doppler- echocardiography: valve insufficiency and ventricular dysfunction.
Prolonged PR interval on ECG
Laboratory
Positive throat culture for group A beta- hemolytic streptococci.
Elevated Erythrocyte sedimentation rate (ESR),
WBC count and differential increased during acute phase of infection
Elevated or rising anti-streptococcal antibody titer (antistreptolysin-O (ASO) titer)
Elevated acute phase reactants: (C-reactive protein)

Medical management
Medical management is in two phases
1. Eradication of infection
 An injection of benzathine penicillin G intramuscularly every 4 weeks
 Administer the same dosage every 3 weeks in areas where rheumatic fever is common, in
patients with carditis, and in high-risk patients

2. Preventive and prophylactic therapy to prevent further damage to valves

 Antibiotic prophylaxis indefinitely for patients at high risk (eg, health care workers,
teachers, daycare workers) for recurrent infection
 Prevention of recurrence through penicillin therapy for 5 years after initial attack
 Carditis and valve disease needs antibiotics for at least 10 years or until age 40 years; in
some cases throughout life if valves are damaged
 Rheumatic heart disease and valve damage require a single dose of antibiotics 1 hour
before surgical and dental procedures to prevent bacterial endocarditis.
 Where there is no evidence of valve damage; not need for prophylaxis.
 Alternative drugs: PO clindamycin (20 mg/kg in children, 600 mg in adults) and PO
azithromycin or clarithromycin (15 mg/kg in children, 500 mg in adults).
 Corticosteroids are used to treat carditis, especially if there is heart failure
 ACE inhibitors, beta blockers and diuretics, in heart failure
 Salicylates or NSAIDS to relieve pain and fever
 Bed rest to maintain optimal cardiac function until inflammation has subsided
SURGICAL MANAGEMENT
 Cummisurotomy can be done to widen the valve.
 Mitral valvulotomy, percutaneous balloon valvuloplasty, or mitral valve replacement to
relieve mitral stenosis
Nursing management
Nursing assessment
SUBJECTIVE DATA
 Past health history: Recent streptococcal infection
 Previous history of rheumatic heart disease,
 Family history of rheumatic fever
 Nutritional-metabolic: Anorexia and weight loss
 Activity-exercise: Palpitations, generalized weakness, fatigue, ataxia etc
 Chest pain
 Migratory joint pain Tenderness (especially large joints)
OBJECTIVE DATA
 Fever
 Subcutaneous nodules
 Erythema marginatum
 Tachycardia, pericardial friction rubs, Murmurs & Peripheral edema
 Chorea-involuntary, purposeless, rapid motions, facial grimaces
 Signs of mono or polyarthritis including swelling, heat, redness, limitation of motion
(especially, knees, ankles, elbows, shoulders, wrists etc)
Nursing diagnoses
1. Pain related to carditis
2. Decreased cardiac output related to valve dysfunction/heart failure
3. Knowledge deficit related to disease condition and long term treatment
4. Anxiety related to disease condition and heart failure
Planning
Goals:
To relieve pain and promote comfort
To improve cardiac output
To improve patient’s knowledge on disease process and need for long term treatment
To alley anxiety
Implementation and rationale
To relieve pain;
 Assess the level of pain, duration, intensity and frequency of pain to enable effective pain
management
 Complete bed rest to provide comfort and to conserve energy
 Provide diversional therapy and psychological support to get the patient’s mind off the pain
 Administer analgesics as needed to relieve pain
To improve cardiac output
 Assess the symptoms of heart failure and decreased cardiac output including diminished
quality of peripheral pulses, cool skin and extremities, increased respiration, increased heart rate,
neck vein distention and presence of edema to detect deviation from normal
 Assess for heart sounds, extra sounds may indicate valve damage
 Monitor intake and output to evaluate renal functions
 Provide bed rest to conserve energy
 Administration of cardiac glycosides e.g. digoxin as prescribed to enhance contractility
 Administer penicillin therapy or its alternative as prescribed to eradicate hemolytic
streptococcus

To enhance knowledge level

 Assess the client’s level of knowledge to ascertain baseline knowledge
 Explain about disease condition and about prophylactic treatment of antibiotics.
 Discuss proper handwashing, disposal of tissues, laundering of handkerchiefs (decrease risk of
exposure to microbes).
 Discuss importance of using patients own toothbrush, soap, and washcloths when living in
group situations to avoid cross infection
 Instruct patient to seek treatment immediately should sore throat occur
 Support patients in long-term antibiotic therapy to prevent relapse (5 years for most adults).
 Instruct patient with valvular disease to use prophylactic penicillin therapy before certain
procedures and surgery
 Counsel patient to maintain good nutrition to enhance immunity

To alley anxiety
 Assess the client’s level of anxiety so as to know the areas of concern
 Clarify the doubts of the client by using non-medical terms and calm, slow speech.
 Explain all activities, procedures and issues that involve the client.
 Explain about the disease conditions and prophylactic treatment.
 Provide anxiolytics as prescribed to calm the patient

Evaluation

 The client verbalizes increased comfort, exhibits relaxed body posture and a calm facial
expression.
 Regular cardiac rhythm, heart rate, blood pressure, respiration and urine output within
normal limit.
 Patient explains disease condition, recognizes need for medication and understands
treatment.
 Client verbalized reduced fear and anxiety
Infective endocarditis
The heart is a vital organ that pumps blood. It has three layers which are endocardium,
myocardium and pericadium.
Infective endocarditis is an inflammation of the inner layer of the heart, the endocardium. It
usually involves the valves and other structures like the intraventricular septum.
Etiology
 Fungus e.g. candida, aspergillus
 Gram negative organisms e.g. pseudomonas
 Other bacteria e.g. staphylococci
 Acute rheumatic fever which damages the valves
 Congenital malformation
 Cardiomyopathy
Risk factors
• Prosthetic (artificial) heart valves
• Previous heart damage
• Dental procedures which lead to introduction of bacteria
• Heart surgery
• Intubations
• Procedures involving gastro intestinal and genitourinary tracts e.g. barium enemas,
sigmoidoscopy, catheterization and cystoscopy
• Reproductive conditions like delivery, abortions and pelvic inflammatory disease
• IV drug users ( drugs of abuse)
• Dysfunctions of heart valves

Pathophysiology
Microbes directly invade the endocardium and accumulate on the valves of the heart or
endocardium. The microbes then proliferate forming vegetation which damages heart valves
leading to poor flow of blood and accumulation of blood in chambers of the heart. The damage
attracts platelets causing clot formation. The clots and vegetation can form emboli which may
obstruct blood flow
Clinical manifestations
Shortness of breath
Shock
Finger clubbing
Myocardial infarction
Malaise
Night sweats
Chest and abdominal pain
Intermittent high fever
Anorexia, weight loss
Cough, back pain and joint pain
Hemorrhages under nails
Osler’s nodes- painful nodules on fingerpads
Roth’s spots- pale hemorrhages in the retina
Heart murmurs
Heart failure

Diagnostic evaluation
 Blood culture to determine specific microorganisms
 Urinalysis to see microscopic hematuria
 Echocardiography to examine wall motion and the valves
 Computerized tomography to rule out heart damage
 Blood urea, nitrogen and creatinine levels to evaluate renal function
 Endocardiography to check valves and ventricular function and presence of vegetation
 White blood cell count rule out infection
Medical management
1. Pharmacotherapy IV antibiotic for 2-6 weeks
2. Antifungal agents e.g. – amphotericin B
Surgery: Valvular replacement
Nursing management
Nursing assessment:
Subjective data
 Past medical history: ask about signs of the disease, the onset, review risk factors like
cardiac failure, shock
 Medication history: any medication taken and its effects
 Family history; any case of similar conditions at home
 Social history: social behaviours that can trigger the problem
 Surgical history: if ever operated on
Objective data:
Assess for temperature elevations, heart murmur, evidence of cough, peripheral edema and
embolism, auscultate for heart sound, monitor arterial blood gas, rapid purse rate, dyspnea,
restlessness and manifestation of heart failure
Nursing diagnoses
1. Impaired gaseous exchange related to fluid accumulation in the lungs as evidenced by
shortness of breath
2. Decreased cardiac output related to valvular dysfunction as evidenced by poor tissue
perfusion
 3. Imbalanced nutrition less than body requirement related to anorexia as evidenced by loss
of weight.
4. Altered thermoregulation related to infection as evidenced by increased body temperature
(fever).
5. Impaired physical mobility related to fatigue
6. Anxiety related to hypoxia or life threatening situation as evidenced by patient
verbalization
Planning
Goals:
To improve gaseous exchange
To improve cardiac output
To ensure adequate nutrition
To regulate body temperature
To conserve energy
To alley anxiety

Implementation/rationale
To improve gaseous exchange
 Position the patient in semi fowlers position to allow room for lung expansion as
abdominal organs are displaced downwards
 Administer oxygen therapy 4-6 l/min to help improve tissue perfusion
 Monitor arterial blood gas- ABG: carbon dioxide, oxygen saturation hourly to detect
signs of respiratory acidosis
 Encourage cough and deep breath to promote chest expansion
To improve cardiac output
 Assess the symptoms of heart failure and decreased cardiac output including diminished
quality of peripheral pulses, cool skin and extremities, increased respiration, increased
heart rate, neck vein distention and presence of edema to detect deviation from normal
 Assess for heart sounds, extra sounds may indicate valve damage
 Monitor intake and output to evaluate renal functions
 Provide bed rest to conserve energy
 Administer inotropic drugs like digoxin that help in increasing contractility of the heart
To ensure adequate nutrition
 Encourage and provide small frequent meals to meet nutritional requirements
To regulate body temperature
 Administer antipyretics to control fever
 Provide tepid sponging to reduce fever through evaporation and conduction

To conserve energy
  Schedule nursing activities to allow rest
 Limit exercise according to patient’s capability

To alley anxiety
 Address patient’s concerns to allay anxiety
 Educate the patient on disease process to enhance coping
 Administered morphine which may help to decrease anxiety

Evaluation
 The client verbalizes increased ease of breathing, maintains semi fowlers, arterial blood
gas- ABG are normal, no respiratory acidosis/alkalosis
 Regular cardiac rhythm, heart rate, blood pressure, peripheral pulses, respiration and
urine output within normal limit. Skin and extremities are warm.
 Patient takes small frequent meals
 Normal body temperature
 Patient verbalizes enough rest
 Patient maintains limited exercise according to capability
 Patient explains disease condition, recognizes need for medication and understands
treatment.
 Client verbalized reduced fear and anxiety

Complications
Chronic heart failure, Shock, Stroke, embolism

Prevention
Antibiotic prophylaxis if patient is undergoing procedures like dental extractions, bronchoscopy,
surgery, etc.
VALVULAR HEART DISEASE
The valves of the heart control the flow of blood through the heart into the pulmonary artery and
aorta by opening and closing in response to the blood pressure changes. The four heart valves
ensure blood flows freely in a forward direction without backward leakage.
Valvular heart disease is defined by damage or defect in one of the four heart valves: the mitral,
aortic, tricuspid or pulmonary.
The mitral and aortic valves are the ones most frequently affected. The mitral and tricuspid
valves control the flow of blood between the atria and the ventricles. The pulmonary valve
controls the flow of blood from the heart to the lungs. The aortic valve governs blood flow
between the heart and the aorta.

Valve damages are classified into:

1. Valvular stenosis
  The valve opening narrows
 Leaflets may become fused or thickened so that the valve cannot open freely
 Obstructs the normal flow of blood
 The chamber behind the stenotic valve is subject to greater stress; must generate more
pressure to force blood through the narrowed opening
 Initially, the heart compensates for the additional workload by gradual hypertrophy and
dilation of the myocardium, but further leads to heart failure.
2. Valvular regurgitation
 Leakage or backflow of blood, results from incomplete closure of the valve due to:
 Scarring and retraction of valve leaflets
 Weakening of supporting structures
 Causes the heart to pump the same blood twice (as the blood comes back into the
chamber)
 The heart dilates to accommodate more blood> Hypertrophy >Heart failure
Types of Valvular Heart Disease
Tricuspid stenosis: Narrowing of the tricuspid orifice that obstructs blood flow from the right
atrium to the right ventricle
Tricuspid regurgitation: Insufficiency of the tricuspid valve causing blood flow from the right
ventricle to the right atrium during systole
Pulmonic stenosis: Narrowing of the pulmonary outflow tract causing obstruction of blood flow
from the right ventricle to the pulmonary artery during systole
Pulmonic regurgitation: Insufficiency of the pulmonic valve causing blood flow from the
pulmonary artery into the right ventricle during diastole
Mitral stenosis: Narrowing of the mitral orifice that impedes blood flow from the left atrium to
the left ventricle
Mitral regurgitation: Insufficiency of the mitral valve causing flow of blood from the left
ventricle (LV) into the left atrium during ventricular systole.
Aortic stenosis: Narrowing of the aortic valve, obstructing blood flow from the left ventricle to
the ascending aorta during systole
Aortic regurgitation: Insufficiency of the aortic valve causing backflow of blood from the aorta
into the left ventricle during diastole
Causes:
 Advanced age (Degeneration/calcification)
 Congenital heart disorders
 Rheumatic fever
 Bacterial endocarditis
 High blood pressure and atherosclerosis
 Myocardial infarction (damage of the muscles that control the heart valves)

Risk factors
Congenital or acquired
Age, Gender, Tobacco use, Hypercholesterolemia, Hypertension, Type II diabetes
General signs and symptoms
Signs and symptoms Many of the symptoms are similar to those associated with congestive heart
failure • Shortness of breath • Wheezing after limited physical exertion • Swelling of the feet,
ankles, hands or abdomen (edema). • Palpitations, chest pain (may be mild). • Fatigue. •
Dizziness or fainting (with aortic stenosis). • Fever (with bacterial endocarditis). • Rapid weight
gain.
Diagnostic procedures
• Heart murmurs on auscultation • X-ray chest • ECG/ ECHO • CT scan /MRI • Cardiac
Catheterization
General Management
Life style changes

 Healthy life choices will improve overall health and heart health and can help slow the
progression of your heart disease
 Healthy Diet • Quit Smoking and Alcohol • Exercise to reduce stress • Weight
maintenance

Medical management
Anticoagulants or Thrombolytic agents • Digitalis (digoxicin) • ACE Inhibitors • Beta-blockers •
Calcium Channel Blockers • Diuretics • Antibiotics

Surgical management
 Minimally invasive valve surgery
 Complex valve repair and replacement
 Trans catheter Procedures –Trans catheter aortic valve replacement (TAVR) –trans
catheter mitral valve repair with Mitral Clip –trans catheter aortic valve fusion –trans
catheter repair of congenital defects
MITRAL STENOSIS
 Almost always rheumatic in origin
 Older people: by heavy calcification of mitral valve
 Congenital (rare)
Clinical features:
 Dyspnea on exertion (pulmonary venous hypertension),
 Fatigue and decreased exercise tolerance (low cardiac output),
 Dry cough, wheezing, Hemoptysis, palpitations,
 Orthopneoa, Paroxysmal nocturnal dyspnea,
 Repeated respiratory infections,
 Dysrhythmias: Atrial fibrillation, Mitral facies - Loud first heart sound, opening snap,
Crepitation’s, pulmonary edema, effusions,
Investigations:
ECG: - Right ventricular hypertrophy,
Chest X-ray: - enlarged Left Atrium & appendage
Echocardiography: - thickened immobile cusps, reduced valve area, enlarged left atrium, reduced
rate of diastolic filling of left ventricle,
Doppler: - pressure gradient across mitral valve.
Cardiac catheterization: - pressure gradient between LA and LV
Management: Medical-surgical
 Anticoagulant to reduce the risk of systemic embolism
 Mitral Balloon valvuloplasty
 Digoxin, beta blockers, or calcium antagonists
 Diuretic to control pulmonary congestion Valve Replacement

MITRAL REGURGITATION:
Etiology:
Congenital: Cleft mitral valve or parachute mitral valve
Acquired: rheumatic heart disease, endocarditis, mitral valve prolapse, connective tissue
disorders like marfan’s syndrome, trauma, chordae tendineae rupture, calcification of mitral
valve, dilated cardiomyopathy, idiopathic
Clinical features
Dyspnea, Fatigue, Weakness, Symptoms of acute pulmonary edema, Puffiness of face
Pulse most probably normal, irregular if atrial fibrillation is present, Widened pulse pressure,
Raised jugular venous pressure
Diagnosis
ECG, Echocardiography, and Color Doppler
Medical-Surgical management
 Salt restricted diet, Diuretics, Vasodilators, Digoxin, Anticoagulants and Long term
antibiotic prophylaxis using benzathine penicillin
 Valve replacement
MITRAL VALVE PROLAPSE
Mitral valves become floppy also known as murmur syndrome or Barlow’s syndrome. It is one
of the most common causes of mild mitral regurgitation
Causes
 Congenital anomalies
 Degenerative myxomatous changes
 Connective tissue disorders like Marfan’s syndrome.
Marfan syndrome is an inherited disorder that affects connective tissue — the fibers that support
and anchor organs and other structures in the body. Marfan syndrome most commonly affects the
heart, eyes, blood vessels and skeleton resulting in aortic dilatation, aneurysm formation, aortic
dissection, aortic regurgitation and mitral valve prolapse.
Clinical manifestations:
 Fatigue & weakness – due to decreased cardiac output – predominant complaint
 Exertional dyspnea & cough – pulmonary congestion, Palpitations – due to atrial
fibrillation (occur in 75% of pts.)
 Edema, ascites – Right- sided heart failure.
 Atrial fibrillation, Cardiomegaly, Signs of pulmonary venous congestion (crepitations,
pulmonary edema, effusions), Signs of pulmonary hypertension & right heart failure
Management: medical-surgical
 Vasodilators (e.g. ACE inhibitors), beta blockers,
 Mitral Valve Repair to treat mitral valve prolapse,
 Diuretics OR If atrial fibrillation presents,  Anticoagulant  Digoxin
 Mitral Valve Replacement
AORTIC STENOSIS
Aortic valve stenosis is narrowing of the orifice between the left ventricle and the aorta.
In adults it is often a result of degenerative calcifications.
Congenital leaflet malformations or an abnormal number of leaflets

Pathophysiology
Progressive narrowing of the valve orifice over several years, the left ventricle overcomes the
obstruction to circulation by contracting more slowly but with greater energy than normal,
increased pressure causes left ventricular hypertrophy.
When these compensatory mechanisms of the heart fail, clinical signs and symptoms develop.

Risk factors
 Diabetes mellitus,
 hypercholesterolemia,
 hypertension
 low levels of high density lipoprotein cholesterol
 rheumatic endocarditis

Clinical Manifestations
 Many patients with mild or moderate aortic stenosis are asymptomatic.
 (CO fails to rise to meet demand) Exertional dyspnea,
 Angina pectoris results from the increased oxygen demands of the hypertrophied left
ventricle
 Orthopnea,
 Exertional syncope(dizziness and fainting)
  Episodes of acute pulmonary edema
 Ejection systolic murmur
 Signs of pulmonary venous congestion- pulmonary edema (e.g. crepitations)
 Pulse pressure may be low (30 mm Hg or less) because of diminished blood flow.
 Blood pressure is usually normal but may be low.
 Paroxysmal nocturnal dyspnea

Medical Management
 Medications for dysrhythmia or left ventricular failure
 Definitive treatment is surgical replacement of the aortic valve.
 Percutaneous valvuloplasty procedures
Investigations:
ECG: - Left ventricular hypertrophy.
Chest X-ray: - May be normal, Enlarged LV & dilated ascending aorta, Calcified valve
ECHO: - Calcified valve with restricted opening, hypertrophied LV
Doppler: - Measurement of severity of stenosis Detection of associated aortic regurgitation
Cardiac catheterization: - To identify coronary artery disease
Management; Medical-Surgical
 Asymptomatic aortic stenosis is kept under review
 Moderate/severe stenosis is valuated every 1-2 years with Doppler echocardiography (to
detect progression in severity)
 Symptomatic severe aortic stenosis; valve Replacement
 Congenital aortic stenosis; Aortic Balloon Valvuloplasty
 Atrial fibrillation or post valve replacement with a mechanical prosthesis; Anticoagulant
AORTIC REGURGITATION
Aortic regurgitation is the flow of blood back into the left ventricle from the aorta during
diastole. It may be caused by inflammatory lesions that deform the leaflets of the aortic valve,
preventing them from completely closing the aortic valve orifice.

Causes
 Congenital-Bicuspid valve or disproportionate cusps
 Infective rheumatic endocarditis, congenital abnormalities,
 Syphilis
 Dissecting aneurysm that causes dilation or tearing of the ascending aorta,
 Blunt chest trauma,
 Deterioration of an aortic valve replacement
 Idiopathic
Pathophysiology
Blood from the aorta returns to the left ventricle during diastole, in addition to the blood
normally delivered by the left atrium
The left ventricle dilates in an attempt to accommodate the increased volume of blood.
It hypertrophies to increase muscle strength to expel more blood with above-normal force, thus
increasing systolic blood pressure.
The arteries attempt to compensate for the higher pressures by reflex vasodilation; the peripheral
arterioles relax, reducing peripheral resistance and diastolic blood pressure.
Clinical Manifestations
 Mild or moderate aortic regurgitation: Usually asymptomatic (because compensatory
ventricular dilatation and hypertrophy occur)
 Some patients are aware of a forceful heartbeat (palpitations)
 Marked arterial pulsations that are visible or palpable at the carotid or temporal arteries
 Exertional dyspnea and fatigue
 Breathlessness (e.g. orthopnea, paroxysmal nocturnal dyspnea
 Angina
 Pulse- Large volume or ‘collapsing’ pulse
 Low diastolic and increased pulse pressure
 Bounding peripheral pulse
Assessment and Diagnostic Findings
 Diastolic murmur
 The pulse pressure (ie, difference between systolic and diastolic pressures) is
considerably widened
 Water-hammer (Corrigan’s) pulse, in which the pulse strikes the palpating finger with a
quick, sharp stroke and then suddenly collapses
 Doppler echocardiography (preferably transesophageal), radionuclide imaging, ECG,
magnetic resonance imaging (MRI), and cardiac catheterization
Medical Management
 Avoid physical exertion, competitive sports, and isometric exercise.
 Vasodilators such as calcium channel blockers (eg, nifedipine )
 ACE inhibitors (eg, captopril, enalapril, lisinopril, ramipril), or hydralazine
 Aortic valvuloplasty or valve replacement performed before left ventricular failure occurs
 Surgery is recommended for any patient with left ventricular hypertrophy, regardless of
the presence or absence of symptoms.
 Treat underlying conditions, such as endocarditis or syphilis
 Annually follow up with echocardiography for evidence of increasing ventricular size.

TRICUSPID STENOSIS:
Usually occurs together with aortic or mitral stenosis. May be due to rheumatic heart disease
Decreased blood flow from right atrium to right ventricle leads to decreased right ventricular
output and then decreased left ventricular filling and finally decreased cardiac output.
Clinical features:
 Symptoms of right- sided Heart failure; Hepatomegaly, Ascites, Peripheral edema, Neck
vein engorgement
 Decreased cardiac output – fatigue, hypotension  Raised JVP
 Mid-diastolic murmur (best heard at lower left or right sternal edge)
Management:
Valve replacement Valvotomy ,
Balloon Valvuloplasty
TRICUSPID REGURGITATION:
Common, and is most frequently as a result of enlargement of right ventricle. Tricuspid valve
allows blood to flow back into the right atrium. Venous congestion & decreased right ventricular
output decrease blood flow towards the lungs
Etiology:
 Rheumatic heart disease
 Endocarditis, particularly in injection drug-users
 Congenital anomaly
 Right ventricular dilatation due to chronic left heart failure
 Right ventricular infarction
 Pulmonary hypertension
Clinical features:
 Usually non-specific Tiredness (reduced forward flow)
 Edema Hepatic enlargement (venous congestion)
 Raised JVP
 Pan systolic murmur (leftsternal edge)
 Pulsatile liver
Management:
 Correction of the cause of right ventricular overload
 Use of diuretic and vasodilator
 Treatment of CCF
 Valve repair
 Valve replacement
PULMONARY STENOSIS:
Clinical features:
 Fatigue, dyspnea on exertion, cyanosis
 Poor weight gain or failure to thrive in infants
 Hepatomegaly, ascites, edema
 Murmur often preceded by an ejection sound (click)
Investigations:
 ECG: - Right ventricular hypertrophy
 Chest x-ray: - Post-stenotic dilatation in the pulmonary artery
 Doppler echocardiography is the definitive investigation
Management:
 Mild to moderate isolated pulmonary stenosis is relatively common and does not usually
progress or require treatment
 Severe pulmonary stenosis percutaneous pulmonary balloon Valvuloplasty  OR surgical
Valvotomy
PULMONARY REGURGITATION
A rare condition usually associated with pulmonary hypertension caused by disease of left side
of the heart, pulmonary vascular disease or Eisenmenger’s syndrome
Blood flows back into right ventricle leads to right ventricle and atrium hypertrophy and finally
symptoms of right- sided heart failure.
Medical /Surgical management:
 Prophylactic antibiotic therapy ( rheumatic fever, infective endocarditis)
 Treatment of heart failure with vasodilators, beta blockers and diuretics
 Low sodium diet
 Anticoagulant therapy is used to treat pulmonary embolization.
 Percutaneous trans-luminal balloon Valvuloplasty: Threading a balloon tipped catheter
from the femoral artery or vein to the stenotic valve so that the balloon may be inflated in
an attempt to separate the valve leaflets.
 Valvuloplasty: It is the repair of cardiac valve• Patient does not require continuous
anticoagulant medication • Usually require cardiopulmonary bypass machine.
 Annuloplasty: repair of valve annulus (junction of the valve leaflet and the muscular
heart wall) Narrows the diameter of the valve’s orifice, useful for valvular regurgitation
 Chordoplasty: It is repair of chordae tendineae done for mitral valve regurgitation
caused by stretched or shortened chordae tendineae
 Valve replacement
NURSING MANAGEMENT OF VALVULAR HEART DISEASE
Nursing Assessment:
 Vital signs: HR, BP, RR measured and compared with previous data for any changes. 
Auscultate heart and lung sounds
 Palpate peripheral pulses
 Assess sign and symptoms of Heart Failure Fatigue, dyspnea with exertion, increase in
coughing, hemoptysis, multiple respiratory infections, Orthopnea, or paroxysmal
nocturnal dyspnea.
  Assess dysrhythmias by palpating the patient’s pulse for strength and rhythm (i.e, regular
or irregular) and asks if the patient has experienced palpitations or felt forceful heartbeats
 Assess for dizziness, syncope, increased weakness, or angina pectoris.
Nursing diagnosis:
1. Decreased cardiac output related to valvular incompetence as evidenced by murmurs,
dyspnea, and peripheral edema.
2. Activity intolerance related to insufficient oxygenation as evidenced by weakness,
fatigue, shortness of breath, BP changes.
3. Risk for fluid volume and electrolyte imbalance related to alteration s in blood volume
4. Deficient knowledge related to lack of experience and exposure to information about
disease and treatment process as evidenced by verbalization of misconception about
measures to prevent complications.
Planning
Goals
To restore cardiac output
To improve activity tolerance
To maintain fluid and electrolyte balance
To enhance patient knowledge on disease process and treatment options

Interventions
To restore Cardiac Output
Monitor cardiovascular status closely
Assess peripheral pulses
Auscultate for heart sounds
Monitor ECG pattern for cardiac dysrhythmias
Measure urine output 1hrly
Rationale: Measures are aimed at ascertaining cardiac hemodynamics and detecting any
deviations from normal
Observe for cardiac failure.

To improve activity tolerance

Provide adequate bed rest, if ambulatory, avoid over exertion. Assess the client’s stamina and
response to exercise to gauge the degree of gradual activity progression. Assess vital signs
before and after exercise. Reduce or discontinue activity if chest pain, vertigo, dyspnea,
confusion, a drop in BP, an irregular pulse or abnormal heart rate develops.
Rationale: This ensures the patient conserves energy and operates within the most comfortable
activity levels
Administered salicylates as prescribed to prevent clot formation

To maintain fluid and electrolyte balance

  Maintaining intake and output chart, monitor urine output 1hrly to evaluate renal
functions
 Weigh daily at same time by same weighing machine.
 Notify physician if weight gain is 1kg or more to rule out fluid retention and edema
 Monitor ECG for electrolyte imbalance
To enhance patient knowledge on disease process and treatment options
 Develop teaching plan for patient and family.
 Provide specific instructions for the following: diet and daily weight, activity
progression, medication regimen, pulse taking, access to emergency medical system.
Involve family in teaching sessions.
 Educate client and family about mechanism of action of anticoagulants, side effects
which need medical attention (bleeding that doesn’t stop after 15 mins, blood in urine,
black tarry stool, unusual bleeding from body orifices, severe headaches, weakness, cold,
blue or painful feet)
 Avoid activities that may cause bleeding, avoid alcoholism,
 Wear medic alert bracelet or ID card
 Avoid foods rich in vitamin k
 Consult with doctor if any other treatment to be started
 Contact emergency department, if fever, dyspnea, bleeding, low urine output
Evaluation
 The cardiac output is restored to maintain organ and tissue perfusion as evident by
normal Central Venous Pressure, arterial pressure, peripheral pulses and urinary output.
 The client will have improved tolerance of activity and progress towards an optimal level
of physical activity.
 The fluid and electrolyte balance is normal as evidenced by normal blood pressure, stable
weight and normal serum electrolyte level.
 The client has improved knowledge about the disease condition and its treatment process
and options.
VASCULAR DISORDERS
The vascular system
Overview
• The vascular system is made up of the vessels that carry blood and lymph through the
body.
• The arteries and veins carry blood throughout the body, delivering oxygen and nutrients
to the body tissues and taking away tissue waste matter.
• The lymph vessels carry lymphatic fluid (a clear, colorless fluid containing water and
blood cells).
• The lymphatic system helps to protect and maintain the fluid environment of the body by
filtering and draining lymph away from each region of the body.
The blood vessels
The vessels of the blood circulatory system are:
• Arteries: - carry oxygenated blood away from the heart to the body.
• Veins: - carry deoxygenated blood from the body back into the heart.
• Capillaries:- Tiny blood vessels between arteries and veins that distribute oxygen-rich
blood to the body

Arterial Assessment
Purpose: To determine adequate tissue perfusion
1. Compare upper & lower limbs
2. Compare bilaterally
3. Compare distal & proximal
Assess for
1. Circulation – presence of pulse means perfusion
2. Motion – muscles need oxygen
3. Sensation – pain, burning, proprioception, numbness

Circulation
Check pulse points
Carotid, Radial, Femoral, dorsalis pedis, posterior tibial, capillary refill

Pulses are based on a scale 0 to 4+

0 = no pulse
1+ = thready pulse
2+ = normal pulse
3+ = bounding pulse
4+ = aneurysm

Motion
 Intermittent Claudication; a condition in which cramping pain in the leg is induced by
exercise, caused by obstruction of the arteries
 Pain with ambulation or elevation, relief with dependent position

Sensation
 The patient reports pain, burning, proprioception, numbness
 Perform physical examination to confirm problems with sensation

Clinical Presentation of Arterial Insufficiency

1. Skin cool, shiny thin, onion like
2. Pain when cold
3. Pain with elevation
4. Distal pulses are reduced or absent
5. Decreased or absent hair
6. Ischemic ulcers
7. Thick nails
Acute arterial insufficiency
The 5 Ps
When present it is a surgical emergency!
1. Pain
2. Pallor
3. Pulselessness
4. Paralysis
5. Paresthesia

ATHEROSCLEROSIS AND ARTERIOSCLEROSIS

Arteriosclerosis is the loss of arterial elasticity, due to hardening and hypertrophy of arterial
walls.
Muscle fibers and the endothelial lining of the walls of small arteries and arterioles become
thickened. The most common disease of the arteries though cause is not fully known.
Atherosclerosis is the accumulation of lipids, calcium, blood components, carbohydrates and
fibrous tissue on the intimal layer of large and medium sized arteries. These accumulations are
referred to as atheromas or plaques.
Atherosclerosis begins in infants and childhood and progresses slowly over the decades, major
targets being the aorta, the coronary and cerebral arteries.
It often produces ischemia of the intestines and lower extremities. It is also a major cause of
abdominal aortic aneurysms.
Risk factors to atherosclerosis
The risk factors are classified into 2:
1. Modifiable risk factors
 Obesity
 Physical inactivity
 High carbohydrate intake
 Nicotine use (i.e., Tobacco smoking, chewing)
 Diet high in lipids
 Hypertension: - increases risk by 60%.
 Diabetes mellitus
 Stress
 Sedentary life style.
 Hyperlipidemia: - low density lipoprotein (bad cholesterol). High density lipoprotein
(good cholesterol).
Non modifiable risk factors
 Age incidences are more as age increases
 Gender, between ages 40 and 60 incidence is more in men, after menopause incidence
increases in women
 Family history
 Genetic abnormalities: - derangements in lipoprotein metabolism such as hyper-
cholesterolemia results in excessively high blood lipid levels.
Clinical manifestations
Are basically attributed to reduced myocardial blood and oxygen supply
 Fatigue
 Chest pain( angina) radiating to shoulders, arms, especially on the left side, jaw, neck or
teeth, presenting as squeezing, burning, crushing tightness in chest & throat
The consequences of atherosclerosis
Symptoms of atherosclerotic disease most often involve the heart, brain, kidneys & lower
extremities:
 Myocardial infarction- Ischemic heart disease
 cerebral infarction (Transient ischemic attack or stroke)
 Subarachnoid hemorrhage
 peripheral vascular disease (gangrene of legs)
 Aneurysms
Diagnostic investigations:
Physical examination includes:-
o Weak pulse below narrowed area of artery
o Decreased blood pressure in affected area
o Bruits sounds over arteries (heard with stethoscope)
o Poor wound healing in the area where blood flow is restricted
Other investigations
 Blood tests for lipid profile
 ECG
 Chest X-ray.
 Echocardiogram.
 Ankle/brachial Index.
 Angiography.
 Stress testing
 Doppler ultrasound
Medical management:
 Anti-cholesterol medications: Example: Statins. (Atorvastatin, fluvastatin,
Lovastatin).Tab Atorvastatin10mg PO OD.
 Anti-platelet medications: Tab. Aspirin 75mg PO OD., Tab. Clopidogrel 75mg PO OD
 Thrombolytic therapy: Injection streptokinase , Anticoagulants- heparin, warfarin
 Antihypertensive: - Beta blockers: E.g. Metaprolol, Atenolol, propanolol. Tab.
Metaprolol 12.5 mg PO OD, Angiotensin-converting enzyme (ACE) inhibitors: Tab.
Enalapril 2.5mg or 5mg. depending on the blood pressure, Calcium channel blockers:
E.g. Tab. Amlodipine 2.5mg, 5mg or 10 mg dose can be adjusted according to the blood
pressure.
 Diuretics: E.g. Tab. Frusemide 20mg
Surgical management:
 Angioplasty: A catheter is inserted into the blocked or narrowed part of artery a second
catheter with a deflated balloon on its tip is then passed through the catheter to the
narrowed area. The balloon is then inflated, compressing the deposits against artery
walls. A mesh tube (stent) is usually left in the artery to help keep the artery open.
 Endarterectomy: fatty deposits are surgically removed from the walls of a narrowed
artery
 Bypass surgery: using a vessel from another part of your body or a tube made of
synthetic fabric allows blood to flow around the blocked or narrowed artery
Nursing management
Nursing Assessment
History (history of presenting illness, past med-surg history, socio-economic history, family
history, medication history)
Physical examination: Vital signs (Temp. Pulse, Resp. Bp), Peripheral pulses, skin color,
capillary refill, auscultate arteries for bruit sounds
Laboratory; Lipid profiles
Radiology; ECG, ECG
 Chest X-ray.
 Echocardiogram.
 Angiography.
 Doppler ultrasound

Nursing diagnosis
1. Pain related to ischemia evidenced by verbalization
2. Altered peripheral tissue perfusion related to reduced arterial blood flow
3. Activity intolerance related to poor vascular supply evidenced by fatigue
4. Risk-prone health behavior related to unhealthy lifestyle choices (e.g., tobacco use, high
calorie/high sodium intake, overweight)
5. Potential for injury due to reduced sensation
6. Deficient knowledge related to lack of information as evidenced by inaccurate follow-
through of instructions
Planning
Goals
Pain relief
Maximize tissue perfusion
Manage activity within limitations
Reduce risk factors
Educate patient to inspect for injury, watch for trauma
Educate patient to enhance knowledge and to promote self-care
Implementation
To relieve pain
 Pain medication can be administered (may not be effective)
 Dependent position may improve comfort
 Maintain fluid volume; in severe stenosis patient must maintain sufficient blood pressure
to avoid complete occlusion
To manage activity
 Monitor claudication
 Teach patient – pain is not harmful, but a body signal for need to rest
 Emphasize: that exercise increases collateral circulation
 Check with doctor about any exercise progression- should be gradual
To maximize tissue perfusion:
 Administer anti-platelet medications, aspirin to reduce risk of clot formation
 Administer anti-coagulants –heparin to dissolve already formed clots
 Administer calcium channel blockers or nitrates; vasodilators which decrease coronary
spasm
 Monitor pulse, ECG detect ischemia.
Risk factor modification:
 Smoking (most significant risk factor) nicotine causes vasospasms and rapid formation of
plagues
 Low fat diet will retard progression of atherosclerosis by reducing fat deposition in the
vessels & controlling hypertension,
 Advice to exercise regularly to consume extra calories
 Control diabetes & hypertension; the two conditions destroy intimal lining of blood
vessels
 Advice to keep body weight near ideal level to reduce circulating free fats and reduce
adipose tissue also reduces workload in extremities
 Encourage adherence of cholesterol lowering medications and other medications.
 Follow up patients on statins to monitor required lowering cholesterol
 Accompany any prescription of medication with dietary control

To prevent injury
 Change position frequently
 Avoid crossing legs & constrictive clothing
 Meticulous foot care (podiatrist)
 Protect from injury
 Keep extremities warm (no heating blanket or hot water bottles!)

To enhance knowledge
 Educate on the nature of atherosclerosis, its prognosis and ways to control disease
progression
 Explain the risk factors related to atherosclerosis and focus on life style changes
 Educate patients about the effect of smoking on the arterial system.
 Educate on importance of adherence to cholesterol lowering medications and other
medications.
 Advice to maintain visits to assess levels of cholesterol in case the patient is on statins
 Emphasize the importance of dietary modification
Evaluation
Patient reports pain relief
Patient exhibits signs of effective tissue perfusion: -pulses adequate in volume, rate and rhythm,
normal BP, normal capillary refill
Patient keeps to activity and rest program
Patient demonstrates willingness to avoid risk factors: - keeps to an exercise program, talks about
stopping smoking, keeps to a low fat diet etc.
Patient is able to identify causes of injury and how to avoid
The patient describes the disease process, its prognosis and treatment modalities including
medication and dietary modification
Prevention
 Regular medical checkups
 Control of blood pressure
 Check cholesterol
 Don’t smoke.
 Exercise regularly
 Maintain a healthy weight
 Eat a heart-healthy diet
 Manage stress
Prognosis
o If arteriosclerosis is left untreated it can be fatal by leading to a stroke or heart attack
o In diabetics the disease progress is fairly fast
ANEURYSM
An aneurysm is a distention of an artery brought by weakening or destruction of the arterial wall.
An aneurysm is a balloon-like bulge in an artery.
Types of aneurysms
Fusiform or spindle-shaped distensions occur mainly in the abdominal aorta and less commonly
in the iliac arteries.
Saccular aneurysms bulge out on one side of the artery. When they occur on the circulus
arteriosus (circle of Willis) in the brain they are called 'berry' aneurysms. They are due to
defective collagen production, atheromatous changes or congenital.
Dissecting aneurysms occur mainly in the arch of the aorta due to infiltration of blood between
the endothelium and tunica media, beginning at a site of endothelial damage.
Micro aneurysms are fusiform or saccular aneurysms, occurring in small arteries and arterioles
in the brain often associated with hypertension. Recurring small strokes (transient ischemic
attacks) are commonly due to thrombosis or to hemorrhage when an aneurysm ruptures.
Location of aneurysms
1. Aortic aneurysm - There are two types of aortic aneurysm - Abdominal aortic aneurysm
(AAA) and - Thoracic aortic aneurysm (TAA)
 Abdominal Aortic Aneurysms occurs in the abdominal portion of the aorta
Causes: Atherosclerosis, Smoking, Hypertension, Vasculitis (infection in the aorta), Cocaine
use, Genetic factors
 Thoracic Aortic Aneurysms occurs in the chest portion of the aorta (above the
diaphragm)
Causes: Atherosclerosis, smoking, hypertension, vasculitis (infection in the aorta), cocaine use,
genetic factors plus: previous aorta injury, traumatic injury - a vehicle accident or a fall and
Marfan syndrome (genetic disorder of the connective tissue) .
2. Cerebral aneurysm - occurs in an artery in the brain, also are called berry aneurysms because
they're often the size of a small berry.
Causes: Weakness in the artery wall (usually present from birth), Hypertension, Arteriosclerosis
3. Peripheral Aneurysm; Common locations include the popliteal, femoral and carotid arteries.
Clinical manifestation:
Abdominal Aortic Aneurysms:
Throbbing feeling in the abdomen (pulsation of distended abdominal aorta)
Steady, gnawing pain in the abdomen that lasts for hours or days
Deep pain in back or the side of the abdomen,
In case of rupture; 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
In case of rupture or dissection; Sudden, severe, sharp or stabbing pain starting in the upper back
and moving down into the abdomen, pain in chest and arms, shock
Cerebral (brain) aneurysm
Very severe headache that occurs suddenly, nausea vomiting, eyesight problems, seizures (fits),
loss of consciousness, confusion, 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
Risk factors:
 Male gender - Men are more likely than women to have aortic aneurysms.
 Age - Abdominal aortic aneurysms are more likely to occur in people aged 65 or older.
 Smoking - damages and weakens the walls of the aorta.
 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.
 History of aneurysms in the arteries of the legs.
 Certain diseases and conditions that weaken the walls of the aorta such as high BP and
atherosclerosis
 Having a bicuspid aortic valve - can raise the risk of having a thoracic aortic aneurysm. A
bicuspid aortic valve has two leaflets instead of the typical three.
 Car accidents or trauma - also can injure the arteries and increase the risk for aneurysms.
Diagnostic test:
 Abdominal or chest X-ray may show calcification that outlines aneurysm
 Ultrasound and Echocardiography: These tests can show the size of an aortic aneurysm
 Computed Tomography Scan (CT scan): shows the size and shape of an aneurysm.
 Magnetic Resonance Imaging (MRI): detects aneurysms, their size and exact location.
 Angiography: shows the amount of damage and blockage in blood vessels.
Management:
Goals:
 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
Medical management:
Aortic aneurysm:
o Lower blood pressures, relax blood vessels, and lower the risk of rupture
o Beta blockers and calcium channel blockers are commonly used
Cerebral aneurysm:
o Analgesics - usually for headaches
 o Calcium channel blockers - reduce the amount of widening and narrowing of blood
vessels
o Vasopressor - raises blood pressure; widens blood vessels which have remained
stubbornly narrowed. The aim is to prevent stroke.
o Anti-seizure drugs - seizures may occur after an aneurysm has ruptures. Examples
include phenytoin and valproic acid
o A ventricular catheter - this can reduce the pressure on the brain caused by
hydrocephalus (excess cerebrospinal fluid), it drains the excess liquid into an external
bag.
o A shunt system - a shunt (flexible silicone rubber tube) and a valve, a drainage channel
that starts in the brain and ends in the patient's abdominal cavity
o Rehabilitation therapy - sometimes a subarachnoid hemorrhage causes brain damage,
resulting in impaired speech and movements. Rehabilitation therapy helps the patient
relearn vital skills.
Surgical management:
Aortic aneurysms
The two main types of surgery to repair aortic aneurysms are:
I. Open Abdominal or Open Chest Repair: This surgery involves a major incision (cut) in
the abdomen or chest, the aneurysm is removed then, the section of aorta is replaced with
a graft made of material such as Dacronor Teflon
II. Endovascular Repair; the aneurysm is not removed instead a graft is inserted into the
aorta to strengthen it (a stent graft). The graft is then expanded to form a stable channel
for blood flow. The graft reinforces the weakened section of the aorta hence prevents
rupture.
Brain aneurysms: two options if the aneurysm has ruptured:
I. Surgical clipping - the aneurysm is closed off. A tiny metal clip is placed on the neck of
the aneurysm to block off the blood flow to it.
II. Endovascular Repair

Nursing management:
Nursing assessment:
History taking
Physical examination
In 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.
In abdominal aortic aneurysm, assess for abdominal (particular left lower quadrant) pain and
intense lower back pain caused by rapid expansion. Be alert for syncope, tachycardia, and
hypotension which may be followed by fatal hemorrhage due to rupture
Nursing diagnosis:
1. Ineffective tissue perfusion (Vital organs) related to aneurysm or aneurysm rupture
2. Acute pain related to pressure of aneurysm on nerves and postoperatively
3. Risk for infection related to surgery
4. Knowledge deficit related to lack of information
Planing
Goal
 Maintaining perfusion of vital organs
 Pain relief
 Infection prevention
 Provide patient education
Nursing interventions:
To maintain perfusion of vital organs
 Monitor for signs and symptoms of hypovolemic shock
 Administer IV fluids as indicated
 Examine neurovascular distal extremities
 Postoperatively: Monitor vital signs frequently. Assess for signs and symptoms of
bleeding - hypotension, tachycardia, tachypnea, diaphoresis
 Monitor urine output hourly.
To relieve 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.
 If throracoabdominal aneurysm repair has been performed, monitor for signs and
symptoms of spinal cord ischemia: - pain, numbness, paresthesia, weakness
To prevent infection:
 Monitor temperature
 Monitor changes in white blood cell (WBC count)
 Monitor operation site for signs of infection
 Administer antibiotics as ordered
Patient education:
 Instruct about medications to control BP and the importance of taking them
 Discuss disease process and signs and symptoms of expanding aneurysm or impending
rupture, or rupture to be reported
  For postsurgical patient, discuss warning signs of postoperative complications (fever,
inflammation of operative site, bleeding and swelling)
 Encourage adequate balanced diet for wound healing
 Encourage patient to maintain an exercise schedule postoperatively
Evaluation
 Patient demonstrates effective tissue perfusion (normal pulses, BP, capillary refill,
absence of dizziness)
 Patient is pain free ad reports increased comfort
 Patient is free from infection post-surgery
 Patient demonstrates knowledge of disease process and treatment modalities
Prevention
 A large percentage of aneurysms are caused by arteriosclerosis.
 The following steps will help prevent the development of arteriosclerosis and aneurysms:
 Quit smoking
 Keep blood pressure under control
 Keep blood cholesterol levels under control
 Eat a healthy, well balanced diet, rich in fruit and vegetables, unrefined carbohydrate,
dietary fiber, good quality fats, and lean protein
 Keep bodyweight within the ideal limits for height
 Get at least 7 hours of good quality sleep each night
 Keep physically active
Complications
 Haemorrhage 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
 A cerebral aneurysm rupture causes:
 Hemorrhagic stroke, cerebral hematoma
GANGRENE
Gangrene refers to the death of body tissue due to either lack of blood flow or a serious bacterial
infection. Gangrene commonly affects the extremities, including toes, fingers and limbs, but it
can also occur in the muscles and internal organs.
It can also be described as localized cell death due to obstructed circulation with severe bacterial
infection.
Causes
o Lack of blood supply; blood provides oxygen, nutrients to the body cells, and immune
system components, such as antibodies. Without a proper blood supply, cells will die
o Severe bacterial infection; if bacteria thrive unchecked for long, tissue death can occur
o Trauma such as gunshot wounds or crushing injuries from car crashes can cause bacteria
to invade tissues deep within the body leading to gangrene
Risk factors
o Diabetes: high blood sugar levels can damage blood vessels, decreasing or interrupting
blood flow
o Blood vessel disease: hardened and narrowed arteries (arteriosclerosis/atherosclerosis)
and blood clots also can block blood flow
o Severe injury or surgery: trauma to the skin and underlying tissue, including frostbite,
increases the risk of developing gangrene, especially with an underlying condition that
affects blood flow to the injured area.
o Smoking: people who smoke have a higher risk of gangrene-nicotine damages vessels
o Obesity: Obesity often accompanies diabetes and vascular disease, but the stress of extra
weight alone can also compress arteries, leading to reduced blood flow and increasing the
risk of infection and poor wound healing.
o Immunosuppression: HIV infection, chemotherapy or radiation therapy reduces the
ability to fight off infections
o Medications or drugs that are injected: In rare instances, certain medications and illegal
drugs that are injected have been shown to cause infection with bacteria that cause
gangrene.
Types of gangrene
1. Dry gangrene
 Dry gangrene is characterized by dry and wrinkled/shrunken skin ranging in color from
brown to purplish blue or black.
 It may develop slowly, occurs most commonly in people who have arterial blood vessel
disease, such as atherosclerosis, or diabetes.
2. Wet gangrene
 Gangrene is referred to as "wet" if there is a bacterial infection in the affected tissue
 Swelling, blistering and a wet appearance are common features of wet gangrene
 It may develop after a severe burn, frostbite or injury
 It often occurs in people with diabetes who unknowingly injure a toe or foot
 Wet gangrene needs immediate treatment because it spreads quickly and can be fatal
3. Gas gangrene
  Gas gangrene typically affects deep muscle tissue; skin appears to have bubbles and
makes a crackling sound when pressed because of the gas within the tissue
 Commonly caused by infection with the bacterium Clostridium perfringens common in
injuries or surgical wound that lack blood supply
 The bacterial infection produces toxins that release gas causing tissue death
 Like wet gangrene, gas gangrene can be life-threatening
4. Internal gangrene
 Affects internal organs, such as intestines, gallbladder or appendix
 Occurs when blood flow to an internal organ is blocked — for example hernia
 Internal gangrene may cause fever and severe pain
 Left untreated, internal gangrene can be fatal

5. Fournier’s gangrene
 Involves the genital organs; men are more often affected, but women can develop this
type of gangrene as well
 It arises due to an infection in the genital area or urinary tract and causes genital pain,
tenderness, redness and swelling
6. Progressive bacterial synergistic gangrene (Meleney's gangrene).
 Rare type of gangrene typically occurs after an operation, with painful skin lesions
developing one to two weeks after surgery.

Pathophysiology
Inadequate exchange of oxygen and other nutrients in the tissue leads to metabolic abnormality.
When cellular metabolism cannot maintain energy balance, cell death (necrosis) occurs.
Alterations in blood vessels at the arterial, capillary, and venous levels may affect cellular
processes and lead to the formation of ulcers
Signs and symptoms
 Skin discoloration — ranging from pale to blue, purple, black, bronze or red,
depending on the type of gangrene
 Swelling or the formation of blisters filled with fluid on the skin
 A clear line between healthy and damaged skin
 Sudden, severe pain followed by a feeling of numbness
 A foul-smelling discharge leaking from a sore
 Thin, shiny skin, or skin without hair
 Skin that feels cool or cold to the touch
 gangrene affecting tissues beneath the surface of the skin, such as gas gangrene or
internal gangrene presents with swelling, severe pain and low-grade fever
  Septic shock can occur if a bacterial infection spreads throughout the body. Signs and
symptoms of septic shock include: low blood pressure, fever, in some cases -
hypothermia, rapid heart rate, lightheadedness, shortness of breath, confusion
Diagnostic Tests
 Abnormally elevated white blood cell count often indicates the presence of an infection.
 Blood culture to isolate infective organism
 Imaging tests; An X-ray, a computerized tomography (CT) scan or a magnetic resonance
imaging (MRI) to view interior body structures and assess the extent to which gangrene
has spread and to visualize any gas that is present under the skin.
 An arteriogram is done by injecting a dye into the bloodstream and X-ray pictures are
taken to determine the blood flow through the arteries.
 Surgery may be performed to determine the extent to which gangrene has spread
 Fluid or tissue culture from a blister for the bacterium Clostridium perfringens, a
common cause of gas gangrene,
 Tissue biopsy for microscopy to determine cell death
Management
 Surgery to remove dead tissue, which helps stop gangrene from spreading and allows
healthy tissue to heal (surgical debridement)
 Repair of damaged blood vessels in order to increase blood flow to the affected area
occasionally, more than one surgery may be required to remove all dead or infected
tissue.
 Reconstructive surgery through skin graft when adequate blood supply has been restored
 Severe cases of gangrene of a toe, finger or limb, may require amputation
 In some cases, the patient will be fitted with an artificial limb (prosthesis).
 Following culture results suitable antibiotics are administered
 Hyperbaric oxygen therapy: patient is placed in a pressurized chamber with pure oxygen,
and the pressure inside the chamber will slowly rise to about 2.5 times normal
atmospheric pressure. This helps in destroying anaerobic bacteria such as Clostridium
perfringens
 Other treatments: supportive care, fluids, nutrients and pain medication to relieve
discomfort.
Nursing management
Nursing Assessment
o Complete history
o Physical examination
o Laboratory and radiological investigations
Nursing Diagnoses
1. Pain related to tissue ischemia
2. Anticipatory grieving related to potential loss of limb evidenced by verbalization
 3. Body image disturbance related to loss of body part evidenced by verbalization

Planning
Goal
Alleviate pain
Lead through anticipatory grieving
Discuss body image and options
Implementation
To alleviate pain
o Administer analgesics such as acetaminophen to relieve pain
o Administer antibiotics to treat bacterial infection, this will reduce inflammation and
promote comfort
To address concerns on anticipatory grieving
o The nurse creates an accepting and supportive atmosphere in which the patient and
family are encouraged to express and share their feelings and work through the grief
process.
o The support from family and friends promotes the patient’s acceptance of the loss.
o Help the patient deal with immediate needs and introduce subjects on rehabilitation and
future independent functioning.
o Refer for Mental health and support group
Evaluation
o Patient reports minimal or no pain
o Patient freely expresses concerns about going through amputation
o Patient develops better coping with body image
Complications
 Gangrene can lead to scarring or the need for reconstructive surgery
 Sometimes, the amount of tissue death is so extensive that requires amputation
 Gangrene that is infected with bacteria can spread quickly to other organs and may be
fatal if left untreated.
Prevention
 Care for diabetes; examine hands and feet daily for cuts, sores and signs of infection,
such as redness, swelling or drainage
 Control blood sugar levels
 Maintain low body weight. Excess weight is a risk factor to diabetes and also places
pressure on arteries, constricting blood flow, risk of infection and slow wound healing
 Stop use of tobacco
 Wash any open wounds with a mild soap and water and keep them clean and dry
  Frostbite reduces blood circulation in an affected area; avoid prolonged exposure to cold
temperatures such as ice.

VARICOSE VEIN
Definition
Varicose veins are defined as dilated, elongated, tortuous and palpable superficial veins as a
result of incompetent valve closure, which results in venous congestion and vein enlargement.
Usually affects the saphenous vein and its branches but can affect other veins.
The vein is so dilated that the valves do not close to prevent backward flow of blood. Such veins
lose their elasticity, become elongated and tortuous and fibrous tissue replaces the tunica media.
Venous System of lower limb Consists of:
 Deep veins which lie below the deep fascia
 Superficial veins which lie outside the deep fascia (carry 10% blood)
 Perforating veins which pass through the deep fascia joining the superficial to the deep
veins
Valves present in superficial veins prevent flow of blood from proximal to distal and from deep
to superficial veins, valves are absent from above groin level
Valves can resist pressure up to 300 mmHg.
Factors helping in venous return
 Negative pressure in thorax during inspiration
 Calf muscle pump: calf muscle contraction helps in pumping blood in the veins
 Arterial pressure transmitted to venous side through capillary bed
 Competent valves ensure forward movement of blood
 Veins lie by the side of arteries, arterial pulsation helps to propel blood in the veins
Sites and effects of varicose veins
Varicose veins of the legs
The great and small saphenous veins and the anterior tibial veins are most commonly affected
causing aching and fatigue of the legs especially during long periods of standing.
 If injured can rupture and cause hemorrhage
 The skin over a varicose vein may become poorly nourished due to stasis of blood,
leading to the formation of varicose ulcers usually on the medial aspects of the leg just
above the ankle.
Haemorrhoids
Sustained pressure on the veins at the junction of the rectum and anus leads to increased venous
pressure, valvular incompetence and the development of hemorrhoids
Common causes are chronic constipation, and the increased pressure in the pelvis towards the
end of pregnancy.
Slight bleeding may occur with passage of stools causing anemia.
Scrotal varicocele
Common in men whose work requires standing for long periods
In bilateral varicocele the increased temperature due to venous congestion may cause depressed
spermatogenesis and result in infertility.
Oesophageal varices
The venous pressure in the liver rises due to liver cirrhosis and right-sided cardiac failure,
pressure rises in the anastomosing veins between the left gastric vein and the azygos vein
causing varicosities to develop in the lower end of the esophagus
Rupture causes severe hemorrhage, and possibly death.
Reticular type and Web type (spider veins) varicose vein
Etiology/predisposing factors
 Long hours of standing, which increase the hydrostatic pressure of gravity, nurses have
higher risk of getting varicose veins
 Heredity: familial tendency but no abnormal genetic factor has been identified
 Gender; females are affected more than males, especially following pregnancy.
 Pregnancy
 Age: there is progressive loss of elasticity in the vein walls with increasing age
 Previous or existing deep vein thrombosis
 Oral contraceptives
 Obesity; superficial veins in the limbs are supported by subcutaneous areolar tissue;
excess adipose tissue may not provide sufficient support.
 Heavy physical activity - gym and boxing
 Lifting heavy object frequently - lifting heavy object would give pressure to both arms
and hands
 Gravity; standing for long periods with little muscle contraction tends to cause pooling of
blood in the lower limbs and pelvis.
 Pressure: veins have thin wall easily compressed by surrounding structures, leading to
increased venous pressure distal to the site of compression
Pathophysiology
Any risk factor or cause will increase venous pressure leading to dilation of veins, valves stretch
and become incompetent, blood reverses back causing further venous distension
Clinical manifestation
 Enlarged veins that are visible on skin causing cosmetic disfigurement
 Dull aches, muscle cramps, and increased muscle fatigue in the lower legs
 Ankle edema and a feeling of heaviness of the legs
 Nocturnal cramps
 Itchy legs, especially in the lower leg and ankle
 Throbbing or cramping in legs
 Discoloration of skin surrounding the varicose veins
Diagnosis
History - Complaints of leg pain, aching, heaviness or fatigue; ankle swelling; history of venous
thrombosis
Physical examination - Visible, dilated, tortuous superficial veins in lower extremities
Investigation:
 Duplex Ultrasound - A non-invasive evaluation of blood flow, measures severity of
valvular reflux
 Trendelenburg test - To determine the underlying cause of superficial venous
insufficiency
 Venography
Conservative management
 Avoiding prolonged standing
 Compression stockings: Crepe bandaging and elastic stockings from toe to thigh, which
reduces edema and reflux and increases venous return
 Elevate limb above the level of heart while lying to facilitate venous return by gravity
 Avoid cross-leg while sitting
 Exercise
 Lose weight
Medical management
Sclerotherapy: injection of a solution (generally salt solution) directly into the vein. The solution
irritates the lining of the blood vessel causing it to collapse and stick together (inducing phlebitis
and fibrosis); blood also clots
Surgical management:
 Ligation and stripping: small incision is made through the skin, the vein is accessed and
tied to prevent pooling of blood
 Radiofrequency ablation: a small cut is made above or below the knee; a catheter is
guided into the vein using an ultrasound scan. A probe is inserted into the catheter that
sends out radiofrequency energy which heats the vein until its walls collapse, closing it
and sealing it. Blood will naturally be redirected to the healthy veins
Nursing management
Assessment
 History - Complaints of leg pain, aching, heaviness or fatigue; ankle swelling; history of
venous thrombosis
 Physical examination - Visible, dilated, tortuous superficial veins in lower extremities
 Investigation :
 Duplex Ultrasound - A non-invasive evaluation of blood flow, measures severity of
valvular reflux
Diagnosis
1. Impaired blood circulation related to venous insufficiency
2. Pain related to tissue ischemia as evidenced by leg pain, aching
 3. Body image disturbance related to tortuous veins visible on lower limbs
Planning
Goals
Improve venous return from peripheral tissue
Relieve pain
Improve perception of body image
Implementation
To improve venous return
 Assess peripheral pulses; capillary refill, skin color, and temperature every 4 hourly to
obtain baseline data
 Assess pain in extremities; use numerical pain scale to evaluate severity to plan for pain
management
 Teach application and use of properly fitted elastic graduated compression stockings;
these compress the veins, promoting venous return from the lower extremities
 Instruct patient to perform regular exercise, such as walking for 20-30 minutes several
times a day to maintain muscle tone, joint mobility, and venous return
 Advice patient to elevate the legs for 15 to 20 minutes several times a day and to sleep
with the legs elevated above the level of the heart to promote venous return
 Encourage patient to wear socks during night time to keep extremities warm this
maintains vasodilatation and increases blood supply
 Advice patient to avoid crossing legs when sitting to prevent impairment of blood flow to
distal tissues
 Advice patient to reduce weight because obesity can cause pressure to lower limbs
 Educate patient about sign & symptom of cellulitis such as severe redness, pain &
increased swelling in the extremities
To relieve pain
Administer acetaminophen or ibuprofen analgesics that manage mild to moderate pain
Elevate the limb to relieve tissue congestion
To improve perception of body image
Discuss possibilities of surgical removal of the tortuous veins
Compression stockings will reduce engorgement
Offer psychological counselling
Evaluation
Adequate venous return from peripheral tissue as evidenced by normal capillary refill, pinkish
and warm skin
Patient verbalizes pain relief and improved comfort
Patient verbalizes worrying less about the site of varicose veins
Complications
  Bleeding
 Thrombophlebitis
 Venous hypertension leading to venous ulcer
 Calcification
 Eczematoid dermatitis and pigmentation

Terminologies:
Thrombosis
A clot forms in the blood vessel
Phlebothrombosis
Development of clot within a vein without inflammation
Thrombophlebitis
Development of clot within an inflamed vein
Embolism
A moving mass (clot) of particles, either solid or gas, in the bloodstream
Thrombophlebitis - a thrombus accompanied by inflammation of the vein (phlebitis). •
Phlebothrombosis - refers to a thrombus with minimal inflammation.
Thromboembolism
Dislodgment and migration of a thrombus, common in phlebothrombosis

PHLEBITIS

Phlebitis is the inflammation of a vein categorized as chemical, mechanical, or bacterial. Two or

more of these types of irritation can occur simultaneously.

 Chemical phlebitis can be caused by an irritating medication or solution (increased pH),

rapid infusion rates, and medication incompatibilities.
 Mechanical phlebitis results from long periods of cannulation, catheters in flexed areas,
catheter gauges larger than the vein lumen, and poorly secured catheters.
 Bacterial phlebitis can develop from poor hand hygiene, lack of aseptic technique, failure
to recognize early signs and symptoms of phlebitis.
Other factors; poor venipuncture technique, catheter in place for a prolonged period, and failure
to adequately secure the catheter
Clinical features
Redness
Warmth area around the insertion site or along the path of the vein,
Pain or tenderness at the site or along the vein, and swelling
Grading of phlebitis
Phlebitis is graded according to the most severe presenting indication.
0 No clinical symptoms
1 Erythema at access site with or without pain
2 Pain at access site Erythema, edema, or both
3 Pain at access site, erythema, edema, or both. Streak formation, palpable venous cord (1 inch
or shorter)
4 Pain at access site with erythema, streak formation, palpable venous cord (longer than 1 inch)
purulent drainage

DEEP VENOUS THROMBOSIS

Definition
Deep vein thrombosis is the formation of a blood clot in one of the deep veins of the body,
usually in the leg.
Deep vein thrombosis and pulmonary embolism collectively make up the condition known as
venous thromboembolism
Etiology:
Virchow's triad describes three factors that contribute to thrombosis: Venous stasis,
Hypercoagulability and Endothelial Injury
1. Venous Stasis
 Prolonged bed rest (4 days or more)
 A cast on the leg
 Limb paralysis from stroke
 Spinal cord injury
 Extended travel in a vehicle
 Age (greater than 65 yrs.)

2. Hypercoagulability
 Surgery and trauma
 Malignancy
 Increased estrogen
 Inherited disorders of coagulation
 Acquired disorders of coagulation

3. Endothelial injury
  Trauma
 Surgery
 Wires connecting to artificial cardiac pacemaker
 Catheters used in dialysis
 Repetitive motion injury
 Central venous catheters: subclavian and internal jugular lines; these lines cause upper
extremity DVT
Pathophysiology
Vessel trauma stimulates the clotting cascade. Platelets aggregate at the point of venous stasis;
platelets and fibrin form the initial thrombus (clot). Red blood cells are trapped in the fibrin
meshwork. The thrombus spreads in the direction of the blood flow. Inflammation is triggered,
causing tenderness, swelling, and erythema. Pieces of thrombus may break loose and travel
through circulation- (emboli). Fibroblasts eventually invade the thrombus, scarring vein wall and
destroying valves. Vessel patency may be restored but valve damage is permanent, affecting
directional flow.
Common clinical manifestations
 Calf pain or tenderness due to ischemia
 Extremities become pale, cold,
 Arterial pulsation is absent
 Numbness, tingling, cramping,
 Swelling with pitting oedema
 Increased skin temperature and fever
 Superficial venous dilatation
 Cyanosis can occur with severe obstruction
Less frequent manifestations of venous thrombosis: - Venous gangrene

Phlegmasia alba dolens: thrombosis is only in major deep veins sparing collateral veins
Phlegmasia cerulea dolens: thrombosis extends to collateral veins.
Clinical examination
 Palpate distal pulses and evaluate capillary refill to assess limb perfusion
 Move and palpate all joints to detect acute arthritis or other joint pathology
 Neurologic evaluation may detect nerve root irritation; sensory, motor, and reflex deficits
should be noted
 Homans sign: pain in the posterior calf or knee with forced dorsiflexion of the foot.
 Lintons sign/Trendelenburg test: After applying torniquet at saphenofemoral junction the
patient is allowed to walk for a short distance, then the limb is elevated in supine position
prominent superficial veins will be observed.
  Moses Sign also known as Bancroft's sign: Patient should be prone during this
examination, knee flexed 90 degrees. The examiner gently squeezes the lower part of the
calf from side to side and observes patient for signs of discomfort and pain.
Diagnostic studies
o Clinical examination alone is able to confirm only 20-30% of cases of DVT
o Blood Tests: the D-dimer
o Imaging studies: venography, radiolabeled fibrinogen, ultrasound, plethysmography,
MRI. Plethysmography measures change in lower extremity volume in response to
certain stimuli.
o Nuclear Medicine Studies
o Because the radioactive isotope incorporates into a growing thrombus, this test can
distinguish new clot from an old clot
Management
The primary objectives of the treatment of DVT are to - prevent pulmonary embolism, reduce
morbidity, and prevent or minimize the risk of developing the postphlebitic syndrome.
General therapeutic measures:
o Bed rest
o Encourage the patient to perform gentle foot & leg exercises every hour
o Increase fluid intake upto 2 L/day unless contraindicated
o Avoid deep palpation

Specific treatment
o Anticoagulation
o Thrombolytic therapy
o Surgery
o Filters
o Compression stockings
o Initial treatment of DVT is with low molecular-weight heparin or unfractionated heparin
for at least 5 days, followed by warfarin (target INR, 2.0–3.0) for at least 3 months.
Surgery
Indications: - when anticoagulant therapy is ineffective, unsafe or contraindicated.
Thrombectomy: this mechanical method of clot removal may involve using intraluminal
catheter with a balloon or other devices. The clots are broken and removed.
A vena cava filter may be placed at the time of thrombectomy; this filter traps large emboli &
prevents pulmonary embolism. Where there is chronic iliac vein compression, balloon
angioplasty with stent placement may successfully treat the patients.
Nursing management
The aim of nursing management of DVT is to prevent DVT in high risk patient, to prevent
existing thrombi from becoming emboli and prevent new thrombi from forming and to monitor
anticoagulant therapy.
Nursing Assessment
Presenting signs and symptoms; if a patient presents with signs and symptoms of DVT, carry out
an assessment of general medical history and a physical examination to exclude other causes.
Nursing Diagnosis
1. Ineffective tissue perfusion related to interruption of venous blood flow
2. Impaired comfort related to vascular inflammation and irritation
3. Deficient knowledge regarding pathophysiology of condition related to lack of
information and misinterpretation
4. Risk for bleeding related to chronic use of anticoagulant therapy
Planning
Goal

 Client will maintain optimal peripheral tissue perfusion in the affected extremity, as
evidenced by strong palpable pulses, reduction in and/or absence of pain, warm, and dry
extremities, and adequate capillary refill.
 Client will report that pain or discomfort is alleviated or controlled.
 Client and/or significant others will verbalize understanding of the disease, treatment, and
prevention.
 Client will not develop bleeding while on anticoagulant therapy
To improve tissue perfusion
 Assess for contributing factors: Central venous catheters, Dehydration, History of
varicosities, Immobility, Leg trauma and surgery, Malignancy, Obesity, Oral
contraceptive use, Pregnancy, Smoking, Venous stasis
 Most clients with DVT are asymptomatic; knowledge of high-risk situations helps in
early detection.
 Assess for the signs and symptoms of deep vein thrombosis (DVT)
 Measure the circumference of the affected leg with a tape measure. Deep vein thrombosis
is suspected if there is a difference of >3 cm between the extremities.
 Maintain adequate hydration to prevent an increased viscosity of blood, which
contributes to venous stasis and clotting.
 Encourage bedrest and keep the affected leg elevated above the heart to decrease
swelling.
 Provide warm, moist heat to the affected site to promote comfort and reduce
inflammation.
 Apply below-knee compression stockings. Ensure that the stockings are the correct size
and are applied correctly; these provide a graduated pressure on the affected leg to help
 return the venous blood to the heart. Inaccurately applied stockings can serve as a
tourniquet and can promote clot formation.
 Administer anticoagulants (heparin/warfarin [Coumadin]) as prescribed to prevent the
formation of new clots by decreasing the normal activity of the clotting mechanism.
Heparin IV or subcutaneous low-molecular-weight heparin is started initially. Oral
anticoagulant therapy (warfarin) will be initiated while the client is still receiving heparin
because the onset of action for warfarin can be up to 72 hours. Heparin will be
discontinued once the warfarin reaches therapeutic levels.
 Monitor for pulmonary embolism- acute and lethal complication of DVT. Manifestations
are: - tachypnea and anxiety, cough without hemoptysis, diaphoresis, dyspnea, crackles
and wheezing.
To improve comfort
 Assess degree and characteristics of discomfort and pain
 Investigate sudden sharp chest pain, dyspnea, tachycardia, and restlessness, or new pain;
these may suggest pulmonary embolism as a complication of DVT.
 Monitor vital signs, noting increased temperature; elevations in heart rate may indicate
discomfort, fever and inflammatory process
 Maintain bed rest during the acute phase to decrease discomfort associated with muscle
contraction and movement
 Encourage client to change position frequently to reduce muscle fatigue, minimize
muscle spasm and maximize circulation to tissues.
 Provide foot cradle to keep the pressure of bedclothes off the affected leg, thereby
reducing pressure discomfort
 Elevation of the legs above the level of heart facilitates blood flow by force of gravity
preventing venous stasis and formation of new thrombi and reduces edema
 Elevate foot of the bed 6 inches (Trendelenburg’s position), with a slight knee bend to
prevent popliteal pressure.
 Apply a warm compress to the affected leg using a 2-hour-on, 2-hour-off schedule around
the clock to relieve pain and improve circulation through vasodilation.
 Administer opioid and non-opioid analgesics to relieve pain and decrease muscle tension
 Administer antipyretics (Acetaminophen) to reduce fever and inflammation
To enhance knowledge regarding pathophysiology and management of the condition
 Assess the client’s understanding of the causes, treatment, and prevention plan
 Instruct in the following signs of pulmonary embolus: Restlessness, Shortness of
breath, sudden chest pain, Tachycardia, Tachypnea
 Instruct on correct medication explaining, dosages and side effects
 Inform on need for regular laboratory testing while on oral anticoagulation
 Discuss and give the client a list of signs and symptoms of excessive anticoagulation
 Provide teaching regarding the safety measures while on anticoagulant therapy such
as the use of an electric razor, soft toothbrush.
  Instruct the client to avoid rubbing or massaging the calf
 Instruct on the correct application of compression stockings

To reduce risk of bleeding

 Monitor anticoagulant therapy through blood sampling every 4-8 hrs. for bleeding time,
PTT, INR & PT.
 Observe for frank bleeding in the urine, tarry or frank blood in the stool,
 bleeding with brushing the teeth,
 Easy subcutaneous bruising and frank pain.
 If invasive studies are necessary e.g., ABG, apply pressure for 30 min at puncture site.
HYPERTENSION
Hypertension is defined as a systolic blood pressure greater than 140 mm Hg and a diastolic
pressure greater than 90 mm Hg, based on two or more measurements taken while seated during
each of two or more outpatient visits.
Classification:
• Normal: systolic less than 120 mm Hg; diastolic less than 80 mm Hg
• Prehypertension: systolic 120 to 139 mm Hg; diastolic 80 to 89 mm Hg
• Stage 1: systolic 140 to 159 mm Hg; diastolic 90 to 99 mm Hg
• Stage 2: systolic >160 mm Hg; diastolic >100 mm Hg
Hypertension is a major risk factor for:
o Atherosclerosis
o Heart failure
o Stroke
o Kidney failure
Prolonged blood pressure elevation damages blood vessels in target organs (heart, kidneys, brain,
and eyes).
Classification of hypertension
1. Essential Hypertension
Also known as Primary or Idiopathic
Account for 90% to 95% of all cases of hypertension
No identifiable medical cause;
It occurs due to
 Familial tendency
 Genetic
 Advancing age
 Diabetes
 High intake of sodium, saturated fats, or alcohol
 Obesity
 Sedentary lifestyle
 Smoking
 Stress
  Increased peripheral resistance and/or increased cardiac output
 increased sympathetic stimulation,
 increased renal water and sodium reabsorption,
 increased renin–angiotensin–aldosterone system activity,
 Decreased vasodilation of the arterioles, or resistance to insulin action.
2. Secondary Hypertension
Secondary hypertension is characterized by elevations in blood pressure with a specific cause
which include
 Adrenal gland tumor
 Arteriosclerosis
 Congenital narrowing (coarctation) of the aorta
 Cushing syndrome
 Hyperaldosteronism (adrenal glands produce an excess of aldosterone)
 Kidney disease (such as glomerulonephritis[inflammation of kidneys]
 renal failure, renal artery stenosis, and renal vascular obstruction
 Medications (such as appetite suppressants, certain cold medications, corticosteroids,
migraine medications, and oral contraceptives)
 Pregnancy (called gestational hypertension)
Clinical Manifestations
Often, a person with hypertension will have no symptoms. If present, signs and symptoms may
include:
 Blurred vision
 Confusion
 Dizziness
 Ear noise or buzzing
 Irregular heart beat
 Nocturia
 Nosebleed
 Papilledema (swelling of the optic disc)
 Headache

Hypertensive Crisis/Urgency
Hypertensive crisis, or hypertensive emergency, an elevated blood pressure must be lowered
immediately (not necessarily to less than 140/90 mm Hg) to halt or prevent target organ damage.
Hypertensive urgency; blood pressure is very elevated but there is no evidence of impending or
progressive target organ damage.
The following drugs are administered to normalize blood pressure within 24 to 48 hours
 Beta-adrenergic blocking agents e.g., labetalol
 ACE inhibitors e.g., captopril
 Alpha2-agonists e.g., clonidine
Monitoring of the patient’s blood pressure and cardiovascular status, vital signs frequently
Hypertensive emergencies and urgencies may occur in:
i. poorly controlled hypertension,
ii. undiagnosed hypertension,
iii. abrupt discontinuation of antihypertensive medications

Clinical findings
 Coronary artery disease with angina or myocardial infarction
 Left ventricular hypertrophy; heart failure.
 Kidneys -nocturia and increased BUN and creatinine levels
 Cerebrovascular -stroke or transient ischemic attack (TIA) i.e., alterations in vision or
speech, dizziness, weakness, a sudden fall, or transient or permanent hemiplegia

Assessment and Diagnostic Methods

History
Physical examination
Laboratory studies
Urinalysis for blood, protein and glucose
Blood urea, electrolytes and creatinine
Blood glucose
Serum total and HDL cholesterol
Creatinine clearance, renin level, 24-hour urine protein
Radiological studies
ECG and echocardiography to assess left ventricular hypertrophy and coronary artery disease
Chest x-ray may reveal cardiomegaly
Medical Management
Goal; to prevent death and complications by achieving BP at or below 140/90 mm Hg a lower
goal pressure of 130/80 mm Hg for people with diabetes mellitus or chronic kidney disease
 Nonpharmacological; weight reduction; restriction of alcohol and sodium; regular
exercise and relaxation, reducing coffee intake, quitting smoking
 DASH (Dietary Approaches to Stop Hypertension) high in fruits, vegetables, eating oily
fish and adopting a diet that is low in saturated fat
 Drug with greatest effectiveness, fewest side effects, and best chance of acceptance
 Two classes of drugs are available as first-line therapy: diuretics and beta-blockers
 Promote compliance by avoiding complicated drug schedules
Drugs
1. Angiotensin Converting Enzyme Inhibitor (ACE I) reduces peripheral vascular resistance
e.g. enalapril
2. Angiotensin Receptor Blockers (ARB) reduces peripheral vascular resistance e.g.
lorsatan
 3. Beta Blocker decrease heart rate and force of contraction e.g. atenolol
4. Calcium channel blocker reduces peripheral vascular resistance e.g. nifedipine
5. Central α2-Blockers Block alpha receptor e.g. Methyldopa (Aldomet)
6. Diuretics reduce circulating fluid volume e.g. furosemide-lasix
7. Direct Arterial Vasodilators reduce after load e.g. Hydralazine (Apresoline)
8. Long-Acting Nitrates reduce after load e.g. Isosorbide mononitrate
9. Peripheral Selective α1 -Blockers reduce after load e.g. Doxazosin, Prazosin, Terazosin
Nursing Management
Assessment
 Monitor blood pressure regularly
 Dietary habits and salt intake
 Assess for signs and symptoms of target organ damage (e.g., angina pain; shortness of
breath; alterations in speech, vision, or balance; nosebleeds; headaches; dizziness; or
nocturia).
 Target organ disease or other disease processes that may place the patient in a high-risk
group at diabetes, CAD, kidney disease
 Cigarette smoking
 Episodes of headache, weakness, muscle cramp, tingling, palpitations, sweating, vision
disturbances
 Medication that could elevate BP: hormonal contraceptives, steroids, NSAIDs, nasal
decongestants, appetite suppressants, tricyclic antidepressants
 Assess extent to which hypertension has affected patient personally, socially, or
financially.
 Other disease processes, such as gout, migraines, asthma, heart failure, and benign
prostatic hyperplasia, which may be helped or worsened by particular hypertension drugs

Nursing Diagnoses
1. Deficient knowledge regarding the relationship between the treatment regimen and
control of the disease process
2. Noncompliance with therapeutic regimen related to side effects of prescribed therapy
Planning
Goals
Understanding of the disease process and its treatment,
Participation in a self-care program,
Absence of complications
Nursing Interventions
Increasing Knowledge
 Explain the meaning of high BP, risk factors, and their influences on the cardiovascular,
cerebral, and renal systems.
 Inform that hypertension is chronic and requires persistent therapy and periodic
evaluation. Effective treatment improves life expectancy; this requires mandatory follow-
up visits.
  Explain the pharmacologic control of hypertension – drugs used will likely produce
adverse effects. – Possibility orthostatic hypotension initially with some drugs, initial
effects such as anorexia, light-headedness, and fatigue, with many medications
 Inform the patient that the goal of treatment is to control BP, reduce the possibility of
complications, and use the minimum number of drugs with the lowest dosage necessary
 Note that dosages are individualized; therefore, they may need to be adjusted because it is
often impossible to predict reactions
 Warn patients that BP is often decreased in dehydration, diarrhea, hemorrhage etc. so BP
should be monitored closely and treatment adjusted.
Encouraging Self- Management
 Ensure the patient's cooperation in redirecting lifestyle in keeping with the guidelines of
therapy, acknowledge the difficulty, and provide support and encouragement
 Plan the patient's medication schedule so that the many medications are given at proper
and convenient times; set up a daily checklist on which the patient can record the
medication taken
 Ensure the patient knows the generic and brand names for all medications and throws
away old medications and dosages so they will not be mixed up with current medications.
 Instruct on proper method of taking BP at home and at work. Inform patient of desired
range and the readings, assist with social support including family members
 Determine recommended dietary plans and provide dietary education as appropriate.
Involve a dietitian to help develop a plan for improving nutrient intake or for weight loss
 Emphasize controlling hypertension with lifestyle changes and medications.
 Advise patient to limit alcohol intake and avoid use of tobacco.
 Recommend support groups for weight control, smoking cessation, and stress reduction
 Assist to develop and adhere to an appropriate exercise regimen.
 Inform about rebound hypertension if medications are suddenly stopped
 Advice on adequate supply of medication
 Medications such as beta blockers may cause sexual dysfunction, provide alternatives
 Advice on when and whom to call if problems arise or information is needed.
Monitoring and Managing Potential Complications
 Assess all body systems during follow-up care to detect evidence of vascular damage
 Question patient about blurred vision, spots, or diminished visual acuity
 Report significant findings promptly for timely studies or changes in medications
Evaluation
 Maintains adequate tissue perfusion
 Complies with self-care program
 Experiences no complications

Potential Complications
• Left ventricular hypertrophy
• Myocardial infarction
• Heart failure
• Transient Ischemic Attack-TIA
• Cerebrovascular accident-CVA
• Renal insufficiency and failure
• Retinal hemorrhage causing vision impairment