CARDIOVASCULAR

DISORDERS
Selline Mukabi
MAIN OBJECTIVE
• The student will acquire appropriate
knowledge, skills and attitude for nursing pts
with cardiac disorders using the nursing
process.
• Be able to manage patients suffering from
vascular disorders using the nursing process.
Cardiac disorders
• Hypertension
• Congestive heart failure
• Rheumatic heart disease
• Coronary heart disease
• Cardiomyopathy
• Dysarhythmias
 CONTENT
Coronary vascular disorders
• Coronary Atherosclerosis
• Angina pectoris
• Myocardial infarction
Vulvular disorders
• Mitral valve prolapse
• Mitral regurgitation
• Mitral stenosis
• Aortic regurgitation
• Aortic stenosis
Infectious diseases of the heart

• Rheumatic Endocarditis
• Infective Endocarditis
• Myocarditis
• Pericarditis
Complications from heart disease
• Heart failure
• Pulmonary edema
• Cardiogenic shock
• Thromboembolism
• Pericardial effusion
• Cardiac Tamponade
• Cardiac Arrest
Vascular disorders- Arterial disorders

• Arteriosclerosis & Atherosclerosis

• Peripheral arterial occlusive disease
• Thrombo angiitis Obliterans (Buerger’s
disease)
• Aortitis
• Aortoiliac disease
• Aneurysm
• Dissecting aorta
• Arterial embolism and arterial thrombosis
• Raynaud’s disease
Venous disorders

• Venous thrombosis, Deep vein thrombosis,

Thrombophlebitis & Phlebothrombosis
• Chronic venous insufficiency
• Varicose veins

• Cor pulmonale
• Hypertension
• Hypertension crisis
• Prevention of cardiovascular disorders in the
community
Disorders to be covered under the following
subheadings:
• Definition
• Types
• Aetiology/predisposing factors
• Pathophysiology
• Clinical features
• Diagnosis
• Treatment
• Prognosis , complications and prevention
• Nursing care
Assignment
 Review Anatomy and physiology of the heart
and blood vessels

 Read and hand in your work on: Epidemiology,

factors contributing to cardiovascular
disorders and prevention of cardiovascular
disorders in the community
 HYPERTENSION
Definition
• A systolic blood pressure greater than 140
mmHg and a diastolic pressure greater than
90 mm Hg based on the average of two or
more accurate blood pressure measurements
taken during two or more contacts with a
health care provider
• Blood pressure is elevated when there is
increased cardiac output plus increased
peripheral resistance
 Types
Primary/essential hypertension- high blood
pressure from unidentified cause(95% of pts
with hypertension)
Secondary hypertension- high blood pressure
related to identified causes (5% of pts with
hypertension)
 Pathophysiology
• For hypertension to occur, there must be a
change in one or more factors affecting the
body’s control systems that monitor or
regulate pressure by affecting peripheral
resistance or cardiac output.
• Single gene mutations have been identified for
a few rare types of hypertension, but most
types of high blood pressure are thought to be
polygenic
 Areas of investigation in primary
hypertension
1. Hyperactivity of sympathetic vasoconstricting
nerves
2. Presence of vasoactive substance released from
the arterial endothelial cells that acts on smooth
muscle, sensitizing it to vasoconstriction
3. Increased cardiac output, followed by arteriole
constriction
4. Excessive dietary sodium intake, sodium
retention, insulin resistance, and
hyperinsulinemia play roles that are not clear
 Causes under secondary hypertension
1. Renal pathology
a. Congenital anomalies, pyelonephritis, renal
artery obstruction, acute and chronic
glomerulonephritis
b. Reduced blood flow to kidney causes release of
renin. Renin reacts with serum protein in
liver(alpha-globulin)- angiotensin I; this plus
angiotensin-converting enzyme(ACE)-angiotensin
II- leads to increased blood pressure
2. Coarctation of aorta (stenosis of aorta)- blood flow
to upper extremities is greater than flow to lower
extremities – hypertension of upper part of the
4. Endocrine disturbances
a. Pheochromocytoma- a tumor of the adrenal gland
that causes release of epinephrine and
norepinephrine and a rise in blood pressure
b. Adrenal cortex tumors lead to an increase in
aldosterone secretion (hyperaldosteronism) and
an elevated blood pressure
c. Cushing syndrome leads to an increase in
adrenocorticosteroids (causing sodium and fluid
retention) and hypertension
d. Hyperthyroidism- causes increased cardiac output
5. Medications such as estrogens,
symphathomimetics, NSAIDs, steroids,
6. Structural and functional changes in the heart
and blood vessels contribute to increases in
blood pressure that occur with age.
• These changes include: accumulation of
atherosclerotic plaque, fragmentation of
arterial elastins, increased collagen deposits
and impaired vasodilatation leading to a
decrease in elasticity of major blood vessels
• These changes results in isolated systolic
hypertension – more common in older adults
and treated as primary/essential hypertension
 Consequences of Hypertension
• Prolonged hypertension damages blood vessels
in the brain, eyes, heart and kidneys and
increases the risk of stroke , angina, myocardial
infarction, blindness, and heart and kidney
failure
• Blood vessel damage occurs through
arteriosclerosis in which smooth muscle cell
proliferation, lipid infiltration, and calcium
accumulation occur in the vascular epithelium
• Damage to heart, brain, eyes, and kidneys is
termed target organ disease; this is the main
object of prevention in pts with high blood
f. Sedentary lifestyle
g. Diabetes mellitus
h. Metabolic syndrome
4. Prevalence in African Americans is 32.4%; in
non Hispanic whites, 23.3%; and in Mexican
Americans, 22.6%
5. In addition to higher prevalence, hypertension
occurs earlier and is more severe in African
Americans
6. Study as shown that only 68% of adults with
hypertension are aware of it, 53% receive
treatment, and only 27% reach good blood
 Clinical manifestations
• Usually asymptomatic, other than high BP
• May cause headache, dizziness, blurred vision
and fatigue when greatly elevated
• Occasionally, retinal changes such as
hemorrhages, exudates (fluid accumulation),
arteriolar narrowing and cotton-wool spots
(small infarctions) occur
• Papilledema (swelling of the optic disk) may
be seen
 Diagnostic evaluation
1. ECG- to determine effects of hypertension on
the heart (left ventricular hypertrophy, ischemia)
or presence of underlying heart disease
2. Chest x-ray- may show cardiomegaly
3. Proteinuria, elevated serum blood urea nitrogen
(BUN), and creatinine levels- indicate kidney
disease as a cause or effect of hypertension; first
voided urine micro-albumin is the earliest sign
4. Serum potassium- decreased in primary
hyperaldosteronism; elevated in Cushing’s
syndrome, both causes of secondary
hypertension
5. Urine (24 hour) for catecholamines- increased
in pheochromocytoma
6. Renal scan to detect renal vascular diseases;
may include ingestion of captopril, an ACE
inhibitor, to detect its effect on renal blood
flow
 Complications
1. Angina pectoris or MI due to decreased coronary
perfusion
2. Left ventricular hypertrophy and CHF due to
consistently elevated aortic pressure
3. Renal failure due to thickening of renal vessels and
diminished perfusion to the glomerulus
4. Transient ischemic attacks (TIAs), stroke or cerebral
hemorrhage due to cerebral ischemia and
arteriosclerosis
5. Retinopathy
6. Accelerated hypertension ( also called malignant
hypertension, occurs when the blood pressure
elevates extremely rapidly, threatening one or more
 Management
• Lifestyle modifications
• Lose weight if BMI is greater than or equal to 27
• Limit alcohol- no more than 1 oz ethanol daily for
men, 0.5 oz for women
• Get regular aerobic exercise equivalent to 30 to 45
minutes of brisk walking most days
• Cut sodium intake to 2.4g or less per day
• Take a diet rich in fruits, vegetables, low –fat dairy
products, and fiber and low in saturated and total
fat, it has been shown to reduce blood pressure
• Stop smoking
• Reduce dietary saturated fat and cholesterol
• Consider reducing coffee intake (five cups per
day has been shown to increase BP in
hypertensive men)
• If, despite lifestyle changes, the BP remains at
or above 140/90 mm Hg(or is not at optimal
level in the presence of other cardiovascular
risk factors) over 3 to 6 months, drug therapy
should be initiated
 Drug therapy
Agents include:
1. Diuretics- lower blood pressure by promoting urinary
excretion of water and sodium to lower blood
volume
2. Beta blockers- beta adrenergic inhibitors that lower
blood pressure by slowing the heart and reducing
cardiac output as well as release of renin from the
kidneys
3. Alpha-receptor blockers- alpha-adrenergic inhibitors
that lower BP by dilating peripheral blood vessels
lowering peripheral vascular resistance
4. Peripheral adrenergic agents- inhibit peripheral
adrenergic release of vasoconstricting
5. Combined alpha and beta blockers- adrenergic
inhibitors that work through both alpha and beta
receptors
6. Angiotensin converting enzyme (ACE) inhibitors-
lower blood pressure by blocking the enzyme that
converts angiotensin I to the potent vasoconstrictor
angiotensin II. These drugs also raise the level of
bradykinin, a potent vasodilator and lower
aldosterone levels
7. Angiotensin II antagonists- similar action to ACE
inhibitors
8. Calcium antagonists (calcium channel blockers)- stop
the movement of calcium into the cells; relax
smooth muscle, which causes vasodilation; and
9. Direct vasodilators- direct smooth muscle relaxants
that primarily dilate arteries and arterioles
• If hypertension is not controlled with the first drug
within 1 to 3 months, three options can be
considered:
a. If the pt has faithfully taken the drug and not
developed any side effects, the dose of the drug
may be increased
b. If the pt has had side effects, another class of drugs
can be substituted
c. A second drug from another class could be added . If
adding the second agent lowers the blood pressure,
the first agent can be slowly withdrawn or, if
necessary, combination therapy will be continued
• The best management of hypertension is to
use the fewest drugs at lowest doses while
encouraging the pt to maintain lifestyle
changes. After blood pressure has been under
control for at least a yr, a slow progressive
decline in drug therapy can be attempted
• If the desired blood pressure is still achieved
with the addition of a second drug, a third
agent or diuretic or both (if not already
prescribed) could be added
 Nursing Interventions
A. Closely monitor pt’s blood pressure
B. Providing Basic education
1. Explain the meaning of high blood pressure,
risk factors and their influences on
cardiovascular, cerebral and renal systems
2. Stress that there can never be total cure, only
control, of essential hypertension; emphasize
the consequences of uncontrolled
hypertension
3. Stress the fact that there may be no
correlation between high blood pressure and
symptoms; the pt cannot tell by the way he or
4. Have the pt recognize that hypertension is chronic and
requires persistent therapy and periodic evaluation.
Effective treatment improves life expectancy;
therefore, follow up health care visits are mandatory
5. Present a coordinated and complementary plan of
guidance
i. Inform the pt the meaning of the various diagnostic
and therapeutic activities to minimize anxiety and to
obtain cooperation
ii. Solicit the assistance of the pt’s
spouse/family/friend- provide information regarding
the total treatment plan
iii. Be aware of the dietary plan developed for this
particular pt
6. Explain the pharmacologic control of
hypertension
a. Explain that the drugs used for effective control
of elevated BP will likely produce side effects
b. Warn the pt of the possibility that orthostatic
hypotension may occur initially with some drug
therapy
i. Instruct the pt to get up slowly to offset the
feeling of dizziness
ii. Encourage pt to sit or lie down immediately if he
or she feels faint
c. Alert the pt to expect initial effects such as
d. Inform the pt 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 to accomplish this
7. Educate the pt to be aware of serious side effects
and report them immediately so that adjustments
can be made in individual pharmacotherapy
8. Note that dosages are individualized; therefore,
they may need to be adjusted because it is often
impossible to predict reactions
9. Warn the pt on vasodilating drugs to use with
caution in certain circumstances that produce
vasodilation- a hot bath, hot weather, febrile illness,
consumption of alcohol- which may exacerbate
[Link] the pt that BP is often decreased when the
circulating blood volume is reduced- as in hydration,
diarrhoea, hemorrhage- so BP shd be monitored
closely and treatment adjusted
A. Encouraging self-management
1. Enlist the pt’s cooperation in redirecting lifestyle in
keeping with guidelines of therapy, acknowledge the
difficulty and provide support and encouragement
2. Develop a plan of instruction for medication self
management
a. Plan the pt’s medication schedule so that the many
medications are given at proper and convenient
times; set up daily checklist on which the pt can
record the medication taken
b. Be sure the pt 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
3. Instruct the pt regarding proper method of
taking BP at home and at work if health care
provider so desires. Inform pt of desired range
and the readings that are to be reported
4. Determine recommended dietary plans and
provide dietary education as appropriate
 HEART FAILURE
• Also called congestive heart failure(CHF)/ CCF
• Is a clinical syndrome that results from the heart’s
inability to pump the amount of blood necessary
to meet the metabolic requirements of the body
due to damaged heart valves, ventricular muscles
or both.
• Results into back pressure of blood with
congestion of organs.
TYPES
LEFT VENTRICULAR HEART FAILURE (LEFT SIDED
FAILURE)
• There is reduced blood flow of arterial blood
from the heart resulting into congestion and
fluid accumulation that affects the lungs causing
fluid oedema.
RIGHT VETRICULAR HEART FAILURE (RIGHT SIDED)
• There is engorgement of neck veins and
peripheral oedema due to poor venous return
 Pathophysiology
• Cardiac compensatory mechanisms (increases in heart
rate, vasoconstriction, heart enlargement) occur to
assist the failing heart
• These mechanisms are able to “ compensate” for the
heart’s inability to pump effectively and maintain
sufficient blood flow to organs and tissue at rest
• Physiologic stressors that increase the workload of the
heart (exercise, infection) may cause these mechanisms
to fail and precipitate the “ clinical syndrome”
associated with a failing heart (elevated
ventricular/atrial pressures, sodium and water
retention, decreased cardiac output, circulatory and
pulmonary congestion)
• The compensatory mechanisms may hasten the onset
 Etiology
• Disorders of heart muscle resulting in
decreased contractile properties of the heart
• Coronary heart disease leading to myocardial
infarction
• Hypertension
• Vulvular heart disease
• Congenital heart disease
• Cardiomyopathies
• Dysrhythmias
• Pulmonary embolism; chronic lung disease
 ctd
• Anesthesia and surgery
• Hemorrhage and anemia
• Transfusions or infusions
• Increased body demands (fever, infection,
pregnancy, arteriovenous fistula)
• Drug-induced…………
• Physical and emotional stress
• Excessive sodium intake…….
 Clinical Manifestations
Left- sided failure(Forward failure)
1. Congestion occurs mainly in the lungs from
backing up of blood into pulmonary veins
and capillaries resulting in:
• Shortness of breath , dyspnea on exertion,
paroxysmal nocturnal dyspnea (due to
reabsorption of dependent edema that has
developed during day), orthopnea, pulmonary
edema
• Cough- may be dry, unproductive; often occurs
at night
 ctd
2. Fatigability- from low cardiac output, nocturia,
insomnia, dyspnea, catabolic effect of chronic
failure
3. Insomnia, restlessness
4. Tachycardia- S3 ventricular gallop
Right-Sided Heart Failure (backward failure)
• Signs and symptoms of elevated pressures and
congestion in systemic veins and capillaries:
1. Edema of ankles; unexplained weight gain
(pitting edema is obvious only after retention
of at least 4.5 kg of fluid)
2. Liver congestion- may produce upper
abdominal pain
3. Distended neck veins
4. Abnormal fluid in body cavities (pleural
space, abdominal cavity
 ctd
5. Anorexia and nausea- from hepatic and
visceral engorgement
6. Nocturia- diuresis occurs at night with rest
and improved cardiac output
7. General weakness and fatigue
 Cardiovascular Findings in Both Types
1. Cardiomegaly (enlargement of the heart)-
detected by physical examination and chest
x-ray
2. Ventricular gallop- evident on auscultation
and ECG
3. Rapid heart rate
4. Development of pulsus alternans (alternation
in strength of beat)
 Diagnostic Evaluation
• ECG may show ventricular hypertrophy and
strain
• Echocardiography may show ventricular
hypertrophy, dilation of chambers, and
abnormal wall motion
• Chest x-ray may show cardiomegaly, pleural
effusion and vascular congestion
• Liver function studies may be altered because
of hepatic congestion
 Complications
• Intractable or refractory heart failure- pt
becomes progressively refractory to therapy
(does not yield to treatment)
• Cardiac dysrhythmias
• Myocardial failure
• Digitalis toxicity- from decreased renal
function, potassium depletion, and low
magnesium levels in the body.
• Pulmonary infarction; pneumonia; emboli
 Management
• Treatment is directed at eliminating excessive
accumulation of body water, increasing the
force and efficiency of myocardial contraction,
and reducing the workload of the heart.
• These goals are achieved through promoting
rest and administering pharmacologic agents:
1. Diuretics: eliminates excess body water and
decrease ventricular pressures
2. Positive Ionotropic Agents
 Increase the heart’s ability to pump more
effectively by improving the contractile force
of the muscle
• Digoxin (Lanoxin) may only be effective in
severe cases of failure
• Dopamine (Intropin) also improves renal blood
flow in low dose range
• Dobutamine (Dobutrex)
• Milrinone (Primacor) and amrinone (Inocor)
are potent vasodilators
3. Vasodilator Therapy

• Decreases the workload of the heart by dilating

peripheral vessels
• By relaxing capacitance vessels (veins and
venules), vasodilators reduce ventricular filling
pressures (preload and volumes)
• By relaxing resistance vessels (arterioles),
vasodilators can reduce impedance to left
ventricular ejection and improve stroke volume
• Vasodilators used in CHF:
a) Nitrates such as nitroglycerin (Tridil), isosorbide
dinitrate (Isordil), nitroglycerin ointment
(Nitrobid)- predominantly dilate systemic veins
 ctd
b. Hydralazine (Apresoline)- predominantly
affects arterioles; reduces arteriolar tone
c. Prazosin (Minipress)- balanced effects on both
arteriole and venous circulation
d. Sodium nitroprusside (Nipride)-
predominantly affects arterioles
e. Morphine sulfate (Duramorph)- decreases
venous return, decreases pain and anxiety and
thus cardiac workload
4. ACE Inhibitors

• Inhibit the adverse effects of angiotensin II

(Potent vasoconstrictor)
• Decreases left ventricular afterload with a
subsequent decrease in heart rate associated
with heart failure, thereby reducing the
workload of the heart and increasing cardiac
output
• Captopril (Capoten) and enalapril (Vasotec)
are commonly used
5. Beta-adrenergic Blocking Agents

• Decrease myocardial workload and protect

against fatal dysrhythmias by blocking
norepinephrine effects of the sympathetic
nervous system
• Metoprolol (Lopressor) or metoprolol CR or XL
(Topco XL) are commonly used
• Carvedilol is a nonselective beta and alpha
blocking agent. Pts may actually experience
increase in general malaise for a 2-to- 3- week
period while they adjust to the medication
Diet
• Restricted sodium
• Restricted fluids

Heart transplantation
• Used in advanced heart failure
 Nursing interventions
A. Maintaining Adequate cardiac output
1. Place pt at physical and emotional rest to
reduce work of heart
a. Provide rest in semirecumbent position or in
arm-chair in air-conditioned environment-
reduces work of heart, increases heart reserve,
reduces blood pressure, decreases work of
respiratory muscles and oxygen utilization,
improves efficiency of heart contraction;
recumbency promotes diuresis by improving
renal perfusion
b. Provide bedside commode- to reduce work of
 ctd
C. Provide for psychological rest- emotional stress
produces vasoconstriction, elevates arterial pressure,
and speeds the heart
i. Promote physical comfort
ii. Avoid situations that tend to promote
anxiety/agitation
iii. Offer careful explanations and answers to the pt’s
questions
2. Evaluate frequently for progression of left
ventricular failure. Take frequent BP readings
a. Observe for lowering of systolic pressure
b. Note narrowing of pulse pressure
c. Note alternations in strong and weak
 ctd
3. Auscultate heart sounds frequently
a. Note presence of S3 or S4 gallop (S3 gallop is a
significant indicator of CHF)
b. Monitor for premature ventricular beats
4. Observe for signs and symptoms of reduced
peripheral tissue perfusion: cool temperature
of skin , facial pallor, poor capillary refill of nail
beds
5. Administer pharmacotherapy
6. Monitor clinical response of pt with respect to
relief of symptoms( lessening dyspnea and
orthopnea, decrease in crackles, relief of
B. Improving oxygenation
1. Raise head of bed 20 to 30 cm – reduces venous
return to heart and lungs; alleviates pulmonary
congestion
2. Auscultate lung fields every 4 hours for crackles and
wheezes in dependent lung fields (fluid
accumulates in areas affected by gravity)
3. Observe for increased rate of respirations (could be
indicative of falling arterial Ph)
4. Observe for Cheyne-Stokes respirations (may occur
in elderly because of a decrease in cerebral
perfusion stimulating a neurogenic response)
5. Position the pt every 2 hours (or encourage the pt
to change position frequently)- to help prevent
 ctd
6. Encourage deep-breathing exercises every 1
to 2 hours- to avoid atelectasis
[Link] small frequent feedings- to avoid
excessive gastric filling and abdominal
distension with subsequent elevation of
diaphragm that causes decrease in lung
capacity
8. Administer oxygen as directed
C. Restoring Fluid Balance
1. Administer prescribed diuretic as ordered
2. Give diuretic early in the morning- nighttime
diuresis disturbs sleep
 ctd
[Link] input and output record- the pt may lose
large volume of fluid after a single dose of
diuretic
[Link] the pt daily- to determine if edema is
being controlled: weight loss should not exceed
0.45 to 0.9 kg/day
5. Assess for weakness, malaise, muscle cramps-
diuretic therapy may produce hypovolemia and
electrolyte depletion, namely hypokalemia.
Hypokalemia may cause weakening of cardiac
contractions and may precipitate digitalis toxicity
in the form of dysrhythmias
6. Give oral potassium as described
 ctd
7. Watch for problems associated with diuretic
therapy including disorders of hyperuricemia,
volume depletion, hyponatremia, magnesium
depletion, hyperglycemia, and diabetes mellitus
8. Watch for signs of bladder distension in the
elderly male with prostatic hyperplasia
9. Observe for symptoms of electrolyte depletion-
lassitude, apathy, mental confusion, anorexia,
decreasing urinary output, azotemia
[Link] IV fluid administration through use of
heparin lock(allows for periodic drug
administration without increasing excessive fluid
intake)
 ctd
[Link] for pitting edema of lower extremities
and sacral area. Use “egg crate” mattress and
sheepskin to prevent pressure sores (poor blood
flow and edema increase susceptibility)
[Link] for the complications of bed rest-
pressure sores(esp in edematous pts),
phlebothrombosis, pulmonary embolism.
[Link] alert to complains of upper quadrant
abdominal pain, poor appetite, nausea and
abdominal distension (may indicate hepatic and
visceral engorgement)
[Link] the pt’s diet. Diet may be limited in
sodium- to prevent, control, or eliminate edema;
D. Improving Activity Tolerance
1. Increase the pt’s activities gradually
a. Assist the pt with self-care activities early in
the day(fatigue sets in as day progresses)
b. Be alert to complains of chest pain or skeletal
pain during and after activities
[Link] the pulse, symptoms, and behavioral
response to increased activity
3. Relieve nighttime anxiety and provide for rest
and sleep- pts with CHF have a tendency to be
restless at night because of cerebral hypoxia
with superimposed nitrogen retention. Give
appropriate sedation- to relieve insomnia and
E. Patient Education and Health Maintenance
1. Explain the disease process to the pt
2. Teach the signs and symptoms of recurrence.
Watch for: gain in weight, swelling of ankles,
feet or abdomen, persistent cough, tiredness,
loss of appetite, frequent urination at night.
3. Review medication regimen
4. Review activity program
5. Restrict sodium as directed
 NSG Dx
• Decreased CO rlt impaired myocardial cells
• Impaired gaseous exchange rlt to
• Impaired tissue perfusion rlt to
• Activity intolerance rlt insufficient blood
supply
 RHEUMATIC HEART DISEASE
(Rheumatic Endocarditis)
• Is damage done to the heart, particularly the
valves , resulting in valve leakage
(regurgitation) and/or obstruction (narrowing
or stenosis)
• There are associated compensatory changes in
the size of the heart’s chambers and the
thickness of chamber walls
 Pathophysiology and Etiology
• Rheumatic fever is as a result of group A
streptococcal infection (rheumatic
fever)resulting into an autoimmune response.
• The autoimmune cells destroy the myosin and
valvular endothelium resulting into
inflammation and scarring of heart tissue
causing cardiac insufficiency.
• It is a preventable disease through early detection and
adequate treatment of streptococcal pharyngitis
Symptoms of streptococcal pharyngitis include:
 Sudden onset of sore throat, throat reddened with
exudates
 Swollen, tender lymph nodes at angle of jaw
 Headache and fever of 38.9 to 40 degrees
 Abdominal pain (children)
• Some cases of streptococcal throat infection are
relatively asymptomatic
 Clinical manifestations
• Polyarthritis; warm and swollen joints
• Carditis
• Chorea (irregular, jerky, involuntary ,
unpredictable muscular movements)
• Erythema marginatum (wavy, thin red-line
rash on trunk and extremities)
• Subcutaneous nodules
• Fever
• Prolonged P-R interval demonstrated by ECG
• Heart murmurs; pleural and pericardial rubs
 Complications
• Valvular heart disease
• Cardiomyopathy
• CHF
 Diagnostic Evaluation
• Throat culture- to determine presence of
streptococcal organisms
• Increased sedimentation rate, WBC count and
differential, and C- reactive protein- increase
during acute phase of infection
• Elevated antistreptolysin titer
 Management
Antimicrobial therapy
• Note that missed doses of antibiotics due to
the pt’s unavailability while off the unit for
diagnostic tests are given after return to the
unit
• Missed antibiotics doses may have irreversible
deleterious consequences
• Notify health care provider if doses will be
missed to ensure that appropriate alternative
measures are taken
• Rest- to maintain optimal cardiac function
• Salicylates- to control fever and pain
 Nursing Interventions
Reducing fever
1. Administer penicillin therapy as prescribed to
eradicate hemolytic streptococcus; an
erythromycin preparation may be used if the
pt is allergic to penicillin
2. Give salicylates as prescribed to suppress
rheumatic activity by controlling toxic
manifestations, to reduce fever and to relieve
joint pain
3. Assess for effectiveness of drug therapy
a. Take and record temperature every 3 hours
Maintaining Adequate Cardiac output
1. Assess for signs and symptoms of acute rheumatic
carditis
a. Be alert to the pt’s complains of chest pain, palpitations,
and/or precordial “tightness”
b. Monitor for tachycardia (usually persistent when the pt
sleeps) or bradycardia
c. Be alert to development of second-degree heart block
or Wenckebach’s disease (acute rheumatic carditis
causes P-R interval prolongation)
2. Auscultate heart sounds every 4 hours
d. Document presence of murmur or pericardial friction
rub
e. Document extra heart sounds (S3 gallop, S4 gallop)
3. Monitor for development of chronic rheumatic
Maintaining activity
• Maintain bed rest for duration of fever or if
signs of active carditis are present
• Provide ROM exercises
• Provide diversional activities that prevent
exertion
• Discuss need for tutorial services with parents
to help child keep up with school work
Patient education and health maintenance
Preventing Recurrence
1. Counsel the pt to maintain adequate nutrition
2. Counsel the pt on hygienic practices
3. Counsel the pt on importance of receiving
adequate rest
4. Counsel the pt to seek help immediately should
sore throat occur

other points
5. Instruct pt to use prophylactic penicillin therapy
before undergoing surgery of GUT, lower GI
tract, and respiratory tract
 NSG Dx
• Decreased CO rlt altered heart valve closure
• Ineffective tissue perfusion rlt reduced blood
supply sec to vasoconstriction
• Impaired gaseous rlt fluid accumulation on the
lungs
• Acute pain rlt inflammation of joints
• Imbalanced nutrition
• Activity intolerance
• Self care deficit
CORONARY HEART DISEASE (CAD)
• Is characterized by the accumulation of fatty
deposits along the innermost layer of the
coronary arteries leading to plaque formation
and narrowing.
 Pathophysiology and Etiology
• The most widely accepted cause of CAD is the
accumulation of lipids (mainly cholesterol) and
fibrous materials (smooth muscle cells) within the
coronary artery lumen
• Increased blood levels of low-density
lipoprotein(LDL- known as the “bad” cholesterol
because it transports cholesterol to body tissues)
irritate and damage the inner layer of the coronary
vessels
• LDL enters the vessel after damaging the
protective barrier, accumulates, and forms fatty
streaks. These are yellow, flat and cause no
significant coronary artery obstruction- develop
 ctd
• Smooth muscle cells (from the middle layer of the
coronary artery) move to the inner layer to engulf
the fatty substance , produce fibrous tissue, and
stimulate calcium deposition
• This cycle continues, resulting in the
transformation of the fatty streak into a fibrous
plaque, and eventually a “complicated” CAD
lesion evolves
• A complicated lesion develops as small blood
vessels grow into the fibrous plaque and the core
of the lesion enlarges and calcifies
• The complicated lesion can cause significant
coronary obstruction by hemorrhage and
 Risk factors
High blood cholesterol levels
Hypertension
Cigarette smoking
Age, male sex, race and family history of CAD
DM, Obesity, sedentary lifestyle and stress
 Clinical manifestations
Stable (Effort) Angina Pectoris
• Chest pain precipitated by physical exertion or
emotional stress; increased oxygen demands
are placed on the heart muscle, but the ability
of the coronary artery to deliver blood to the
muscle is impaired because of obstruction by a
significant coronary lesion (75%narrowing of
the vessel)
• Rest and nitroglycerin relieve the pain
1. Character- substernal chest pain, pressure,
heaviness or discomfort. Other sensations
include a squeezing , aching, burning,
 ctd
Pain may be mild or severe and typically
presents with a gradual buildup of discomfort
and subsequent gradual fading away
May produce numbness or weakness in arms,
wrists, or hands
Associated symptoms include diaphoresis,
nausea, indigestion, dyspnea, tachycardia, and
increase in blood pressure
[Link]- behind middle or upper third of
sternum; the pt generally will make a fist over
the site of the pain(positive Levine sign;
indicates diffuse deep visceral pain) rather than
 ctd
3. Radiation- usually radiates to neck, jaw,
shoulders, arms, hands, and posterior
intrascapular area. Pain occurs more
commonly on the left side than the right
4. Duration- usually lasts 1 to 5 minutes after
stopping activity; nitroglycerin relieves pain
within 1 minute
5. Other precipitating factors- exposure to hot or
cold weather, eating a heavy meal, and sexual
intercourse increase the workload of the heart
and, therefore , increase oxygen demand
 Unstable (preinfarction) Angina Pectoris
• Chest pain occurring at rest; no increase in oxygen
demand is placed on the heart muscle, but an acute
lack of blood flow to the muscle occurs because of
coronary artery spasm aggravated by presence of an
enlarged plaque or hemorrhage/ulceration of a
complicated lesion. Critical narrowing of the vessel
lumen occurs abruptly in either instance.
 A change in frequency, duration, and intensity of
stable angina symptoms is indicative of progression to
unstable angina
 Unstable angina pain lasts longer than 10 minutes, is
unrelieved by rest or sublingual nitroglycerin, and
mimics signs and symptoms of impending myocardial
 Silent Ischemia
• The absence of chest pain with documented
evidence of an imbalance between myocardial
oxygen supply and demand (S-T depression of
1mm or more) as determined by ECG, exercise
stress test, or ambulatory (Holter) ECG
monitoring
Silent ischemia most commonly occurs in the
early morning hours (6am to 12pm
Arousal causes an increase in sympathetic
stimulation and blood viscosity, and coronary
vessel tone increase in the morning , causing
silent ischemic episodes
 Complications
• Sudden death due to lethal dysrhythmias
• Congestive heart failure (CHF)
• Myocardial infarction (MI)
 Diagnostic Evaluation
1. Characteristic chest pain and clinical history
2. Nitroglycerin test- relief of pain with nitroglycerin
3. ECG stress testing- progressive increases of speed
and elevation of walking on a treadmill increase
the work load of the heart. ST and T wave
changes occur if myocardial ischemia is induced
4. Radionuclide imaging- a radioisotope, thallium
201, injected during exercise is imaged by
camera. Low uptake of the isotope by heart
muscle indicates regions of ischemia induced by
exercise. Images taken during rest show a
reversal of ischemia in those regions affected
 ctd
5. Radionuclide ventriculography (gated blood pool
scanning)- red blood cells tagged with a
radioisotope are imaged by camera during
exercise and at rest. Wall motion abnormalities of
the heart can be detected and ejection fraction
estimated
6. Cardiac catheterization- coronary angiography
performed during the procedure determines the
presence, location, and extent of coronary lesions
7. Positron emission tomography (PET)- Cardiac
perfusion imaging with high resolution to detect
very small perfusion differences due to stenotic
arteries. Not available in all settings
 Management
1. Drug therapy
Nitrates- cause generalized vasodilation
throughout the body
Beta blockers- inhibit sympathetic stimulation
of receptor that are located in the conduction
system of the heart and in the heart muscle
Calcium channel blockers- inhibit movement of
calcium within the heart muscle and coronary
vessels; promote vasodilation and
prevent/control coronary artery spasm
Antilipid agents- decrease cholesterol and
triglyceride
 ctd
3. Percutaneous Transluminal Angioplasty (PTCA)
4. Intracoronary Atherectomy
5. Intracoronary Stent
6. Coronary Artery Bypass surgery
7. Transmyocardial Revascularization
8. Lifestyle Modification
 Cessation of smoking
 Control of high blood pressure
 Lowering of blood cholesterol level
 Dietary modifications
 Folate and B- complex vitamins for
hyperhomocystinemia
 Nursing Interventions
A. Relieving pain
1. Determine intensity of pt’s angina
2. Place pt in comfortable position
3. Administer oxygen if prescribed
4. Obtain blood pressure, apical heart rate, and
respiratory rate
5. Obtain a 12-lead ECG as directed
6. Administer antiaginal medication as prescribed
7. Report findings to health Care providers
8. Monitor for relief of pain, and note duration of
anginal episode
 ctd
9. Take vital signs every 5 to 10 minutes until
angina pain subsides
[Link] for progression of stable angina to
unstable angina: increase in intensity of pain,
pain occurring at rest and at low levels of
exertion, pain lasting longer than 15 minutes
[Link] level of activity that precipitated
anginal episode
[Link] specific activities pt may engage in
that are below the level at which anginal pain
occurs
[Link] the importance of notifying nursing
 ctd
B. Maintaining Cardiac output
1. Monitor carefully pt’s response to drug therapy
2. Be sure to remove previous nitrate patch or
paste before applying new paste or pad
(prevents hypotension)
3. Be alert to adverse reaction related to abrupt
discontinuation of beta blocker and calcium
channel blocker therapy. These drugs must be
tapered to prevent a “rebound phenomenon”:
tachycardia, increase in chest pain,
hypertension
4. Report all untoward drug effects to health care
C. Decreasing anxiety
1. Anxiety and fear put an increased stress on the
heart, requiring the heart to use more oxygen
2. Rule out physiologic etiologies for increasing or new
onset of anxiety before administering prn sedatives
3. Assess pt for signs of hypoperfusion auscultate heart
and lung sounds, obtain a rhythm strip and
administer oxygen as prescribed. Notify health care
provider immediately
4. Document all assessment findings, health care
provider notification and response , and
interventions and response
5. Explain to the pt and family reasons for
hospitalization, diagnostic tests and therapies
administered
 ctd
6. Answer the pt’s questions with concise
explanations
7. Administer medications to relieve pt’s anxiety
as directed
8. Explain to the pt the importance of anxiety
reduction to assist in control of angina- teach
relaxation techniques
9. Discuss measures to be taken when an
anginal episode occurs
D. Patient education and health
maintenance
1. Instruct pt and family about CAD
2. Identify suitable activity label to prevent
angina- participate in a normal daily program
of activities that do not produce chest
discomfort, SOB, and undue fatigue
3. Instruct about appropriate use of
medications and side effects
4. Counsel on risk factors and lifestyle changes
 INFECTIVE ENDOCARDITIS
( Bacterial endocarditis)
• Is an infection of the inner lining of the heart
caused by direct invasion of bacteria or other
organisms leading to deformity of the valve
leaflets
 Pathophysiology and Etiology

• When the inner lining of the heart (endocardium)

becomes inflamed, a fibrin clot (vegetation)
forms
• The fibrin clot may become colonized by
pathogens during transient episodes of
bacteremia resulting from invasive procedures
(venous/arterial cannulation, dental work causing
gingival bleeding, GI tract surgery, liver biopsy
and sigmoidoscopy), indwelling catheters, urinary
tract infections, and wound/skin infections
• Platelets and fibrin surround the invading
microorganisms, forming a protective covering
and causing the infected vegetation to enlarge
 ctd

a. The enlarged vegetation (the basic lesion of

endocarditis) can deform, thicken, stiffen, and
scar the free margins of valve leaflets as well
as the fibrous ring (annulus) supporting the
valve
b. The vegetation/s may also travel to various
organs/tissues (spleen, kidney, coronary
artery, brain and lungs) and obstruct blood
flow
c. The “protective covering” surrounding the
vegetation makes it difficult for white blood
cells and antimicrobial agents to infiltrate and
 ctd
• Causal organisms include:
a) Bacteria
i. Streptococcus viridans- bacteremia occurs after
dental work or upper respiratory infection
ii. Staphylococcus aureus – bacteremia occurs after
cardiac surgery or parenteral drug abuse
iii. Enterococci (penicillin resistant group D
streptococci)- bacteremia usually occurs in elderly
pts (over age 60) with genitourinary tract infection
b) Fungi (Candida albicans, Aspergillus)
c) Rickettsieae
• Infective endocarditis may develop on a heart valve
already injured by rheumatic fever, congenital
 ctd
• Infective endocarditis may be acute or
subacute, depending on the microorganisms
involved. Acute IE manifests rapidly with danger
of intractable heart failure and occurs more
commonly on the normal heart valves
• Subacute IE manifests a prolonged chronic
course with a lesser chance of complications
and occurs more commonly on damaged or
defective valves
• IE may follow cardiac surgery, especially when
prosthetic heart valves are used. Foreign bodies
such as pacemakers, patches, grafts, and dialysis
 ctd
• High incidence among drug abusers, in whom
the disease mainly affects normal valves,
usually the tricuspid
• Hospitalized pts with indwelling catheters,
those on prolonged IV therapy or prolonged
antibiotic therapy, and those on
immunosuppressive drugs or steroids may
develop fungal endocarditis
• Relapse due to metastatic infection is possible,
usually within the first 2 months after
completion of antibiotic regimen
 Clinical Manifestations
• Severity of manifestations depends on
invading microorganism
General Manifestations
1. Fever, chills, sweats (fever may be absent in
elderly or in patients with uremia)
2. Anorexia, weight loss, weakness
3. Cough, back and joint pain (especially in pts
over age 60)
4. Splenomegaly
 ctd
Skin and Nail Manifestations
1. Petechiae- (small, purplish, hemorrhagic
spots) -conjunctiva, mucus membranes
2. Splinter hemorrhages(reddish-brown lines
and streaks) in nail beds
3. Osler’s nodes- painful red nodes on pads of
fingers and toes; usually late sign of infection
and found with a subacute infection
4. Janeway’s lesions- light pink macules on palms
or soles, nontender, may change to light tan
within several days, fade in 1 to 2 weeks.
Usually an early sign of endocardial infection
 ctd
Heart manifestations
• New pathologic or changing murmur- no murmur
with other signs and symptoms may indicate right
heart infection
• Tachycardia- related to decreased cardiac output
Central Nervous system manifestations
• Localized headaches
• Transient cerebral ischemia
• Altered mental status, aphasia
• Hemiplegia
• Cortical sensory loss
• Roth spots on fundi of the eyes(hemorrhages with
 ctd
Pulmonary manifestations
o Usually occur with right-sided heart involvement
• Pneumonitis, pleuritis, pulmonary edema, pulmonary
infiltrates
Embolic phenomena
• Lung- hemoptysis, chest pain, shortness of breath
• Kidney- hematuria
• Spleen- pain in upper left quadrant of abdomen
radiating to left shoulder
• Heart- myocardial infarction
• Brain- sudden blindness, paralysis, brain abscess,
meningitis
• Blood vessels- mycotic aneurysms
•
 Diagnostic Evaluation
Varied clinical manifestations and similarities to
other diseases make early diagnosis of IE
difficult
• Blood cultures- at least two positive serial
blood cultures isolating bacteria or fungi
• Elevated sedimentation rate, tests indicative
of anemia, mild leukocytosis, urine
abnormalities indicating nephrosis
• ECG- usually normal
• Echocardiography- identification of
vegetations and assessment of location and
 Complications
• Severe heart failure due to vulvular
insufficiency
• Uncontrolled/refractory infection
• Embolic episodes (ischemia or necrosis of
extremities and organs)
• Conduction disturbances
 Management
• Antimicrobial therapy based on sensitivity of
causative agent- penicillin G is usually the
medication of choice for 2-6 wks
• Urine cultures obtained after 48 hours to
assess efficacy of drug therapy
• Close follow-up by cardiologist
• Supplemental nutrition
• Surgical intervention for:
a. Acute destructive valvular lesion- excision of
infected valves or removal of prosthetic valve
 ctd
b) Hemodynamic impairment
c) Recurrent emboli
d) Infection that cannot be eliminated with
antimicrobial therapy
e) Drainage of abscess or empyema- for pts with
localized abscess or empyema
f) Repair of peripheral or cerebral mycotic
aneurysm
 Nursing Interventions
• Maintaining adequate cardiac output
• Maintaining tissue perfusion
• Maintaining normothermia
• Improving nutritional status
• Reducing anxiety
• Pt education and health maintenance for pts
at risk for infective endocarditis and those
who have had regarding possible relapse
 MYOCARDIAL INFARCTION
• Refers to a dynamic process by which one or
more regions of the heart muscle experience a
severe and prolonged decrease in oxygen
supply because of insufficient coronary blood
flow; subsequently, necrosis or “ death” to the
myocardial tissue occurs
• The onset of the myocardial infarction process
may be sudden or gradual, and the
progression of the event to completion takes
approximately 3 to 6 hours
 Pathophysiology and Etiology
1. Acute coronary thrombosis (partial or total)-
associated with 90% of MIs
• Severe coronary artery disease (greater than
70% narrowing of the artery) precipitates
thrombus formation
• Intramural hemorrhage into atheromatous
plaques causes the lesion to enlarge and
occlude the vessel; dissecting hemorrhage can
also occur
• The plaque ruptures into the vessel lumen,
and a thrombus forms on top of the ulcerated
lesion, with resultant vessel occlusion
 ctd

2. Other etiologic factors include coronary artery spasm,

coronary artery embolism, infectious diseases causing
arterial inflammation, hypoxia, anemia, and severe
exertion or stress on the heart in the presence of
significant coronary artery disease
3. Different degrees of damage occur to the heart
muscle:
 Zone of necrosis- death to the heart muscle caused by
extensive and complete oxygen deprivation;
irreversible damage
 Zone of injury- region of the heart muscle surrounding
the area of necrosis; inflamed and injured, but still
viable if adequate oxygenation can be restored
 ctd
4. Zone of ischemia- region of the heart muscle
surrounding the area of injury, which is
ischemic and viable; not endangered unless
extension of the infarction occurs
5. According to the layers of the heart muscle
involved, MIs can be classified as:
a. Transmural (Q wave) infarction- area of
necrosis occurs throughout the entire
thickness of the heart muscle
b. Subendocardial (nontransmural/non-Q)
Infarction- area of necrosis is confined to the
innermost layer of the heart lining the
 ctd
5. Location of MI is identified as the location of the
damaged heart muscle within the left ventricle: inferior,
anterior, lateral, and posterior or right ventricle
a. Left ventricle is the most common and dangerous
location of an MI, because it is the main pumping
chamber of the heart
b. Right ventricular infarctions commonly occur in
conjunction with damage to the inferior and/or
posterior wall of the left ventricle
6. Region of the heart that becomes damaged-
determined by the coronary artery that becomes
obstructed
7. The amount of heart muscle damage and the location
of the MI- determine prognosis
 Clinical Manifestations
1. Chest pain
a. Severe, diffuse steady substernal pain of a
crushing and squeezing nature
b. Not relieved by rest or sublingual vasodilator
therapy, but requires narcotics
c. May radiate to the arms (commonly the left),
shoulders, neck, back, and/or jaw
d. Continues for more than 15 minutes
e. May produce anxiety and fear, resulting in an
increase in heart rate, BP, and respiratory rate
2. Diaphoresis, cool clammy skin, facial pallor
 ctd
4. Bradycardia or tachycardia
5. Premature ventricular and/or atrial beats
6. Palpitations, severe anxiety, dyspnea
7. Disorientation, confusion, restlessness
8. Fainting, marked weakness
9. Nausea, vomiting, hiccups
[Link] symptoms: epigastric or abdominal
distress, dull aching or tingling sensations,
SOB, extreme fatigue
 Complications
1. Rhythm disturbances
2. Cardiac failure
a. Infarct expansion (thinning and dilation of
the necrotic zone)
b. Infarct extension (additional heart muscle
necrosis occurring after 24 hours of acute
infarction)
c. CHF (with 20% to 35% left ventricle damage)
d. Cardiogenic shock
e. Reinfarction
f. Ischemic cardiomyopathy
 ctd
3. Cardiac rupture
4. Papillary muscle rupture
5. Ventricular mural thrombus
6. Thromboemboli
7. Ventricular aneurysm
8. Cardiac tamponade
9. Pericarditis (2 to 3 days after MI)
[Link] problems- depression, personality
changes
 Diagnostic Evaluation
ECG changes
1. Generally occur within 2 to 12 hours, but may
take 72 to 96 hours
2. Necrotic, injured and ischemic tissue alters
ventricular depolarization and repolarization
a. S-T segment depression and T wave inversion
indicate a pattern of ischemia
b. S-T elevation indicates an injury pattern
c. Q waves indicate tissue necrosis and are
permanent. A pathologic Q wave is one that
is greater than 3mm in depth or greater than
 Elevation of Serum Enzymes and Isoenzymes

1. Enzymes are drawn in a serial pattern, usually on

admission and every 6 to 24 hours until three samples
are obtained; enzyme activity is then is correlated to
the extent of heart muscle damage
2. Enzymes commonly evaluated include creatinine kinase
(CK), lactic dehydrogenase(LDH), and aspartate amino
tranferase (AST)
3. CK and LDH can be broken down further into iso-
enzymes, which are more organ specific
a. CK-MB is specific to heart muscle and thus the most
sensitive enzyme for determining heart muscle damage
b. LDH1 and LDH2 are specific to heart muscle and thus
elevated
Other findings
1. Elevated cardiac troponins
2. Elevated myoglonins
3. White blood cell count and sedimentation rate
elevate due to inflammatory process associated
with the damaged heart muscle
4. Radionuclide imaging allows recognition of areas
of decreased perfusion
5. PET determines the presence of reversible heart
muscle injury and irreversible or necrotic tissue;
extent to which the injured heart muscle has
responded to treatment also can be determined
6. Cardiac muscle dysfunction noted on
 Management
• Therapy is aimed at the protection of ischemic
and injured heart tissue to preserve muscle
function, reduce the infarct size, and prevent
death

Oxygen Therapy
• Improves oxygenation to ischemic heart
muscle
Pain control
• Endogenous catecholamine release during
pain imposes an increased workload on the
heart muscle, thus causing an increase in
oxygen demand
1. Opiate analgesic therapy
a. Morphine is used to relieve pain, to improve
cardiac hemodynamics by reducing preload
and after load, and to provide anxiety relief
b. Meperidine (Demerol) is useful for pain
management in those pts allergic to
morphine or sensitive to respiratory
 ctd
2. Vasodilator therapy
a. Nitroglycerin (sublingual, IV, Paste) promotes
venous (low-dose) and arterial (high-dose)
relaxation as well as relaxation of coronary
vessels and prevention of coronary spasm
b. Myocardial oxygen demand is reduced with
subsequent pain relief
c. Persistent chest pain requires prompt action
(IV nitroglycerin)
3. Anxiolytic therapy
d. Benzodiazepines are used with analgesics
when anxiety complicates chest pain and its
Pharmacologic Therapy
1. Thrombolytic agents, such as tissue
plasminogen activator (Activase),
streptokinase (Streptase), and reteplase
(Retavase), reestablish blood flow in coronary
vessels by dissolving obstructing thrombus
2. Adjunctive therapy aimed at preventing
fibrinogen from adhering to activated
platelets may include administration of
eptifibatide (Integrilin) or abciximab (ReoPro),
or, to prevent platelet activation, asprin
3. Anticoagulation therapy is useful as an
adjunct to thrombolytic therapy
 ctd
4. Beta- adrenergic blocking agents improve
oxygen supply and demand, decrease
sympathetic stimulation to the heart, promote
blood flow in the small vessels of the heart, and
have antidysrhythmic effects
5. Antidysrthmic therapy – lidocaine (Xylocaine)
decreases ventricular irritability, which
commonly occurs after MI
6. Calcium channel blockers improve the balance
between oxygen supply and demand by
decreasing heart rate, blood pressure and
dilating coronary vessels. Diltiazem is the only
 ctd
• Percutaneous Transluminal Coronary
Angioplasty (PTCA)- Mechanical opening of
the coronary vessel
• Surgical Revascularization- coronary artery
bypass
 Nursing Interventions
1. Reducing pain- includes oxygen
administration by nasal cannula if prescribed,
and encouraging pt to take deep breaths-
may decrease incidence of dysrhythmias by
allowing the heart to be less ischemic and
less irritable; may reduce infarct size,
decrease anxiety, and resolve chest pain
2. Alleviating anxiety
3. Increasing activity tolerance- promote rest
with early gradual increase in mobilization-
prevents deconditioning, which occurs with
bed rest
 ctd
4. Maintaining hemodynamic stability
• Monitor BP every 2 hours or as directed
• Monitor respiration and lung fields every 2-4
hours or as prescribed
• Evaluate the heart rate and heart sounds
every 2-4 hours or as directed
• Note presence of jugular venous distension
and liver engorgement
• Evaluate the major arterial pulses
• Take body temp every 4 hours or as directed
• Observe for presence of edema
 ctd
• Monitor skin color and temperature
• Be alert to change in mental status, such as confusion,
restlessness, disorientation
• Employ hemodynamic monitoring as indicated
• Evaluate urine output (30ml/hr)
• Monitor for life-threatening dysrhythmias (common
within 24 hours following infarctions)
5. Preventing bleeding
6. Maintaining tissue perfusion- observe for persistent
and/or recurrence of signs and symptoms of ischemia:
chest pain, diaphoresis, hypotension, may indicate
extension of MI and/reocclusion of coronary vessel
7. Strengthening coping abilities
 PULMONARY HEART DISEASE
(Cor Pulmonale)
• Is an alteration in the structure or function of
the right ventricle resulting from a disease
affecting lung structure or function or its
vasculature (except when this alteration
results from disease of the left side of the
heart or from congenital heart disease)
• Cor pulmonale refers to heart disease caused
by lung disease
 Pathophysiology
• Condition that deprives lungs of oxygen:
hypoxemia hypercapnia acidosis
circulatory complications hypertension
right heart enlargement right heart failure
 Etiology
• Pulmonary vascular disease
• Pulmonary embolism
• COPD
 Clinical manifestations
1. Increasing dyspnea and fatigue; progressive
dyspnea (orthopnea, paroxysmal nocturnal
dyspnea), chronic cough
2. Distended neck veins, peripheral edema,
hepatomegally
3. Bibasilar crackles and split second heart
sound on auscultation of chest
4. Manifestations of carbon dioxide narcosis-
headache, confusion, somnolence, coma
 Diagnostic Evaluation
1. ABGs- decreased Pao2 and pH, increased
Paco2
2. PFTs may show airway obstruction
3. Electrocardiogram changes are consistent
with right ventricular hypertrophy
4. Chest x-ray show right heart enlargement
5. Echocardiogram shows right heart
enlargement
 Complications
• Respiratory failure
• Dysrhythmias
 Management
Goal: treatment of underlying lung disease and
management of heart disease
1. Long-term, low-flow oxygen to improve oxygen
delivery to peripheral tissues, thus decreasing cardiac
work and lessening sympathetic vasoconstriction.
2. Diuretics to lower pulmonary artery pressure (PAP) by
reducing total blood volume and excess fluid in the
lungs
3. Pulmonary vasodilators such as nitroprusside
(Nitropress); hydralazine (Apresoline); calcium channel
blockers to dilate pulmonary bed and reduce
pulmonary vascular resistance
4. Bronchodilators to improve lung function
5. Mechanical ventilation, pt in respiratory failure
 Nursing interventions
Improving Gas Exchange
• Monitor ABG values and/or oxygen saturation
as a guide in assessing adequacy of ventilation
• Use continuous low-flow oxygen as directed to
reduce PAP
• Avoid central nervous system depressants
(narcotics, hypnotics). They have depressant
action on respiratory centers and mask
symptoms of hypercapnia
• Monitor for signs of respiratory infection,
because infection causes carbon dioxide
retention and hypoxemia
Attaining fluid balance
• Watch alterations in electrolyte levels,
especially potassium, which can lead to
disturbances of cardiac rhythm
• Employ ECG monitoring when necessary, and
monitor closely for dysrhythmias
• Limit physical activity until improvement is
seen
• Restrict sodium intake based on evidence of
fluid retention
Patient Education and Health Maintenance
• Emphasize the importance of stopping cigarette
smoking as a major cause of pulmonary heart
disease
• Teach the pt to recognize and treat infections
immediately
• Inform the pt of interrelationship among infection,
air pollution and cardiopulmonary disease
• Explain to the pt/family that restlessness,
depression, and poor sleeping, as well as irritable
and angry behavior, may be characteristic; pt
should improve with rise in O2 and CO2 levels in
ABG values
• Explain the treatment and need to have low-flow
 MYOCARDITIS
• Is an inflammatory process involving the
myocardium
 Pathophysiology and Etiology
• Focal or diffuse inflammation of the
myocardium; may be acute or chronic
• May follow infectious process- viral (especially
coxsackie group B, and may develop after
influenza A or B, herpes simplex), bacterial,
mycotic, parasitic, protozoal, rickettsial, and
spirochetal infections
• May be associated with chemotherapy
(especially doxorubicin (Adriamycin) )or
immunosuppressive therapy
• Conditions such as sarcoidosis and collagen
diseases may lead to myocarditis
 Clinical manifestations
• Symptoms depend on type of infection, degree of
myocardial damage, capacity of myocardium to
recover, and host resistance. Can be acute or chronic
and can occur at any age. Symptoms may be minor
and go unnoticed
 Fatigue and dyspnea
 Palpitations
 Occasional primordial discomfort
• Cardiac enlargement
• Abnormal heart sounds: murmur, S3 or S4 or friction
rubs
• Signs of CHF ( E.g. pulsus alternant, dyspnea, crackles
• Fever with tachycardia
 Diagnostic Evaluation
• Transient ECG changes- S-T segment flattened,
T wave inversion, conduction defects,
extrasystoles, supraventricular and ventricular
ectopic beats
• Elevated WBC count and sedimentation rate
• Chest x-ray- show heart enlargement and lung
congestion
• Elevated antibody titers (antistreptolysin-
o(ASO titer as in rheumatic fever)
• Stool and throat cultures isolating bacteria or
a virus
 Management
• Treatment objectives are targeted toward
management of complications
• Diuretic and digoxin (Lanoxin) therapy for CHF and
atrial fibrillation
• Antidysrhythmic therapy (usually quinidine or
procainamide)
• Strict bed rest to promote healing of damaged
myocardium
• Antimicrobial therapy if causative bacteria is
isolated
Complications
• CHF
 Nursing interventions
• Reducing fever
• Maintaining cardiac output
• Reducing fatigue
• Pt education and health maintenance
 PERICARDITIS
 Pericarditis- is an inflammation of the
pericardium, the membranous sac enveloping
the heart. It is often a manifestation of a more
or generalized disease
 Pericardial effusion- is an outpouring of fluid
into the pericardial cavity seen in pericarditis
 Constrictive pericarditis- is a condition in
which a chronic inflammatory thickening of
the pericardium compresses the heart so it is
unable to fill normally during diastole
 Pathophysiology and Etiology
1. Acute idiopathic pericarditis is the most
common and typical form; etiology unknown
2. Other causes include:
a. Infection
i. Viral ( influenza, coxsackievirus)
ii. Bacterial – Staphylococcus, meningococcus,
streptococcus, pneumococcus, gonococcus,
Mycobacterium tuberculosis
iii. Fungal
iv. Parasitic
b. Connective tissue disorders ( lupus
 ctd
c. Myocardial infarctions; early, 24 to 72 hours;
or late 1 week to 2 years after MI (Dressler’s
syndrome)
d. Malignant disease; thoracic irradiation
e. Chest trauma, heart surgery, including
pacemaker implantation
f. Drug induced (procainamide (pronestyl));
phenytoin (Dilantin)
 Clinical Manifestations
 Pain in anterior chest, aggravated by thoracic
motion- may vary from mild to sharp and severe;
located in pre-cordial area-epigastrium (may be
felt beneath clavicle, neck, scapular region)- may
be relieved by leaning forward
 Pericardial friction rub- scratchy, grating, or
creaking sound occurring in the presence of
pericardial inflammation
 Dyspnea- from compression of heart and
surrounding thoracic structures
 Fever, sweating, chills- due to inflammation of
pericardium

 Diagnostic Evaluation
• Echocardiogram- most sensitive method for
detecting pericardial effusion
• Chest x-ray- may show heart enlargement
• ECG- to evaluate for MI
• WBC and differential elevations indicating
infection
• Antinuclear antibody serologic tests elevated
in lupus erythematosus
• PPD test positive in tuberculosis; ASO titers-
elevated if rheumatic fever is present
 ctd
• Pericardiocentesis- for examination of
pericardial fluid for etiologic diagnosis
• BUN- to evaluate for uremia

Complications
• Cardiac tamponade
• CHF
• Hemopericardium (especially pts post-MI
receiving anticoagulants)
 Management
• Bacterial pericarditis- penicillin or other
antimicrobial agents
• Rheumatic fever- penicillin G and other
antimicrobial agents
• Tuberculosis- antituberculosis chemotherapy
• Fungal pericarditis- amphotericin B and
fluconazole
• Systemic lupus erythematosus- steroids
• Renal pericarditis- dialysis, indomethacin
(indocin), biochemical control of end-stage
renal disease
 ctd
• Neoplastic pericarditis- intrapericardial
instillation of chemotherapy; radiotherapy
• Postmyocardial infarction syndrome- bed rest,
asprin, prednisone
• Postpericardiotomy syndrome ( after open-
heart surgery)- treat symptomatically
• Emergency pericardiocentesis if cardiac
tamponade develops
• Partial pericardiectomy (pericardial “
window”) or total pericardiectomy for
recurrent constrictive pericarditis
 Nursing Interventions
1. Reducing discomfort- pain relief, relieve anxiety,
reassure pt, bed rest, comfortable position
2. Maintaining cardiac output:
 Assess heart rate, rhythm, BP, respirations at least
hourly in the acute phase
 Assess for signs of cardiac tamponade- increased
heart rate, decreased BP, Presence of paradoxical
pulse, distended neck veins, restlessness, muffled
heart sounds
 Prepare for emergency pericardiocentesis or surgery
 Assess for signs of CHF
 Monitor closely for development of dysrhythmias
 ARTERIOSCLEROSIS AND
ATHEROSCLEROSIS
 Arteriosclerosis- is an arterial disease manifested by
a loss of elasticity and hardening of the vessel wall.
More commonly known as “ hardening of arteries”, it
is a normal stage of the aging process and generally
occurs uniformly throughout the arterial system
 Atherosclerosis- is the most common type of
arteriosclerosis, manifested by formation of
atheromas (patchy lipoidal degeneration of the
intima)
• Lesions or plaques form throughout the arterial wall,
reducing the size of the vessel and limiting the flow
 ctd
• Over time, atherosclerotic lesions can
completely occlude the lumen by buildup of
the plaque material and may contribute to
thrombus formation
 Pathophysiology and Etiology
 Etiology thought to be a reaction to injury:
• Endothelial cell injury causes increased
platelet and monocyte aggregation to site of
injury
• Smooth muscle cells migrate and proliferate
• Matrix of collagen and elastic fibers forms
 Atherosclerotic lesions are two types: fatty
streaks and fibrous plaques
 Risk factors
Heredity
Increasing age
Male gender
Cigarette smoking
Hypertension
Elevated blood cholesterol levels
DM
Obesity
Physical inactivity
Stress
 Clinical Manifestations
• May affect entire vascular system or one
segment of the vascular tree
• Symptoms are based on area affected
1. Brain (cerebroarteriosclerosis)- transient
ischemic attacks (TIA); stroke or
cerebrovascular accident (CVA); visual
disturbances such as amaurosis fugax, which
is described by pts as a shade over portion of
the eye
2. Heart (coronary artery disease, CAD)- angina,
MI,CHF
 ctd
3. Gastrointestinal tract (aortic occlusive
disease, aortic aneurysm, and mesenteric
ischemia)- abdominal pain, unintentional
weight loss, lower back pain
4. Kidneys (renal artery stenosis)- renal
insufficiency, poorly controlled hypertension
5. Extremities (lower extremity arterial occlusive
disease)- intermittent claudication (pain in
legs associated with exercise), rest pain, tissue
loss( with or without presence of infection
and/or gangrene), embolic events
6. Decreased or absent pulses; bruits
 Diagnostic Evaluation
(Specific to body system affected)
1. Arteriography of involved area may show stenosis
and increased collateral circulation
2. CT scan
3. MRI/MRA
4. Noninvasive testing of the vascular system:
Duplex studies, Sequential Doppler studies, Pulse
volume resistance, Ankle-branchial index (ABI)
5. ECG, holter monitoring, exercise stress
monitoring, myocardial imaging, and cardiac
catheterization may be done to evaluate coronary
artery disease
 Complications
• Long term complications are related to the
specific body system affected.
1. Brain- long and short-term disabilities
associated with stroke
2. Heart- stable/unstable angina, MI, CHF
3. Aorta- ischemic bowel, aneurysms,
impotence, renal failure, nephrectomy
4. Lower extremities- intermittent claudication,
non-healing ulcers, infections/gangrene,
amputation
 Management
Medical management
• Modification of risk factors
• Prescriptive mx- anticoagulants, antiplatelet
therapy, lipid lowering agents, anti-
hypertensives
• Specific treatment for end-organ dysfunction
• Vascular rehabilitation/exercise
 Surgical Mx
1. Endovascular procedures:
a. Percutaneous transluminal angioplasty (PTA)
with or without placement of intralumenal
stent
b. Endovascular grafting
c. Rotational atherectomy
d. Laser angioplasty
2. Surgical revascularization of the affected
vessels including: Embolectomy,
Thrombectomy, Endarterectomy, Bypass
 Nursing interventions and patient
Education
• Attention is directed to reducing risk factors
• Encourage active lifestyle to promote
cardiovascular health
 VENOUS THROMBUS
• Phlebitis - is an inflammation in the wall of a
vein. The term is used clinically to indicate a
superficial and localized condition that can be
treated with application of heat
• Superficial thrombophlebitis - is a condition in
which a clot forms in a vein secondary to
phlebitis or because of partial obstruction of
the vein. More commonly seen in the greater
or lesser saphenous veins of the lower
extremities
 ctd
 Phlebothrombosis- is the formation of a
thrombus or thrombi in a vein
• Deep veins of the lower extremities are most
commonly involved
 Deep vein thrombosis (DVT)- is thrombosis of
deep rather than superficial veins. Two
serious complications are pulmonary
embolism and postphlebitic syndrome
 Pathophysiology and Etiology
• Three antecedent factors are believed to play
a significant role in the development of
venous thromboses: (Virchow's triad)
a) stasis of blood,
b) injury to the vessel wall
c) altered blood coagulation
• Usually two of the three factors occur before
thrombosis develops
 Thrombosis related situations
 Venous stasis- following operations, childbirth, or bed
rest for any prolonged illness
 Prolonged sitting or as a complication of varicose veins
 Injury (bruise) to a vein; may result from direct trauma
or internal trauma as from IV catheters, infusion of
medications, and/or infiltration of medications
 Extension of an infection of tissues surrounding the
vessel
 Continuous pressure of a tumour, aneurysm, or
excessive weight gain in pregnancy
 Unusual activity in a person who has been sedentary
 Hypercoagulability associated with malignant disease,
blood dyscrasias
 High risk factors
1. Malignancy
2. Previous venous insufficiency
3. Conditions causing prolonged bed rest- MI,
CHF, Sepsis, traction, end-stage cancer,
HIV/AIDS
4. Leg trauma- fractures, cast, joint
replacements
5. General surgery- over 40 yrs of age
6. Obesity, smoking
 Clinical Manifestations
1. DVT may occur asymptomatically or may
produce severe pain, fevers, chills, malaise
and swelling and cyanosis of affected arm or
leg
2. Superficial thrombophlebitis produces visible
and palpable signs such as heat, pain,
swelling, erythema, tenderness, and
induration (hardening) along the length of
the affected vein
3. Extensive vein involvement may cause
lymphadenitis
 Diagnostic Evaluation
• Venous duplex/color duplex ultrasound is
commonly done. This noninvasive test allows for
visualization of the thrombus, including any free
floating or unstable thrombi that may cause
emboli. Most effective in the detection of
thrombus in the lower extremities
• Impedance plethysmography (IPG): a noninvasive
measurements of the changes in calf volume
corresponding to changes in blood volume
brought about by temporary venous occlusion
with a high-pneumatic cuff. Electrodes measure
electrical impedance as cuff is deflated. Slow
decrease in impedance indicates diminished blood
 ctd
• RF testing: radioctive fibrinogen is
administered intravenously. Images are taken
through nuclear scanning 12 to 24 hours; the
radioctive fibrinogen will be concentrated at
the area of clot formation
• Venography: intravenous injection of a radio-
contrast agent. The vascular tree is visualized
and obstruction is identified
• Coagulation profiles: APTT, PT/INR, circulating
fibrin, monomer complexes, fibrinopeptide A,
serum fibrin, protein C and S, antithrombin III
levels. Detect intravascular coagulation
 Management
GOAL: To prevent propagation of the thrombus,
prevent recurrent thrombus formation, prevent
pulmonary emboli, and limit venous valvular
damage

Anticoagulation
 To prevent embolization
• Heparin is given IV initially, followed by 3 to 6
months of oral anticoagulant therapy
• Heparin and enoxaparin may also be given
subcutaneously as prophylaxis for the
prevention of DVT, especially in postoperative
Thrombolytic therapy
• May be used in life- or limb-threatening
situations
• Most effective in dissolving existing clots
within the first 24 hours of thrombolic event

Nonpharmacologic therapies
• For artificial thrombophlebitis and as an
adjunct to anticoagulation with DVT
1. Bed rest- usually recommended for 5 days.
Prevents muscle contraction with walking,
which may dislodge clots
 ctd
2. Elevation of affected extremity- at least 10 to
20 degrees above the level of the heart to
enhance venous return and decrease swelling
3. Compression- promotes venous return and
reduces swelling
4. Dry heat- warm water bottles
5. Moist heat- hydrotherapy, whirlpool bath,
warm compresses
Surgery
Placement of a filter into the inferior vena
cava to prevent pulmonary embolism in a pt
who cannot tolerate prolonged anticoagulant
therapy
Thrombectomy may be necessary for severely
compromised venous drainage of the
extremity

Complications
• Pulmonary embolism
• Postphlebitic syndrome
 Nursing Interventions
Relieving pain
• Elevate legs
• Apply warm compresses or heating pad
• Administer acetaminophen(Tylenol), codeine, or
other analgesic as needed. Avoid the use of
aspirin (or aspirin-containing drugs) and NSAIDs
during anticoagulant therapy to prevent further
risk of bleeding
Preventing bleeding
• Handle pt carefully while turning and positioning
• Maintain pressure on IV and venipuncture sites
for at least 5 minutes. Apply ice if pt is prone to
 ctd
• Assist with ambulation and keep walkways free
from clutter to prevent falls
• Observe carefully and report any possible signs of
bleeding
• Have antidotes to reverse anticoagulants being
used
Preventing other hazards of immobility
• Prevent venous stasis by proper positioning in bed
• Initiate active exercises unless contraindicated, in
which case use passive exercises
• Encourage adequate fluid intake, frequent changes
of position, and effective coughing and deep-
 ctd
• Be alert for signs of pulmonary embolism-
chest pain, dyspnea, anxiety, and
apprehension- and report immediately
• After the acute phase (5-7 days), apply elastic
stockings as directed. Remove twice daily and
check for skin changes, pressure points and
calf tenderness
• Encourage ambulation when allowed (usually
after 5-7 days, when clot has fully adhered to
vessel wall)
Patient education and health maintenance
 VARICOSE VEINS
 Primary varicose veins- bilateral dilatation and
elongation of saphenous veins; deeper veins
are normal
• As the condition progresses, because of
hydrostatic pressure and vein weakness, the
vein walls become distended, with asymmetric
dilatation, and some of the valves become
incompetent. The process is irreversible
 Secondary varicose veins result from
obstruction of deep veins
 ctd
• Telangectasias (spider veins) are dilated
superficial capillaries , arterioles and venules.
They may be cosmetically unattractive but do
not pose a threat to circulation
 Pathophysiology and Etiology
• Dilatation of the veins prevents the valve
cusps from meeting; this results in increased
back-up pressure, which is passed into the
next lower segment of the vein. The
combination of vein dilatation and valve
incompetence produces the varicosity
• Varicosities may occur elsewhere in the body
(esophageal and hemorrhoidal veins) when
flow or pressure is abnormally high
Predisposing factors:
• Hereditary weakness of the vein wall or valves
• Long-standing distension of veins brought
about by pregnancy, obesity, or prolonged
standing
• Old age- loss of tissue elasticity
 Clinical manifestations
• Disfigurement due to large, discolored,
tortuous leg veins
• Easy leg fatigue, cramps in leg, heavy feeling,
increased pain during menstruation, nocturnal
muscle cramps
 Diagnostic Evaluation
1. Walking tourniquet test- to demonstrate
presence or absence of vulvular incompetence
of communicating veins
A tourniquet is snugly fasted around the lower
extremity just above the highest noted
varicosities
The pt is directed to walk briskly for 2 minutes
Failure of varicosities to empty suggests
valvular incompetence of communicating
veins distal to tourniquet
 ctd
2. Photoplethysmography- a noninvasive
technique to observe venous flow
hemodynamics by noting changes in the blood
content of the skin; used to detect
incompetence in valves located inside the vein
3. Doppler ultrasound- can detect accurately and
rapidly the presence or absence of venous
reflux in deep or superficial vessels
4. Venous outflow and reflux plethysmography-
able to detect deep venous occlusion
 ctd
5. Ascending and descending venography- an
invasive technique that can demonstrate
venous occlusion and patterns of collateral
flow. This test is expensive; it may not be
required if a careful history, physical exam and
lab testing are done
 Management
1. Conservative therapies such as encouraging
weight loss if appropriate and avoiding
activities that cause venous stasis by
obstructing venous flow
2. Surgery may be considered for ulceration,
bleeding, and cosmetic purposes in selected
pts, if patency of deep veins is ensured
3. Surgical procedures- a single method or
combination of methods is tailored to meet
the needs of the individual:
 ctd
a. Sclerosing injection- may be combined with ligation
or limited to treatment of isolated varicosities. The
affected vessel may be sclerosed by injecting
sodium tetradecyl sulfate or similar sclerosing
agent. Compression bandage is then applied
without interruption for six weeks; inflamed
endothelial surfaces adhere by direct contact
b. Multiple vein ligation
c. Ligation and stripping of the greater and lesser
saphenous systems. This is the most effective
procedure
d. Venous reconstruction or venous valvular transplant
e. Laser therapy- uses a laser fiber tip that seals the
vein (decompressed)
 Complications
• Hemorrhage due to weakening of the vein
wall and pressure on it
• Skin infection and breakdown, producing
ulcers (rare in primary varices)
 Nursing Interventions
Promoting tissue integrity postoperatively
1. Maintain elastic compression bandages from
toes to groin. Monitor neurovascular status of
feet ( color, warmth, capillary refill, sensation,
pulses) to prevent compromise from swelling
2. Elevate legs about 30 degrees, providing support
for the entire leg. Check that knee gatch is
positioned for straight incline
3. Monitor for signs of bleeding, especially in the
first 24 hours
4. If incisional bleeding occurs, elevate the leg
above the level of the heart, apply pressure over
the site, and notify the surgeon
 ctd
5. Be alert for complains of pain over bony
prominences of the foot and ankle; if the
elastic bandage is too tight, loosen it- later,
have it reapplied
6. Maintain IV infusion for fluids and antibiotics
as ordered
7. After removal of compression bandages
(about 7 days postoperatively), observe or
teach pt to observe for signs of cellulitis or
incisional infection
8. Encourage use of elastic stockings for several
weeks to months following surgery
Relieving pain
• Administer analgesics
• Encourage mostly bed rest the first day with
legs elevated . The second day encourage
ambulation for 5 to 10 mins every 2 hours
• Advise, when ambulatory, to avoid prolonged
standing, sitting, or crossing or dangling legs
to prevent obstruction
Patient Education and health maintenance
Postoperative instructions
 Instruct pt to:
• Wear pressure bandages or elastic stockings-
usually 3 to 4 wks after surgery
• Elevate legs about 30 degrees and provide
adequate support for entire leg
• Take analgesics for pain
• Report signs such as sensory loss, calf pain, or
fever to the health care provider
• Avoid dangling of legs
• Walk as able
 ctd
• Note that complains of patchy numbness can
be expected but should disappear in less than
a yr
• Follow conservative mx instructions to prevent
recurrence
Conservative management
 Instruct pt to:
• Avoid activities that cause venous stasis by
obstructing venous flow- wearing tight garters,
sitting or standing for prolonged period of time,
crossing legs at knees for prolonged period
while seated
• Control excessive weight gain
• Wear firm elastic support, from toe to thigh
when in upright position
• Elevate foot of bed 15 to 20cm for night
sleeping
•
 VASOSPASTIC DISORDER
( Raynaud’s phenomena)
• Raynaud’s phenomenon or syndrome is a
vasospastic disorder that is brought on by an
unusual sensitivity to cold or to emotional
stress
 Pathophysiology and Etiology
• The condition is a form of intermittent
arteriolar vasoconstriction that results in
coldness, pain, and pallor of fingertips, toes,
or tip of nose
• The cause is unknown, although it may be
secondary to connective tissue and other
immunologic disorders
• Episodes may be triggered by emotional
factors or by unusual sensitivity to cold
• Most common in women between ages 16
and 40 and seen much more frequently in cold
 Clinical manifestations
1. Intermittent arteriolar vasoconstriction
resulting in coldness, pain, pallor
2. Involvement of the fingers appears to be
asymmetric; thumbs are less often involved
3. Characteristic color changes: white-blue-red
a. White- blanching, dead-white appearance if
spasm is severe
b. Blue- cyanotic, relatively stagnant blood flow
c. Red- a reactive hyperemia on rewarming
4. Occasionally, there is alteration of the
fingertips
 Diagnostic evaluation
• Clinical symptoms must last at least 2 years to
confirm the diagnosis
• Tests may be done to rule out secondary
disease processes such as chronic arterial
occlusive or connective tissue disease
 Management
• Avoidance of trigger and aggravating factors
• Calcium channel blockers are frequently used to
prevent or reduce muscle spasm
• Nitroglycerin or sympatholytics such as reserpine
(serpasil), guanethidine (Ismelin) or prasozin
(Minipress) may be helpful for some. Side effects
such as headache, dizziness, and orthostatic
hypotension may be prohibitive
• Antiplatelet agents such as aspirin or dipyridamole
(persantine) may be given to prevent total
occlusion
• Sympathectomy- removal of the sympathetic
ganglia or division of their branches may offer some
 Complications
• Chronic disease may cause atrophy of skin and
muscles
• Ulceration, gangrene and amputation (rare)
 Nursing Interventions
Minimizing sensory alteration
• Assist pt in avoiding exposure to cold; e.g. use
of gloves to handle cold items
• Encourage pt to stop smoking
• Help pt to understand the need to avoid
stressful situations
• Offer pt options for stress management
• Administer and teach pt about drug therapy
• Need to take drugs every day to prevent or
minimize symptoms
 ctd
• Follow orthostatic hypotension precaution if on
sympatholytics
• Advise pt that episode may be terminated by
placing hands (or feet) in warm water
Relieving pain
• Explain to pt that pain may be experienced when
spasm is relieved- hyperemic phase
• Administer or teach self- administration of
analgesics
• Reassure pt that pain is temporary; persistent
pain, ulceration, or signs of infection should be
reported
References
1. Hinkle. J and cheerer, K. (2014) Brunner and
suddart. 14th edition. Philadephia.
2. Lewis S. Dirken S. Heitkemper M. bucher l
and camera. I. (2011). Medical surgical
Nursing: Assessment and management of
clinical problem 8th Edition. USA. Mosby
Elservier Inc.