Mindanao State University

COLLEGE OF HEALTH SCIENCES

Marawi City

Alterations in Cardiovascular Function

A requirement presented to

Professor Norhanie A. Lininding

In partial fulfillment for the course

NSG 124 - XxYy1

(Care of Mother and Child at Risk or with Problems)

Second Sem, S.Y. 2022-2023

Submitted by:

Monisha A. Lucman

Raymah M. Mahdi

Norjannah M. Malawani

April 28, 2023

 TRANPOSITION OF THE GREAT ARTERIES (TGA)
TGA occurs when the two main blood vessels coming out of the heart — the aorta and the
pulmonary artery — are transposed, or switched in position. The aorta is positioned in front
of the pulmonary artery instead of behind it.

2 Types of Tranposition of the Great Arteries:

Dextro transposition of the great arteries (D-TGA)
• Aorta have switched places. This type of TGA almost always needs to be repaired in the
first year of life.
• Circulation of deoxygenated blood is returned to the body and is never oxygenated. And
circulation of oxygenated blood is returned to the lungs and is never deoxygenated.
Levo transposition of the great arteries (L-TGA)
• Ventricles have switched places. This type of TGA, in the absence of other heart defects,
may not require repair early in life.
• Circulation of deoxygenated blood is partially oxygenated before returning to the body.
And circulation of oxygenated blood is partially deoxygenated before returning to the
lungs.

ASSESSMENT
Symptoms
• Cyanosis (bluish skin, lips and nails from • Rapid heart rate
not getting enough oxygen-rich blood) • Slow weight gain
• Fast or labored breathing • Weak pulse
• Low appetite • Tachypneic
• Poor feeding

Tests that can confirm a TGA diagnosis include:

• Chest X-ray • Pulse oximetry
• Electrocardiogram (ECG)

MEDICAL MANAGEMENT
Treatments that can help a baby’s heart and lungs before surgery include:
• Intravenous (IV) medication to help the heart and lungs work better
• Prostaglandin E1, a medication that helps blood flow through the heart
• Supplemental oxygen or a ventilator (a machine that helps do the work of breathing)

SURGICAL Management
• Jatene procedure - Includes dissecting both the pulmonary artery and aorta above their
respective valves and switching the vessels to the appropriate location. The final
component of the surgical repair is removing the coronary arteries from the base of the
original aorta and surgically placing them in an appropriate spot on the new aortic root,
now coming off of the left ventricle.
• Cardiopulmonary bypass - Reimplantation of the coronary arteries, however this may
produces other potential complications; Ischemia. Poor myocardial function, decreased
cardiac output & impair ventricular function, and long segment narrowing of the
pulmonary artery.

NURSING MANAGEMENT
Nursing care before surgery includes ensuring their oxygen saturation remains normal for this
defect, which is 75% to 85%; monitoring for signs of increased pulmonary blood flow; and
supporting the family as they wait for their newborn to undergo heart surgery.
 CONGESTIVE HEART FAILURE (CHF)
Is a long-term condition where the heart is too weak to pump efficiently. And because it can't
pump efficiently, it can't provide the proper cardiac output that your body needs to maintain
its metabolic needs.

RELATED TERMS:
• Preload: the volume of blood in the ventricles at the point just before contraction; it is an
indicator of circulating blood volume.
• Contractility: ability to modulate the rate and force of fiber shortening
• Afterload: amount of resistance met by the ventricles upon ejection
• Compliance: the ability of the ventricles to stretch and fill

ASSESSMENT
Symptoms (CHF is more difficult to detect in infants because it may be more subtle)
• Breathlessness • Dyspnea
• Rapid respirations • Weigh Loss (caloric expenditure is
• Diaphoretic greater than the caloric intake)

Right-sided failure (Increased venous pressure)

• Hepatomegaly • Periorbital edema (Edema is uncommon
• Jugular venous distention in children)

Left-sided failure (Increased pulmonary pressures)

Can ultimately lead to right-sided failure, as excessive pressure in the pulmonary system
prevents blood from leaving the right ventricle.
• Rales • Shortness of breath
• Tachypnea

Clinical Findings
• Hepatomegaly • Enlarged heart (Chest radiograph, with or
• Cardiac gallop without pulmonary edema

THERAPEUTIC MANAGEMENT
Management of heart failure is twofold:
a) symptomatically manage the patient and
b) treat the underlying cause of the heart failure

Goals:
• The goal is to decrease any fluid overload, enhance myocardial contractility, and decrease
afterload in order to ensure adequate perfusion and decrease the work of the heart.
• Be certain that outcomes established for the care of a child with congestive heart disease
are realistic in light of the child’s overall condition and are individualized for each child.
Not all children may be able to attain “normal” vital signs, but they should be comfortable
and be able to participate in their regular daily activities, regardless of the actual heart rate
or respiratory rate.
• Interventions focus on helping support heart function and helping parents deal with this
crisis until the child is stabilized and the underlying condition can be treated, if possible.
 PERSISTENT PULMONARY HYPERTENSION
ETIOLOGY
Persistent pulmonary hypertension, also called persistent fetal circulation, occurs due to an
abnormal transition from fetal to extrauterine circulation. It can also result from poor lung
vascularization in conditions such as congenital diaphragmatic hernia.

RISK FACTORS
• Breathed in their own bowel movements before birth (meconium aspiration)
• Lack of oxygen before or during birth
• Infection in their lungs or blood
• Abnormal development of the heart or lungs
• Been born to a mother with diabetes mellitus
• Been born large for gestational age (LGA).

SIGNS AND SYMPTOMS

At birth, or within the first hours after birth, the baby will have:
• Fast breathing and a fast heart rate • Low amount of oxygen carried in the
• Grunting or moaning when breathing blood (oxygen saturation) even after
• Retractions – the skin between and under getting oxygen
the ribs pulls in during fast and hard • Lower oxygen saturation in the baby’s
breathing legs than in the right wrist
• Cyanosis • Low blood pressure

DIAGNOSTIC LABORATORIES
The following tests may be done to diagnose PPHN:
• Echocardiogram (echo): This painless test uses sound waves to take a picture of the heart
and blood vessels. It will show how the blood flows through the body.
• X-rays: A camera takes a picture of the lungs and can also see if the heart is too large.
• Blood tests: These tests will show changes in the number of blood cells and the level of
other things like salt, sugar, and acids in the blood. They help to tell how well your baby
uses oxygen or if they have an infection.
• Pulse oximeter: This checks oxygen saturation levels.

MEDICAL MANAGEMENT
The goal of treatment is to increase oxygen levels in the blood, open the blood vessels in the
lungs, and maintain a normal blood pressure. This is done with oxygen, medicines, and fluids.
Your baby may get oxygen by:
• Nasal cannula: A small tube with prongs is placed in the nostrils and hooked up to
oxygen.
• Continuous Positive Air Pressure (CPAP): This machine gently pushes air or oxygen
into the lungs.
• Ventilator: This machine will breathe for your baby until the baby can breathe on their
own. The physician will put a breathing tube down their windpipe. This is called
intubation (in-too-BAY-shun). The breathing tube is then hooked up to the ventilator. The
ventilator is programmed to give your baby even and regular breaths.
• High frequency oscillation ventilation: This is a special type of ventilator. It can deliver
rapid, short bursts of air through a breathing tube.
The types of medicines given are:
• Blood pressure medicine: to keep the blood pressure at the right level
• Antibiotics: to treat or prevent infection
• Sedatives: to help your baby rest and stay calm. When the baby is calm, the machines
that give him oxygen can work better and he may need to use less.
• Surfactant: to help the lungs work better. Surfactant allows the lungs to use oxygen and
get rid of carbon dioxide. It is given to the baby through a breathing tube.
If other treatments don’t work, very severe PPHN may be treated with:
• Nitric oxide – This is a gas that helps expand the blood vessels in the lungs.
• Extracorporeal membrane oxygenation (ECMO) – Your baby’s blood is pumped
through a machine that acts as a lung. It puts oxygen right into the blood. It also takes out
carbon dioxide before pumping the blood back into the baby. If your baby needs ECMO,
their health care provider will explain it to you.

DRUGS OF CHOICE
• Blood pressure medicine: to keep the blood pressure at the right level
• Antibiotics: to treat or prevent infection
• Sedatives: to help your baby rest and stay calm. When the baby is calm, the machines that
give him oxygen can work better and he may need to use less.
• Surfactant: to help the lungs work better. Surfactant allows the lungs to use oxygen and
get rid of carbon dioxide. It is given to the baby through a breathing tube.

SURGICAL MANAGEMENT
Some people with pulmonary hypertension may need surgery. The 3 types of surgery
currently used are:
• Pulmonary endarterectomy – an operation to remove old blood clots from the
pulmonary arteries in the lungs in people with chronic thromboembolic pulmonary
hypertension
• Balloon pulmonary angioplasty – a new procedure where a tiny balloon is guided into
the arteries and inflated for a few seconds to push the blockage aside and restore blood
flow to the lung; it may be considered if pulmonary endarterectomy is not suitable, and
has been shown to lower blood pressure in the lung arteries, improve breathing, and
increase the ability to exercise
• Atrial septostomy – a small hole is made in the wall between the left and right atria of the
heart using a cardiac catheter, a thin, flexible tube inserted into the heart’s chambers or
blood vessels; it reduces the pressure in the right side of the heart, so the heart can pump
more efficiently and the blood flow to the lungs can be improved
• Transplant – in severe cases, a lung transplant or a heart-lung transplant may be needed;
this type of surgery is rarely used because effective medicine is available

NURSING DIAGNOSIS
• Decreased cardiac output related to arrhythmias secondary to pulmonary hypertension, as
evidenced by palpitations, heart rate of above 120 bpm (tachycardia)
• Acute Pain related to increased strain in cardiac muscles secondary to pulmonary
hypertension, as evidenced by pain score of 10 out of 10, heart rate of above 120 bpm,
respiratory rate of higher than 60 cpm, and restlessness
• Ineffective Breathing Pattern related to pulmonary hypertension secondary to chronic
obstructive pulmonary disorder (COPD) as evidenced by nasal flaring, pursed lip
breathing, and use of accessory muscles.

NURSING INTERVENTIONS
• Assess the patient’s vital signs and characteristics of heartbeat at least every 4 hours.
Assess heart sounds via auscultation.
• Observe for signs of decreasing peripheral tissue perfusion such as slow capillary refill,
facial pallor, cyanosis, and cool, clammy skin.
• Administer prescribed medications for pulmonary hypertension.
• Assess the patient’s vital signs and characteristics of pain at least 30 minutes after
administration of medication.
• Administer supplemental oxygen, as prescribed.
• Discontinue if SpO2 level is within the target range, or as ordered by the physician.
 RHEUMATIC FEVER
ETIOLOGY
Rheumatic fever is an autoimmune disease that occurs as a reaction to a group A β-hemolytic
streptococcal infection, specifically, a pharyngitis. Inflammation from the immune response
leads to inflammatory lesions being found in the heart, blood vessels, brain, and joints.
• GABHS infection. Rheumatic fever only develops in children and adolescents following
group A beta-hemolytic streptococcal (GABHS) pharyngitis, and only infections of the
pharynx initiate or reactivate rheumatic fever.
• Molecular mimicry. So-called molecular mimicry between streptococcal and human
proteins is felt to involve both the B and T cells of peripheral blood, with infiltration of the
heart by T cells; some believe that an increased production of inflammatory cytokines is
the final mechanism of the autoimmune reaction that causes damage to cardiac tissue in
RHD.
• Streptococcal antigens. Streptococcal antigens, which are structurally similar to those in
the heart, include hyaluronate in the bacterial capsule, cell wall polysaccharides (similar to
glycoproteins in heart valves), and membrane antigens that share epitopes with the
sarcolemma and smooth muscle.
• Decrease in regulatory T-cells. Decreased levels of regulatory T-cells have also been
associated with rheumatic heart disease and with increased severity.

RISK FACTOR
Things that may increase the risk of rheumatic fever include:
• Genes. Some people have one or more genes that might make them more likely to develop
rheumatic fever.
• Specific type of strep bacteria. Certain strains of strep bacteria are more likely to
contribute to rheumatic fever than are other strains.
• Environmental factors. A greater risk of rheumatic fever is associated with overcrowding,
poor sanitation and other conditions that can cause strep bacteria to easily spread among
many people.

SIGNS AND SYMPTOMS

Rheumatic fever signs and symptoms can include:
• Carditis • Jerky, uncontrollable body movements
• Polyarthritis (Sydenham chorea) — most often in the
• Chorea hands, feet and face
• Subcutaneous nodules • Outbursts of unusual behavior, such as
• Erythema marginatum crying or inappropriate laughing, that
• Fever accompanies Sydenham chorea
• Painful and tender joints — most often in • Small, painless bumps beneath the skin
the knees, ankles, elbows and wrists • Polyarthralgia
• Pain in one joint that migrates to another • Prolonged PR interval
joint • Increased ESR
• Red, hot or swollen joints
• Chest pain
• Fatigue
• Flat or slightly raised, painless rash with
a ragged edge
• Heart murmur
DIAGNOSTIC LABORATORY
• Throat culture. Throat cultures for GABHS infections usually are negative by the time
symptoms of rheumatic fever or rheumatic heart disease (RHD) appear; make attempts to
isolate the organism prior to the initiation of antibiotic therapy to help confirm a diagnosis
of streptococcal pharyngitis and to allow typing of the organism if it is isolated
successfully.
• Rapid antigen detection test. This test allows rapid detection of group A streptococci
(GAS) antigen, allowing the diagnosis of streptococcal pharyngitis to be made and
antibiotic therapy to be initiated while the patient is still in the physician’s office.
• Antistreptococcal antibodies. Clinical features of rheumatic fever begin when
antistreptococcal antibody levels are at their peak; thus, these tests are useful for
confirming previous GAS infection; antistreptococcal antibodies are particularly useful in
patients who present with chorea as the only diagnostic criterion.
• Acute-phase reactants. C-reactive protein and erythrocyte sedimentation rate are elevated
in individuals with rheumatic fever due to the inflammatory nature of the disease; both
tests have high sensitivity but low specificity for rheumatic fever.
• Heart reactive antibodies. Tropomyosin is elevated in persons with acute rheumatic
fever.
• Rapid detection test for D8/17. This immunofluorescence technique for identifying the
B-cell marker D8/17 is positive in 90% of patients with rheumatic fever and may be useful
for identifying patients who are at risk of developing rheumatic fever.
• Chest radiography. Cardiomegaly, pulmonary congestion, and other findings consistent
with heart failure may be observed on chest radiograph in individuals with rheumatic fever.
• Echocardiography. In individuals with acute RHD, echocardiography identified and
quantitated valve insufficiency and ventricular dysfunction.

MEDICAL MANAGEMENT
• Anti-inflammatory. Treatment of the acute inflammatory manifestations of acute
rheumatic fever consists of salicylates and steroids; aspirin in anti-inflammatory doses
effectively reduces all manifestations of the disease except chorea, and the response
typically is dramatic.
• Corticosteroids. If moderate to severe carditis is present as indicated by cardiomegaly,
third-degree heart block, or CHF, add PO prednisone to salicylate therapy.
• Anticonvulsant medications. For severe involuntary movements caused by Sydenham
chorea, your doctor might prescribe an anticonvulsant, such as valproic acid (Depakene)
or carbamazepine (Carbatrol, Tegretol, others).
• Antibiotics. Your child’s doctor will prescribe penicillin or another antibiotic to eliminate
remaining strep bacteria.
• Surgical care. When heart failure persists or worsens after aggressive medical therapy for
acute RHD, surgery to decrease valve insufficiency may be lifesaving; approximately 40%
of patients with acute rheumatic fever subsequently develop mitral stenosis as adults.
• Diet. Advise nutritious diet without restrictions except in patients with CHF, who should
follow a fluid-restricted and sodium-restricted diet; potassium supplementation may be
necessary because of the mineralocorticoid effect of corticosteroid and the diuretics if used.
• Activity. Initially, place patients on bed rest, followed by a period of indoor activity
before they are permitted to return to school; do not allow full activity until the APRs have
returned to normal; patients with chorea may require a wheelchair and should be on
homebound instruction until the abnormal movements resolve

DRUGS OF CHOICE
• Antibiotics. The roles for antibiotics are to (1) initially treat GABHS pharyngitis, (2)
prevent recurrent streptococcal pharyngitis, rheumatic fever (RF), and rheumatic heart
disease (RHD), and (3) provide prophylaxis against bacterial endocarditis.
• Anti-inflammatory agents. Manifestations of acute rheumatic fever (including carditis)
typically respond rapidly to therapy with anti-inflammatory agents; aspirin, in anti-
inflammatory doses, is DOC; prednisone is added when evidence of worsening carditis
and heart failure is noted.
• Therapy for congestive heart failure. Heart failure in RHD probably is related in part to
the severe insufficiency of the mitral and aortic valves and in part to pancarditis; therapy
traditionally has consisted of an inotropic agent (digitalis) in combination with diuretics
(furosemide, spironolactone) and afterload reduction (captopril)

SURGICAL MANAGEMENT
• If the heart valves are damaged as a result of rheumatic fever, eventually you or your child
may need heart valve repair or heart valve replacement

NURSING DIAGNOSIS
• Acute pain related to inflammation
• Risk for infection related to Chronic recurrence of disease
• Activity Intolerance related to Joint pain and swelling

NURSING INTERVENTIONS
• Assess the child’s pain perception using an appropriate scale every 2 to 3 hours.
• Assess the child’s mobility and physical activity level.
• Monitor pulse rate, and blood pressure; observe for dyspnea, use of accessory muscles,
and skin color before and after activity.
• Assess changes in behavior, such as high-pitched crying, irritability, restlessness, refusal
to move, facial grimace, and aggressive or dependent behavior.
• Examine affected joints, degree of joint pain, and level of joint movement.
• Elevate involved extremities above heart level.
• Maintain bed rest during the acute stage of the disease.
• Advise positional changes every 2 hours while maintaining body alignment.
• Apply bed cradle under outside covers over painful joints.
• Encourage the use of nonpharmacologic interventions such as imagery, relaxation,
distraction, cutaneous stimulation, and heat application.
• Provide toys, and games for quiet, sedentary play.
• Stress the importance of limited activity or the amount of joint movement allowed.
• Teach parents and children about the need for analgesia and that it will help him/her to
feel better.
• Educate parents in proper body positioning and handling of affected parts.
• Administer salicylates and anti-inflammatory medications as prescribed, and advise the
child that the medication will decrease the pain; administer a sustained action analgesic
before bedtime or 1 hour before anticipated movement.
• Teach the children and family members good proper hand hygiene.
• Ensure that the child’s room and equipment are clean and disinfected to prevent the spread
of infection.
• Encourage the children to follow a diet rich in fruits, vegetables, whole grains, and lean
proteins.
• Notify the physician immediately of any upper respiratory infections, elevated temperature,
joint pain, or non-compliance to antibiotic therapy.
• Encourage and teach the child active range-of-motion exercises.
• Instruct the child to resume activity gradually once asymptomatic at rest and indicators of
acute inflammation have resolved
• Encourage the child to increase fluid intake as indicated and allow a dietary intake of low
sodium and low sugar diet.
 KAWASAKI DISEASE
Kawasaki disease (mucocutaneous lymph node syndrome) is defined as an acute febrile
syndrome associated with generalized vasculitis affecting all blood vessels throughout the
body, including the coronary arteries.
The vasculitis can lead to the formation of coronary artery aneurysms which will predispose
the child to thrombus formation and a high risk of myocardial infarction.

ETIOLOGY
• It has an unknown etiology. • There is also a strong suggestion of an
• Does seem to be a genetic predisposition infectious precursor.
to the syndrome.

RISK FACTORS
• Age: Mostly affects children younger than 5.
• Sex: Boys are slightly more likely than girls to develop the disease.
• Ethnicity: More common in people of Asian or Pacific Island descent.

SIGNS AND SYMPTOMS

Kawasaki disease has no imaging or laboratory test that can diagnose it. However, there are
clinical criteria to help with the diagnosis of kawasaki disease.
• Prolonged fever (>100.4°F [39°C]) of 5 or more days
• Four or more of the following symptoms:
• Changes in hands and feet (erythema, edema, peeling)
• Polymorphous exanthema (diffuse maculopapular rash of the trunk and
extremities)
• Bilateral conjunctivitis without exudates
• Changes in lips and mouth (erythema, strawberry tongue, dry, cracked lips)
• Cervical lymphadenopathy (>1.5 cm diameter, usually unilateral)

3 Phases of Kawasaki Disease:

Acute Phase (Week 1 and 2)
Children are very irritable and uncomfortable from the fever and inflammatory process that
causes joint pain.
Subacute Phase (Week 3 and 4)
The fever, rash, and lymph node swelling go away, but other symptoms may remain. Some
symptoms associated are irritability, poor appetite, some eye redness, and peeling skin in the
hands and feet.
Convalescent Phase (Week 6 and 8)
All symptoms are gone, but a blood test show there is still abnormal inflammation in the
body. Ends when lab values returns to normal

Changes in laboratory data may help support diagnosis or rule out other diseases
The changes mandate a thorough investigation into possible causes for the child’s symptoms
(e.g., viral infection, scarlet fever, juvenile rheumatoid arthritis, etc.) If no definitive cause is
determined and the child’s symptoms fit the criteria listed above, the child is given the
diagnosis of Kawasaki disease.
• Thrombocytosis • Elevated liver enzymes
• Leukocytosis
• Mild anemia • Elevated erythrocyte sedimentation rate
(ESR) and C-reactive protein (CRP)
DIAGNOSTIC LABORATORY
• Electrocardiogram (ECG or EKG): Electrodes are attached to the skin to measure the
electrical impulses of the heartbeat. Kawasaki disease can cause heart rhythm problems.
• Echocardiogram (cardiac ultrasound): Uses ultrasound images to show how well the
heart is working and can help identify problems with the coronary arteries.
• Blood tests: CBC, ESR, CRP, GGT

MEDICAL MANAGEMENT
Treatment for Kawasaki disease is focused on addressing the immediate symptoms and
preventing any long-term consequences.
• Children are treated with 2 g/kg of intravenous immune globulin (IVIG). This dose may be
repeated if the fever does not break.
• High-dose aspirin at 80 to 100 mg/kg divided four times a day is also continued for 48 to
72 hours after the fever breaks. The aspirin is then continued at a low dose of 3 to 5
mg/kg/day once a day for 6 to 8 weeks with no evidence of coronary artery abnormalities.
If abnormalities occur, aspirin may be continued indefinitely.

DRUG OF CHOICE
• Gamma globulin: Infusion of an immune protein (gamma globulin) through a vein
(intravenously) can lower the risk of coronary artery problems. This helps to reduce
inflammation in the vessels.
• Aspirin: High doses of aspirin might help treat inflammation. Aspirin can also decrease
pain, joint inflammation and fever. The aspirin dose will likely be lowered once the fever
has been gone for 48 hours.

NURSING DIAGNOSIS
• Hyperthermia related to inflammatory disease process as evidenced by fever as high as
39°C that last for more than 5 days
• Impaired skin integrity related to peripheral erythema as evidenced by erythematous
generalized rash
• Impaired oral mucous membrane related to dehydration as evidenced by dry mouth

NURSING MANAGEMENT
a) Promoting comfort and rest of the child, and preventing dehydration
Skin:
• Provide tepid sponge bath for fever.
• Remove wet and wrinkled bed linens.
• Instruct intake of adequate fluid intake.
• Instruct intake of protein-rich foods such as eggs, beans, and chicken.
Eyes:
• Darken room; Provide cool cloth to cover eyes or instruct to let child wear sunglasses.
• Instruct child to avoid rubbing eyes.
• Provide artificial tear drops as required by physician.
Lips and Mouth:
• Provide soft food, nonirritating foods such as gelatin.
• Provide mouth care every 1-4 hours with special mouth swabs; soft tooth brush only
when healing occurred.
• Apply petroleum to dry and cracked lips.
Dehydration:
 • Monitor urinary output.
• Monitor intravenous infusion hourly.
• Asses skin turgor to aid in assessment of hydration status.
• Instruct patient to maintain adequate intake of water.
b) Carrying out continual cardiac monitoring and assessment for complications
• Take vital signs every 2 hours.
• Ensure proper functioning of cardiac monitor, observe for and report signs of
arrhythmias, myocarditis and congestive heart failure.
c) Monitor child for signs of aspirin toxicity when high-dose aspirin is prescribed
d) Provide for emotional support and diversional activities appropriate for age
• Explain procedure to the child.
• Provide soft toys and quiet play.
• Provide play therapy.
• Allow the child to have periods of uninterrupted rest.
e) Provide emotional support for the parents who are distressed and concerned about their
child’
• Involve the parents in comforting the child and care of child.
• Provide health education.
• Encourage parents to verbalize their concerns, fears, and questions.
 INFECTIOUS ENDOCARDITIS
Infective endocarditis is inflammation and infection of the endocardium or valves of the heart.
Bacteria travel through your bloodstream and attach to damaged tissue in your endocardium,
forming colonies (vegetations). These colonies release toxins and enzymes that destroy
healthy cells and prevent healing.
It is noted in children with and without heart disease. The incidence of infective endocarditis
in children is rare but may be increasing due to the increased survival of children with
congenital heart disease.

ETIOLOGY
The infection is generally caused by Streptococcus viridans and Staphylococcus aureus,
although fungal organisms have also been noted.

RISK FACTORS
Risk factors include the presence of a prosthetic heart valve, structural or congenital heart
disease, intravenous drug use, and a recent history of invasive procedures.
• Congenital heart defects • Damaged heart valves
• Long-term catheter use • Artificial heart valves
• Poor dental health • Implanted heart device

SIGNS AND SYMPTOMS

2 Presentation of Infective Endocarditis:
Acute Presentation
• Systemic response to infection
• Children have high-spiking fevers
• Severely ill and toxic in appearance.
• Symptoms of congestive heart failure (CHF) may be present.
• Murmurs are frequently noted due to destruction of the cardiac valve tissue.
Subacute Presentation
• Persistent low-grade fever • Fatigue
• Malaise • Rigors
• Weight loss, • Diaphoresis
• Arthralgias

Diagnostic Testing
• Positive blood cultures are necessary for a diagnosis of infective endocarditis.
• Echocardiogram is extremely helpful in allowing for visualization of the vegetations as
well as the damage to the heart itself such as valve destruction and perforation, rupture of
chordae, and development of valvar leaks.
• Other laboratory studies will reveal proteinuria or hematuria, a normochromic,
leukocytosis, and an increased elevated erythrocyte sedimentation rate (ESR).

MEDICAL MANAGEMENT
Treatment is aimed at the underlying bacterial infection but an extended course of antibiotics
is necessary as the organisms are imbedded in a fibrin platelet matrix in high concentrations.
• Once sensitivity is determined, treatment is typically for 4 to 6 weeks of IV therapy. This
will necessitate the insertion of a PICC in children so they may go home and receive home
nursing services to administer their antibiotic therapy.
• Lesions will heal, but children may be left with long-term sequelae such as renal
dysfunction from thrombi or leaky cardiac valves from primary damage.
• All children diagnosed with endocarditis must receive prophylactic antibiotics prior to
some invasive procedures including dental work.

DRUG OF CHOICE
Antibiotics: Antibiotics are usually given through the vein (intravenous or IV) for several
weeks.

SURGICAL MANAGEMENT
Infective endocarditis surgery: If the heart valves are damaged or developed severe heart
infection, the child may need surgery to clear away bacteria, and have heart valve repair or
heart valve replacement. Repair or replacement procedure depends on the type and severity of
heart valve damage.

NURSING DIAGNOSIS
• Hyperthermia secondary to infective process of endocarditis as evidenced by temperature
of 38.7 degrees Celsius, rapid breathing, profuse sweating, and chills
• Decreased cardiac output secondary to valvular dysfunction from infective process as
evidenced by fatigue and inability to do ADLs as normal
• Impaired gas exchange related to alveolar inflammation due to increased ventricular
pressure secondary to endocarditis, as evidenced by productive cough, crackles heard on
auscultation, shortness of breath, pallor noted on the conjunctiva, nailbeds, and buccal
mucosa and fatigue.

NURSING MANAGEMENT
• Monitor patient’s vital signs.
• Remove excessive clothing, blankets and linens. Adjust the room temperature.
• Administer the prescribed antibiotic and anti-pyretic medications.
• Provide tepid sponge bath.
• Elevate the head of the bed.
• Assess the patient’s breathing pattern, respiratory rate, auxiliary muscle use, indications of
air hunger, lung excursion, cyanosis, and any notable changes in the patient’s vital signs.
• Auscultate the patient’s lung fields to check the presence of crackles with the use of a
stethoscope.
• Determine and monitor the patient’s oxygen saturation, WBC count, and ABG levels as
indicated and report any deviation from the normal values.
• Assess the patient skin color, and observe the color of the mucous membranes, and nail
beds to see if there is peripheral cyanosis.
• Instruct patient to have proper rest periods and to get a night of adequate sleep.
• Administer supplemental oxygen, as prescribed. Discontinue if SpO2 level is above the
target range, or as ordered by the physician.
• Have airway emergency equipment at the ready at all times.
• Educate the parents to understand the symptoms and indications of endocarditis.
• Assess characteristics of heart beat at least every 4 hours. Assess heart sounds via
auscultation. Observe for signs of decreasing peripheral tissue perfusion such as slow
capillary refill, facial pallor, cyanosis, and cool, clammy skin.
• Educate patient and parents on stress management, deep breathing exercises, and
relaxation techniques.
 REFERENCES
Maternal and Child Health Nursing. Care of the Childbearing and Childrearing Family. 8th
Edition. (2017) Lippincott Williams & Wilkins 530 Wallnut Street Philadelphia
Transposition of the Great Arteries (TGA) Ari Michael Cedars, M.D. (2010)
Hopkinsmedicine.org
Congestive Heart Failure (CHF) Michelle Llamas, BCPA, Sophia Clifton (2023)
Drugwatch.com
Living with Congestive Heart Failure (CHF) Nita Crighton (2022) Encompasshealth.com
Belleza, M. (2022). Rheumatic Fever. https://nurseslabs.com/rheumatic-fever/
Centers for Disease Control and Prevention. (2022). Rheumatic Fever.
https://www.cdc.gov/groupastrep/diseases-public/rheumatic-fever.html#
Nies, M. (n.d.). Pulmonary Hypertension in Children.
https://www.hopkinsmedicine.org/health/conditions-and-diseases/high-blood-pressure-
hypertension/pulmonary-hypertension-in-children#
Pulmonary hypertension. (2022). Mayo Clinic. https://www.mayoclinic.org/diseases-
conditions/pulmonary-hypertension/diagnosis-treatment/drc-20350702#
Persistent Pulmonary Hypertension of the Newborn (PPHN). (2022). Nationwide Children’s.
https://www.nationwidechildrens.org/conditions/persistent-pulmonary-hypertension-of-
the-newborn-pphn
Barnes, B. (n.d.). Kawasaki Disease. https://www.hopkinsmedicine.org/health/conditions-
and-diseases/kawasaki-disease
Martin, P. (2023). 6 Kawasaki Disease Nursing Care Plans. https://nurseslabs.com/kawasaki-
disease-nursing-care-plans/5/
Kawasaki Disease. (2021). Mayo Clinic. https://www.mayoclinic.org/diseases-
conditions/kawasaki-disease/symptoms-causes/syc-20354598\
Infective Endocaditis. (2022). Cleveland Clinic.
https://my.clevelandclinic.org/health/diseases/23068-infective-endocarditis
Infective Endocarditis Surgery. (2022). Cleveland Clinic.
https://my.clevelandclinic.org/health/treatments/17125-infective-endocarditis-surgery
Curran, A, (n.d.). Endocarditis Nursing Diagnosis and Nursing Care Plan.
https://nursestudy.net/endocarditis-nursing-diagnosis/