FINALS Lecture: NCM 109: Maternal Cause: rhinovirus, respiratory syncytial virus,

adenovirus, parainfluenza virus, and influenza virus.

and Child Nursing at Risk or with
Problems (Acute and Chronic)
Nursing Care of Children with Alteration
Oxygenation
Choanal Atresia
Is an obstruction of the posterior nares that prevents an
infant from drawing air through the nose and down into
the nasopharynx
This condition is congenital and may be caused by an
obstructing membrane or more rarely, a bony growth.
Types: unilateral and bilateral
Etiology: Nasal cavities extend posteriorly during
development under the influence of the posteriorly
directed fusion of the palatal process; thinning of the
membrane occur, which separates the nasal cavities
from oral cavities. By the 38th day of development, the
two layered membrane consisting of nasal or oral
epithelia ruptures and form the choanae ( posterior nares
). Failure of this rupture result in choanal atresia.
Assessment
 Signs of respiratory distress after birth as they
attempt to breathe through their nose.
 Passing of a soft #8 or # 10 French catheter
through the posterior nares to the stomach
confirms presence of atresia.
 Holding the newborn mouth’s closed and then
gently compressing first one nostril and then the
other. If atresia is present, infant will struggle and
become cyanotic.
 Noisy breathing
 Feeding difficulties
 Infant’s color improves when they open their
mouth to cry.
 Become cyanotic when feeding.
Treatment
Local piercing of obstructing membrane
Surgical removal of bony growth
Assessment
 Nasal congestion
in
 Watery rhinitis
 Low-grade fever
 Mucous membrane of the nose becomes
edematous and inflamed
 Posterior rhinitis may lead to Pharyngitis
 May lead to cough
 Swollen, palpable cervical lymph nodes
Therapeutic Management
 Antibiotics (secondary Bacterial infection)
 Antipyretic
 Do not give aspirin for children below 18 years old.
 Saline nose drops or nasal spray to liquefy nasal
secretions.
 Remove nasal mucus before feeding.
 Cool mist vaporizer loosen nasal secretions
Croup (Laryngotracheo bronchitis)
It is an acute inflammatory condition of the larynx,
trachea, and major bronchi.
It primarily affects children between 6 months to 3 years
of age, the origin is usually viral.
In children between 3 and 6 years old, it may occur.
In bacterial form commonly “ haemophilus influenzae”.
It usually spread by breathing in airborne droplets
containing viruses or by having contact with
infected objects.
Assessment
 Slightly elevated temperatures
 Barking cough (croupy cough)
 Inspiratory stridor
 Marked retraction.
 Diagnostic tests:
o Pulse oximetry – an oximeter is a small
machine that measures the amount of oxygen
in the blood.

IV fluid to maintain their glucose and fluid level until Therapeutic Management
surgery
 Cool moist air combined with corticosteroid given by
Avoid bottle feeding because it may cause aspiration to nebulizer or cool mist tent.
the lungs.  Insertion of a large bore needle into the trachea
followed by tracheostomy (done only if the child is in
Acute Nasopharyngitis hospital)
Common colds  Tracheotomy – an incision into trachea is made to
open upon a passage for the air to enter proximal to
Most frequent infectious disease in children the laryngeal obstruction.
 Corticosteroid
Aspiration Therapeutic management
Inhalation of foreign object into the airway.  Bronchoscopy – to remove foreign body.
 Assess child closely for signs of bronchial
When foreign object such as coin or peanut,
edema and airway obstruction.
immediate reaction is choking and hard forceful
 Obtain frequent v/s – increase pulse and RR
coughing.
suggest increase edema and obstruction.
Series of back blows or subdiaphragmatic  NPO for at least an hour.
abdominal thrust may be used.  Once gag reflex is present, offer cool fluid
cautiously.
 Apply cool moist air or ice collar – reduce
edema.
Bronchitis

Inflammation of the major bronchi and trachea

Bronchial Obstruction
Aspirated foreign object lodge in the right bronchus
obstructing a portion or all of the right lung.
The alveoli distal to the obstruction will collapse as
the air remaining in them becomes absorbed
(atelectasis)
Characterized by fever and cough in conjunction
with nasal congestion.
Causative agents: influenza viruses, adenovirus,
Mycoplasma pneumoniae.
Assessment
 Mild URTI for 1-2 days after which they
develop fever and a dry hacking cough.
 Symptoms may last for a week or 2 wks.
 Rhonchi and coarse crackles.
 Chest X-ray – reveal diffuse alveolar
hyperinflation and markings in hilus of the
lung.
Therapeutic Management

Hyperinflation and pneumothorax may occur The aim is to relieve respiratory, reduce fever and
maintain adequate hydration.
Assessment
Antibiotic for bacterial infection.
 The child coughs violently and dyspneic
 Hemoptysis Bronchiolitis
 Fever
Inflammation and edema of the fine
 Purulent sputum
bronchioles and small bronchi
 Leukocytosis
 Localized wheezing Usually d/t viral illness
 Respiratory distress
 Diagnostic exam The most common cause: RSV –
respiratory syncytia virus)
o Chest X-ray
Other causative agents include adenovirus,
parainfluenza and influenza virus
Allergy triggers
Occurs under 2 years of age and has a peak
Environmental (tobacco smoke)
incidence between 3 and 6 months of age most
commonly during the winter and early spring Indoor Irritants (mice and cockroaches)
months.
Outdoor Irritants (pollen, grasses, pollution)
Assessment
Viral respiratory illness
 Congestion
 Rhinorrhea ASSESSMENT:
 Fever  Dry cough
 Cough  Difficulty exhaling
 Wheezing  Dyspnea
 Retraction  Wheezing on expiration
Therapeutic Management  Decrease O2 saturation
 Chest tightness
For children with less symptoms:
Physical assessment
 Antipyretics
 Adequate hydration Wheezing evident by auscultation
 Nasal suctioning Hyper resonant by percussion (air filled lungs)
 Nasal saline
 Avoidance of tobacco exposure Retractions –chest wall is drawn inward with
breaths because of use of intercostal accessory
For severe illness muscles to achieve full breaths.
• Hospitalization Assume sitting or standing position for comfort.
• Prophylactic:
o Palivizumab (monoclonal antibody) Pulmonary Function Studies - Spirometry is
to prevent RSV for infant with helpful in evaluating asthma in children.
gestational age less than 29 weeks Good pulmonary functions depends on the ff:
or less than 1 year of age with
preexisting health condition.  Good ventilations
 Adequate transfer of gases across the
Asthma alveolar capillary membrane
Chronic inflammatory disease of the airways that  Adequate volume and distribution of
causes airway hyper responsiveness, mucosal pulmonary capillary blood flow to body cells
edema and mucus production. Asthma means Note: normal expiratory rate is 2 or 3 seconds but
“panting” due to narrowed bronchioles due to bronchospasm
Risk Factors expiratory rate is more than 10 seconds.

• Genetic Peak Expiratory Flow Rate

• Environmental exposures such as:  Measure gross changes in peak expiratory
o Allergens flow
o Stress
o Pollution Peak Flow Meter
• Note : these affects body’s immune  Place the number indicator at the bottom
• Response  Place meter in the mouth, deep breath and
Inflammation, bronchoconstriction, increased blows out as hard as possible
mucus production.  Repeat 2 more times
  Record the highest number achieved as • Teach and encourage the cause of
PFM results diaphragmatic breathing and coughing
 Done daily for 2 weeks techniques.
• Administer antibiotics are prescribed.
MANAGEMENT:
• Encourage the patient to be immunized against
Four components influenza and streptococcus pneumoniae.

1. Measure of asthma assessment and Cystic Fibrosis

monitoring (history, PA, objective testing)
2. Education of home self management.
3. Control of environmental factors
4. Pharmacologic therapy (quick relief and
Long acting medication.
Primary goal in Asthma Management- prevention of
airway inflammation.
Short acting ß-agonist – mild intermittent asthma,
e.g. Albuterol
Inhaled corticosteroid – persistent and severe
symptoms, e.g. Fluticasone propionate, prednisone
Treatment:
Most common fatal autosomal recessive disease
among the Caucasian population.
Inherited multi-system disorder among children and
adults characterized by obstruction and infection of
airways and by maldigestion and its consequences.
It is the major cause of several lung disease in
children and is responsible for most exocrine
pancreatic insufficiency during early life.
The disease is characterized by a thick mucus
secretion, particularly in the pancreas and the
lungs, as well as electrolyte abnormalities in sweat
gland secretion.

Methylanthines – such as aminophylline and An abnormality of the long arm of chromosome 7

theophylline, are used because of their results in the inability to transport small molecules
bronchodilating effects. They relax bronchial across cell membranes, leading to dehydration of
smooth muscle, increase movements of mucus in epithelial cells in the airway and pancreas.
the airways and potentiate contraction of
Pancreas Involvement
diaphragm.
Acinar cells of
Anticholinergics – maybe particularly beneficial to
pancreas normally
asthmatics, who are not candidates for beta agonist
produce lipase,
and methylscanthines because of underlying
trypsin and
cardiac disease.
amylase- enzymes
Mast cell inhibitors – chromolyn sodium, a mast that digest fat,
cell inhibitor, is an integral part of the treatment of protein and
asthma. It prevents the release of chemical carbohydrate.
mediators of anaphylaxis, thereby resulting in
These enzyme
bronchodilation and decrease in airway
secretions may be
inflammation.
so thick that they plug ducts, resulting to atropy of
Nursing Intervention acinar cells and an inability to produce enzymes.

• Administer bronchodilators as prescribed. Absence of pancreatic enzymes in the duodenum

• Evaluate Effectiveness of mini nebulizer of results to inability to digest fat, protein and some
IPPB treatments. sugars.
• Instruct and encourage patient in diaphragmatic
• Steatorrhea- bowel become large, bulky,
breathing and effective coughing.
and greasy and foul.
• Administer oxygen by the method prescribed.
• Malnutrition
• Give patient 6-8 glasses of fluids day unless
• Malabsorption of fat soluble vitamins
cor pulmonale is present.
(A,D,E).
• Meconium is thick and tenacious
Lung Involvement
The anteroposterior diameter of the chest is
enlarged.
Thickened mucus pools in the bronchioles and
often results in frequent infections.
Atelectasis may occur because of absorption of air
from alveoli behind blocked bronchioles.
Clubbed fingers may occur
Sweat testing- more than 60 meq/L of sodium
chloride (normal-20meq/L).
Duodenal Analysis-done by passing NGT into
duodenum, secretion aspirated for analysis of ph,
trypsin content, & pancreatic enzyme assay
Stool analysis- stool is collected and analyzed for
fat content.
Pulmonary testing- Chest X-ray and pulmonary
function test to determine the extent of atelectasis
and emphysema.

Sweat Gland Involvement Therapeutic management

The level of chloride to sodium in perspiration is It is collaborative to reduce the involvement of the
increased 2 to 5 times above normal resulting to pancreas, lungs, and sweat glands.
“salty” perspiration.
• Antibiotic treatment
Assessment • Expectorants
• Mild analgesics/antipyretics
 Screening test
• (Aspirin / acetaminophen)
 Chromosomal abnormality
 Abnormal chloride concentration in Nursing Interventions
 Perspiration.
 Absence of pancreatic enzyme in the • Bed rest
 Duodenum • Immunization
 Presence of immunoreactive trypsinogen • Increase fluid intake
 In blood. • Protect patient from fatigue and chilling
 In newborn- fails to regain normal • Good hygiene
Birth weight 7 to 10 days after birth
Secondary to infant’s inability to
Absorb milk fat.
 Poor weight gain
 Meconium ileus
 In undiagnosed children- complains of
Increased hunger and steatorrhea
Stool.
 Respiratory infection – wheezing and
Rhonchi, hyperresonant chest, cough
And clubbing fingers.
Diagnostic Test
 Assessment
Systolic murmur at second intercostal space, left
upper sternal border or left clavicular area.
If defect is large - Rales , congestion, increased
work of breathing, difficulty feeding or failure to
Nursing Care of Children with Alteration in thrive.
Cardiovascular Function
Severity of symptoms depend on the amount of
Congenital Heart Defects blood shunting to the lungs.

Classification Confirmed by echocardiogram.

A. Increasing pulmonary blood flow

B. Decreasing pulmonary blood flow
C. Obstruction to systemic blood flow
D. Single ventricle defect
Cyanotic heart disease – when venous blood from
the right side of the heart mixes with blood in the
left side
Acyanotic heart disease – the blood shunts from
the left to the right. Management
Medical Management
• Diuretics (Furosemide)
• Increased caloric intake
• PDA closure – left heart dilation
• Indomethacin, NSAID, and Prostaglandin
facilitate closure of PDA
Older children-
• Closure of PDA through catheterization
• Surgical closure of PDA for premature baby
Atrial Septal Defect (ASD)

Defect that increases Pulmonary Blood Flow A portion of atrial septal tissue does not completely
form.
Patent Ductus Arteriosus
Secundum type defect- most common type located
Occurs when the fetal at the center of the atrial septum.
shunt fails to close after
several days of life. Primum defect- found low in the atrial septum near
the IVC
Incidence in premature
ranges from 20% to 60% Sinus venosus defect- found high in the septum
where the pulmonary veins enter the left atrium.
If ductus arteriosus does
not close after birth, it allows blood to flow from the Acyanotic defect that allows blood to flow from high
aorta (area of high pressure) through the PDA and pressure left atrium to low pressure right atrium.
into the main pulmonary artery (area of low
pressure)
Acyanotic defect as blood flowing from aorta is
fully oxygenated.

Assessment
If defect is small
• Undetected, requires no intervention
If defect is large enough
• Rales
• Congestion
• Tiring with activity
• Poor weight gain
• Murmur at left upper sternal border
• ASD is confirmed with an echocardiogram
Management
• Management is based on the size of defect and
child’s age.
• Diuretics
• Closure of ASD-if defect is 5mm or larger
• Median sternotomy incision
• Cardiopulmonary bypass.
Ventricular Septal Defect
Occur when a portion of ventricular septum does
not completely close.
Is an abnormal opening in the septum between the
right and the left ventricles
It may vary in size from very small defects (Roger’s
defect) to very large defects, and may occur in
either the membranous or muscular portion of the
ventricular septum.
Assessment
 Acyanotic defect that allows blood flow from left
side of the heart to the right side of the heart.
 This increases pulmonary blood flow and
ultimately increases the volume of blood
returning to the heart causing left heart dilation.
 Murmur at left lower sternal border
 Symptoms are similar to those found with PDA
or ASD
 Symptoms of CHF (Tachypnea, poor feeding,
failure to thrive)
 Condition confirmed by echocardiogram
Management
• Small defects closes spontaneously
• Diuretics (Furosemide)
• Increase in caloric density of milk formula
• Closure of VSD by catheterization or surgically
(median sternotomy)
Atrioventricular Septal Defect (AVSD)
This defect comprises several congenital heart
defects.
A primum ASD, a high VSD and failure of the
tricuspid and mitral valve to develop and attach
correctly.
Pathophysiology
• Blood freely mixes between right and left side.
• Pulmonary blood flow can significantly increase
• Complete AVSD allows for right to left shunting.
• The atria can become dilated through
regurgitation of blood through the incompetent
valves.
Assessment
 Symptoms of CHF
 Diagnosis is confirmed with echocardiogram
 Cardiac catheterization to measure pulmonary
measures and confirm reactivity with the
administration of oxygen or nitric oxide.
Management
• Furosemide, Digoxin, ACE inhibitor (captopril,
enalapril)
• Surgical correction by 3 months of age if there
is increase pulmonary pressures.
• Pulmonary artery band- band surgically
placed around the pulmonary artery that
constricts it to increase the resistance within the
pulmonary artery.
• Surgical repair – consist of closing atrial and
vsds and repairing the mitral and tricuspid
valve.
• Surgical intervention goal is to repair the mitral
valve so no stenosis and minimal regurgitation
exist.
• Artificial valve replacement
Defect with Mixed Blood Flow
Transposition of the Great Arteries
Second most common congenital defect
Described as reversal of the great arteries.
The aorta coming off of the right ventricle and
pulmonary artery arising from the left ventricle.
Pathophysiology
This defect results in 2 separate circulations; the
right manages the systemic circulation, and the left
manages the pulmonary circulation.
For life to be sustained, there must be
accompanying defect that provides for the mixing of
oxygenated and unoxygenated blood between the
two circulations.
The mixing of oxygenated and unoxygenated blood
occurs through one or more of the following shunts:
A. Atrial septal defect
B. Ventricular septal defect
C. Patent ductus arteriosus
D. Patent foramen ovale
Assessment
Clinical manifestations:
Influenced predominantly by the extent
intercirculatory mixing:
A. Cyanosis – usually developing shortly after
birth ( degree depends on the type of
associated malformations )
B. Congestive heart failure – manifested by
tachypnea cardiomegaly, hepatomegaly clinical
manifestations:\
C. Fatigability
D. Slow weight gain
E. Clubbing of the fingers and toes
Diagnostic Test
• Chest X-ray - cardiomegaly, narrow
mediastinum, egg-shaped cardiac silhouette,
increased
• Vascular markings ( decreased vascular
markings in children with associated pulmonary
stenosis ).
• ECG - right axis deviation, right or biventricular
hypertrophy.
• Echocardiogram- confirm the diagnosis
• Laboratory tests:
o Polycythemia
o Thrombocytopenia
Management
Surgical correction: Jatene Procedure or arterial
switch.
Palliative procedures
a. Rashkind procedure - the creation of an atrial
septal defect with a balloon catheter during
cardiac catheterization.
b. Blalock-Hanlon procedure - surgical creation of
an atrial septal defect.Management
c. Pulmonary artery banding (indicated for infants
with ventricular septal defects with large
pulmonary blood flow ).
d. Systemic-pulmonary anastomosis (indicated for
some infants with severe pulmonary stenosis ).
Complete correction
a. Mustard procedure – with
cardiopulmonary bypass, the atrial septum
is removed and a baffle of Dacron velour
and / or pericardium is sutured in place in
such a way that the pulmonary venous blood
is directed toward the right ventricle and
the systemic venous blood is directed
toward the left ventricle.
of b. Senning procedure – with cardiopulmonary
bypass, the systemic and pulmonary returns are
rerouted by arranging flaps of the interatrial
septum and right atrial free wall to form the new
venous channels.
c. Rastelli procedure - the surgery of choice for
transposition with ventricular septal defect and
ventricular outflow-tract obstruction.
d. C.2 with cardiopulmonary bypass, the
ventricular septal defect is closed in such a way
that the left ventricle communicates with the
aorta. The pulmonary artery is ligated, and the
 right ventricle is connected to the distal portion 3. Overriding of aorta
of the pulmonary artery by means of a valve 4. Right ventricular hypertrophy
bearing tubular graft.
Pathophysiology
e. As with other types of congenital cardiac
surgery, the question of optimum timing for Obstruction of the blood flow from the right ventricle
surgery is controversial. Increasingly, total to the pulmonary circulation is caused by
correction is recommended when feasible. obstruction at the pulmonary valve level or the
infundibular area of the right ventricle below the
Anomalous Pulmonary Venous Return and
pulmonary valve.
Truncus Arteriosus
Unoxygenated blood is shunted from the right
Two rare, uncommon cyanotic defects.
ventricle through the ventricular septal defect
APVR is a result of failure of pulmonary venous directly to the aorta.
connections to unite with the left atrium in the utero.
The right ventricle is hypertrophied because of high
Requires urgent surgical intervention right ventricular pressure.
Clinical Manifestations:
• Are variable and depend on the size of the
ventricular septal defect and the degree of right
ventricular outflow obstruction.
• Cyanosis:
o Not cyanotic at birth but may develop
cyanosis as they grow and stenosis
TA is characterized by single arterial vessel that becomes relatively more severe.
originates from the heart, overrides the ventricular o Cyanosis may at first be observed only
septum, and supplies all of the systemic, coronary,
with exertion and crying but may also be
and pulmonary blood flow.
cyanotic even at rest.
The pulmonary arteries arise at some point along o Hypercyanotic spell
this large vessel. o Infundibular stenosis may be minimal so
that cyanosis never develops “pink
Defect that Decrease Pulmonary Blood Flow tetralogy”.
Tetralogy of Fallot  Clubbing of the fingers and toes
 Squatting (posture assumed
Prevalence: 4 to 5 per 10,000 live birth once the child reached the
This defect accounts for about 7% to 10% of cases walking stage )
of congenital heart disease  Slow weight gain
 Dyspnea on exertion
 Hypoxic spells, transient cerebral
Ischemia
Diagnostic Evaluation
Auscultation
a. Single second sound (aortic
component )
b. Systolic ejection murmur at the second
and third interspaces to the left of the
sternum.
Four components of Defect c. Prominent ejection click heard
1. Right ventricular-outflow stenosis or atresia immediately after the first heart sound.
2. Ventricular septal defec Chest X-ray
 a. Heart size normal
b. Pulmonary segment small and concave
(“boot-shaped heart”)
c. Diminished pulmonary vascular markings
ECG – right axis deviation; right ventricular
hypertrophy
Laboratory data
a. Polycythemia
b. Increased hematocrit
Treatment
Goal is to improve oxygenation of arterial blood.
Palliative
a. Blalock-Taussig shunt – anastomosis
between the right or left subclavian artery
and the right pulmonary artery (preferred
method)
b. Waterston shunt - anastomosis between
the posterior lateral aspect of the ascending
aorta and the right pulmonary artery.
Total correction
a. Removal of shunt if previously performed.
b. With cardiopulmonary bypass, ventricular
septal defect is repaired and right
ventricular-outflow obstruction is relieved.
c. Total correction is increasingly being
advocated for all infants in whom pulmonary
arteries are of sufficient size.
Defects with obstruction to obstruction to
systemic blood flow
Coarctation of the Aorta
Is the narrowing or constriction of the vessel at any
point; most commonly the constriction is located
just distal to the origin of the left subclavian artery
in the vicinity of the ductus arteriosus.
Pathophysiology:
The narrowing of the aorta obstructs blood flow
through the constricted segment of the aorta thus
increasing left ventricular pressure and workload.
Collateral vessels develop, arising chiefly from
the branches of the subclavian and the
intercostals arteries, bypassing contracted
segment of the aorta and supplying circulation to
the lower extremities.
Clinical Manifestations:
Usually asymptomatic in childhood – growth and
development normal.
May demonstrate: occasional fatigue, headache,
nose bleeds, leg cramps
Absent or greatly reduced femoral pulsations.
Hypertension in upper extremities and diminished
blood pressure in lower extremities
Symptoms secondary to hypertension (rare in
children)
Severe anomalies cause symptoms in infants,
including growth failure, tachypnea, dyspnea,
peripheral edema, and severe congestive heart
failure.
Diagnostic Evaluation:
• Auscultation – non-specific systolic murmur
heard along the sternal border.
• Chest X-ray – prominent aorta; rib notching is
common finding in children over 10 years of
age.
• Seriously ill infants demonstrate significant
cardiomegaly with increased pulmonary
vascularity.
• ECG – normal or varying degrees of left • Narrow pulse pressure: weak peripheral pulses,
ventricular hypertrophy treatment: Systolic heart murmur, left ventricular
• Infants – vigorous management of congestive hypertrophy.
heart failure and surgical correction is indicated
Diagnostic Evaluation:
for infants who present in the first 6 months of
life with heart failure. Auscultation
• Older child – surgical resection is
recommended for children between the ages 2- a. Harsh, low pitched systolic ejection murmur,
4 years with significant coarctation. maximal at the second right intercostals space,
radiates to apex, back and neck.
Treatment: b. Ejection click at fourth interspace to the left of
the sternum (mild to moderate cases). Single
Surgery – resection of the coarcted segment and
or narrowly split-second heart sound
end-to-end anastomosis or graft.
o Chest X-ray – dilated ascending aorta and
varying degrees of left ventricular
enlargement.
o ECG – normal or left ventricular hypertrophy.
Strain pattern
o T- wave inversion) is evidence of severe
stenosis.
Aortic Valvular Stenosis o S-T segment depression indicates
myocardial ischemia.
Occurs when there is
an obstruction to the left Treatment
ventricular outflow at
• Beta blocker or Calcium channel blocker-
the level of the valve.
prevent ventricular hypertrophy
Most common form of • Cardiac catheterization
aortic stenosis; others • Aortic Valvulotomy or Prosthetic Valve
being hypertrophic Replacement (indicated for children who are
subaortic and symptomatic or have evidence of left ventricular
supravalvular. strain on electrocardiogram ).

Pathophysiology: Single-Ventricle Defect

• Obstruction of blood flow through the aortic A variety of congenital anomalies such as mitral
valve into the aorta atresia, aortic atresia,
• Increased left ventricular pressure (to overcome
Or pulmonary atresia.
resistance of the obstructed valve)
• Results to myocardial ischemia (imbalance Hypoplastic left heart syndrome is a rare disorder
between the increased O2 requirement of the which results when there is a poor or no flow to the
hypertrophied left ventricle and the amount of left ventricle secondary to mitral or aortic stenosis
oxygen that can be supplied to the or atresia.
myocardium).
Clinical manifestations:
• Rarely symptomatic during infancy
• Severe cases may demonstrate evidence of
decreased cardiac output.
• Faint peripheral pulses or exercise intolerance
• Older children may experience chest pain,
dyspnea and fatigue with exertion.

Rheumatic Fever
Is a systemic disease characterized by
inflammatory lesions of connective tissue and
endothelial tissue.
Etiology: unknown; thought to be autoimmune
response to group A beta hemolytic streptococcus
specifically, pharyngitis.
Preceded by streptococcal infection of the throat or
URT at an interval of several days to several
weeks.
Pathophysiology:
• Aschoff body - pathologic lesion;
• Exudative and proliferative inflammatory
reactions of the mesenchymal tissue of the
heart, joints, blood vessels and subcutaneous
tissues;
• May involve the leaflets and/or chordae
tendineae of the heart valves, most frequently
the mitral and / or aortic valves.
Clinical Manifestations:
A. Major manifestations:
a. Carditis – manifested with significant
murmurs, signs of pericarditis, cardiac
enlargement, or congested heart failure.
b. Polyarthritis - migratory and manifested by
swelling, heat, redness and tenderness;
pain and limitation of motion of two or more
joints;
According to Jones Criteria: diagnosed as RHF if
there are two major manifestation, or one major
and two minor manifestations.
c. Sydenham chorea - purposeless,
involuntary, rapid movements often
associated with muscle weakness.
d. Erythema marginatum – an evanescent,
pink rash have pale centers and round or
wavy margins.
i. Vary greatly in size, occur mainly in
trunk and extremities.
ii. Erythema is transient, migrates from
place to place, and may be brought out
by the application of heat.
e. Subcutaneous nodules - firm and painless
nodules seen or felt over the extensor
surface of certain joints, particularly elbows,
knees, and wrists, in the occipital region, or
over the spinous processes of the thoracic
and lumbar vertebrae; the skin overlying
them moves freely and is not inflamed.
B. Minor manifestations:
Clinical
a. History of previous rheumatic fever or
evidence of preexisting rheumatic heart
disease.
b. Arthralgia - pain in one or more joints
without evidence of inflammation,
tenderness to touch or limitation of motion.
c. Fever - temperature in excess of 38.5˚c.
Laboratory:
a. ESR elevated.
b. C-reactive protein – positive
c. ECG changes – mainly P-R interval
d. Prolongation
e. Leukocytosis
C. Evidence of streptococcal infection:
a. Increased titer of streptococcal antibodies
(ant streptolysin O or ASO titer )
b. Positive throat culture for group A
streptococci
c. Recent scarlet fever
Treatment:
• Salicylates or NSAIDS - control fever and joint
manifestations
• Steroids – for severe carditis
• Phenobarbital or diazepam for Chorea
• Pen G Na 600,000 – 1.2 M units, or
Erythromycin
• Surgical intervention to repair or replace the
valve.
Nursing Interventions:
1. Bed rest and close attention to changes in
cardiac findings
2. Treatment of streptococcal infection
3. Management of fever A nondilated left ventricle cavity, systolic
4. Alleviate child’s anxiety. hypercontractility, diastolic dysfunction and
5. Decrease cardiac workload. obstruction of left ventricle outflow
6. Provide comfort.
This is the most common cardiovascular disorder
7. Prevent recurrent attack – prophylactic
with an autosomal genetic etiology.
antimicrobial therapy.
Assessment
Cardiomyopathy
• Limited exercise capacity as primary
Is a disorder of the heart muscle and is common
symptoms
cause of heart failure in children and the most
• CHF clinical symptoms
common cause of heart transplantation in children
• Chest pain
older than 1 year of age.
• Echocardiogram confirms diagnosis.
Dilated Cardiomyopathy
Management
Severe disease of the heart muscle characterized
• Aimed at reducing symptoms and prolonged
by dilation of the left ventricle with reduced left
survival.
ventricle systolic function and normal ventricular
• Beta blocker therapy (metoprolol)
wall thickness.
• Calcium channel blocker (verapamil)
Cause: genetic account for 40% of cases, • Pacemakers
myocarditis, and unknown / idiopathic • Surgical removal of any LVOT obstruction
Assessment Restrictive Cardiomyopathy
Children Characterized by restrictive filling and reduce
diastolic volume of either or both ventricles with
• Exercise intolerance
normal or near-normal systolic function and wall
• Dyspnea on exertion
thickness.
• Palpitation
• Chest pain Cause: idiopathic
• Syncope
Prognosis is poor – half of children dying within 2
• Cardiovascular collapse
years of diagnosis.
Infant
• Respiratory distress
• Poor feeding
• Easy fatigability Arrhythmogenic Right Ventricular
• Altered heart and respiratory rate. Cardiomyopathy
• Chest X-ray – Cardiomegaly, Pulmonary
edema, and pleural effusion. A rare inherited disease of the hear that cause
ventricular tachyarrhythmias and sudden death in
Treatment young people and athletes.
• Supportive and nonspecific if there is no It results in fibro-fatty replacement of the right
identifiable cause. ventricle and the subepicardial region of the left
• Aimed at controlling symptoms of CHF. ventricle.
o ACE inhibitor
o Beta blockers Assessment
o Inhibition of renin-angiotensin system. • Palpitations
• Heart transplant • Syncope
• Sudden cardiac arrest during exercise
Hypertrophic Cardiomyopathy
• Diagnosis – patient and family history, 12 lead
Is characterized by hypertrophy of the left ventricle. ECG evaluation, and echocardiogram.
Management
• No treatment
• Management through restriction of physical
exercise, antiarrhythmic drugs, beta blocker
therapy, and implantable cardioverter
defibrillator (ICD)