Nursing Care of a Family

When a Child Has a

Cardiovascular Disorder
FACTUM PER

ANNA IRISH BELEN, RN MSN

OBJECTIVES
1. Describe common cardiovascular disorders of childhood.
2. Assess a child with a cardiovascular dysfunction.
3. Formulate nursing diagnoses for a child with a cardiovascular disorder.
4. Establish outcomes based on the priority needs of a child with a
cardiovascular disorder that can help the family manage seamless transitions
across different healthcare settings.
5. Implement nursing care for a child with a cardiovascular disorder
6. Evaluate expected outcomes for achievement and effectiveness of care.
7. Integrate knowledge of cardiovascular disorders with the interplay of
nursing process, and Family Nursing to promote quality maternal and child
health nursing care.
Measures:

• Physical activity or aerobic physical activity for muscle

strengthening activity.
• Reduce consumption of calories from solid fats and added sugars.
• Increase consumption of dark green vegetables, red and orange
vegetables, beans,
and peas to the diets
• Encouraging a low-fat diet, caution parents not to start their children
on reduced-fat diets until they are 2 years old to allow for
myelination of nerve cells.
The Cardiovascular System
The heart acts as a pump; the blood, which provides the fluid and cells for transport of oxygen, nutrients, regulatory
substances, antibodies, and the evacuation of waste products; and the blood vessels, which provide the means and routes for
transport throughout the body.
Fetal Cirvulation
ASSESSMENT
General Appearance

❖Distal extremities for color and measure capillary refill time, as these are
indicators of poor tissue perfusion

❖The mucous membranes of the mouth are the most accurate site to assess
for cyanosis, so always assess the buccal membrane and lips for a blue
color

❖Cool, cyanotic extremities in newborns is termed acrocyanosis and is a

normal finding in the first 24 to 48 hours of life.
Physical Examination

Evaluate for the apical impulse, thrills, lifts, or heaves. Deviations in the PMI can be indicators of an enlarged heart due to
illness, heart failure, or congenital heart defects.
A thrill is a vibration felt secondary to significant cardiac murmurs.
A lift is a forceful cardiac contraction that causes the hand to move up.
A heave is a very forceful cardiac contraction that actually causes the hand to move up and laterally.

Cardiac auscultation
Heart Sound
(S1) produced by the mitral and tricuspid valve closing.

(S2) is produced by closure of the aortic and pulmonic (semilunar) valves.

(S3) is produced from the rapid filling of the ventricles in early diastole

(S4) is produced by atrial contraction in late diastole and is always pathologic.

Heart murmurs turbulent flow through an abnormal valve, vessel, or chamber

Innocent murmur of infancy
F

low of blood through the slightly smaller branch

pulmonary arteries and specifically through the left pulmonary artery. It is a high-pitched,
harsher murmur heard best at the left upper sternal border with transmission of sounds to
the axillae and the left upper back area. This is
typically noted after birth and should disappear by the time the child turns 6 months of age,
as the pulmonary arteries have grown.
Venous hum - 2 to 8 years of age; is an innocent continuous murmur heard when the child is sitting or standing
but will change in quality if the child’s head is turned to the opposite side and will disappear completely if the
child lies supine.

Continuous murmur - persistent patent ductus arteriosus. It is noted at the left upper sternal border or out to
the left clavicular area and will not change in quality when the child changes position.

Regurgitant aortic and pulmonic valves- diastolic murmur heard immediately after the second heart sound
Diagnostic Tests
Laboratory Testing
Potassium - lost with most diuretics

Calcium - necessary for myocardial contractility and to prevent dysrhythmias

Sodium - indicator of fluid status

Creatine kinase (CK), CK-MB and Troponin levels - for myocardial damage due to arrhythmia,
inflammation, or infection.

C-reactive protein (CRP) - indicator of an active infectious process.

Erythrocyte sedimentation rate (ESR) - inflammation such as occurs with rheumatic fever, Kawasaki
syndrome, or myocarditis

B-Type natriuretic peptide (BNP) - substance secreted from the ventricles in response to changes in pressure
that occur when heart failure develops and worsens; N= <100 pg/ml

Arterial blood gas (pH and base status), carbon dioxide, oxygen, and bicarbonate levels
Electrocardiography - records the electrical signal from the heart
Electrocardiogram
❖heart rate
❖rhythm
❖state of the myocardium
❖presence or absence of hypertrophy
❖ischemia
❖necrosis
❖Inadequate cardiac circulation
❖Abnormalities of conduction
❖Effect of various drugs
❖Electrolyte imbalances
Holter/Event Monitor - gives a complete account of every
heart beat the child experiences
Echocardiography - high-frequency sound waves
Transthoracic Echocardiogram

❖Detailed information about heart structure and function.

❖size of chambers
❖thickness of walls;
❖relationship of major vessels to chambers
❖motion, and
❖pressure gradients across valves
❖velocity of blood flow
❖estimate pressures in the heart chambers and lungs and provide
Transesophageal echocardiogram (TEE)
provides high-quality images of intracardiac structures because of the absence of
interfering structures such as lung and bone.
Computed Tomography/Magnetic Resonance Imaging
Provides excellent anatomic imaging of the chest structures, including the coronary
arteries, through the
use of radiation.

Cardiac magnetic resonance imaging (MRI) can provide information regarding cardiac
anatomy and function, blood flow measurement, tissue characterization, myocardial
perfusion, and viability.
Exercise Stress Testing
Evaluates a child’s clinical condition during periods of increased myocardial demand.
Cardiac Catheterization - Uses fluoroscopy that allows for direct measurements of pressure as well
as visualization of the heart and all blood vessels with the aid of a contrast medium. Corrective procedures can also be
performed in the catheterization lab, such as atrial and ventricular septal defect closure, patent ductus arteriosus closure, or
valve replacement.
Congestive Heart Failure

❖Congenital heart defects

❖Acquired disorders

❖Understanding components of adequate cardiac function.

❖Heart Rate X Stroke Volume = Cardiac Output (volume of blood pumped by the
ventricles each minute)

❖Stroke volume is affected by the following factors:

• Preload: the volume of blood in the ventricles at the point just before contraction
• Contractility: ability to modulate the rate and force of fiber shortening
• Afterload: resistance against which the ventricles must pump.
• Compliance: the ability of the ventricles to stretch and fill
Congestive heart failure (CHF)
Inability of the heart to supply adequate oxygenated blood to meet the metabolic demands of
the body. Excessive workload.

Etiology - inability to meet metabolic demands, decreased filling, or obstruction of flow

Outcomes – Either one side or both sides of the heart are unable to pump effectively and will
eventually fail if the root problem is not corrected.

Nuerohormone – responseis to decreased cardiac output is peripheral vasoconstriction and

fluid retention.

Nervous system - provides a rapid response by increasing heart rate (chronotropy), stimulates
myocardial contractility (inotropy), and promotes regional vasoconstriction.
❖Activation of the renin–angiotensin–aldosterone system (RAAS) stimulates renal fluid
retention to expand vascular volume.

❖Heart eventually becomes overloaded from the extra volume and cannot maintain
adequate contractility against the increased afterload.

❖ Vasoconstriction

❖Redistribution of blood flow to ensure adequate perfusion of vital organs occur at the
expense of skin, intestinal, and renal blood flow.
Right-sided failure
❖leads to hepatomegaly
❖increased venous pressure noted in
❖jugular venous distention in older
children
❖periorbital edema
❖manifests with an enlarged liver,
which is palpable below the costal
margin
Left-sided failure
❖increased pulmonary pressures
❖Rales
❖Tachypnea
❖shortness of breath
❖back pressure causes blood to
accumulate in the pulmonary system
❖orthopnea
❖use of accessory muscles to support
their breathing
❖intercostal, substernal, and/or
suprasternal retractions
Digoxin - positive inotropic and negative chronotropic effect; increases
contractility

Angiotensin-converting enzyme (ACE) inhibitors - reduce afterload by

blocking the conversion of angiotensin I to angiotensin II, a potent
vasoconstrictor. They also block the activation of the RAAS and decrease
adrenergic activity. This causes vasodilation, improves tissue perfusion, and
reduces congestion by natriuresis.

Diuretics - increase the excretion of sodium and water, which in turn

relieves the symptoms of fluid overload and congestion
Congenital Heart
Defects
“increasing pulmonary blood flow,”
“decreasing pulmonary blood flow,”
“obstruction tosystemic blood flow.

cyanotic heart disease - venous blood from the right side of the
heart mixes with blood on the left side

acyanotic heart disease - oxygenated blood from the left side mixes
with blood in the right side of the
heart and goes back to the lungs again.
DEFECTS THAT
INCREASE
PULMONARY
BLOOD FLOW
Patent Ductus Arteriosus
Occurs when the ductus arteriosus does not close after birth, it allows blood to flow from the aorta (area of high
pressure) through the PDA and into the main pulmonary artery (area of low pressure).

The shunted blood then returns to the left atrium of the heart and repeats the cycle. This extra blood flow increases
pulmonary circulation.
Assessment
❖ Echocardiobragm
❖ Produces a systolic murmur early in life
❖ continuous murmur as the child ages.
❖ Rales for large
❖ Congestion
❖ increased work of breathing
❖ difficulty feeding
❖ Over time, the left heart can become dilated

Management
❖ Caloric concentration to child weight
❖ Furosemide
❖ Indomethacin, a nonsteroidal anti-inflammatory and prostaglandin inhibitor, can be utilized to facilitate closure
❖ PDA closure.
❖ PDA is done via a left-sided thoracotomy incision for infants
Atrial Septal Defect
Created when a portion of the atrial septal tissue does not completely form.
secundum most common type defect that is located in the center of the atrial septum
primum defect found low in the atrial septum near the IVC.
sinus venosus defects found high in the septum where the pulmonary veins enter the left atrium. Allows
communication of one or more of the pulmonary veins with the right atrium.
Assessment
❖ confirmed with an echocardiogram
❖ pulmonary overcirculation
❖ Rales
❖ Congestion
❖ tiring with activity
❖ poor weight gain
❖ right heart may also dilate as a result of the increased volume

Management
❖ Closure to decrease the incidence of supraventricular dysrhythmias and prevent pulmonary vascular
disease.
❖ 8mm or larger with evidence of increased pulmonary blood flow, the child will be referred for closure
immediately.
❖ A secundum ASD is typically closed in the catheterization lab
❖ Sinus venosus and primum defects for surgical closure; median sternotomy incision
Ventricular Septal Defect
The most common defect found in children, either in isolation or combined with other defects. VSDs may
be single or multiple and are defined based on their anatomical location
Assessment and Management

❖ The child may be medically managed to allow for spontaneous closure of the defect as the child grows.

❖ Some children will have an audible murmur but no symptoms of pulmonary overcirculation.

❖ If the child does exhibit signs of pulmonary overload, such as tachypnea, retractions, or rales, management
will include use of a diuretic such as furosemide

❖ Increase in the caloric density of the child’s formula or breast milk

❖ can be closed in the catheterization lab; others are closed surgically.

❖ Surgically closed through a median sternotomy (entering the chest cavity through the sternum)
Atrioventricular Septal Defect

Several congenital heart defects:

❖ a primum ASD
❖ a high VSD
❖ failure of the tricuspid and mitral valves to develop and attach correctly

Varying degrees of abnormality:

❖ mild septal defects
❖ complete lack of central septa
❖ incompetent valves on both sides

Complete AVSD, blood freely mixes between the right and left sides.

20% of children with Down syndrome who have heart disease, have this type of congenital cardiac
disorder
Assessment

❖ with symptoms of CHF

❖ increase pulmonary blood flow
❖ cardiac catheterization may be performed before surgical correction to measure pulmonary pressures and
❖ confirm reactivity with the administration of oxygen or nitric oxide, both of which should cause pulmonary
pressures to decrease.

Management

❖ medications such as furosemide, digoxin, and an ACE inhibitor

❖ concentrated feeds to help maintain weight.
❖ Children with Down syndrome are typically referred for surgical correction by 3 months of age or earlier if
with signs of increased pulmonary pressures.
❖ Other Children repair by 5 or 6 months of age
❖ Pulmonary artery band surgically placed around the pulmonary artery that constricts it to increase the resistance
within the pulmonary artery, thus decreasing some of the overall pulmonary blood flow and preventing too
much pulmonary circulation and long-term pulmonary vascular changes.

❖ Surgical repair of an AVSD consists of closing atrial and VSDs and repairing the mitral and tricuspid valves to
make them functional.
Transposition of the Great Arteries
❖reversal of the great arteries.
❖aorta coming off of the right ventricle
❖pulmonary artery arising from the left ventricle
❖oxygenated blood returns from the lungs to the left atrium, to the left ventricle, and then
proceeds back through the pulmonary artery and to the lungs again
❖deoxygenated blood returns from the body to the right atrium, the right ventricle, and
proceeds back out the aorta, supplying deoxygenated blood to the systemic circulation
❖mixing of oxygenated and deoxygenated blood
❖possible for the child to experience increased pulmonary blood flow
❖A prostaglandin E1 (PGE1) infusion is started immediately after birth to maintain
patency of the ductus arteriosus and encourage mixing of blood.

❖More effective mixing occurs through a patent foramen ovale (PFO). Opening will
have to be enlarged through a balloon atrial septostomy. Catheter through the IVC
to the right atrium and across the foramen ovale. Once the catheter has crossed into
the left atrium, a balloon is inflated at the end of that catheter, and the catheter is
vigorously pulled back through the septum, effectively creating a larger ASD.

❖Surgical correction within the first 14 days

❖The repair, termed an arterial switch or Jatene procedure, includes dissecting

both the pulmonary artery and aorta above their respective valves and switching the
vessels to the appropriate location.
Anomalous Pulmonary Venous Return and Truncus
Arteriosus
Failure of the pulmonary venous connections to unite with the left atrium in
utero. Instead, they return to another vessel (left innominate, portal, or
coronary sinus vein) or

directly to the right atrium, and the oxygenated pulmonary blood return
drains back into the right side of the heart. This can be seen with one, two, or
three of the veins (partial APVR), or all four veins (total APVR), draining to
the venous side. Total APVR requires urgent surgical intervention. Partial
PVR, if only one vessel, can be missed because it may cause no significant
clinical effects.
DEFECTS THAT
DECREASE
PULMONARY
BLOOD FLOW
Tetralogy of Fallot
cyanotic defect is defined by four components: pulmonary artery stenosis, VSD, overriding aorta, and right ventricular
hypertrophy occurs secondary to the pulmonary stenosis.
DEFECTS WITH
OBSTRUCTION
TO SYSTEMIC
BLOOD FLOW
Coarctation of the Aorta

❖ Narrowing of the segment in aortic arch

❖ absent femoral pulse
❖ ECG: left ventricle hypertrophy
❖ Management: close heart surgery; Balloon angioplasty
Aortic Stenosis
❖ Obstruction out the left ventricle below or above the aortic valve.
❖ The narrowing prevents blood from passing freely from the left ventricle of the heart into the aorta.
❖ Increased pressure and hypertrophy occur in the left ventricle
❖ If this pressure becomes severe, pressure in the left atrium will increase as well, resulting in back pressure through
the pulmonary veins to the lungs, causing pulmonary edema
Assessment
The child may be free of symptoms if severe, there is decreased
cardiac output as evidenced by faint pulses, hypotension, tachycardia.

Therapeutic Management
Balloon angioplasty or surgical repair.
Stabilization with a beta-blocker or a calcium channel blocker
SINGLE-VENTRICLE
DEFECTS
Surgical Management of a Hypoplastic Left Heart Syndrome Defect
Cardiac Surgery
SINUS ARRHYTHMIA
❖child’s heart rhythm based on their respiratory pattern
❖breathing in, the heart rate slow down and as they
❖exhalation, there is a slight increase in rate.

SINUS BRADYCARDIA
❖heart rate that is less than the stated normal for a child’s age
❖normal as seen in athletes
❖May be secondary to medications such as beta-blockers

SINUS TACHYCARDIA
❖heart rate that is greater than the stated normal for a child’s age
❖may be expected as with a fever, anxiety, or pain may be
❖secondary to medications such as albuterol
❖may be an indicator of a pathologic state such as dehydration, anemia, or infection.
SUPRAVENTRICULAR TACHYCARDIA

❖ heart rate greater than 220 beats/min in an infant and greater than 160 beats/min
❖ chest pain
❖ racing heart
❖ tired and dizzy
❖ ECG demonstrates a very narrow complex with P waves that are not visible
Acquired Heart
Disease
KAWASAKI DISEASE
❖ Mucocutaneous lymph node syndrome
❖ an acute febrile syndrome associated with generalized vasculitis
❖ affecting all blood vessels throughout the body, including the coronary arteries
Therapeutic Management

❖antipyretics
❖IV fluids
❖high-dose intravenous
immunoglobulin
❖high-dose aspirin
RHEUMATIC FEVER

❖ autoimmune disease that occurs as a reaction to a group A β-hemolytic streptococcal infection, pharyngitis
❖ Inflammation from the immune response leads to inflammatory lesions being found in the heart, blood vessels,
brain, and joints.
❖ Approximately 10 days after recovery from the pharyngitis, the autoimmune response begins, lasts many weeks
and gradually damages the left heart valves.
Therapeutic Management

❖penicillin therapy
❖Oral nonsteroidal anti-inflammatory
agents to reduce inflammation and
joint pain.
❖Phenobarbital and diazepam (Valium)
are both effective in reducing the
purposeless movements of chorea.
CARDIOMYOPATHY
disorder of the heart muscle

Dilated Cardiomyopathy
❖ Dilation of the left ventricle with reduced left ventricle systolic function and ventricular wall thickness.
❖ Children typically present with exercise intolerance, dyspnea on exertion, palpitations, chest pain, syncope, or possible
cardiovascular collapse.
❖ Cardiomegaly, pulmonary venous congestion, pulmonary edema, and pleural effusions
❖ ECG typically shows sinus tachycardia
❖ Echocardiogram presence of a dilated ventricle with poor systolic function.
❖ Treatment ACE inhibitors, beta-blockers, and inhibition of the renin–angiotensin system.
Hypertrophic Cardiomyopathy
hypertrophy of the left ventricle, a nondilated left ventricle cavity, systolic hypercontractility, diastolic dysfunction,
obstruction of left ventricle outflow secondary to mitral–septal contact during systole (hypertrophic obstructive
cardiomyopathy).
Chest pain is also very common at rest or with activity.

❖ Management: Beta-blocker therapy

▪ decrease the contractile force
▪ myocardial workload and oxygen demand.
▪ increase diastolic filling by slowing the heart rate
▪ relieves chest pain and dyspnea

❖ Calcium channel blockers, specifically verapamil, have a negative chronotropic effect which increases the diastolic
relaxation
❖ pacemakers and surgical removal of any LV Outflow Tract obstruction
Restrictive Cardiomyopathy

❖restrictive filling and reduced diastolic volume of either or both ventricles

❖This leads to poor cardiac output and ultimately symptoms of heart failure.
❖Prognosis is poor

Arrhythmogenic Right Ventricular Cardiomyopathy

❖rare inherited disease of the heart that causes ventricular tachyarrhythmias

❖fibro-fatty replacement of the right ventricle and the subepicardial region of the left
ventricle.
❖Unfortunately, there is no treatment for this disorder, only management through
restriction of physical exercise, antiarrhythmic drugs, beta-blocker therapy
INFLAMMATORY
PROCESSES
Inflammatory processes that impact the heart can be secondary to an infectious process
(viral or bacterial)
Myocarditis

❖ acute or chronic inflammatory process affecting the myocardium

❖ caused by a wide variety of toxins, drugs, or infectious agents, most commonly viral agents such as
coxsackievirus, adenovirus, or parvovirus.

Pericarditis

❖ inflammation of the pericardial membrane with or without accumulation of excess pericardial fluid.
❖ Presentation frequently includes chest pain which can be sharp, precordial, radiating, and worse with inspiration
or cough.
❖ It is characteristically positional, and patients feel better when sitting up and leaning forward.
❖ Fever is also common.

Infective Endocarditis

❖ inflammation and infection of the endocardium or valves of the heart.

❖ peripherally inserted central catheters (PICCs) similarly may injure the endocardial or endothelial layer
allowing for the deposition of red blood cells, platelets, and fibrin.
❖ Bacteria then can adhere to the damaged endothelial layer
Thank You!!!
Thank You!!!
SOURCE:
Maternal and Child Health Nursing

JoAnne Silbert-Flagg
Adele Pillitteri