The cardiovascular system in children is dynamic and undergoes significant changes from fetal circulation to extrauterine life. Congenital heart defects (CHDs) are the most common birth defects and a primary focus in paediatric cardiology. Acquired heart conditions also affect children, though less frequently than CHDs. Understanding these conditions, their presentation, and nursing management is crucial for paediatric nurses.

Congenital Heart Defects (CHDs)

Congenital heart defects are structural abnormalities of the heart or great vessels present at birth. They arise from errors during fetal cardiac development. CHDs are broadly classified based on their haemodynamic effects:

1. Defects with Increased Pulmonary Blood Flow (Acyanotic)

These defects allow blood to flow from the high-pressure left side of the heart to the low-pressure right side, shunting oxygenated blood back to the lungs. This leads to increased blood volume in the lungs and right ventricle workload.

• Atrial Septal Defect (ASD): An abnormal opening between the atria.

  • Pathophysiology: Blood shunts from the left atrium (LA) to the right atrium (RA), increasing blood flow to the lungs.
  • Clinical Manifestations: Often asymptomatic in early childhood. May present with a soft systolic ejection murmur at the upper left sternal border, fatigue, dyspnea on exertion, poor growth, and recurrent respiratory infections. Large defects can lead to right atrial and ventricular enlargement.
  • Diagnostic Evaluation: Echocardiogram is diagnostic. Chest X-ray may show cardiomegaly and increased pulmonary vascular markings. ECG may show right axis deviation.
  • Nursing Management:
    • Monitor for signs of heart failure (tachypnea, tachycardia, poor feeding, hepatomegaly).
    • Manage respiratory infections promptly.
    • Provide nutritional support for growth (e.g., high-calorie formula).
    • Prepare child and family for surgical or transcatheter closure if indicated.
    • Post-operative care: Monitor vital signs, incision site, signs of infection, arrhythmias, and manage pain.

• Ventricular Septal Defect (VSD): An abnormal opening between the ventricles. This is the most common CHD.

  • Pathophysiology: Blood shunts from the left ventricle (LV) to the right ventricle (RV), increasing pulmonary blood flow. The size of the defect determines the severity.
  • Clinical Manifestations: Small VSDs may be asymptomatic. Moderate to large VSDs can cause a harsh holosystolic murmur at the left lower sternal border, tachypnea, poor feeding, failure to thrive, diaphoresis during feeding, and signs of congestive heart failure (CHF).
  • Diagnostic Evaluation: Echocardiogram is diagnostic. Chest X-ray may show cardiomegaly and increased pulmonary vascularity. ECG may show left and/or right ventricular hypertrophy.
  • Nursing Management:
    • Similar to ASD, with a strong emphasis on CHF management (diuretics, digoxin, ACE inhibitors as prescribed).
    • Monitor feeding tolerance and provide strategies for adequate caloric intake (e.g., smaller, more frequent feeds, NG tube feeding if necessary).
    • Educate parents on signs of worsening CHF and medication administration.
    • Prepare for surgical patch closure or transcatheter device closure.

• Patent Ductus Arteriosus (PDA): Failure of the fetal ductus arteriosus (connecting the aorta and pulmonary artery) to close after birth.

  • Pathophysiology: Blood shunts from the aorta to the pulmonary artery, leading to increased pulmonary blood flow.
  • Clinical Manifestations: Small PDA may be asymptomatic. Larger PDA presents with a continuous “machinery-like” murmur heard best at the upper left sternal border, bounding peripheral pulses, wide pulse pressure, tachypnea, poor feeding, and signs of CHF. Higher risk in premature infants.
  • Diagnostic Evaluation: Echocardiogram is diagnostic. Chest X-ray may show cardiomegaly and increased pulmonary vascular markings.
  • Nursing Management:
    • Administer indomethacin or ibuprofen (prostaglandin inhibitors) as prescribed in premature infants to promote ductal closure.
    • Monitor respiratory status, oxygen saturation, and signs of CHF.
    • Provide supportive care, including fluid management and nutritional support.
    • Prepare for surgical ligation or transcatheter coil embolization/device closure if medical management fails or in older infants/children.

2. Defects with Decreased Pulmonary Blood Flow (Cyanotic)

These defects obstruct pulmonary blood flow, or there is mixing of deoxygenated blood with systemic circulation, resulting in cyanosis.

• Tetralogy of Fallot (TOF): Characterized by four defects:

  1. Ventricular Septal Defect (VSD)
  2. Pulmonary Stenosis (obstruction of right ventricular outflow)
  3. Overriding Aorta (aorta positioned over the VSD)
  4. Right Ventricular Hypertrophy
  • Pathophysiology: The degree of pulmonary stenosis determines the severity of cyanosis. Deoxygenated blood from the right ventricle shunts through the VSD into the aorta, or blood flow to the lungs is severely restricted.
  • Clinical Manifestations: Cyanosis (may be present at birth or develop in the first few months), “tet spells” or hypercyanotic spells (acute episodes of hypoxia and cyanosis, often during crying or feeding), clubbing of fingers and toes, polycythemia, poor growth, systolic murmur.
  • Diagnostic Evaluation: Echocardiogram is diagnostic. Chest X-ray may show a “boot-shaped” heart and decreased pulmonary vascular markings. ECG shows right ventricular hypertrophy.
  • Nursing Management:
    • Monitor for and manage hypercyanotic spells: place infant in knee-chest position, administer oxygen, morphine sulfate as prescribed, and IV fluids. Calm the child.
    • Educate parents on recognizing and managing tet spells.
    • Prevent dehydration, as it can increase risk of thromboembolism due to polycythemia.
    • Provide nutritional support.
    • Prepare for palliative shunt (e.g., Blalock-Taussig shunt) or complete surgical repair.
    • Post-operative care: Monitor for arrhythmias, low cardiac output, and residual VSD or pulmonary stenosis.

• Pulmonary Atresia (PA): Absence of the pulmonary valve, preventing blood flow from the right ventricle to the pulmonary artery. Often associated with an intact ventricular septum (PA/IVS) or a VSD. Blood flow to the lungs depends on a PDA or bronchial collaterals.

  • Pathophysiology: Severe obstruction to pulmonary blood flow. Deoxygenated blood cannot reach the lungs via the normal pathway.
  • Clinical Manifestations: Severe cyanosis shortly after birth (once PDA begins to close), tachypnea, poor feeding.
  • Diagnostic Evaluation: Echocardiogram is diagnostic.
  • Nursing Management:
    • Immediate prostaglandin E1 infusion to maintain patency of the ductus arteriosus.
    • Stabilize respiratory and cardiovascular status.
    • Prepare for staged surgical procedures (e.g., shunt, Glenn, Fontan).
    • Provide supportive care and family education.

3. Obstructive Defects (Acyanotic or Cyanotic depending on severity and associated lesions)

These defects impede blood flow out of the ventricles. Pressure load is placed on the ventricle proximal to the obstruction, leading to ventricular hypertrophy.

• Coarctation of the Aorta (CoA): Narrowing of the aorta, typically near the insertion of the ductus arteriosus.

  • Pathophysiology: Obstruction to systemic blood flow. Increased pressure proximal to the defect (upper extremities) and decreased pressure distal to the defect (lower extremities).
  • Clinical Manifestations: Cardinal sign: higher blood pressure in the upper extremities compared to the lower extremities. Bounding pulses in the arms, weak or absent femoral pulses. Infants may present with severe CHF and shock once the ductus arteriosus closes. Older children may be asymptomatic or complain of headaches, leg cramps with exercise, or epistaxis. A systolic murmur may be heard.
  • Diagnostic Evaluation: Echocardiogram is diagnostic. Chest X-ray may show cardiomegaly and rib notching (in older children due to collateral circulation). Four-limb blood pressure measurement is crucial.
  • Nursing Management:
    • Monitor blood pressure in all four extremities.
    • Assess for signs of CHF and manage accordingly.
    • Prostaglandin E1 infusion in neonates with critical coarctation to maintain ductal patency.
    • Prepare for balloon angioplasty or surgical repair.
    • Post-procedure/operative care: Monitor for re-coarctation, hypertension, and neurological complications.

• Aortic Stenosis (AS): Narrowing of the aortic valve, obstructing blood flow from the left ventricle to the aorta.

  • Pathophysiology: Increased workload on the left ventricle leading to LV hypertrophy. Can lead to decreased cardiac output and pulmonary congestion.
  • Clinical Manifestations: Varies with severity. Infants with critical AS present with faint pulses, hypotension, tachycardia, poor feeding, and CHF. Older children may have exercise intolerance, chest pain, dizziness, syncope, and a systolic ejection murmur.
  • Diagnostic Evaluation: Echocardiogram is diagnostic. ECG may show LV hypertrophy.
  • Nursing Management:
    • Monitor for signs of low cardiac output and CHF.
    • Activity restrictions may be necessary for moderate to severe AS.
    • Prepare for balloon valvuloplasty or surgical valve repair/replacement.
    • Educate on infective endocarditis prophylaxis if indicated.

• Pulmonary Stenosis (PS): Narrowing of the pulmonary valve, obstructing blood flow from the right ventricle to the pulmonary artery. (Also a component of TOF).

  • Pathophysiology: Increased workload on the right ventricle leading to RV hypertrophy.
  • Clinical Manifestations: Mild PS often asymptomatic. Moderate to severe PS may cause dyspnea on exertion, fatigue, cyanosis (if RA pressure exceeds LA pressure leading to right-to-left shunting through a patent foramen ovale), and a systolic ejection murmur.
  • Diagnostic Evaluation: Echocardiogram is diagnostic. ECG may show RV hypertrophy.
  • Nursing Management:
    • Monitor for signs of right-sided heart failure (rare in isolation).
    • Prepare for balloon valvuloplasty or surgical valvotomy.

4. Mixed Defects (Cyanotic)

These defects involve mixing of oxygenated and deoxygenated blood in the systemic circulation, leading to desaturation and cyanosis. Pulmonary blood flow may be increased or decreased.

• Transposition of the Great Arteries (TGA): The aorta arises from the right ventricle, and the pulmonary artery arises from the left ventricle. Two separate parallel circulations. Survival depends on mixing of blood through a PDA, ASD, and/or VSD.

  • Pathophysiology: Deoxygenated blood circulates through the body, and oxygenated blood circulates through the lungs.
  • Clinical Manifestations: Severe cyanosis usually evident within hours of birth, particularly as the PDA closes. Tachypnea, signs of CHF may develop. Murmurs may be present if associated defects exist.
  • Diagnostic Evaluation: Echocardiogram is diagnostic. Chest X-ray may show “egg on a string” appearance of the heart.
  • Nursing Management:
    • Immediate prostaglandin E1 infusion to maintain ductal patency.
    • Oxygen therapy (use with caution as it can reduce pulmonary vascular resistance and worsen mixing in some cases, but generally given for hypoxia).
    • Balloon atrial septostomy may be performed to improve mixing.
    • Prepare for arterial switch operation usually within the first few weeks of life.
    • Monitor for electrolyte imbalances, hypoglycemia, and acidosis.

• Truncus Arteriosus: A single large vessel (truncus) arises from both ventricles, overriding a VSD, and supplies the systemic, pulmonary, and coronary circulations.

  • Pathophysiology: Complete mixing of oxygenated and deoxygenated blood. Pulmonary blood flow is usually increased due to lower pulmonary vascular resistance.
  • Clinical Manifestations: Cyanosis (variable), signs of CHF (tachypnea, poor feeding, diaphoresis), bounding peripheral pulses, single second heart sound, harsh systolic murmur.
  • Diagnostic Evaluation: Echocardiogram is diagnostic.
  • Nursing Management:
    • Manage CHF with diuretics and digoxin.
    • Nutritional support.
    • Prepare for early surgical repair (closure of VSD, separation of pulmonary arteries from truncus, and creation of a conduit from RV to pulmonary arteries).
    • Monitor for conduit stenosis and arrhythmias post-operatively.

• Hypoplastic Left Heart Syndrome (HLHS): Underdevelopment of the left side of the heart, including the left ventricle, mitral valve, aortic valve, and ascending aorta. Systemic circulation is dependent on the PDA.

  • Pathophysiology: The right ventricle pumps blood to both the pulmonary and systemic circulations (via the PDA).
  • Clinical Manifestations: Symptoms appear as the PDA closes: cyanosis, tachypnea, poor perfusion, shock, single second heart sound. Rapid deterioration.
  • Diagnostic Evaluation: Echocardiogram is diagnostic.
  • Nursing Management:
    • Immediate prostaglandin E1 infusion.
    • Avoid supplemental oxygen (can decrease pulmonary vascular resistance, shunting blood away from systemic circulation).
    • Careful fluid and electrolyte management.
    • Supportive care, including respiratory support if needed.
    • Prepare for staged surgical palliation (Norwood, Glenn, Fontan procedures) or cardiac transplantation.
    • Extensive family support and education due to complex, long-term management.

Acquired Cardiovascular Conditions in Children

1. Congestive Heart Failure (CHF)

CHF is a clinical syndrome where the heart is unable to pump enough blood to meet the metabolic demands of the body. It can be a complication of many CHDs, as well as acquired conditions.

• Pathophysiology: Can result from volume overload (e.g., VSD, PDA), pressure overload (e.g., AS, CoA), decreased contractility (e.g., cardiomyopathy, myocarditis), or high cardiac output demands (e.g., severe anemia). Compensatory mechanisms (tachycardia, ventricular dilation, hypertrophy) eventually fail.
• Clinical Manifestations:
  • Infants: Tachypnea (often first sign), tachycardia, difficulty feeding (tires easily, sweats with feeds), poor weight gain/failure to thrive, periorbital edema, hepatomegaly, irritability, frequent respiratory infections.
  • Older Children: Exercise intolerance, dyspnea on exertion, fatigue, cough (especially nocturnal), wheezing, peripheral edema, ascites, jugular venous distension (less common in young children), orthopnea.
• Diagnostic Evaluation: Based on clinical signs and symptoms. Chest X-ray (cardiomegaly, pulmonary congestion), Echocardiogram (cardiac function, underlying cause), ECG (arrhythmias, ventricular hypertrophy), BNP levels (elevated).
• Nursing Management:
  • Improve Cardiac Function: Administer medications as prescribed:
    • Digoxin: Increases contractility, decreases heart rate. Monitor for toxicity (bradycardia, arrhythmias, nausea, vomiting, anorexia). Check apical pulse before administration.
    • ACE inhibitors (e.g., Captopril, Enalapril): Reduce afterload, promote vasodilation. Monitor blood pressure, renal function, potassium levels.
    • Beta-blockers (e.g., Carvedilol): Decrease heart rate and blood pressure, improve ventricular function (used cautiously).
  • Remove Accumulated Fluid and Sodium (Decrease Preload):
    • Diuretics (e.g., Furosemide, Spironolactone): Monitor intake and output, daily weights, electrolytes (especially potassium).
    • Fluid restriction may be necessary.
    • Sodium restriction (less common in infants, more applicable to older children).
  • Decrease Cardiac Demands:
    • Provide a neutral thermal environment.
    • Treat infections promptly.
    • Reduce effort of breathing (semi-Fowler’s position).
    • Cluster care to allow for rest periods.
    • Provide small, frequent, high-calorie feedings. Gavage feeding may be needed if oral feeding causes distress.
  • Improve Tissue Oxygenation and Decrease Oxygen Consumption:
    • Administer oxygen as prescribed (use cautiously in certain defects).
    • Monitor oxygen saturation.
    • Maintain patent airway.
  • Family Support and Education: Teach parents about medications, signs of worsening CHF, feeding techniques, and when to seek medical attention.

2. Infective Endocarditis (IE)

An infection of the endocardial surface of the heart, most commonly affecting the heart valves. Often occurs in children with underlying CHDs, prosthetic valves, or previous IE.

• Pathophysiology: Endothelial damage allows microorganisms (usually bacteria, sometimes fungi) to adhere and colonize, forming vegetations. These vegetations can embolize and cause systemic complications.
• Clinical Manifestations: Often insidious onset. Low-grade fever, malaise, fatigue, anorexia, weight loss, myalgias, arthralgias. New or changed heart murmur. Splinter hemorrhages (under nails), Osler nodes (painful nodules on fingers/toes), Janeway lesions (painless macules on palms/soles), Roth spots (retinal hemorrhages). Splenomegaly. Signs of embolization (stroke, hematuria).
• Diagnostic Evaluation: Blood cultures (multiple sets) are critical. Echocardiogram (to identify vegetations). Elevated ESR and CRP. Modified Duke criteria used for diagnosis.
• Nursing Management:
  • Administer high-dose intravenous antibiotics for a prolonged period (typically 4-6 weeks) as prescribed.
  • Monitor vital signs, especially temperature.
  • Assess for signs of embolization and complications (CHF, arrhythmias).
  • Provide comfort measures.
  • Educate family on the importance of completing the antibiotic course.
  • Teach about prophylactic antibiotics before certain dental or surgical procedures for at-risk children.

3. Rheumatic Fever (RF) and Rheumatic Heart Disease (RHD)

RF is an inflammatory disease that can develop as a delayed sequela to a Group A Streptococcal (GAS) pharyngeal infection. RHD is the cardiac manifestation of RF, involving damage to the heart valves.

• Pathophysiology: An autoimmune reaction where antibodies produced against GAS cross-react with host tissues, particularly cardiac, joint, brain, and skin tissues.
• Clinical Manifestations (Jones Criteria for Diagnosis – need 2 major or 1 major and 2 minor, plus evidence of preceding GAS infection):
  • Major Manifestations:
    • Carditis: Inflammation of all parts of the heart (pancarditis) – endocarditis (mitral valve most common), myocarditis, pericarditis. New murmur, tachycardia, cardiomegaly, CHF, pericardial friction rub.
    • Polyarthritis: Migratory inflammation of large joints (knees, ankles, elbows, wrists). Painful, swollen, red, warm.
    • Chorea (Sydenham’s Chorea): Involuntary, purposeless movements, emotional lability, muscle weakness.
    • Erythema Marginatum: Non-pruritic, macular rash with a clear center and serpiginous border, usually on trunk and proximal limbs.
    • Subcutaneous Nodules: Firm, painless nodules over bony prominences (e.g., elbows, knees, spine).
  • Minor Manifestations: Fever, arthralgia, prolonged PR interval on ECG, elevated ESR/CRP.
  • Evidence of preceding GAS infection: Positive throat culture or rapid strep test, elevated or rising streptococcal antibody titer (ASO or Anti-DNase B).
• Diagnostic Evaluation: Based on Jones criteria. Throat culture, ASO titer, ESR, CRP, ECG, Echocardiogram (to assess for carditis and valvular damage).
• Nursing Management:
  • Eradicate GAS infection: Administer penicillin (or alternative if allergic) as prescribed.
  • Anti-inflammatory therapy: Aspirin (for arthritis and fever), corticosteroids (for severe carditis). Monitor for side effects.
  • Supportive care: Bed rest during acute phase, especially with carditis. Manage fever and joint pain.
  • Management of CHF if present.
  • Prevention of recurrence: Long-term secondary prophylaxis with penicillin (IM monthly or oral daily) is crucial to prevent further attacks and worsening RHD. Duration depends on severity of RHD.
  • Education: Importance of completing antibiotic therapy for strep throat, recognizing symptoms of RF, and adherence to prophylactic regimen.

4. Kawasaki Disease (Mucocutaneous Lymph Node Syndrome)

An acute, self-limiting vasculitis of unknown etiology that predominantly affects young children. The most serious complication is the development of coronary artery aneurysms.

• Pathophysiology: Widespread inflammation of small and medium-sized blood vessels, including the coronary arteries.
• Clinical Manifestations (Diagnosis based on fever for ≥ 5 days plus ≥ 4 of 5 principal clinical features, or fever and <4 features with coronary abnormalities):
  • Principal Clinical Features:
    1. Changes in extremities: Erythema and edema of hands and feet in acute phase; periungual desquamation (peeling) in subacute phase.
    2. Polymorphous rash: Usually generalized, non-vesicular.
    3. Bilateral bulbar conjunctival injection: Non-purulent.
    4. Changes in lips and oral cavity: Erythema and cracking of lips (“strawberry tongue”), diffuse erythema of oropharyngeal mucosa.
    5. Cervical lymphadenopathy: Usually unilateral, >1.5 cm.
  • Other findings: Irritability, abdominal pain, diarrhea, vomiting, arthritis, urethritis.
• Phases of Illness:
  • Acute Phase (1-2 weeks): Abrupt onset of high fever, unresponsive to antibiotics. Presence of principal clinical features. Myocarditis may occur.
  • Subacute Phase (2-4 weeks): Resolution of fever and most acute symptoms. Desquamation of fingers and toes. Highest risk for coronary artery aneurysm development. Thrombocytosis.
  • Convalescent Phase (6-8 weeks after onset): All clinical signs resolved. Lab values return to normal. Continues until ESR normalizes. Coronary complications may persist.
• Diagnostic Evaluation: No specific diagnostic test. Diagnosis is clinical. Echocardiogram is essential to assess for coronary artery abnormalities, myocarditis, and pericardial effusion. Elevated ESR, CRP, WBC count, platelet count (thrombocytosis in subacute phase).
• Nursing Management:
  • Administer High-Dose Intravenous Immunoglobulin (IVIG): Reduces incidence of coronary artery aneurysms. Given within first 10 days of illness if possible. Monitor for allergic reactions.
  • Administer High-Dose Aspirin Therapy: Initially for anti-inflammatory effects, then lower dose for antiplatelet effects. Monitor for aspirin toxicity (tinnitus, headache, dizziness, confusion).
  • Monitor Cardiac Status: Frequent vital signs, assess for signs of CHF, arrhythmias. Serial echocardiograms as ordered.
  • Symptomatic Relief: Mouth care, cool compresses for fever, quiet environment, manage irritability.
  • Parent Education: Disease process, importance of follow-up (especially cardiology for coronary artery monitoring), medication administration, signs of complications. Long-term follow-up is essential, particularly if coronary aneurysms develop.

5. Cardiomyopathies

A group of diseases affecting the heart muscle itself, impairing its ability to pump effectively. Can be primary (idiopathic) or secondary to other conditions.

• Types:
  • Dilated Cardiomyopathy (DCM): Most common type in children. Ventricular dilation and impaired systolic function.
  • Hypertrophic Cardiomyopathy (HCM): Inappropriate left ventricular hypertrophy, often asymmetrical. Impaired diastolic function. Risk of sudden cardiac death.
  • Restrictive Cardiomyopathy (RCM): Rare in children. Stiff, noncompliant ventricles impair diastolic filling.
  • Arrhythmogenic Right Ventricular Dysplasia (ARVD): Fibrofatty replacement of right ventricular myocardium, leading to arrhythmias and RV dysfunction.
• Clinical Manifestations: Vary widely depending on type and severity. May include signs of CHF (tachypnea, poor feeding, fatigue, edema), arrhythmias (palpitations, syncope), chest pain, sudden cardiac death (especially with HCM and ARVD).
• Diagnostic Evaluation: Echocardiogram is key. ECG, Chest X-ray, cardiac MRI, genetic testing (for some types like HCM). Cardiac catheterization and biopsy may be needed.
• Nursing Management:
  • Focus on managing symptoms of CHF (see CHF management).
  • Administer medications as prescribed (beta-blockers, ACE inhibitors, diuretics, antiarrhythmics).
  • Monitor for and manage arrhythmias.
  • Activity restrictions may be necessary, especially for HCM.
  • Nutritional support.
  • Genetic counseling for familial forms.
  • Support for child and family coping with chronic illness.
  • Education on emergency preparedness (e.g., CPR, automated external defibrillator (AED) for high-risk patients).
  • Preparation for potential heart transplantation if medical management fails.

General Nursing Considerations for Paediatric Cardiovascular Conditions:

• Assessment: Thorough cardiovascular assessment (heart rate, rhythm, murmurs, pulses, perfusion, blood pressure in all four limbs if indicated), respiratory assessment, fluid status, growth and development.
• Oxygenation: Monitor oxygen saturation, administer oxygen as ordered, position for optimal lung expansion.
• Nutrition: High-calorie intake to support growth and increased metabolic demands. Small, frequent feedings. Enteral tube feeding may be necessary.
• Fluid Management: Monitor intake and output, daily weights. Fluid restriction or liberal fluids as indicated by specific condition and physician orders.
• Activity Management: Balance rest with developmentally appropriate activity. Activity restrictions may be needed for certain conditions.
• Medication Administration: Accurate calculation and administration of cardiac medications. Monitor for therapeutic effects and side effects. Parent education on medication administration.
• Pain Management: Assess and manage pain, especially post-operatively or during procedures.
• Psychosocial Support: Address anxiety and fear in child and family. Provide emotional support. Refer to social work, child life specialists, and support groups as needed.
• Family-Centered Care: Involve family in care planning and decision-making. Provide thorough education about the child’s condition, treatment plan, home care, and emergency management.
• Prevention of Complications: Infection control, endocarditis prophylaxis if indicated, monitoring for signs of worsening condition.
• Transition to Adult Care: For adolescents with chronic CHDs, prepare them for transition to adult cardiology services.