340 heart defects
Assessment of Cardiac Function in Children
History
Parental concerns about any symptoms, family history of cardiovascular diseases, or congenital defects.
Mother’s health & pregnancy history, including complications during pregnancy such as gestational diabetes, hypertension, or infections that could impact fetal development.
Family History of cardiac diseases, including genetic conditions or hereditary aspects that may predispose the child to cardiovascular issues.
Inspection
Nutritional state, noting whether the child shows signs of malnutrition or obesity which can affect cardiac health.
Color (skin and mucous membranes) to detect signs of cyanosis, pallor, or flushing, indicating circulatory problems.
Chest deformities, such as pectus excavatum or pectus carinatum, which can affect heart function.
Unusual pulsations that may indicate structural abnormalities or increased heart workload.
Respiratory excursion as decreased movement can signify underlying respiratory or cardiovascular conditions.
Digital clubbing, which can be a sign of chronic low oxygen levels due to invalid heart or lung conditions.
Assessment of a Child With Possible Cardiovascular Disorder
Palpation and Percussion
Chest palpation to assess for vibrations indicating turbulence in blood flow.
Abdomen for organomegaly which can suggest liver or GI issues secondary to heart failure.
Peripheral pulses to evaluate perfusion; compare strength and regularity across extremities to identify discrepancies.
Auscultation
Heart rate and rhythm, including pattern abnormalities which may indicate arrhythmias.
Blood Pressure monitoring (both arms, one leg) to evaluate systemic vascular resistance and hemodynamic status.
Character of heart sounds, noting diastolic and systolic murmurs, clicks, or rubs which can indicate valvular or structural heart disorders.
Diagnostic Evaluation
Chest X-Ray: Provides crucial information about heart size, shape, and position, as well as lung vascularity.
ECG: Evaluates the electrical activity of the heart, identifies arrhythmias, and assesses chamber enlargement.
Complete Blood Count (CBC): Detects polycythemia, which can lead to blood clots and signify chronic hypoxemia.
Echocardiogram: Non-invasive imaging tool to visualize internal structures of the heart such as chambers, valves, and flow dynamics.
Arterial Blood Gas (ABG): Assesses gas exchange and acid-base balance; may reveal hypoxia or hypercapnia.
Cardiac Catheterization: Can be both diagnostic and interventional; assists in evaluating anatomical and functional heart characteristics.
Cardiac Catheterization
Types of Procedures
Diagnostic: Utilized to determine the presence and extent of cardiovascular disease.
Interventional: To fix structural heart problems, such as closing septal defects, or balloon dilation of stenotic valves.
Electrophysiology studies: Assess the electrical conduction system of the heart, identifying areas of abnormal conduction.
Right side catheterization is more common in children: This is due to safety, simpler access, and higher success rates in identifying structural defects allows access to the left side of the heart.
Pre-procedural Care
Comprehensive Nursing Assessment to evaluate the child's overall health status and readiness for the procedure.
NPO (nothing by mouth) for 4-6 hours to prevent aspiration during sedation.
Clarify morning medications with the physician to determine if they should be taken or withheld.
IV Fluids: Assess if needed to maintain hydration status.
Developmentally appropriate psychological preparation to reduce anxiety and help the child understand the procedure.
Sedation assessment: Determine if sedation is needed and tailor based on the child’s age and health status.
Post-procedural Care; Cardiac Catheterization
Observation for Complications
Monitor color and level of consciousness to detect neurological or oxygenation issues post-procedure.
Vital Signs:
Take heart rate for one full minute; pay special attention to blood pressure as fluctuations can indicate complications.
Assess respiratory status, looking for signs of compromised airflow or lung function.
Monitor distal extremities; pulses distal to the catheterization site may be weaker for the first few hours, assessing for potential occlusion.
Inspect the dressing for bleeding to prevent hematoma formation.
Manage fluid intake: both IV and oral; ensuring proper hydration post-procedure.
Watch for signs of hypoglycemia due to NPO status and manage accordingly.
Monitor signs of stroke; look for confusion, weakness in the face or arm, slurred speech, and loss of balance urgently.
Discharge Planning Following Cardiac Catheterization
Pressure dressing for 24 hours to stabilize the catheterization site and prevent bleeding.
No tub baths for 3 days; may shower the next day, avoiding submersion that may cause site infection.
Rest and quiet activities for 3 days to encourage healing without strain.
Can return to school after 3 days but avoid strenuous activities until cardiologist clearance is obtained.
Return to a regular diet gradually, considering individual dietary needs based on recovery and cardiac health.
Manage pain with Ibuprofen or Tylenol, following recommended dosing guidelines.
Educate family on signs and symptoms of infection such as fever or unusual site discharge.
Protecting the Catheterization Site
A. Teach the parents to "double diaper" until the site heals to prevent direct friction or pressure on the site.
B. Cover the dressing with plastic film, sealing edges with tape to keep it dry and clean.
C. Place absorbent drapes under the child and leave the diaper off until the site heals to minimize moisture.
Developmental Considerations
Heart size: At birth, ventricles are equal in size which may affect functional capacity with growth.
Less compliance: Muscle fibers of the heart are underdeveloped in infancy, resulting in limited functional capacity to manage cardiac demands effectively.
Normal O2 saturation: Ranges from 95% to 100% indicates optimal respiratory function; significant drops warrant investigation for cardiovascular or pulmonary issues.
Physiology of infants and young children: Characterized by thin chest walls and minimal subcutaneous fat & muscle, impacting both insulation and protection of the organs.
Fetal Circulation vs. Adult Circulation
Key Differences
The liver and lungs are bypassed via shunts:
Ductus Arteriosus: Bypasses the lungs; closes after birth typically within days.
Foramen Ovale: Bypasses the lungs; closes shortly after birth due to pressure changes.
Ductus Venosus: Bypasses the liver; closes functionally soon after birth.
Fetal circulation ensures vital organs receive maximum concentration of oxygenated blood.
Closure of Fetal Shunts
All shunts typically close at birth or shortly thereafter due to:
Decreased maternal hormone Prostaglandin E, which maintains shunt patency in utero.
Increased O2 saturation at birth that induces shunt closure.
Pressure changes within the heart as the newborn takes first breaths and circulation changes post delivery.
General Clinical Findings for Cardiac Defects
Dyspnea or difficulty breathing during exertion or normal activities.
Feeding difficulties and failure to thrive evident in infants struggling with heart workload.
Stridor or choking spells which may indicate respiratory distress or obstructive issues.
Heart rate >200; respiratory rate 60 in infants indicating significant distress.
Recurrent respiratory infections due to compromised cardiovascular function.
In older children: poor physical development, delayed milestones, decreased exercise tolerance, indicating reduced oxygenation.
Cyanosis and clubbing of fingers and toes possibly due to chronic low oxygen states.
Squatting or knee-chest position as a compensatory action to improve venous return.
Heart murmurs that can indicate significant underlying abnormalities.
Excessive perspiration particularly when feeding or at rest, signaling heart strain.
Signs of heart failure requiring immediate evaluation.
Classification of Cardiovascular Disorders
Congenital Heart Disease: Defects present at birth that may affect cardiovascular performance.
Acquired Cardiac Disorders: Develop after birth due to various factors such as infections, diseases, or trauma impacting heart function over time.
Cardiac Hemodynamics (Normal vs. Abnormal)
Normal:
Right atrium (RA), left atrium (LA), right ventricle (RV), left ventricle (LV), pulmonary artery (PA), aorta (AO) functioning harmoniously, allowing for effective systemic and pulmonary circulation.
Abnormal: Changes depend on defect and can arise from structural anomalies, leading to altered pressure and blood flow distribution.
Congenital Heart Defects (Clinical Consequences)
Left to Right Shunting
Caused by defects that allow blood to flow from the left side of the heart to the right, resulting in
Symptoms of congestive heart failure (CHF) due to increased blood volume on the right side of the heart, leading to edema and pulmonary congestion.
Decreased Pulmonary Blood Flow
Caused by defects that restrict blood flow to the lungs, leading to hypoxia and cyanosis due to inadequate oxygenation.
Congestive Heart Failure (CHF)
Definition: A condition resulting from structural or functional abnormalities leading to volume or pressure overload primarily affecting the ventricles preventing adequate blood circulation.
Contributing Factors
Congenital heart defects that impair effective circulation.
Poor myocardial function due to various factors including ischemia or hypertrophy.
Protein-loss enteropathy affecting nutrition and contributing to heart stress.
Other systemic diseases such as chronic anemia or thyroid dysfunction influencing heart function as secondary care factors.
Clinical Manifestations of CHF
Pulmonary Venous Congestion
Symptoms include tachypnea, wheezing, crackles, cough, dyspnea on exertion indicating impaired gas exchange.
Irritability and fatigue with play as children struggle to manage daily activities.
Nasal flaring and cyanosis as responses to hypoxia or respiratory distress.
Systemic Venous Congestion
Symptoms include hepatomegaly, ascites, edema, neck vein distention indicating fluid overload.
Weight gain not attributable to nutrition but retention, indicative of CHF.
Impaired Myocardial Function
Symptoms such as tachycardia, weak peripheral pulses, gallop rhythm indicating heart strain.
Hypotension, extended capillary refill, and cool extremities indicating shock or inadequate perfusion, fatigue, oliguria, and pallor that signal deteriorating status.
Therapeutic Management of CHF
Improve cardiac function through medications and procedural interventions.
Remove accumulated fluid & sodium via diuretics to alleviate edema and improve heart workload.
Decrease cardiac demands through rest and supportive therapies.
Improve tissue oxygenation & decrease oxygen consumption via supplemental O2 and managing activity levels.
Medications in CHF
Furosemide (Lasix): Monitor potassium levels due to risks of hypokalemia; encourage potassium-rich foods.
ACE Inhibitors: Monitor blood pressure and renal function; most are potassium-sparing, assisting cardiac efficiency.
Digitalis: Helps improve myocardial contractility, enhancing cardiac output under careful monitoring for toxicity.
Digitalis Administration Rules
Administer medication at regular intervals (1 hour before or 2 hours after meals) for optimal absorption; timing aids effectiveness.
Check apical heart rate for 1 minute prior to administration (hold if < 90-110 in infants & children, < 70 in older children) to prevent bradycardia.
Do not mix with food or other fluids. Monitor potassium levels prior to administration and adjust based on prescription guidelines.
If vomiting occurs after administration, do not repeat the dose to avoid overdosing.
If a dose is missed, administer if less than 4 hours late; otherwise, omit and notify practitioner for further instruction.
Digoxin Toxicity
Symptoms
Nausea and vomiting as initial symptoms indicating potential toxicity; often first signs.
Bradycardia presenting with decreased heart rate may signal overdose.
Anorexia or loss of appetite secondary to gastrointestinal disturbances.
Neurologic and visual disturbances (e.g., diplopia), indicating potential effects on the central nervous system.
Management
Monitor for dysrhythmias due to risk for hyperkalemia when serum levels rise; follow protocols for safely correcting electrolyte imbalances.
Digibind (Digoxin immune Fab fragments) may be administered for toxicity treatment, effectively neutralizing digoxin effects.
Effect of Digoxin on Potassium
Digoxin toxicity can cause hyperkalemia due to blocking the sodium-potassium pump in cells, leading to serious complications if untreated.
Conversely, hypokalemia increases the risk of digoxin toxicity as it enhances digoxin binding, necessitating careful monitoring of both.
Home Care for Children with CHF
Detailed Nursing Instructions
Monitor fluid intake and output meticulously to prevent volume overload or dehydration; facilitate accurate daily weights as part of the regimen.
Educate family on recognizing signs of worsening conditions; empower caregivers to act swiftly upon the first signs of distress.
Ensure a nutritious diet to meet high caloric needs while considering smaller more frequent feedings to ease the workload on the heart.
Discuss the symptoms of respiratory infections and the importance of vaccinations to reduce risk of exacerbating the child's condition.
Acyanotic Heart Defects
Increased Pulmonary Blood Flow typically includes greater volume flow directed to the lungs resulting potentially in congestive heart failure due to overload yet maintained oxygenation.
Atrial Septal Defect (ASD) represents abnormal communication between the atria, potentially requiring surgical intervention.
Ventricular Septal Defect (VSD) can lead to significant volume overload on the heart, often necessitating surgical closure at a specific age.
Patent Ductus Arteriosus (PDA) occurs when the ductus fails to close post-birth, requiring interventional strategies such as Indomethacin or surgical closure for management.
Clinical Management of Increased Pulmonary Blood Flow Defects
ASD: Surgical intervention for severe cases via Dacron patch closure or device closure for those with significant shunting.
VSD: Management may require surgical intervention outages with a focus on timed closures to optimize functional outcomes.
PDA: Potential treatments include administering Indomethacin and evaluating the need for closure via surgical methods based on symptoms and hemodynamic status.
Obstructive Lesions
Coarctation of the Aorta is characterized by narrowing of the aorta leading to differential blood pressures in arms and legs requiring surgical intervention.
Aortic Stenosis presents with valvular obstruction affecting systemic flow and may require balloon dilation or surgical replacement of the valve.
Pulmonic Stenosis involves narrowing at the outflow tract from the right ventricle, often leading to hypertrophy and requiring interventional procedures.
Clinical Consequences
Patients present with signs of CHF and decreased peripheral perfusion; close monitoring is essential.
Therapeutic Management
Surgical repair is typically required, especially in coarctation scenarios where life-threatening hypertension can occur if untreated.
Cyanotic Heart Defects
Decreased Pulmonary Blood Flow conditions such as Tetralogy of Fallot, Tricuspid Atresia, and others hallmark reduced oxygenation and blood saturation.
Clinical Considerations
Can present with cyanosis, polycythemia from chronic hypoxia, and clubbing resulting from longstanding low oxygen states.
Management Strategies
Consistent monitoring and family education on managing cyanotic episodes (e.g., recognizing hypercyanotic spells) are paramount to prevent complications and ensure safety.