Pediatric Cardiac Defects (copy)

The Child with Cardiovascular Dysfunction

Presenter: Jessie Seeck, STLCC - Wildwood

Types of Cardiovascular Disorders

1. Congenital Heart Disease

• Congenital Heart Defects: Structural abnormalities of the heart present at birth. These defects can affect the normal blood flow through the heart and can lead to significant health issues if not detected and treated early.

2. Acquired Cardiac Disorders

• Acquired Cardiovascular Diseases: Conditions that develop after birth due to factors such as infection, autoimmune disease, or other health conditions. Both congenital and acquired disorders can lead to symptoms of heart failure in varying degrees.

Both types can cause Heart FAILURE to some degree.

History and Physical Examination

History

• Maternal Health History: Comprehensive history should include maternal conditions during pregnancy like {gestational diabetes, lupus, history of infections RUBELLA, and any use of teratogenic medications DILATIN}. These factors significantly contribute to the risk of congenital heart disease (CHD).

• Family History: Investigate any family history of cardiovascular issues, as genetic predispositions can play a critical role in the development of heart conditions in children.

Physical Assessment

• Techniques: Key assessment techniques include inspection, palpation, percussion, and auscultation.

Diagnostic Evaluation

A thorough diagnostic evaluation is critical for identifying cardiovascular dysfunction in children. Methods may include:

• Echocardiogram: Provides images of the heart structure and function.

• Electrocardiogram (EKG): Measures the electrical activity of the heart.

• Holter Monitor: Continuous monitoring to detect arrhythmias.

• Chest X-ray: Helps to assess heart size and pulmonary blood flow.

• Cardiac MRI: Advanced imaging for detailed cardiovascular evaluation.

• Comprehensive Blood Counts (CBC) and Arterial Blood Gases (ABGs): Evaluate overall health and oxygenation.

• Hyperoxia Test: Assesses the degree of hypoxemia.

• Cardiac Catheterization: Invasive procedure that allows direct measurements and possible therapeutic interventions.

Nursing Care Management

Pre-procedural Care

• Assessment: Document allergies, signs of infections, and baseline vitals including O2 saturation. Pre-operative considerations must take into account the child's age and weight for proper anesthesia management.

  • s/s of infection - diaper rash

  • assess/mark pulses

  • include parents and patients in care, age appropriate explanations. In addition, ensure to discuss the procedure and recovery expectations with both the child and their parents to alleviate anxiety and promote understanding.

  • NPO 6-8 HOURS BEFORE.

Post-procedural Care

• Monitoring: Intensive monitoring for complications should include';

  • Heart monitor/ pulse o2 /temp

  • Color checks and pulses on extremities/

  • Count pulse for full minute.

  • Vitals q15 / BP (HYPOTENSION RISK)

  • Dressing- check for bleeding.

  • Fluid intake r/f hypovolemia/dehydration

  • Blood glucose- infants are at greater r/f hypoglycemia, should receive IV fluids with dextrose.

    Family Centered Care: Essential for post-catheterization teaching, including instructions about bandage changes, cleanliness maintenance, restrictions on activities, and signs of potential infections. Discuss pain management and strategies for returning to school or sports.

    • bed rest

    • diaper wearer - prevent cath site infection.

    • Change dressing x 2 days

    • avoid baths and swimming x 1 week.

    • regular diet

    • Tylenol for pain

    • rest/calm activities x 3 days

    • KEEP FOLLOW UP VISIT

Importance of Maternal Health in Cardiovascular Dysfunction

Maternal health factors that significantly affect Congenital Heart Disease include:

• Diabetes: Elevated blood sugar levels can affect fetal heart development.

• Lupus: An autoimmune disease that can increase risk for CHD.

• Substance Use: Alcohol and illicit drugs negatively affect fetal cardiovascular health.

• Infections: Maternal infections, like Rubella, pose risks during pregnancy.

• Teratogenic Drugs: Some medications, such as Dilantin, contribute to heart defects.

Child Physical Examination Indicators

Signs of cardiovascular dysfunction include:

• Failure to Thrive: Poor growth patterns can indicate underlying cardiac issues.

• Cyanosis: A bluish discoloration of the skin, indicating low oxygen levels.

• Respiratory Excursions: Inadequate respiratory effort may signify heart distress.

• Clubbing of Fingers: Indicates chronic hypoxia often associated with congenital heart disease.

• Organomegaly: Hepatomegaly or splenomegaly may suggest increased pressure in the vascular system.

• Peripheral Pulses: Regular assessment is crucial for rate, rhythm, and amplitude to evaluate perfusion.

• Auscultation: Identifying abnormal heart rates such as tachycardia, bradycardia, irregular rhythms, and murmurs.

Circulatory Changes at Birth

Upon birth, critical circulatory changes occur:

• Cord Clamping and Lung Expansion: Trigger the functional closure of fetal shunts, essential for normal circulation.

  • Umbilical vein and umbilical arteries, before birth the umbilical vein delivers oxygen and nutrients to the fetus.

• Foramen Ovale: Closes as the pressure gradient changes in the atria.

• Ductus Arteriosus: Begins closure with increased oxygen levels in the blood post-natally.

Normal Fetal and Newborn Heart Anatomy

Key structures include:

• Superior vena cava, Patent ductus arteriosus, Foramen ovale, Pulmonary artery, Ligamentum arteriosus, and Mitral and Tricuspid valves, which are all critical for evaluating congenital heart anomalies.

Congenital Heart Defects Categories

Classification based on blood flow:

• Increased Pulmonary Blood Flow (Acyanotic): Conditions such as Ventricular Septal Defect (VSD), Atrial Septal Defect (ASD), and Patent Ductus Arteriosus (PDA).

  • Ventral Septal Defect (VSD)= hole between the ventricles.

    • Can close spontaneously

    • S/S: s/s of heart failure, murmur- loud systolic at left sternal border.

    • Treatment- surgery to suture or patch the hole.

  • Atrial Septal Defect (ASD) = hole in septum that separates left and right atria. Often asymptomatic in childhood but may lead to heart failure or arrhythmias if untreated.

    • S/S; Heart failure, systolic murmur with wide fix splitting of S2.

    • Treatment: Closure with cardiac cath or surgical closure.

  • Patent Ductus Arteriosus (PDA) = failure of the ductus arteriosus to close after birth, leading to increased blood flow to the lungs and potential pulmonary congestion.

    • S/S: machine hum murmur, bounding pulses, wide pulse pressure

    • Treatment: Indomethacin- NSAID(goes in the whole and closes it) , coils to occlude PDA during cardiac cath.

• Obstruction to Blood Flow (Acyanotic): Includes defects that restrict normal blood flow, such as pulmonary stenosis and aortic stenosis.

  • Coarctation of the aorta- narrowing of the aorta, occurs after blood is supplied to upper extremities. Lower extremities are not getting much.

    • S/S- upper extremities (hypertension, bounding pulses) lower extremity( poor perfusion, pallor, skin is cool, weak pulses)

    • Treatment- balloon angioplasty or stents to open up the narrowed section of the aorta or remove narrow section.

      • Manage hypertension with blood pressure medication'

  • Aortic Stenosis- narrowing of the aortic valve, which separates with left ventricle from the aorta. This decreases blood flow to the whole body.

    • S/S- Hypotension, decreased pulses, tachycardia(heart is trying to compensate for the hypotension), poor feeding, exercise intolerance.

      • Infants- faint pulses, hypotension, tachycardia, poor feeding intolerance.

      • Children- intolerance of exercise dizziness, CP

    • Treatment- cath lab balloon dilation or valvotomy to try to open the narrowed valve.

      • Serious defect- treatments rarely completely repair, sudden episodes of myocardial ischemia can lead to SCD.

  • Pulmonary Stenosis- narrowing of the pulmonary vein, which separates the right ventricle from the pulmonary artery. This obstructs blood flow to the lungs.

    • May be asymptomatic at birth.

      • S/S- systolic ejection murmur, cyanosis, cardiomegaly(enlarged heart), and heart failure.

  • Treatment: cath lab Balloon dilation or valvotomy, try to open that narrowed valve. Infants- brock procedure (through ventricle) children- valvotomy with CPB.

IF YOU APPLY 02 TO A BABY WITH AN ACYANOTIC DEFECT IT WILL DO NOTHING.

• Decreased Pulmonary Blood Flow (Cyanotic): Examples include Tricuspid Atresia and Tetralogy of Fallot.

• Mixed Blood Flow (Cyanotic): Conditions like Transposition of the Great Vessels and Hypoplastic Left Heart Syndrome.

Increased Pulmonary Blood Flow Defects

• Characteristics: These defects are marked by left-to-right shunting; common symptoms include signs of heart failure, systolic murmurs, dyspnea, and poor growth.

• Examples: VSD treatment options can be surgical or non-surgical.

Obstructive Congenital Heart Defects

• Examples and Symptoms:

  • Pulmonary Stenosis: Often asymptomatic at birth; balloon angioplasty or surgery may be needed.

  • Aortic Stenosis: Symptoms can present variably; treatment may include dilation and valve replacement.

  • Coarctation of the Aorta: Revealed through a high BP in the upper body with weak pulses in lower extremities; may require dilation or surgery.

Decreased Pulmonary Blood Flow Defects

• Examples Include:

  • Tricuspid Atresia: pulmonary stenosis and transposition of the great arteries. There is complete mixing of deoxygenated and oxygenated blood in the left side of the heart, which results in systemic desaturation, and varying amounts of pulmonary obstruction, which causes decreased pulmonary blood flow. Requires surgical intervention and presents varying symptoms based on the patient’s age.

    • S/S- cyanosis, tachycardia, dyspnea, clubbing of fingernails.

      • Infants (cyanosis)

      • Child (clubbing/chronic hypoxia, activity intolerance, poor feeding)

    • Treatment: multiple surgery’s, shunt placement,

  • Tetralogy of Fallot: Presents severe episodes of cyanosis at birth; nursing care should include high-calorie feeds and close monitoring of respiratory rates. Mix of Four different defects (Prove That You Know All Four)

    • Pulmonary stenosis, right ventricular hypertrophy, Overriding aorta, Ventricular septa defect.

    • S/S: cyanosis- “tet” spells (place patient in knee chest position to increase blood flow to lungs), systolic murmur present.

    • Treatment: Surgical repair in first few months.

Mixed Blood Flow Defects

• Conditions include:

  • Transposition of Great Vessels: Surgical intervention is essential; survival relies on the presence of PDA/VSD. Aorta and pulmonary artery connections are reveres. Blood flow is opposite- deoxygenated blood in the right ventricle is being pumped out to the body. Oxygenated blood is being pumped back into the lungs.

    • S/S- Heart failure, SOB, cardiomegaly(enlarged heart), cyanosis, hypoxia, murmurs, fatigue, poor growth.

    • TX: Prostaglandins- help keep PDA(patent ductus arteriosus open to allow mixing of blood until the child can get surgery. Surgery within 1st week of life.

      • Jatene procedure- arterial switch operation

  • Truncus Arteriosus: A single vessel shared between the right and left ventricles causes complex symptoms. Usually will have VSD- mixing of blood.

    • S/S- Heart failure, murmurs, cyanosis, poor feeding.

    • TX: Surgical repair within first few months of life.

  • Hypoplastic Left Heart Syndrome: Characterized by an underdeveloped left side leading to severe cyanosis if untreated. Will have PDA or ASD also.

    • S/S- cyanosis, heart failure, cold extremities, lethargy.

      • IF PDA or ASD close the child will rapidly deteriorate.

    • Treatment: Prostaglandin to keep PDA open until surgery. 3 diff stages of surgery. Complex surgery- parents need to know how to monitor 02 levels, weight gain (poor weight gain= poor prognosis).

Management of Heart Failure in Children

Goals

• Improve cardiac function and promote effective tissue oxygenation.

• Nursing strategies may involve medications such as Digoxin, diuretics, managing fluid intake restrictions, and minimizing cardiac demand.

Digoxin Care

• Administration Guidelines: Monitor heart rate and understand toxicity signs; accurate dosage calculation is vital. Safety in administration and proper storage are critical for efficacy and safety.

  • Count apical pulse for 1 minutre

  • Hold med if

    • 90-110 for infants/young kids

    • 70- older children

    • 60 in adults

  • Rinse month if liquid (cavities)

  • vomit or missing a dose do not take another or double up.

• Digoxin Toxicity

  • 0.8-2mcg/L is safe range

  • s/s- bradycardia, anorexia, N/V, visual changes (halos around lights).

  • Draw a dig level if any concerns.

Acquired Cardiovascular Disorders

Kawasaki Disease (red Kawasaki motorcycle)

Clinical Manifestations

Symptoms to be vigilant for include high fever, rashes, lymph node swelling, and risk of developing coronary artery aneurysms—a serious complication leading to heart failure.

• Systemic inflammation of the blood vessels in the body (vasculitits). Cause is unknown, possibly due to an exaggerated immune response to an infection in a susceptible child.

• 3 phases- acute, subacute, convulsant phase.

• Acute phase: Characterized by a sudden onset of symptoms, including prolonged fever, irritability, and conjunctival injection.

  • S/S: high fever(over 102) x 1-2 weeks and antipyretics do not help. Various areas of redness or erythema on the body, red eyes without drainage, chapped and cracked lips (red), oral mucosal membrane will be red, and palms and soles will be red, arthritis, possibly cardiac symptoms ( dysrhythmias and myocarditis).

• Subacute phase: Marked by a decrease in fever and the appearance of complications such as coronary artery aneurysms, with potential for thrombosis.

  • S/S- fever has resolved, arthritis is present, peeling skin around nails/palms/soles.

• Convalescent phase: This phase involves gradual recovery, where symptoms resolve but laboratory markers of inflammation may remain elevated.

  • s/s: no clinical manifestations, labs( elevated CRP/ESR (r/t inflammation), albumin will be decreased.

Diagnosis:

• Fever x 5 days, four of the five symptoms:

  • CREAM

    • C- conjunctivitis (redness of eyes)

    • R- rash

    • E- extremity changes(redness to hands/feet

    • A- adenopathy (enlarged lymph nodes in neck)

    • M- mucosal changes (red lips/cracked, red mucous membranes, strawberry tongue.

• Treatment: Intravenous immunoglobulin (IVIG), high dose aspirin(ONLY OKAY IN A FEW CONDITIONS)

• Nursing care:

  • closely monitor cardiac function r/t carditis

  • resp status

  • daily weights/ I&O

  • Supportive care: skin, mouth, irritable babies, clear lquies/soft foods.

  • family teaching- no live immunizations for 11 months (MMR and Varicella)

Nursing Management

Treatment typically includes IVIG and supportive measures. Continuous monitoring is vital for early detection of deterioration.

Pediatric Vitals

Pay close attention to age-specific vital signs for blood pressure, pulse rates, and respiration rates to ensure proper monitoring of children’s overall cardiovascular health.

Quick Review Questions

1. How to respond to hypercyanotic spells?

2. Signs of Digoxin toxicity in children?

3. What are the manifestations and treatment protocols for Kawasaki Disease?

4. Cyanosis that worsens with crying is a typical sing of congenital heart defects, particularly tetralogy of Fallot.

5. Aspirin and immunoglobulin (IVIG) are main treatments for Kawasaki disease.

6. A sudden increase in respiratory rate (24 to 40 breaths per minute) could indicate respiratory distress or complications such as pneumothorax, fluid overload, or heart failure. IMMEDIATE INTERVENTION TO ASSESS AND STABILIZE THE CHILD.

7. Before administering digoxin, ASSESS CHILDS PULSE RATE!! (90-110 beats per min for infant/young child.)

8. In tetralogy of Fallot “tet spell” occurs due to decrease in oxygenation, often precipitated by crying or stress. Place child in knee to chest position to increase systemic vascular resistance and help relieve the cyanosis by improving pulmonary blood flow.

9. Do not limit fluids for Kawasaki disease due to dehydration.

10. Atrial septal defect (ASD), typically causes a soft, systolic murmur at then upper left sternal border due to increased blood flow through the right atrium and ventricle.

11. Patent ductus arteriosus (PDA), CONTINUOUS “MACHINE LIKE” MURMUR, due to continuous blood flow btwn the aorta and pulmonary artery.

12. A potential complication of Kawasaki disease is the development of coronary artery aneurysms (SUDDEN ONSET OF CHEST PAIN).

13. Coarctation of the aorta is a narrowing of the aorta that obstructs blood flow to the lower body. Blood pressure is higher in the upper extremities and lower in the lower extremities.

14. Ventricular septal defect (VSD) causes increased blood flow to the lungs and can lead to heart failure. S/S- tachypnea, poor feeding, and difficulty breathing. Priority= assess and manage heart failure.

15. Patent ductus arteriosus (PDA) causes blood to flow abnormally between the aorta and pulmonary artery, leading to increased blood flow to the lungs. S/S(tachypnea, bounding pulses, and poor feeding) due to increased cardiac workload.

16. Transposition of the great arteries (TGA)- the aorta and pulmonary artery are switched, which causes poorly oxygenated blood to circulate to the body and oxygenated blood to circulate to the lungs. S/S- SEVERE CYANOSIS THAT DOES NOT IMPROVE WITH OXYGEN THERAPY.

17. Echocardiogram is the most appropriate diagnostic tool to confirm congenital heart defects.

18. In infants with Atrial septal defect (ASD)- there is an increased flow of blood to the lungs. S/S- HF, tachypnea, poor feeding, failure to thrive.

19. Children with mitral valve prolapse (MVP) may need to limit intense physical activity or competitive sports. Regular follow ups are important, monitor for dizziness and fainting.