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Common Cardiovascular Disorders in Children
Congenital Heart Defects Congestive Heart Failure Acquired Heart Disease
Fetal Shunts
ductus venosus: accessory (extra) vein, carries oxygenated blood to fetal liver from umbilical vein
foramen ovale: shunts oxygenated blood from right atrium to left atrium (hole in the atrial septum)
ductus arteriosus: accessory (extra) artery, shunts deoxygenated blood away from lungs to descending aorta to umbilical cord to placenta
Fetal Circulation of Oxygenated Blood
Oxygenated blood flows from placenta into the umbilical vein to fetal liver through ductus venosus
then inferior vena cava with the remaining unoxygenated blood from fetal legs & abdomen
Fetal Circulation of Oxygenated Blood
Inferior Vena cava empties into Right atrium
Little oxygenated blood flows into right ventricle to be pumped through the pulmonary artery to the lungs (because the lungs are not inflating)
Fetal Circulation of Oxygenated Blood
Most of the oxygenated blood in the right atrium is shunted through the foramen ovale into the left atrium
Then oxygenated blood travels from the left atrium, into the left ventricle, and pumped into the aorta to the body
Fetal circulation of Deoxygenated blood
Deoxygenated blood returns though the superior vena cava into the right atrium, right ventricle and into the pulmonary artery
Because resistance is high in the pulmonary artery, blood flows through the opening in the pulmonary artery- the ductus arteriosus, into the aorta, into the fetal arterial system and into the 2 umbilical arteries back to the placenta
How does the fetus receive sufficient oxygen from the
maternal blood supply?
Fetal hemoglobin carries 20-30% more oxygen than maternal hemoglobin
Fetal hemoglobin concentration is 50% greater than mother’s
Fetal heart rate 120-160bpm (increases cardiac output)
Transition from intrauterine to extrauterine life
Cord is clamped, neonate initiated respirations
O2 levels rise = greater pressure in the left atrium, decreased pressure in the right atrium leading to an immediate closure of the foramen ovale
Transition from intrauterine to extrauterine life
After O2 circulates systemically, over 24 hours, the pressure in the left ventricle will become greater than the pulmonary artery and closes the ductus arterosis
The absent flow of blood through the umbilicus gradually closes the ductus venosus over 12 hr to 2 weeks
Cardiac Catheterization
Primary method to measure extent of cardiac disease in children
Shows type and severity of the CHD Insert tiny catheter through an artery in arm,
leg or neck into the heart Take blood samples and measure pressure,
measure o2 saturation, and as an intervention Sedation or anesthesia Outpatient vs Hospital
Cardiac Catheterization Pre-Op
NPO 4-6 hrs Check for known allergies, history
of recent fever, signs and symptoms of infection
Cardiac Catheterization-Post Op
Monitor closely (cardiac monitor, continuous pulse ox) VS q 15
Assess dressing at insertion site for infection, hematoma
Dressing must remain dry for 1st 48-72 hrs
No blood drawn from extremity used Palpate a pulse distal to the dressing to
assure blood flow to extremity is not obstructed: keep extremity straight for 48 hrs after procedure
Congestive Heart Failure
heart doesn’t pump blood well enough –can not provide adequate cardiac output due to impaired myocardial contractility
Causes in children:• Defects
• Acquired heart disease
• Infections
Congestive Heart Failure
Most common cause in children is congenital heart defects• Increased volume load or increased pressure
in heart Excess volume and pressure builds up in
lungs leading to labored breathing builds up in rest of body leading to edema (edema is a late sign in children)
Congestive Heart Failure Symptoms
1st sign: tachycardia tire easily rapid, labored breathing decreased urine output fluid and sodium are retained increased sweating, pallor edema
CHF Diagnosis and Treatment
CXR- shows enlargement Echocardiogram- dilated heart
vessels, hypertrophy, increase in heart size
Tx-aimed at reducing volume overload, improve contractility
May require surgery
Congestive Heart Failure Medical Management
1. Digoxin- Helps strengthen the heart muscle, enables it to pump more efficiently
1st line tx Dosing depends on wt and age Need HR, EKG, drug levels Parent teaching
2. ACE (Angiotension-converting-enzyme) inhibitors- dilates the blood vessels making it easier for the heart to pump blood forward into the body
Congestive Heart Failure Medical Management
Diuretics- Helps the kidneys remove excess fluid from the body• Potassium sparing• Potassium wasting
• Potassium supplements- given along with wasting diuretics
Lasix-1st agent for children-lose K esp. when taken with digoxin
Congenital Heart Disease
35 different types Common to have multiple defects Range from mild to life threatening and
fatal Genetic and environmental causes Caused by:
• Defect or
• Failure of shunt closure
Types of CHD
Acynotic defects• Septal defects
• VSD• ASD
• PDA Obstructive (Cyanotic) defects
• Pulmonic Stenosis• Coarctation of the aorta
Cyanotic defects• Transposition of the greater vessels• Tetrology of Fallot• Hypoplastic left heart
Septal Defects- increased pulmonary blood flow
Left to right shunting (acyanotic defect)• Increased cardiac
workload• Excessive pulmonary
blood flow• Right ventricular strain,
dilation, hypertrophy• CHF, pulmonary HTN,
bacterial endocarditis• Ventral Septal Defect• Atrial Septal Defect
Ventricular Septal Defect
Most common CHD High Pressure in LV
forces blood back to RV
Results in increased pulmonary blood flow (heart must pump extra blood), higher than normal artery pressure
Ventricular Septal Defect
S/S: vary with the size of the defect 4-8 weeks of age develop loud, harsh
systolic heart murmur Right ventricular hypertrophy 20-60% close spontaneously cardiac cath shows: O2 level of RV higher
than normal large defects: develop CHF, poor feeding,
failure to thrive
Ventricular Septal Defect
Treatment: Small defects: followed by cardiologist,
prophylactic ABX Large defect: open heart surgery with
cardiopulmonary bypass, will suture or patch hole closed• If child is not stable for open heart surgery:
pulmonary artery banding: narrowing of pulmonary artery to reduce blood flow to lungs
VSD Medical Management
For infants not medically stable for surgery or awaiting surgery-
Digoxin: to improve cardiac output; check apical pulse first, don’t give if HR < 100 bmp in infants and < 70 bpm in children
Digoxin toxicity: vomiting, bradycardia
Oxygen
Atrial Septal Defect
Pressure in LA is greater than RA (blood flows left to right)
Oxygen rich blood leaks back to RA to RV and is then pumped back to lungs, results in ventricular hypertrophy
Few if any symptoms, over time may experience fatigue and dyspnea on exertion
Atrial Septal Defect Clinical Presentation
Large defect may cause CHF Harsh systolic murmur Second heart sound is split: “fixed
splitting” ** diagnostic of ASD pulmonary valve closes later than
aortic valve Echocardiogram: shows enlarged
right side of heart, increased pulmonary circulation
ASD Management
Nonsurgical management: prosthetic umbrella patch
Surgical management: open-heart with CP bypass, edges are sutured or will use Silastic patch to cover hole
Diuretics to control symptoms until repair is performed
Patent Ductus Arteriosus
Failure of ductus arteriosus to close completely at birth
Blood from the aorta flows into the pulmonary arteries to be reoxygenated in the lungs, returns to LA and LV
Not enough oxygenated blood is getting out o nourish the body
More common in preemies
Patent Ductus Arteriosus
Preterm infants: present with CHF and respiratory distress
Fullterm infants: may be asymptomatic with a continuous “machinery” type murmur
Tire easily, growth retardation (shorter, weigh less, less muscle mass), prone to frequent respiratory tract infections
Patent Ductus Arteriosus
Chest radiographs (x-ray) show enlarged LA and LV
Medical management: Indomethacin (prostaglandin inhibitor that stimulates ductus to constrict)
Surgical management: ductus is divided and ligated (usually performed in first year of life to decrease risk of bacterial endocarditis
Obstructive Defects- decreased pulmonary blood
flow
Right to left shuntDefect present that obstructs LV
flow Pulmonic Stenosis Coarctation of the Aorta
Pulmonary Stenosis
Obstruction of the right ventricular outflow tract
Decreased pulmonary blood flow Right ventricular hypertrophy High ventricular pressure may cause
blood to back up into right atrium and force foramen ovale to open to allow blood to flow from right to left atrium
Pulmonary Stenosis
Usually asymptomatic Systolic ejection murmur with a palpable thrill Enlarged heart on x-ray Severe: right ventricular failure, CHF, if there is right to left
shunting through the foramen ovale, mild to moderate cyanosis
Pulmonary Stenosis
Medical Management: If asymptomatic: cardiac follow-up Prophylactic ABX
Surgical Management: Pulmonary balloon valvuloplasty via
cardiac cath if unsuccessful: valvotomy
Coarctation of Aorta
Localized constriction of the aorta at or near the insertion site of the ductus arteriosus
Reduces cardiac output (impedes blood flow from heart to body)
Aortic pressure is high proximal to the constriction and low distal to the constriction
Coarctation of Aorta
S/S: related to severity of the constriction and presence of associated cardiac defects
Mild: asymptomatic, sys. murmur, diminished pulses in lower ext
Severe: poor lower body perfusion, metabolic acidosis, CHF, systemic hypertension
In both: BP is 20mmHg higher in arms than in lower extremities
Treatment of Coarctation of Aorta
Symptomatic newborn treated with: Digoxin diuretics to manage CHF may also receive PGE1
(prostaglandin) infusions to maintain ductal patency and improves perfusion to lower extremities
surgical repair within first 2 years
Cynaotic Defects
Decreased pulmonary blood flow• Transposition of the greater vessels• Tetrology of Fallot• Hypoplastic left heart
Tetralogy of Fallot Consists of 4 Parts:
VSD RV hypertrophy Overriding aorta Pulmonic Stenosis:
impedes blood flow to the lungs, forces unoxygenated blood through the VSD & into aorta
S/STetralogy of Fallot
The degree of pulmonic stenosis governs the onset and severity of symptoms.
Mild: little to no right to left shunting infant has “tet spells” hypercyanotic episodes
Mod-severe: some cyanotic at birth when PDA closes, other infants become increasingly cyanotic over the first few months of life
Tetralogy of Fallot
Tire easily especially with exertion, difficulty feeding and gaining weight,
Other signs: chronic hypoxemia
Management Tetralogy of Fallot
Over time may have hypercyanotic episodes (tet spells)
often preceded by crying, feeding or stooling, worsening cyanosis, increased respiratory rate, may lose consciousness
Treatment of tet spells: calm infant, knee-chest position, O2 Do not leave alone- cyanosis can cause LOC, death
Tetralogy of Fallot
Medical management: Symptomatic newborn: PGE1 infusion to
maintain ductal patency Older infants: close monitoring for
worsening of hypoxia Surgical management: done at 3-12 months
of age, in stages primary open-heart repair: close VSD, open
pulmonary valve, remove obstructing muscle
Hypoplastic Left Heart Syndrome
pulmonary venous blood is shunted through foramen ovale into right atrium
mixed blood travels through the right ventricle to the pulmonary artery, patent ductus arteriosus
as ductus begins to close in first few days of life infant becomes symptomatic
Hypoplastic Left Heart Syndrome
symptoms: CHF hypoperfusion,
shock grayish-blue
color dyspnea hypotension
DiagnosisClinical presentation and echo (increased size in right side)
Hypoplastic Left Heart Syndrome
Medical Management: PGE1 to keep ductus arteriosus open Correct acid-base and electrolyte
imbalances
Surgical management: Heart transplant Three-stage repair
Transposition of Great Arteries
Aorta is connected to RV (unoxygenated blood goes to body)
Pulmonary artery is attached to LV (oxygen rich blood is recirculated to lungs)
Survival depends on mixing these two circulations through the fetal structures (foramen ovale and ductus arteriosus)
Transposition of Great Arteries
Cyanosis apparent at birth or shortly after, no response to oxygen
Prompt diagnosis and treatment needed for survival
Arterial switch procedure: redirects blood flow, may be done in stages within 1st year
Caring for the Child with a Congenital Heart Defect
Nursing Care: taking infant home before corrective surgery
Provide parents with information about care
Review steps for follow-up care, emergency management (s/s respiratory distress, CPR)
Key: promote normalcy within the limits of the child’s condition
Caring for the Child with a Congenital Heart Defect
Preoperative:undergoing corrective surgery
Explain procedures to parents and child, assure understanding
Encourage child and parents to express fears
Prepare child for surgery and post-op, show models of equipment (chest tube)
Caring for the Child with a Congenital Heart Defect
Postoperative: Monitor cardiac output Support respiratory function Maintain fluid and electrolyte balance Promote comfort (IV morphine,
sedatives) Promote healing and recovery
Hypertension
Primary HTN• Caused by increased body mass• Genetics
Secondary HTN• Cause is from an underlying condition
such as kidney disease or heart defects
Hypertension
No set systolic and diastolic number for diagnosis
Need to compare to child’s age, gender and height
If 3 different readings are above the 95th percentile for that child then diagnosis is confirmed
Hypertension
Managed by eliminating the primary cause if possible• Exercise, life style modification
ACE inhibitors ARBs Beta-Blockers Ca Channel Blockers
Infective Endocarditis
Inflammation of the lining of the valves and arteries
Caused by bacterial and fungal infections in the blood stream that infects an already existing injured endocardium
Children at risk: cardiac defects, severe valve disorders
Infective Endocarditis
Symptoms:• Fever, fatigue, headache, N/V, new or
changed murmur, CHF, dyspnea Treatment:
• Antibiotics IV for 2-8 weeks, surgery to replace valves, treatment of CHF
Rheumatic Fever
Acute RF is leading cause of acquired heart disease (but has decreased in US b/c abx)
Inflammatory autoimmune condition Seen in children age 5-15 Usually follows untreated strep A
infection (pharyngitis) Causes scarring of the mitral valves
Rheumatic Fever
Management: Treat infection Treat other symptoms Streptococcal prophylaxis
• PCN IM every monthor
• PCN PO BID (if allergic Sulfadiazine PO QD)
Kawasaki Disease
Acquired heart disease in children under age 5
Boys>girls Asian decent Multisystem vasculitis (inflammation of
blood vessels) 3 stages of illness Affects the coronary arteries Occurs due to antibody vascular injury
post infection
Kawasaki Disease first stage day 1-14
Prolonged fever Bilateral, nonpurulent conjunctivitis Changes in mouth (erythema, fissures,
crusting of lips, strawberry tongue) Induration of hands and feet Erythema of palms and soles Erythemous rash Enlarged cervical lymph nodes
Kawasaki Diseasesecond stage day 15-25
Fever and most of the previous symptoms resolve
Extreme irritability develops Anorexia Lip cracking and fissuring Desquamation of fingers and toes Arthritis Vascular changes in myocardium and
coronary arteries
Kawasaki DiseaseThird phase- day 26-40
Lasts until erythrocyte sed rate returns to normal and all symptoms disappear
Beau’s lines may appear
Management
Prevent or reduce coronary artery damage
Gamma-globulin IV in a dosage of 2gm/kg over a 12h infusion
High dose aspirin therapy at same time (80-100mg/kg/day once daily), continued through weeks 6-8 of disease
A parent of a toddler with Kawaski’s disease tells the nurse “I just don’t know what to do with my child. He’s never acted like this before.” The nurses best reply is:
1. Don’t worry. This type of behavior is typical for a toddler
2. Irritability is part of Kawasaki’s disease. Please don’t be embarrassed
3. Perhaps your child would benefit from stricter limits4. You seem to be in need of a referral to our Child
Guidance Center
When assessing a child for signs and symptoms of rheumatic fever, which symptoms should the nurse anticipate?
1. Tachycardia and joint pain2. Bradycardia and swollen joints3. Loss of coordination and pruritic rash4. Bradycardia and fever
Which nursing intervention is most effective in preventing rheumatic fever in children?
1. Refer children with sore throats for a throat culture
2. Include an ECG in the child’s yearly physical examination
3. Assess the child for a change in the quality of the pulse
4. Assess the child’s blood pressure
Which is most beneficial in achieving the goal of preventing infection in a child with cardiac disease?
1. Give the child extra immunizations2. Keep the child on daily prophylactic
antibiotics3. Keep the child away from others who are ill4. Place the child in protective isolation
A newborn with patent ductus arteriousus is scheduled to receive indomethacin. The nurse administers this medication to:
1. Open the ductus arteriosus2. Close the ductus arteriosus3. Enlarge the ductus arteriosus4. Maintain the size of the ductus
arteriosus
Which congenital heart defect necessitates that the nurse take upper and lower extremity blood pressure readings?
1. Coarctation of the aorta2. Tetralogy of Fallot3. Ventricular septal defect4. Patent ductus arteriosus
An infant with ventricular septal defect develops congestive heart failure and is placed on digoxin therapy twice a day. The infant vomits the morning dose of digoxin. The most appropriate nursing intervention is to:
1. Notify the pediatrician as soon as possible2. Take the infant’s pulse for 1 minute and repeat the
dose of digoxin3. Skip the dose and give twice the amount at the next
dose4. Repeat the dose and chart that the infant vomited the
first dose
The parents of a newborn with ventricular septal defect ask why their baby is being sent home instead of undergoing immediate open heart surgery. The nurse’s best response is:
1. Your baby’s condition is too serious for immediate open heart surgery
2. Ventricular septal defects are not repaired until the infant is older
3. Your baby has a small defect, and we hope that is closes spontaneously
4. Your baby must be fully immunized before surgery
When reviewing the chart of an infant with tetralogy of Fallot, the nurse should anticipate which laboratory findings?
1. Anemia2. Polycythemia3. Increased white blood cell count4. Decreased hematocrit