Cardiovascular Stressors
and Adaptation
Common Cardiovascular
Disorders in Children
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Congenital Heart Defects
Congestive Heart Failure
Acquired Heart Disease
Review of Normal
Circulation
Fetal Shunts
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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
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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
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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)

What happens to the
shunts after birth?
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
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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
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NPO 4-6 hrs
Check for known allergies,
history of recent fever, signs
and symptoms of infection
Cardiac CatheterizationPost Op
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Monitor closely (cardiac monitor,
continuous pulse ox) VS q 15
Assess dressing at insertion site for
infection, hematoma
Dressing must remain dry for 1st 4872 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
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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
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1st sign: tachycardia
tire easily
rapid, labored breathing
decreased urine output
fluid and sodium are retained
increased sweating, pallor
edema
CHF Diagnosis and
Treatment
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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
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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
Normal Blood Flow
Pressure in left is higher than
right side
Types of CHD

Acynotic defects
• Septal defects
• VSD
• ASD
• PDA

Obstructive (Cyanotic) defects

Cyanotic defects
• Pulmonic Stenosis
• Coarctation of the aorta
• 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
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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
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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
VSD Medical Management
For infants not medically stable for
surgery or awaiting surgeryDigoxin: 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
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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
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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
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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
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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
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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
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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 Defectsdecreased pulmonary
blood flow
Right to left shunt
Defect present that obstructs LV
flow
 Pulmonic Stenosis
 Coarctation of the Aorta
Pulmonary Stenosis
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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
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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
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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
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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
Coarctation of Aorta
Diagnosis-clinical exam, echo
Treatment is based on severity
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:

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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
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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
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
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
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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
Diagnosis
Clinical
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
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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
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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
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Preoperative:undergoing corrective
surgery
Explain procedures to parents and
child, assure understanding
Encourage child and parents to
express fears
Prepare child for surgery and postop, 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
Acquired Heart Diseae
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HTN
Endocarditis
Rheumatic Fever
Kawasaki Disease
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
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
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
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ACE inhibitors
ARBs
Beta-Blockers
Ca Channel Blockers
Infective Endocarditis
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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
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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
S/S:
 Polyarthritis
 Carditis
 Chorea
 Erythema marginatum
 Subcutaneous nodules
Rheumatic Fever

Diagnosis- clinical symptoms
and +ASO titer
Rheumatic Fever
Management:
 Treat infection
 Treat other symptoms
 Streptococcal prophylaxis
• PCN IM every month
or
• PCN PO BID (if allergic Sulfadiazine PO
QD)
Kawasaki Disease
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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
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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 Disease
second stage day 15-25
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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 Disease
Third 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

Kawasaki Disease
Nursing care:
 Administer meds
 Comfort measures
 Hydration
 Parental support
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.
2.
3.
4.
Don’t worry. This type of behavior is typical for a
toddler
Irritability is part of Kawasaki’s disease. Please
don’t be embarrassed
Perhaps your child would benefit from stricter
limits
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.
2.
3.
4.
Tachycardia and joint pain
Bradycardia and swollen joints
Loss of coordination and pruritic
rash
Bradycardia and fever
Which nursing intervention is most effective
in preventing rheumatic fever in children?
1.
2.
3.
4.
Refer children with sore throats for a
throat culture
Include an ECG in the child’s yearly
physical examination
Assess the child for a change in the
quality of the pulse
Assess the child’s blood pressure
Which is most beneficial in achieving the
goal of preventing infection in a child
with cardiac disease?
1.
2.
3.
4.
Give the child extra immunizations
Keep the child on daily prophylactic
antibiotics
Keep the child away from others who are
ill
Place the child in protective isolation
A newborn with patent ductus
arteriousus is scheduled to receive
indomethacin. The nurse
administers this medication to:
1.
2.
3.
4.
Open the ductus arteriosus
Close the ductus arteriosus
Enlarge the ductus arteriosus
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 aorta
2. Tetralogy of Fallot
3. Ventricular septal defect
4. 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.
2.
3.
4.
Notify the pediatrician as soon as possible
Take the infant’s pulse for 1 minute and repeat
the dose of digoxin
Skip the dose and give twice the amount at the
next dose
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.
2.
3.
4.
Your baby’s condition is too serious for immediate
open heart surgery
Ventricular septal defects are not repaired until
the infant is older
Your baby has a small defect, and we hope that is
closes spontaneously
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. Anemia
2. Polycythemia
3. Increased white blood cell count
4. Decreased hematocrit
An infant with tetralogy of Fallot
becomes hypoxic following a
prolonged bout of crying. The
nurse’s first action should be to:
1. Administer oxygen
2. Administer morphine
3. Place the infant in the knee-chest
position
4. Comfort the infant