Describe the common cardiovascular disorders of
childhood.
Assess a child with a cardiovascular dysfunction.
Formulate nursing diagnoses for a child with a
cardiovascular disorder.
Establish appropriate outcomes based on the priority
needs of a child with a cardiovascular disorder.
Plan nursing care for a child with a cardiovascular
disorder.
Implement nursing care for a child with a
cardiovascular disorder.
Evaluate expected outcomes for achievement and
effectiveness of nursing care.
Consists of 3 main parts:
1. Heart
2. Blood
3. Blood vessels
HEART
CIRCULATION
It is calculated by
multiplying stroke
volume (the
volume of blood a
ventricle ejects
during systole) by
the heart rate
(beats per minute).
Preload.
Afterload.
Contractility.
HEART SOUNDS
DIAGNOSTIC TESTS
1. Chest X-ray
2. Laboratory Testing
3. Electrocardiogram
4. Holter/Event Monitor - Worn for 24 to 72
hours and gives a complete account of every heart beat of the child
Can be worn for 30 days
5. Transthoracic echocardiogram
6. CT scan or MRI
7. Exercise Stress Testing
8. Cardiac Catheterization
•CONGENITAL HEART DEFECTS
Defects that Increase Pulmonary Blood Flow
• Patent Ductus Arteriosus
• Atrial Septal Defect
• Ventricular Septal Defect
• Atrioventricular Septal Defect
• Transposition of the Great Arteries
• Anomalous Pulmonary Venous Return
• Truncus Arteriosus
Defects that Decrease Pulmonary Blood Flow
• Tetralogy of Fallot
Defects With Obstruction to Systemic Blood Flow
• Coarctation of Aorta
• Aortic Stenosis
Single Ventricle Defects
• Hypoplastic Left Heart Syndrome (HLHS)
Acyanotic Heart Disease
◦ Left-to-right shunts
Patent ductus arteriosus
Atrial septal defect
Ventricular septal defect
Atrioventricular septal defect
Blood flows from
the aorta through
the PDA and back
to the pulmonary
artery and lungs,
causing inc. LV
workload and
increase
pulmonary
vascular
congestion
Ifdefect is small, child
may be asymptomatic
A loud machine like
murmur is one of the
characteristic
Child may have frequent
Resp. infections
Child may have CHF
with poor feeding,
fatigue,
hepatosplenomegaly,
poor weight gain ,
tachypnea and
irritability.
Tachycardia
Diagnostic test: ECG
Indomethacin - NSAID
Furosemide - diuretic
Surgical Mgt:
Cardiac catheterization
with a device placed in
the duct to occlude flow
An abnormal communication
between the L AND R atria;
results when the Atrial Septal
tissue does not fuse properly
during embryonic devt.
Bloodflows from
the higher –
pressure left
atrium across the
ASD into the lower
pressure right
atrium
Increased blood
return to the right
heart leads to right
ventricular volume
overload and right
ventricular dilation.
Increased pulmonary
blood flow leads to
elevated PA
pressures.
Most
infants tend to be
asymptomatic.
Symptoms may vary with sizes
of defects, fatigue and
dyspnea on exertion
Slow weight gain and
frequent respirations may
occur
Systolic ejection murmur
may be auscultated, usually
most prominent at the 2 nd
ICS
Tachycardia,
Echocardiography
with Doppler
reveals the
enlarged R side of
the heart and
pulmonary
circulation.
Cardiac
catheterization
demonstrates
the separation
of the R atrial
septum and the
O2 saturation in
the R atrium
Closure of
suture
Pericardial
patch
The
most common CHD, is
an abnormal opening
between the right and left
ventricles
Thedegree of this defect
vary from a pinhole
between the R&L ventricles
to an absent septum
Blood flows from the high-
pressure LV across the VSD
into low pressure RV and into
pulmonary artery, resulting in
pulmonary overcirculation.
Symptoms vary w/ size of
defect, age and amount of
resistance, usually the child is
asymptomatic.
Failure to thrive, excessive
sweating, fatigue.
More susceptible to
pulmonary infections
Decreased CO=tachycardia
RVH =increase pulmonary
vascular resistance
Loud harsh murmur
Small VSD
[Link] no med mgt.
[Link] repair indicated
[Link] endocarditis
precaution.
Large VSD
CHF management:
digoxin and diuretics
and afterload reduction
Avoid O2
Surgical repair :
One stage approach patch
closure of VSD
Two stage Approach:1st surgery
is to band the pulmonary
artery (close heart) to restrict
pulmonary bld flow.
2nd surgery is to patch close VSD
and remove PA band.
A left to right shunt occurs at
the atrial and ventricular
levels; AV valve regurgitation
may be significant, sometimes
producing a direct LV to RA
shunt.
Result in enlargement of all 4
cardiac chambers.
Overtime, the increase in
pulmonary blood flow,
pulmonary artery pressure, and
pulmonary vascular resistance
may lead to reversal shunt
direction with cyanosis
Small : asymptomatic
Large : Cause Heart Failure, with
dyspnea when feeding, poor growth,
tachypnea ,diaphoresis and
arrhythmias
Surgical Repair: Single stage
complete repair
Elective Surgery for partial
defect
TRANSPOSITION OF THE GREAT ARTERIES
TRANSPOSITION OF THE GREAT ARTERIES
➢ The aorta arises from the RV and the
pulmonary artery arises from the LV
Oxygenated blood returns from the lungs
to the LA, to the LV, and then proceeds
back through the pulmonary artery and to
the lungs again.
Deoxygenated blood returns from the
body to the RA, to the RV and proceeds out
back to the aorta, supplying deoxygenated
blood to systemic circulation
TRANSPOSITION OF THE GREAT ARTERIES
• Management
surgical correction, within the first 14 days
of life
Arterial switch or Jatene procedure –
cutting both the PA and aorta above their
respective valves and switching the vessels
to the appropriate location
ANOMALOUS PULMONARY VENOUS RETURN
ANOMALOUS PULMONARY VENOUS RETURN
➢ APVR a result of failure of the pulmonary
venous connections to unite with the left
atrium – instead they return directly to the
RA, O2nated blood drains back into the
right side of the heart
TRUNCUS ARTERIOSUS
➢ TA – single arterial vessel that originates
from the heart; overrides the ventricular
septum; and supplies all of the systemic,
coronary and pulmonary blood flow
TRUNCUS ARTERIOSUS
Blood ejected from the ventricles
enters the common artery and flows
either the lungs or aortic arch.
Pressure in both ventricles is high and
blood flow to the lungs is marked
increased.
Neonateswith this defect appear normal;
however, as pulmonary vascular resistance
decreases after birth, severe pulmonary
edema and CHF common develop cyanotic
CHD.
Marked cyanosis, especially on exertion
LVH, dyspnea, Marked activity
intolerance and retarded growth.
Loud systolic murmur best heard at
the lower left sternal border and
radiating throughout the chest.
Surgical
repair is necessary in the 1st
few months of life, the mortality rate
associated with surgery is greater than
10%.
w/o surgery, children die w/in 1 yr.
•CONGENITAL HEART DEFECTS
Defects that Increase Pulmonary Blood Flow
• Patent Ductus Arteriosus
• Atrial Septal Defect
• Ventricular Septal Defect
• Atrioventricular Septal Defect
• Transposition of the Great Arteries
• Anomalous Pulmonary Venous Return
• Truncus Arteriosus
Defects that Decrease Pulmonary Blood Flow
• Tetralogy of Fallot
Defects With Obstruction to Systemic Blood Flow
• Coarctation of Aorta
• Aortic Stenosis
Single Ventricle Defects
• Hypoplastic Left Heart Syndrome (HLHS)
TETRALOGY OF FALLOT
➢ Allows deoxygenated blood to be ejected
across the VSD and into the aorta
A heart defect that features four problems:
1. a hole between the lower chambers of
the heart
2. an obstruction from the heart to the
lungs
3. The aorta (blood vessel) lies over the
hole in the lower chambers
4. The muscle surrounding the lower right
chamber becomes overly thickened
Hereditary
Vitamin deficiency
Viral infection: rubella
Radiation and drugs: Thalidomide, alcohol
and phenytoin
Down syndrome, Turner’s syndrome
Club feet, cryptorchidism, and micromegaly
Maternal dietary deficiency
Maternal age > 40 & Maternal IDDM
Cyanosis of mucous membranes of
the lips, mouth, and pharynx, and
in the fingernails and toenails
Skin is a dusky, bluish color
Clubbing of the fingers and toes
occurs by 1 to 2 years of age
Exercise causes severe dyspnea
Assume a knee-chest position when
they lie down
Limit their exercise to their level of
tolerance
Squatting position
After a short rest, the child resumes
activity
Paroxysmal dyspneic attacks ( anoxic
“blue” spells)
Restless, cyanotic and gasps for
breath
Weak cry may be heard
Short episodes may be followed by
sleep
Prolonged episodes may lead to
unconsciousness, convulsions,
hemiparesis, or death
Occur with no warning, although they
may follow feeding, an emotional
upset, or defecation
Do not grow and develop normally.
Small and their nutritional status is
poor.
Mental slowness may result from
chronic hypoxia of the brain.
May be able to play for a short time.
Removal of the shunt
Cardiopulmonary bypass
Elective repair is usually
performed during the
infant’s 1st year of life, but
palliative repairs may be
warranted for infants who
cannot undergo primary
repair.
•Done at 1 to 2 years of age.
•During hypoxic episode, administering
oxygen
•Knee–chest position
•Morphine sulfate generally reduces
symptoms
•Propranolol (Inderal, a beta-blocker) may be
given orally to aid pulmonary artery dilation.
• A temporary or palliative surgical repair,
called the Blalock-Taussig procedure
• Subclavian artery is used in a Blalock-Taussig
procedure –no palpable pulse in the R arm
after this procedure.
• BP and venipunctures should be avoided in
the affected arm.
Assessment
* systolic murmur at L upper sternal
border
*hypercyanotic spells
Management
*surgical repair at 3-6 months of age
* closure of VSD, repair of stenotic
pulmonary valve
•CONGENITAL HEART DEFECTS
Defects that Increase Pulmonary Blood Flow
• Patent Ductus Arteriosus
• Atrial Septal Defect
• Ventricular Septal Defect
• Atrioventricular Septal Defect
• Transposition of the Great Arteries
• Anomalous Pulmonary Venous Return
• Truncus Arteriosus
Defects that Decrease Pulmonary Blood Flow
• Tetralogy of Fallot
Defects With Obstruction to Systemic Blood Flow
• Coarctation of Aorta
• Aortic Stenosis
• Pulmonic Stenosis
Restrictedblood flow
trough the narrowed aorta
increases the pressure on
the LV and causes dilatation
of the proximal aorta and
LV hypertrophy, w/c may
led to LV failure
The child may be
asymptomatic or may
experience the classic
difference in BP and pulse is
bounding in the UE and dec. or
absent in the LE.
Epistaxis,headaches,
fainting and lower leg
cramps
Repairinvolves
surgical removal
of the stenotic
area.
Nonsurgical repair
via balloon
angioplasty
ECG, echocardiography,
and chest x ray may reveal
left sided heart
enlargement resulting from
back pressure
Adefect that primary
involves an obstruction to
LV outflow of the valve.
LVpressure inc. to overcome
resistance of the obstructed
valve and allow blood to flow
into the aorta, eventually
producing LVH
myocardialinfarction may
develop as the inc.
O2 demands of the
hypertrophied LV go unmet
ECG reveals LV
Hypertrophy
Cardiac catheterization
demonstrates degree of
stenosis
Faintpulse , hypotension, tachycardia,
and poor feeding pattern
Exercise intolerance, chest pain, and
dizziness when standing for long
periods
A systolic ejection murmur maybe
heard best at 2nd ICS
Treatment
Balloon angioplasty can be
used to dilate the narrow
valve
Adefect that involves
obstruction of blood flow
from the right ventricle
RVpressure increases
leading to RV Hypertrophy
and eventually RV failure
may occur
Maybe asymptomatic or may
have mild cyanosis or CHF
A systolic murmur may be
heard over the pulmonic area:
a thrill may be heard if
stenosis is severe
In
severe cases, decreased
exercise tolerance,
dyspnea, precordial pain
and generalized cyanosis
may occur
Balloon angioplasty techniques are
being widely used to treat PS
Surgical valvulotomy
➢ Inadequate cardiac
output: systemic &
pulmonary
CIRCULATION.
➢ Pulmonary hypertension
➢ Systolic or Diastolic
overloading of the heart
chambers
➢ Lack of adequate tissue
oxygenation.
Murmurs
Decreased exercise tolerance
Dyspnea
Tachycardia and tachypnea
Recurrent respiratory infection
Cyanosis and polycythemia
Tissue hypoxia
Growth retardation
Cardiac failure
Areas that need care from parents. This
information can be group into the
following:
Care during episode of dyspnea
Need for comfort and rest
Nutritional needs
Medications
Psychosocial needs
Continuing care
Family relationship
Financial responsibilities
Providing Preoperative Care
Preoperative Assessment
◦ Admission history and physical
examination
◦ Preoperative Studies
◦ Baseline VS
◦ Height and weight measurement
◦ Additional Nursing Observations
Introduction to the environment
Introduction to the equipment
Introduction to the postoperative
procedure
Post operative assessment and
management
Cardiopulmonary functioning
Gastrointestinal and Renal
functioning
CNS functioning
Cardiovascular
Arrhythmias
Hypotension
Hypovolemia
Cardiac failure
Respiratory complications:
Accumulation of mucus in the
respiratory tract
Pneumonia
Pneumothorax
Renal function impaired in ability to
excrete waste, I and O
CNC – embolus and increase cerebral
blood flow.
CHF
-most commonly acquired heart
disease in children
➢ due to a congenital heart disorder or
a disease such as rheumatic fever,
Kawasaki disease, or infectious
endocarditis.
CHF results when the
myocardium of the
heart cannot pump and
circulate enough blood
to supply oxygen and
nutrients to body cells
Blood pools in the heart (excessive
preload) or in the pulmonary or
venous systems.
Lessens the effectiveness of the
heart's pumping action (myocardium
is weakened).
Severe anemia, hypocalcemia, and
myocarditis: may contribute to the heart's
inability to function effectively.
- most apt to occur in children under 1 year
of age (Fulton & Freed, 2004).
Ventricular hypertrophy
As blood flow to the kidneys decreases, the
GFR slows, resulting in stimulation of the
renin-angiotensin system.
Causes fluid and sodium retention.
Aldosterone secretion by the adrenal
glands further promotes sodium
retention in an attempt to increase
blood flow to the kidneys.
ADH secretion by the pituitary is also
increased to help retain fluid. This
additional fluid can result in
dependent edema.
Reduces preload with diuretics,
Inotropic drugs (heart-strengthening) drug,
and reducing afterload with vasodilators.
Commonly used diuretics include furosemide
(Lasix) and spironolactone (Aldactone).
The most common drug used to increase
contractility and slow tachycardia is
DIGOXIN.
Drugs that decrease afterload include:
[Link] (an arterial vasodilator),
[Link] (calcium channel blocker)
3. nitroprusside (direct-acting vasodilator)and
4. captopril (angiotensin-converting
enzyme ACE inhibitor) (Karch, 2004).
Realistic in light of the child's condition
Individualized for each child.
Focus on helping support heart function and
Help parents deal with this crisis until the
child's heart is again strong enough to
maintain strong heart.
results due to presence of pulmonary
vascular resistance present at birth.
It occurs most often in full-term infants who
have experienced perinatal asphyxia from
conditions
Supportive therapy
[Link], high-frequency oscillatory
ventilation
2. IV glucose to provide calories.
3. Antibiotics to combat infection.
an autoimmune disease
reaction to group A beta-hemolytic
streptococcal infection (Hoffman, 2003).
leads to fibrin deposits on the endocardium
and valves, in particular the mitral valve, as
well as in the major body joints.
Thedisease often follows
an attack of pharyngitis,
tonsillitis, scarlet fever,
“strep throat,” or
impetigo, because the
organism common to
these infections is a
group A beta-hemolytic
streptococcus.
The full course of RF is 6 to 8
weeks.
Bed rest only during the acute
phase of illness or until
congestive heart disease is
not present, the ESR
decreases, and the C-reactive
protein level and pulse rate
return to normal.
Pulse rate is a valuable
sign of improvement.
Obtaining an apical pulse
for a full minute is
preferred.
Ordered when the child is
asleep as well as when the
child is awake to measure
the effect of activity on
the pulse rate.
Penicillin therapy or a single intramuscular
injection of benzathine penicillin.
Oral ibuprofen.
Corticosteroids
-Possible side effects of corticosteroid
therapy include hirsutism, a round moon face
(Cushing's syndrome), and an increased
susceptibility to infection.
Phenobarbital and Diazepam.
Digoxin and Diuretics
Mild cases of streptococcal pharyngitis, RF
occurs in about 0.3% of children.
Severe streptococcal infections, the attack
rate may be as high as 1% to 3% (Hoffman,
2003).
Either amoxicillin or penicillin is used to
eliminate streptococci (upper respiratory
tract). – a drug level must be maintained for
10 to 14 days to be effective.
Erythromycin is used in children sensitive to
penicillin.
Usually the child's symptoms will fade before
then, and if the parents are not cautioned
about the importance of the drug, they may
give the drug for only 2 or 3 days and then
discontinue it.
Prevent valve damage from occurring a
second time.
Must take prophylactic antibiotic therapy for
at least 5 years after the initial attack, or until
they are 18 years of age.
If some valve involvement is present,
physicians advocate maintaining the child on
penicillin indefinitely.
Penicillin may be prescribed as monthly
injections of benzathine penicillin G or daily
oral doses of aqueous penicillin (penicillin V).
Known as mucocutaneous lymph node
syndrome
a febrile, multisystem disorder that occurs
almost exclusively in children before the age
of puberty.
Common in boys under 4 years of age.
higher in late winter and spring.
Vasculitis (inflammation of blood vessels) is
the principal (and life-threatening) finding -
can lead to formation of aneurysm and
myocardial infarction (Callahan, 2003).
Cause is unknown.
Genetically predisposed individuals
after exposure to unidentified
infectious agent (perhaps an upper
respiratory infection)
Altered immune function occurs.
Increase in antibody production
creates circulating immune
(antibody–antigen) complexes that
bind to the vascular endothelium
and cause inflammation.
The inflammation of blood vessels leads to:
1. Aneurysms
2. Platelet accumulation, and the
3. Formation of thrombi or
4. Obstruction in the heart and blood vessels.
The signs and symptoms are divided into
major and minor symptoms
Heart involvement is the most serious.
Child usually has a systolic murmur from
mitral insufficiency and prolonged P-R and
Q-T intervals on the ECG that reflect
inflammation and slowing of impulse
conduction.
Chorea (sudden involuntary movement of the limbs) is a
striking symptom.
Loss of voluntary muscles occurs most often
in children to 7 and 14 years of age (rarely
after age 20).
Occurs more frequently in girls than boys
(Hoffman, 2003).
Dysfunctional speech from chorea may be
demonstrated by asking the child to count
rapidly. Children with chorea begin with clear
speech, but then suddenly the sounds become garbled or
they cannot speak for several seconds.
If asked to protrude the tongue - children
cannot keep from making undulating, jerky
movements.
If asked to extend their arms in front of them,
they soon hyperextend their wrists and
fingers.
Hand grasp may be weak or may consist of
spasmodic contractions and relaxation.
If asked to smile, the facial expression may
change rapidly from a “Cheshire cat” grin to a
flat, expressionless affect or grimace.
Full course of 6 to 8 weeks.
Bed rest only during the acute
Monitoring vital signs is essential during the
acute phase.
Obtaining apical pulse for a full minute is
preferred. (monitor either asleep as well as
when the child is awake to measure the effect
of activity on the pulse rate).
Penicillin therapy or a single intramuscular
injection of benzathine penicillin is used to
eliminate group A beta-hemolytic
streptococci completely from the child's
body.
Oral ibuprofen
Corticosteroids
Possible side effects of corticosteroid therapy
include hirsutism, a round moon face
(Cushing's syndrome), and an increased
susceptibility to infection.
POST-QUIZ