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Chapter 21: Cardiovascular Dysfunction (ASD, VSD, COA, PDA, TOF, TGA), Page 1 of 17

HEART MURMURS
These sounds are produced by blood passing through a defective valve, great vessel, or other
heart structure.
Murmurs are classified by: intensity (grade I-IV), location, radiation, timing, and quality.
Innocent or functional murmur: an abnormal sound made by the healthy/normal heart as blood
flows- there is no defect, heart is fine.
Parents need to be explained that child will not have any restrictions based on innocent heart
murmur.

(benign)

CLASSIFICATIONS OF CONGENITAL HEART DISEASE (CHD): Acyanotic vs. Cyanotic


pulmonary blood flow (acyanotic)
pulmonary blood flow (cyanotic)
Obstructive (acyanotic)
Mixed-blood flow (cyanotic)
CYANOTIC / ACYANOTIC DEFECTS
CYANOTIC DEFECTS
ACYANOTIC DEFECTS
Decreased pulmonary
1. Tetralogy of Fallot (TOF) blood flow
3. Atrial Septal Defect (ASD) No SBE
Turns blue when
2. Transposition of the greater arteries (TGA) 4. Ventricular Septal Defect (VSD) Yes SBE child cries.
Mixed blood flow
5. Patent Ductus Arteriosus (PDA) SBE FOR 1yr post-op
6. Coarctation of the Aorta (COA) Yes SBE Obstructive defects
ASD- ATRIAL SEPTAL DEFECT [left-to-right shunt]

Hole in
the wall
in the top
of the
heart.

Left side has more


pressure which
goes into right side
and back into lungs.

An opening (hole) between the atria allowing blood from the higher pressure left atria to enter the lower

pressure right atria.


Degree of symptoms depends on the size of the hole. A child with a small ASD will have virtually no

Increased
pulmonary
blood flow

Chapter 21: Cardiovascular Dysfunction (ASD, VSD, COA, PDA, TOF, TGA), Page 2 of 17

clinical symptoms but will have a significant murmur (the smaller the hole, the louder the murmur, the less
severe the symptoms). The smaller ASD can close spontaneously.
The child with a large ASD will exhibit S&S of CHF.
REPAIR OF ASD
Repair can be performed in two ways
Open or closed heart surgery (depending on the type of defect and age of the patient)
An umbrella closure performed in the cardiac cath lab.
A child with a ASD does not require SBE prophylaxis (subacute bacterial endocarditis proplylaxis).
VSD- VENTRICULAR SEPTAL DEFECT left-to-right shunt

Midline
defect
LV is pumping
chamber so pushes
to RV and RV get
hypertrophy and
baby gets CHF.

An opening (hole) between the right and left ventricle. VSD are the most common birth defect in
children. Can range from a pin point sized hole to a large opening (virtually no septal wall present).
Causes increased pulmonary blood flow and left-to-right shunting of blood flow, this increased flow
causes increased work load on the RV predisposing the child to CHF, RV hypertrophy and b.e.
A VSD is an acyanotic defect. However, in very LARGE VSDs there is virtually no septal wall
accompanied by significant congestive heart failure and cyanosis may be present.
NURSING INTERVENTION (VSD)
Small frequent feeding of high caloric infant formula.
o Must be monitored closely to be assured formula is being mixed correctly.
Left-to-Right----Oygenated
o Feeding log
Parental education
Lots of teaching!
Right-to-Left----Deoxygenated SHUNTING
Teach parents S&S of CHF
(Blue baby)
o Medication administration Digoxin, lasix, give bananas
o Teach parents S&S of infection (especially RSV Sept-March)
Parental support
Provide referrals to support groups

Chapter 21: Cardiovascular Dysfunction (ASD, VSD, COA, PDA, TOF, TGA), Page 3 of 17

Referrals and assistance to help with the high price of increased calorie formula (can be as high as
$400 a month)
Frequent weights (outpatient: minimum of weekly, inpatient: daily)
Referral to EI if child is not meeting developmental milestones
(Early interventions)

ASSESSMENT OF THE CHILD WITH A SIGNIFICANT VSD


Child will exhibit S&S of CHF:
Tachypnea, dyspnea
Poor growth = FTT
Decreased fluid (formula) intake
Palpable cardiac thrill
Systolic murmur at lower sternal border
MEDICAL TREATMENT OF A CHILD WITH VSD
Pharmacologic management of CHF (digoxin, Lasix).
Increased caloric intake to meet increased metabolic demands (increased BMR)
o High calorie infant formula. Commercial infant formula is 20kcal/oz. concentration by
adding less water or more formula powder, increasing kcal/oz.; can go up to 30kcal/oz.

Synagis vaccine Sept- March for RSV.

(immunoglobulin)

Give synagis until 2yrs old.

Should not go

higher than
30kcal/oz.

SURGICAL REPAIR OF VSD


The vast majority of small VSDs close spontaneously.
The moderate-large VSD will require open heart surgery to repair. Can't put an umbrella, need to sow a patch.
Age of repair depends on the degree of CHF. Wait until child is 1yr old
The child with a VSD will require SBE prophylaxis for life.
ASD/VSD REPAIR
ASD
Spontaneous closure of ASDs can occur in the infant/young child. The surgical repair is called an
ASD repair, a closed heart repair. A patch is sewn over the opening. Age of repair depends on the
size of the ASD. Very high success rate, minimal surgical risk & mortality. Smaller defects can be
closed in the cardiac cath lab using an umbrella like device, the umbrella is placed at the opening
and seals the hole. Being used in limited sites in the U.S. as the device can migrate out of the ASD
and move into pulmonary circulation.
Child with ASD does not require SBE prophylaxis.
VSD
Called a VSD repair. It is an open heart procedure; child needs to go on cardiopulmonary bypass.
A patch of gortex is sewn over defect. Age of repair depends on size of VSD/degree of CHF. Very
high success rate, minimal surgical risk.
Child with a VSD will need bacterial endocarditis prophylaxis for life.

Chapter 21: Cardiovascular Dysfunction (ASD, VSD, COA, PDA, TOF, TGA), Page 4 of 17

COA - COARCTATION OF THE AORTA

Left arm
Right arm
Brain
Blood gets

BP is very high causing


headaches and nose
bleeds

backed up
so it goes
Legs, gut and kidneys
don't get circulation.

Lungs
get
edema

A localized narrowing (coarctation) of the aorta; aorta is pinched closed.


Will cause increased pressure proximal to the defect (head and upper extremities) and decreased pressure to
distal (body and lower extremities)
Clinical Manifestations of COA (dependent on the degree of coarctation):
Increased BP
Everyone should get pulses in all 4 extremities.
Bounding pulses in arms
Decreased BP in lower extremities
Absent femoral pulses
Cool lower extremities
DEGREE OF COA
In infants with a significant COA, there can be S&S of CHF with rapid progression to the infant being
critically ill with acidosis and hypotension. At this stage they will require intubation and inotropic support
until repair can be completed.
With a milder degree of coarctation, the defect might not be diagnosed until it begins to produce symptoms
(dizziness, headache, numbness in lower extremities, epistaxis (nose bleed), syncope) Some children are
not diagnosed until adolescence.

Chapter 21: Cardiovascular Dysfunction (ASD, VSD, COA, PDA, TOF, TGA), Page 5 of 17

REPAIR OF COA
Can be achieved in 2 ways:
1. Balloon angioplasty of the coarcted area, done in the cardiac cath lab. A balloon catheter is
threaded up to the area of the coarctation and opened in the coarcted area. In some cases just
ballooning the area will work, in others a stent is needed to keep the aorta open. The potential for a
re-COA is possible requiring an additional procedure.
2. Surgical repair (closed heart repair, no cardiopulmonary bypass is required). A resection with an
end-to-end anastomosis (surgical connection between 2 structures) of the aorta is performed.
A child with a COA will require SBE prophylaxis for life.
PDA: PATENT DUCTUS ARTERIOSUS left-to-right shunt

The failure of the fetal ductus arterious (the artery connecting the pulmonary artery and the
aorta) to close within the first few weeks of life. In utero the PDA allows the blood to pass
between the aorta and pulmonary artery, bypassing the lungs. It normally closes within the first
72 hrs to 1 week after birth.
Depending on how large the PDA is, when a large ductus stays open (patent), systemic BP
becomes greater than pulmonary BP and the additional blood begins to shunt from the aorta
across the ductus to the pulmonary artery, this is a left-to-right shunt.
This shunt from the aorta, across the duct, to the pulmonary artery (left-to-right shunt):
increases the workload of the left side of the heart and RV, which
increases pulmonary vascular congestion and pulmonary vascular resistance, which
may cause increased right ventricular pressure and RV hypertrophy.
Symptoms: tachycardia, dyspnea, machine-like murmurs, cardiomegaly(enlarged heart), subclavian thrill, bounding
pulse, widened pulse pressure
Diagnosis: made by echocardiogram, ECG not useful
Murmur heard on auscultation. Close PDA in neonate with Indomethacin. In Transposition of Great Vessels (TGA) you need to
keep it open using Prostagladins.

PDA- congenial
disorder in the heart
where in a neonate
ductus arteriosus
fails to close at birth.
Initial there is a leftto-right shunt and
child is
asymptomatic. Later
on in life, reversal of
shunt develops
called Eissenmenger
Syndrome. When
reversal of shunt
deleveops, i.e-rightto-left(pulmona ry
artery to aorta)
deoxygenated blood
will enter systemic
circulation and
cyanosis occurs.

Chapter 21: Cardiovascular Dysfunction (ASD, VSD, COA, PDA, TOF, TGA), Page 6 of 17

Three are 3 methods of closure:


1. Indomethicin IV during neonatal period (in smaller neonates or preemies)
2. Closed heart procedure in which the ductus is ligated (tied off) requires a thoractomy, very easy
procedure (for moderate-large PDA).
3. In cardiac cath lab, a coil is place in the ductus to seal it off. Minimally invasive, this method
can only be used in small-moderate size PDA.
Reason for closure: to prevent bacterial endocarditis. Child with a PDA will need bacterial endocarditis
prophylaxis prior to closure and for one year after closure.
TETRALOGY OF FALLOT- TOF right-to-left shunt

Four defects
1. Pulmonic valve stenosis ---the valve and the vessel
2. Right ventricular hypertrophy (right ventricle wall is large and thick)---blood gets backed causing hypertrophy
3. Ventricular septal defect (VSD)
4. Overriding aorta (extends down to the level of the VSD) ---the aorta sits in what would have been the middle of the
heart

These four defects combine to allow blood flow to bypass the lungs and enter the left side of the heart,
sending unoxygentated blood to the systemic circulation. This is called a right-to-left shunt.
1. The exit is narrow
2. The child looks really blue-O2 sat in the 70's

Chapter 21: Cardiovascular Dysfunction (ASD, VSD, COA, PDA, TOF, TGA), Page 7 of 17

TREATMENT AND SURGICAL REPAIR OF TOF


Degree of clinical manifestations and symptoms will depend on the degree of pulmonic stenosis.
For the child born with significant PS (the child born cyanotic):
Oxygen administration
Correction of metabolic acidosis
Immediate infusion of Prostaglandin E1 to keep PDA open to allow for mixing of blood.
Palliative surgery to improve oxygenation and allow for mixing of blood:
o Blalock-Taussig shunt - provision of blood to the pulmonary arteries from the left or right
subcalivan arteries; or
o Balloon septostomy - the widening of a foramen ovale, patent foramen ovale (PFO), or
atrial septal defect (ASD) via cardiac catheterization (heart cath) using a balloon catheter.
This procedure allows a greater amount of oxygenated blood to enter the systemic
circulation in some cases of cyanotic congenital heart defect (CHD).
ASSESSMENT OF A CHILD WITH UNREPAIRED TOF
Body thinks doesn't
Clubbing of fingers/toes
Exercise/activity intolerance
have RBC's because
Polycythemia (excess # of RBCs)
Systolic murmur in pulmonic region
doesn't have enough
Metabolic acidosis
Cyanosis
oxygen so makes

Poor growth FTT

excess RBC's.

O2 saturations as low as 50%

TET (HYPERCYANOTIC) SPELL -- ALWAYS ON NCLEX


They are hypercyanotic spells when there is an increase in the right-to-left shunting of blood (poorly
oxygenated blood is getting to systemic circulation).
TET spells can be precipitated by:
Crying
Defecation
Cold
Feedings
TREATMENT FOR TET SPELLS
Older unrepaired child will assume a squatting position to decrease perfusion to lower extremities. This is
rarely seen in the U.S., most children are repaired.
Put child in knee chest position to increase blood flow to upper extremities
Administration of oxygen--- Do this first!!!!
IV administration of morphine sulfate

Chapter 21: Cardiovascular Dysfunction (ASD, VSD, COA, PDA, TOF, TGA), Page 8 of 17

TRANSPOSITION OF THE GREATER ARTERIES - TGA

Ductal dependent defect


The greater vessels (aorta and pulmonary artery) positions are switched.

The pulmonary artery leaves from the left ventricle and the aorta leaves from the right ventricle.
(normal heart: aorta from the left ventricle with oxygenated blood going to systemic circulation,
pulmonary artery from the right ventricle with unoxygentated blood going to the lungs)

There must be an additional defect PDA, PFO (patent foramen ovale), or VSD to allow for the
mixing of unoxygentated and oxygenated blood or the neonate will not receive any
oxygenated blood into circulation.
This child is born cyanotic and needs immediate intervention to sustain life.
The patency of the PDA must be maintained with an infusion of Prostaglandin E1.
TGA is a ductal dependent defect if the PDA closes the child will have severe hypoxia (SaO 2 can
be as low as 20%) severe cyanosis and acidosis. Death will follow very quickly.
The birth of a child with known or suspected TGA is a true medical emergency.
Metabolic

TREATMENT (AT BIRTH) FOR TGA


IV access
Intubation and mechanical ventilation
Infusion of PGE 1 at 0.1mg/kg/min to maintain patency of PDA
Pharmacologic paralysis and sedation
Correction of metabolic acidosis
Transfer to NICU with Pediatric cardiology services

TGA- the pulmonary artery(to the lungs) and aorta


(leads to all arteries in the body) are switched.
Blood comes into heart thru RA to RV supposed to get
pumped thru PA into lungs and cones back
oxygenated thru LA goes into LV and pumped thru
back by LV. But in TGA the PA plugs into LV and aorta
in right side receiving deoxygenated blood. Blue blood
is getting pumped into aorta and red blood pumped
back into lungs. There's no mixture so this defect is
fatal. Usually TGA comes with VSD ventricular septal
defect which defect that allows blood to mix, lifesustaining, at least some O2 into body. Some
newborns have ductus arteriosus provides
communication between both loops.

SURGICAL TREATMENT FOR TGA


Emergency procedure if child is too unstable for repair, duct is closing, O.R. not ready, or surgery
cannot be performed immediately.
An artificial opening is made between the atria via a balloon septostomy (balloon catheter is
threaded up to the atria and a hole is made), this is performed in the cardiac cath lab. It will
allow the mixing of oxygenated and unoxygentated blood.

Chapter 21: Cardiovascular Dysfunction (ASD, VSD, COA, PDA, TOF, TGA), Page 9 of 17

ARTERIAL SWITCH FOR TGA


Procedure should be done within the first few days (in rare cases weeks) after birth.
The aorta and pulmonary artery are resected at the level of the valves and reimplanted to their
proper anatomical position.
Coronary arteries must also be resected.
During the post operative period (first 24 hours) the child is critically ill with the potential
for leaking around the multiple suture sites, arrhythmias, hemorrhage and LV dysfunction.
After the initial postoperative period (with no significant complications) there is a very
good prognosis.
SURGICAL REPAIR OF CONGENITAL HEART DISEASE TYPES OF CHD REPAIR
Open heart procedure:
A median sternotomy is performed and child is put on cardiopulmonary bypass
Closed heart procedure
A thoractomy is performed and heart is repaired without cardiopulmonary bypass
Cardiopulmonary bypass
A procedure / perfusion machine that acts as the heart & lungs while heart is repaired. Child is
connected to machine, heart stopped with meds injected directly into the heart, machine takes
over systemic perfusion. During open heart surgery the heart is NOT beating. After procedure is
completed, heart is restarted by cardioversion, machine removed, chest closed.
PGE1 / PROSTAGLANDIN E1 / ALPROSTADIL
Directly affects vascular and ductus arteriosus smooth muscle, causing vasodilation.
Indications for usage: to maintain patency of patent ductus arteriosus.
Dosage: 0.05 0.1 mcg/kg/min
PGE1 (PROSTAGALNDIN)
Adverse reactions:
o CNS: seizures
o CV: profound flushing, bradycardia, hypotension, tachycardia, cardiac arrest, edema
o GI: Diarrhea
o Heme: DIC
o Metabolic: Hypokalemia
o Resp: apnea (occurs most commonly in infants under 2.2kg)
o Other: Fever, sepsis
Special precautions:
o Child on PGE must be taken care of by staff trained in Pediatric critical care (not NICU)
with high level of staffing, this patient requires 1:1 nursing care.
INDOMETHICIN (PROSTAGLANDIN INHIBITOR)
Non-steroidal anti-inflammatory agent.
Used in Pediatrics to inhibit prostaglandin synthesis to close the patent ductus arteriosus.
Used only in neonates, frequently in the very premature infant (on high vent settings) with a
moderate-large PDA.
Infant can be given up to three doses
o
o
o

First dose: 0.2mg 0.25 mg/kg/IV


Three does given at 12-24 hour intervals until duct is closed.
If indomethicin fails to close duct, surgical intervention will be required.

Chapter 21: Cardiovascular Dysfunction (ASD, VSD, COA, PDA, TOF, TGA), Page 10 of 17

CAUSES OF CHD
Chromosomal/genetic = 10% - 12%
Maternal or environmental = 1% - 2%
o Maternal drug use

Fetal alcohol syndrome50% have CHD o


Maternal illness

Rubella in first 7 weeks of pregnancy


50% risk of defects including PDA and
pulmonary branch stenosis

CM, toxoplasmosis, other viral illnesses cardiac defects


IDMs = 10% risk of CHD (VSD, cardiomyopathy, TGA most common)

Multifactorial = 85%

ACUTE RHEUMATIC FEVER


ETIOLOGY:
An immune reaction to untreated group A streptococcal infection, usually pharyngitis. It typically
presents after a 2-6 week period following pharyngitis with one or more of the major or minor
manifestations. It is a self-limiting disease, but may cause significant cardiac valve damage.
PATHOLOGY:
Rheumatic Fever is classified by the Jones Criteria who are divided into major and minor criteria:
MAJOR CRITERIA - RF
1. Carditis the most serious manifestation, changes on EKG; new murmur; mitral or aortic
regurgitation.
2. Polyarthritis common, edema / swelling, inflammation effusion in joint tissue, limited motion,
tenderness, erythema. Large joints, knees, hips, elbows, wrists, shoulders. Migratory type of
arthritis, migrates to a different joint q1-2 days. accompanies the acute febrile period in the first
1-2 weeks of the illness. Reversible.
3. Erythema marginatum uncommon, distinct pink macular rash with clear center usually on trunk
/proximal extremities, elicited by application of local heat. Will resolve.
4. Subcutaneous nodules uncommon, small (0.5-1 cm) nodules, firm, non-tender, present over bony
prominences of elbows, knees, knuckles, ankles, scapulae, scalp and vertebrae. Persist indefinitely
but will resolve.
5. Chorea (Sydenhams disease) St. Vitus Dance- uncommon, presents weeks to months after
infection has resolved. Characterized by sudden, aimless, irregular movements of the extremities,
involuntary facial grimacing, speech disturbances, emotional labiality, and profound muscle
weakness.
It is exaggerated by anxiety and attempts at fine, deliberative motor activity, relieved by rest, sleep.
Reflects streptococcal infection of vascular tissue of brain and CNS. Increases in severity over first
2 weeks, reaches a plateau and begins to diminish and resolve over a 10 week period.

Chapter 21: Cardiovascular Dysfunction (ASD, VSD, COA, PDA, TOF, TGA), Page 11 of 17

MINOR CRITERIA - RF
1. Fever (101-102)
2. Arthralgia (joint pain)
3. Previous RF
4. Leukocytosis (5-20 is normal WBC range)
5. Elevated ESR and C reactive protein
ESR - Erythrocyte sedimentation rate
C-reactive protein a protein normally found in serum with inflammatory conditions.
before ESR (within 24-48hrs). Disappears when suppressed with salicylates, steroids.
6. Prolonged PR interval on EKG
CRITERIA FOR DIAGNOSIS OF RF
RF is diagnosed by the presence of:
one major criteria + 2 minor criteria; or
2 major + evidence of recent GABHS infection (scarlet fever, positive throat culture)
TREATMENT AND NURSING CARE OF RF:
Bed rest during acute febrile phase to decrease workload of the heart. Provide child with
quiet diversional activities in bed.
NSAID's (Motrin) for arthritic pain
Steroids for severe, life-threatening carditis only, since they do not reduce valve damage. Teach parents
that steroids, ex. Prednisone cannot be discontinued suddenly, must be tapered down slowly.
Penicillin to eradicate strep, erythromycin for penicillin allergy
Penicillin prophylaxis is essential part of treatment: Bicillin 1.2 million units IM monthly, for a
MINIMUM of 10 years. Drastically reduces permanent damage to mitral and aortic valves.
PREVENTION OF RF
RF can be prevented by doing throat cultures of all school-age children suspected of strep
infection with GABHS.
Patient/ parent teaching- abxs must be taken for full prescribed course.
PROPHYLAXIS FOR DENTAL WORK, INFECTION, AND INVASIVE PROCEDURES.
KAWASAKIS SYNDROME Only disease aspirin is given to reduce inflammation.
Multisystem disorder involving vasculitis (inflammation of the inner lining of arteries, veins and
capillaries). Also called mucocutaneous lymph node syndrome.
Characterized as an acute febrile illness associated with systemic vasculitis. Approximately 20%
have cardiovascular complications.
ETIOLOGY/PATHOPHYSIOLOGY:
Unknown cause, generally affects young children less than 3 years,
M > F, children under 1 year of age are most seriously affected by KD and are at the greatest risk
for cardiac involvement.
Asians > Blacks > Caucasians
Increased incidence in winter to early spring
Seasonal epidemics every 2-3 years
Specific triggers - bacterial: strep, viral: retrovirus

Chapter 21: Cardiovascular Dysfunction (ASD, VSD, COA, PDA, TOF, TGA), Page 12 of 17

DIAGNOSTIC CRITERIA FOR KS


The child must exhibit FIVE of the following six criteria, including fever.
1. Fever 5 or more days
2. Bilateral conjunctival injection (inflammation) without exudation
3. Changes in the oral mucosal membranes dryness, erythema and fissuring of lips; strawberry
tongue, oropharyngeal reddening
4. Changes in extremities peripheral edema, erythema of the palms and soles, and periungual
desquamation (peeling) of the hands and feet
5. Polymorphous rash
6. Cervical lymphadenopathy (one lymph node >1.5cm)
KAWASAKIS THREE PHASES OF ILLNESS
1. Acute phase: from onset of fever till resolution of fever (5-21days). Fever, high-spiking
39.5- 40.5, does not respond to antibiotic / antipyretic therapy or anything at all.
Conjunctival exanthema (widespread rash): begins shortly after fever
Swollen hands/feet
Rash: begins 5 days after fever, fine, erythematosus
Enlarged cervical lymph nodes
Child is VERY irritable
ESR & platelet count are verywith potential for thrombosis occlusion of coronary arteries
Cardiac: arrhythmias gallop rhythm, CHF with shock, pericarditis, pericardial effusion, cardiac
tamponade, mitral or aortic valve regurgitation.
2. Subacute phase: from resolution of fever to disappearance of all clinical symptoms. Occurs 3-4
week after onset of fever. Lasts for 2-4 weeks.
Peripheral extremity change: desquamation of fingers, toes palms of hands & feet.
Changes in oral mucosa, dryness and fissuring of the lips, oropharyngeal redness, strawberry
tongue.
Cardiac: Coronary artery vasculitis, dilatation and or aneurysms of coronary arteries. Can first
be detected at approx. 10 days. Peak occurrence for CA involvement is 3-4 weeks after onset
3. Convalescent phase: ESR & platelet count returns to normal, usually lasts about 10-12 weeks.
NEUROLOGIC COMPLICATIONS OF KS
Extreme irritability and lethargy (thing we need to remember for exam)
Aseptic meningitis (25%)
Hemiparesis or paralysis of extremities, ataxia
Increased ICP
Mild sensorineuronal hearing loss
TREATMENT DURING ACUTE PHASE
High dose IVImmunoGlobulin (2g/kg), over 12hrs. Follow institutional policy on blood/blood
product transfusions
IVIG in conjunction with high dose ASA tx (80-100mg/kg/qd)-reduces fever and decreases
probability of cardiac aneurysm formation. This is the only condition in which you give aspirin
to a child.
Once fever has subsided, ASA dose is decreased to antiplatelet dose (3-5mg/kg/qd). This low dose
ASA is continued for 6-8 weeks. Monitor aspirin levels damage to renal and GI systems.

Chapter 21: Cardiovascular Dysfunction (ASD, VSD, COA, PDA, TOF, TGA), Page 13 of 17

NURSING CONSIDERATIONS
Child needs both cardiology and infectious disease consult. Both specialties need to manage this
child.
Continuous monitoring of cardiac status (EKG daily/echocardiogram)
I&O
Daily weight
Assessment and prevention of dehydration (child is VERY prone to dehydration because their oral
cavity is a mess between the fissures and not eating)
During IVIG infusion, follow protocol for blood transfusion
Follow institutional policy on blood product transfusions
Most nursing care focuses on symptomatic relief
Skin care (when skin starts to desquamanate)
Mouth care
FAMILY IMPACT KAWASAKI'S SYNDROME
The length of illness can be as long as 19 weeks - with a week or more in the hospital.
Economic consequences of the length of the childs illness can be devastating.
BACTERIAL ENDOCARDITIS PREVENTION/PROPHYLAXIS
SBE (Systemic bacterial endocarditis or Subacute bacterial endocarditis)
Endocarditis is an infection of valves and inner lining of the heart. It most commonly occurs in persons
with congenital or acquired heart disease, (but can occur in a person without any heart disease). It is most
often a complication of bacteremia in the child with acquired or congenital heart disease.
The most common bacteria causing bacterial endocarditis in children with CHD is Streptococcus Viridians.
B.E. occurs when organisms enter the blood stream from site of localized infection. The organism begins to
grow on endocardial tissue, tricuspid, aortic, pulmonic or aortic valves.
The most common site of entry is the mouth from dental work, with dental work it is any
invasive oral procedure.
The patient with CHD is especially at risk with a dental cleaning.
Other sources : GU system, the heart after cardiac surgery, respiratory system after an invasive
procedure (such as a bronchoscopy), through breaks in the skin which develop into a localized
infections and other invasive procedures of the GI/GYN systems.
In the childbearing female, this includes childbirth.
If a procedure is considered a dirty procedure the patient with CHD is at risk of getting BE.
PREVENTION OF BACTERIAL ENDOCARDITIS
To prevent BE, a patient with CHD must be premedicated with antibiotics 1 hour prior to the procedure
being performed. If the patient is NPO for the procedure, antibiotics must be given IM or IV.
The antibiotic of choice is Amoxicillin 50mg/kg (max. 2g) PO 1 hour prior to procedure.
o If NPO or unable to take oral medication for another reason, Ampicillin 50mg/kg IM/IV,
maximum dose 2g, hour prior to procedure.
o If the patient is penicillin sensitive the alternative drugs are azithromycin, Clairthromycin,
Clindamycin.

Chapter 21: Cardiovascular Dysfunction (ASD, VSD, COA, PDA, TOF, TGA), Page 14 of 17

CONGESTIVE HEART FAILURE IN THE PEDIATRIC PATIENT


Occurs when the heart cannot pump the blood returning to the right side of the heart or it cannot provide
adequate circulation to meet the needs of organs and tissues in the body.
The components in CHF are: preload, circulatory volume, after load and contractility
Causes of CHF in the pediatric patient include:
High output state, related to CHD wherein there is pulmonary blood flow returning to the right
side of the heart: VSD, PDA.
Low output states where there are left sided heart obstructions causing the heart to pump harder
to bypass the obstruction: COA, TOF.
Any child with any form of CHD is vulnerable to CHF.
Heart valve damage
Pulmonary disease
Endocarditis
Significant anemia
Arrhythmias
Hypertension
Cardiomyopathy
Hemorrhage
One-sided heart failure is very rare in children; if one ventricle fails the other also starts showing S&S
of failure (and very quickly, unlike the adult pt w/ CHF).
Right-sided failure: RV unable to pump blood effectively into the pulmonary artery, which results
in increased pressure in the RA and systemic venous circulation. Systemic hypertension and
hepatosplenomegaly result.
Left sided heart failure: the LV is unable to pump blood into the systemic circulation, resulting in
increased pressure in the LA and pulmonary veins. The lungs become congested with blood,
causing elevated pulmonary pressure and pulmonary edema
S &S OF CHF IN THE CHILD
The earliest sign of CHF in the pediatric patient is tachycardia at rest
S&S of CHF in the infant:
Diaphoresis (esp. the scalp & face) while eating
Fatigue (infant struggles to eat and falls asleep during feedings)
Irritability
Gallop Rhythm (S3, S4 )
Anorexia
Poor perfusion to lower extremities from decreased cardiac output:
Cool, pale extremities
Weak peripheral pulses
Slow capillary refill (>2 sec)
Mottled skin
Oliguria

Chapter 21: Cardiovascular Dysfunction (ASD, VSD, COA, PDA, TOF, TGA), Page 15 of 17

Signs of pulmonary congestion:

Tachypnea
Dyspnea
Nasal flaring
Cyanosis
Intercostal retraction
Wheezing
Orthopena (dyspnea while lying down)
Dry, persistent cough, hoarseness
BMR
Edema: first seen in eyelids, face,
spreading to extremities

FTT = Poor Weight Gain


o Infant is struggling to breathe, has
decreased PO intake
o Weight gain from increased fluid retention
Activity intolerance
Developmental delays (esp. in gross motor)
Fluid retention can lead to ascites, pleural
effusion, neck vein distension (hard to see in
infants due to their short, fat necks)

PHARMACOLOGIC MANAGEMENT OF CHF


Digoxin: increases force of systolic contractions, leading to decreased diastolic volume; slower
conduction increases renal perfusion & renal output, which in turn decreases venous congestion.
No blood
Furosemide: a diuretic that increase fluid output, monitor closely for hypokalemia, there is no
+
levels in peds.
Na restriction as with adults
Digoxin
toxicity
Ace Inhibitors: Capoten/Enalapril block conversion of angiotensin I to angiotensin II (which
assumed if
normally causes vasodilatation and decreases systemic and pulmonary vascular resistance, which
+
throwing up,
in turn decreases BP. Also inhibits aldosetrone secretion (decrease in preload, decrease from Na
dose based
retention of H2O).
Synagis: All children with CHD ages birth2 years from Sept-March
on weight.
Potassium supplementation: for replacement of K+ lost with diuretic therapy
Potassium sparing diuretics: aldactone

NON-PHARMACOLOGIC MANAGEMENT OF CHF


cardiac demand:
o keep infant warm, decrease cold stress
o semi-fowlers to respiratory effort
Frequent position changes to decrease edema
Skin care (edematous areas)
Prompt recognition and treatment of infections (especially respiratory)
Allow for periods of uninterrupted rest
O2 administration (if cyanosis present)
High calorie, low volume diet.
Parent education of S&S of increasing CHF.
DIGOXIN
Inotropic action: increases force & velocity of myocardial contraction. In pts with CHF it
increases contractile force and boosts cardiac output.
When starting Digoxin in pediatric patients with CHD, children must be digitalized, which means
to give their loading does in three doses, 8 hours apart.

Cardiac glycoside
Antiarhythmic

Chapter 21: Cardiovascular Dysfunction (ASD, VSD, COA, PDA, TOF, TGA), Page 16 of 17

DIGOXIN SAFETY/ADMINISTRATION
If a dose is missed and it is less than 4 hours since scheduled time, dose can be given and the
following dose given at regular time.
If more than 4 hours has lapsed, hold that dose and resume with next scheduled dose.
If two or more consecutive doses are missed, advise parent to call the cardiologist NEVER
increase or double up on dose.
If child has concurrent illness (V/D, high fever advise parent to call cardiologist for
further instructions).
If child goes to a baby sitter or day care, try to schedule doses so they are at home for
administration. If this is not possible
o DO NOT under any circumstance give child-care provider the bottle of Digoxin; give
individual doses drawn up in a syringe.
o Parent must understand rationale behind this.
Drug must be given in a TB 1mL or 3mL syringe, never use dropper provided in bottle or any other
measuring device.
ADVERSE REACTIONS OF DIGOXIN
CNS
Fatigue
Muscle weakness
Agitation/ Hallucinations
Headache/ Dizziness
EENT
Yellow green halos around visual images (hard to assess in pediatric pts)
Blurred vision
Light flashes
Photophobia
GI
Anorexia / N / V / D
All difficult for children to verbalize

Digoxin is brand
specific. Need to use the
same brand!

PATIENT/PARENT TEACHING DIGOXIN ADMINSTRATION SAFETY


Drug must be inaccessible to ALL children; an overdose will kill a child in minutes.
Provide parent with detailed written instructions to take home.
Provide parent with a chart for administration.
Provide parent with phone number of poison control.
Provide parent with adequate supply of appropriate sized syringes.
Do not administer with food or liquid.
If child vomits after dose DO NOT repeat. Give next dose as scheduled, if child vomits the 2nd
dose, advise parent to call the cardiologist.

NURSING CONSIDERATIONS IN PEDIATRIC DIGOXIN ADMINISTRATION


Prescribed dose and amount drawn up in syringe must be verified with another pediatric RN before
administration (even if this is not the policy in your institution).
During digitalizing dosing closely monitor HR and BP.
Assess K+ levels and UO before administering.
Assess HR before administration.

Chapter 21: Cardiovascular Dysfunction (ASD, VSD, COA, PDA, TOF, TGA), Page 17 of 17

There is no margin of error in pediatric digoxin administration overdose = death.


MAINTENANCE DIGOXIN DOSES
AGE
PO
Full term infant
8-10mcg/kg
1 mo 2 years
10-12mcg/kg

IV
6-8 mcg/kg
7.5-9 mcg/kg

2 10 years

6-8 mcg/kg

8-10mcg/kg

Children under 10 years, two divided doses q12


Children over 10, QD.
We are not responsible to remember the individual range of Digoxin dosages for each age group but we are
responsible to know how a TDD is administered and calculated in a pediatric patient and ALL safety
considerations.
st

1 dose
nd

dose

TDD - Total Digitalizing Dose


of TDD
of TDD, 8 hours after first dose,
rd

EKG must be done before 3 dose.


rd

3 dose

of TDD 8 hours after 2

nd

dose

Dose# of TDD is 60mg @4am


Dig 50mg/mL
DOSE
1.
2.
3.
Total

TIME mL
150
4am 3
75
12pm 1.5-----ECG
758pm 1.5
300
6mL

***Can't be less than 8hrs between doses!***