Transcript Alterations in Cardiovascular Function 7

Alterations in Cardiovascular
Function
Ball & Bindler
Donna Hills APN EdD
Blood Flow
Transition from fetal to
pulmonary circulation
•
•
•
•
•
•
•
the umbilical cord is cut
systemic vascular resistance is increased
pressure in the L side of the heart increases
foramen ovale closes
breathing is initiated
pulmonary vascular resistance falls
blood that was shunted through the PDA
now goes to the lungs.
FIGURE 26–1 Fetal circulation. Blood leaves the placenta and enters the fetus through the umbilical vein. The ductus venosus, the
foramen ovale, and the ductus arteriosus allow the blood to bypass the fetal liver and lungs. After circulating through the fetus, the blood
returns to the placenta through the umbilical arteries. From Ladewig, P. W., London, M. L., Moberly, S., & Olds, S. B. (2002).
Contemporary Maternal-Child Nursing Care (8th ed,. p. 51 ). Upper Saddle River, NJ: Prentice Hall.
Jane W. Ball and Ruth C. Bindler
Child Health Nursing: Partnering with Children & Families
© 2006 by Pearson Education, Inc.
Upper Saddle River, New Jersey 07458
All rights reserved.
FIGURE 26–2 A, Fetal (prenatal) circulation. B, Pulmonary (postnatal) circulation. LA, left atrium; LV, left ventricle; RA, right atrium;
RV, right ventricle.
Jane W. Ball and Ruth C. Bindler
Child Health Nursing: Partnering with Children & Families
© 2006 by Pearson Education, Inc.
Upper Saddle River, New Jersey 07458
All rights reserved.
Ductus Arteriosus
• an opening in fetal circ. between the
pulmonary artery (PA) and aorta (Ao).
• in fetal circulation, most of the blood
bypasses the lungs and returns to systemic
circulation by way of the PDA (PA to Ao).
• In transition to pulmonary circulation, the
PDA constricts over 10-15hrs; permanent
closure should occur by 3wks of age,
UNLESS SATURATION REMAINS LOW
FIGURE 26–3 Normal pressure gradients and oxygen saturation levels in the heart chambers and great vessels. The ventricle on the
right side of the heart has a lower pressure during systole than the left ventricle because less pressure is needed to pump blood to the lungs
than to the rest of the body.
Jane W. Ball and Ruth C. Bindler
Child Health Nursing: Partnering with Children & Families
© 2006 by Pearson Education, Inc.
Upper Saddle River, New Jersey 07458
All rights reserved.
Hypoxemia in the infant
• below 95% pulse oximetry.
• cyanosis results from hypoxemia
• perioral cyanosis indicates central
hypoxemia
• acrocyanosis does not.
Response to Hypoxemia
• acute: HR increases
• chronic: bone marrow produces more RBC
to increase the amount of Hgb available for
oxygen transport.
• Hct>50 is called polycythemia.
• increased blood viscosity increases risk of
thromboembolism.
Cardiac Functioning
• 02 requirements are high the first few weeks
of life
• normally, HR increases to provide adequate
oxygen transport
• infant has little cardiac output reserve
capacity
• cardiac output depends almost completely
on HR until the heart is fully developed
(age 5 yr).
Compliance in the infant
• in infancy, muscle fibers are less developed
and organized
• results in less functional capacity or less
compliance
• less compliance means the infant is unable
or less able to distend or expand the
ventricles to achieve an increase stroke
volume in order to compensate for
increased demands.
Severe Hypoxemia
• children respond with bradycardia
• cardiac arrest generally results from
prolonged hypoxemia related to respiratory
failure or shock
• in adults, hypoxemia usually results from
direct insult to the heart.
• therefore, in children, bradycardia is a
significant warning sign of cardiac arrest.
• approp Rx for hypoxemia reverses brady.
Case Study
• Dylan is a 3 mo old with Down Syndrome
and VSD, admitted for CHF. His birth
weight was 7 lb 9 oz; a week ago he
weighed 12 lb at the pediatrician’s office
and now weighs 12.10 lb. He is breathing
72 bpm with a HR of 190 and a sat of 91%.
He is diaphoretic and is not taking his usual
3 oz formula every 3-4 hours. He has had 4
moderately wet diapers in the past 24 hrs.
Study questions for case study
• Identify abnormal assessment data for
Dylan
• What other data would you collect? (Hx and
assessment)
• What is your priority nursing action?
• What other nursing interventions would you
do for him? For his mother?
Down Syndrome
• A trisomy genetic abnormality; ;usually on
chromo 21.
• Classic characteristics:
– Some degree of mental retardation with variable
functional deficit
– Microcephaly, flattened forehead, wide short neck.
Epicanthal eye folds, simian palmar crease, protruding
tongue, low set ears, short broad hands, hearing loss,
hypotonia.
– Increased incidence of DM, CHD and Leukemia
What aspects of Down Syndrome
have an affect on his ability to
maintain optimal health?
• Protruding tongue
• Hypotonia
• Slower to reach milestones, compounded by
hypotonia
Pulmonary Artery Hypertension
• irreversible condition that results from R
sided heart circulation being overloaded and
therefore shunting excessive blood to the
lungs.
• overloads the R side of the heart, overloads
the pulmonary system causing increased
pulmonary vascular resistance (life
threatening).
Obstructive Congenital Defects
• due to abnormally small pulmonary vessels
• which restrict flow of blood, so the heart
hypertrophies to work harder to provide the
blood flow to organs.
• however, CO increases initially but
eventually hypertrophied muscle becomes
ineffective.
• initially R sided failure, progressing to L
sided and eventual bilateral failure
Congestive Heart Failure
• cardiac output is inadequate to meet the
body’s needs
• may result from:
– congenital heart defect that causes increased
pulmonary blood flow or obstruction of blood
outflow tract
– problems with heart contractility
– pathology that requires a high cardiac output
(severe anemia, acidosis, respiratory disease).
CHF in the infant
•
•
•
•
•
can be subtle
good assessment skills are a must
tires easily, especially during feeding
(initial) weight loss
diaphoresis, irritability, frequent infection.
FIGURE 26–4
failure.
Jooti is receiving intravenous fluids and oxygen. Her condition is being continuously monitored for congestive heart
Jane W. Ball and Ruth C. Bindler
Child Health Nursing: Partnering with Children & Families
© 2006 by Pearson Education, Inc.
Upper Saddle River, New Jersey 07458
All rights reserved.
CHF in older children
•
•
•
•
exercise intolerance
dyspnea
abdominal pain or distention
peripheral edema.
Symptoms of progressive disease
• tachycardia, tachypnea, pallor or cyanosis,
F/G/R, cough, crackles.
• fluid volume overload: periorbital and facial
edema, JVD, hepatomegaly, ascites.
• not mentioned in the book: increased weight
gain, bounding pulses, edema of dependent
body parts.
FIGURE 26–4
failure.
Jooti is receiving intravenous fluids and oxygen. Her condition is being continuously monitored for congestive heart
Jane W. Ball and Ruth C. Bindler
Child Health Nursing: Partnering with Children & Families
© 2006 by Pearson Education, Inc.
Upper Saddle River, New Jersey 07458
All rights reserved.
FIGURE 26–5 Infants with cardiac conditions often require supplemental feedings to provide sufficient calories for growth and
development. The parents of this infant girl have been taught how to give her nasogastric feedings at home.
Jane W. Ball and Ruth C. Bindler
Child Health Nursing: Partnering with Children & Families
© 2006 by Pearson Education, Inc.
Upper Saddle River, New Jersey 07458
All rights reserved.
Cardiomegaly
• occurs at the heart attempts to maintain CO
• if CHF is not adequately treated, precursors
of Cardiogenic Shock arise: cyanosis, weak
peripheral pulses, cool extremities,
hypotension, heart murmurs
• clarification: not all heart murmurs are
heralding cardiogenic shock.
Clinical diagnosis
• based upon clinical assessment: tachycardia,
respiratory distress, crackles.
• cxray could show cardiac enlargement,
venous congestion, PE, atelectasis.
• cardiac echo: defects or dysfunction
• EKG: tachycardia, bradycardia, ventricular
hypertrophy
Goals of Management
• make the heart work efficiently
• remove excess fluid
• improve systemic circulation without
overloading the pulmonary circulation
Medication therapy
• positive inotropic effect and afterload reducing agents
– Digitalis
• Digoxin
– ACE inhibitors (Angiotensin-converting
enzyme inhibitors)
• Lisinopril
– Beta Blockers
• Indural (Propranolol)
– Diuretics: Lasix, HCThiazide, aldactone.
Supportive treatment
• oxygen
• fluids, as indicated( in CHF, fluids may be
restricted).
• increased calories or concentrated
formula(prescribed)
• air way support/management
• rest and spacing of activity/rest periods
Surgical treatment
• cardiac catheterization, which may include
procedural treatment in the cath lab
• valve replacement
• conduit placement
• cardiac transplant
FIGURE 26–6
Interventional catheterization, balloon valvuloplasty to open the pulmonary valve.
Jane W. Ball and Ruth C. Bindler
Child Health Nursing: Partnering with Children & Families
© 2006 by Pearson Education, Inc.
Upper Saddle River, New Jersey 07458
All rights reserved.
Developmental Assessment
• the child may be unable to reach
developmental milestones until CHF is
adequately controlled
• Taylor activity to child’s ability.
• Energy must be adequate for motor
milestones to improve.
• Dev. Assessment: DDST II: followed Q 23mos in infancy/toddler.
• limit contact with other children: risk of inf.
Congenital Heart Disease(CHD)
• refers to a defect in the heart, great vessels
or persistence of a fetal structure
• occurs in 1% live births
• higher incidence in still births and aborted
fetuses
• incidence has declined over past 25 yrs d/t
techno advances in intrauterine assessment,
surgical techniques and intensive care
Factors that increase risk for
having a child with CHD
• family hx of CHD
• maternal age >35yr
• coexisting maternal disease: DM, collagen
vascular disease, PKU
• exposure to teratogens or rubella infection
CHD
• most CHD develop during first 8 wks of
gestation
• usually result of combined genetic and
environmental interaction
–
–
–
–
fetal exposure to drugs:phenytoin & lithium
maternal viral infections:rubella
maternal metabolic disorders: DM, PKU
maternal complic of preg ie incr age, antepartal
bleeding
CHD etiologies cont.
– genetic factors: familial patterns
– chromosomal abnormalities: most common is
Down’s syndrome with 40% occurrence rate of
CHD.
• defects are divided into cyanotic and
acyanotic (in pure form).
Acyanotic Heart Defects
• constitutes the majority of heart defects in
children
• two types: obstructive and non-obstructive
• obstructive: PS, AoS, Coarc.
• non-obstructive:PDA, ASD, AV canal
(endocardial cushing defect), VSD.
Cyanotic Heart Defects
• generally caused by a valvular or vascular
formation
• ex: Tetralogy of Fallot, Transposition,
hypoplastic LV, tricuspid atresia, pulmonary
atresia, truncus arteriosus, and total
anomalous venous return.
Acyanotic; non-obstructive
lesions
•
•
•
•
PDA
ASD
AV canal
VSD
Pathophysiology of Acyanotic,
non-obstructive CHD
• openings in the septal wall cause a L to R
shunt
• oxygenated blood mixes with deoxygenated
blood
• volume overload to the pulmonary system
• can cause CHF
• PHT occurs d/t chronic volume overload to
the lungs if uncorrected.
Patent Ductus Arteriosus
• common; 9-12% of all CHD
• persistant fetal structure
• when the PDA remains open, blood is
shunted from the Aorta to the Pulmonary
artery, therefore increasing blood flow to
the lungs: L to R.
• bounding pulses, dyspnea, tachypnea, FTT.
• at risk for freq URI and endocarditis, CHF.
• continuous systolic murmur and thrill palp.
Treatment of a PDA
• surgical ligation; transcatheter closure
>18mos of age.
• Indomethacin may stimulate closure in
premies
• Prostaglandin helps to keep the PDA open
until surgical correction is optimal.
• left untreated, LVH, pulmonary
hypertension (PHT) and vascular
obstructive disease develop.
Atrial Septal Defect; ASD
•
•
•
•
opening in the atrial shunting
L to R shunting
accounts for 6-10% of CHD
small to moderate size may go undiagnosed
until preschool years or later
• sx of large ASD: CHF, tiring easily, poor
growth
• soft systolic murmur heard in pulmonic
space; wide S2 split.
Treatment of ASD
• Echo shows RV overload and shunt size
• cxray and EKG may be normal unless a
large shunt
• surgery to close or a patch via catheter
during Cardiac Cath.
• atrial arrhythmias can be a late sx or
associated with a large ASD involving
conduction system in the septum
FIGURE 26–7 A, Septal occluder used to close an atrial septal defect (ASD) and less commonly to close a ventricular septal defect
(VSD). B, Coil used to close a patent ductus arteriosus (PDA). The coil of wire covered with tiny fibers occludes the ductus arteriosis when
a thrombus forms in the mass of fabric and wire.
Jane W. Ball and Ruth C. Bindler
Child Health Nursing: Partnering with Children & Families
© 2006 by Pearson Education, Inc.
Upper Saddle River, New Jersey 07458
All rights reserved.
FIGURE 26–8 A child with atrial septal defect repair. Surgery is performed with this type of defect to prevent pulmonary vascular
obstructive disease as an adult.
Jane W. Ball and Ruth C. Bindler
Child Health Nursing: Partnering with Children & Families
© 2006 by Pearson Education, Inc.
Upper Saddle River, New Jersey 07458
All rights reserved.
Atrioventricular Canal:
Endocardial Cushing Defect
• accounts for 4-5% of CHD
• partial or complete ASD/VSD with some
degree of involvement of mitral/tricuspid
valves variable
• associated with Down’s syndrome
• severity of sx depends on degree of mitral
regurgitation.
• sx in infants: CHF, tachypnea, tachycardia,
FTT, incr URI, systolic murmur (LLSB)
Treatment of AV Canal
• surgery during infancy to prevent PHT
• patches placed over septal defects; mitral
valve replacement
• arrhythmias and mitral valve insufficiency
occur post/op
• no difference between short term survival
rates in infants with or without Down’s
syndrome.
Ventricular Septal Defect; VSD
•
•
•
•
opening in the ventricular septum
shunts L to R; increases pulmonary bld flow
most common: accounts for 20% CHD
only 15% large enough to generate
symptoms: tachypnea, dyspnea,, FTT,
reduced fluid intake, CHF, PHT.
• systolic murmur ; LLSB
• most small VSD close spontaneously
Treatment of VSD
• if no sx CHF or PHT, treatment is
conservative
• surgical patching during infancy if FTT
• closure by transcatheter device during CC
for some defects: Rashkind procedure.
• prophylaxis for infective endocarditis is
required
• high risk for surgical repair in first few
months of life
Acyanotic; obstructive lesions
• PS
• AoS
• Coarctation of the Aorta
Pathophysiology of Acyanotic,
obstructive CHD
• narrowing across the valves causes pressure
overload and hypertrophy of the closest
ventricle
• child will have a murmur
• some experience fatigue and exercise intol
d/t inability to increase CO
• many are asympto and grow normally
• older children: exercise induced dizziness
and syncope: requires immediate attention
Pulmonary Stenosis: PS
• narrowing of the pulmonary valve or
valvular area
• obstructs flow to the PA
• increases pre-load; results in RVH
• second most common CHD
• accounts for 8-12% of CHD
• systolic murmur with fixed split S2 in
Pulmonic area.
Treatment of PS
• dx usually made at birth with murmur
ascultated
• cxray may show heart enlargement
• EKG may demonstrate RVH
• echo provides info re pressure gradient
across the valve
• may dilate during CC using balloon
valvuloplasty or valvular replacement
• lifelong endocarditis prophylaxis is required
Aortic Stenosis: AoS
• narrowing of the aortic valve; obstructs
blood flow to systemic circulation
• accounts for 3-6% of CHD; progressive
during childhood
• often associated with bicuspid rather than
normal tricuspid aortic valve.
• asymptomatic, grow normally; BP wnl but
may have a narrow pulse pressure
• systolic m; thrill in Ao; c.p. after exer.
Treatment of AoS
• cxray and EKG are usually normal if mild
• echo can reveal number of valve leaflets,
pressure gradient across the valve, and size
of the aorta.
• surgical valvuloplasty or dilated with
balloon during card. cath.
• valvular replacement
• requires lifelong SBE prophylaxis
• c/p, syncope or sudden death poss. s/p ex.
Coarctation of the Aorta
•
•
•
•
narrowing or obstruction of descending Ao.
obstructs systemic blood flow
accounts for 5-8% CHD
grow normally but constriction is
progressive
• lower BP in LE and higher in UE, neck,
head.
• pulse weak or absent in LE; full/bounding
in UE
Treatment of Coarc
• EKG shows LVH
• cxray reveals enlargement and pulm venous
congestion and constricted aorta
• balloon dilation in card cath or surgical
resection/anastomosis/patch.
• risks of reoccurrance, persistent HTN in
adulthood, 20% develop post-coarctectomy
syndrome (abdominal pain and distention).
• SBE prophylaxis needed.
Cyanotic Heart Defects
• Tetralogy of Fallot
• Transposition of the Great Vessels
• caused by malformation or a combination of
defects that prevent adequate level of
oxygenation
• R to L shunt occurs resulting in chronic
hypoxemia and cyanosis.
Pathophysiology of Cyanotic
Heart Disease
• P02 is lower than normal; PC02 rises
• hypoxemia becomes progressively worse as
respiratory center overreacts and incr
respiratory effort
• incr resp effort attempts to incr CO;
contributes to a downward spiral without
intervention
• at risk for thromboembolism d/t hypoxemia
causing polycythemia
Clinical Manifestations of
Cyanotic Heart Disease
• chronic hypoxemia causes fatigue,
clubbing, exertional dyspnea, delayed
milestones, tire easily with feeding, reduced
growth, CHF
• hypercyanotic (hypoxic) spells: incr rate
and depth of respir, incr cyanosis, incr HR,
pallor and poor perfusion, agitation and
irritability.
FIGURE 26–13 Clubbing of the fingers is one manifestation of a cyanotic defect in an older child. What neurologic signs may be
associated with such a defect?
Jane W. Ball and Ruth C. Bindler
Child Health Nursing: Partnering with Children & Families
© 2006 by Pearson Education, Inc.
Upper Saddle River, New Jersey 07458
All rights reserved.
Cyanotic Spell
• most signif prob to develop in infants and
toddlers with cyanotic heart disease
• brought on by crying, feeding, exercise,
warm bath, or straining to defecate
• during a hypoxic spell, child will often
squat knee to chest to decrease venous
return (by incr systemic vascular resistance)
from LE which decr CO and relieves the
cyanotic spell.
Tetralogy of Fallot
• combination of four defects
–
–
–
–
•
•
•
•
pulmonary stenosis: degree determines severity
VSD
over-riding of the aorta
RVH
accounts for 10% of CHD
elevated R sided pressures: R to L shunt
xray: boot shaped heart d/t RVH
risk for metabolic acidosis and syncope.
Treatment of TOF
• total repair is done by 6 mo if cyanotic
spells
• surgery is not necessarily currative, but
most have improved quality of life and
improved longevity
• residual problems: arrhythmias and RV
dysfunction
• lifelong SBE required
Transposition of the Great
Arteries: TGA
• position of the PA and Ao are switched
• life threatening at birth;cyanosis, hypoxia,
acidosis
• cyanosis does not improve with 02 admin
• survival depends upon a patent DA and
foramen ovale
• accounts for 5% of CHD
• may be assoc with an ASD or VSD
Treatment of TGA
• xray show egg on a string
• prostaglandin E1 used to keep PDA open
until palliative procedure
• corrective surgery (artery switch) usually
performed by 1 wk of age
• balloon atrial septostomy during card cath
may be used to open foramen ovale
• survival depends upon surgery; risk for
arrhy, SBE, RV failure, sudden death LT.
FIGURE 26–9 This infant has a congenital heart defect with decreased blood flow. What is the prognosis for an infant who has either of
the most common malformations—tetralogy of Fallot or transposition of the great vessels?
Jane W. Ball and Ruth C. Bindler
Child Health Nursing: Partnering with Children & Families
© 2006 by Pearson Education, Inc.
Upper Saddle River, New Jersey 07458
All rights reserved.
FIGURE 26–10
A child with a cyanotic heart defect squats (assumes a knee–chest position) to relieve cyanotic spells.
Jane W. Ball and Ruth C. Bindler
Child Health Nursing: Partnering with Children & Families
© 2006 by Pearson Education, Inc.
Upper Saddle River, New Jersey 07458
All rights reserved.
FIGURE 26–12 Place the infant who has a hypercyanotic spell in the knee–chest position. This position increases systemic vascular
resistance in the lower extremities.
Jane W. Ball and Ruth C. Bindler
Child Health Nursing: Partnering with Children & Families
© 2006 by Pearson Education, Inc.
Upper Saddle River, New Jersey 07458
All rights reserved.
Murmurs in children
• are not necessarily indicative of pathology
but require a careful assessment and
possibly a cardiac workup
• innocent murmurs are more prevalent than
pathologic murmurs
• caused by increased turbulence of blood
flow
• heard especially well in a child with a thin
chest wall
Patent Ductus Arteriosus Murmur
Pearls
• some VSD’s close spontaneously with time
• weight gain or growth of the child may
increase the probability of success of
cardiac surgery
• defects that cause PHT are corrected in
infancy to prevent irreversible pulmonary
vascular disease.
• major complication of acyanotic heart
defects: PHT
Cardiac Catheterization
• used to be used for diagnosis, now more
commonly used for treatment
• potential complications: perf of PA, allergic
reaction to contrast media, arrhythmias,
hypotension, stroke, vascular compromise
in the leg, and bleeding
• post cath: activity is limited and pressure
dressing is applied
• risks: thrombosis, hemorrhage, dehydration
Nursing care of the child
undergoing heart surgery
• parents may need genetic counseling; fetal
echo can id structural heart defects as early
as 18-20 weeks; some intrauterine
procedures available.
• ICU care post-op with intubation and
sedation
• will have an arterial line; may have chest
tubes
Heart Transplantation
• improved statistical survival to 5 yrs (65%)
d/t improved immunosuppressive protocols
and surgical techniques
• infection and rejection are the major causes
of M&M
• immunosuppressive drugs: cyclosporine A,
azathioprine, and corticosteroids
– drugs can cause physical side effects
– prevents immunization with live viruses
Pulmonary Artery Hypertension:
PHT
• incr load to the lungs causes pulmonary
vascular changes in an attempt to decrease
the blood flow
• inflammation, hypertrophy of the pulm
vessels and fibrosis develop
• pulmonary venous hypertension develops
and leads to R to L shunting, with R sided
heart function impaired.
• life threatening: irreversible
Acquired Heart Diseases
•
•
•
•
•
•
Rheumatic Fever
Infective Endocarditis
Cardiac Arrhythmias
Kawasaki Disease
Hyperlipidemia
Hypertension
Rheumatic Fever
• inflammatory connective tissue disorder
that follows initial infection by group A
beta-hemolytic streptococci
• may lead to permanent mitral or aortic valve
damage
• sx: migratory polyarthritis, subcutaneous
nodules, erythema marginatum, fevers, St.
Vitus dance (chorea movements)
• dx: Jones criteria and an elevated ASO
Treatment for Rheumatic Fever
• antibiotics to treat the strept infection: pcn,
erythromycin
• asa for joint pain and fever
• monitored by cardiac echo (serial)
• steroids for severe carditis with CHF
• SBE prophylaxis
• long term antibiotics until adulthood
– daily oral or 1x/mo IM (Pen G)
Infective Endocarditis
• inflammation of the lining, valves, and
arterial vessels of the heart
• caused by bacterial, enterococci and fungal
infections
• significant M&M for children with CHD,
prosthetic valves and shunts, and in
immunocompromised children with long
term central venous catheters.
SBE Prophylaxis
• Prophylaxis for infective bacterial
endocarditis
• aka SBE prophylaxis ;systemic bacterial
endocarditis prophylaxis
• see Table 14-4 p 489 in B&B
• commonly given before dental procedures
to prevent oral bacteria from entering the
blood stream and seeding in the area of
defect, causing a bacterial endocarditis
Cardiac Arrhythmias
• not uncommon in children
• sinus tachycardias;sinus bradycardias, SVT.
– May occur with an acute condition and then
resolve
• sinus arrhythmia:variation of normal
– increased HR with inspir/decr with expir.
Supraventricular Tachycardia:
SVT
• pathologic tachycardia
• abrupt onset of a rapid heart rate >200
• recurrent or prolonged SVT can cause
symptoms, CHF or shock
• rx with vagal stimulation (ice to the face),
or valsalva maneuver (hold breath or
straining)
• meds used: Adenosine or Amiodarone
• cardioversion or ablation if needed
Long QT Syndrome
• inherited genetic disorder that puts the child
at risk for ventricular fibrillation and sudden
death
• may also result from electrolyte imbalance,
malnutrition (anorexia and bulimia),
myocarditis and CNS trauma
• speculation that it may be associated with
SIDS (unproven)
• no warning; results in death
Kawasaki Syndrome
• acute systemic inflammatory disease
• aka mucocutaneous lymph node syndrome
• most common cause of acquired heart
disease
• etiology unknown
• 3 stages:
– acute, subacute and convalescent
• dx based upon clinical signs
Diagnostic Criteria for Kawasaki
Syndrome
• fever > 102.2 x 5 days plus 4 of the
following:
• bilateral conjunctivitis
• strawberry tongue; cracks/fissures of lips
• palmar/plantar erythema, induration,then
desquamation
• maculopapular rash on trunk
• acute cervical lymphadenitis
FIGURE 26–14
This child shows many of the signs of the acute stage of Kawasaki syndrome.
Jane W. Ball and Ruth C. Bindler
Child Health Nursing: Partnering with Children & Families
© 2006 by Pearson Education, Inc.
Upper Saddle River, New Jersey 07458
All rights reserved.
Treatment of Kawasaki
Syndrome
• high dose ASA and IgG given early
significantly decreases the risk of cardiac
involvement
• greatest risks are coronary artery lesions
and cardiac aneurysms
• monitor for cardiac involvement for
months: aneurysms, early atherosclerosis,
arrhythmias, CHF, coronary stenosis, MI
and potential death.
FIGURE 26–15 This child has returned for one of her frequent follow-up visits to assess her cardiac status after treatment for Kawasaki
syndrome. Notice the lips that show the inflammation and cracking.
Jane W. Ball and Ruth C. Bindler
Child Health Nursing: Partnering with Children & Families
© 2006 by Pearson Education, Inc.
Upper Saddle River, New Jersey 07458
All rights reserved.
Dyslipidemia
• fam hx incr risk of CAD d/t high levels of
LDL and cholesterol
• total lipid panel, nutritional history and life
style needs to be considered.
• children need fats to grow, metabolize
vitamins and produce hormones
• high fat/sat fat diet is not recommended.
• long term studies of effect of childhood
lipid levels on life span inconclusive
Hypertension
• 1-3% of the pedi population
• unknown cause = essential or primary HTN
• underlying kidney or cardiac
disease=secondary HTN
• children’s BP in >90th at incr risk for adult
HTN
• HTN in adol correlates with obesity and
elevated serum lipid level