FETAL AND NEONATAL
Purkinje fibers/ cells
4 temporary shunts (pathway)
1.ductus arteriosus - becomes ligamentum
arteriosum
2.Ductus venosus – becomes ligamentum venosum
3.Foramen ovale – becomes ligamentum teres
(butas sa right ventricle and left atrium)
4.Umbilical vessels art vein / umbilical arteries –
medial umbilical ligaments
Heart CONDUCTION SYSTEM
Sinoatrial Node (SA node)
• Primary pacemaker of the heart
• Inherent firing rate of 60 to 100 impulses per
minute
Atrioventricular Node (AV node)
• Located in the right atrial wall near the
tricuspid valve
Coordinates the incoming electrical
impulses from the atria and after a slight
delay relays the impulse to ventricles
• 40 to 60 impulses per minute
Bundle of His
Specialized conducting tissue
Right bundle branch – conducting impulses to the
right ventricle
Left bundle branch – conducting impulses to the left
ventricle
*Divides into the left anterior and posterior
bundle branches
• Terminal point in the conduction system
• Specialized to rapidly conduct impulses
through the thick walls of the ventricles
• 30 to 40 impulses per
CONGENITAL HEART DEFECTS
▪ Most common is VSD
▪ Incidence: 1% of or about 40,000 births per
year
▪ 25% of babies with CHD are critical and
generally needs surgery or other
procedures in their 1st year of life (CDC)
▪ 15% of CHD are associated with genetic
conditions
▪ 28% of kids with CHD have another
recognized anomaly (trisomy 21,)
4 hemodynamic problems
Acyanotic (left to right shunting)
1.Increase of pulmonary blood flow
✓ Atrial septal defect
✓ Ventricular septal defect
✓ Patent ductus arteriosus
✓ Atrioventricular canal
2.Obstruction of blood flow from ventricle
✓ Coarctation aorta
✓ Aortic stenosis
✓ Pulmonic stenosis
Cyonotic (right to left shunting)
3.Decrease of pulmonary blood flow
✓ Tetralogy of fallot
✓ Tricuspid atresia
*atresia (sarado)
4.Mixed blood flow
✓ Transposition of great arteries
✓ Total anomalous pulmonary venous return
✓ Truncus arteriosus
✓ Hypoplastic left heart syndrome
(makipot,sarado na ang aorta)
Congenital heart disease (CHD) 2. NPO WITH IVF
Increased Pulmonary Blood flow (ACYANOTIC) 3. GET HEIGHT AND WEIGHT
1.ATRIAL SEPTAL DEFECT (ASD) 4. MARK THE PEDAL PULSES - DORSALIS AND
POSTERIOR TIBIAL PULSES
6. ORIENT CHILD AND PARENTS TO CC ROOM
POST CARDIAC CATHERIZATION
INTERVENTION
1.CHECK THE VITAL SIGNS
2.GIVE DIURETIC
3.CHECK PEDAL PULSES
▪ Abnormal opening between atria → blood 4.IMMOBILIZE THE AFFECTED LIMB AMD
from higher pressure (LA) to flow into lower APPLY PRESSURE
pressure (RA).
▪ Increase O2 blood into R side of heart *Femoral artery 6-8 hours
RA & RV enlargement
*Femoral vein 4-6 hours
▪ Cardiac failure is unusual in uncomplicated
ASD *Open heart surgery - tatapalan yung butas gamit
▪ May be asymptomatic if small defect ang Teflon material
Dyspnea
▪ Fatigue and poor growth Medication
▪ Soft systolic murmur in pulmonic area 1.Cardiac glycoside (energy drug)
(splitting S2)
▪ May develop CHF Ex: lanoxin
▪ Surgical treatment: Surgical Dacron patch *Below 100 heart beats do not give lanoxin
closure
– Open repair with C-P bypass during 2.Duretics-lasix
school age
3.Antihypertensive
Non-surgical: may be closed using devices
during cardiac catheterization Nursing Management:
TYPES OF ASD • Explain to parents the purpose of tests and
procedures
ASD1 ostium primum - Ang butas ay below of
septum • Teach parents ways to support nutrition,
reduce stress on heart, promote rest, and
ASD2 ostium secundum- gitna ang butas support growth and development during
preoperative period
ASD3 sinus venosus - above ng septum ang
• Teach parents signs of congestive heart
butas
failure and infection
Cardiac catheterization • Prepare parents and child for surgery by
visiting intensive care unit, explaining
Purpose:
equipment and sounds
▪ Diagnostic • Prepare older child for post-operative
▪ Therapeutic/intervention experience, including coughing and deep
▪ Electrophysiologic studies breathing and need for movement
• Teach need for antibiotic prophylaxis to
PRE-CARDIAC CATHERIZATION prevent subacute bacterial endocarditis
INTERVENTION
1.BASELINE VITAL SIGNS
2.VENTRICULAR SEPTAL
• Defect in ventricular septum – error in early
fetal development
• abnormal opening between the right and left
ventricles
• Can occur anywhere in muscle or
membranous ventricular septum
• 20-25% of all CHDs are VSD
• Pressure LV → RV and systemic arterial
circulation resistance → pulmonary
circulation, blood flows through the defect
and into the pulmonary artery
• RV becomes enlarged (Hypertrophied), over
time the RA may also become distended
• Symptoms:
Tachypnea, dyspnea
Poor growth, reduced fluid intake
Palpable thrills
Systolic murmur at left lower sternal border
May develop CHF
• Medications:
Furosemide: a diuretic which removes
excess fluid out of the body
Digoxin: helps the heart pump more
forcefully
Angiotensin-converting enzyme (ACE)
inhibitor: relaxes blood vessels and help
heart to pump more easily
• Surgical repair with bypass (procedure of
choice)
• Pulmonary artery banding (if not too
large) or patch
• Eisenmenger syndrome - right to left
shunting of blood becomes cyanotic
SMALL DEFECT VSD THERE ARE 2 OPTIONS
1. WAIT FOR SPONTANEOUS CLOSURE
2. OPEN HEART SURGERY THE APPROACH IS
PURSE-STRING
LARGE DEFECT - OPEN HEART APPROACH
DACRON/TEFLON PATCH
3.PATENT DUCTUS ARTERIOSUS (pda)
• Ductus SHOULD close by about age 15
hours after birth
• Some shunting of blood may occur up to 24
hours of life
• DUCTUS closes because increase in
arterial oxygen concentration that follows
initiation of pulmonary function
• Prostaglandin E leads to closure of PDA
Allows blood to flow from left to right and
pulmonary blood flow
• No communication from pulmonary artery to
aorta
• Small PDA: asymptomatic
• Bounding peripheral pulses
• Widened pulse pressure (>25)
• Loud machine-like murmur at upper left
sternal border (Left intraclavicular area)
• Complication for Large PDA: CHF with
tachypnea, dyspnea, and hoarse cry
• Definitive diagnosis: ECHO
Medical
(Premature) INDOMETHACIN to close
PDA’s; surgical ligation if meds fail
Prophylactic antibiotics to prevent bacterial
endocarditis
Surgery >> between age 1-2
year
2 approaches:
1. Lateral sternotomy
2. Median sternotomy
4.OBSTRUCTIVE DEFECTS
• Blood flow in heart meets an area of
anatomic narrowing (stenosis) →
obstruction to blood flow
• Pressure in ventricle & great arteries before
obstruction is increased; pressure in area
beyond obstruction is
• Decreased
• Location of narrowing near the valve:
Valvular: site of valve itself
Subvalvular: narrowing in vent below valve
(ventricular outflow tract)
Supravalvular: narrowing in great art
above valve
• (+) pressure load on ventricle – decrease
CO
• s/s CHF
• Mild obstruction: asymptomatic
• Severe stenosis: hypoxemia (rare)
5.COARCTATION OF AORTA
Descending aorta - kumikipot
UE/HEAD • Clinical manifestations:
Signs of decreased CO: faint pulses,
1.PINKISH
hypotension, poor feeding, tachycardia
2.BOUNDING PULSE Murmur; exercise intolerance
Chest pain, dizziness with standing
3.WELL DEVELOPED • Treatment
4.HEADACHE – Balloon angioplasty to dilate the valve;
Surgery: Konne procedure (valve
5.HIGH BP replacement)
LE • May require repeat procedures

1.CYANOTIC 7.PULMONARY STENOSIS

2. UNDERDEVELOPED • Pulmonary valve is stenosed

3. CLOD CLAMMY SKIN
4. LOW BP
Approach:
PGE1- Prostaglandin
Cc - balloon angioplasty
Valvotomy/valvuloplasty/ commissurotomy
Signs of CHF in infants:
• Condition can deteriorate rapidly
• Older kids may complain of dizziness,
headache, fainting and epistaxis from
hypertension
• Patient at risk for ruptured aorta, aortic
aneurysm, or stroke
• Treatment: non-surgical
– balloon angioplasty. Usually, effective
• Surgical: does not require bypass since
defect is outside pericardium
• Post-op complication is hypertension
Usually done before age 2 yrs.
Risk of recurrence
6.AORTIC STENOSIS
• Narrowing of aortic valve usually malformed
in BI- rather than TRI- cuspid valve
• Causes increased resistance in left
ventricle, decreased CO, L ventricular
hypertrophy and pulmonary vascular
congestion
• L ventricular wall is hypertrophied>>
increased pulmonary vascular resistance &
pulmonary hypertension
• LVH >> decrease coronary artery
perfusion & increase risk of MI
• Narrowing at entrance to pulmonary artery
>> R ventricular hypertrophy and decreased
pulmonary blood flow
• Extreme form of PS: Pulmonary atresia
(total fusion of the commissures and no
blood flow to lungs)
• PS >> RVH, R ventricular failure >> R atrial
pressure increases and may reopen
foramen ovale
• Shunts unoxygenated blood to L atrium >>
systemic cyanosis
• May lead to CHF
• Often have PDA as well
• Cardiomegaly on CXR
• Treatment: Balloon angioplasty to dilate the
valve
Surgical treatment – Breck procedure
(Bypass to do valvotomy)
Usually, can repair with catheterization
DEFECTS OF DECREASED PULMONARY
BLOOD FLOW (CYANOTIC)
• Obstruction of pulmonary blood flow +
anatomic defect (ASD/ VSD) between R & L
side of heart
• Difficulty of blood exiting R heart via
pulmonary artery → increase R side
pressure > L pressure
→ desaturated blood shunt R to L →
desaturated blood in systemic circulation
• Hypoxemia, usually cyanotic
1.TETRALOGY OF FALLOT
four heart defects:
1. Ventricular Septal Defect
2. Pulmonary stenosis
 3. Right ventricular hypertrophy
4. Overriding aorta
• Hemodynamics vary widely
-Depends on extent of pulmonic valve
stenosis & size of VSD
-If VSD is large, pressures are equal in R
and L ventricles. Blood is shunted in the
direction of the least resistance (pulmonary
or systemic vascular resistance)
• PVR is > than systemic vascular resistance,
shunt will be R to L
• Clinical manifestations:
• “TET SPELLS” or “blue spells” with acute
episodes of cyanosis and hypoxia
Anoxic after feeding or with crying.
• RISK of emboli, LOC, sudden death,
seizures
• Repairs: usually indicated when Tet spells
and hyper cyanotic spells increase
Stage 1: Blalock or modified Blalock
shunt
>> blood to pulmonary arteries from L or R
subclavian artery
Complete repair: usually in 1st year of life.
Repair of VSD, resect stenosed area, and
patch R ventricular outflow\
2.TRICUSPID ATRESIA
• Failure of tricuspid valve to develop
• No communication from R atrium to R
ventricle
• Blood flows thru an ASD or a patent FO to L
side of the heart thru a VSD to R ventricle to
lungs
• Often associated with PS and TGS
• Complete mixing unO2 and O2 blood in L
side of the heart → systemic desaturation,
pulmonary obstruction
→ decrease pulmonary blood flow
• At birth: presence of patent FO (or ASD) is
required to permit blood flow across septum
into L atrium
– PDA allows blood flow to pulmonary
artery for oxygenation
• Manifestations: cyanosis, tachycardia,
dyspnea, hypoxemia, clubbing
At risk for bacterial endocarditis, brain
abcess, stroke
• Treatment: NB – pulmonary blood flow
depends on PDA
Continuous infusion of PGE 1 until Sx
Palliative: shunt (pulmonary-to- systemic art
anastamosis)
Pulmonary artery banding
Modified Fontan procedure
TATLONG SAKIT SA PUSO NA AGAD
NANGINGITIM
1. TRICUSPID ATRESIA - WALANG PAG
DADAANAN NG DUGO MULA SA RIGHT ATRIUM
TO R VENTRICLE AND LUNGS
APPROACH:
- PGE1
*FONTAN PROCEDURE - Gumagawa ng
dugtungan sa pagitan ng right atrium to pulmonary
artery
*BI-DIRECTIONAL GLEN SHUNT - superior vena
cava to pulmonary artery
2.TRANSPOSITION OF THE GREAT VESSELS -
*Atrial switching either senning approach (enough
na yung pag dugtong) or mustard approach
(additional na pag dugtong)
3.HYPOPLASTIC LEFT HEART SYNDROME
MIXED DEFECTS
• Survival on postnatal period depends on
mixing of blood from pulmonary systemic
circulation within cardiac chambers
• Blood is mixed from pulmonary and
systemic circulations within the heart
chambers >> Relative desaturation of blood
in systemic blood flow
• Cardiac output decreases because of
volume load on ventricle
• Signs of desaturation, cyanosis, and CHF,
but variable depending on anatomy
• Degree of cyanosis not always visible &
signs of CHF
TGA: severe cyanosis in 1st day of life →
CHF (later)
Truncus arteriosus: severe CHF 1st few
weeks of life and mild desaturation
1.HYPOPLASTIC LEFT HEART SYNDROME
• Left side of the heart is underdeveloped
• Left ventricle is small and aortic atresia
 • Most blood flows across patent foramen
ovale to R atrium – to R ventricle and out
the pulmonary
• Descending aorta receives blood from the
PDA to supply the systemic circulation
• PDA closure >> rapid deterioration and CHF
• Treatment: Keep ductus open with
Prostaglandin E infusion
Surgical Treatment:
Norwood procedure to create a new aorta
using the main pulmonary artery and
creation of large ASD
Bidirectional Glenn Shunt at 6-9 months
age to reduce volume load on the R
ventricle
Modified Fontan procedure, similar to
Tricuspid atresia repair
Transplant may be an option for some
parts. Mortality rate is very high (30%- 50%)
2.TRANSPOSITION OF THE GREAT VESSELS
• Pulmonary artery leaves the L ventricle and
the aorta exits from the R ventricle
• No communication between the systemic
and pulmonary circulations
• Must have PDA or Septal defect to permit
blood flow
• Rare defect
Furosemides, Thiazides, Spirinolactone
Fluid restriction
Sodium restriction
• Decrease cardiac demands
Bed rest, treat infection
Preserve body temperature; reduce effort of
breathing (semi-fowlers)
Sedate an irritable child
• Improve tissue oxygenation & decrease O2
consumption
O2 vasodilator
Cool humidified O2
DISTURBANCES IN CIRCULATION
ACQUIRED CARDIOVASCULAR DISORDERS
1.CONGESTIVE HEART FAILURE
• Inability of the heart to pump and adequate
amount of blood to the systemic circulation
at normal filling pressures to meet the
metabolic demands of the body
• Due to structural deformity in children
(septal defects) → increased blood volume
& pressure in the heart → MYOCARDIAL
FAILURE
• Can occur with cardiomyopathy, dysrythmia,
severe electrolyte imbalances
• Could also be due to excess demands on a
normal cardiac muscle (sepsis / severe
anemia)
TYPE OF CONGESTIVE HEART FAILURE
A. RIGHT SIDED HEART FAILURE
RV unable to pump blood to Pulmonary
Artery → increased pressure in RA and in
the systemic venous circulation Systemic
venous HPN →
hepatosplenomegaly
B. LEFT SIDED HEART FAILURE
– LV unable to pump blood to the systemic
circulation → increased LA pressure and
pulmonary vv → congestion in lungs →
increased pulmonary pressure →
pulmonary edema → pulmonary HPN
Signs and symptoms of CHF
• Each side of the heart depends on the
adequate function of the other
• Failure of one chamber affects the opposite
chamber
• If not corrected, it may lead to cardiac
damage → inadequate CO → decreased
supply to the kidneys → Na and H2O
resorption → hypervolemia, increased
workload on the heart, pulmonary and
systemic
CONGESTIVE HEART FAILURE in Children
Impaired myocardial function
Tachycardia, fatigue, weakness, restless, pale, cool
extremities, decreased BP, decreased urine output
Pulmonary congestion
Tachypnea, dyspnea, respiratory distress, exercise
intolerance cyanosis, wheezes
Systemic venous congestion
Peripheral and periorbital edema, weight gain,
ascites, hepatomegaly, neck vein distention
CHF Treatment
Goals:
• Improved cardiac function
Digitalize – Digoxin
 Increased CO, decreased size and venous
pressure, relieve
edema
• Lanoxin (Pedia) – more rapid in onset
– Oral / IV doses x 24 hours followed by
maintenance dose (BID) to maintain blood
levels (Digitalizing Dose)
• ACE Inhibitors (Capoten / Enalapril)
(-) normal function of R-A system in kidney
Blocks conversion of AI to AII (Vasodilator)
Captopril – can be given smaller doses
• Remove accumulated Fluid and Sodium
✓ Diuretics – mainstay of treatment to
eliminate excess H2O and salt
✓ Bidirectional glenn
• Keep hct and blood viscosity within
acceptable limits (hydrate)
• Monitor for anemia, Fe supplementation,
blood transfusion
• Respiratory infection or reduce pulmonary
function can worsen hypoxemia
✓ Aggressive pulmonary hygiene
✓ CPT, antibiotics
✓ O2
OBJECTIVE IN THE MANAGEMENT OF CHF
1. Increase myocardial contractility by giving
cardiac glucoside
2. Decrease fluid overload - diuretic/weighing
3. decrease oxygen demands - complete bed rest
without bathroom privilege, do all nursing care
4. Prevent respiratory infection - reposition
5. Collaboration with dietician
6. Emotional support
2.ENDOCARDITIS (Bacterial Infective
Endocarditis)
• BE, IE or subacute bacterial endocarditis
(SBE)
• Infection in valves and endocardium
• Sequelae of sepsis in child with cardiac
disease of congenital anomaly
• Affects children with valvular abnormalities,
prosthetic valves, recent heart surgery with
invasive lines and RHD with valve
involvement, drug abuse
• Staph aureus, strep viridians (most
common), candida albicans, gram negative
bacteria
• Enter blood system thru: dental (most
common), UTI, cardiac catheterization,
surgery, etc.
• Organism in endocardium → vegetations
(verrucae) → fibrin deposits → platelet
thrombi → invade adjacent tissues
(mitral/aortic valves)
→ breaks off and embolize elsewhere
(spleen, kidney, CNS) → death
• Diagnostics
✓ Based on clinical manifestations
✓ Blood c/s: definitive diagnosis
✓ ECG/CXR (cardiomegaly)
✓ Increased ESR, increased WBC,
anemia, microscopic hematuria
✓ 2D-echo – vegetations, valve
function
• Clinical manifestation
✓ Insidious onset, unexplained fever
(low grade, intermittent)
✓ Anorexia, malaise, weight loss
✓ Extracardiac emboli
✓ Splinter h’ge – thin black lines under
nails
✓ Osler nodes – red, painful,
intradermal nodes on pads of
phalanges
✓ Laneway lesions – painless h’ges on
panes and soles
✓ Petechiae on oral mucous membrane
✓ May be present: CHF, dysrythmia,
new murmur
• Therapeutic management
✓ High dose antibiotics: Penicillin,
ampicillin, methicillin, cloxacillin,
streptomycin, or gentamycin
✓ IV/IM x 4 weeks at least
✓ Amphoterecin or flucytosine for
fungal infections
✓ Treat 2-8 weeks. If antibiotics is
unsuccessful
>> CHF develops, vulvular
damage
✓ Should be instituted immediately
✓ Blood c/s periodically to evaluate
response to antibiotics
 ✓ Prophylaxis before dental
procedures, bronchoscopy, T&A,
surgeries, childbirth
✓ Prophylaxis: 1 hour before
procedures (IV) or may use PO in
some cases
✓ Family dentist should be advised of
existing heart problems
3.Rheumatic Fever (RF)
Inflammatory disease occurs after Group A Beta-
haemolytic streptococcal throat infection
Self-limiting
– Affects joints, skin, brain,
serious surfaces, and heart
Risk factors:
Age and sex: (5-15 years old) female
Housing and socioeconomic status
Season: rainy season
Genetic predisposition
4 affectations
• Heart, pan carditis, joints - polyarthralgia
and SC nodules, skin - erythma
marginatum, cnd - syndenhams chore
Clinical Manifestations
✓ Acute febrile-like illness (2-3 weeks after
streptococcal throat infection)
✓ Non-specific
Fever
Joint pain
Loss of appetite
Muscle ache
✓ Specific
Joints (swelling and pain of larger joints like
knee, ankle, elbow and wrist occurring in
rapid succession – “migratory arthritis”)
Heart (causes inflammation of the whole
layers of the heart – PANCARDITIS) –
Palpitation, chest pain, shortness of breath,
leg swelling, etc.
Skin & subcutaneous tissues (non-itching
macular rash and painless mobile nodules
over joints and spines)
Central Nervous System (a late
manifestation) – abnormal movements of
the limbs with muscle weakness and
emotional labiality.
Diagnostic approach: Modified Jones Criteria
2 major or 1 major + 2 minor manifestations + strep
infection
MAJOR
Carditis – tachycardia out of proportion to degree of
fever
-Cardiomegaly, murmur, muffled heart sounds
-Pericardial friction rub, pericardial pain, changes in
ECG
-Involves endocardium, pericardium, and
myocardium
» Most commonly the mitral valve
Polyarthritis
- Arthritis is reversible and migrates, especially in
large joints (knees, elbow, hips, shoulders, wrists)
- Swollen, hot, red, painful joints, after 1-2 days →
affects different joints
Clinical Manifestations (Modified Jones Criteria)
MAJOR
Erythma marginatum – rash
• Transitory, non pruritic
• Trunk and proximal portion of extremities
• Red macule with clear center wavy, well-
dermacated border
Subcutaneous nodules
• Small nontender nodules
• Bony prominences – hands, feet, elbows,
scalp, scapulae, vertebrae
• Persistent indefinitely after onset of the
disease and resolve with no resulting
damage
St. Vitus Dance – The Fifth Manifestation
(Sydenham’s
Chorea)
• St. Vitus Dance (aka, chorea) reflects CNS
involvement
• Definition: Chorea refers to sudden, aimless
movements of extremities, involuntary facial
grimaces, speech disturbances, emotional
lability and muscle weakness
• Worse with anxiety and relieved by rest
MINOR
• Arthralgia
• Fever
LABORATORY
• Increased ESR, CRP
– Supporting evidence of antecedent group,
A Strep Infection
• Throat c/s, rapid Ag test
• ASO titer (most reliable – 80% children)
• AntiDNAse. ESR, CRP
ECG, CXR – evidence of heart involvement
TREATMENT
Goals:
✓ Eradication of haemolytic strep
✓ Prevention of permanent cardiac
damage
✓ Palliation of other symptoms
✓ Prevention or recurrence of RF
Prevention of RHD
Treatment of streptococcal tonsillitis / pharyngitis
✓ Penicillin G – IM x 1
✓ Penicillin V – oral x 10 days
✓ Sulfa – oral x 10 days
✓ Erythromycin (if allergic to above) – oral x
10 days
Treatment of recurrent RF
– Same as above
Salicylates (ASA) – control inflammatory process
esp. joints, dec fever and discomfort
Bed rest – during febrile phase but need not be
strict
Should be followed medically x 5 years at least
NURSING CONSIDERATIONS
• Encourage compliance with drug
• Encourage adherence to tx’c plan
(+) poor compliance: monthly injections
• Facilitate recovery from illness
• Provide emotional support
• Prevent disease
Interventions during homecare
• Provide rest and adequate nutrition
• Once fever is over, resume moderate
activities, improve appetite
• Carditis: most disturbing and frustrating
manifestation
• Gradual
• Mistaken for nervousness, clumsiness,
inattentiveness
• Limits physical activity
• Stress parents and teachers: illness is
temporary and disappears in time
Rheumatic Heart Disease (RHD)
- Most common complication of RF
- Damage to valves leading to stenosis or
regurgitation with resultant hemodynamic dist.
4.KAWASAKI DISEASE
• Mucocutaneous LN syndrome
• Acute systemic vasculitis
• < 5 y/o (Peak: toddlers)
• Self-limiting but 20% children without
treatment develop
Area involved: CVS
Initially: Inflammation arterioles, venules,
capilliaries → formation coronary artery aneurysm
Death: result of coronary thrombosis or severe scar
formation & stenosis of main coronary artery
Myocardial infarction from thrombosis
No specific diagnostic test
IRRITABILITY – hallmark of Kawasaki Disease
Persists in 2 weeks
- Help family adjust to the disorder
- Educate family
- Help family cope with effects of the disorder
- Prepare child and family for surgery
Surgical Interventions
- Open-Heart
- Closed heart procedures
- Staged procedures
- Prepare child and family for procedures
Postoperative Care of the Child
- Monitor vital signs and A/V pressures
- Intraarterial monitoring of BP
- Intracardiac monitoring
- Respiratory needs
- Rest, comfort and pain management
- Fluid management
- Progression of activity
Postoperative Complications
CHF – due to excessive pulmonary blood flow or
fluid overload
Hypoxia – inadequate pulmonary blood flow /
respiratory problems
Dysrythmias
- Early post op period
- Due to electrolyte imbalance (hypokalemia)
& surgical intervention to septum /
myocardium
- ECG pattern, apical pulses x 1 minute
Cardiac tamponade
- Compression of heart by blood and other
effusion (clots) in pericardial sac → restricts
normal heart movement
- Rising and equalizing RA and LA pressures,
narrowing pulse pressure, tachycardia,
dyspnea, apprehension, abrupt stop to
chest tube drainage from mediastinal tubes
- 2-D echo to confirm the diagnosis
Decreased cardiac output syndrome
Signs of Shock: decreased BP, decreased pulse
pressure,
cool extremities, metabolic acidosis, oliguria
Aggressively treated with IV inotropes (dopamine,
dobutamine, milrinone)
Decreased peripheral perfusion
Capillary refill time, skin color, warm/cold
extremities, pulses (strong/weak)
Pulmonary changes
Areas of atelectasis common after Sx
Treatment: Pericardiocentesis
6 criteria
1.fever 5days or more
2. Polymorphous rashes
3. Bilateral conjunctivitis without exudates
4. Cervical lymph node
5. Changes mucous membrane - strawberry
younger peeling of skin
3 stages
1. Acute stage last for the 1st to 10 days of illness;
give immunoglobulin
2. Subacute stage
3. Convalescent