Download Cardiovascular Alterations

Cardiovascular Alterations
NUR 264
Pediatrics
Angela J. Jackson, RN, MSN
Cardiovascular Alterations:
Developmental Differences
Heart sounds are higher pitched
Pulse rate is higher
Chest wall is thinner because of lack of
subcutaneous tissue and muscle
Cardiac output is dependent on heart
rate until 5 years old
Systolic murmur maybe present with
fever and anemia without heart disease
Fetal Circulation
Foramen ovale
closes shortly after
birth
Ductus venosus
closes when
umbilical cord is
clamped
Ductus arteriosus
closes within 24
hours of birth
Congenital Heart Defects:
Acyanotic Disorders
Acyanotic: oxygenated blood shunts from left
to right where it mixes with unoxygenated
blood
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Atrial septal defect
Ventricular septal defect
Patent ductus arteriosus
Atrioventricular canal
Coarctation of the aorta
Aortic stenosis
Pulmonic stenosis
Congenital Heart Defects:
Cyanotic Disorders
Cyanotic: unoxygenated blood shunts from
right to left where it mixes with oxygenated
blood. Blood pumped through aorta to
peripheral tissues has decrease oxygen
resulting in cyanosis
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Tetralogy of Fallot
Tricuspid atresia
Transposition of great arteries
Truncus arteriosus
Hypoplastic left heart syndrome
Congenital Heart Defects:
General Clinical Manifestations
Chest enlargement or asymmetry
Abnormal heart sounds: murmurs
Abnormal B/P readings
Increased pulse and respirations
Weak, muffled cry in infants
Poor exercise tolerance, especially with feedings
Posturing dyspnea with activity or stress
Cyanosis: mucous membranes, nail beds, lips,
extremities, decreased cap refill, doesn’t pink with O2
administration
Congenital Heart Defects:
General Clinical Manifestations
Clubbing of fingers and toes @ 1-2 years of age in
response to hypoxia
CHF: early signs – tachypnea, dyspnea, retractions,
grunting, tachycardia, diaphoresis on upper lip and
forehead late signs – hepatomegaly, edema. Risk of
left-sided heart failure
Polycythemia
Poor feeding, poor growth
Squatting
Frequent respiratory infections
Congenital Heart Defects:
Nursing Care
Monitor vital signs
Provide O2 to keep saturations at prescribed
level
Adequate nutrition:
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Infants: small frequent feedings, burp frequently,
provide extra calories (24 calories /oz), soft nipple
for bottle feeding, bottle for 20 minutes then tube
feed rest of formula, feed before hungry to avoid
crying.
Children: avoid empty calorie foods, well-balanced
meals, healthy snacks
Congenital Heart Defects:
Nursing Care
Prevent cold stress
Decrease energy expenditure: plan nursing care to
allow for rest, prevent crying
Skin care: decreased blood flow to periphery
Medication administration: cardiac drugs, diuretics,
anticoagulants, antibiotic prophylaxis
Position: knee-chest, DO NOT interfere with
squatting
Prepare family and client for diagnostic studies,
surgery
Promote growth and development
Teach parents to treat child normally, use discipline,
don’t overprotect
Congenital Heart Defects:
Nursing Care
Cardiac Catheterization Care:
 Cardiac Cath may be performed to obtain pressure
gradients, O2 concentrations
 Pre-op: NPO 4-6 hours prior to procedure, obtain
consent, check pulse strength, educate
parents/child about procedure
 Post-op care: keep extremity straight, check
pressure dressing on site, check pulse distal
to site, NO BP on extremity, do
neurovascular checks on extremity, monitor
for dysrhythmias, hematoma, thrombus
formation, infection. Monitor I&O as contrast
medium may cause diuresis
Cardiovascular Alterations:
Atrial Septal Defect (ASD)
Abnormal
connection between
the right and left
atria
Accounts for
approximately 7% of
all congenital heart
disease
ASD: Pathophysiology
Normal increased pressure on the left
side of the heart causes blood to flow
from left to right through the ASD
Leads to increased volume on the right
side of the heart
Increase in right atrial, right ventricular
and pulmonary artery size
ASD: Clinical Manifestations
Usually asymptomatic
May have a soft systolic murmur
May have a widely split S2, unaffected
by respiratory pattern (increased blood
flow prolongs right ventricular
emptying, causing a delay in pulmonic
valve closure)
ASD: Diagnosis
Physical exam (detection of a murmur)
Chest x-ray (increased heart size)
Echocardiogram identifies the location
and size of the defect
ASD: Treatment
Diuretics may be given preoperatively for
symptoms of CHF
The defect may close spontaneously during
the first 2 years of life
Surgery is performed in the preschool age
child
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Defect is stitched closed or patched
Insertion of an implantable umbrella through a
large femoral vessel may also be an option
Main complications of repair are atrial arrhythmias
or heart block
Ventricular Septal Defect
(VSD)
An abnormal
connection between
the right and left
ventricles
May be located in
various positions
along the septum
Most common
congenital heart
defect
VSD: Pathophysiology
Normally increased pressure on the left side
of the heart causes blood shunt from left to
right through the VSD
The blood recirculates through the pulmonary
artery to the lungs
Increased pulmonary blood flow leads to left
heart enlargement and pulmonary venous
congestion
The degree of shunting depends on the size
of the defect and pulmonary resistance
VSD: Clinical Manifestations
An infant with a small VSD may be
asymptomatic
Moderate to large defects result in CHF
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Tachypneic
Diaphoretic
Easily fatigued
Underweight for age
Poor feeding (tires before a feeding is completed)
VSD: Diagnosis
Physical exam
Loud, harsh pansystolic murmur
heard best at the left lower sternal
border
Chest x-ray reveals cardiomegaly with
an increase in pulmonary blood flow
Echocardiogram identifies the size and
location of the defect
VSD: Treatment
75-80% of small VSD close in the first two
years of life
Large defects are unlikely to close
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Treated medically for first few months
Digoxin and diuretics for symptoms of CHF
High calorie formula for growth
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May need NGT feedings
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Surgical repair
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Performed between 3 and 12 months of life
Earlier in infants with failure to thrive
Defect is closed with a patch of the child’s own pericardium
Patent Ductus Arteriosus
(PDA)
The ductus
arteriosus
remains open
Incidence in preterm
infants: 45%
Incidence in term
infants: 5-10&
PDA: Pathophysiology
Left to right shunt
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Blood from high pressure aorta flows
directly to low pressure pulmonary artery
Degree of shunting depends on size of
defect, as well as pulmonary vascular
resistance
Increased pulmonary blood flow can
contribute to CHF
PDA: Clinical Manifestations
and Diagnosis
Clinical manifestations
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Small PDA: asymptomatic
Large PDA: signs and symptoms of CHF
Diagnosis
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Continuous murmur best heard below the
left clavicle
Normal chest x-ray
Diagnosed with echocardiogram
PDA: Treatment
May be closed with infusion of
indomethacin in preterm infants
Surgical closure in full-term,
symptomatic infants
Elective closure in older, asymptomatic
children before age 5
Pulmonary Stenosis
Narrowing of the
pulmonary valve and
obstruction to blood
flow from the right
ventricle to the lungs
Obstruction may be:
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At the valve (Valve
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Before the valve
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After the valve
stenosis)
(subvalve stenosis)
(supravalve stenosis)
Pulmonary Stenosis:
Pathophysiology
Right ventricular pressure increases
because of obstruction of blood flow
from the RV to the pulmonary artery.
This may result in RV failure
Decreased amount of blood flow is able
to get to the lungs
Increased exertion may result in
cyanosis
Pulmonary Stenosis: Clinical
Manifestations and Diagnosis
Clinical Manifestations
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Mild to moderate PS may be asymptomatic
Severe PS: dyspnea upon exertion, fatigue,
cyanosis
Murmur discovered on physical exam
Diagnosis
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Physical exam
Chest x-ray normal (severe PS may have
cardiomegaly)
Echocardiogram demonstrates size and function of
RV and anatomy of pulmonary valve
Pulmonary Stenosis:
Treatment
Neonates with critical PS require
infusion of prostaglandins to maintain
patency of the ductus arteriosus in
order to provide adequate blood flow to
the lungs until surgery can be
performed
Surgical repair
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Balloon valvuloplasty performed in the cardiac
catheterization lab
Surgical valvotomy
Tetralogy of Fallot
Made up of four
components
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VSD
Pulmonary stenosis
Right ventricular
hypertrophy
Overriding aorta
Degree of pulmonary
stenosis is the most
important component
Most common cyanotic
heart defect
Tetralogy of Fallot:
Pathophysiology
Large VSD leads to equal pressures in
right and left ventricles
Amount of pulmonary blood flow and
the amount of cyanosis is dependant on
the degree of pulmonary stenosis
Tetralogy of Fallot: Clinical
Manifestations and Diagnosis
Clinical Manifestations
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Dependant upon degree of PS, may be mildly or
profoundly cyanotic
Loud systolic murmur noted at birth
Hypercyanotic spells (“tet spells”) may be
brought on by crying, feeding or defecating
Diagnosis
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Echocardiogram
Chest x-ray often normal. May exhibit bootshaped heart
Tetralogy of Fallot: Treatment
Preoperative management of hypercyanotic spells:
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Place infant in knee-chest position. (Older children will squat)
this decreases systemic venous return of unoxygenated blood and
increases systemic vascular resistance, reducing right to left
shunting and allowing more blood flow to the lungs
Children in the hospital may be treated with morphine to relieve
symptoms of agitation and break the cycle of hyperpnea. Other
treatment includes: IV fluids to decrease blood viscosity,
supplemental O2, IV phenylephrine to increase systemic vascular
resistance.
Infants with multiple hypercyanotic spells may need a palliative
modified Blalock-Taussing (BT) shunt to assure pulmonary blood
flow until complete surgical repair is performed
Tetralogy of Fallot: Treatment
Surgery:
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Performed between 6 and 12 months of
age
The pulmonary artery is widened and the
VSD is closed
If a BT shunt is in place, it is taken down
or occluded at the time of the definitive
repair
Aortic Stenosis (AS)
Narrowing of the aortic
valve
Causes obstruction to
left ventricular outflow
Increased afterload
Increased ventricular
work
Left ventricular
hypertrophy
AS: Clinical Manifestations and
Diagnosis
Clinical Manifestations
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Infants usually grow normally, diagnosis made when older
child is referred for evaluation of a murmur. Older children
may also have:
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Exertional fatigue
Dyspnea
Angina
Syncope with severe AS
Diagnosis
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Physical exam
Echocardiogram
LV and aorta pressure gradients (less than 25 mm Hg are
considered mild)
Aortic Stenosis: Treatment
Infants:
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administration of prostaglandins to
keep the ductus arteriosus open
Aortic valvotomy
Children:
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Balloon valvuloplasty
Valve replacement
Hypoplastic Left Heart Syndrome
(HLHS)
Lack of development
of the left ventricle
secondary to mitral
valve atresia or
aortic atresia
Small, hypoplastic
left ventricle not
capable of any
cardiac function
HLHS: Clinical Manifestations and
Diagnosis
Clinical Manifestations
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Cyanosis develops within hours of birth
Hypotension, tachycardia, cyanosis,
tachypnea
One-third will present in cardiovascular
collapse
Diagnosis
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Physical exam
Echocardiogram
HLHS: Treatment
Three treatment options
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No intervention
Cardiac transplantation
Palliative surgery
Acute Rheumatic Fever
Autoimmune reaction to an untreated
or partially treated group A
streptococcal pharyngitis
Develops 2-6 weeks after infection
Three organ systems affected: heart,
central nervous system and the
joints
Acute Rheumatic Fever:
Clinical Manifestations
Valvulitis: inflammation of the heart valves – one of
the most significant clinical features. New systolic
murmur reflects mitral regurgitation
Polyarthritis: most frequent benign major
manifestation. Arthritis is migratory, there is
tenderness, pain, swelling, heat and limitation of
movement in the affected joints
Erythema marginatum: fine, pink rash noted on the
trunk and extremities, becomes more pronounced
with heat. Always seen with carditis or polyarthritis
Subcutaneous nodules: firm, painless nodules over
the extensor surfaces of the elbows, knees and
wrists. Always accompany carditis
Acute Rheumatic Fever:
Diagnosis
Physical examination
Laboratory findings
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Elevated sed rate and C-reactive protein
(inflammation)
ASO titers, anti-DNAse B (detects strep
infection)
EKG
ECHO: most sensitive tool for diagnosis of
valvar disease
Acute Rheumatic Fever:
Treatment
Penicillin for eradication of strep
bacteria
Aspirin as an anti-inflammatory agent
Bedrest until inflammation has resolved
Repeat ECHO
Antibiotic prophylaxis
Frequent follow-up
Kawasaki Disease
(Acute Systemic Vasculitis)
Vasculitis of multiple systems in the body, especially
the coronary arteries
First 10 days of the disease: infiltration of vessel
walls with inflammatory cells causing inflammation
and hypertrophy of blood vessels.
Day 10 to day 40, decrease in inflammation.
Vessels have undergone destructive changes.
Coronary artery aneurysm can develop
After 40 days, progressive fibrosis and healing of
coronary artery abnormalities occurs. Aneurysms
and dilation usually regress in one to two years
Kawasaki Disease: Clinical
Manifestations
Abrupt onset of high fever lasting more than 5 days
Conjunctival infection, photophobia
Diffuse red rash
Red strawberry tongue, cracked red lips
Hands and feet swollen, palms and soles red, tips of
fingers and toes peel, progressing to palms and soles
Cervical lymphadenopathy
Tachycardia, gallop rhythm, CHF
Irritability
Painful joints, aseptic meningitis, sterile pyuria,
diarrhea
Kawasaki Disease: Diagnosis
Physical exam
Elevated WBC, sed rate, platelet count
Pyuria
Elevated liver function tests
ECHO for coronary aneurysms
Kawasaki Disease: Treatment
IV immune globulin: 2gm/kg IV over 10-12
hours, may repeat with 1gm/kg)
Aspirin 100mg/kg/day in 4 divided doses
until fever subsides, then 3-5mg/dg daily for
6-8 weeks
Solu-medrol may be used with IVIG
Coumadin if aneurysms >8mm
Thrombolytics for vessel occlusion
Coronary angioplasty, coronary artery bypass
and graft or heart transplant for severe
coronary artery disease
Kawasaki Disease: Nursing
Considerations
VS, I%O, daily weight
Supportive treatment – analgesics, fever
reduction, soft foods, fluids, monitor calories
Assess for S/S of CHF
IVIG administration, monitor VS and side
effects
Parental involvement
Discharge planning for medication
administration, follow-up with cardiologist
Questions?