Module 5 – Pediatric Cardiac Disorders
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Transcript Module 5 – Pediatric Cardiac Disorders
Pediatric Cardiac Disorders
http://www.rnceus.com
http://www.childrensheartinstitute.org/
http://depts.washington.edu/physdx/heart/de
mo.html
http://www.texasheart.org/education/cme/exp
lore/events/eventdetail_5469.cfm
http://www.med.ucla.edu/wilkes/inex.htm
http://www.texasheart.org/education/cme/exp
lore/events/eventdetail_5469.cfm
http://www.youtube.com/watch?v=J2R8MOo
Qtd8&NR=1
Day 15
Day 20
Day 22
Day 24
Day 28
Day 33
Day 37
Day 50
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Fetal Circulation
Main Blood Flow
Placenta Umbilical
Vein Liver Ductus
Venosus Inferior
Vena Cava
Vena Cava Right
Atrium Foramen
Ovale Left Atrium
Left Ventricle
Aorta Body
Fetal Circulation
Secondary Route:
Right Atrium
Right Ventricle
Pulmonary Artery
Ductus Arteriosus
(so does not go to lungs)
Aorta
Body
Fetal Circulation
Third route of blood flow
Right Atrium
Right Ventricle
Pulmonary Artery
Lungs (needs to perfuse the
lungs and upper body with
oxygen)
Left Atrium
Left Ventricle
Aorta
Body
Transition from Fetal Circulation to
Pulmonary circulation
The umbilical arteries and vein and the ductus
venosus become non-functional
Decreased pulmonary vascular resistance and
increased pulmonary blood flow
Increase in pressure of the left atrium, decrease
pressure in right atrium, causing closure of
foramen ovale.
Pulmonary resistance is less than systematic
resistance so there is left-to-right shunting
resulting in closure of the ductus arteriosus.
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Infants increase cardiac output by increasing
rate.
In young children, heart rate is usually higher
and stroke volume is lower than in adults.
Sinus arrhythmias are normal findings in
infants.
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Chest wall is thinner in children than in adults,
with little musculature.
Tip of xiphoid process may protrude slightly.
Point of maximal impulse is located at the 4th
intercostal space in the child younger than 7
years old.
Apical impulse may be visible in children.
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Assessment
History
Physical
Diagnostic
Diagnostic Data
CBC
Chest x-ray
Pulse oximetry
ECG
Echocardiography
Cardiac Cath
MRI
Angiography
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Congestive Heart Failure
Congestive heart failure
The inability of the myocardium to circulate
enough oxygenated blood to meet the
demands of the body.
When the heart fails, cardiac output is
diminished. Heart rate, preload,
contractitility, and afterload are affected.
Peripheral tissue is not adequately
perfused.
Congestion in lungs and periphery
develops.
Etiology and Pathophysiology
Congenital defects – allow blood to flow from
the left side of the heart to the right so that
extra blood is pumped to the pulmonary
system rather than through the aorta when the
ventricle contracts.
Obstructive congenital defects – restricts the
flow of blood so the heart hypertrophies to
work harder to force blood through the
narrowed structures. The hypertrophied
muscle becomes ineffective.
Other defects which weaken the heart muscle.
Compensatory Mechanisms
Stimulation of the sympathetic nervous system
which releases norepinephrine from the adrenals.
This stimulates blood vessels to constrict and an
increase in the heart rate.
Tachycardia increases venous return to the heart
which stretches the myocardial fibers and
increases preload. Only successful for short
period of time.
Increased renin and ADH secretion caused by
decrease renal perfusion. Resultant increase in
Na and H2O retention to increase fluid to the
heart and leading to edema
CHF in Children
Impaired myocardial function
Tachycardia
Diminished pulses
Capillary refill > 2 seconds
Pallor
cool extremities;
Hypotension
Oliguria
Slide 23
CHF in Children
Pulmonary congestion
Tachypnea
Dyspnea – even @ rest
respiratory distress– like what????
exercise intolerance
cyanosis
Slide 24
CHF in Children
Systemic venous congestion
periorbital edema
Peripheral edema
weight gain
ascites
hepatomegaly
Slide 25
CHF in Children
High Metabolic Rate
Failure to Thrive
Slow weight gain
Clinical Manifestations
1.
2.
3.
4.
5.
6.
7.
Pump Fails – cannot meet the demands of the
body = CHF
How do you know when something is wrong?
Tires easily during feeding
Periorbital edema, weight gain
Rales and rhonchi
Dyspnea, orthopnea, tachypnea
Diaphoretic / sweating
Tachycardia
Weight
Pathophysiology of CHF
Slide 28
Treatment of Congestive Heart Failure
Medication Therapy
Digoxin– increases contractility and decreases
heart rate.
Heart Rate Parameters??????
ACE-inhibitors - arterial vasodilator / afterload
reducing agent
Diuretics - enhance renal secretion of sodium and
water by reducing circulating blood volume and
decreasing preload.
Beta Blocker - increases contractility
Treatment of Congestive Heart Failure
Diet – ????? sodium, small frequent feedings
(be sure you can pick the right foods for a low NA diet.
Nursing care:
Measure intake and output – weighing diapers
Observe for changes in peripheral edema and
circulation
If ascites present – take serial abdominal
measurements to monitor changes.
Skin care
Turning schedule
Congenital Cardiac Anomalies
Defects that increase pulmonary
blood flow
Patent Ductus Arterious
Atrial septal defects
Ventricular septal defects
Atrial Septal Defect
1. Oxygenated blood is shunted
from left to right side of the
heart via defect
2. A larger volume of blood
than normal must be
handled by the right side of
the heart hypertrophy
3. Extra blood then passes
through the pulmonary
artery into the lungs,
causing higher pressure
than normal in the blood
vessels in the lungs
congestive heart failure
Treatment
Medical Management
Cardiac Catheterizaton
Medications – digoxin
Amplatzer septal occluder
Open-heart Surgery
Cardiac Catheterization
Pre-care:
History and Physical
Lab work – EKG, ECHO cardiogram, CBC
NPO
Preprocedural teaching
Post Care:
Monitor vital signs
Monitor extremity distal to the catheter instertion,
Keep leg immobilized
Vital signs
Check for bleeding at insertion site
Measure I&O
Treatment
Device Closure – Amplatzer septal
occluder
During cardiac catheterization the occluder is placed in the
Defect
Ventricular Septal Defect
1. Oxygenated blood is shunted
from left to right side of the
heart via defect
2. A larger volume of blood
than normal must be
handled by the right side of
the heart hypertrophy
3. Extra blood then passes
through the pulmonary
artery into the lungs,
causing higher pressure
than normal in the blood
vessels in the lungs
congestive heart failure
Treatment
Surgical repair with a patch inserted
Patent Ductus Arteriosus
1. Blood shunts from
aorta (left) to the
pulmonary artery
(right)
2. Returns to the lungs
causing increase
pressure in the lung
3. Congestive heart
failure
Treatment for PDA
Medical Mangement
Medication
Indomethacin - inhibits prostaglandin‘s
Promotes closure of the ductus
arteriosus
Surgery
Ligate the
ductus arteriosus
Treatment for PDA
Cardiac Catheterization
Insert coil – tiny fibers
occlude the ductus
arteriosus when a
thrombus forms in
the mass of fabric and
wire
Defects with decrease pulmonary
blood flow and mixed defects
Pulmonic stenosis
Tetralogy of fallot
Transposition of the great arteries
Truncus arteriosus
Pulmonic Stenosis
Narrowing of entrance that
decreases blood flow
Treatment:
Medications – Prostaglandin E 1 to keep the
PDA open
Cardiac Catheterization
Baloon Valvuloplasty
Surgery
Valvotomy
Tetralogy of Fallot
Four defects are:
1.
2.
3.
4.
Signs and Symptoms
1.
Failure to thrive
2.
Squatting
3.
Lack of energy
4.
Infections
5.
Polycythemia
6.
Clubbing of fingers
7.
Cerebral absess
8.
Cardiomegaly
Treatment
Surgical interventions
Blalock – Taussig or Potts procedure –
increases blood flow to the lungs.
Open heart surgery
Transposition of Great Vessels
Aorta arises from the right
ventricle, and the pulmonary
artery arises from the left
ventricle - which is not
compatible with survival
unless there is a large defect
present in ventricular or
atrial septum.
artery
aorta
Truncus arteriosus
A single arterial trunk
arises from both
ventricles that supplies
the systemic,
pulmonary, and
coronary circulations. A
vsd and a single,
defective, valve also
exist.
Entire systemic
circulation supplied from
common trunk.
Defects obstructing Systemic blood
flow
•
•
Aortic stenosis
Coarctation of the Aorta
Coarctation of the Aorta
1. Narrowing of Aorta causing
obstruction of left
ventricular blood flow
2. Left ventricular hypertrophy
Signs and Symptoms
1.
B/P in upper extremities
2.
B/P in lower extremities
3.
Radial pulses full/bounding and
femoral or popliteal pulses weak
or absent
4. Leg pains, fatigue
5.
Nose bleeds
Treatment
Goals of management are to improve ventricular
function and restore blood flow to the lower body.
Medical management with Medication
A continuous intravenous medication,
prostaglandin (PGE-1), is used to open the ductus
arteriosus (and maintain it in an open state)
allowing blood flow to areas beyond the
coarctation.
Baloon Valvoplasty
Surgery for Coarctation of Aorta
1. Resect
narrow
area
2. Anastomosis
Ask Yourself ?
Laboratory analysis on a child with Tetralogy
of Fallot indicates a high RBC count. The
polycythemia is a compensatory mechanism
for:
a. Tissue oxygen need
b. Low iron level
C. Low blood pressure
d. Cardiomegaly
Acquired Cardiac Diseases
RHEUMATIC FEVER
A systemic inflammatory (collagen) disease of
connective tissue that usually follows a group A
beta-hemolytic streptococcus infection.
This disorder causes changes in the entire heart
(especially the valves), joints, brain, and skin
tissues.
Rheumatic Fever
Assessment
Jones Criteria
Major
Minor
Treatment
Antibiotic Therapy
Aspirin
MAJOR Manifestations
Carditis
Polyarthritis
Chorea
Erythema Marginatum
Subcutaneous nodules
MINOR
Arthralgia
Fever
ESR
C-reactive protein
Prolonged PR Interval
59
Subacute Bacterial Endocarditis /
Ineffective Endocarditis:
Microorganisms grow on the
endocardium, forming vegetations,
deposits of fibrin, and platelet thrombi.
The lesion may invade adjacent tissues
such as aortic and mitral valves.
Subacute Bacterial Endocarditis /
Ineffective Endocarditis:
Assessment
Diagnosis – blood cultures
Treatment
Antibiotics
Patient teaching – take antibiotics prior to
surgery, dental work, etc.
Kawasaki Disease
Multisystem vasculitis – inflammation of
blood vessels in the body especially the
coronary arteries with antigen-antibody
complexes.
Kawasaki Disease
Signs and Symptoms / Treatment
Three Phases of clinical manifestations:
Acute
Subacute
Convalesant
Treatment
Aspirin
Gamma Globulin
Nursing Care
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Kawasaki Disease
Which phase of Kawasaki is this child
exhibiting?
Inflamed, Cracked,
Peeling Lips
Strawberry tongue
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Promote adequate cardiac output and
oxygenation
Position
Neck slightly
hyperextented to
keep airway open
Knee-chest or
squatting to relieve
“Tet” spells
77
Promote adequate cardiac output and
oxygenation
Pharmacologic
agents
Digoxin
Vasodilators
ACE inhibitors
78
Reduce workload of heart to conserve
energy
Avoid extremes of temperature
Organize care
Semi-folwer’s position
Feed no longer than 30 minutes
Diuretics if ordered
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Energy is conserved which reduces
workload of the heart
Vital signs within parameters for
the child’s age, weight, height
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Promote adequate nutrition
Low sodium formulas
High calorie with low volume
I&O
Gavage feedings if needed
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Prevent infection
Standard precautions
Limit contacts with crowds
Report early signs & symptoms of
infection
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Promote optimal growth &
development
(Outcome)
Fluid and caloric requirements are met to
enable physical growth to progress at
consistent rate.
Development progresses.
83
Meet teaching needs of patient, family
(Outcome)
Family and child demonstrate adequate coping
mechanisms to deal with CHD.
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Fluid and caloric requirements are met to
enable physical growth to progress at a
consistent rate.
The child/family verbalize understanding of the
type of CHD, its treatment and prognosis.
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Preparing Children for Surgery
Infants
Separation from parents
Stranger Anxiety
Toddlers
Need visuals
Preschool
May view as punishment
Misconceptions about happenings in
surgery
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School Age
Adolescent
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What materials would you use to
teach
Preschool age
School age
Adolescent
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