Transcript Cardiovascular dysfunction in Children

Chapter 48
Cardiovascular Dysfunction
in Children
Fetal Circulation
Blood enters through the umbilical vein
Oxygenation blood enters the right atrium via the
inferior vena cava
Right atrium is at higher pressure than left in fetal
circulation
Blood from IVC goes straight across to left atrium
Blood from SVC goes down to the right ventricle
Major portion of blood from RV is shunted
through the ductus arteriosis to the descending
aorta
Circulatory Changes at Birth
Pulmonary vasodilatation with the first breath
causes a drop in pulmonary pressure.
Systemic pressure rises with the removal of the
placenta
This causes a closure in the foramen ovale
The ductus arteriosus closes in response to the
increase oxygen in the blood as well as “other
factors”
Page 1558 in text book
Older Classification of CHD
Cyanotic/Acyanotic heart defects
Doesn’t necessarily mean that a child with
acyanotic heart defect will not show
cyanosis at some point
Definition based on whether the flow of
blood is deoxygenated into oxygenated or
oxygenated into deoxygenated
Newer Classification of CHD
Hemodynamic Characteristics
- increased pulmonary blood flow
-decreased pulmonary blood flow
-obstruction of blood flow out of the heart
-mixed blood flow
Classification Chart
Increase Pulmonary Blood Flow
Atrial Septal Defect
Ventricular Septal Defect
Patent Ductus Arteriosus
Atrioventricular Canal Defect
Oxygenated blood returns to the right ventricle
and recirculates to the lungs
Increased blood volume on the right side
Increase pulmonary and decreased systemic
The left to right shut of IPBV
Atrial Septal Defect
Atrial Septal Defect
Some children with small defects are
asymptomatic
Some of these defects (secondum) may
close spontaneously
Surgery may be recommended at school age
to prevent progressive pulmonary
involvement
Ventricular Septal Defect
Ventricular Septal Defect
Can develop into congestive heart failure
and cyanotic heart symptoms.
Remember that blood flows from area of
high pressure to low pressure, if congestive
heart failure occurs pressure in the right
ventricle will become higher and now blood
going from right ventricle will go into left
ventricle
Patent Ductus Arteriosis
Patent Ductus Arteriosis
May go unnoticed in infancy
Dyspnea with full and bounding radial pulse
Wide pulse pressure
Infants may respond to indomethacin drug
therapy for closure
Surgery performed in infancy
At risk for endocarditis and pulmonary
vascular obstructive disease
Obstructive Defects
Obstruct blood flow from the ventricles
because of a narrowing of a vessel
Coarctation of the Aorta
Aortic Stenosis
Pulmonic Stenosis
Coarctation of the Aorta
Coarctation Facts
Increase pressure proximal to the defect and
decreased pressure distal to the defect
Marked difference between blood pressure and
pulses of the upper and lower extremities
Sometimes not detected until late childhood
Screening of newborns: femoral pulses
High risk for hypertension, rupture aorta, aortic
aneurysm or stroke.
Aortic Stenosis
Aortic Stenosis
Narrowing or stricture of the aortic valve
Causes resistance to blood flow in the LV,
decreased cardiac output, left ventricular
hypertrophy and pulmonary vascular congestion
Manifestations: decreased output, faint pulses,
hypotension, tachycardia, poor feeding.
Children show signs of exercise intolerance, chest
pain and dizziness when standing too long
Pulmonic Stenosis
Pulmonic Stenosis
Narrowing at the entrance to the pulmonary
artery
Causes right ventricular hypertrophy and
decreased pulmonary blood flow
Right ventricular failure can result in
eventual reopening of the foramen ovale
and shunting of unoxygenated blood into
the left atrium
Decreased Pulmonary Blood Flow
Unoxygenated blood passes into the aorta or
general circulation.
defined as cyanotic heart disease in the “old
school” method of classifying
Right to left shunting of the blood
Tetralogy of Fallot
Tricuspid Atresia
Tetralogy of Fallot
Stenosis of the
pulmonary valve
Hypertrophy of the
right ventricle
Dextroposition of the
aorta (blood from both
ventricles are entering
it)
VSD
Tetralogy of Fallot
Tetralogy of Fallot
Surgery most likely
Cyanosis increases with age as well as clubbing of
the nails
TET position; Child sits in squatting position to
breath more easily
Polycythemia to compensate for lack of oxygen
TET spells; put infant in TET position to diminish
IV prostaglandin to open ductus arteriosus if
oxygen levels are critically low soon after birth
TET Spell explanation
The arterial oxygen saturation of babies
with tetralogy of Fallot can suddenly
drop markedly. This phenomenon,
called a "tetralogy spell," usually results
from a spasm in the heart that
decreases pulmonary blood flow and
increases right to left shunting.
TET spell care
1577 “Guidelines”
Older children would squat during these
spells to decrease the systemic venous
return and thus increase the systemic
vascular resistance and thus decrease the
right to left shunting.
Tricuspid Atresia
Tricuspid Valve
Closed
ASD
VSD
PDA (sometimes)
Underdeveloped Right
Ventricle
Tricuspid Atresia
Tricuspid Atresia
Mixing of blood on the left side of the heart
Decreased pulmonary blood flow.
Prostaglandin E may be used to keep the
PDA open until surgery is performed. (to
keep pulmonary blood flow going)
Mixed Blood Flow Defects
Complex cardiac anomalies
Transposition of the Aorta
Total anomalous pulmonary venous return
Truncus arteriosus
Hypoplastic left heart syndrome
They are called mixed defects because
survival depends on mixing of blood from
the pulmonary and systemic circulations
within the heart chambers.
Transposition of the Arteries
Transposition of the Aorta
With associated defects
Transposition of the Aorta
Associated defects must be present to
permit life
Most common defect Patent Foramen Ovale
IV prostaglandin to keep ductus arteriosis
patent
Surgery is indicated
Explanation of the ventricles
Even when a good bit of mixing of oxygen-poor (blue)
and oxygen-rich (red) blood can occur, other
problems are present. The left ventricle, which in
TGA is connected to the pulmonary artery, is the
stronger of the two ventricles since it normally has to
generate a lot of force to pump blood to the body.
The right ventricle, connected to the aorta in TGA, is
the weaker of the two ventricles. Because the right
ventricle is weaker, it may not be able to pump blood
efficiently to the body, and it will enlarge under the
strain of the job. The left ventricle may pump blood
into the lungs more vigorously than needed, leading
to strain in the blood vessels in the lungs.
Total anomalous pulmonary
venous return
Total anoumalous pulmonary
venous return
Failure of pulmonary
veins to connect to
Left Atrium
Atrial Septal Defect
Corrective repair in
early infancy
Truncus Arteriosis
Truncus Arteriosis
Blood flows preferentially to lower pressure
pulmonary arteries
Patient at risk for pulmonary vascular
disease due to this
Early repair in first months of life
Hypoplastic Left Heart Syndrome
HLHS four defects
Hypoplastic ascending aorta and aortic
arch.
Hypoplastic left ventricle.
Large patent ductus arteriosus supplying the
only source of blood flow to the body.
Atrial septal defect allowing blood returning
from lungs to reach the single ventricle.
Hypoplastic Left Heart Syndrome
Hypoplastic Left Heart Syndrome
Underdeveloped left ventricle
Aortic Atresia
Blood from Left Atrium flows to Right
through patent foramen ovale
Descending aorta receives blood from the
PDA
Pts become rapidly symptomatic when PDA
closes
Digoxin for the little ones
Lanoxin 50mcg (.05 mg) per ml
Usually given bid after “loading dose”
High risk for toxicity
If more than 1 ml for infant prescribed very high
index of suspicion of wrong dose!
Heart rates <70 child and <90-100 infant
Usually hospital protocol is second practitioner
checking order and amount before administering
See page 1572 home care box for further info
Digoxin Toxicity in children
Gastrointestinal
Nausea
Vomiting
Anorexia
Cardiac
Bradycardia
dysrhythmias
Bacterial Endocarditis
Infection in the valves and inner lining of the heart
Children with CHD at risk due to damage done by
turbulent flow of blood in the heart
Turbulent flow “roughens” the lining making
bacteria stick to it
Procedures in which bacteria enter the blood
stream: dental, tonsillectomy, adenoidectomy,
bronchoscopy, other surgery
Endocarditis manifestations
Fever
Anorexia
Malaise
Weight loss
Extracardiac emboli formation
Splinter hemorrhages, osler nodes, janeway
lesions
Endocarditis management
Prevention; prophylaxis management
Education on early detection
Long term IV antibiotic therapy
Review box 48-8 and 48-9 1584-85
High Risk Conditions
Congenital heart disease (septal defects,
valve disease, cyanotic heart disease)
Acquired valve disease
Prosthetic valve
IV drug use
Previous episode of bacterial endocarditis
Surgical systemic to pulmonary shunts and
conduits
Central venous catheters
Rheumatic Fever Manifestations
Carditis
Polyarthritis
Erythema Marginatum
Chorea
Subcutaneous Nodes
See guidelines page 1585
Erythema Marginatum
Subcutaneous Nodules
Rheumatic Fever Manifestations
Rheumatic Fever Management
Antibiotics to elimination of infection
Long term chemoprophylaxis
Management of heart failure if occurred
Pain relief; anti-inflammatory
Aspirin is drug of choice for joint disease
Skin care due to bed rest
Careful monitoring I/O
Kawasaki Disease
Reactions to toxins produced by previous
infection
Causes inflammation of the vessel walls
often resulting in aneurysm
Manifestations: THINK RED
Kawasaki Disease, manifestations
High fever
Conjunctivitis without discharge
Strawberry tongue
Inflamed mouth
Inflamed pharyngeal membranes
Erythematous skin rash with peeling
Irritability
Enlarged lymph nodes
Swollen joints
Photophobia
Kawasaki Disease
Kawasaki Disease
Kawasaki Disease
Kawasaki Disease, management
IV gamma globulin
Salicylate therapy for antithrombus and anti
inflammatory properties
Warfarin may be prescribed
Postpone immunizations after the
administration of immune globulin
Rheumatic Fever
Affects:
Joints
Heart; scars the mitral valves
CNS
Skin
Subcutaneous Tissues
Is a reaction to group A beta hemolytic
Streptococcus