cardiac disorder pedia
TRANSCRIPT
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Cardiac Lecture
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Cardiac
Ball & Bindler
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Focused Health History
Family history of defects / early cardiac
disease / siblings with defects
Maternal history of stillborns or miscarriages
Congenital anomalies / genetic anomalies /
fetal alcohol syndrome / Down Syndrome and
Turner Syndrome
Maternal exposure to rubella
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Focused Health History
Heart murmur
Tires while eating
Low weight for height
Sweats while eating (diaphoretic)
Cyanosis, worsens with feeding or activity
level
Irritable weak cry
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Focused Health History
In the older child additional symptoms may
include:
Chest pain
Decreased activity level
Syncope
Slight of build
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Focused Physical Assessment
General appearance
Integumentary system
Face, nose, and oral cavity
Thorax and lung
Cardiovascular system
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Heart Sounds
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Heart Murmurs
These sounds are produced by blood passing
through a defective valve, great vessel, or
other heart structure.
Murmurs are classified by: intensity, location,radiation, timing, and quality.
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Pulses
Alert:
Weaker pulses or lower blood pressure in the
lower extremities may indicate coarctation of
the aorta (COA)
Bounding pulses can indicate a patent ductus
arteriosus (PDA) or aortic insufficiency.
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Vital Signs
Heart rate: tachycardia in the absence of
fever, crying, or stress may indicate cardiac
pathology.
Tachypnea, even with rest, chest retractionsindicate respiratory distress, possibly
resulting from congestive heart failure
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Knee-chest Position
Child with a cyanotic heartdefect squats (assumes a knee-chest position) to relievecyanotic spells. Some times called tet spells. Ball &
Bindler
Nurse puts infant in knee-chestposition. Whaley & Wong
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First Breath
Pulmonary alveoli open up
Pressure in pulmonary tissues decreases
Blood from the right heart rushes to fill the
alveolar capillaries Pressure in right side of heart decreases
Pressure in left side of heart increases
Pressure increases in aorta
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Treatment Modalities
Palliative procedures
Pulmonary artery banding
Shunts
Corrective procedures
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Diagnostic Test
Chest x-ray to define silhouette of the heart. Heart size, shape, pulmonary markings, and
cardiomegaly.
Electrocardiogram ECG or EKG to defineelectrical activity of the heart.
Echo-cardiogram to visualize anatomicstructures.
Non-invasive
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Cardiac Conduction
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Echo-Cardiogram
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Cardiac Catheterization
An invasive test to diagnose or treat cardiac
defects.
Visualizes heart and vessels.
Measures oxygen saturation of chambers.
Measures intra-cardiac pressures.
Determines muscle function and pumping action
of the heart.
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Toxicity to Dye
Watch for signs of toxicity to the dye usedduring the procedure. Increased temperature
Urticaria Wheezing
Edema
Dyspnea
Headache*Allergy response
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Pre-cardiac Catheterization
Assess vital signs with blood pressure.
Hemoglobin and hematocrit
Pedal pulses
NPO
Hold digoxin
IV if child is polycythemic
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Post-cardiac Catheterization
Vital sign, with apical pulse, and blood
pressure q 15 minutes for first hour.
Apical pulse for 1 minute to check for
bradycardia or dysrhythmias.
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Post-cardiac Catheterization
Assess pulses below the cath site.
Record quality and symmetry of pulses.
Assess temperature and color of affected
extremity.
Check dressing for bleeding or hematoma
formation.
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Home Care Instructions
Keep dressing in place for 24 hours.
Keep site dry and clean.
Observe site for redness, swelling, drainage,
or bleeding. Check temperature.
Avoid strenuous exercise.
Acetaminophen for pain. Keep follow-up appointment
Pre-procedure medications as ordered.
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Left to Right Shunt
Pressures on the left side of the heart are
normally higher than the pressures in the
right side of the heart. If there is an abnormal
opening in the septum between the right andleft sides, blood flows from left to the right.
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Left to Right Shunt
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Clinical Manifestations
Dyspnea and pulmonary edema due to the
lungs receiving blood under high pressure
from the right ventricle.
Increased number of respiratory infections
due to blood pooling in the the lungs
promoting bacterial growth.
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Right to Left Shunts
Occurs when pressure in the right side of the heart
is greater than the left side of the heart.
Resistance of the lungs in abnormally high
Pulmonary artery is restricted
Deoxygenated blood from the right side shunts to
the left side
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Right to Left Shunt
Hole in septum + obstructive lesion =
Deoxygenated blood from the right side of the
heart shunts to the left side of the heart and
out into the body.
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Clinical Manifestations
Hypoxemia = the result of decreased tissue
oxygenation.
Polycythemia = increased red blood cell
production due to the bodys attempt tocompensate for the hypoxemia.
Increase viscosity of the blood = heart has to
pump harder.
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Potential Complications
Thrombus formation due to sluggish
circulation.
Brain abscess or stroke due to the un-
oxygenated blood bypassing the filteringsystem of the lungs.
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Heart Failure
Major manifestation of cardiac disease
Under 1 year of age due to congenital
anomaly
Over 1 year with no congenital anomaly may
be due to acquired heart disease
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Clinical Manifestations of HF
Systemic Venous Congestion
Weight gain, hepatomegaly, edema, jugular vein
distension
Pulmonary Venous Congestion Tachypnea, dyspnea, cough, wheezes
Compensatory Response
Tachycardia, cardiomegaly, diaphoretic, fatigue,failure to grow
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Digoxin Therapy
Digoxin increases the force of the myocardial
contraction.
Take an apical pulse with a stethoscope for 1 full
minute before every dose of digoxin. Ifbradycardia is detected.
< 100 beats / min for infant and toddler
< 80 beats in the older child
< 60 beats in the adolescent
* Call physician before administering the drug.
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Signs of Digoxin Toxicity
Bradycardia
Arrhythmia
Nausea, vomiting, anorexia
Dizziness, headache
Weakness and fatigue
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Interventions
Fluid restriction
DiureticsLasix (potassium wasting) orAldactone (potassium sparing)
Bed rest Oxygen
Small frequent feedingssoft nipple withsupplemental NG for adequate calorie intake
Pulse oximeter
Sedatives if needed
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Feeding
Small frequent feedings
Soft nipple to easy energy needed to suck
24 calorie formula for added calories
NG feed if not taking in adequate calories to
gain weight
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Patent Ductus Arteriosus
PDA
Incidence 10%
One of the most common benign defects
Ductus normally closes within hours of birth
Connection between the pulmonary artery
(low pressure) and aorta (high pressure)
High risk for pulmonary hypertension
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PDA
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Diagnosis and Treatment
Diagnosis by
Chest x-rayenlarged heart and dilated
pulmonary artery
Echo-cardiogramshow the opening betweenpulmonary artery and aorta
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Treatment
Indomethocin given poconstricts the
muscle in the wall of the PDA and promotes
closure
Cardiac Catheterizationcoil is placed in theopen duct and acts like a plug
Closed heart surgerysmall incision made
between ribs on left hand side and PDA isligated or tied and cut
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Atrial Septal Defect
ASD
10% of defects
Blood in left atrium flows into right atrium
Pulmonary hypertension
Reduced blood volume in systemic circulation
If left untreated may lead to pulmonary
hypertension, congestive heart failure or
stroke as an adult.
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ASD
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Diagnosis and Treatment
Diagnosis: heart murmur may be heard in the
pulmonary valve area because the heart is
forcing an unusually large amount of blood
through a normal sized valve. Echocardiogram is the primary method used
to diagnose the defectit can show the hole
and its size and any enlargement of the rightatrium and ventricle in response to the extra
work they are doing.
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Treatment
Surgical closure of the atrial septal defect
After closure in childhood the heart size will
return to normal over a period of four to six
months. No restrictions to physical activity post
closure
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Ventricular Septal Defect
VSD
30% of defects
Opening in the ventricular septum
Left-to-right shunt
Right ventricular hypertrophy
Deficient systemic blood flow
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VSD
Small holes generally are asymptomatic
Medium to moderate holes will cause
problems when the pressure in the right side
of the heart decreases and blood will start toflow to the path of least resistance (from the
left ventricle through the VSD to the right
ventricle and into the lungs) This will generally lead to CHF
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Treatment VSD
CHF: diuretics of help get rid of extra fluid in
the lungs
Digoxin if additional force needed to squeeze
the heart FTT or failure to grow may need higher
calorie concentration
Will need prophylactic antibiotics beforedental procedures if defect is not repaired
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Surgical Repair
Over a period of years the vessels in thelungs will develop thicker wallsthe pressurein the lungs will increase and pulmonaryvascular disease
If pressure in the lungs becomes too high theun-oxygenated blood with cross over to theleft side of the heart and un-oxygenated
blood with enter the circulatory system. If the large VSD is repaired these changes
will not occur.
f A
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Coarctation of Aorta
COA
7 % of defects
Congenital narrowing of the descending aorta
80% have aortic-valve anomalies
Difference in BP in arms and legs (severe
obstruction)
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Di i d T
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Diagnosis and Treatment
In 50% the narrowing is not severe enough to
cause symptoms in the first days of life.
When the PDA closes a higher resistance
develops and heart failure can develop. Pulses in the groin and leg will be diminished
Echocardiogram will show the defect in the
aorta
T
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Treatment
Prostaglandin may given to keep the PDA open to
reduce the pressure changes
The most common repair is resection of the
narrowed area with re-anastomosis of the two ends
Surgical complicationskidney damage due to
clamping off of blood flow during surgery
High blood pressure post surgerymay need to be
on antihypertensives Antibiotic prophylactic need due to possible aortic
valve abnormalities.
T l f F ll (TOF)
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Tetralogy of Fallot (TOF)
6% of defects
Most common cardiac malformation
responsible for cyanosis in a child over 1 year
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TOF
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TOF
Four Components
VSD
Pulmonary stenosisnarrowing of pulmonary
valve Overriding of the aortaaortic valve is enlarged
and appears to arise from both the left and right
ventricles instead of the left ventricle
Hypertrophy of right ventriclethickening of themuscular walls because of the right ventricle
pumping at high pressure
Cli i l M if i
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Clinical Manifestations
Dependent on degree of right ventricular
outflow obstruction.
Right-to-left shunt
Clubbing of digits
tet spells - treated by flexing knees forward
and upward
Severe irritability due to low oxygen levels
Di i
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Diagnosis
Cyanosis
Oxygen will have little effect on the cyanosis
Loud heart murmur
Echocardiogramdemonstrates the four
defects characteristic of tetralogy
T
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Treatment
If oxygen levels are extremely low prostaglandinsmay be administered IV to keep the PDA open
Complete repair is done when the infant is about 6
months of age
Correction includes
Closure of the VSD with dacron patch
The narrowed pulmonary valve is enlarged
Coronary arteries will be repaired Hypertrophy of right heart should remodel within a few
months when pressure in right side is reduced
L T O t
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Long Term Outcomes
Leaky pulmonary valve that can lead to
pulmonary insufficiency
Arrhythmias after surgery
Heart blockoccasionally a pacemaker isnecessary
Periodic echocardiogram and exercise stress
test or Holter evaluation
A ti St i
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Aortic Stenosis
6% of defects
Aortic valve: has two rather than three
leaflets. Leaflets are thickened or fused.
Obstruction of blood flow from left ventricle
Mild symptoms: dizziness, syncope, angina,
fatigue
30% incidence of sudden death
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A ti St i
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Aortic Stenosis
Causes obstruction to blood flow between the
left ventricle and aorta.
Most common form is obstruction of the valve
itself When the aortic valve does not open properly
the left ventricle must work harder to eject
blood into the aorta. Left ventricular muscle becomes
hypertrophied.
Di i
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Diagnosis
Heart murmur or AS is a turbulent noise
caused by ejection of blood through the
obstructed valve.
Electrocardiogram is usually normal Echocardiogram will show the obstruction
and rule out other heart anomalies
Exercise stress testprovides information onimpact of the stenosis on heart function
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Hypoplastic Left Heart
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Hypoplastic Left Heart
One of the most complex defects seen in thenewborn and the most challenging of all the
congenital defects
All the structures on the left side of the heartare severely underdeveloped.
Mitral and aortic valves are either completely
closed or are very smallleft ventricle is tinyaorta is small and often only a few
millimeters in diameter
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HLH
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HLH
Life threatening shock develops when theductus arteriosis closes
Low oxygen saturationswill not increase
with oxygen administration Pulses will be weak in all extremities
Plan to deliver infant in a hospital capable of
providing the aggressive treatment needed
Treatment
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Treatment
Three staged procedure to reconfigure thecardiovascular system
Norwoodright ventricle becomes the systemic
ventricle pumping blood to the body Glenn done at 3-6 months
Fontan done at 2 -3 years of age
Long Term Complications
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Long Term Complications
Easily tiring when participating in sports orother exercises
Formation of blood clotsheparin or
Coumadin use Heart arrhythmiaspace maker
Cardiac failure
Bacterial Endocarditis
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Bacterial Endocarditis
Infection of endocardial surface of the heart
History of CHD, Kawasaki Disease,
Rheumatic Fever, or prosthetic valves are
more susceptible to infection Prophylactic antibiotics with dental care,
throat, intestinal, urinary or vaginal infections
or surgery.
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Kawasaki Disease
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Kawasaki Disease
Acute-self limiting disease
Generalized vasculitis
Peak incidence 6 months to 2 years
More common in males and Japanese
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Clinical Manifestations
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Clinical Manifestations
High fever
Conjunctivitisno drainage
Strawberry tongue
Edema of hands and feed
Reddening of palms and soles
Lymph node swelling
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Edema Hands and Feet
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EdemaHands and Feet
Peeling Finger Tips
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Peeling Finger Tips
Blood Values
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Blood Values
Elevated WBC
Elevated ESR
Elevated platelets
Interdisciplinary Interventions
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Interdisciplinary Interventions
Intravenous gamma globulin
High dose of ASA while in hospital
Low dose ASA upon discharge
Base-line echocardiogram to assess
coronary artery status