Transcript Cardiac

Cardiac Lecture
Jan Bazner-Chandler
CPNP, CNS, MSN, RN
Cardiac
Ball & Bindler
Health History
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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
Present Health History
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Heart murmur
Tires while eating
Low weight for height
Sweats while eating (diaphoretic)
Cyanosis, worsens with feeding or activity
level
Irritable weak cry
Health History
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In the older child additional symptoms may
include:
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Chest pain
Decreased activity level
Syncope
Slight of build
Heart Sounds
Heart Sounds
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Use both the bell (for low frequency) and the
diaphragm (for high frequency)
Quality: distinct S1 and S2
Rate matches radial pulse
Intensity
Rhythm
Heart Sounds
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Heart sounds should be crisp and distinct in
children.
S1 is the first heart sound, produced by
closure of the tricuspid and mitral valves
when ventricular contraction begins.
S2 is produced by the closure of the aortic
and pulmonic valves.
Heart Murmurs
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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.
Clubbing of Fingers
Clubbing of Fingers
Whaley & Wong
Bowden text
Knee-chest Position
Nurse puts infant in knee-chest
position.
Whaley & Wong
Child with a cyanotic heart
defect squats (assumes a knee-chest position) to relieve
cyanotic spells. Some times called “tet” spells.
Ball &
Bindler
First Breath
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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
Treatment Modalities
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Palliative procedures
Pulmonary artery banding
Shunts
Corrective procedures
Diagnostic Test
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Chest x-ray to define silhouette of the heart.
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Heart size, shape, pulmonary markings, and
cardiomegaly.
Electrocardiogram to define electrical activity
of the heart.
Echo-cardiogram to visualize anatomic
structures.
Non-invasive
Cardiac Conduction
Cardiac Catheterization
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An invasive test to diagnose or treat cardiac
defects.
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Visualizes heart and vessels.
Measures oxygen saturation of chambers.
Measures intra-cardiac pressures.
Determines muscle function and pumping action
of the heart.
Pre-cardiac Catheterization
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Assess vital signs with blood pressure.
Hemoglobin and hematocrit
Pedal pulses
NPO
Hold digoxin
IV if child is polycythemic
Post-cardiac Catheterization
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Vital sign, with apical pulse, and blood
pressure q 15 minutes for first hour.
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Apical pulse for 1 minute to check for
bradycardia or dysrhythmias.
Toxicity to Dye
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Watch for signs of toxicity to the dye used
during the procedure.
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Increased temperature
Urticaria
Wheezing
Edema
Dyspnea
Headache
*Allergy response
Home Care Instructions
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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.
Post-cardiac Catheterization
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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.
Right to Left Shunts
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Occurs when pressure in the right side of the heart
is greater than the left side of the heart.
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Resistance of the lungs in abnormally high
Pulmonary artery is restricted
Deoxygenated blood from the right side shunts to
the left side
Right to Left Shunt
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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.
Clinical Manifestations
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Hypoxemia = the result of decreased tissue
oxygenation.
Polycythemia = increased red blood cell
production due to the body’s attempt to
compensate for the hypoxemia.
Increase viscosity of the blood = heart has to
pump harder.
Potential Complications
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Thrombus formation due to sluggish
circulation.
Brain abscess or stroke due to the unoxygenated blood bypassing the filtering
system of the lungs.
Left to Right Shunt
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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 and
left sides, blood flows from left to the right.
Clinical Manifestations
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The infant is not cyanotic.
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Tachycardia due to pushing increased blood
volume.
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Cardiomegaly due to increased workload of
the heart.
Clinical Manifestations
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Dyspnea and pulmonary edema due to the
lungs receiving blood under high pressure
from the right ventricle.
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Increased number of respiratory infections
due to blood pooling in the the lungs
promoting bacterial growth.
Congestive Heart Failure
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Major manifestation of cardiac disease.
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Under 1 year of age due to congenital
anomaly.
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Over 1 year with no congenital anomaly may
be due to acquired heart disease.
Cardinal Signs of CHF
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Tachycardia
Cardiomegaly
Tachypnea
Hepatomegaly
Digoxin Therapy
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Digoxin increases the force of the myocardial
contraction.
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Take an apical pulse with a stethoscope for 1 full
minute before every dose of digoxin. If
bradycardia is detected.
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< 100 beats / min for infant and toddler
< 80 beats in the older child
< 60 beats in the adolescent
* Call physician before administering the drug.
Signs of Digoxin Toxicity
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Bradycardia
Arrhythmia
Nausea, vomiting, anorexia
Dizziness, headache
Weakness and fatigue
Interventions
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Fluid restriction
Diuretics – Lasix (potassium wasting) or
Aldactone (potassium sparing)
Bed rest
Oxygen
Small frequent feedings – soft nipple with
supplemental NG for adequate calorie intake
Pulse oximeter
Sedatives if needed
Supplemental Feeding
Infants with cardiac
conditions often require
supplemental feeding
to provide sufficient
nutrients for growth.
Ball and Bindler
Cardiac Heart Defects
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http://www.cincinnatichildrens.org/health/hear
t-encyclopedia/anomalies/
Patent Ductus Arteriosus
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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
Diagnosis and Treatment
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Diagnosis by
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Chest x-ray – enlarged heart and dilated
pulmonary artery
Echo-cardiogram – show the opening between
pulmonary artery and aorta
Treatment
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Indomethocin given po – constricts the
muscle in the wall of the PDA and promotes
closure
Cardiac Catheterization – coil is placed in the
open duct and acts like a plug
Closed heart surgery – small incision made
between ribs on left hand side and PDA is
ligated or tied and cut
Atrial Septal Defect
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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.
Diagnosis and Treatment
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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 defect – it can show the hole
and its size and any enlargement of the right
atrium and ventricle in response to the extra
work they are doing.
Treatment
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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
Ventricular Septal Defect
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VSD
30% of defects
Opening in the ventricular septum
Left-to-right shunt
Right ventricular hypertrophy
Deficient systemic blood flow
VSD
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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 to
flow 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
Diagnosis and Treatment
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Diagnosis – heart murmur – clinical pearl a
louder murmur may indicate a smaller hole
due to the force that is needed for the blood
to get through the hole.
Electrocardiogram – to see if there is a strain
on the heart
Chest x-ray – size of heart
Echocardiogram – shows size of the hole and
size of heart chambers
Treatment VSD
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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 before
dental procedures if defect is not repaired
Surgical Repair
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Over a period of years the vessels in the
lungs will develop thicker walls – the pressure
in the lungs will increase and pulmonary
vascular disease
If pressure in the lungs becomes too high the
un-oxygenated blood with cross over to the
left side of the heart and un-oxygenated
blood with enter the circulatory system.
If the large VSD is repaired these changes
will not occur.
Coarctation of Aorta
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COA
7 % of defects
Congenital narrowing of the descending aorta
80% have aortic-valve anomalies
Difference in BP in arms and legs (severe
obstruction)
Diagnosis and Treatment
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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
Treatment
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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 complications – kidney damage due to
clamping off of blood flow during surgery
High blood pressure post surgery – may need to be
on antihypertensives
Antibiotic prophylactic need due to possible aortic
valve abnormalities.
Pulmonary Stenosis
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PS
7% of defects
Obstruction of blood flow from right ventricle
Hypertrophy of right ventricle
If severe cyanosis due to right-to-left shunt
Pulmonary Valvar Stenosis
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In pulmonary valvar stenosis the pulmonary
valve leads to narrowing and obstruction
between the right ventricle and the pulmonary
artery.
Thickened tissue become less pliable and
increases the obstruction
Right ventricle must work harder to eject
blood into the pulmonary artery.
Diagnosis and Treatment
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Diagnosis: heart murmur is heard – clicking
sound when the thickened valve snaps to an
open position.
Electrocardiogram would be normal
Echocardiogram most important non-invasive
test to detect and evaluate pulmonary
stenosis
Cardiac Catheterization – to measure
pressures and measure the stenosis
Treatment
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Cardiac Catheterization to dilate the valve
and open up the obstruction.
Open- heart procedure would only needed for
more complex valve anomaly.
Tetralogy of Fallot (TOF)
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6% of defects
Most common cardiac malformation
responsible for cyanosis in a child over 1 year
TOF
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Four Components
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VSD
Pulmonary stenosis – narrowing of pulmonary
valve
Overriding of the aorta – aortic valve is enlarged
and appears to arise from both the left and right
ventricles instead of the left ventricle
Hypertrophy of right ventricle – thickening of the
muscular walls because of the right ventricle
pumping at high pressure
Clinical Manifestations
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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
Diagnosis
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Cyanosis
Oxygen will have little effect on the cyanosis
Loud heart murmur
Echocardiogram – demonstrates the four
defects characteristic of tetralogy
Treatment
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If oxygen levels are extremely low prostaglandins
may be administered IV to keep the PDA open
Complete repair is done when the infant is about 6
months of age
Correction includes
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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
Long Term Outcomes
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Leaky pulmonary valve that can lead to
pulmonary insufficiency
Arrhythmias after surgery
Heart block – occasionally a pacemaker is
necessary
Periodic echocardiogram and exercise stress
test or Holter evaluation
Aortic Stenosis
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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
Aortic Stenosis
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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.
Diagnosis
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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 test – provides information on
impact of the stenosis on heart function
Treatment
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Cardiac catheterization – balloon dilation of the
narrowed valve.
Surgical valvotomy if the closed procedure does not
work – often done when patient is older when
severe calcium deposits further obstruct the valve.
Recurrent valve obstruction is a complication and if
valve replacement is done too early the child may
outgrow the valve.
Antibiotic prophylaxis especially if valve replacement
Hypoplastic Left Heart
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One of the most complex defects seen in the
newborn and the most challenging of all the
congenital defects
All the structures on the left side of the heart
are severely underdeveloped.
Mitral and aortic valves are either completely
closed or are very small – left ventricle is tiny
– aorta is small and often only a few
millimeters in diameter
HLH
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Life threatening shock develops when the
ductus arteriosis closes
Low oxygen saturations – will 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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Three staged procedure to reconfigure the
cardiovascular system
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Norwood – right 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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Easily tiring when participating in sports or
other exercises
Formation of blood clots – heparin or
Coumadin use
Heart arrhythmias – pace maker
Cardiac failure
Bacterial Endocarditis
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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.
Kawasaki Disease
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Acute-self limiting disease
Generalized vasculitis
Peak incidence 6 months to 2 years
More common in males and Japanese
http://www.aafp.org/afp/990600ap/3093.html
Clinical Manifestations
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High fever
Conjunctivitis
Strawberry tongue
Edema of hands and feed
Reddening of palms and soles
Lymph node swelling
Edema – Hands and Feet
Peeling Finger Tips
Blood Values
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Elevated WBC
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Elevated ESR
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Elevated platelets
Management
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Intravenous gamma globulin
High dose of ASA while in hospital
Low dose ASA upon discharge
Base-line echocardiogram to assess
coronary artery status