pediatric cardiac disorders. mo.html
TRANSCRIPT
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Pediatric Cardiac Disorders
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http://www.rnceus.com
http://www.childrensheartinstitute.org/
http://depts.washington.edu/physdx/heart/demo.html
http://www.texasheart.org/education/cme/explore/events/eventdetail_5469.cfm
http://www.med.ucla.edu/wilkes/inex.htm
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http://www.texasheart.org/education/cme/explore/events/eventdetail_5469.cfm
http://www.youtube.com/watch?v=J2R8MOoQtd8&NR=1
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Day 15 Day 20 Day 22
Day 24
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Day 28 Day 33
Day 37Day 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
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Fetal Circulation
Secondary Route:
Right Atrium Right Ventricle Pulmonary Artery
Ductus Arteriosus
(so does not go to
lungs)
Aorta Body
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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
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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
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Diagnostic Data
CBC Chest x-ray Pulse oximetry ECG Echocardiography Cardiac Cath MRI Angiography
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Congestive Heart Failure
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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.
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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.
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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
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Slide 23
CHF in Children
Impaired myocardial function Tachycardia Diminished pulses Capillary refill > 2 seconds Pallor cool extremities; Hypotension Oliguria
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Slide 24
CHF in Children
Pulmonary congestion Tachypnea Dyspnea – even @ rest respiratory distress– like
what???? exercise intolerance cyanosis
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Slide 25
CHF in Children
Systemic venous congestion periorbital edema Peripheral edema weight gain ascites hepatomegaly
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CHF in Children
High Metabolic Rate Failure to Thrive Slow weight gain
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Clinical Manifestations Pump Fails – cannot meet the demands
of the body = CHFHow do you know when something is
wrong?
1. Tires easily during feeding2. Periorbital edema, weight gain3. Rales and rhonchi4. Dyspnea, orthopnea, tachypnea5. Diaphoretic / sweating6. Tachycardia7. Weight
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Slide 28
Pathophysiology of CHF
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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
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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
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Congenital Cardiac Anomalies
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Defects that increase pulmonary blood flow
Patent Ductus ArteriousAtrial septal defects
Ventricular septal defects
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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
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Treatment
Medical Management Medications – digoxin
Cardiac Catheterizaton - Amplatzer septal occluder
Open-heart Surgery
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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
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Treatment
Device Closure – Amplatzer septal occluder
During cardiac catheterization the occluder is placed in the Defect
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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
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Treatment
Surgical repair with a patch inserted
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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
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Treatment for PDA
Medical Mangement Medication
Indomethacin - inhibits prostaglandin‘s
Promotes closure of the ductus arteriosus
Surgery
Ligate the ductus arteriosus
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Treatment for PDA
Cardiac Catheterization
Insert coil – tiny fibers occlude the ductus arteriosus when a
thrombus forms in the mass of fabric and
wire
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Pulmonic stenosisTetralogy of fallot
Transposition of the great arteries
Truncus arteriosus
Defects with decrease pulmonary blood flow and
mixed defects
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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
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Tetralogy of Fallot
Four defects are:
1.
2.
3.4.
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Signs and Symptoms1. Failure to thrive
2. Squatting
3. Lack of energy
4. Infections
5. Polycythemia
6. Clubbing of fingers
7. Cerebral absess
8. Cardiomegaly
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Treatment
Surgical interventions Blalock – Taussig or Potts
procedure – increases blood flow to the lungs.
Open heart surgery
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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
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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.
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Defects obstructing Systemic blood flow
•Aortic stenosis•Coarctation of the Aorta
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Coarctation of the Aorta1. Narrowing of Aorta
causing obstruction of left ventricular blood flow
2. Left ventricular hypertrophy
Signs and Symptoms
11 B/P in upper extremities
11 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
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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
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Surgery for Coarctation of Aorta
1. Resect
narrow
area
2. Anastomosis
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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
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Acquired Cardiac Diseases
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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.
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Rheumatic Fever
Assessment Jones Criteria
Major Minor
Treatment Antibiotic Therapy Aspirin
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MAJOR Manifestations
Carditis Polyarthritis Chorea Erythema Marginatum Subcutaneous nodules
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MINOR
Arthralgia Fever ESR C-reactive protein Prolonged PR Interval
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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.
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Subacute Bacterial Endocarditis / Ineffective Endocarditis:
Assessment
Diagnosis – blood cultures
Treatment Antibiotics
Patient teaching – take antibiotics prior to surgery, dental work, etc.
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Kawasaki Disease
Multisystem vasculitis – inflammation of blood vessels in the body especially the coronary arteries with antigen-antibody
complexes.
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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
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Promote adequate cardiac output and oxygenation
Pharmacologic agents
Digoxin
Vasodilators
ACE inhibitors
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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.
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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
‘ The Pedi-Cardiac Lecture ’ Part 3 Pediatric Cardiovascular Disorders Jerry Carley MSN, MA, RN, CNE
‘ The Pedi-Cardiac Lecture ’ Part 2 Pediatric Cardiovascular Disorders Jerry Carley MSN, MA, RN, CNE