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Congenital heart defect (present at birth) Tetralogy of Fallot terta=4 fallot=name who discovered it.
most common Tetralogy of Fallot ventricular defect
Tetralogy of Fallot causes death during first yr
faster HR/met rate higher, thin chest wall, can't increase their sv as the older child or adult, heart n great vessels dev during first 3-8 wks,high pitched heart sounds greater intensity pedi diff in the heart and circulation
Two types of cardiac defects congenital (anatomic, resulting in abnormal function) acquired ( strep infection, acute glomerulonephritis)
secondary cause of cardiac defects strep acute glomerulonephritis
is a heart defect, present at birth (congenital), that results in low blood oxygen levels. Cyanotic heart disease
Cyanotic heart diseases caused by congenital anomalies: Genetic and chromosomal syndromes, such as Down syndrome, n Turner syndrome
feeding is key failure to thrive, poor wgt gain, sweats while eating, irritable weak cry cm of cardiac failure
decrease in the amt of oxygen to the extremities. The hands and feet turn blue. Acrocyanosis
diag for Acrocyanosis cxr-heart size, shape, cadiomeglay, ecg or ekg, echo
question to ask parent r/t cardiac dysfuntion describe how baby feeds
rr (40-60 norm), hr 160 @ rest = tachy, skin color; pallor around mouth, clubbing fingers late sign, ck peri pulses, bp norm s/b 90/50 if cardiac issue take on all 4 extremities physical assessment cardiac dsyfunction
invasive test to diag or treat cardiac defects; visualize heart n vessels, measure o2 sat, intra pressures, muscle function Diag catheterization fix pt with ductus
disease in which the proportion of blood volume that is occupied by rbc increases.The overproduction of rbc b/c process in the bone marrow or a reaction to chronically low oxygen levels Polycythemia (thick blood)
NPO 4-6hr b4, hold digi, iv if polycythemic,warm bc dye used preprocedural considerations cardiac cath
in creased temp,urticaria(hives),wheezing,edema,dyspnea,h/a signs of toxicity to dye (pretreat with benadryl)
assess pulses below the site, record quality pulses,temp, color, *ck dressing for bleeding or hematoma, extremity 24-48degrees post-cath
a heart defect present at birth that does not produce blue discoloration of the skin and mucous membranes under normal circumstances.Blood is properly oxygenated. ex atrial septal defecet acyanotic heart defect (L->R shunt)
atrial/ventricle septal defect;ductus arteriosus;coarctations of aorta can be responsible for acyanotic (L->R shunt)
in this shunting there is increased pulmonary blood flow and decreased systemic blood flow L>R
the infant is not usually cyanotic, fatigue, failure to thrive, frequent resp infections cm left to right shunts
NIC r/t L>R shunt risk for infection education nutrition:q 3 hr feed ->no energy to eat so increase cal for feed
ductus arteriosus does not close. Patent ductus arteriosus (PDA) acyanotic heart defect (L->R shunt)
widened pulse pressure, bounding pulses (ex 120/50) phy growth and activity slowed cm PDA -acyanotic heart defect (L->R shunt)
successful in preterm infans and some newborn; PDA Patent ductus arteriosus, medications indomethacin (suppresses prosteglandins) or a special form of ibuprofen are often the first choice.
holes in the wall that separates the right and left ventricles of the heart. is one of the most common congenital heart defects Ventricular septal defect VSD
Shortness of breath;Fast breathing;Hard breathing from what defect Paleness Failure to gain weight Fast heart rate Sweating while feeding Frequent respiratory infections cm:Ventricular septal defect VSD
increased pressures on the left-sided heart, directs blood flow through the VSD in a _>_ shunting L>R
non surgical treatment: device closure during cardiac cath;Surgical repair by direct closure or silastic patch nic postop prior to pt must be on abx prophilacticall so no endocarditis
baby is in the womb, an opening between the upper chambers of the heart (atria) to allow blood to flow around the lungs.usually closes around the time when the baby is born. If it doesnt close, its a atrial septal defect, or ASD acyanotic heart defect (L->R shunt)
is a hole in the wall between the two upper chambers of your heart. The condition is present from birth (congenital). atrial septal defect (ASD)
is a narrowing of the aorta;Pale skin Irritability Heavy sweating Difficulty breathing Coarctation of the aorta
narrowing of the aorta increases pressure proximal to the narrowing and decreased pressure distal to the obstruction Coarctation of the aorta
CM; high bp and bounding pulse in the arms, or weak or absent femoral pulses, and cool lower extremities w/ lower bp;Older children may experience h/a and fainting & nosebleeds because of htn cm of COA ;Coarctation of the aorta
prostaglanddin given to keep the PDA open to reduce the pressure changes, the most common repair is resection of the narrowed area w/re-anastomosis of the 2 ends Treatment of COA (Coarctation of the aorta), very acute infant /like to correct before symptoms appear
Occurs when pressure in the right side>left side. Deoxygenated blood on the right side shunts to the left Cyanotic defects; right to left shunts
Hypoxemia, Polycythemia, increased viscosity of the blood = heart has to pump harder. Major risk air can have direct access, so filter on IV to prevent air embolism Clinical manifestations right to left shunting. Need adequate fluids, patient is anemic b/c not keeping up w/hgb stores, may give prostaglandans
Potential complications right to left shunts Thrombus formation due to sluggish circulation
It is made up of four components, vsd, pulmonary stenosis, right ventricular hypertrophy, and an overriding aorta Tetrology of fallott
right ventricle is hypertrophied b/c of resistance to pumping blood thro pulmonary artery r/t stenoses or narrowing Tetrology of fallott
infant May be cyanotic at birth or have mild cyanosis that progress over the first year. blue /tet spells related to anoxia. finger clubbing, squatting polycythemia, and poor growth Clinical manifestations Tetrology of fallott
#1: place infant in knee-chest position first,Calm approach, admin 100% oxygen by blow-by Treating hypercyanotic spells
Cyanotic, O2 will not work, loud manner, Echo,All iv lines should have filters, Diagnosis or cyanotic defect
Closure of the VDS w. dacron patch, if oxygen levels are low prostaglanddin may be administered iv to keep the PDA open treatment of TOF
long term outcomes of leaky pulmonary valve -> pulmonary insufficiency, heart block TOF
is a defect in which the great vessels (aorta and pulmnary artery) are transposed or reversed. the aorta comes off the R vent and the pul artery off the L vent Transposition of the great vessels
on-o2 blood ent the RA to RV then flows out aorta to body; oxy blood from lungs ent LA to LV and the flows out pulm artery back to the lungs; there is a parallel circulation w no o2 blood get to systemic circulation Transposition of the great vessels
cyanosis w/in first few hrs of birth; most important cm in cm TOGA (big babies)
IV prostaglandin E maybe initiated to keep the ductus open and increase mixing of blood n provide an oxygen sat of 75% to maint co; procedure of choice arterial switch performed 1st wk of life treatment TOGA
CHF,Rheumatic Fever, Endocarditis, Kawasaki Disease,HTN, & Hyperlipidemia acquired cardiovascular d/o
cm of cardiac disease usually acyonotic defects; <1y due to congenital anomaly; > 1y w/no congenial anomaly may be due to acquired heart disease. CHD
systemic venous congestion (wgt gain,lrg liver, endema,jvd) Pulmonary VC (tachpnea,dyspnea,cough,wheeze) Compensatory response (tachy,lrg heart,sweating,fatigue,failure to grow) CM of CHF weigh 2x day r/t edema;take BP b4 captopril;watch K+ w/digi, may need K+ suppl can mix in juice
Improve cardiac function (rest & meds digoxin);remove edema (lasix); decrease cardiac demands; improve oxygen therapeutic mgt CHF
bradycardia, arrhythmia, N/V=anorexia (main sigh in kids), dizzy, h/a,weak,fatique are CM of what digoxin toxicity (store safely b/c it tastes good)
why use tuburecula syrings BID 9am-9pm with digoxin b/c must be very accurate
inflammatory disease occure after group A B-hemolytic strep pharyngitits, affects joints,skin,serous surfaces, and heart RF & Rheumlatic Heart disease
edu r/t rheumatic heart disease All antibiotics must be taken
Polyarthritis, on and off rash, swollen joints, involuntary movement of legs and arms, may notice a change in handwriting-> trouble walking Manifestations of RF Jones criteria
nic r/t RF Jones criteria Early treatment and recognition of a strep infection
Inflammation of the heart structures heart valves with RF Endocarditis
Once a month injection or oral pcn eurythromycin RF w/out carditis is Rheumatic fever prophylaxis
Five years or until 21 years of age whichever is longer is treatment for Rheumatic fever prophylaxis
prophylactic antibiotics 1hr b4 dental care, throat,intestina, urinary or vaginal infections or surgery is critical to prevention of infective endocarditis
unexplaned fever, malaise, anorexia & wgt loss, spinter hemorrhages; osler nodes(bumps on fingers), janeway lesions(peeling hands n feet); petechiae on oral mucous membranes CM Infective Endocarditis
high dose of abx iv for 4-8wks; edu r/t f/u visits for cardiac eval, echo monitoring and blood cultures therapeutic mgt of Infective Endocarditis
an acute systemic inflammation of vessels usually cardiovascular, start sm then takes off; can have aortic aneurysm; in children <5 Kawasaki Disease (KD;Mucocutaneous Lymph Node Syndrome
High fever (104) lasting >5 days, conjunctivits b/c eye vessels ruptured b/c of inflammation; strawberry tongue,red lips, cracked lips; polymorphous erythematous rash; chg in hands n feet r/t lrg amt of peeling. CM of KD
give rapid to prevent reaction to IV IgG; monitor VS ofter; cardiac monitor; RUN saline Medical Mgt #1 IV gamma globulin; asa 80-100mg/kg/day fever
Pediatric Indicators of Cardiac Dysfunction Poor feeding Tachypnea 40-60 is norm, tachycardia >160 @ rest Failure to thrive, poor weight gain, activity intolerance Developmental delays Positive prenatal history Positive family history of cardiac disease
Cyanosis w/in the first few hours of birth is the most important clinical finding of this Clinical Manifestations TOGA (Transposition of the Great Vessels)
There is almost always a patent ______ _____ present foramen ovale
______should be suspected in an otherwise healthy newborn with acute cyanosis that is not responsive to oxygen TGA Transposition of the Great Vessels
CHF Rheumatic Fever Endocarditis Kawasaki Disease Hypertension Hyperlipidemia Acquired Cardiovascular Disorders
Is a Major cm of cardiac disease CHF
Most common cause in infants is CHD r/t either volume overload or pressure overload on the heart >excessive volume or pressure can contribute to pulmonary edema congenital heart disease is the most common cause of CHF
Acquired heart disease is the most common cause in older children or adolescents, cardiomyopathy, endocarditis, myocarditis congestive heart failure as a result of acquired
Systemic Venous Congestion indicates right ventricular failure Weight gain, hepatomegaly, edema, jugular vein distension (seen in the older child > 10-12 years), changes in urine output
Tachypnea, retractions, nasal flaring, dyspnea, cough, wheezes Oxygen saturation may fall Pulmonary Venous Congestion r/t leaking of fluid into the alveoli and interstitium of the lung leading to pulmonary edema
Cool mottled extremities,weak,thready pulses indicate poor perfusion Excessive sweating is caused by sns BP is usually maint; therefore, hypotension is a late sign Growth failure & poor wgt gain are common in infants and children with CH Cardiac Manifestations of CHF r/t cardiomegaly
Take an apical pulse with a stethoscope for 1 full minute before every dose of digoxin ___ beats / min for infant and toddler ____beats in the older child ____beats in the adolescent < 100 < 80 < 60
Inflammatory disease occurs after group A β-hemolytic streptococcal pharyngitis Self-limiting Affects joints, skin, brain, serous surfaces, and heart Rheumatic Fever (RF)
Most common complication of RF Damage to valves as result of RF Rheumatic Heart Disease (RHD)
Carditis Polyarthritis Erythema Marginatum Chorea Subcutaneous Nodes Manifestations of RF Jones Criteria
Eradication of hemolytic streptococci Prevention of permanent cardiac damage Palliation of the other symptoms Prevention of recurrences Therapeutic Management of RF
Duration of Secondary Rheumatic Fever Prophylaxis RF with carditis and residual persistent valvular disease 10 years or until 40 years of age (whichever is longer), sometimes lifelong prophylaxis
Duration of Secondary Rheumatic Fever Prophylaxis RF with carditis but no residual heart disease 10 years or until 21 years of age (whichever is longer)
Duration of Secondary Rheumatic Fever Prophylaxis RF without carditis 5 years or until 21 years of age (whichever is longer
Penicillin G IM X 1 Penicillin V PO q 10 days Sulfa PO q 10 days Erythromycin (if allergic to above) PO q 10 days trmt of streptococcal tonsillitis and pharyngitis and trmt of recurrent RF
Insidious onset Unexplained fever Malaise Anorexia and weight loss Characteristic findings: Splinter hemorrhages, Osler nodes, Jane way lesions, petechiae on oral mucous membranes Clinical Manifestations of Infective Endocarditis
Trmt w/ high doses of abx iv for 4-8 weeks a PICC line will be inserted,Bed rest and quiet activities ,Parent edu r/t follow-up visits for cardiac evaluation, echocardiograph monitoring, and blood cultures Therapeutic Management of Infective Endocarditis
in children <5 years old,Boys are affected more than girls,asian,Epidemics occur in the winter and spring,multisystem vasculitis (inflammation of the blood vessels) Kawasaki Disease (KD or Mucocutaneous Lymph Node Syndrome)
High fever lasting >5 days Conjunctivitis Oral changes: strawberry tongue,erythema of lips and oropharynx,cracked lips Polymorphous erythematous rash Changes in hands and feet:tense edema, diffuse erythema, desquamation Kawasaki Disease (KD or Mucocutaneous Lymph Node Syndrome)
Med mgt of Kawasaki Disease (KD or Mucocutaneous Lymph Node Syndrome) Intravenous immune globulin (IVIG) is administered during the first 10 days of illness
IVIG s/b admin 2 gm./kg over 10-12 hours IV for mgt of KD. Why use IVIG IVIG causes rapid resolution of symptoms, reduces the incidence of coronary artery aneurysms;IVIG is a blood product the nurse should be familiar with hospital guidelines prior to administration
Med mgt Kawasaki Disease using ASA Initial therapy of 80-100 mg/kg/day in 4 divided doses until fever subsides (anti-inflammatory dose) The dosage is then chgd to 3-5 mg/kg/day as one dose for 6-8 wks until platelet count has returned to norm or indef if there are cardiac abnormalities
Med mgt Kawasaki Disease if aneurysm noted Anticoagulation with warfarin is recommended in children with giant aneurysms to prevent coronary artery thrombosis and occlusion
Medication Concerns R/t KD r/t asa Give aspirin with meals to prevent GI upset
Medication Concerns R/t KD If flu or chickenpox is suspected child on aspirin it should be discontinued or changed to dipyridamole (Persantine)
Medication Concerns R/t KD IVIG is a blood product IVIG is a blood product
Medication Concerns R/t KD IVIG administration IVIG is a blood product Frequent monitoring of vital signs should occur during the first hour or two of administration
Medication Concerns R/t KD IVIG administration If an adverse reaction If an adverse reaction is noted (rash, fever, shaking, shills) discontinue infusion immediately and notify practitioner
Promote comfort;Small, frequent feedings; Passive rom exercises;Cool baths;Gentle oral care Encourage fluids Monitor for complications Kawasaki Disease Nursing Considerations
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. patent ductus arteriosus (PDA) or aortic insufficiency.
(Prostaglandin Inhibiter) – given by mouth, constricts the muscle in the wall of the PDA and promotes closure Indomethocin
coil is placed in the open duct and acts like a plug Cardiac Catheterization
– small incision made between ribs on left hand side and PDA is ligated or tied and cut (Surgical ligation via left thoracotomy or Visually Assisted Thoroscopic Surgery/VATS Closed heart surgery
is an abnormal connection between the right and left ventricles VSD
Pulmonary vascular resistance falls in the first few weeks of life This can dramatically change intracardiac blood flow patterns A newborn with this may not demonstrate symptoms until the Pulmonary Vascular Resistance falls a VSD
May be asymptomatic CHF is common Characteristic loud holosystolic murmur heard at left sternal border (often not heard at birth) Signs and symptoms consistent with acyanotic defects: tachpyneic, diaphoretic, fatigue, FTT Clinical Manifestations VSD
is an abnormal connection between the right and left atria ASD
Surgical closure ;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 atrial septal defect
Stenosis or narrowing located within the thoracic aorta Coarctation of Aorta
Classic clinical finding: High blood pressure and bounding pulses in the arms, weak or absent femoral pulses, and cool lower extremities with lower blood pressure in lower extremities Clinical Manifestations COA
How to Determine Arm or Leg Gradients for BP Subtract the leg systolic pressure from the arm systolic pressure This will equal the gradient Example: Right arm 150/70, right leg 100/68 gradient is 150-100 = 50 mm Hg Measurements less than 20 mm Hg are associated with mild coarctation
Deoxygenated blood from the right side shunts to the left side Cyanotic Defects Right to Left Shunts
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. Clinical Manifestations Right to Left Shunting
TOF is made up of 4 components: VSD, pulmonary stenosis, right ventricular hypertrophy, and an overriding aorta
narrowing of the pulmonary valve and outflow tract or area below the valve, that creates and obstruction of blood flow from the right ventricle to the pulmonary artery TOF Pulmonary stenosis:
the aortic valve is enlarged and appears to arise from both the left and right ventricles instead of the left ventricle TOF Overriding Aorta:
the right ventricle is pumping at high pressure and becomes thickened and enlarged TOF Right Ventricular hypertrophy:
TOF; Acute episodes of cyanosis and hypoxia, called _____ associated with anoxia result from stressing the infant blue spells or tet spells,This leads to an increase in R>L shunting
Created by: troop27



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