Nursing Care of the Newborn with a Congenital Heart Defect – Flashcards
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Ductus Venosus
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Blood bypasses the liver Closes when the umbilical cord is clamped & cut
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Foremen Ovale
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Blood bypasses the lunges Closes after birth with the change in pressure in cardiac chambers
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Ductus Arteriosus
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Allows for mixing of blood Closes after birth with the first few breaths
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Acyanotic Defects
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An obstruction of blood flow from the ventricles or a defect that causes increased flow of blood to the lungs Congestion in lungs may cause increased resistance of the pulmonary vessels & pulmonary hypertension Pulmonary congestion, increases work of heart & lungs; increase fatigue & growth slowed Atrial septal defect Ventricular septal defect Patent ductus arteriosus Atrioventricular canal *Obstruction of blood flow from ventricles:* Coarctation of the aorta Aortic stenosis Pulmonic stenosis
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Acyanotic Congenital Defects Signs & Symptoms
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Increase fatigue Murmur Increase risk of endocarditis CHF Growth restriction
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Atrial Septal Defect (ASD)
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Abnormal opening between the atria Allows blood form the higher pressure left atrium to flow into the lower pressure right atrium Foramen ovale fails to close
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ASD Assessment
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Often asymptomatic if small May develop CHF Characteristic murmur
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ASD Diagnostic Procedure
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Characteristic murmur Chest radiography film (cardiomegaly)
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ASD Treatment
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May close on its own Primary closure Secondary closure
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Primary Closure of ASD
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Opening is repaired with sutures alone if the defect is small
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Secondary Closure of ASD
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May involve sewing a synthetic patch made of Dacron material over the opening
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Ventricular Septal Defect (VSD)
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Abnormal opening between the right & left ventricles Left to right shunting of blood flow is caused by the higher pressure in the left ventricle The shunting of blood causes an increased load on the right ventricle The increased blood volume is pumped into the lungs
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Assessment of VSD
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CHF is common Characteristic murmur
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VSD Planning & Intervention
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Occasionally spontaneous closure occurs during first year of life in children having small or moderate defect Surgical patching if failure to thrive occurs Prophylactic antibiotics treatment to prevent endocarditis
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Surgical Treatment of VSD
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Small defects are fixed using simple stitching of the hole with thread Large defects are fixed using knitted Dacron patch sewn over opening
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Patent Ductus Arteriosus (PDA)
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Failure of the ductus arteriosus to close Allows blood to flow from the higher pressure aorta to the lower pressure pulmonary artery, causing a left to right shunt Additional blood is re-circulated through the lungs & returned to the left atrium & left ventricle Increases pulmonary vascular congestion
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PDA Assessment
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Maybe asymptomatic or show signs of CHF Characteristic machinery-like murmur Widened pulse pressure & bounding pulses result from runoff of blood from the aorta to the pulmonary artery
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PDA Interventions
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In preterm infants & some newborns, administration of indomethacin sodium
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indomethacin sodium for PDA
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Potent inhibitor of prostaglandin synthesis, causes closure of patent ductus arteriosus 75 to 80% of the time
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PDA Treatment
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Surgical ligation of the patent vessel Now use visual-assisted thoracoscope surgery (VATS) to place a clip on the ductus Nonsurgical is the use of coils to occlude the PDA in the cath lab
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Atrioventricular Canal Defect (AVC)
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Low atrial septal defect with a high ventricular defect Allows blood to flow between all 4 chambers The direction & pathways of flow are generally from left to right but determined by pulmonary & systemic resistance, left & right ventricular pressures & compliance of each chamber
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AVC Assessment
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Usually have moderate to severe CHF Characteristic murmur Mild cyanosis that increases with crying High risk for developing pulmonary vascular obstructive disease
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AVC Diagnostic Procedures
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Chest radiograph fil findings depend on shunt size; in moderate or large shunts, heart enlargement might be present Echocardiogram Doppler studies can reveal ductal flow, enlargement of left atrium & left ventricle is indicative of CHF
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AVC Treatment
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Surgical repair consists of patch closure of the septal defects & reconstruction of the AV valve tissue
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Coarctation of the Aorta (COAC)
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Narrowing of the aorta near the ductus arteriosus Increase blood flow above the narrowing Decreased blood flow below the narrowing Restricts blood flow leaving the heart Narrowing or constriction of the descending aorta Progressive disorder that leads to CHF
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COAC Assessment
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Bounding upper extremity pulses & weak lower extremity pulses Maybe high blood pressure & bounding pulses in arms, weak or absent femoral pulses & cool lower extremities with lower blood pressure Signs of CHF Condition deteriorates rapidly
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Therapeutic Management of COAC
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Resection of the coarcted portion or enlargement of the constricted section Residual permanent hypertension after repair seems to be related to age & time of repair so advised within first 2 years of life Balloon angioplasty as primary intervention
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Aortic Stenosis (AS)
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Narrowing of aortic valve This narrowing causes resistance of blood flow in the left ventricle, decreased cardiac output, left ventricle hypertrophy & pulmonary vascular congestion (pulmonary edema)
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AS Assessment
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Severe defects have signs of decrease cardiac output with faint pulses, hypotension, tachycardia & poor feeding Children have activity intolerance, chest pain, dizziness when standing for a long period
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AS Treatment
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Dilating narrowed valve with balloon angioplasty in catheterization lab
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Pulmonary Stenosis (PS)
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Narrowing at the entrance to the pulmonary artery Resistance to blood flow causes right ventricular hypertrophy & decrease pulmonary blood flow Prevents oxygen-poor blood in the right side of the heart from traveling normally to the lungs to pick up oxygen If right ventricular failure develops, right atrial pressure will increase & this may result in reopening of the foramen ovale, shunting of un-oxygenated blood into the left atrium & systemic cyanosis If severe CHF An associated defect such as PDA partially compensates for the obstruction
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PS Assessment
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Maybe asymptomatic Some have mild cyanosis Newborns with severe narrowing will have cyanosis Characteristic murmur
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Diagnostic Test for PS
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Chest x-ray shows cardiomegaly
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PS Treatment
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In infants, transventricular valvotomy (Brock) procedure In children, pulmonary valvotomy with cardiopulmonary bypass Non-surgical treatment id balloon angioplasty techniques, most common
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Cyanotic Defects
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Blood flow to the lungs decreases or venous blood & oxygenated blood are mixed in circulation decreasing the oxygen to tissues When venous blood from the right side flows through an abnormal opening to the left side, it is called a right to left shunt *Decreased pulmonary blood flow:* Tetralogy of fallot Tricuspid atresia *Mixed blood flow:* Transportation of great arteries Truncus arteriosus Hypoplastic left heart syndrome
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Tetralogy of Fallot (TOF)
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4 defects
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4 Defects of TOF
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Pulmonic stenosis Ventricular septal defect Overriding aorta Right ventricular hypertrophy
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TOF Assessment
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Some infants may be cyanotic at birth, other mild cyanosis that progresses over the first year of life as the PS worsens
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TOF Treatment
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Palliative shunt Complete repair in first year if life
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Tricuspid Atresia
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Failure of the tricuspid valve to develop No communication from the right atrium to the right ventricle Blood floes through an ASD to the left side of the heart & through a VSD to the right ventricle & out to the lungs
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Tricuspid Atresia Assessment
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Cyanosis is usually seen in the newborn Tachycardia & dyspnea
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Management of Tricuspid Atresia
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Neonate pulmonary blood flow depends on the patency of the ductus arteriosus Newborns will be given alprostadil (Prostaglnadin E1) until surgical intervention
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Transposition of Great Arteries
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Aorta exits from right ventricle Pulmonary artery exits from left ventricle No communication between pulmonic & systemic circulations Pulmonary artery originates from left ventricle, blood travels from the left ventricle to the pulmonary artery then to the lungs & then back into the left atrium
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Transposition of Great Arteries Pathophysiology
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There are two closed circulation pathways Survival depends on ductus arteriosus *remaining open* to mix oxygenated & deoxygenated blood (give prostaglandin E1)
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Transposition of Great Arteries Assessment
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Depends on type & size of the associated defects, children with minimum communication are severely cyanotic & depressed at birth Those with large septal defects or a PDA maybe less severely cyanotic but may have symptoms of CHF
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Therapeutic Management of Transposition of Great Arteries
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Prostaglandin E1 to temporarily increase blood mixing if oxygen saturation of 75% or less to maintain cardiac output Cardiac catheter (a balloon atrial septostomy - Rashkind procedure) Corrective surgical procedures - arterial switch procedure
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Truncus Arteriosus
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Defect of the great vessels (aorta & pulmonary artery) Aorta & pulmonary artery do not form as separate arteries Instead, a large artery called the truncus comes from the heart Blood form both ventricles mixes in the common great artery causing desaturation & hypoxemia
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Truncus Arteriosus Assessment
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Most infants are symptomatic & moderate to severe CHF & variable cyanosis, poor growth & activity intolerance
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Truncus Arteriosus Treatment
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Surgical, early repair, multiple surgeries, use of homograft
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Hypoplastic Left Heart Syndrome
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Underdevelopment of the left side of the heart, resulting in a hypoplastic left ventricle & aortic atresia Inability of the heart to supply the oxygen needs of the body
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Hypoplastic Left Heart Syndrome Assessment
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Patients are usually symptomatic in the first week of life with cyanosis & CHF when the PDA starts to close with progressive deterioration & decreased cardiac output Usually fatal in the first months of life without intervention
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Hypoplastic Left Heart Syndrome Treatment
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Prostaglandin E1 given to prevent closure of patent ductus arteriosus Several staged surgeries
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Hypoplastic Left Heart Syndrome Therapeutic Management
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Improved cardiac function digoxin (Lanoxin) is used almost exclusively Improve tissue oxygensation
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digoxin (Lanoxin) for Hypoplastic Left Heart Syndrome
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Observe signs of toxicity Calculate & administer correct dose Apical pulse is always checked before Not given if <90 bpm in infants/young children <70 bpm in older children
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Oxygenation Administration for Hypoplastic Left Heart Syndrome
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Oxygen hood is preferred with young infants to provide increased concentration of gas Administered only with an appropriate order
