Neonatal Cardiology

1. Neonatal Cardiology Susan Hicks, RN Nurse Manager, NICU/ICN Madigan Healthcare System

2. Objectives • Discuss the physiological adaptation from fetal to newborn circulation • Describe how to perform a thorough cardiac assessment on a neonate • Identify ductal dependent lesions and nursing care for these infants • Identify the common Arrythmias in the newborn period

3. Transition to Extrauterine Life • Placenta receives 50% of fetal cardiac output and is the organ of gas exchange in utero • Low pulmonary blood flow (8-10% of cardiac output) due to high pulmonary vascular resistance • Ductal patency is maintained by low oxygen tension in utero and the vasodilating effect of prostaglandin E2

4. Fetal Circulation

5. Cardiopulmonary Adaptation at Birth • Umbilical cord is clamped which increases systemic vascular resistance • The three major fetal shunts functionally close during transition • Surfactant is secreted into the amniotic fluid by the fetal lung by about 20 weeks gestation and increases in quantity throughout gestation and can support extrauterine breathing by about 34 weeks

6. Ductal Closure • Increasing arterial oxygenation from the lungs and decreasing prostaglandin levels are potent stimulus’ to constrict the ductus arteriosus • Foramen ovale functionally closes related to increase in left atrial and left ventricular pressures • Ductus venosus closes because of absent umbilical venous return- becomes ligimentum venosum

7. Cardiac Assessment • Heart Rate • Cardiac output= Heart rate times stroke volume • Rhythm • arrhythmias are common in the neonatal period and are frequently benign

8. Murmur • Caused by turbulent blood flow • Pathological vs. innocent • Note location, intensity, radiation quality and pitch • Occur in 60% of neonates in the first 48 hours of life

9. Murmurs • Grade 1- barely audible • Grade 2- soft but immediately audible • Grade 3- moderate intensity without a thrill • Grade 4- loud, can be heard with stethoscope barely on the chest • Grade 5- very loud, heard with stethoscope slightly removed from the chest

10. Color/ Cyanosis • Central vs. Peripheral • assess central color on mucous membranes paying attention to intrapartal history • acrocyanosis common in newborn period related to circulatory changes • Cardiac vs. Pulmonary • cyanosis not responsive to oxygenation should bring suspicion of cardiac disease

11. Cardiac Assessment • Perfusion • Capillary Refill time • Pulses • Brachial, femoral (Central) • tibial, radial (peripheral) • right vs. left • right preductal • left - postductal • bounding common in premature infants

12. Blood Pressure • Use appropriate sized cuff for accuracy • Norms dependent on weight, age • Decreases 3-4 hours postnatally, increases to plateau at 4-6 days of age • Follow blood pressures for trending

13. Cardiac Diagnosis • CXR- rule out pulmonary disease, assess heart size • EKG • Cardiac Echo • Blood Gas- low PaO2, normal CO2 • hyper-oxygen test- pre and post ductal saturation

14. Neonatal Cardiac Disease • Approximately 1% of infants born in the United States each year have some form of congenital heart disease. • Major structural defects in the heart can occur if there is an interference with the maternal-placental fetal unit during the first seven weeks of gestation when cardiac development occurs

15. Neonatal Cardiac Disease • Causes of congenital heart disease include chromosomal, genetic, maternal, environmental, or multifactorial

16. Chromosomal Abnormalities • Many chromosomal abnormalities are associated with structural heart defects. • Almost half of the infants with Down’s syndrome have some form of congenital heart disease • The most common defects in Down’s include endocardial cushing defects and ventral septal defects

17. Maternal Factors • Maternal factors include maternal illness and drug ingestion. • Rubella during the first 7 weeks of pregnancy carries a 50% risk of congenital rubella with congenital defects of multiple organ systems.

18. Maternal Factors • Maternal drug use may also cause congenital heart disease. Fifty percent of newborns with Fetal Alcohol Syndrome have some form of congenital heart disease • Infants of Diabetic Mothers have a 10% chance of having and infant with a heart defect,usually VSD and Transposition of the Great Arteries

19. Environmental Factors • Environmental factors as causes of congenital heart disease have only recently begun to be recognized • More research is needed

20. Cyanotic Heart Defects or Ductal Dependent lesions • Cyanotic heart defects are those that produce a right-to-left shunt through the heart, thus decreasing pulmonary blood flow. • Cyanosis is usually present within the first few days of life and worsens with the closure of the PDA as blood supply is bypassing the lungs. These are then referred to as Ductal Dependent Lesions.

21. Coarctation of the Aorta • Constriction of the aorta distal to the left subclavian artery, usually at insertion site of the Ductus • Left to right shunt. • Decreased pulses and BP in lower extremities • Treat CHF, surgical repair

22. Transposition of the Great Arteries • Position of the great arteries are reversed. • Oxygenated blood from lungs enters left heart and goes back to lungs via Pulmonary artery. • Desaturated blood enters the right atrium and leaves via the aorta. • Left to right mixing is required for survival. • PGE, septostomy, surgical repair.

23. X-Ray Transpositon of the Great Arteries Commonly referred to as an “egg lying on it’s side”

24. Tetralogy of Fallot • Most common cyanotic heart lesion • Pulmonary stenosis, VSD, Aorta overrides VSD, right ventricular hypertrophy • Dynamics depend on degree of pulmonary stenosis • Surgical repair

25. X-Ray Tetralogy of Fallot Commonly thought to look “boot shaped”

26. Pulmonary Atresia • Complete obstruction of the pulmonary valve resulting in hypoplastic Right ventricle and tricuspid valve atresia • Right to left shunt via the foramen ovale • Dependent on PDA for mixing

27. X-Ray of Pulmonary Atresia Commonly with little vascular markings and may also be seen as “snowman”

28. Tricuspid Atresia • Failure of tricuspid valve to develop • Right to left shut via the foramen ovale • If VSD present, some blood from the left to the right ventricle and to lungs • PGE to create mixing via the PDA • Surgical correction, good survival rate

29. X-Ray Tricuspid Atresia Little vascular marking, heart appears smaller than normal.

30. Persistent Pulmonary Hypertension of the Newborn • Hypoxia and acidosis create pulmonary vasoconstriction • lungs become high resistance • blood flows path of least resistance • Treatment-correct acidosis, ventilate, NO

31. Ebstein’s Anomaly • Anomaly of the tricuspid valve – occurs in less than 1% of all congenital heart defects • Downward displacement of the Tricuspid valve into the RV. • Portion of RV is incorporated into the RA. • A PFO or ASD with a right-to-left shunt present

32. Ebstein’s Anomaly • Massive heart noted at birth if severe • 18% of symptomatic newborns dies the neonatal period • 30% die before 10 yrs of age • Median age of death is about 20 yrs.

33. X-Ray Ebstein’s Anomaly

34. Ductal Dependent Lesions • What will you see? • Infant who is cyanotic and does NOT respond to O2. • Infant becomes increasingly cyanotic and/or tires easily with feedings in first few days as duct closes • Usually appear comfortable but may exhibit s/s of respiratory distress • Xray may show CHF already

35. Ductal Dependent Lesions • Nursing Care • Monitor VS very closely • Observe SaO2 closely – may not want sats high d/t defect and shunting of blood • STRICT I&O!!! CHF can result easily • Pre/Post Sats may be ordered • Sedate if necessary, Ventilate if necessary (may have underlying respiratory issue also)

36. Ductal Dependent Lesions • Nursing Treatment includes • medications (prostaglandin infusion, inotrops, and correction of metabolic acidosis) • surgical intervention (balloon septostomy) to maintain mixing between the right and left heart thus increasing pulmonary blood flow • corrective surgical repair Bottom line: When in doubt start prostagland! Transport these infants asap to a cardiac care center

37. Arrythmias Bradycardia • Etiology • Usually secondary to respiratory or apnea • Clinical Signs • Decreased heart rate (<100), regular QRS complex • Treatment • Treat underlying respiratory disorder (methylzanthines), stimulation

38. Supraventricular Tachycardia (SVT) Etiology • Abnormal stimulation of the AV node, heart disease usually not present

39. SVT Treatment • Vagal stimulation (the diving reflex) • Adenosine • Cardioversion - synchronized, 0.5-1.0 joules per kg

40. SVT • Clinical Signs • Heart rate persistently >200-220 • Heart rate does not change based on infant’s activity • Usually absent p waves on EKG • Signs of circulatory collapse and decreased cardiac output • Eventually, congestive heart failure

41. Arrythmias