The Child with Cardiovascular Dysfunction

1. The Child with Cardiovascular Dysfunction Chapter 25

2. Fetal Circulation Structures • Umbilical vein; umbilical arteries • Foramen ovale • Ductus arteriosus • Ductus venosus

3. Changes at Birth • (Note to instructor: Image available in Electronic Image Collection)

4. Pediatric Indicators of Cardiac Dysfunction • Poor feeding/SOB/fatigue/cyanosis • Tachypnea/ tachycardia/diaphoresis • Syncope/chest pain/dizziness/palpitations • Failure to thrive/poor weight gain/activity intolerance/ hx frequent respiratory infections • Developmental delays • + Prenatal history—maternal exposure to infection, drugs, birth complications • + Family history of cardiac disease

5. Diagnostics: Cardiac Catheterization • May be diagnostic or interventional • May be left or right-sided • Pre-procedure interventions: • Education—procedure and touch senses • Assessment • Accurate ht & wt • Allergies • Mark pulses • Pulse ox

6. Cardiac Cath cont’d • Postprocedure interventions: • Keep extremity straight 4-6h • Assess 6 Ps • Routine postop VS (apical) • I&O d/t contrast • Pulse ox • Observe for hematoma or hemorrhage • Home care p. 894

7. Two Types of Cardiac Defects • Congenital • Anatomic anomalies present at birth that result in abnormal cardiac function • Acquired • Disease process after birth • Infection • Autoimmune response • Environmental factors • Familial tendencies

8. Causes of CHD • Chromosomal/genetic = 10%-12% • Maternal or environmental = 1%-2% • Maternal drug use • Fetal alcohol syndrome—50% have CHD • Maternal illness • Rubella in 1st 7 wks of pregnancy→50% risk of defects including PDA and pulmonary branch stenosis • CMV, toxoplasmosis, other viral illnesses>> cardiac defects • Mothers with chronic illness such as DM or lupus are more likely to have babies with CHDs • Multifactorial = 85%

9. CHD • Incidence: 5-8 per 1000 live births • About 2-3 of these are symptomatic in first year of life • Major cause of death in first year of life (after prematurity) • Most common anomaly is VSD • 28% of kids with CHD have another recognized anomaly (trisomy 21, 13, 18, +++ )

10. Classification of CHD • Hemodynamic characteristics • Increased pulmonary blood flow (patent ductus arteriosus) • Decreased pulmonary blood flow (Tetralogy of Fallot) • Obstruction of blood flow out of the heart (coarctation of aorta) • Mixed blood flow (transposition of great arteries)

11. Patent Ductus Arteriosus (PDA)

12. PDA cont’d • Failure to close within first weeks of life • Causes left to right shunt • Additional blood is re-circulated thru lungs and comes back to left side • Causes increased workload on both ventricles • May have S/S CHF; machinery–like murmur; wide pulse pressure; bounding pulses • Treated medically with indomethacin IV; placement of a coil thru interventional cardiac cath; or surgically with VATS and placing a clip on the ductus

13. Tetralogy of Fallot (TOF)

14. TOF cont’d • 4 defects: VSD, pulmonic stenosis, overriding aorta, right ventricular hypertrophy • Blood mixes in ventricles but depending on large vessel resistance, shunt could be either direction • Blood from both ventricles is distributed systemically • Infant/Child has tet spells which are relieved by squatting or knee chest position (915). Will also have murmur. • Complete surgical repair is tx of choice—repair of VSD, resection of stenosis with pericardial patch over surgical site to enlarge ventricle

15. Coarctation of Aorta (COA)

16. COA cont’d • Narrowing of aorta near PDA • Increased pressure in head and upper extremities; decreased in lower • S/S include HBP and bounding pulses in arms, LBP and weak or absent pulses in legs; CHF; dizziness, HA, syncope, epistaxis • Tx: angioplasty, resection with anastomosis, grafting

17. Transposition of Great Vessels (TGV or TGA)

18. TGV cont’d • PA comes from LV, goes to lungs and back to LV; aorta comes from RV goes to body and back to RV • No communication between the pulmonary and systemic circulation • Patent foramen ovale or VSD must be present to sustain life, but will cause CHF • S/S range from moderately to severely cyanotic depending on size of septal defect; CHF sx, murmur • Tx includes prostaglandin E1 and septostomy (Rashkind procedure) to increase mixing until surgery; arterial switch is surgery of choice

19. CHF in Children • Impaired myocardial function • Tachycardia, fatigue, weakness, restless, pale, cool extremities, diaphoresis, decrease BP, decrease urine output, gallop rhythm • Pulmonary congestion • Tachypnea, dyspnea, respiratory distress (grunting, flaring, retractions), exercise intolerance, cyanosis • Systemic venous congestion • Peripheral and periorbital edema, weight gain, ascites, hepatomegaly, JVD

20. CHF cont’d • Treatment goals are to decrease fluid overload, increase oxygenation, improve output, decrease O2 demand of heart • Lasix—decreases overload • Digoxin—improves output—need to double check dosage with another nurse—infants rarely receive > 1 mL (50 mcg) • ACEIs, bedrest, nutritional support—decreases O2 demand • Oxygen therapy

21. CHF—Nursing interventions • VS, heart and lung sounds, pulses • Monitor tissue perfusion, O2 tx • Maintain rest, nutrition • Monitor fluid status • Edema, dehydration, fontanels • JVD, hepatomegaly, periorbital and peripheral edema • I&O, daily wts, specific gravity