Cardiovascular Stressors and Adaptation

1. Cardiovascular Stressors and Adaptation

2. Common Cardiovascular Disorders in Children • Congenital Heart Defects • Congestive Heart Failure • Acquired Heart Disease

3. Review of Normal Circulation

4. How to Understand Congenital Defects • Think of blood as: • Red highly O2 saturated • Blue unsaturated • Purplemedium O2 saturated (mixed) • Lavender- reduced volume of medium O2 saturated (mixed) • Pink Low O2 saturated • Light Blue Reduced volume of unsaturated

5. Fetal Circulation

6. Fetal Shunts • ductusvenosus: accessory (extra) vein, carries oxygenated blood from umbilical vein into lower venous system • foramen ovale: shunts mixed blood from right atrium to left atrium (hole in the atrial septum) • ductusarteriosus: accessory (extra) artery, shunts mixed blood away from lungs to descending aorta

7. How does the fetus receive sufficient oxygen from the maternal blood supply? • Fetal hemoglobin carries 20-30% more oxygen than maternal hemoglobin • Fetal hemoglobin concentration is 50% greater than mother’s • Fetal heart rate 120-160bpm (increases cardiac output)

8. What happens to the shunts after birth?

9. Transition from intrauterine to extrauterine life • Cord is clamped, neonate initiated respirations • O2 levels rise = greater pressure in the left atrium, decreased pressure in the right atrium leading to an immediate closure of the foramen ovale

10. Transition from intrauterine to extrauterine life • After O2 circulates systemically, over 24 hours, the pressure in the left ventricle will become greater than the pulmonary artery and closes the ductus arterosis • The absent flow of blood through the umbilicus gradually closes the ductus venosus over 12 hr to 2 weeks

11. Cardiac Defects Either: • Ductal closure failure (no structural abnormality) • Structural abnormality

12. Diagnosis • Assessment findings • Results of diagnostic testing • Cardiac Catherization

13. Cardiac Catheterization • Primary method to measure extent of cardiac disease in children • Shows type and severity of the CHD • Insert tiny catheter through an artery in arm, leg or neck into the heart • Take blood samples and measure pressure, measure o2 saturation, and as an intervention • Sedation or anesthesia • Outpatient vs Hospital

14. Cardiac Catheterization-Post Op • Monitor closely (cardiac monitor, continuous pulse ox) VS q 15 • Assess dressing at insertion site for infection, hematoma • Dressing must remain dry for 1st 48-72 hrs • No blood drawn from extremity used • Palpate a pulse distal to the dressing to assure blood flow to extremity is not obstructed: keep extremity straight for 48 hrs after procedure

15. If Congenital Defect is suspected or confirmed, • Intervention is Important to Prevent CHF

16. Congestive Heart Failure • Heart doesn’t pump blood well enough –can not provide adequate cardiac output due to impaired myocardial contractility • Causes in children: • Defects • Acquired heart disease • Infections

17. Congestive Heart Failure • Most common cause in children is congenital heart defects • Increased volume load or increased pressure in heart • Excess volume and pressure builds up in lungs leading to labored breathing • Builds up in rest of body leading to edema

18. Congestive Heart Failure Symptoms • 1st sign: tachycardia • tire easily • rapid, labored breathing • decreased urine output • fluid and sodium are retained • increased sweating, pallor • peripheral edema

19. CHF Diagnosis and Treatment • CXR- shows enlargement • Echocardiogram- dilated heart vessels, hypertrophy, increase in heart size • Tx-aimed at reducing volume overload, improve contractility • May require surgery

20. Congestive Heart Failure Medical Management Digoxin- Helps strengthen the heart muscle, enables it to pump more efficiently • 1st line tx • Dosing depends on wt and age • Digoxin toxicity: vomiting, bradycardia • Need HR, EKG, drug levels check apical pulse first, don’t give if HR < 100 bmp in infants and < 70 bpm in children • Parent teaching

21. Congestive Heart Failure Medical Management Diuretics- Helps the kidneys remove excess fluid from the body • Potassium sparing • Potassium wasting • Potassium supplements- given along with wasting diuretics Lasix-1st agent for children-lose K esp. when taken with digoxin

22. Congenital Heart Disease • 35 different types • Common to have multiple defects • Range from mild to life threatening and fatal • Genetic and environmental causes

23. Blood Flows From High to Low Pressure Higher pressure Lower Pressure

24. Types of CHD • Acynotic defects- purple blood (too much to lungs) • Septal defects • VSD • ASD • PDA • Obstructive Cyanotic defects-reduced flow (lungs/body) • PulmonicStenosislight blue blood (lungs) • Coarctation of the aorta pink blood (body) • Cyanotic defects- from poor perfusion (lungs and body) • Tetrology of Fallotlight blue & purple blood • Hypoplastic left heart lavender blood • Transposition of the greater vessels

25. Septal Defects- increased pulmonary blood flow • Left to right shunting (acyanotic defect) • Sends already sat blood back to lungs • Increased cardiac workload • Excessive pulmonary blood flow • Right ventricular strain, dilation, hypertrophy

26. Ventricular Septal Defect • Most common CHD • High Pressure in LV forces blood back to RV • Results in increased pulmonary blood flow (heart must pump extra blood), higher than normal artery pressure

27. Ventricular Septal Defect • S/S: vary with the size of the defect • 4-8 weeks of age develop loud, harsh systolic heart murmur • Right ventricular hypertrophy • 20-60% close spontaneously • cardiac cath shows: O2 level of RV higher than normal • large defects: develop CHF, poor feeding, failure to thrive

28. Ventricular Septal Defect Treatment: • Small defects: followed by cardiologist, prophylactic ABX • Large defect: open heart surgery with cardiopulmonary bypass, will suture or patch hole closed • If child is not stable for open heart surgery: pulmonary artery banding: narrowing of pulmonary artery to reduce blood flow to lungs

29. VSD Medical Management For infants not medically stable for surgery or awaiting surgery- • Digoxin: to improve cardiac output; • Oxygen

30. Atrial Septal Defect • Pressure in LA is greater than RA (blood flows left to right) • Oxygen rich blood leaks back to RA to RV and is then pumped back to lungs, results in ventricular hypertrophy • Few symptoms at birth, over time may experience fatigue and dyspnea on exertion

31. Atrial Septal Defect Clinical Presentation • Large defect may cause CHF • Harsh systolic murmur • Second heart sound is split: “fixed splitting” ** diagnostic of ASD • pulmonary valve closes later than aortic valve- risk for pulm edema • Echocardiogram: shows enlarged right side of heart, increased pulmonary circulation

32. ASD Management • Nonsurgical management: prosthetic patch • Surgical management: open-heart with CP bypass, edges are sutured or will use patch to cover hole • Diuretics to control symptoms until repair is performed

33. Patent Ductus Arteriosus • Failure of ductus arteriosus to close completely at birth • Blood from the aorta flows into the pulmonary arteries to be reoxygenated in the lungs, returns to LA and LV • More common in preemies H to L

34. Patent Ductus Arteriosus • Preterm infants: present with CHF and respiratory distress • Fullterm infants: may be asymptomatic with a continuous “machinery” type murmur • Tire easily, growth retardation (shorter, weigh less, less muscle mass), prone to frequent respiratory tract infections

35. Patent Ductus Arteriosus • Chest radiographs (x-ray) show enlarged LA and LV • Medical management: Indomethacin (prostaglandin inhibitor that stimulates ductus to constrict) • Surgical management: ductus is divided and ligated (usually performed in first year of life to decrease risk of bacterial endocarditis

36. Acyanotic Defects • VSD & ASD • Rt CHF • Pulm edema • Pulm htn • PDA • Pulm edema • Pulm htn

37. Obstructive Defects- decreased pulmonary blood flow Right to left shunt unsat blood into sat blood • Pulmonic Stenosis • Coarctation of the Aorta

38. Pulmonary Stenosis • Obstruction of the right ventricular outflow tract • Decreased pulmonary blood flow

39. Pulmonary Stenosis Symptoms • Right ventricular hypertrophy • High ventricular pressure may cause blood to back up into right atrium and force foramen ovale to open to allow blood to flow from right to left atrium • Mild-Mod: Usually asymptomatic except for Systolic ejection murmur with a palpable thrill • If Severe: right ventricular failure, CHF, if there is right to left shunting through the foramen ovale, mild to moderate cyanosis

40. Pulmonary Stenosis Medical Management: • If asymptomatic: cardiac follow-up • Prophylactic ABX Surgical Management: • Pulmonary balloon valvuloplasty via cardiac cath • if unsuccessful: valvotomy

41. Coarctation of Aorta • Localized constriction of the aorta at or near the insertion site of the ductus arteriosus • Reduces cardiac output (impedes blood flow from heart to body=pink blood) • Aortic pressure is high proximal to the constriction and low distal to the constriction-CVA Higher pressure Pink Blood

42. Coarctation of Aorta • S/S: related to severity of the constriction and presence of associated cardiac defects • Mild: asymptomatic, sys. murmur, diminished pulses in lower ext • Severe: poor lower body perfusion, metabolic acidosis, CHF, systemic hypertension • In both: BP is 20mmHg higher in arms than in lower extremities

43. Coarctation of Aorta Diagnosis-clinical exam, echo Treatment is based on severity

44. Treatment of Coarctation of Aorta Symptomatic newborn treated with: • Digoxin • diuretics to manage CHF • may also receive PGE1 (prostaglandin) infusions to maintain ductal patency and improves perfusion to lower extremities- although will cause inc pulm flow • surgical repair within first 2 years

45. Cynaotic Defects • Decreased pulmonary blood flow (light blue blood to lungs) • Transposition of the greater vessels • Tetrology of Fallot • Hypoplastic left heart

46. VSD RV hypertrophy Overriding aorta Pulmonic Stenosis: impedes blood flow to the lungs, forces unoxygenated blood through the VSD & into aorta Tetralogy of Fallot Consists of 4 Parts: Blood is purple Blood is light blue

47. S/STetralogy of Fallot • The degree of pulmonic stenosis governs the onset and severity of symptoms. • Mild: little to no right to left shunting infant has “tet spells” hypercyanotic episodes • Mod-severe: some cyanotic at birth when PDA closes, other infants become increasingly cyanotic over the first few months of life

48. Tetralogy of Fallot • Tire easily especially with exertion, difficulty feeding and gaining weight, • Other signs: chronic hypoxemia

49. Management Tetralogy of Fallot • Over time may have hypercyanotic episodes (tet spells) • often preceded by crying, feeding or stooling, worsening cyanosis, increased respiratory rate, may lose consciousness Treatment of tet spells: • knee-chest position then apply O2 • Do not leave alone- cyanosis can cause LOC, death

50. Tetralogy of Fallot Medical management: • Symptomatic newborn: PGE1 infusion to maintain ductal patency • Older infants: close monitoring for worsening of hypoxia • Surgical management: done at 3-12 months of age, in stages • primary open-heart repair: close VSD, open pulmonary valve, remove obstructing muscle