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Cardiovascular Stressors and Adaptation

Cardiovascular Stressors and Adaptation. Common Cardiovascular Disorders in Children. Congenital Heart Defects Congestive Heart Failure Acquired Heart Disease. Review of Normal Circulation. How to Understand Congenital Defects. Think of blood as: Red highly O2 saturated

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Cardiovascular Stressors and Adaptation

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  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

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