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Care of Child with Cardiovascular Disorders

Care of Child with Cardiovascular Disorders. Dr. Manal Kloub. CHD CHF Hypoxemia Acyanotic disorders Increased pulmonary flow PDA ASD VSD. Cyanotic disorders Obstructive AS PS COA Decreased pulmonary flow TOF Mixed defects TGV or TGA Hypoplastic heart. Outline.

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Care of Child with Cardiovascular Disorders

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  1. Care of Child with Cardiovascular Disorders Dr. Manal Kloub

  2. CHD CHF Hypoxemia Acyanotic disorders Increased pulmonary flow PDA ASD VSD Cyanotic disorders Obstructive AS PS COA Decreased pulmonary flow TOF Mixed defects TGV or TGA Hypoplastic heart Outline

  3. Heart Anatomy and Physiology

  4. Cardiac Conduction

  5. First Breath • Pulmonary alveoli open up • Pressure in pulmonary tissues decreases • Blood from the right heart rushes to fill the alveolar capillaries • Pressure in right side of heart decreases • Pressure in left side of heart increases • Pressure increases in aorta

  6. Congenital Heart Diseases♥ Definition: • It includes primarily anatomic abnormalities present at birth that results in abnormal cardiac functions • The newborn’s heart begins to beat at 28 days of gestation • The heart is completely developed on the 9th week of intrauterine life

  7. Incidence: CHD • 4 – 10/100 live births • Major cause of death during 1st year of life after prematurity • Affect both sexes differently • It is more likely to be with other congenital anomalies e.g. T.E fistula, Renal agenecies and diaphragmatic hernia.

  8. Etiology: CHD • Factors associated with increased incidence: • Prenatal factors: • Maternal rubella • Radiation • Alcoholism • age >40 yrs • Insulin dependent diabetes • fetal intra uterine cardiac viral disease

  9. Etiology: CHD • Genetic factors: although the influence is multifactorial there is high risk of CHD in children who have: • a sibling with a heart defect • a parent with CHD • chromosomal aberration e.g. Down’s syndrome • Born with other congenital anomalies

  10. Altered Hemodynamics • Blood flows from high pressure to area of lower pressure and with lower resistance, in response to the pumping action of the heart • The higher the pressure gradient the greater the rate of flow • The higher the resistance the less the rate of flow

  11. Normally the pressure in the Rt side is lower than the Lt side of the heart • The resistance in the pulmonary circulation and vessels entering or leaving these chambers have corresponding pressure • So if there is septal defect, blood will flow from Lt to Rt known as left to right shunt, and no desaturated blood flows directly into the Lt side of the heart so it is acyanotic defect

  12. Cyanotic defects are due to: • Change in the pressure causing blood to flow Rt - to - Lt Shunt. • Due to increased pulmonary flow through the pulmonary vascular resistance • Or obstruction to the blood flow through the pulmonary valve and aorta • Or due to mixing of the blood between pulmonary and systemic circulation e.g. truncus arteriosus (the pulmonary artery and the aorta are one single vessel that overrides both ventricles

  13. Classification and clinical consequences of congenital Heart Diseases: • Depending on the severity of the cardiac defect and the altered hemodynamics TWO principal clinical consequences can occur: 1st Consequence is Congestive Heart Failure 2nd Consequence is Hypoxemia

  14. Congestive Heart Failure • It is the inability of the heart to pump adequate blood to the systemic circulation to meet the metabolic demands of the body. • It is a symptom caused by cardiac defect not a disease in itself, it is due to increased work load on normal myocardium

  15. Congestive Heart Failure • Major manifestation of cardiac disease. • Under 1 year of age due to congenital anomaly. • Over 1 year with no congenital anomaly may be due to acquired heart disease. In children failure of one chamber causes change in the opposite chamber

  16. Pathophysiology of CHF Two categories • Rt sided failure; the Rt ventricle is unable to pump blood to pulmonary artery resulting in increase in the pressure in the Rt atrium and systemic venous circulations leading to liver and spleen enlargement and occasionally edema. • Lt sided failure, the left ventricle is unable to pump blood into the systemic circulation leading to increased pressure in the Lt atrium and pulmonary veins. The lungs become congested leading to increased pulmonary pressure and pulmonary edema.

  17. Congestive heart failure leads to: • cardiac muscles damage • decrease the cardiac output • decrease the flow of blood to the kidneys • increase the reabsorption of Na and water and increase blood volume • increase systemic congestion • Distention in neck veins and peripheral veins • Edema and hepatomegaly • Forehead sweating due to sympathetic response

  18. Cardiac Congestion: Tachycardia Cardiomegaly Pale cool extremities Weak peripheral pulses Low blood pressure Gallop Rhythm heart beats Pulmonary Congestion: Tachypnea Dyspnea Cyanosis Wheezing Grunting Retractions with flaring nares Cough and hoarseness of voice Clinical S & S of CHF

  19. Exercise intolerance Orthopnea Sweating Decreased urine output Weakness Fatigue Restlessness Anorexia Systemic Venous Congestion: Weight gain (due to edema) Hepatomegaly Peripheral edema especially periorbital area Ascites Neck vein distension Clinical S & S of CHF

  20. ♥ Therapeutic management Goals: • Improve cardiac function • Remove accumulated fluid and Na • Decrease cardiac demands • Improve tissue oxygenation and decrease O2 consumption

  21. Interventions • Fluid restriction • Diuretics – Lasix (potassium wasting) or Aldactone (potassium sparing) • Bed rest • Oxygen therapy • Small frequent feedings – soft nipple with supplemental NG for adequate calorie intake • Pulse oximeter • Sedatives if needed

  22. Improving Myocardial efficiency By giving: Digitalis glycosides (Lanoxin /Digoxin) • Increase cardiac output • Decrease heart size • Decrease venous pressure • Decrease edema • Regulate heart rate • Digoxin increases the force of the myocardial contraction.

  23. Digoxin Therapy • Take an apical pulse with a stethoscope for 1 full minute before every dose of digoxin. If bradycardia is detected. • < 100 beats / min for infant and toddler • < 80 beats in the older child • < 60 beats in the adolescent Nursingalert * Call physician before administering the drug*

  24. Signs of Digoxin Toxicity • Extreme Bradycardia • Arrhythmia • Nausea, vomiting, anorexia • Dizziness, headache • Weakness and fatigue

  25. Supplemental Feeding Infants with cardiac conditions often require supplemental feeding to provide sufficient nutrients for growth.

  26. Angiotensin-converting enzyme (Captopril/capotin): • Inhibit the normal function of rennin angiotensin in the kidney and vasodilatation occur, decrease pulmonary and systemic vascular resistance which decreases B/P and cardiac after load • Remove accumulated fluid and Na: • Diuretics. frusamide (Lasix). Thiazide and Spironolactone. • Possible restriction of fluids and decrease Na • Observe fluid intake and out put and Signs of dehydration • Potassium supplement, because Diuretics increase potassium loss

  27. Decrease cardiac demand: • Decrease physical activities, by bed rest, observe body temp. • Treat any infections • Improve breathing ; semi sitting position and sedate irritable children • Increase tissue oxygenation and decrease O2 consumption by applying the mentioned measures and giving humidified cool O2

  28. 2nd Consequence Hypoxemia • Referred to arterial O2 tension (or pressure PaCo2), that is less than normal can be identified by ↓ SaO2 or ↓PaO2 Hypoxia: • Reduction in tissue oxygenation that results from ↓oxygen saturation and PaO2 which results in impaired cellular process Cyanosis: • Blue discoloration of mucus membrane, skin nail beds due to reduced O2 saturation, results from the presence of deoxygenated hemoglobin in a concentration of 5g/dl of blood or more.

  29. Cyanosis occurs when O2 saturation is 75% - 85% • May not reflect arterial hypoxemia because both O2 saturation and amount of circulating hemoglobin are involved • In severe anemia no cyanosis despite severe hypoxemia, because hemoglobin level may be too low to produce blue color • On the contrary, in polycythemia there is cyanosis and normal PaO2 • In Heart defects Hypoxemia and Cyanosis result from desaturated venous blood entering the systemic circulation

  30. Squatting (rarely seen) Polycythemia (increased number of RBC) Clubbing of the finger Hypercyanotic spells Clinical manifestations of Hypoxemia

  31. Hypercyanotic spells • Hypercyanotic spells: • Cyanosis • Hyperapneia (increased depth of breathing) • ↑Rt -to-Lt Shunt. • Rare < 2 months of age • More common in >1year of age increase in the morning and during feeding, crying and defecation • Possible consequences : • CVA • Brain abscess • ↓Development

  32. Congenital Heart Diseases TYPES OF DEFECTS and Classification 1st Acyanotic ♥ 2nd Cyanotic ♥ ↑Pulmonary Obstruction to ↓Pulmonary Mixed blood flow blood flow flow flow ↓ ↓ ↓ ↓ ASD Tetralogy TPOGA VSD Coarctation of of Fallots Truncus the aorta arteriosis. PDA Tricuspid Hypoplastic Pulmonic stenosis Artesia Lt Heart syndrome

  33. Right to Left Shunts • Occurs when pressure in the right side of the heart is greater than the left side of the heart. • Resistance of the lungs in abnormally high • Pulmonary artery is restricted • Deoxygenated blood from the right side shunts to the left side

  34. Right to Left Shunt • Hole in septum + obstructive lesion = Deoxygenated blood from the right side of the heart shunts to the left side of the heart and out into the body.

  35. Clinical Manifestations • Hypoxemia = the result of decreased tissue oxygenation. • Polycythemia = increased red blood cell production due to the body’s attempt to compensate for the hypoxemia. • Increase viscosity of the blood = heart has to pump harder.

  36. Potential Complications • Thrombus formation due to sluggish circulation. • Brain abscess or stroke due to the un-oxygenated blood bypassing the filtering system of the lungs.

  37. Left to Right Shunt • Pressures on the left side of the heart are normally higher than the pressures in the right side of the heart. If there is an abnormal opening in the septum between the right and left sides, blood flows from left to the right.

  38. Clinical Manifestations • The infant is not cyanotic. • Tachycardia due to pushing increased blood volume. • Cardiomegaly due to increased workload of the heart.

  39. Clinical Manifestations • Dyspnea and pulmonary edema due to the lungs receiving blood under high pressure from the right ventricle. • Increased number of respiratory infections due to blood pooling in the the lungs promoting bacterial growth.

  40. ♥Acyanotic Defects: • Lt – to – Rt shunting through an abnormal opening or obstructive lesions leading to decrease blood flow to various parts of the body. • The most common clinical manifestation is heart failure. Some of them may be asymptomatic (ASD, VSD, PDA)

  41. Patent Ductus Arteriosus

  42. Patent Ductus Arteriosus:(PDA) • The fetal ductus artery connecting the aorta and the pulmonary artery fails to close within few weeks after birth, so the blood flows from the high pressure of the aorta to the lower pressure of the pulmonary artery (Lt – to –Rt shunt • Ductus normally closes within hours of birth • Connection between the pulmonary artery (low pressure) and aorta (high pressure)

  43. Patent Ductus Arteriosus Incidence: • Incidence 10% • It is most common cardiac anomaly • One of the most common benign defects • The ratio is: 2 ♀: 1♂ • High risk for pulmonary hypertension

  44. Clinical Manifestations: PDA • Might be asymptomatic • Show signs of CHF • Machinery - like murmur • Widened pulse pressure • Bounding pulses resulting from runoff of blood from aorta to pulmonary artery • Risk of bacterial endocarditis and pulmonary vascular obstructive disease in later life from chronic excessive pulmonary blood flow

  45. Diagnosis tests • Diagnosis by • Chest x-ray – enlarged heart and dilated pulmonary artery • Echo-cardiogram – show the opening between pulmonary artery and aorta

  46. Treatment: PDA • Medical management by using Endomethacin (Prostaglandin inhibitor) which constricts the muscle in the wall of the PDA and promotes closure • Nonsurgical treatment where coil is placed in the open duct and acts like a plug used during catheterization procedure • Surgical Management via small incision made between ribs on left hand side and PDA is ligated or tied and cut off Prognosis is good with less than 1% mortality

  47. Atrial Septal Defect (ASD)

  48. Atrial Septal Defect (ASD) • An abnormal opening between atria with a Lt-to-Rt Shunt. Blood in left atrium flows into right atrium. • 10% of defects • Reduced blood volume in systemic circulation

  49. Clinical Manifestations (ASD) • May be asymptomatic • May develop CHF • Characteristic murmur • Pt is at risk for atrial dysrythmia ( may be due to atrial enlargement and stretching of conduction fibers) • At risk for pulmonary vascular obstructive disease, and emboli formation later in life due to chronic increased pulmonary blood flow If left untreated may lead to pulmonary hypertension, congestive heart failure or stroke as an adult.

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