Anatomy & Physiology

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2 Anatomy & Physiology Heart is divided into four chambers, two atrias & two ventricles. Atrioventricular valves (tricuspid & mitral) separate the atria from ventricles. they open & close to control flow of blood into ventricles. The simelunar valve (pulmonary & aortic), they open & close to prevent the backflow of blood to ventricles. The pulmonary artery carry deoxygenated blood from right ventricle to lungs, after process of gas exchange occur, oxygenated blood is transmitted again into left atrium by pulmonary veins and through mitral valve to the left ventricle. And then to the body by aorta. 2

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6 Fetal Circulation During pregnancy blood is transferred from placenta through umbilical vein into the ductus venosus (opining into the inferior vena cava). Then blood is carried to the right atrium in which is forced into the left atrium by an opining between the two atriums called foramen ovale. Blood is transferred into the left ventricles and to the whole body through aorta. Some blood pass into the right ventricle, in which it moved to the lungs by the pulmonary artery. But, the majority of this blood pass into the aorta by an opining between aorta & pulmonary artery called ductus atreriousus. 6

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8 After birth, the newborn start breathing which increase the lung expansion, helping in shifting of blood into the lungs by the pulmonary artery not into the aorta by the ductus arteriosus as during pregnancy. This will lead to increase pulmonary blood flow & decrease pulmonary vascular resistance. Also leading to increase blood returned to the left atrium through pulmonary veins & this leads to increase pressure in the left atrium. The increasing pressure stimulate the closure of the foramen ovale and. Ductus arteriosus close in response to increase O2 saturation after hours and permanently after days. 8 Transition from fetal to pulmonary circulation

9 Pediatric differences 1- Cardiac functioning: The heart s muscle fibers are less develops & less organized, resulting in limited functional capacity. The heart muscle is fully developed at 5 years of age & the heart muscle fiber at 9 years of age. The heart weight increase by six times at one year. Heart rate is high due to increase metabolic rate & O2 requirements. 9

10 Laboratory tests 1. Cardiac catheterization. 2. Chest radiograph study. 3. Echocardiogram. 4. ECG 5. MRI 6. Arterial blood gases. 7. CBC 10

11 Congenital Heart Diseases Refer to a defect in the heart or great vessels or persistence of a fetal structure after birth. Most of the CHD develops during the first 8 weeks of gestation. Some genetic or environmental factors found to be related to the CHD, such as: 1. Fetal exposure to drugs such as warfarin, lithium, alcohol. 2. Maternal viral infection such as rubella. 3. Genetic factors. 4. Chromosomal abnormalities such as Down syndrome. 5. Maternal complication during pregnancy. 11

12 Classifications CHD previously were categorized as to whether the child have or did not have cyanosis (cyanotic or acyanotic). But now they are classified according to their pathophysiology & hemodynamics. Theses categories include The following: 1. Increase pulmonary blood flow 2. Decreased pulmonary blood flow. 3. Obstructed systemic blood flow. 4. Mixed defects in which infant survival is dependent upon mixing of systemic & pulmonary blood. 12

13 CHD that increase pulmonary blood flow These defects includes: 1. Patent ductus arteriosus. 2. Atrial septal defect 3. Ventricular septal defect 13

14 Patent ductus arteriosus (PDA) Pathophysiology: In this anomaly, the ductus arteriosus does not close after birth. Leading blood to shift from aorta to the pulmonary artery ( because the pressure in the aorta is higher than it in the pulmonary artery). Leading to increase blood shunted into the lungs and increased pulmonary vascular resistance & pulmonary blood pressure in response. This will leads to right ventricular hypertrophy to overcome the increasing pulmonary vascular resistance & deliver the blood to the lungs. 14

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16 It is a common problem in preterm infants & present in nearly all preterm infant less than 27 weeks gestation Clinical manifestations: Dyspnea; tachycardia; full, bounding pulse; hypotension, crackles. Intercostal retractions & growth retardation. Contentious murmur in diastole & systole. Diagnostic procedure: Chest radiograph; ECG; will show left & right ventricular hypertrophy. 16

17 Clinical Therapy Surgical ligation of PDA. Intravenous indomethacin often stimulate the closure of the ductus atreriosus. Thranscatheter closure by obstructive device is needed in children over 18 months. Prognosis: No long term interventions if treated before pulmonary vascular disease develops. 17

18 Arterial Septal Defect (ASD) It is an opening in the atrial septum that permits left to right shunting of blood. It can be small as when the foramen ovale fail to close, or large as when the septum may be completely absent. As the pressure in the left atrium is higher than in the right atrium; blood will shifts from the left to the right atrium. Leading to increase pressure on pulmonary system & right sided hypertrophy. 18

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20 Clinical manifestations: Infant & young children may have no symptoms, small to moderate size ASDs may not be diagnosed until preschool years or later. CHF, easy tiring, poor growth in large ASDs. Diagnostic procedure: Echocardiogram identified dilated right ventricle. Radiograph & ECG reviles right sided hypertrophy. 20

21 Clinical Therapy Spontaneous closure occur within the first 4 years of life. surgery is needed when symptoms of CHF occur. Prognosis: if not treated, person may develop signs of CHF. 21

22 Ventricular Septal Defect (VSD) An opening in the ventricular septum leads blood to shunts from the left ventricle to the right ventricle. Leading to increase pressure in the right side of the heart, hypertrophy occur in response. Clinical manifestations: Only large VSDs causes symptoms of CHF. Systolic murmur is heard. 22

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24 Diagnostic procedures: Echocardiogram identified dilated right ventricle. Radiograph & ECG reviles right & left sided hypertrophy. Treatment: Small VSDs lose within 6 months of life. Surgical patch is used when poor growth is evident. Closure of VSD by catheterization. Prognosis: Highest risk associated with surgical repair in the few months of life. 24

25 Nursing interventions for defects that increase pulmonary blood flow Psychological assessment. Assess parents needs. Psychosocial support. Genetic counseling for future pregnancy Pain management ( after surgery), e.g. use a pillow or stuffed animal held against the chest to reduce the pain from coughing & deep breathing. Promote respiratory function. Chest physiotherapy. Mange fluid & nutrition, encourage parents to bring favored food to the child if he tolerate it. 25

26 CHD that decreased pulmonary blood flow & mixed defects ## defects that decrease pulmonary flow: 1. Pulmonic stenosis. 2. Tetrology of fallot. 3. Tricuspid atresia. 4. Pulmonary atresia. ## Mixed defects: 1. Coarctation of aorta. 2. Aortic stenosis. 3. Mitral stenosis. 26

27 Pathophysiology: Pulmonic stenosis. Stenosis in the pulmonic valve. The stenosis can be at the valve area, above or below it. The stenosis obstruct the blood flow into the pulmonary artery leading to increased preload (the volume of blood in ventricles at the end of diastole). leading to right ventricle hypertrophy. 27

28 Pulmonary stenosis 28

29 Normal valve Pulmonary stenosis 29

30 Clinical manifestations: Children with mild stenosis have no symptoms. In moderate stenosis, dyspnea & fatigue occur on exertion. In sever cases, heart failure & chest pain occur with exertion. Load systolic murmur is heard. Thrill is felt in the pulmonic area. Diagnostic tests: Chest radiograph show an enlarged pulmonary artery with normal heart size. The ECG show right sided hypertrophy. 30

31 Clinical Therapy Dilation by balloon valvuloplasty, performed during cardiac catheterization. Surgical valvotomy is used with other defects presents such as VSD. Prognosis: It does not increase in severity, lifelong infective endocarditis prophylaxis is necessary. 31

32 Tetrology of fallot It consists of four defects: pulmonary stenosis, right ventricular hypertrophy, ventricular septal defect (VSD), & overriding of the aorta. Some children have fifth defect, an open foramen ovale. Presence of VSD leads blood to shunt from left ventricle to the right ventricle increase pressure in right ventricle hypertrophy. Presence of pulmonary stenosis leads to increase accumulation of blood in right ventricle increase pressure in right ventricle hypertrophy. 32

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34 Tetrology of fallot 34

35 Clinical Manifestation Hypoxia; cyanosis. Systolic murmur is heard in the pulmonic area. Thrill is palpated in the palmonic area. poor growth. Clubbing nail. Hypoxia episodes. Metabolic acidosis. Toddler with uncorrected or partially corrected defect, assume knee to chest position to decrease venous return. 35

36 Diagnostic tests: Chest radiograph. The ECG shows right ventricular hypertrophy. The echocardiogram shows the VSD, the size of the pulmonary artery. Cardiac catheterization provides details about the anatomic defects. Clinical therapy: Treating he cyanotic episodes by placing the child on knee-chest position, giving oxygen. Total repair performed before the age of 6 months when the infant has hypercyanotic episode. 36