congenital heart diseases.pptx

CONGENITAL HEART DISEASES Presented by Sharoon rufan RN, BSN  Objectives  At the end of this presentation the students will be able to  Explain Fetal circulation  Elaborate Congenital malformations of heart  Define Rheumatic heart disease  understand pharmacological mana...

CONGENITAL HEART DISEASES Presented by Sharoon rufan RN, BSN  Objectives  At the end of this presentation the students will be able to  Explain Fetal circulation  Elaborate Congenital malformations of heart  Define Rheumatic heart disease  understand pharmacological management and Nursing Care approaches while dealing  Fetal circulation  Fetal circulation refers to the unique circulatory system present in an unborn baby (fetus) during pregnancy. The fetal circulatory system is adapted to allow the exchange of nutrients, oxygen, and waste products between the fetus and the mother while the baby is developing in the womb. It differs significantly from the circulatory system present after birth, as certain structures and pathways are not needed until  Important structures of fetal circulation  Placenta: The placenta is an organ that develops during pregnancy and acts as a bridge between the mother's blood supply and the fetus. Oxygen and nutrients are exchanged through the placental membrane, while waste products are eliminated from the fetal bloodstream.  Umbilical Cord: The umbilical cord connects the fetus to the placenta. It contains two umbilical arteries that carry deoxygenated blood from the fetus to the placenta and one umbilical vein that carries  continue...  Foramen Ovale: In the fetal heart, there is a small opening called the foramen ovale between the two atria (upper chambers). This opening allows some of the oxygen-rich blood returning from the placenta to bypass the fetal lungs and flow directly into the left atrium.  Ductus Arteriosus: Another important fetal adaptation is the ductus arteriosus, a blood vessel that connects the pulmonary artery (leading to the lungs) to the aorta (leading to the body's systemic  continue...  Ductus Venosus: This vessel shunts a portion of the oxygenated blood from the umbilical vein directly into the inferior vena cava, bypassing the liver. This helps supply oxygen and nutrients to the developing fetal tissues. continue...  Changes after birth  After birth, several changes occur as the baby begins to breathe air and adapt to life outside the womb:  First Breath: When the baby takes its first breath, the lungs expand, and pulmonary blood flow increases. This decrease in resistance in the pulmonary circulation causes the closure of the ductus arteriosus.  continue...  Closure of Foramen Ovale: As blood flows into the lungs, pressure in the left atrium increases, leading to the closure of the foramen ovale. This prevents blood from shunting directly between the atria.  Closure of Ductus Venosus: With the umbilical cord clamped and cut after birth, blood flow through the ductus venosus ceases. This vessel will eventually close and become a  Congenital heart diseases  Congenital heart diseases (CHDs) are a group of structural or functional abnormalities in the heart that are present at birth. These conditions can affect the heart's chambers, valves, blood vessels, and electrical conduction system. these diseases vary in severity, ranging from mild conditions that might not require treatment Types of congenital heart diseases  1.Acynotic (a.increased pulmonary blood flow)  1.Atrial Septal Defect (ASD): An opening in the wall (septum) between the heart's upper chambers (atria). This can lead to abnormal blood flow between the atria. Types of the atrial septal defect  Ostium primum (ASD 1): Opening at lower end of septum; may be associated with mitral valve abnormalities  Ostium secundum (ASD 2): Opening near center of septum  Sinus venosus defect: Opening near junction of superior vena cava and right atrium.  Pathophysiology  left atrial pressure slightly exceeds right atrial pressure, blood flows from the left to the right atrium, causing an increased flow of oxygenated blood into the right side of the heart. Despite the low pressure difference, a high rate of flow can still occur because of low pulmonary vascular resistance and the greater distensibility of the right atrium, which further reduces flow resistance. This volume is well tolerated by the right ventricle because it is delivered under much lower pressure than with a VSD. Although there is right atrial and ventricular enlargement, cardiac failure is unusual in an uncomplicated ASD.  Surgical treatment  Surgical patch closure (pericardial patch or Dacron patch) is done for moderate to large defects. Open repair with cardiopulmonary bypass is usually performed before school age. 2.Ventricular Septal Defect (VSD)  Ventricular Septal Defect (VSD): A hole in the septum between the heart's lower chambers (ventricles), allowing blood to flow between them.  Pathophysiology  Because of the higher pressure within the left ventricle and because the systemic arterial circulation offers more resistance than the pulmonary circulation, blood flows through the defect into the pulmonary artery. The increased blood volume is pumped into the lungs, which may eventually result in increased pulmonary vascular resistance. Increased pressure in the right ventricle as a result of left-to-right shunting and pulmonary resistance causes the muscle to hypertrophy. If the right ventricle is unable to accommodate the increased workload, the right atrium may also enlarge as it attempts to overcome the resistance offered by incomplete right ventricular emptying.  Surgical management  Complete repair (procedure of choice): Small defects are repaired with sutures. Large defects usually require that a knitted Dacron patch be sewn over the opening. 3.Atrioventricular Canal Defect  Incomplete fusion of the endocardial cushions. Consists of a low ASD that is continuous with a high VSD and clefts of the mitral and tricuspid valves, which create a large central AV valve that allows blood to flow between all four chambers of the heart  Pathophysiology  The alterations in hemodynamics depend on the severity of the defect and the child's pulmonary vascular resistance. Immediately after birth, while the newborn's pulmonary vascular resistance is high, there is minimum shunting of blood through the defect. When this resistance falls, left-to-right shunting occurs, and pulmonary blood flow increases. The resultant pulmonary vascular engorgement predisposes the child to development of HF. 4.Patent Ductus Arteriosus (PDA)  Patent Ductus Arteriosus (PDA): Failure of the fetal ductus arteriosus (artery connecting the aorta and pulmonary artery) to close within the first weeks of life. The continued patency of this vessel allows blood to flow from the higher pressure aorta to the lower pressure pulmonary artery, which causes a left- to-right shunt.  Pathophysiology  The hemodynamic consequences of PDA depend on the size of the ductus and the pulmonary vascular resistance. At birth, the resistance in the pulmonary and systemic circulations is almost identical so that the resistance in the aorta and pulmonary artery is equalized. As the systemic pressure comes to exceed the pulmonary pressure, blood begins to shunt from the aorta across the duct to the pulmonary artery (left-to-right shunt). The additional blood is recirculated through the lungs and returned to the left atrium and left ventricle. The effects of this altered circulation are increased workload on the left side of the heart, increased pulmonary vascular congestion and possibly resistance, and potentially increased right ventricular pressure and hypertrophy.  Medical management  Administration of indomethacin (a prostaglandin inhibitor) has proved successful in closing a PDA in preterm infants and some newborns. 1.Acynotic (b. obstruction to the blood flow to the ventricles)  1.Coarctation of the Aorta: Localized narrowing near the insertion of the ductus arteriosus, which results in increased pressure proximal to the defect (head and upper extremities) and decreased pressure distal to the obstruction (body and lower extremities).  Clinical manifestations  The patient may have high BP and bounding pulses in the arms, weak or absent femoral pulses, and cool lower extremities with lower BP. There are signs of HF in infants. In infants with critical coarctation, the hemodynamic condition may deteriorate rapidly with severe acidosis and hypotension.  Surgical treatment  Repair is by resection of the coarcted portion with an end-to-end anastomosis of the aorta or enlargement of the constricted section using a graft of prosthetic material or a portion of the left subclavian artery. 2.Aortic Stenosis  Narrowing or stricture of the aortic valve, causing resistance to blood flow in the left ventricle, decreased cardiac output, left ventricular hypertrophy, and pulmonary vascular congestion. The prominent anatomic consequence of AS is the hypertrophy of the left ventricular wall, which eventually leads to increased end-diastolic pressure, resulting in pulmonary venous and pulmonary arterial hypertension.  Pathophysiology  A stricture in the aortic outflow tract causes resistance to ejection of blood from the left ventricle. The extra workload on the left ventricle causes hypertrophy. If left ventricular failure develops, left atrial pressure will increase; this causes increased pressure in the pulmonary veins, which results in pulmonary vascular congestion (pulmonary edema).  Clinical manifestations:  Newborns with critical AS demonstrate signs of decreased cardiac output with faint pulses, hypotension, tachycardia, and poor feeding. Children show signs of exercise intolerance, chest pain, and dizziness when standing for a long period.  Surgical treatment  Balloon dilation in the catheterization laboratory is the first-line procedure.  Aortic valve replacement  3.Pulmonic Stenosis  Narrowing at the entrance to the pulmonary artery. Resistance to blood flow causes right ventricular hypertrophy and decreased pulmonary blood flow.  Pathophysiology  When PS is present, resistance to blood flow causes right ventricular hypertrophy. If right ventricular failure develops, right atrial pressure will increase, and this may result in reopening of the foramen ovale, shunting of unoxygenated blood into the left atrium, and systemic cyanosis. If PS is severe, HF occurs.  Surgical treatment  In infants, transventricular (closed) valvotomy (Brock procedure) is the surgical treatment. 2.cynotic (Decreased pulmonary blood flow) 1.Tetralogy of Fallot: The classic form includes four defects: (1) Ventricular Septal Defect, (2) Pulmonary Stenosis, (3) overriding aorta, and (4) right ventricular hypertrophy.  Pathophysiology  The alteration in hemodynamics varies widely, depending primarily on the degree of PS but also on the size of the VSD and the pulmonary and systemic resistance to flow. Because the VSD is usually large, pressures may be equal in the right and left ventricles. Therefore, the shunt direction depends on the difference between pulmonary and systemic vascular resistance. If pulmonary vascular resistance is higher than systemic resistance, the shunt is from right to left. If systemic resistance is higher than pulmonary resistance, the shunt is from left to right. PS decreases blood flow to the lungs and consequently the amount of oxygenated blood that returns to the left side of the heart. Depending on the position of the aorta, blood from both ventricles may be distributed systemically.  Clinical manifestations  Some infants may be acutely cyanotic at birth; others have mild cyanosis that progresses over the first year of life as the PS worsens. There is a characteristic systolic murmur that is often moderate in intensity. There may be acute episodes of cyanosis and hypoxia, called blue spells or tet spells. Anoxic spells occur when the infant's oxygen requirements exceed the blood supply, usually during crying or after feeding.  Surgical treatment  Complete repair: Elective repair is usually performed in the first year of life. Indications for repair include increasing cyanosis and the development of hypercyanotic spells.  Tricuspid Atresia  The tricuspid valve fails to develop; consequently there is no communication from the right atrium to the right ventricle. Blood flows through an ASD or a patent foramen ovale to the left side of the heart and through a VSD to the right ventricle and out to the lungs.  Pathophysiology  At birth, the presence of a patent foramen ovale (or other atrial septal opening) is required to permit blood flow across the septum into the left atrium; the PDA allows blood flow to the pulmonary artery into the lungs for oxygenation. A VSD allows a modest amount of blood to enter the right ventricle and pulmonary artery for oxygenation. Pulmonary blood flow usually is diminished.  Clinical manifestations  Cyanosis is usually seen in the newborn period. There may be tachycardia and dyspnea. Older children have signs of chronic hypoxemia with clubbing.  Surgical treatment  Palliative treatment is the placement of a shunt (pulmonary–to–systemic artery anastomosis) to increase blood flow to the lungs. If the ASD is small, an atrial septostomy is performed during cardiac catheterization. 2.Cynotic( mixed defects)  1.Transposition of the Great Vessels: The pulmonary artery leaves the left ventricle, and the aorta exits from the right ventricle with no communication between the systemic and pulmonary circulations.  Pathophysiology  Associated defects, such as septal defects or PDA, must be present to permit blood to enter the systemic circulation or the pulmonary circulation for mixing of saturated and desaturated blood.  Clinical manifestations  These depend on the type and size of the associated defects. Newborns with minimum communication are severely cyanotic and have depressed function at birth. Those with large septal defects or a PDA may be less cyanotic but have symptoms of HF. Heart sounds vary according to the type of defect present. Cardiomegaly is usually evident a few weeks after birth.  Therapeutic management  The administration of IV prostaglandin E1 may be initiated to keep the ductus arteriosus open to temporarily increase blood mixing and provide an oxygen saturation of 75% or to maintain cardiac output. During cardiac catheterization or under echocardiographic guidance, a balloon atrial septostomy (Rashkind procedure) may also be performed to increase mixing by opening the atrial septum.  Rheumatic heart disease  Rheumatic heart disease (RHD) is a serious condition that can result from untreated or inadequately treated streptococcal throat infections, particularly streptococcal pharyngitis (strep throat). It is an inflammatory disease that affects the heart and its valves, often leading to permanent damage.  Causes  RHD is caused by an autoimmune response to an infection with group A Streptococcus bacteria. When the body's immune system reacts to the streptococcal infection, it can also mistakenly attack and damage the heart valves and other parts of the heart.  Sign and Symptoms  : The symptoms of RHD can vary widely and may include shortness of breath, fatigue, chest pain, palpitations, and swollen ankles or legs. In severe cases, RHD can lead to heart failure and other complications.  Valve Damage: RHD most commonly affects the heart valves, particularly the mitral valve. The inflammation can cause scarring, thickening, and deformities in the valves, which can disrupt blood flow through the heart.  Diagnostics  Diagnosis of RHD involves a combination of medical history, physical examination, and diagnostic tests such as echocardiography (ultrasound of the heart), electrocardiography (ECG), and sometimes cardiac catheterization.  Prevention  The primary prevention of RHD involves promptly and adequately treating streptococcal infections, particularly strep throat, with appropriate antibiotics to prevent the development of acute rheumatic fever (ARF), which is a precursor to RHD. In some cases, long-term antibiotic prophylaxis might be recommended for individuals at high risk of developing RHD  Treatment  Treatment for RHD focuses on managing the symptoms, preventing further damage, and addressing complications. Medications such as antibiotics (for ongoing prophylaxis), anti- inflammatory drugs, and medications to manage heart failure might be prescribed. In cases of severe valve damage, surgical interventions such as valve repair or replacement might be necessary.  Nursing management  Assess and record heart rate, respiratory rate, blood pressure (BP), and any signs or symptoms of decreased cardiac output every 2 to 4 hours and as necessary.  Administer cardiac drugs on schedule. Assess and record any side effects or any signs and symptoms of toxicity. Follow hospital protocol for administration.  Keep accurate record of intake and output.  Weigh infant on same scale at same time of day as previously. Document results and compare to previous weight.  continue...  Administer diuretics on schedule. Assess and record effectiveness and any side effects noted.  Offer small, frequent feedings to infant's tolerance.  Organize nursing care to allow infant uninterrupted rest. Refrences  Hawes, H., & Scotchmer, C. (1993). What children need to know and pass on about child development Children for health London: The Child to Child Trust, UNICEEF.  Wong, D. L. (2005). Whaley and Wong’s nursing care of infants and  children, St. Louis: Mosby. Thank you!!!