The Child with Cardiovascular Dysfunction



The Child with Cardiovascular Dysfunction


Margaret L. Schroeder, Amy Delaney and Annette L. Baker



Learning Objectives


On completion of this chapter the reader will be able to:


• Design a plan for assisting children during cardiac diagnostic procedures.


• Demonstrate an understanding of the hemodynamics, distinctive manifestations, and therapeutic management of congenital heart disease.


• Outline a care plan for an infant or child with heart failure.


• Describe the care for a child who has hypoxia.


• Describe the care for an infant or a child with a congenital heart defect and its surgical repair.


• Discuss the nurse’s role in helping the child and family cope with congenital heart disease.


• Differentiate between rheumatic fever and rheumatic heart disease.


• List the criteria for selected cholesterol screening of children.


• Discuss the assessment and management of hypertension in children and adolescents.


• Outline a care plan for a child with Kawasaki disease.


• Describe the emergency treatment for shock, including anaphylaxis.


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http://evolve.elsevier.com/wong/essentials





Cardiovascular Dysfunction


image Animation—Structure of the Heart


image Cardiovascular disorders in children are divided into two major groups, congenital heart disease and acquired heart disorders. Congenital heart disease (CHD) includes primarily anatomic abnormalities present at birth that result in abnormal cardiac function. The clinical consequences of congenital heart defects fall into two broad categories, heart failure (HF) and hypoxemia. Acquired cardiac disorders are disease processes or abnormalities that occur after birth and can be seen in the normal heart or in the presence of congenital heart defects. They result from various factors, including infection, autoimmune responses, environmental factors, and familial tendencies. The pathophysiology review found in Figure 25-1 describes the flow of blood through the heart.


image
FIG 25-1 Diagram showing serially connected pulmonary and systemic circulatory systems and how to trace the flow of blood. Right heart chambers propel unoxygenated blood through the systemic circulation. LA, Left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle. (From McCance KL, Heuther SE: Pathophysiology: the biological basis for disease in adults and children, ed 6, St. Louis, 2010, Mosby.)


History and Physical Examination


Taking an accurate health history is an important first step in assessing an infant or child for possible heart disease. Parents may have specific concerns, such as an infant with poor feeding or fast breathing, or a 7-year-old who can no longer keep up with friends on the soccer field. Others may not realize that their child has a medical problem because their baby has always been pale and fussy.


Asking details about the mother’s health history, pregnancy, and birth history is important in assessing infants. Mothers with chronic health conditions, such as diabetes or lupus, are more likely to have infants with heart disease. Some medications, such as phenytoin (Dilantin), are teratogenic to fetuses. Maternal alcohol use or illicit drug use increases the risk of congenital heart defects. Exposures to infections, such as rubella, early in pregnancy may result in congenital anomalies. Infants with low birth weight resulting from intrauterine growth restriction are more likely to have congenital anomalies. High-birth-weight infants have an increased incidence of heart disease.


A detailed family history is also important. There is an increased incidence of congenital cardiac defects if either parent or a sibling has a heart defect. Some diseases, such as Marfan syndrome, and some cardiomyopathies are hereditary. A family history of frequent fetal loss, sudden infant death, and sudden death in adults may indicate heart disease. Congenital heart defects are seen in many syndromes such as Down and Turner syndromes.


The physical assessment of suspected cardiac disease begins with observation of general appearance and then proceeds with more specific observations. The following are supplementary to the general assessment techniques described for physical examination of the chest and heart in Chapter 6:






Diagnostic Evaluation


A variety of invasive and noninvasive tests may be used in the diagnosis of heart disease (Table 25-1). Some of the more common diagnostic tools that require nursing assessment and intervention are described here.



TABLE 25-1


PROCEDURES FOR CARDIAC DIAGNOSIS


























































PROCEDURE DESCRIPTION
Chest radiography (x-ray) Provides information on heart size and pulmonary blood flow patterns
ECG Graphic measure of electrical activity of heart
 Holter monitor 24-hour continuous ECG recording used to assess dysrhythmias
Echocardiography Use of high-frequency sound waves obtained by a transducer to produce an image of cardiac structures
 Transthoracic Done with transducer on chest
  M-mode One-dimensional graphic view used to estimate ventricular size and function
  Two-dimensional Real-time, cross-sectional views of heart used to identify cardiac structures and cardiac anatomy
  Doppler Identifies blood flow patterns and pressure gradients across structures
 Fetal Imaging fetal heart in utero
 TEE Transducer placed in esophagus behind heart to obtain images of posterior heart structures or in patients with poor images from chest approach
Cardiac catheterization Imaging study using radiopaque catheters placed in a peripheral blood vessel and advanced into heart to measure pressures and oxygen levels in heart chambers and visualize heart structures and blood flow patterns
 Hemodynamics Measures pressures and oxygen saturations in heart chambers
 Angiography Use of contrast material to illuminate heart structures and blood flow patterns
 Biopsy Use of special catheter to remove tiny samples of heart muscle for microscopic evaluation; used in assessing infection, inflammation, or muscle dysfunction disorders; also to evaluate for rejection after heart transplant
 EPS Special catheters with electrodes employed to record electrical activity from within heart; used to diagnose rhythm disturbances
Exercise stress test Monitoring of heart rate, blood pressure, ECG, and oxygen consumption at rest and during progressive exercise on a treadmill or bicycle
Cardiac MRI Noninvasive imaging technique; used in evaluation of vascular anatomy outside of heart (e.g., COA, vascular rings), estimates of ventricular mass and volume; uses for MRI are expanding

COA, Coarctation of the aorta; ECG, electrocardiography; EPS, electrophysiology; MRI, magnetic resonance imaging; TEE, transesophageal echocardiography.



Electrocardiogram

Bedside cardiac monitoring with the electrocardiogram (ECG) is commonly used in pediatrics, especially in the care of children with heart disease. The bedside monitor provides valuable information about heart rate and rhythm through a graphic display of the ECG tracing and a digital display. An alarm can be set with parameters for individual patient requirements and will sound if the heart rate is above or below the set parameters. Gelfoam electrodes are commonly used and placed on the right side of the chest (above the level of the heart) and on the left side of the chest, and a ground electrode is placed on the abdomen. Electrodes should be changed every 1 or 2 days because they irritate the skin. Bedside monitors are an adjunct to patient care and should never be substituted for direct assessment and auscultation of heart sounds. The nurse should assess the patient, not the monitor.



Nursing Tip


Electrodes for cardiac monitoring are often color coded: white for right, green (or red) for ground, and black for left. Always check to ensure that these colors are placed correctly.



Echocardiography

Echocardiography is one of the most frequently used tests for detecting cardiac dysfunction in children. Recent improvements in echocardiographic techniques have made it increasingly possible to confirm the diagnosis without resorting to cardiac catheterization. In more and more cases, a prenatal diagnosis of CHD can be made by fetal echocardiography.


Echocardiography involves the use of ultra-high-frequency sound waves to produce an image of the heart’s structure. A transducer placed directly on the chest wall delivers repetitive pulses of ultrasound and processes the returned signals (echoes).


Although the test is noninvasive, painless, and associated with no known side effects, it can be stressful for children. The child must lie quietly in the standard echocardiographic positions; crying, nursing, or sitting up often leads to diagnostic errors or omissions. Therefore, infants and young children may need a mild sedative; older children benefit from psychologic preparation for the test. The distraction of a video or movie is often helpful.



Cardiac Catheterization

image Animation—Catheter Placement, Umbilical Vein


image Cardiac catheterization is an invasive diagnostic procedure in which a radiopaque catheter is inserted through a peripheral blood vessel into the heart. The catheter is usually introduced through percutaneous technique, in which the catheter is threaded through a large-bore needle that is inserted into the vein. The catheter is guided through the heart with the aid of fluoroscopy. After the tip of the catheter is within a heart chamber, contrast material is injected, and films are taken of the dilution and circulation of the material (angiography). Types of cardiac catheterizations include:



Diagnostic catheterizations—These studies are used to diagnose congenital cardiac defects, particularly in symptomatic infants and before surgical repair. They are divided into right-sided catheterizations, in which the catheter is introduced through a vein (usually the femoral vein) and threaded to the right atrium (most common), and left-sided catheterizations, in which the catheter is threaded through an artery into the aorta and into the heart.


Interventional catheterizations (therapeutic catheterizations)—A balloon catheter or other device is used to alter the cardiac anatomy. Examples include dilating stenotic valves or vessels or closing abnormal connections (Table 25-2).



Electrophysiology studies—Catheters with tiny electrodes that record the impulses of the heart directly from the conduction system are used to evaluate dysrhythmias and sometimes destroy accessory pathways that cause some tachydysrhythmias.



Nursing Care Management


Cardiac catheterization has become a routine diagnostic procedure and may be done on an outpatient basis. However, it is not without risks, especially in neonates and seriously ill infants and children. Possible complications include acute hemorrhage from the entry site (more likely with interventional procedures because larger catheters are used), low-grade fever, nausea, vomiting, loss of pulse in the catheterized extremity (usually transient, resulting from a clot, hematoma, or intimal tear), and transient dysrhythmias (generally catheter induced) (Uzark, 2001). Rare risks include stroke, seizures, tamponade, and death.



Preprocedural Care

A complete nursing assessment is necessary to ensure a safe procedure with minimum complications. This assessment should include accurate height (essential for correct catheter selection) and weight. Obtaining a history of allergic reactions is important because some of the contrast agents are iodine based. Specific attention to signs and symptoms of infection is crucial. Severe diaper rash may be a reason to cancel the procedure if femoral access is required. Because assessment of pedal pulses is important after catheterization, the nurse should assess and mark the pulses (dorsalis pedis, posterior tibial) before the child goes to the catheterization room. The presence and quality of pulses in both feet are clearly documented. Baseline oxygen saturation using pulse oximetry in children with cyanosis is also recorded.


Preparing the child and family for the procedure is the joint responsibility of the patient care team. School-age children and adolescents benefit from a description of the catheterization laboratory and a chronologic explanation of the procedure, emphasizing what they will see, feel, and hear. Older children and adolescents may bring earphones and favorite music so they can listen during the catheterization procedure. Preparation materials such as picture books, videotapes, or tours of the catheterization laboratory may be helpful. Preparation should be geared to the child’s developmental level. The child’s caregivers often benefit from the same explanations. Additional information, such as the expected length of the catheterization, description of the child’s appearance after catheterization, and usual postprocedure care, should be outlined. (See also Prepare the Child and Family for Invasive Procedures, p. 845.)


Methods of sedation vary among institutions and may include oral or intravenous (IV) medications (see Chapter 22). The child’s age, heart defect, clinical status, and type of catheterization procedure planned are considered when sedation is determined. General anesthesia may be needed for some interventional procedures. Children are allowed nothing by mouth (NPO) for 4 to 6 hours or more before the procedure according to institutional guidelines. Infants and patients with polycythemia may need IV fluids to prevent dehydration and hypoglycemia.



Postprocedural Care

Patients may recover from the procedure in a recovery unit; their hospital room; or, occasionally, an intensive care unit (ICU). Patients are placed on a cardiac monitor and a pulse oximeter for the first few hours of recovery. The most important nursing responsibility is observation of the following for signs of complications:



• Pulses, especially below the catheterization site, for equality and symmetry (Pulse distal to the site may be weaker for the first few hours after catheterization but should gradually increase in strength.)


• Temperature and color of the affected extremity because coolness or blanching may indicate arterial obstruction


• Vital signs, which are taken as frequently as every 15 minutes, with special emphasis on heart rate, which is counted for 1 full minute for evidence of dysrhythmias or bradycardia


• Blood pressure (BP), especially for hypotension, which may indicate hemorrhage from cardiac perforation or bleeding at the site of initial catheterization


• Dressing, for evidence of bleeding or hematoma formation in the femoral or antecubital area


• Fluid intake, both IV and oral, to ensure adequate hydration (Blood loss in the catheterization laboratory, the child’s NPO status, and diuretic actions of dyes used during the procedure put children at risk for hypovolemia and dehydration.)


• Blood glucose levels for hypoglycemia, especially in infants, who should receive dextrose-containing IV fluids



image Nursing Alert


If bleeding occurs, direct continuous pressure is applied 2.5 cm (1 inch) above the percutaneous skin site to localize pressure over the vessel puncture.


Depending on hospital policy, the child may be kept in bed with the affected extremity maintained straight for 4 to 6 hours after venous catheterization and 6 to 8 hours after arterial catheterization to facilitate healing of the cannulated vessel. If younger children have difficulty complying, they can be held in the parent’s lap with the leg maintained in the correct position. The child’s usual diet can be resumed as soon as tolerated, beginning with sips of clear liquids and advancing as the condition allows. The child is encouraged to void to clear the contrast material from the blood. Generally, there is only slight discomfort at the percutaneous site. To prevent infection, the catheterization area is protected from possible contamination. If the child wears diapers, the dressing can be kept dry by covering it with a piece of plastic film and sealing the edges of the film to the skin with tape. However, the nurse must be careful to continue observing the site for any evidence of bleeding (see Family-Centered Care box and Critical Thinking Case Study).



image Family-Centered Care


After Cardiac Catheterization




Modified from Children’s Hospital (Boston) Cardiovascular Program, 1996.



image Critical Thinking Case Study


Cardiac Catheterization


Tommy, a 3-year-old boy with tetralogy of Fallot, has just returned to his hospital room from the cardiac catheterization recovery room. His mother calls you to the bedside to tell you that he is vomiting and bleeding. You arrive to find Tommy anxious, pale, crying, and sitting in a puddle of blood.




Congenital Heart Disease


The incidence of CHD in children is approximately 5 to 8 per 1000 live births (Park, 2008). About 2 or 3 in 1000 infants will be symptomatic during the first year of life with significant heart disease that requires treatment (Hoffman and Kaplan, 2002). CHD is the major cause of death (other than prematurity) in the first year of life. Although there are more than 35 well-recognized cardiac defects, the most common heart anomaly is ventricular septal defect (VSD).


The exact cause of most congenital cardiac defects is unknown. Most are thought to be a result of multiple factors, including a complex interaction of genetic and environmental influences. Some risk factors are known to be associated with increased incidence of congenital heart defects. Maternal risk factors include chronic illnesses such as diabetes or poorly controlled phenylketonuria, alcohol consumption, and exposure to environmental toxins and infections. Family history of a cardiac defect in a parent or sibling increases the likelihood of a cardiac anomaly. The risk of CHD increases if a first-degree relative (parent or sibling) is affected. The familial risk is higher with left-sided obstructive lesions.


Congenital heart anomalies are often associated with chromosomal abnormalities, specific syndromes, or congenital defects in other body systems. Down syndrome (trisomy 21) and trisomies 13 and 18 are highly correlated with congenital heart defects. Syndromes associated with heart defects include DiGeorge syndrome, a syndrome characterized by deletion of part of chromosome 22q11 (interrupted aortic arch, truncus arteriosus, tetralogy of Fallot, and posterior malaligned VSDs); Noonan syndrome (pulmonic valve anomalies and cardiomyopathy); Williams syndrome (aortic and pulmonic stenosis); and Holt-Oram syndrome (upper limb anomalies and atrial septal defect [ASD]). Extracardiac defects such as tracheoesophageal fistula, renal abnormalities, and diaphragmatic hernia are seen in association with heart anomalies.



Circulatory Changes at Birth


image Blood carrying oxygen and nutritive materials from the placenta enters the fetal system through the umbilicus via the large umbilical vein. The blood then travels to the liver, where it divides. Part of the blood enters the portal and hepatic circulation of the liver, and the remainder travels directly to the inferior vena cava (IVC) by way of the ductus venosus. Oxygenated blood enters the heart by way of the IVC. Because of the higher pressure of blood entering the right atrium, it is directed posteriorly in a straight pathway across the right atrium and through the foramen ovale to the left atrium. In this way, the better-oxygenated blood enters the left atrium and ventricle to be pumped through the aorta to the head and upper extremities. Blood from the head and upper extremities entering the right atrium from the superior vena cava is directed downward through the tricuspid valve into the right ventricle. From there it is pumped through the pulmonary artery, where the major portion is shunted to the descending aorta via the ductus arteriosus. Only a small amount flows to and from the nonfunctioning fetal lungs (Fig. 25-2, A).


image
FIG 25-2 Changes in circulation at birth. A, Prenatal circulation. B, Postnatal circulation. Arrows indicate direction of blood flow. Although four pulmonary veins enter the left atrium (LA), for simplicity, this diagram shows only two. LV, Left ventricle; RA, right atrium; RV, right ventricle.

image Animation—Fetal Circulation


Before birth, the high pulmonary vascular resistance created by the collapsed fetal lung causes greater pressures in the right side of the heart and the pulmonary arteries. At the same time, the free-flowing placental circulation and the ductus arteriosus produce a low vascular resistance in the remainder of the fetal vascular system. With the cessation of placental blood flow from clamping of the umbilical cord and the expansion of the lungs at birth, the hemodynamics of the fetal vascular system undergo pronounced and abrupt changes (Fig. 25-2, B).


With the first breath, the lungs are expanded, and increased oxygen causes pulmonary vasodilation. Pulmonary pressures start to fall as systemic pressures, given the removal of the placenta, start to rise. Normally, the foramen ovale closes as the pressure in the left atrium exceeds the pressure in the right atrium. The ductus arteriosus starts to close in the presence of increased oxygen concentration in the blood and other factors.



Altered Hemodynamics


To appreciate the physiology of heart defects, it is necessary to understand the role of pressure gradients, flow, and resistance within the circulation. As blood is pumped through the heart, it (1) flows from an area of high pressure to one of low pressure and (2) takes the path of least resistance. In general, the higher the pressure gradient, the faster the rate of flow; the higher the resistance, the slower the rate of flow.


Normally, the pressure on the right side of the heart is lower than that on the left side, and the resistance in the pulmonary circulation is less than that in the systemic circulation. Vessels entering or exiting these chambers have corresponding pressures. Therefore, if an abnormal connection exists between the heart chambers (e.g., a septal defect), blood will necessarily flow from an area of higher pressure (left side) to one of lower pressure (right side). Such a flow of blood is termed a left-to-right shunt. Anomalies resulting in cyanosis may result from a change in pressure so that the blood is shunted from the right to the left side of the heart (right-to-left shunt) because of either increased pulmonary vascular resistance or obstruction to blood flow through the pulmonic valve and artery. Cyanosis may also result from a defect that allows mixing of oxygenated and deoxygenated blood within the heart chambers or great arteries, such as occurs in truncus arteriosus.



Classification of Defects


There are typically two classification systems used to categorize congenital heart defects. Traditionally, cyanosis, a physical characteristic, has been used as the distinguishing feature, dividing anomalies into acyanotic defects and cyanotic defects. In clinical practice, this system is problematic because children with acyanotic defects may develop cyanosis. Also, more often, those with cyanotic defects may appear pink and have more clinical signs of HF.


A more useful classification system is based on hemodynamic characteristics (blood flow patterns within the heart). These blood flow patterns are (1) increased pulmonary blood flow; (2) decreased pulmonary blood flow; (3) obstruction to blood flow out of the heart; and (4) mixed blood flow, in which saturated and desaturated blood mix within the heart or great arteries. As a comparison, Figure 25-3 outlines both classification systems. With the hemodynamic classification system, the clinical manifestations of each group are more uniform and predictable. Defects that allow blood flow from the higher pressure left side of the heart to the lower pressure right side (left-to-right shunt) result in increased pulmonary blood flow and cause heart failure (HF). Obstructive defects impede blood flow out of the ventricles; whereas obstruction on the left side of the heart results in HF, severe obstruction on the right side causes cyanosis. Defects that cause decreased pulmonary blood flow result in cyanosis. Mixed lesions present a variable clinical picture based on the degree of mixing and amount of pulmonary blood flow; hypoxemia (with or without cyanosis) and HF usually occur together. Using this classification system, the clinical presentation and management of the most common defects are outlined in the following sections and Box 25-1.



Box 25-1   Defects with Increased Pulmonary Blood Flow



Atrial Septal Defect


image



Description—Abnormal opening between the atria, allowing blood from the higher pressure left atrium to flow into the lower pressure right atrium. There are three types of ASD:



Pathophysiology—Because 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. Pulmonary vascular changes usually occur only after several decades if the defect is left unrepaired.


Clinical manifestations—Patients may be asymptomatic. They may develop HF. There is a characteristic systolic murmur with a fixed split second heart sound. There may also be a diastolic murmur. Patients are at risk for atrial dysrhythmias (probably caused by atrial enlargement and stretching of conduction fibers) and pulmonary vascular obstructive disease and emboli formation later in life from chronically increased pulmonary blood flow.


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. In addition, the sinus venosus defect requires patch placement, so the anomalous right pulmonary venous return is directed to the left atrium with a baffle. ASD 1 type may require mitral valve repair or, rarely, replacement of the mitral valve.


Nonsurgical treatment—ASD 2 closure with a device during cardiac catheterization is becoming commonplace and can be done as an outpatient procedure. The Amplatzer Septal Occluder is most commonly used. Smaller defects that have a rim around them for attachment of the device can be closed with a device; large, irregular defects without a rim require surgical closure. Successful closure in appropriately selected patients yields results similar to those from surgery but involves shorter hospital stays and fewer complications. Patients receive low-dose aspirin for 6 months (Rome and Kreutzer, 2004).


Prognosis—Operative mortality is very low (<1%).



Ventricular Septal Defect


image



Description—Abnormal opening between the right and left ventricles. May be classified according to location: membranous (accounting for 80%) or muscular. May vary in size from a small pinhole to absence of the septum, which results in a common ventricle. VSDs are frequently associated with other defects, such as pulmonary stenosis, transposition of the great vessels, PDA, atrial defects, and COA. Many VSDs (20%–60%) close spontaneously. Spontaneous closure is most likely to occur during the first year of life in children having small or moderate defects. A left-to-right shunt is caused by the flow of blood from the higher pressure left ventricle to the lower pressure right ventricle.


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.


Clinical manifestations—HF is common. There is a characteristic loud holosystolic murmur heard best at the left sternal border. Patients are at risk for BE and pulmonary vascular obstructive disease.


Surgical treatment



Nonsurgical treatment—Device closure during cardiac catheterization is being performed in some centers under investigational protocols. One device has been approved for closure of muscular defects, and another is in clinical trials. Early results are encouraging, with successful defect closure and few complications (Rome and Kreutzer, 2004).


Prognosis—Risks depend on the location of the defect, the number of defects, and the presence of other associated cardiac defects. Single-membranous defects are associated with low mortality (<2%); multiple muscular defects can carry a higher risk (Jacobs, Mavroudis, Jacobs, and others, 2004).



Atrioventricular Canal Defect


image



Description—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. The directions and pathways of flow are determined by pulmonary and systemic resistance, left and right ventricular pressures, and the compliance of each chamber, although flow is generally from left to right. It is the most common cardiac defect in children with Down syndrome.


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.


Clinical manifestations—Patients usually have moderate to severe HF. There is a loud systolic murmur. There may be mild cyanosis that increases with crying. Patients are at high risk for developing pulmonary vascular obstructive disease.


Surgical treatment



Prognosis—Operative mortality is less than 5% (Jacobs, Mavroudis, Jacobs, and others, 2004). A potential later problem is mitral regurgitation, which may require valve replacement.



image Patent Ductus Arteriosus


image



Description—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.


    image Case Study—Patent Ductus Arteriosus


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.


Clinical manifestations—Patients may be asymptomatic or show signs of HF. There is a characteristic machinery-like murmur. A widened pulse pressure and bounding pulses result from runoff of blood from the aorta to the pulmonary artery. Patients are at risk for BE and pulmonary vascular obstructive disease in later life from chronic excessive pulmonary blood flow.


Medical management—Administration of indomethacin (a prostaglandin inhibitor) has proved successful in closing a PDA in preterm infants and some newborns.


Surgical treatment—Surgical division or ligation of the patent vessel is performed via a left thoracotomy. In a newer technique, video-assisted thoracoscopic surgery, a thoracoscope and instruments are inserted through three small incisions on the left side of the chest to place a clip on the ductus. The technique is used in some centers and eliminates the need for a thoracotomy, thereby speeding postoperative recovery.


Nonsurgical treatment—Coils to occlude the PDA are placed in the catheterization laboratory in many centers. Preterm or small infants (with small-diameter femoral arteries) and patients with large or unusual PDAs may require surgery.


Prognosis—Both surgical and nonsurgical procedures can be done at low risk with less than 1% mortality. PDA closure in very preterm infants has a higher mortality rate because of the additional significant medical problems.

Related posts:

  1. Pain Assessment and Management in Children
  2. Family Influences on Child Health Promotion
  3. Health Promotion of the Adolescent and Family
  4. The Child with Cerebral Dysfunction

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Jan 16, 2017 | Posted by in NURSING | Comments Off on The Child with Cardiovascular Dysfunction

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