Cardiac Disorders



Cardiac Disorders



Objectives



1. Define the vocabulary terms listed


2. Describe the changes from fetal to neonatal circulation


3. Summarize the symptoms of a congenital heart defect with increased pulmonary blood flow


4. Discuss the corrective interventions for a child with mixed heart defects


5. Develop a teaching plan for an older child who is scheduled for a cardiac catheterization


6. List the symptoms for an infant with CHF


7. List three major and two minor manifestations of acute rheumatic fever as determined by the modified Jones criteria


8. Identify the priority nursing care for a child with rheumatic fever



Key Terms















imagehttp://evolve.elsevier.com/Price/pediatric/



Cardiovascular System


The four-chambered heart begins development as a single tube around the third week of gestation and becomes the first fully functioning system by the eighth week of gestation. Some of these defects occur before mothers are aware of their pregnancy. Cardiac defects can be evident at birth or may not be identified until a later age. The heart is a vital organ and when parents are confronted with cardiac problems, fear and anxiety become overwhelming. Families who may not have a basic understanding of the cardiovascular system are being overloaded with new terms and information.


Heart defects are the most common birth defect and are the leading cause of birth defect-related deaths. The incidence rate of infants born with a congenital heart defect is about one per 125 deliveries (March of Dimes, 2006). With the advancement in diagnosis and treatment, about 85% of children live into adulthood. This has created a new subspecialty, the adult with congenital heart disease.


Fetal circulation differs from normal circulation as the organ of oxygenation is the placenta. Oxygenated blood from the placenta flows through the umbilical vein to the liver and inferior vena cava. A small portion of the blood supports the hepatic tissue, while the rest flows through the ductus venosus into the inferior vena cava. As blood enters the right atrium, most of the flow is directed through the foramen ovale (a septum connection between the right and left atrium) to the left side of the heart and out the aorta. The remaining blood continues to flow to the right ventricle and out the pulmonary arteries to the lungs. Since the lungs are not functioning, only a small amount of the oxygenated blood is needed to provide nutrients to lung tissue. The majority of this oxygenated flow is diverted again through the ductus arteriosus (a connection between the pulmonary artery and the aorta) into the aorta. The oxygenated blood is distributed to the rest of the body and is returned through the umbilical arteries to the placenta (Figure 12-1).


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FIGURE 12-1 Diagram of fetal circulation showing the placenta, umbilical vein, and umbilical arteries. The fetal bypasses are also shown. These are ductus venosus, ductus arteriosus, and foramen ovale.

During the birthing process, the dynamics of blood flow changes as the lungs become the organ of oxygenation. Blood flow no longer needs to bypass the lungs, resulting in the closure of the fetal shunts (i.e., the ductus venosus, foramen ovale, and ductus arteriosus). While the ductus venosus and foramen ovale usually close quickly, the ductus arteriosus may take several days to close.


Closures of these shunts impact the pressures in the heart. During fetal circulation, the pressure is higher on the right side of the heart. The closure of the shunts will result in higher left-sided pressures. Direction of blood flow is impacted by the pressures in various parts of the heart. Blood flow will move from an area of higher pressure to an area of lower pressure.


Murmurs are generated by turbulence of blood flow through the heart. They are classified as systolic, diastolic, or continuous. They are graded from 1 to 6 based on increasing loudness. Murmurs may be thought of as functional (innocent) or organic (from improper heart formation). Functional murmurs are caused by the sound of blood passing through a normal heart. Organic murmurs result from blood passing through abnormal openings or normal openings that have not yet closed. Most heart murmurs in the newborn period have been found to be functional, may come and go (transient), and tend not to be serious. However, murmurs should be reported to the physician and the newborn should be checked periodically to rule out other possibilities.



Congenital Heart Disease


A baby born with congenital heart disease (CHD) has a defect in the structure of the heart or in one or more of the large blood vessels that lead to and from the heart. The heart or vessels have failed to develop properly during the gestational period.


Research indicates that most congenital defects are a result of genetic-environmental interactions; that is, they are multifactorial. Genetic factors that may increase the risks include a history of CHD in other family members and chromosomal abnormalities such as Down syndrome. Environmental risk factors include alcoholism, cocaine use, rubella, exposure to Coxsackie virus, diabetes mellitus, ingestion of lithium salts, use of Accutane, and advanced maternal age.


Therefore, the nurse must stress the need for good prenatal care and impress on the parents the value of regular checkups at baby clinics. Many organic heart murmurs have been detected early in infancy at a periodic checkup. A careful health history is particularly useful.



Classification


In the past, congenital heart defects were divided into two groups: cyanotic and acyanotic. This categorization has proved inaccurate because children with acyanotic defects may develop cyanosis and those with cyanotic disease may be pink in color. Presently, defects are classified according to the effect the defect has on the movement of circulating blood. The study of blood circulation is termed hemodynamics (hemo, blood; dynamis, power). Defects can be classified as (1) defects with increased pulmonary blood flow, (2) obstructive defects, (3) defects with decreased pulmonary blood flow, and (4) mixed defects. A list of the hemodynamics and the heart defect(s) associated with each is given in Box 12-1.



Box 12-1   Hemodynamics and Examples of Congenital Heart Disease






The flow of blood through abnormal openings or vessels is called shunting. The direction of the shunt flow is determined by the pressures in the connecting chambers or vessels. Flow will move from a high to a low pressure area. Normally the right side of the heart has a lower pressure than the left side. Flow from the left side to the right is referred to as “left to right shunt.” The flow of oxygenated blood into unoxygenated blood results in no mixed blood gaining access to the systemic system. Flow from the right to the left side is called “right to left shunt.” This flow of unoxygenated blood into oxygenated blood results in mixed blood circulating in the systemic system.



Diagnostic Tools


Several diagnostic tools can be used in evaluation of a child with CHD. Not all testing is necessary for each child. The tools include laboratory tests, electrocardiogram, Holter monitor, event recorder, chest radiography, echocardiogram, MRI, and cardiac catheterization. The diagnostic procedures listed in Box 12-2 can be used in identifying the type of heart defect.



Box 12-2   Diagnostic Procedures in Congenital Heart Disease




Cardiac catheterization is an invasive procedure that provides information about anatomy, cardiac pressures, oxygen saturations, and cardiac function. Sedation is necessary to ensure that the child does not move. Older children and families should be prepared for the procedure. Discussing the sounds and sights of the cath lab and post op care may help decrease anxiety. Following the procedure, the child will have a cardiac monitor and pulse oximetry. The nurse will need to monitor the following:




imageSafety Alert


The pressure dressing placed over the insertion site is monitored per hospital policy. The infant’s diaper area should also be monitored as any bleeding can flow down the child’s groin crease. Any wetness or bleeding should be immediately reported, and pressure should be applied above the insertion site. Dressings should not be removed to view the site until ordered.


The child’s extremity should be kept straight for 4 to 6 hours depending on hospital policy. Encouraging parents to hold the child may help in decreasing the child’s anxiety. Discharge instructions should include signs of infection, fever management, activity restrictions, and bathing guidelines.



Signs and Symptoms


The symptoms, as indicated in Box 12-3, depend on the location and type of heart defect. Some children have mild cases and can lead a fairly normal life with medical management. Others are treated medically until the optimal time for surgery. Heart transplantation is an option in some cases.



Box 12-3   General Signs and Symptoms in Congenital Heart Disease




The child with CHD may be small for age, and his or her condition may be classified as a physiologic failure to thrive. This is the result of the difficulty the child has feeding and breathing at the same time. In addition, it takes energy to suck and infants may spend more energy eating than gained from their formula. Exercise intolerance may first be identified when the infant experiences dyspnea while feeding or it may not be evident until later, when the child tends to be more active. The older child may assume a squatting position to decrease venous return by occluding the femoral veins and thus lessen the workload of the right side of the heart. The infant can gain this same effect by being placed in the knee-chest position.


Hematocrit and hemoglobin concentration impact the effectiveness of oxygen transportation. Hematocrit (the percent of erythrocytes volume in a given volume of blood) is normally 35% to 49% in infants and children. Hematocrit can range from 44% to 72% in newborns. Hemoglobin (the iron-containing pigment that carries oxygen) can range from 11% to 15% in children. When the body determines there is hypoxemia (decreased oxygen in blood), it compensates by increasing the number of red blood cells to carry oxygen to the tissues. This is known as polycythemia. When there is an increase in the number of red blood cells, the hematocrit will also be elevated. This results in an increased viscosity of the blood and increased cardiac workload. “Thick” blood causes an increased risk for thromboembolism and cardiovascular accident.


Hypoxia is a result of inadequate oxygenation and can present with cyanosis in children with heart defects. Cyanosis can be generalized or localized such as in the hands, feet, or lips or around the mouth. Cyanosis may be constant or transient and can be influenced by the child’s behavior such as crying. Crying can improve or worsen the cyanosis. Overt cyanosis can be difficult to observe in children with dark skin. For these children, cyanosis can be detected in the mucous membranes of the mouth, on the palms of the hands, or on the bottom of the feet. Chronic hypoxia can result in long-lasting pooling of the blood in the capillaries resulting in clubbing of the fingers and/or toes (Figure 12-2). The child may also present with a pale or mottled appearance. Arterial oxygen saturation can differ with each type of defect. Ideally, oxygen saturation is between 95% and 98% in normal children, and saturations below 88% can result in cyanosis. Some of the defects have saturations much lower than 88%. Assessment of the heart rate of a child with hypoxemia is important as hypoxemia can result in bradycardia.


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FIGURE 12-2 Clubbing in fingers caused by poor oxygenation.


imageNursing Brief


Bradycardia can be a warning sign of an impending cardiac arrest. Prolonged hypoxemia and respiratory arrest result in cardiac arrest in children rather than a primary cardiac arrhythmia as seen in adults. Nursing assessment of hypoxemia is a priority for a child with a cardiac defect.


Finally, many CHD children tend to have frequent respiratory infections because of pulmonary vascular congestion. The amount of dyspnea does vary, and in more acute cases, it is accompanied by flaring of the nostrils, mouth breathing, and sternal retractions. The child has more trouble breathing when flat in bed than when being held upright. Signs of air hunger are irritability, restlessness, and a weak and hoarse cry. Increased respirations over 60 per minute in an infant can indicate distress.


Some common nursing diagnoses associated with CHD are listed in Box 12-4. The normal heart is illustrated in Figure 12-3.



Box 12-4   Nursing Diagnoses Associated with Congenital Heart Disease




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FIGURE 12-3 The normal heart.


Congestive Heart Failure. 

A child with a severe heart defect may develop congestive heart failure (CHF). It is not a disease in itself but rather symptoms caused by an underlying heart defect. CHF occurs if the heart is unable to maintain adequate cardiac output to meet body demands. Early symptoms may be subtle. The infant, who requires a longer time period for feeding and has a decrease in intake, may fail to gain weight and be irritable and fatigued. Tachycardia and tachypnea with increased work of breathing (grunting, nasal flaring, wheezing, coughing, retractions) may be observed. As CHF progresses, periorbital and facial edema, vein distention, hepatomegaly, and splenomegaly can appear. A decrease in perfusion results in decreased urine output, diaphoresis, mottling, cyanosis, and pallor.



Defects with Increased Pulmonary Blood Flow 


Patent Ductus Arteriosus. 

The ductus arteriosus (PDA) is the passageway by which the blood crosses from the pulmonary artery to the aorta and avoids the deflated lungs in the fetus. This vessel closes shortly after birth; however, when it does not close, blood continues to pass from the aorta, where the pressure is higher, into the pulmonary artery. This causes oxygenated blood to recycle through the lungs, overburdening the pulmonary circulation and making the heart work harder. A machine-like murmur may be heard. The symptoms of this disorder may go unnoticed during infancy. However, with growth, the child experiences dyspnea, pulses becomes full and bounding on exertion, and there may be failure to thrive. The parents may report frequent respiratory infections, which are a result of pulmonary congestion. Symptoms will depend on the amount of blood flowing through the ductus.


Patent ductus arteriosus is one of the most common cardiac anomalies (Figure 12-4). The word patent means open. PDA occurs twice as frequently in females as in males. In the premature infant, indomethacin or ibuprofen may be administered to facilitate closure of the ductus (Sadowski, 2009). If drug treatment is not successful, other nonsurgical intervention may be tried. Recent interventional devices such as coils or the Amplatzer PDA device (Figure 12-5) have provided closure for small ducts during cardiac catheterization. Occluder device risks include leaking and occlusions (Park, 2008). For large ducts, surgical repair includes ligation of the ductus through a left thoracotomy or with video-assisted thoracoscopic surgery (VATS). If this condition is left uncorrected, the child eventually could develop CHF or endocarditis. The prognosis for a corrected PDA is excellent.


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FIGURE 12-4 Patent ductus arteriosus.

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FIGURE 12-5 Amplatzer devices used with ASD, VSD, and PDA.


Atrial Septal Defect. 

Atrial septal defect (ASD) is one of the more common congenital heart anomalies (Figure 12-6). The incidence is higher in females than in males. There is an abnormal opening between the right and left atria. Blood that contains oxygen is forced from the left atrium to the right atrium. This type of arteriovenous shunt does not produce cyanosis unless the blood flow is reversed by heart failure. Most children do not have symptoms, but CHF and failure to thrive may be present in those with large openings. Currently, the defect can be repaired either with open heart surgery or percutaneous occluder devices (e.g., the Amplatzer ASD; see Figure 12-5) during cardiac catheterization. Open heart surgery requires the child being placed on the heart-lung machine during the procedure and has all the risks of a surgical procedure. Occluder devices can be used with openings located in certain places along the septum and openings with a small diameter. The occluder devices require shorter hospital stays. The child may require antimicrobial prophylaxis for potential infective endocarditis, and low-dose aspirin or an antiplatelet such as Plavix for clot prevention (Ferri, 2011). Both surgical and nonsurgical procedures have good results.


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FIGURE 12-6 Atrial septal defect.

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Dec 22, 2016 | Posted by in NURSING | Comments Off on Cardiac Disorders

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