After studying this chapter, you should be able to: evolve.elsevier.com/McKinney/mat-ch/ CLINICAL REFERENCE Review of the Heart and Circulation Normal Cardiac Anatomy and Physiology The heart is a muscular pump divided into four chambers. The two upper chambers are the atria, and the two lower chambers are the ventricles. The atria are referred to as the filling chambers and the ventricles as the pumping chambers. There are two atrioventricular (AV) valves, the tricuspid valve and the mitral valve, and two semilunar valves, the pulmonary valve and the aortic valve. In normal blood flow, desaturated venous blood returning from the body flows from the superior vena cava and inferior vena cava into the right atrium. It then moves through the tricuspid valve into the right ventricle and is pumped into the main pulmonary artery and branch pulmonary arteries to the pulmonary circulation. In the lungs, carbon dioxide is removed, and oxygen is added to the blood. This richly oxygen-saturated blood returns from the pulmonary circulation to the left side of the heart through the pulmonary veins and into the left atrium. From the left atrium, it flows through the mitral valve into the left ventricle and is pumped into the aorta and systemic circulation. Mechanical contraction of the heart muscle starts with electrical stimulation. This electrical stimulation is normally initiated by a group of cells called the sinus node, located at the superior vena cava and right atrial junction. The electrical impulse spreads through the atrium to the relay station, the AV node, and is then transmitted to the ventricles through the bundle of His, the bundle branch system, and finally the Purkinje fibers. The result is rhythmic atrial electrical stimulation and then contraction, followed by ventricular stimulation and contraction. The electrocardiogram records this electrical activity. The P wave reflects atrial depolarization; the QRS complex reflects ventricular depolarization; the T wave reflects ventricular repolarization. Each cardiac cycle consists of this electrical activity, which produces depolarization and subsequent repolarization of the cardiac muscle—more simply, a heartbeat. The venous (or right) side of the heart is normally a lower-pressure system compared with the higher arterial (or left) side of the heart. The right ventricle has a range of normal pressure of 18 to 30/0 to 5 mm Hg and pulmonary artery pressure of 20 to 30/8 to 12 mm Hg. The left ventricle has a range of normal pressure of 90 to 140/5 mm Hg (age dependent), and the aorta has a normal pressure of about 100/60 mm Hg (age dependent). On average, the left-sided pressures are four to five times higher than those on the right side. In addition, the venous circulation normally has lower oxygen saturations, in the range of 65% to 80%. This compares with the arterial circulation, which has a normal range of 95% to 100%. Congenital or acquired malformations or anomalies in any of the cardiac structures can affect blood flow, pressures, and oxygen saturations, thereby altering hemodynamic stability. Fetal Circulation Fetal circulation differs from neonatal circulation in three areas: the process of gas exchange, the pressures within the systemic and pulmonary circulations, and the existence of anatomic structures that assist in the delivery of oxygen-rich blood to vital organ systems. In the fetus, oxygenation (gas exchange) takes place at the placenta. Oxygen and nutrients are carried by blood in the umbilical vein, which travels through the fetal liver to the inferior vena cava. A small amount of blood travels into the hepatic circulation to provide oxygen and nutrients to the hepatic tissue. Liver function is minimal in the fetus, so very little blood supply is required. The remainder of the blood flows into the inferior vena cava through a fetal structure, the ductus venosus. The inferior vena cava empties blood into the right atrium. The trajectory (direction) of the blood flow, as well as the pressure in the right atrium, propels most of this blood through a second fetal structure, the foramen ovale, into the left atrium. This richly oxygenated blood travels through the left ventricle into the aorta, feeding the coronary arteries and the brain—the two most oxygen-needy organ systems. Blood returning from the upper body enters the right atrium through the superior vena cava. This blood is directed primarily through the tricuspid valve and the right ventricle into the pulmonary artery. Resistance in the pulmonary circulation is very high because the lungs are collapsed and filled with fluid. A very small amount of blood flows through the branch pulmonary arteries to provide oxygen and nutrients to the pulmonary tissue. Most of the blood flows through a third fetal structure, the ductus arteriosus, to the descending aorta. This blood is then distributed to the organ systems and tissues in the lower portion of the body and returns to the placenta for gas exchange through two umbilical arteries. Transitional and Neonatal Circulation Major changes in the circulatory system occur at birth. With the neonate’s first breath, gas exchange is transferred from the placenta to the lungs. The fetal shunts (ductus venosus, ductus arteriosus, foramen ovale) functionally close in response to pressure changes in the systemic and pulmonary circulations and to increased blood oxygen content. Pulmonary vascular resistance begins to decrease, and pulmonary blood flow markedly increases. Closure of the ductus arteriosus, along with the increased pulmonary blood flow, enhances left ventricular filling. The increase in systemic arterial pressure as a result of clamping the umbilical cord at delivery and placental separation from the fetus increases the workload of the left ventricle, and the neonatal heart now functions on its own. The neonatal circulation is now normal. In some neonates, it may take several days for the fetal shunts to close. COMMON DIAGNOSTIC TESTS FOR CARDIAC DISORDERS
IV, Intravenous. Cardiovascular alterations in children are either congenital or acquired. Congenital heart disease (CHD) denotes one or more structural abnormalities that develop before birth, although the clinical symptoms may not be present in the newborn period. Acquired heart disease, such as the cardiomyopathies, Kawasaki disease, or rheumatic fever, develops after birth and may be seen both in children with normal hearts and in those with CHD. Over the past 3 decades, there have been major advances in the diagnosis and management of CHD. Because of these advances, approximately 90% of infants born with CHD can be expected to live into adulthood. To appreciate each defect or combination of multiple defects and their effect on a child’s life, an understanding of normal cardiac anatomy and physiology, including development of the heart, circulation (including fetal, transitional, and postnatal), normal structures, and function is required. Congenital cardiac defects are some of the most frequently seen congenital defects in infants and children and have an overall incidence of 8 in every 1000 live births (American Heart Association [AHA], 2011). As interventional cardiology becomes more effective, more adults are living with congenital heart disease (CHD); the prevalence of CHD in adults is approximately 4 per 1000 (AHA, 2011). Although the nongenetic etiology and risk factors for CHD are not fully known, maternal diabetes mellitus, maternal infection during pregnancy, maternal smoking, maternal obesity, and maternal exposure to some chemicals and pollutants have been implicated (AHA, 2011). Children with certain genetic conditions or defects have an extremely high incidence of cardiac disorders, including children with chromosome aberrations, most specifically trisomy 21 (Down syndrome), in which the incidence of CHD is approximately 50% (Park, 2008). Other congenital conditions that increase the risk for CHD include Turner syndrome in girls (single X chromosome), Klinefelter variant in boys (genetically having additional X chromosomes), and children with Marfan syndrome or with velocardiofacial syndrome (DiGeorge syndrome) (Park, 2008). A family history of CHD increases the risk. Congenital heart defects can be classified according to structural abnormalities, functional alterations, or both (Table 46-1). Historically, defects were simply classified according to whether they were cyanotic or acyanotic. Currently, these classifications are subdivided into groups that are defined by blood flow patterns. These include presence of increased pulmonary blood flow, normal to decreased pulmonary blood flow, obstructive lesions, and miscellaneous complex lesions. TABLE 46-1 CLASSIFICATION OF CONGENITAL HEART DISEASE
ASD, Atrial septal defect; AVSD, atrioventricular septal defect; HF, heart failure; PDA, patent ductus arteriosus; VSD, ventricular septal defect. ∗Also classified as a lesion that decreases cardiac outflow. Clinical signs of congenital cardiac defects can manifest any time during the newborn period, infancy, or early childhood. The degree of symptoms, indications for medical, surgical, or transcatheter interventions, and chronicity of the condition depend on the diagnosis. Abnormal blood flow from one part of the circulatory system to another is called a shunt. A shunt occurs when (1) there is an abnormal opening or connection between the cardiac chambers or great arteries, (2) the pressure is higher on one side of the heart compared with the other (pressure gradient), and (3) the oxygen saturation is increased or decreased in the normally desaturated or fully saturated blood. It is important to remember that the venous or right side is usually a low-pressure, desaturated (average 70%) system and the arterial or left side is usually a high-pressure, fully saturated (95% to 100%) system. The combination of pressure differences and the size of the abnormal opening determine the extent of shunting. Generally, the amount of blood flow to the lungs through the pulmonary artery is the same as the amount of blood flow to the systemic circulation through the aorta. This ratio of pulmonary to systemic blood flow is described as the pulmonary-to-systemic ratio (QP/QS ratio) and is usually 1:1. Patients with CHD may have normal, increased, or decreased QP/QS blood flow ratios. Understanding the principles of shunting and normal saturations in each of the heart’s chambers helps clarify the blood flow direction in CHD. There are two primary physiologic consequences of CHD in children. These include heart failure and cyanosis. The definition of heart failure (HF) is the heart’s inability to circulate blood to maintain sufficient cardiac output to meet the metabolic demands of the body. Despite the causes of HF, the heart initially responds to the need for increased cardiac output by increasing the heart rate. Over time the heart may become enlarged (cardiomegaly), causing the muscle walls of the heart to grow weak and inefficient. This can reduce blood volume in the body, which causes the body’s arteries to constrict and force the heart to work even harder. This poor function causes congestion in the body and/or lung tissues (pulmonary edema). The etiology of HF in neonates, infants, and children differs from that for adults. In infants and children, HF is most often related to an underlying congenital cardiac defect that causes volume or pressure overload, but may also develop from many other etiologies, including acquired heart disease. Examples of acquired heart disease include cardiomyopathies, dysrhythmias, infections (e.g., endocarditis, myocarditis), and tumors. Damage to the heart also can occur as a result of inborn metabolic disorders and exposure to certain drugs, and toxins (Park, 2008). Many times the symptoms can be treated by drugs. If there is an anatomic defect, correction of the cause either by surgery or transcatheter intervention is often needed. Defects that lead to volume overload and cause symptoms of HF in infants and children include left-to-right shunts (e.g., atrial septal defects [ASDs], ventricular septal defects [VSDs], common AV canal defect [CAVC], and patent ductus arteriosus [PDA]). These defects allow excess blood to pass from the left side of the heart to the right, causing the heart to work harder to pump this extra volume to the lungs. Defects that lead to pressure overload and cause symptoms of HF mainly include left-side heart obstructive lesions (e.g., critical aortic stenosis, severe aortic coarctation, congenital mitral stenosis, and hypoplastic left heart syndrome) (Park, 2008). These defects cause the heart to pump harder against an obstruction in order to get blood to the body. This extra work, over time, will cause the heart muscle to enlarge (hypertrophy) and become inefficient. Defects that are acquired and cause symptoms of HF include primary myocardial diseases that attack the heart muscle and cause it to weaken. Dysrhythmias disrupt the delicate balance of the electrical or conduction system of the heart; cause the heart rate to be slow, fast, or erratic; and, over time, lead to poor cardiac output. The incidence of HF in infants and children is difficult to estimate because of improvements in surgical options. The earliest clinical manifestations of HF are often subtle. The infant may have mild tachypnea (70 to 100 breaths per minute) at rest and sometimes difficulty feeding. Parents may report that feedings take longer and the child requires frequent rest periods. This type of history describes a scenario where less nutrition is consumed while more energy is expended, resulting in fewer calories being consumed, although metabolic demands are increased. Feedings therefore provide little satisfaction, and the infant may appear hungry and irritable soon after a feeding. Over time, the infant fails to gain weight and eventually develops a condition known as failure to thrive (FTT). Children with HF may also exhibit respiratory-related symptoms. They may complain of dyspnea (particularly on exertion) and tachypnea. They are often described as having less energy than their peers. They may exhibit diaphoresis and complain of decreased appetite. This is due to chronic abdominal pain, usually related to poor circulation and decreased perfusion to the abdominal organs. This can also lead to failure to gain weight. Other clinical manifestations of HF include an abnormal cardiac rhythm known as a gallop; periorbital and facial edema, neck vein distention (in older children), hepatomegaly, and PATHOPHYSIOLOGY Heart Failure When a child develops heart failure (HF), hemodynamic and neurohormonal changes occur in response to decreased cardiac output. Cardiac output is a function of stroke volume and heart rate. Stroke volume (SV) is defined as the amount of blood ejected from the heart with each heartbeat. It is expressed in liters per minute (L/min). Cardiac output equals heart rate multiplied by stroke volume. Other factors affecting cardiac output include preload, afterload, and contractility. Neurohormonal changes include the stimulation of both the sympathetic nervous system and the renin-angiotensin system. Maintaining blood pressure, blood flow, and oxygen delivery to vital organs is the goal of this compensatory system. With decreased cardiac output, there is stimulation of the sympathetic nervous system. Initially this leads to increased heart rate, contractility, and stroke volume; increased systemic vascular resistance (afterload); and selective peripheral vasoconstriction. Tachycardia, although beneficial to compensate for early HF, increases myocardial oxygen consumption, decreases the diastolic filling time and resting phase of the heart, and decreases coronary artery perfusion.∗ Decreased cardiac output also causes the renal system to have decreased renal blood flow and a diminished glomerular filtration rate. This leads to increased stimulation of the renin-angiotensin-aldosterone system. Sodium and water are reabsorbed, leading to fluid retention and thereby increasing intravascular volume. Initially, this volume retention increases preload and cardiac output. Later, the myocardium becomes more edematous, and ventricular function decreases from volume and pressure overload. The pulmonary system is also affected by this increased volume, and interstitial edema develops. In addition, myocardial oxygen consumption increases and may exceed the oxygen availability. Finally, myocardial muscle can undergo cellular and muscular mass changes, or hypertrophy. Without intervention, heart failure progresses until the compensatory mechanisms are no longer effective. ∗Bernstein, D. (2011). The cardiovascular system. In R. Kliegman, B. Stanton, J. St. Geme, et al. (Eds.), Nelson textbook of pediatrics (19th ed., pp 1527-1604.). St. Louis: Saunders. splenomegaly; and decreased peripheral perfusion, decreased urine output, mottling, and cyanosis or pallor. |
Chapter 19: Nursing Care of the child With an Alteration in Perfusion/Cardiovascular Disorder
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