Congenital heart defects are not uncommon among neonatal patients. The prompt identification of a life-threatening anomaly is essential for rapid intervention and a positive treatment outcome. Cardiac defects may be identified in the newborn nursery with thorough and systematic physical assessment, including inspection, palpation, auscultation, and measurement of blood pressure and oxygen saturations. The ability of the nurse to identify irregular findings during physical assessment aids rapid identification and treatment.
Introduction
Congenital Heart Defects are the Second Leading cause of death among children in the first year of life, yet prenatal screening alone picks up less than 25 percent of affected fetuses. Of cardiac lesions associated with death in the first two weeks, the most frequent are coarctation of the aorta, aortic stenosis, interrupted aortic arch, hypoplastic left heart syndrome, transposition of the great arteries, pulmonary atresia, and critical pulmonary stenosis. Nurses play an important role in the detection and assessment of congenital heart disease. One study found that 90 percent of newborn congenital heart defects could be identified prior to discharge when experienced nurses used a systematic approach to physical assessment and referral. A thorough cardiac examination of all newborns is essential to determine which patients need further examination and treatment. This article presents the steps of a thorough neonatal cardiac examination and provides an overview of several specific cardiac lesions.
History
An infant who is only a few hours old has a relatively short medical history; however, information can be gathered about the pregnancy and the child’s family that might suggest an increased risk of cardiac problems such as congenital heart disease. One of the most common risk factors for congenital heart disease is a positive family history. It is important to know whether a sibling or first-degree relative has been diagnosed with structural heart defect or if the family has a history of known heritable syndromes associated with heart abnormalities. Prenatal testing can also provide valuable information about the presence of genetic conditions associated with heart disease. Chorionic villus sampling (offered at 10 to 12 weeks gestational age) and amniocentesis (offered at 15 to 20 weeks) are diagnostic prenatal tests that can identify several conditions associated with congenital heart disease in the neonate, including trisomies 13, 18, and 21.
Many factors at play during pregnancy affect the proper structural formation of the fetal heart. Prenatal exposure to infections, such as with Epstein-Barr virus or rubella virus, poor maternal control of diabetes mellitus during pregnancy, and exposure to teratogenic drugs, are risk factors for congenital cardiac disease. Prescription medications as well as herbal preparations and over-the-counter medications taken during pregnancy should be identified when teratogenic substances are considered, especially amphetamines, anticonvulsants, trimethadione, lithium, and sex hormones. Fetal echocardiograms can be performed as early as 18–20 weeks gestational age to identify lesions such as hypoplastic left heart syndrome, tricuspid atresia, pulmonary atresia, truncus arteriosus, tetralogy of Fallot, atrioventricular septal defects, large ventricular septal defects, transposition of the great arteries, and other complex lesions. Prenatal indications for fetal cardiac echocardiogram include the presence of certain fetal, maternal, and familial factors associated with high risk of structural, functional, or rhythm-associated cardiac defects and/or nuchal thickening in the first trimester, associated with trisomy 22, Turner syndrome, and left-sided obstructive lesions.
Physical Examination
All newborns should have a complete physical examination within the first two hours of life. The nurse should start by examining the patient’s overall appearance. The infant’s coloring should be noted. Pallor may indicate anemia, whereas ruddiness may be a sign of polycythemia. Central cyanosis, a bluish discoloration of the skin that is best visualized in highly vascular areas such as the lips and mucous membranes, is a pathologic condition caused by decreased arterial oxygen saturation. Peripheral cyanosis is caused by increased oxygen extraction from hemoglobin in the extremities secondary to vasomotor instability, vasoconstriction, obstruction, elevated venous pressure, low cardiac output, or polycythemia; affected areas appear pale and cool to the touch. Peripheral cyanosis is common in neonates and, alone, is not an indication of pathology. The level of oxygen saturation at which cyanosis can be seen is dependent upon total hemoglobin concentration. Central cyanosis becomes apparent when levels of deoxygenated blood in capillary beds exceed 3 g/dL. Cyanosis can be detected among polycythemic patients at higher oxygen saturations than among anemic patients. Because polycythemic patients have more red blood cells and therefore reach the visibility threshold of 3 g/dL reduced hemoglobin more rapidly than anemic patients, central cyanosis is associated with a much lower oxygen saturation in an anemic patient than in a polycythemic patient. Skin mottling may also occur as peripheral perfusion is decreased. This spider web appearance at the surface of the skin occurs due to compensatory vasoconstriction that helps redistribute blood to vital organs.
Although respiratory complications outnumber congenital heart defects in the neonatal population, deteriorating respiratory status may be a sign of underlying cardiac problems. The nurse should observe for signs and symptoms of respiratory distress, such as tachypnea, retractions, grunting, and nasal flaring. These can be late indicators of cardiac failure and are caused by pulmonary edema secondary to insufficient emptying or overload of the left ventricle. In an infant, tachypnea is defined as a resting respiratory rate of 60–120 breaths per minute. Heart rate should be measured, and infants who are consistently tachycardic or bradycardic should be referred for evaluation. Tachycardia, a heart rate above 160 beats per minute, often occurs as the heart attempts to compensate for low cardiac output. Tachycardia has been associated with myocarditis and cardiomyopathy. Bradycardia, a rate of less than 90 beats per minute, is associated with long QT syndrome and atrioventricular block. In newborns with suspected cardiac compromise, blood pressures should be taken in each extremity and compared. A difference between upper and lower extremities greater than 15 mmHg systolic, when measured with an appropriately sized cuff, is abnormal and suggestive of coarctation of the aorta. A blood pressure cuff with a bladder width that measures approximately 40 percent of the upper arm circumference produces the most accurate results.
After a general physical assessment, the heart should be assessed systematically beginning with inspection and palpation. Upon inspection, a precordial bulge on the left side of the chest wall suggests cardiac enlargement; a substernal heave is suggestive of right ventricular hypertrophy secondary to pulmonary stenosis. The nurse should palpate for a precordial thrill resulting from disturbed high-velocity blood flow within the heart. Upon auscultation, the first and second heart sounds (S1 and S2) should be identified as well as any additional heart sounds. In neonates, the components of S2 may be split with inspiration and become one sound with expiration, but this can be difficult to appreciate in the neonate with a rapid heart rate. Because of the high respiratory rate of most infants, splitting at any point during the cardiac cycle may be considered normal. Pathologic sounds associated with S2 include loud pulmonary valve closure, seen with pulmonary artery hypertension; wide split, associated with right ventricular volume overload or delayed right ventricular conduction; and wide fixed split, associated with atrial septal defect. S3 and S4 can be distinguished from S1 and S2 because they are lower-frequency sounds best heard with the bell of the stethoscope. S3 is usually considered nonpathologic from birth until early adulthood; it is a diastolic heart sound caused by rapid, passive, ventricular filling, which causes reverberation within the ventricle that begins after ventricular relaxation has occurred. The health care provider should be aware that there are a few instances when S3 is not considered a normal finding, including when the sound is associated with right-to-left shunting lesions with significant regurgitation, left ventricular cardiomyopathy, and congestive heart failure. S4 is rare below the age of 40 and is considered an abnormal finding in the neonatal population. S4 occurs just before S1 during active ventricular filling and is associated with decreased ventricular compliance, which may occur in neonates with conditions such as coronary artery disease, hypertrophic obstructive cardiomyopathy (thickened cardiac muscle), aortic stenosis, systemic hypertension, pulmonary artery hypertension, tricuspid valve stenosis, and Ebstein’s anomaly.
After cardiac auscultation, the nurse should assess peripheral pulses, including the radial, posterior tibial, and femoral, for rate, rhythm, and character, also noting whether or not pulses are symmetric. Unequal pulses in the upper extremities or between the upper and lower extremities and weak or absent femoral pulses are hallmark indicators of coarctation of the aorta. Weak pulses may be a sign of poor perfusion caused by low cardiac output, obstruction, or shunting of blood to vital organs as a result of hypoxemia causing vasoconstriction in the extremities, whereas bounding pulses may indicate the presence of fluid volume overload, a patent ductus arteriosus, or right-to-left cardiac shunt, all of which result in excess fluid presence in the systemic circuit. Capillary refill should be assessed by blanching the skin over a bony area, such as the chest, and counting the number of seconds until color completely returns to the area; a normal reperfusion time is less than three seconds.
Pulse Oximetry
In the neonate, a pulse oximetry sensor is placed around the wrist or foot where blood vessels are close to the surface of the skin to measure the oxygen saturation of hemoglobin in the bloodstream. Pulse oximetry is a noninvasive tool that uses red and infrared wavelengths to determine light absorbency of arterial blood, producing a meaningful number representing the percentage of hemoglobin saturated with oxygen. It has been suggested that routine pulse oximetry would be a rapid and cost-effective screening tool for early diagnosis of congenital heart defects.
In a study by Arlettaz and colleagues, only 35 percent of newborns with cyanotic congenital heart defects presented with a murmur versus 100 percent of those with noncyanotic heart defects. No infants with cyanotic heart disease exhibited oxygen saturation greater than or equal to 95 percent. These results suggest that the presence of a murmur does not correlate well with severity of the cardiac lesion and that pulse oximetry should be used to screen all infants with or without audible heart murmurs.
The use of pulse oximetry as a screening tool to detect cardiac defects before clinical manifestation may still be of some benefit, especially, in infants who will deteriorate rapidly or show only subtle signs of physical decline. Early pulse oximetry measurement of a postductal extremity may also prove useful in regions with lower prenatal detection rates of critical congenital heart defects and with the growing trend to discharge infants from the hospital earlier in life, when physical signs of heart abnormalities may not yet be apparent. Further large-scale studies of the use of pulse oximetry in all neonates will need to be done to determine the utility and cost-effectiveness of such a screening tool.
Measuring Pre- and Postductal Oxygen Saturations
Measurement of preductal and postductal oxygen saturations may provide valuable information about blood shunting as the result of conditions such as persistent pulmonary hypertension of the newborn (PPHN). PPHN results in severe hypoxia and acidosis in term or near-term infants and occurs in the presence of extremely elevated pulmonary vasular resistance. High pulmonary pressures cause blood to shunt from the right side of the heart to the left through a patent ductus arteriosus (PDA) or foramen ovale. The ductus arteriosus connects to the aorta distal to the brachiocephalic artery, which splits into the right subclavian and right carotid arteries supplying blood to the upper right side of the body. The rest of the body receives blood that is partially deoxygenated due to blood flow through the PDA. High pressure in the pulmonary vasculature, such as occurs with PPHN, causes deoxygenated blood in the pulmonary artery to travel the path of least resistance to the aorta through the PDA instead of continuing through the pulmonary circuit. Therefore, oxygen saturations are higher when measured on the right hand or wrist (preductally) than on the left hand or wrist, left foot, or right foot (postductally). The accuracy of this test is limited when right-to-left shunting occurs at an atrial level; in these cases, no difference would be found between preductal and postductal saturations despite the presence of a serious cardiac condition.
Hyperoxia Test
The hyperoxia test can be used to distinguish pulmonary and cardiac causes of central cyanosis. Arterial oxygen tension is measured first preductally and then postductally while the patient breathes 100 percent oxygen. A transcutaneous oxygen monitor is used to assess whether oxygen tension, measured in millimeters of mercury, rises significantly with oxygen administration, indicating a pulmonary, as opposed to a cardiac, abnormality. If hypoxemia is caused by right-to-left shunting, then increasing the percentage of inspired oxygen has little effect because the shunted blood is not yet oxygenated in the lungs. Results of an abnormal or ambiguous test should be confirmed with an arterial blood gas measurement from the right radial artery. The hyperoxia test is not part of a routine cardiac examination of the neonate.
Cardiac Murmurs
Heart murmurs result from turbulent blood flow in or around the heart. They may be innocent or abnormal, but they are not uncommon. Frommelt identified murmurs in 60 percent of healthy newborns. Most identified neonatal cardiac murmurs are either benign or due to minor abnormalities of transitional circulation. Congenital heart defects of clinical significance have been found to affect only about 1 percent of infants. Cardiac murmurs are described by their intensity and timing. The timing of the murmur is identified as systolic, diastolic, or continuous. Systolic murmurs fall between the first and the second heart sound. Innocent murmurs are almost always systolic in nature; systole is normally associated with high pressures and turbulent blood flow caused by cardiac contraction. Diastole is usually a period of low-pressure, low-turbulence blood flow during ventricular refilling. These murmurs are caused by either turbulent blood flow through the low-pressure system, as with stenosis or increased blood flow across the mitral or tricuspid valve, or a leak in the high-pressure system caused by aortic or pulmonic valve regurgitation, neither of which is found under normal circumstances within the heart. Therefore, diastolic murmurs are more often associated with pathologic origins than are systolic murmurs.
Like diastolic murmurs, continuous murmurs are associated with pathology more often than systolic murmurs. They are not confined to systole or diastole as they can be heard throughout the cardiac cycle. Their place of origin is an area of turbulent blood flow that lies beyond the pulmonary or aortic valves. A “machinery-like” continuous murmur is classically heard in the presence of a PDA. One example of an innocent continuous murmur that is common in infants and children is the cervical venous hum, audible in the low anterior part of the neck and caused by high-pressure flow in the internal jugular and subclavian veins. Gentle compression of the jugular veins or turning the patient’s head toward the murmur should eliminate the humming sound. A murmur may be absent in the presence of serious heart disease if the velocity of blood at the site of the defect is not high enough to produce a murmur, if ventricular function is significantly decreased, or if pulmonary resistance is significantly increased. The location at which a murmur is auscultated may help identify the site of the defect. An echocardiogram is used to diagnose specific cardiac lesions. Common indications for neonatal echocardiogram include suspected PDA, PPHN, hemodynamic instability, and congenital heart disease in the presence of cyanosis, heart murmur, tachypnea, a genetic syndrome, noncardiac congenital malformations, arrhythmia, abnormal fetal echocardiogram, and maternal diabetes.
Summary
Before life-saving interventions can occur in a health care setting, assessment is central to the identification of a problem. Nurses in the nursery are in a unique position to be the first to identify serious cardiac abnormalities within this vulnerable population. A thorough physical assessment using a systematic approach is important to ensure that each child receives the same careful assessment, because infants may be seriously compromised without showing obvious signs or symptoms of acute illness. The examination begins with inspection of the infant’s overall appearance and attainment of vital signs. It is important to remember that infants with life-threatening heart defects do not always present with audible cardiac murmurs. A thorough cardiac examination should be done using inspection, palpation, and auscultation. Four-point blood pressures should be taken and pulse oximetry used to evaluate for indications of coarctation of the aorta and cyanotic heart disease.
Astute assessment skills are essential for any nurse serving the newborn population, because early detection could ultimately mean more rapid intervention and better treatment outcomes.
Source: Neonatal Network, 07-13-2010
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