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Acute Respiratory Care of the Newborn
Acute Respiratory Care of the Newborn JAN NUGENT, RN, MSN Respiratory problems account for most of the morbidity and mortality in the neonatal period. Etiology of respiratory difficulties and specific nursing assessments and interventions relevant to the neonate experiencing respiratory distress are discussed.
Many of the respiratory disorders of the newborn are unique to that period of development. Understanding the process of fetal lung maturation and differentiation as well as the adaptive transitional changes which occur in the cardiovascular and respiratory systems during the first 24 hours of life is essential in comprehending the pathogenesis of these problems. This information is available in the literature and will not be reviewed here. 1-4 CAUSES OF RESPIRATORY DISTRESS There are many respiratory disorders in the newborn period. By far, the most common are hyaline membrane disease, transient tachypnea of the newborn and meconium aspiration syndrome. Hyaline Membrane Disease Hyaline membrane disease, the most common form of neonatal respiratory distress, accounts for 18% of all neonatal deaths in the United state^.^ Hyaline membrane disease occurs in infants born prior to term and of appropriate size for gestational age.6 T h e pathogenesis of hyaline membrane disease is directly re-
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lated to the immaturity of the lung in respect to its capacity to synthesize and regenerate the surface active material surfactant. Surfactant effectively lowers surface tension in alveoli and thereby promotes alveolar stability and the establishment of a functional residual capacity.6 Without surfactant, alveolar collapse occurs at the end of expiration. Each breath becomes as difficult as the first and as the infant tires, atelectasis becomes progressively more pronounced. Progressive atelectasis is the hallmark of hyaline membrane disease. Atelectasis greatly reduces tidal volume, lung compliance, functional residual capacity, and alveolar ventilation. Atelectasis also contributes significantly to an uneven ventilation-perfusion ratio. T h e negative correlation between alveolar ventilation and right-toleft shunts (ie., the less the ventilation, the greater the shunt) is significant. This combination of atelectasis and pulmonary hypoperfusion secondary to intra- and extrapulmonary shunting of blood produces the typical clinical pict u r e of progressive hypoxia, hypercapnia, and metabolic a c i d o ~ i s . ~ A striking feature of hyaline membrane disease is early onset of symptoms, usually before six hours
of life. T h e infant will demonstrate tachypnea, nasal flaring, grunting, see-saw (paradoxical) respirations, and cyanosis. T h e infant will become progressively more obtunded and flaccid. Auscultation of lung fields will reveal diminished breath sounds. As the disease progresses, characteristic “sandpaper” breath sounds can be detected on inspiration and expiration. Characteristic x-ray findings are illustrated in Figure 1. T h e natural course of the disease is one of increasing severity of respiratory distress and poor lung function until 48 to 72 hours of life. Symptoms then will begin to abate as pulmonary type I1 cell regeneration occurs and surfactant production is reestablished.6 Treatment is aimed at overcoming and preventing atelectasis. Therapeutic measures consist of oxygen therapy, continuous positive airway pressure, and positive pressure ventilation. Hypothermia must be avoided; metabolic acidosis and hypotension must be corrected; and fluid, electrolyte, and glucose needs must be met. Transient Tachypnea of the Newborn T h e pathognomonic hallmark of transient tachypnea of the new-
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Figure 1. Anteroposterior chest film demonstrates x-ray manifestations of hyaline membrane disease. Note homogenous, bilaterally symmetrical reticulogranular pattern with diffuse air bronchogranis. In severe hyaline membrane disease, hypoaeration is also evident and is demonstrated by increased doming of both hemidiaphragms at the level of the seventh rib.
born, (respiratory distress, type 11) is delayed resorption of fetal lung fluid. Transient tachypnea of the
newborn occurs in term as well as preterm infant^.^ Predisposing conditions are prematurity and ce-
Figure 2. Anteropoaterior chest film demonstrated x-ray manifestations of transient tachypnea in the newborn. Bilateral diffuse perihilar and central lung fluid with fluid in the fissure are shown. Concoinitant hyperaeration of lungs is noted as both hemicli;ipliragms are at the level of the tenth rib.
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sarean section. Absent in the delivery of these infants is the thoracic squeeze, which will mechanically clear up to one-third of the fluid from the lungs. Initially, transient tachypnea of the newborn may be difficult to distinguish from hyaline membrane disease. Clinically, tachypnea, substernal retraction, flaring, and grunting are seen. Auscultation of breath sounds reveals adequate air entry and scattered rales. Mild hypoxia and hypercapnia may be present. T h e radiographic pattern of transient tachypnea of the newborn is demonstrated in Figure 2. T h e clinical course demonstrates mild to moderate respiratory distress from two to four hours after birth. T h e symptoms peak at 36 hours, and gradual recovery usually occurs by 72 hours of life. Treatment consists of oxygen supplementation and supportive health care m a i n t e n a n ~ e . ~
Meconium Aspiration Syndrome Meconium aspiration is a significant cause of neonatal morbidity and death. T h e reported incidence of meconium-stained amniotic fluid is 10% of all pregnancies; approximately 10% of infants with meconiuni-stained amniotic fluid have evidence of respiratory distress.' Massive meconium aspiration occurs most frequently in term, postterm, and small-for-gestational-age infants. This syndrome rarely is encountered in preterm infants.' T h e pathogenesis of meconium aspiration has two components: fetal asphyxia, followed by aspiration of meconium into the tracheobronchial tree. Intrauterine hypoxia initiates a vagal reflex which results in passage of meconium into the amniotic fluid. Usually, meconium then is aspirated into the lower airways during the first respiratory efforts made outside the birth canal. At this point, a large negative pressure is gener-
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ated inside the chest and any fluid in the nasopharynx or trachea will be pulled d o w n into the smaller airways. T h e presence of meconium in lower airways will produce varying degrees of complete and partial airway obstruction. Partial airway obstruction results in air trapping and overinflation of distal alveolar sacs. Complete obstruction produces alveolar collapse. Meconium in the lung produces a severe inflammatory reaction resulting in a chemical pneumonitis that reduces the diffusing capacity of the lung. Together these conditions produce the clinical picture of hypoxemia, intra- and extrapulmonary shunting, C O P retention, and pulmonary air leaks.' In meconium aspiration, t h e spectrum of severity of clinical symptoms correlates grossly with the amount of meconium aspirated into the lungs. Infants with meconium aspiration syndrome, usually have low Apgar scores and demonstrate tachypnea, retractions, and cyanosis shortly after birth. The infant's chest frequently will be overdistended a n d barrelshaped with increased anteriorposterior diameter; breath sounds are poor and usually obscured by coarse bronchial sounds; expiration is prolonged. Palpation of the abdomen may demonstrate t h e liver well below the intercostal margins. Displacement of the liver is secondary t o depression of the diaphragm by air trapping and overexpansion of the lung. T h e radiographic pattern of meconium aspiration syndrome is demonstrated in Figure 3. Pneumomediastinum, p n e u m o t h o r a x , a n d pleural fluid frequently a r e found. Initial blood gases will reveal hypoxia, and respiratory and metabolic acidosis.* Successful treatment of meconium aspiration syndrome is dependent on prompt removal of meconium from the airway. Consistent use of intrapartum naso-
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Figure 3. Anteroposterior chest film denionstrates x-ray manifestations of meconium aspiration syndrome. Note bilateral, asymmetrical infiltrates. In severe meconiuni aspiration syndrome, lungs will be hyperaerated with Iiemidi;tphragn~sflattened below the ninth rib.
pharyngeal suctioning via DeLee suction of oronasal pharynx at the time of the delivery of the infant's head prior to the first extrauterine gasp, immediate visualization of vocal cords, and efficient tracheal suctioning will significantly reduce morbidity and mortality.' Positive pressure ventilation ( Z . P . , bagging) should not be applied prior to suctioning. Once initial suctioning is complete, the infant then can be ventilated with high oxygen concentrations to ensure adequate oxygenation and elimination of CO2. When meconium does reach the lower airways, treatment is directed toward clearance of the meconium by postural drainage and chest physiotherapy. Supplemental oxygen will be necessary, and if hypoxia and hypercapnia are severe, intubation and mechanical ventilation will be required. Because of reduced lung compliance and increased airway resistance, high peak inspiratory pressures and fast frequency ventilation with low inspiratory/expiratory ratio will be needed. Although life saving, this type of mechanical venti-
lation, together with damage produced by meconium, makes the occurrence of pulmonary air leaks (pneumothorax, pneumomediastinum) a common complication in these infants. Other complications the nurse should be alert to are persistent fetal circulation, seizures secondary to cerebral edema resulting from asphyxia, and sepsis secondary to bacterial pneumonia. Although n o evidence supports their use, prophylactic antibiotics a r e frequently administered in consideration of the latter complication.' Supportive measures to prevent hypoglycemia, electrolyte imbalances, a n d hypothermia should be instituted.
RESPIRATORY ASSESSMENT OF T H E NEWBORN I t is essential that the neonatal nurse be skilled in the principles of respiratory assessment. Early recognition of an infant in respiratory distress is as critical to the infant's well-being as the subsequent mea-
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sures taken to improve the infant’s respiratory status. Nursing assessment of the neonate in respiratory distress includes anticipatory identification of infants vulnerable to respiratory disorders, recognition of neonatal respiratory distress, and an ability to make acute serial observations while concurrently evaluating the infant’s response to treatment. This process involves the collection and documentation of perinatal history, clinical observations, and laboratory data.
IDENTIFICATION OF INFANTS AT RISK Perinatal History In many instances, neonatal respiratory distress is predictable. T h e nurse must be aware of highrisk factors or events in the mother’s and neonate’s prenatal history that would be pertinent to assessment of the infant. T h e nurse then can anticipate which infants are at risk and subsequently identify what measures to take to prevent unnecessary deterioration of the infant’s condition. Factors that identify infants at risk for respiratory distress are maternal analgesia, bleeding or diabetes, infection, meconiumstained amniotic fluid, cesarean section, asphyxia, hypothermia, prematurity, postmaturity, smallor large-for-gestation, and erythroblastosis fetalis. Assessment begins with determining the physical status of the neonate immediately after birth. Assessment includes Apgar score, physical examination to rule out gross anomalies, estimation of gestational age, and classification of the infant as appropriate-smallor large-for-gestational-age. Recognizing infants as preterm, postterm, small- or large-for-dates will help the nurse anticipate inherent problems and make preparations necessary to facilitate treatment. 34s
Inspection Clinical observations of respiratory function are gathered primarily via inspection and auscultation. Inspection of infants at risk for respiratory dysfunction should begin in the delivery room and continue at frequent intervals in the nursery. Respiratory difficulties can be recognized by simple and methodical observation of the infant. T h e infant’s color and quality of respiration need to be inspected before disturbing the infant. At birth, infants are seldom completely pink. A transient generalized cyanosis may be present for the first five to six minutes of life. Acryocyanosis involving hands, feet, and circumoral area may be evident at delivery and for a short time thereafter. However, a sustained, generalized cyanosis is clearly indicative of distress. T h e infant’s respirations should be counted for a minimum of 60 seconds: Normal respiratory rates range between 40 to 60 breaths per minute. T h e nurse should note any periodic breathing or apnea by observing the infant’s respiratory pattern. Periodic breathing, i.e., short cessation of breathing for up to 10 seconds, is a frequent normal finding in premature infants. Periodic breathing is not associated with cyanosis or bradycardia, and should not be confused with apnea. Apnea is of longer duration and is often accompanied by cyanosis and/or bradycardia. Periodic breathing occurs rarely during the first 24 hours of life; apnea may occur at any time. Nursing assessment also includes inspection of thoracic shape, size, and symmetry of movement. Respiratory movements should be symmetrical and predominantly diaphragmatic with a relatively immobile thoracic cage. T h e abdomen will rise and fall with inspiration and expiration. Asymmetry of thoracic size or movement may
indicate pathology, i.e., pneumothorax, chylothorax, or diaphragmatic hernia. T h e anteroposterior diameter of the chest should be compared with the lateral diameter. In infants, this ratio is usually 1:1. An increased anteroposterior diameter is indicative of overexpanded lungs (transient tachypnea of the newborn, meconium aspiration syndrome). T h e infant’s ribs are flexible and slight sternal retractions may be evident. Retractions indicate obstruction to airflow at any level of the respiratory tract; more than slight retractions are abnormal. Respiratory dysfunction will be demonstrated by tachypnea, expiratory grunting, retractions, nasal flaring, cyanosis, pallor, apnea, bradycardia, hypothermia, and hypotonia. Quantitating the signs of respiratory distress with the Silverman-Anderson score or the Miller score may be usefuLg All signs of respiratory distress should be documented and reported immediately to the physician.
Auscultation Auscultation of the chest will help the nurse assess air flow and detect any obstruction of the airway. T h e quality of information gathered by auscultation is in direct proportion to the skill of the listener. T h e neonate’s diminutive chest size can distort breath sounds; localization of findings is often impossible and absence of breath sounds in one part of the lung may not be appreciated because breath sounds from unaffected areas are transmitted from one region to another. However, the experienced listener can qualify air exchange, and detect atelectasis and pneumothorax, rales, and rhonchi. Decreased breath sounds occur in hyaline membrane disease, meconium aspiration syndrome, atelectasis, pneumothorax, and emphysema. Rales are crackling sounds
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produced in terminal bronchioles and alveoli when air rushes through fluid within them. Rales are occasionally heard in hyaline membrane disease but are more pronounced in transient tachypnea of the newborn and meconium aspiration syndrome. Rhonchi a r e coarse snoring sounds produced by air rushing through fluid in large bronchi. Rhonchi can be cleared with endotracheal suctioningrales cannot. Rhonchi are commonly heard in meconium aspiration syndrome. Breath sounds should be auscultated bilaterally and methodically. A stethoscope with a small diaphragm (Figure 4) should be used to prevent interference from extraneous noise and assist in isolating breath sounds. T h e examiner should move the stethoscope down the chest auscultating breath sounds both anteriorly and laterally along the midaxillary line. Breath sounds, produced by the movement of air in the bronchioles and alveoli, are normally soft- and low-pitched and should be heard equally over all lung fields. T h e duration of the sounds on inspiration is greater than on expiration. T h e nurse should note diminished breath sounds, particularly when there is a discrepancy between the two lungs and adventitious breath sounds (rales, rhonchi). T h e physician should be notified of any abnormal findings and their location should be recorded, ie., diminished breath sounds in left lower lobe, rales noted bilaterally. Heart sounds must be auscultated: Heart rate should be noted, the first and second heart sound differentiated, murmurs noted, and the infant’s point of maximal impulse located. T h e point of maximal impulse is normally in the fifth intercostal space to the left of the sternum in the midclavicular line; displacement of the point of maximal impulse can lead to suspicion
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Figure 4. Correct technique for auscultation of breath sounds laterally along the midaxillary line. Note appropriate size of stethoscope diaphragm.
of pneumothorax, diaphragmatic hernia, or dextrocardia. T h e nurse needs to determine if respiratory distress is of pulmonary o r extrapulmonary origin. This determination can be accomplished by following a few guidelines. Respiratory distress of cardiac origin presents with tachypnea, but breathing is usually not labored o r obstructed. Heart sounds are loud and rapid: a murmur or gallop rhythm may be audible. Infants with cyanotic heart disease do not improve with 100% oxygen. Hepatomegaly (more than 3 cm below the intercostal margin) may be present, as well as x-ray manifestations of cardiomegaly.
Diagnostic Measures Once the nurse has assessed that an infant is clinically demonstrating signs of respiratory distress, the physician should be notified and orders for confirming x-ray information, laboratory data, and therapeutic measures should be obtained. T h e nurse should be familiar with the common x-ray manifestations of hyaline membrane dis-
ease, transient tachypnea of the newborn, and meconium aspiration syndrome. T o assure good radiographic results and avoid unnecessary radiation exposure, the infant must be correctly positioned for the x-ray procedures. Usually, anteroposterior and lateral views of the chest are requested. Chest films should be taken during inspiratory phase of respiration. T h e infant’s gonads should always be covered with a small lead shield. All nursery personnel need to wear a lead apron when assisting with any x-ray procedure. T h e presence of respiratory pathology often is confirmed by blood gas data. T h e nurse needs to know and understand blood gas normals, be able to recognize and characterize deviations from the norm (ie., respiratory acidosis, metabolic acidosis), and understand the impact that various disease processes have on blood gases (Tables 1, 2, and 3). Table 1 provides guidelines for normal blood gas values. These values may vary slightly with individual laboratories. Arterial blood samples provide the most reliable blood gas data. If arterial blood is not easily ob-
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Table 1. Normal Blood Gas Values in the Neonate Source
Arterial
CaDillarv
PH PO2 PCO* HCOs Base excess/deficit
7.35-7.45 50-80 mm Hg 35-45 mm Hg 22-26 mEq/L. 2 -2
7.35-7.45 40-50 mm Hg 35-45 mm Hg 22-26 mEq/L. -2 2
+
+
Table 2. Classification of Blood Gases as Related to Acid-base Disturbances
Disturbance
Blood DH
PCO*
HC03
Base excessldeficit
Respiratory Acidosis uncompensated compensated
<7.35 normal
T T
normal T
normal excess > +2
Respiratory alkalosis uncompensated compensated
>7.45 normal
1 1.
normal 1
normal deficit > -2
Metabolic acidosis uncompensated compensated
<7.35 normal
normal 1.
1
1
deficit > -2 deficit > -2
Metabolic alkalosis uncompensated compensated
>7.45 normal
normal T
T T
excess > +2 excess > +2
tained, capillary blood gases may be of value, especially if a transcutaneous pop monitor (TcpO2) is used simultaneously. Capillary samples will indicate the status of pH and pC02 but are unreliable indicators of p02. If properly calibrated and positioned, the TcpOp will provide reliable continuous recording of pop. Knowledge of theory, calibration and operation of the Tcp02 is of paramount importance if reliable clinical data are to be obtained. Selection of a proper skin
site is critical. For neonatal monitoring, commonly used sites are the upper part of the chest, abdomen, and inner aspect of the thigh. The site should have good capillary blood flow with as little fat as possible. Bony prominences should be avoided. Ensure an airtight seal between the Tcp02 electrode and skin surface by cleaning the skin with an alcohol swab. The skin site should be changed and the electrode recalibrated at least every four hours. If an infant requires oxygen
therapy and/or assisted ventilation, a reliable method of obtaining blood gases must be established. T h e method chosen to monitor blood gases will depend upon the severity of the infant’s pulmonary disease (Table 4). After the initial assessment and recognition of an infant in respiratory distress, the nurse must continue to assess and correlate clinically the infant’s physical findings and blood gas data throughout the course of the disease. Pertinent nursing observations should be reported to the physician and systematically documented. A 24-hour flow sheet (Figure 5 ) is usually ideal for this purpose. Observations that should be recorded at one- to two-hour intervals are quality of respirations, breath sounds, color, tone, activity, and vital signs (temperature, pulse, respirations, and blood pressure). Response to therapy and any communication with the physician should be documented. The nursing flow sheet as well as a respiratory therapy flow sheet with all blood gas data should be at the neonate’s bedside for easy reference. Nurses play an important role in detecting significant changes, assessing response to medical management, and providing supportive nursing care.
NURSING INTERVENTIONS Multidisciplinary Approach Successful, comprehensive treatment of an infant in respiratory distress depends upon close teamwork between physician, nurse,
Table 3. Classification of Frequently Found Blood Gas Abnormalities by Disease
Respiratory Acidosis
Disease
Hypoxia
Hyaline membrane disease Transient tachypnea of the newborn Meconium aspiration syndrome
J
J
J
minimal
J
J
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Respiratory Alkalosis
Metabolic Acidosis
Metabolic Alkalosis
occasional -
J
-
minimal
-
J
-
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and respiratory therapist. T h e physician determines the course of therapy; the nurse and respiratory therapist support the therapy via ongoing assessment a n d implementation of appropriate interventions. Hence, the three disciplines work together to develop a plan of care that is communicated to all members of the health-care team.
Table 4. Blood Gas Monitoring Technidues
Indwelling catheter
Steady state gases Easy access once placed Allows continuous blood pressure monitoring
Potential for major complications: thrombi, emboli, infection, exsanguination, and arterial spasm
Intermittent punctures
Allows access to arterial blood when no catheter in place
Potential for major complications: carpal tunnel syndrome, median nerve damage, and thrombi Patient may not be in a steady state, i.e., may be crying or breath-holding,which will cause fluctuations in Pa02
Capillary sampling (arterialized)
Accurate pH, PCO2 Good for chronic conditions, i.e., bronchopulmonary dysplasia Low complication rate Can be performed easily
Not reliable for PO2
Transcutaneous monitoring
Noninvasive Continuous record of PO2
pH, PC02, electrodes not yet commercially available May be unreliable if skin perfusion is decreased Sophisticated setup required Complications; skin burns and erosion
Implications for Nursing Practice
The infant manifesting respiratory distress has both' specific respiratory care a n d supportive health care needs. These needs are interrelated and must be dealt with effectively if the infant is to achieve and maintain optimal physiologic functioning. STANDARDS FOR RESPIRATORY CARE
Specific respiratory health care needs of an infant in respiratory distress are 1) maintenance of adequate oxygenation and ventilation, and 2) correction of acid-base balance. These needs initially are met by providing the appropriate oxygen therapy, i.e., increasing ambient oxygen, continuous positive airway pressure, or controlled mechanical ventilation. The maintenance of adequate oxygenation is imperative as the sequential effects of hypoxia (acidosis, persistent pulmonary hypertension, and ischemic injury to heart, kidney, and brain) are cataclysmic. Oxygen, although lifesaving, is a drug and must be administered carefully. Infants requiring oxygen therapy must be monitored closely in three ways: clinically, by a knowledgable nurse and physician; technically, by cardiorespiratory, temperature, and blood pressure monitors; and serially, by laboratory data via blood gas determinations. If the infant cannot receive all of the components of care, he/she should be
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Disadvantaaes
Advantages
Adapted from and used with permission of author and publisher. Phillips B, McQuintty J: Blood gases: technical aspects and interpretation. In: Goldsmith J, Karotkin E, eds. Assisted ventilation of the neonate. Philadelphia: Saunders, 1981:220.
transferred immediately to a newborn intensive care unit. T h e purpose of administering oxygen is to increase the amount of oxygen delivered to the tissues. An infant's P a 0 2 should be maintained between 50 to 80 mm Hg." T h e concentration, humidity, and temperature of inspired oxygen should be precisely regulated. T h e toxic effects of oxygen on eyes (retrolental fibroplasia) and lungs (bronchopulmonary dysplasia) must be appreciated." Hyperoxemia (Pa02 > 100 mm Hg) must be avoided. All preterm infants receiving oxygen therapy should undergo a dilated fundoscopic examination prior to discharge. N o infant should be exposed unnecessarily to high concentrations of oxygen. All infants should be weaned
from oxygen as soon as it is clinically feasible. Blood gas measurements are essential for safe oxygen administration. Blood gas measuring capabilities should be available on a 24hour basis and performed using micro-technique blood volumes (0.3 cc). Provision of an adequate thermal environment is an important factor in decreasing metabolic oxygen requirements and improving the survival of infants with severe respiratory failure. Hypothermia significantly increases oxygen consumption and promotes pulmonary vasoconstriction. These conditions promote hypoxia and acidosis which notably decrease surfactant production. Hypoxic infants have a diminished thermo-
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genic response to chilling. At a P a 0 2 of 40 mm Hg, thermogenesis is reduced; at a PaOz of 30 mm Hg, the thermogenesis is abolished." Neutral thermal environment is best achieved by using an isolette or an open bed radiant warmer. The use of servo-control is recommended to keep an infant's temperature at the prescribed level. All inspired gases should be warmed to the infant's neutral thermal range and ventilator gases maintained at 97°F (36°C). The infant's axillary temperature should be monitored and recorded at one- to two-hour intervals. Axillary temperature needs to be maintained between 97°F and 98°F (36°C to 36.6"C).
Oxygen Per Hood Using an isolette to administer oxygen is problematic. Concentrations greater than 30% cannot be maintained effectively, and steady oxygen equilibrium is impossible due to the need to open the portholes. If higher concentrations are required, an oxygen hood should be used. Prescribed oxygen levels should be ordered in exact concentrations, i.e., percent or fraction of inspired oxygen (FIO2),not in liters per minute. The precise provision of oxygen between 2 1 to 100% requires separate sources of compressed air and oxygen that are connected to a blender or mixing chamber. Table 5 outlines specific nursing responsibilitiesand interventions when using an oxygen hood.
Table 5. Nursing Responsibilities and Interventions for Use of Oxygen Hood
Responsibility
Interventions
Maintain prescribed F102
Know how to operate and calibrate oxygen analyzer Place sensor near infant's nose (Figure 6) Analyze and document FIO, hourly Avoid fluctuations in oxygen concentration
Maintain patent airway and optimal position
When supine, slightly hyperextend neck with roll under neck and shoulders; place in prone position if umbilical artery catheter not in place Gently suction nasal passages and oropharynx as needed; aspirate stomach every 4 hours Do not restrict air exchange with nasogastric tube or phototherapy eye pads
Prevent drying of mucous membranes
Humidify (sterile water) all inspired gases Give oral care with glycerin swabs as needed
Prevent cold stress
Warm all inspired gases to infant's neutral thermal range Keep thermometer in h o d at all times (Figure 6) Maintain constant temperature in hood Note and document hood temperature with vital signs
Prevent COPbuildup in hood
Provide at least a 2 liter flow of gas through hood
Monitor clinical response to oxygen therapy
An arterial blood gas should be obtained at least every 4 hours, and 10 to 20 minutes after each change in F102 Notify physician if PaO, >80 or (50 mm Hg; PC02 >50 mm Hg; pH <7.30. Monitor hourly: skin color, breath sounds, quality of respirations, and vital signs Alert physician to changes in clinical status
has greatly increased the survival rate of infants in respiratory distress.I3 Treatment with constant
positive airway pressure involves attaching a system that applies constant distending pressure to the
CONSTANT POSITIVE AIRWAY PRESSURE The application of constant positive airway pressure in the treatment of hypoxemia is one of the most important advances in neonatal respiratory therapy in the last decade. Since first described by Gregory et al. in 197 1, this therapy
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Figure 6. Correct positioning of oxygen analyzer sensor. Note thermometer in hood.
airway throughout the respiratory cycle to a spontaneously breathing infant. T h e main effect of constant positive airway pressure is that it opens and stabilizes atelectatic al-
veoli and thereby decreases intrapulmonary shunting, increases functional residual capacity, and improves ventilatory capacity. T h e intended net effect is a dramatic
Table 6. Nursing Responsibilitiesand Intervention for Use of Constant Positive Airway Pressure Responsibility
Intervention
Maintain prescribed constant positive airway pressure
Check manometer readings frequently Document distending pressure on flow sheet Adjust pressure when infant is quiet Be alert for leaks or loose connections Maintain nasal prongs securely and properly angled in nares (Figure 7)
Maintain prescribed F102
Monitor in-line oxygen concentrations hourly Document F102 on flow sheet
Maintain adequate humidity
Constant positive airway pressure tubing should be fogged evenly with humidity Avoid excessive humidity which causes pooling and increases danger of near-drowning
Maintain adequate temperature of inspired gases
Maintain in-line thermometer in system close to infant In-line temperature should be 1 to 2 degrees below body temperature Check and document temperature with vital signs
Prevent airway obstruction
Suction endotracheal tube, nares, and oral pharynx as needed (Table 7) Clean nasal prongs every 2 hours
Be alert for signs of pneumothorax
Auscultate and document quality of breath sounds hourly Pneumothorax is evidenced by decreased breath sounds and chest movement, shift in point of maximal impulse, bradycardia, cyanosis, and decreased pulse pressure Action: ventilate with 100% oxygen, alert physician, call for stat chest x-ray, prepare for needle aspiration and/or chest tube placement
Prevent abdominal distention
Insert orogastric tube, leave open to atmospheric pressure Periodically use syringe to decompress stomach
Prevent skin breakdown
Secure prongs or endotrachealtube to prevent excessive movement or displacement (Figure 7) Keep skin dry and clean Support constant positive airway pressure tubing to prevent excessive pressure points Turn infant every 2 hours Use of water bed may be indicated
Maintain good oral hygiene
Assess nares and mouth frequently for irritation; apply antibiotic ointment if indicated Apply glycerine to prevent cracking or drying of mouth
Monitor clinical response to constant positive airway pressure
Obtain arterial blood gas at least every 4 hours and 10 to 20 min past change in pressure or F102 Be alert for hypercapnea (PC02 > 50 mm Hg), hypoxia (PO2 < 50 mm Hg), and acidosis (pH < 7.30) Monitor temperature, pulse, respiration, and blood pressure every 1 to 2 hours Observe closely: skin color, quality of respirations, and peripheral perfusion
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improvement in oxygenation, reduction of carbon dioxide levels, and a decrease in the work of breathing.14 Constant positive airway pressure is most effective in atelectatic disease, i.?., respiratory distress syndrome: use is indicated if an infant has a P a 0 2 less than 50 mm Hg while breathing 60% oxygen. Distending pressures should be kept as low as possible, compatible with oxygenation, to reduce the incidence of adverse cardiopulmonary effects. Usually, an initial pressure of four to six cm H 2 0 is applied and increased by two-cm increments until adequate oxygenation is achieved.14 T h e aim of constant positive airway pressure therapy is to apply the level of pressure necessary to expand but not overdistend the majority of alveoli. Infants should be weaned from constant positive airway pressure in two-cm increments once the F I 0 2 can be maintained at 40% oxygen. To avoid a decrease of physiologic functional residual capacity, constant positive airway pressure should not be reduced below two to four cm H2O.I4 Constant positive airway pressure can be applied by way of an endotracheal tube, nasopharyngeal tube, face mask, hood chamber, or nasal prongs: Each has its own advantages a n d disadvantages." Endotracheal intubation or nasal prong systems are the most widely used. Table 6 outlines appropriate constant positive airway pressure nursing responsibilities and interventions. T h e nurse must be aware of and alert to the serious complications that can develop from the use of constant positive airway pressure. Pulmonary a i r leaks (pneumothorax, interstitial emphysema) increase during distending pressure therapy. Cardiac output can be impaired by excessive transmission of pressure to thoracic veins which reduces venous return to the heart.
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Excessive constant positive airway pressure can cause decreased lung compliance with h ypoven tilation. Constant positive airway pressure must be monitored carefully and constant positive airway pressure decreased if there is any indication of deleterious cardiopulmonary effects, it., hypotension, metabolic acidosis, decreased peripheral perfusion, or hypercapnea.
Mechanical Ventilation Mechanical ventilation should be considered when apnea is protracted, when constant positive airway pressure has failed (PaO:, is less than 50 mm Hg in 100% oxygen at distending pressures of 10 to 12 crn H,O), or when blood gases reveal respiratory failure. Generally, a pH of less than 7.25, a Pa02 of less than 50 mm Hg, and a PaC02 of greater than 60 nim Hg in 60% oxygen indicate a need for some form of respiratory assistance. Various types of ventilators are available. “-”Because mechanical ventilation is associated with potentially hazardous complications, all nursing personnel must be thoroughly familiar with the operating principles of the particular ventilator used in their intensive care unit. Regardless of the type of ventilator used, the goal of mechanical ventilation is to achieve adequate alveolar ventilation and maximal oxygenation. Individual parameters of ventilator function, i . ~ . , F 1 0 2 , peak inspiratory pressure (PIP),positive end expiratory pressure (PEEP), respiratory rate, and inspiration/expiration (1:E) ratio are modified to achieve physiological blood gases. Standard approach o r uniformity in values for the specific parameters of mechanical ventilation required to produce optimal therapy do not exist. However, various philosophies of mechanical venti-
May/June 1981JOGN Nursing (Supplement)
Figure 7. Correct positioning of nasal constant positive airway pressure prongs. Foam “bonnet” holds prongs securely, preventing pressure points. A surgical face mask also may be used for “bonnet.”
lation (high frequency, slow rate, etc.) are a d ~ o c a t e d . ’ ~Establish.’~ ing appropriate ventilator settings requires teamwork between the physician, nurse, and respiratory therapist. T h e nurse must have a working knowledge of ventilator settings as well as the various philosophies governing their Nursing care of the neonate requiring mechanical ventilation demands acute, close observation. Repeated documentation of each infant’s response to changes in parameters and pattern of his ventilation is necessary. Blood gases must be followed carefully. T h e immediate environment surrounding the ventilated infant should provide all monitoring and technical equipment needed to provide safe care (Lt., cardiorespiratory monitor, suction equipment, resuscitation bag and mask, etc). Use of appropriate alarm systems on the ventilator or on the patient will greatly reduce serious complications associated with mechanical failure. Recommended alarms are high and low pressure, power disconnect, high and low oxygen, ap-
nea, heart rate, and blood pressure. l7 T h e airway (endotracheal tube) must be kept patent. Endotracheal intubation and subsequent oxygen therapy decrease ciliary activity and accelerate mucus production. Adequate chest physiotherapy is required to aid outflow of pulmonary secretions and assure patent airway. Various authors have described the technique of chest physiotherapy (percussion, vibration and suctioning) in detai1.19*20 T h e frequency of chest physiotherapy should depend upon individual patient need. Strict adherence to every two hour scheduling of chest physiotherapy should be avoided as accepted methods of chest physiotherapy have potentially detrimental side effects, ie., hypoxia, bradycardia, apnea, and cardiac arrest. T h e nurse should evaluate the need for chest physiotherapy by assessing the degree of atelectasis, volume of secretions, and stability of the infant’s condition. Muscle relaxants may be a useful adjunct to care when an infant’s
41s
own respiratory efforts interfere with ventilator therapy and hypoventilation results. T h e struggling infant generates increased intrathoracic pressure with decreased venous return and is at increased risk for pulmonary air leaks. Muscle relaxants improve oxygenation, decrease the incidence of pulmonary air leaks, and significantly reduce periods of increased intracranial pressure.21s22 Pancuronium (Pavulon@),a longlasting, competitive neuromuscular blocking agent, is the drug most frequently used in neonates. Curare seldom is used because of significant cardiovascular effects, ie., hypotension. When given intravenously, Pavulon produces maximum paralysis within two to four minutes. Pavulon has been shown to moderately increase blood pressure and heart rate. Pavulon does not alter the sensation of pain. Recommended dosage ranges from 0.03 to 0.1 mg/kg. T h e duration of paralysis varies from one to several hours and is prolonged by acidosis, hypokalemia, aminoglycosides, and decreased renal function.*' T h e primary hazard during paralysis is hypoxia due to accidental extubation or disconnection from the ventilator. T h e paralyzed neonate is entirely dependent on mechanical ventilation, and careful observation is mandatory. T h e infant's condition and response to respiratory paralysis after each administration of Pavulon need to be monitored. T h e effect on clinical condition should be noted by frequent assessment of color, vital signs, breath sounds, and blood gases. Ventilation parameters may need adjustment as hypoxic episodes have occurred following initial paralysis.24 T h e effects of Pavulon are reversed by simultaneously and slowly administering atropine, 0.02 mg/kg I.V., and neostigmine, 0.08 mg/kg I.V. The nurse should allow 15 to 20 minutes for complete action. In-
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Table 7. Nursing Responsibilities and Interventions for Use of Ventiiator ~~
Responsibility Maintain patent airway Alert to extubation
Provide CPT* regimen Maintain prescribed ventilator parameters (PIP,t PEEP,+ F102, rate, I:E ratios) Assess infant's response to mechanical ventilation Arterial blood gases
Clinical
Detect malfunctioning equipment Preventive measures
Occurrence of malfunction
Safe administration of muscle relaxants
Intervention
Clinically evidendd by audible crying, distinct ventilator sounds auscultated in stomach, decreased breath sounds, and sudden deterioration in color and heart rate Action: remove tube, ventilate with bag and mask, place orogastric tube to decompress stomach, set up for reintubation Follow prescribed technic for percussion vibration and suctioningignZ0;frequency dictated by individual assessment Have working knowledge of ventilator Check and record ventilator parameters hourly Properly humidify inspired gases (Table 6) Keep in-line temperature of gases 97OF (36OC) (Table 6)
Obtain blood gas 10 to 20 min postparameter change Subsequent gases should be obtained at least every 4 hours Use blood gas data to assess ventilation (PCO2). oxygenation (PO2), acid-base balance (pH, HC03), and response to therapy Follow serially to detect deterioration, i.e., acidosis, hypoxia, hypercapnea Auscultate breath sounds hourly to assess: quality of ventilation, adequate placement of endotrachealtube or occurrence of pneumothorax (Table 6) Assess vital signs: temperature, pulse, respirations, and blood pressure hourly Observeclosely for deterioration in color, heart rate, blood pressure, activity, and tone Document findings on flow sheet
Check ventilator parameters frequently Maintain alarms ON at all times Check all connections hourly to make sure they are snug Respond promptly to sounding of alarm Evidenced by sounding of alarm, sudden change in ventilator parameters, and sudden deterioration of infant Action: remove infant from ventilator, ventilate with bag, and get assistance in locating problem Know dosage, side effects, antidotes Maintain all alarm systems ON Close observation is imperative Assess respiratory paralysis after each administration of drug; note duration of effect and any changes in cardiorespiratory systems2' Maintain good alignment of body parts Cred6 bladder every 2 hours as needed Assess need for continuation of neuromuscular block prior to each dose (Continuedon page 43s)
May/June 1983 JOGN Nursing (Supplement)
spiratory acidosis (inadequate ventilation) will only further increase the level of COP.
Table 7. (Continued) Intervention
Responsibility Prevent decubiti formation
Maintain good oral hygiene Prevent gastrointestinal insufflation
Evidenced by inflammation or skin breakdown Keep skin clean, dry and free from pressure points Turn infant every 1 to 2 hours Use waterbed if pressure points occur Secure endotracheal tube to prevent excessive movement See Table 6 Insert orogastric tube Aspirate with a syringe to decompress stomach every 2 hrs ~~
* CPT-Chest
physiotherapy. t PIP-Peak inspiratory pressure. PEEP-Positive end expiratory pressure. 0 I:E ratio-lnspiration/expiration ratio.
+
dications for discontinuation of respiratory paralysis are improved arterial blood gases in the presence of lowered respiratory parameters ( F 1 0 2 less than 60%). A thorough nursing protocol for neonatal respiratory paralysis is available in the 1iteratu1-e.~~ Mechanical ventilation is associated with various serious complications. T h e nurse must be aware of pulmonary air leaks and deterioration secondary to mechanical failure. T h e latter consists of extubation, endotracheal tube plugs, disconnected tubes, and ventilator apparatus malfunction. These mechanical problems can be rectified by alert nursing personnel before irreversible harm is done. Table 7 outlines nursing responsibilities and interventions for mechanical ventilation. Weaning the infant from the ventilator begins as soon as the respiratory disease stabilizes and ventilatory need decreases. T h e decrease in ventilatory settings is determined by improvement in arterial blood gases and clinical response. T h e weaning process is gradual. Close observation for respiratory deterioration is necessary. Extubation is feasible when an infant maintains normal blood gases and has good respiratory effort on constant positive airway pressure of two cm to four cm and
May/June 1983 JOGN Nursing (Supplement)
40% oxygen. After extubation, infants will be placed in an oxyhood or on nasal prong constant positive airway pressure. ACID-BASE BALANCE Acid-base derangements accompany respiratory problems in the newborn. Respiratory and metabolic acidosis are encountered most frequently. There is a direct correlation between quality of ventilation and the level of PaC02. Normal ventilation will reflect normal PaC02; hypoventilation will reflect elevated PaCO,; and hyperventilation will reflect decreased PaC02. Respiratory acidosis is due to retention of carbon dioxide or hypoventilation. Consequently, the only effective treatment is to ventilate, thereby reducing COP levels. Metabolic acidosis occurs as a result of tissue anoxia and anaerobic metabolism. Improving oxygenation, reestablishing adequate perfusion with volume expansion, and alkali therapy are all therapeutic. Slow (1 mEq/min) intravenous infusion of NaHC03 1 to 3 mEq/ kg diluted at least 1:l with sterile water accelerates correction of severe metabolic acidosis. NaHC03 should not be given until adequate ventilation is established. Giving bicarbonate in the presence of re-
SUPPORTIVE MEASURES In addition to respiratory management, the following supportive measures must be monitored carefully: thermoregulation, fluid, electrolyte and caloric balance, maintenance of normal blood pressure, protection from infection, and conservation of energy. Key components of care are included in outlines of nursing care. PARENT SUPPORT To provide comprehensive respiratory care, the nurse must support and care for the infant’s family as well. Support should be given in four areas: listening, communicating, educating, and providing parent-infant interaction. From admission through discharge, the nurse must meet the needs of the family. As each aspect of care is determined individually for each patient, so are the approaches to the primary caregivers. Referral to appropriate resource personnel is essential to insure optimal outcome.
CONCLUSION T h e care of the neonate with an acute respiratory disease is challenging and complex. Care of these infants requires knowledge of embryonic development, pulmonary pathophysiology, acid-base principles, and appropriate management of respiratory problems. Assessment skills and technical expertise are essential. Finally, the nurse must support the parents by listening, communicating, educating, and promoting parent-infant interaction.
References 1. Moore K. Before we are born. Philadelphia: WB Sauders, 1974: 125-9.
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2. King R. Pulmonary surfactant. J Appl Physiol 1982;53:1-8. 3. Avery M, Fletcher B, Williams R. The lung and its disorders in the newborn infant. In: Major problems in clinical pediatrics. Philadelphia: WB Saunders, 1981:348. 4. Oehler J. Family-centered neonatal nursing care. Philadelphia: JB Lippincott, 1981: 186-96. 5. Hein H, Brown C. Neonatal mortality review: a basis for improving care. Pediatrics 1981; 68:504-9. 6. Stahlman M. Acute respiratory disorders in the newborn. In: Avery G, ed. Neonatology. Philadelphia:JB Lippincott, 1981:37687. 7. Wesenburg R. T h e newborn chest. Hagerstown, Md.: Harper & ROW,1973~43-124. 8. Bancalari E, Berlin J. Meconium aspiration and other asphyxia1 disorders. Clin Perinatol 1978; 5:3 17-34. 9. Affonso D, Harris T. Care of the high risk neonate. In: Clark A, Affonso D, eds. Childbearing: a nursing perspective. Philadelphia: FA Davis, 1979:841-4. 10. Bancalari E. Pulmonary function testing and other diagnostic laboratory procedures. In: Thibeault D, Gregory G, eds. Neonatal pulmonary care. Menlo Park, Ca.: Addison-Wesley, 1979:123-4. 11. Korones S. Complications. In: GoldsmithJ, Karotkin E, eds. Assisted ventilation of the neonate.
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12. 13.
14.
15. 16. 17.
18.
19.
Philadelphia: WB Saunders, 1981:181-206. Sinclair J. Thermal control in premature infants. Ann Rev Med 1972;23:129. Gregory G, Kitterman J, Phibbs R, Tooley A, Hamilton W. Treatment of the idiopathetic respiratory distress syndrome with continuous positive airway pressure (CPAP). N Engl J Med 1971; 284~1333-40. Gregory G. Continuous positive airway pressure (CPAP). In: Thibeault D, Gregory G, eds. Neonatal pulmonary care. Menlo Park, Ca.: Addison-Wesley, 1979:207-16. Affonso D, Harris T. Continuous positive airway pressure. Am J Nurs 1976;76:570-3. McPherson SP. Respiratory therapy equipment. 2nd ed. St. Louis: CV Mosby, 1981:168-365. Fox W, Shatack J. Positive pressure ventilation: pressure and time-cycled ventilators. In: Goldsmith J, Karotkin E, eds. Assisted ventilation of the neonate. Philadelphia: WB Saunders, 1981: 101-26. Hakanson D. Positive pressure ventilation: volume cycled ventilators. In: Goldsmith J, Karotkin E, eds. Assisted ventilation of the neonate. Philadelphia: WB Saunders, 1981:128-5 1. Nugent J, Hanks H. Pulmonary care. In: GoldsmithJ, Karotkin E, eds. Assisted ventilation of the neonate. Philadelphia: WB Saunders, 1981:67-80.
20. Thibeault D, Nelson P. Pulmonary care of infants with endotracheal tubes. In: Thibeault D, Gregory G, eds. Neonatal pulmonary care. Menlo Park, Ca.: AddisonWesley, 1979:237-52. 2 1. Crone R, Favorito J. The effects of pancuronium bromide on infants with hyaline membrane disease. J Pediatr 1980;97:991-3. 22. Finer N , Tomney P. Controlled evaluation of muscle relaxation in the ventilated neonate. Pediatrics 1981;67:64 1-6. 23. Nugent S, Laravuso R, Rogers M. Pharmacology and use of muscle relaxants in infants and children. J Pediatr 1979;20:481-7. 24. Cohen S, Perez R, Strodtbeck F. Newborn respiratory paralysis for severe respiratory distress: a nursing protocol. Dimensions of Critical Care Nursing 1982;1:340-9.
Address for correspondence: Jan Nugent, RN, Unit Directer, NICU, Ochsner Foundation Hospital, 1516Jefferson Highway, N e w Orleans, LA 70121.
Jan Nugent is the unit director of newborn intensive care unit, intermediate nursery, and nurse practitioner activities at Ochsner Foundation Hospital of New Orleans, Louisiana. She holds a BSN from the University of Southwestern Louisiana and an MSN from the University of California in San Francisco. Ms. Nugent is a member of NAACOG.
May/June 1983 JOGN Nursing (Supplement)
Many of the respiratory disorders of the newborn are unique to that period of development. Understanding the process of fetal lung maturation and differentiation as well as the adaptive transitional changes which occur in the cardiovascular and respiratory systems during the first 24 hours of life is essential in comprehending the pathogenesis of these problems. This information is available in the literature and will not be reviewed here. 1-4 CAUSES OF RESPIRATORY DISTRESS There are many respiratory disorders in the newborn period. By far, the most common are hyaline membrane disease, transient tachypnea of the newborn and meconium aspiration syndrome. Hyaline Membrane Disease Hyaline membrane disease, the most common form of neonatal respiratory distress, accounts for 18% of all neonatal deaths in the United state^.^ Hyaline membrane disease occurs in infants born prior to term and of appropriate size for gestational age.6 T h e pathogenesis of hyaline membrane disease is directly re-
May/June 1983JOGN Nursing (Supplement)
0090-031 1/83/0513-0031~$01.50
lated to the immaturity of the lung in respect to its capacity to synthesize and regenerate the surface active material surfactant. Surfactant effectively lowers surface tension in alveoli and thereby promotes alveolar stability and the establishment of a functional residual capacity.6 Without surfactant, alveolar collapse occurs at the end of expiration. Each breath becomes as difficult as the first and as the infant tires, atelectasis becomes progressively more pronounced. Progressive atelectasis is the hallmark of hyaline membrane disease. Atelectasis greatly reduces tidal volume, lung compliance, functional residual capacity, and alveolar ventilation. Atelectasis also contributes significantly to an uneven ventilation-perfusion ratio. T h e negative correlation between alveolar ventilation and right-toleft shunts (ie., the less the ventilation, the greater the shunt) is significant. This combination of atelectasis and pulmonary hypoperfusion secondary to intra- and extrapulmonary shunting of blood produces the typical clinical pict u r e of progressive hypoxia, hypercapnia, and metabolic a c i d o ~ i s . ~ A striking feature of hyaline membrane disease is early onset of symptoms, usually before six hours
of life. T h e infant will demonstrate tachypnea, nasal flaring, grunting, see-saw (paradoxical) respirations, and cyanosis. T h e infant will become progressively more obtunded and flaccid. Auscultation of lung fields will reveal diminished breath sounds. As the disease progresses, characteristic “sandpaper” breath sounds can be detected on inspiration and expiration. Characteristic x-ray findings are illustrated in Figure 1. T h e natural course of the disease is one of increasing severity of respiratory distress and poor lung function until 48 to 72 hours of life. Symptoms then will begin to abate as pulmonary type I1 cell regeneration occurs and surfactant production is reestablished.6 Treatment is aimed at overcoming and preventing atelectasis. Therapeutic measures consist of oxygen therapy, continuous positive airway pressure, and positive pressure ventilation. Hypothermia must be avoided; metabolic acidosis and hypotension must be corrected; and fluid, electrolyte, and glucose needs must be met. Transient Tachypnea of the Newborn T h e pathognomonic hallmark of transient tachypnea of the new-
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Figure 1. Anteroposterior chest film demonstrates x-ray manifestations of hyaline membrane disease. Note homogenous, bilaterally symmetrical reticulogranular pattern with diffuse air bronchogranis. In severe hyaline membrane disease, hypoaeration is also evident and is demonstrated by increased doming of both hemidiaphragms at the level of the seventh rib.
born, (respiratory distress, type 11) is delayed resorption of fetal lung fluid. Transient tachypnea of the
newborn occurs in term as well as preterm infant^.^ Predisposing conditions are prematurity and ce-
Figure 2. Anteropoaterior chest film demonstrated x-ray manifestations of transient tachypnea in the newborn. Bilateral diffuse perihilar and central lung fluid with fluid in the fissure are shown. Concoinitant hyperaeration of lungs is noted as both hemicli;ipliragms are at the level of the tenth rib.
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sarean section. Absent in the delivery of these infants is the thoracic squeeze, which will mechanically clear up to one-third of the fluid from the lungs. Initially, transient tachypnea of the newborn may be difficult to distinguish from hyaline membrane disease. Clinically, tachypnea, substernal retraction, flaring, and grunting are seen. Auscultation of breath sounds reveals adequate air entry and scattered rales. Mild hypoxia and hypercapnia may be present. T h e radiographic pattern of transient tachypnea of the newborn is demonstrated in Figure 2. T h e clinical course demonstrates mild to moderate respiratory distress from two to four hours after birth. T h e symptoms peak at 36 hours, and gradual recovery usually occurs by 72 hours of life. Treatment consists of oxygen supplementation and supportive health care m a i n t e n a n ~ e . ~
Meconium Aspiration Syndrome Meconium aspiration is a significant cause of neonatal morbidity and death. T h e reported incidence of meconium-stained amniotic fluid is 10% of all pregnancies; approximately 10% of infants with meconiuni-stained amniotic fluid have evidence of respiratory distress.' Massive meconium aspiration occurs most frequently in term, postterm, and small-for-gestational-age infants. This syndrome rarely is encountered in preterm infants.' T h e pathogenesis of meconium aspiration has two components: fetal asphyxia, followed by aspiration of meconium into the tracheobronchial tree. Intrauterine hypoxia initiates a vagal reflex which results in passage of meconium into the amniotic fluid. Usually, meconium then is aspirated into the lower airways during the first respiratory efforts made outside the birth canal. At this point, a large negative pressure is gener-
May/June 1983 JOGN Nursing (Supplement)
ated inside the chest and any fluid in the nasopharynx or trachea will be pulled d o w n into the smaller airways. T h e presence of meconium in lower airways will produce varying degrees of complete and partial airway obstruction. Partial airway obstruction results in air trapping and overinflation of distal alveolar sacs. Complete obstruction produces alveolar collapse. Meconium in the lung produces a severe inflammatory reaction resulting in a chemical pneumonitis that reduces the diffusing capacity of the lung. Together these conditions produce the clinical picture of hypoxemia, intra- and extrapulmonary shunting, C O P retention, and pulmonary air leaks.' In meconium aspiration, t h e spectrum of severity of clinical symptoms correlates grossly with the amount of meconium aspirated into the lungs. Infants with meconium aspiration syndrome, usually have low Apgar scores and demonstrate tachypnea, retractions, and cyanosis shortly after birth. The infant's chest frequently will be overdistended a n d barrelshaped with increased anteriorposterior diameter; breath sounds are poor and usually obscured by coarse bronchial sounds; expiration is prolonged. Palpation of the abdomen may demonstrate t h e liver well below the intercostal margins. Displacement of the liver is secondary t o depression of the diaphragm by air trapping and overexpansion of the lung. T h e radiographic pattern of meconium aspiration syndrome is demonstrated in Figure 3. Pneumomediastinum, p n e u m o t h o r a x , a n d pleural fluid frequently a r e found. Initial blood gases will reveal hypoxia, and respiratory and metabolic acidosis.* Successful treatment of meconium aspiration syndrome is dependent on prompt removal of meconium from the airway. Consistent use of intrapartum naso-
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Figure 3. Anteroposterior chest film denionstrates x-ray manifestations of meconium aspiration syndrome. Note bilateral, asymmetrical infiltrates. In severe meconiuni aspiration syndrome, lungs will be hyperaerated with Iiemidi;tphragn~sflattened below the ninth rib.
pharyngeal suctioning via DeLee suction of oronasal pharynx at the time of the delivery of the infant's head prior to the first extrauterine gasp, immediate visualization of vocal cords, and efficient tracheal suctioning will significantly reduce morbidity and mortality.' Positive pressure ventilation ( Z . P . , bagging) should not be applied prior to suctioning. Once initial suctioning is complete, the infant then can be ventilated with high oxygen concentrations to ensure adequate oxygenation and elimination of CO2. When meconium does reach the lower airways, treatment is directed toward clearance of the meconium by postural drainage and chest physiotherapy. Supplemental oxygen will be necessary, and if hypoxia and hypercapnia are severe, intubation and mechanical ventilation will be required. Because of reduced lung compliance and increased airway resistance, high peak inspiratory pressures and fast frequency ventilation with low inspiratory/expiratory ratio will be needed. Although life saving, this type of mechanical venti-
lation, together with damage produced by meconium, makes the occurrence of pulmonary air leaks (pneumothorax, pneumomediastinum) a common complication in these infants. Other complications the nurse should be alert to are persistent fetal circulation, seizures secondary to cerebral edema resulting from asphyxia, and sepsis secondary to bacterial pneumonia. Although n o evidence supports their use, prophylactic antibiotics a r e frequently administered in consideration of the latter complication.' Supportive measures to prevent hypoglycemia, electrolyte imbalances, a n d hypothermia should be instituted.
RESPIRATORY ASSESSMENT OF T H E NEWBORN I t is essential that the neonatal nurse be skilled in the principles of respiratory assessment. Early recognition of an infant in respiratory distress is as critical to the infant's well-being as the subsequent mea-
33s
sures taken to improve the infant’s respiratory status. Nursing assessment of the neonate in respiratory distress includes anticipatory identification of infants vulnerable to respiratory disorders, recognition of neonatal respiratory distress, and an ability to make acute serial observations while concurrently evaluating the infant’s response to treatment. This process involves the collection and documentation of perinatal history, clinical observations, and laboratory data.
IDENTIFICATION OF INFANTS AT RISK Perinatal History In many instances, neonatal respiratory distress is predictable. T h e nurse must be aware of highrisk factors or events in the mother’s and neonate’s prenatal history that would be pertinent to assessment of the infant. T h e nurse then can anticipate which infants are at risk and subsequently identify what measures to take to prevent unnecessary deterioration of the infant’s condition. Factors that identify infants at risk for respiratory distress are maternal analgesia, bleeding or diabetes, infection, meconiumstained amniotic fluid, cesarean section, asphyxia, hypothermia, prematurity, postmaturity, smallor large-for-gestation, and erythroblastosis fetalis. Assessment begins with determining the physical status of the neonate immediately after birth. Assessment includes Apgar score, physical examination to rule out gross anomalies, estimation of gestational age, and classification of the infant as appropriate-smallor large-for-gestational-age. Recognizing infants as preterm, postterm, small- or large-for-dates will help the nurse anticipate inherent problems and make preparations necessary to facilitate treatment. 34s
Inspection Clinical observations of respiratory function are gathered primarily via inspection and auscultation. Inspection of infants at risk for respiratory dysfunction should begin in the delivery room and continue at frequent intervals in the nursery. Respiratory difficulties can be recognized by simple and methodical observation of the infant. T h e infant’s color and quality of respiration need to be inspected before disturbing the infant. At birth, infants are seldom completely pink. A transient generalized cyanosis may be present for the first five to six minutes of life. Acryocyanosis involving hands, feet, and circumoral area may be evident at delivery and for a short time thereafter. However, a sustained, generalized cyanosis is clearly indicative of distress. T h e infant’s respirations should be counted for a minimum of 60 seconds: Normal respiratory rates range between 40 to 60 breaths per minute. T h e nurse should note any periodic breathing or apnea by observing the infant’s respiratory pattern. Periodic breathing, i.e., short cessation of breathing for up to 10 seconds, is a frequent normal finding in premature infants. Periodic breathing is not associated with cyanosis or bradycardia, and should not be confused with apnea. Apnea is of longer duration and is often accompanied by cyanosis and/or bradycardia. Periodic breathing occurs rarely during the first 24 hours of life; apnea may occur at any time. Nursing assessment also includes inspection of thoracic shape, size, and symmetry of movement. Respiratory movements should be symmetrical and predominantly diaphragmatic with a relatively immobile thoracic cage. T h e abdomen will rise and fall with inspiration and expiration. Asymmetry of thoracic size or movement may
indicate pathology, i.e., pneumothorax, chylothorax, or diaphragmatic hernia. T h e anteroposterior diameter of the chest should be compared with the lateral diameter. In infants, this ratio is usually 1:1. An increased anteroposterior diameter is indicative of overexpanded lungs (transient tachypnea of the newborn, meconium aspiration syndrome). T h e infant’s ribs are flexible and slight sternal retractions may be evident. Retractions indicate obstruction to airflow at any level of the respiratory tract; more than slight retractions are abnormal. Respiratory dysfunction will be demonstrated by tachypnea, expiratory grunting, retractions, nasal flaring, cyanosis, pallor, apnea, bradycardia, hypothermia, and hypotonia. Quantitating the signs of respiratory distress with the Silverman-Anderson score or the Miller score may be usefuLg All signs of respiratory distress should be documented and reported immediately to the physician.
Auscultation Auscultation of the chest will help the nurse assess air flow and detect any obstruction of the airway. T h e quality of information gathered by auscultation is in direct proportion to the skill of the listener. T h e neonate’s diminutive chest size can distort breath sounds; localization of findings is often impossible and absence of breath sounds in one part of the lung may not be appreciated because breath sounds from unaffected areas are transmitted from one region to another. However, the experienced listener can qualify air exchange, and detect atelectasis and pneumothorax, rales, and rhonchi. Decreased breath sounds occur in hyaline membrane disease, meconium aspiration syndrome, atelectasis, pneumothorax, and emphysema. Rales are crackling sounds
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produced in terminal bronchioles and alveoli when air rushes through fluid within them. Rales are occasionally heard in hyaline membrane disease but are more pronounced in transient tachypnea of the newborn and meconium aspiration syndrome. Rhonchi a r e coarse snoring sounds produced by air rushing through fluid in large bronchi. Rhonchi can be cleared with endotracheal suctioningrales cannot. Rhonchi are commonly heard in meconium aspiration syndrome. Breath sounds should be auscultated bilaterally and methodically. A stethoscope with a small diaphragm (Figure 4) should be used to prevent interference from extraneous noise and assist in isolating breath sounds. T h e examiner should move the stethoscope down the chest auscultating breath sounds both anteriorly and laterally along the midaxillary line. Breath sounds, produced by the movement of air in the bronchioles and alveoli, are normally soft- and low-pitched and should be heard equally over all lung fields. T h e duration of the sounds on inspiration is greater than on expiration. T h e nurse should note diminished breath sounds, particularly when there is a discrepancy between the two lungs and adventitious breath sounds (rales, rhonchi). T h e physician should be notified of any abnormal findings and their location should be recorded, ie., diminished breath sounds in left lower lobe, rales noted bilaterally. Heart sounds must be auscultated: Heart rate should be noted, the first and second heart sound differentiated, murmurs noted, and the infant’s point of maximal impulse located. T h e point of maximal impulse is normally in the fifth intercostal space to the left of the sternum in the midclavicular line; displacement of the point of maximal impulse can lead to suspicion
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Figure 4. Correct technique for auscultation of breath sounds laterally along the midaxillary line. Note appropriate size of stethoscope diaphragm.
of pneumothorax, diaphragmatic hernia, or dextrocardia. T h e nurse needs to determine if respiratory distress is of pulmonary o r extrapulmonary origin. This determination can be accomplished by following a few guidelines. Respiratory distress of cardiac origin presents with tachypnea, but breathing is usually not labored o r obstructed. Heart sounds are loud and rapid: a murmur or gallop rhythm may be audible. Infants with cyanotic heart disease do not improve with 100% oxygen. Hepatomegaly (more than 3 cm below the intercostal margin) may be present, as well as x-ray manifestations of cardiomegaly.
Diagnostic Measures Once the nurse has assessed that an infant is clinically demonstrating signs of respiratory distress, the physician should be notified and orders for confirming x-ray information, laboratory data, and therapeutic measures should be obtained. T h e nurse should be familiar with the common x-ray manifestations of hyaline membrane dis-
ease, transient tachypnea of the newborn, and meconium aspiration syndrome. T o assure good radiographic results and avoid unnecessary radiation exposure, the infant must be correctly positioned for the x-ray procedures. Usually, anteroposterior and lateral views of the chest are requested. Chest films should be taken during inspiratory phase of respiration. T h e infant’s gonads should always be covered with a small lead shield. All nursery personnel need to wear a lead apron when assisting with any x-ray procedure. T h e presence of respiratory pathology often is confirmed by blood gas data. T h e nurse needs to know and understand blood gas normals, be able to recognize and characterize deviations from the norm (ie., respiratory acidosis, metabolic acidosis), and understand the impact that various disease processes have on blood gases (Tables 1, 2, and 3). Table 1 provides guidelines for normal blood gas values. These values may vary slightly with individual laboratories. Arterial blood samples provide the most reliable blood gas data. If arterial blood is not easily ob-
35s
Table 1. Normal Blood Gas Values in the Neonate Source
Arterial
CaDillarv
PH PO2 PCO* HCOs Base excess/deficit
7.35-7.45 50-80 mm Hg 35-45 mm Hg 22-26 mEq/L. 2 -2
7.35-7.45 40-50 mm Hg 35-45 mm Hg 22-26 mEq/L. -2 2
+
+
Table 2. Classification of Blood Gases as Related to Acid-base Disturbances
Disturbance
Blood DH
PCO*
HC03
Base excessldeficit
Respiratory Acidosis uncompensated compensated
<7.35 normal
T T
normal T
normal excess > +2
Respiratory alkalosis uncompensated compensated
>7.45 normal
1 1.
normal 1
normal deficit > -2
Metabolic acidosis uncompensated compensated
<7.35 normal
normal 1.
1
1
deficit > -2 deficit > -2
Metabolic alkalosis uncompensated compensated
>7.45 normal
normal T
T T
excess > +2 excess > +2
tained, capillary blood gases may be of value, especially if a transcutaneous pop monitor (TcpO2) is used simultaneously. Capillary samples will indicate the status of pH and pC02 but are unreliable indicators of p02. If properly calibrated and positioned, the TcpOp will provide reliable continuous recording of pop. Knowledge of theory, calibration and operation of the Tcp02 is of paramount importance if reliable clinical data are to be obtained. Selection of a proper skin
site is critical. For neonatal monitoring, commonly used sites are the upper part of the chest, abdomen, and inner aspect of the thigh. The site should have good capillary blood flow with as little fat as possible. Bony prominences should be avoided. Ensure an airtight seal between the Tcp02 electrode and skin surface by cleaning the skin with an alcohol swab. The skin site should be changed and the electrode recalibrated at least every four hours. If an infant requires oxygen
therapy and/or assisted ventilation, a reliable method of obtaining blood gases must be established. T h e method chosen to monitor blood gases will depend upon the severity of the infant’s pulmonary disease (Table 4). After the initial assessment and recognition of an infant in respiratory distress, the nurse must continue to assess and correlate clinically the infant’s physical findings and blood gas data throughout the course of the disease. Pertinent nursing observations should be reported to the physician and systematically documented. A 24-hour flow sheet (Figure 5 ) is usually ideal for this purpose. Observations that should be recorded at one- to two-hour intervals are quality of respirations, breath sounds, color, tone, activity, and vital signs (temperature, pulse, respirations, and blood pressure). Response to therapy and any communication with the physician should be documented. The nursing flow sheet as well as a respiratory therapy flow sheet with all blood gas data should be at the neonate’s bedside for easy reference. Nurses play an important role in detecting significant changes, assessing response to medical management, and providing supportive nursing care.
NURSING INTERVENTIONS Multidisciplinary Approach Successful, comprehensive treatment of an infant in respiratory distress depends upon close teamwork between physician, nurse,
Table 3. Classification of Frequently Found Blood Gas Abnormalities by Disease
Respiratory Acidosis
Disease
Hypoxia
Hyaline membrane disease Transient tachypnea of the newborn Meconium aspiration syndrome
J
J
J
minimal
J
J
36s
Respiratory Alkalosis
Metabolic Acidosis
Metabolic Alkalosis
occasional -
J
-
minimal
-
J
-
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and respiratory therapist. T h e physician determines the course of therapy; the nurse and respiratory therapist support the therapy via ongoing assessment a n d implementation of appropriate interventions. Hence, the three disciplines work together to develop a plan of care that is communicated to all members of the health-care team.
Table 4. Blood Gas Monitoring Technidues
Indwelling catheter
Steady state gases Easy access once placed Allows continuous blood pressure monitoring
Potential for major complications: thrombi, emboli, infection, exsanguination, and arterial spasm
Intermittent punctures
Allows access to arterial blood when no catheter in place
Potential for major complications: carpal tunnel syndrome, median nerve damage, and thrombi Patient may not be in a steady state, i.e., may be crying or breath-holding,which will cause fluctuations in Pa02
Capillary sampling (arterialized)
Accurate pH, PCO2 Good for chronic conditions, i.e., bronchopulmonary dysplasia Low complication rate Can be performed easily
Not reliable for PO2
Transcutaneous monitoring
Noninvasive Continuous record of PO2
pH, PC02, electrodes not yet commercially available May be unreliable if skin perfusion is decreased Sophisticated setup required Complications; skin burns and erosion
Implications for Nursing Practice
The infant manifesting respiratory distress has both' specific respiratory care a n d supportive health care needs. These needs are interrelated and must be dealt with effectively if the infant is to achieve and maintain optimal physiologic functioning. STANDARDS FOR RESPIRATORY CARE
Specific respiratory health care needs of an infant in respiratory distress are 1) maintenance of adequate oxygenation and ventilation, and 2) correction of acid-base balance. These needs initially are met by providing the appropriate oxygen therapy, i.e., increasing ambient oxygen, continuous positive airway pressure, or controlled mechanical ventilation. The maintenance of adequate oxygenation is imperative as the sequential effects of hypoxia (acidosis, persistent pulmonary hypertension, and ischemic injury to heart, kidney, and brain) are cataclysmic. Oxygen, although lifesaving, is a drug and must be administered carefully. Infants requiring oxygen therapy must be monitored closely in three ways: clinically, by a knowledgable nurse and physician; technically, by cardiorespiratory, temperature, and blood pressure monitors; and serially, by laboratory data via blood gas determinations. If the infant cannot receive all of the components of care, he/she should be
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Disadvantaaes
Advantages
Adapted from and used with permission of author and publisher. Phillips B, McQuintty J: Blood gases: technical aspects and interpretation. In: Goldsmith J, Karotkin E, eds. Assisted ventilation of the neonate. Philadelphia: Saunders, 1981:220.
transferred immediately to a newborn intensive care unit. T h e purpose of administering oxygen is to increase the amount of oxygen delivered to the tissues. An infant's P a 0 2 should be maintained between 50 to 80 mm Hg." T h e concentration, humidity, and temperature of inspired oxygen should be precisely regulated. T h e toxic effects of oxygen on eyes (retrolental fibroplasia) and lungs (bronchopulmonary dysplasia) must be appreciated." Hyperoxemia (Pa02 > 100 mm Hg) must be avoided. All preterm infants receiving oxygen therapy should undergo a dilated fundoscopic examination prior to discharge. N o infant should be exposed unnecessarily to high concentrations of oxygen. All infants should be weaned
from oxygen as soon as it is clinically feasible. Blood gas measurements are essential for safe oxygen administration. Blood gas measuring capabilities should be available on a 24hour basis and performed using micro-technique blood volumes (0.3 cc). Provision of an adequate thermal environment is an important factor in decreasing metabolic oxygen requirements and improving the survival of infants with severe respiratory failure. Hypothermia significantly increases oxygen consumption and promotes pulmonary vasoconstriction. These conditions promote hypoxia and acidosis which notably decrease surfactant production. Hypoxic infants have a diminished thermo-
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genic response to chilling. At a P a 0 2 of 40 mm Hg, thermogenesis is reduced; at a PaOz of 30 mm Hg, the thermogenesis is abolished." Neutral thermal environment is best achieved by using an isolette or an open bed radiant warmer. The use of servo-control is recommended to keep an infant's temperature at the prescribed level. All inspired gases should be warmed to the infant's neutral thermal range and ventilator gases maintained at 97°F (36°C). The infant's axillary temperature should be monitored and recorded at one- to two-hour intervals. Axillary temperature needs to be maintained between 97°F and 98°F (36°C to 36.6"C).
Oxygen Per Hood Using an isolette to administer oxygen is problematic. Concentrations greater than 30% cannot be maintained effectively, and steady oxygen equilibrium is impossible due to the need to open the portholes. If higher concentrations are required, an oxygen hood should be used. Prescribed oxygen levels should be ordered in exact concentrations, i.e., percent or fraction of inspired oxygen (FIO2),not in liters per minute. The precise provision of oxygen between 2 1 to 100% requires separate sources of compressed air and oxygen that are connected to a blender or mixing chamber. Table 5 outlines specific nursing responsibilitiesand interventions when using an oxygen hood.
Table 5. Nursing Responsibilities and Interventions for Use of Oxygen Hood
Responsibility
Interventions
Maintain prescribed F102
Know how to operate and calibrate oxygen analyzer Place sensor near infant's nose (Figure 6) Analyze and document FIO, hourly Avoid fluctuations in oxygen concentration
Maintain patent airway and optimal position
When supine, slightly hyperextend neck with roll under neck and shoulders; place in prone position if umbilical artery catheter not in place Gently suction nasal passages and oropharynx as needed; aspirate stomach every 4 hours Do not restrict air exchange with nasogastric tube or phototherapy eye pads
Prevent drying of mucous membranes
Humidify (sterile water) all inspired gases Give oral care with glycerin swabs as needed
Prevent cold stress
Warm all inspired gases to infant's neutral thermal range Keep thermometer in h o d at all times (Figure 6) Maintain constant temperature in hood Note and document hood temperature with vital signs
Prevent COPbuildup in hood
Provide at least a 2 liter flow of gas through hood
Monitor clinical response to oxygen therapy
An arterial blood gas should be obtained at least every 4 hours, and 10 to 20 minutes after each change in F102 Notify physician if PaO, >80 or (50 mm Hg; PC02 >50 mm Hg; pH <7.30. Monitor hourly: skin color, breath sounds, quality of respirations, and vital signs Alert physician to changes in clinical status
has greatly increased the survival rate of infants in respiratory distress.I3 Treatment with constant
positive airway pressure involves attaching a system that applies constant distending pressure to the
CONSTANT POSITIVE AIRWAY PRESSURE The application of constant positive airway pressure in the treatment of hypoxemia is one of the most important advances in neonatal respiratory therapy in the last decade. Since first described by Gregory et al. in 197 1, this therapy
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Figure 6. Correct positioning of oxygen analyzer sensor. Note thermometer in hood.
airway throughout the respiratory cycle to a spontaneously breathing infant. T h e main effect of constant positive airway pressure is that it opens and stabilizes atelectatic al-
veoli and thereby decreases intrapulmonary shunting, increases functional residual capacity, and improves ventilatory capacity. T h e intended net effect is a dramatic
Table 6. Nursing Responsibilitiesand Intervention for Use of Constant Positive Airway Pressure Responsibility
Intervention
Maintain prescribed constant positive airway pressure
Check manometer readings frequently Document distending pressure on flow sheet Adjust pressure when infant is quiet Be alert for leaks or loose connections Maintain nasal prongs securely and properly angled in nares (Figure 7)
Maintain prescribed F102
Monitor in-line oxygen concentrations hourly Document F102 on flow sheet
Maintain adequate humidity
Constant positive airway pressure tubing should be fogged evenly with humidity Avoid excessive humidity which causes pooling and increases danger of near-drowning
Maintain adequate temperature of inspired gases
Maintain in-line thermometer in system close to infant In-line temperature should be 1 to 2 degrees below body temperature Check and document temperature with vital signs
Prevent airway obstruction
Suction endotracheal tube, nares, and oral pharynx as needed (Table 7) Clean nasal prongs every 2 hours
Be alert for signs of pneumothorax
Auscultate and document quality of breath sounds hourly Pneumothorax is evidenced by decreased breath sounds and chest movement, shift in point of maximal impulse, bradycardia, cyanosis, and decreased pulse pressure Action: ventilate with 100% oxygen, alert physician, call for stat chest x-ray, prepare for needle aspiration and/or chest tube placement
Prevent abdominal distention
Insert orogastric tube, leave open to atmospheric pressure Periodically use syringe to decompress stomach
Prevent skin breakdown
Secure prongs or endotrachealtube to prevent excessive movement or displacement (Figure 7) Keep skin dry and clean Support constant positive airway pressure tubing to prevent excessive pressure points Turn infant every 2 hours Use of water bed may be indicated
Maintain good oral hygiene
Assess nares and mouth frequently for irritation; apply antibiotic ointment if indicated Apply glycerine to prevent cracking or drying of mouth
Monitor clinical response to constant positive airway pressure
Obtain arterial blood gas at least every 4 hours and 10 to 20 min past change in pressure or F102 Be alert for hypercapnea (PC02 > 50 mm Hg), hypoxia (PO2 < 50 mm Hg), and acidosis (pH < 7.30) Monitor temperature, pulse, respiration, and blood pressure every 1 to 2 hours Observe closely: skin color, quality of respirations, and peripheral perfusion
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improvement in oxygenation, reduction of carbon dioxide levels, and a decrease in the work of breathing.14 Constant positive airway pressure is most effective in atelectatic disease, i.?., respiratory distress syndrome: use is indicated if an infant has a P a 0 2 less than 50 mm Hg while breathing 60% oxygen. Distending pressures should be kept as low as possible, compatible with oxygenation, to reduce the incidence of adverse cardiopulmonary effects. Usually, an initial pressure of four to six cm H 2 0 is applied and increased by two-cm increments until adequate oxygenation is achieved.14 T h e aim of constant positive airway pressure therapy is to apply the level of pressure necessary to expand but not overdistend the majority of alveoli. Infants should be weaned from constant positive airway pressure in two-cm increments once the F I 0 2 can be maintained at 40% oxygen. To avoid a decrease of physiologic functional residual capacity, constant positive airway pressure should not be reduced below two to four cm H2O.I4 Constant positive airway pressure can be applied by way of an endotracheal tube, nasopharyngeal tube, face mask, hood chamber, or nasal prongs: Each has its own advantages a n d disadvantages." Endotracheal intubation or nasal prong systems are the most widely used. Table 6 outlines appropriate constant positive airway pressure nursing responsibilities and interventions. T h e nurse must be aware of and alert to the serious complications that can develop from the use of constant positive airway pressure. Pulmonary a i r leaks (pneumothorax, interstitial emphysema) increase during distending pressure therapy. Cardiac output can be impaired by excessive transmission of pressure to thoracic veins which reduces venous return to the heart.
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Excessive constant positive airway pressure can cause decreased lung compliance with h ypoven tilation. Constant positive airway pressure must be monitored carefully and constant positive airway pressure decreased if there is any indication of deleterious cardiopulmonary effects, it., hypotension, metabolic acidosis, decreased peripheral perfusion, or hypercapnea.
Mechanical Ventilation Mechanical ventilation should be considered when apnea is protracted, when constant positive airway pressure has failed (PaO:, is less than 50 mm Hg in 100% oxygen at distending pressures of 10 to 12 crn H,O), or when blood gases reveal respiratory failure. Generally, a pH of less than 7.25, a Pa02 of less than 50 mm Hg, and a PaC02 of greater than 60 nim Hg in 60% oxygen indicate a need for some form of respiratory assistance. Various types of ventilators are available. “-”Because mechanical ventilation is associated with potentially hazardous complications, all nursing personnel must be thoroughly familiar with the operating principles of the particular ventilator used in their intensive care unit. Regardless of the type of ventilator used, the goal of mechanical ventilation is to achieve adequate alveolar ventilation and maximal oxygenation. Individual parameters of ventilator function, i . ~ . , F 1 0 2 , peak inspiratory pressure (PIP),positive end expiratory pressure (PEEP), respiratory rate, and inspiration/expiration (1:E) ratio are modified to achieve physiological blood gases. Standard approach o r uniformity in values for the specific parameters of mechanical ventilation required to produce optimal therapy do not exist. However, various philosophies of mechanical venti-
May/June 1981JOGN Nursing (Supplement)
Figure 7. Correct positioning of nasal constant positive airway pressure prongs. Foam “bonnet” holds prongs securely, preventing pressure points. A surgical face mask also may be used for “bonnet.”
lation (high frequency, slow rate, etc.) are a d ~ o c a t e d . ’ ~Establish.’~ ing appropriate ventilator settings requires teamwork between the physician, nurse, and respiratory therapist. T h e nurse must have a working knowledge of ventilator settings as well as the various philosophies governing their Nursing care of the neonate requiring mechanical ventilation demands acute, close observation. Repeated documentation of each infant’s response to changes in parameters and pattern of his ventilation is necessary. Blood gases must be followed carefully. T h e immediate environment surrounding the ventilated infant should provide all monitoring and technical equipment needed to provide safe care (Lt., cardiorespiratory monitor, suction equipment, resuscitation bag and mask, etc). Use of appropriate alarm systems on the ventilator or on the patient will greatly reduce serious complications associated with mechanical failure. Recommended alarms are high and low pressure, power disconnect, high and low oxygen, ap-
nea, heart rate, and blood pressure. l7 T h e airway (endotracheal tube) must be kept patent. Endotracheal intubation and subsequent oxygen therapy decrease ciliary activity and accelerate mucus production. Adequate chest physiotherapy is required to aid outflow of pulmonary secretions and assure patent airway. Various authors have described the technique of chest physiotherapy (percussion, vibration and suctioning) in detai1.19*20 T h e frequency of chest physiotherapy should depend upon individual patient need. Strict adherence to every two hour scheduling of chest physiotherapy should be avoided as accepted methods of chest physiotherapy have potentially detrimental side effects, ie., hypoxia, bradycardia, apnea, and cardiac arrest. T h e nurse should evaluate the need for chest physiotherapy by assessing the degree of atelectasis, volume of secretions, and stability of the infant’s condition. Muscle relaxants may be a useful adjunct to care when an infant’s
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own respiratory efforts interfere with ventilator therapy and hypoventilation results. T h e struggling infant generates increased intrathoracic pressure with decreased venous return and is at increased risk for pulmonary air leaks. Muscle relaxants improve oxygenation, decrease the incidence of pulmonary air leaks, and significantly reduce periods of increased intracranial pressure.21s22 Pancuronium (Pavulon@),a longlasting, competitive neuromuscular blocking agent, is the drug most frequently used in neonates. Curare seldom is used because of significant cardiovascular effects, ie., hypotension. When given intravenously, Pavulon produces maximum paralysis within two to four minutes. Pavulon has been shown to moderately increase blood pressure and heart rate. Pavulon does not alter the sensation of pain. Recommended dosage ranges from 0.03 to 0.1 mg/kg. T h e duration of paralysis varies from one to several hours and is prolonged by acidosis, hypokalemia, aminoglycosides, and decreased renal function.*' T h e primary hazard during paralysis is hypoxia due to accidental extubation or disconnection from the ventilator. T h e paralyzed neonate is entirely dependent on mechanical ventilation, and careful observation is mandatory. T h e infant's condition and response to respiratory paralysis after each administration of Pavulon need to be monitored. T h e effect on clinical condition should be noted by frequent assessment of color, vital signs, breath sounds, and blood gases. Ventilation parameters may need adjustment as hypoxic episodes have occurred following initial paralysis.24 T h e effects of Pavulon are reversed by simultaneously and slowly administering atropine, 0.02 mg/kg I.V., and neostigmine, 0.08 mg/kg I.V. The nurse should allow 15 to 20 minutes for complete action. In-
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Table 7. Nursing Responsibilities and Interventions for Use of Ventiiator ~~
Responsibility Maintain patent airway Alert to extubation
Provide CPT* regimen Maintain prescribed ventilator parameters (PIP,t PEEP,+ F102, rate, I:E ratios) Assess infant's response to mechanical ventilation Arterial blood gases
Clinical
Detect malfunctioning equipment Preventive measures
Occurrence of malfunction
Safe administration of muscle relaxants
Intervention
Clinically evidendd by audible crying, distinct ventilator sounds auscultated in stomach, decreased breath sounds, and sudden deterioration in color and heart rate Action: remove tube, ventilate with bag and mask, place orogastric tube to decompress stomach, set up for reintubation Follow prescribed technic for percussion vibration and suctioningignZ0;frequency dictated by individual assessment Have working knowledge of ventilator Check and record ventilator parameters hourly Properly humidify inspired gases (Table 6) Keep in-line temperature of gases 97OF (36OC) (Table 6)
Obtain blood gas 10 to 20 min postparameter change Subsequent gases should be obtained at least every 4 hours Use blood gas data to assess ventilation (PCO2). oxygenation (PO2), acid-base balance (pH, HC03), and response to therapy Follow serially to detect deterioration, i.e., acidosis, hypoxia, hypercapnea Auscultate breath sounds hourly to assess: quality of ventilation, adequate placement of endotrachealtube or occurrence of pneumothorax (Table 6) Assess vital signs: temperature, pulse, respirations, and blood pressure hourly Observeclosely for deterioration in color, heart rate, blood pressure, activity, and tone Document findings on flow sheet
Check ventilator parameters frequently Maintain alarms ON at all times Check all connections hourly to make sure they are snug Respond promptly to sounding of alarm Evidenced by sounding of alarm, sudden change in ventilator parameters, and sudden deterioration of infant Action: remove infant from ventilator, ventilate with bag, and get assistance in locating problem Know dosage, side effects, antidotes Maintain all alarm systems ON Close observation is imperative Assess respiratory paralysis after each administration of drug; note duration of effect and any changes in cardiorespiratory systems2' Maintain good alignment of body parts Cred6 bladder every 2 hours as needed Assess need for continuation of neuromuscular block prior to each dose (Continuedon page 43s)
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spiratory acidosis (inadequate ventilation) will only further increase the level of COP.
Table 7. (Continued) Intervention
Responsibility Prevent decubiti formation
Maintain good oral hygiene Prevent gastrointestinal insufflation
Evidenced by inflammation or skin breakdown Keep skin clean, dry and free from pressure points Turn infant every 1 to 2 hours Use waterbed if pressure points occur Secure endotracheal tube to prevent excessive movement See Table 6 Insert orogastric tube Aspirate with a syringe to decompress stomach every 2 hrs ~~
* CPT-Chest
physiotherapy. t PIP-Peak inspiratory pressure. PEEP-Positive end expiratory pressure. 0 I:E ratio-lnspiration/expiration ratio.
+
dications for discontinuation of respiratory paralysis are improved arterial blood gases in the presence of lowered respiratory parameters ( F 1 0 2 less than 60%). A thorough nursing protocol for neonatal respiratory paralysis is available in the 1iteratu1-e.~~ Mechanical ventilation is associated with various serious complications. T h e nurse must be aware of pulmonary air leaks and deterioration secondary to mechanical failure. T h e latter consists of extubation, endotracheal tube plugs, disconnected tubes, and ventilator apparatus malfunction. These mechanical problems can be rectified by alert nursing personnel before irreversible harm is done. Table 7 outlines nursing responsibilities and interventions for mechanical ventilation. Weaning the infant from the ventilator begins as soon as the respiratory disease stabilizes and ventilatory need decreases. T h e decrease in ventilatory settings is determined by improvement in arterial blood gases and clinical response. T h e weaning process is gradual. Close observation for respiratory deterioration is necessary. Extubation is feasible when an infant maintains normal blood gases and has good respiratory effort on constant positive airway pressure of two cm to four cm and
May/June 1983 JOGN Nursing (Supplement)
40% oxygen. After extubation, infants will be placed in an oxyhood or on nasal prong constant positive airway pressure. ACID-BASE BALANCE Acid-base derangements accompany respiratory problems in the newborn. Respiratory and metabolic acidosis are encountered most frequently. There is a direct correlation between quality of ventilation and the level of PaC02. Normal ventilation will reflect normal PaC02; hypoventilation will reflect elevated PaCO,; and hyperventilation will reflect decreased PaC02. Respiratory acidosis is due to retention of carbon dioxide or hypoventilation. Consequently, the only effective treatment is to ventilate, thereby reducing COP levels. Metabolic acidosis occurs as a result of tissue anoxia and anaerobic metabolism. Improving oxygenation, reestablishing adequate perfusion with volume expansion, and alkali therapy are all therapeutic. Slow (1 mEq/min) intravenous infusion of NaHC03 1 to 3 mEq/ kg diluted at least 1:l with sterile water accelerates correction of severe metabolic acidosis. NaHC03 should not be given until adequate ventilation is established. Giving bicarbonate in the presence of re-
SUPPORTIVE MEASURES In addition to respiratory management, the following supportive measures must be monitored carefully: thermoregulation, fluid, electrolyte and caloric balance, maintenance of normal blood pressure, protection from infection, and conservation of energy. Key components of care are included in outlines of nursing care. PARENT SUPPORT To provide comprehensive respiratory care, the nurse must support and care for the infant’s family as well. Support should be given in four areas: listening, communicating, educating, and providing parent-infant interaction. From admission through discharge, the nurse must meet the needs of the family. As each aspect of care is determined individually for each patient, so are the approaches to the primary caregivers. Referral to appropriate resource personnel is essential to insure optimal outcome.
CONCLUSION T h e care of the neonate with an acute respiratory disease is challenging and complex. Care of these infants requires knowledge of embryonic development, pulmonary pathophysiology, acid-base principles, and appropriate management of respiratory problems. Assessment skills and technical expertise are essential. Finally, the nurse must support the parents by listening, communicating, educating, and promoting parent-infant interaction.
References 1. Moore K. Before we are born. Philadelphia: WB Sauders, 1974: 125-9.
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2. King R. Pulmonary surfactant. J Appl Physiol 1982;53:1-8. 3. Avery M, Fletcher B, Williams R. The lung and its disorders in the newborn infant. In: Major problems in clinical pediatrics. Philadelphia: WB Saunders, 1981:348. 4. Oehler J. Family-centered neonatal nursing care. Philadelphia: JB Lippincott, 1981: 186-96. 5. Hein H, Brown C. Neonatal mortality review: a basis for improving care. Pediatrics 1981; 68:504-9. 6. Stahlman M. Acute respiratory disorders in the newborn. In: Avery G, ed. Neonatology. Philadelphia:JB Lippincott, 1981:37687. 7. Wesenburg R. T h e newborn chest. Hagerstown, Md.: Harper & ROW,1973~43-124. 8. Bancalari E, Berlin J. Meconium aspiration and other asphyxia1 disorders. Clin Perinatol 1978; 5:3 17-34. 9. Affonso D, Harris T. Care of the high risk neonate. In: Clark A, Affonso D, eds. Childbearing: a nursing perspective. Philadelphia: FA Davis, 1979:841-4. 10. Bancalari E. Pulmonary function testing and other diagnostic laboratory procedures. In: Thibeault D, Gregory G, eds. Neonatal pulmonary care. Menlo Park, Ca.: Addison-Wesley, 1979:123-4. 11. Korones S. Complications. In: GoldsmithJ, Karotkin E, eds. Assisted ventilation of the neonate.
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12. 13.
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Philadelphia: WB Saunders, 1981:181-206. Sinclair J. Thermal control in premature infants. Ann Rev Med 1972;23:129. Gregory G, Kitterman J, Phibbs R, Tooley A, Hamilton W. Treatment of the idiopathetic respiratory distress syndrome with continuous positive airway pressure (CPAP). N Engl J Med 1971; 284~1333-40. Gregory G. Continuous positive airway pressure (CPAP). In: Thibeault D, Gregory G, eds. Neonatal pulmonary care. Menlo Park, Ca.: Addison-Wesley, 1979:207-16. Affonso D, Harris T. Continuous positive airway pressure. Am J Nurs 1976;76:570-3. McPherson SP. Respiratory therapy equipment. 2nd ed. St. Louis: CV Mosby, 1981:168-365. Fox W, Shatack J. Positive pressure ventilation: pressure and time-cycled ventilators. In: Goldsmith J, Karotkin E, eds. Assisted ventilation of the neonate. Philadelphia: WB Saunders, 1981: 101-26. Hakanson D. Positive pressure ventilation: volume cycled ventilators. In: Goldsmith J, Karotkin E, eds. Assisted ventilation of the neonate. Philadelphia: WB Saunders, 1981:128-5 1. Nugent J, Hanks H. Pulmonary care. In: GoldsmithJ, Karotkin E, eds. Assisted ventilation of the neonate. Philadelphia: WB Saunders, 1981:67-80.
20. Thibeault D, Nelson P. Pulmonary care of infants with endotracheal tubes. In: Thibeault D, Gregory G, eds. Neonatal pulmonary care. Menlo Park, Ca.: AddisonWesley, 1979:237-52. 2 1. Crone R, Favorito J. The effects of pancuronium bromide on infants with hyaline membrane disease. J Pediatr 1980;97:991-3. 22. Finer N , Tomney P. Controlled evaluation of muscle relaxation in the ventilated neonate. Pediatrics 1981;67:64 1-6. 23. Nugent S, Laravuso R, Rogers M. Pharmacology and use of muscle relaxants in infants and children. J Pediatr 1979;20:481-7. 24. Cohen S, Perez R, Strodtbeck F. Newborn respiratory paralysis for severe respiratory distress: a nursing protocol. Dimensions of Critical Care Nursing 1982;1:340-9.
Address for correspondence: Jan Nugent, RN, Unit Directer, NICU, Ochsner Foundation Hospital, 1516Jefferson Highway, N e w Orleans, LA 70121.
Jan Nugent is the unit director of newborn intensive care unit, intermediate nursery, and nurse practitioner activities at Ochsner Foundation Hospital of New Orleans, Louisiana. She holds a BSN from the University of Southwestern Louisiana and an MSN from the University of California in San Francisco. Ms. Nugent is a member of NAACOG.
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