THE 1ST BREATH : Transition to Pulmonary Respiration Successful establishment of adequate lung function at birth is dependent on airway patency, functional lung development, and maturity of respiratory control. Fetal lung fluid must be removed and replaced with gas. This process begins before birth as active sodium transport across the pulmonary epithelium drives liquid from the lung lumen into the interstitium with subsequent absorption into the vasculature. Increased levels of circulating catecholamines, vasopressin, prolactin, and glucocorticoids enhance lung fluid adsorption and trigger the change in lung epithelia from a chloride secretory to a sodium reabsorptive mode. Functional residual capacity (FRC) must be established and maintained in order to develop a ventilation-perfusion relationship that will provide optimal exchange of oxygen and carbon dioxide between alveoli and blood . During vaginal delivery, intermittent compression of the thorax facilitates removal of lung fluid. Surfactant lining the alveoli enhances the aeration of gas-free lungs by reducing surface tension, thereby lowering the pressure required to open alveoli. Although spontaneously breathing infants do not need to generate an opening pressure to create airflow, infants requiring positive pressure ventilation at birth require an opening pressure of 13–32 cm H20 and are more likely to establish FRC if they generate a spontaneous, negative pressure breath. Expiratory esophageal pressures associated with the 1st few spontaneous breaths in term newborns range from 45 to 90 cm H2O. This high pressure, due to expiration against a partially closed glottis, may aid in the establishment of FRC but would be difficult to mimic safely using artificial ventilation. There is accumulating evidence that the inspiratory phase of the 1st breath should be prolonged in order to establish FRC in infants who fail to establish spontaneous respirations. The higher pressures needed to initiate respiration are required to overcome the opposing forces of surface tension (particularly in small airways) and the viscosity of liquid remaining in the airways, as well as to introduce about 50 mL/kg of air into the lungs, 20–30 mL/kg of which remains after the 1st breath to establish FRC. Air entry into the lungs displaces fluid, decreases hydrostatic pressure in the pulmonary vasculature, and increases pulmonary blood flow. This, in turn, increases the blood volume of the lung and the effective vascular surface area available for fluid uptake. The remaining fluid is removed via the pulmonary lymphatics, upper airway, mediastinum, and the pleural space. Fluid removal may be impaired after cesarean section or as a result of surfactant deficiency, endothelial cell damage, hypoalbuminemia, high pulmonary venous pressure, or neonatal sedation. Initiation of the 1st breath is due to a decline in PaO2 and pH and a rise in PaCO2 as a result of interruption of the placental circulation, a redistribution of cardiac output, a decrease in body temperature, and various tactile and sensory inputs. The relative contribution of these stimuli to the onset of respiration is uncertain. When compared with term infants, low birthweight (LBW) infants who have a very compliant chest wall may be at a disadvantage in drawing the 1st breath. The FRC is lowest in the most immature infants because of the decrease in alveolar number. Abnormalities in ventilation-perfusion ratio are greater and persist for longer periods in LBW infants and may result in hypoxemia and hypercarbia as a result of atelectasis, intrapulmonary shunting, hypoventilation, and gas trapping. The smallest immature infants have the most profound disturbances, which may resemble RDS. BREATHING PATTERNS IN NEWBORNS. During sleep in the 1st months of life, normal full-term infants may have infrequent episodes when regular breathing is interrupted by short pauses. This periodic breathing pattern, which shifts from a regular rhythmicity to cyclic brief episodes of intermittent apnea, is more common in premature infants, who may have apneic pauses of 5–10 sec followed by a burst of rapid respirations at a rate of 50–60/min for 10–15 sec. They rarely have an associated change in color or heart rate, and it often stops without apparent reason. Intermittent periodic breathing persists beyond 36 wks postconceptional age (PCA; gestational age at birth plus postnatal age) in the premature infant. The duration of periodic breathing, however, decreases between 33 and 35 wk PCA. If an infant is hypoxic, an increase in inspired oxygen concentration often converts periodic to regular breathing. Periodic breathing, a normal characteristic of neonatal respiration, has no prognostic significance. Respiratory Tract Disorders Respiratory disorders are the most frequent cause of admission for neonatal intensive care in both term and preterm infants. Signs and symptoms include cyanosis, grunting, nasal flaring, retractions, tachypnea, decreased breath sounds with rales and/or rhonchi, pallor, and apnea. A wide variety of pathologic lesions may be responsible for respiratory disturbances (see Tables 98-1 and 98-2 ), including hyaline membrane disease (HMD; respiratory distress syndrome [RDS]), aspiration (meconium or amniotic fluid) syndrome, pneumonia, sepsis, congenital heart disease, heart failure, pulmonary hypertension, choanal atresia, hypoglycemia, hypoplasia of the mandible with posterior displacement of the tongue, macroglossia, malformation of the epiglottis, malformation or injury of the larynx, cysts or neoplasms of the larynx or chest, pneumothorax, lobar emphysema, pulmonary sequestration, cystic adenomatoid malformations, pulmonary agenesis or hypoplasia, congenital pulmonary lymphangiectasis, tracheoesophageal fistula, avulsion of the phrenic nerve, hernia or eventration of the diaphragm, intracranial lesions, neuromuscular disorders, and metabolic disturbances. It is occasionally difficult to distinguish respiratory from cardiovascular causes or sepsis on the basis of clinical signs alone. Any sign of postnatal respiratory distress is an indication for immediate examination and diagnostic evaluation, including a blood gas or pulse oximetry determination and x-ray of the chest. Timely and appropriate therapy is essential to prevent ongoing injury and improve outcome. As a result of important advances in understanding the pathophysiology of respiratory disease, neonatal and infant deaths from early respiratory disease have declined markedly. The challenge is not only to continue to improve survival, but also to reduce short- and long-term complications related to early lung disease. Transient Tachypnea of the Newborn Transient tachypnea usually follows uneventful normal preterm or term vaginal delivery or cesarean delivery. It may be characterized by the early onset of tachypnea, sometimes with retractions, or expiratory grunting and, occasionally, cyanosis that is relieved by minimal oxygen (
Posted on: Mon, 18 Aug 2014 09:13:26 +0000
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