NEONATAL RESUSCITATION FETAL PULMONARY
Category: Child Health
Abstract : neonatal resuscitation - Respiratory adaptation Following birth, for the lungs to operate as a functional respiratory unit providing adequate gas exchange, the airways and the alveoli must be cleared of fetal lung fluid; an increase in pulmonary blood flow also must occur. In utero, most of the blood flow is shunted away from the lungs and directed to the placenta where fetoplacental gas exchan
neonatal resuscitation - Respiratory adaptation
Following birth, for the lungs to operate as a functional respiratory unit providing adequate gas exchange, the airways and the alveoli must be cleared of fetal lung fluid; an increase in pulmonary blood flow also must occur. In utero, most of the blood flow is shunted away from the lungs and directed to the placenta where fetoplacental gas exchange occurs.
Fetal pulmonary vascular resistance is high, and the fetal systemic vascular resistance is low. Within minutes of delivery, the newborn's pulmonary vascular resistance may decrease by 8- to 10-fold, causing a corresponding increase in neonatal pulmonary blood flow. At birth, the lungs must transition rapidly to become the site for gas exchange, or cyanosis and hypoxia rapidly develop.
An understanding of the structure and function of the fetal pulmonary vascularity and the subsequent transition to neonatal physiology is important to assist with adaptation effectively during resuscitation. In utero, the lungs develop steadily from early in gestation. Respiratory development is classified into 4 stages. Based on this information, it is easy to see why infants neonates born before approximately 23-24 weeks' gestational age often do not have sufficient lung development for survival because of the absence of a capillary network adjacent to the immature ventilatory units.
Fetal pulmonary physiology
The fetal lung is filled with approximately 20 mL fluid at term. Fetal airways, alveoli, and terminal saccules are open and stable at normal fetal lung volumes, distended by lung fluid. A constant flow of this fluid is secreted into the alveolar spaces throughout development, which contributes to the fetal amniotic fluid. Pulmonary and bronchial circulation also develops as the alveoli appear. Because of the compressive effect of the fetal lung fluid and the low partial pressure alveolar oxygen (paO2) in utero, the pulmonary capillary bed and pulmonary blood vessels remain constricted. High vascular resistance and low pulmonary blood flow results.
The placenta provides the respiratory function for the fetus. Two major characteristics of placental circulation enable the placenta to maintain adequate oxygenation of the fetus. First, the placenta has a multivillous circulation that allows for maximum exposure of maternal and fetal blood. Second, several factors result in the lowering of maternal pH and increasing of fetal pH, which results in increased transfer of oxygen by the maternal and fetal hemoglobins.
Maternal blood, carrying oxygen on adult hemoglobin, releases oxygen to the fetal circulation and accepts both carbon dioxide and various byproducts of metabolism from the fetal circulation. These transfers result in a decrease in the maternal placental blood pH and a corresponding shift of the maternal oxygen-dissociation curve to the right, which results in a lower affinity of the hemoglobin for oxygen and the release of additional oxygen to the fetal hemoglobin. The corresponding shift in the fetal oxygen-dissociation curve to the left allows the fetal hemoglobin to bind more oxygen.
Fetal "breathing" begins at approximately 11 weeks and increases in strength and frequency throughout gestation. Fetal respirations are controlled by chemoreceptors located in the aorta and at the bifurcation of the common carotid. These areas sense both pH and partial pressure of carbon dioxide (pCO2). A reflex response to altered pH and pCO2 is present at approximately 18 weeks' gestation; however, the fetus is not able to regulate this response until approximately 24 weeks of gestation. Recent studies have indicated that this response cannot be elicited in utero even when the pH and pCO2 are altered, leading researchers to believe that this response is suppressed in utero and is not activated until birth. Studies also suggest that the low paO2 in utero may be the mechanism that inhibits continuous breathing, and when paO2 is increased, continuous breathing is stimulated.
Neonatal pulmonary physiology
As discussed above, the fetal airways and alveoli are filled with lung fluid that needs to be removed before respiration. Only a portion of this fetal lung fluid is removed physically during delivery. During the thoracic squeeze, 25-33% of the fluid may be expressed from the oropharynx and upper airways, although this amount may be markedly less. Thoracic recoil allows for passive inspiration of air into the larger bronchioles. Effective transition requires that any remaining liquid be quickly absorbed to allow effective gas exchange.
A recent study showed that the decrease in lung fluid begins during labor. Using lamb fetuses, the researchers were able to show that the production of lung fluid is decreased on onset of labor. The subsequent reduction in lung fluid was associated with improved gas exchange and acid-base balance. In addition, labor is associated with an increase in catecholamine levels that stimulate lymphatic drainage of the lung fluid. These findings could account for the increased incidence of transient tachypnea of the newborn after a repeat cesarean section without labor. After birth, lung fluid is removed by several mechanisms, including evaporation, active ion transport, passive movement from Starling forces, and lymphatic drainage. Active sodium transport by energy-requiring sodium transporters, located at the basilar layer of the pulmonary epithelial cells, drive liquid from the lung lumen into the pulmonary interstitium where it is absorbed by the pulmonary circulation and lymphatics.
The first breath must overcome the viscosity of the lung fluid and the intraalveolar surface tension. This first breath must generate high transpulmonary pressure, which also helps drive the alveoli fluid across the alveolar epithelium. With subsequent lung aeration, the intraparenchymal structures stretch and gasses enter the alveoli, resulting in increased paO2 and pH. The increased paO2 and pH result in pulmonary vasodilation and constriction of the ductus arteriosus.
Lung expansion and aeration also is a stimulus for surfactant release with the resultant establishment of an air-fluid interface and development of functional residual capacity (FRC). Normally, 80-90% of FRC is established within the first hour of birth in the term neonate with spontaneous respirations. The pulmonary vascularity is stimulated to dilate by chemical mediators, nitric oxide, and prostaglandins. Nitric oxide is released when pulmonary blood flow and oxygenation increases. The formation of certain prostaglandins, such as prostacyclin, is induced by the presence of increased oxygen tension. Prostacyclin acts on the pulmonary vascular smooth muscle bed to induce pulmonary vasodilation. Prostacyclin has a short half-life in the bloodstream and, therefore, does not affect the systemic circulation.
Two major physiologic responses have been described for the initial lung inflation in the neonate. The first response is the "rejection response," in which the neonate responds to positive pressure lung inflation with a positive intraesophageal pressure to resist the inflation. That is to say, the infant actively resists attempts to inflate the lungs by generating an active exhalation. This response acts to not only reduce lung inflation, but also may cause high transient inflation pressures.
The second response is Head's paradoxical response in which the neonate responds to positive pressure lung inflation with an inspiratory effort, causing a negative intraesophageal pressure. This inspiratory effort, with the resultant negative, pressure produces a fall in inflation pressures but results in a transient increase in tidal volume.
Of course, the neonate may demonstrate no response to the inflation attempt, not generating any change in intraesophageal pressure during the positive pressure inflation, and passive inflation subsequently results. It is important to recognize that these physiologic responses to positive pressure inflation in the delivery room may cause large variability in the tidal volume and intrapulmonary pressures, despite constant delivery of inflation pressure.
Stimuli for the first breath may be multifactorial. The environmental changes that occur with birth (eg, tactile and thermal changes, increased noise and light) activate a number of sensory receptors that may help initiate and maintain breathing. Clamping of the cord removes the low resistance placenta, causing an increase in systemic vascular resistance and consequently causing an increase in both systemic blood pressure and pulmonary blood flow. Certain evidence also suggests that the increased arterial paO2 following the initial breaths may be responsible for the development of continuous breathing via hormonal or chemical mediators that are still undefined.
When the newborn lungs fill with air, the paO2 should rise gradually. In term infants with a persistent hypoxia, an initial increase in ventilation occurs, followed by a decrease in ventilation occurs. This effect is even more profound in premature infants whose CNS is not as mature. The carotid bodies and peripheral chemoreceptors located at the bifurcation of the common carotids are stimulated during hypoxia to increase minute ventilation. In asphyxiated infants who cannot increase minute ventilation (eg, because of extreme prematurity or sedation), profound bradycardia may result.
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