The decision for initiation of assisted ventilation should be individualized. Factors to consider include underlying disease and its expected natural history, birth weight, gestational age, postnatal age, chest radiographic appearance, progression of clinical signs, serial arterial blood gas tension measurements, and pH measurements. The criteria indicating a need for mechanical ventilation are difficult to define, and there is lack of unanimity about a particular threshold for PaO
2, partial pressure of CO
2 (PaCO
2), or FiO
2. In general, the PaO
2 should be maintained at or above 50 mm Hg because of reasonable oxyhemoglobin saturation at this level, but the maximal level of inspired O
2 dictating intubation and application of assisted ventilation remains controversial. A trend of rising PaCO
2 with concomitant decrease in pH or onset of apnea indicates a need for mechanical assistance. After assisted ventilation is initiated, the generally accepted goals are to maintain the PaO
2 between 45 and 70 mm Hg, PaCO
2 between 45 and 60 mm Hg, and pH at 7.25 or more, minimizing PIP and FiO
2, and optimizing MAP (P
AW[gas]) and PEEP. These general guidelines must be interpreted and often must be modified to provide optimal support for the individual patient (
42).
Because acute lung disease is usually more severe and protracted in more immature infants, criteria for intervention for infants weighing less than 1,000 g differ from those for larger or older infants. For example, a 750-g infant with RDS has a high probability of developing apnea, fatigue, or both, and most of these infants require assisted ventilation even if the FiO
2 need is less than 40%. A 2,500 g, 36-week-old infant with RDS has greater muscular and caloric reserve and is able to sustain rapid ventilatory rates and higher respiratory work for several days without assistance. Infants of gestational age 35 to 39 weeks and older than 24 hours who develop respiratory failure with RDS may benefit from surfactant treatment (
43).
Physiologic Considerations
An understanding of the effects of mechanical ventilation on the lungs requires knowledge of the interplay among thoracic mechanics, including pulmonary compliance and airway resistance, lung volumes, respiratory control mechanisms, and alveolar gas exchange.
Lung compliance, that is change in lung volume per unit pressure change, in units of mL/cm H2O depends on the elastic properties of the tissue, which are influenced by the lung volume and abnormalities such as tissue inflammation and edema. Compliance is low if there is alveolar collapse or overdistention. Expansion from alveolar collapse requires inflation pressures of 12 to 20 cm H2O in preterm infants with RDS to achieve tidal volumes of 3 to 5 mL/kg. The lungs of infants with RDS have areas of collapse and overexpansion, and there is nonuniformity of compliance. Other conditions, such as pneumothorax, lobar atelectasis or consolidation, and pulmonary edema, decrease compliance. The most relevant measure of compliance, specific compliance, is calculated by normalizing compliance by EEV, the functional equivalent of FRC measured during positive-pressure ventilation. Very low or high values for EEV will reduce compliance. Changes in compliance, EEV, and gas exchange are not concordant, at least not during RDS. This has limited the value of bedside measurements of compliance, particularly without concomitant measurements in EEV. Chest wall compliance usually is high and does not present a problem to mechanical ventilation.
Airway resistance (cm H2O/L/s) is inversely related to the fourth power of the radius during laminar air flow. Airway resistance is high in infants, increasing with low lung volumes and with obstruction of the airway. High rates of air flow increase resistance by producing turbulence in the airways.
Resistance and compliance determine the rate at which lung areas inflate and deflate. An increase in airway resistance increases the time required for air to reach the alveoli; a decrease in compliance results in less time required to reach equilibrium. The product of resistance and compliance is the pulmonary time constant. Changes in resistance or compliance can alter the pattern or distribution of ventilation, and recognition of the variations in the time constant (e.g., short with poor compliance, prolonged with increased airway resistance) helps determine respirator settings. Unfortunately, a single time constant does not exist for all lung areas during complex pulmonary disorders. Thus, all conventional positive-pressure ventilators produce areas of overinflation and underinflation of gas exchanging areas, each contributing to suboptimal gas exchange.
Because RDS should result in a short time constant, short inspiratory times are permissible, and MAP should be increased to improve oxygenation. With meconium aspiration or airway edema, the time constant is slower, and sufficient time for expiration is important to avoid gas trapping, overdistention of the lungs, and possible air leak. If the expiratory time (TE) is shorter than the time constant of the lung for expiration, overdistention results. If the overall time constant for the lung is longer than the imposed ventilator inspiratory time (TI), inadequate ventilation could result. Unequal time constants coexisting in different parts of the lung are most likely to occur if pulmonary abnormalities are unevenly distributed, as in pneumonia, meconium aspiration, pulmonary interstitial emphysema, pneumothorax, or CLD, in which case the optimal TI or TE becomes difficult to determine.
The circulatory effects of mechanically applied pressure to the alveoli are important. Normal breathing results in negative intrapleural pressure that enhances venous return and cardiac output. Positive-pressure breathing can impede venous return and may diminish cardiac output. Pressure during inspiration decreases the pulmonary capillary circulation as long as alveolar pressure exceeds capillary pressure and can affect total pulmonary blood flow and hence gas exchange.