Which flow pattern occurs in airways at high flow rates and high pressure gradients

Barotrauma

Elevated peak inspiratory pressures and mean airway pressures have been implicated as being traumatic to the lung parenchyma. High peak inspiratory pressures are associated with pneumothorax, whereas elevated mean airway pressures are associated with pneumothorax and reduction in cardiac output.73 It is not clear whether high peak inspiratory pressures are a primary or secondary phenomenon associated with the generation of pneumothorax. It is possible that nonhomogeneous lung ventilation (areas of poorly ventilated and well-ventilated alveoli in close proximity) results in pressure gradients across the interstitium and alveoli and the potential for rupture. However, it is a common clinical strategy to try to limit peak inspiratory pressure and mean airway pressure as much as possible. Animal studies have demonstrated in normal lungs that higher volume per respiration is associated with greater transudation of fluid across the pulmonary capillary membrane. Originally it was believed to be the result of the difference in pressure, but studies in animal models have now shown that it is not the pressure that causes edema genesis but the change in gas volume.74 As a precaution, strategies have been developed to lower the peak inspiratory pressure in the hope of reducing complications secondary to mechanical ventilation.

Barotrauma is the most commonly associated complication of mechanical ventilation, with the literature suggesting an incidence of between 7% and 25%.75 Much of the difference depends on the case mix in a particular study as well as the definition of barotrauma used. Some investigators identify only patients with overt bronchopleural fistula requiring chest tube drainage as having barotrauma, and include the presence of interstitial air in the definition. There also appears to be an association between higher incidence of pneumothorax and greater peak inspiratory pressures. Interestingly, however, investigators demonstrated equal incidences of pneumothorax for high-frequency ventilation and standard mechanical ventilation.76,77 The patients in the studies had significantly low peak inspiratory pressure, but the incidence of pneumothorax remained the same. The conclusion of the two investigating teams was that the incidence of pneumothorax is more closely related to the underlying disease than to the level of peak inspiratory pressure. Patients who have necrotizing processes within the lung have a tendency to have a higher rate of pneumothorax than patients who do not. Additionally, in other studies, patients in whom hyperinflation resulted from severe airway obstruction had a marked tendency to have pneumothorax.78,79

At present, many investigators believe that pneumothorax is secondary to inhomogeneous ventilation, regardless of the underlying disease in the lung. Necrotizing lung processes, however, result in rupture of alveolar sacs with lower airway pressures than nonnecrotizing processes.

Barotrauma is usually evidenced by a sudden increase in peak inspiratory pressure on the ventilator pressure manometer. If the barotrauma results in a tension pneumothorax, there is usually significant hemodynamic compromise, with an increase in heart rate and a decrease in blood pressure. A reduction in arterial saturation is usually noted in these patients as well. Such patients must be attended to very rapidly. Auscultation of the chest should demonstrate reduced breath sounds on the side of the pneumothorax. A shift of the mediastinum away from a tension pneumothorax is usually evident as well (Fig. 9-9). Under these circumstances, the insertion of a needle into the second intercostal space in the midclavicular line on the appropriate side is indicated to relieve the intrathoracic pressure and restore hemodynamic function.

In the event that the patient is not hemodynamically compromised and a simple pneumothorax is suspected, a chest radiograph should be obtained immediately, and a chest tube should then be placed under more controlled circumstances. Even when the pneumothorax is small, it is probably not prudent for it to be left undrained in a patient who is receiving positive-pressure ventilation. When a large pneumothorax develops and chest tubes are inserted, a large percentage of the VT generated by the ventilator may be exhausted through the chest tube drainage, resulting in significant alveolar hypoventilation. This occurs because there is less resistance for the gas to move across the chest tube than to enter the lung. Some studies have shown that under these circumstances, high-frequency jet ventilation may result in a more uniform distribution of gas because of the smaller VT employed.80 There are no data yet to suggest that the smaller VT with less leakage across the thoracostomy tube results in earlier closure of pneumothorax after it occurs. Currently, several high-frequency ventilators are available, and anecdotal data have suggested better outcomes in patients without good response to conventional ventilation.

Barotrauma may also manifest as rupture toward the mediastinal surface of the lungs. The earliest sign on the chest radiograph is mediastinal air or air shadows in the pericardial or pleural mediastinal planes. Subcutaneous emphysema is often palpated in these circumstances and can become quite extensive, with air migrating through the tissue planes up to the head, down through the abdomen into the groin, and even into the lower extremities. Cosmetically this migration is very unattractive, although from a clinical standpoint subcutaneous emphysema does not appear to have any significant adverse effects on the patient. There is no way to drain subcutaneous emphysema; however, after the air leak stops, the migrated air is usually quickly reabsorbed, and the subcutaneous emphysema dissipates on its own.

Volume Monitoring and Targeting

The continuous monitoring of VT allows rapid weaning of PIP as the mechanical conditions of the lung improve. This can be achieved by a manual decrease of PIP as VT increases, or automatically by using volume-targeted ventilation where weaning is achieved automatically independent of the clinician, who only sets the VT targeted by the ventilator. Evidence from randomized trials using volume-targeting strategies suggest that faster weaning from mechanical ventilation can be achieved, although the results have not been entirely consistent (Singh et al, 2006; Sinha et al, 1997).

Volume Monitoring and Volume-Targeted Ventilation During Weaning

The continuous monitoring of VT allows rapid reduction of PIP as the mechanical conditions of the lung improve. This can be achieved by a manual decrease of PIP as the VT increases or automatically by use of volume-targeted ventilation where weaning is achieved automatically independent of the clinician, who only sets the VT targeted by the ventilator. Evidence from randomized trials using volume-targeting strategies suggests that faster weaning off mechanical ventilation can be achieved, although the results have not been entirely consistent (Sinha et al., 1997; Singh et al., 2006).

Pressure‐Cycled Mode

With pressure‐cycled ventilation, inspiration is terminated when a preset peak inspiratory pressure is reached. The delivered volume (i.e., tidal volume) with each respiration is dependent on pulmonary and thoracic compliance, airway resistance, and respiratory effort. Flow is delivered in a decelerating pattern, in which inspiratory flow tapers off as the lung inflates and varies from breath to breath. The advantage of this type of ventilation is that it allows for a homogeneous gas distribution throughout the lungs. Studies have suggested that patients are more comfortable breathing spontaneously while receiving ventilation via the pressure‐cycled mode. However, because the tidal volume is variable with this mode of ventilation, inconsistent alveolar minute ventilation can occur, resulting in potentially inadequate ventilation. Therefore, pressure‐cycled ventilators are less useful than volume‐cycled ventilation in critically ill patients with rapidly changing respiratory mechanics. If pulmonary compliance decreases or airway resistance increases, hypoventilation might result. This form of ventilation requires constant and aggressive monitoring of respiratory mechanics and is less favored in the ED setting.

Manipulating the ventilator settings

Various parameters can be preset on most ventilators, including the respiratory rate, PIP, PEEP, inspiratory time, and gas flow rate. When adjusting these parameters it is necessary to consider the pathologic condition present in the lung. Infants with primary pulmonary hypertension have very compliant lungs that are easily overdistended. In these patients adequate minute ventilation may be achieved with low PIP and PEEP, a short inspiratory time, and a moderate respiratory rate. Conversely a child with ARDS has noncompliant lungs and may require a relatively high PIP and PEEP, a short inspiratory time, and a high respiratory rate to achieve adequate alveolar ventilation. Obstructive disorders such as meconium aspiration syndrome and asthma have a longer time constant and require ventilation at a slower rate. After determining the initial settings, however, the patient's response must be evaluated and adjustments must be made to stay abreast of dynamic changes in pulmonary compliance and resistance that occur over time.

SURFACTANT AND MECHANICAL VENTILATION

Several studies have shown that ventilator modes with large tidal volumes and high peak inspiratory pressures during mechanical ventilation affect the pulmonary surfactant system.33 The exact mechanism by which the surfactant system is affected by mechanical ventilation is not yet entirely clear. One factor is that the surfactant in the alveolar lining is actively removed from the alveolus toward the larger airways; this can lead to a shortage of surfactant at the alveolar level that can cause the changes in surface tension characteristics in the lung seen during or after prolonged periods of mechanical ventilation.34

During end-expiration, the surfactant molecules covering the alveolar epithelium are compressed on the small alveolar area (leading to low surface tension or high surface pressure), thus preventing the alveoli from collapse. When the surface of the alveolus is smaller than the surface occupied by the surfactant molecules, the molecules are squeezed out of the surface of the alveolus and are forced toward the airways. These surfactant molecules are then unavailable to the alveoli and are eventually cleared from these alveoli. During the following inflation of the alveoli, the surface is replenished with surfactant molecules from the underlying hypophase, in which surfactant molecules in micelles are stored for later use. During the next expiration, the mechanism repeats itself, and again surfactant molecules are forced out of the alveolus and are subsequently replenished from the hypophase, in a continuing cycle.35

The amount of surfactant that must be produced and subsequently secreted by the alveolar type II cells is proportional to the loss of surface active molecules during the breathing cycle. When production and secretion of new surfactant molecules keep pace with consumption, no surfactant deficiency can occur, as in a normal, healthy lung.

Thus, mechanical ventilation should take place at a lung volume equal to or higher than the functional residual capacity level with the smallest possible volume and pressure changes. Another factor that may be important is that mechanical ventilation, especially in nonhomogeneous lungs, creates severe shear forces between open and closed airways and possible overstretch of the epithelium during the breathing cycle, thereby resulting in necrosis and desquamation of bronchiolar and alveolar epithelium.36 The overstretch of the intercellular junctions of the epithelium leads to increased permeability, with resulting surfactant inhibition.

Gross and Narine37 were the first to show that conversion of active into nonactive surfactant subfractions depends on cyclic changes in surface area in vitro. To maintain an adequate pool of functional surfactant subfraction in the air spaces in vivo, it is necessary to maintain a balance among secretion, uptake, and clearance of the active and nonactive surfactant subfractions.38 In vivo studies by Veldhuizen and colleagues39,40 in rabbits attributed the surfactant conversion to a change in alveolar surface area associated with mechanical ventilation. These investigators found that changing the respiratory rate did not affect the rate of conversion, but conversion of surfactant subfractions depended on tidal volume and time.40

Role of Pulmonary Graphics in Ventilator Management

Pulmonary graphics along with numeric estimates of pulmonary function constitute important tools to help manage significant pulmonary and airway problems. To effectively use this tool, one must understand how a given ventilator works, interpret the displayed graphics, and determine the underlying pulmonary pathophysiology. Bedside pulmonary graphics can assist the clinician in determining the many factors involved in a given patient’s abnormal pulmonary function. These factors include (1) compliance, (2) resistance, (3) tidal volume, (4) under- or overinflation, (5) effect of end-expiratory pressure, and (6) the patient’s own support (positive or negative). When ventilator parameters are changed, graphics will help determine if the alterations improve or worsen the patient’s status.

Continuous Flow Versus Demand Flow

Some ventilators that can provide pressure-regulated ventilation have both inspiratory and expiratory valves. Once PIP is reached, both inspiratory and expiratory valves close and the lung is held in inflation until the end of inspiration. For use in infants, ventilators were modified to provide continuous flow throughout the respiratory cycle.14 A continuous flow device refers to a ventilator in which the flow of respiratory gas occurs throughout the respiratory cycle. Most infant ventilators are continuous flow devices (e.g., Infant Star, Baby Bird). In most continuous flow infant ventilators, inspiratory valves are lacking, and the cycling is controlled by the exhalation valve. Closure of the exhalation valve begins inspiration, and the flow of gas going through the circuit is diverted to the patient. If the inspiratory flow rate is low (1 to 3 L/kg) and if the PIP is not limited, the tidal volume delivered by the patient can be calculated from the inspiratory flow rate and the inspiratory time. This would result in a time-cycled, volume-regulated breath. For pressure-control ventilation, the flow rates used are usually higher (4 to 10 L/kg). Once the preset PIP is reached, the excess flow is vented through a pressure relief valve, and the lungs are maintained in inflation throughout the rest of inspiration. During exhalation, there is continuous flow of gas, allowing the patient to breathe from the circuit rather than open a demand valve. A demand flow ventilator refers to a ventilator that allows inspiratory flow of gas to the patient between ventilator breaths through a demand valve that is opened by the patient’s inspiratory efforts. Work of breathing is higher with a demand flow ventilator compared with a continuous flow device because of the effort required to open the demand valve.

Volume-Targeted Ventilation

With volume-targeted ventilation, the clinician sets the desired Vt value and the ventilator automatically adjusts the PIP to deliver the set VT. As the mechanical characteristics of the lung improve and the contribution of spontaneous breathing effort increases, the ventilator delivers lower pressures.35 Thus, volume-targeted ventilation achieves automatic weaning from the PIP independent of the clinician, who only has to decide what VT is delivered by the ventilator in combination with the infant's effort. There is evidence from randomized trials and a meta-analysis that volume-targeting strategies can achieve faster weaning from mechanical ventilation and possibly reduce the incidence of bronchopulmonary dysplasia.36-38