Mechanical Ventilation in Pediatric Surgical Disease

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Mechanical Ventilation in Pediatric Surgical Disease

Amazingly, ventilation via tracheal cannulation was performed as early as 1543 when Vesalius demonstrated the ability to maintain the beating heart in animals with open chests.1 This technique was first applied to humans in 1780, but there was little progress in positive-pressure ventilation until the development of the Fell–O’Dwyer apparatus. This device provided translaryngeal ventilation using bellows and was first used in 1887 (Fig. 7-1).2,3 The Drinker–Shaw iron lung, which allowed piston-pump cyclic ventilation of a metal cylinder and concomitant negative-pressure ventilation, became available in 1928 and was followed by a simplified version built by Emerson in 1931.4 Such machines were the mainstays in the ventilation of victims of poliomyelitis in the 1930s through the 1950s.

In the 1920s, the technique of tracheal intubation was refined by Magill and Rowbotham.5,6 In World War II, the Bennett valve, which allowed cyclic application of high pressure, was devised to allow pilots to tolerate high-altitude bombing missions.7 Concomitantly, the use of translaryngeal intubation and mechanical ventilation became common in the operating room as well as in the treatment of respiratory insufficiency. However, application of mechanical ventilation to newborns, both in the operating room and in the intensive care unit (ICU), lagged behind that for children and adults.

The use of positive-pressure mechanical ventilation in the management of respiratory distress syndrome (RDS) was described in 1962.8 It was the unfortunate death of Patrick Bouvier Kennedy at 32 weeks gestation in 1963 that resulted in additional National Institutes of Health (NIH) funding for research in the management of newborns with respiratory failure.9 The discovery of surfactant deficiency as the etiology of RDS in 1959, the ability to provide positive-pressure ventilation in newborns with respiratory insufficiency in 1965, and demonstration of the effectiveness of continuous positive airway pressure in enhancing lung volume and ventilation in patients with RDS in 1971 set the stage for the development of continuous-flow ventilators specifically designed for neonates.1012 The development of neonatal ICUs (NICUs), hyperalimentation, and neonatal invasive and noninvasive monitoring enhanced the care of newborns with respiratory failure and increased survival in preterm newborns from 50% in the early 1970s to more than 90% today.13

Physiology of Gas Exchange during Mechanical Ventilation

The approach to mechanical ventilation is best understood if the two variables of oxygenation and carbon dioxide elimination are considered separately.14

Carbon Dioxide Elimination

The primary purpose of ventilation is to eliminate carbon dioxide, which is accomplished by delivering tidal volume (Vt) breaths at a designated rate. The product (Vt × rate) determines the minute volume ventilation (image). Although CO2 elimination is proportional to image, it is, in fact, directly related to the volume of gas ventilating the alveoli because part of the image resides in the conducting airways or in nonperfused alveoli. As such, the portion of the ventilation that does not participate in CO2 exchange is termed the dead space (Vd).15 In a patient with healthy lungs, this dead space is fixed or ‘anatomic’, and consists of about one-third of the tidal volume (i.e., Vd/Vt = 0.33). In a setting of respiratory insufficiency, the proportion of dead space (Vd/Vt) may be augmented by the presence of nonperfused alveoli and a reduction in Vt. Furthermore, dead space can unwittingly be increased through the presence of extensions of the trachea such as the endotracheal tube, a pneumotachometer to measure tidal volume, an end-tidal CO2 monitor, or an extension of the ventilator tubing beyond the ‘Y.’

Tidal volume is a function of the applied ventilator pressure and the volume/pressure relationship (compliance), which describes the ability of the lung and chest wall to distend. At the functional residual capacity (FRC), the static point of end expiration, the tendency for the lung to collapse (elastic recoil) is in balance with the forces that promote chest wall expansion.15 As each breath develops, the elastic recoil of both the lung and chest wall work in concert to oppose lung inflation. Therefore, pulmonary compliance is a function of both the lung elastic recoil (lung compliance) and that of the rib cage and diaphragm (chest wall compliance).

The compliance can be determined in a dynamic or static mode. Figure 7-2 demonstrates the dynamic volume/pressure relationship for a normal patient. Note that application of 25 cmH2O of inflating pressure (ΔP) above static FRC at positive end-expiratory pressure (PEEP) of 5 cmH2O generates a Vt of 40 mL/kg. The lung, at an inflating pressure of 30 cmH2O when compared with ambient (transpulmonary) pressure, is considered to be at total lung capacity (TLC) (Table 7-1). Note that the loop observed during both inspiration and expiration is curvilinear. This is due to the resistance that is present in the airways and describes the work required to overcome air flow resistance. As a result, at any given point of active flow, the measured pressure in the airways is higher during inspiration and lower during expiration than at the same volume under zero-flow conditions. Pulmonary compliance measurements, as well as alveolar pressure measurements, can be effectively performed only when no flow is present in the airways (zero flow), which occurs at FRC and TLC. The change observed is a volume of 40 mL/kg and pressure of 25 cmH2O or 1.6 mL/kg/cmH2O. This is termed effective compliance because it is calculated only between the two arbitrary points of end inspiration and end expiration.

As can be seen from Figure 7-3, the volume/pressure relationship is not linear over the range of most inflating pressures when a static compliance curve is developed. Such static compliance assessments are most commonly performed via a large syringe in which aliquots of 1–2 mL/kg of oxygen, up to a total of 15–20 mL/kg, are instilled sequentially with 3 to 5-second pauses. At the end of each pause, zero-flow pressures are measured. By plotting the data, a static compliance curve can be generated. This curve demonstrates how the calculated compliance can change depending on the arbitrary points used for assessment of the effective compliance (Ceff).16

Alternatively, the pulmonary pressure/volume relationship can be assessed by administration of a slow constant flow of gas into the lungs with simultaneous determination of airway pressure.17,18 A curve may be fitted to the data points to determine the optimal compliance and FRC.19 The compliance will change as the FRC or end-expiratory lung volume (EELV) increases or decreases. For instance, as can be seen in Figure 7-3, at low FRC (point A), atelectasis is present. A given ΔP will not optimally inflate alveoli. Likewise, at a high FRC (point C), because of air trapping or application of high PEEP, the lung is already distended. Application of the same ΔP will result only in over distention and potential lung injury with little benefit in terms of added Vt. Thus, optimal compliance is provided when the pressure/volume range is on the linear portion of the static compliance curve (point B). Clinically, the compliance at a variety of FRC or PEEP values can be monitored to establish optimal FRC.20

Finally, it is important to recognize that a portion of the Vt generated by the ventilator is actually compression of gas within both the ventilator tubing and the airways. The ratio of gas compressed in the ventilator tubing to that entering the lungs is a function of the compliance of the ventilator tubing and the lung. The compliance of the ventilator tubing is 0.3–4.5 mL/cmH2O.21 A change in pressure of 15 cmH2O in a 3 kg newborn with respiratory insufficiency and a pulmonary compliance of 0.4 mL/cmH2O/kg would result in a lung Vt of 18 mL and an impressive ventilator tubing/gas compression volume of 15 mL if the tubing compliance were 1.0 mL/cmH2O. The relative ventilator tubing/gas compression volume would not be as striking in an adult. The ventilator tubing compliance is characterized for all current ventilators and should be factored when considering Vt data. The software in many ventilators corrects for ventilator tubing compliance when displaying Vt values.

Typical ventilator rate requirements in patients with healthy lungs range from 10 breaths/min in an adult to 30 breaths/min in a newborn. The Vt is maintained at 5–10 mL/kg, resulting in a image of about 100 mL/kg/min in adults and 150 mL/kg/min in newborns. In healthy lungs, these settings should provide sufficient ventilation to maintain normal PaCO2 levels of approximately 40 mmHg, and should generate peak inspiratory pressures between 15–20 cmH2O above an applied PEEP of 5 cmH2O. Clinical assessment by observing chest wall movement, auscultation, and evaluation of gas exchange determines the appropriate Vt in a given patient.

Oxygenation

In contrast to CO2 determination, oxygenation is determined by the fraction of inspired oxygen (FiO2) and the degree of lung distention or alveolar recruitment, determined by the level of PEEP and the mean airway pressure (Paw) during each ventilator cycle. If CO2 was not a competing gas at the alveolar level, oxygen within the pulmonary capillary blood would simply be replaced by that provided at the airway, as long as alveolar distention was maintained. Such apneic oxygenation has been used in conjunction with extracorporeal carbon dioxide removal (ECCO2R) or arteriovenous CO2 removal (AVCO2R), in which oxygen is delivered at the carina, whereas lung distention is maintained through application of PEEP.22,23 Under normal circumstances, however, alveolar ventilation serves to remove CO2 from the alveolus and to replenish the PO2, thereby maintaining the alveolar/pulmonary capillary blood oxygen gradient.

Rather than depending on the degree of alveolar ventilation, oxygenation predominantly is a function of the appropriate matching of pulmonary blood flow to inflated alveoli (ventilation/perfusion [image] matching).15 In normal lungs, the PEEP should be maintained at 5 cmH2O, a pressure that allows maintenance of alveolar inflation at end expiration, balancing the lung/chest wall recoil. An FiO2 of 0.50 should be administered initially. However, one should be able to wean the FiO2 rapidly in a patient with healthy lungs and normal image matching. Areas of ventilation but no perfusion (high image), such as in the setting of pulmonary embolus, do not contribute to oxygenation. Therefore, hypoxemia supervenes in this situation once the average residence time of blood in the remaining perfused pulmonary capillaries exceeds that necessary for complete oxygenation. Normal residence time is threefold that required for full oxygenation of pulmonary capillary blood.

However, the common pathophysiology observed in the setting of respiratory insufficiency is that of minimal or no ventilation, with persistent perfusion (low image), resulting in right-to-left shunting and hypoxemia. Patients with the acute respiratory distress syndrome (ARDS) have collapse of the posterior, or dependent, regions of the lungs when supine.24,25 As the majority of blood flow is distributed to these dependent regions, one can easily imagine the limited oxygen transfer and large shunt secondary to image mismatch and the resulting hypoxemia that occurs in patients with ARDS. Attempts to inflate the alveoli in these regions, such as with the application of increased PEEP, can reduce image mismatch and enhance oxygenation.

Just as partial pressure of CO2 in the pulmonary artery (PaCO2) is used to evaluate ventilation, partial pressure of oxygen in pulmonary arterial blood (PaO2) and arterial oxygen saturation (SaO2) levels are the measures most frequently used to evaluate oxygenation. Lung oxygenation capabilities are also frequently assessed as a function of the difference between the ideal alveolar and the measured systemic arterial oxygen levels (A–a gradient), the ratio of the PaO2 to the FiO2 (P/F ratio), the physiologic shunt (image), and the oxygen index (OI).

image

where FiO2 is the fraction of inspired oxygen, PB is the barometric pressure, PH2O is the partial pressure of water, and RQ is the respiratory quotient or the ratio of CO2 production (VCO2) to oxygen consumption (VO2).

image

where CvO2, CaO2, and CiO2 are the oxygen contents of venous, arterial, and expected pulmonary capillary blood, respectively.

image

where Paw represents the mean airway pressure.15

The overall therapeutic goal of optimizing oxygenation parameters is to maintain oxygen delivery (DO2) to the tissues. Three variables determine DO2: cardiac output (Q), hemoglobin concentration (Hgb), and arterial blood oxygen saturation (SaO2). The product of these three variables determines DO2 by the relation:

image

Note that the contribution of the PaO2 to DO2 is minimal and may be disregarded in most circumstances. If the hemoglobin concentration of the blood is normal (15 g/dL) and the hemoglobin is fully saturated with oxygen, the amount of oxygen bound to hemoglobin is 20.4 mL/dL (Fig. 7-4). In addition, approximately 0.3 mL of oxygen is physically dissolved in each deciliter of plasma, which makes the oxygen content of normal arterial blood equal to approximately 20.7 mL O2/dL. Similar calculations reveal that the normal venous blood oxygen content is approximately 15 mL O2/dL.

Typically, DO2 is four to five times greater than the associated oxygen consumption (VO2). As DO2 increases or VO2 decreases, more oxygen remains in the venous blood. The result is an increase in the oxygen hemoglobin saturation in the mixed venous pulmonary artery blood (image). In contrast, if the DO2 decreases or VO2 increases, relatively more oxygen is extracted from the blood, and therefore less oxygen remains in the venous blood. A decrease in image is the result. In general, the image serves as an excellent monitor of oxygen kinetics because it specifically assesses the adequacy of DO2 in relation to DO2 (DO2/VO2 ratio) (Fig. 7-5).26 Many pulmonary arterial catheters contain fiber optic bundles that provide continuous mixed venous oximetry data. Such data provides a means for assessing the adequacy of DO2, rapid assessment of the response to interventions such as mechanical ventilation, and cost savings due to a diminished need for sequential blood gas monitoring.26,27 If a pulmonary artery catheter is unavailable, the central venous oxygen saturation (image) may serve as a surrogate of the image.28

Four factors are manipulated in an attempt to improve the DO2/VO2 ratio: cardiac output, hemoglobin concentration, SaO2, and VO2. The result of various interventions designed to increase cardiac output, such as volume administration, infusion of inotropic agents, administration of afterload-reducing drugs, and correction of acid–base abnormalities, can be assessed by the effect on the image. One of the most efficient ways to enhance DO2 is to increase the oxygen-carrying capacity of the blood. For instance, an increase in hemoglobin from 7.5 g/dL to 15 g/dL will be associated with a twofold increase in DO2 at constant cardiac output. However, blood viscosity is also increased with blood transfusion, which may result in a reduction in cardiac output.29 The SaO2 can often be enhanced through application of supplemental oxygen and mechanical ventilation.

Assessment of the ‘best PEEP’ identifies the level at which DO2 and image are optimal without compromising compliance.30,31 Evaluation of the best PEEP should be performed in any patient requiring an FiO2 greater than 0.60 and may be determined by continuous monitoring of the image as the PEEP is sequentially increased from 5 cmH2O to 15 cmH2O over a short period. The point at which the image is maximal indicates optimal DO2. The use of PEEP with mechanical ventilation is limited, however, by the adverse effects observed on cardiac output, the effect of barotrauma, and the risk for ventilator-induced lung injury with application of peak inspiratory pressures greater than 30–40 cmH2O.32,33 Furthermore, oxygen consumption can be elevated secondary to sepsis, burns, agitation, seizures, hyperthermia, hyperthyroidism, and increased catecholamine production or infusion. A number of interventions may be applied to reduce VO2, such as sedation and mechanical ventilation. Paralysis may enhance the effectiveness of mechanical ventilation while simultaneously reducing VO2.34,35 In the appropriate setting, hypothermia may be induced with an associated reduction of 7% in VO2 with each 1°C decrease in core temperature.36

Mechanical Ventilation

As discussed earlier, failure of gas exchange (CO2 elimination or oxygenation) may be an indication for mechanical ventilation. The ventilator can also be used to reduce the work of breathing and decrease VO2. Finally, mechanical ventilation is used in patients who are unable to breathe independently for neurologic reasons (primary hypoventilation, traumatic brain injury, inability to protect airway).

The Mechanical Ventilator and Its Components

The ventilator must overcome the pressure generated by the elastic recoil of the lung at end inspiration plus the resistance to flow at the airway. To do so, most ventilators in the ICU are pneumatically powered by gas pressurized at 50 pounds per square inch (psi). Microprocessor controls allow accurate management of proportional solenoid-driven valves, which carefully control infusion of a blend of air or oxygen into the ventilator circuit while simultaneously opening and closing an expiratory valve.37 Additional components of a ventilator include a bacterial filter, a pneumotachometer, a humidifier, a heater/thermostat, an oxygen analyzer, and a pressure manometer. A chamber for nebulizing drugs is usually incorporated into the inspiratory circuit. The Vt is not usually measured directly. Rather, flow is assessed as a function of time, thereby allowing calculation of Vt. The modes of ventilation are characterized by three variables that affect patient and ventilator synchrony or interaction: the parameter used to initiate or ‘trigger’ a breath, the parameter used to ‘limit’ the size of the breath, and the parameter used to terminate inspiration or ‘cycle’ the breath (Fig. 7-6).38

Gas flow in most ventilators is triggered either by time (controlled breath) or by patient effort (assisted breath). Controlled ventilation modes are time triggered: the inspiratory phase is concluded once a desired volume, pressure, or flow is attained, but the expiratory time will be the difference between the inspiratory time and the preset respiratory cycle time. In the assist mode, the ventilator is pressure or flow triggered. With the former, a pressure generated by the patient of approximately −1 cmH2O will trigger the initiation of a breath. The sensitivity of the triggering device can be adjusted so that patient work is minimized. Other ventilators detect the reduction in constant ventilator tubing gas flow that is associated with patient initiation of a breath. Detection of this decrease in flow results in initiation of a positive-pressure breath.

The magnitude of the breath is controlled or limited by one of three variables: pressure, volume, or flow. When a breath is volume, pressure, or flow ‘controlled,’ it indicates that inspiration concludes once the limiting variable is reached. Pressure-controlled or pressure-limited modes are the most popular for all age groups, although volume-control ventilation may be of advantage in preterm newborns.39,40 In the pressure modes, the respiratory rate, the inspiratory gas flow, the PEEP level, the inspiratory/expiratory (I/E) ratio, and the Paw are determined. The ventilator infuses gas until the desired peak inspiratory pressure (PIP) is provided. Zero-flow conditions are realized at end inspiration during pressure-limited ventilation. Therefore, in this mode, PIP is frequently equivalent to end-inspiratory pressure (EIP) or plateau pressure.

In many ventilators, the gas flow rate is fixed, although some ventilators allow manipulation of the flow rate and therefore the rate of positive-pressure development. Those with rapid flow rates will provide rapid ascent of pressure to the preset maximum, where it will remain for the duration of the inspiratory phase. This ‘square wave’ pressure pattern results in decelerating flow during inspiration (Fig. 7-7). Airway pressure is ‘front loaded,’ which increases Paw, alveolar volume, and oxygenation without increasing PIP.41 However, one of the biggest advantages of pressure-controlled or pressure-limited ventilation is the ability to avoid lung over-distention and barotrauma/volutrauma (discussed later). The disadvantage of pressure-controlled or pressure-limited ventilation is that delivered volume varies with airway resistance and pulmonary compliance, and may be reduced when short inspiratory times are applied (Fig. 7-8).42 For this reason, both Vt and image must be monitored carefully.

Volume-controlled or volume-limited ventilation requires delineation of the Vt, respiratory rate, and inspiratory gas flow. Gas will be inspired until the preset Vt is attained. The volume will remain constant despite changes in pulmonary mechanics, although the resulting EIP and PIP may be altered. Flow-controlled or flow-limited ventilation is similar in many respects to volume-controlled or volume-limited ventilation. A flow pattern is predetermined, which effectively results in a fixed volume as the limiting component of inspiration.

The ventilator breath is concluded based on one of four variables: volume, time, pressure, or flow. With volume-cycled ventilation, inspiration is terminated when a prescribed volume is obtained. Likewise, with time-, pressure-, or flow-cycled ventilation, expiration begins after a certain period has passed, the airway pressure reaches a certain value, or when the flow has decreased to a predetermined level, respectively.

A factor that limits inspiration suggests that the chosen value limits the level of the variable during inspiration, but the inspiratory phase does not necessarily conclude once this value is attained. For instance, during ‘pressure-limited’ ventilation, gas flow continues until a given pressure limit is attained. However, the inspiratory phase may continue beyond that point. The limitation only controls the magnitude of the breath but does not always determine the length of the inspiratory phase. In contrast, during pressure-controlled ventilation, both gas flow and the inspiratory phase terminate once the preset pressure is reached because pressure is used to limit the magnitude of the breath and the gas flow.

Modes of Ventilation (Table 7-2)

Synchronized Intermittent Mandatory Ventilation

In the SIMV mode, the ventilator synchronizes IMV breaths with the patient’s spontaneous breaths (Fig. 7-9). Small, patient-initiated negative deflections in airway pressure (pressure triggered) or decreases in the constant ventilator gas flow (bias flow) passing through the exhalation valve (flow triggered) provide a signal to the ventilator that a patient breath has been initiated. Ventilated breaths are timed with the patient’s spontaneous respiration, but the number of supported breaths each minute is predetermined and remains constant. Additional constant inspired gas flow is provided for use during any other spontaneous breaths. Advances in neonatal ventilators have provided the means for detecting small alterations in bias flow. As such, flow-triggered SIMV can be applied to newborns, which appears to enhance ventilatory patterns and allows ventilation with reduced airway pressures and FiO2.44,45 SIMV may be associated with a reduction in the duration of ventilation and the incidence of air leak in newborns in general, as well as in those premature infants with bronchopulmonary dysplasia (BPD) and intraventricular hemorrhage.46,47

Assist-Control Ventilation

In the spontaneously breathing patient, brain stem reflexes dependent on cerebrospinal fluid levels of CO2 and pH can be harnessed to determine the appropriate breathing rate.15 As in SIMV, with assist-control ventilation (ACV) the assisted breaths can be either pressure triggered or flow triggered. The triggering-mechanism sensitivity can be set in most ventilators. In contrast to SIMV, the ventilator supports all patient-initiated breaths. This mode is similar to IMV but allows the patient inherently to control the ventilation and minimizes patient work of breathing in adults and neonates.48,49 Occasionally, patients may hyperventilate, such as when they are agitated or have neurologic injury. Heavy sedation may be required if agitation is present. A minimal ventilator rate below the patient’s assist rate should be established in case of apnea.

Pressure Support Ventilation

Pressure support ventilation (PSV) is a pressure- or flow-triggered, pressure-limited, and flow-cycled mode of ventilation. It is similar in concept to ACV, in that mechanical support is provided for each spontaneous breath and the patient determines the ventilator rate. During each breath, inspiratory flow is applied until a predetermined pressure is attained.50 As the end of inspiration approaches, flow decreases to a level below a specified value (2–6 L/min) or a percentage of peak inspiratory flow (at 25%). At this point, inspiration terminates. Although it may apply full support, PSV is frequently used to support the patient partially by assigning a pressure limit for each breath that is less than that required for full support.51 For example, in the spontaneously breathing patient, PSV can be sequentially decreased from full support to a PSV 5–10 cmH2O above PEEP, allowing weaning while providing partial support with each breath.52,53 Thus, Vt during PSV may be dependent on patient effort. PSV provides two advantages during ventilation of spontaneously breathing patients: (1) it provides excellent support and decreases the work of breathing associated with ventilation; and (2) it lowers PIP and Paw while higher Vt and cardiac output levels may be observed.50,54,55

Pressure-triggered SIMV and PSV can be applied to newborns. Inspiration is terminated when the peak airway flow decreases to a set percentage between 5–25%. This flow cutoff for inspiration, known as the termination sensitivity, can be adjusted. The higher the termination sensitivity value, the shorter is the inspiratory time. The termination sensitivity function also may be disabled, at which point ventilation is time cycled instead of flow cycled. There is a reduction in work of breathing and sedation requirements when SIMV with pressure support is applied to newborns.

Proportional Assist Ventilation

Proportional assist ventilation (PAV) is an intriguing approach in the spontaneously breathing patient. It relies on the concept that the combined pressure generated by the ventilator (Paw) and respiratory muscles (Pmus) is equivalent to that required to overcome the resistance to flow of the endotracheal tube/airways (Pres) and the tendency for the inflated lungs to collapse.59

With PAV, airway pressure generation by the ventilator is proportional at any instant to the respiratory effort (Pmus) generated by the patient. Small efforts, therefore, result in small breaths, whereas greater patient effort results in development of a greater Vt. Inspiration is patient triggered and terminates with discontinuation of patient effort. Rate, Vt, and inspiratory time are entirely patient controlled. The predominant variable controlled by the ventilator is the proportional response between Pmus and the applied ventilator pressure. This proportional assist (Paw/Pmus) can be increased until nearly all patient effort is provided by the ventilator.60 Patient work of breathing, dyspnea, and PIP are reduced.61,62 Elastance and resistance are set, as is applied PEEP. Vt is variable, and the risk of atelectasis is present. PAV produces similar gas exchange with lower airway pressures when compared with conventional ventilation in infants.63 Compared with preterm newborns being ventilated with the assist-control mode and with IMV, preterm newborns managed with PAV maintained gas exchange with lower airway pressures and a decrease in the oxygenation index by 28%.64 Chest wall dynamics also are enhanced.65 PAV represents an exciting first step in servoregulating ventilators to patient requirements. Additional studies using neutrally adjusted ventilation are also underway and certain populations (obstructive lung disease and small children) may benefit from the increased patient-ventilator synchrony.66,67

Continuous Positive Airway Pressure

During continuous positive airway pressure (CPAP), pressures greater than those of ambient pressure are continuously applied to the airways to enhance alveolar distention and oxygenation.68 Both airway resistance and work of breathing may be substantially reduced. Since ventilation is unsupported, this mode requires that the patient provides all of the work of breathing and CPAP should be avoided in patients with hypovolemia, untreated pneumothorax, lung hyperinflation, or elevated intracranial pressure, and in infants with nasal obstruction, cleft palate, tracheoesophageal fistula, or untreated congenital diaphragmatic hernia. CPAP is frequently applied via nasal prongs, although it can be delivered in adult patients with a nasal mask.

Bilevel Control of Positive Airway Pressure (BiPAP)

Although sometimes used in the setting of acute lung injury, BiPAP is frequently used for home respiratory support by varying airway pressure between one of two settings: the inspiratory positive airway pressure (IPAP) and the expiratory positive airway pressure (EPAP).69,70 With patient effort, a change in flow is detected, and the IPAP pressure level is developed. With reduced flow at end expiration, EPAP is re-established. Therefore, this device provides both ventilatory support and airway distention during the expiratory phase; however, BiPAP ventilators should be used only to support the patient who is spontaneously breathing. In fact, in a randomized trial of noninvasive ventilation (NIV) in a subset of pediatric patients with lung injury, NIV improved hypoxemia and decreased the rate of endotracheal intubation.71 In neonates, a multicenter randomized trial demonstrated decreased days of mechanical ventilation, chronic lung disease, and mortality when early CPAP was used instead of intubation and surfactant in preterm infants.72

Inverse Ratio Ventilation

In the setting of respiratory failure, it would be helpful to enhance alveolar distention to reduce hypoxemia and shunt. One means to accomplish this is to maintain the inspiratory plateau pressure for a longer proportion of the breath.73 The inspiratory time may be prolonged to the point at which the I/E ratio may be as high as 4 : 1.74 In most circumstances, however, the I/E ratio is maintained at approximately 2 : 1. Inverse ratio ventilation (IRV) is usually performed during pressure-controlled ventilation (PC-IRV), although prolonged inspiratory times can be applied during volume-controlled ventilation by adding a decelerating flow pattern or an end-inspiratory pause to the volume-controlled ventilator breath.75 One advantage of IRV is the ability to recruit alveoli that are associated with high-resistance airways that inflate only with prolonged application of positive pressure.76 Unfortunately, IRV is associated with a profound sense of dyspnea in patients who are awake and spontaneously breathing. Therefore, heavy sedation and pharmacologic paralysis is required during this ventilator mode.

As Et is reduced, the risk for incomplete expiration, identified by the failure to achieve zero-flow conditions at end expiration, is increased. This results in ‘auto-PEEP’ or a total PEEP greater than that of the preset or applied PEEP. Care should be taken to recognize the presence of auto-PEEP and to incorporate it into the ventilation strategy to avoid barotrauma.77 IRV also may negatively affect cardiac output and, therefore, decrease DO2.78 Some studies using IRV revealed an increase in Paw and oxygenation while protecting the lungs by reducing PIP.7982 Other reports suggest that early implementation of IRV in severe ARDS enhances oxygenation and allows reduction in FiO2, PEEP, and PIP.83 On the contrary, a number of studies have failed to demonstrate enhanced gas exchange with this mode of ventilation. Some series have suggested that IRV is less effective at enhancing gas exchange than is application of PEEP to maintain the same mean airway pressure.84 Overall, it appears that oxygenation is determined primarily by the mean airway pressure rather than specifically by the application of IRV. As such, the usefulness of IRV remains in question.85

Airway Pressure Release Ventilation

Airway pressure release ventilation (APRV) is a unique approach to ventilation in which CPAP at high levels is used to enhance mean alveolar volume while intermittent reductions in pressure to a ‘release’ level provide a period of expiration (Fig. 7-10). Re-establishment of CPAP results in inspiration and return of lung volume back to the baseline level. The advantage of APRV is a reduction in PIP of approximately 50% in adult patients with ARDS when compared with other more conventional modes of mechanical ventilation.86,87 Spontaneous ventilation also is allowed throughout the cycle, which may enhance cardiac function and renal blood flow.88,89 Some data suggest that image matching may beimproved and dead space reduced.90,91 In performing APRV, tidal volume is altered by adjusting the release pressure. Conceptually, ventilator management during APRV is the inverse of other modes of positive-pressure ventilation in that the PIP, or CPAP, determines oxygenation, while the expiratory pressure (release pressure) is used to adjust Vt and CO2 elimination.

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