Special Feature: Optimal Ventilator Settings in Respiratory Failure From the Viewpoint of Pulmonary Mechanics
By Jun Takezawa, MD
Types of Respiratory Failure
Although respiratory failure is usually classified as insufficiency in pulmonary oxygenation and respiratory muscle pump performance, it also can be classified depending on lung mechanics—the lung with low compliance, high airway resistance, and a combination of the both. This classification is useful in determining optimal ventilator settings in patients with various types of respiratory failures independently of their pathogenesis.1
Respiratory Failure with Respect to Respiratory Mechanics
While lung compliance is decreased in pneumonia, the acute respiratory distress syndrome (ARDS), and atelectasis, airway resistance is increased in bronchial asthma. Increases in both compliance and airway resistance can be observed in patients with emphysema (usually with chronic obstructive pulmonary disease [COPD]) complicated with bronchial asthma, which requires the most sophisticated ventilator settings.
Optimal Settings for Full Ventilatory Support
Condition 1: The Lung with Decreased Compliance. The lung with low compliance requires high alveolar pressure (Palv) to provide the usual tidal volume (VT, 10-12 mL/kg). During controlled ventilation, this can be accomplished by allowing the development of high peak inspiratory airway pressure (PIP). Because pulmonary oxygenation is related to the mean airway pressure (mPaw), achieving the desired VT can be accomplished by adopting the following 3 methods; increasing PIP, positive end-expiratory pressure (PEEP), and inspiration-to-expiration (I/E) ratio.2 No other methods, which do not result in an increase in mPaw, contribute to improve partial pressure alveolar oxygen (PaO2).
Because plateau pressure (Pplat) is limited to be less than 30-35 cmH2O for avoiding over-distension of the alveoli and ventilator-induced lung injury, and if sufficient PaO2 cannot be obtained, the remaining options should be considered. Although the optimal PEEP, which is advocated to be set as equal to or more than lower inflection point (Pinf) on the relaxed pressure-volume curve, the measurement of Pinf is extremely difficult and time-consuming. Under usual clinical settings, optimal PEEP can be chosen on a trial-and-error basis. Another option is to increase the I/E ratio. This can be accomplished by prolonging the end-inspiratory period (Pplat or pause time). The I/E ratio can be increased until auto-PEEP develops. The decrease in expiratory time (TE) without development of auto-PEEP may result in hypercapnia, which can be allowed as permissive hypercapnia.
Condition 2: The Lung with High Airway Resistance. The target of optimal ventilator settings for the lung with high airway resistance is to provide maximal alveolar ventilation without the development of either auto-PEEP or high alveolar distending pressure. The highest alveolar pressure should be limited to be less than 30-35 cm H2O, as in the lung with low compliance. Airway pressure during inspiration does not reflect alveolar pressure because of the presence of high airway resistance. The discrepancy between PIP and Pplat increases with an increase in airway resistance. Therefore, PIP can be increased until the alveolar pressure reaches 30-35 cm H2O. The alveolar pressure is estimated by using end-inspiratory airway occlusion (Pplat).
In order to measure auto-PEEP, either the end-expiratory occlusion or the end-inspiratory occlusion method can be used. The end-expiratory airway occlusion method measures the airway pressure at the end of expiration after occlusion of airway opening, which subsequently becomes the same as alveolar pressure. The end-inspiratory occlusion method measures the difference between alveolar pressure (Pplat) at the given ventilator settings and that measured after prolonging the expiratory time (TE).3 The presence of auto-PEEP can easily be demonstrated by disconnecting the ventilator from the patient or by stopping providing ventilator breaths and observing the reduction in central venous pressure (CVP), pulmonary capillary wedge pressure (Pcwp), and mean pulmonary artery pressure. The lowest value of these parameters should be used for evaluation of cardiac performance. Counter-PEEP can be used when a dynamic component of airway resistance is present; in other situations, provision of counter-PEEP results in an increase in alveolar pressure, and no changes in the level of auto-PEEP.
Auto-PEEP
Auto-PEEP is the alveolar pressure, which exceeds the airway opening pressure at the end of expiration. Because the clinician cannot detect or monitor auto-PEEP by means of the ventilator’s routine pressure readouts, this phenomenon can cause patient harm without being recognized. Examples of this harm include 1) barotrauma (volutrauma); 2) a decrease in cardiac output due to decreased venous return, increased pulmonary resistance, and decreased ventricular filling pressure; 3) Increased ICP due to an increase in intravascular volume of intracranial capacitance vessels; and 4) Trigger failure of the ventilator during partial ventilatory assist.
The development of auto-PEEP can be understood by considering the time constant of the lung (t), as shown in Figure 1. The lung can be passively inflated or deflated following the single exponential curve, where t can be calculated, as compliance times resistance (C × R). An expiratory time exceeding 4 × t is required for the lung volume to return to the baseline level. Therefore, a subsequent ventilator breath that starts within 4 time constants (t × 4) results in the development of auto-PEEP. Thus, auto-PEEP develops depending on VT, t, and TE.
The optimal ventilator settings for full ventilatory support are shown in Figure 2. The ventilator strategies to improve oxygenation and to facilitate optimal CO2 elimination are shown separately. When hypercapnia persists despite use of the algorithm shown, high-frequency oscillatory ventilation is one possibility for promotion of CO2 elimination.
Partial Ventilatory Support Maximum Transalveolar Pressure (Ptalv)
During partial ventilatory support, with the patient doing a portion of the total work of breathing, because inspiratory effort is partially supported by the ventilator, the driving pressure to inflate the lung is a function of both alveolar pressure from the airways and pleural pressure, which is in the opposite direction: Ptalv = (Palv-Ppl), which can be approximated as trans-pulmonary pressure (Ptp). The maximum Palv, which is restricted to be less than 30-35 cm H2O during full ventilatory support, can be used to restrict Ptp to be less than 30-35 cm H2O during partial ventilatory support. However, because Ptp cannot be monitored routinely during partial ventilatory support, allowable PIP cannot be determined unless esophageal pressure is monitored.
Patient-Ventilator Dyssynchrony
Another problem during partial ventilatory support is patient-ventilator dyssynchrony. Both inspiratory trigger delay and expiration cycling mismatch cause patient-ventilator dyssynchrony. Inspiratory trigger delay loads additional inspiratory work to the patient. Inspiratory trigger delay occurs in the lung with low compliance and high resistance, as well as in the lung with auto-PEEP.
As shown in Figure 3, a significant trigger delay (approximately 500 msec) is present in triggering the ventilator. Because no change in lung volume occurs in this trigger phase, no inspiratory work can be calculated. However, patient places significant efforts to trigger the ventilator. Another finding in this figure is the expiration cycling delay. Approximately 500 msec is present from the end of inspiratory effort to the end of ventilatory breath.
In Figure 3, Diaphragmatic electromyographic (EMG) activity is shown at the top, indicating patient inspiratory effort; airway pressure is shown in the middle, and esophageal pressure (Pes, representing pleural pressure) is shown on the bottom. The start and end of inspiration are shown. (Adapted, with permission, from Imsand C, Feihl F, Perret C, Fitting JW. Regulation of inspiratory neuromuscular output during synchronized intermittent mechanical ventilation. Anesthesiology. 1994;80[1]:13-22.)
If alveolar rupture occurs it is likely a function of the maximum Ptp. Ptp may not always become greatest during the initial inspiratory phase in partial ventilatory support. It can become greatest even during the expiratory phase. Whichever phase produces the greatest Ptp, the chance of alveolar rapture increases during partial ventilatory support as compared to full ventilatory support, because of patient-ventilator dyssynchrony (between Ppl and Palv).
On the other hand, premature termination of inspiratory flow during pressure support ventilation (PSV) is observed in the lung with low compliance. This is mostly due to the incorporation of high inspiratory flow termination criteria in the ventilator’s algorithm (eg, 5 L/min or 25% of the peak inspiratory flow), which allows the ventilator to stop delivering flow to the patient, even though the patient is still in the inspiratory phase. This problem can be overcome by adjusting the termination flow criterion to a lower value. Although pressure control ventilation (PCV) has been advocated to overcome this limitation of PSV, variation of both VT and TI becomes too large to permit synchronization by the set TI in PCV. Therefore, PCV should be only used as full ventilatory support and should not be used as partial ventilatory support.
Summary
In summary, ventilator strategy to improve pulmonary gas exchange in respiratory failure is established in FVS. Optimal ventilator settings can be easily understood, when pulmonary mechanics is taken into account. However, optimal ventilator settings for PVS are still unknown. Patient-ventilator dyssynchrony is still a remaining problem to be solved in terms of developing barotraumas and imposing respiratory work of breathing on patients with respiratory failure.
References
1. Pierson DJ. Types of respiratory dysfunction in disease. In: Pierson DJ, Kacmarek RM, eds. Foundations of Respiratory Care. New York, NY: Churchill Livingstone; 1992:197-205.
2. Marini JJ, Ravenscraft SA. Mean airway pressure. Physiologic determinants and clinical importance Part 1. Physiologic determinants and measurement. Crit Care Med. 1992;20:1461-1472.
3. Marini JJ, Ravenscraft SA. Mean airway pressure. Physiologic determinants and clinical importance
Part 2. Clinical implications. Crit Care Med. 1992; 20:1604-1616.
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