Special Feature
Pressures, Volumes, Outcomes, and Physiology in Mechanical Ventilation
By Dean R. Hess, PhD RRT, Respiratory Care, Massachusetts General Hospital, Department of Anesthesiology, Harvard Medical School, Boston, is Associate Editor for Critical Care Alert.
Dr. Hess reports no financial relationship to this field of study.
There is little debate that tidal volume (VT) should be lowered in patients with acute lung injury (ALI) or the acute respiratory distress syndrome (ARDS). The pivotal trial of more than 800 patients conducted by the ARDS Network1 reported significantly lower mortality for a VT target of 6 mL/kg predicted body weight (range 4-8 mL/kg) compared to a VT of 12 mL/kg. Translated to evidence-based medicine terms, the number-needed-to-treat from this trial was 12 patients: for every 12 mechanically ventilated patients with ALI/ARDS treated with a VT of 6 mL/kg rather 12 mL/kg, 1 additional life is saved. Mechanical ventilation, a life-support technology, can increase the risk of death if set improperly or, if set properly, can increase the likelihood of survival.
The ARDS Network protocol1 also calls for monitoring of plateau pressure (PPLAT). PPLAT is measured using an end-inspiratory breath-hold maneuver. This is easily accomplished on modern ventilators with the press of a button, which closes both the inspiratory and expiratory valves, allowing pressure in the lungs to equilibrate with proximal airway pressure. In this way, pressure measured at the proximal airway estimates the alveolar pressure at end-inhalation. Thus, PPLAT is an estimation of peak alveolar pressure. The ARDS Network protocol targeted PPLAT ≤ 30 cm H2O. If PPLAT > 30 cm H2O, the protocol calls for a reduction in VT to as low as 4 mL/kg. If severe acidosis or patient-ventilator dys-synchrony occurs, the protocol allows VT to be increased to as much as 8 mL/kg provided that PPLAT remains ≤ 30 cm H2O.
When Might We be Fooled by the PPLAT?
Alveolar injury is likely the result of excessive trans-pulmonary pressure (PTP) rather than VT or alveolar pressure per se. PTP is the difference between the pressure in the alveolus (PPLAT) and the pressure outside the alveolus. The pressure outside the alveolus is pleural pressure (PPL). During passive positive pressure ventilation (ie, no spontaneous inspiratory efforts by the patient), PPL is determined by VT and chest wall compliance. During active breathing efforts, PPL is determined by the magnitude of the inspiratory efforts by the patient.
Imagine the scenario in Figure 1 (below). In this case, the chest wall compliance is reduced, as might occur with abdominal compartment syndrome or chest wall burns. When the lungs are passively inflated to an alveolar pressure (PPLAT) of 30 cm H2O, the pleural pressure increases by 15 cm H2O. In this case, the PTP is only 15 cm H2O. One might argue that there is reduced risk of ventilator-induced lung injury (VILI) in this case and that a higher PPLAT might be safe. In fact, the restrictive effects of a stiff chest wall may be protective against VILI, as has been shown in experimental animal models.2
Imagine now the scenario in which the ventilator is set for pressure-controlled ventilation of 20 cm H2O and PEEP of 10 cm H2O (Figure 1). Thus, the ventilator will target an alveolar pressure (PPLAT) of 30 cm H2O. If the patient makes an active inspiratory effort, the ventilator will deliver more flow (and volume) to maintain the PPLAT constant. If the inspiratory effort of the patient decreases the pleural pressure by 15 cm H2O, note that the PTP is 45 cm H2O, which might be sufficiently high to produce VILI. In animal models, VILI resulted from either high positive pressure applied inside the lungs or high negative pressure applied outside the lungs.2
Evaluation of PPLAT demands consideration of the pleural pressure because PTP is determined not only by PPLAT but also by PPL as well. Although it has been argued to focus on PPLAT rather than VT in the context of preventing VILI,(3)3 it might not be so simple. A lower PPLAT does not necessarily decrease the risk of VILI. Imagine the case in which the alveolar pressure is 30 cm H2O and the PPL is 5 cm H2O. In another case, the alveolar pressure is 15 cm H2O during pressure-controlled (or pressure support) ventilation and the PPL decreases by 10 cm H2O as the result of the inspiratory effort of the patient. One can argue that the PTP and VT are the same in both scenarios.
How Can We Estimate PPL at the Bedside?
The traditional approach to assessing PPL is the use of an esophageal balloon, which consists of a thin catheter with multiple small holes in the distal 5-7 cm of its length.4 A 10-cm balloon is placed over the distal end of the catheter to prevent the holes in the catheter from being occluded by esophageal tissue, and the balloon is inflated with a small amount of air (0.5-1 mL). The proximal end of the catheter is attached to a pressure transducer. The proximity of the esophagus to the pleural space allows use of esophageal pressure (PES) as an estimate of PPL. However, PES accurately reflects PPL only if the pressure measured in the balloon is an accurate measure of the pressure in the esophagus, the transmural pressure of the esophagus is zero, there is no compression of the esophagus by the heart or other intrathoracic structures, and the pressure in the mediastinum surrounding the esophagus is equal to PPL.
PES may be affected by measurement artifacts such as the elastic recoil of the balloon (worsened by balloon over-inflation), elastic recoil of the esophagus, active esophageal contraction, or pressure transmitted from surrounding structures. Moreover, PES varies with lung volume and body position. Upright-to-supine differences in PPL are attributed to artifact caused by direct compression of the esophagus by mediastinal contents such as the heart. It follows that absolute values of PES are unpredictable and of questionable value for clinical purposes.5 However, changes in PES closely reflect changes in PPL and hence changes in PES are useful when assessing respiratory system mechanics.
Measurement of PES is invasive, requires special equipment, and is not commonly available for the care of mechanically ventilated patients. While PES is the standard method of estimating PPL, PPL changes during lung inflation are transmitted to other structures in the mediastinum. In 1965, Comroe suggested that an intra-thoracic vein with its thin wall is capable of transmitting PPL and might therefore be an acceptable alternative to the esophagus for PPL measurement.6 Respiratory variation in central venous pressure is easily detected at the bedside during mechanical ventilation and varies from a positive deflection when the respiratory muscles are completely inactive to negative swings during large inspiratory efforts. Chieveley-Williams et al7 compared ΔPES to changes in central venous pressure (ΔPCVP) and reported that useful information can be obtained from ΔPCVP during mechanical ventilation. In an experimental model, Valenza et al8 recently reported that ΔPCVP was similar to ΔPES.
Talmor et al9 used PES to estimate the influence of the chest wall on PPL and PTP in patients with acute respiratory failure. They subtracted 5 cm H2O from each value of PES to correct for artifacts attributable to body position and balloon pressure and then calculated PTP from the difference between airway opening pressure (PAO) and corrected PES:
PTP = PAO - PES + 5 cm H2O
They reported a wide range of calculated PTP at all values of PAO, supporting the concern that PAO is influenced by chest wall mechanics. They suggested that, by using this approach, ventilator settings could be more appropriately customized to accommodate inter-individual variations in lung and chest wall mechanics. Although this approach is attractive, it is potentially flawed by the assumption that corrected PES accurately reflects PPL. The approach suggested by Talmor and associates9 cannot be recommended without further confirmation and evidence that this results in improved patient outcomes.5
Volume-controlled vs Pressure-controlled Ventilation
An area of some debate is whether a lung-protective ventilatory strategy can be achieved using pressure-controlled ventilation rather than volume-controlled ventilation as used by the ARDS Network protocol. This question can be addressed by examination of the equation of motion for the respiratory system:
PVENT = VT / C + V × R - PMUS
where PVENT is the pressure applied by the ventilator, VT is tidal volume, C is respiratory system compliance, V is flow, R is airways resistance, and PMUS is the pressure generated by the respiratory muscles.
During volume-controlled ventilation, the ventilator controls V and VT. Thus, an active inspiratory effort of the patient (PMUS) results in a decrease in alveolar and proximal airway pressure. The result is the characteristic scooped-out appearance of the airway pressure graphic during active breathing efforts during volume-controlled ventilation. Because VT and V are fixed, the equation of motion predicts that PPLAT and PPL should be reduced by equivalent amounts with active inspiratory efforts. In other words, PTP is not affected. Although this may be uncomfortable for the patient, volume-controlled ventilation protects the patient from increases in PTP in the presence of active inspiratory efforts.
During pressure-controlled ventilation, the ventilator controls PVENT. In this case, an active inspiratory effort of the patient (PMUS) results in an increase in V and VT. The increase in PMUS increases PTP and VT, both of which are a potential source of VILI. Note that this applies to all pressure-controlled modes, including airway pressure-release ventilation (APRV). Theoretically, vigorous inspiratory efforts may result in large PTP swings during the high pressure phase of APRV.
How Low Can We Go?
Another controversial issue is whether a PPLAT of ≤ 30 cm H2O is sufficient or whether lower levels are better. In other words, should the VT be lowered even if PPLAT is ≤ 30 cm H2O?3 This was addressed by a secondary analysis of the data from the ARDS Network, in which mortality was lower with a lower PPLAT. That would suggest that mortality is reduced by a reduction in PPLAT, even if PPLAT ≤ 30 cm H2O.10 On day 1 of enrollment in the original ARDS Network trial, patients in the lowest quartile of PPLAT randomized to a VT of 12 mL/kg had a PPLAT of 16-26 cm H2O and a mortality of 34%. However, patients in the lowest quartile of PPLAT who were randomized to a VT of 6 mL/kg had a PPLAT of 10 to 20 cm H2O and a mortality of only 23%. A recent study by Terragni et al11 reported alveolar overdistention in two-thirds of patients with PPLAT < 30 on 6 mL/kg VT.
A Lower PPLAT for Everyone?
If lower PPLAT is associated with improved survival in ALI/ARDS, and if a lower PPLAT is achieved with use of smaller VT, should VT and PPLAT be decreased in all mechanically ventilated patients, whether or not ALI/ARDS is present? Although no randomized controlled trial has addressed this question, lower levels of evidence are accumulating to support that a lower VT and PPLAT should be considered in all mechanically ventilated patients. Several studies have shown that higher VT is associated with a greater risk of developing ALI/ARDS in patients whose lungs are essentially normal at the time of intubation.12-14 Another study showed a lower risk of ALI/ARDS following implementation of a protocol to limit VT to a maximum 10 mL/kg predicted body weight in all patients and a recommendation to use 6-8 mL/kg PBW for patients at any risk of ALI/ARDS.15 In patients with severe brain injury, the use of high VT was recently reported as a predictor of ALI.16
Shultz et al17 recently addressed the question, "What Tidal Volumes Should Be Used in Patients without Acute Lung Injury?", and recommend that the use of lower VT should be considered in all mechanically ventilated patients whether they have ALI or not. Prospective studies should be performed to evaluate optimal ventilator management strategies for patients without ALI.
Concluding Comments
Evidence is clear that VT and PPLAT should be targeted to 6 mL/kg predicted body weight and ≤ 30 cm H2O, respectively, in patients with ALI/ARDS. Evidence is also suggestive of a benefit with a lower VT and PPLAT, suggesting that the lowest possible VT and PPLAT should be targeted in patients with ALI/ARDS. Accumulating evidence suggests that lower VT and PPLAT should also be targeted in patients who do not have ALI/ARDS. The message to the bedside clinician is that we should be treating the lungs as gently as possible during positive pressure ventilation.
References
- ARDS Network. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. The Acute Respiratory Distress Syndrome Network. N Engl J Med. 2000;342:1301-1308.
- Dreyfuss D, Saumon G. Ventilator-induced lung injury: lessons from experimental studies. Am J Respir Crit Care Med. 1998;157:294-323.
- Steinberg KP, Kacmarek RM. Respiratory controversies in the critical care setting. Should tidal volume be 6 mL/kg predicted body weight in virtually all patients with acute respiratory failure? Respir Care. 2007;52:556-564.
- Benditt JO. Esophageal and gastric pressure measurements. Respir Care. 2005;50:68-75.
- Hager DN, Brower RG. Customizing lung-protective mechanical ventilation strategies. Crit Care Med. 2006;34:1554-1555.
- Comroe J. Physiology of respiration. Year Book Medical Publishers, 1965.
- Chieveley-Williams S, et al. Central venous and bladder pressure reflect transdiaphragmatic pressure during pressure support ventilation. Chest. 2002;121:533-538.
- Valenza F, et al. Static and dynamic components of esophageal and central venous pressure during intra-abdominal hypertension. Crit Care Med. 2007;35:1575-1581.
- Talmor D, et al. Esophageal and transpulmonary pressures in acute respiratory failure. Crit Care Med. 2006;34:1389-1394.
- Hager DN, et al. ARDS Clinical Trials Network. Tidal volume reduction in patients with acute lung injury when plateau pressures are not high. Am J Respir Crit Care Med. 2005;172:1241-1245.
- Terragni PP, et al. Tidal hyperinflation during low tidal volume ventilation in acute respiratory distress syndrome. Am J Respir Crit Care Med. 2007;175:160-166.
- Fernandez-Perez ER, et al. Intraoperative tidal volume as a risk factor for respiratory failure after pneumonectomy. Anesthesiology. 2006;105:14-18.
- Gajic O, et al. Ventilator settings as a risk factor for acute respiratory distress syndrome in mechanically ventilated patients. Intensive Care Med. 2005;31:922-926.
- Gajic O, et al. Ventilator-associated lung injury in patients without acute lung injury at the onset of mechanical ventilation. Crit Care Med. 2004;32:1817-1824.
- Yilmaz M, et al. Toward the prevention of acute lung injury: protocol-guided limitation of large tidal volume ventilation and inappropriate transfusion. Crit Care Med. 2007;35:1660-1666.
- Mascia L, et al. Brain IT group. High tidal volume is associated with the development of acute lung injury after severe brain injury: An international observational study. Crit Care Med. 2007;35:1815-1820.
- Shultz MJ, et al. What tidal volumes should be used in patients without acute lung injury? Anesthesiology. 2007;106:1226-1231.
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