Protective lung strategies should be initiated. These include:
a) Increasing the level of PEEP to maintain an adequate PaO2 and to maintain lung recruitment.
b) Reducing the FiO2 to < .6 (using PEEP and/or accepting PaO2 levels 55-60 mmHg)
b) Restricting the peak airway pressures by using low tidal volume ventilation and Pressure Control (if needed)
c) Restricting the tidal volume to approximately 4-8 cc/kg (~6 cc/kg) (using higher respiratory rates and accepting mild respiratory acidosis if required)
Acute Lung Injury
Inflammation leads to an increased permeability at the alveolar-capillary membrane. This results in an increase in the amount of fluid which leaks into the pulmonary interstitium. Interstitial fluid collections cause surrounding alveoli to collapse and decreases the lung's compliance (or stretchability).
As alveoli begin to collapse, an imbalance between the amount of ventilation and the amount of perfusion begins to develop. Blood flowing past areas of reduced ventilation (V/Q mismatch) will pick up less oxygen than blood traveling past normal gas exchange units. In severe disease, some alveoli will be completely airless (shunt units). These areas of reduced or absent ventilation lead to a lowering of the oxygen saturation of the blood reaching the left side of the heart.
As the number of diseased alveoli increase, the arterial oxygen saturation drops, producing a more severe decline in the PaO2:FiO2 gradient. A PaO2:FiO2 gradient < 300 indicates acute lung injury and < 200 indicates Acute Respiratory Distress Syndrome (ARDS). If the low PaO2 is due primarily to V/Q mismatch, the PaO2 will improve if the FiO2 is increased. If the patient has a large number of alveoli that are airless or nearly airless, the PaO2 will not improve with FiO2 levels. PEEP will be needed to correct this type of hypoxemia.
Factors that contribute to Acute Lung Injury:
1) Too Low
PEEP acts like an alveolar "splint" to prevent the alveoli from closing at the end of each breath. If the level of PEEP is not high enough, diseased alveloi will collapse during exhalation as soon as the airway pressure drops below a critical point. During inspiration, hiring airway pressures are required to reopen these diseased alveoli and deliver a breath. Higher airway pressures can lead to barotrauma. The repetetive opening (recruitment) and closing (derecruitment) during inspiration and expiration causes harm to the alveolar wall and leads to more inflammation.
the Repetitive Alveolar Opening and Closing
To prevent derecruitment of the alveoli with subsequent alveolar trauma, PEEP should be increased to a level that is high enough to maintain an adequate PaO2 with an FiO2 level < .6. It is also used to keep a larger portion of the alveoli open or recruited. Peak inspiratory pressure requirements can be reduced by keeping the alveoli in an open state. This is referred to as "open lung ventilation".
In addition to the benefit that PEEP has on maintaining alveolar patency, PEEP can improve the ratio between ventilation and perfusion. Because pulmonary edema collects in the dependent areas of the lung, the majority of the gas exchange abnormalities develop in these dependent areas. Blood flow (perfusion) is enhanced in dependent lung regions. This combination of decreased ventilation and increased perfusion exaggerates the V/Q imbalance in these areas (e.g. the lower lobes of a supine patient). PEEP > 10-12 cmH20 helps to open collapsed alveoli to recruit more gas exchange units and improve the V/Q balance.
When lungs become non-compliant, higher airway pressures and large tidal volumes are believed to contribute to overstretching of the alveoli. Because the lung disease is not uniform, more of the tidal volume will be directed toward the healthiest and least resistant alveoli. This can lead to overdistention, particularly in the most compliant parts of the lung. This over stretching can cause cause additional inflammation and is believed to worsen the lung injury. There is evidence that lower tidal volumes improve patient outcomes. Low tidal volume ventilation will reduce both the volume (and potential for overdistention)and the peak airway pressures. High peak airway pressures are believed to increase the risk for barotrauma. Pressure Control can also be used to help keep the airway pressures below a goal of ~30-35 cmH20.
Brower, R et al. Ventilation with Lower Tidal Volumes as Compared with Traditional Tidal Volumes for Acute Lung Injury and the Acute Respiratory Distress Syndrome. New England Journal of Medicine. Early release for May 4, 2000.
MacIntyre, N. Clinically available new strategies for mechanical ventilatory support. Chest 1993; 104:560-565.
Parker JC, Hernandez LA, Peevy KJ. Mechanisms of ventilator-induced lung injury. Crit Care Med 1993;21:131-43.
Ranieri VM, Suter PM, Tortorella C, et al. Effect of mechanical ventilation on inflammatory mediators in patients with acute respiratory distress syndrome: a randomized controlled trial.JAMA 1999;282:54-61.
Slutsky AS, Tremblay LN. Multiple system organ failure: is mechanical ventilation a contributing factor? Am J Respir Crit Care Med 1998;157:1721-5.
Slutsky, A. Mechanical Ventilation: ACCP Consensus Conference. Chest 1993; 104:1833- 59.[Erratum, Chest 1994;106:656.]
Tremblay L, Valenza F, Ribeiro SP, Li J, Slutsky AS. Injurious ventilatory strategies increase cytokines and c-fos m-RNA expression in an isolated rat lung model. J Clin Invest 1997;99:944-52.
Tsuno K, Miura K, Takeya M, Kolobow T, Morioka T. Histopathologic pulmonary changes from mechanical ventilation at high peak airway pressures. Am Rev Respir Dis 1991;143:1115-20.
Webb, A., Shapiro, M., Singer, M., Suter, P. Textbook of Critical Care. London, UK: Oxford Books, 1999, Page(s) 1309-1332.
Clinical Educator, CCTC
February 16, 2007