chanical ventilation such as barotrauma/volutrauma and infection are critical considerations. Because patients with ARDS experience substantially reduced


lung volumes caused by alveolar damage, atelectasis, and alveolar edema, the use of large mechanical tidal volumes are to be avoided to prevent over-distension of the lungs and volutrauma. Alveolar over-distension has been correlated with surfactant degra- dation, epithelial and endothelial membrane disruption, cytokine release, and pulmonary tissue inflammation. Volutrauma may de- velop from increased airway pressure with alveolar over-distension, or from shear forces applied during opening and closing of small airways. Therefore, the current trend is to ventilate these patients with tidal volumes based on about 6 ml/kg of ideal body weight and positive end-expiratory pressure (PEEP), along with attempting to achieve plateau pressures of less than 35 cm H2O. ARDS patients generally receive various levels of PEEP to pre-


vent the opening and closing of alveoli during ventilation. PEEP is further added to improve oxygenation and to avoid using high FIO2s (i.e., > 0.60) and to prevent alveolar derecruitment. Inverse ratio ventilation (IRV), e.g., I:E ratio of 2:1, is used to


improve oxygenation by increasing the patient’s mean airway pres- sure (mean Paw). During IRV the tidal volume is delivered slowly with a longer inspiratory time and with a lower driving pressure. Expiratory time is shortened and less time is allowed for recruited alveoli to collapse. These strategies have the potential effect of im- proving oxygenation. Lung injury resulting from high ventilation pressures, i.e., barotrauma, must be avoided. For I:E ratios greater than 1.5:1, neuromuscular blockade of the patient is essential. Permissive hypercapnia is the intentional reduction of me-


chanical ventilation for the avoidance of alveolar over-distension, i.e., volutrauma. PaCO2 levels are deliberately allowed to rise to levels as high as 100 torr. The arterial pH is maintained somewhere around 7.20 to 7.25; however, the pH deemed acceptable is de- termined on an individual basis. The pH is controlled by the pa- tient’s renal compensation and the administration of NaH2CO3. The PaO2 is maintained at greater than 60 torr. This ventilatory strategy is generally implemented when the plateau pressure (alve- olar pressure) climbs to potentially dangerous levels. A number of measures are taken to establish permissive hy-


percapnia. The PaCO2 is permitted to increase, while the pH is al- lowed to decrease as a result of sedating the patient. Carbon dioxide production is minimized by instituting neuromuscular blockade and sedation, reducing the patient’s body temperature, and limiting the patient’s intake of glucose. Tracheal gas insufflation may be instituted to flush out carbon dioxide from the patient’s anatomic dead space, but studies regarding the effectiveness of tra- cheal gas insufflation are inconclusive. Permissive hypercapnia should not be used on patients who have an elevated intracranial pressure because the high PaCO2 may increase cerebral perfusion significantly. The use of permissive hypercapnia was advanced by Hickling, et al in the early 1990s, and has been associated with a lower mortality rate among patients with ARDS. Placing mechanically ventilated ARDS patients in the prone


position produces a short-term improvement in the patient’s oxy- genation status. Long-term influence is uncertain. The physiology underlying this maneuver has not been elucidated. The speculation is the gravitational effects on pulmonary blood flow and the intra- pleural pressure gradient improves ventilation-perfusion ratios. Prone positioning demands vigilance regarding the displace-


ment of the endotracheal tube and vascular lines. Thoracic com- pliance sometimes decreases when the patient is placed in the


The 12th Annual Focus Conference May 10-12, 2012


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www.Foocus.com Focus Journal Fall 2011 9


prone position. The consequence is higher airway pressure with volume ventilation, or a decreased tidal volume with pressure ventilation. Trials of high frequency jet ventilation and high frequency


oscillatory ventilation have been conducted. However, the data supporting the use of these methods of mechanical ven- tilation for ARDS patients are inconclusive. A variety of pharmacologic agents have been studied


within the context of ARDS, but none have demonstrated a re- duction in the mortality rate. Inhaled nitric oxide (NO) di- lates


the pulmonary vasculature, improves


ventilation-perfusion mismatching, and improves oxy- genation. Yet, the use of NO neither decreases the dura- tion of mechanical ventilation, nor the mortality rate associated with ARDS. Corticosteroids have been used as anti-inflammatory


agents. The administration of corticosteroids before the onset of signs and symptoms of ARDS, or during the early stage of ARDS has not proved efficacious. Similarly, the instillation of pulmonary surfactant into the lungs of ARDS patients has had no significant clinical benefit. Respiratory therapists must have a firm understanding


of the various etiologic factors associated with ARDS and must be vigilant of the signs and symptoms of this syn- drome in order to be prepared to take definitive action once the onset of this condition emerges. Once support- ive care has been initiated, the respiratory therapist must work to avoid or to minimize the risk of volutrauma/baro- trauma, and apply strategies to improve oxygenation and to avert the devastation of multiple organ system failure.


Alright, I’ve arrived


Now cut that cord, I’ve gotta’ get to FOCUS.


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