Autor: Dean R. Hess, PhD, RRT

Associate Professor of Anesthesia, Harvard Medical School

Assistant Director of Respiratory Care, Massachusetts General Hospital

Boston, MA USA

   

MECHANICAL VENTILATION OF THE TRAUMA PATIENT

 

Introduction

Trauma patients may require mechanical ventilation secondary to respiratory center depression or the Acute Respiratory Distress Syndrome (ARDS). Although usually administered with an endotracheal tube, mechanical ventilation can be applied by face mask in carefully selected patients. It has become increasingly accepted that mechanical ventilation, although often life-saving, can contribute to lung injury. This has led to implementation of lung-protective ventilation strategies. Mechanical ventilation of the trauma patient can be complicated by chest trauma, burns, inhalation injury, and head trauma.

 

ARDS

In 1994, a consensus definition was recommended for ARDS: acute onset of respiratory failure, bilateral infiltrates on chest radiograph, pulmonary artery wedge pressure less than or equal to 18 mm Hg, or the absence of clinical evidence of left atrial hypertension, PaO2/FIO2 less than or equal to 300 (acute lung injury) or PaO2/FIO2 less than or equal to 200 (ARDS). The difference between acute lung injury (ALI) and ARDS is that ALI includes a milder form of the same syndrome. A recent epidemiologic study using these definitions reported an incidence of about 79 per 100,000 for ALI and 59 per 100,000 for the acute ARDS. The clinical disorders commonly associated with ARDS can be divided into those associated with direct injury to the lung (pulmonary ARDS) and those that cause indirect lung injury in the setting of a systemic process (extrapulmonary ARDS). Causes of ARDS due to direct lung injury include pneumonia, aspiration of gastric contents, pulmonary contusion, fat emboli, near-drowning, inhalational injury, and reperfusion pulmonary edema after lung transplantation or pulmonary embolectomy. Common causes of ARDS due to indirect lung injury include sepsis, severe trauma with shock and multiple transfusions, cardiopulmonary bypass, drug overdose, acute pancreatitis, and transfusions of blood products. Trauma is a risk factor for ARDS and the mortality of ARDS associated with severe trauma has been reported at about 25%.

 

Ventilator-Induced Lung Injury

It has become increasingly accepted that mechanical ventilation can contribute to lung injury. Traditional barotrauma (eg, pneumothorax) is relatively uncommon, and the role of oxygen toxicity in humans is controversial. The modern concept of ventilator-induced lung injury is described in the context of alveolar over-distention (volutrauma), alveolar de-recruitment (atelectrauma), and biochemical injury and inflammantion to the lung parenchyma (biotrauma). Ventilator-induced lung injury is a subtle injury that can cause ARDS, progression of existing ARDS, multiple organ dysfunction syndrome, and death.

 

Volutrauma is alveolar over-distention due to an excessive inflation volume. This results in a biophysical injury in the lungs causing increased alveolar-capillary permeability. Alveolar over-distention is commonly assessed by measurement of the end-inspiratory plateau pressure (Pplat). However, it should be appreciated that alveolar distention is determined by the transpulmonary pressure, which is determined by both the pressure inside the alveolus (Pplat) and pressure outside the alveolus (pleural pressure). This becomes an important consideration in patients with a stiff chest wall (e.g., abdominal compartment syndrome, chest wall burns). Ventilator-induced lung injury can also result from cyclic closing and re-opening of alveoli (atelectrauma). This injury is ameliorated by use of positive end-expiratory pressure (PEEP) sufficient to avoid alveolar de-recruitment. Avoiding high inspiratory pressures also avoids opening collapsed alveoli which may prevent atelectrauma but promote hypoxemia. Ventilating the lungs in a manner that promotes alveolar over-distention and de-recruitment increases inflammation in the lungs (biotrauma). Inflammatory mediators (cytokines, chemokines) may translocate into the pulmonary circulation secondary to increased alveolar-capillary permeability, resulting in systemic inflammation. How the lungs are ventilated may thus play a role in systemic inflammation. Systemic inflammation arising from the lungs can lead to multiple organ dysfunction syndrome.

 

Selection of Tidal Volume

When traditional tidal volumes of 10 to 15 mL/kg are used in patients with ALI/ARDS receiving mechanical ventilation, the resulting alveolar pressures are frequently elevated, reflecting over-distention particularly of the less-affected lung regions. Three small, prospective, randomized trials of traditional versus lower tidal volume ventilation in patients with or at risk for ALI/ARDS did not demonstrate beneficial effects of a modestly lower tidal volume. In contrast to these, Amato et al randomized patients with ARDS to a low tidal volume (£6 mL/kg) or a traditional tidal volume (12 mL/kg). They reported a reduced mortality with the lower tidal volume, although mortality in the traditional tidal volume group was high (71% compared with 38% in the protective ventilation group). In the ARDSnet trial, 861 patients were randomized to receive a relatively low tidal volume of 6 mL/kg predicted body weight (PBW), which was nearly 5 mL/kg measured weight, versus a tidal volume of 12 mL/kg PBW. The lower tidal volume was associated with 31% mortality, whereas ventilation with the conventional tidal volume was associated with 40% mortality. Tidal volume was reduced further to a minimum of 4 mL/kg PBW if the Pplat was > 30 cm H2O. The results of the ARDSnet trial suggest that for every 12 patients with ALI/ARDS who are ventilated using this strategy, one life can be saved. This is very compelling evidence to adopt this approach to the ventilation of patients with ALI/ARDS. Although this study enrolled patients with a variety of etiologies, 10% of the patients had ARDS resulting from trauma. Post-hoc analysis revealed no difference in mortality for trauma patients for the two tidal volumes, and the overall mortality in this group was low (11%). In trauma patients receiving the lower tidal volume, there was a higher proportion of patients achieving unassisted breathing by day 28 (80% vs 70%) and a lower cumulative incidence of nonpulmonary organ failure with the lower tidal volume (49% vs 65%).

 

An area of controversy is whether pressure-controlled ventilation should be used as part of a lung protective ventilation strategy. Theoretically, any ventilator mode can be used provided that tidal volume delivery and transpulmonary pressure are limited. A common reason given for using pressure control or pressure support ventilation is to allow the patient to augment inspiratory flow and tidal volume. This results in a higher transpulmonary pressure and tidal volume, which violates the goal of volume and pressure limitation. It should be noted that Pplat is not an accurate reflection of transpulmonary pressure if the patient is making active breathing efforts such as with pressure control or pressure support ventilation. There is enthusiasm for new approaches to mechanical ventilation, such as the use of high frequency ventilation and airway pressure-release ventilation. The role, if any, for new ventilator modes in the management of patients with ALI/ARDS is unclear. Evidence is lacking for a survival benefit of new ventilatory modes compared with the ARDSnet approach.

 

Selection of Positive End-expiratory Pressure

An appropriate level of PEEP is an important part of a lung protective ventilatory strategy. Zero end-expiratory pressure is likely harmful in patients with ALI/ARDS. A criticism of the original ARDSnet study was that the level of PEEP was too low. Advocates of the open-lung approach to mechanical ventilation argued that a higher level of PEEP was needed in patients with ARDS [24]. Pursuant to this, the ARDSnet conducted a study of higher versus lower PEEP in patients with ARDS. In this study, 549 patients with ALI/ARDS were randomized to receive mechanical ventilation with either lower or higher PEEP levels, set according to different combinations of PEEP and FIO2 to maintain PaO2 at 55 to 80 mmHg or SpO2 at 88% to 95%. FIO2 was lower and PaO2/FIO2 was higher in patients who received the higher level of PEEP. Lung compliance was also higher in patients receiving the higher level of PEEP. However, mortality before hospital discharge was not significantly different between the groups (about 25% in each group). These results suggest that mechanical ventilation with a tidal volume of 6 mL/kg PBW and a Pplat less than or equal to 30 cm H2O, clinical outcomes were similar whether a lower or higher PEEP level is used. However, the study was relatively small, and a modest benefit (or harm) from higher PEEP may have gone undetected. A larger multi-center trial comparing modest versus higher levels of PEEP is ongoing. It is important to note that an important impediment to the use of higher levels of PEEP is the associated increase in end-inspiratory alveolar pressure. The setting of PEEP is often a compromise among the maintenance of alveolar recruitment, the avoidance of alveolar over-distention, and hemodynamic compromise.

 

There has been some enthusiasm for the use of the pressure-volume (PV) curve to set PEEP. Traditional critical-care teaching has been that the lower inflection point presumably represents the pressure at which a large number of alveoli are recruited, and the upper inflection point represents the pressure at which a large number of alveoli are overdistended. Thus, it would seem reasonable to set the PEEP above the lower inflection point and the Pplat below the upper inflection point. The use of a super syringe is the traditional method to measure the PV curve. Precise volumes of gas are added to the endotracheal tube and the pressure at each step change in volume is measured. The PV curve is then plotted as volume as a function of pressure. It can also be measured by setting a slow constant flow on the ventilator and observing the ventilator display of the PV curve, but this measurement includes the effect of airway resistance. The role of the PV curve to set the ventilator is presently unclear, and many limitations to its clinical use exist. The measurement requires sedation and often paralysis. It can be difficult to identify the inflection points, and there can be considerable inter-observer variability. Separation of the effect of the chest wall from the effect of the lungs on the PV curve requires measurement of esophageal pressure. The deflation limb may be more useful than inflation limb, but the inflation limb is most commonly measured. Lung function is heterogeneous with ARDS, and the PV curve treats the lungs as a single compartment. It is now accepted that recruitment may occur throughout the entire PV curve, and the upper inflection point may represent the end of recruitment rather than the point of over-distention. Clearly, more evidence is needed before the PV curve can be recommended for routine use to set the ventilator.

 

Adjuncts to Mechanical Ventilation

In recent years, there has been enthusiasm for various adjuncts to mechanical ventilation in patients with ALI/ARDS. Inhaled nitric oxide results in an increase in PaO2 in the many patients with ARDS, but evidence for a survival benefit is lacking. Likewise, prone position results in a higher PaO2 in many patients with ARDS; however, a survival benefit has not been demonstrated. Recruitment maneuvers have been used in an attempt to open the collapsed alveoli in patients with ARDS. A recruitment maneuver is a sustained increase in airway pressure, typically performed by increasing the PEEP setting on the ventilator to 30 to 40 cm H2O for 30 to 40 s, after which a sufficient amount of PEEP is applied to keep the lungs open. Recruitment maneuvers increase the PaO2 in some, but not all, patients with ARDS. Even in patients who respond to a recruitment maneuver with an increase in PaO2, the effect is short-lived. In a randomized, controlled trial conducted by the ARDSnet, improvements in arterial oxygenation for patients receiving a recruitment maneuver and a sham maneuver were similar. Despite the initial enthusiasm for lung recruitment maneuvers in patients with ARDS, it remains unknown whether they are safe and if they affect survival.

 

Weaning from Mechanical Ventilation

Readiness for a trial of spontaneous breathing can usually be assessed from a commonsense screen for resolution of the cause of respiratory failure, gas exchange, ability to initiate an inspiratory effort (e.g., sedation), and hemodynamic stability. Weaning parameters are of limited usefulness. The available evidence supports that a trial of spontaneous breathing is the best means of determining when a patient is able to sustain spontaneous breathing. Weaning success is lower with SIMV mode than trials of spontaneous breathing or pressure support ventilation. Protocol approaches to weaning improve patient outcomes. Finally, the need for a ventilator should be separated from the need for an airway; some patients need an artificial airway but do not require ventilatory assistance.

 

Trauma-Specific Considerations

Chest trauma

Patients with blunt or penetrating chest trauma may require mechanical ventilation. In patients with lung contusion, lung protective ventilation strategies similar to those used with other forms of ARDS should be employed. Mechanical ventilation in the patient with lung contusion can be problematic if it is unilateral, resulting in differing lung mechanics. The presence of air leak can also complicate mechanical ventilation – particularly with a large airway tear. If the patient has cardiac contusion, this may complicate mechanical ventilation strategies. Rib fractures, particularly flail chest, can be the source of considerable pain and are often associated with other injuries such as pneumothorax, hemothorax, and pulmonary contusion.

 

Inhalation injury

A number of issues should be considered related to mechanical ventilation of the patient with inhalation injury. Carbon monoxide poisoning should be suspected and, if present, 100% oxygen should be administered and hyperbaric oxygen therapy should be considered if available. Thermal and chemical injury to the upper airway can result in life-threatening upper airway obstruction necessitating endotracheal intubation. Inhalation injury ARDS is managed using lung protective ventilation strategies (i.e., avoid over-distention and provide adequate PEEP). Chemical injury to the airway can trigger bronchospasm, which is usually treated with inhaled bronchodilators. Airway plugging necessitates aggressive bronchial hygiene and bronchoscopy. These patients are also at increased risk for ventilator-associated pneumonia.

 

Burn injury

Burn injury can be associated with cardiogenic and non-cardiogenic pulmonary edema, both of which can present challenges during mechanical ventilation. As in patients with other traumatic injuries, lung protective ventilation strategies should be used. Another challenge during mechanical ventilation is a decreased chest wall compliance, which requires escharotomy in severe cases. These patients are at increased risk for ventilator-associated pneumonia.

 

Head injury

Ventilator setting in these patients should be selected with consideration of the potential effects on cerebral perfusion pressure. Mechanical ventilation of these patients can be complicated by neurogenic pulmonary edema, which may result in both cardiogenic and noncardiogenic pulmonary edema. A concern in this patient population is the effect of PEEP on cerebral perfusion pressure. The available evidence suggests that modest levels of PEEP (£10 cm H2O), if indicated, has minimal detrimental effects on intracranial pressure and cerebral perfusion pressure. In these patients, hypercapnia, hypocapnia, and hypoxemia are avoided. Generally, iatrogenic hyperventilation is discouraged.

 

Conclusions

Mechanical ventilation, a life support technique, is associated with attributable mortality if it is set incorrectly. For patients with ALI/ARDS, the available evidence supports the use of a lower tidal volume and two large trials have reported unprecedented low mortalities with a strategy that targets a tidal volume of 6 mL/kg PBW with further reduction for Pplat > 30 cm H2O. Zero end-expiratory pressure is likely harmful during mechanical ventilation of patients with ALI/ARDS. However, evidence is lacking for a survival benefit if a high PEEP level is set compared to a modest level of PEEP. Although adjunctive measures such as recruitment maneuvers, prone position, and inhaled nitric oxide may improve oxygenation, evidence is lacking that these measures improve survival. Ventilator weaning should focus on use of spontaneous breathing trials. Specific considerations are necessary for mechanical ventilation of patients with chest trauma, inhalation injury, burns, and acute head injury.

 

References

Kallet RH. Evidence-based management of acute lung injury and acute respiratory distress syndrome. Respir Care 2004; 49:793.

Frank JA, Matthay MA. Science review: mechanisms of ventilator-induced injury. Crit Care 2003; 7:233.

Eisner MD, Thompson T, Hudson LD, et al. Efficacy of low tidal volume ventilation in patients with different clinical risk factors for acute lung injury and the acute respiratory distress syndrome. Am J Respir Crit Care Med 2001; 164:231.

The Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med 2000; 342:1301.

Brower RG, Lanken PN, MacIntyre N, et al. Higher versus lower positive end-expiratory pressures in patients with the acute respiratory distress syndrome. N Engl J Med 2004, 351:327

Slutsky AS: Ventilator-induced lung injury: from barotrauma to biotrauma. Respir Care 2005; 50:646.

Amato MB, Barbas CS, Medeiros DM, et al. Effect of a protective-ventilation strategy on mortality in the acute respiratory distress syndrome. N Engl J Med 1998; 338:347.

Harris RS. Pressure-volume curves of the respiratory system. Respir Care 2005; 50:78.

Taylor RW, Zimmerman JL, Dellinger RP, et al. Low-dose inhaled nitric oxide in patients with acute lung injury: a randomized controlled trial. JAMA 2004; 291:1603.

Hess DR, Bigatello LM. Lung recruitment: the role of recruitment maneuvers. Respir Care 2002; 47:308.

Oczenski W, Hörmann C, Keller C, et al. Recruitment maneuvers after a positive end-expiratory pressure trial do not induce sustained effects in early adult respiratory distress syndrome. Anesthesiology 2004; 101:620.

Brower RG, Morris A, MacIntyre N, et al. Effects of recruitment maneuvers in patients with acute lung injury and acute respiratory distress syndrome ventilated with high positive end-expiratory pressure. Crit Care Med 2003; 31:2592.

McCall JE, Cahill TJ. Respiratory Care of the Burn Patient. Journal Burn Care Rehab 2005; 26:200.

Rubenfeld GD, Caldwell E, Peabody E, et al. Incidence and outcomes of acute lung injury. N Engl J Med 2005; 353:1685.

Wanek S, Mayberry JC. Blunt thoracic trauma: flail chest, pulmonary contusion, and blast injury. Crit Care Clin 2004; 20:71.

Stocchetti N, Maas AIR, Chieregato A, et al. Hyperventilation in Head Injury. Chest 2005; 127:1812.

Michaels AJ. Management of post traumatic respiratory failure. Crit Care Clin 2004; 20:83. 

 

Dirección: Cañar 607 y Coronel, Segundo Piso. Guayaquil - Ecuador

E-mail:  info@ecuadortrauma.com 

Teléfonos: (593-4) 2344259 - 2447551 - 2292725 Celular:  09-9757784 Fax: 2290408

Esta página está hospedada en www.medicosecuador.com

Desea más información? Búsquela en medicosecuador.com