eMedicine Specialties > Pulmonology > Mechanical Ventilation

Barotrauma and Mechanical Ventilation

Author: Guy W Soo Hoo, MD, MPH, Clinical Professor of Medicine, Geffen School of Medicine at the University of California at Los Angeles; Director, Medical Intensive Care Unit, Pulmonary and Critical Care Section, West Los Angeles Healthcare Center, Veteran Affairs Greater Los Angeles Healthcare System
Contributor Information and Disclosures

Updated: Apr 2, 2009

Introduction

Background

Barotrauma is a well-recognized complication of mechanical ventilation.  Although most frequently encountered in patients with the acute respiratory distress syndrome (ARDS), it can occur in any patient receiving mechanical ventilation. In addition, barotrauma can occur in patients with a wide range of underlying pulmonary conditions (eg, asthma, chronic obstructive pulmonary disease, interstitial lung disease, Pneumocystis jiroveci [Pneumocystis carinii] pneumonia).

In clinical medicine, barotrauma is used to describe the manifestations of extra-alveolar air during mechanical ventilation. Early descriptions of barotrauma refer to rupture of the lung after forceful exhalation against a closed glottis, such as pulmonary injury after a deep-sea dive (eg, breath-holding while pearl diving). Although nonmechanically ventilated patients may have barotrauma, most cases occur in patients receiving mechanical ventilation.

The clinical presentation can vary, ranging from absent symptoms with the subtle radiographic findings of pulmonary interstitial emphysema (PIE) to respiratory distress or cardiac arrest due to a large tension pneumothorax. Other manifestations include subcutaneous emphysema, pneumopericardium, pneumomediastinum, and even pneumoperitoneum, singly or in combination. Barotrauma was once the most frequent and easily recognized complication of mechanical ventilation. However, now evident is that barotrauma represents only one of the mechanisms underlying the broad category of ventilator-induced lung injury (VILI). As the term suggests, the lung injury associated with barotrauma is mediated by increased alveolar pressures. Other manifestations of VILI have been termed volutrauma, atelectotrauma, and biotrauma (cytokine and chemokine mediated) to reflect the major pathophysiologic events behind the injury.

Pathophysiology

An appreciation of the pathophysiology of barotrauma in mechanically ventilated patients improves the understanding of its clinical manifestations. It is important to recognize that lung involvement in persons with ARDS is heterogenous and that some portions of the lungs are more adversely affected than others. This involvement can lead to maldistribution of mechanically delivered tidal volume, with some alveoli subjected to more distension than others. Pressures between adjacent alveoli may initially equilibrate, but alveolar pressures eventually increase, creating a pressure gradient between the alveoli and adjacent perivascular sheath. This gradient may result in rupture of the alveoli adjacent to the perivascular sheath, with ensuing passage of air into the perivascular sheath, and proximal dissection into the mediastinum. This condition is often referred to as perivascular interstitial emphysema or PIE.

In persons with PIE, alveolar air is further decompressed by dissecting along lines of least resistance. These pathways include subcutaneous tissues, where the air produces subcutaneous emphysema, or along tissue planes, resulting in pneumopericardium, pneumoperitoneum, or subpleural air cysts. In the mediastinum, air can track along tissue planes, creating a pneumomediastinum, whereas increased pressures that rupture through the mediastinal pleura produce a pneumothorax. This is the most dreaded manifestation of barotrauma, and continued accumulation of air during mechanical ventilation can progress to a tension pneumothorax, sometimes with catastrophic consequences. In many patients, radiographic evidence of barotrauma (eg, PIE, pneumomediastinum) can be noted before any clinical manifestations are evident and, certainly, before a pneumothorax occurs.

Given the description above, alveolar overdistension is the key element in the development of barotrauma. In this sense, barotrauma is a misnomer because barotrauma suggests the presence of elevated pressures in its pathogenesis. Current concepts suggest that high tidal volume ventilation produces the alveolar disruption that triggers the aforementioned chain of events. Therefore, VILI seen with high tidal volume is most accurately termed volutrauma, and it has been the basis for recent clinical trials that have established a low tidal volume approach to mechanical ventilation.

On the other hand, transalveolar pressure, a measure of alveolar distension, provides another indication of the risk of barotrauma. The concept is the same, with overdistended alveoli leading to disruption in the alveolar epithelium and decompression of air as previously outlined. The plateau pressure provides the best estimate of transalveolar pressure, and some have argued that this is the key risk factor for the development of barotrauma.

Other aspects of VILI include atelectotrauma, which describes the injury associated with repeated opening and closing (recruitment and collapse) of collapsed alveoli during mechanical ventilation. Biotrauma has been used to describe the release of inflammatory cytokines and chemokines as a result of VILI. These cytokines have both pulmonary and systemic effects and may contribute to mortality. The last 2 components have not been implicated as direct causes of barotrauma, but they may contribute to the development of abnormal lung parenchyma and lung mechanics, which, in turn, may increase the risk of barotrauma.

Also important is to recognize that the effects of VILI are greater in patients with preexisting lung disease or those with acute lung injury (ALI) or ARDS compared with persons with healthy lungs. These differences can be gleaned from the differences in barotrauma in a large cohort evaluated on the basis of underlying lung disease. Patients with chronic obstructive lung disease have the lowest incidence of barotrauma (2.9%). The incidence is highest in persons with chronic interstitial lung disease (10%), and patients with ARDS have an intermediate rate (6.5%). This observation underscores the heterogeneity of lung disease and regional differences in lung compliance.

Frequency

United States

The incidence of barotrauma in mechanically ventilated patients varies widely and is reported to be as low as 0.5% in postoperative patients and as high as 87% in patients with ARDS. The underlying condition of the lungs obviously plays a significant role in the development of barotrauma. Patients with ARDS have the highest incidence of barotrauma, at 40-60%, with the associated mortality rate in a similar range.

Notably, however, the incidence of barotrauma in persons with ARDS and all mechanically ventilated patients has decreased markedly over the past decade. In a retrospective analysis of more than 5000 patients, barotrauma was noted in approximately 3% of all mechanically ventilated patients and in slightly more than 6% of persons with ARDS. As is discussed in subsequent sections, the change in the incidence of barotrauma is most likely related to changes in the approach to mechanical ventilation, specifically with respect to ventilator settings and the use of lower tidal volumes in conjunction with a reduction in plateau pressures.

International

No international or geographic influences are known to affect the incidence of barotrauma. Any differences are likely small and more a reflection of the underlying disease status of the patients and of differences in ventilator management in those locations than of any ethnic or environmental influence.

International multicenter trials involving patients with ARDS revealed a decrease in the incidence of barotrauma similar to that observed in the United States, to a range of 8-15%. This decline in the incidence of barotrauma is also associated with a decline in the mortality rate from ARDS, although not of the same magnitude as the decline in barotrauma.

Mortality/Morbidity

The morbidity and mortality attributed to barotrauma is related to the severity of its manifestations in the patient.

• PIE or air along tissue planes (eg, subcutaneous emphysema, pneumomediastinum) may be the only manifestation in some patients. This finding is more of a radiographic diagnosis than a clinical entity and is without clinical significance. However, it can be a harbinger of a pneumothorax. In one series, mediastinal emphysema led to a subsequent pneumothorax in 42% of patients.
• Pneumothoraces can be life threatening, especially if they are not recognized and not treated. However, the effect of barotrauma on morbidity and mortality is mixed. In the 2000 Acute Respiratory Distress Syndrome Network trial of low versus high tidal volume, the incidence of barotrauma was similar between the groups, although the mortality rate was lower in the low tidal volume group.¹ Other series of patients with ARDS have not identified pneumothoraces as a cause of increased mortality in these patients. Although a pneumothorax is a risk factor for mortality, it is more likely a reflection of the severity of the underlying lung disease than a cause of death. In one series of patients with ARDS, less than 2% of 66 deaths were directly attributable to a pneumothorax.

Early ventilator practices using high tidal volumes and resulting in high peak inspiratory pressures and plateau pressures may confound some of these data. In early series, the incidences of barotrauma and subsequent mortality were high and were associated with the barotrauma. When low tidal volumes are used along with low plateau pressures, the incidence of barotrauma decreases. Although barotrauma did not appear to influence mortality in an interventional trial comparing low with high tidal volume, an observational study of more than 5000 ICU patients showed that barotrauma increased the median length of mechanical ventilation and ICU stay by 2 days and increased the mortality rate by 12% (39% vs 51%).²

To provide perspective, the mortality rate from ARDS has been steadily decreasing over the past few decades, approaching or exceeding 70% in the early 1980s and declining to 30-40%.

Race

No ethnic predisposition to barotrauma is reported.

Sex

No sex differences are known regarding the development of barotrauma.

Age

As a complication of mechanical ventilation, age is not expected to influence barotrauma. However, the incidence of ALI does increase with age, especially for individuals in whom sepsis is a risk factor for the development of ARDS. Additionally, note that lung compliance normally decreases with age, and this may be a factor in the risk for barotrauma in older patients.

Clinical

History

The main historical consideration with respect to the risk of barotrauma in mechanically ventilated patients is their risk for developing ALI and ARDS. Patients are often intubated and unable to communicate, but historical data may be elicited from their medical records. The widely accepted definition of ALI and ARDS outlines a process characterized by an acute onset, bilateral infiltrates observed on chest radiographs, information that excludes cardiogenic pulmonary edema (pulmonary artery wedge pressure <18 mm Hg), and a low ratio of partial pressure of oxygen to fraction of inspired oxygen (PaO₂/FIO₂ ratio), which is defined as less than or equal to 300 for ALI and less than 200 for ARDS.

Some differences in ARDS may be based on whether the inciting cause involves direct lung injury (eg, pneumonia, gastric acid aspiration, pulmonary contusion) or indirect lung injury (eg, sepsis, trauma with shock, acute pancreatitis, multiple transfusions).

Although a mechanically ventilated patient with ARDS may be at risk for barotrauma, patients with blunt trauma, severe pneumonia, chronic obstructive pulmonary disease, or underlying interstitial lung disease may also be at risk. Iatrogenic pneumothoraces can occur in patients who undergo intravascular catheter placement into the internal jugular or subclavian. Among patients receiving mechanical ventilation, the finding of barotrauma implies VILI, although barotrauma related to the underlying lung disease is possible, especially if it occurs early in the patient's course.

In the isolated patient who may be able to communicate, reports of increased dyspnea, chest pain, discomfort, or subcutaneous air (in the chest or neck) may herald the development of barotrauma.

Physical

As discussed in the Introduction, the manifestations of barotrauma span the entire clinical spectrum, from totally asymptomatic to full cardiac arrest. The severity of the presentation depends on the amount of extra-alveolar air present. In some individuals, the diagnosis is made only on the basis of chest radiographic findings.

Because patients usually cannot communicate because of intubation, signs of respiratory distress (eg, tachypnea, patient-ventilator discoordination, use of accessory muscles [eg, neck muscle], diaphoresis, tachycardia) may be the earliest indicators of barotrauma.

• Systemic gas embolism is the most dramatic extrathoracic manifestation of barotrauma. This occurs in the context of the described thoracic manifestations, including lung cysts and pneumothoraces. Effects include cerebral air embolism with infarcts, myocardial injury, and livido reticularis. Some speculate that other clinical findings, such changes in sensorium, seizures, and cardiac dysrhythmias without a clearly identified cause, may also be related to episodic systemic gas embolization. Fortunately, this complication is rare and preventable with a strategy of low tidal volume ventilation.³
• The increased intrathoracic pressures that occur in mechanically ventilated patients may affect venous drainage of extrathoracic sites. This increase can affect venous return from the brain and abdomen, a change that may be of concern when the pressures in these areas are already elevated (eg, from cerebral edema or abdominal compartment syndrome). This process provides another impetus to adopt a ventilator strategy (ie, low tidal volume) that translates into lowered intrathoracic pressures. Of course, barotrauma only worsens the pressures in the extrathoracic areas. If the pressures in these areas are monitored, a sudden increase may herald barotrauma as opposed to a problem in the area monitored.
• VILI and alveolar overdistension may also activate cytotoxic and proinflammatory pathways. This is often referred to as biotrauma and represents a mechanical transduction injury in which the injurious physical effects of mechanical ventilation lead to the release of a host of chemokines and cytokines. Findings in both animal and human investigations have shown increases in leukocytes, tumor necrosis factor, interleukin 6, and interleukin 8 with high tidal volumes, with a reduction in levels in subjects given low tidal volumes. These cytokines are the same as those implicated in systemic inflammatory response syndrome and sepsis; this observation provides insight into another possible benefit of low tidal volume ventilation.

Causes

Barotrauma is one of the manifestations of VILI. In a multivariate analysis, the risk of barotrauma was increased in mechanically ventilated patients who had asthma, chronic interstitial lung disease, or ARDS and in those who developed ARDS during mechanical ventilation. Although barotrauma can occur in patients without ARDS, ARDS has always been the major risk factor for barotrauma in mechanically ventilated patients.

Because the current understanding of the pathophysiology underlying barotrauma is related to high tidal volumes that cause alveolar overdistension and alveolar rupture, it follows that barotrauma is related to the ventilator settings used in mechanical ventilation. Barotrauma has been associated with high peak inspiratory airway pressures (>40 cm water) and plateau pressures (>35 cm water); however, its association with high tidal volumes has not been confirmed. The Acute Respiratory Distress Syndrome Network trial to compare high and low tidal volumes demonstrated a mortality benefit with low tidal volumes, but incidences of barotrauma did not differ between the groups.

Plateau pressures provide an estimate of transalveolar pressure. Transalveolar pressure is a function of both the tidal volume and the underlying compliance of the lung. Therefore, plateau pressures can reasonably be used as another measure of the risk of barotrauma. Although the exact value of the optimal plateau pressure is debated, the general consensus is that a plateau pressure of less than 30 cm water is protective.

Pneumothoraces can also occur in situations unrelated to mechanical ventilation. These include cases involving primary or secondary spontaneous pneumothoraces (underlying lung disease), pneumothoraces associated with invasive procedures, use of inhalational drugs, blunt or penetrating chest trauma, or menses (catamenial). Patients with these conditions may develop a pneumothorax that requires mechanical ventilation. Although the events may be temporally separate, distinguishing a pneumothorax unrelated to mechanical ventilation from one due to mechanical ventilation may be difficult when it occurs.

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