Failure to detect this complication of mechanical ventilation can be catastrophic, from both a physical and financial viewpoint.

Today’s respiratory care director must manage a department that is a cost center, not the revenue center of yesterday. Managers must identify and track those diagnosis-related groups that have the potential to generate immense costs. One of the more expensive procedures is mechanically ventilating a patient for prolonged periods. If a patient should develop infection or experience volutrauma during the period of ventilation, the delay in extubation may be catastrophic, from both a physical and financial point of view.

One of the most frequently encountered complications of mechanical ventilation is volutrauma. This broad term is commonly used to define extra-alveolar air as it migrates from a ruptured alveolus into surrounding tissue spaces. This complication of mechanical ventilation may be transparent to the bedside clinician, as with pulmonary hyperinflation, or it may be life threatening, as in the case of untreated tension pneumothorax.

The first reports of pulmonary volutrauma appears in the surgical literature.1,2 In more recent years, with the introduction of more sophisticated mechanical ventilators, a broader awareness of the many forms volutrauma may take has developed. In the past, the damage was thought to be the result of the application of excessive pressure commonly know as barotrauma. Recently, however, volutrauma has been proposed as a more appropriate term because it is now believed that overdistension of the lungs via excessive inflation volume is a more realistic explanation.

Physical Costs

Inordinately large tidal volume delivery has been positively identified as a contributing factor in volutrauma.3,4 Once the gas has dissected the bronchovascular sheath, it then spreads throughout the thorax, manifesting itself as pneumomediastinum, subcutaneous emphysema, pneumopericardium, pneumoperitoneum, pulmonary interstitial emphysema, air embolism, and pneumothorax. The professional literature has documented this phenomenon for more than 50 years.5

Mechanically ventilated patients have been reported6-10 to experience a 4 percent to 15 percent incidence of pneumothorax. Patients with lung conditions conducive to volutrauma (such as adult respiratory distress syndrome, aspiration pneumonia, and restrictive lung disease) may require higher peak airway pressures when volume-oriented ventilation is used, and may experience significantly higher incidence rates.7,10,11

Haake et al9 reported volutrauma in 40 percent of their mechanically ventilated patients requiring peak airway pressures of more than 70 cm H2O. It was also reported7 that there was an increased incidence of extra-alveolar gas in patients requiring peak airway pressures of more than 40 cm H2O. Other researchers have noted higher levels of positive end-expiratory pressure (PEEP) as a contributor to volutrauma. Recent research,12,13 however, suggests that transalveolar pressure may actually be the major factor, while peak airway pressure and PEEP play a more minor role. Regardless of the primary cause of volutrauma, it is commonly accepted three factors must be present in some combination for this phenomenon to occur: underlying lung disease, overdistension, and elevated pressures.

Detection And Treatment

Bedside clinicians must be able to recognize, diagnose, and treat pneumothorax occurring during mechanical ventilation without delay. Clinical assessment skills must be keenly developed by bedside practitioners, as patient assessment continues to play a more vital part in health care. The intensive care unit (ICU) patient is at far more risk than other patients for multisystem organ failure and must be continuously monitored. Any form of distress requires immediate therapeutic action. Patient assessment must- become a natural component of every patient interaction.14 Kacmarek15 relates, for example, that there are specific signs and symptoms associated with pneumothorax that occur during mechanical support. These include

  • decreased chest wall compliance, which results in an increase in peak airway pressure, a decrease in tidal volume, and activation of the ventilator’s high-pressure and low-tidal-volume or minute-ventilation alarms;
  • increased intrathoracic pressure manifesting itself as early hypertension and tachycardia that change to hypotension and bradycardia as tension pneumothorax progresses;
  • a reduction in variables normally found during physical assessment, such as reduced breath sounds, diminished chest movement, and changes in percussion resonance on the affected side; and
  • signs that commonly indicate respiratory distress, such as ventilator asynchrony, agitation, and increased work of breathing.

    All of these, however, manifest themselves after the fact. It is of extreme importance to identify the at-risk patient and to implement an early ventilatory strategy that will minimize the patient’s exposure to predisposing factors for volutrauma. Strategies such as permissive hypercapnia, inverse-ratio ventilation, and pressure-controlled ventilation are newer approaches currently in use, yet the use of any mechanical ventilatory strategy must be monitored closely. The value designated airway pressure on most ventilator displays is not peak airway pressure at all. This pressure, unless sensed within the trachea using a special catheter, is a reflection of the pressure within either the mechanical ventilator tubing or the Y. Peak airway pressure truly reflects alveolar pressure only during a static maneuver such as an inspiratory hold.

    Few clinicians take into consideration the fact that peak airway pressure is a reflection of alveolar pressure only when the ventilator design, patient circuit, and resistive properties of the airways, including the tracheostomy or endotracheal tube, are also taken into consideration. A much more important variable in the management of the at-risk patient is the relationship of alveolar pressure to pleural pressure. It is the transmural pressure (alveolar pressure minus pleural pressure) that has the greatest potential to create volutrauma.

    When initiating mechanical ventilatory support, the ideal application should be selected to guarantee adequate gas exchange, reduce both the physiological work of breathing and the imposed work of breathing, and reinforce normal alveolar function without injuring the nondiseased lung segments. Scanlan16 suggests that the health care team should establish measurable clinical objectives to guide the course of ventilatory support toward patient/ventilator separation. These objectives should provide clear and concise directions for all bedside practitioners and allow for individual tailoring of support to each patient’s needs.

    Marcy17 reported that normal lungs are inflated to their total capacity at a transalveolar pressure of approximately 35 cm H2O. He states that when pressures exceed 35 to 40 cm H2O, there is certainly overdistension present; alveoli that are susceptible to rupture may do so. Routine determination of the adequacy of mechanical ventilatory support is frequently based on subjective clinical assessment supported by objective data (such as arterial blood gas levels, chest radiographs, and selected ventilator parameters). As a result, clinicians are frequently unable to detect subtle changes that may occur, and they often consider the patient to be fighting the ventilator. This diagnosis can frequently be supported by the fact that the monitored ventilator parameters agree with those selected by bedside personnel. In actuality, patient-ventilator asynchrony is present, and it may go undetected by conventional assessment parameters.

    Overdistension may go unnoticed unless there is some form of graphical presentation of waveforms and loops available. Bedside pulmonary monitoring does not replace clinical judgment, but it adds a distinct set of objective variables to the ventilation equation that the clinician can use to improve patient care. Loops using both airway pressure and esophageal pressure versus volume are able to display the inflation pressure-volume relationship during inspiration and the passive or active relationship during exhalation. This capability of visualizing pressure-volume loops in “real time” offers a distinct advantage: a proactive method of removing one of the factors associated with volutrauma.

    Financial Costs

    There is no question that ICU patients consume a large share of health care resources. A direct association between mechanical ventilation and rising health care expense is a common perception. In 1980, Davis et al18 reported, in their study of 100 medical/surgical patients mechanically ventilated for more than 48 hours, an 87 percent increase in hospital charges, compared with those for all other types of hospitalized patients. Of the total charges, respiratory care services represented 16.8 percent.

    In a 1985 multicenter study19 of 3,884 medical and surgical patients at 12 different medical centers, costs for patients requiring mechanical ventilation for 7 or more days rose an average of $48,500 above costs for normally weaned patients. Furthermore, this was an enormous jump of $61,100 over the cost for ICU patients who did not require mechanical support.

    In 1993, Civetta20 hypothesized in an editorial that patients whose conditions were misdiagnosed and who were placed in a failure-to-wean category might represent a potential of 192,000 cases per year nationwide. In his experience, if a nosocomially acquired infection were to occur, an additional 2 to 3 weeks of unexpected support might be added to the length of required mechanical ventilation. In applying these data to the number of available ICU beds, one finds that the potential unnecessary expense could be as much as $1.5 billion per year.

    The longer patients are exposed to mechanical support, the more likely they are to be subjected to an incident that may inhibit a good outcome. Gluck et al21 reported, in their 1993 study of 16 patients (control, n=8, and test, n=8) transferred to a chronic ventilator unit and randomized into two study protocols, that the test group monitored via esophageal manometry required fewer days of withdrawal from ventilatory support before a determination of weaning failure could be diagnosed (8.4 ñ3 versus 12ñ6.2). They noted, furthermore, that the test group was weaned in fewer days when compared with the control group (16.4ñ6.5 versus 24.7ñ10.3). Taking Civetta’s figure of a $4,000-per-day cost for ventilated patients, this amounts to a potential savings of over $32,000 per patient. A multicenter trial22 designed to support the original findings resulted in the same positive results. Subsequent independent reports23,24 have also confirmed the advantages of using newer technology to improve patient care, reduce lengths of stay, and minimize ICU costs.

    Because the incurred costs associated with mechanical support are so high, it is important to make good cost-benefit decisions based on expected outcomes. Administrative managers must trend and interpret outcomes data, even though variations in patient populations make this job extremely difficult. If clinical tools are available that prove to aid in reducing the number of ventilator days and/or predicting the failure of a weaning trial prior to the patient’s crashing, we must embrace such technologies.


    Airway pressure measurements are routinely captured and evaluated during mechanical ventilation. Respiratory care flow sheets devote considerable space to assessing peak pressure, mean pressure, static pressure, PEEP, and a variety of other pressure measurements based on the value shown on the ventilator’s airway pressure gauge. If these measurements accurately reflected alveolar pressure and the resultant volume changes within the lungs, whether volutrauma is caused by pressure or volume would be clinically irrelevant.

    Current professional literature suggests that there are sufficient indicators to warrant a strong suspicion that high peak airway pressure, by itself, is not the primary cause of volutrauma. Instead, overdistension of the lung appears to be a more likely cause. The bedside clinician must not lose sight of other conditions–such as resistance of the artificial or conducting airways, active use of auxiliary respiratory muscles, and pressure loss due to ventilator design and/or patient circuit resistance–that change any relationship between monitored volumes and peak airway pressure.

    It is always important to minimize pulmonary exposure to high inflating pressures, but not at the expense of ventilation and oxygenation when the ventilator’s peak airway pressure indication is the foundation upon which a treatment decision is based. Pleural pressure more accurately reflects the events leading up to volutrauma, and it allows the bedside clinician to take a proactive position before a catastrophic event. If volutrauma and nosocomially acquired infections can be minimized, ventilator days can be reduced, mortality rates can be improved, and the adverse financial impact of mechanical ventilation can be reduced.

    Larry Boutcher, PhD, RRT, RCP, is the director of clinical education for the Associate Degree Respiratory Therapy Program at Victor Valley College, Victorville, Calif.


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