RCPs have made huge strides in optimizing the management of artificially ventilated lungs through providing basic lung function needs such as optimal temperature and humidity and attempting to eliminate every possible source of nosocomial infection.

 The human lung is a mighty yet fragile organ that constantly interacts with the surrounding environment, while effectively transporting oxygen and carbon dioxide into and out of the individual. When committed to a mechanical ventilator, a necessary but unnatural marriage occurs. It is the RCP’s role to serve the lung by ensuring proper temperature, humidity, and gas exchange. We must simultaneously protect the lung from mechanical malfunctions, human error, infections, and the onslaughts of volume and pressure that can result in ventilator-induced lung injury.

Maintaining the Airway
While focusing attention on contemporary modes of ventilation and other higher order patient care issues, it can be easy to overlook the basics, including simple airway management. A secure airway is essential to ventilator management, and without it, all other issues become moot. “The rate of unplanned extubation (accidental extubation or self-extubation) has been reported as 2% to 13%.”1 Whether secured with adhesive tape, twill tape, or commercially available devices, it is essential that the endotracheal (ET) tube and cuff pressures be evaluated routinely and repositioned periodically to prevent tissue necrosis and sores. Securing and/or repositioning the tube should never be undertaken single-handedly; one clinician should perform the procedure while another stabilizes the tube position. Optimal cuff pressure to create an effective seal while minimizing aspiration or tracheal wall injury is normally 25 to 35 cm H2O.

The upper airway is the conduit between the lungs and the lower respiratory tract. By substituting an artificial airway, important functions are compromised or bypassed. These include the jobs of providing warmth, humidification, filtration, removal of debris, and facilitation of expectoration and speech. The upper airway represents an essential component of the immune system that is lost when ventilator support is required—a significant factor when considering lung protection strategies.

Ventilator-Associated Pneumonia
Ventilator-associated pneumonia (VAP) is a nosocomial infection occurring in patients after 48 hours of mechanical ventilation. It is typically accompanied by fever, increased leukocyte production, and purulent secretions. Vastly differing rates of VAP are reported, principally because there is not a consistent standard for diagnosis, beyond the occurrence of a new infiltrate presenting (usually after 48 hours) in a mechanically ventilated patient.

Identification of VAP typically includes:

  • Appearance of a new infiltrate or consolidation that is evident on chest x-ray.
  • New onset of purulent secretions or change in the character of the sputum.
  • Pathogenic organisms isolated by blood culture and/or transtracheal aspirate or bronchial lavage. Cultures are best obtained via bronchoscopy, which produces the most consistent results, but traditional acquisition via a suction trap is also commonly used.

VAP rates can be determined by dividing the number of VAPs identified and dividing this figure by the total ventilator days times 1,000:

VAP number
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Ventilator days X 1,000

Active or Passive Humidification?
Once upon a time, RCPs spent considerable time draining wet ventilator tubing into bedside buckets before the contents blocked airflow or emptied into the patient’s lungs. Eventually, inline water traps collected the condensate while eliminating the need to disconnect the patient from the ventilator when disposing of the water. Heat moisture exchangers (HMEs) are passive systems and have more recently become en vogue. They eliminate the need for a heated humidifier and the associated condensation as well as many of the other challenges previously associated with active systems. They are also economical, efficient, convenient, and dependable. Consequently, HMEs continue to provide an attractive tool for use with short-term or postoperative patients.

However, the policy of using HMEs for all patients all the time is currently being challenged when applied to long-term ventilatory support. When VAP becomes a concern, a recursion from passive to active humidification is winning favor. Many investigators believe the heat and moisture provided by HMEs may be insufficient to promote optimal mucokinesis over a long term, especially if high minute volumes are required.

When the patient is disconnected from the ventilator, some machines generate significant flows through the circuit, which may aerosolize contaminated fluids, increasing the risk of lung infections. Consequently, a reduction or elimination of ventilator circuit changes and a commitment not to break the circuit have been successfully pursued.

When applied to VAP, ventilator circuit change frequency has been one of the foremost topics of investigation. Frequent ventilator circuit changes, once a standard practice, have been reconsidered, with “the optimum protocol for ventilator tubing changes …still [considered to be] uncertain, but evidence suggests that tubing-change intervals should be at seven days, and accumulating evidence suggests that ventilatory circuits need not be changed at any regular interval.”1 Numerous studies have determined that intervals of 7 days between circuit changes have shown no difference in VAP rates. The practice is easy to implement, cost-effective, and safe. Circuit change intervals substantially longer than 7 days are currently being investigated.

Gary Hospodar, MAOM, RRT, an independent consultant in Santa Fe, NM, has studied the issue and presented his findings at the 48th American Association for Respiratory Care International Respiratory Congress in Tampa, Fla. He described a 6-month investigative study, which embraced four components intended to reduce VAP.

  • Use of in-line suction catheters, which were changed every 7 days. RCPs were allowed the option of changing the catheters more frequently if they deemed it necessary, but the 7-day standard replaced the former 24-hour frequency of change. Suctioning was performed when clinically indicated, not as a matter of thoughtless routine.
  • Ventilator circuit changes every 30 days. This replaced the former 7-day circuit change frequency. In addition to dramatically decreasing the frequency of ventilator changes, a policy of maintaining a closed, virtually unbroken system was invoked.
  • Implementation of active (heated) humidification systems. The active systems were intended to enhance mucociliary activity that may be compromised with passive systems. The molecular water produced by modern heated humidifiers is not thought to pose an important risk of pneumonia in ventilated patients.
  • Education of the entire clinical care team. Hospodar emphasized this as a key element to the success of the investigation. Revisiting the essential importance of hand washing, double gloving, and use of personal protection devices was stressed. Most important, all members of the team, including physicians, nurses, infection control specialists, and ancillary personnel, were indoctrinated with the goals of the study.

Another commonly overlooked, but potential source of infection may come from the ubiquitous oral suction tips that are typically used and reused to remove oral secretions. While these tools are useful for many patients and caregivers in a variety of circumstances, their potential as a source for VAP infections was considered. Hospodar eliminated the use of these tools, favoring single-use alternatives for oral care and suction.

Dean Hess, PhD, RRT, FAARC, is affiliated with the Department of Respiratory Care, Massachusetts General Hospital, Boston, and Harvard Medical School. He suggests, “VAP is more likely the result of what is aspirated around the cuff of the endotracheal tube than what is inhaled from the ventilator circuit” and “rather than refer to these infections as VAP, perhaps we should refer to them as ET associated pneumonia.”2 Hospodar adds that VAP is likely a result of numerous sources, and agrees that it is a mistake to focus on any individual component, such as ventilator tubing or suction catheters.

Hospodar’s investigation also demonstrated that improved patient care could also be cost-effective. His investigation showed a decrease from $17.81 to $7.79 in operational supply expenses—a 56% reduction. In addition to the savings in supply costs, staff labor time is naturally reduced.

When RCPs report for duty clearly suffering from a cold or flu, perhaps even running a fever, there are often no mechanisms to send the offender home to bed. This is surprising in an industry that embraces quality improvement and has policies and procedures to deal with virtually any other event. The popular work ethic that often encourages workers to “tough it out” when they are ill is in direct conflict with everything else we value. Colds and flu can admittedly be hard to quantify, but when RCPs report for duty suffering from a contagious illness, they put everyone around them at risk. Respiratory care departments should be performing a careful self-examination with consideration as to how employee illness may impact patient care.

Ventilator-Induced Lung Injury
Ventilator-induced lung injury may result from oxygen toxicity, biotrauma, atelectrauma, and volutrauma. Acute lung injury (ALI) is caused by alveolar overdistention caused by high peak inflation volume (volutrauma), and high peak alveolar pressures.1

  • Oxygen Toxicity. High oxygen concentrations can result in oxygen toxicity, which can create acute respiratory distress syndrome (ARDS)-like changes in the lungs. Consequently, the fractional inspired oxygen (Fio2) should be set as low as possible, while maintaining oxygen saturations above 90%. Positive end-expiratory pressure (PEEP) can enhance alveolar recruitment while simultaneously enhancing oxygenation and permitting an Fio2 of below 60% to maintain acceptable oxygenation levels.
  • Biotrauma. Biotrauma is an inflammatory process that can result from ventilating the lungs in a manner that promotes alveolar overdistention. “Inflammatory mediators such as cytokines and chemokines may translocate into the pulmonary circulation, causing systemic inflammation. The manner in which the lungs are ventilated therefore may play a role in systemic inflammation.”1
  • Atelectrauma. The implementation of lung protection strategies for patients with acute lung injury and ARDS has been an important step in optimizing patient outcomes; however, while the application of low VT ventilation is clearly beneficial, “it will not prevent injury from repetitive alveolar opening and closing, and may promote alveolar collapse,”3 or atelectrauma. Consequently, investigators are taking a close look at maneuvers intended to recruit alveoli into useful service. Plateau pressure is reflective of alveolar pressure and should be kept below 30 cm H2O, while PEEP is used to enhance alveolar recruitment.
  • Volutrauma. The overdistention of alveoli caused by high peak inflation volume is also associated with high peak alveolar pressures. “The main determinant of volutrauma seems to be the end-inspiratory volume (the overall lung distension), rather than the VT or FRC (which depends on PEEP). Consequently, a consensus has emerged as to the importance of monitoring and limiting inspiratory plateau pressure (which reflects end-inspiratory volume better than does peak pressure).”4

ARDS is an inflammatory lung condition that usually occurs in conjunction with catastrophic medical conditions, such as pneumonia, shock, sepsis, and trauma. Approximately 150,000 Americans are affected each year, and more than 40% die.5 The ARDSnet (Acute Respiratory Distress Syndrome Clinical Network) is a monumental national trial, federally funded by the National Institutes of Health (NIH) and the National Heart, Lung, and Blood Institute (NHLBI). It is currently studying the effects of numerous treatment modalities to optimize care for patients with ARDS and ALI. ARDSnet has 10 clinical centers composed of 23 hospitals, and one clinical coordinating center. Several studies have been concluded, and information about these as well as ongoing studies can be accessed at www.ardsnet.org.

The information gathered by the investigators is evaluated even as the studies are conducted. Fran Piedalue, RRT, clinical coordinator for respiratory care at University of Colorado Hospital, Denver, says, “Statisticians perform an interim analysis on a predetermined enrollment number to consider the efficacy versus futility for each study.” Consequently, some studies are concluded early, when the effectiveness (or lack of it) has been determined.

“The prognosis of ARDS seems to have improved over the years for reasons that are yet unclear, but may be related in part to the lower VT used in most intensive care units at present.”4 Indeed, one of the most significant ARDSnet studies that has been concluded showed that limiting tidal volume to 6 mL/kg or less (typically 4 to 6 mL/kg) can minimize the undesirable effects of larger tidal volumes. The test study was intended to enroll 1,000 patients, but was concluded early because the results were overwhelmingly clear. “The decision [to conclude the study] was recommended by the study’s Data Safety and Monitoring Board (DSMB)…based on data on the first 800 patients, which showed approximately 25% fewer deaths among patients receiving small, rather than large, breaths of air from a mechanical ventilator.”5

The resulting lower minute volumes create an increasingly acidic state, and clinicians have traditionally been uncomfortable with resulting arterial blood gas values that fall outside the “normal” range; however, rather than risk increased injury to the lungs from the effects of volume and pressure, an elevated partial pressure of arterial carbon dioxide (Paco2) was accepted. With this resulting “permissive hypercapnea, the clinical concern generally is related to pH, not Paco2 [and] most investigators agree that a pH above 7.25 is acceptable.”1

Current studies under way by the ARDSnet clinical trials include:

  • Late Steroid Rescue (LSR study). While it has already been determined that corticosteroids are not effective in treating early ARDS, the study is designed to determine if the administration of cortico-steroids, in the form of methylprednisolone sodium succinate, in severe late-phase (after 7 days) ARDS will reduce mortality and morbidity.
  • Pulmonary Artery Catheter (PAC study). Evaluating the use of a pulmonary artery catheter vs a less invasive alternative, the central venous catheter, for management of patients with ALI and ARDS. The study is combined with a concurrent study evaluating a “Fluid Conservative” vs “Fluid Liberal” management strategy in patients with ALI or ARDS.

Studies concluded by the ARDSnet clinical trial due to lack of efficacy included:

  • Ketoconazole Study. Tested whether the administration of ketoconazole early after the onset of ALI or ARDS will reduce mortality and morbidity. It was concluded early due to lack of efficacy.
  • Lisofylline Study. Tested whether the administration of lisofylline early after the onset of ALI or ARDS would reduce mortality and morbidity. It was concluded early due to lack of efficacy.
  • ALVEOLI Study. Investigated the hypothesis that mortality from ALI and ARDS would be reduced with a mechanical ventilation strategy designed to prevent lung injury from repeated collapse of bronchioles and alveoli at end-expiration. It compared clinical outcomes of patients with acute ALI and ARDS treated with a higher end-expiratory lung volume/lower Fio2 vs a lower end-expiratory lung volume/higher Fio2 ventilation strategy. It was concluded early due to a lack of efficacy.

Lung protection strategies for providing life-sustaining ventilator support while minimizing morbidity and mortality continue to evolve and improve. The introduction of new methods combined with a continued willingness to challenge and question long-accepted notions has led to dramatically improved patient outcomes. The optimal management of ARDS continues to be evolving, most notably as a result of the comprehensive ARDSnet studies, with implications that will undoubtedly benefit other ventilator management challenges as well. By providing basic lung function needs, including optimal temperature and humidity, minimizing the effects of volume and pressure, and attempting to eliminate every possible source of nosocomial infection, we have made huge strides in optimizing the management of artificially ventilated lungs. RCPs are leading the way in the process, as investigators, inventors, and instigators of positive change and evolution.

John A. Wolfe, RRT, CPFT, is a contributing writer for RT Magazine.

1. Hess DR, MacIntyre NR, Mishoe SC, Galvin WF, Adams AB, Saposnich AB. Respiratory Care Principles and Practice. Philadelphia: WB Saunders Co; 2002.
2. Hess DR. Mechanical ventilation strategies: what’s new and what’s worth keeping? Respir Care. 2002;47:1008-1009.
3. Hess DR, Bigatello LM. Lung recruitment: the role of recruitment maneuvers. Respir Care. 2002;47:308-318.
4. Dreyfuss D, Saumon G. Ventilator-induced lung injury. Am J Respir Crit Care Med. 1998;157:294-323.
5. National Institutes of Health; National Heart, Lung, and Blood Institute. News Release; March 15, 1999.