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Clinicians have long been aware that substantial lung injury results when mechanical ventilation imposes too much stress on the pulmonary parenchyma. Evidence is accruing that substantial injury may also result when the ventilator imposes too little stress on the respiratory muscles. Through adjustment of ventilator settings and administration of pharmacotherapy, the respiratory muscles may be rendered almost (or completely) inactive. Research in animals has shown that diaphragmatic inactivity produces severe injury and atrophy of muscle fibers. Human data have recently revealed that 18 to 69 hours of complete diaphragmatic inactivity associated with mechanical ventilation decreased the cross-sectional areas of diaphragmatic fibers by half or more. The atrophic injury seems to result from increased oxidative stress leading to activation of protein-degradation pathways. Scientific understanding of ventilator-induced respiratory muscle injury has not reached the stage where meaningful controlled trials can be done, and thus, it is not possible to give concrete recommendations for patient management. In the meantime, clinicians are advised to select ventilator settings that avoid both excessive patient effort and excessive respiratory muscle rest. The contour of the airway pressure waveform on a ventilator screen provides the most practical indication of patient effort, and clinicians are advised to pay close attention to the waveform as they titrate ventilator settings. Research on ventilator-induced respiratory muscle injury is in its infancy and portends to be an exciting area to follow.

Objectives: To address the issues of Prevention and Management of Acute Renal Failure in the ICU Patient, using the format of an International Consensus Conference., Methods and Questions: Five main questions formulated by scientific advisors were addressed by experts during a 2-day symposium and a Jury summarized the available evidence: (1) Identification and definition of acute kidney insufficiency (AKI), this terminology being selected by the Jury; (2) Prevention of AKI during routine ICU Care; (3) Prevention in specific diseases, including liver failure, lung Injury, cardiac surgery, tumor lysis syndrome, rhabdomyolysis and elevated intraabdominal pressure; (4) Management of AKI, including nutrition, anticoagulation, and dialysate composition; (5) Impact of renal replacement therapy on mortality and recovery., Results and Conclusions: The Jury recommended the use of newly described definitions. AKI significantly contributes to the morbidity and mortality of critically ill patients, and adequate volume repletion is of major importance for its prevention, though correction of fluid deficit will not always prevent renal failure. Fluid resuscitation with crystalloids is effective and safe, and hyperoncotic solutions are not recommended because of their renal risk. Renal replacement therapy is a life-sustaining intervention that can provide a bridge to renal recovery; no method has proven to be superior, but careful management is essential for improving outcome.

Rationale: Exercise-induced dynamic hyperinflation contributes to decreased exercise tolerance in chronic obstructive pulmonary disease (COPD). It is unknown whether respiratory retraining (ventilation-feedback [VF] training) can affect exercise-induced dynamic hyperinflation and increase exercise tolerance., Objectives: To determine whether patients with COPD would achieve longer exercise duration if randomized to a combination of exercise training plus VF training than either form of training on its own., Methods: A total of 64 patients randomized to 1 of 3 groups: VF plus exercise (n = 22), exercise alone (n = 20), and VF alone (n = 22)., Measurements and Main Results: Exercise duration before and after 36 training sessions and exercise-induced dynamic hyperinflation and respiratory pattern before and after training were measured. In the 49 patients who completed training, duration of constant work-rate exercise was 40.0 (+/- 20.4) minutes (mean +/- SD) with VF plus exercise, 31.5 (+/- 17.3) minutes with exercise alone, and 16.1 (+/- 19.3) minutes with VF alone. Exercise duration was longer in VF plus exercise than in VF alone (P < 0.0001), but did not reach predetermined statistical significance when VF plus exercise was compared with exercise alone (P = 0.022) (because of multiple comparisons, P

Objectives: Tube feeding might increase gastric burden of pathogenic bacteria and predispose patients to ventilator-associated pneumonia. We sought to determine whether a tube feeding formula acidified using potassium sorbate could reduce gastric burden of potentially pathogenic bacteria., Design: Prospective, randomized, double-blind trial., Setting: RML Specialty Hospital, a facility with expertise in weaning patients from prolonged mechanical ventilation., Patients: Thirty patients recovering from prolonged mechanical ventilation., Intervention: Patients were randomized to receive either a standard tube feeding formula (n=14) or a formula acidified using potassium sorbate to a pH of 4.25 (n=16)., Measurements and Results: Weekly quantitative cultures of gastric aspirates. The number of colony-forming units (CFUs) per patient was higher in the control than in the treatment group (53%+/-11% vs 9%+/-3.4%, threshold of >or=100,000 CFU/mL fluid, P=.003). The number of organisms isolated in each patient per week was higher among patients receiving standard tube feeding formula than among patients receiving acidified formula (0.91 +/- 0.20 vs 0.13 +/- 0.05 organisms per patient per week, threshold of >or=100,000 CFU/mL fluid, P=.0014). There was no difference in the incidence of gastrointestinal bleeding or ventilator-associated pneumonia between study groups., Conclusion: Tube feeding formula acidified using potassium sorbate was well tolerated and reduced gastric bacterial burden in patients recovering from prolonged mechanical ventilation.

Mechanically ventilated patients are subject to few pathophysiologic disturbances that have such intuitive importance as abnormal function of the respiratory output. Abnormal function of the respiratory output plays a fundamental role in all aspects of mechanical ventilation: in determining which patients require mechanical ventilation, in determining the interaction between a patient and the ventilator, and in determining when a patient can tolerate discontinuation of mechanical ventilation. Monitoring indexes such as the rate of rise in electrical activity of the diaphragm, Po.1, (dP/dt)max, and Pmus, has provided insight into the performance of the respiratory centers in critically ill patients, but these methods require considerable refinement. A large body of research on measurements of energy expenditure of the respiratory muscles, such as pressure-time product, and measurements of inspiratory effort, such as the tension-time index, is currently accumulating. Several challenges, however, lay ahead regarding these indices. First, there is the need to identify the correct level of pressure generation and respiratory muscle effort that should be attained in the day-to-day management of mechanically ventilated patients. The correct titration of ventilator setting should not cause iatrogenic muscle damage because the support is excessive or insufficient. One of the challenges in reaching this goal is that for the same patient, different underlying pathologic conditions (eg, sepsis or ventilator-associated muscle injury) may require different levels of support. Second, many of the measurements of pressure generation and effort have been confined to the research laboratory. Modifications of the technology to achieve accurate measurements in the intensive care unit-outside of the research laboratory--are needed. To facilitate individual titration of ventilator settings, the new technologies must provide easier access to quantification of drive, pressure output, and effort. Finally, more research is needed to define the effect of monitoring respiratory output on patient outcome and containment of costs.

We present a case of unilateral airflow obstruction during forced exhalations. The patient presented with episodic dyspnea and wheezing, particularly when he lay in the right lateral decubitus position. Spirometry revealed symmetric, marked reductions in forced expiratory volume in the first second and forced vital capacity values, while plethysmography demonstrated a near-normal total lung capacity. Bronchoscopy revealed a polypoid lesion in the right main bronchus, of which biopsy specimens demonstrated adenoid cystic carcinoma. Following a right pneumonectomy, total lung capacity was markedly reduced; interestingly, however, spirometry was essentially unchanged. This case is an elegant illustration of the effects of respiratory maneuvers and body position on airway caliber.