Management strategies to effect change in intensive care units: lessons from the world of business. Part I. Targeting quality improvement initiatives.

The business community has developed strategies to ensure the quality of the goods or services they produce and to improve the management of multidisciplinary work teams. With modification, many of these techniques can be imported into intensive care units (ICUs) to improve clinical operations and patient safety. In Part I of a three-part ATS Seminar series, we argue for adopting business management strategies in ICUs and set forth strategies for targeting selected quality improvement initiatives. These tools are relevant to health care today as focus is placed on limiting low-value care and measuring, reporting, and improving quality. In the ICU, the complexity of illness and the need to standardize processes make these tools even more appealing. Herein, we highlight four techniques to help prioritize initiatives. First, the "80/20 rule" mandates focus on the few (20%) interventions likely to drive the majority (80%) of improvement. Second, benchmarking--a process of comparison with peer units or institutions--is essential to identifying areas of strength and weakness. Third, root cause analyses, in which structured retrospective reviews of negative events are performed, can be used to identify and fix systems errors. Finally, failure mode and effects analysis--a process aimed at prospectively identifying potential sources of error--allows for systems fixes to be instituted in advance to prevent negative outcomes. These techniques originated in fields other than health care, yet adoption has and can help ICU managers prioritize issues for quality improvement.

Management strategies to effect change in intensive care units: lessons from the world of business. Part III. Effectively effecting and sustaining change.

Reaping the optimal rewards from any quality improvement project mandates sustainability after the initial implementation. In Part III of this three-part ATS Seminars series, we discuss strategies to create a culture for change, improve cooperation and interaction between multidisciplinary teams of clinicians, and position the intensive care unit (ICU) optimally within the hospital environment. Coaches are used throughout other industries to help professionals assess and continually improve upon their practice; use of this strategy is as of yet infrequent in health care, but would be easily transferable and potentially beneficial to ICU managers and clinicians alike. Similarly, activities focused on improving teamwork are commonplace outside of health care. Simulation training and classroom education about key components of successful team functioning are known to result in improvements. In addition to creating an ICU environment in which individuals and teams of clinicians perform well, ICU managers must position the ICU to function well within the hospital system. It is important to move away from the notion of a standalone ("siloed") ICU to one that is well integrated into the rest of the institution. Creating a "pull-system" (in which participants are active in searching out needed resources and admitting patients) can help ICU managers both provide better care for the critically ill and strengthen relationships with non-ICU staff. Although not necessary, there is potential upside to creating a unified critical care service to assist with achieving these ends.

Management strategies to effect change in intensive care units: lessons from the world of business. Part II. Quality-improvement strategies.

The success of quality-improvement projects relies heavily on both project design and the metrics chosen to assess change. In Part II of this three-part American Thoracic Society Seminars series, we begin by describing methods for determining which data to collect, tools for data presentation, and strategies for data dissemination. As Avedis Donabedian detailed a half century ago, defining metrics in healthcare can be challenging; algorithmic determination of the best type of metric (outcome, process, or structure) can help intensive care unit (ICU) managers begin this process. Choosing appropriate graphical data displays (e.g., run charts) can prompt discussions about and promote quality improvement. Similarly, dashboards/scorecards are useful in presenting performance improvement data either publicly or privately in a visually appealing manner. To have compelling data to show, ICU managers must plan quality-improvement projects well. The second portion of this review details four quality-improvement tools-checklists, Six Sigma methodology, lean thinking, and Kaizen. Checklists have become commonplace in many ICUs to improve care quality; thinking about how to maximize their effectiveness is now of prime importance. Six Sigma methodology, lean thinking, and Kaizen are techniques that use multidisciplinary teams to organize thinking about process improvement, formalize change strategies, actualize initiatives, and measure progress. None originated within healthcare, but each has been used in the hospital environment with success. To conclude this part of the series, we demonstrate how to use these tools through an example of improving the timely administration of antibiotics to patients with sepsis.

Prenatal and postnatal polycyclic aromatic hydrocarbon exposure, airway hyperreactivity, and Beta-2 adrenergic receptor function in sensitized mouse offspring.

Despite data associating exposure to traffic-related polycyclic aromatic hydrocarbons (PAH) in asthma, mechanistic support has been limited. We hypothesized that both prenatal and early postnatal exposure to PAH would increase airway hyperreactivity (AHR) and that the resulting AHR may be insensitive to treatment with a ß 2AR agonist drug, procaterol. Further, we hypothesized that these exposures would be associated with altered ß 2AR gene expression and DNA methylation in mouse lungs. Mice were exposed prenatally or postnatally to a nebulized PAH mixture versus negative control aerosol 5 days a week. Double knockout ß 2AR mice were exposed postnatally only. Prenatal exposure to PAH was associated with reduced ß 2AR gene expression among nonsensitized mice offspring, but not increases in DNA methylation or AHR. Postnatal exposure to PAH was borderline associated with increased AHR among sensitized wildtype, but not knockout mice. In the first study that delivers PAH aerosols to mice in a relatively physiological manner, small effects on AHR and ß 2AR gene expression, but not ß 2AR agonist drug activity, were observed. If confirmed, the results may suggest that exposure to PAH, common ambient urban pollutants, affects ß 2AR function, although the impact on the efficacy of ß 2AR agonist drugs used in treating asthma remains uncertain.

The use of nonphysician providers in adult intensive care units.

In the United States there are not currently enough critical care-trained practitioners to provide care to all critically ill patients. With calls for "high-intensity" staffing and 24-hour coverage of our intensive care units, the board-certified intensivists we do have are being stretched ever more thin. Nonphysician providers (physician assistants and nurse practitioners) are being used with increasing frequency in critical care settings to provide care to critically ill patients. In this review, we explore the impact of introducing nonphysician providers into the adult intensive care unit.

Polycyclic aromatic hydrocarbons impair function of ß2-adrenergic receptors in airway epithelial and smooth muscle cells.

Incomplete combustion produces a pollutant mixture that includes polycyclic aromatic hydrocarbons (PAHs). Previous work by the Columbia Center for Children's Environmental Health (CCCEH) and others linked exposure to PAH with symptoms of asthma and other adverse health effects in young children. Inhaled ß(2)-adrenergic agonists are mainstays in the treatment of reactive airway diseases. These exogenous catecholamines engage membrane-bound ß(2)-adrenergic receptors (ß(2)AR) on airway epithelial and smooth muscle cells to cause airway dilation. We hypothesized that exposure to PAH might similarly interfere with the function of ß(2)AR in airway epithelial or smooth muscle cells, reducing the efficacy of a medication important for the treatment of asthma symptoms. A PAH mixture was devised, based on ambient levels measured prenatally among a cohort of pregnant women participating at the CCCEH. Primary airway epithelial and smooth muscle cells were exposed to varying concentrations of the PAH mixture, and expression, function, and signaling of ß(2)AR were assessed. Murine tracheal epithelial cells and human airway smooth muscle cells, after exposure to a PAH mixture, exhibited reduced expression and function of ß(2)AR. These findings support our hypothesis that environmentally relevant PAHs can impede ß(2)AR-mediated airway relaxation, and suggest a new paradigm where air pollutants not only contribute to the pathogenesis of childhood asthma, but also diminish responsiveness to standard therapy.

Impact of nonphysician staffing on outcomes in a medical ICU.

BACKGROUND: As the number of ICU beds and demand for intensivists increase, alternative solutions are needed to provide coverage for critically ill patients. The impact of different staffing models on the outcomes of patients in the medical ICU (MICU) remains unknown. In our study, we compare outcomes of nonphysician provider-based teams to those of medical house staff-based teams in the MICU. METHODS: We conducted a retrospective review of 590 daytime (7:00 am-7:00 pm) admissions to two MICUs at one hospital. In one MICU staffed by nurse practitioners and physician assistants (MICU-NP/PA) there were nonphysicians (nurse practitioners and physicians assistants) during the day (7:00 am-7:00 pm) with attending physician coverage overnight. In the other MICU, there were medicine residents (MICU-RES) (24 h/d). The outcomes investigated were hospital mortality, length of stay (LOS) (ICU, hospital), and posthospital discharge destination. RESULTS: Three hundred two patients were admitted to the MICU-NP/PA and 288 to the MICU-RES. Mortality probability model III (MPM(0)-III) predicted mortality was similar (P = .14). There was no significant difference in hospital mortality (32.1% for MICU-NP/PA vs 32.3% for MICU-RES, P = .96), MICU LOS (4.22 ± 2.51 days for MICU-NP/PA vs 4.44 ± 3.10 days for MICU-RES, P = .59), or hospital LOS (14.01 ± 2.92 days for MICU-NP/PA vs 13.74 ± 2.94 days for MICU-RES, P = .86). Discharge to a skilled care facility (vs home) was similar (37.1% for MICU-NP/PA vs 32.5% for MICU-RES, P = .34). After multivariate adjustment, MICU staffing type was not associated with hospital mortality (P = .26), MICU LOS (P = .29), hospital LOS (P = .19), or posthospital discharge destination (P = .90). CONCLUSIONS: Staffing models including daytime use of nonphysician providers appear to be a safe and effective alternative to the traditional house staff-based team in a high-acuity, adult ICU.

Coma with absent brainstem reflexes resulting from zolpidem overdose.

Zolpidem is a nonbenzodiazepine hypnotic with a favorable adverse effect profile. There are single reports of respiratory decompensation associated with zolpidem overdose. We report a case ofa young woman with depression who developed deep coma with respiratory failure and a loss of brainstem reflexes as a result of zolpidem overdose. Supportive management led to a complete recovery of neurologic function. Acute zolpidem overdose should be considered in the differential diagnosis of coma with absent brainstem reflexes.

Prenatal allergen and diesel exhaust exposure and their effects on allergy in adult offspring mice.

BACKGROUND: Multiple studies have suggested that prenatal exposure to either allergens or air pollution may increase the risk for the development of allergic immune responses in young offspring. However, the effects of prenatal environmental exposures on adult offspring have not been well-studied. We hypothesized that combined prenatal exposure to Aspergillus fumigatus (A. fumigatus) allergen and diesel exhaust particles will be associated with altered IgE production, airway inflammation, airway hyperreactivity (AHR), and airway remodeling of adult offspring. METHODS: Following sensitization via the airway route to A. fumigatus and mating, pregnant BALB/c mice were exposed to additional A. fumigatus and/or diesel exhaust particles. At age 9-10 weeks, their offspring were sensitized and challenged with A. fumigatus. RESULTS: We found that adult offspring from mice that were exposed to A. fumigatus or diesel exhaust particles during pregnancy experienced decreases in IgE production. Adult offspring of mice that were exposed to both A. fumigatus and diesel exhaust particles during pregnancy experienced decreases in airway eosinophilia. CONCLUSION: These results suggest that, in this model, allergen and/or diesel administration during pregnancy may be associated with protection from developing systemic and airway allergic immune responses in the adult offspring.

Vascular inflammation in obesity and sleep apnea.

BACKGROUND: Unrecognized obstructive sleep apnea (OSA) is highly prevalent in obesity. Both obesity and OSA are associated with vascular endothelial inflammation and increased risk for cardiovascular diseases. We investigated directly whether the endothelial alterations that are attributed commonly to obesity are in fact related to OSA. METHODS AND RESULTS: Seventy-one subjects with a body mass index ranging from normal to obese underwent attended polysomnography. To assess vascular inflammation and oxidative stress directly, we quantified the expression of nuclear factor-kappaB and nitrotyrosine by immunofluorescence in freshly harvested venous endothelial cells. To evaluate basal endothelial nitric oxide (NO) production and activity, we quantified the expression of endothelial NO synthase (eNOS) and phosphorylated eNOS. Vascular reactivity was measured by brachial artery flow-mediated dilation. Expression of eNOS and phosphorylated eNOS and flow-mediated dilation were significantly lower, whereas expression of nitrotyrosine was significantly greater in OSA patients (n=38) than in OSA-free subjects (n=33) regardless of central adiposity. Expression of nuclear factor-kappaB was greater in obese OSA patients than in obese OSA-free subjects (P=0.004). Protein expression and flow-mediated dilation were not significantly affected by increasing body mass index or central obesity in OSA patients and in OSA-free subjects. After 4 weeks of continuous positive airway pressure therapy, flow-mediated dilation and expression of eNOS and phosphorylated eNOS significantly increased whereas expression of nitrotyrosine and nuclear factor-kappaB significantly decreased in OSA patients who adhered to continuous positive airway pressure >/=4 hours daily. CONCLUSIONS: Untreated OSA rather than obesity is a major determinant of vascular endothelial dysfunction, inflammation, and elevated oxidative stress in obese patients.

Relationship between ICU design and mortality.

BACKGROUND: Architectural design of health-care facilities can influence patient safety; however, it is unknown whether patient outcomes are significantly affected by ICU design. METHODS: Six hundred sixty-four patients admitted to the medical ICU (MICU) of Columbia University Medical Center during 2008 were included in this retrospective study. Patient outcome measures, which included hospital mortality, ICU mortality, ICU length of stay (LOS), and ventilator-free days, were compared based on random room assignment. Rooms that were not visible from the MICU central nursing station were designated as low-visible rooms (LVRs), whereas the remaining rooms were designated as high-visible rooms (HVRs). RESULTS: Overall hospital mortality did not differ among patients assigned to LVRs vs HVRs; however, severely ill patients (those with Acute Physiology and Chronic Health Evaluation II scores > 30) had significantly higher hospital mortality when admitted to an LVR than did similarly ill patients admitted to an HVR (82.1% and 64.0%, n = 39 and 75, respectively; P = .046). ICU mortality showed a similar pattern. ICU LOS and ventilator-free days did not differ significantly between groups. CONCLUSIONS: Severely ill patients may experience higher mortality rates when assigned to ICU rooms that are poorly visualized by nursing staff and physicians.

Endothelial repair capacity and apoptosis are inversely related in obstructive sleep apnea.

PURPOSE: To investigate the impact of obstructive sleep apnea (OSA) on endothelial repair capacity and apoptosis in the absence of potentially confounding factors including obesity. PATIENTS AND METHODS: Sixteen patients with a body mass index <30 and newly diagnosed OSA and 16 controls were studied. Circulating levels of endothelial progenitor cells, a marker of endothelial repair capacity, and endothelial microparticles, a marker of endothelial apoptosis, were quantified before and after four-week therapy with continuous positive airway pressure (CPAP). Endothelial cell apoptotic rate was also quantified in freshly harvested venous endothelial cells. Vascular reactivity was measured by flow-mediated dilation. RESULTS: Before treatment, endothelial microparticle levels were greater and endothelial progenitor cell levels were lower in patients with OSA than in controls (P < 0.001 for both). Levels of endothelial microparticles and progenitors cells were inversely related (r = -0.67, P < 0.001). Endothelial progenitor cell levels increased after effective treatment (P = 0.036). CONCLUSIONS: In the absence of any co-morbid conditions including obesity, OSA alone impairs endothelial repair capacity and promotes endothelial apoptosis. These early endothelial alterations may underlie accelerated atherosclerosis and increased cardiovascular risk in OSA.

Inflammation, oxidative stress, and repair capacity of the vascular endothelium in obstructive sleep apnea.

BACKGROUND: Indirect evidence implicates endothelial dysfunction in the pathogenesis of vascular diseases associated with obstructive sleep apnea (OSA). We investigated directly whether dysfunction and inflammation occur in vivo in the vascular endothelium of patients with OSA. The effects of continuous positive airway pressure (CPAP) therapy on endothelial function and repair capacity were assessed. METHODS AND RESULTS: Thirty-two patients with newly diagnosed OSA and 15 control subjects were studied. Proteins that regulate basal endothelial nitric oxide (NO) production (endothelial NO synthase [eNOS] and phosphorylated eNOS) and inflammation (cyclooxygenase-2 and inducible NOS) and markers of oxidative stress (nitrotyrosine) were quantified by immunofluorescence in freshly harvested venous endothelial cells before and after 4 weeks of CPAP therapy. Vascular reactivity was measured by flow-mediated dilation. Circulating endothelial progenitor cell levels were quantified to assess endothelial repair capacity. Baseline endothelial expression of eNOS and phosphorylated eNOS was reduced by 59% and 94%, respectively, in patients with OSA compared with control subjects. Expression of both nitrotyrosine and cyclooxygenase-2 was 5-fold greater in patients with OSA than in control subjects, whereas inducible NOS expression was 56% greater. Expression of eNOS and phosphorylated eNOS significantly increased, whereas expression of nitrotyrosine, cyclooxygenase-2, and inducible NOS significantly decreased in patients who adhered to CPAP > or = 4 hours daily. Baseline flow-mediated dilation and endothelial progenitor cell levels were lower in patients than in control subjects, and both significantly increased in patients who adhered to CPAP > or = 4 hours daily. CONCLUSIONS: OSA directly affects the vascular endothelium by promoting inflammation and oxidative stress while decreasing NO availability and repair capacity. Effective CPAP therapy is associated with the reversal of these alterations.

Clinical review: airway hygiene in the intensive care unit.

Maintenance of airway secretion clearance, or airway hygiene, is important for the preservation of airway patency and the prevention of respiratory tract infection. Impaired airway clearance often prompts admission to the intensive care unit (ICU) and can be a cause and/or contributor to acute respiratory failure. Physical methods to augment airway clearance are often used in the ICU but few are substantiated by clinical data. This review focuses on the impact of oral hygiene, tracheal suctioning, bronchoscopy, mucus-controlling agents, and kinetic therapy on the incidence of hospital-acquired respiratory infections, length of stay in the hospital and the ICU, and mortality in critically ill patients. Available data are distilled into recommendations for the maintenance of airway hygiene in ICU patients.

Overexpression of the Na-K-ATPase alpha2-subunit improves lung liquid clearance during ventilation-induced lung injury.

Mechanical ventilation with high tidal volumes (HV(T)) impairs lung liquid clearance (LLC) and downregulates alveolar epithelial Na-K-ATPase. We have previously reported that the Na-K-ATPase alpha(2)-subunit contributes to LLC in normal rat lungs. Here we tested whether overexpression of Na-K-ATPase alpha(2)-subunit in the alveolar epithelium would increase clearance in a HV(T) model of lung injury. We infected rat lungs with a replication-incompetent adenovirus that expresses Na-K-ATPase alpha(2)-subunit gene (Adalpha(2)) 7 days before HV(T) mechanical ventilation. HV(T) ventilation decreased LLC by approximately 50% in untreated, sham, and Adnull-infected rats. Overexpression of Na-K-ATPase alpha(2)-subunit prevented the decrease in clearance caused by HV(T) and was associated with significant increases in Na-K-ATPase alpha(2) protein abundance and activity in peripheral lung basolateral membrane fractions. Ouabain at 10(-5) M, a concentration that inhibits the alpha(2) but not the Na-K-ATPase alpha(1), decreased LLC in Adalpha(2)-infected rats to the same level as sham and Adnull-infected lungs, suggesting that the increased clearance in Adalpha(2) lungs was due to Na-K-ATPase alpha(2) expression and activity. In summary, we provide evidence that augmentation of the Na-K-ATPase alpha(2)-subunit, via gene transfer, may accelerate LLC in the injured lung.

Alveolar epithelial beta2-adrenergic receptors.

beta(2)-adrenergic receptors are present throughout the lung, including the alveolar airspace, where they play an important role for regulation of the active Na(+) transport needed for clearance of excess fluid out of alveolar airspace. beta(2)-adrenergic receptor signaling is required for up-regulation of alveolar epithelial active ion transport in the setting of excess alveolar edema. The positive, protective effects of beta(2)-adrenergic receptor signaling on alveolar active Na(+) transport in normal and injured lungs provide substantial support for the use of beta-adrenergic agonists to accelerate alveolar fluid clearance in patients with cardiogenic and noncardiogenic pulmonary edema. In this review, we summarize the role of beta(2)-adrenergic receptors in the alveolar epithelium with emphasis on their role in the regulation of alveolar active Na(+) transport in normal and injured lungs.