Adoption of low tidal volume ventilation in the emergency department: A quality improvement intervention.

BACKGROUND: Ventilator tidal volumes of >8 mL/kg of predicted body weight (PBW) may increase the risk of lung injury. We sought to evaluate the impact of a quality improvement intervention among intubated Emergency Department (ED) patients to protocolize the prescription of low tidal volume ventilation. METHODS: In this before-and-after study, the average tidal volume delivered to ED patients receiving volume assist-control ventilation was compared before (2007-2014) and after (2015-2016) implementation of a ventilator initiation protocol (the quality improvement intervention). The intervention emphasized 1) measurement of the patient's height to calculate PBW and therefore tailor the tidal volume to estimated lung size (<8 mL/kg PBW), and 2) focused education and reference materials for ED physicians and respiratory therapists. RESULTS: Among ventilated ED patients meeting inclusion criteria in the before (N = 2185) and after (N = 774) cohorts, the mean (±SD) tidal volume decreased from 9.0 ±â€¯1.4 mL/kg to 7.2 ±â€¯0.9 mL/kg PBW following the intervention (absolute difference 1.8 mL/kg, 95% confidence interval 1.7 to 1.9 mL/kg, p < 0.001). The proportion of patients receiving low tidal volume ventilation increased after the intervention (72%), as compared to before (23%). Low tidal volume ventilation continued to be utilized at 24 h after ICU admission in patients who remained intubated in the cohort following the intervention (mean tidal volume 7.3 mL/kg PBW). CONCLUSIONS: Pairing a ventilator initiation protocol with focused education and resources for emergency physicians and respiratory therapists was associated with a significant reduction in tidal volume delivered to ED patients.

Impact of Chest Wall Modifications and Lung Injury on the Correspondence Between Airway and Transpulmonary Driving Pressures.

OBJECTIVE: Recent interest has arisen in airway driving pressure (DP(AW)), the quotient of tidal volume (V(T)), and respiratory system compliance (C(RS)), which could serve as a direct and easily measured marker for ventilator-induced lung injury risk. We aimed to test the correspondence between DP(AW) and transpulmonary driving pressure (DP(TP))-the quotient of V(T) and lung compliance (C(L)), in response to intra-abdominal hypertension and changes in positive end-expiratory pressure during different models of lung pathology. DESIGN: Well-controlled experimental setting that allowed reversible modification of chest wall compliance (C(CW)) in a variety of models of lung pathology. SETTING: Large animal laboratory of a university-affiliated hospital. SUBJECTS: Ten deeply anesthetized swine. INTERVENTIONS: Application of intra-abdominal pressures of 0 and 20 cm H2O at positive end-expiratory pressure of 1 and 10 cm H2O, under volume-controlled mechanical ventilation in the settings of normal lungs (baseline), unilateral whole-lung atelectasis, and unilateral and bilateral lung injuries caused by saline lavage. MEASUREMENTS AND MAIN RESULTS: Pulmonary mechanics including esophageal pressure and calculations of DP(AW), DP(TP), C(RS), C(L), and C(CW). When compared with normal intra-abdominal pressures, intra-abdominal hypertension increased DP(AW), during both "normal lung conditions" (p < 0.0001) and "unilateral atelectasis" (p = 0.0026). In contrast, DP(TP) remained virtually unaffected by changes in positive end-expiratory pressure or intra-abdominal pressures in both conditions. During unilateral lung injury, both DPA(W) and DP(TP) were increased by the presence of intra-abdominal hypertension (p < 0.0001 and p = 0.0222, respectively). During bilateral lung injury, intra-abdominal hypertension increased both DP(AW) (at positive end-expiratory pressure of 1 cm H2O, p < 0.0001; and at positive end-expiratory pressure of 10 cm H2O, p = 0.0091) and DP(TP) (at positive end-expiratory pressure of 1 cm H2O, p = 0.0510; and at positive end-expiratory pressure of 10 cm H2O, p = 0.0335). CONCLUSIONS: Our data indicate that DP(AW) is influenced by reductions in chest wall compliance and by underlying lung properties. As with other measures of pulmonary mechanics that are based on unmodified P(AW), caution is advised in attempting to attribute hazard or safety to any specific absolute value of DP(AW).

Value and limitations of transpulmonary pressure calculations during intra-abdominal hypertension.

OBJECTIVE: To clarify the effect of progressively increasing intra-abdominal pressure on esophageal pressure, transpulmonary pressure, and functional residual capacity. DESIGN: Controlled application of increased intra-abdominal pressure at two positive end-expiratory pressure levels (1 and 10 cm H2O) in an anesthetized porcine model of controlled ventilation. SETTING: Large animal laboratory of a university-affiliated hospital. SUBJECTS: Eleven deeply anesthetized swine (weight 46.2 ± 6.2 kg). INTERVENTIONS: Air-regulated intra-abdominal hypertension (0-25 mm Hg). MEASUREMENTS: Esophageal pressure, tidal compliance, bladder pressure, and end-expiratory lung aeration by gas dilution. MAIN RESULTS: Functional residual capacity was significantly reduced by increasing intra-abdominal pressure at both positive end-expiratory pressure levels (p ≤ 0.0001) without corresponding changes of end-expiratory esophageal pressure. Above intra-abdominal pressure 5 mm Hg, plateau airway pressure increased linearly by ~ 50% of the applied intra-abdominal pressure value, associated with commensurate changes of esophageal pressure. With tidal volume held constant, negligible changes occurred in transpulmonary pressure due to intra-abdominal pressure. Driving pressures calculated from airway pressures alone (plateau airway pressure--positive end-expiratory pressure) did not equate to those computed from transpulmonary pressure (tidal changes in transpulmonary pressure). Increasing positive end-expiratory pressure shifted the predominantly negative end-expiratory transpulmonary pressure at positive end-expiratory pressure 1 cm H2O (mean -3.5 ± 0.4 cm H2O) into the positive range at positive end-expiratory pressure 10 cm H2O (mean 0.58 ± 1.2 cm H2O). CONCLUSIONS: Despite its insensitivity to changes in functional residual capacity, measuring transpulmonary pressure may be helpful in explaining how different levels of positive end-expiratory pressure influence recruitment and collapse during tidal ventilation in the presence of increased intra-abdominal pressure and in calculating true transpulmonary driving pressure (tidal changes of transpulmonary pressure). Traditional interpretations of respiratory mechanics based on unmodified airway pressure were misleading regarding lung behavior in this setting.

Experimental intra-abdominal hypertension attenuates the benefit of positive end-expiratory pressure in ventilating effusion-compressed lungs*.

OBJECTIVE: To test the ability of positive end-expiratory pressure to offset the reduction of resting lung volume caused by intra abdominal hypertension, unilateral pleural effusion, and their combination. DESIGN: : Controlled application of intrapleural fluid, raised abdominal pressure and their combination before and after positive end-expiratory pressure in an anesthetized porcine model of controlled ventilation. SETTING: Large animal laboratory of a university-affiliated hospital. SUBJECTS: Fourteen deeply anesthetized swine (weight 30-35 kg). INTERVENTIONS: Unilateral pleural effusion instillation (13 mL/kg), intra-abdominal hypertension (15 mm Hg), and simultaneous pleural effusion/intra abdominal hypertension. MEASUREMENTS: Tidal compliance, end-expiratory lung aeration by gas dilution functional residual capacity, and quantitative analyses of computerized tomograms of the lungs at the extremes of the tidal cycle. MAIN RESULTS: Positive end-expiratory pressure of 10 cm H2O (positive end-expiratory pressure 10) increased mean functional residual capacity by 368 mL when pleural effusion was present and by 184 mL when intra-abdominal hypertension was present. When pleural effusion and intra-abdominal hypertension were simultaneously applied, positive end-expiratory pressure 10 failed to improve tidal compliance and increased functional residual capacity by only 77 mL, whereastidal recruitment during ventilation remained substantial. CONCLUSIONS: The presence of intra-abdominal hypertension negates most of the positive end-expiratory pressure 10 benefit in reversing pleural effusion-induced de-recruitment. Relief of intra-abdominal hypertension may be instrumental to the treatment of pleural effusion-associated lung restriction and cyclical tidal collapse and reopening.

Agreement between functional residual capacity estimated via automated gas dilution versus via computed tomography in a pleural effusion model.

BACKGROUND: The measurement of functional residual capacity (FRC) in ventilated patients could help track the extent of acute lung disease, monitor recruitment of unstable lung units, or guide the use of PEEP. Quantitative analysis of computed tomography (CT) images of the lungs is currently the accepted standard for FRC measurement (FRC-CT), but is impractical for routine use. Gas dilution and gas tracer technologies, while attractive for research applications, require specialized equipment and skills missing from the clinical setting. We simultaneously evaluated FRC-CT and FRC determined by a ventilator-incorporated wash-in/wash-out (FRC-WI/WO) method in an animal model of unilateral pleural effusion that varied the fluid volume instilled and the applied PEEP. METHODS: A swine model (n = 6) of unilateral pleural effusion was created by injecting boluses of radio-opaque fluid (iopromide) (13 mL/kg and then 26 mL/kg) into the right thoracic cavity. FRC-CT and FRC-WI/WO were simultaneously obtained, at 2 PEEP levels, at baseline and at both pleural-effusion volumes. RESULTS: A correlation coefficient (r²) of 0.89 between FRC-CT and FRC-WI/WO revealed concordance between the techniques, with directional agreement and acceptable bias and precision under all tested conditions. CONCLUSIONS: We found excellent concordance between FRC-WI/WO and FRC-CT in an animal model of unilateral pleural effusion that stressed the capability of this technology. The technical advantage of the wash-in/wash-out technique is its incorporation into ventilator operation without requiring adjustments to ventilation.

Ventilation patterns influence airway secretion movement.

BACKGROUND: Retention of airway secretions is a common and serious problem in ventilated patients. Treating or avoiding secretion retention with mucus thinning, patient-positioning, airway suctioning, or chest or airway vibration or percussion may provide short-term benefit. METHODS: In a series of laboratory experiments with a test-lung system we examined the role of ventilator settings and lung-impedance on secretion retention and expulsion. Known quantities of a synthetic dye-stained mucus simulant with clinically relevant properties were injected into a transparent tube the diameter of an adult trachea and exposed to various mechanical-ventilation conditions. Mucus-simulant movement was measured with a photodensitometric technique and examined with image-analysis software. We tested 2 mucus-simulant viscosities and various peak flows, inspiratory/expiratory flow ratios, intrinsic positive end-expiratory pressures, ventilation waveforms, and impedance values. RESULTS: Ventilator settings that produced flow bias had a major effect on mucus movement. Expiratory flow bias associated with intrinsic positive end-expiratory pressure generated by elevated minute ventilation moved mucus toward the airway opening, whereas intrinsic positive end-expiratory pressure generated by increased airway resistance moved the mucus toward the lungs. Inter-lung transfer of mucus simulant occurred rapidly across the "carinal divider" between interconnected test lungs set to radically different compliances; the mucus moved out of the low-compliance lung and into the high-compliance lung. CONCLUSIONS: The movement of mucus simulant was influenced by the ventilation pattern and lung impedance. Flow bias obtained with ventilator settings may clear or embed mucus during mechanical ventilation.

Positional effects on the distributions of ventilation and end-expiratory gas volume in the asymmetric chest-a quantitative lung computed tomographic analysis.

BACKGROUND: Body positioning affects the configuration and dynamic properties of the chest wall and therefore may influence decisions made to increase or decrease ventilating pressures and tidal volume. We hypothesized that unlike global functional residual capacity (FRC), component sector gas volumes and their corresponding regional tidal expansions would vary markedly in the setting of unilateral pleural effusion (PLEF), owing to shifting distributions of aeration and collapse as posture changed. METHODS: Six deeply anesthetized swine underwent tracheostomy, thoracostomy, and experimental PLEF with 10 mL/kg of radiopaque isotonic fluid randomly instilled into either pleural space. Animals were ventilated at VT = 10 mL/kg, frequency = 15 bpm, I/E = 1:2, PEEP = 1 cmH2O, and FiO2 = 0.5. Quantitative lung computed tomographic (CT) analysis of regional aeration and global FRC measurements by nitrogen wash-in/wash-out technique was performed in each of these randomly applied positions: semi-Fowler's (inclined 30° from horizontal in the sagittal plane); prone, supine, and lateral positions with dependent PLEF and non-dependent PLEF. RESULTS: No significant differences in total FRC were observed among the horizontal positions, either at baseline (p = 0.9037) or with PLEF (p = 0.58). However, component sector total gas volumes in each phase of the tidal cycle were different within all studied positions with and without PLEF (p = < .01). Compared to other positions, prone and lateral positions with non-dependent PLEF had more homogenous VT distributions among quadrants (p = .051). Supine position was associated with most dependent collapse and greatest tendency for tidal recruitment (48 vs ~ 22%, p = 0.0073). CONCLUSIONS: Changes in body position in the setting of effusion-caused chest asymmetry markedly affected the internal distributions of gas volume, collapse, ventilation, and tidal recruitment, even though global FRC measurements provided little indication of these potentially important positional changes.

Time course of physiologic variables in response to ventilator-induced lung injury.

BACKGROUND: The time course of the physiological derangements that result from ventilator-induced lung injury has not been adequately described. Similarly, the regional topographies of pleural pressure and tissue edema have not been carefully mapped for this injury process. METHODS: Lung injury was induced in 9 normal pigs by ventilating for 6 hours at a transpulmonary pressure of 35 cm H(2)O, with the animals in the supine position. Eight additional normal pigs received right thoracotomy to place pleural-surface-pressure sensors prior to an identical period and intensity of injurious ventilation. Gas exchange and lung mechanics were tracked in all the animals. Cytokines (tumor necrosis factor alpha, interleukin 6, and interleukin 8) in peripheral blood were assayed at 2 hour intervals, beginning at the onset of mechanical ventilation, from all the animals. RESULTS: After a brief "induction" period, P(aO(2)) and tidal volume declined steadily in the animals that were ventilated to induce lung injury. The rate of decline was greater in the animals that received thoracotomy. The pleural pressure gradient steadily increased from ventral to dorsal. The serum cytokine levels did not evolve with developing injury, but cytokines were elevated at the onset of ventilation. Tissue edema, as assessed by the ratio of wet weight to dry weight, was greater in the thoracotomized animals than in the nonthoracotomized animals, and tissue edema tended to be greater in the caudal lung regions than in the cephalad lung regions. CONCLUSIONS: Following the induction period, the development of ventilator-induced lung injury progressed steadily and then plateaued, as assessed by quantitative physiology variables during 6 hours of ventilation at a transpulmonary pressure of 35 cm H(2)O. Greater injury developed in animals that had a coexisting potential insult (thoracotomy). Injury development was not paralleled by bloodborne inflammatory cytokines.

A proposed curvilinearity index for quantifying airflow obstruction.

BACKGROUND: Though forced expiratory volume in the first second (FEV(1)) is the primary indicator of airway obstruction, curvilinearity in the expiratory flow-volume curve is used to support the quantitative assessment of obstruction via FEV(1). Currently there is no available index to quantify a pathological contour of curvilinearity. STUDY PURPOSE: We propose a "curvature" index (k(max)) and compare FEV(1) values to the index with a sequential sample of spirometry data. METHODS: The hyperbolic function b(0)Q + b(1)Q V + b(2)V = 1 (in which Q = flow rate, V = volume, and b(0), b(1), and b(2) are estimated from the patient's flow-volume data) is fit to a fixed segment of the descending phase of the expiratory flow-volume curve. A previously developed biomechanical interpretation of this relationship associates the coefficient b(1) with the rate of airway-resistance-increase as exhaled volume increases. A global curvature index k(max)=b(1)/2(b(0)b(2)+b(1)) is defined to quantify the curvilinearity phenomenon. We used statistics software to determine the k(max) of spirometry data from 67 sequential patients, and to determine the relationship of k(max) to FEV(1). RESULTS: Individual k(max) estimates appeared to correspond well with the degree of curvilinearity observed and were related in an exponential manner to FEV(1). CONCLUSIONS: We defined a curvature index to quantify the curvilinearity phenomenon observed in the expiratory limb of flow-volume loops from patients with obstructive lung disease. This index uses data from a major segment of the flow-volume curve, and our preliminary data indicate an exponential relationship with FEV(1). This new index allows the putative association between curvilinearity and obstructive lung disease to be examined quantitatively in clinical practice and future studies.

The Effect of Compartmental Asymmetry on the Monitoring of Pulmonary Mechanics and Lung Volumes.

BACKGROUND: Esophageal pressure measurement for computation of transpulmonary pressure (Ptp) has begun to be incorporated into clinical use for evaluating forces across the lungs. Gaps exist in our understanding of how esophageal pressure (and therefore Ptp), a value measured at a single site, responds when respiratory system compartments are asymmetrically affected by whole-lung atelectasis or unilateral injury as well as changes in chest wall compliance. We reasoned that Ptp would track with aerated volume changes as estimated by functional residual capacity (FRC) and tidal volume. We examined this hypothesis in the setting of asymmetric lungs and changes in intra-abdominal pressure. METHODS: This study was conducted in the animal laboratory of a university-affiliated hospital. Models of unilateral atelectasis and unilateral and bilateral lung injury exposed to intra-abdominal hypertension (IAH) in 10 deeply sedated mechanically ventilated swine. Atelectasis was created by balloon occlusion of the left main bronchus. Unilateral lung injury was induced by saline lavage of isolated right lung. Diffuse lung injury was induced by saline lavage of both lungs. The peritoneum was insufflated with air to create a model of pressure-regulated IAH. We measured esophageal pressures, airway pressures, FRC by gas dilution, and oxygenation. RESULTS: FRC was reduced by IAH in normal lungs (P < .001) and both asymmetric lung pathologies (P < .001). Ptp at end-expiration was decreased by IAH in bilateral (P = .001) and unilateral lung injury (P = .003) as well as unilateral atelectasis (P = .019). In the setting of both lung injury models, end-expiratory Ptp showed a moderate correlation in tracking with FRC. CONCLUSIONS: Ptp tracks with aerated lung volume in the setting of thoracic asymmetry and changes in intra-abdominal pressure. However, used alone, it cannot distinguish the relative contributions of air-space distention and recruitment of lung units.

Evaluation of resistance in 8 different heat-and-moisture exchangers: effects of saturation and flow rate/profile.

INTRODUCTION: When endotracheal intubation is required during ventilatory support, the physiologic mechanisms of heating and humidifying the inspired air related to the upper airways are bypassed. The task of conditioning the air can be partially accomplished by heat-and-moisture exchangers (HMEs). OBJECTIVES: To evaluate and compare with respect to imposed resistance, different types/models of HME: (1) dry versus saturated, (2) changing inspiratory flow rates. MATERIALS AND METHODS: Eight different HMEs were studied using a lung model system. The study was conducted initially by simulating spontaneous breathing, followed by connecting the system directly to a mechanical ventilator to provide pressure-support ventilation. RESULTS: None of the encountered values of resistance (0.5\N3.6 cm H(2)O/L/s) exceeded the limits stipulated by the previously described international standard for HMEs (International Standards Organization Draft International Standard 9360-2) (not to exceed 5.0 cm H(2)O with a flow of 1.0 L/s, even when saturated). The hygroscopic HME had less resistance than other types, independent of the precondition status (dry or saturated) or the respiratory mode. The hygroscopic HME also had a lesser increase in resistance when saturated. The resistance of the HME was little affected by increases in flow, but saturation did increase resistance in the hydrophobic and hygroscopic/hydrophobic HME to levels that could be important at some clinical conditions. CONCLUSIONS: Resistance was little affected by saturation in hygroscopic models, when compared to the hydrophobic or hygroscopic/hydrophobic HME. Changes in inspiratory flow did not cause relevant alterations in resistance.

Tracheal gas insufflation during late exhalation efficiently reduces PaCO(2) in experimental acute lung injury.

OBJECTIVE: Tracheal gas insufflation (TGI) reduces PaCO(2) by flushing the tracheal and mechanical deadspace, and may have its maximum benefit when TGI gas is unopposed by significant expiratory gas flow. Thus, limiting TGI to the late expiratory period may diminish tracheal exposure to TGI gas while preserving the efficacy of TGI. This study examined the gas exchange consequences of such late-expiratory TGI. DESIGN AND SETTING: Randomized controlled trial, animal study. MATERIALS: Eleven pigs. INTERVENTIONS: After stable lung injury was established using oleic acid 11 pigs were ventilated using a standardized lung protective strategy. Phasic expiratory TGI was applied for 30 min stages during the last 20%, 40%, 60%, and 100% of expiration in random sequence. PaCO(2) was continuously measured via an indwelling blood gas analysis system. MEASUREMENTS AND RESULTS: PaCO(2) at baseline was 86.1+/-4.7 mmHg, and decreased progressively with increasing TGI duration of 20%, 40%, and 60%, but not 100%, of expiration (PaCO(2)=75.7+/-5.2, 68.8+/-3.6, 65.1+/-5.3 and 65.2+/-5.2 mmHg, respectively). For all stages the reduction in PaCO(2) relative to baseline was significant. Trends of increasing PaO(2) and airway pressure with increasing TGI duration were noted and most likely associated with a TGI-induced increase in lung volume. CONCLUSIONS: Under these conditions confining TGI to the final 60% of expiration achieved effective PaCO(2) reduction, not significantly different from panexpiratory TGI, while limiting exposure of the trachea to TGI gas, and reducing the potential for TGI-induced hyperinflation. These findings suggest that TGI is most effectively applied in a phasic manner in late expiration, with its duration titrated to effect.

Distal projection of insufflated gas during tracheal gas insufflation.

Tracheal gas insufflation (TGI) flushes expired gas from the ventilator circuitry and central airways, augmenting CO2 clearance. Whereas a significant portion of this washout effect may occur distal to the injection orifice, the penetration and mixing behavior of TGI gas has not been studied experimentally. We examined the behavior of 100% oxygen TGI injected at set flow rates of 1-20 l/min into a simulated trachea consisting of a smooth-walled, 14-mm-diameter tube. Models incorporating a separate coaxial TGI injector, a rough-walled trachea, and a bifurcated trachea were also studied. One-hundred percent nitrogen, representing expiratory flow, passed in the direction opposite to TGI at set flow rates of 1-25 l/min. Oxygen concentration within the "trachea" was mapped as a function of axial and radial position. Three consistent findings were observed: 1) mixing of expiratory and TGI gases occurred close to the TGI orifice; 2) the oxygenated domain extended several centimeters beyond the endotracheal tube, even at high-expiratory flows, but had a defined distal limit; and 3) more distally from the site of gas injection, the TGI gas tended to propagate along the tracheal wall, rather than as a central projection. We conclude that forward-directed TGI penetrates a substantial distance into the central airways, extending the compartment susceptible to CO2 washout.

Publication, citations, and impact factors of leading investigators in critical care medicine.

INTRODUCTION: Critical care medicine research is reported in major medical journals that can be accessed via computerized search engines such as PubMed (National Library of Medicine) or Web of Science (Thomson ISI [Institute for Scientific Information]). The crediting of report citations to specific journals or individuals is a rapidly developing and highly controversial evaluative process. METHODS: We conducted a citation analysis to measure the research and publication accomplishments of critical care medicine investigators, by tallying their numbers of published reports and numbers of citations to their reports. Major investigators were identified from the author indexes of major critical care medicine publications. From the Web of Science the number of publications and citations of their works were determined for 224 investigators for the period 1997 through August 2003. We calculated the individual researcher's "impact factor" by dividing the number of citations (made by other researchers to a given researcher's reports) by the number of articles that researcher had published. To estimate which countries are producing the most research on mechanical ventilation, we studied the abstract books from the 2001, 2002, and 2003 American Thoracic Society annual international conferences and tallied the number of posters (pertaining to mechanical ventilation) from the various countries. We then calculated a "country factor" as the number of posters per million population of the source country. RESULTS: We considered 44, 576 citations in 3,755 publications. Using criteria selected to recognize original works, J L Vincent published the greatest number of reports (129). M A Matthay received the most citations (2,056). G U Meduri had the highest impact factor (25.32). There was a balance between the number of leading investigators from Europe and North America. Relative to its population size, Canada warrants leadership acknowledgement in critical care medicine, considering its number of leading investigators and poster presentations. CONCLUSIONS: From criteria selected to attribute original work to specific authors we identified 20 leading critical care medicine investigators, as measured by number of publications, citations, and impact factors. We also report a country factor based on posters (on mechanical ventilation) presented at the 2001-2003 international conferences of the American Thoracic Society.

Characteristics of demand oxygen delivery systems: maximum output and setting recommendations.

BACKGROUND: Demand oxygen delivery systems (DODS) allot oxygen by interrupting the oxygen flow during exhalation, when it would mostly be wasted. Because DODS conserve oxygen by various methods, there are important performance differences between DODS. We studied certain performance factors that have not previously been carefully examined. METHODS: A bench model was constructed to simulate a nose, airway, and alveolar chamber. A breathing simulator generated 4 respiratory patterns, at frequencies of 15, 20, 25, and 30 breaths/min. Eighteen models of DODS were tested at 4 settings, each up to the maximum output, and compared to continuous-flow oxygen. The variable of interest was the fraction of inspired oxygen (F(I)O(2)) in the alveolar chamber, which was measured for each condition. RESULTS: The DODS differed from continuous-flow oxygen, delivering 0.5-2.1 times (mean = 1.13 times) the F(I)O(2) increase at similar settings. During maximum output the DODS showed a wide range of F(I)O(2), from 0.27 to 0.46. There was a direct relationship between volume output per pulse in the first 0.6 s of inhalation and the delivered F(I)O(2). CONCLUSIONS: DODS settings were not equivalent to continuous-flow oxygen in a bench model assessment; with equivalent settings the DODS tended to deliver greater F(I)O(2) than did continuous-flow oxygen. The maximum output capacity differed markedly among the DODS, and the user should know the device's capacity. A volume-referenced setting system for DODS should be adopted that would allow more predictable oxygen prescription and delivery via DODS.

Ventilator-induced lung injury.

Ventilator-induced lung injury has been established as a significant risk to patients receiving PPV. Animal studies have provided definitive experimental data that support the existence of VILI. Clinical studies have implied the role of VILI in ARDS and ALI patients. In patients who have ARDS or ALI, however, VILI cannot be distinguished from exacerbation of the primary condition. Animal and clinical studies that clearly show elevated levels of cytokines when PPV is applied beyond certain limits support the concept that an inflammatory process is activated by PPV. Whether the induction of inflammatory mediators contributes to the mortality or morbidity of the ventilated patient has not been established. A potential role for anti-inflammatory therapeutic agents is promising. Therefore, the following considerations can guide the clinical care of ventilator patients: Alveolar pressure exposure (plateau pressure) should be limited to less than 32 cm H2O. Positive end-expiratory pressure should be applied to avoid end-expiratory collapse and reopening. Tidal volume should be set at approximately 6 mL/kg or further guided by plateau pressure limitation. Although studies suggest that reducing Ti, flow, and f may be important in avoiding VILI, there are no current guidelines. The results of preliminary studies investigating the preventative potential of respiratory acidosis, prone positioning, or careful vascular pressure management seem promising. Inflammatory response in VILI has been established, but a role for intervention, such as general or specific suppression of the response, has not been established.

Experimental intra-abdominal hypertension influences airway pressure limits for lung protective mechanical ventilation.

BACKGROUND: Intra-abdominal hypertension (IAH) and abdominal compartment syndrome (ACS) may complicate monitoring of pulmonary mechanics owing to their impact on the respiratory system. However, recommendations for mechanical ventilation of patients with IAH/ACS and the interpretation of thoracoabdominal interactions remain unclear. Our study aimed to characterize the influence of elevated intra-abdominal pressure (IAP) and positive end-expiratory pressure (PEEP) on airway plateau pressure (PPLAT) and bladder pressure (PBLAD). METHODS: Nine deeply anesthetized swine were mechanically ventilated via tracheostomy: volume-controlled mode at tidal volume (VT) of 10 mL/kg, frequency of 15, inspiratory-expiratory ratio of 1:2, and PEEP of 1 and 10 cm H2O (PEEP1 and PEEP10, respectively). A tracheostomy tube was placed in the peritoneal cavity, and IAP levels of 5, 10, 15, 20, and 25 mm Hg were applied, using a continuous positive airway pressure system. At each IAP level, PBLAD and airway pressure measurements were performed during both PEEP1 and PEEP10. RESULTS: PBLAD increased as experimental IAP rose (y = 0.83x + 0.5; R = 0.98; p < 0.001 at PEEP1). Minimal underestimation of IAP by PBLAD was observed (-2.5 ± 0.8 mm Hg at an IAP of 10-25 mm Hg). Applying PEEP10 did not significantly affect the correlation between experimental IAP and PBLAD. Approximately 50% of the PBLAD (in cm H2O) was reflected by changes in PPLAT, regardless of the PEEP level applied. Increasing IAP did not influence hemodynamics at any level of IAP generated. CONCLUSION: With minimal underestimation, PBLAD measurements closely correlated with experimentally regulated IAP, independent of the PEEP level applied. For each PEEP level applied, a constant proportion (approximately 50%) of measured PBLAD (in cm H2O) was reflected in PPLAT. A higher safety threshold for PPLAT should be considered in the setting of IAH/ACS as the clinician considers changes in VT. A strategy of reducing VT to cap PPLAT at widely recommended values may not be warranted in the setting of increased IAP.

Non-pulmonary factors strongly influence the stress index.

PURPOSE: A quantitative measure of the airway pressure-time tracing during passive inflation [stress index (SI)] has been suggested as an indicator of tidal lung recruitment and/or overinflation. If reliable, this simple index could help guide positive end-expiratory pressure (PEEP) and tidal volume selection. The compartment surrounding the lungs should impact airway pressure and could, therefore, affect SI validity. To explore the possibility, we determined SI in a swine model of pleural effusion (PLEF). METHODS: Unilateral PLEF was simulated by instilling fluid (13 ml/kg-moderate, 26 ml/kg-large) into the right pleural space of five anesthetized, paralyzed, mechanically ventilated pigs. Animals were ventilated with constant flow ventilation: tidal volume (V (T)) 9 ml/kg, f set to end-tidal CO2 (ETCO2) of 30-40 mmHg, inspiratory to expiratory ratio (I/E) 1:2, PEEP 1 or 10 cmH2O. Respiratory system mechanics and computed tomography (CT) were acquired at end-inspiration and end-expiration to determine % tidal recruitment and overinflation. RESULTS: Prior to PLEF instillation, SI values derived at PEEP = 1 and 10 cmH2O were 0.90 and 1.22, respectively. Moderate PLEF increased these SI values to 1.06 and 1.24 and large PLEF further increased SI to 1.23 and 1.27 despite extensive tidal recruitment and negligible overdistention by CT. The initial half of the tidal pressure curve produced SI values (range 0.82-1.17) that were significantly lower than those of the second half (0.98-1.37). CONCLUSIONS: In the presence of pleural fluid, SI indicated overinflation when virtually none was present and tidal lung recruitment predominated. When the extrapulmonary environment is abnormal, caregivers are advised to interpret the SI with caution.