Mean Airway Pressure As a Predictor of 90-Day Mortality in Mechanically Ventilated Patients.

OBJECTIVES: To determine the association between mean airway pressure and 90-day mortality in patients with acute respiratory failure requiring mechanical ventilation and to compare the predictive ability of mean airway pressure compared with inspiratory plateau pressure and driving pressure. DESIGN: Prospective observational cohort. SETTING: Five ICUs in Lima, Peru. SUBJECTS: Adults requiring invasive mechanical ventilation via endotracheal tube for acute respiratory failure. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Of potentially eligible participants (n = 1,500), 65 (4%) were missing baseline mean airway pressure, while 352 (23.5%) were missing baseline plateau pressure and driving pressure. Ultimately, 1,429 participants were included in the analysis with an average age of 59 ± 19 years, 45% female, and a mean PaO2/FIO2 ratio of 248 ± 147 mm Hg at baseline. Overall, 90-day mortality was 50.4%. Median baseline mean airway pressure was 13 cm H2O (interquartile range, 10-16 cm H2O) in participants who died compared to a median mean airway pressure of 12 cm H2O (interquartile range, 10-14 cm H2O) in participants who survived greater than 90 days (p < 0.001). Mean airway pressure was independently associated with 90-day mortality (odds ratio, 1.38 for difference comparing the 75th to the 25th percentile for mean airway pressure; 95% CI, 1.10-1.74) after adjusting for age, sex, baseline Acute Physiology and Chronic Health Evaluation III, baseline PaO2/FIO2 (modeled with restricted cubic spline), baseline positive end-expiratory pressure, baseline tidal volume, and hospital site. In predicting 90-day mortality, baseline mean airway pressure demonstrated similar discriminative ability (adjusted area under the curve = 0.69) and calibration characteristics as baseline plateau pressure and driving pressure. CONCLUSIONS: In a multicenter prospective cohort, baseline mean airway pressure was independently associated with 90-day mortality in mechanically ventilated participants and predicts mortality similarly to plateau pressure and driving pressure. Because mean airway pressure is readily available on all mechanically ventilated patients and all ventilator modes, it is a potentially more useful predictor of mortality in acute respiratory failure.

Role of nasal positive end expiratory pressure valve as an alternative treatment for obstructive sleep apnoea in Chinese patients.

BACKGROUND AND OBJECTIVE: As compliance of continuous positive airway pressure (CPAP) for treatment of obstructive sleep apnoea (OSA) is often suboptimal, a less cumbersome treatment is desirable. We explored the clinical usefulness of nasal positive end expiratory pressure (nPEEP) valves. METHODS: Symptomatic OSA patients (apnoea hypopnea index (AHI) >5/h by polysomnography (PSG) or >10/h by type III devices), who declined CPAP, were recruited. A nPEEP valve was attached to each nostril before bed. After successful acclimatization for 1 week, treatment was continued for 4 weeks. The nPEEP valves provided expiratory resistance to build up PEEP. PSG was performed at week 4. RESULTS: Among 196 subjects, 46 (23%) failed acclimatization and 14 (7%) withdrew. Among the 120 patients with a valid PSG, 72 (60%) and 75 (63%) had >50% reduction in mean (standard deviation) overall AHI 26 (16)/h to 18 (18)/h and mean supine AHI 31 (19)/h to 11(16)/h, respectively, P < 0.001. Compared with responders, patients with <50% reduction in AHI had a higher mean overall AHI (30/h vs 23/h, P = 0.03), higher mean supine AHI (35/h vs 26/h, P = 0.04), more severe mean oxygen desaturation nadir (76.7% vs 82.7%, P < 0.01) and longer mean period of desaturation <90% SaO2 (7.7 vs 2.4, P = 0.02). Breathing discomfort and dry mouth were the most common side effects. Compared with a dental device, there was a larger mean reduction in supine AHI using nPEEP (29 (14)/h vs 16 (17)/h). CONCLUSION: nPEEP valves were useful in selected patients with mild or positional-related OSA.

Dynamic laryngeal narrowing during exercise: a mechanism for generating intrinsic PEEP in COPD?

INTRODUCTION: Patients with COPD commonly exhibit pursed-lip breathing during exercise, a strategy that, by increasing intrinsic positive end-expiratory pressure, may optimise lung mechanics and exercise tolerance. A similar role for laryngeal narrowing in modulating exercise airways resistance and the respiratory cycle volume-time course is postulated, yet remains unstudied in COPD. The aim of this study was to assess the characteristics of laryngeal narrowing and its role in exercise intolerance and dynamic hyperinflation in COPD. METHODS: We studied 19 patients (n=8 mild-moderate; n=11 severe COPD) and healthy age and sex matched controls (n=11). Baseline physiological characteristics and clinical status were assessed prior to an incremental maximal cardiopulmonary exercise test with continuous laryngoscopy. Laryngeal narrowing measures were calculated at the glottic and supra-glottic aperture at rest and peak exercise. RESULTS: At rest, expiratory laryngeal narrowing was pronounced at the glottic level in patients and related to FEV1 in the whole cohort (r=-0.71, p<0.001) and patients alone (r=-0.53, p=0.018). During exercise, glottic narrowing was inversely related to peak ventilation in all subjects (r=-0.55, p=0.0015) and patients (r=-0.71, p<0.001) and peak exercise tidal volume (r=-0.58, p=0.0062 and r=-0.55, p=0.0076, respectively). Exercise glottic narrowing was also inversely related to peak oxygen uptake (% predicted) in all subjects (r=-0.65, p<0.001) and patients considered alone (r=-0.58, p=0.014). Exercise inspiratory duty cycle was related to exercise glottic narrowing for all subjects (r=-0.69, p<0.001) and patients (r=-0.62, p<0.001). CONCLUSIONS: Dynamic laryngeal narrowing during expiration is prevalent in patients with COPD and is related to disease severity, respiratory duty cycle and exercise capacity.

Hemodynamic consequences of auto-PEEP.

Auto-positive end-expiratory pressure (PEEP) is a common but frequently unrecognized problem in critically ill patients. It has important physiologic consequences and can cause shock and cardiac arrest. Treatment consists of relieving expiratory airflow obstruction and reducing minute ventilation delivered by positive pressure ventilation. Sedation and fluid management are important adjunctive therapies. This analytic review discusses the prevalence, pathophysiology, and hemodynamic consequences of auto-PEEP and an approach to its treatment.

Dynamic hyperinflation and auto-positive end-expiratory pressure: lessons learned over 30 years.

Auto-positive end-expiratory pressure (auto-PEEP; AP) and dynamic hyperinflation (DH) may affect hemodynamics, predispose to barotrauma, increase work of breathing, cause dyspnea, disrupt patient-ventilator synchrony, confuse monitoring of hemodynamics and respiratory system mechanics, and interfere with the effectiveness of pressure-regulated ventilation. Although basic knowledge regarding the clinical physiology and management of AP during mechanical ventilation has evolved impressively over the 30 years since DH and AP were first brought to clinical attention, novel and clinically relevant characteristics of this complex phenomenon continue to be described. This discussion reviews some of the more important aspects of AP that bear on the care of the ventilated patient with critical illness.

Neural respiratory drive in obesity.

BACKGROUND: The load imposed on ventilation by increased body mass contributes to the respiratory symptoms caused by obesity. A study was conducted to quantify ventilatory load and respiratory drive in obesity in both the upright and supine postures. METHODS: Resting breathing when seated and supine was studied in 30 obese subjects (mean (SD) body mass index (BMI) 42.8 (8.6) kg/m(2)) and 30 normal subjects (mean (SD) BMI 23.6 (3.7) kg/m(2)), recording the electromyogram of the diaphragm (EMGdi, transoesophageal multipair electrode), gastric and oesophageal pressures. RESULTS: Ventilatory load and neural drive were higher in the obese group as judged by the EMGdi (21.9 (9.0) vs 8.4 (4.0)%max, p<0.001) and oesophageal pressure swings (9.6 (2.9) vs 5.3 (2.2) cm H(2)O, p<0.001). The supine posture caused an increase in oesophageal pressure swings to 16.0 (5.0) cm H(2)O in obese subjects (p<0.001) and to 6.9 (2.0) cm H(2)O in non-obese subjects (p<0.001). The EMGdi increased in the obese group to 24.7 (8.2)%max (p<0.001) but remained the same in non-obese subjects (7.0 (3.4)%max, p = NS). Obese subjects developed intrinsic positive end-expiratory pressure (PEEPi) of 5.3 (3.6) cm H(2)O when supine. Applying continuous positive airway pressure (CPAP) in a subgroup of obese subjects when supine reduced the EMGdi by 40%, inspiratory pressure swings by 25% and largely abolished PEEPi (4.1 (2.7) vs 0.8 (0.4) cm H(2)O, p = 0.009). CONCLUSION: Obese patients have substantially increased neural drive related to BMI and develop PEEPi when supine. CPAP abolishes PEEPi and reduces neural respiratory drive in these patients. These findings highlight the adverse respiratory consequences of obesity and have implications for the clinical management of patients, particularly where the supine posture is required.

Central airway occlusion underestimates intrinsic positive end-expiratory pressure: a numerical and physical simulation.

Intrinsic positive end-expiratory pressure (PEEP) occurs when airway outflow is higher than zero at end-expiration. Differences in the time constant among alveolar units may result in an uneven distribution of intrinsic PEEP. The authors conducted a computer simulation of a 2-compartment respiratory system and calculated intrinsic PEEP for each alveolar unit and confirmed it with a test-lung experiment. Ventilator settings, including respiratory rate, inspiratory time, pause time, and external PEEP, were tested at various values in combination with various airway resistance and alveolar compliance values. The simulation was performed by calculating the flow, pressure, and volume every millisecond. The data demonstrated that the larger the difference of time constant between 2 respiratory units, the greater the difference in intrinsic PEEP between the units. A higher respiratory frequency and a larger percentage of inspiratory time resulted in an increase in the intrinsic PEEP at the central airway, as well as a wide difference in the intrinsic PEEP between airway units. These phenomena were confirmed by a 2-compartment test-lung study. The authors demonstrated and verified an uneven distribution of intrinsic PEEP in 2 different experiments, which raised a warning that some respiratory units might have much higher intrinsic PEEP than the intrinsic PEEP measured clinically.

Hyperinflation and intrinsic positive end-expiratory pressure: less room to breathe.

Clinically, the symptoms and limited exercise capabilities of patients with chronic obstructive pulmonary disease (COPD) correlate better with changes in lung volumes than with airflow measurements. The realization of the clinical importance of hyperinflation has been overshadowed for decades by the use of forced expiratory volume during 1 s (FEV(1)) and the ratio of the FEV(1) to the forced expiratory vital capacity (FEV(1)/FVC) to categorize the severity and progression of COPD. Hyperinflation is defined as an elevation in the end-expiratory lung volume or functional residual capacity. When severe hyperinflation encroaches upon inspiratory capacity and limits vital capacity, it results in elevated intrinsic positive end-expiratory pressure (PEEPi) that places the diaphragm at a mechanical disadvantage and increases the work of breathing. Severe hyperinflation is the major physiologic cause of the resulting hypercarbic respiratory failure and patients' inability to transition (i.e. wean) from mechanical ventilatory support to spontaneous breathing. This paper reviews the basic physiologic principles of hyperinflation and its clinical manifestations as demonstrated by PEEPi. Also reviewed are the adverse effects of hyperinflation and PEEPi in critically ill patients with COPD, and methods for minimizing or counterbalancing these effects.

Ventilatory strategies in the neonatal and paediatric intensive care units.

Mechanical ventilation is a common form of support in the modern day intensive care unit (ICU). In order for the clinician better to understand and apply mechanical ventilation, it is important that they understand the physiological principles of ventilation. This review describes these basic concepts; parameters of mechanical ventilation, high frequency ventilation and non-invasive ventilation. An overview of ventilatory strategies for four common diseases seen in paediatric and neonatal ICUs will be discussed.

Study of tracheal dyskinesia impact on the cardiac hemodynamics.

BACKGROUND: Tracheal dyskinesia (TD) was recently recognized as a possible mechanism for acute pulmonary edema (Elamin and Firdose, J Bronchol 2004;11:118-21; Khan and Elamin Eur Respir J 2005;26:319). This study was designed to evaluate possible impact of TD on cardiac hemodynamics. METHODS: Patients were prospectively assigned to either study "A" or control "B" groups (TD >50% or <50%, respectively) diagnosed by bronchoscopy or dynamic chest computed tomography. The cardiac hemodynamics was assisted by impedance cardiography (BioZ; CardioDynamics, San Diego, CA) at rest and during coughing. The latter was repeated after 5 minutes of rest. RESULTS: Thirteen patients were assigned to group A and 14 to group B. There was higher incidence of hypertension, diabetes mellitus, and history of congestive heart failure in group A compared with group B. The percentage of TD was 85% +/- 10.0% versus 25% +/- 2.5%, in the A and B groups, respectively (P < 0.05). Stroke volume index (normal = 35-65 mL/beat/body surface area) was significantly reduced in group A 29.68 [95% confidence interval (CI), 25.557-33.818] compared with group B 38.321 (95% CI, 35.199-41.444; P < 0.05). In addition, the velocity index (representative of aortic blood velocity) was 32.188 (95% CI, 20.841-43.534, P < 0.049) in group A compared with 46.786 (95% CI, 38.209-55.363) in group B, and the left ventricular ejection time measured in milliseconds was 265.813 (95% CI, 246.065-285.560 in group A, P < 0.004) compared with 303.821(95% CI, 288.894-318.749) in group B. CONCLUSION: This prospective study demonstrated the importance of recognizing TD as a pathologic entity and the need to consider TD in the workup of acute pulmonary edema especially if other tests were unrevealing.

Driving Pressure and Hospital Mortality in Patients Without ARDS: A Cohort Study.

BACKGROUND: Driving pressure (ΔP) is associated with mortality in patients with ARDS and with pulmonary complications in patients undergoing general anesthesia. Whether ΔP is associated with outcomes of patients without ARDS who undergo ventilation in the ICU is unknown. Our objective was to determine the independent association between ΔP and outcomes in mechanically ventilated patients without ARDS on day 1 of mechanical ventilation. METHODS: This was a retrospective analysis of a cohort of 622 mechanically ventilated adult patients without ARDS on day 1 of mechanical ventilation from five ICUs in a tertiary center in the United States. The primary outcome was hospital mortality. The presence of ARDS was determined using the minimum daily Pao2 to Fio2 (PF) ratio and an automated text search of chest radiography reports. The data set was validated by first testing the model in 543 patients with ARDS. RESULTS: In patients without ARDS on day 1 of mechanical ventilation, ΔP was not independently associated with hospital mortality (OR, 1.01; 95% CI, 0.97-1.05). The results of the primary analysis were confirmed in a series of preplanned sensitivity analyses. CONCLUSIONS: In this cohort of patients without ARDS on day 1 of mechanical ventilation and within the limits of ventilatory settings normally used by clinicians, ΔP was not associated with hospital mortality. This study also confirms the association between ΔP and mortality in patients with ARDS not enrolled in a trial and in hypoxemic patients without ARDS.

Expiratory Flow Limitation During Mechanical Ventilation.

Expiratory flow limitation (EFL) is present when the flow cannot rise despite an increase in the expiratory driving pressure. The mechanisms of EFL are debated but are believed to be related to the collapsibility of small airways. In patients who are mechanically ventilated, EFL can exist during tidal ventilation, representing an extreme situation in which lung volume cannot decrease, regardless of the expiratory driving forces. It is a key factor for the generation of auto- or intrinsic positive end-expiratory pressure (PEEP) and requires specific management such as positioning and adjustment of external PEEP. EFL can be responsible for causing dyspnea and patient-ventilator dyssynchrony, and it is influenced by the fluid status of the patient. EFL frequently affects patients with COPD, obesity, and heart failure, as well as patients with ARDS, especially at low PEEP. EFL is, however, most often unrecognized in the clinical setting despite being associated with complications of mechanical ventilation and poor outcomes such as postoperative pulmonary complications, extubation failure, and possibly airway injury in ARDS. Therefore, prompt recognition might help the management of patients being mechanically ventilated who have EFL and could potentially influence outcome. EFL can be suspected by using different means, and this review summarizes the methods to specifically detect EFL during mechanical ventilation.

Assessment of Factors Related to Auto-PEEP.

BACKGROUND: Previous physiological studies have identified factors that are involved in auto-PEEP generation. In our study, we examined how much auto-PEEP is generated from factors that are involved in its development. METHODS: One hundred eighty-six subjects undergoing controlled mechanical ventilation with persistent expiratory flow at the beginning of each inspiration were enrolled in the study. Volume-controlled continuous mandatory ventilation with PEEP of 0 cm H2O was applied while maintaining the ventilator setting as chosen by the attending physician. End-expiratory and end-inspiratory airway occlusion maneuvers were performed to calculate respiratory mechanics, and tidal flow limitation was assessed by a maneuver of manual compression of the abdomen. RESULTS: The variable with the strongest effect on auto-PEEP was flow limitation, which was associated with an increase of 2.4 cm H2O in auto-PEEP values. Moreover, auto-PEEP values were directly related to resistance of the respiratory system and body mass index and inversely related to expiratory time/time constant. Variables that were associated with the breathing pattern (tidal volume, frequency minute ventilation, and expiratory time) did not show any relationship with auto-PEEP values. The risk of auto-PEEP ≥5 cm H2O was increased by flow limitation (adjusted odds ratio 17; 95% CI: 6-56.2), expiratory time/time constant ratio <1.85 (12.6; 4.7-39.6), respiratory system resistance >15 cm H2O/L s (3; 1.3-6.9), age >65 y (2.8; 1.2-6.5), and body mass index >26 kg/m(2) (2.6; 1.1-6.1). CONCLUSIONS: Flow limitation, expiratory time/time constant, resistance of the respiratory system, and obesity are the most important variables that affect auto-PEEP values. Frequency expiratory time, tidal volume, and minute ventilation were not independently associated with auto-PEEP. Therapeutic strategies aimed at reducing auto-PEEP and its adverse effects should be primarily oriented to the variables that mainly affect auto-PEEP values.

Oxygen consumption and PEEPe in ventilated COPD patients.

The intrinsic positive-end-expiratory pressure (PEEPi) increases the inspiratory load, the cost of breathing and thus oxygen consumption (V(O2)). It has been shown that applying an extrinsic positive-end-expiratory pressure (PEEPe) reduces the inspiratory threshold load but the optimal PEEPe level is still in debate. We hypothesize that the best level of PEEPe could induce a decrease in V(O2) by reducing the V(O2) demands from PEEPi. Nine mechanically ventilated COPD patients were included. The level of PEEPe was determined in accordance with the static PEEPi. V(O2) was measured using an automatic gas analyser during synchronized intermittent mandatory ventilation (SIMV): without PEEPe, with a PEEPe equal to 50% of static PEEPi and with a PEEPe equal to 100% of static PEEPi. Static PEEPi appeared to be significantly correlated with the degree of airflow obstruction (FEV1) (P<0.05). Applying a PEEPe equal to static PEEPi resulted in a significant decrease in V(O2) (P<0.05) whereas the change in V(O2) proved to be unpredictable for a PEEPe level of 50% of static PEEPi. In conclusion, V(O2) decreases progressively when increasing PEEPe up to a level equal to 100% of static PEEPi. Thus, in mechanically ventilated COPD patients with a FEV1 < or = 1000 ml, applying a PEEPe of 5 cmH2O should be recommended.

Measurement of air trapping, intrinsic positive end-expiratory pressure, and dynamic hyperinflation in mechanically ventilated patients.

Severe airflow obstruction is a common cause of acute respiratory failure. Dynamic hyperinflation affects tidal ventilation, increases airways resistance, and causes intrinsic positive end-expiratory pressure (auto-PEEP). Most patients with asthma and chronic obstructive pulmonary disease have dynamic hyperinflation and auto-PEEP during mechanical ventilation, which can cause hemodynamic compromise and barotrauma. Auto-PEEP can be identified in passively breathing patients by observation of real-time ventilator flow and pressure graphics. In spontaneously breathing patients, auto-PEEP is measured by simultaneous recordings of esophageal and flow waveforms. The ventilatory pattern should be directed toward minimizing dynamic hyperinflation and auto-PEEP by using small tidal volume and preserving expiratory time. With a spontaneously breathing patient, to reduce the work of breathing and improve patient-ventilator interaction, it is crucial to set an adequate inspiratory flow, inspiratory time, trigger sensitivity, and ventilator-applied PEEP. Ventilator graphics are invaluable for monitoring and treatment decisions at the bedside.

Auto-positive end-expiratory pressure: mechanisms and treatment.

Auto-positive end-expiratory pressure (auto-PEEP) is a common problem in patients receiving full or partial ventilatory support, as well as in those ready to be weaned from the ventilator. Physicians should be alert for it and take measures to reduce it, as it can have serious consequences.