Total Minute Ventilation Research Articles

Alveolar target ventilation and dead space in children under anaesthesia: The proventiped cohort study.

Ventilator settings in children under anaesthesia remain difficult because of the changes in the physiology and the high dead space. To determine the alveolar minute-volume to sustain normocapnia in children under mechanical ventilation. A prospective observational study. This study was performed between May and October 2019 in a tertiary care children's hospital. Children between 2 months and 12 years, weighing between 5 and 40 kg, admitted for general anaesthesia. Volumetric capnography was used to estimate the alveolar and dead space volume (Vd). Total and alveolar minute ventilation in (ml kg-1 min-1) over 100 breaths. Sixty patients were included comprising 20 per group: 5 to 10 kg (group 1), 10 to 20 kg (group 2), 20 to 40 kg (group 3). Seven patients were excluded for aberrant capnographic curves. After normalisation to weight, the median [IQR] tidal volume per kilogram was similar between the three groups: 6.5 ml kg-1 [6.0 to 7.5 ml kg-1], 6.4 ml kg-1 [5.7 to 7.3 ml kg-1], 6.4 ml kg-1 [5.3 to 6.8 ml kg-1]; P = 0.3. Total Vd (in ml kg-1) was negatively correlated to weight (r = -0.62, 95% confidence interval -0.41 to -0.76, P < 0.001). The total normalised minute ventilation (ml kg-1 min-1) to obtain normocapnia was higher in group 1 than in group 2 and in group 3; 203 ml kg-1 min-1 [175 to 219 ml kg-1 min-1], 150 ml kg-1 min-1 [139 to 181 ml kg-1 min-1] and 128 ml kg-1 min-1 [107 to 157 ml kg-1 min-1]; P < 0.001 (mean ± SD), but (mean ± SD) alveolar minute ventilation was similar between the three groups; 68 ± 21 ml kg-1 min-1. Total dead space volume (including apparatus dead space) represents a major component of tidal volume in children less than 30 kg, when using large heat and moisture exchanger filters. The total minute ventilation necessary to achieve normocapnia decreased with increasing weight, while the alveolar minute ventilation remained constant. ClinicalTrials.gov, identifier: NCT03901599.

Utilization of Airway Pressure Release Ventilation as a Rescue Strategy in COVID-19 Patients: A Retrospective Analysis.

Background:Airway Pressure Release Ventilation (APRV) is a pressure controlled intermittent mandatory mode of ventilation characterized by prolonged inspiratory time and high mean airway pressure. Several studies have demonstrated that APRV can improve oxygenation and lung recruitment in patients with Acute Respiratory Distress Syndrome (ARDS). Although most patients with COVID-19 meet the Berlin criteria for ARDS, hypoxic respiratory failure due to COVID-19 may differ from traditional ARDS as patients often present with severe, refractory hypoxemia and significant variation in respiratory system compliance. To date, no studies investigating APRV in this patient population have been published. The aim of this study was to evaluate the effectiveness of APRV as a rescue mode of ventilation in critically ill patients diagnosed with COVID-19 and refractory hypoxemia.Methods:We conducted a retrospective analysis of patients admitted with COVID-19 requiring invasive mechanical ventilation who were treated with a trial of APRV for refractory hypoxemia. PaO2/FIO2 (P/F ratio), ventilatory ratio and ventilation outputs before and during APRV were compared.Results:APRV significantly improved the P/F ratio and decreased FIO2 requirements. PaCO2 and ventilatory ratio were also improved. There was an increase in tidal volume per predicted body weight during APRV and a decrease in total minute ventilation. On multivariate analysis, higher inspiratory to expiratory ratio (I: E) and airway pressure were associated with greater improvement in P/F ratio.Conclusions:APRV may improve oxygenation, alveolar ventilation and CO2 clearance in patients with COVID-19 and refractory hypoxemia. These effects are more pronounced with higher airway pressure and inspiratory time.

Typical within and between person variability in non-invasive ventilator derived variables among clinically stable, long-term users

BackgroundDespite increasing capacity to remotely monitor non-invasive ventilation (NIV), how remote data varies from day to day and person to person is poorly described.MethodsSingle-centre, 2-month, prospective study of clinically stable...

Prediction of readiness to decannulation from venovenous extracorporeal membrane oxygenation.

The criteria and process for liberation from extracorporeal membrane oxygenation in patients with severe acute respiratory distress syndrome are not standardized. The predictive accuracy of the oxygen challenge test as a diagnostic test in determining weaning and decannulation from venovenous extracorporeal membrane oxygenation was tested. A single-centre, retrospective, observational cohort study. Tertiary referral severe respiratory failure centre in a university hospital in the United Kingdom. 253 adults with severe acute respiratory distress syndrome requiring extracorporeal membrane oxygenation. None. Patients had median age: 43 years (interquartile range: 32-52) years, extracorporeal membrane oxygenation days: 9 (interquartile range: 6-14) and acute physiology and chronic health evaluation II score 17.5 (interquartile range: 15-20). Oxygen challenge test value (PaO2-OCT) with best prediction was 31 kPa (232 mmHg; sensitivity 0.74; specificity 0.70; area under curve 0.77 (confidence interval: 0.73-0.81)). PaO2-OCT did not perform well as a prospective test to identify readiness to decannulation. Only 24 patients (10%) were decannulated 48 hours after their first positive oxygen challenge test (true positive) and 73.4% patients were false positives (positive oxygen challenge test but not decannulated). True positives had higher tidal volume (541 ± 218 vs 368 mL ± 210; p < 0.05) and minute ventilation (9.34 ± 5.36 vs 6.33 L/min ± 4.43; p < 0.05). Blood flow (3.17 ± 0.23 vs 3.53 L/min ± 0.56; p < 0.05), sweep gas flow (1.42 ±1.83 vs 3.74 L/min ± 2.43; p < 0.05) and extracorporeal membrane oxygenation minute volume at time of first positive oxygen challenge test was lower in true positives (1.66 ± 2.26 vs 4.82 ± 3.43 L/min). This was a strong predictor for decannulation within 48 hours (area under curve: 0.88, confidence interval: 0.88-0.89). In severe acute respiratory distress syndrome requiring venovenous extracorporeal membrane oxygenation, the PaO2-OCT is a poor predictor of readiness to decannulate from extracorporeal membrane oxygenation. Additional factors involved in the control of respiratory drive and carbon dioxide clearance, particularly native lung dead space and total minute ventilation, should be assessed.

Effect of a Single Session of Intermittent Hypoxia on Erythropoietin and Oxygen‐Carrying Capacity

Intermittent hypoxia, defined as alternating bouts of breathing hypoxic and normoxic air, has the potential to improve oxygen‐carrying capacity through an erythropoietin‐mediated increase in hemoglobin mass. The purpose of this study was to determine the effect of a single exposure of intermittent normobaric hypoxia on erythropoietin levels and hemoglobin mass in young healthy individuals. Nineteen healthy individuals (10 women and 9 men, age: 24 ± 4 years, height: 174 ± 11 cm, weight: 72.2 ± 12.2 kg) participated in the study. Participants were randomly assigned to an intermittent hypoxia group (Hyp, n = 10) or a placebo intermittent normoxia group (Norm, n = 9). Intermittent hypoxia consisted of five 4‐min hypoxic cycles at a targeted arterial oxygen saturation of 90% interspersed with 4‐min normoxic cycles. Air was made hypoxic by titrating nitrogen to a breathing circuit connected to a tank of compressed air. Nitrogen was not added to the breathing circuit in the intermittent normoxia condition. Pulmonary gas exchange, arterial oxygen saturation, and hemodynamics, using finger plethysmography, were continuously assessed during the intervention. Erythropoietin levels were measured before and two hours following the completion of the protocol. Hemoglobin mass was assessed using the carbon monoxide rebreathing technique the day before and seven days after exposure to intermittent hypoxia or normoxia. As anticipated, the intermittent hypoxia group had a lower arterial oxygen saturation than the intermittent normoxia group during the intervention (Hyp: 89 ± 1 vs. Norm: 98 ± 1%, p &lt; 0.01), which was equivalent to a lower fraction of inspired oxygen (Hyp: 0.119 ± 0.008, Norm: 0.209 ± 0.001, p &lt; 0.01). Erythropoietin levels did not significantly increase following exposure to intermittent hypoxia (Hyp: 8.2 ± 4.5 to 9.0 ± 4.8, Norm: 8.9 ± 1.7 to 11.1 ± 2.1 mU/ml, p = 0.56). Hemoglobin mass did not change following exposure to intermittent hypoxia (Hyp: 10.6 ± 1.4 to 10.2 ± 1.4, Norm: 9.7 ± 1.6 to 9.4 ± 1.5 g/kg, p = 0.48). Exposure to intermittent hypoxia did not affect mean arterial pressure (Hyp: 91 ± 6 to 90 ± 6, Norm: 93 ± 12 to 93 ± 12 mmHg, p = 0.84) or heart rate (Hyp: 68 ± 8 to 74 ± 9, Norm: 68 ± 8 to 68 ± 8 mmHg, p = 0.27). Respiratory rate, tidal volume, end‐tidal CO2 and total minute ventilation were not affected by intermittent hypoxia. Thus, a 40‐min session of intermittent hypoxia was not sufficient to elicit a rise in erythropoietin levels or oxygen‐carrying capacity in young healthy individuals. A longer exposure to intermittent hypoxia at a lower arterial oxygen saturation may be necessary to trigger an erythropoietin‐mediated increase in hemoglobin mass in young healthy individuals.

Volume Guaranteed Ventilation During Neonatal Transport.

To compare tidal volumes, inflating pressures and other ventilator variables of infants receiving synchronized intermitted mandatory ventilation with volume guarantee during emergency neonatal transport with those of infants receiving synchronized intermitted mandatory ventilation without volume guarantee. Retrospective observational study. A regional neonatal emergency transport service. We enrolled 77 infants undergoing emergency neonatal transfer. Forty-five infants were ventilated with synchronized intermittent mandatory ventilation with volume guarantee and 32 with synchronized intermitted mandatory ventilation without volume guarantee. Infants received synchronized intermitted mandatory ventilation with or without volume guarantee during interhospital emergency neonatal transport using a Fabian + nCPAP evolution neonatal ventilator (Software Version: 4.0.1; Acutronic Medical Instruments, Hirzel, Switzerland). We downloaded detailed ventilator data with 0.5 Hz sampling rate. We analyzed data with the Python computer language and its data science packages. The mean expiratory tidal volume of inflations was lower and less variable in infants ventilated with volume guarantee than in babies ventilated without volume guarantee (group median 4.8 vs 6.0 mL/kg; p = 0.001). Babies ventilated with synchronized intermittent mandatory ventilation with volume guarantee had on average lower and more variable peak inflating pressures than babies ventilated without volume guarantee (group median 15.5 vs 19.5 cm H2O;p = 0.0004). With volume guarantee, a lower proportion of the total minute ventilation was attributed to ventilator inflations rather than to spontaneous breaths between inflations (group median 66% vs 83%; p = 0.02). With volume guarantee, babies had fewer inflations with tidal volumes greater than 6 mL/kg and greater than 8 mL/kg (group medians 3% vs 44% and 0% vs 7%, respectively; p = 0.0001). The larger tidal volumes in the non-volume guarantee group were not associated with significant hypocapnia except in one case. During neonatal transport, synchronized intermittent mandatory ventilation with volume guarantee ventilation reduced the occurrence of excessive tidal volumes, but it was associated with larger contribution of spontaneous breaths to minute ventilation compared with synchronized intermitted mandatory ventilation without volume guarantee.

Severe diaphragmatic dysfunction with preserved activity of accessory respiratory muscles in a critically ill child: a case report of failure of neurally adjusted ventilatory assist (NAVA) and successful support with pressure support ventilation (PSV)

BackgroundNeurally adjusted ventilatory assist (NAVA) is an alternative to pressure support ventilation (PSV) potentially improving patient-ventilator interaction. During NAVA, diaphragmatic electrical activity (EAdi) is used to trigger the ventilator and perform a proportional respiratory assistance. We present a case in which the presence of severe bilateral diaphragmatic dysfunction led to a failure of NAVA. On the contrary, the preserved activity of the accessory inspiratory muscles allowed a successful respiratory assistance using PSV.Case presentationA 10-year-old girl developed quadriplegia after neurological surgery. Initially, no spontaneous breathing activity was present and volume controlled ventilation was necessary. Two months later spontaneous inspiratory efforts were observed and a maximal negative inspiratory force of − 20 cmH2O was recorded. In addition, a NAVA nasogastric tube was placed. The recorded EAdi signal, despite showing a phasic activity, had a very low amplitude (1–2 μV). Two brief (15 min) breathing trials to compare PSV (pressure support = 8 cmH2O) with NAVA (Gain = 5 cmH2O/μV, inspiratory trigger = 0.3 μV) were performed. On PSV, the patient was well adapted with stable tidal volumes, respiratory rates, minute ventilation, end-tidal and venous carbon dioxide levels. When switched to NAVA, her breathing pattern became irregular and she showed clear sign of increased work of breathing and distress: tidal volume dropped and respiratory rate rose, leading to an increase in total minute ventilation. Nevertheless, end-tidal and venous carbon dioxide rapidly increased (from 49 to 55 mmHg and from 52 to 57 mmHg, respectively). An electromyographic study documented an impairment of the diaphragm with preserved activity of the accessory inspiratory muscles.ConclusionsWe document the failure of mechanical assistance performed with NAVA due to bilateral diaphragmatic dysfunction in a critically ill child. The preserved activity of some accessory respiratory muscles allowed to support the patient effectively with pressure support ventilation, i.e. by applying a pneumatic trigger. The present case underlines (i) the importance of the integrity of the respiratory centers, phrenic nerves and diaphragm in order to perform NAVA and (ii) the possible diagnostic role of EAdi monitoring in complex cases of weaning failure.

Respiratory load compensation and perception during 10‐breath sustained inspiratory resistive loading in normal subjects

Increased load on the respiratory system is a key feature in various respiratory diseases, accompanied by ventilatory compensatory behavior and breathlessness. This increased inspiratory load is often prolonged, ranging from minutes to days, and requires the individual to adjust their breathing pattern to sustain alveolar ventilation and minimize the work of breathing, i.e. load compensation. Experimentally, this is often studied by breathing through resistive (R) loads. Most prior load compensation studies have used single breath loads within a range of adaptability for most individuals (0–40 cmH2O/l/s) to determine the load compensation mechanisms. However, during exacerbations of lung diseases, the individual must load compensate for multiple breaths against increasing load magnitudes that may exceed their ability to sustain alveolar ventilation. The aim of this study was to investigate load compensation in normal subjects when breathing for multiple breaths (10) through loads of increasing magnitudes greater than their expected ability to sustain alveolar ventilation. A threshold for load decompensation was hypothesized. Healthy participants were tested while breathing through a circuit with inspiratory flow‐resistive loads (R's: 0–100 cmH20/L/s). The loads were presented in random block order, each for 10 consecutive breaths and separated by unloaded breathing periods. The loads were presented in 2 trials, 2 times each per trial. Subjects estimated their perceived load intensity in one trial and unpleasantness in the other trial. A load compensation index (LCI) was calculated using breath phase duration and airflow. For R=0–25 cmH2O/L/s, respiratory load pattern was a load magnitude dependent increased maximum inspiratory pressure, decreased airflow, increased inspiratory duration and decreased expiratory duration. This resulted in a relatively constant total breath time, inspiratory volume, minute ventilation, PCO2, PO2 and LCI. However, decompensation was observed for R50 and R100 leading to declining minute ventilation and LCI. The results suggest, however, that increasing the duration of the R=50–100 load presentations would likely lead to hypoventilation and respiratory failure. The perception of inspiratory R load intensity and unpleasantness increased with load magnitude. The results suggest that high magnitude loads and/or long durations of loaded breathing result in increased affective response and decompensating respiratory pattern indicating that the individual is no longer able to sustain ventilation under these conditions.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Optimization techniques in respiratory control system models

One of the most complex physiological systems whose modeling is still an open study is the respiratory control system where different models have been proposed based on the criterion of minimizing the work of breathing (WOB). The aim of this study is twofold: to compare two known models of the respiratory control system which set the breathing pattern based on quantifying the respiratory work; and to assess the influence of using direct-search or evolutionary optimization algorithms on adjustment of model parameters. This study was carried out using experimental data from a group of healthy volunteers under CO2 incremental inhalation, which were used to adjust the model parameters and to evaluate how much the equations of WOB follow a real breathing pattern. This breathing pattern was characterized by the following variables: tidal volume, inspiratory and expiratory time duration and total minute ventilation. Different optimization algorithms were considered to determine the most appropriate model from physiological viewpoint. Algorithms were used for a double optimization: firstly, to minimize the WOB and secondly to adjust model parameters. The performance of optimization algorithms was also evaluated in terms of convergence rate, solution accuracy and precision. Results showed strong differences in the performance of optimization algorithms according to constraints and topological features of the function to be optimized. In breathing pattern optimization, the sequential quadratic programming technique (SQP) showed the best performance and convergence speed when respiratory work was low. In addition, SQP allowed to implement multiple non-linear constraints through mathematical expressions in the easiest way. Regarding parameter adjustment of the model to experimental data, the evolutionary strategy with covariance matrix and adaptation (CMA-ES) provided the best quality solutions with fast convergence and the best accuracy and precision in both models. CMAES reached the best adjustment because of its good performance on noise and multi-peaked fitness functions. Although one of the studied models has been much more commonly used to simulate respiratory response to CO2 inhalation, results showed that an alternative model has a more appropriate cost function to minimize WOB from a physiological viewpoint according to experimental data.

Higher Levels of Spontaneous Breathing Induce Lung Recruitment and Reduce Global Stress/Strain in Experimental Lung Injury

Spontaneous breathing (SB) in the early phase of the acute respiratory distress syndrome is controversial. Biphasic positive airway pressure/airway pressure release ventilation (BIPAP/APRV) is commonly used, but the level of SB necessary to maximize potential beneficial effects is unknown. Experimental acute respiratory distress syndrome was induced by saline lung lavage in anesthetized and mechanically ventilated pigs (n = 12). By using a Latin square and crossover design, animals were ventilated with BIPAP/APRV at four different levels of SB in total minute ventilation (60 min each): (1) 0% (BIPAP/APRV0%); (2) greater than 0 to 30% (BIPAP/APRV>0-30%); (3) greater than 30 to 60% (BIPAP/APRV>30-60%); and (4) greater than 60% (BIPAP/APRV>60%). Gas exchange, hemodynamics, and respiratory variables were measured. Lung aeration was assessed by high-resolution computed tomography. The distribution of perfusion was marked with Ga-labeled microspheres and evaluated by positron emission tomography. The authors found that higher levels of SB during BIPAP/APRV (1) improved oxygenation; (2) decreased mean transpulmonary pressure (stress) despite increased inspiratory effort; (3) reduced nonaerated lung tissue, with minimal changes in the distribution of perfusion, resulting in decreased low aeration/perfusion zones; and (4) decreased global strain (mean ± SD) (BIPAP/APRV0%: 1.39 ± 0.08; BIPAP/APRV0-30%: 1.33 ± 0.03; BIPAP/APRV30-60%: 1.27 ± 0.06; BIPAP/APRV>60%: 1.25 ± 0.04, P < 0.05 all vs. BIPAP/APRV0%, and BIPAP/APRV>60% vs. BIPAP/APRV0-30%). In a saline lung lavage model of experimental acute respiratory distress syndrome in pigs, levels of SB during BIPAP/APRV higher than currently recommended for clinical practice, that is, 10 to 30%, improve oxygenation by increasing aeration in dependent lung zones without relevant redistribution of perfusion. In presence of lung recruitment, higher levels of SB reduce global stress and strain despite an increase in inspiratory effort.

Utility of end-tidal carbon dioxide monitoring in critically ill children.

Carbon dioxide is produced in the tissues as a byproduct of aerobic metabolism, then transported to the lungs by the venous circulation and is finally eliminated during the expiratory phase of ventilation. End-tidal CO2(ETCO2) is defined as the peak CO2 value during expiration and is dependent on adequate pulmonary blood flow to the ventilating areas of the lung. ETCO2 in healthy subjects differs normally by <5 mmHg from the arterial CO2(PaCO2). An increased ETCO2-PaCO2 gap can be found in association with a decreased pulmonary blood flow and/or increased dead-space. Capnometry is the measurement of CO2 concentration of tidal gas at the airway opening. Capnography is the graphic display of the measured CO2. Capnography is an important non-invasive technique that can monitor CO2 production, pulmonary perfusion and alveolar ventilation as well as respiratory patterns.[1] Capnography has been shown to be effective as a tool for early detection of complications during anesthesia including, hypoventilation, esophageal intubation and circuit disconnection. Tinker et al.[2] concluded after a closed claim analysis for the American Society of Anesthesiology that the application of capnography and pulse oximetry together could have helped prevent 93% of avoidable anesthesia mishaps identified in their study. Capnometry is now a standard of care during administration of general anesthesia, for confirmation of placement of endotracheal tube after intubation and during transportation of an intubated patient. It has been increasingly used in intubated ventilated patients in intensive care units to safely wean patients, decrease the number of arterial blood gases, detect endotracheal displacement and prevent hypercarbia. Nasal ETCO2 monitoring is useful during procedural sedation and post-operative monitoring in the recovery room. In addition, volumetric capnography can be used as a non-invasive method to measure cardiac output. In this journal, Mehta and colleagues presented their data showing good correlation between ETCO2 and PaCO2 in neonates and children.[3] As expected correlation between ETCO2 and PaCO2 was weaker when P/F ratio was 200. Although, the mean bias with the Bland-Altman plot was low in neonates as well as children the limits of agreement is large suggesting variability of PaCO2-ETCO2 gap in their sample. Their findings confirm previously published data in neonates. The gradient between PaCO2 and ETCO2 depends upon the amount of dead space during ventilation.[4] Many variables influence the percentage of dead space to total minute ventilation. Decreased pulmonary blood flow, pulmonary disease or hyperinflation of lungs can lead to increased dead space and consequently high PaCO2-ETCO2 gap. An important limitation of using ETCO2 as a surrogate for PaCO2 measurement is that the PaCO2-ETCO2 gap changes from patient to patient based on underlying pulmonary and cardiovascular conditions and ventilation strategies and within the same patient with significant changes in the cardiopulmonary condition. In a stable patient ETCO2 monitoring can be used as trending tool during weaning or after the change in ventilator setting. Periodic measurement of PaCO2 is necessary to make sure the PaCO2-ETCO2 gap is not significantly altered. Mehta et al.[3] confirmed previous reports of ETCO2 monitoring as a valid tool in sick, mechanically ventilated neonates and children. In addition to monitoring ventilation status, continuous ETCO2 is useful in early detection of dislodgement of endotracheal tube. Waveform of capnography may be useful in detecting certain type of pulmonary pathology, such as obstructive airway disease. ETCO2 monitoring is a valuable tool during cardiopulmonary resuscitation (CPR). ETCO2 levels fall to low levels at the onset of cardiac arrest, increases with effective CPR and returns to normal levels at return of spontaneous circulation. Although there are no absolute contraindications of use of ETCO2 monitoring there few limitations for its use.[5] Large main stream capnometers can add dead space and may cause kinking of endotracheal tubes. Fortunately, most modern capnometers add a small amount dead space and are of light weight. Gas sampling rate from a side stream capnometer can lead to auto triggering and sometimes inadequate tidal volume delivery in very small neonates. Secretions and condensation in the tubing and leaks in the ventilator circuit can affect the accuracy of ETCO2. End-tidal carbon dioxide monitoring is a useful tool in the management of acutely ill and is becoming a standard of care in many clinical situations. In ventilated patients, ETCO2 monitoring is best used as a trending device for ventilation in addition to detecting endotracheal position.

APRV Mode in Ventilator Induced Lung Injury (VILI)

Ventilator-Induced Lung Injury (VILI), being a significant iatrogenic complication in the ICU patients, is associated with high morbidity and mortality. Numerous approaches, protocols and ventilation modes have been introduced and examined to decrease the incidence of VILI in the ICU patients. Airway pressure release ventilation (APRV), firstly introduced by Stock and Downs in 1987, applies higher Continuous Positive Airway Pressure (CPAP) levels in prolonged periods (P and T high) in order to preserve satisfactory lung volume and consequently alveolar recruitment. This mode benefits a time-cycled release phase to a lower set of pressure for a short period of time (P and T low i.e. release time) (1,2). While some advantages have been introduced for APRV such as efficiently recruited alveoli over time, more homogeneous ventilation, less volutrauma, probable stabilization of patent alveoli and reduction in atelectrauma, protective effects of APRV on lung damage only seem to be substantial if spontaneous breathing responds to more than 30% of total minute ventilation (3). APRV in ARDS patients should be administered cautiously; T low&lt;0.6 seconds, for recruiting collapsed alveoli; however overstretching of alveoli especially during P high should not be neglected and appropriate sedation considered. The proposed advantages for APRV give the impression of being outstanding; however, APRV, as a non-physiologic inverse ratio mode of ventilation, might result in inflammation mainly due to impaired patient-ventilator interaction explaining the negative or minimally desirable effects of APRV on inflammation (4). Consequently, continuous infusion of neuromuscular blocking drugs during ARDS has been reported to reduce mortality (5). There are insufficient confirming data on the superiority of APRV above other ventilatory methods in regard to oxygenation, hemodynamics, regional blood flow, patient comfort and length of mechanical ventilation. Based on current findings and the concept that ARDS is not a syndrome that should be treated, but rather prevented, APRV does not seem to be an ideal mode for prevention of ARDS in mechanically ventilated subjects especially in those with concurrent intra-cranial hypertension and large broncho-pleural fistulae (5). If APRV is opted for ARDS patients, it is recommended to use appropriate sedation and T low&lt; 0.6 seconds for recruiting collapsed alveoli and be cautious regarding overstretching of alveoli especially during P high. Currently APRV is recommended for carefully-selected and not all ALI/ ARDS patient.

Feasibility of early spontaneous breathing in acute respiratory distress syndrome

Airway pressure release ventilation (APRV) is as a pressure preset mode that allows unrestricted spontaneous breathing throughout the entire ventilator cycle. In ARDS, this mode may decrease the need for sedation, increase alveolar recruitment and improve hemodynamic tolerance. The aim of this study is to assess the feasibility of a protocol combining APRV settings and sedation adaptation in order to obtain levels of spontaneous breathing between 10 and 50% of total minute ventilation.

Effects of instrumental dead space reduction during weaning from synchronized ventilation in preterm infants

A majority of the modalities of synchronized ventilation in preterm infants require the use of flow sensors that can increase dead space and may adversely affect ventilator weaning. The objective of this study was to assess the effects of flow sensor dead space during synchronized intermittent mandatory ventilation (SIMV) weaning in preterm infants. Twelve preterm infants (gestational age 25+/-2 weeks, birth weight 705+/-158 g, age: 31+/-186 days, SIMV rate: 25+/-8 breaths min(-1), peak inspiratory pressure 18+/-2 cm H(2)O, positive end-expiratory pressure: 5+/-0.5 cm H(2)O, pressure support: 9+/-3 cm H(2)O, fraction of inspired oxygen: 34+/-6%) underwent two 2.5-h weaning periods during which SIMV rate was reduced twice by 5 breaths min(-1) at 30-min intervals as tolerated, with and without reduction of flow sensor dead space, in random sequence. A 30-min baseline was obtained before each weaning period. Dead space was reduced by flushing the flow sensor with a continuous gas leak flow in the endotracheal tube connector. Transcutaneous CO(2) tension during SIMV weaning periods without and with reduced dead space did not differ from baseline, whereas total minute ventilation and tidal volume were lower during the SIMV weaning period with reduced dead space. Three infants did not tolerate SIMV weaning without while one infant did not tolerate weaning with reduced dead space. SIMV weaning elicited a compensatory rise in spontaneous ventilation. When flow sensor dead space was reduced during SIMV weaning, gas exchange was maintained with lower minute ventilation. Instrumental dead space imposes a ventilatory burden during SIMV weaning in small preterm infants.

Hyperventilation in Response to Progressive Reduction in Central Blood Volume to Near Syncope

There is little evidence to support the usefulness in monitoring respiration during casualty triage and transport as an early indicator of hemorrhage severity and trauma patient outcome. We, therefore, tested the hypothesis that hyperventilation can be elicited by progressive reductions in central blood volume independent of metabolic stimuli. Progressive central hypovolemia was induced in 10 healthy subjects (5 men, 5 women) by applying lower body negative pressure (LBNP). The LBNP protocol consisted of a 5-min controlled rest period (0% LBNP) followed by progressive 5-min chamber decompressions until the onset of hemodynamic decompensation (LBNP(max)). During each LBNP stage, total minute ventilation volume (V(E)), tidal volume (V(T)), respiratory rate, oxygen uptake (Vo2), end-tidal CO2 (E(T)co2), arterial oxygen saturation (S(p)o2), and venous blood pH and lactate were measured. Compared with baseline, Vo2, S(p)o2, Po2, Pco2, pH, and lactate were unaltered throughout LBNP. V(E) was unaltered through 80% of LBNP tolerance, but increased by 54% during LBNP(max) as a result primarily of elevated V(T), while E(T)Co2 was reduced. Increased V(E) at LBNP(max) combined with reduced E(T)co2 in the absence of changes in blood and systemic metabolic stimuli support the hypothesis that severe reductions in central blood volume drive hyperventilation. The endogenous "respiratory pump" may be a protective strategy to optimize cardiac filling in conditions of central hypovolemic hypotension, but its late appearance indicates that respiratory parameters may not be useful as a clinical metric for early prediction of patient outcome during hemorrhage.

Pressure Support Ventilation and Biphasic Positive Airway Pressure Improve Oxygenation by Redistribution of Pulmonary Blood Flow

Spontaneous breathing (SB) activity may improve gas exchange during mechanical ventilation mainly by the recruitment of previously collapsed regions. Pressure support ventilation (PSV) and biphasic positive airway pressure (BIPAP) are frequently used modes of SB, but little is known about the mechanisms of improvement of lung function during these modes of assisted mechanical ventilation. We evaluated the mechanisms behind the improvement of gas exchange with PSV and BIPAP. Five pigs (25-29.3 kg) were mechanically ventilated in supine position, and acute lung injury (ALI) was induced by surfactant depletion. After stabilization, BIPAP was initiated with lower continuous positive airway pressure equal to 5 cm H2O and the higher continuous positive airway pressure titrated to achieve a tidal volume between 6 and 8 mL/kg. The depth of anesthesia was reduced, and when SB represented > or = 20% of total minute ventilation, PSV and BIPAP + SB were each performed for 1 h (random sequence). Whole chest helical computed tomography was performed during end-expiratory pauses and functional variables were obtained. Pulmonary blood flow (PBF) was marked with IV administered fluorescent microspheres, and spatial cluster analysis was used to determine the effects of each ventilatory mode on the distribution of PBF. ALI led to impairment of lung function and increase of poorly and nonaerated areas in dependent lung regions (P < 0.05). PSV and BIPAP + SB similarly improved oxygenation and reduced venous admixture compared with controlled mechanical ventilation (P < 0.05). Despite that, a significant increase of nonaerated areas in dependent regions with a concomitant decrease of normally aerated areas was observed during SB. In five of six lung clusters, redistribution of PBF from dependent to nondependent, better aerated lung regions were observed during PSV and BIPAP + SB. In this model of ALI, the improvements of oxygenation and venous admixture obtained during assisted mechanical ventilation with PSV and BIPAP + SB were explained by the redistribution of PBF toward nondependent lung regions rather than recruitment of dependent zones.

The effect of two levels of pressure support ventilation on tidal volume delivery and minute ventilation in preterm infants

Objective:To study the effect of different levels of pressure support ventilation (PSV) on respiratory parameters in preterm infants during the weaning phase of mechanical ventilation.Design/methods:In this quasi-experimental crossover study, a...

Metabolic and Respiratory Variables during Pressure Support versus Synchronized Intermittent Mandatory Ventilation

Background: Mechanically ventilated patients interact and respond differently to different modes of ventilatory support. Objectives: To assess changes in metabolic and respiratory variables during equivalent changes with either pressure support ventilation (PSV) or volume-cycled synchronized intermittent mandatory ventilation (SIMV) in non-tracheostomized patients without known obstructive pulmonary disease receiving short-term mechanical ventilation in the intensive care unit. Methods: Fourteen patients receiving volume-cycled SIMV at 12 breaths/min (SIMV_100%) were included in the study. The PSV level (PSV_100%) resulting in a minute volume and respiratory rate equivalent to that during SIMV_100% was determined for each patient. Then each patient underwent trials at 66% and 33% of initial ventilator support with volume-cycled SIMV (SIMV_66% and SIMV_33%) and PSV (PSV_66% and PSV_33%) in random order. At the end of each trial, oxygen consumption (v̇O₂), carbon dioxide production (v̇CO₂), measured energy expenditures (MEE), peak inspiratory flow, total respiratory frequency, tidal volume, minute ventilation, occlusion pressure (P_0.1) and inspiratory duty cycle (T_i/T_tot) were measured. Results: There were smaller changes in v̇O₂, v̇CO₂ and MEE when equivalent changes were applied with PSV (15.7 ± 4.4; 12.5 ± 2.2 and 15 ± 3.5%) compared with volume-cycled SIMV (32.7 ± 7.7; 23 ± 5.2 and 30.7 ± 6.8%; p < 0.05). P_0.1 and T_i/T_tot were significantly smaller during PSV (2.64 ± 0.28 and 0.38 ± 0.03 cm H₂O) than volume-cycled SIMV (4.01 ± 0.21 and 0.43 ± 0.02 cm H₂O; p < 0.05). Conclusions: Changes in the level of PSV resulted in smaller changes in metabolic and respiratory variables compared with equivalent changes in the level of volume-cycled SIMV support. PSV may be more suitable for progressive respiratory muscle reloading.

Metabolic and ventilatory physiology of the Barrow Island golden bandicoot ( Isoodon auratus barrowensis) and the northern brown bandicoot ( Isoodon macrourus)

Metabolic and ventilatory parameters were measured for the smallest and largest Isoodon bandicoots; the arid-adapted Barrow Island golden bandicoot ( Isoodon auratus barrowensis) and the tropical northern brown bandicoot ( Isoodon macrourus). I. a. barrowensis has a number of physiological characteristics that aid its tolerance of high T a and survival in a hot and dry climate, including a low and labile body temperature, a very low basal metabolic rate, low total evaporative water loss, and an effective panting mechanism. I. macrourus generally has an “average” physiology for a bandicoot despite its size, although a number of its physiological characteristics aid survival in (sub)tropical conditions. These include a low body temperature, low total evaporative water loss and minute ventilation at high ambient temperatures, and an average thermal conductance. These data support the theory that phylogeny is a more important predictor of bandicoot physiology than habitat/distribution.

A Single Ventilator for Multiple Simulated Patients to Meet Disaster Surge

ObjectivesTo determine if a ventilator available in an emergency department could quickly be modified to provide ventilation for four adults simultaneously.MethodsUsing lung simulators, readily available plastic tubing, and ventilators (840 Series Ventilator; Puritan‐Bennett), human lung simulators were added in parallel until the ventilator was ventilating the equivalent of four adults. Data collected included peak pressure, positive end‐expiratory pressure, total tidal volume, and total minute ventilation. Any obvious asymmetry in the delivery of gas to the lung simulators was also documented. The ventilator was run for almost 12 consecutive hours (5.5 hours of pressure control and more than six hours of volume control).ResultsUsing readily available plastic tubing set up to minimize dead space volume, the four lung simulators were easily ventilated for 12 hours using one ventilator. In pressure control (set at 25 mm H2O), the mean tidal volume was 1,884 mL (approximately 471 mL/lung simulator) with an average minute ventilation of 30.2 L/min (or 7.5 L/min/lung simulator). In volume control (set at 2 L), the mean peak pressure was 28 cm H2O and the minute ventilation was 32.5 L/min total (8.1 L/min/lung simulator).ConclusionsA single ventilator may be quickly modified to ventilate four simulated adults for a limited time. The volumes delivered in this simulation should be able to sustain four 70‐kg individuals. While further study is necessary, this pilot study suggests significant potential for the expanded use of a single ventilator during cases of disaster surge involving multiple casualties with respiratory failure.