Tidal Volume Variability Research Articles

Respiration and heartbeat signal detection from airflow at airway in rat by catheter flow sensor with temperature compensation function

We previously proposed an evaluation method for detecting both respiration and heartbeat signals from the airflow at the mouth (Kawaoka et al 201518th Int. Conf. on Solid-State Sensors, Actuators and Microsystems; Kawaoka et al 2015 IEEE Sensors; Kawaoka et al 2016 Technical Digest IEEE Micro Electro Mechanical Systems Conf.). In the current study, we developed a catheter flow sensor with temperature compensation that uses MEMS technologies and used it to directly detect the breathing airflow in the airway of a rat. The temperature sensors were integrated with the catheter flow sensor. Heaters working as airflow and temperature sensors were produced on polymer film by using the same fabrication process so that the temperature coefficients of their resistances would coincide. As a result, the variation in sensor outputs due to the airflow temperature changes ranging from 20 °C to 34 °C was suppressed to less than 2.5%. The developed catheter flow sensor was inserted into the airway of a rat to detect both respiration and heartbeat signals. The accuracy of the breathing airflow measurements was improved thanks to the temperature compensation. The tidal volume variations between the expired and inspired air were suppressed to within 5%. Heartbeat signal information was extracted from the measured breathing waveforms by applying a discrete Fourier transform.

Variability of Tidal Volume in Patient-Triggered Mechanical Ventilation in ARDS

Limiting tidal volume (VT) in patients with ARDS may not be achieved once patient-triggered breaths occur. Furthermore, ICU ventilators offer numerous patient-triggered modes that work differently across brands. We systematically investigated, using a bench model, the effect of patient-triggered modes on the size and variability of VT at different breathing frequencies (f), patient effort, and ARDS severity. We used a V500 Infinity ICU ventilator connected to an ASL 5000 lung model whose compliance was mimicking mild, moderate, and severe ARDS. Thirteen patient-triggered modes were tested, falling into 3 categories, namely volume control ventilation with mandatory minute ventilation; pressure control ventilation, including airway pressure release ventilation (APRV); and pressure support ventilation. Two levels of f and effort were tested for each ARDS severity in each mode. Median (first-third quartiles) VT was compared across modes using non-parametric tests. The probability of VT > 6 mL/kg ideal body weight was assessed by binomial regression and expressed as the odds ratio (OR) with 95% CI. VT variability was measured from the coefficient of variation. VT distribution over all f, effort, and ARDS categories significantly differed across modes (P < .001, Kruskal-Wallis test). VT was significantly greater with pressure support (OR 420 mL, 95% CI 332-527 mL) than with any other mode except for variable pressure support level. Risk for VT to be > 6 mL/kg was significantly increased with spontaneous breaths patient-triggered by pressure support (OR 19.36, 95% CI 12.37-30.65) and significantly reduced in APRV (OR 0.44, 95% CI 0.26-0.72) and pressure support with guaranteed volume mode. The risk increased with increasing effort and decreasing f. Coefficient of variation of VT was greater for low f and volume control-mandatory minute ventilation and pressure control modes. APRV had the greatest within-mode variability. Risk of VT > 6 mL/kg was significantly reduced in APRV and pressure support with guaranteed volume mode. APRV had the highest variability. Pressure support with guaranteed volume could be tested in patients with ARDS.

Optimization of Variable Ventilation for Physiology, Immune Response and Surfactant Enhancement in Preterm Lambs.

Preterm infants often require mechanical ventilation due to lung immaturity including reduced or abnormal surfactant. Since cyclic stretch with cycle-by-cycle variability is known to augment surfactant release by epithelial cells, we hypothesized that such in vivo mechanotransduction improves surfactant maturation and hence lung physiology in preterm subjects. We thus tested whether breath-by-breath variability in tidal volume (VT) in variable ventilation (VV) can be tuned for optimal performance in a preterm lamb model. Preterm lambs were ventilated for 3 h with conventional ventilation (CV) or two variants of VV that used a maximum VT of 1.5 (VV1) or 2.25 (VV2) times the mean VT. VT was adjusted during ventilation to a permissive pCO2 target range. Respiratory mechanics were monitored continuously using the forced oscillation technique, followed by postmortem bronchoalveolar lavage and tissue collection. Both VVs outperformed CV in blood gas parameters (pH, SaO2, cerebral O2 saturation). However, only VV2 lowered PaCO2 and had a higher specific respiratory compliance than CV. VV2 also increased surfactant protein (SP)-B release compared to VV1 and stimulated its production compared to CV. The production and release of proSP-C however, was increased with CV compared to both VVs. There was more SP-A in both VVs than CV in the lung, but VV2 downregulated SP-A in the lavage, whereas SP-D significantly increased in CV in both the lavage and lung. Compared to CV, the cytokines IL-1β, and TNFα decreased with both VVs with less inflammation during VV2. Additionally, VV2 lungs showed the most homogeneous alveolar structure and least inflammatory cell infiltration assessed by histology. CV lungs exhibited over-distension mixed with collapsed and interstitial edematous regions with occasional hemorrhage. Following VV1, some lambs had normal alveolar structure while others were similar to CV. The IgG serum proteins in the lavage, a marker of leakage, were the highest in CV. An overall combined index of performance that included physiological, biochemical and histological markers was the best in VV2 followed by VV1. Thus, VV2 outperformed VV1 by enhancing SP-B metabolism resulting in open alveolar airspaces, less leakage and inflammation and hence better respiratory mechanics.

A new global and comprehensive model for ICU ventilator performances evaluation

BackgroundThis study aimed to provide a new global and comprehensive evaluation of recent ICU ventilators taking into account both technical performances and ergonomics.MethodsSix recent ICU ventilators were evaluated. Technical performances were assessed under two FIO2 levels (100%, 50%), three respiratory mechanics combinations (Normal: compliance [C] = 70 mL cmH2O−1/resistance [R] = 5 cmH2O L−1 s−1; Restrictive: C = 30/R = 10; Obstructive: C = 120/R = 20), four exponential levels of leaks (from 0 to 12.5 L min−1) and three levels of inspiratory effort (P0.1 = 2, 4 and 8 cmH2O), using an automated test lung. Ergonomics were evaluated by 20 ICU physicians using a global and comprehensive model involving physiological response to stress measurements (heart rate, respiratory rate, tidal volume variability and eye tracking), psycho-cognitive scales (SUS and NASA-TLX) and objective tasks completion.ResultsFew differences in terms of technical performance were observed between devices. Non-invasive ventilation modes had a huge influence on asynchrony occurrence. Using our global model, either objective tasks completion, psycho-cognitive scales and/or physiological measurements were able to depict significant differences in terms of devices’ usability. The level of failure that was observed with some devices depicted the lack of adaptation of device’s development to end users’ requests.ConclusionsDespite similar technical performance, some ICU ventilators exhibit low ergonomics performance and a high risk of misusage.

Increased circadian variations in chemoreflex sensitivity in chronic heart failure

Respiratory function follows a circadian pattern, and rhythmic changes in carotid body sensitivity to blood gases may contribute to these oscillations in ventilation. Recent studies have demonstrated that the isolated rat carotid body shows enhanced responses to hypoxic and hypercapnic stimulation in the presence of melatonin, a nocturnally released hormone. Carotid body dysfunction is known to occur in several pathological conditions, including chronic heart failure (CHF). CHF is characterized by tonic hyperactivity and exaggerated reactivity of the carotid bodies to hypoxia and hypercapnia. Thus, we've begun to examine circadian rhythms in chemoreflex breathing in CHF to determine if the already heightened hypoxic and hypercapnic responses in CHF are further augmented during the night. Male Sprague‐Dawley rats were divided into either control or CHF groups. Heart failure was induced via coronary ligation. Chemoreflex breathing was assessed during the day and then again 12 hours later during the night. Animals were exposed to room air (baseline), hypoxia (10 % O2) and hypercapnia (5 % CO2). Percent change in respiratory rate from day to night were similar between CHF (17.1 % increase) and control (16.9 % increase) rats when exposed to room air, but hypoxic and hypercapnic challenges induced large circadian differences in CHF (hypoxia: 20.9 % increase; hypercapnia: 23.9 % increase) but not in control (hypoxia: 8.2 % increase; hypercapnia: 13.9 % increase) rats. CHF rats also showed robust night time circadian differences in tidal volume when exposed to room air (31.6 % increase), hypoxia (27.9 % increase), and hypercapnia (43.8 %). In contrast, circadian variations in tidal volume were attenuated in control rats (room air: 11 % increase; hypoxia: 15.6 % increase; hypercapnia: 11.0 % increase). Minute ventilation showed similar differences between CHF and control rats with CHF significantly augmenting circadian variations. CHF rats showed a 53.1 % increase in minute ventilation during the night, and a 52.9 % increase and a 78.2 % increase in response to hypoxia and hypercapnia, respectively. Control rats, in contrast, showed only a 27.7 % increase in minute ventilation to room air, a 25.1 % increase in response to hypoxia, and a 26.9 % increase in response to hypercapnia. Therefore, the data suggest that circadian rhythms in ventilatory responses are amplified in CHF. Future research may directly assess the contribution of the carotid bodies to this phenomenon.

Lung and Heart Dose Variability During Radiation Therapy of Non-Small Cell Lung Cancer

Toinvestigate the hypothesis that positional and anatomic variations during radiation therapy induce changes in lung and heart volumes and associated radiation doses. In this longitudinal investigation, variations in lung and heart volumes and standard dose parameters of mean lung dose, lung V20Gy, mean heart dose, and heart V40Gy were analyzed on weekly 4-dimensional CT scans of 15 lung cancer patients during conventionally fractionated radiochemotherapy. Tumor, individual lunglobes, and heart were delineated on the mid-ventilation phase of weekly 4-dimensional CT scans. Lung lobes and heart were also contoured on individual breathing phases of pre-, mid-, and end-of-treatment scans. Planning dose was transferred to consecutive scans via rigid registration. Volume and dose variations were assessed relative to the initial planning scan. Interfraction lung volume variability relative to week 0 was twice as large as tidal volume variability (8.0%±5.3% vs 4.0%±3.3%, P=.003). Interfraction lung volume variation ranged between 0.8% and 17.1% for individual patient means. Lower lung lobes had larger volume variability compared with upper lobes (13.5%±8.1% vs 7.0%±5.0%, P<.00001). Average mean lung dose variation was 0.5Gy (range, 0.2-1.0Gy for individual patient means) and average lung V20Gy variation 0.9% (range, 0.2%-1.6%). Average heart volume variation was 7.2% (range, 3.4%-12.6%). Average mean heart dose variation was 1.2Gy (range, 0.1-3.0Gy) and average heart V40Gy variation 1.4% (range, 0%-4.2%). Anatomic and positional variations during radiation therapy induce changes in radiation doses to lung and heart. Repeated lung and heart dose assessment will provide a better estimate of the actual delivered dose and will improve prediction models for normal tissue toxicity, if assessed in larger cohorts.

A Novel Respiratory Motion Perturbation Model Adaptable to Patient Breathing Irregularities

To develop a physical, adaptive motion perturbation model to predict tumor motion using feedback from dynamic measurement of breathing conditions to compensate for breathing irregularities. A novel respiratory motion perturbation (RMP) model was developed to predict tumor motion variations caused by breathing irregularities. This model contained 2 terms: the initial tumor motion trajectory, measured from 4-dimensional computed tomography (4DCT) images, and motion perturbation, calculated from breathing variations in tidal volume (TV) and breathing pattern (BP). The motion perturbation was derived from the patient-specific anatomy, tumor-specific location, and time-dependent breathing variations. Ten patients were studied, and 2 amplitude-binned 4DCT images for each patient were acquired within 2weeks. The motion trajectories of 40 corresponding bifurcation points in both 4DCT images of each patient were obtained using deformable image registration. An in-house 4D data processing toolbox was developed to calculate the TV and BP as functions of the breathing phase. The motion was predicted from the simulation 4DCT scan to the treatment 4DCT scan, and vice versa, resulting in 800 predictions. For comparison, noncorrected motion differences and the predictions from a published 5-dimensional model were used. The average motion range in the superoinferior direction was 9.4±4.4mm, the average ΔTV ranged from 10 to 248mm3 (-26% to 61%), and the ΔBP ranged from 0 to 0.2 (-71% to 333%) between the 2 4DCT scans. The mean noncorrected motion difference was 2.0±2.8mm between 2 4DCT motion trajectories. After applying the RMP model, the mean motion difference was reduced significantly to 1.2 ± 1.8 mm (P=.0018), a 40% improvement, similar to the 1.2 ± 1.8mm(P=.72) predicted with the 5-dimensional model. A novel physical RMP model was developed with an average accuracy of 1.2±1.8mm for interfraction motion prediction, similar to that of a published lung motion model. This physical RMP was analytically derived and is able to adapt to breathing irregularities. Further improvement of this RMP model is under investigation.

Assessment of an alternative calibration technique to record breathing pattern and its variability with respiratory inductive plethysmography.

Recent literature has raised doubts on the existing calibration methods for respiratory inductive plethysmography (RIP) which can lead to erroneous estimation of tidal volume. This study sought to validate an alternative calibration method to record tidal volume and tidal volume variability during rest and exercise by comparing the measurements obtained from a RIP device against a pneumotachograph (PT) for breath-by-breath analysis. 11 healthy individuals were recruited. Tidal volume and variability were simultaneously recorded during 30min of rest and 20min of exercises. Pearson correlation coefficients for group mean tidal volume between PT and RIP were 0.8 during rest and exercises. No statistical significant difference was observed in tidal volume variability between devices during rest and exercises. This study provides support for an alternative calibration method, which addresses existing limitations. The simplicity of equipment set up process and no need to perform subject cooperated calibration procedure will improve the respiratory monitoring process.

Comparison of different degrees of variability in tidal volume to prevent deterioration of respiratory system elastance in experimental acute lung inflammation

BackgroundVariable ventilation improves respiratory function, but it is not known whether the amount of variability in tidal volume (VT) can be reduced in recruited lungs without a deterioration of respiratory system elastance. MethodsAcute lung inflammation was induced by intratracheal instillation of lipopolysaccharide in 35 Wistar rats. Twenty-eight animals were anaesthetized and ventilated in volume-controlled mode. Lungs were recruited by random variation of VT (mean 6 ml kg−1, coefficient of variation 30%, normal distribution) for 30 min. Animals were randomly assigned to different amounts of VT variability (n+7 for 90 min per group): 30, 15, 7.5, or 0%. Lung function, diffuse alveolar damage, and gene expression of biological markers associated with cell mechanical stress, inflammation, and fibrogenesis were assessed. Seven animals were not ventilated and served as controls for post-mortem analyses. ResultsA VT variability of 30%, but not 15, 7.5, or 0%, prevented deterioration of respiratory system elastance [Mean (SD) −7.5 (8.7%), P<0.05; 21.1 (9.6%), P<0.05; 43.3 (25.9), P<0.05; and 41.2 (16.4), P<0.05, respectively]. Diffuse alveolar damage was lower with a VT variability of 30% than with 0% and without ventilation, because of reduced oedema and haemorrhage. A VT variability of 30, 15, or 7.5% reduced the gene expression of amphiregulin, cytokine-induced neutrophil chemoattractant-1, and tumour necrosis factor α compared with a VT variability of 0%. ConclusionsIn this model of acute lung inflammation, a VT variability of 30%, compared with 15 and 7.5%, was necessary to avoid deterioration of respiratory system elastance and was not associated with lung histological damage.

Assisted Ventilation in Patients With Acute Respiratory Distress Syndrome

BACKGROUND: In patients with acute respiratory distress syndrome (ARDS), the use of assisted mechanical ventilation is a subject of debate. Assisted ventilation has benefits over controlled ventilation, such as preserved diaphragm function and improved oxygenation. Therefore, higher level of patient of ventilator assist may be preferable in ARDS. However, assisted modes may also increase the risk of high tidal volumes and lung-distending pressures. The current study aims to quantify how differences in freedom to control the ventilator affect lung-protective ventilation, breathing pattern variability, and patient-ventilator interaction. METHODS: Twelve patients with ARDS were ventilated in a randomized order with assist pressure control ventilation (PCV), pressure support ventilation (PSV), and neurally adjusted ventilatory assist (NAVA). Transpulmonary pressure, tidal volume, diaphragm electrical activity, and patient-ventilator interaction were measured. Respiratory variability was assessed using the coefficient of variation of tidal volume. RESULTS: During inspiration, transpulmonary pressure was slightly lower with NAVA (10.3 +/- 0.7, 11.2 +/- 0.7, and 9.4 +/- 0.7 cm H2O for PCV, PSV, and NAVA, respectively; P < 0.01). Tidal volume was similar between modes (6.6 [5.7 to 7.0], 6.4 [5.8 to 7.0], and 6.0 [5.6 to 7.3] ml/kg for PCV, PSV, and NAVA, respectively), but respiratory variability was higher with NAVA (8.0 [6.4 to 10.0], 7.1 [5.9 to 9.0], and 17.0 [12.0 to 36.1] % for PCV, PSV, and NAVA, respectively; P < 0.001). Patient-ventilator interaction improved with NAVA (6 [5 to 8] % error) compared with PCV (29 [14 to 52] % error) and PSV (12 [9 to 27] % error); P < 0.0001. CONCLUSION: In patients with mild-to-moderate ARDS, increasing freedom to control the ventilator maintains lung-protective ventilation in terms of tidal volume and lung-distending pressure, but it improves patient-ventilator interaction and preserves respiratory variability.

Increased ventilatory variability and complexity in patients with hyperventilation disorder.

It has been hypothesized that hyperventilation disorders could be characterized by an abnormal ventilatory control leading to enhanced variability of resting ventilation. The variability of tidal volume (VT) often depicts a nonnormal distribution that can be described by the negative slope characterizing augmented breaths formed by the relationship between the probability density distribution of VT and VT on a log-log scale. The objectives of this study were to describe the variability of resting ventilation [coefficient of variation (CV) of VT and slope], the stability in respiratory control (loop, controller and plant gains characterizing ventilatory-chemoresponsiveness interactions) and the chaotic-like dynamics (embedding dimension, Kappa values characterizing complexity) of resting ventilation in patients with a well-defined dysfunctional breathing pattern characterized by air hunger and constantly decreased PaCO2 during a cardiopulmonary exercise test. Compared with 14 healthy subjects with similar anthropometrics, 23 patients with hyperventilation were characterized by increased variability of resting tidal ventilation (CV of VT median [interquartile]: 26% [19-35] vs. 36% [28-48], P = 0.020; slope: -6.63 [-7.65; -5.36] vs. -3.88 [-5.91; -2.66], P = 0.004) that was not related to increased chemical drive (loop gain: 0.051 [0.039-0.221] vs. 0.044 [0.012-0.087], P = 0.149) but that was related to an increased ventilatory complexity (Kappa values, P < 0.05). Plant gain was decreased in patients and correlated with complexity (with Kappa 5 - degree 5: Rho = -0.48, P = 0.006). In conclusion, well-defined patients suffering from hyperventilation disorder are characterized by increased variability of their resting ventilation due to increased ventilatory complexity with stable ventilatory-chemoresponsiveness interactions.

Sigh-induced changes of breathing pattern in preterm infants.

Sighs are thought to play an important role in control of breathing. It is unclear how sighs are triggered, and whether preterm birth and lung disease influence breathing pattern prior to and after a sigh in infants. To assess whether frequency, morphology, size, and short-term variability in tidal volume (VT) before, during, and after a sigh are influenced by gestational age at birth and lung disease (bronchopulmonary dysplasia, BPD) in former preterm infants and healthy term controls measured at equivalent postconceptional age (PCA). We performed tidal breathing measurements in 143 infants during quiet natural sleep at a mean (SD) PCA of 44.8 (1.3) weeks. A total of 233 sighs were analyzed using multilevel, multivariable regression. Sigh frequency in preterm infants increased with the degree of prematurity and severity of BPD, but was not different from that of term controls when normalized to respiratory rate. After a sigh, VT decreased remarkably in all infants (paired t-test: P < 0.001). There was no major effect of prematurity or BPD on various indices of sigh morphology and changes in VT prior to or after a sigh. Short-term variability in VT modestly increased with maturity at birth and infants with BPD showed an earlier return to baseline variability in VT following a sigh. In early infancy, sigh-induced changes in breathing pattern are moderately influenced by prematurity and BPD in preterm infants. The major determinants of sigh-related breathing pattern in these infants remain to be investigated, ideally using a longitudinal study design.

Pressure regulated volume controlled ventilation versus synchronized intermittent mandatory ventilation in COPD patients suffering from acute respiratory failure

BackgroundVolume controlled ventilation (VC) allows a set tidal volume to be guaranteed but it causes excessive airway pressures that may lead to barotrauma. Pressure controlled ventilation (PC) limits ventilator-induced lung injury but has a disadvantage of variable tidal volume delivery. Pressure-regulated volume controlled ventilation is a kind of dual-control ventilation that combines the advantages of both volume controlled and pressure controlled ventilation. ObjectiveTo compare the pressure regulated volume controlled ventilation (PRVC) versus traditional synchronized intermittent mandatory ventilation (SIMV) in chronic obstructive pulmonary disease (COPD) patients suffering from acute respiratory failure. Patients and methodsThis prospective study was carried on 30 COPD patients suffering from acute respiratory failure, divided in two groups: group 1 patients were ventilated using the SIMV mode and group 2 patients were ventilated using the PRVC mode. The arterial blood gas (ABG) parameters, ventilation data, complications and prognosis were compared in the two groups. ResultsThe ABG parameters improved better in the PRVC group after 6 and 48h. The peak inspiratory pressure (PIP) values were lower in the PRVC group. There were fewer complications (33% in group 2 versus 86% in group 1). The prognosis was better in PRVC group as 13 patients (86%) were weaned, 1 patient (7%) died and 1 patient (7%) failed to be weaned. On the other hand, 6 patients (40%) were weaned, 3 patients (20%) died and 6 patients (40%) failed to be weaned in the SIMV group. ConclusionThe PRVC mode is better than the volume controlled SIMV mode in ventilating COPD patients with acute exacerbations and type II respiratory failure.

Assisted Ventilation in Patients with Acute Respiratory Distress Syndrome: Lung-distending Pressure and Patient-Ventilator Interaction.

In patients with acute respiratory distress syndrome (ARDS), the use of assisted mechanical ventilation is a subject of debate. Assisted ventilation has benefits over controlled ventilation, such as preserved diaphragm function and improved oxygenation. Therefore, higher level of "patient control" of ventilator assist may be preferable in ARDS. However, assisted modes may also increase the risk of high tidal volumes and lung-distending pressures. The current study aims to quantify how differences in freedom to control the ventilator affect lung-protective ventilation, breathing pattern variability, and patient-ventilator interaction. Twelve patients with ARDS were ventilated in a randomized order with assist pressure control ventilation (PCV), pressure support ventilation (PSV), and neurally adjusted ventilatory assist (NAVA). Transpulmonary pressure, tidal volume, diaphragm electrical activity, and patient-ventilator interaction were measured. Respiratory variability was assessed using the coefficient of variation of tidal volume. During inspiration, transpulmonary pressure was slightly lower with NAVA (10.3 ± 0.7, 11.2 ± 0.7, and 9.4 ± 0.7 cm H2O for PCV, PSV, and NAVA, respectively; P < 0.01). Tidal volume was similar between modes (6.6 [5.7 to 7.0], 6.4 [5.8 to 7.0], and 6.0 [5.6 to 7.3] ml/kg for PCV, PSV, and NAVA, respectively), but respiratory variability was higher with NAVA (8.0 [6.4 to 10.0], 7.1 [5.9 to 9.0], and 17.0 [12.0 to 36.1] % for PCV, PSV, and NAVA, respectively; P < 0.001). Patient-ventilator interaction improved with NAVA (6 [5 to 8] % error) compared with PCV (29 [14 to 52] % error) and PSV (12 [9 to 27] % error); P < 0.0001. In patients with mild-to-moderate ARDS, increasing freedom to control the ventilator maintains lung-protective ventilation in terms of tidal volume and lung-distending pressure, but it improves patient-ventilator interaction and preserves respiratory variability.

Design and Evaluation of an Intelligent Remote Tidal Volume Variability Monitoring System in E-Health Applications.

A reliable long-term monitoring and diagnosis of breath disorders at an early stage provides an improvement of medical act, life expectancy, and quality of life while decreasing the costs of treatment and medical services. Therefore, a real-time unobtrusive monitoring of respiration patterns, as well as breath parameters, is a critical need in medical applications. In this paper, we propose an intelligent system for patient home care, capable of measuring respiration rate and tidal volume variability via a wearable sensing technology. The proposed system is designed particularly for the goal of diagnosis and treatment in patients with pathological breathing, e.g., respiratory complications after surgery or sleep disorders. The complete system was comprised of wearable calibrated accelerometer sensor, Bluetooth low energy, and cloud database. The experiments are conducted with eight subjects and the overall error in respiration rate calculation is obtained 0.29%±0.33% considering SPR-BTA spirometer as the reference. We also introduce a method for tidal volume variability estimation while validated using Pearson correlation. Furthermore, since it is essential to detect the critical events resulted from sudden rise or fall in per breath tidal volume of the patients, we provide a technique to automatically find the accurate threshold values based on each individual breath characteristics. Therefore, the system is able to detect the major changes, precisely by more than 98%, and provide immediate feedback such as sound alarm for round-the-clock respiration monitoring.

Acute Activation of Carotid Chemoreceptors Increases Ventilatory Instability in Healthy Humans

Patients with sleep apnea exhibit ventilatory instability and increased carotid chemoreceptor activity. Whether ventilatory instability is directly related to altered chemoreceptor activity has not been examined in humans. Therefore we tested the hypothesis that acute activation of the carotid chemoreflex with hypoxia (10% O2) would increase breathing variability (assessed by coefficient of variation of tidal volume {%CV}) and blunting the peripheral chemoreflex with IV dopamine would attenuate the response. To test this hypothesis, nine healthy subjects (3 M/6 F) were studied on two separate study days: 1) saline or 2) low‐dose dopamine infusion. Individualized dopamine dose (1‐4 mg/kg/min), that maximally blunted chemoreflex sensitivity, was identified during a separate screening visit. Respiratory rate (RR), tidal volume (TV), end tidal CO2 (ETCO2)and O2 (ETO2) were measured. Baseline measures were similar between days. Saline infusion did not affect RR, TV, end tidal gases, or %CV. However, dopamine infusion significantly increased %CV (25 ± 5 to 32 ± 6 %; p&lt;0.05) and ETCO2 (0.3 ± 0.1 %; p&lt;0.0001) without affecting RR, or TV. Hypoxia increased %CV during saline infusion (18 ± 3 to 29 ± 3%; p&lt;0.05), and this effect was blunted during dopamine infusion (31 ± 6 to 38 ± 6%; p&gt;0.05). These data indicate hypoxia increases respiratory variability and this effect is mediated by the carotid chemoreceptors. Furthermore, the effect of increased chemoreceptor drive on ventilatory instability, such as that seen in sleep apnea, may be blunted by low‐dose dopamine in humans. These data provide a potential therapeutic target for improving ventilatory instability in human disease.&#x0D; Funding:NIH DK090541

Physiologic comparison of neurally adjusted ventilator assist, proportional assist and pressure support ventilation in critically ill patients

To compare, in a group of difficult to wean critically ill patients, the short-term effects of neurally adjusted ventilator assist (NAVA), proportional assist (PAV+) and pressure support (PSV) ventilation on patient–ventilator interaction. Methods: Seventeen patients were studied during NAVA, PAV+ and PSV with and without artificial increase in ventilator demands (dead space in 10 and chest load in 7 patients). Prior to challenge addition the level of assist in each of the three modes tested was adjusted to get the same level of patient's effort. Results: Compared to PSV, proportional modes favored tidal volume variability. Patient effort increase after dead space was comparable among the three modes. After chest load, patient effort increased significantly more with NAVA and PSV compared to PAV+. Triggering delay was significantly higher with PAV+. The linear correlation between tidal volume and inspiratory integral of transdiaphragmatic pressure (PTPdi) was weaker with NAVA than with PAV+ and PSV on account of a weaker inspiratory integral of the electrical activity of the diaphragm (∫EAdi)–PTPdi linear correlation during NAVA [median (interquartile range) of r2, determination of coefficient, 16.2% (1.4–30.9%)]. Conclusion: Compared to PSV, proportional modes favored tidal volume variability. The weak ∫EAdi–PTPdi linear relationship during NAVA and poor triggering function during PAV+ may limit the effectiveness of these modes to proportionally assist the inspiratory effort.

The volume dependence of stress relaxation in the rat respiratory system

ABSTRACTAim: To investigate the volume dependence of respiratory system stress relaxation in anesthetized, positive-pressure ventilated rats. Materials and methods: The effects on respiratory system stress relaxation of changing the end inflation volume while keeping tidal volume constant, and of changing the tidal volume while maintaining constant end inflation volume, were separately studied by the end-inflation occlusion method. These changes were obtained by inflating the respiratory system starting from different volumes above functional residual capacity. Results: We found that: (1) a simple exponential equation well describe the visco-elastic pressure drop for different inflation modalities; (2) the stress relaxation-linked, visco-elastic pressure drop, increases with increasing the tidal volume and keeping the end-inflation volume constant, but is independent from the end-inflation lung volume at constant tidal volumes; (3) time constant values show a significant increment with end-inflation volume at constant tidal volume but result independent from tidal volume variation at constant end-inflation volume. Conclusions: Stress relaxation-linked pressure dissipation increases with increasing tidal volume independently from end-inspiratory volume.

Variabilité ventilatoire et assistance ventilatoire en réanimation

Ventilation is not monotonous. In contrast, the breathing pattern components vary with time, not only with respect to homeostatic adjustment needs, but also from one cycle to another (often referred to as the “anharmonic” period). These breath-by-breath variations in tidal volume and its components are a result of the complex and chaotic nature — in mathematical terms — of the central ventilator command that creates the tidal volume. Respiratory variability reflects “healthy’ breathing, whereas decreasing variability of the breathing pattern components is a reflection of “poor health”. This decrease may be due to central command changes or, it may be due to the “filtering” of the central variability changes in regards to the mechanical loads: the complexity of the ventilatory flow and its breath-by-breath variability is related to both the neuro-mechanical coupling and the load-capacity adequacy. Thus, in intensive care, low ventilatory variability predicts mechanical ventilation weaning failure and is also an independent risk factor of death. Moreover, in animal models, the addition of extrinsic variability has shown improvements in both lung mechanics and gas exchange. The restoration of a natural variability through new mechanical ventilation modes may prove beneficial.

Carotid body denervation improves autonomic and cardiac function and attenuates disordered breathing in congestive heart failure

In congestive heart failure (CHF), carotid body (CB) chemoreceptor activity is enhanced and is associated with oscillatory (Cheyne-Stokes) breathing patterns, increased sympathetic nerve activity (SNA) and increased arrhythmia incidence. We hypothesized that denervation of the CB (CBD) chemoreceptors would reduce SNA, reduce apnoea and arrhythmia incidence and improve ventricular function in pacing-induced CHF rabbits. Resting breathing, renal SNA (RSNA) and arrhythmia incidence were measured in three groups of animals: (1) sham CHF/sham-CBD (sham-sham); (2) CHF/sham-CBD (CHF-sham); and (3) CHF/CBD (CHF-CBD). Chemoreflex sensitivity was measured as the RSNA and minute ventilatory (VE) responses to hypoxia and hypercapnia. Respiratory pattern was measured by plethysmography and quantified by an apnoea-hypopnoea index, respiratory rate variability index and the coefficient of variation of tidal volume. Sympatho-respiratory coupling (SRC) was assessed using power spectral analysis and the magnitude of the peak coherence function between tidal volume and RSNA frequency spectra. Arrhythmia incidence and low frequency/high frequency ratio of heart rate variability were assessed using ECG and blood pressure waveforms, respectively. RSNA and VE responses to hypoxia were augmented in CHF-sham and abolished in CHF-CBD animals. Resting RSNA was greater in CHF-sham compared to sham-sham animals (43±5% max vs. 23 ± 2% max, P<0.05), and this increase was not found in CHF-CBD animals (25±1% max, P<0.05 vs. CHF-sham). Low frequency/high frequency heart rate variability ratio was similarly increased in CHF and reduced by CBD (P<0.05). Respiratory rate variability index, coefficient of variation of tidal volume and apnoea-hypopnoea index were increased in CHF-sham animals and reduced in CHF-CBD animals (P<0.05). SRC (peak coherence) was increased in CHF-sham animals (sham-sham 0.49±0.05; CHF-sham 0.79±0.06), and was attenuated in CHF-CBD animals (0.59±0.05) (P<0.05 for all comparisons). Arrhythmia incidence was increased in CHF-sham and reduced in CHF-CBD animals (213±58 eventsh(-1) CHF, 108±48 eventsh(-1) CHF-CBD, P<0.05). Furthermore, ventricular systolic (3.8±0.7 vs. 6.3±0.5ml, P<0.05) and diastolic (6.3±1.0 vs. 9.1±0.5ml, P<0.05) volumes were reduced, and ejection fraction preserved (41±5% vs. 54±2% reduction from pre-pace, P<0.05) in CHF-CBD compared to CHF-sham rabbits. Similar patterns of changes were observed longitudinally within the CHF-CBD group before and after CBD. In conclusion, CBD is effective in reducing RSNA, SRC and arrhythmia incidence, while improving breathing stability and cardiac function in pacing-induced CHF rabbits.