Tidal volumes and volume ventilators.
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Humans↗
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Results for “Tidal Volume”
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Tidal volume losses of volume-limited ventilators.
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Humans↗
Influence of low tidal volumes on gas exchange in acute respiratory distress syndrome and the role of recruitment maneuvers.
UNLABELLED: BACKGROUND Use of a low tidal volume (V(T)) strategy in the treatment of acute respiratory distress syndrome can lead to a decrease in oxygenation. This study evaluated the safety and efficacy of a recruitment maneuver (RM) in this setting. METHODS: Twelve patients with acute respiratory distress syndrome were studied within 48 hours of diagnosis. Baseline gas exchange, hemodynamics, and respiratory mechanics were determined and patients were placed on a V(T) of 6 mL/kg. Measurements were repeated and an RM of 30 cm H20 for 40 seconds was performed. Measurements were repeated at 30 minutes and 2 hours post-RM. RESULTS: Decreasing V(T) resulted in a decrease in arterial oxygenation (from 91 +/- 9 mm Hg to 75 +/- 9 mm Hg, p < 0.01), an increase in shunt (from 19 +/- 3.7% to 23 +/- 5%, p < 0.01), and a decrease in lung compliance (from 37 mL/cm H2O to 33 mL/cm H2O, < 0.05). At 30 minutes post-RM, oxygenation improved to 99 +/- 16 mm Hg, shunt decreased to 17 +/- 3%, and lung compliance improved to 39 mL/cm H2O (p < 0.05). Two hours later, oxygenation fell (86 +/- 12 mm Hg), shunt increased (20 +/- 3%), and compliance diminished (36 mL/cm H2O). There were no hemodynamic or barotraumatic complications. CONCLUSION: An RM transiently improves gas exchange during low V(T)ventilation. RMs are well tolerated and no hemodynamic consequences were seen.
Accidents, Traffic↗
Early changes in lung gene expression due to high tidal volume.
The purpose of this study was to use gene expression profiling to understand how adult rat lung responds to high tidal volume (HV) ventilation in vivo. HV ventilation for 30 minutes did not cause discernable lung injury (in terms of altered mechanics or histology) but caused obvious injury when continued for 90 minutes. However, at 30-minute ventilation, HV caused significant upregulation of 10 genes and suppression of 12 genes. Among the upregulated genes were transcription factors, stress proteins, and inflammatory mediators; the downregulated genes were exemplified by metabolic regulatory genes. On the basis of cluster analysis, we studied Egr-1, c-Jun, heat shock protein 70, and interleukin (IL)-1beta in further detail. Temporal studies demonstrated that Egr-1 and c-Jun were increased early and before heat shock protein 70 and IL-1beta. Spatial studies using in situ hybridization and laser capture microscopy revealed that all four genes were upregulated primarily in the bronchiolar airway epithelium. Furthermore, at 90 minutes of HV ventilation, a significant increase in intracellular IL-1beta protein was observed. Although there are limitations to gene array methodology, the current data suggest a global hypothesis that (1). the effects of HV are cumulative; (2). specific patterns of gene activation and suppression precede lung injury; and (3). alteration of gene expression after mechanical stretch is pathogenic.
Animals↗
Influence of tidal volume on the compliance of the respiratory system in mechanically ventilated newborn infants.
We measured the compliance of the respiratory system (Crs) at 4 different tidal volumes (VT = 2.5, 5.0, 7.5, 10.0 ml/kg) in 29 mechanically ventilated newborn infants and determined the VT associated with the highest Crs ("optimal" VT) and with the lowest Crs ("worst" VT). Crs depended on the VT in all newborn infants investigated. The "optimal" VT most frequently observed was 2.5 and 5.0 ml/kg and the "worst" VT most frequently observed was 2.5 and 10.0 ml/kg. Mean Crs at the "optimal" VT was 62.3% higher than at the "worst" VT. The "optimal" VT was lower (2.5 ml/kg) in newborn infants with controlled ventilation than in newborn infants with intermittent mandatory ventilation (5.0 ml/kg). We conclude that it may be useful to determine the VT associated with the highest Crs in order to avoid unnecessarily high inflation pressures for the mechanical ventilation of newborn infants. Further studies are needed to assess long-term effects of such a Crs guided respirator therapy.
Humans↗
The dead space to tidal volume ratio in the diagnosis of pulmonary embolism.
In order to assess the value of the measurement of the physiologic dead space (VD) to tidal volume (VT) ratio in pulmonary embolism (PE), a prospective study was performed in hospital inpatients suspected to have PE (n = 110; mean age +/- SD, 52.2 +/- 15.5 yr). In 16 of 29 patients in whom the diagnosis of PE was excluded on the basis of a normal radioisotope perfusion scan and/or normal pulmonary angiogram, VD/VT was less than 40%; in the other 13 patients, a VD/VT greater than 40% was associated with an abnormal spirogram. In all patients in whom PE was angiographically diagnosed (n = 16), VD/VT was greater than 40%. In the remaining 65 patients, a high probability of PE was rarely (6%) associated with a normal VD/VT, whereas in patients with a low probability of PE, 71% had normal VD/VT values. These data indicate that a VD/VT value of less than 40% makes the diagnosis of PE extremely unlikely, whereas VD/VT value greater than 40% in the presence of a normal spirogram is highly suggestive of PE. The diagnostic sensitivity of a VD/VT greater than 0.4 with a normal spirogram as a positive test of PE, and a VD/VT less than 0.4 excluding the diagnosis of PE was 100%, whereas the specificity was 94%; applying Bayesian analysis, the probability of a correct diagnosis of PE using these criteria in a similar population would be 90.5%, and of excluding PE, 96.7%. Thus, as a diagnostic test in PE, VD/VT measurement is comparable, in terms of sensitivity and specificity, to radioisotope lung scanning.
Adult↗
Routine use of pressure-volume loops during mechanical ventilation. Determination of optimal combination of flow, tidal volume, and positive end-expiratory pressure.
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Humans↗
The influence of PEEP and tidal volume on central blood volume.
BACKGROUND AND OBJECTIVE: Measurement of central blood volumes (CBV), such as global end-diastolic volume (GEDV) and right ventricular end-diastolic volume (RVEDV) are considered appropriate estimates of intravascular volume status. However, to apply those parameters for preload assessment in mechanically ventilated patients, the influence of tidal volume (TV) and positive endexpiratory airway pressure (PEEP) on those parameters must be known. METHODS: In 13 mechanically ventilated piglets, the effect of low (10 mL kg(-1)) and high (20 mL kg(-1)) TVs on CBV was investigated in absence and presence of PEEP (0 and 15 cm H(2)O). GEDV, RVEDV, right heart (RHEDV) and left heart end-diastolic volume (LHEDV) were measured by thermodilution. Blood flow on the descending thoracic aorta measured with an ultrasonic flow-probe served to determine stroke volume (SV). Measurements were performed during baseline conditions, after volume loading with previously extracted haemodilution blood (20 mL kg(-1)) and following haemorrhage (30 mL kg(-1)). RESULTS: Application of PEEP decreased GEDV and SV significantly (P < 0.05). Augmenting TV did not reduce GEDV systematically, but significantly reduced SV (P < 0.05). Changes in ventilator settings only influenced RVEDV following volume loading (P < 0.05). RHEDV and LHEDV decreased following application of PEEP, but only RHEDV decreased after augmenting TV at baseline and following volume loading. Correlation of SV with parameters of CBV was r = 0.487 (P < 0.01) for GEDV, r = 0.553 (P < 0.01) for RVEDV, r = 0.596 (P < 0.01) for RHEDV and r = 0.303 (P < 0.01) for LHEDV. CONCLUSION: Application of PEEP decreases CBV and SV. Augmenting TV reduces SV but not CBV. There is a moderate correlation between parameters of CBV and cardiac performance.
Animals↗
Ventilation with smaller tidal volumes: a quantitative systematic review of randomized controlled trials.
In this quantitative systematic review we assessed the effects of ventilation with smaller tidal volume (VT) on morbidity and mortality in patients aged 16 yr or older affected by acute lung injury and acute respiratory distress syndrome. Five randomized trials (1202 patients) comparing ventilation using smaller VT and/or low airway driving pressure (plateau pressure 30 cm H2O or less), resulting in VT of 7 mL/kg or less versus ventilation that uses VT in the range of 10 to 15 mL/kg, were identified after a systematic search of The Cochrane Central Register of Controlled Trials, MEDLINE, EMBASE, CINAHL, databases of current research, reference lists, and "gray literature." Mortality at day 28 was significantly reduced by lung-protective ventilation (relative risk [RR], 0.74; confidence interval [CI], 0.61-0.88), whereas beneficial effect on long-term mortality was uncertain (RR, 0.84; CI, 0.68-1.05). The comparison between small and conventional VT was not significantly different if a plateau pressure less than or equal to 31 cm H2O in the control group was used (RR, 1.13; CI, 0.88-1.45). Clinical heterogeneity, such as different lengths of follow-up and higher plateau pressures in control arms in two trials, make the interpretation of the combined results difficult.
Adult↗
A method for measuring tidal volume and lung compliance in intubated neonates in the presence of endotracheal tube leakage.
Leakage around the uncuffed endotracheal tube is a major cause of error in the measurement of tidal volume and compliance in intubated neonates. A correction for the leakage can be made if the intratracheal pressure is measured during inflation provided the compliance is linear and the inflation flow is held constant. A two parameter function is given that describes the pressure-time relationship under the above mentioned conditions. The validity of the function has been tested using a model of the system tube-trachea-lung. In practice, the calculation is done from data obtained by graphical analysis of the pressure-time curve.
Animals↗
Adjusting positive end-expiratory pressure and tidal volume in acute respiratory distress syndrome according to the pressure-volume curve.
BACKGROUND: Management of acute respiratory distress syndrome (ARDS) patients implies the selection of the adequate ventilatory parameters, essentially PEEP and tidal volume (Vt), to prevent ventilator-induced lung injury. These parameters should be reset as the lung injury evolves. Among the different methods proposed for the adjustment of the ventilator, the measurement of the P-V curve has emerged as a useful, although debated, tool. Our aim has been to study the relationship between the different inflection points of the P-V curve in ARDS patients, and to assess the changes in the empiric PEEP and Vt (PEEP(emp), V(temp) following its use. METHODS: P-V curves were measured in 27 patients (lung injury score [LIS] >or= 2, 69 measurements) by means of the low-flow continuous inflation method. RESULTS: A lower inflection point (LIP) was found in all patients and, although it correlated with the PEEP(emp), there was only a fair concordance, so the PEEP was modified in 80% of the cases. The expiratory inflection point (EIP) was significantly lower than the LIP (6.3 +/- 1.7 vs. 8.1 +/- 3.2, P = 0.008). An upper inflection point was observed in 16 measurements (23%) and the Vt was reset in 20% of the cases. Both PEEP and Vt were readjusted on 10 occasions (14%). Only the EIP was significantly higher on the first 3 days of mechanical ventilation. The LIS was correlated with all the inflection points. There were no differences for any parameter independent of the cause of the ARDS (pulmonary/extrapulmonary). CONCLUSIONS: The quasi-static measurement of the P-V curve is a simple method, easy to interpret, for objective adjustment of the ventilatory parameters in ARDS patients as the lung injury evolves. The implementation of this strategy may vary the empiric clinical practice. The role of the EIP for the evaluation of the severity of lung injury deserves further investigation.
Acute Disease↗
Effects of mean airway pressure and tidal volume on lung and chest wall mechanics in the dog.
Dependencies of the dynamic mechanical properties of the respiratory system on mean airway pressure (Paw) and the effects of tidal volume (VT) are not completely clear. We measured resistance and dynamic elastance of the total respiratory system (Rrs and Ers), lungs (RL and EL), and chest wall (Rcw and Ecw) in six healthy anesthetized paralyzed dogs during sinusoidal volume oscillations at the trachea (50-300 ml; 0.4 Hz) delivered at mean Paw from -9 to +23 cmH2O. Changes in end-expiratory lung volume, estimated with inductance plethysmographic belts, showed a typical sigmoidal relationship to mean Paw. Each dog showed the same dependencies of mechanical properties on mean Paw and VT. All elastances and resistances were minimal between 5 and 10 cmH2O mean Paw. All elastances, Rrs, and RL increased greatly with decreasing Paw below 5 cmH2O. Ers and EL increased above 10 cmH2O. Ecw, Ers, Rcw, and Rrs decreased slightly with increasing VT, but RL and EL were independent of VT. We conclude that 1) respiratory system impedance is minimal at the normal mean lung volume of supine anesthetized paralyzed dogs; 2) the dependency of RL on lung volume above functional residual capacity is dependent on VT and respiratory frequency; and 3) chest wall, but not lung, mechanical behavior is nonlinear (i.e., VT dependent) at any given lung volume.
Air Pressure↗
Contribution of chemical feedback loops to breath-to-breath variability of tidal volume.
We tested whether chemical feedback loops contribute to the breath-to-breath correlations seen in respiratory cycle parameters. We have analyzed tidal volume (VT) of seven anesthetized, vagotomized, spontaneously breathing rats and the peaks of the 'integrated' phrenic neurograms (P) of another twelve anesthetized, vagotomized, paralyzed and artificially ventilated rats. Animals were studied while breathing 100% O2, 4% CO2 in O2 and/or room air. Our analysis consisted of fitting a first-order autoregressive (AR1) model to each measured variable in steady-state conditions. We found that: (1) breath-to-breath fluctuations of VT could be described by a first-order autoregressive model in which the fluctuation of VT on each breath from its mean level is correlated with that of the immediately preceding breath; (2) breath-to-breath fluctuations of P were not correlated with those of previous breaths, because successive values of P were uncorrelated random variables. Hypercapnia enhanced correlations in VT (3 rats) but not in P (12 rats). We propose that breath-to-breath correlations of VT in anesthetized, vagotomized and spontaneously breathing rats may reflect the effects of noise in respiratory chemical feedback loops.
Animals↗
The effects of tidal volume demand on work of breathing during simulated lung-protective ventilation.
BACKGROUND: Lung-protective ventilation (LPV) can result in a ventilator tidal volume (V(T)) below patient V(T) demand, which may elevate work of breathing (WOB). Increasing the ventilator inspiratory flow may not sufficiently reduce WOB, because the patient's flow-time requirements may exceed the ventilator's flow-time delivery pattern. We investigated (1) the effects of V(T) demand on WOB during LPV and (2) which ventilator pattern best reduced WOB while achieving LPV goals. METHODS: A standard WOB lung model simulated assisted breathing. Using 3 ventilators (Hamilton Veolar, Hamilton Galileo, and Dräger Evita 2 dura), we tested volume-control ventilation with a constant flow pattern (VCV-CF), volume-control ventilation with a decelerating flow (VCV-DF), and pressure-control ventilation (PCV). Simulated V(T) demand was increased from 50-125% of the ventilator-delivered V(T) (400 mL) as ventilator inspiratory time (T(I)) was decreased (0.95, 0.80, 0.65, and 0.45 s) relative to simulated T(I) (0.8 s). WOB was measured with a pulmonary mechanics monitor. RESULTS: During VCV-CF and VCV-DF, a V(T) demand of > or = 100% drastically increased WOB, attributable to imposed WOB from the inspiratory valve. Increasing inspiratory flow by using the decelerating flow pattern and/or decreasing T(I) reduced WOB, but generally not to normal levels. "Double-triggered" breaths, with excessive V(T) delivery, often occurred when ventilator T(I) was well below simulated T(I). PCV was most effective in reducing WOB, but V(T) delivery exceeded the LPV target unless T(I) was reduced. CONCLUSIONS: Given our dual goals of reducing both WOB and V(T) during LPV, VCV-DF with relatively brief T(I) appeared to be the best option, followed by PCV with a relatively brief T(I).
Computer Simulation↗
The effect of a bellows leak in an Ohmeda 7810 ventilator on room contamination, inspired oxygen, airway pressure, and tidal volume.
We investigated the effect of a small bellows leak (bellows full at end-expiration) on inspired oxygen fraction (Fio(2)), exhaled tidal volume (Vt), airway pressure, and room contamination in an oxygen-driven anesthesia ventilator (Ohmeda 7810, Madison, WI). CO(2) concentration at the ventilator exhalation valve, Fio(2), Vt, and airway pressure were measured (n = 3) while ventilating a CO(2)-producing test lung at 8 breaths/min and an inspiratory/expiratory ratio of 1:2, with and without a bellows leak (4-mm-long tear). Set Vt was 400, 600, 800, and 1000 mL. Fresh gas flow (FGF) was 0.3 L/min O(2) and (a) 5.0 L/min air, (b) 2.0 L/min air, and (c) 0.2 L/min nitrogen. There was no clinical difference in Fio(2), Vt, PIP (peak inspiratory pressure) and PEEP (positive end-expiratory pressure), with and without a 4-mm bellows tear, at all FGFs and Vt settings. CO(2) at the ventilator exhalation valve was always nonzero with a bellows leak, indicating that CO(2)-laden circuit gas was contaminating the drive gas via the bellows leak. A 4-mm bellows tear in an Ohmeda 7810 ventilator allows anesthetic gases to contaminate ambient air but does not cause clinically significant changes in Fio(2), exhaled Vt, PIP, or PEEP.
Air Pressure↗
Tidal volume and respiratory timing derived from a portable ventilation monitor.
STUDY OBJECTIVES: To determine the accuracy of a portable magnetometer designed to measure tidal volume (VT), inspiratory time (TI), and expiratory time (TE). PARTICIPANTS: Fourteen healthy subjects. DESIGN: Subjects breathed over a sixfold range of VTs while at rest (sitting and standing) and during treadmill exercise. We then compared VT, TI, and TE measured by magnetometry (VTmag, TImag, and TEmag) with VT, TI, and TE measured by spirometry (VTspiro, TIspiro, and TEspiro, respectively). SETTING: Pulmonary function and exercise physiology laboratories. MEASUREMENTS AND RESULTS: The sternal-umbilical distance and the anteroposterior displacements of the rib cage and abdomen were measured with two pairs of magnetometer coils. VT was calculated from the sum of these three signals, and was simultaneously measured using a spirometer or flow meter. A total of 1,111 breaths were analyzed for the resting condition, and 1,163 breaths were analyzed for the exercise condition. We found that VTmag was highly correlated with VTspiro at rest (R2 = 0.90) and during exercise (R2 = 0.79) for pooled data. The slope of this relationship approached the line of identity. The mean percentage differences between VTmag and VTspiro were 10.1 +/- 6.6% at rest and 13.5 +/- 8.6% with exercise. By Bland-Altman analysis, the mean differences between VTmag and VTspiro were 38 mL at rest with changes in posture, and 182 mL during exercise. TImag and TIspiro values and TEmag and TEspiro values also were highly correlated (R2 = 0.97 and R2 = 0.95, respectively) for pooled data. CONCLUSION: A portable magnetometer system can give useful measures of VT, TI, and TE over a wide range of VTs in sitting, standing, and exercising subjects.
Adult↗
Evaluation of the dead space to tidal volume ratio as a predictor of extubation failure.
OBJECTIVE: The objective of this study was to evaluate the ratio of dead space to tidal volume (VD/VT) as a predictor of extubation failure of children from mechanical ventilation. METHODS: From September 2001 to January 2003 we studied a cohort consisting of all children (1 day-15 years) submitted to mechanical ventilation at a pediatric intensive care unit who were extubated and for whom pre-extubation ventilometry data were available, including the VD/VT ratio. Extubation success was defined as no need for any type of ventilatory support, invasive or otherwise, within 48 hours. Patients who tolerated extubation, with or without noninvasive support, were defined as success-R and compared with those who were reintubated. Statistic analysis was based on a VD/VT cutoff point of 0.65. RESULTS: During the study period 250 children received mechanical ventilation at the pediatric intensive care unit. Eighty-six of these children comprised the study sample. Twenty-one children (24.4%) met the criteria for extubation failure, with 11 (12.8%) of these requiring non-invasive support and 10 (11.6%) reintubation. Their mean age was 16.8 (+/-30.1) months (median = 5.5 months). The mean VD/VT ratio for all cases was 0.62 (+/-0.18). Mean VD/VT ratios for patients with successful and failed extubations were 0.62 (+/-0.17) and 0.65 (+/-0.21) (p = 0.472), respectively. Logistic regression failed to reveal any statistically significant correlation between VD/VT ratio and success or failure of extubation (p = 0.8458), even for patients who were reintubated (p = 0.5576). CONCLUSIONS: In a pediatric population receiving mechanical ventilation due to a variety of etiologies, the VD/VT ratio was unable to predict the populations at risk of extubation failure or of reintubation.
Adolescent↗
Effect of anatoxin-a(s) from Anabaena flos-aquae NRC-525-17 on blood pressure, heart rate, respiratory rate, tidal volume, minute volume, and phrenic nerve activity in rats.
The effects of anatoxin-a(s) [antx-a(s)] from the cyanobacterium Anabaena flos-aquae NRC-525-17 on mean arterial blood pressure, heart rate, respiratory rate, tidal volume, minute volume, and phrenic nerve activity were evaluated in anesthetized Sprague-Dawley rats. Anatoxin-a(s) was administered by continuous intravenous infusion. The initial effect of the toxin was to slow the heart rate and reduce arterial blood pressure, followed by much more pronounced reductions in these parameters. The marked decline in heart rate and blood pressure frequently occurred before there was a large decrease in respiratory minute volume [reduced by only 15.4 +/- 3% (mean +/- S.E.) compared to the predose period], suggesting that antx-a(s) has an important muscarinic action on the cardiovascular system in vivo. Phrenic nerve amplitude increased, but, nevertheless, tidal and minute volumes decreased progressively, indicating that antx-a(s), unlike most low-molecular-weight organophosphorus cholinesterase inhibitors, does not have any remarkable inhibitory action on central mediation of respiration.
Animals↗