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PubMed1978

A graphic approach to assessing interrelationships among minute ventilation, arterial carbon dioxide tension, and ratio of physiologic dead space to tidal volume in patients on respirators.

A graphic analysis of the relationships among minute ventilation, arterial PCO2, and the ratio of physiologic dead space to tidal volume is presented for the bedside clinical evaluation of patients receiving continuous respiratory support. With simultaneous measurement of minute ventilation and arterial PCO2, the graph can be used to determine the patient's ratio of dead space to tidal volume. This information can subsequently be used (1) for respirator adjustments to obtain the desired arterial PCO2; (2) to assess the severity of ventilation/perfusion unevenness; and (3) to follow the patient's response to respiratory therapy. It provides the clinician with a conceptual tool with which he can assess the status of a patient's gas exchange and more accurately evaluate and plan his course of treatment.

Carbon Dioxide↗

PubMed1986

Effect of tidal volume on ventilation maldistribution.

To examine the effect of changing tidal volume (VT) on ventilation distribution, we studied multiple breath nitrogen washouts in 4 normal subjects breathing with a VT of 0.6, 1.0 or 1.5 L. We used a recently developed technique of analysis (Crawford et al., 1985) that distinguishes inhomogeneity of gas concentrations due to the interaction of convection and diffusion in the lung periphery (DCDI) from ventilation maldistribution among larger units determined at more proximal branchpoints (CDI). The results indicate that increases in VT reduce the inhomogeneity due to DCDI but increase that due to CDI. In view of the VT dependence of physiological dead space, derived from arterial PCO2, we speculate that the increase in CDI has a dominant effect on gas exchange.

Breath Tests↗

PubMed2002

Pulmonary hemodynamic and tidal volume changes during exercise in heart failure.

BACKGROUND: Impairment of lung mechanics, increase of pulmonary artery pressure and limitation of exercise capacity are common findings in chronic heart failure. The objective of the present study was to evaluate whether pulmonary mechanics are correlated with pulmonary hemodynamics, whether both are correlated with the functional capacity and whether the time course of their changes during exercise correlates with the exercise capacity. METHODS: We performed a cardiopulmonary exercise test (breath by breath analysis of ventilation and gas exchange, cycloergometer, 25 W increments every 3 min) with pulmonary hemodynamic monitoring in 38 heart failure patients. The parameters were analyzed at rest, 1 min after the work rate increase and at peak exercise. RESULTS: A significant linear correlation with peak oxygen consumption was found at rest for: mean pulmonary artery pressure (mPAP, r = -0.56), right atrial pressure (RAP, r = -0.42), pulmonary wedge pressure (PWP, r = -0.53), and total pulmonary (TPR, r = -0.53) and pulmonary vascular resistances (PVR, r = -0.45); after 1 min of exercise for: cardiac index (CI, r = 0.49), mPAP (r = -0.57), RAP (r = -0.60), PWP (r = -0.45), and TPR (r = -0.67) and PVR (r = -0.38); at peak exercise for: tidal volume (r = 0.63), CI (r = 0.63), RAP (r = -0.43), TPR (r = -0.65) and PVR (r = -0.43). A significant linear correlation with peak oxygen consumption was found, for the increment between rest and 1 min of exercise, for RAP (r = -0.58) and CI (r = 0.42) and, for the increments between rest and peak exercise, for tidal volume (r = 0.79) and CI (r = 0.61) and, for the ratio between the increment between rest and 1 min of exercise/increment between rest and peak exercise, for mPAP (r = -0.42), RAP (r = 0.51) and CI (r = -0.54). The same ratio of increment of mPAP (r = 0.39) and CI (r = 0.36) correlated with that of tidal volume. CONCLUSIONS: This study provides evidence of a strong correlation between the respiratory function and pulmonary vascular pressure changes during exercise in heart failure.

Adult↗

PubMed1987

Alterations in ventilatory pattern and ratio of dead-space to tidal volume.

The effects of alterations in ventilatory pattern on the simultaneously measured physiologic and anatomic dead-spaces (VDphys and VDan, respectively) and the dead-space to tidal volume ratio (VD-VT) were studied in 17 healthy normal subjects (13 men, four women, ages 21 to 36 years). There were no significant changes in VDan with increases in respiratory frequency (f) or tidal volume (VT). The VDphys increased (mean change +0.153 L, p less than 0.05) with increase in VT (mean increase +0.84 L, p less than 0.01), but did not alter significantly with a twofold increase in f, at control VT. Increase in VT significantly reduced VD/VT (mean change -10.4 percent, p less than 0.05), but increase in f, at control VT, did not significantly alter VD/VT. These results indicate that in normal subjects, increase in VT alters ventilation/perfusion matching in the lungs, whereas an increase in f, at constant VT, has no effect on ventilation/perfusion matching. Increases in VD/VT cannot, therefore, be ascribed to alterations in ventilatory pattern where either VT, or f, or both are increased.

Adult↗

PubMed1989

Positive end-expiratory pressure: implications for tidal volume changes in anesthesia machine ventilation.

In clinical practice, the addition of positive end-expiratory pressure (PEEP) into a standard anesthesia circle circuit decreases the delivered tidal volume (DTV) to a patient. We studied the magnitude of the delta DTV/delta PEEP relationship in two commonly used anesthesia systems. In addition, the magnitude of the delta DTV/delta PEEP relationship varies with both pulmonary compliance and volume of gas contained in the patient's breathing system between the ventilator and PEEP valve site, and this was also evaluated. Routine monitoring of expired tidal volume should be used whenever PEEP is added to an anesthesia circuit.

Anesthesia, Closed-Circuit↗

PubMed1987

Tidal volume changes due to the interaction of anesthesia machine and anesthesia ventilator.

Tidal volume (VT) delivered by mechanical ventilation during anesthesia may be influenced by factors related not only to the patient and the breathing circuit, but also to the interaction between the anesthesia machine and the anesthesia ventilator. To characterize this interaction, we studied in a test lung the effect of fresh-gas-flow (FGF) (0.25, 2.5, 5, and 10 L/min), inspiratory-to-expiratory time ratio (I:E) (1:1, 1:2, and 1:3), and ventilatory frequency (8, 12, and 16 breaths/min) at fixed ventilator bellows excursions of 300, 600, and 900 ml. The influence of these variables was also estimated mathematically for a pediatric situation: a bellows excursion of 50 ml at 20 and 30 breaths/min. Each variable studied was associated with an increase, sometimes dramatic, in the delivered VT compared with that which was set. The VT augmentation was greatest at the highest FGF rate, largest I:E ratio, and slowest respiratory rate. Because the magnitude of the augmentation is independent of the VT setting, the percent increase is much larger for pediatric settings. For example, with VT set at 50 ml, delivered VT ranged from 71 ml (FGF 2.5 L/min, I:E 1:3, and 30 breaths/min) to 300 ml (FGF 10 L/min, I:E 1:1, and 20 breaths/min). Thus it is possible in the pediatric situation to increase the delivered VT by sixfold without changing the ventilator bellows excursion. The magnitude of the changes was slightly larger for the VT settings for adult patients because of the slower respiratory rate. This VT augmentation can be predicted by the product of FGF (ml/s) and inspiratory time (seconds).(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, General↗

PubMed1998

Vital capacity and tidal volume preoxygenation with a mouthpiece.

We have measured oxygen wash-in in 20 volunteers undergoing preoxygenation with a face mask, mouthpiece alone and a mouthpiece with a noseclip, in a crossover study. Tidal volume breathing and maximal deep breath techniques were studied with each type of equipment. When tidal volume breathing was used, the face mask and mouthpiece with noseclip were comparable, but the mouthpiece alone achieved a lower end-expiratory oxygen concentration than the two other methods after 3 min (P < 0.001 and P < 0.01), and after 5 min (P < 0.05 in each case). Conversely, during preoxygenation with vital capacity breaths, the mouthpiece and mouthpiece with noseclip were comparable, and both were more effective than the face mask (P < 0.001). In a second study, 20 patients who had undergone preoxygenation before induction of anaesthesia were asked later if they would have preferred the face mask or mouthpiece for this procedure. Significantly more patients (14 of 18 who expressed a preference) favoured the mouthpiece (P < 0.05; confidence limits 0.56-0.92).

Cross-Over Studies↗

PubMed2005

[Effect of different tidal volume ventilation on rat bronchial and alveolar epithelial cell apoptosis].

OBJECTIVE: To investigate the changes in bronchial and alveolar epithelial cell apoptosis after mechanical ventilation with different tidal volumes and explore the mechanism and significance of cell apoptosis in ventilation-induced lung injury. METHODS: Thirty healthy male Sprague-Dawley rats were randomly divided into groups A, B and C to receive tracheotomy under anesthesia for ventilation with different tidal volumes (VT) for 4 h (VT of 10 ml/kg in group A, 20 ml/kg in group B and 40 ml/kg in group C). Lung histopathology was assessed after the ventilation and compared between the 3 groups. The severity of lung injury and bronchial epithelial edema was evaluated, and the extent and location of cell apoptosis in the bronchus and lung tissues were studied by transferase d-UTP end-labeling (TUNEL) assay and immunohistochemistry. RESULTS: After mechanical ventilation for 4 h, lung injury and bronchial epithelial edema increased with the increment of VT. By TUNEL assay, the apoptosis index of both alveolar and bronchial epithelial cells was found to increase with VT. Immunohistochemical study identified enhanced caspase-3 expression in the cytoplasm and nuclei of airway and alveolar epithelial cells and vascular endothelial cells in rats with high VT ventilation, and the enhancement was especially obvious in the bronchial epithelial cells. CONCLUSION: Mechanical ventilation with different VTs causes consistent changes in histopathology, cell apoptosis and caspase-3 expression in rats, which support the presumption that cell apoptosis plays an important role in the pathogenesis of high VT ventilation-induced lung injury.

Animals↗

PubMed1991

Tidal volume reduction in ARDS. Effect on cardiac output and arterial oxygenation.

During continuous positive pressure ventilation (CPPV), mean airway pressure and lung volume will be influenced both by the tidal volume (VT) employed and the amount of positive end-expiratory pressure (PEEP). The effect of varying levels of CPPV on PaO2 and cardiac output (Q) has been previously assessed by adjusting the level of PEEP at constant VT. This study examined the influence of a 200-ml reduction in VT, at a constant PEEP of 15 cm H2O, on the PaO2 and Q of 21 patients with adult respiratory distress syndrome (ARDS). The relationship between change in Q and change in total respiratory system compliance (Cst) after VT reduction was also examined. VT reduction from 14.1 +/- 0.8 ml/kg to 11.2 +/- 0.9 ml/kg yielded an increase in Q (+ 15 +/- 12 percent, p less than 0.01) without a significant change in PaO2 (-6.3 +/- 15.0 mm Hg, p = 0.08). Cst increased with VT reduction (+ 3.1 +/- 1.8 ml/cm H2O). There was only a modest correlation (r = +0.42, p = 0.06) between delta Q percent and delta Cst following VT reduction. VT reduction at high level PEEP may yield a significant improvement in Q and net O2 delivery, but the degree of hemodynamic improvement is variable and is not reliably predicted noninvasively by measurement of Cst.

Adult↗

PubMed1990

Preoxygenation in parturients: a comparison of 4, 6 and 8 vital capacity breaths to 5 minutes of tidal volume breathing.

We compared the difference in denitrogenation (by intermittent measurement of arterial tension, PaO2) in 45 parturients at term when preoxygenated with 4, 6 or 8 rapid vital capacity breaths and 5 minutes of tidal volume breathing. Oxygen, at 8 litres min-1, was delivered through a facemask via a circle absorber with a 2 litre reservoir bag. Higher PaO2 was produced with 5 minutes of tidal volume breathing. This differed significantly from the PaO2 produced by 4, 6 or 8 rapid vital capacity breaths (p less than 0.01).

Adult↗

PubMed2003

High tidal volume upregulates intrapulmonary cytokines in an in vivo mouse model of ventilator-induced lung injury.

Mechanical ventilation has been demonstrated to exacerbate lung injury, and a sufficiently high tidal volume can induce injury in otherwise healthy lungs. However, it remains controversial whether injurious ventilation per se, without preceding lung injury, can initiate cytokine-mediated pulmonary inflammation. To address this, we developed an in vivo mouse model of acute lung injury produced by high tidal volume (Vt) ventilation. Anesthetized C57BL6 mice were ventilated at high Vt (34.5 +/- 2.9 ml/kg, mean +/- SD) for a duration of 156 +/- 17 min until mean blood pressure fell below 45 mmHg (series 1); high Vt for 120 min (series 2); or low Vt (8.8 +/- 0.5 ml/kg) for 120 or 180 min (series 3). High Vt produced progressive lung injury with a decrease in respiratory system compliance, increase in protein concentration in lung lavage fluid, and lung pathology showing hyaline membrane formation. High-Vt ventilation was associated with increased TNF-alpha in lung lavage fluid at the early stage of injury (series 2) but not the later stage (series 1). In contrast, lavage fluid macrophage inflammatory protein-2 (MIP-2) was increased in all high-Vt animals. Lavage fluid from high-Vt animals contained bioactive TNF-alpha by WEHI bioassay. Low-Vt ventilation induced minimal changes in physiology and pathology with negligible TNF-alpha and MIP-2 proteins and TNF-alpha bioactivity. These results demonstrate that high-Vt ventilation in the absence of underlying injury induces intrapulmonary TNF-alpha and MIP-2 expression in mice. The apparently transient nature of TNF-alpha upregulation may help explain previous controversy regarding the involvement of cytokines in ventilator-induced lung injury.

Animals↗

PubMed1987

Tidal volumes required to maintain isocapnia at frequencies from 3 to 30 Hz in the dog.

We ventilated seven mongrel dogs with high frequency oscillatory ventilation (HFO) at frequencies from 3 to 30 Hz. At each frequency, the tidal volume required to achieve isocapnia (VTiso) was measured by plethysmography. In an individual dog, VTiso could be related to frequency by an equation of the form VTiso = KfA. A was similar for the seven dogs, A = -0.54 +/- 0.03. K varied from 179 to 325 cc- Hz-A, reflecting differences between the dogs in dead space, CO2 production and gradient for gas transport. This relation is consistent with that predicted from the data of previous investigators who used different ventilators, circuits and methodology. From 3 to 30 Hz, VTiso decreased from 1.2 to 0.4 times anatomic plus equipment dead space, but minute volumes required to maintain isocapnia increased from 6 to 18 times those required during conventional ventilation. We conclude that low tidal volume ventilation is also high minute volume ventilation.

Animals↗

PubMed1983

Interaction of hypoxia and hypercapnia on ventilation, tidal volume and respiratory frequency in the anaesthetized rat.

1. Ventilation ( V(E)), tidal volume (V(T)), respiratory frequency (f) and arterial and end-tidal gas tensions were measured in seventy-one tracheostomized New Zealand white rats ( approximately 405 g) anaesthetized with an initial dose of pentobarbitone followed by repeated small doses to ensure that a weak limb-withdrawal reflex remained.2. O(2) consumption (1.2 ml (s.t.p.d.) min(-1) 100 g(-1)), CO(2) production (1.0 ml (s.t.p.d.) min(-1) 100 g(-1)), heart rate (357 min(-1)), V(E) (43 ml min(-1) 100 g(-1)), P(a,CO2) (34 mmHg) and P(a,O2) (84 mmHg) in the control periods did not change significantly during the course of the experiment.3. Inspirates of 21% O(2) with 2-10% CO(2), 15, 10 or 7.5% O(2) with either no or sufficient CO(2) to maintain normocapnia and 15 or 10% O(2) with 4, 6 or 8% CO(2) were tested. Steady-state responses were measured after 2 min of exposure.4. Hypoxic-hypercapnic interaction on V(E), V(T) and f determined by a three-inspirate test ((i) hypoxia alone, (ii) hypercapnia and (iii) these hypoxic and hypercapnic levels combined) yielded various conclusions depending on the level of asphyxia examined. Essentially, the milder the asphyxia the more the interaction appeared additive or even multiplicative and the stronger the asphyxia the more the interaction appeared occlusive. However, this test is unsuitable for accurately showing interactions because the P(a,O2) achieved in asphyxia was higher than in hypoxia and the asphyxial P(a,CO2) was lower than in hypercapnia.5. For isoxic conditions (P(a,O2) = 97, 77 and 51 mmHg), V(E) and V(T) were related linearly to P(a,CO2) whilst f was related hyperbolically with convexity upwards (P(a,O2) 97 mmHg) or downwards (P(a,O2) 77 and 51 mmHg).6. For isocapnic conditions (P(a,CO2) = 33, 40 and 48 mmHg), V(E) and V(T) were inversely related to P(a,O2) with a hyperbolic curve (convexity downwards) whilst f was inversely and linearly related (P(a,CO2) 33 mmHg) or constant (P(a,CO2) 40 and 48 mmHg).7. Multivariate analyses showed that the hypoxic-hypercapnic interaction was additive for V(T) but occlusive for V(E) and f and the occlusion was more severe in the latter. This was illustrated graphically for the variable plotted against P(a,CO2) or P(a,O2) as parallel shifts in regression lines for V(T), flatter regression lines for V(E) during asphyxia and a virtually constant f during asphyxia.8. V(E) responses and sensitivities to hypoxia and hypercapnia, the shape of V(E), V(T) and f regression lines against P(a,O2) and P(a,CO2) and the type of hypoxic-hypercapnic interaction on each variable in the rat were compared with other species.9. Possible causes of the occlusive hypoxic-hypercapnic interaction in the rat were considered.

Anesthesia, Intravenous↗

PubMed2004

Mechanical ventilation with moderate tidal volumes synergistically increases lung cytokine response to systemic endotoxin.

Previous animal studies have identified a role for activation of innate immunity in the pathogenesis of ventilator-associated lung injury. These studies have used large tidal volume ventilation to study the effect of alveolar overdistension on induction of inflammatory pathways. We hypothesized an alternative mechanism for the pathogenesis of lung injury in which moderate tidal volume ventilation does not independently cause clinical inflammation but rather interacts with innate immune activation by bacterial products, resulting in an enhanced inflammatory response. We measured cytokine expression and lung injury in normal and lipopolysaccharide (LPS)-treated anesthetized rabbits randomized to either spontaneous respiration or mechanical ventilation. Outcome parameters were analyzed by two-way factorial analysis of variance to identify synergism between ventilation and systemic LPS. Mechanical ventilation alone resulted in minimal cytokine expression in the lung but did enhance LPS-induced expression of tumor necrosis factor-alpha, the CXC chemokines interleukin-8 and growth-related protein-alpha, and the CC chemokine monocyte chemoattractant protein-1. Increased mRNA expression and activation of the transcription factors nuclear factor-kappaB and activator protein-1 accompanied the cytokine responses. We conclude that moderate volume ventilation strategies augment the innate immune response to bacterial products in the lung and may play a role in the development of acute lung injury in patients with sepsis.

Albumins↗

PubMedDate not supplied

Influence of tidal volume, respiratory rate, and supplemental oxygen flow on delivered oxygen fraction using a mouth to mask ventilation device.

We examined the influence of the following parameters in determining the FiO2 delivered to a pediatric lung model using the mouth-to-mask method of resuscitation: rate of ventilation, inspiratory tidal volumes, and supplemental oxygen flow. With a ventilator rate of 20/min and tidal volumes (Vt) < or = 100 mL, an FiO2 of approximately .50 was observed with a supplemental oxygen flow of 5 L/min. Increasing the supplemental oxygen flow to 15 L/m did not appreciably increase the FiO2 (FiO2 = .53 versus FiO2 = .60, respectively), but did cause a significant and unintended increase in Vt. Similar results were noted with a ventilator rate of 12/min and Vt < or = 100 mL (FiO2 = .68 versus FiO2 = .73, respectively). We also observed a potentially hazardous situation involving the positioning of the supplemental oxygen port that might result in high inspiratory pressures (stacking of breaths) to the pediatric patient. We believe additional testing is warranted prior to widespread use of this device in children.

Child↗

PubMed2001

[Effects of positive end-expiratory pressure, tidal volume and perflubron doses on gas exchange during partial liquid ventilation].

The efficacy of gas exchange during partial liquid ventilation (PLV) may be affected by positive end-expiratory pressure (PEEP), tidal volume (TV) and perflubron (PFOB) dose. The purpose of the present study was to clarify which factors were important for improving gas exchange during PLV. Fourteen rabbits were anesthetized and tracheostomized. Lung was introduced with intravenous oleic acid combined with saline lung lavage. After obtaining control data, PFOB 7.5 ml.kg-1 was instilled into the trachea, and ventilation settings were changed sequentially [1. TV: 10 ml.kg-1 (mTV), 2. mTV with PEEP, 3. TV: 15 ml.kg-1 (hTV), 4. hTV with PEEP]. PEEP level was set to the lower inflection point. The PFOB dose was increased to 15 ml.kg-1 and measurements were repeated under each ventilation setting. PEEP increased PaO2 in all ventilation settings. In hTV ventilation settings, incremental dose of PFOB significantly increased PaO2. The PaO2 values of all hTV ventilation settings were significantly higher than those of corresponding ventilation setting of mTV. Pulmonary compliance was significantly decreased with PEEP in hTV ventilation in addition to 15 ml.kg-1 PFOB. The results suggested that adequate gas tidal volume was the most important factor for improving gas exchange during PLV. However, PEEP or larger dose of PFOB should be avoided because they may decrease pulmonary compliance.

Animals↗

PubMed1993

Noninvasive monitoring of tidal volume with an extensometer: laboratory and clinical studies.

The extensometer or "rubbery ruler" (RR) is a new torso transducer with potential application in the field of respiratory pattern analysis. This paper determines whether the RR can measure tidal volume over a clinically useful time frame following spirometric calibration. Laboratory testing identified no error or baseline drift during 774,000 controlled stretches. Clinical testing in a variety of patients demonstrated that 96.6% of derived spirometric values were contained within an error range of +15.2% to -16.9% of spirometrically measured tidal volume and that accuracy did not change over a period of one hour. These results are encouraging and suggest that this device merits further investigation.

Adult↗

PubMed2005

[Positive end-expiratory pressure and tidal volume titration after recruitment maneuver in a canine model of acute respiratory distress syndrome].

OBJECTIVE: To investigate the mechanisms of alveolar derecruitment and titration of positive end-expiratory pressure (PEEP) and tidal volume (V(T)) after recruitment maneuver (RM) in acute respiratory distress syndrome (ARDS). METHODS: Eighteen dogs with oleic acid induced ARDS were ventilated with volume controlled ventilation [VCV, PEEP 16 cm H2O, V(T) 10 ml/kg, respiratory rate (RR) 30 breaths/min] and the steady state in this mode was defined as baseline (0 min). All animals accepted RM by using pressure controlled ventilation [PEEP 35 cm H2O and peak inspiratory pressure (PIP) 50 cm H2O for 1 min] and then randomly assigned into three groups and ventilated by VCV for 4 h: low V(T) and moderate PEEP group (LVMP group, V(T) 10 ml/kg, PEEP 16 cm H2O, RR 30 breaths/min), low V(T) and low PEEP group (LVLP group, V(T) 10 ml/kg, PEEP 10 cm H2O, RR 30 breaths/min) and moderate V(T) and low PEEP group (MVLP group, V(T) 15 ml/kg, PEEP 10 cm H2O, RR 20 breaths/min). Oxygenation, lung mechanics, hemodynamics and lung injury score were measured. RESULTS: (1) The average lower inflection pressure (LIP) was identified as (16.0 +/- 2.1) cm H2O. (2) PaO(2) in the LVMP group [(371 +/- 64) mm Hg at 30 min and (365 +/- 51) mm Hg at 60 min] was higher than that in the LVLP and the MVLP group [(243 +/- 112), (242 +/- 97) mm Hg at 30 min and (240 +/- 108), (232 +/- 87) mm Hg at 60 min, respectively; all P < 0.05], but no significant differences were observed among three groups from the second hour after RM to the end of the experiment. Better ventilation profiles were observed in the MVLP group. (3) Compared with baseline, marked cardiac compromise with higher airway plateau pressure (Pplat) and lower static respiratory compliance (Cst) were found in the LVMP group, while improvement was observed in other two groups. Cst in the MVLP group was slightly higher than that in the LVLP group. (4) No significant differences of lung injury were found from bronchoalveolar lavage fluid (BALF) analysis. CONCLUSIONS: Higher PEEP close to LIP maybe useful in preventing alveolar recollapse and improving oxygenation, but harmful to hemodynamics and may increase the risk of lung jury. Lower PEEP combined with moderate tidal volume after RM may be a more reasonable approach than conventional lung protective ventilation.

Animals↗