Dead Space Volume Research Articles

Inbred strain variation in lung function.

The purpose of the present study was to determine the strain-specific phenotype variance of lung function parameters among common inbred laboratory mouse strains. In accordance with the "Mouse Phenome Project" run by The Jackson Laboratory (http://www.jax.org/phenome), lung volumes, lung mechanics, and diffusing capacity of 16 males and 16 females of the strains C3H/HeJ, BALB/cByJ, C57B1/6J, A/J, FVB/J, 129SV/ImJ, and SWR/J were determined in a standardized manner. The defined respiratory maneuvers for lung function testing were performed with a custom-made, computer-controlled servo-ventilator in anesthetized animals. Sex differences within the strains were found in most (83%) of the absolute lung function parameters. Usually, normalization to body or lung size completely compensates for the observed gender differences. There was great diversity between strains for all of the lung function parameters studied; for example, the total lung capacity as well as the pulmonary diffusing capacity for carbon monoxide varied by 50% and the static lung compliance by a factor of almost two among the strains. Little, but statistically significant variability was detectable for the dead space volume and the respiratory system resistance. There was no clear-cut evidence for any strain exhibiting either the smallest or the largest values for all parameters studied, suggesting that there were no simple allometric relationships of lung size between the strains. Well-established genealogical relationships among strains were not constantly reflected in phenotype similarities of pulmonary function. Therefore, these data strongly support heritable genetic traits for pulmonary function. Moreover, it constitutes a basis for further genetic lung function-related studies.

Pathophysiologic Mechanisms Underlying Apnea of Prematurity

After completing this article, readers should be able to: 1. Characterize the unique features of neonatal respiratory control mechanisms. 2. Clarify how immature respiratory control contributes to neonatal apnea. 3. Identify the contribution of upper airway obstruction to episodes of mixed apnea. Idiopathic apnea of prematurity is a common disorder that requires therapeutic intervention to avoid potential morbidity in preterm infants who require neonatal intensive care. Severe, recurrent apneic episodes may lead to multiple investigations to rule out secondary disorders leading to apnea (see accompanying article in this issue). Although the incidence of neonatal apnea is inversely related to gestational age and is probably as high as 100% in the most immature preterm infants, the onset may be delayed by the presence of lung disease in the first days of life. Apnea of prematurity, especially if severe or persistent, has been associated with poor developmental outcome in school-age children, although a cause-and-effect relationship is difficult to establish. The definition of apnea varies among studies. Apnea of prematurity has been defined most widely as cessation of breathing in excess of 15 seconds’ duration, typically accompanied by desaturation and bradycardia. However, shorter episodes of apnea, and even periodic breathing, may be accompanied by bradycardia or hypoxemia. Prolonged desaturation episodes also have been reported in the absence of apnea or bradycardia, both in healthy preterm infants and in infants who have chronic lung disease. These episodes might represent obstructive apnea, hypoventilation, or possibly intrapulmonary right-to-left shunting, although episodes of desaturation and bradycardia almost always are preceded by apnea or hypoventilation. Apnea is classified traditionally into three categories based on the presence or absence of upper airway obstruction: central, obstructive, and mixed apneas. Central apnea is characterized by total cessation of inspiratory efforts with no evidence of obstruction. In obstructed apnea, the infant tries to breathe against …

Removal of deadspace volume from arterial catheter: How muchis enough?

OBJECTIVE: To evaluate the amount of volume needed to be removed from arterial catheter systems to compensate for "deadspace" and to allow an accurate measurement of pH and hemoglobin (Hb). DESIGN: Twenty patients undergoing heart surgery were evaluated in a steady state after the induction of anesthesia before surgery. Six blood samples were removed from the arterial catheter, the total volume of which was 1.5 mL at 30-sec intervals and measured for pH and Hb. The first sample was then taken after removing 1.5 mL from the tubing. In subsequent samples, the volume removed before sampling increased by 0.5-mL intervals. All other samples were compared with sample number 6, in which 4 mL of volume were removed before measurements. RESULTS: The first three samples with volumes of 1.5, 2.0, and 2.5 mL before measurement were inaccurate compared with sample number 6 (p <.000), giving artificially low values for both pH and Hb. There was no significant difference between the values measured in sample numbers 4, 5, and 6 (3.0, 3.5, and 4.0 mL, respectively). CONCLUSION: The amount of volume needed to be removed before measurement from an arterial catheter system, the volume of which is 1.5 mL, is 3 mL to achieve accurate measurements of pH and Hb. Removal of less volume results in an artificially low measurement.

Nitric oxide inhalation increases alveolar gas exchange by decreasing deadspace volume.

To test the hypothesis that nitric oxide inhalation facilitates CO2 elimination by decreasing alveolar deadspace in an ovine model of acute lung injury. Prospective, placebo-controlled, randomized, crossover model. University research laboratory. Eleven mixed-breed adult sheep. To induce acute lung injury, hydrochloric acid was instilled into the tracheas of paralyzed sheep receiving controlled mechanical ventilation. Each sheep breathed 0 ppm, 5 ppm, and 20 ppm nitric oxide in random order. Estimates of alveolar deadspace volumes and arterial-to-end tidal CO2 partial pressure differences were used as indicators of CO2 elimination efficiency. At a constant minute ventilation, nitric oxide inhalation caused dose-independent decreases in Paco2 (p <.05), alveolar deadspace (p <.01), and arterial-to-end tidal CO2 partial pressure differences (p <.01). We found that estimates of arterial-to-end tidal CO2 partial pressure differences may be used to predict alveolar deadspace volume (r2 =.86, p <.05). Estimates of arterial-to-end tidal CO2 partial pressure differences are reliable indicators of alveolar deadspace. Both values decreased during nitric oxide inhalation in our model of acutely injured lungs. This finding supports the idea that nitric oxide inhalation facilitates CO2 elimination in acutely injured lungs. Future studies are needed to determine whether nitric oxide therapy can be used to reduce the work of breathing in selected patients with cardiopulmonary disorders.

Estudio comparativo de distintos métodos de drenaje pleural en un modelo experimental de neumotórax

To observe the usefulness of several procedures for draining pneumothorax in an animal model and to identify the best pleural drainage system with minimal impairment of respiratory function. Thirty-four New Zealand white rabbits weighting 1687 +/- 78 g and aged a mean 59 days were randomly placed in groups as follows. Unilateral pneumothorax was induced in the first problem group (P1) rabbits (n = 10) by thoracostomy, with pleural drainage. In the second problem group (P2) of rabbits (n = 10), bilateral pneumothorax was similarly induced by thoracostomy with pleural drainage. The control groups underwent unilateral (C1; n = 7) and bilateral (C2; n = 7) thoracostomy and drainage. Every 7 minutes the chest tube was connected successfully in each animal to an underwater seal with a dead-space volume of 35.58 ml (neonatal Bülau unit) or to a 3,940 ml system (chest drainage unit) and to pleural aspirations of -5 and -20 cmH2O. We analyzed mortality, fluctuations of the hydrostatic column of the underwater seal, heart rate (HR), respiratory rate (RR), PaCO2, SaO2, pH and arterial blood gas measures. Intraoperative mortality was significantly higher (particularly in the P2 group) when connection was to a large volume system without aspiration. Recovery after pneumothorax was more satisfactory with aspiration of -5 and -20 cmH2O. The results suggest that a pleural drainage unit with a large dead space between the pleural cavity and the underwater seal is a frequent cause of respiratory failure or insufficiency. We believe that when an underwater seal without pleural suction is applied, the Bülau unit should be used with the smallest possible volume.

Estimation of pulmonary blood flow from sinusoidal gas exchange during anaesthesia: a theoretical study.

We simulated the use of simultaneous sinusoidal changes of inspired O2 and N2O (Williams et al., J Appl Physiol, 1994; 76: 2130-9) at fractional concentrations up to 0.3 and 0.7, respectively, to estimate FRC and pulmonary blood flow (PBF) during anaesthesia, using O2 as an insoluble indicator. Hahn's approximate equations, which neglect the effect of pulmonary uptake and excretion on expiratory flow, estimate dead space and alveolar volume (VA) with systematic errors less than 10%, but yield systematic errors in PBF which are approximately proportional to FIN2O in magnitude. A correction factor (1 - P)-1 for Hahn's equations for PBF (where P is the mean partial pressure of the soluble indicator) reduces the dependence of PBF estimates of FIN2O, and the solution of equations describing the simultaneous mass balance of both indicators yields accurate results for a wide range of mean FIN2O. However, PBF estimates are sensitive to measurement errors and a third gas must be present to ensure that the indicator gases behave independently.

The Newton valve revisited: an in-vitro study of ventilator circuit dead space

A laboratory study was conducted to investigate the volume (length) of the ventilator circuit dead space (VCD) tubing at which dilution of an inspired gas by ventilator driving gas first occurs using three lung models. Various lengths of two VCD tubing materials [Portex (Sims Portex Ltd, Kent, UK) 10 mm bore smooth-walled silicon and Intersurgical (Wokingham, Berks, UK) 22 mm corrugated plastic] were interposed between a T-piece circuit and Nuffield 200 ventilator (Penlon, Abingdon, Oxon, UK) with a Newton valve attached. Dilution of inspired gas by the ventilator driving gas was first detected during ventilation of infant and child lung models when the VCD was 7 ml (6 cm) and 77 ml (102 cm), respectively, using Portex tubing, and 24 ml (6.5 cm) and 105 ml (29 cm), respectively, using Intersurgical tubing. No dilution occurred using the neonatal model. Dilution of the inspired anaesthetic gases by ventilator driving gas may occur in paediatric practice if the VCD volume (length) is inadequate. This risk is greatest in the child.

Serotonin reuptake inhibition does not enhance short term modulation of the exercise ventilatory response

Increased respiratory dead space causes a serotonin (5-HT) dependent augmentation of the exercise ventilatory response known as short term modulation (STM). Contrary to predictions, 5-HT reuptake inhibition with fluoxetine failed to enhance, and even impaired STM with large dead space volumes (0.4–0.6 L). In this study, we tested the hypotheses that: (1) fluoxetine similarly impairs STM with smaller dead space volumes (0.2 L); whereas (2) acute 5-HT release and reuptake inhibition with fenfluramine would enhance STM. Ventilatory and blood gas measurements were made on five goats (37–58 kg) during rest and exercise, with the mask alone or with increased dead space (0.2 L). STM protocols were performed following chronic fluoxetine (≥21 days, 1 mg/kg, SQ, SID) and acute fenfluramine administration (1 mg/kg, IV). Following fluoxetine, STM was partially impaired. Fenfluramine had no detectable effects on STM. The data suggest that: (1) chronic fluoxetine diminishes STM, possibly via down-regulation of relevant 5-HT receptors, and (2) drugs that release 5-HT acutely do not enhance STM.

Alveolar dead space as a predictor of severity of pulmonary embolism.

To determine whether the alveolar dead space volume (V(D)alv), expressed as a percentage of the alveolar tidal volume (V(D)alv/V(T)alv), can predict the degree of vascular occlusion caused by pulmonary embolism (PE). Fifty-three subjects with suspected PE were prospectively studied. Pulmonary embolism was diagnosed in 33 by high-probability ventilation/perfusion (V/Q) scan (n = 19) or by pulmonary arteriography (PAG, n = 14). Pulmonary embolism was excluded by PAG in 20 subjects. The V(D)alv/V(T)alv was determined from volumetric capnography and arterial blood gas analysis, which permits measurement of the physiologic dead space, V(D)phys (mL) = [(PaCO2 - PeCO2)/PaCO2]. tidal volume. Airway dead space (V(D)aw) was subtracted to yield the alveolar dead space [(V(D)phys - V(D)aw) = V(D)alv (mL)]; the percentage of alveolar volume occupied by alveolar dead space per breath = V(D)alv/V(T)alv x 100%. Percentage perfusion defect was determined from V/Q scans by a radiologist blinded to other data. Regression analysis was performed to show correlation between V(D)alv/V(T)alv and defect on V/Q scan or systolic pulmonary arterial pressure (SPAP). For subjects with PE, the mean perfusion defect on lung scan was 38 +/- 22%; the mean V(D)alv = 208 +/- 115 mL, V(T)alv = 452 +/- 251 mL, and V(D)alv/V(T)alv = 43 +/- 18%. Regression of V(D)alv/V(T)alv vs perfusion defect yielded r2 = 0.41. Regression of V(D)alv/V(T)alv vs pulmonary artery pressures yielded r2 = 0.59. For subjects without PE, V(D)alv/V(T)alv = 27 +/- 14% and V(D)alv = 89 +/- 66 mL. The V(D)alv/V(T)alv correlates with the lung perfusion defect and the pulmonary artery pressures in subjects with PE. These findings show the potential for V(D)alv/V(T)alv to quantify the embolic burden of PE.

Ventilation heterogeneity in excised lobes: effect of tidal volume.

Although several factors are known to influence nonuniformity of ventilation, including lung mechanical properties (regional structure and compliance), external factors (chest wall, pleural pressure, heart), and ventilatory parameters (tidal and preinspiratory volume, flow rate), their relative contributions are poorly understood. We studied five excised, unperfused, canine right-middle lobes under varied levels of tidal volume (VT), thus eliminating many factors affecting heterogeneity. Multiple-breath washouts of N(2) were analyzed for anatomic dead space volume (VD(anat)), nonuniformity of N(2) washout, and nonuniformity between joined acinar regions vs. that occurring between larger joined regions. Approximately 80% of ventilation heterogeneity was found among joined acinar regions at resting levels of VT, but increasing VT reduced intra-acinar heterogeneity to about 25% of that found at resting levels. Increasing VT had essentially no effect on VD(anat) and heterogeneity among larger joined regions. The results indicate that the magnitude of VT is a major influence on the dominant intra-acinar component of ventilation heterogeneity and that VT effects on VD(anat) are likely due to perfusion and/or influences normally external to the lobar structure.

Pressure support ventilation in patients with acute lung injury.

To assess the success rate of pressure support ventilation (PSV) in acute lung injury patients undergoing continuous positive pressure ventilation (CPPV), to study physiologic changes after the transition from CPPV to PSV, and to investigate differences between patients who succeed and patients who fail PSV according to predetermined criteria. Observational study. General intensive care unit in a teaching hospital. We studied 48 patients having acute lung injury, as defined by a PaO2/F(IO2) <300 mm Hg and the presence of bilateral infiltrates on chest radiograph, and ventilated with CPPV. We included patients with PaO2 >80 mm Hg, at positive end-expiratory pressure of <15 cm H2O and with F(IO2) up to 1.0. After enrollment, PSV was instituted and patients were strictly monitored during the following 48 hrs. Subjects who met any of the predefined PSV failure criteria during this period were returned to CPPV (Group F). PSV was continued in the remaining patients (Group S). Gas exchange, respiratory mechanics, and hemodynamics measurements were collected before switching from CPPV to PSV and were repeated at 24 hrs after beginning PSV, or immediately before return to CPPV in Group F patients. The physiologic deadspace volume to tidal volume ratio (V(D)/V(T)) was obtained by the Enghoff's equation from the measurement of the mixed expired CO2 fraction. PSV resulted in a significant PaCO2 decrease (49.2+/-10.9 mm Hg to 44.4+/-7.2 mm Hg) and significant increases in minute volume (V(E))(9.0+/-2.3 L/min to 12.0+/-4.0 L/min) and arterial blood pH (7.405+/-0.054 to 7.435+/-0.064), with stable oxygenation and hemodynamics. In patients who were hypercapnic (PaCO2 >50 mm Hg) during CPPV, the V(E) increase was higher than in normocapnic patients. In the latter patients, PaCO2 and pH did not change significantly going from CPPV to PSV. A total of 38 patients (79%) were allocated to Group S and the remaining 10 patients were included in Group F. In Group S, positive endexpiratory pressure of 9.4+/-2.9 cm H2O (range, 3-14 cm H2O) and a PSV level of 14.9+/-3.8 cm H2O (range, 9-22 cm H2O) were applied. In Group F, positive end-expiratory pressure of 8.9+/-3.1 cm H2O (range, 5-15 cm H2O) and a PSV level of 21.6+/-4.6 cm H2O (range, 16-31 cm H2O) were adopted. Compared with Group S, Group F had a longer duration of intubation (20.2+/-19.2 days vs. 9.2+/-13.5 days), a lower static compliance of the respiratory system (30.4+/-16.5 mL/cm H2O vs. 41.7+/-15.0 mL/cm H2O), and a higher V(D)/V(T) (0.70+/-0.09 vs. 0.52+/-0.10), but similar oxygenation and positive end-expiratory pressure. V(E) was higher in Group F during both CPPV and PSV. In a relatively high proportion of the investigated patients, PSV was successful. The institution of PSV led to no major changes in oxygenation or in hemodynamics. PSV was associated with increases in V(E) and respiratory frequency. In patients who had been hypercapnic during CPPV, PaCO2 decreased despite a compensated pH. Compared with PSV success patients, patients who failed PSV appeared to be sicker, as shown by the higher duration of respiratory support, increased ventilatory needs, and decreased respiratory system compliance, despite similar arterial oxygenation and positive end-expiratory pressure.

Influence of media-packing ratio on performance of anaerobic hybrid reactors

In this study, the influence of media-packing ratio on the performances of anaerobic hybrid reactors (AHRs) at low, medium and high organic loading rates was evaluated by conducting COD profile, granulation and tracer studies. Four laboratory upflow anaerobic hybrid reactors, each with a total unpacked volume of 7.85 l, with varying packing depths, were operated at organic loading rates from 1 to 24 g COD/l d. The media-packing ratios were 75%, 60%, 40% and 20% of the total reactor height in the AHRs. Three types of soluble COD profiles along the reactor height were observed when the organic loading rate was gradually increased. When operated at 1 and 2 g COD/l d the COD profiles along the reactor height from bottom to top showed a plug-flow regime. From 4 to 12 g COD/l d the COD profiles were distorted in the reactors with 20%, 40% and 60% packing, while at 16 g COD/l d and above the COD profile indicated homogeneity in each reactor, suggesting a perfectly-mixed regime. The distorted COD profiles were considered to be caused by the non-ideal flow pattern prevalent in the reactors. The dead-space volume and the bypass flowrate due to short-circuiting were determined using the Cholette and Cloutier model. A `distortion index' (DI), which was calculated from the ratio of the average COD value of the sludge bed over the average COD value of the reactor, was used to describe distortion of the COD profile. The distortion index correlated well with the short-circuiting fraction.

An IBM PC-based system for the assessment of cardio-respiratory function using oscillating inert gas forcing signals.

An IBM PC-based real-time data acquisition, monitoring and analysis system was developed for the assessment of cardio-respiratory function, i.e. airway dead space, alveolar volume and pulmonary blood flow, using oscillating inert inspired gas forcing signals. The forcing gas mixture was generated by an in-house sinusoid gas delivery unit. The system interfaced with a mass spectrometer and an airway flow transducer, and performed real-time tracking of the breath-by-breath end-inspired, end-expired and mixed-expired concentrations. It calculated the cardiorespiratory parameters using two, i.e. continuous and tidal, in-house mathematical models of the lungs. The system's performance was evaluated using a mechanical bench lung, laboratory subjects and awake adults breathing spontaneously. Its predictive accuracy was compared with the measured volumes of the bench lung; single breath CO2 test for airway dead space and N2 washout for alveolar volume in laboratory subjects and awake adults; and thermal dilution technique for pulmonary blood flow in laboratory subjects. Close agreements were found between the true and predicted airway dead space, i.e. mean differences of -12.39%, 14.47% and -17.49%, respectively, and that of alveolar volume, i.e. -8.03%, -3.62% and 7.22%, respectively, in the bench lung, laboratory subject and awake adult studies; and that of pulmonary blood flow (-23.81%) in the laboratory subjects using the continuous lung model. Even closer agreements were observed for airway dead space (-5.8%) and alveolar volume (-4.01%) of the bench lung and for pulmonary blood flow (-8.47%) in the laboratory subjects using the tidal lung model. A system was developed to deliver, monitor and analyse on-line, and in real-time, output data from the sinusoid forcing technique. The technique was administered using the system in various subjects, and produced favourable predictions.

In vitro and in vivo assessment of the Ventrak 1550/Capnogard 1265 for single breath carbon dioxide analysis in neonates

The Ventrak 1550/Capnogard 1265 (V&C) enables deadspace (VD) measurements to be made in neonates. The aim of our studies was to validate the V&C device for VD measurement in vitro (lung model) and in vivo (adult rabbits). Methods of measurement of VD using the V&C (automatic computation, interactive carbon dioxide-volume plot analysis, Bohr equation) were tested by comparing known added deadspace volumes (VDadd) with calculated VDadd. After producing a change in alveolar (VDalv) and physiological (VDphys) deadspace by in vivo broncho-alveolar lavage, VDalv and VDphys computed automatically were compared with values calculated by the Bohr-Enghoff equations. VDadd was slightly underestimated (absolute error in mean: automatically -0.61 ml; interactively -0.55 ml; Bohr -0.54 ml). The higher the VDadd, the lower the absolute errors and coefficients of variation (cv). The highest cv occurred for automatic analysis (approximately 11%) compared with < 6% for interactive analysis or the Bohr equation. Average differences between results calculated automatically and by the Bohr-Enghoff equation were -0.79 ml for VDalv (95% confidence interval -2.02 to 0.44 ml) and -0.23 ml for VDphys (-0.6 to 0.14 ml). We conclude that the V&C can be used in newborn infants undergoing mechanical ventilation, if changes in VD are < 5 ml, interactive analysis or the Bohr equation should be used.

Improved accuracy and extended flow range for a Fleisch pneumotachograph.

A large linear flow range and a small instrumental dead space volume are incompatible properties for a pneumotachometer (PTM). The linearity of a Fleisch number 2 PTM is studied for flows up to 6 litre s-1 (nominal range 0-2 litre s-1) with various up- and downstream geometries. It is hypothesised that using an array of calibration factors (conductance; flow/pressure), instead of a single calibration factor over the entire flow range, could improve accuracy and also extend the applicable flow range. The conductance against pressure characteristics are calculated with a previously described weighted averaging technique based on multiple strokes from a precision syringe. A single conductance value gives stroke volume errors in the range of -5 to 3% (0-2 litre s-1) and -6 to 11% (0-6 litre s-1) for validation using the same geometry as for calibration. The pressure dependent conductance improves accuracy to within -3% and 1% independent of flow range. However, for validation using a different geometry than for calibration, errors range from -5% to +8%. The degree of non-linearity varies between the geometries (range 3-15%) and is highest when using a one-directional valve upstream of the PTM and a Y-shaped connector. In conclusion, a pressure-dependent conductance improves accuracy and can also be used to extend the applicable flow range up to at least three times the nominal flow range.

A plastic plate facilitating the monitoring of fluid absorption during general anaesthesia

A plastic plate facilitating the monitoring of fluid absorption during general anaesthesia

Intermittent CPAP during General Anesthesia

Department of Anesthesiology, MDC 59; University of South Florida; College of Medicine; 12901 Bruce B. Downs Boulevard; Tampa, Florida;jdowns@com1.med.usf.eduIn Reply:-We appreciate Dr. Fletcher's careful review of our article and considerate comments. We considered the ratio PaCO(2):minute ventilation to be a simple calculation of ventilatory efficiency in the restrictive setting of cardiopulmonary and metabolic stability with "…relatively constant PaCO(2) and carbon dioxide production…" [1] We did not and would not advise use of the calculation in a setting of variable CO2production, alveolar ventilation, or PaCO(2). As a separate measure, we calculated the P(a-et)CO(2) and confirmed that intermittent CPAP results in more efficient ventilation than traditional controlled mechanical ventilation (CMV). Fletcher also referred to an increase in alveolar ventilation, which was precluded by study design. We produced equivalent levels of alveolar ventilation during CMV and intermittent CPAP, as evidenced by similar PaCO(2) values, but with significantly less total ventilation during the latter. Using the calculation P(a-et)CO(2)/PaCO(2) as an indication of the fraction of unperfused, but ventilated alveoli [2] we found a mean alveolar deadspace of 4% during intermittent CPAP and 17% during CMV.It is well known that an inspiratory pause applied during CMV may result in a smaller calculated physiologic deadspace. [3] It is less apparent that "conducting airways," which define the "anatomic" deadspace, are reduced in volume by an end-inspiratory pause. It also is not clear that CPAP will have a pulmonary effect similar to that observed with conventional positive pressure ventilation with an inspiratory plateau. Our data clearly support a significant decrease in alveolar deadspace during intermittent CPAP. To test Fletcher's hypothesis that a decrease in anatomic deadspace might account for the observed increase in efficiency of ventilation during intermittent CPAP, we calculated the difference in mean anatomic and alveolar deadspace (VD) volumes during CMV and intermittent CPAP, using data in the manuscript [1] and standard equations. [4] We assumed a normal anatomic deadspace of 194 ml during CMV. During intermittent CPAP alveolar V (D) was 15 ml, anatomic VD139 ml, and total physiologic VD153 ml. During CMV alveolar VDwas 74 ml, anatomic VD194 ml, as assumed, and total physiologic VD268 ml. We observed that intermittent CPAP caused modest decrease in calculated anatomic VDcompared with CMV, of 28%. More important however, was the fivefold increase in alveolar deadspace generated by controlled ventilation. Overall physiologic VDwas 74% higher during CMV than during intermittent CPAP, emphasizing our conclusion that intermittent CPAP provides more efficient ventilation.John B. Downs, M.D.Department of Anesthesiology, MDC 59; University of South Florida; College of Medicine; 12901 Bruce B. Downs Boulevard; Tampa, Florida;jdowns@com1.med.usf.edu(Accepted for publication December 17, 1998.)

Angiotensin-converting enzyme inhibition facilitates alveolar-capillary gas transfer and improves ventilation-perfusion coupling in patients with left ventricular dysfunction.

The backward effects of left ventricular dysfunction include alterations in alveolar-capillary gas transfer and ventilation-perfusion coupling. Because the angiotensin-converting enzyme (ACE) is highly concentrated in the vascular endothelium of the lungs, we examined whether ACE inhibitors may influence the pulmonary function in patients with congestive heart failure. In 20 patients with idiopathic cardiomyopathy, pulmonary function and exercise capacity were evaluated at baseline and 6 and 12 months after treatment with enalapril (10 mg twice a day) was started. The study also included 19 age- and sex-matched control subjects with mild primary hypertension and normal left ventricular function who were given enalapril as a standard treatment of high blood pressure. In congestive heart failure, forced expiratory volume in 1 second, vital capacity, and total lung capacity did not vary significantly with enalapril; alveolar-capillary diffusion of carbon monoxide (DL(CO)) increased toward normal; exercise tolerance time, peak exercise oxygen uptake (peak VO2), minute ventilation and tidal volume (peak VT) also increased; and the ratio of volume of dead space (VD) to VT (peak VD/VT) at peak exercise reduced. Changes in peak VO2 showed a direct correlation with those in DL(CO) and an inverse correlation with those in peak VD/VT. Results at 6 and 12 months were comparable. Enalapril did not affect these variables in the control population. In patients with idiopathic cardiomyopathy heart failure, but not in control subjects, gas transfer and ventilation-perfusion improved with ACE inhibition. These pulmonary changes may contribute to the associated increase in exercise tolerance.

Lung carbon dioxide elimination rate (LCO2) correlates with physiologic deadspace volume during mechanical ventilatory support

Society of Critical Care Medicine; 28th Educational and Scientific Symposium; San Francisco, California, USA; January 23-27, 1999: Poster Presentations: Poster Hall

Abnormal Increases in Physiologic Deadspace Volume at a Critical Mean Airway Pressure

Abnormal Increases in Physiologic Deadspace Volume at a Critical Mean Airway Pressure