Volumetric capnography in patients with acute lung injury: effects of positive end-expiratory pressure.

The aim of the study was to analyse the effects of positive end-expiratory pressure (PEEP) on volumetric capnography and respiratory system mechanics in mechanically ventilated patients. Eight normal subjects (control group), nine patients with moderate acute lung injury (ALI group) and eight patients with acute respiratory distress syndrome (ARDS group) were studied. Respiratory system mechanics, alveolar ejection volume as a fraction of tidal volume (VAE/VT), phase III slopes of expired CO2 beyond VAE and Bohr's dead space (VD/VT(Bohr)) at different levels of PEEP were measured. No differences in respiratory system resistances were found between the ALI and ARDS groups. VD/VT(Bohr) and expired CO2 slope beyond VAE were higher in ALI patients (0.52+/-0.01 and 13.9+/-0.7 mmHg x L(-1), respectively) compared with control patients (0.46+/-0.01 and 7.7+/-0.4 mmHg x L(-1), p<0.01, respectively) and in ARDS patients (0.61+/-0.02 and 24.9+/-1.6 mmHg x L(-1), p<0.01, respectively) compared with ALI patients. VAE/VT differed similarly (0.6+/-0.01 in control group, 0.43+/-0.01 in ALI group and 0.31+/-0.01 in ARDS group, p<0.01). PEEP had no effect on VAE/VT, expired CO2 slope beyond VAE and VD/VT(Bohr) in any group. A significant correlation (p<0.01) was found between VAE/VT and expired CO2 slope beyond VAE and lung injury score at zero PEEP. Indices of volumetric capnography are affected by the severity of the lung injury, but are unmodified by the application of positive end-expiratory pressure.     

Airway insufflation: physiologic effects on acute and chronic gas exchange in humans

Reduction in dead space through conventional tracheostomy has been used to treat patients with chronic CO2 retention. The insufflation of air directly into the trachea by transtracheal catheter (airway insufflation, AI) provides reductions in dead space as great or greater than those of tracheostomy. The physiologic effects of AI on gas exchange have not been adequately studied because instillation of gases into the trachea contaminates minute ventilation (VL), dead space volume (VD), tidal volume (VT), and other indices of gas exchange, as measured by usual technics. We overcame this problem by devising special methods of measuring inspired and expired ventilation, alveolar and dead space ventilation, and VT and VD by using pneumotachographic timing of inspiration and expiration so that true inspired and expired ventilation were calculated. We studied 5 patients with chronic CO2 retention from either COPD, scoliosis, or muscular dystrophy (annual average PaCO2 = 45 to 75 mm Hg) during 75 min of AI with serial gas exchange and arterial blood gas measurements. AI at about 5 L/min of room air through the trachea in 5 patients reduced VL by 18% (from 7.91 to 6.48 L/min), VT by 25% (from 450 to 338 ml), and VD by 37% (from 223 to 141 ml), while not affecting PaCO2 (from 51.8 to 48.2 mm Hg) or PaO2 (from 65.1 to 63.4 mm Hg). In 2 patients, AI administered continuously for 4 to 12 months (as 30 to 50% O2) maintained PaCO2 as well as or better than breathing enriched O2 from a tracheal collar via an open tracheostomy.(ABSTRACT TRUNCATED AT 250 WORDS)     

慢性阻塞性肺疾病患者运动高峰时肺内气体交换对运动能力的影响

目的 探讨COPD患者在运动高峰时肺内气体交换对最大运动能力的影响.方法 对42例男性稳定期COPD患者及26例健康男性进行功率递增至症状自限的踏车运动,同步实时测定摄氧量和二氧化碳产生量,在运动高峰时抽取桡动脉血,测定并计算PaO2、PaCO2、死腔容积与潮气容积比值(VD/VT)和P(A-a)O2.分别对两组资料进行正态性检验,符合正态分布的资料以x-±s表示,两组间比较采用独立样本t检验,最大摄氧量与运动高峰时的血气参数进行相关因素分析.结果 COPD组的最大摄氧量[(16±4)ml·kg-1·min-1]明显低于对照组[(19±6)ml·kg-1·min-1];PaCO2[(43±3)mm Hg,1 mm Hg=0.133 kPa]、VD/VT(0.35±0.11)和P(A-a)O2[(33±11)mm Hg]均明显高于对照组[(40±5)mm Hg、0.27±0.08和(15±7)mm Hg];最大摄氧量与VD/VT呈显著负相关(r=-0.734,P＜0.01).结论 VD/VT增加导致通气效率降低,这是引起COPD患者运动能力减低的一个重要原因.     

Single breath CO2 measurements of deadspace in ducks

We measured deadspace (VD) in ducks using CO2 expirograms (plots of expired PCO2 vs expired volume) obtained during artificial ventilation at different tidal volumes (VT) and respiratory system volumes (VRS). Conventional analysis of the expirograms for Bohr and Fowler VD indicated both were larger than anatomic VD. Most expirograms at VT less than or equal to 100 ml had terminal slopes greater than predicted for lung gas and violated the usual assumptions of the Fowler calculation. Bohr VD was not affected by VRS but increased with VT. This can be explained by expired PCO2 not reaching lung values at low VT and an expiratory mesobronchial ventilatory shunt. We propose a measure of mesobronchial shunt corresponding to a volume of gas exhaled in one breath from caudal air sacs through the mesobronchus (VM). VM/VT changes with pump vs constant flow ventilation indicating sensitivity of VM to flow pattern. We estimate mesobronchial shunting is greatest at the beginning of expiration and approaches zero only near the end of a 200 ml expiration with constant flow ventilation.     

健康成人二氧化碳通气当量与生理死腔的相关性研究

目的:通过健康成人二氧化碳通气当量(EqCO2)和生理死腔/潮气量(VD/VT)比率的相关性探讨,用无创的方法代替有创的方法研究呼吸生理。方法:28例受试者行心肺运动试验,同步实时测定分钟通气量(VE)和二氧化碳产生量(VCO2),计算出静态二氧化碳通气当量(EqCO2rest)、无氧阈二氧化碳通气当量(EqCO2AT)及最大运动状态下二氧化碳通气当量(EqCO2max)。并分别在运动前及运动高峰时抽取动脉血,根据改良Bohr的公式,得出实际生理死腔/潮气量比率(VD/VT)。结果:正常人静态时EqCO2rest与VD/VTrest有显著相关关系(r=0.601,P=0.011);运动高峰时EqCO2max与VD/VTmax无相关性(r=-0.223,P=0.334),且EqCO2AT和EqCO2max较EqCO2rest明显下降,差异有统计学意义(P<0.001),EqCO2max与EqCO2AT比较也有下降,但差异无统计学意义(P=0.417)。结论:正常成人静息状态下用无创方法测定EqCO2可反映实际VD/VT。     

Mechanisms of periodic breathing during exercise in patients with chronic heart failure

BACKGROUND: Periodic breathing (PB) in heart failure (HF) is attributed to many factors, including low cardiac output delaying the time it takes pulmonary venous blood to reach the central and peripheral chemoreceptors, low lung volume, lung congestion, augmented chemoreceptor sensitivity, and the narrow difference between eupneic carbon dioxide tension and apneic/hypoventilatory threshold. METHODS AND RESULTS: We measured expired gases, ventilation, amplitude, and duration of PB in 23 patients with PB during progressive exercise tests done with 0 mL, 250 mL, or 500 mL of added dead space. Periodicity of PB remained constant despite heart rate, oxygen consumption, and minute ventilation increasing. Within each PB cycle, starting from the beginning of exercise, the largest (peak) tidal volume approached maximum observed tidal volume, while the smallest (nadir) tidal volume increased as exercise power output increased. PB ceased when nadir tidal volume reached peak tidal volume. End-tidal carbon dioxide increased with added dead space, and PB ceased progressively earlier during the exercise done with increased dead space. CONCLUSION: Circulatory delay does not contribute to the PB observed in exercising HF patients. The pattern of gradually increasing nadir tidal volume during exercise and the effect of dead space on both PB ceasing and end-tidal carbon dioxide suggest that low tidal volume and carbon dioxide apnea threshold are important contributors to PB that occurs during exercise in HF.     

Diffusing Capacity for Carbon Monoxide is Linked to Ventilatory Demand in Patients with Chronic Obstructive Pulmonary Disease

Abstract

Dyspnea is deemed to result from an imbalance between ventilatory demand and capacity. The single-breath diffusing capacity for carbon monoxide (DLCO) is often the best correlate to dyspnea in COPD. We hypothesized that DLCO contributes to the assessment of ventilatory demand, which is linked to physiological dead space /tidal volume (VD/VT) ratio. An additional objective was to assess the validity of non-invasive measurement of transcutaneous P_CO2 allowing the calculation of this ratio. Forty-two subjects (median [range] age: 66 [43–80] years; 12 females) suffering mainly from moderate-to-severe COPD (GOLD stage 2 or 3: n = 36) underwent pulmonary function and incremental exercise tests while taking their regular COPD treatment. DLCO% predicted correlated with both resting and peak physiological VD/VT ratios (r = ?0.55, p = 0.0015 and r = ?0.40, p = 0.032; respectively). The peak physiological VD/VT ratio contributed to increase ventilation (increased ventilatory demand), to increase dynamic hyperinflation and to impair oxygenation on exercise. Indirect (MRC score) and direct (peak Borg score/% predicted V˙O2) exertional dyspnea assessments were correlated and demonstrated significant relationships with DLCO% predicted and physiological VD/VT at peak exercise, respectively. The non-invasive measurement of transcutaneous P_CO2 both at rest and on exercise was validated by Bland-Altman analyses. In conclusion, DLCO constitutes and indirect assessment of ventilatory demand, which is linked to exertional dyspnea in COPD patients. The assessment of this demand can also be non invasively obtained on exercise using transcutaneous PCO₂ measurement.     

The efficacy of a custom-fabricated nasal mask on gas exchange during nasal intermittent positive pressure ventilation.

Commercially available nasal masks have a large mask volume and give rise to considerable air leaks around the mask during nasal intermittent positive pressure ventilation (NIPPV) which may reduce alveolar ventilation (VA per breath). The effects of a custom-fabricated nasal mask (F-mask) versus a commercially available mask (C-mask) on arterial blood gas measurements, dead space including both physiological and apparatus dead space (VD), air leak and VA per breath were compared in patients with restrictive thoracic disease during short-term NIPPV sessions while using a volume cycled ventilator with equivalent settings for both masks. The mask volume of the C-mask was significantly larger than that of the F-mask (p<0.003). The arterial carbon dioxide tension (Pa,CO2) during NIPPV with either the F-mask (5.56+/-1.35 kPa) (mean+/-SD) or the C-mask (6.87+/-0.96 kPa) was significantly lower than during spontaneous breathing (7.75+/-0.81 kPa; p<0.003), but the Pa,CO2 decreased more during NIPPV with the F-mask than with the C-mask (p<0.003). The VD was significantly smaller (p<0.03), the air leak was significantly less (p<0.03), and the VA per breath was significantly larger (p<0.03) during NIPPV with the F-mask than with the C-mask. In conclusion, nasal intermittent positive pressure ventilation with the F-mask was more effective than nasal intermittent positive pressure ventilation with the commercially available mask due to its smaller dead space and less air leak. Further studies are needed to extend these results to all the commercially available-masks.     

Efficacy of diaphragmatic breathing in patients with chronic obstructive pulmonary disease

This study investigated the effects of diaphragmatic breathing (DB) on ventilation and breathing pattern, seeking to identify predictors of its efficacy in patients with chronic obstructive pulmonary disease (COPD). Twenty-nine patients with moderate and severe COPD were monitored using respiratory inductance plethysmography and metabolic gas analysis. After 4 minutes of natural breathing, subjects completed 2 minutes of DB followed by 4 minutes of natural breathing. Dyspnea was measured using a visual analogue scale. Diaphragmatic mobility was assessed using chest radiography. DB was associated with a significant increase in tidal volume and reduction in breathing frequency, leading to higher ventilation and oxygen saturation, with a reduction in dead space ventilation and ventilatory equivalent for carbon dioxide. A total of 10 subjects with moderate (5) and severe (5) COPD performed DB with asynchronous thoracoabdominal motion, worsening the dyspnea, and decreasing the gain of tidal volume. Diaphragmatic mobility, inspiratory muscular strength, lower scores for dyspnea and hypoxemia as well as coordinated thoracoabdominal motion are associated with effective DB. In patients with COPD, DB can improve breathing pattern and ventilatory efficiency without causing dyspnea in patients whose respiratory muscular system is preserved.     

Breathing pattern and gas exchange at peak exercise in COPD patients with and without tidal flow limitation at rest.

Expiratory flow limitation (FL) at rest is frequently present in chronic obstructive pulmonary disease (COPD) patients. It promotes dynamic hyperinflation with a consequent decrease in inspiratory capacity (IC). Since in COPD resting IC is strongly correlated with exercise tolerance, this study hypothesized that this is due to limitation of the maximal tidal volume (VT,max) during exercise by the reduced IC. The present study investigated the role of tidal FL at rest on: 1) the relationship of resting IC to VT,max; and 2) on gas exchange during peak exercise in COPD patients. Fifty-two stable COPD patients were studied at rest, using the negative expiratory pressure technique to assess the presence of FL, and during incremental symptom-limited cycling exercise to evaluate exercise performance. At rest, FL was present in 29 patients. In the 52 patients, a close relationship of VT,max to IC was found using non-normalized values (r=0.77; p < 0.0001), and stepwise regression analysis selected IC as the only significant predictor of VT,max. Subgroup analysis showed that this was also the case for patients both with and without FL (r=0.70 and 0.76, respectively). In addition, in FL patients there was an increase (p < 0.002) in arterial carbon dioxide partial pressure at peak exercise, mainly due to a relatively low VT,max and consequent increase in the physiological dead space (VD)/VT ratio. The arterial oxygen partial pressure also decreased at peak exercise in the FL patients (p < 0.05). In conclusion, in chronic obstructive pulmonary disease patients the maximal tidal volume, and hence maximal oxygen consumption, are closely related to the reduced inspiratory capacity. The flow limited patients also exhibit a significant increase in arterial carbon dioxide partial pressure and a decrease in arterial oxygen partial pressure during peak exercise.     

The increased ventilatory response to exercise in chronic heart failure: relation to pulmonary pathology.

OBJECTIVE: To assess the exercise limitation of patients with chronic heart failure (CHF) and its relation to possible pulmonary and ventilatory abnormalities. SETTING: A tertiary referral centre for cardiology. METHODS: The metabolic gas exchange responses to maximum incremental treadmill exercise were assessed in 55 patients with CHF (mean (SD) age 57.9 (13.0) years; 5 female, 50 male) and 24 controls (age 53.0 (11.1) years; 4 female, 20 male). Ventilatory response was calculated as the slope of the relation between ventilation and carbon dioxide production (VE/VCO2 slope). RESULTS: Oxygen consumption (VO2) was the same at each stage in each group. Ventilation (VE) was higher in patients at each stage. Patients had a lower peak VO2 and a steeper VE/VCO2 slope than controls. Dead space ventilation as a fraction of tidal volume (VD/VT) was higher in patients at peak exercise, but dead space per breath was greater in controls at peak exercise (0.74 (0.29) v 0.57 (0.17) litres/breath; P = 0.002). End tidal CO2 was lower in patients at all stages, and correlated with peak VO2 (r = 0.58, P < 0.001). Alveolar oxygen tension was higher in patients at each stage than in controls. CONCLUSIONS: Patients with CHF have an increased ventilatory response at all stages of exercise. Although this is accompanied by an increase in VD/VT, there is hyperventilation relative to blood gases. It is more likely that the excessive ventilation is not due to a primary pulmonary pathology, but rather, the increase in dead space is likely to be a response to increased ventilation.     

Effect of breathing pattern on dead space ventilation VD/VT during exercise

In order to assess the effect of breathing pattern on measurements of dead space ventilation (VD/VT) during exercise, we studied 6 patients with the complaint of exertional dyspnea. They had essentially normal resting pulmonary function studies and the only abnormality noted during an initial exercise study was an elevated VD/VT associated with a rapid respiratory rate. A second exercise study was then performed during which they were coached to breathe at a slower rate and larger tidal volume. During the exercise study with coaching, the VD/VT response was normal. We conclude that breathing pattern during exercise influences VD/VT and that an increase in total minute ventilation which is accomplished by a preferential increase in respiratory rate may result in an abnormally high VD/VT.     

Ventilatory and cerebrovascular responses in normocapnic and hypercapnic COPD patients.

This study investigated the hypothesis that hypercapnia in some chronic obstructive pulmonary disease (COPD) patients may be related to a high cerebrovascular response to carbon dioxide (CO2). The relationship between responses of ventilation and of cerebral blood volume (CBV) to acute changes in carbon dioxide tension in arterial blood (Pa,CO2) was measured in 17 chronic hypercapnic (Pa,CO2 >6.0 kPa) and 16 normocapnic (Pa,CO2 < or = 6.0 kPa) COPD patients, who were matched for degree of airway obstruction (forced expiratory volume in one second 27% predicted). Results were compared with 15 age-matched healthy subjects. CBV was measured using near infrared spectroscopy during normo- and hypercapnia and related to inspired minute ventilation (V'I) and mouth occlusion pressure (P0.1). Hypercapnia (end-tidal pressure of carbon dioxide (deltaPET,CO2) > 1 kPa) was induced by giving adequate amounts of CO2 in the inspired air. During normocapnia, CBV (mL x 100 g(-1)) was 2.41+/- 0.66 and 2.90 +/- 0.60 (mean +/- SD) in the normocapnic and chronic hypercapnic patients, respectively, which was significantly lower compared to healthy subjects (3.53 +/- 0.77). All slopes of CO2 responsiveness (deltaCBV/deltaPa,CO2, deltaV'I/deltaPa,CO2, deltaP0.1/deltaPa,CO2) were significantly lower in both COPD groups relative to healthy subjects, but were not significantly different between the COPD groups. A poor but positive correlation between ventilatory and cerebrovascular CO2 responsiveness (deltaCBV/deltaPa,CO2 and deltaV'I/deltaPa,CO2) was found in COPD patients and healthy subjects. The findings do not support the hypothesis of abnormal cerebrovascular responses to carbon dioxide in hypercapnic chronic obstructive pulmonary disease patients.     

Effects of inspiratory flow waveforms on lung mechanics,gas exchange,and respiratory metabolism in COPD patients during mechanical ventilation

STUDY OBJECTIVE: The clinical usefulness of varying inspiratory flow waveforms during mechanical ventilation has not been adequately studied. The aim of this study was to compare the effects of three different respiratory waveforms on the pulmonary mechanics, gas exchange, and respiratory metabolism of ventilated patients with COPD. DESIGN: A randomized and comparative trial of consecutive patients. SETTING: Medical ICUs of a 2,000-bed university hospital. PATIENTS: Fifty-four patients with COPD were enrolled. INTERVENTIONS: Constant, decelerating, and sine waveforms were applied to each patient in a random order. MEASUREMENTS AND RESULTS: With tidal volume, inspiratory time, and inspiratory frequency being kept constant, the decelerating waveform produced statistically significant reductions of peak inspiratory pressure, mean airway resistance, physiologic dead space ventilation (VD/VT), PaCO(2), and symptom score. There was also a significant increase in alveolar-arterial oxygen pressure difference with the decelerating flow waveform, but there were no significant changes in mean airway pressure, arterial oxygenation, heart rate, mean BP, and other hemodynamic measurements. In addition, assessment on the work of breathing (WOB) revealed that ventilator WOB values were reduced with the decelerating waveform. Oxygen consumption and carbon dioxide output were virtually not affected by changing inspiratory flow waveforms. Except for VD/VT, the effects of constant square and sine waveforms were similar to each other and could not be separated statistically. CONCLUSIONS: The most favorable flow pattern for ventilated patients with COPD appeared to be the decelerating waveform. There are possibilities for the improvement of ventilation in these patients by selecting an appropriate inspiratory flow.     

Arterial to end-tidal CO2 difference in respiratory disease.

The difference in CO2 tension between arterial blood and end-tidal alveolar gas (a-end-tidal)DCO2 was found to correlate fairly well with the VD/VT ratio in 13 healthy subjects and 50 patients with pulmonary diseases (r = 0.74), and to discriminate between healthy subjects and patient groups at least as effectively as did the VD/VT ratio. An increase in breathing frequency from 8 to 32/min, without simultaneous change in alveolar ventilation, was associated with a mean increase in (a-end-tidal) DCO2 of several mmHg in both the healthy subjects and the patient groups. It is concluded that measurement of (a-end-tidal)DCO2 seems to be a clinically useful alternative to measurement of VD/VT ratio for evaluation of the wasted ventilation component, provided that the effect of the breathing frequency on (a-end-tidal) DCO2 is taken into account.     

Sleep hypoventilation in hypercapnic chronic obstructive pulmonary disease: prevalence and associated factors.

Sleep hypoventilation (SH) may be important in the development of hypercapnic respiratory failure in chronic obstructive pulmonary disease (COPD). The prevalence of SH, associated factors, and overnight changes in waking arterial blood gases (ABG), were assessed in 54 stable hypercapnic COPD patients without concomitant sleep apnoea or morbid obesity. Lung function assessment, anthropomorphic measurements, and polysomnography with ABG measurement before and after sleep were conducted in all patients. Transcutaneous carbon dioxide tension (Pt,CO2) was measured in sleep, using simultaneous arterial carbon dioxide tension (Pa,CO2) for in vivo calibration and to correct for drift in the sensor. Of the patients, 43% spent > or = 20% of sleep time with Pt,CO2 > 1.33 kPa (10 mmHg) above waking baseline. Severity of SH was best predicted by a combination of baseline Pa,CO2, body mass index and per cent rapid-eye movement (REM) sleep. REM-related hypoventilation correlated significantly with severity of inspiratory flow limitation in REM, and with apnoea/hypopnoea index. Pa,CO2 increased mean+/-SD 0.70+/-0.65 kPa (5.29+/-4.92 mmHg) from night to morning, and this change was highly significant. The change in Pa,CO2 was strongly correlated with severity of SH. Sleep hypoventilation is common in hypercapnic chronic obstructive pulmonary disease, and related to baseline arterial carbon dioxide tension, body mass index and indices of upper airway obstruction. Sleep hypoventilation is associated with significant increases in arterial carbon dioxide tension night-to-morning, and may contribute to long-term elevations in arterial carbon dioxide tension.     

Ventilatory response to low levels of CO2

Ventilation and Pa(CO2), were measured in six subjects after 10-12 min of breathing 1-2% CO2 during hyperoxia and hypoxia. These inspired CO2 concentrations were achieved in two ways: by enriching the inspirate with CO2 and by having the subjects breathe through dead spaces of 100-400 cm3. Breathing through dead space gave the same results as CO2 enrichment of the inspirate when the effect of the dead spaces on mean inspired CO2 was allowed for. During hyperoxia all subjects demonstrated isocapni hyperpnea in response to mean inspired CO2 concentrations of 1%; ventilation increased without change in PA(CO2). When mean inspired CO2 concentration approximated 1.5% two subjects showed isocapnic hyperpnea, and one subject demonstrated isocapnic hyperpnea in response to mean inspired CO2 concentrations of 2%. The increase in PA(CO2) observed in each subject in response to 2% CO2 in O2 correlated negatively with the slope of that subject's rebreathing CO2 response curve. Hypoxia (PA(O2Y = 45-50 mm Hg) depressed the response to 1% CO2 in that, while hypoxic, no subject showed isocapnic hyperpnea in response to 1% CO2. The isocapnic hyperpnea we observed was chiefly due to increased tidal volume, and was therefore not analogous to the isocapnic hyperpnea observed by others in dogs in response to increases of CO2 in lung gas. When low levels of CO2 produced an increase in PA(CO2) the associated change in ventilation (delta Ve/delta PA(CO2)was much less than that observed while rebreathing 7% CO2. Isocapnic hyperpnea in response to low levels of CO2 is common among normal individuals, and is depressed by hypoxia; the stimulus responsible for this response is unknown.     

Accuracy of capnography in nonintubated surgical patients.

Previous studies have reported mixed results when correlating etCO2 and PaCO2 in mechanically ventilated patients with underlying respiratory disease. However, the utility and accuracy of capnography in nonintubated patients, without chronic pulmonary disease, has received little attention. We studied 25 nonintubated surgical patients to (1) examine the correlation between PaCO2 and etCO2 and (2) describe the relationship between dead space (VD/VT), venous admixture and P(a-et)CO2. End tidal CO2 was lower than PaCO2 by an average of 3.6 mm Hg. Regression analysis found a close correlation between dead space and the P(a-et)CO2 gradient (r = 0.77, p < 0.001), while venous admixture was of lesser importance (r = 0.47). Capnographic estimates of PaCO2 can be useful for continuously monitoring the respiratory status of nonintubated spontaneously breathing patients weaned from mechanical ventilation. This may be of particular value in trauma victims and in selected surgical patients without underlying respiratory disease in whom other injuries require continued critical care.     

呼出气CO2容积曲线对肺部疾病换气功能障碍的诊断与评价

目的 评价无创肺换气功能诊断技术即呼出气CO2容积曲线(VCap)对肺部疾病慢性阻塞性肺疾病(chronic obstructive pulmonary disease.COPD)、支气管哮喘(简称哮喘)和间质性肺疾病(ILD)患者换气功能障碍的诊断价值及临床意义.方法 对照组(医院对照)94人,平均年龄(61.59±8.73)岁.COPD组287例.平均年龄(64.31±11.71)岁.根据COPD肺功能分级标准分4级:COPD Ⅰ级(9例)、COPD Ⅱ级(141例)、COPD Ⅲ级(75例)、COPDⅣ级(62例).哮喘组251例,平均年龄(57.86±13.54)岁.根据气道阻塞程度分4级(分级标准同COPD):轻度阻塞(6例)、中度阻塞(113例)、重度阻塞(100例)、极重度阻塞(32例).ILD组45例,平均年龄(56.42±13.97)岁.主要分析变量:最大呼出气二氧化碳浓度、Ⅲ相斜率(dC/dV3)、呼出气最高CO2浓度的25%～50%时的容积与潮气容积的比值(Vm25-50/VT)、呼出气最高CO2浓度的50%～75%时的容积与潮气容积的比值(Vm50-75/VT).结果 ①ILD、哮喘和COPD分别与对照组比较:Vm25-50/VT、Vm50-75/VT、FeCO2max、dC/dV3,差异有统计学意义(P<0.01);②轻度哮喘和轻度COPD组比较:Vm50-75/VT,dC/dV3差异无统计学意义;中、重度组比较:Vms50-75/VT,dC/dV3差异有统计学意义(P<0.01);哮喘合并肺气肿和COPD(肺气肿)组比较差异无统计学意义;③Vm50-75/VT和dC/dV3用于COPD(肺气肿)的评价敏感度分别为98.3%和96.5%.特异度分别为91.4%和86.1%.结论 ①COPD、哮喘和ILD患者VCap形态异常.dC/dV3增高并且与疾病的严重程度有关,示肺内气体分布不均,系气道阻力增高和(或)肺顺应性改变导致吸入气体分布不均和呼出气体非同步排空所致,ILD相对于COPD和哮喘则气体分布不均更为突出;②变量Vm50-75/VT间接反映肺泡死腔量,相对受生理因素及通气量的影响小,与常规肺功能指标均有较好的相关性,可作为评价肺部疾病换气功能障碍即肺泡死腔增大,通气血流/灌注失调间接指标.③Vm50-75/VT%≥10%和dC/dV3≥1.3%/L用于评价肺气肿有较高敏感度和特异度.     

Elevated pulmonary artery systolic storage volume associated with improved ventilation-to-perfusion ratios in acute respiratory failure.

The possibility that an elevated pulmonary artery systolic storage volume (PASSV) correlates with improved overall ratios of ventilation-to-perfusion and hence benefits gas exchange in acute respiratory failure was examined. We examined this by assessing the correlation between PASSV and both the physiologic dead space to tidal volume ratio (VD/VT) and intrapulmonary shunt fraction (Qsp/Qt). The VD/VT and Qsp/Qt were used as an index of distribution of ventilation-to-perfusion as well as efficiency of pulmonary gas exchange. Twenty-eight patients suffering from acute respiratory failure were included. All required mechanical ventilation. PASSV was calculated from the pulmonary artery (PA) compliance and mean PA systolic distending pressure. Pulmonary arteriolar pressures were computed by Fourier analysis. PA compliance was derived from the PA time constant and the PA resistance. Storage volume fraction of stroke volume index (PASSV/SVI) was used to compare individual variations. There were inverse linear relationships between PASSV/SVI and VD/VT (r = 0.693, p less than 0.0001), and between PASSV/SVI and Qsp/Qt (r = 0.427, p = 0.012). Also, a direct correlation was found between VD/VT and PA time constant (r = 0.503, p = 0.002). The patients were divided into two groups based on PASSV/SVI to evaluate the effect of other hemodynamic data on PASSV. Comparison of the two groups revealed that VD/VT and Qsp/Qt were lower (p less than 0.0001, and p = 0.018, respectively), PA time constant was higher (p less than 0.001), and right ventricular stroke-work index was higher (p = 0.005) in the group with a high PASSV/SVI. There were no differences in other hemodynamic data between the two groups. These data suggest that an elevated PASSV may indeed benefit gas exchange in acute respiratory failure.