Gas mixing in dog lungs during high frequency ventilation studied by partial washout-single exhalation technique

Gas mixing was studied in 10 anesthetized paralyzed dogs during high-frequency low tidal ventilation (HFV). After simultaneous washin of ethane (1%) and washout of resident argon (0.9%) the gas inflow was switched to atmospheric air for varied time intervals leading to varied levels of C2H6 washout and Ar washin. After the stop of HFV at predetermined test gas washout/washin levels, a constant-flow exhalation by a servo ventilator was performed and expirograms of C2H6 and Ar were recorded. Measurements were performed at varied ventilation frequencies (10-40 Hz), stroke volumes (20-40 ml), lung volumes (730-830 ml), expiratory flow rates (0.1-0.01 L/sec), breath-holding prior to exhalation (0-12 sec) and test gas washout levels achieved by varying the washout time (1 to 65 sec) before onset of exhalation. The expirograms showed a close to linearly rising alveolar plateau. They were analyzed for series dead space and alveolar slope which was normalized to the initial-to-final partial pressure difference. The normalized slopes of C2H6 washout and Ar washin were averaged, whereby the effect of shrinking lung volume due to continuing CO2/O2 exchange at low R was assumed to be suppressed. The slope was little affected by changes of stroke volume, decreased slightly with increasing frequency, and decreased considerably with breath-holding or increasing lung volume. As washout progressed, the alveolar slope first increased, attained a maximum at about half-washout and thereafter decreased. The finite values of the alveolar slope indicated that intrapulmonary gas mixing during HFV was incomplete. The slopes were larger than expected from diffusion calculations on symmetrically branching lung models. The behavior of the slope at varied washout levels suggested involvement of parallel ventilation/volume inhomogeneity coupled with sequential emptying.     

Effects of rehabilitation on chest wall volume regulation during exercise in COPD patients.

In order to investigate underlying mechanisms, the present authors studied the effect of pulmonary rehabilitation on the regulation of total chest wall and compartmental (ribcage, abdominal) volumes during exercise in patients with chronic obstructive pulmonary disease. In total, 20 patients (forced expiratory volume in one second, mean +/- SEM 39 +/- 3% predicted) undertook high-intensity exercise 3 days x week(-1) for 12 weeks. Before and after rehabilitation, the changes in chest wall (cw) volumes at the end of expiration (EEV) and inspiration (EIV) were computed by optoelectronic plethysmography during incremental exercise to the limit of tolerance (W(peak)). Rehabilitation significantly improved W(peak) (57+/-7 versus 47+/-5 W). In the post-rehabilitation period and at identical work rates, significant reductions were observed in minute ventilation (35.1+/-2.7 versus 38.4+/-2.7 L x min(-1)), breathing frequency (26+/-1 versus 29+/-1 breaths x min(-1)) and EEV(cw) and EIV(cw) (by 182+/-79 and 136+/-37 mL, respectively). Inspiratory reserve volume was significantly increased (by 148+/-70 mL). Volume reductions were attributed to significant changes in abdominal EEV and EIV (by 163+/-59 and 125+/-27 mL, respectively). The improvement in W(peak) was similar in patients who progressively hyperinflated during exercise and those who did not (24 and 26%, respectively). In conclusion, pulmonary rehabilitation lowers chest wall volumes during exercise by decreasing the abdominal volumes. The improvement in exercise capacity following rehabilitation is independent of the pattern of exercise-induced dynamic hyperinflation.     

Regional pulmonary function in intra-emphysematous bulla and peri-emphysematous bulla]

We have measured regional alveolar volume and regional ventilation of emphysematous lesions and periemphysematous lesions with positron emission tomography and N-13 gas in 10 patients. The purpose of the study was to investigate how emphysematous lesion develops. The subjects were all male (except one) who put on a mask in supine position, and were connected with a spirometer. We gave N-13 gas in this closed circuit and had the gas rebreathed by the subjects. After activity reached equilibrium in closed circuit, an equilibrium scan was made. We took "activity gas" from the closed circuit and measured activity by well counter during equilibrium to get quantitative alveolar volume. The activity in closed circuit during equilibrium showed activity in the thoracic unit. After equilibrium, we used air to wash out radioactive gas from the circuit. During washout we took 3 sequential images. The decreased rate of activity in the region of interest from these 3 sequential washout images was expressed in a monoexponential curve. The index of monoexponential denotes V/V. Alveolar volume in emphysematous lesions was 34.8 +/- 19.5 ml/100ml thoracic volume, and V/V in these lesions was 0.27 +/- 0.21/min. On the other hand alveolar volume in periemphysematous lesions was 76.5 +/- 13.1 ml/100ml thoracic volume, and V/V was 0.38 +/- 0.22/min. Thus alveolar volume in periemphysematous lesions was relatively high. These results indicate that the effect of emphysematous lesions as compared with periemphysematous lesions was not direct compression of alveolar space. The direct effect was compression to the bronchiole of peripheral lesions, and check valve mechanism occurred in the bronchiole causing peripheral lesions resulting in the destruction of the alveolar wall.     

Pulmonary gas exchange and oxygen uptake during exercise in patients with type 1 diabetes mellitus.

In order to investigate pulmonary gas exchange and cardiopulmonary performance in Type 1 diabetes, 36 patients underwent a progressive incremental exercise test on a cycle ergometer. Cardiopulmonary variables were measured, and arterial blood gases determined on samples obtained from an indwelling catheter in the radial artery. The results were compared with those from 40 control subjects. In the patients, the maximum power (Wmax) and maximum oxygen uptake (VO2max) were lower than in the control subjects (Wmax 186 +/- 52 (+/- SD) vs 233 +/- 48 W, p less than 0.05; VO2max 2.56 +/- 0.71 vs 3.17 + 0.77 l min-1, p less than 0.05). At comparable levels of power output, however, no significant abnormality was observed in the difference between alveolar and arterial oxygen pressure (P(A-a)O2), and the ratio of physiological dead space to tidal volume (VD/VT ratio). These data indicate that in Type 1 diabetic patients, despite their reduced maximum oxygen uptake, gas transfer during exercise is not limited and thus does not contribute to the impairment of exercise capacity.     

Effects of cardiac oscillations on acinar gas mixing during pulmonary edema.

We used a previously reported technique (Mackenzie et al., J. Appl. Physiol. 68: 2013-2018, 1990) to measure the effects of severe pulmonary edema on acinar cardiogenic gas mixing in anesthetized dogs. We also tested how increases in lung volume affected gas mixing in healthy lungs and during pulmonary edema. Cardiogenic gas mixing was evaluated by measurement of the rate of washout of xenon133 injected into an occluded pulmonary artery during apnea. The rate constant of xenon133 washout was 0.40 min-1 (+/- 0.06 SE) in the healthy lung at functional residual capacity. It decreased (P < 0.05) to 0.08 min-1 (+/- 0.03) when lung volume was raised 500 ml. Pulmonary edema was induced by injection of oleic acid (0.06 mg.kg-1) into the right atrium over a 4-min period; clinical signs of severe pulmonary edema were present after 90 min. The rate constant for xenon133 washout (0.07 +/- 0.03 min-1) was less than in the healthy lung (P < 0.05), and was not changed after lung volume was increased (P > 0.05). We conclude that, in the presence of severe pulmonary edema: (1) acinar resistance is increased and/or magnitude of cardiogenic oscillations is decreased; and (2) salutary effects of increased lung volume are not due to enhancement of cardiogenic gas mixing.     

Nitrogen washout during tidal breathing with superimposed high-frequency chest wall oscillation

In order to assess the efficacy of high-frequency chest wall oscillation (HFCWO) superimposed on tidal ventilation, multiple-breath nitrogen washout curves were obtained in 7 normal seated subjects. To maintain a regular breathing pattern throughout the study, the subjects breathed synchronously with a Harvard ventilator set at a constant tidal volume and frequency for each subject during a trial period. Washout curves were obtained during 3 different maneuvers performed in random order. Series A was the control condition with no superimposed HFCWO. In Series B and C, HFCWO at 5 Hz was superimposed on the regulated tidal breathing; the magnitude of the oscillatory tidal volume measured at the airway opening was 20 ml for Series B and 40 ml for Series C. The nitrogen washout was clearly faster in Series C than in Series A for each subject. In Series B, there was an interindividual variability, with a washout rate either equal to that in Maneuver A or in Maneuver C, or intermediate between the two. When these washout curves were analyzed in terms of a simple monocompartment model, the time constant of the washout was found to decrease by 16 +/- 11% in Series B, and 25 +/- 7% in Series C compared with that in Series A. In this group of normal subjects, the correction of any inhomogeneity in the distribution of the ventilation is unlikely to explain these results because of the close fit of all washout curves to a monoexponential model. It is postulated that during inspiration HFCWO enhances gas mixing in the lung periphery and that during expiration it improves gas mixing in the airways.(ABSTRACT TRUNCATED AT 250 WORDS)     

Ventilation and gas exchange during exercise in sickle cell anemia

Adults with sickle cell anemia (SCA) have restrictive lung impairment, increased alveolar dead space, and hypoxemia. These factors, together with increased anaerobic metabolism, are thought to cause exercise hyperventilation. To assess the role of each of these in children, 34 patients with SCA and 16 control subjects performed pulmonary function and exercise tests. Twenty-eight patients with SCA had spirometric values and lung volumes, and all but two patients with SCA had arterial saturation greater than 91% during exercise. Despite a low VO2max (30.07 +/- 6.55 ml/min/kg), the ventilatory anaerobic threshold (VAT) in the patients occurred at a similar %VO2max as in the control subjects (69 +/- 9% versus 63 +/- 12%). The slope of the delta VE/delta VCO2 relationship for sub-VAT work was steeper in the patients (29.4 +/- 6.5 versus 24.7 +/- 5.2, p = 0.01), and the ventilatory equivalent for CO2 (VE/VCO2) in steady-state exercise was greater in the patients than in the control subjects (33.2 +/- 3.5 versus 30.8 +/- 3.5, p = 0.03). End-tidal PCO2 did not differ (38.3 +/- 3.0 versus 39.2 +/- 3.1), indicating equivalent alveolar ventilation. The patients had a higher dead space:tidal volume ratio (VD/VT) than did the control subjects (0.204 +/- 0.033 versus 0.173 +/- 0.024, p = 0.0005). The PaCO2 was significantly lower in those with lower Hb, but there was no difference in pH. In conclusion, children with SCA have an increased exercise ventilatory response caused in part by increased physiologic dead space, and in part by their low Hb. The greater dead space may be the result of sickle cells impairing capillary perfusion to ventilated alveoli.     

死腔负荷对慢性阻塞性肺疾病患者肺功能及呼吸肌功能和运动耐力的影响

目的评价死腔负荷对肺通气功能和呼吸肌的影响,测试呼吸肌氧耗的检测方法,探讨呼吸肌氧耗在慢性阻塞性肺疾病(COPD)运动耐力下降中的作用.方法 26例中度COPD患者和29名年龄相近健康对照者在300 ml呼吸管路死腔(长46 cm)负荷下,完成30 W或55 W功率恒定运动试验,并在死腔负荷下检测运动前、后肺功能和运动中分钟通气量((V·)E)和摄氧量((V·)O2).结果无论COPD或健康对照组,在静息状态或运动后,增加死腔对用力肺活量(FVC)、一秒钟用力呼气容积(FEV1)和FEV1/FVC无显著影响.COPD组静息死腔负荷下FVC、FEV1和FEV1/FVC分别为(3.03±0.15)L、(1.95±0.09)L和(64.9±2.5)%;55 W运动后上述指标分别为(3.03±0.18)L、(2.00±0.13)L和(66.3±3.2)%(P均＞0.05).每例受试个体,无论静息或运动中,附加死腔均导致(V·)E和(V·)O2在原有基础上显著增加,卸除死腔后(V·)E和(V·)O2回落.死腔负荷下(V·)O2的增加量(Δ(V·)O2)在静息和30 W运动时,COPD组和健康对照组之间差异无显著性.在55 W运动时,COPD组Δ(V·)O2显著高于健康对照组[(272±24)ml/min与(194±19)ml/min,P<0.05].结论本组患者呼吸管路加长46 cm(300 ml死腔),伴随中等强度运动未导致COPD患者气流阻塞的进一步加重,也未出现明显呼吸肌疲劳征象.COPD患者呼吸肌具有氧耗优势,呼吸肌与肢体运动肌摄氧比例不平衡,可能是导致COPD患者运动耐力下降的因素之一.     

Effect of a deep breath on gas mixing and diffusion in the lung

We examined the effect of a previous deep breath on both inert gas mixing and the single breath diffusing capacity (DLCOSB) during submaximal single breath maneuvers in normal subjects. Single breath washouts were performed either immediately after a deep breath or after breathing tidally for 10 min. Maneuvers consisted of inhaling test gas from functional residual capacity to 50% inspiratory capacity and, after either 0 or 6 s of breath holding, exhaling slowly back to residual volume. We measured the Fowler dead space, the Phase III slope of the alveolar plateau of the He washout (delta He/L), the amplitude of the cardiogenic oscillations (Oc), closing capacity, mixing efficiency (Emix) and DLCOSB using the three equation method. For maneuvers immediately after a deep breath we found that delta He/L was steeper and the Oc were larger for washouts with 6 s but not 0 s of breath holding, while Emix was significantly lower and DLCOSB significantly higher for both the 0 s and the 6 s breath holding maneuvers. We conclude that a deep breath increases DLCOSB but simultaneously also increases convective-dependent inhomogeneity in the lung.     

Comparison of oxygen uptake during bicycle exercise in patients with chronic heart failure and in normal subjects

Prediction of oxygen uptake (VO2) during exercise from relations established in normal subjects between VO2 and work load in watts (W) may be inaccurate in patients with chronic heart failure because these patients could manifest delayed VO2 kinetics at final stages of exercise. To test the hypothesis that even at low levels of work, patients exhibit a lower VO2 than do normal subjects, 77 patients with heart failure and 27 control subjects with a normal heart or with disease other than heart failure underwent bicycle exercise with respiratory gas analysis. Work load was increased by 10 W/min from an initial 20 W. VO2 (ml/min per kg) was measured every 15 s. The delta VO2/delta W ratio was significantly reduced only in the most severely impaired patients in heart failure class C-D (8.75 +/- 2.14 versus 11.05 +/- 0.38, p less than 0.05). Class B patients showed a lower ratio at a work load of greater than or equal to 80 W, whereas class C-D patients manifested a lower ratio at greater than or equal to 20 W. Even with a low incremental work rate protocol, compared with sedentary normal subjects or patients without heart failure, patients with heart failure demonstrate impaired oxygen uptake. This observation suggests the presence of anaerobic metabolism or delayed VO2 uptake, or both; accordingly, indirect estimates of VO2 requirements derived from intensity or duration of exercise in such patients are overestimated.     

Tidal volume change and gas mixing in the lung

Changing the depth and the frequency of breathing affects the efficiency of ventilation. This has been studied in eight normal subjects using the technique of nitrogen washout whilst breathing a mixture of 79% argon and oxygen. The signals were converted to digital data at 50 Hz and all calculations were then done with the computer. The size of the dead space of the conducting airways (series dead space, VdS) and of the alveolar dead space (VdA) has been measured for carbon dioxide (CO2) and oxygen (O2). The nitrogen (N2) decay curve was computed allowing the calculation of first breath (AMEsb) and multi breath (AMEmb) alveolar mixing efficiency. The increase in VdS per 100 ml increase in tidal volume (Vt) was 3.7 ml for CO2 and 3.3 for O2. As VdS increased, VdA also increased by 11.1 ml for CO2 and 19.1 ml for O2, for each 100 ml increase in Vt. Whilst VdA and VdS increase with increasing Vt, the proportion of VdA + VdS in each breath diminishes with such an increase, the net result is that, for each 100 ml increase in Vt, alveolar ventilation increases by 86 ml for CO2 and 78 ml for O2. The increase of absolute values and the different behaviour of N2, AMEsb and AMEmb show a progressive decrease of the parallel component of the intra-pulmonary ventilation distribution with increasing Vt. It appears that the pattern of ventilation, as well as minute ventilation, plays a role in the effectiveness of ventilation.     

Intraregional gas mixing in humans during high frequency oscillations

We measured the effect of high frequency oscillation (HFO) on gas mixing in the human lung. In seven healthy, seated subjects the alveolar slope of the single breath nitrogen washout was used to assess the effects of HFO on gas mixing. A reduction in slope was interpreted as reflecting improved gas mixing within topographical lung regions. The alveolar slope was measured after 0, 10, 20 and 30 sec of control breathhold or HFO applied at the subject's TLC. We found that HFO reduced the alveolar slope more than did control breathhold. The difference in the slopes was greater with longer durations, increased stroke volume (SV) and frequency (f) of oscillations. The reduction in alveolar slope correlated better with SV than with f. We conclude that to the extend that a change in the slope in the alveolar plateau reflects intraregional mixing, this mixing is more dependent on SV than on f.     

Alveolar-capillary membrane conductance is the best pulmonary function correlate of exercise ventilation efficiency in heart failure patients

BACKGROUND: In heart failure (HF), changes in lung mechanics and gas diffusion are limiting factors to exercise. Their contribution to an increased exercise ventilation to CO2 production (VE/VCO2) slope is undefined. METHODS: A total of 67 stable HF patients underwent cardiopulmonary exercise and pulmonary function tests, including forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1), maximal voluntary ventilation (MVV), total lung capacity (TLC) and alveolar diffusing capacity with its subcomponents (alveolar-capillary membrane conductance (D(m)) and capillary blood volume (V(c))). RESULTS: Patients showed a mild restrictive pattern (FEV1=85+/-15% and FVC=75+/-13% of normal predicted) and a moderate D(m) reduction (32+/-12 ml min(-1) mm Hg(-1)). Average peak VO(2) was 15.6+/-4.0 ml min(-1) kg(-1) and the VE/VCO2 slope was 39.6+/-11.0. At simple Spearman correlation analysis, all variables, but V(c), correlated with peak VO2; only D(m) correlated with VE/VCO2 slope. At partial Spearman correlation, all variables lost the peak VO2 correlation, and D(m) still inversely correlated with VE/VCO2 slope (r=-0.35; p=0.005). In patients with a high VE/VCO2 slope (cutoff value 34), despite comparable lung volumes, D(m) was significantly more depressed (30+/-13 vs. 35+/-10 ml min(-1) mm Hg(-1); p<0.01). CONCLUSIONS: Pulmonary function tests and alveolar gas diffusing capacity poorly correlate with peak VO2. D(m) impairment rather than lung volumes correlates with exercise ventilation efficiency. This finding further adds to the pathophysiological relevance of an abnormal gas exchange in HF patients.     

Detecting abnormalities in left ventricular function during exercise by respiratory measurement

The degree of exercise-induced cardiac dysfunction and its relation to the anaerobic threshold were evaluated in 23 patients with chronic heart disease. A symptom-limited exercise test was performed with a cycle ergometer with work rate increased by 1 W every 6 seconds. Left ventricular function, as reflected by ejection fraction, was continuously monitored with a computerized cadmium telluride detector after the intravenous injection of technetium-labeled red blood cells. The anaerobic threshold (mean, 727 +/- 166 ml/min) was determined by the noninvasive measurement of respiratory gas exchange. As work rate rose, the left ventricular ejection fraction increased but reached a peak value at the anaerobic threshold and then fell below resting levels. Ejection fraction at rest, anaerobic threshold, and peak exercise were 41.4 +/- 11.3%, 46.5 +/- 12.0%, and 37.2 +/- 11.0%, respectively. Stroke volume also increased from rest (54.6 +/- 17.0 ml/beat) to the point of the anaerobic threshold (65.0 +/- 21.2 ml/beat) and then decreased at peak exercise (52.4 +/- 18.7 ml/beat). The slope of the plot of cardiac output versus work rate decreased above the anaerobic threshold. The anaerobic threshold occurred at the work rate above which left ventricular function decreased during exercise. Accurate determination of the anaerobic threshold provides an objective, noninvasive measure of the oxygen uptake above which exercise-induced deterioration in left ventricular function occurs in patients with chronic heart disease.     

Left ventricular response to submaximal exercise in endurance-trained athletes and sedentary adults.

This investigation examines the hypothesis that athletes increase stroke volume with submaximal exercise through an augmentation of left ventricular (LV) end-diastolic volume and a reduction of LV end-systolic volume, whereas sedentary adults only increase stroke volume modestly, because LV end-diastolic volume does not increase. Upright bicycle exercise was performed by 17 endurance-trained male athletes and 15 sedentary men. M-mode echocardiograms were obtained during submaximal exercise at predetermined heart rates. Athletes, at a heart rate of 130 beats/min, increased their stroke volume 67% from 72 +/- 18 ml to 120 +/- 26 ml (p less than 0.001). This resulted from an increase of LV end-diastolic volume from 119 +/- 23 to 152 +/- 28 ml (p less than 0.001) and a reduction in LV end-systolic volume from 46 +/- 14 to 31 +/- 9 ml (p less than 0.001). Sedentary men at the same heart rate increased stroke volume 22% from 63 +/- 15 to 77 +/- 21 ml (p less than 0.05). LV end-diastolic volume did not change (96 +/- 20 vs 97 +/- 28 ml) (p = not significant), but LV end-systolic volume decreased (33 +/- 11 vs 20 +/- 9 ml) (p less than 0.001). In conclusion, athletes increased cardiac output through a more prominent augmentation of stroke volume than sedentary subjects at submaximal exercise. This was accomplished through an augmentation of LV end-diastolic volume. This may have a conserving effect on myocardial oxygen consumption at these levels of exercise.     

Gas trapping in normal infants and in infants with cystic fibrosis

Two different methods for estimating trapped gas volume have been described in the literature. The purpose of this study was to use both of these methods to estimate and compare trapped gas volumes in normal infants and infants with cystic fibrosis (CF). Thirty normal infants and 29 infants with CF, ages 1 month to 3 years, were studied. Pulmonary function tests, including raised volume forced expiratory flows, plethysmographic functional residual capacity (FRC(pleth)), and fractional lung volumes, were measured. Then functional residual capacity was measured by nitrogen washout (FRC(nitrogen)). Following nitrogen washout, lungs were then inflated three times to 30 cm H(2)O, using 100% oxygen. This process was repeated until no further nitrogen could be washed from the lungs. The volume of trapped gas (tg) was calculated from the total additional amounts of nitrogen expired following lung inflations. The difference between FRC(pleth) and FRC(nitrogen) provided a second estimate of trapped gas volume (delta V). Mean tg and delta V values for normal infants were 2.5 +/- 3.5 ml and 15.6 +/- 30.4 ml, respectively. Mean tg and delta V values for infants with CF were 5.8 +/- 7.7 ml and 33.2 +/- 43.8 ml, respectively. Both tg and delta V did not differ significantly between normal infants and infants with CF. Measured following raised volume forced expiratory maneuvers, delta V and tg do not distinguish infants with CF from normal infants as well as do other currently available tests of infant lung function.     

Measurement of the Fowler dead space in patients with pulmonary emphysema using C18O2

In patients with lung emphysema, changes in lung volumes as well as changes in airway resistance are well known. The change in airway resistance is caused by obstruction of central airways, which is supposed to reduce the respiratory dead space. Until now, it was not possible to measure the respiratory dead space in patients with lung emphysema using the method of Fowler [2], because in this method distinction of the three phases of an inert gas expirogram is essential. While this distinction is easy in healthy subjects (fig. 1; expirogram 3), the separation of the three phases in patients with lung emphysema is not possible due to gradual transition of phase II into phase III in these patients (fig. 1; expirogram 2). The use of C18O2 as tracer gas allows to separate phase II and phase III even if the patients have severe emphysema (fig. 1; expirogram 1). CO2 labeled with the stable oxygen isotope 18O (C18O2) is completely taken up in the gas exchanging region of the lung, but not from the conducting airways. Therefore C18O2 is only expired from the dead space of the lung, but not from the alveolar region. Hence, C18O2 allows exact measurement of the respiratory dead space in patients with lung emphysema. 21 healthy nonsmoking subjects and 29 patients with clinical signs of lung emphysema participated in this study. There was a good correlation between respiratory dead space, measured by the use of Ar-gas and C18O2-gas in healthy subjects (fig. 2). This indicates, that the use of C18O2 is a valid method to measure the functional dead space. As expected, there was also a correlation between the airway resistance and respiratory dead space in patients with lung emphysema (fig. 3), but not in healty subjects. There was no significant difference of the mean values of the respiratory dead space between these two groups (223 +/- 43 ml in healthy subjects vs. 227 +/- 52 ml in patients), even though there were large differences in airway resistance (0.20 +/- 0.10 kPa/l/s vs. 0.49 +/- 0.27 kPa/l/s). This may be due to a loss of alveolar function in the area of the terminal bronchioli, which is typical for emphysematous patients. This entails a shift of functional dead space towards lung periphery and therefore causes an increase of the volume of functional dead space. But this enlargement may be compensated by the volume reduction, caused by the airway obstruction. Hence, these two oppositional mechanisms may result in only minimal change of dead space volume.     

Vasodilatory behavior of skeletal muscle arterioles in patients with nonedematous chronic heart failure

During maximal upright exercise, blood flow to working skeletal muscle is frequently reduced in patients with nonedematous chronic heart failure. It has been speculated that this reduced muscle flow may be caused in part by an intrinsic impairment of skeletal muscle vasodilatory capacity. To test this hypothesis, forearm blood flow and resistance were compared during forearm exercise and in response to transient forearm ischemia (10 min) in 22 patients with heart failure and in 11 normal subjects. During forearm exercise, both groups exhibited comparable forearm blood flows (ml/min/100 ml) (0.2 W: normal 5.9 +/- 3.1, heart failure 6.5 +/- 2.8; 0.4 W: normal 8.2 +/- 5.5, heart failure 8.2 +/- 3.6; 0.6 W: normal 11.5 +/- 6.8, heart failure 11.8 +/- 4.8 [all p = NS]) and forearm vascular resistance (mm Hg/ml/min/100 ml) (0.2 W: normal 23.1 +/- 12.4, heart failure 18.5 +/- 7.8; 0.4 W: normal 16.9 +/- 7.7, heart failure 14.7 +/- 6.4; 0.6 W: normal 13.1 +/- 7.7, heart failure 10.3 +/- 4.1 [all p = NS]). Ten minutes of forearm ischemia, an intervention that produces maximal forearm vasodilation, also resulted in comparable forearm vascular resistances in both groups (normal 4.1 +/- 2.4, heart failure 3.8 +/- 1.3 mm Hg/ml/min/100 ml/p = NS). These data suggest that skeletal muscle vasodilatory capacity is not intrinsically impaired in patients with nonedematous chronic heart failure.     

Moment ratio analysis of multiple breath nitrogen washout in infants with lung disease.

Measurement of lung volumes at end expiratory level and assessment of ventilation inhomogeneity is important for respiratory management in infants with lung disease. This study compared multiple breath nitrogen washout was compared with body plethysmography to measure functional residual capacity in infants and assessed ventilation inhomogeneity using mean dilution numbers and alveolar based gas dilution numbers. Measurements were performed in 23 infants with lung disorders, eleven had wheezing bronchitis, four bronchopulmonary disease, and eight cystic fibrosis. Mean age was 11.2+/-5.8 months. Functional residual capacity of nitrogen washout (29.8+/-11.4 mL x kg(-1)) was significantly (p<0.05) lower than the plethysmographically measured functional residual capacity (40.3+/-11.4 mL x kg(-1)). Tidal volumes before nitrogen washout (90.4+/-35.1 mL) were significantly larger than at the end of the washout (72.2+/-26.9 mL). Alveolar based gas dilution numbers (6.7+/-2.3) were significantly lower (p<0.001) than mean dilution numbers (10+/-5.7). Functional residual capacity determination by nitrogen washout and plethysmography in infants with lung disease showed evidence of air trapping and ventilation inhomogeneity. Ventilation inhomogeneities are best described by alveolar based dilution numbers, since rebreathing of 100% oxygen changes ventilation pattern.