Modification of pulmonary gas mixing by postural changes

Mixing for two gases of markedly different gaseous diffusivity, helium (He) (mol wt = 4) and sulfur hexafluoride (SF6) (mol wt = 146) has been studied by a rebreathing method in different postures. In nine normal subjects duplicate measurements were made in the erect (seated), supine, and lateral decubitus posture, at a constant tidal volume (700 ml) and frequency (1 Hz) starting from functional residual capacity (FRC). Additional measurements were made on four of the subjects, rebreathing seated erect at a volume similar to the relaxed FRC supine and supine at a volume similar to the relaxed FRC seated. In the supine posture the mean breath number to reach 99% equilibrium (n99), was not significantly different for the two gases, 8.9 for He and 9.8 for SF6. There was a difference (P less than 0.01) when erect; n99 (He) = 8.2 and n99 (SF6) = 10.9. The greatest He-SF6 difference (P less than 0.001) was in the lateral decubitus position n99 (He) = 10.1 and n99 (SF6) = 15.9. The mean relaxed FRC as percent of seated was 71% supine and 75% in lateral decubitus posture. Rebreathing seated at a lower volume did not abolish the He-SF6 mixing difference nor did rebreathing at a higher volume when supine induce a He-SF6 mixing difference. Thus the effect of posture on gas mixing cannot be due solely to lung volume and must represent a convective and diffusive dependent change in the distribution of ventilation per unit lung volume.     

High-frequency ventilation of ducks and geese

We studied gas exchange in anesthetized ducks and geese artificially ventilated at normal tidal volumes (VT) and respiratory frequencies (fR) with a Harvard respirator (control ventilation, CV) or at low VT-high fR using an oscillating pump across a bias flow with mean airway opening pressure regulated at 0 cmH2O (high-frequency ventilation, HFV). VT was normalized to anatomic plus instrument dead space (VT/VD) for analysis. Arterial PCO2 was maintained at or below CV levels by HFV with VT/VD less than 0.5 and fR = 9 and 12 s-1 but not at fR = 6 s-1. For 0.4 less than or equal to VT/VD less than or equal to 0.85 and 3 s-1. less than or equal to fR less than or equal to 12 s-1, increased VT/VD was twice as effective as increased fR at decreasing arterial PCO2, consistent with oscillatory dispersion in a branching network being an important gas transport mechanism in birds on HFV. Ventilation of proximal exchange units with fresh gas due to laminar flow is not the necessary mechanism supporting gas exchange in HFV, since exchange could be maintained with VT/VD less than 0.5. Interclavicular and posterior thoracic air sac ventilation measured by helium washout did not change as much as expired minute ventilation during HFV. PCO2 was equal in both air sacs during HFV. These results could be explained by alterations in aerodynamic valving and flow patterns with HFV. Ventilation-perfusion distributions measured by the multiple inert gas elimination technique show increased inhomogeneity with HFV. Elimination of soluble gases was also enhanced in HFV as reported for mammals.(ABSTRACT TRUNCATED AT 250 WORDS)     

Physiological dead space during high-frequency ventilation in dogs

Tidal volumes used in high-frequency ventilation (HFV) may be smaller than anatomic dead space, but since gas exchange does take place, physiological dead space (VD) must be smaller than tidal volume (VT). We quantified changes in VD in three dogs at constant alveolar ventilation using the Bohr equation as VT was varied from 3 to 15 ml/kg and frequency (f) from 0.2 to 8 Hz, ranges that include normal as well as HFV. We found that VD was relatively constant at tidal volumes associated with normal ventilation (7-15 ml/kg) but fell sharply as VT was reduced further to tidal volumes associated with HFV (less than 7 ml/kg). The frequency required to maintain constant alveolar ventilation increased slowly as tidal volume was decreased from 15 to 7 ml/kg but rose sharply with attendant rapid increases in minute ventilation as tidal volumes were decreased to less than 7 ml/kg. At tidal volumes less than 7 ml/kg, the data deviated substantially from the conventional alveolar ventilation equation [f(VT - VD) = constant] but fit well a model derived previously for HFV. This model predicts that gas exchange with volumes smaller than dead space should vary approximately as the product of f and VT2.     

Effect of altitude relocations upon AaDo2 at rest and during exercise.

The supine pulmonary venous admixture (shunt) has been measured at Cerro de Pasco, 4,350 m altitude in eight subjects native to high altitude (HAN) under resting condition. Alveolar-arterial O2 tension difference (AaDO2) was also determined at rest and during exercise. The same subjects were studied again after 10 days' sojourn at sea level in Lima at 150 m altitude. They were compared with four subjects from sea level (SLN) who were studied first at Lima and after 2 and 10 days at Cerro de Pasco. At altitude, AaDO2 was smaller in HAN than SLN both at rest and during exercise. Shunt was the same in both groups. It is concluded that HAN show more even ventilation/perfusion relationship (VA/Q) at altitude, probably due to their high pulmonary artery pressure. On the contrary, SLN show less even VA/Q on altitude exposure, since their shunt decreased 37%. At sea level, HAN increased their AaDO2 due partially to an increase of 110% in their shunt, and in part due to less even VA/Q as shown by augmented VD/VT ratios. Each group tended to have a more effective gas exchange in its own environment.     

Effect of increased inspired CO2 on respiratory dead space in ponies

The objective of the present study was to determine the effect of elevated inspired CO2 on respiratory dead space (VD) of 12 normal, 8 carotid body-denervated (CBD), 7 hilar nerve-denervated (HND), and 6 CBD+HND ponies. The Fowler technique was used to determine VD on a breath-by-breath basis while the ponies breathed room air and inspired CO2 at 3 and 6%. During room air breathing, tidal volume (VT) and VD were greater in HND ponies than in normal and CBD ponies (P less than 0.05), and VT was less and VD/VT was greater after CBD than before CBD. For all groups. VD, VT, and breathing frequency (f) increased and VD/VT decreased significantly (P less than 0.01) with increasing inspired CO2. During CO2 breathing, VT and VD were higher (P less than 0.05) in the HND ponies than in all other groups, the decrease (P less than 0.05) in VD/VT was greatest in the CBD+HND group, and f was lower in the HND and HND+CBD than in the normal and CBD ponies. In addition, when inspired CO2 was increased from 0 to 6%, the decrease in VD/VT was greater and the increase in arterial PCO2 was less (P less than 0.05) after CBD than before CBD. For 70% of the ponies in all groups, VD increased linearly with increases in VT; for most of the remainder, VD tended to plateau at higher values of VT.     

Respiratory adaptations to dead space loading during maximal incremental exercise

We examined the effects of dead space (VD) loading on breathing pattern during maximal incremental exercise in eight normal subjects. Addition of external VD was associated with a significant increase in tidal volume (VT) and decrease in respiratory frequency (f) at moderate and high levels of ventilation (VI); at a VI of 120 l/min, VT and f with added VD were 3.31 +/- 0.33 liters and 36.7 +/- 6.7 breaths/min, respectively, compared with 2.90 +/- 0.29 liters and 41.8 +/- 7.3 breaths/min without added VD. Because breathing pattern does not change with CO2 inhalation during heavy exercise (Gallagher et al. J. Appl. Physiol. 63: 238-244, 1987), the breathing pattern response to added VD is probably a consequence of alteration in the PCO2 time profile, possibly sensed by the carotid body and/or airway-pulmonary chemoreceptors. The increase in VT during heavy exercise with VD loading indicates that the tachypneic breathing pattern of heavy exercise is not due to mechanical limitation of maximum ventilatory capacity at high levels of VT.     

Obesity alters regional ventilation in lateral decubitus position

Alterations of regional ventilation were determined as a function of body position in five morbidly obese subjects using 81mKr to assess ventilation (V) and 127Xe at equilibrium to determine lung volume (V). With subjects in seated and supine positions, the left lung contributed an average of 43% of the total V/V. When the apical-basal gradient within each lung was examined in subjects in the seated position, V/V was greatest in the dependent (basal) regions in half of the subjects, whereas the others showed greater V/V near the upper lung regions. All obese subjects preferentially ventilated the nondependent lung in both the left and right lateral decubitus positions. In a control group of three nonobese subjects, V/V was found to be equally distributed between left and right lungs in both the seated and supine positions. In contrast with the results in the obese group, V/V was slightly greater in the dependent lung in both lateral decubitus positions. Although the combination of 127Xe images and He-dilution measurement of functional residual capacity in the lateral decubitus positions indicated a reduction in the volume of the dependent lung of the obese when compared with values in the seated position, other factors affecting the mechanical function of either the diaphragm or the intercostal muscles could also have produced these positional alterations of ventilation.     

Effects of body posture and tidal volume on inter- and intraregional ventilation distribution in healthy men.

The influences of body posture and tidal volume (VT) on inter- and intraregional ventilation inhomogeneity were assessed by normalized phase III slope (Sn(III)) analysis of multiple-breath washout recordings of SF(6) and He in 11 healthy men. Washouts with target VT of 750, 1,000, and 1,250 ml were performed standing and supine. A linear-fit method was used to establish the contributions of convection-dependent (interregional) (cdi) and diffusion-convection interaction-dependent (intraregional) inhomogeneity (dcdi). Overall inhomogeneity was defined as the sum of cdi and dcdi. The difference in first-breath Sn(III) for SF(6) vs. He, the (SF(6) - He)Sn(III), served as an index of intra-acinar inhomogeneity. Multiple-regression analysis revealed greater cdi supine vs. standing (P < 0.001) but no significant effects of posture on dcdi or overall inhomogeneity. Larger VT were associated with greater cdi (P < 0.001), particularly when supine, but reduced dcdi (P < 0.001), overall inhomogeneity (P < 0.001), and (SF(6) - He)Sn(III) (P = 0.031). In conclusion, during resting breathing overall and intraregional ventilation inhomogeneities remain unchanged when the supine posture is assumed and improve with larger VT, but supine posture and larger breaths result in greater interregional inhomogeneities.     

Effect of increased gas density on pulmonary gas exchange in man.

Pulmonary gas exchange was measured in seven resting supine subjects breathing air or a dense gas mixture containing 21% O2 in sulfur hexafluoride (SF6). The mean value of the alveolar-arterial oxygen difference (AaDO2) decreased from 12.4 on air to 7.0 on SF6 (P less than 0.01), and increased again to 13.4 when air breathing resumed (P less than 0.01). No differences occurred between gas mixtures for O2 consumption, respiratory quotient, minute ventilation, breathing frequency, heart rate, or blood pressure, and the improved oxygen transfer could not be attributed to changes in cardiac output or mixed venous oxygen content in the one subject in which they were measured. These results are best explained by an altered distribution of ventilation during dense gas breathing, so that the ventilation-perfusion ratio (VA/Q) variance was reduced. Of several considered mechanisms, we favor one in which SF6 promotes cardiogenic gas mixing between peripheral parallel units having different alveolar gas concentrations. This mechanism allows for observed increases in arterial carbon dioxide tension and dead space-to-tidal volume ratio during dense gas breathing, and suggests that intraregional VA/Q variance accounts for at least one-half of the resting AaDO2 in healthy supine young men.     

Effects of posture on the venodilatory response to nitroglycerin

To determine the effects of posture on the venodilatory response to nitroglycerin (TNG), the change in forearm venous volume after inflation of an upper arm cuff to 30 mmHg above cuff zero (VV[30]) was measured during control conditions and after TNG (0.8 mg spray) in 18 healthy young volunteers in the supine position and the sitting position. VV[30] was 3.24 +/- 0.98 ml/100 ml arm in the supine position and 2.46 +/- 1.32 ml/100 ml arm in the sitting position. TNG increased VV[30] by 0.56 +/- 0.19 ml/100 ml arm in supine subjects, but by only 0.38 +/- 0.17 ml/100 ml arm in sitting subjects (P = 0.013). When limb volume was measured in the forearm and calf without using a cuff to produce venous congestion, the increase in limb volume with TNG was significantly greater in the sitting than in the supine position. Because the fall in both systolic and diastolic pressure and the rise in heart rate were significantly greater after TNG was administered in the sitting position, it is suggested that a greater reflex venoconstriction occurred in this posture, which antagonized the TNG-induced increase in venous distensibility. In the seated position, the effect of gravity more than compensated for the impaired venodilatory response to TNG. These results suggest that TNG causes a greater reduction in venous return to the heart when administered in the sitting position than in the supine position.     

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.     

Cardiovascular effects of static carotid baroreceptor stimulation during water immersion in humans

We hypothesized that the more-pronounced hypotensive and bradycardic effects of an antiorthostatic posture change from seated to supine than water immersion are caused by hydrostatic carotid baroreceptor stimulation. Ten seated healthy males underwent five interventions of 15-min each of 1) posture change to supine, 2) seated water immersion to the Xiphoid process (WI), 3) seated neck suction (NS), 4) WI with simultaneous neck suction (-22 mmHg) adjusted to simulate the carotid hydrostatic pressure increase during supine (WI + NS), and 5) seated control. Left atrial diameter increased similarly during supine, WI + NS, and WI and was unchanged during control and NS. Mean arterial pressure (MAP) decreased the most during supine (7 +/- 1 mmHg, P < 0.05) and less during WI + NS (4 +/- 1 mmHg) and NS (3 +/- 1 mmHg). The decrease in heart rate (HR) by 13 +/- 1 beats/min (P < 0.05) and the increase in arterial pulse pressure (PP) by 17 +/- 4 mmHg (P < 0.05) during supine was more pronounced (P < 0.05) than during WI + NS (10 +/- 2 beats/min and 7 +/- 2 mmHg, respectively) and WI (8 +/- 2 beats/min and 6 +/- 1 mmHg, respectively, P < 0.05). Plasma vasopressin decreased only during supine and WI, and plasma norepinephrine, in addition, decreased during WI + NS (P < 0.05). In conclusion, WI + NS is not sufficient to decrease MAP and HR to a similar extent as a 15-min seated to supine posture change. We suggest that not only static carotid baroreceptor stimulation but also the increase in PP combined with low-pressure receptor stimulation is a possible mechanism for the more-pronounced decrease in MAP and HR during the posture change.     

Fluid conservation in athletes: responses to water intake, supine posture, and immersion

The roles of antidiuretic hormone (ADH) and aldosterone in the elicited diuretic responses of trained and untrained men to seated, supine, and head-out water immersed conditions were studied. Volunteers were comprised of groups of six untrained individuals, six trained swimmers, and six trained runners. Each subject underwent three protocols, six hours in a seated position, supine position, or immersion (35 degrees C water). The last two protocols were preceded and followed by 1 h of seated position. After 10 h of fasting, 0.5% body wt of water was drunk. One hour later the trained groups had higher urine osmolalities (P less than 0.05) and urinary excretion rates of ADH (P less than 0.05) and lower urine flow rates (P less than 0.05) than untrained subjects. Throughout the sitting protocol, urinary ADH was also higher in both trained groups (P less than 0.05). Both supine posture and immersion resulted in significant decreases in urinary ADH in the untrained subjects (P less than 0.05) but no changes wer noted in swimmers and only during the second hour of immersion in the runners (P less than 0.05). The natriuresis and kaliuresis were greater during immersion than in the supine position but plasma renin activity, measured only in trained groups, and plasma aldosterone, measured in the untrained group, were decreased similarly with both protocols. The increases in urinary sodium excretion and urine flow rate were lower in trained than untrained subjects during the supine and immersion protocols (P less than 0.05). The data are compatible with an increased osmotic but decreased volume sensitivity of ADH control in trained men.     

Effect of high-intensity exercise on the VE-VCO2 relationship

The intrinsic relationship between ventilation (VE) and carbon dioxide output (VCO2) is described by the modified alveolar ventilation equation VE = VCO2 k/PaCO2(1-VD/VT) where PaCO2 is the partial pressure of CO2 in the arterial blood and VD/VT is the dead space fraction of the tidal volume. Previous investigators have reported that high-intensity exercise uncouples VE from VCO2; however, they did not measure the PaCO2 and VD/VT components of the overall relationship. In an attempt to provide a more complete analysis of the effects of high-intensity exercise on the VE-VCO2 relationship, we undertook an investigation where five subjects volunteered to perform three steady-state tests (SS1, SS2, SS3) at 60 W. One week after SS1 each subject was required to perform repeated 1-min bouts of exercise corresponding to a work rate of approximately 140% of maximal oxygen uptake (VO2max). Two and 24 h later the subjects performed SS2 and SS3, respectively. This exercise intervention caused PaCO2 during SS2 and SS3 to be regulated (P less than 0.01) approximately 4 Torr below the control (SS1) value of 38.8 Torr. Additionally, significant alterations were noted for VCO2 with corresponding values of 1.15 (SS1), 1.10 (SS2), and 1.04 (SS3) l/min. No changes were noted in either VD/VT or VE. In summary, it seems reasonable to suggest that the disproportionate increase in VE with respect to VCO2 noted in earlier work does not reflect an uncoupling. Rather the slope of the VE-VCO2 relationship is increased in a predictable manner as described by the modified alveolar ventilation equation.     

Effects of posture and bronchoconstriction on low-frequency input and transfer impedances in humans.

We simultaneously evaluated the mechanical response of the total respiratory system, lung, and chest wall to changes in posture and to bronchoconstriction. We synthesized the optimal ventilation waveform (OVW) approach, which simultaneously provides ventilation and multifrequency forcing, with optoelectronic plethysmography (OEP) to measure chest wall flow globally and locally. We applied an OVW containing six frequencies from 0.156 to 4.6 Hz to the mouth of six healthy men in the seated and supine positions, before and after methacholine challenge. We measured mouth, esophageal, and transpulmonary pressures, airway flow by pneumotachometry, and total chest wall, pulmonary rib cage, and abdominal volumes by OEP. We computed total respiratory, lung, and chest wall input impedances and the total and regional transfer impedances (Ztr). These data were appropriately sensitive to changes in posture, showing added resistance in supine vs. seated position. The Ztr were also highly sensitive to lung constriction, more so than input impedance, as the former is minimally distorted by shunting of flow into alveolar gas compression and airway walls. Local impedances show that, during bronchoconstriction and at typical breathing frequencies, the contribution of the abdomen becomes amplified relative to the rib cage. A similar redistribution occurs when passing from seated to supine. These data suggest that the OEP-OVW approach for measuring Ztr could noninvasively track important lung and respiratory conditions, even in subjects who cannot cooperate. Applications might range from routine evaluation of airway hyperreactivity in asthmatic subjects to critical conditions in the supine position during mechanical ventilation.     

Lung mechanics in individuals with spinal cord injury: effects of injury level and posture.

Individuals with spinal cord injury (SCI) exhibit reduced lung volumes and flow rates as a result of respiratory muscle weakness. These features have not, however, been investigated in relation to the combined effects of injury level and posture. Changes in forced vital capacity (FVC), forced expiratory volume in 1 s (FEV(1)), FEV(1)/FVC, forced expiratory flow at 50% vital capacity (FEF(50)), inspiratory capacity (IC), and expiratory reserve volume (ERV) were assessed by injury level in the seated and supine positions in 74 individuals with SCI. The main findings were 1) FVC, FEV(1), and IC increased with descending SCI level down to T(10), below which they tended to level off; 2) supine values of FVC and FEV(1) tended to be larger in the supine compared with the seated posture down to injury level T(1), caudad to which they were less than when seated; 3) IC increased proportionately more down to injury level L(1), below which it declined slightly and plateaued; 4) ERV was measurable even at high cervical injuries, was generally smaller in the supine position, reached peak values in both positions at T(10) injury level, and then rapidly declined at lower levels; 5) when subjects were separated according to current, former, and never smokers, only formerly smoking paraplegic individuals demonstrated spirometric values significantly less than paraplegic individuals who never smoked. Changes in spirometric measurements in SCI are dependent on injury level and posture. These findings support the concept that the increase in vital capacity in supine position is related to the effect of gravity on abdominal contents and increase in IC.     

Left ventricular hemodynamics during exercise recovery

The directional response of human left ventricular stroke volume during exercise recovery is unclear. Stroke volume has been reported to increase and decrease over exercise values during early recovery. The confounding variable may be posture. With the use of pulsed Doppler ultrasound, we tested the hypothesis that there is a significant difference between seated and supine stroke index (SI) during passive recovery from seated ergometer exercise. Thirteen subjects aged 26 +/- 2 yr performed two seated cycle ergometer exercise tests to 70% of predicted maximum heart rate (HR). Recovery was supine on one test and seated on the other. Cardiac index (CI), HR, and SI were calculated during rest, exercise, and 10 min of recovery. At rest, SI and CI were significantly (P less than 0.01) less and HR significantly (P less than 0.01) greater when the subjects were seated than when they were supine. At the last exercise work load, no significant differences were found in any measured variable between tests. During recovery, supine SI was maximal 180 s postexercise (99 +/- 14 ml/m2) and exceeded (P less than 0.01) resting supine (81 +/- 14 ml/m2) and peak exercise (77 +/- 14 ml/m2) SI by 22 and 29%, respectively. Seated SI was constant at peak exercise levels for 2 min. Seated and supine recovery CI never exceeded exercise values. Systolic and diastolic blood pressure recovery curves were similar in the two postures. We conclude that posture significantly affects SI during recovery from submaximal seated exercise. These results have implications for choice of recovery posture after stress testing in cardiac patients where it is desirable to minimize ventricular loading.     

Adrenergic mechanisms do not contribute to age-related decreases in calf venous compliance

Limb venous compliance decreases with advancing age, even in healthy humans. To test the hypothesis that adrenergic mechanisms contribute to age-associated reductions in limb venous compliance, we measured calf venous compliance before and during acute systemic α- and β-adrenergic blockade in eight young (27 ± 1 yr old, mean ± SE) and eight older healthy men (67 ± 2 yr old). Calf venous compliance was determined in supine subjects by inflating a thigh-collecting cuff to 60 mmHg for 8 min and then decreasing it (1 mmHg/s) to 0 mmHg while calf volume was indexed with a strain gauge. The slope (·10?3) of the pressure-compliance relation (compliance= β? + 2·β?·cuff pressure), which is the first derivative of the quadratic pressure-volume relation [(Δlimb volume) = β?+ β?·(cuff pressure) + β?·(cuff pressure)2] during reductions in cuff pressure, was used to quantify calf venous compliance. Calf venous compliance was ～30% lower (P < 0.01) in older compared with young men before adrenergic blockade. In response to adrenergic blockade calf venous compliance did not increase in young (-2.62 ± 0.14 and -2.29 ± 0.18 ml·dl?1·mmHg?1, before and during blockade, respectively) or older men (-1.78 ± 0.27 and -1.68 ± 0.21 ml·dl?1 ·mmHg?1). Moreover, during adrenergic blockade differences in calf venous compliance between young and older men observed before adrenergic blockade persisted. Collectively, these data strongly suggest that adrenergic mechanisms neither directly restrain calf venous compliance in young or older men nor do they contribute to age-associated reductions in calf venous compliance in healthy men.     

Local gas transport in eucapnic ventilation: effects of gravity and breathing frequency

The effects of body position and respiratory frequency (f) on regional gas transport during eucapnic conventional ventilation (CV) and high-frequency ventilation (HFV) were assessed from the washout of nitrogen 13 (13NN) using positron-emission tomography. In one protocol, six dogs were ventilated with CV or HFV at f = 6 Hz and tidal volume (VT) selected supine for eucapnia. A coronal cross section of the lung base was studied in the supine, prone, and right and left lateral decubitus positions. In a second protocol, six dogs were studied prone: apical and basal cross sections were studied in CV and in HFV with f = 3 and 9 Hz at eucapnic VT. Regional alveolar ventilation per unit of lung volume (spVr) was calculated for selected regions and analyzed for gravity-dependent cephalocaudal and right-to-left gradients. In both CV and HFV, nonuniformity in spVr was highest supine and lowest prone. In CV there were vertical gradients of spVr in all body positions: nondependent less ventilated than dependent regions, particularly in the supine position. In HFV there was a moderate vertical gradient in spVr in addition to a preferentially ventilated central region in all body positions. Overall lung spV was unaffected by body position in CV but in HFV was highest supine and lowest prone. Nonuniformity in eucapnic prone HFV was unaffected by f and always higher than in CV.(ABSTRACT TRUNCATED AT 250 WORDS)     

Relationship for gas transport during high-frequency ventilation in dogs

Alveolar ventilation during high-frequency ventilation (HFV) was estimated from the washout of the positron-emitting isotope (nitrogen-13-labeled N2) from the lungs of anesthetized paralyzed supine dogs by use of a positron camera. HFV was delivered at a mean lung volume (VL) equal to the resting functional residual capacity with a ventilator that generated tidal volumes (VT) between 30 and 120 ml, independent of the animal's lung impedance, at frequencies (f) from 2 to 25 Hz, with constant inspiratory and expiratory flows and an inspiration-to-expiration time ratio of unity. Specific ventilation (SPV), which is equivalent to ventilation per unit of compartment volume, was found to follow closely the relation: SPV = 1.9(VT/VL)2.1 X f. From this relation and from arterial PCO2 measurements we found an expression for the normocapnic settings of VT and f, given VL and body weight (W). We found that the VL was an important normalizing parameter in the sense that VT/VL yielded a better correlation (r = 0.91) with SPV/f than VT/W (r = 0.62) or VT alone (r = 0.8).