Biomedical subjects

H K Chang

Publications and source records attributed to H K Chang.

At least 127 records · Page 7Linked to original sources

PubMed1984

Ventilation by high-frequency oscillation of thorax or at trachea in rats.

The efficiency of ventilation by high-frequency oscillation (HFO) applied to the thorax (external HFO) has been compared with that of HFO applied through a tracheal cannula (internal HFO) in a group of normal rats. Anesthetized, paralyzed, tracheotomized rats were placed in a whole-body plethysmograph. External HFO was achieved by varying the pressure surrounding the animal by means of a piston pump connected to the body plethysmograph; internal HFO was obtained in the same animals by connecting the pump to the tracheal cannula. Arterial CO2 and O2 partial pressures were measured in blood sampled from a carotid artery and were compared for external and internal HFO applied at 20 Hz with matched tidal volumes of 0.8, 1.4, 1.9, and 2.4 ml/kg. With increasing tidal volume, the mean arterial CO2 partial pressure decreased progressively from 68 to 30 Torr and was identical in the two modes of HFO; no difference was noted for the CO2 elimination or for the arterial O2 partial pressure. These results indicate that, in terms of gas exchange, external and internal HFO are equally efficient in normal rats.

Animals↗

PubMed1984

Mechanisms of gas transport during ventilation by high-frequency oscillation.

Ventilation by high-frequency oscillation (HFO) presents some difficulties in understanding exactly how gas is transported in the lung. However, at a qualitative level, five modes of transport may be identified: 1) direct alveolar ventilation in the lung units situated near the airway opening; 2) bulk convective mixing in the conducting airways as a result of recirculation of air among units of inhomogeneous time constants; 3) convective transport of gases as a result of the asymmetry between inspiratory and expiratory velocity profiles; 4) longitudinal dispersion caused by the interaction between axial velocities and radial transports due to turbulent eddies and/or secondary swirling motions; and 5) molecular diffusion near the alveolocapillary membrane. These modes of transport are not mutually exclusive and certainly interact. It is therefore difficult to make quantitative predictions about the overall rate of transport. Qualitatively, it may now be stated with confidence that convective transport in the tracheobronchial tree is very important during HFO as in normal breathing and that increasing tidal volume is more effective than increasing frequency in improving gas exchange during HFO. To optimize the gas transport efficiency of HFO, future research should focus on identifying the rate-limiting mode of transport for a given set of geometric and dynamic conditions.

Animals↗

PubMed1984

Alveolar ventilation during high-frequency oscillation: core dead space concept.

To assess the role of direct alveolar ventilation during high-frequency ventilation, we studied convective gas mixing during high-frequency oscillation with tidal volumes close to the dead space volume in a simple physical model. A main conduit representing a large airway was connected with a rigid sphere (V = 77, 517, and 1,719 cm3) by a small circular tube (d = 0.3 and 0.5 cm; L = 5, 10, and 20 cm). The efficiency of sinusoidal oscillations (f = 5, 20, and 40 Hz) applied at one end of the main conduit was assessed from the washout of a CO2 mixture from the sphere; to flush CO2 from the main fluid line, a constant flow of air was used. The decay in CO2 concentration measured in the sphere was exponential and therefore characterized by a measured time constant (tau m). Taking the small tube volume as the ventilatory dead space (VD), an effective tidal volume (VT*) was computed from tau m and compared with the tidal volume (VT) obtained separately from the pressure variation in the sphere. The discrepancy between these two tidal volumes has been found to be uniquely dependent on the ratio VT/VD within the range of VT/VD studied (0.5-2.2). For VT/VD less than 1.2, VT* was larger than VT, indicating that the conventional concept of alveolar ventilation does not apply. From the partition of the oscillatory flow in the small tube into two regions, the core and the unsteady boundary layer, we theoretically computed the proportions of the sinusoidal flow (or tidal volume) and the dead space for each region.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1984

Pulmonary arterial and venous pressures measured with small catheters in dogs.

To further subdivide the pressure drops across the arterial, middle, and venous segments obtained from the occlusion technique, we compared the pressures at the distal end of the arterial segment (Pa') and the proximal end of the venous segment (Pv') measured with this technique, with the pressures measured with 1.2-mm catheters in a small artery (Psa) and a small vein (Psv) of left lower lobes of dogs perfused in situ. The arterial (Pa) and venous (Pv) pressures were monitored and blood flow kept constant. Under control conditions the mean Pa, Psa, Pa', Pv', Psv, and Pv were 18.1, 13.0, 11.3, 9.2, 8.4, and 0.7 mmHg, respectively, suggesting that 29 and 44% of the total pulmonary vascular resistance (PVR) were in arteries and veins with diameters larger than at least 1.2 mm. Serotonin and histamine increased the pressure drops in arteries and veins, respectively, both larger and smaller than 1.2 mm. The small catheter pressures increased with flow rate. Microvascular pressures calculated from occlusion and small catheter measurements were higher than those calculated from the formula assuming 40% of PVR on the venous side. Our data suggest that a substantial proportion of resistance in the lung may lie in larger arteries and veins, the fraction of resistance in vessels under 1.2 mm increases with vasoconstrictors, the arterial and venous segments include muscular vessels under 1.2 mm, and calculation of microvascular pressures assuming 40% of the resistance in the veins may be misleading, especially when vasomotor tone is increased.

Animals↗

PubMed1984

Tracheal mucus clearance in high-frequency oscillation. II: Chest wall versus mouth oscillation.

We compared the tracheal mucus clearance rate (TMCR) in anesthetized dogs during spontaneous breathing (SB), ventilation by high-frequency oscillation at the airway opening (HFO/AO), and ventilation by high-frequency oscillation of the chest wall (HFO/CW). The HFO/AO was carried out by using a piston pump with a high impedance transverse flow at the proximal end of the endotracheal tube; HFO/CW was effected by creating rapid pressure oscillations in an air-filled cuff wrapped around the lower thorax of the animal, causing small tidal volumes at the mouth. The TMCR was measured by observing the rate of displacement of a charcoal marker in the lower trachea; a fiberoptic bronchoscope was used to deposit the marker before each experiment and to relocate it after a 5-min run. In 7 dogs, mean TMCR during control (SB) was 8.9 +/- 3.5 mm/min. At 13 Hz with an oscillatory tidal volume (VTO) of 1.5 ml/kg, mean TMCR was 240% of control with HFO/CW (p less than 0.001) and 76% of control with HFO/AO (NS). During HFO/AO at 20 Hz and a VTO of 3 ml/kg, mean TMCR was 97% of control. We conclude that high-frequency ventilation by rapid chest wall compression enhances tracheal mucus clearance when compared with spontaneous breathing, whereas high-frequency oscillation at the mouth does not.

Animals↗

PubMed1983

Mechanical ventilation with superimposed high frequency oscillation in the normal rat.

The gas exchange efficacy of high frequency oscillations superimposed on conventional mechanical ventilation (CMV-HFO) was assessed in 24 normal rats. These animals were anesthetized, paralyzed, tracheotomized and placed in a body box in order to measure the magnitude of the CMV tidal volume and that of the superimposed oscillations. The frequency of oscillations was 20 Hz and the mechanical ventilator delivered a tidal volume of 5 ml/kg at a rate of 50 min-1 which corresponded to a slight alveolar hypoventilation. Four groups of animals were studied with two magnitudes of oscillation (0.75 and 1.25 ml/kg) and with two different volumes of instrumental dead space. Blood gases were measured during CMV-HFO and during CMV alone from blood samples taken from a carotid artery. There were no significant differences in arterial PCO2 during these two modes of ventilation except a decrease in the group with large amplitude oscillations and a small dead space in which the oscillations alone could ensure quasi-normal gas exchange. By contrast in 20 out of 24 animals there was a decrease of alveolar - arterial oxygen difference with CMV-HFO even in the case of small oscillations and a large dead space. These results suggest that VA/Q homogeneity is improved by interregional and/or intraregional redistribution of ventilation due to the high frequency oscillations superimposed on conventional mechanical ventilation.

Animals↗

PubMed1983

Site of pulmonary hypoxic vasoconstriction studied with arterial and venous occlusion.

We applied the arterial and venous occlusion technique in an in situ, isolated left lower lobe preparation of a dog lung to compare the effects of hypoxia with the effects of airway pressure elevation, and the infusion of serotonin, norepinephrine, and histamine. The total arteriovenous pressure drop across the lobe was partitioned longitudinally into pressure drops across the relatively indistensible arteries (delta Pa) and veins (delta Pv) and across the middle distensible vessels (delta Pm). Hypoxia increased primarily delta Pm, as did elevation of airway pressure, whereas the vasoactive drugs increased either delta Pa or delta Pv. The increases in pulmonary arterial pressure (Pa) caused by hypoxia and by elevation of airway pressure were independent of blood flow rate, but increases in Pa induced by the vasoactive drugs were dependent on flow rate. We conclude that in the dog hypoxia acts primarily on small distensible vessels, whereas pulmonary vasoactive drugs constrict the relatively indistensible arteries and veins. It is possible that the increase in pulmonary vascular resistance during hypoxia did not involve smooth muscle contraction.

Animals↗

PubMed1983

Ventilation by high-frequency chest wall compression in dogs with normal lungs.

In 6 anesthetized and paralyzed supine dogs, ventilation by high-frequency chest wall compression (HFCWC) was accomplished by a piston pump rapidly oscillating the pressure in a modified double blood pressure cuff wrapped around the lower thorax. Testing applied frequencies at 3, 5, 8, and 11 Hz, applied peak cuff pressures ranged from 30 to 230 cmH2O. This produced swings of esophageal pressure as high as 18 cmH2O and peak oscillatory air flow ranging from 0.7 to 1.6 L/s. Oscillatory tidal volume declined with increasing frequency and ranged from a mean of 61 to 45 ml. After 30 min of applied HFCWC, arterial blood gas determinations revealed a mean PaCO2 of 29.3 mmHg at 5 Hz, 35 mmHg at 3 Hz, 36 mmHg at 8 Hz, and 51 mmHg at 11 Hz. Mean PaO2 improved from ventilator control values at 3 Hz, remained unchanged at 5 and 8 Hz, and declined at 11 Hz. In 2 dogs breathing spontaneously, HFCWC applied at 5 and 11 Hz resulted in a reduction in spontaneous minute ventilation, mainly by a reduction in spontaneous tidal volume, whereas arterial blood gas values changed slightly. One dog ceased to breath spontaneously within 5 min of application of HFCWC as the PaCO2 fell below control values. We conclude that in dogs with normal lungs, HFCWC may assist spontaneous ventilation. In paralyzed dogs, HFCWC may be of sufficient magnitude to cause hyperventilation.

Animals↗

PubMed1983

Enhanced tracheal mucus clearance with high frequency chest wall compression.

The clearance of mucus in the trachea during high frequency chest wall compression (HFCWC) was studied in nine anesthetized dogs. High frequency chest wall compression was applied by oscillating the pressure in a thoracic cuff such that it produced oscillatory tidal volumes of 25 to 100 cc at frequencies of 3 to 17 Hz. The tracheal mucus clearance rate (TMCR) was determined by direct observation of the rate of displacement of a charcoal particle spot by means of a fiberoptic bronchoscope. Baseline TMCR during spontaneous breathing averaged 8.2 +/- 5.6 mm/min in the 9 dogs. The TMCR during 2 min of HFCWC was increased at 5, 8, 11, 13, 15, and 17 Hz but not at 3 Hz. The enhancement of clearance was most pronounced in the range of 11 to 15 Hz, reaching a peak value of 340% of control at 13 Hz. These studies suggest that HFCWC might be of considerable potential benefit as a mode of chest physiotherapy.

Animals↗

PubMed1982

Effects of unequal pressure swings and different waveforms on distribution of ventilation: a non-linear model simulation.

In an attempt to understand the role of unequal pleural pressure swings and of different waveforms of pleural pressure variation in the distribution of ventilation during cyclic breathing, a mathematical model simulation was performed. The computer model which incorporates non-linear resistances and compliances as well as sinusoidal, square, and triangular waveforms of pleural pressure variations indicates that the distribution of ventilation is insensitive to the waveform of the pleural pressure. The distribution is also little changed by the depth of breathing (amplitude), but it is affected significantly by the pattern of different pressures over the regions of the model. For sinusoidal, triangular, and low amplitude square wave pleural pressures with equal amplitudes on both compartments, air was distributed preferentially to the lower compartment under the influence of the static pressure difference. With unequal amplitudes, more air flowed to the compartment experiencing the larger pressure swing. This was virtually independent of the waveform and of the amplitudes of the pleural pressure variation. Comparison of the present results with a constant flow model reveals that the overall distribution of tidal air during cyclic breathing is very different from the results obtained in constant rate inspiration experiments or in bolus distribution experiments. New experiments performed under cyclic breathing conditions are thus indicated.

Humans↗

PubMed1982

A model study of flow dynamics in human central airways. Part I: axial velocity profiles.

We measured detailed steady inspiratory and expiratory velocity profiles in a 3:1 scale model of the human central airways. The model was constructed out of acrylic plastic, mounted vertically, and connected to a specially designed steady-flow system. Laterally introduced hot-wire anemoneter probes were used to record axial velocities along 4 diameters at each of the 12 pre-drilled stations of measurement; the flow distribution among the five lobar bronchi was controlled by distally positioned linear resistors. Whether with a flat entrance profile or entering as a narrow jet, the inspiratory flow velocity profiles in the frontal plane showed a high degree of asymmetry in all branches, with peak velocities near the inner wall of the bifurcation. In the sagittal plane the velocity profiles were nearly symmetric, exhibiting a single peak near the center in the frontal plane and almost flat in the sagittal plane. Overall, the velocity profiles were more sensitive to airway geometry than to flow rate. The only site of flow separation was observed in the right upper lobar bronchus. The most evident modification of axial velocity profiles in a single branch was found in the left main bronchus during expiratory flow.

Humans↗

PubMed1982

A model study of flow dynamics in human central airways. Part II: secondary flow velocities.

Secondary velocity components perpendicular to the tube axis were measured in a 3 : 1 scale model of the human central airways. Slanted hot-wire probes were introduced axially in order to measure the secondary velocities at about 12 points for each of the 7 stations investigated. Secondary velocities in the inspiratory direction never exceeded a mean value of 18% of the mean axial velocity. Secondary velocities in the expiratory direction reached a mean value of 21.5% of the mean axial velocity. In the inspiratory direction, two unequal eddies were formed in the left main bronchus and in the right upper lobe. Moreover, maximum velocities were observed near the wall and the decay of secondary velocities in the left main bronchus was observed. The secondary flow patterns observed in the left upper and lower lobes after the secondary bifurcation were difficult to recognize, although they seemed to be more influenced by the second bifurcation. The complexity of the flow pattern was reinforced by viscous effects acting near the wall. In the expiratory direction, only two stations in the trachea were measured; four uneven eddies seemed to have existed, with the ventral eddies appearing to be predominant. Overall, the secondary velocity magnitudes as well as the patterns of eddies were very dependent on the geometry of the model used.

Humans↗

PubMed1982

Partitioning of pulmonary vascular resistance in dogs by arterial and venous occlusion.

We perfused in situ isolated left lower lung lobes at a steady flow rate in zone 3 condition. When the lobar arterial inflow was suddenly occluded, the arterial pressure (Pa) fell rapidly and then more slowly. When the lobar venous outflow was suddenly occluded, the venous pressure (Pv) rose rapidly and then continued to rise more slowly. The rapid changes in Pa and Pv with inflow and outflow occlusion, respectively, represent the pressure drops across the arterial (delta Pa) and venous (delta Pv) relatively indistensible vessels. The total arteriovenous pressure difference (delta Pt) minus delta Pa + delta Pv gives the pressure drop across the vessels in the middle (delta Pm) that are much more distensible. Serotonin and histamine infusion increased delta Pa and delta Pv, respectively, but left delta Pm unchanged. delta Pa and delta Pv, but not delta Pm, increased as flow rate was increased. The studies with varying flow rate and venous pressures suggested that the arteries and veins became resistant to distension when their transmural pressures exceeded 10--5 Torr, respectively. Under the conditions studied, the middle nonmuscular segment contributed a major fraction of the vascular compliance and less than 16% of the total resistance. The muscular arteries and veins contributed equally to the remaining resistance. We conclude that the arterial and venous occlusion method is a useful technique to describe the resistance and compliance of different segments of the pulmonary vasculature.

Animals↗

PubMed1982

Resistance of mucus-lined tubes to steady and oscillatory airflow.

We examined the effects of quantity and physical properties of mucus on resistance to steady and oscillatory flows in a circular tube. Gels with similar rheological properties to canine tracheal mucus were prepared from hog gastric mucin or locust bean gum cross-linked with Na2B4O7. A horizontal straight tube (D 1.85 cm) was lined with these mucus simulants to depths ranging from 0.3 to 1.0 mm. The pressure difference over a 50-cm portion of the tube and the volumetric flow rate were determined simultaneously. Low-amplitude oscillatory flow were generated with a modified Harvard pump. For steady flow, the resistance at low Reynolds number (Re) increased with increasing gel depth only to the extent expected for simple constriction of the tube cross-sectional area. The same was true for oscillatory (0.25--6 Hz) flow resistance at low flow amplitude (corresponding to Re less than 4,000). No effect of gel cross-link density at low Re was observed. At high steady-flow rates, and for high-amplitude oscillatory flow, resistance increased beyond that predicted for simple constriction. Plots of friction factor (f) vs. Re showed a critical point (Recrit) of the order of 1.5 x 10(4), at which f increased sharply. Recrit, which corresponded to the onset of wave formation in the lining layer, was insensitive to changes in gel depth. However, gel cross-link density did affect the onset of wave formation: in oscillatory flow Recrit was shifted to higher Re, and the rise in f in steady flow was blunted with high degrees of cross-linking. The existence of Recrit and its association with wave formation are consistent with predictions based on two-phase flow theory.

Airway Resistance↗

PubMed1982

Effect of lung inflation on pulmonary vascular resistance by arterial and venous occlusion.

To explain the changes in pulmonary vascular resistance (PVR) with positive- and negative-pressure inflation (PPI and NPI, respectively), we studied their effects in isolated canine left lower lobes perfused at constant flow rate. The venous pressure was kept constant relative to atmospheric pressure during lung inflation. The total arteriovenous pressure drop (delta Pt) was partitioned with the arterial and venous occlusion technique into pressure drops across arterial and venous segments (large indistensible extra-alveolar vessels) and a middle segment (small distensible extra-alveolar and alveolar vessels). PPI caused a curvilinear increase in delta Pt due to a large Starling resistance effect in the alveolar vessels associated with a small volume-dependent increase in the resistance of alveolar and extra-alveolar vessels. NPI caused an initial decrease in delta Pt due to reduction in the resistance of extra-alveolar vessels followed by an increase in delta Pt due to a volume-dependent increase in the resistance of all vessels. In conclusion, we provided for the first time evidence that lung inflation results in a volume-dependent increase in the resistance of both alveolar and extra-alveolar vessels. The data suggest that while the volume-related changes in PVR are identical with PPI and NPI, there are pressure-related changes that can be different between the two modes of inflation.

Animals↗

PubMed1981

Redistribution of pulmonary blood flow during experimental air embolism.

The effect of experimental pulmonary air embolism on pulmonary perfusion was studied in 14 closed-chest, anesthetized, paralyzed dogs. During constant-rate air infusion through a femoral vein, regional distribution of lung perfusion was measured with radioactive xenon boluses injected via a catheter positioned distally to the pulmonary valve. The results obtained from nine prone dogs indicate a large shift of blood perfusion toward the dependent areas of the lung during air embolism; the results obtained in five supine dogs were similar but statistically less significant. Concomitant with the perfusion shift, pulmonary arterial pressure increased, more acutely during the first 30 min. Switching from air to N2O-O2 ventilation accentuated the perfusion shift, which may be reverted towards control values by intravenous administration of 0.4 mg of isoproterenol. Other alterations observed included moderate increase of pulmonary resistance and decrease of cardiac output. It is concluded, based on these results and an adjunct model study, that the observed changes were predominantly due to aggregation of air bubbles in the upper part of the pulmonary vasculature.

Airway Resistance↗

PubMed1981

Fluid dynamic factors in tracheal pressure measurement.

Because tracheal pressure measurement generally involves the use of a cannula or an endotracheal tube, fluid dynamic factors may cause a considerable artifact. We present a theoretical explanation of the observed apparent paradox in which the resistance of a tracheal cannula or an endotracheal tube is isolation was found to exceed the resistance of the airways plus the cannula or the tube in situ. By estimating the viscous dissipation and the kinetic energy change in a conduit with sudden variation of cross-sectional area, a predictive model is derived. The predictions are verified by a series of in vitro experiments with both steady and oscillatory flows. The experiments showed that the pressure recorded from the sidearm of a tracheal cannula or endotracheal tube contains an error which, in general, increased with the mean Reynolds' number of the through flow and also depends on the diameter ratio between the trachea and the tube or cannula, the position of the pressure tap, and the frequency of ventilation. When feasible, direct measurement with a needle in the trachea is suggested as a way to avoid the possible artifacts arising from the use fo a side tap of the cannula. Theoretical considerations, as well as in vitro and animal experiments, indicate that adding a properly chosen expansion to the tracheal cannula makes it possible to alter inspiratory and expiratory pressures selectively. This device may prove useful in control of breathing studies.

Airway Resistance↗

PubMed1981

Time course of phrenic activity and respiratory pressures during airway occlusion in cats.

The morphology of integrated ("moving time average") phrenic electroneurograms (EPHR) and of tracheal (Ptr) and transdiaphragmatic (Pdi) pressure waves during occluded inspirations was studied in eight anesthetized cats breathing air and various hypercapnic and hypoxic mixtures. The shape of the rising part of EPR-, Ptr-, and Pdi-time profiles varied between animals (from convex to concave), but in each animal it remained virtually unchanged by hypoxia and hypercapnia. The shape of the Ptr and Pdi occlusion waves reflected the shape of EPHR. The relationship of EPHR to Pdi and Ptr did not change with chemical drive. It is concluded that central inspiratory activity (CIA) (as reflected by EPHR and its mechanical transforms Pdi and Ptr) increases in amplitude with stimulation of breathing but that the profile of CIA remains essentially unchanged. However, substantial differences in the time course development of phrenic activity, Pdi, and Ptr exist between cats. The fixed interrelationships among EPHR, Pdi, and Ptr indicate a proportional increase in activity among all inspiratory muscles with increased chemical drive.

Airway Obstruction↗