Distribution of ventilation-perfusion ratios in dogs with normal and abnormal lungs

1975 ◽  
Vol 38 (6) ◽  
pp. 1099-1109 ◽  
Author(s):  
P. D. Wagner ◽  
R. B. Laravuso ◽  
E. Goldzimmer ◽  
P. F. Naumann ◽  
J. B. West

We have recently described a new method for measuring distributions of ventilation-perfusion ratios (VA/Q) based on inert gas elimination. Here we report the initial application of the method in normal dogs and in dogs with pulmonary embolism, pulmonary edema, and pneumonia. Characteristic distributions appropriate to the known effects of each lesion were observed. Comparison with traditional indices of gas exchange revealed that the arterial PO2 calculated from the distributions agreed well with measured values, as did the shunts indicated by the method and by the arterial PO2 while breathing 100 per cent 02. Also the Bohr dead space closely matched the dispersion of ventilation in realtion to VA/Q. Assumptions made in the method were critically evaluated and appear justified. These include the existence of a steady state of gas exchange, an alveolar-end-capillary diffusion equilibration, and the fact that all of the observered VA/Q inequality occurs between gas exchange units in parallel. However, theoretical analysis suggests that the method can detect failure of diffusion equilbration across the blood-gas barrier should it exist. These results suggest that the method is well-suited to clinical investigation of patients with pulmonary disease.

1986 ◽  
Vol 60 (2) ◽  
pp. 391-397 ◽  
Author(s):  
S. Lahiri ◽  
S. Matsumoto ◽  
A. Mokashi

We studied the responses of the ganglioglomerular nerve (GGN) efferents to brief periods of hypoxia and hypercapnia and to several levels of steady-state arterial PO2 and PCO2 and to intravascular injection of cyanide in thirteen anesthetized cats. The cats breathed spontaneously. A branch of the GGN which was cut close to the carotid body was divided into several filaments, and the activity of each filament was tested until clean and identifiable action potentials were obtained. The GGN efferent activity, breath-by-breath inspiratory volume, tracheal PO2 and PCO2 and arterial blood pressure were recorded simultaneously. We found that the GGN contained spontaneously active fibers which showed a range of responses to the respiratory stimuli. Fifty-eight percent of the filaments with dominant cardiovascular rhythm showed the least response to blood gas stimuli. Forty-two percent showed clear responses to hypoxia and hypercapnia. These responses developed slowly with the onset of the stimulus but decreased promptly with the withdrawal of the stimulus. These GGN efferents were also promptly stimulated by sodium cyanide. The steady-state response curve to hypoxia was hyperbolic and to hypercapnia it was linear. Some of these fibers showed stronger respiratory rhythms than others. The responses of these GGN efferents were associated with the respiratory responses to hypoxia and hypercapnia. For the same respiratory drive, however, the steady-state hypoxic stimulus elicited a greater GGN response than did hypercapnia.


2009 ◽  
Vol 297 (6) ◽  
pp. R1625-R1634 ◽  
Author(s):  
John B. West

Two opposing selective pressures have shaped the evolution of the structure of the blood-gas barrier in air breathing vertebrates. The first pressure, which has been recognized for 100 years, is to facilitate diffusive gas exchange. This requires the barrier to be extremely thin and have a large area. The second pressure, which has only recently been appreciated, is to maintain the mechanical integrity of the barrier in the face of its extreme thinness. The most important tensile stress comes from the pressure within the pulmonary capillaries, which results in a hoop stress. The strength of the barrier can be attributed to the type IV collagen in the extracellular matrix. In addition, the stress is minimized in mammals and birds by complete separation of the pulmonary and systemic circulations. Remarkably, the avian barrier is about 2.5 times thinner than that in mammals and also is much more uniform in thickness. These advantages for gas exchange come about because the avian pulmonary capillaries are unique among air breathers in being mechanically supported externally in addition to the strength that comes from the structure of their walls. This external support comes from epithelial plates that are part of the air capillaries, and the support is available because the terminal air spaces in the avian lung are extremely small due to the flow-through nature of ventilation in contrast to the reciprocating pattern in mammals.


1995 ◽  
Vol 79 (3) ◽  
pp. 918-928 ◽  
Author(s):  
J. E. Souders ◽  
S. C. George ◽  
N. L. Polissar ◽  
E. R. Swenson ◽  
M. P. Hlastala

Exchange of inert gases across the conducting airways has been demonstrated by using an isolated dog tracheal preparation and has been characterized by using a mathematical model (E. R. Swenson, H. T. Robertson, N. L. Polissar, M. E. Middaugh, and M. P. Hlastala, J. Appl. Physiol. 72: 1581–1588, 1992). Theory predicts that gas exchange is both diffusion and perfusion dependent, with gases with a higher blood-gas partition coefficient exchanging more efficiently. The present study evaluated the perfusion dependence of airway gas exchange in an in situ canine tracheal preparation. Eight dogs were studied under general anesthesia with the same isolated tracheal preparation. Tracheal perfusion (Q) was altered from control blood flow (Qo) by epinephrine or papaverine instilled into the trachea and was measured with fluorescent microspheres. Six inert gases of differing blood-gas partition coefficients were used to measure inert gas elimination. Gas exchange was quantified as excretion (E), equal to exhaled partial pressure divided by arterial partial pressure. Data were plotted as ln [E/(l-E)] vs. In (Q/Qo), and the slopes were determined by least squares. Excretion was a positive function of Q, and the magnitude of the response of each gas to changes in Q was similar and highly significant (P < or = 0.0002). These results confirm a substantial perfusion dependence of airway gas exchange.


1985 ◽  
Vol 58 (2) ◽  
pp. 506-513
Author(s):  
H. I. Modell ◽  
P. Beeman ◽  
J. Mendenhall

Available data relating duration of +GZ stress to blood gas exchange status is limited. Furthermore, studies focusing on pulmonary gas exchange during +GZ stress when abdominal restriction is imposed have yielded conflicting results. To examine the time course of blood gas changes occurring during exposure to +GZ stress in dogs and the influence of G-suit abdominal bladder inflation on this time course, seven spontaneously breathing pentobarbital-anesthetized adult mongrel dogs were exposed to 60 s of up to +5 GZ stress with and without G-suit abdominal bladder inflation. Arterial and mixed venous blood were sampled for blood gas analysis during the first and last 20 s of the exposure and at 3 min postexposure. Little change in blood gas status was seen at +3 GZ regardless of G-suit status. However, with G-suit inflation, arterial PO2 fell by a mean of 14.7 Torr during the first 20 s at +4 Gz (P less than 0.01, t test) and 20.6 Torr at +5 GZ (P less than 0.01). It continued to fall an additional 10 Torr during the next 40 s at both +4 and +5 GZ. Arterial PO2 was still 5–10 Torr below control values (P less than 0.05) 3 min postexposure. A second series of experiments paralleling the first focused on blood gas status during repeated exposure to acceleration. Blood gas status was assessed in five dogs during the late 20 s of two 60-s exposures separated by 3 min at 0 GZ. No significant differences between the initial and repeated exposures were detected. The data indicate that G-suit abdominal bladder inflation promotes increased venous admixture.


PEDIATRICS ◽  
1976 ◽  
Vol 57 (5) ◽  
pp. 681-690
Author(s):  
R. Huch ◽  
A. Huch ◽  
M. Albani ◽  
M. Gabriel ◽  
F. J. Schulte ◽  
...  

Results are reported concerning the clinical application of the transcutaneous Po2 method (tc Po2 method) according to Huch et al. for monitoring arterial Po2. Thirty long-term continuous tc Po2 recordings were made in 22 ventilated children and infants with cardiorespiratory problems in four different pediatric intensive care units (Zürich, Göttingen, Kassel, and Mainz). These recordings were compared with 132 arterial Po2 determinations made during the same period of time. There was a linear relationship and a close correspondence between arterial Po2 and tc Po2 (r = .94). The continuous recordings have shown that the variability of Po2 is much greater than assumed so far by single blood gas analysis. This fact restricts greatly the value of single samples. Continuous tc Po2 monitoring has proved to be a great help in optimal respirator setting.


1979 ◽  
Vol 46 (2) ◽  
pp. 240-248 ◽  
Author(s):  
I. H. Young ◽  
P. D. Wagner

The potential effect of intrapulmonary variations in hematocrit on gas exchange has been studied in theoretical models of the lung containing maldistribution of both hematocrit (Hct) and ventilation-perfusion (VA/Q) ratio. Hematocrit inequality enhanced gas exchange when units of low VA/Q were given a low Hct, arterial PO2 rising by as much as 14 Torr and PCO2 falling by up to 2 Torr depending on the particular distributions of Hct and VA/Q, whereas gas exchange was depressed when units of low VA/Q had a high Hct. After measuring inert gas solubilities in both dog and human blood of different Hct, the effect of Hct inequality on inert gas exchange was similarly assessed. Solubility was found to increase with HCT for less soluble gases. Because of this, conditions for enhancement of inert and O2 exchange by HCt inequality coincided, and it was found that in general the effects on O2 and inert gas transfer were quantitatively internally consistent. Even when Hct inequality was extreme, the resulting perturbation of inert gas concentrations was sufficiently small that the main features of the recovered VA/Q distributions were unaltered.


1979 ◽  
Vol 46 (3-4) ◽  
pp. 209-222 ◽  
Author(s):  
John W. Evans
Keyword(s):  

1988 ◽  
Vol 65 (4) ◽  
pp. 1686-1692 ◽  
Author(s):  
A. A. Balgos ◽  
D. C. Willford ◽  
J. B. West

Previous studies on normal subjects and patients with polycythemia have given conflicting results of the effect of polycythemia on pulmonary gas exchange. We studied acutely induced normovolemic polycythemia in the dog and measured arterial blood gases and ventilation-perfusion (VA/Q) relationships using the multiple inert gas elimination technique. The mean base-line hematocrit of 43 +/- 5% was increased to 57 +/- 4 and 68 +/- 8%, respectively, after two exchange transfusions of packed erythrocytes. Subsequent plasma exchange transfusions returned the mean hematocrit to 44 +/- 4%. Polycythemia caused no significant arterial hypoxemia; indeed there was a slight improvement in the alveolar-arterial PO2 difference. The multiple inert gas elimination measurements showed no increase in VA/Q inhomogeneity with no increase in log SD ventilation (V) or log SD blood flow (Q). There was a shift of mean V and mean Q to high VA/Q areas because of a decrease in cardiac output, presumably caused by increased blood viscosity. This study showed no deleterious effects on pulmonary gas exchange within the hematocrit range of 36-76%.


1987 ◽  
Vol 63 (4) ◽  
pp. 1567-1571 ◽  
Author(s):  
S. Javaheri ◽  
L. J. Teppema

We designed experiments to study changes in ventral medullary extracellular fluid (ECF) PCO2 and pH during hypoxemia. Measurements were made in chloralose-urethan-anesthetized spontaneously breathing cats (n = 12) with peripherial chemodenervation. Steady-state measurements were made during normoxemia [arterial PO2 (PaO2) = 106 Torr], hypoxemia (PaO2 = 46 Torr), and recovery (PaO2 = 105 Torr), with relatively constant arterial PCO2 (approximately 44 Torr). Mean values of ventilation were 945, 683, and 1,037 ml/min during normoxemia, hypoxemia, and recovery from hypoxemia, respectively. Ventilatory depression occurred in each cat during hypoxemia. Mean values of medullary ECF PCO2 were 57.7 +/- 7.2 (SD), 59.4 +/- 9.7, and 57.4 +/- 7.2 Torr during normoxemia, hypoxemia, and recovery to normoxemia, respectively; respective values for ECF [H+] were 60.9 +/- 8.0, 64.4 +/- 11.6, and 62.9 +/- 9.2 neq/l. Mean values of calculated ECF [HCO3-] were 22.8 +/- 3.0, 21.7 +/- 3.3, and 21.4 +/- 3.1 meq/l during normoxemia, hypoxemia, and recovery, respectively. Changes in medullary ECF PCO2 and [H+] were not statistically significant. Therefore hypoxemia caused ventilatory depression independent of changes in ECF acid-base variables. Furthermore, on return to normoxemia, ventilation rose considerably, still independent of changes in ECF PCO2, [H+], and [HCO3-].


1957 ◽  
Vol 191 (3) ◽  
pp. 423-427 ◽  
Author(s):  
William S. Yamamoto

Steady state measurements of metabolic gas exchange, ventilation and body temperature were made in anesthetized (urethane) Wistar rats breathing gas mixtures in compositions ranging from 20 to 30% oxygen, 0 to 10% carbon dioxide, and nitrogen. Metabolic rate was caused to vary by interrupted electrical stimulation of limb muscles. From 218 such determinations a regression was calculated, Vcoco2 = 0.00843 V (0.999Fe – Fi) – 0.091. It is concluded that the coco2 exchange of rats is similar to those reported in man and dog. Particular care was taken to assure a steady (constant) state at the time of measurement. Homeostatic defense against internally produced CO2 is good, whereas that against environmental CO2 changes is poor.


Sign in / Sign up

Export Citation Format

Share Document