Ventilation-perfusion relationships during induced normovolemic polycythemia in dogs

1988 ◽  
Vol 65 (4) ◽  
pp. 1686-1692 ◽  
Author(s):  
A. A. Balgos ◽  
D. C. Willford ◽  
J. B. West
Keyword(s):  
Gas Exchange ◽  
Blood Gases ◽  
Normal Subjects ◽  
Pulmonary Gas Exchange ◽  
Inert Gas ◽  
Base Line ◽  
Slight Improvement ◽  
Arterial Blood ◽  
The Mean ◽  
Arterial Po2

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%.

scholarly journals Noninvasive measurement of pulmonary gas exchange: comparison with data from arterial blood gases

2019 ◽  
Vol 316 (1) ◽  
pp. L114-L118 ◽  
Author(s):  
John B. West ◽  
Daniel L. Wang ◽  
G. Kim Prisk ◽  
Janelle M. Fine ◽  
Amy Bellinghausen ◽  
...  
Keyword(s):  
Gas Exchange ◽  
Blood Gases ◽  
Normal Subjects ◽  
Pulmonary Gas Exchange ◽  
Oxygen Deficit ◽  
Noninvasive Method ◽  
Arterial Blood Gases ◽  
Noninvasive Technique ◽  
Arterial Blood ◽  
End Tidal

A new noninvasive method was used to measure the impairment of pulmonary gas exchange in 34 patients with lung disease, and the results were compared with the traditional ideal alveolar-arterial Po2 difference (AaDO2) calculated from arterial blood gases. The end-tidal Po2 was measured from the expired gas during steady-state breathing, the arterial Po2 was derived from a pulse oximeter if the [Formula: see text] was 95% or less, which was the case for 23 patients. The difference between the end-tidal and the calculated Po2 was defined as the oxygen deficit. Oxygen deficit was 42.7 mmHg (SE 4.0) in this group of patients, much higher than the means previously found in 20 young normal subjects measured under hypoxic conditions (2.0 mmHg, SE 0.8) and 11 older normal subjects (7.5 mmHg, SE 1.6) and emphasizes the sensitivity of the new method for detecting the presence of abnormal gas exchange. The oxygen deficit was correlated with AaDO2 ( R2 0.72). The arterial Po2 that was calculated from the noninvasive technique was correlated with the results from the arterial blood gases ( R2 0.76) and with a mean bias of +2.7 mmHg. The Pco2 was correlated with the results from the arterial blood gases (R2 0.67) with a mean bias of −3.6 mmHg. We conclude that the oxygen deficit as obtained from the noninvasive method is a very sensitive indicator of impaired pulmonary gas exchange. It has the advantage that it can be obtained within a few minutes by having the patient simply breathe through a tube.

Pulmonary gas exchange during exercise in women: effects of exercise type and work increment

2000 ◽  
Vol 89 (2) ◽  
pp. 721-730 ◽  
Author(s):  
Susan R. Hopkins ◽  
Rebecca C. Barker ◽  
Tom D. Brutsaert ◽  
Timothy P. Gavin ◽  
Pauline Entin ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Gas Exchange ◽  
Blood Gases ◽  
Random Order ◽  
Pulmonary Gas Exchange ◽  
Male Athletes ◽  
Prediction Limit ◽  
Fast Running ◽  
Arterial Blood ◽  
Exercise Induced

Exercise-induced arterial hypoxemia (EIAH) has been reported in male athletes, particularly during fast-increment treadmill exercise protocols. Recent reports suggest a higher incidence in women. We hypothesized that 1-min incremental (fast) running (R) protocols would result in a lower arterial Po 2 (PaO2 ) than 5-min increment protocols (slow) or cycling exercise (C) and that women would experience greater EIAH than previously reported for men. Arterial blood gases, cardiac output, and metabolic data were obtained in 17 active women [mean maximal O2 uptake (V˙o 2 max) = 51 ml · kg−1 · min−1]. They were studied in random order (C or R), with a fastV˙o 2 max protocol. After recovery, the women performed 5 min of exercise at 30, 60, and 90% ofV˙o 2 max (slow). One week later, the other exercise mode (R or C) was similarly studied. There were no significant differences in V˙o 2 maxbetween R and C. Pulmonary gas exchange was similar at rest, 30%, and 60% of V˙o 2 max. At 90% ofV˙o 2 max, PaO2 was lower during R (mean ± SE = 94 ± 2 Torr) than during C (105 ± 2 Torr, P < 0.0001), as was ventilation (85.2 ± 3.8 vs. 98.2 ± 4.4 l/min btps, P < 0.0001) and cardiac output (19.1 ± 0.6 vs. 21.1 ± 1.0 l/min, P < 0.001). Arterial Pco 2 (32.0 ± 0.5 vs. 30.0 ± 0.6 Torr, P < 0.001) and alveolar-arterial O2 difference (A-aDo 2; 22 ± 2 vs. 16 ± 2 Torr, P < 0.0001) were greater during R. PaO2 and A-aDo 2 were similar between slow and fast. Nadir PaO2 was ≤80 Torr in four women (24%) but only during fast-R. In all subjects, PaO2 atV˙o 2 max was greater than the lower 95% prediction limit calculated from available data in men ( n = 72 C and 38 R) for both R and C. These data suggest intrinsic differences in gas exchange between R and C, due to differences in ventilation and also efficiency of gas exchange. The PaO2 responses to R and C exercise in our 17 subjects do not differ significantly from those previously observed in men.

Validation of measurements of ventilation-to-perfusion ratio inequality in the lung from expired gas

2003 ◽  
Vol 94 (3) ◽  
pp. 1186-1192 ◽  
Author(s):  
G. Kim Prisk ◽  
Harold J. B. Guy ◽  
John B. West ◽  
James W. Reed
Keyword(s):  
Gas Exchange ◽  
Respiratory Exchange Ratio ◽  
Blood Gases ◽  
Inert Gas ◽  
Phase Iii ◽  
Strongly Correlated ◽  
Arterial Blood Gases ◽  
Arterial Blood ◽  
Expired Gas ◽  
The Relationship

The analysis of the gas in a single expirate has long been used to estimate the degree of ventilation-perfusion (V˙a/Q˙) inequality in the lung. To further validate this estimate, we examined three measures ofV˙a/Q˙ inhomogeneity calculated from a single full exhalation in nine anesthetized mongrel dogs under control conditions and after exposure to aerosolized methacholine. These measurements were then compared with arterial blood gases and with measurements of V˙a/Q˙ inhomogeneity obtained using the multiple inert gas elimination technique. The slope of the instantaneous respiratory exchange ratio (R slope) vs. expired volume was poorly correlated with independent measures, probably because of the curvilinear nature of the relationship due to continuing gas exchange. When R was converted to the intrabreathV˙a/Q˙ (iV˙/Q˙), the best index was the slope of iV˙/Q˙ vs. volume over phase III (iV˙/Q˙slope). This was strongly correlated with independent measures, especially those relating to inhomogeneity of perfusion. The correlations for iV˙/Q˙ slope and R slope considerably improved when only the first half of phase III was considered. We conclude that a useful noninvasive measurement ofV˙a/Q˙ inhomogeneity can be derived from the intrabreath respiratory exchange ratio.

Oxygen-induced alteration of ventilation-perfusion relationships in rats

1979 ◽  
Vol 47 (5) ◽  
pp. 1112-1117 ◽  
Author(s):  
W. E. Truog ◽  
M. P. Hlastala ◽  
T. A. Standaert ◽  
H. P. McKenna ◽  
W. A. Hodson
Keyword(s):  
Gas Exchange ◽  
Pulmonary Gas Exchange ◽  
Inert Gas ◽  
Base Line ◽  
Small Animals ◽  
Difference Curve ◽  
Oxygen Breathing ◽  
Anesthetized Rats ◽  
Effect Of Oxygen ◽  
Breathing Room

The effect of oxygen breathing on shunt and ventilation-perfusion ratios (VA/Q) in anesthetized rats was studied using a modification of the multiple inert gas elimination technique. Base-line analyses showed hypoxemia in some animals breathing room air (arterial O2 tensions 48-70 Torr) associated with intrapulmonary shunts ranging from 0 to 22%, and variable low VA/Q lung regions as determined by calculation of the inert gas arterial-alveolar difference curve. Of nine rats that breathed 100% oxygen for 30 min, three showed increases in shunt (0% leads to 19%, 1.5% leads to 16%, 11% leads to 40%). These three animals had larger preexisting low VA/Q regions than the six that developed no shunt (0.48 +/- 0.15 vs. 0.17 +/- 0.03 (mean +/- SD); P less than 0.05). These data are compatible with the theory of absorption atelectasis. This study documents the usefulness of the inert gas elimination technique for studying pulmonary gas exchange problems in small animals.

Cardiorespiratory and cellular changes with interleukin 2 infusion in sheep

1989 ◽  
Vol 66 (1) ◽  
pp. 128-134 ◽  
Author(s):  
F. L. Glauser ◽  
D. E. Bechard ◽  
G. G. DeBlois ◽  
A. A. Fowler ◽  
R. E. Merchant ◽  
...  
Keyword(s):  
Interleukin 2 ◽  
Blood Gases ◽  
Base Line ◽  
Duration Of Treatment ◽  
Protein Ratio ◽  
Arterial Blood ◽  
Cellular Changes ◽  
Recombinant Interleukin 2 ◽  
Arterial Po2 ◽  
Lung Lymph

Recombinant interleukin 2 (rIL-2) administration, a new form of therapy for patients with far-advanced cancer, is associated with a "third space" syndrome, i.e., pulmonary edema, respiratory distress, and hypoxemia, which limits the dose and duration of treatment. To extend our knowledge regarding this toxicity, we established a sheep chronic lung lymph fistula model and measured hemodynamics, arterial blood gases, caudal mediastinal (lung) lymph flow (QL), and blood and lung lymph cellular changes before, during, and after (recovery) a 3-day continuous rIL-2 infusion (9 x 10(5) U/kg). Moderate systemic hypotension, mild pulmonary hypertension, and an increase in alveolar-arterial PO2 gradient was present on day 3 of rIL-2 infusion. QL increased from a base line of 1.9 +/- 0.2 to a maximum of 4.3 +/- 1.1 ml/15 min on day 3 of rIL-2 infusion. At no time was there a change in lymph-to-plasma protein ratio. The leukocyte count increased significantly to 16.1 +/- 4.5 x 10(3) cells/mm3 at recovery day 1. The percentage of blood lymphocytes decreased significantly by day 1 of rIL-2 infusion, returned to base-line levels on day 3, and significantly increased on day 2 of recovery. Lung lymph lymphocytes decreased significantly on days 1 and 2 of rIL-2 infusion. There was a shift in their size; i.e., their area increased from 32 +/- 7 to 57 +/- 19 micron 2 (P less than 0.05) by day 2 of rIL-2 infusion. By day 1 of recovery, lung lymph lymphocyte counts increased significantly.(ABSTRACT TRUNCATED AT 250 WORDS)

Pulmonary gas exchange during exercise in athletes. I. Ventilation-perfusion mismatch and diffusion limitation

1994 ◽  
Vol 77 (2) ◽  
pp. 912-917 ◽  
Author(s):  
S. R. Hopkins ◽  
D. C. McKenzie ◽  
R. B. Schoene ◽  
R. W. Glenny ◽  
H. T. Robertson
Keyword(s):  
Gas Exchange ◽  
Aerobic Capacity ◽  
Maximal Exercise ◽  
Cycle Ergometer ◽  
Pulmonary Gas Exchange ◽  
Inert Gases ◽  
Inert Gas ◽  
Diffusion Limitation ◽  
Maximal Aerobic Capacity ◽  
Arterial Blood

To investigate pulmonary gas exchange during exercise in athletes, 10 high aerobic capacity athletes (maximal aerobic capacity = 5.15 +/- 0.52 l/min) underwent testing on a cycle ergometer at rest, 150 W, 300 W, and maximal exercise (372 +/- 22 W) while trace amounts of six inert gases were infused intravenously. Arterial blood samples, mixed expired gas samples, and metabolic data were obtained. Indexes of ventilation-perfusion (VA/Q) mismatch were calculated by the multiple inert gas elimination technique. The alveolar-arterial difference for O2 (AaDO2) was predicted from the inert gas model on the basis of the calculated VA/Q mismatch. VA/Q heterogeneity increased significantly with exercise and was predicted to increase the AaDO2 by > 17 Torr during heavy and maximal exercise. The observed AaDO2 increased significantly more than that predicted by the inert gas technique during maximal exercise (10 +/- 10 Torr). These data suggest that this population develops diffusion limitation during maximal exercise, but VA/Q mismatch is the most important contributor (> 60%) to the wide AaDO2 observed.

scholarly journals Measuring the efficiency of pulmonary gas exchange using expired gas instead of arterial blood: comparing the “ideal” Po2 of Riley with end-tidal Po2

2020 ◽  
Vol 319 (2) ◽  
pp. L289-L293
Author(s):  
John B. West ◽  
Matthew A. Liu ◽  
Phoebe C. Stark ◽  
G. Kim Prisk
Keyword(s):  
Gas Exchange ◽  
Present Report ◽  
Oxygen Affinity ◽  
Normal Subjects ◽  
Pulmonary Gas Exchange ◽  
Oxygen Deficit ◽  
Arterial Blood ◽  
The Difference ◽  
End Tidal ◽  
The Ideal

When using a new noninvasive method for measuring the efficiency of pulmonary gas exchange, a key measurement is the oxygen deficit, defined as the difference between the end-tidal alveolar Po2 and the calculated arterial Po2. The end-tidal Po2 is measured using a rapid gas analyzer, and the arterial Po2 is derived from pulse oximetry after allowing for the effect of the Pco2 on the oxygen affinity of hemoglobin. In the present report we show that the values of end-tidal Po2 and Pco2 are highly reproducible, providing a solid foundation for the measurement of the oxygen deficit. We compare the oxygen deficit with the classical ideal alveolar-arterial Po2 difference (A-aDO2) as originally proposed by Riley, and now extensively used in clinical practice. This assumes Riley’s criteria for ideal alveolar gas, namely no ventilation-perfusion inequality, the same Pco2 as arterial blood, and the same respiratory exchange ratio as the whole lung. It transpires that, in normal subjects, the end-tidal Po2 is essentially the same as the ideal value. This conclusion is consistent with the very small oxygen deficit that we have reported in young normal subjects, the significantly higher values seen in older normal subjects, and the much larger values in patients with lung disease. We conclude that this noninvasive measurement of the efficiency of pulmonary exchange is identical in many respects to that based on the ideal alveolar Po2, but that it is easier to obtain.

Oxygen respiratory gas analysis by sine-wave measurement: a theoretical model

1996 ◽  
Vol 81 (2) ◽  
pp. 985-997 ◽  
Author(s):  
C. E. Hahn
Keyword(s):  
Gas Exchange ◽  
Dead Space ◽  
Venous Blood ◽  
Sine Wave ◽  
Inert Gas ◽  
Mixed Venous Blood ◽  
Arterial Blood ◽  
Partial Pressures ◽  
The Mean ◽  
Mixed Venous

A sinusoidal forcing function inert-gas-exchange model (C. E. W. Hahn, A. M. S. Black, S. A. Barton, and I. Scott. J. Appl. Physiol. 75: 1863–1876, 1993) is modified by replacing the inspired inert gas with oxygen, which then behaves mathematically in the gas phase as if it were an inert gas. A simple perturbation theory is developed that relates the ratios of the amplitudes of the inspired, end-expired, and mixed-expired oxygen sine-wave oscillations to the airways' dead space volume and lung alveolar volume. These relationships are independent of oxygen consumption, the gas-exchange ratio, and the mean fractional inspired (FIO2) and expired oxygen partial pressures. The model also predicts that blood flow shunt fraction (Qs/QT) is directly related to the oxygen sine-wave amplitude perturbations transmitted to end-expired air and arterial and mixed-venous blood through two simple equations. When the mean FIO2 is sufficiently high for arterial hemoglobin to be fully saturated, oxygen behaves mathematically in the blood like a low-solubility inert gas, and the amplitudes of the arterial and end-expired sine-wave perturbations are directly related to Qs/QT. This relationship is independent of the mean arterial and mixed-venous oxygen partial pressures and is also free from mixed-venous perturbation effects at high forcing frequencies. When arterial blood is not fully saturated, the theory predicts that QS/QT is directly related to the ratio of the amplitudes of the induced-saturation sinusoids in arterial and mixed-venous blood. The model therefore predicts that 1) on-line calculation of airway dead space and end-expired lung volume can be made by the addition of an oxygen sine-wave perturbation component to the mean FIO2; and (2) QS/QT can be measured from the resultant oxygen perturbation sine-wave amplitudes in the expired gas and in arterial and mixed-venous blood and is independent of the mean blood oxygen partial pressure and oxyhemoglobin saturation values. These calculations can be updated at the sine-wave forcing period, typically 2–4 min.

Mechanism of improvement in pulmonary gas exchange during growth in awake piglets

1988 ◽  
Vol 65 (3) ◽  
pp. 1055-1061 ◽  
Author(s):  
P. J. Escourrou ◽  
B. P. Teisseire ◽  
R. A. Herigault ◽  
M. O. Vallez ◽  
A. J. Dupeyrat ◽  
...  
Keyword(s):  
Gas Exchange ◽  
Dead Space ◽  
Pressure Difference ◽  
Age Groups ◽  
Pulmonary Gas Exchange ◽  
Inert Gas ◽  
Diffusion Limitation ◽  
Significant Difference ◽  
Arterial Po2 ◽  
And Diffusion

Previous studies have shown a lower arterial PO2 (PaO2) in infants and young animals than in adults. To investigate the mechanism of this impairment of gas exchange we studied 13 piglets from 12 to 65 days of age. Two days after instrumentation we measured the distribution of ventilation-perfusion ratios (VA/Q) by use of the multiple inert gas technique on awake animals. We showed that PaO2 is lower in young animals, increasing from 72 +/- 11.5 Torr before 2 wk to 102 Torr at 2 mo. This hypoxemia is due to an enlarged alveolar-arterial O2 pressure difference that significantly decreases with age. This impairment in gas exchange is not due to shunting (0.6 +/- 1.3%). Mean dead space (36 +/- 11%) was not related to age. Mean modes of perfusion and ventilation did not differ significantly between age groups. However, the dispersion of perfusion as expressed by its logSD decreased significantly with age, whereas dispersion of ventilation remained constant. Furthermore, in the young animals only, a significant difference was evidenced between measured alveolar-arterial PO2 gradient and the value predicted by the inert gas model. We therefore conclude that the impairment of gas exchange in piglets is due to two mechanisms: VA/Q mismatch and diffusion limitation for O2.

scholarly journals Passive body movement and gas exchange in the frilled lizard (Chlamydosaurus kingii) and goanna (Varanus gouldii).

1998 ◽  
Vol 201 (15) ◽  
pp. 2307-2311 ◽  
Author(s):  
P B Frappell ◽  
J P Mortola
Keyword(s):  
Gas Exchange ◽  
Partial Pressure ◽  
Body Mass ◽  
Time Course ◽  
Body Movement ◽  
Blood Gases ◽  
Pulmonary Gas Exchange ◽  
Body Movements ◽  
Arterial Blood Gas ◽  
Arterial Blood

The saccular lung in lizards is large and highly compliant compared with mammalian lungs, and these properties led us to question to what extent body movements could affect pulmonary gas exchange and the partial pressure of arterial blood gases. Specimens of two species of lizards, the frilled lizard (Chlamydosaurus kingii, approximately 600 g body mass) and the goanna (Varanus gouldii, approximately 1400 mass), were anaesthetised, maintained at approximately 36 degreesC and mechanically hyperventilated to lower the arterial partial pressure of carbon dioxide (PaCO2) to below apnoeic threshold. Respiratory system compliance (Crs) averaged 0. 112 ml kg-1 Pa-1 (goanna) and 0.173 ml kg-1 Pa-1 (frilled lizard), which is approximately 7-11 times the predicted value for a mammal of similar body mass. Mechanical ventilation was interrupted, and the changes in PaCO2 and PaO2 were monitored over the following 10 min as the animal was either left immobile or subjected to imposed lateral body movements. During the post-hyperventilation apnoea, PaCO2 increased whereas PaO2 did not always fall, sometimes even increasing, suggesting a reduction in the importance of pulmonary shunts. No significant differences were detected in the time course of changes in arterial blood gas levels or heart rate between runs with or without body movement. We conclude that in these species of lizards, despite the high Crs, lateral chest wall movements neither hinder nor favour pulmonary gas exchange.

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