Ventilation-perfusion relationships after hemorrhage and resuscitation: an inert gas analysis

1983 ◽  
Vol 54 (4) ◽  
pp. 1131-1140 ◽  
Author(s):  
N. B. Robinson ◽  
E. Y. Chi ◽  
H. T. Robertson
Keyword(s):  
Blood Flow ◽  
Hemorrhagic Shock ◽  
Dead Space ◽  
Pulmonary Blood Flow ◽  
Autologous Blood ◽  
Regional Distribution ◽  
Gas Analysis ◽  
Inert Gas ◽  
Base Line ◽  
Dead Space Ventilation

Previous investigations suggest that ventilation-perfusion (VA/Q) relationships after hemorrhagic shock are primarily dependent on regional distribution of pulmonary blood flow and implicated early VA/Q heterogeneity secondary to disproportionate redistribution of pulmonary blood flow to dependent lung regions. Multiple inert gas elimination analysis, as described by Wagner et al. (J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 36: 588–599, 1974), was applied to a standard hemorrhagic shock preparation to test this hypothesis. Soon after hemorrhage, VA/Q distributions shifted homogeneously into high VA/Q compartments, preserving base-line VA/Q relationships around a new mean VA/Q ratio. Although the mean VA/Q and VA/Q distribution returned to base line after resuscitation with autologous blood, absolute dead space ventilation persisted. Gas exchange defects included increased Bohr dead space ventilation, which could be attributed to 1) a homogeneous shift of VA/Q distributions into high VA/Q compartments, and 2) new absolute dead space ventilation associated with observed intravascular leukostasis and vascular occlusion. In contrast to previous investigations, these data suggest that VA/Q heterogeneity does not occur after hemorrhage, but rather pulmonary blood flow decreases proportionately throughout all lung regions, preserving base-line VA/Q patterns around a new mean VA/Q ratio.

Effect of common dead space on VA/Q distribution in the dog

1990 ◽  
Vol 68 (6) ◽  
pp. 2488-2493 ◽  
Author(s):  
K. Tsukimoto ◽  
J. P. Arcos ◽  
W. Schaffartzik ◽  
P. D. Wagner ◽  
J. B. West
Keyword(s):  
Blood Flow ◽  
Tidal Volume ◽  
Dead Space ◽  
Volume Ratio ◽  
Inert Gas ◽  
Base Line ◽  
Heavy Exercise ◽  
The Common ◽  
Technique Comparison ◽  
Condition B

Several previous studies have shown worsening ventilation-perfusion (VA/Q) relationships in humans during heavy exercise at sea level. However, the mechanism of this deterioration remains unclear because of the correlation with ventilatory and circulatory variables. Our hypothesis was that the decrease in the series dead space-to-tidal volume ratio during exercise might be partly responsible because mixing in the common dead space can reduce apparent inequality. We tested this notion in 10 resting anesthetized normocapnic dogs passively hyperventilated by increase tidal volume and a) inspired CO2 or b) external dead space. We predicted less apparent VA/Q inequality in condition b because of mixing in the added dead space. After base-line measurements, conditions a and b were randomly assigned, and after a second set of base-line measurements they were repeated in the reverse order in each dog. VA/Q inequality was measured by the multiple inert gas elimination technique. Comparison of conditions a and b demonstrated that additional external dead space improved (P less than 0.001) the blood flow distributions as hypothesized [log standard deviation of perfusion = 0.49 +/- 0.02 (SE) in condition b and 0.61 +/- 0.03 in condition a with respect to 0.52 +/- 0.03 at base line]. This study suggests that the increased tidal volume during exercise could uncover VA/Q inequality not evident at rest because of the higher ratio of common dead space to tidal volume at rest.

On-line determination of pulmonary blood flow using respiratory inert gas analysis

1993 ◽  
Vol 40 (12) ◽  
pp. 1250-1259 ◽  
Author(s):  
K. Gan ◽  
I. Nishi ◽  
I. Chin ◽  
A.S. Slutsky
Keyword(s):  
Blood Flow ◽  
Pulmonary Blood Flow ◽  
Gas Analysis ◽  
Inert Gas ◽  
On Line

Pulmonary blood flow determined by continuous analysis of pulmonary N2O exchange

1975 ◽  
Vol 38 (5) ◽  
pp. 913-918 ◽  
Author(s):  
R. L. Stout ◽  
H. U. Wessel ◽  
M. H. Paul
Keyword(s):  
Mathematical Model ◽  
Blood Flow ◽  
Lung Tissue ◽  
Dead Space ◽  
Measurement Errors ◽  
Pulmonary Blood Flow ◽  
Gas Flow ◽  
Inert Gas ◽  
Response Measurement ◽  
Clinical Method

Measurement of mean pulmonary blood flow (Qp) as a function of pulmonary inert gas (N2O) uptake was studied with the aid of a mathematical model, fast response measurement of gas flow and gas concentrations at the mouth, and digital computer analysis of the data. The model treats the total pulmonary inert gas uptake as the sum of dead space, alveolar, lung tissue, and pulmonary blood flow uptakes. Analysis of any two breaths during breathing of a gas mixture (39 percent N2O, 21 percent O2, 40 percent N2 or He) in terms of the soluble (N2O) and the insoluble (N2 or He) inert gas yields two simultaneous equations with two unknowns which can be solved for Qp. No assumptions are required about the magnitude of the alveloar, dead space, or lung tissue volumes and constant FRC is not a requirement. The validity of the mathematical model and its sensitivity to known measurement errors was studied by computer simulation of respiratory gas exchange for N2O and N2. Comparison of Qp (N2O) with the direct Fick method (O2) in five anesthetized dogs showed agreement within plus or minus 20 percent. The proposed method has promise as a clinical method for determination of cardiac output on a breath-to-breath basis during regular breathing at rest or during exercise.

Effect of alveolar hypoxia on regional pulmonary perfusion

1984 ◽  
Vol 56 (2) ◽  
pp. 338-342 ◽  
Author(s):  
P. H. Neumann ◽  
C. M. Kivlen ◽  
A. Johnson ◽  
F. L. Minnear ◽  
A. B. Malik
Keyword(s):  
Blood Flow ◽  
Pulmonary Blood Flow ◽  
Regional Distribution ◽  
Flow Distribution ◽  
Relative Increase ◽  
Pulmonary Perfusion ◽  
Base Line ◽  
Dependent Lung ◽  
Mean Pulmonary Arterial Pressure ◽  
Alveolar Hypoxia

We examined the effects of varying levels of alveolar hypoxia on regional distribution of pulmonary blood flow (QL) in control-ventilated sheep. Regional distribution of QL was measured using 15-micron-diam labeled microspheres during the base-line period and at two levels of hypoxemia (arterial O2 partial pressure 44 and 20 Torr). During the base-line period, regional distribution of QL in the prone position was uniform [14 +/- 4% (SE) of QL/g bloodless dry lung wt in the upper lung and 16 +/- 2% of QL/g in the dependent lung]. During hypoxemia, however, the regional distribution of QL increased in the upper lung (20 +/- 3% of QL/g) while it decreased in the dependent lung (10 +/- 2% of QL/g). The degree of flow distribution was proportional to the severity of hypoxemia. The flow distribution was not associated with significant increases in pulmonary blood flow (2.0 +/- 0.4----2.4 +/- 0.5----2.6 +/- 0.1 l/min) but was associated with increases in mean pulmonary arterial pressure (17.8 +/- 1.3----21.7 +/- 1.1----29.0 +/- 3.8 Torr). Therefore alveolar hypoxia results in a relative increase in regional pulmonary perfusion to the upper lung, which depends on the level of pulmonary hypertension. The increased upper lung perfusion may be due to recruitment in the upper lung or to vasodilation in this region.

Assessment of cardiorespiratory function using oscillating inert gas forcing signals

1994 ◽  
Vol 76 (5) ◽  
pp. 2130-2139 ◽  
Author(s):  
E. M. Williams ◽  
J. B. Aspel ◽  
S. M. Burrough ◽  
W. A. Ryder ◽  
M. C. Sainsbury ◽  
...  
Keyword(s):  
Blood Flow ◽  
Nitrous Oxide ◽  
Dead Space ◽  
Confidence Limit ◽  
Pulmonary Blood Flow ◽  
Mean Difference ◽  
Alveolar Volume ◽  
Single Breath ◽  
Cardiorespiratory Function ◽  
Airway Dead Space

A theoretical model (Hahn et al. J. Appl. Physiol. 75: 1863–1876, 1993) predicts that the amplitudes of the argon and nitrous oxide inspired, end-expired, and mixed expired sinusoids at forcing periods in the range of 2–3 min (frequency 0.3–0.5 min-1) can be used directly to measure airway dead space, lung alveolar volume, and pulmonary blood flow. We tested the ability of this procedure to measure these parameters continuously by feeding monosinusoidal argon and nitrous oxide forcing signals (6 +/- 4% vol/vol) into the inspired airstream of nine anesthetized ventilated dogs. Close agreement was found between single-breath and sinusoid airway dead space measurements (mean difference 15 +/- 6%, 95% confidence limit), N2 washout and sinusoid alveolar volume (mean difference 4 +/- 6%, 95% confidence limit), and thermal dilution and sinusoid pulmonary blood flow (mean difference 12 +/- 11%, 95% confidence limit). The application of 1 kPa positive end-expiratory pressure increased airway dead space by 12% and alveolar volume from 0.8 to 1.1 liters but did not alter pulmonary blood flow, as measured by both the sinusoid and comparator techniques. Our findings show that the noninvasive sinusoid technique can be used to measure cardiorespiratory lung function and allows changes in function to be resolved in 2 min.

Effects of Vaporized Perfluorocarbon on Pulmonary Blood Flow and Ventilation/Perfusion Distribution in a Model of Acute Respiratory Distress Syndrome

2001 ◽  
Vol 95 (6) ◽  
pp. 1414-1421 ◽  
Author(s):  
Matthias Hübler ◽  
Jennifer E. Souders ◽  
Erin D. Shade ◽  
Nayak L. Polissar ◽  
Carmel Schimmel ◽  
...  
Keyword(s):  
Blood Flow ◽  
Oleic Acid ◽  
Gas Exchange ◽  
Lung Injury ◽  
Repeated Measures ◽  
Pulmonary Blood Flow ◽  
Analysis Of Covariance ◽  
Inert Gas ◽  
Low Flow ◽  
Repeated Measures Analysis

Background Perfluorocarbon (PFC) liquids are known to improve gas exchange and pulmonary function in various models of acute respiratory failure. Vaporization has been recently reported as a new method of delivering PFC to the lung. Our aim was to study the effect of PFC vapor on the ventilation/perfusion (VA/Q) matching and relative pulmonary blood flow (Qrel) distribution. Methods In nine sheep, lung injury was induced using oleic acid. Four sheep were treated with vaporized perfluorohexane (PFX) for 30 min, whereas the remaining sheep served as control animals. Vaporization was achieved using a modified isoflurane vaporizer. The animals were studied for 90 min after vaporization. VA/Q distributions were estimated using the multiple inert gas elimination technique. Change in Qrel distribution was assessed using fluorescent-labeled microspheres. Results Treatment with PFX vapor improved oxygenation significantly and led to significantly lower shunt values (P < 0.05, repeated-measures analysis of covariance). Analysis of the multiple inert gas elimination technique data showed that animals treated with PFX vapor demonstrated a higher VA/Q heterogeneity than the control animals (P < 0.05, repeated-measures analysis of covariance). Microsphere data showed a redistribution of Qrel attributable to oleic acid injury. Qrel shifted from areas that were initially high-flow to areas that were initially low-flow, with no difference in redistribution between the groups. After established injury, Qrel was redistributed to the nondependent lung areas in control animals, whereas Qrel distribution did not change in treatment animals. Conclusion In oleic acid lung injury, treatment with PFX vapor improves gas exchange by increasing VA/Q heterogeneity in the whole lung without a significant change in gravitational gradient.

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