How does increased cardiac output increase shunt in pulmonary edema?

1982 ◽  
Vol 53 (5) ◽  
pp. 1273-1280 ◽  
Author(s):  
P. H. Breen ◽  
P. T. Schumacker ◽  
G. Hedenstierna ◽  
J. Ali ◽  
P. D. Wagner ◽  
...  

In pulmonary edema, the relationship between cardiac output (QT) and shunt (QS/QT) may be due to a diffusion barrier for O2 transfer (incomplete alveolar-capillary equilibration) or to redistribution of increased pulmonary blood flow toward edematous units. We compared transfer of O2 and multiple inert gases in the left (LLL) and right (RLL) lower lobes and in the whole lungs of eight dogs having oleic acid edema in LLL. When mean QT was increased from 3.0 to 5.5 l X min-1 during O2 ventilation, relative perfusion of LLL did not increase but QS/QT increased because LLL shunt increased from 56 to 78%. We conclude that increased pulmonary blood flow is not redistributed toward edematous regions, but we cannot exclude such redistribution within LLL and other slightly edematous lobes. In LLL, inert gas shunt and O2 shunt were not systematically different during O2 ventilation, and lobar venous PO2 measured during air ventilation was not different from that predicted by inert gas transfer. We conclude that diffusion limitation for O2 does not contribute to QS/QT or to the increase in QS/QT when QT increases. Conceivably, increased QT increased QS/QT by increasing edema or hematocrit in edematous regions.

2019 ◽  
Vol 9 (4) ◽  
pp. 204589401989453 ◽  
Author(s):  
Stefan Stadler ◽  
Nicoletta Mergenthaler ◽  
Tobias J. Lange

Background Cardiac output is a prognostic marker in patients with pulmonary hypertension. Pulmonary blood flow as a surrogate for cardiac output can be measured non-invasively by inert gas rebreathing. We hypothesized that pulmonary blood flow can predict outcome in patients with pulmonary hypertension. Methods From January 2009 to January 2012, we measured pulmonary blood flow by inert gas rebreathing in outpatients with pulmonary hypertension. Patients with pulmonary hypertension confirmed by right heart catheterization and a valid inert gas rebreathing maneuver were followed until January 2016. The investigated outcome was all-cause mortality. Results We included 259 patients (mean age 65 ± 13 years, 53% female) with pulmonary hypertension and classified into groups 1 (n = 103), 2 (n = 26), 3 (n = 80), and 4 (n = 50) according to the current pulmonary hypertension classification system. The median time between pulmonary hypertension diagnosis and inert gas rebreathing was 9 (IQR 0; 36) months. During a median follow-up time of 51 (IQR 20; 68) months, 109 patients (42%) died. Parameters significantly associated with survival (in order of decreasing statistical strength) were diffusion capacity of the lung for carbon monoxide (DLCO), 6-minute walk distance (6-MWD), age, NTpro-BNP, WHO functional class, group 3 pulmonary hypertension, and tricuspid annular plane systolic excursion (TAPSE), while baseline hemodynamics and pulmonary blood flow were not. In multivariable Cox regression analysis, DLCO, age, 6-MWD, and TAPSE remained significant and independent predictors of the outcome. DLCO as the strongest parameter also significantly predicted survival in aetiological subgroups except for group 4. Conclusions DLCO is a strong and independent predictor for survival in patients with pulmonary hypertension of different aetiologies, while pulmonary blood flow measured by inert gas rebreathing is not.


2001 ◽  
Vol 95 (6) ◽  
pp. 1414-1421 ◽  
Author(s):  
Matthias Hübler ◽  
Jennifer E. Souders ◽  
Erin D. Shade ◽  
Nayak L. Polissar ◽  
Carmel Schimmel ◽  
...  

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.


1972 ◽  
Vol 84 (3) ◽  
pp. 371-376 ◽  
Author(s):  
Elmer Treat ◽  
Harvey Ulano ◽  
Marc Pfeffer ◽  
Walter Massion ◽  
Linda L. Shanbour ◽  
...  

1986 ◽  
Vol 71 (s15) ◽  
pp. 36P-36P ◽  
Author(s):  
A.H. Kendrick ◽  
A. Rozkovec ◽  
M. Papouchado ◽  
J. West ◽  
J.E. Bees ◽  
...  

PEDIATRICS ◽  
1971 ◽  
Vol 47 (5) ◽  
pp. 870-879
Author(s):  
Zuhdi Lababidi ◽  
D. A. Ehmke ◽  
Robert E. Durnin ◽  
Paul E. Leaverton ◽  
Ronald M. Lauer

In 20 children without shunts or valvular insufficiency, duplicate dye dilution and impedance cardiac outputs (ICO) were carried out. The duplicate dye dilutions had a standard deviation 0.259 L/min/m2, while duplicate ICO had a standard deviation 0.192 L/min/m2 (F = 1.82, p < 0.05). Of 53 sequential estimates, cardiac outputs measured by both indicator dye dilution and ICO had a 5.5% mean difference. In 21 subjects with left to right shunts, the ICO related well with pulmonary blood flow (r = 0.92) rather than systemic flow (r = 0.21). In 13 subjects with aortic insufficiency, sequential Fick and ICO had a 50% mean difference; the impedance measurement was found to be higher in every case. These data indicate that the impedance cardiograph can provide a noninvasive measure of cardiac output when there are no shunts or valvular insufficiencies. In subjects with left to right shunts the impedance cardiograph provides a measure of the pulmonary blood flow. When aortic insufficiency exists the impedance cardiograph is distorted such that it is consistently higher than Fick cardiac output.


1980 ◽  
Vol 49 (5) ◽  
pp. 834-840 ◽  
Author(s):  
A. B. Malik ◽  
H. van der Zee ◽  
P. H. Neumann ◽  
N. B. Gertzberg

Regional pulmonary blood flow was determined in dogs during varying degrees of pulmonary edema induced by infusing 179.2-659.4 ml/kg normal saline over 2-3 h. Pulmonary hemodynamics and regional blood flows were measured during the base-line period and at 30 min postinfusion. The degree of pulmonary edema was determined by the final extravascular lung water-to-bloodless dry lung weight ratio (W/D). In dogs developing gross alveolar edema (W/D of 10.70 +/- 0.88 vs. 3.10 +/- 0.30 in controls), the blood flow was shifted to either upper or dependent lung regions. The shift to the upper regions was associated with an increased (P < 0.05) pulmonary arterial pressure (Ppa), whereas the shift to the dependent lung was not associated with a significant change in Ppa. Breathing 100% O2 did not prevent these shifts, suggesting that they were not due to localized hypoxic pulmonary vasoconstriction. The flow distribution patterns were also not related to regional differences in edema. In contrast to the changes during fulminant edema, blood flow distribution did not change after moderate levels of pulmonary edema (W/D of 6.03 0.69), suggesting that gross alveolar flooding is required for a redistribution of pulmonary blood flow. Flow redistribution to the upper lung during airway flooding may be due to increase in Ppa, whereas the increased flow in the dependent lung during the same degree of edema may be due to "bulging" of alveolar vessels into the air spaces, secondary to a decrease in surface activity.


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