scholarly journals Pulmonary gas exchange following rapid intravenous saline infusion

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
G. Kim Prisk ◽  
I. Mark Olfert ◽  
Tatsuya J Arai ◽  
Richard M Hinds ◽  
Kun Lun Huang ◽  
...  
2010 ◽  
Vol 108 (1) ◽  
pp. 53-59 ◽  
Author(s):  
G. Kim Prisk ◽  
I. Mark Olfert ◽  
Tatsuya J. Arai ◽  
Peter D. Wagner ◽  
Susan R. Hopkins

Rapid infusion of intravenous saline, a model of pulmonary interstitial edema, alters the distribution of pulmonary perfusion, raises pulmonary capillary blood volume, and increases bronchial wall thickness in humans. We hypothesized that infusion would disrupt pulmonary gas exchange by increasing ventilation/perfusion (V̇a/Q̇) inequality as opposed to a diffusive impairment in O2 exchange. Seven males (26 ± 3 yr; FEV1: 110 ± 16% predicted.) performed spirometry and had V̇a/Q̇ mismatch measured using the multiple inert gas elimination technique, before and after 20 ml/kg iv of normal saline delivered in ∼30 min. Infusion increased thoracic fluid content from transthoracic impedance by 12% ( P < 0.0001) and left FVC unchanged but reduced expiratory flows (FEF25–75 falling from 5.1 ± 0.4 to 4.2 ± 0.4 l/s, P < 0.05). However, V̇a/Q̇ mismatch as measured by the log standard deviation of the ventilation (LogSDV̇) and perfusion (LogSDQ̇) distributions remained unchanged; LogSDV̇: 0.40 ± 0.03 pre, 0.38 ± 0.04 post, NS; LogSDQ̇: 0.38 ± 0.03 pre, 0.37 ± 0.03 post, NS. There was no significant change in arterial Po2 (99 ± 2 pre, 99 ± 3 mmHg post, NS) but arterial Pco2 was decreased (38.7 ± 0.6 pre, 36.8 ± 1.2 mmHg post, P < 0.05). Thus, infusion compressed small airways and caused a mild degree of hyperventilation. There was no evidence for a diffusive limitation to O2 exchange, with the measured-predicted alveolar-arterial oxygen partial pressure difference being unaltered by infusion at FiO2 = 0.125 (4.3 ± 1.0 pre, 5.2 ± 1.0 post, NS). After infusion, the fraction of perfusion going to areas with V̇a/Q̇ < 1 was increased when a subject breathed a hyperoxic gas mixture [0.72 ± 0.06 (FiO2 = 0.21), 0.80 ± 0.06 (FiO2 = 0.30), P < 0.05] with similar effects on ventilation in the face of unchanged V̇a and Q̇. These results suggest active control of blood flow to regions of decreased ventilation during air breathing, thus minimizing the gas exchange consequences.


1999 ◽  
Vol 87 (1) ◽  
pp. 132-141 ◽  
Author(s):  
Steven Deem ◽  
Richard G. Hedges ◽  
Steven McKinney ◽  
Nayak L. Polissar ◽  
Michael K. Alberts ◽  
...  

Severe anemia is associated with remarkable stability of pulmonary gas exchange (S. Deem, M. K. Alberts, M. J. Bishop, A. Bidani, and E. R. Swenson. J. Appl. Physiol. 83: 240–246, 1997), although the factors that contribute to this stability have not been studied in detail. In the present study, 10 Flemish Giant rabbits were anesthetized, paralyzed, and mechanically ventilated at a fixed minute ventilation. Serial hemodilution was performed in five rabbits by simultaneous withdrawal of blood and infusion of an equal volume of 6% hetastarch; five rabbits were followed over a comparable time. Ventilation-perfusion (V˙a/Q˙) relationships were studied by using the multiple inert-gas-elimination technique, and pulmonary blood flow distribution was assessed by using fluorescent microspheres. Expired nitric oxide (NO) was measured by chemiluminescence. Hemodilution resulted in a linear fall in hematocrit over time, from 30 ± 1.6 to 11 ± 1%. Anemia was associated with an increase in arterial [Formula: see text] in comparison with controls ( P < 0.01 between groups). The improvement in O2 exchange was associated with reducedV˙a/Q˙heterogeneity, a reduction in the fractal dimension of pulmonary blood flow ( P = 0.04), and a relative increase in the spatial correlation of pulmonary blood flow ( P = 0.04). Expired NO increased with anemia, whereas it remained stable in control animals ( P < 0.0001 between groups). Anemia results in improved gas exchange in the normal lung as a result of an improvement in overallV˙a/Q˙matching. In turn, this may be a result of favorable changes in pulmonary blood flow distribution, as assessed by the fractal dimension and spatial correlation of blood flow and as a result of increased NO availability.


Respiration ◽  
1978 ◽  
Vol 35 (3) ◽  
pp. 136-147 ◽  
Author(s):  
P. Jebavý ◽  
J. Fabián ◽  
M. Henzlová ◽  
A. Belán

1992 ◽  
Vol 9 (3) ◽  
pp. 252-257 ◽  
Author(s):  
Th. Wanke ◽  
D. Formanek ◽  
M. Auinger ◽  
H. Zwick ◽  
K. Irsigler

2009 ◽  
Vol 10 (1_suppl) ◽  
pp. S3-S6 ◽  
Author(s):  
Neil MacGillivray

The paper reviews the work of Dr Thomas Latta who during the cholera epidemic of 1831—32 pioneered the use of intravenous saline infusion in the treatment of cholera. The reaction of the medical profession to this new therapy is described and the reasons for the profession’s failure to acknowledge the importance of this advance is analysed. The reasons why the name of Thomas Latta and his contribution did not survive his death in 1833 are discussed and the contributions of twentieth century scholars in remembering his work are highlighted.


2009 ◽  
Vol 106 (6) ◽  
pp. 1902-1908 ◽  
Author(s):  
Roberto Rodríguez-Roisin ◽  
Mitra Drakulovic ◽  
Diego A. Rodríguez ◽  
Josep Roca ◽  
Joan Albert Barberà ◽  
...  

Chronic obstructive pulmonary disease (COPD) is characterized by a decline in forced expiratory volume in 1 s (FEV1) and, in many advanced patients, by arterial hypoxemia with or without hypercapnia. Spirometric and gas exchange abnormalities have not been found to relate closely, but this may reflect a narrow range of severity in patients studied. Therefore, we assessed the relationship between pulmonary gas exchange and airflow limitation in patients with COPD across the severity spectrum. Ventilation-perfusion (V̇A/Q̇) mismatch was measured using the multiple inert gas elimination technique in 150 patients from previous studies. The distribution of patients according to the GOLD stage of COPD was: 15 with stage 1; 40 with stage 2; 32 with stage 3; and 63 with stage 4. In GOLD stage 1, AaPo2 and V̇A/Q̇ mismatch were clearly abnormal; thereafter, hypoxemia, AaPo2, and V̇A/Q̇ imbalance increased, but the changes from GOLD stages 1–4 were modest. Postbronchodilator FEV1 was related to PaO2 ( r = 0.62) and PaCO2 ( r = −0.59) and to overall V̇A/Q̇ heterogeneity ( r = −0.48) ( P < 0.001 each). Pulmonary gas exchange abnormalities in COPD are related to FEV1 across the spectrum of severity. V̇A/Q̇ imbalance, predominantly perfusion heterogeneity, is disproportionately greater than airflow limitation in GOLD stage 1, suggesting that COPD initially involves the smallest airways, parenchyma, and pulmonary vessels with minimal spirometric disturbances. That progression of V̇A/Q̇ inequality with spirometric severity is modest may reflect pathogenic processes that reduce both local ventilation and blood flow in the same regions through airway and alveolar disease and capillary involvement.


Sign in / Sign up

Export Citation Format

Share Document