Pulmonary gas exchange response to exercise- and mannitol-induced bronchoconstriction in mild asthma

2008 ◽  
Vol 105 (5) ◽  
pp. 1477-1485 ◽  
Author(s):  
Phillip A. Muñoz ◽  
Federico P. Gómez ◽  
Hernán A. Manrique ◽  
Josep Roca ◽  
Joan A. Barberà ◽  
...  
Keyword(s):  
Blood Flow ◽  
Gas Exchange ◽  
Minute Ventilation ◽  
Forced Expiratory Volume ◽  
Pulmonary Gas Exchange ◽  
Slow Recovery ◽  
Airway Narrowing ◽  
Asthmatic Patients ◽  
Response To Exercise ◽  
Blood Flow Redistribution

Both exercise (EIB) and mannitol challenges were performed in asthmatic patients to assess and compare their pulmonary gas exchange responses for an equivalent degree of bronchoconstriction. In 11 subjects with EIB [27 ± 4 (SD) yr; forced expiratory volume in 1 s (FEV1), 86 ± 8% predicted], ventilation-perfusion (V̇a/Q̇) distributions (using multiple inert gas elimination technique) were measured 5, 15, and 45 min after cycling exercise (FEV1 fall, 35 ± 12%) and after mannitol (33 ± 10%), 1 wk apart. Five minutes after EIB, minute ventilation (V̇e; by 123 ± 60%), cardiac output (Q̇t, by 48 ± 29%), and oxygen uptake (V̇o2; by 54 ± 25%) increased, whereas arterial Po2 (PaO2; by 14 ± 11 Torr) decreased due to moderate V̇a/Q̇ imbalance, assessed by increases in dispersions of pulmonary blood flow (log SDQ̇; by 0.53 ± 0.16) and alveolar ventilation (log SDV̇; by 0.28 ± 0.15) (dimensionless) ( P < 0.01 each). In contrast, for an equivalent degree of bronchoconstriction and minor increases in V̇e, Q̇t, and V̇o2, mannitol decreased PaO2 more intensely (by 24 ± 9 Torr) despite fewer disturbances in log SDQ̇ (by 0.27 ± 0.12). Notwithstanding, mannitol-induced increase in log SDV̇ at 5 min (by 0.35 ± 0.15) was similar to that observed during EIB, as was the slow recovery in log SDV̇ and high V̇a/Q̇ ratio areas, at variance with the faster recovery of log SDQ̇ and low V̇a/Q̇ ratio areas. In asthmatic individuals, EIB provokes more V̇a/Q̇ imbalance but less hypoxemia than mannitol, primarily due to postexercise increases in V̇e and Q̇t benefiting PaO2. V̇a/Q̇ inequalities during both challenges most likely reflect uneven airway narrowing and blood flow redistribution generating distinctive V̇a/Q̇ patterns, including the development of areas with low and high V̇a/Q̇ ratios.

Mechanisms of improvement in pulmonary gas exchange during isovolemic hemodilution

1999 ◽  
Vol 87 (1) ◽  
pp. 132-141 ◽  
Author(s):  
Steven Deem ◽  
Richard G. Hedges ◽  
Steven McKinney ◽  
Nayak L. Polissar ◽  
Michael K. Alberts ◽  
...  
Keyword(s):  
Blood Flow ◽  
Fractal Dimension ◽  
Gas Exchange ◽  
Spatial Correlation ◽  
Pulmonary Blood Flow ◽  
Minute Ventilation ◽  
Flow Distribution ◽  
Pulmonary Gas Exchange ◽  
Normal Lung ◽  
Blood Flow Distribution

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.

Pulmonary blood flow and ventilation-perfusion heterogeneity

1991 ◽  
Vol 71 (1) ◽  
pp. 252-258 ◽  
Author(s):  
K. B. Domino ◽  
B. L. Eisenstein ◽  
F. W. Cheney ◽  
M. P. Hlastala
Keyword(s):  
Blood Flow ◽  
Standard Deviation ◽  
Gas Exchange ◽  
Minute Ventilation ◽  
Lower Lobe ◽  
Left Pulmonary Artery ◽  
Pulmonary Gas Exchange ◽  
Ventilation Distribution ◽  
Anesthetized Dogs ◽  
The Right

We studied the independent influence of changes in perfusion on pulmonary gas exchange in the left lower lobe (LLL) of anesthetized dogs. Blood flow to the LLL (QLLL) was raised 50% (increased QLLL) or reduced 50% (decreased QLLL) from baseline by partial occlusion of the right or left pulmonary artery, respectively. Minute ventilation and alveolar PCO2 of the LLL remained constant throughout the study. We determined ventilation-perfusion distributions of the LLL using the multiple inert gas elimination technique. Increased QLLL impaired LLL pulmonary gas exchange. All dispersion indexes and all arterial-alveolar difference areas increased (P less than 0.01). Decreased QLLL increased the log standard deviation of the perfusion distribution (P less than 0.05) and reduced the log standard deviation of the ventilation distribution (P less than 0.01) but did not affect the dispersion indexes or alveolar-arterial difference areas. We conclude that ventilation-perfusion heterogeneity is increased by independent changes in perfusion from normal baseline blood flow, even when ventilation and alveolar gas composition remain constant.

Ventilation-perfusion imbalance and chronic obstructive pulmonary disease staging severity

2009 ◽  
Vol 106 (6) ◽  
pp. 1902-1908 ◽  
Author(s):  
Roberto Rodríguez-Roisin ◽  
Mitra Drakulovic ◽  
Diego A. Rodríguez ◽  
Josep Roca ◽  
Joan Albert Barberà ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Gas Exchange ◽  
Pulmonary Disease ◽  
Forced Expiratory Volume ◽  
Pulmonary Gas Exchange ◽  
Airflow Limitation ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Gold Stage ◽  
Stage 1

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.

Unilateral lung edema: effects on pulmonary gas exchange, hemodynamics, and pulmonary perfusion distribution

2000 ◽  
Vol 89 (4) ◽  
pp. 1513-1521 ◽  
Author(s):  
Klaus Slama ◽  
Mareike Gesch ◽  
Johannes C. Böck ◽  
Sylvia M. Pietschmann ◽  
Walter Schaffartzik ◽  
...  
Keyword(s):  
Blood Flow ◽  
Gas Exchange ◽  
Pulmonary Artery ◽  
Venous Pressure ◽  
Pulmonary Gas Exchange ◽  
The Other ◽  
Lung Edema ◽  
Pulmonary Perfusion ◽  
Central Venous ◽  
Fluorescent Microspheres

Two types of unilateral lung edema in sheep were characterized regarding their effects on pulmonary gas exchange, hemodynamics, and distribution of pulmonary perfusion. One edema type was induced with aerosolized HCl (0.15 M, pH 1.0) and the other with NaCl (0.15 M, pH 7.4). Both aerosols were nebulized continuously for 4 h into left lungs. In HCl-treated animals, pulmonary gas exchange deteriorated [from a partial arterial O2 pressure-to-inspired O2 fraction ratio (PaO2 /Fi O2 ) of 254 at baseline to 187 after 4 h HCl]. In addition, pulmonary artery pressure and total pulmonary vascular resistance increased (from 16 to 19 mmHg and from 133 to 154 dyn · s · cm−5, respectively). In NaCl-treated animals, only the central venous pressure significantly increased (from 7 to 9 mmHg). Distribution of pulmonary perfusion (measured with fluorescent microspheres) changed differently in both groups. After HCl application, 6% more blood flow was directed to the treated lung, whereas, after NaCl, 5% more blood flow was directed to the untreated lung. HCl and NaCl treatment both induce an equivalent lung edema, but only HCl treatment is associated with gas exchange alteration and tissue damage. Redistribution of pulmonary perfusion maintains gas exchange during NaCl treatment and decreases it during HCl inhalation.

Intrapulmonary blood flow redistribution during hypoxia increases gas exchange surface area

1982 ◽  
Vol 52 (6) ◽  
pp. 1575-1580 ◽  
Author(s):  
R. L. Capen ◽  
W. W. Wagner
Keyword(s):  
Carbon Monoxide ◽  
Blood Flow ◽  
Cardiac Output ◽  
Gas Exchange ◽  
Surface Area ◽  
Vascular Resistance ◽  
Diffusing Capacity ◽  
Capillary Recruitment ◽  
Blood Flow Redistribution ◽  
Exchange Surface

We have previously shown that airway hypoxia causes pulmonary capillary recruitment and raises diffusing capacity for carbon monoxide. This study was designed to determine whether these events were caused by an increase in pulmonary vascular resistance, which redistributed blood flow toward the top of the lung, or by an increase in cardiac output. We measured capillary recruitment at the top of the dog lung by in vivo microscopy, gas exchange surface area of the whole lung by diffusing capacity for carbon monoxide, and blood flow distribution by radioactive microspheres. During airway hypoxia recruitment occurred, diffusing capacity increased, and blood flow was redistributed upward. When a vasodilator was infused while holding hypoxia constant, these effects were reversed; i. e., capillary “derecruitment” occurred, diffusing capacity decreased, and blood flow was redistributed back toward the bottom of the lung. The vasodilator was infused at a rate that left hypoxic cardiac output unchanged. These data show that widespread capillary recruitment during hypoxia is caused by increased vascular resistance and the resulting upward blood flow redistribution.

The effect of blood flow and diffusion impairment on pulmonary gas exchange: A computer model

1987 ◽  
Vol 20 (5) ◽  
pp. 497-506 ◽  
Author(s):  
Wesley M. Granger ◽  
David A. Miller ◽  
Ina C. Ehrhart ◽  
Wendell F. Hofman
Keyword(s):  
Blood Flow ◽  
Gas Exchange ◽  
Computer Model ◽  
Pulmonary Gas Exchange ◽  
And Diffusion

Effect of increased gas density on pulmonary gas exchange in man

1976 ◽  
Vol 41 (2) ◽  
pp. 206-210 ◽  
Author(s):  
L. D. Wood ◽  
A. C. Bryan ◽  
S. K. Bau ◽  
T. R. Weng ◽  
H. Levison
Keyword(s):  
Gas Exchange ◽  
Sulfur Hexafluoride ◽  
Minute Ventilation ◽  
Volume Ratio ◽  
Carbon Dioxide Tension ◽  
Mean Value ◽  
Pulmonary Gas Exchange ◽  
Arterial Oxygen ◽  
Dense Gas ◽  
The One

Pulmonary gas exchange was measured in seven resting supine subjects breathing air or a dense gas mixture containing 21% O2 in sulfur hexafluoride (SF6). The mean value of the alveolar-arterial oxygen difference (AaDO2) decreased from 12.4 on air to 7.0 on SF6 (P less than 0.01), and increased again to 13.4 when air breathing resumed (P less than 0.01). No differences occurred between gas mixtures for O2 consumption, respiratory quotient, minute ventilation, breathing frequency, heart rate, or blood pressure, and theimproved oxygen transfer could not be attributed to changes in cardiac output or mixed venous oxygen content in the one subject in which they were measured. These results are best explained by an altered distribution of ventilation during dense gas breathing, so that the ventilation-perfusion ratio(VA/Q) variance was reduced. Of several considered mechanisms, we favor onein which SF6 promotes cardiogenic gas mixing between peripheral parallel units having different alveolar gas concentrations. This mechanism allows forobserved increases in arterial carbon dioxide tension and dead space-to-tidal volume ratio during dense gas breathing, and suggests that intraregionalVA/Q variance accounts for at least one-half of the resting AaDO2 in healthysupine young men.

scholarly journals Gas exchange and ventilation–perfusion relationships in the lung

2014 ◽  
Vol 44 (4) ◽  
pp. 1023-1041 ◽  
Author(s):  
Johan Petersson ◽  
Robb W. Glenny
Keyword(s):  
Carbon Dioxide ◽  
Blood Flow ◽  
Gas Exchange ◽  
Minute Ventilation ◽  
Work Of Breathing ◽  
Arterial Oxygen Tension ◽  
Supplemental Oxygen ◽  
Arterial Oxygen ◽  
Respiratory Drive ◽  
Clinical Scenarios

This review provides an overview of the relationship between ventilation/perfusion ratios and gas exchange in the lung, emphasising basic concepts and relating them to clinical scenarios. For each gas exchanging unit, the alveolar and effluent blood partial pressures of oxygen and carbon dioxide (PO2andPCO2) are determined by the ratio of alveolar ventilation to blood flow (V′A/Q′) for each unit. Shunt and lowV′A/Q′ regions are two examples ofV′A/Q′ mismatch and are the most frequent causes of hypoxaemia. Diffusion limitation, hypoventilation and low inspiredPO2cause hypoxaemia, even in the absence ofV′A/Q′ mismatch. In contrast to other causes, hypoxaemia due to shunt responds poorly to supplemental oxygen. Gas exchanging units with little or no blood flow (highV′A/Q′ regions) result in alveolar dead space and increased wasted ventilation,i.e.less efficient carbon dioxide removal. Because of the respiratory drive to maintain a normal arterialPCO2, the most frequent result of wasted ventilation is increased minute ventilation and work of breathing, not hypercapnia. Calculations of alveolar–arterial oxygen tension difference, venous admixture and wasted ventilation provide quantitative estimates of the effect ofV′A/Q′ mismatch on gas exchange. The types ofV′A/Q′ mismatch causing impaired gas exchange vary characteristically with different lung diseases.

scholarly journals Ventilatory response to exercise of elite soccer players

2014 ◽  
Vol 9 ◽  
Author(s):  
Adriano Di Paco ◽  
Giosuè A. Catapano ◽  
Guido Vagheggini ◽  
Stefano Mazzoleni ◽  
Matteo Levi Micheli ◽  
...  
Keyword(s):  
Maximal Exercise ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Lung Function Test ◽  
Peak Oxygen Uptake ◽  
Forced Expiratory Volume ◽  
Soccer Players ◽  
Ventilatory Parameters ◽  
Response To Exercise

Background: The purpose of this study was to evaluate the role of ventilatory parameters in maximal exercise performance in elite soccer players. Methods: From September 2009 to December 2012, 90 elite soccer players underwent evaluation of lung function test and ergospirometry by means of an incremental symptom-limited treadmill test. Results were analyzed according to i) maximal exercise velocity performed (Hi-M: high-performers, >18.65 km/h; Lo-M: low-performers, <18.65 km/h) and ii) usual role in the team. Results: Hi-M showed higher peak minute ventilation (V_ Epeak: 158.3 ± 19.5 vs 148.0 ± 18.54 L/min, p = 0.0203), and forced expiratory volume at first second (5.28 ± 0.50 vs 4.89 ± 0.52 liters, p < 0.001) than Lo-M, independently of playing role. Moreover, a significant correlation between peak oxygen uptake and V_ E (r = 0.57, p < 0.001) was found. Conclusions: Ventilatory response plays a role in the assessment of exercise capacity in elite soccer players.

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