Gas exchange in nonperfused dog lungs

1981 ◽  
Vol 51 (5) ◽  
pp. 1261-1267 ◽  
Author(s):  
J. W. Shepard ◽  
V. D. Minh ◽  
G. F. Dolan
Keyword(s):  
Gas Exchange ◽  
Minute Ventilation ◽  
Left Lung ◽  
Co2 Concentration ◽  
Gas Transfer ◽  
O2 Uptake ◽  
Tissue Metabolism ◽  
End Tidal

Gas exchange was studied under conditions of zero perfusion both in situ and in vitro. Six dogs, anesthetized with pentobarbital sodium, underwent surgical interruption of both pulmonary and bronchial circulations to the left lung. Despite the absence of perfusion, O2 uptake for the left lung ranged from 0.76 to 0.98 ml/min, whereas CO2 elimination greatly exceeded O2 uptake ranging from 1.68 to 4.34 ml/min. In addition, CO2 output was observed to vary directly with the level of minute ventilation (VE) and inversely with end-tidal CO2 concentration. To investigate the mechanisms responsible for these findings we studied 20 excised, ventilated, but nonperfused dog lungs to evaluate the relative roles of tissue metabolism and transpleural diffusion to gas exchange. The results obtained with these excised lungs under conditions of varying VE and extrapleural gas concentrations indicate that the high respiratory exchange ratios observed in situ can be explained by the greater rate with which CO2 diffuses through the pleura, and that reduced ventilation decreases total gas transfer by decreasing the transpleural partial pressure driving gradient. Our data further document that the concentration of CO2 in alveolar gas may differ significantly from that present in inspired gas under conditions of ventilation-perfusion ratio equal to infinity, and that tissue metabolism as well as transpleural diffusion contribute to gas exchange in nonperfused lung.

Pulmonary gas exchange in humans during exercise at sea level

1986 ◽  
Vol 60 (5) ◽  
pp. 1590-1598 ◽  
Author(s):  
M. D. Hammond ◽  
G. E. Gale ◽  
K. S. Kapitan ◽  
A. Ries ◽  
P. D. Wagner
Keyword(s):  
Gas Exchange ◽  
Sea Level ◽  
Minute Ventilation ◽  
Normal Subjects ◽  
Inert Gas ◽  
Diffusion Limitation ◽  
O2 Uptake ◽  
Heavy Exercise ◽  
Blood Temperature ◽  
O2 Diffusion

Previous studies have shown both worsening ventilation-perfusion (VA/Q) relationships and the development of diffusion limitation during exercise at simulated altitude and suggested that similar changes could occur even at sea level. We used the multiple-inert gas-elimination technique to further study gas exchange during exercise in healthy subjects at sea level. Mixed expired and arterial respiratory and inert gas tensions, cardiac output, heart rate, minute ventilation, respiratory rate, and blood temperature were recorded at rest and during steady-state exercise in the following order: rest, minimal exercise (75 W), heavy exercise (300 W), heavy exercise breathing 100% O2, repeat rest, moderate exercise (225 W), and light exercise (150 W). Alveolar-to-arterial O2 tension difference increased linearly with O2 uptake (VO2) (6.1 Torr X min-1 X 1(-1) VO2). This could be fully explained by measured VA/Q inequality at mean VO2 less than 2.5 l X min-1. At higher VO2, the increase in alveolar-to-arterial O2 tension difference could not be explained by VA/Q inequality alone, suggesting the development of diffusion limitation. VA/Q inequality increased significantly during exercise (mean log SD of perfusion increased from 0.28 +/- 0.13 at rest to 0.58 +/- 0.30 at VO2 = 4.0 l X min-1, P less than 0.01). This increase was not reversed by 100% O2 breathing and appeared to persist at least transiently following exercise. These results confirm and extend the earlier suggestions (8, 21) of increasing VA/Q inequality and O2 diffusion limitation during heavy exercise at sea level in normal subjects and demonstrate that these changes are independent of the order of performance of exercise.

Immediate effects of cigarette smoking on cardiorespiratory responses to exercise

1985 ◽  
Vol 58 (6) ◽  
pp. 1975-1981 ◽  
Author(s):  
G. L. Hirsch ◽  
D. Y. Sue ◽  
K. Wasserman ◽  
T. E. Robinson ◽  
J. E. Hansen
Keyword(s):  
Gas Exchange ◽  
Cigarette Smoking ◽  
Pulse Pressure ◽  
Minute Ventilation ◽  
Cardiovascular Responses ◽  
Co2 Production ◽  
Blood Levels ◽  
Maximal Aerobic Capacity ◽  
Arterial Blood ◽  
End Tidal

To determine the acute action of cigarette smoking on cardiorespiratory function under stress, the immediate effects of cigarette smoking on the ventilatory, gas exchange, and cardiovascular responses to exercise were studied in nine healthy male subjects. Each subject performed an incremental exercise test to exhaustion on two separate days, one without smoking (control) and one after smoking 3 cigarettes/h for 5 h. The order of the two tests was randomized. Arterial blood gases and pH were measured during rest and all levels of exercise; CO blood levels confirmed the absorption of cigarette smoke. In addition, minute ventilation (VE), end-tidal PCO2 and PO2, O2 uptake (VO2), CO2 production, directly measured blood pressure, electrocardiogram, and heart rate (HR) were recorded every 30 s. The dead space-to-tidal volume ratio (VD/VT), maximal aerobic capacity (VO2max), and anaerobic threshold (AT) were determined from the gas exchange data. Cigarette smoking resulted in a significantly lower VO2max, AT, and VO2/HR (O2 pulse) and a significantly higher HR, pulse-pressure product, and pulse pressure (P less than 0.05) compared with the control. Additionally, a trend toward a higher VD/VT and arterial-end-tidal PCO2 difference was found during exercise after smoking. We conclude that cigarette smoking causes immediate detrimental effects on cardiovascular function during exercise, including tachycardia, increased pulse-pressure product, and impaired O2 delivery. The acute effects on respiratory function were less striking and primarily limited to abnormalities reflecting ventilation-perfusion mismatching.

scholarly journals Estimation of bubble-mediated air–sea gas exchange from concurrent DMS and CO<sub>2</sub> transfer velocities at intermediate–high wind speeds

2017 ◽  
Vol 17 (14) ◽  
pp. 9019-9033 ◽  
Author(s):  
Thomas G. Bell ◽  
Sebastian Landwehr ◽  
Scott D. Miller ◽  
Warren J. de Bruyn ◽  
Adrian H. Callaghan ◽  
...  
Keyword(s):  
Wind Speed ◽  
Gas Exchange ◽  
North Atlantic ◽  
Gas Transfer ◽  
Data Set ◽  
Wind Speeds ◽  
Wide Range ◽  
Carbon Dioxide Co2 ◽  
The Impact

Abstract. Simultaneous air–sea fluxes and concentration differences of dimethylsulfide (DMS) and carbon dioxide (CO2) were measured during a summertime North Atlantic cruise in 2011. This data set reveals significant differences between the gas transfer velocities of these two gases (Δkw) over a range of wind speeds up to 21 m s−1. These differences occur at and above the approximate wind speed threshold when waves begin breaking. Whitecap fraction (a proxy for bubbles) was also measured and has a positive relationship with Δkw, consistent with enhanced bubble-mediated transfer of the less soluble CO2 relative to that of the more soluble DMS. However, the correlation of Δkw with whitecap fraction is no stronger than with wind speed. Models used to estimate bubble-mediated transfer from in situ whitecap fraction underpredict the observations, particularly at intermediate wind speeds. Examining the differences between gas transfer velocities of gases with different solubilities is a useful way to detect the impact of bubble-mediated exchange. More simultaneous gas transfer measurements of different solubility gases across a wide range of oceanic conditions are needed to understand the factors controlling the magnitude and scaling of bubble-mediated gas exchange.

Measurement and analysis of gas exchange during exercise using a programmable calculator

1980 ◽  
Vol 49 (3) ◽  
pp. 456-461 ◽  
Author(s):  
D. Y. Sue ◽  
J. E. Hansen ◽  
M. Blais ◽  
K. Wasserman
Keyword(s):  
Gas Exchange ◽  
Respiratory Exchange Ratio ◽  
Minute Ventilation ◽  
Co2 Production ◽  
O2 Consumption ◽  
Exercise Tests ◽  
Programmable Calculator ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
End Tidal

Although exercise testing is useful in the diagnosis and management of cardiovascular and pulmonary diseases, a rapid comprehensive method for measurement of ventilation and gas exchange has been limited to expensive complex computer-based systems. We devised a relatively inexpensive, technically simple, and clinically oriented exercise system built around a desktop calculator. This system automatically collects and analyzes data on a breath-by-breath basis. Our calculator system overcomes the potential inaccuracies of gas exchange measurement due to water vapor dilution and mismatching of expired flow and gas concentrations. We found no difference between the calculator-derived minute ventilation, CO2 production, O2 consumption, and respiratory exchange ratio and the values determined from simultaneous mixed expired gas collections in 30 constant-work-rate exercise studies. Both tabular and graphic displays of minute ventilation, CO2 production, O2 consumption, respiratory exchange ratio, heart rate, end-tidal O2 tension, end-tidal CO2 tension, and arterial blood gas value are included for aid in the interpretation of clinical exercise tests.

Effects of beta-adrenergic blockade on ventilation and gas exchange during exercise in humans

1983 ◽  
Vol 54 (5) ◽  
pp. 1306-1313 ◽  
Author(s):  
E. S. Petersen ◽  
B. J. Whipp ◽  
J. A. Davis ◽  
D. J. Huntsman ◽  
H. V. Brown ◽  
...  
Keyword(s):  
Heart Rate ◽  
Gas Exchange ◽  
Time Constant ◽  
Minute Ventilation ◽  
Work Rate ◽  
Beta Blockade ◽  
Adrenergic Blockade ◽  
O2 Uptake ◽  
Beta Adrenergic ◽  
Co2 Partial Pressure

The effects of beta-adrenergic blockade induced by intravenous propranolol hydrochloride (0.2 mg/kg) on ventilatory and gas exchange responses to exercise were studied during tests in which the work rate was either increased progressively or maintained at a constant load in six healthy young male subjects. Heart rate during exercise decreased by about 20% and cardiac output, as estimated by a modification of the method of Kim et al. (J. Appl. Physiol. 21: 1338–1344, 1966), by about 15%. The relation between work rate and O2 uptake (VO2) was unaffected by propranolol, whereas maximal O2 uptake (VO2max) decreased by 5% and the anaerobic threshold, estimated noninvasively, was lowered by 23%. The relations between CO2 output (VCO2) and end-tidal CO2 partial pressure (PCO2) and between VCO2 and minute ventilation (VE) were both unaffected. The time constants for changes of VO2, VCO2, and VE during on-transients from unloaded pedaling to either a moderate (ca. 50% VO2max) or a heavy (ca. 67% VO2max) work rate in the control studies were in agreement with previously reported values, i.e., 42, 60, and 69 s, respectively. beta-Blockade was associated with a significantly increased time constant for VO2 of 61 s but with less consistent and insignificant changes for VCO2 and VE. There was a small but significant increase of the time constant for heart rate from 40 to 45 s. It is concluded that propranolol exerts its primary influence during exercise on the cardiovascular system without any discernible effect on ventilatory control.

Coupling of ventilation to pulmonary gas exchange during nonsteady-state work in men

1983 ◽  
Vol 54 (2) ◽  
pp. 587-593 ◽  
Author(s):  
D. H. Wasserman ◽  
B. J. Whipp
Keyword(s):  
Gas Exchange ◽  
Minute Ventilation ◽  
Normal Subjects ◽  
Load Cycle ◽  
Constant Load ◽  
Response Dynamics ◽  
Co2 Output ◽  
Exercise Ventilation ◽  
Nonsteady State ◽  
End Tidal

During steady-state exercise, ventilation increases in proportion to CO2 output (VCO2), regulating arterial PCO2. To characterize the dynamics of ventilatory coupling to VCO2 and O2 uptake (VO2) in the nonsteady-state phase, seven normal subjects performed constant-load cycle ergometry to a series of subanaerobic threshold work rates. Each bout consisted of eight 6-min periods of alternating loaded and unloaded cycling. Ventilation and gas exchange variables were computed breath by breath, with the time-averaged response dynamics being established off-line. Ventilation increased as a linear function of VCO2 in all cases, the relationship being identical in the steady- and the nonsteady-state phases. Ventilation, however, bore a curvilinear relation to VO2, the kinetics of the latter being more rapid. Owing to the kinetic disparity between expired minute ventilation (VE) and VO2, there was an overshoot in the direction of change in VE/VO2 and end-tidal PO2 during the work-rate transition. In contrast, there was no overshoot in the direction of change in VE/VCO2 and end-tidal PCO2 throughout the nonsteady-state period. These data suggest that the exercise hyperpnea is coupled to metabolism in men via a signal proportional to VCO2 in both the nonsteady and steady states of moderate exercise.

Defining origin of positive slope in hypercapnic ventilatory response curve

1991 ◽  
Vol 261 (3) ◽  
pp. R747-R751
Author(s):  
Z. Lorinc ◽  
J. Derr ◽  
M. Snider ◽  
R. Lydic
Keyword(s):  
Ventilatory Response ◽  
Minute Ventilation ◽  
Complex Function ◽  
Co2 Concentration ◽  
Positive Slope ◽  
Hypercapnic Ventilatory Response ◽  
Joint Point ◽  
Respiratory Stimulant ◽  
End Tidal ◽  
Derived Data

The sensitivity to CO2 as a respiratory stimulant has traditionally been studied by exposing organisms to progressively increasing levels of inspired CO2 while measuring the corresponding increase in minute ventilation (V). Plots of V as a function of end-tidal CO2 concentration reveal a complex function with a "dogleg" shape. Only the positive slope of the V function is taken as an index of chemosensitivity, but the starting points for such analyses are often chosen arbitrarily. This paper examined the hypotheses that the range of CO2 concentrations over which V slopes are compared may be mathematically defined and that arbitrary choices of this analytic range may influence conclusions about the hypercapnic ventilatory response (HCVR). Three mathematical models attempted to define the origin of the positive slope for the HCVR curve using empirically derived data. The results revealed good agreement that the origin of the positive HCVR slope may be reliably defined by a point that joins the horizontal and positive slope of the HCVR curve. In addition to identifying the "joint-point" statistic, the results suggest that arbitrarily defining the range of CO2 values over which V is analyzed can be replaced by quantitative approaches for identifying the origin of the ventilatory response to hypercapnia.

Breathing pattern and metabolic behavior during anticipation of exercise

1986 ◽  
Vol 60 (4) ◽  
pp. 1306-1312 ◽  
Author(s):  
M. J. Tobin ◽  
W. Perez ◽  
S. M. Guenther ◽  
G. D'Alonzo ◽  
D. R. Dantzker
Keyword(s):  
Mental Arithmetic ◽  
Minute Ventilation ◽  
Influencing Factor ◽  
Random Order ◽  
Co2 Concentration ◽  
Cortical Activity ◽  
Respiratory Center ◽  
The Face ◽  
Metabolic Behavior ◽  
End Tidal

The mechanisms responsible for the marked increase in ventilation at the onset of exercise are incompletely defined. A conditioned response to exercise anticipation has been suggested as an influencing factor, but systematic measurements have not been made during the transition from rest to the time when exercise is anticipated but has not yet commenced. We tested the hypothesis that cortical activity associated with the anticipation of exercise causes hyperpnea, which is at least partly responsible for the increased ventilation at the onset of exercise. To assess the influence of continuous cortical activity in the absence of exercise anticipation the subjects performed mental arithmetic tasks. Fifteen subjects performed the two experiments in a random order. Ventilation was measured noninvasively using a calibrated respiratory inductive plethysmograph and end-tidal CO2 concentration (FETCO2) was monitored at the nasal vestibule. Both exercise anticipation and mental arithmetic caused an increase in minute ventilation (VI) (P less than 0.01) and mean inspiratory flow (VT/TI, P less than 0.01), which reflects respiratory center drive, although the derivation differed in that the former was volume based, whereas the latter was due to alteration in timing. Despite the increase in VI, FETCO2 remained constant in both instances. In a complementary study the constant FETCO2 in the face of increased VI was shown to be due to increased CO2 output. The results show that the mere anticipation of exercise causes an increase in ventilation. The mechanism responsible for this hyperpnea cannot be due solely to respiratory center activation because of the constancy of FETCO2 and the associated alterations in cardiac and metabolic behavior.

scholarly journals Control of ventilation during exercise in patients with central venous-to-systemic arterial shunts

1988 ◽  
Vol 64 (1) ◽  
pp. 234-242 ◽  
Author(s):  
K. E. Sietsema ◽  
D. M. Cooper ◽  
J. K. Perloff ◽  
J. S. Child ◽  
M. H. Rosove ◽  
...  
Keyword(s):  
Gas Exchange ◽  
Minute Ventilation ◽  
Venous Blood ◽  
Work Rate ◽  
Moderate Intensity ◽  
Moderate Intensity Exercise ◽  
Arterial Circulation ◽  
Arterial Blood ◽  
Constant Work Rate ◽  
End Tidal

The diversion of systemic venous blood into the arterial circulation in patients with intracardiac right-to-left shunts represents a pathophysiological condition in which there are alterations in some of the potential stimuli for the exercise hyperpnea. We therefore studied 18 adult patients with congenital (16) or noncongenital (2) right-to-left shunts and a group of normal control subjects during constant work rate and progressive work rate exercise to assess the effects of these alterations on the dynamics of exercise ventilation and gas exchange. Minute ventilation (VE) was significantly higher in the patients than in the controls, both at rest (10.7 +/- 2.4 vs. 7.5 +/- 1.2 l/min, respectively) and during constant-load exercise (24.9 +/- 4.8 vs. 12.7 +/- 2.61 l/min, respectively). When beginning constant work rate exercise from rest, the ventilatory response of the patients followed a pattern that was distinct from that of the normal subjects. At the onset of exercise, the patients' end-tidal PCO2 decreased, end-tidal PO2 increased, and gas exchange ratio increased, indicating that pulmonary blood was hyperventilated relative to the resting state. However, arterial blood gases, in six patients in which they were measured, revealed that despite the large VE response to exercise, arterial pH and PCO2 were not significantly different from resting values when sampled during the first 2 min of moderate-intensity exercise. Arterial PCO2 changed by an average of only 1.4 Torr after 4.5-6 min of exercise. Thus the exercise-induced alveolar and pulmonary capillary hypocapnia was of an appropriate degree to compensate for the shunting of CO2-rich venous blood into the systemic arterial circulation.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Estimation of bubbled-mediated air/sea gas exchange from concurrent DMS and CO<sub>2</sub> transfer velocities at intermediate-high wind speeds

2017 ◽  
Author(s):  
Thomas G. Bell ◽  
Sebastian Landwehr ◽  
Scott D. Miller ◽  
Warren J. de Bruyn ◽  
Adrian Callaghan ◽  
...  
Keyword(s):  
Wind Speed ◽  
Gas Exchange ◽  
North Atlantic ◽  
Gas Transfer ◽  
High Wind ◽  
Wind Speeds ◽  
Wide Range ◽  
Carbon Dioxide Co2 ◽  
The Impact

Abstract. Simultaneous air/sea fluxes and concentration differences of dimethylsulfide (DMS) and carbon dioxide (CO2) were measured during a summertime North Atlantic cruise in 2011. This dataset reveals significant differences between the gas transfer velocities of these two gases (Δkw) over a range of wind speeds up to 21 m  s−1. These differences occur at and above the approximate wind speed threshold when waves begin breaking. Whitecap fraction (a proxy for bubbles) was also measured and has a positive relationship with Δkw, consistent with enhanced bubble-mediated transfer of the less soluble CO2 relative to that of the more soluble DMS. However, the correlation of Δkw with whitecap fraction is no stronger than with wind speed. Models used to estimate bubble-mediated transfer from in situ whitecap fraction under-predict the observations, particularly at intermediate wind speeds. Examining the differences between gas transfer velocities of gases with different solubilities is a useful way to detect the impact of bubble-mediated exchange. More simultaneous gas transfer measurements of different solubility gases across a wide range of oceanic conditions are needed to understand the factors controlling the magnitude and scaling of bubble-mediated gas exchange.

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