Exercise performance with added dead space in chronic airflow obstruction

1984 ◽  
Vol 56 (4) ◽  
pp. 1020-1026 ◽  
Author(s):  
S. E. Brown ◽  
R. R. King ◽  
S. M. Temerlin ◽  
D. W. Stansbury ◽  
C. K. Mahutte ◽  
...  
Keyword(s):  
Exercise Capacity ◽  
Dead Space ◽  
Exercise Performance ◽  
Airflow Obstruction ◽  
Co2 Production ◽  
Base Line ◽  
Arterial Pco2 ◽  
Maximum Exercise ◽  
Ventilatory Mechanics ◽  
Arterial Po2

Individuals with chronic airflow obstruction (CAO) are thought to have limited exercise tolerance primarily because of impaired ventilatory mechanics. We studied the effects of added external dead space (DS) on exercise capacity [maximum O2 consumption (VO2max)], maximum exercise ventilation (VEmax), and blood gases (arterial PO2, PCO2, pH) in 22 patients with CAO [forced expired volume at 1 s (FEV1) = 0.96 +/- 0.41 liter]. Maximum exercise testing (Emax) was performed by incremental cycle ergometry. Patients exercised at base line (BL) and with DS (0.25 liter if FEV1 less than 0.8, and 0.50 liter if FEV1 greater than 0.8 liter), in random-order single-blind fashion. DS resulted in a 12.2% increase in VEmax (P less than 0.001); tidal volume increased (P less than 0.025) while respiratory frequency was unchanged. The VO2max and maximum CO2 production decreased (P less than 0.001) with DS. Arterial PCO2 at rest and at exhaustion increased with DS (P less than 0.001). The pH and arterial PO2 showed small declines at rest and at Emax. Thus, at the lower maximum work load achieved with DS, the patients ventilated more and tolerated a higher arterial PCO2 and a lower arterial PO2 and pH before stopping from dyspnea as compared with the BL exercise run. In contrast, the VO2max of nine normal control subjects was unaffected by the addition of DS. Although VEmax can be increased in CAO patients with DS, this increase is not sufficient to prevent further CO2 retention or a decrease in exercise capacity. We conclude that exercise performance is limited primarily by impaired ventilatory mechanics in CAO.

Inspiratory airway CO2 loading in the pony

1984 ◽  
Vol 57 (4) ◽  
pp. 1097-1103 ◽  
Author(s):  
H. W. Shirer ◽  
J. A. Orr ◽  
J. L. Loker
Keyword(s):  
Tidal Volume ◽  
Dead Space ◽  
Blood Gases ◽  
Minute Volume ◽  
Arterial Pco2 ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
Airway Dead Space ◽  
Arterial Po2 ◽  
Stimulation Of

To determine if CO2-sensitive airway receptors are important in the control of breathing, CO2 was preferentially loaded into the respiratory airways in conscious ponies. The technique involved adding small amounts of 100% CO2 to either the latter one-third or latter two-thirds of the inspiratory air in an attempt to raise CO2 concentrations in the airway dead space independent of the arterial blood. Arterial blood gas tensions (PCO2 and PO2) and pH, as well as respiratory output (minute volume, tidal volume, and respiratory rate), were measured in a series of 20 experiments on 5 awake ponies. Elevation of airway CO2 to approximately 12% by addition of CO2 to the latter portion of the inspiratory tidal volume did not alter either ventilation or arterial blood gases. When CO2 was added earlier in the inspiratory phase to fill more of the airway dead space, a small but significant increase in minute volume (2.1 l X min-1 X m-2) and tidal volume (0.1 l X m-2) was accompanied by an increase in arterial PCO2, arterial PO2, and a fall in pH (0.96 Torr, 10.5 Torr, 0.007 units, respectively). A second series of 12 experiments on 6 awake ponies using radiolabeled 14CO2 determined that the increases in breathing were minimal when compared with the large increase that occurred when these animals inhaled 6% 14CO2 (12.7 l X min-1 X m-2). Also, stimulation of systemic arterial or central nervous system chemoreceptors cannot be eliminated from the response since significant amounts of 14CO2 were present in the arterial blood when this marker gas was added to the latter two-thirds of the inspiratory tidal volume. The results, therefore, provide no evidence for CO2-sensitive airway receptors that can increase breathing when stimulated during the latter part of the inspiratory cycle.

Metabolic-ventilatory interaction in conscious rats: effect of hypoxia and ambient temperature

1994 ◽  
Vol 76 (4) ◽  
pp. 1594-1599 ◽  
Author(s):  
C. Saiki ◽  
T. Matsuoka ◽  
J. P. Mortola
Keyword(s):  
Blood Pressure ◽  
Metabolic Rate ◽  
Ambient Temperature ◽  
Blood Gases ◽  
Male Rats ◽  
Co2 Production ◽  
O2 Consumption ◽  
Arterial Pco2 ◽  
Open Flow ◽  
Arterial Po2

Previous studies have indicated that the hypometabolic response to hypoxia depends on ambient temperature (Ta), being more pronounced in the cold. If metabolic rate were an important contributor to the level of ventilation (VE), the magnitude of the hyperpneic response to hypoxia should also depend on Ta. We tested this hypothesis on adult conscious male rats. In normoxia, a drop in Ta from 25 to 10 degrees C increased O2 consumption and CO2 production (VO2 and VCO2, respectively, measured by an open-flow technique) and VE (measured with the barometric method) by 80 and 60%, respectively, with no changes in blood gases. At both Ta, hypoxia (10% inspired O2, 33–35 Torr arterial PO2) induced the same degree of hyperventilation, i.e., the same drop in arterial PCO2 (about -13 Torr). The hyperventilation at 25 degrees C Ta was achieved exclusively by an increase in VE, whereas at 10 degrees C Ta the hyperpnea was minimal (+15%) and accompanied by a drop (-30%) in VO2 and VCO2. Diaphragmatic electromyograms confirmed the VE results. Changes in blood pressure were similar at both Ta. Addition of 3% CO2 to the inspired air further increased VE, indicating that the hypoxic rat was not breathing at its maximal VE at either Ta. We conclude that, in the rat, changes in metabolic rate play an important role in the VE response to hypoxia and that Ta influences the response because of its effect on the degree of hypoxic hypometabolism.

Ventilatory and diaphragmatic EMG responses to negative-pressure ventilation in airflow obstruction

1988 ◽  
Vol 65 (4) ◽  
pp. 1621-1626 ◽  
Author(s):  
D. O. Rodenstein ◽  
D. C. Stanescu ◽  
G. Cuttita ◽  
G. Liistro ◽  
C. Veriter
Keyword(s):  
Negative Pressure ◽  
Phase Locking ◽  
Minute Ventilation ◽  
Airflow Obstruction ◽  
Chronic Obstructive Lung Disease ◽  
Chronic Obstructive ◽  
Arterial Pco2 ◽  
Negative Pressure Ventilation ◽  
Inspiratory Activity ◽  
Arterial Po2

To assess the responses of patients with chronic obstructive lung disease (COLD) to negative-pressure ventilation (NPV), we studied eight naive patients with moderate to severe COLD before (control) and during NPV with "low" (-10-cmH2O) and "high" (-30-cmH2O) pressure swings in a Drinker tank respirator. Tidal volume (VT) and minute ventilation (VE) were recorded from a Respitrace and diaphragmatic electromyogram (DEMG) from a bipolar esophageal electrode. During short, 5-min runs of "low" and "high" NPV, VT did not change and VE increased in a borderline significant way at -30-cmH2O NPV. Peak integrated DEMG amplitude did not change with respect to control during short runs of NPV. However, when NPV was maintained for 20-60 min, a significant (though small, 20%) decrease in peak DEMG amplitude was observed with respect to control. By contrast, in a ninth patient habituated to NPV, the decrease in peak DEMG amplitude during a 5-min run of NPV was 60%. Significant increases in arterial PO2 (at -10- and -30-cmH2O NPV) and decreases in arterial PCO2 (at -30-cmH2O NPV) were found during NPV for the whole group of patients. One-to-one phase locking between the respirator and patients was the most common pattern of entrainment observed. However, 1:1 phase locking did not preclude the presence of dissociation between the two pacemakers. We conclude that short runs of NPV in naive patients do not result in changes in DEMG, as opposed to immediate and nearly complete cessation of inspiratory activity in trained patients.

Physiological dead space increases during initial hours of chronic hypoxemia with or without hypocapnia

1994 ◽  
Vol 77 (3) ◽  
pp. 1526-1531 ◽  
Author(s):  
E. B. Olson
Keyword(s):  
Dead Space ◽  
Minute Ventilation ◽  
Volume Ratio ◽  
Whole Body ◽  
Co2 Production ◽  
Sprague Dawley ◽  
Arterial Pco2 ◽  
Physiological Dead Space ◽  
Production Ratio ◽  
Arterial Blood

A whole body plethysmograph was used to determine the minute ventilation-to-CO2 production ratio (VE/VCO2) of intact unrestrained unanesthetized adult male Sprague-Dawley rats during 7 days of hypoxemia (arterial PO2 approximately 50 Torr). In one set of rats, normocapnia (arterial PCO2 approximately 40 Torr) was maintained. Arterial blood gases and acid-base status were determined, and arterial PCO2 was used to calculate alveolar ventilation-to-VCO2 ratio (VA/VCO2) in all situations when inhaled CO2 was not elevated. In normoxia VE/VCO2 = 25 +/- 1 (mean +/- 95% confidence limits); after 12 h of hypoxemia, VE/VCO2 was maximal, 61 +/- 5 in hypoxemic hypocapnia and 200 +/- 55 in hypoxemic normocapnia. Between 2 and 7 days of hypoxemia, VE/VCO2 had plateaued, 42 +/- 3 in hypoxemic hypocapnia and 95 +/- 19 in hypoxemic normocapnia. Dead space-to-tidal volume ratio (VD/VT) = (VE/VCO2 - VA/VCO2)/(VE/VCO2), and in normoxia VD/VT = 0.17 +/- 0.04. In hypoxemic hypocapnia, VD/VT measured between 1 and 5 h was 0.38 +/- 0.04. It remained elevated at 0.29 +/- 0.04 after 24 h, but after 4-7 days in hypoxemic hypocapnia, VD/VT had recovered to 0.15 +/- 0.03. It is postulated that the disproportionate increase in VE/VCO2 observed during the first 24 h of exposure to hypoxemic normocapnia (compared with elevated steady-state plateau levels maintained from 2 to 7 days sojourn) reflects an immediate transient increase of physiological dead space on exposure to hypoxemia.

Metabolic response to ambient temperature and hypoxia in sinoaortic-denervated rats

1994 ◽  
Vol 266 (2) ◽  
pp. R387-R391 ◽  
Author(s):  
T. Matsuoka ◽  
A. Dotta ◽  
J. P. Mortola
Keyword(s):  
Significant Contribution ◽  
Metabolic Response ◽  
Acute Hypoxia ◽  
Co2 Production ◽  
Adult Rats ◽  
Arterial Pco2 ◽  
Open Flow ◽  
Ambient Temperatures ◽  
Colonic Temperature ◽  
Arterial Po2

We tested the hypothesis that the sinoaortic afferents may contribute to normoxic thermogenesis and to the magnitude of the hypometabolic response to hypoxia. Adult rats were either sinoaortic denervated (SAX; n = 20) or sham operated (Sham; n = 20). A few days after the operation, gaseous metabolism [O2 uptake (VO2) and CO2 production (VCO2)] was measured with an open-flow system at ambient temperatures (Tamb) of 20, 25, 30, and 35 degrees C as the animal was resting awake. At thermoneutrality (Tamb 30 degrees C) or higher Tamb there was no difference in VO2 or VCO2. Below thermoneutrality, metabolic rate was significantly lower in SAX than in Sham animals (-14 and -16% at 20 and 25 degrees C, respectively). Colonic temperature and arterial PO2 were also slightly less, whereas arterial PCO2 and pH, mean arterial pressure, and heart rate did not differ significantly between the two groups. Exposure to acute hypoxia (10% inspired O2, 20-30 min) at Tamb 20 and 25 degrees C significantly reduced VO2 in both groups to a similar value; hence, at either Tamb, the metabolic drop during hypoxia in Sham animals was larger than that in SAX animals. Hypercapnia (5% CO2 breathing) did not change VO2 in either group. We conclude that in the rat at Tamb slightly below thermoneutrality, the sinoaortic afferents 1) provide a small but significant contribution to normoxic thermogenesis and 2) are not required for the manifestation of the drop in metabolism during hypoxia.

Determinants of Maximum Exercise Capacity in Patients with Chronic Airflow Obstruction

CHEST Journal ◽  
1989 ◽  
Vol 96 (2) ◽  
pp. 267-271 ◽  
Author(s):  
Thomas A. Dillard ◽  
Steven Piantadosi ◽  
Krishnan R. Rajagopal
Keyword(s):  
Exercise Capacity ◽  
Airflow Obstruction ◽  
Maximum Exercise

Effects of High- and Low-Carbohydrate Meals on Maximum Exercise Performance in Chronic Airflow Obstruction

CHEST Journal ◽  
1991 ◽  
Vol 100 (3) ◽  
pp. 792-795 ◽  
Author(s):  
James D. Frankfort ◽  
Claudia E. Fischer ◽  
David W Stansbury ◽  
David L. McArthur ◽  
Stephen E. Brown ◽  
...  
Keyword(s):  
Exercise Performance ◽  
Airflow Obstruction ◽  
Maximum Exercise ◽  
Low Carbohydrate

Increased Dead Space Ventilation Mediates Reduced Exercise Capacity in Systolic Heart Failure

2016 ◽  
Vol 193 (11) ◽  
pp. 1292-1300 ◽  
Author(s):  
Kirk Kee ◽  
Christopher Stuart-Andrews ◽  
Matthew J. Ellis ◽  
Jeremy P. Wrobel ◽  
Kris Nilsen ◽  
...  
Keyword(s):  
Heart Failure ◽  
Exercise Capacity ◽  
Dead Space ◽  
Systolic Heart Failure ◽  
Dead Space Ventilation

Increases in coronary vein CO2 during cardiac resuscitation

1990 ◽  
Vol 68 (4) ◽  
pp. 1405-1408 ◽  
Author(s):  
C. V. Gudipati ◽  
M. H. Weil ◽  
R. J. Gazmuri ◽  
H. G. Deshmukh ◽  
J. Bisera ◽  
...  
Keyword(s):  
Spontaneous Circulation ◽  
Co2 Production ◽  
Acid Base ◽  
Coronary Vein ◽  
Arterial Pco2 ◽  
Control Value ◽  
Great Cardiac Vein ◽  
Aortic Blood ◽  
Highly Correlated ◽  
Mixed Venous

We investigated the aortic, mixed venous, and great cardiac vein acid-base changes in eight domestic pigs during cardiac arrest produced by ventricular fibrillation and during cardiopulmonary resuscitation (CPR). The great cardiac vein PCO2 increased from a control value of 52 +/- 2 to 132 +/- 28 (SD) Torr during CPR, whereas the arterial PCO2 was unchanged (39 +/- 4 vs. 38 +/- 4). The coronary venoarterial PCO2 gradient, therefore, increased remarkably from 13 +/- 2 to 94 +/- 29 Torr. The simultaneously measured great cardiac vein lactate concentrations increased from 0.24 +/- 0.06 to 7.3 +/- 2.34 mmol/l. Much more moderate increases in the lactate content of aortic blood from 0.64 +/- 0.25 to 2.56 +/- 0.27 mmol/l were observed. Increases in great cardiac vein PCO2 and lactate were highly correlated during CPR (r = 0.91). After successful CPR, the coronary venoarterial PCO2 gradient returned to normal levels within 2 min after restoration of spontaneous circulation. Lactate content was rapidly reduced and lactate extraction was reestablished within 30 min after CPR. These studies demonstrate marked but reversible acidosis predominantly as the result of myocardial CO2 production during CPR.

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