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

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.

1993 ◽  
Vol 75 (1) ◽  
pp. 285-293 ◽  
Author(s):  
J. Qvist ◽  
W. E. Hurford ◽  
Y. S. Park ◽  
P. Radermacher ◽  
K. J. Falke ◽  
...  

Korean female unassisted divers (cachido ama) breath-hold dive > 100 times to depths of 3–7 m during a work day. We sought to determine the extent of arterial hypoxemia during normal working dives and reasonable time limits for breath-hold diving by measuring radial artery blood gas tensions and pH in five cachido ama who dove to a fixed depth of 4–5 m and then continued to breath hold for various times after their return to the surface. Eighty-two blood samples were withdrawn from indwelling radial artery catheters during 37 ocean dives. We measured compression hyperoxia [arterial PO2 = 141 +/- 24 (SD) Torr] and hypercapnia (arterial PCO2 = 46.6 +/- 2.4 Torr) at depth. Mean arterial PO2 near the end of breath-hold dives lasting 32–95 s (62 +/- 14 s) was decreased (62.6 +/- 13.5 Torr). Mean arterial PCO2 reached 49.9 +/- 5.4 Torr. Complete return of these values to their baseline did not occur until 15–20 s after breathing was resumed. In dives of usual working duration (< 30 s), blood gas tensions remained within normal ranges. Detailed analysis of hemoglobin components and intrinsic oxygenation properties revealed no evidence for adaptive changes that could increase the tolerance of the ama to hypoxic or hypothermic conditions associated with repetitive diving.


1984 ◽  
Vol 57 (6) ◽  
pp. 1704-1709 ◽  
Author(s):  
C. J. Allen ◽  
N. L. Jones ◽  
K. J. Killian

Changes in expired alveolar O2 and CO2 were measured breath-by-breath in six healthy male subjects (mean age 30 yr, mean weight 80 kg) at rest, 600 kpm/min, and 1,200 kpm/min. Changes were expressed in relation to expired volume (liters) and time (s) and separated into an initial dead-space component using the Fowler method applied to expired CO2 and O2, and alveolar slope. The alveolar slopes with respect to time (dPACO2, dPAO2, Torr/s) increased in relation to CO2 output (VCO2, 1/min, STPD) and O2 intake (VO2, 1/min, STPD) but were reduced by increasing tidal volume (VT, liters, BTPS): dPACO2 = 2.7 + 4.6(VCO2) - 1.9(VT) (r = 0.97); and dPAO2 = 2.3 + 5.5(VO2) - 1.9(VT) (r = 0.96). From the alveolar slopes, tidal volume, and airway dead-space volume, mean expired alveolar PO2 and PCO2 (PAO2, PACO2) were calculated. There was no change in arterialized capillary PCO2 (PaCO2) between rest (38.9 +/- 0.66 Torr) and heavy exercise (38.2 +/- 2.18 Torr), but mean PACO2 rose from 36.7 +/- 0.55 to 40.8 +/- 1.67 Torr during heavy exercise. There was no change in arterialized capillary (mean = 84.3 +/- 0.7 Torr) or alveolar (mean = 107.2 +/- 1.03 Torr) PO2. Exercise increases the fluctuations in alveolar gas composition leading to discrepancies between the PCO2 in mean alveolar gas and arterial blood to an extent that is dependent on VCO2 and VT.


1994 ◽  
Vol 76 (1) ◽  
pp. 120-126 ◽  
Author(s):  
C. Prefaut ◽  
F. Anselme ◽  
C. Caillaud ◽  
J. Masse-Biron

To determine whether exercise induces hypoxemia in highly trained older “master” athletes (MA), as it does in certain elite endurance-trained young athletes (YA), 10 MA (65.3 +/- 2.6 yr), 10 control subjects (CS; 68.3 +/- 2.2 yr), and 10 endurance-trained YA (23.3 +/- 1.1 yr) performed an incremental exercise test. During testing, blood samples for arterial blood gas analysis were drawn during the last 20 s of each load. Lung exchanges were measured using a breath-by-breath automated exercise device. Exercise-induced hypoxemia (EIH) appeared in all MA and 8 of 10 YA, whereas there were no changes in the blood gases of CS. In MA, arterial PO2 decreased significantly from 40% of maximal O2 uptake onward and was associated with a significant increase in the ideal alveolar-arterial O2 difference from 60% onward. The MA also showed a lower ventilation for a given absolute load compared with CS. In all subjects arterial PCO2 rose slightly but significantly during the work, but this increase was most marked in MA. The EIH differed between MA and YA in the following ways: 1) all MA showed a drop in arterial PO2 during exercise, 2) this drop appeared earlier and was significantly greater for a given load in MA, and 3) EIH appeared at a lower level of training regimen in MA. This hypoxemia was at first isolated, probably at least partially due to relative hypoventilation, and then was associated with a widened ideal alveolar-arterial O2 difference, which may have been due to an increase in extravascular lung water.(ABSTRACT TRUNCATED AT 250 WORDS)


1991 ◽  
Vol 70 (4) ◽  
pp. 1796-1809 ◽  
Author(s):  
S. L. Adamson ◽  
I. M. Kuipers ◽  
D. M. Olson

The role of umbilical cord occlusion in the initiation of breathing at birth was investigated by use of 16 unanesthetized fetal sheep near full term. Artificial ventilation with high-frequency oscillation was used to control fetal arterial blood gas tensions. At baseline, PCO2 was maintained at control fetal values and PO2 was elevated to between 25 and 50 Torr. In the first study on six intact and four vagotomized fetuses, arterial PCO2 and PO2 were maintained constant during two 30-min periods of umbilical cord occlusion. Nevertheless, the mean fetal breathing rate increased significantly when the umbilical cord was occluded. In the second study on six intact fetuses, hypercapnia (68 Torr) was imposed by adding CO2 to the ventilation gas. When the umbilical cord was occluded, there was a significantly greater stimulation of breathing (rate, incidence, and amplitude) in response to hypercapnia than in response to hypercapnia alone. During cord occlusion, plasma prostaglandin E2 concentration decreased significantly. Results indicate that cord occlusion stimulates breathing possibly by causing the removal of a placentally produced respiratory inhibitor such as prostaglandin E2 from the circulation.


1986 ◽  
Vol 61 (2) ◽  
pp. 599-602 ◽  
Author(s):  
P. S. Clifford ◽  
J. T. Litzow ◽  
R. L. Coon

Previous investigators have assumed that during exercise there is a tight coupling of ventilation with CO2 delivery to the lungs such that arterial blood remains isocapnic. We measured arterial blood gases in a group of 10 beagle dogs in which arterial blood sampling could be accomplished via exteriorized carotid artery loops and in six of the same dogs following chronic pulmonary denervation. Samples were taken at rest, at 15-s intervals during the first minute of unrestrained treadmill exercise at 5.0 km/h, 0% grade, and then at 2 and 3 min at the same work load. Mean resting arterial PCO2 for the control dogs was 37.1 Torr. At the onset of exercise arterial PCO2 fell progressively to a nadir of 34.6 Torr during the 30- to 45-s sampling period. Samples at 2 and 3 min remained significantly hypocapnic (PCO2 = 34.8 Torr). The arterial PCO2 and pH responses to exercise in the lung-denervated dogs were not significantly different from those of the control dogs, although arterial PO2 was lower at rest and during exercise following denervation of the lungs. The arterial hypocapnia exhibited in intact beagle dogs at the onset of exercise persists into the steady state and suggests that there is not a tight coupling of ventilation with pulmonary CO2 delivery. The similarity of the response in lung-denervated dogs suggests that intrapulmonary receptors with afferents in the vagi are not the primary mediators of the ventilatory response to exercise.


PEDIATRICS ◽  
1965 ◽  
Vol 35 (1) ◽  
pp. 20-26
Author(s):  
Norman S. Talner ◽  
S. K. Sanyal ◽  
Katherine H. Halloran ◽  
Thomas H. Gardner ◽  
Nelson K. Ordway

Studies of arterial blood gases and acid-base equilibrium in twenty infants in congestive heart failure have revealed the following alterations: (1) elevation of arterial Pco2, (2) diminution of arterial Po2, (3) lowered pH. These findings demonstrate the presence of respiratory insufficiency in infants with pulmonary congestion and cardiac decompensation. Studies of serum electrolytes have shown in some infants a hyponatremia and hypochloremia present prior to the use of therapeutic agents and these alterations may influence response to digitalis and diuretic agents.


Healthcare ◽  
2021 ◽  
Vol 9 (1) ◽  
pp. 74
Author(s):  
Pietro Elias Fubini ◽  
Laurent Suppan

Shortness of breath is a common complaint among patients in emergency medicine. While most common causes are usually promptly identified, less frequent aetiologies might be challenging to diagnose, especially in the pre-hospital setting. We report a case of prehospital dyspnoea initially ascribed to pulmonary oedema which turned out to be the result of profound metformin-associated metabolic acidosis. This diagnosis was already made during the prehospital phase by virtue of arterial blood gas measurement. Pre-hospital measurement of arterial blood gases is therefore feasible and can improve diagnostic accuracy in the field, thus avoiding unnecessary delay and potential harm to the patient before initiating the appropriate therapeutic actions.


Arterial blood gas (ABGs) analysis forms the cornerstone of emergency respiratory investigation. In many situations values obtained dictate management strategy and facilitate decision-making. It is an uncomfortable procedure for the patients and if repeated ABGs are required, consider whether less invasive measures, such as respiratory rate, pulse oximetry or capillary blood gas measurements could be used....


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