A Comparison of the Ventilatory Response to Carbon Dioxide by Steady-State and Rebreathing Methods during Metabolic Acidosis and Alkalosis

1973 ◽  
Vol 45 (2) ◽  
pp. 239-249 ◽  
Author(s):  
R. A. F. Linton ◽  
P. A. Poole-Wilson ◽  
R. J. Davies ◽  
I. R. Cameron
Keyword(s):  
Carbon Dioxide ◽  
Steady State ◽  
Metabolic Acidosis ◽  
Normal Subjects ◽  
Respiratory Response ◽  
Acid Base ◽  
Co2 Response ◽  
Significant Change ◽  
Response Line ◽  
Rebreathing Methods

1. The rebreathing and steady-state methods for assessing the response to inhaled carbon dioxide were compared in six normal subjects under control conditions and during metabolic acidosis and alkalosis. 2. The slopes of the CO2 response lines obtained with the two methods under control conditions were not significantly different. 3. Metabolic acidosis and alkalosis produced a significant change in the intercept of the response line when this was assessed with the steady-state technique. The slope of the response lines did not change significantly in alkalosis but there was probably a small increase during acidosis. 4. Using the rebreathing technique there was no significant change in intercept in acidosis and alkalosis, but the slope varied significantly from control values. 5. It is concluded that the two methods of assessing the respiratory response to inhaled CO2 are comparable under normal acid-base conditions. This similarity does not hold in metabolic changes of the acid-base state.

Stability of cerebrospinal fluid pH in chronic acid-base disturbances in blood

1965 ◽  
Vol 20 (3) ◽  
pp. 443-452 ◽  
Author(s):  
R. A. Mitchell ◽  
C. T. Carman ◽  
J. W. Severinghaus ◽  
B. W. Richardson ◽  
M. M. Singer ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Active Transport ◽  
Respiratory Acidosis ◽  
Normal Subjects ◽  
Respiratory Alkalosis ◽  
Regulation Of Respiration ◽  
Respiratory Drive ◽  
Acid Base ◽  
Peripheral Chemoreceptors ◽  
Mean Values

In chronic acid-base disturbances, CSF pH was generally within the normal limits (7.30–7.36 units, being the range including two standard deviations of 12 normal subjects). The mean values of CSF and arterial pHH, respectively, were: 1) metabolic alkalosis, 7.337 and 7.523; 2) metabolic acidosis, 7.315 and 7.350; 3) respiratory alkalosis, 7.336 and 7.485; and 4) respiratory acidosis (untreated), 7.314 and 7.382. Other investigators report similar values. The constancy of CSF pH cannot be explained by a poorly permeable blood-CSF barrier in chronic metabolic acidosis and alkalosis, nor can it be explained by respiratory compensation. It cannot be explained by renal compensation in respiratory alkalosis (high altitude for 8 days), although it may be explained by renal compensation in respiratory acidosis. The former three states suggest that active transport regulation of CSF pH is a function of the blood-CSF barrier. Since CSF pH is constant, so also must that portion of the respiratory drive originating in the superficial medullary respiratory chemoreceptors be constant. Ventilation changes in chronic acid-base disturbances thus may result from changes in the activity of peripheral chemoreceptors, in response to changes in arterial pH, arterial PO2, and possibly in neuromuscular receptors. regulation of respiration; medullary respiratory; chemoreceptors; peripheral chemoreceptors; metabolic acidosis and alkalosis; respiratory acidosis and alkalosis; active transport; blood-brain barrier; pregnancy Submitted on July 27, 1964

Respiratory Response to Carbon Dioxide after Propranolol in Normal Subjects

Respiration ◽  
1979 ◽  
Vol 37 (4) ◽  
pp. 197-200 ◽  
Author(s):  
E. Bosisio ◽  
M. Sergi ◽  
R. Sega ◽  
A. Libretti
Keyword(s):  
Carbon Dioxide ◽  
Normal Subjects ◽  
Respiratory Response

The Respiratory Response to Inhaled Carbon Dioxide in Man after 3 Hours Exposure to 3% Carbon Dioxide

1978 ◽  
Vol 55 (3) ◽  
pp. 309-316
Author(s):  
K. Prowse ◽  
C. Duvivier ◽  
R. Peslin ◽  
P. Sadoul
Keyword(s):  
Carbon Dioxide ◽  
Response Curve ◽  
Minute Ventilation ◽  
Control Period ◽  
Respiratory Pattern ◽  
Significant Shift ◽  
Respiratory Response ◽  
Response Curves ◽  
Significant Change ◽  
Acclimatization Period

1. The respiratory response to inhaled 3% and 6% CO2 was measured in 10 normal subjects after a 3 h acclimatization period to 3% CO2 in an environmental chamber. Control studies were carried out after a 3 h period of breathing air in the chamber. 2. At the end of the acclimatization period studies were carried out during 20 min periods breathing 3% CO2, 6% CO2 and air. 3. At 2-min intervals during the studies measurements were made of tidal volume (Vt), breathing frequency (fR), minute ventilation (V̇e), viscous pulmonary rate of work (Ẇp) and total viscous rate of work across the lungs and apparatus (Ẇt). Blood gas tensions were measured at the end of this period. 4. After acclimatization to 3% CO2 there was a significant shift in the response curves V̇e/Pa,co2 and Ẇt/Pa,co2 such that subjects showed higher Pa,co2 values for given values of V̇e or Ẇt. There was no significant change in the slope of the response curves. 5. No correlation was found between the slope of the response curve after the control period breathing air and the degree of shift of the response curve. 6. There was no difference in respiratory pattern or in pulmonary resistance. 7. Similar results were found in two subjects studied after 24 h acclimatization to 3% CO2 but one subject also showed a significant change in the slope of the V̇e/Pa,co2 curve.

The Effect of Bendrofluazide and Frusemide on the Ventilatory Response to Carbon Dioxide and Hypoxia in Normal Man

1974 ◽  
Vol 47 (4) ◽  
pp. 377-385 ◽  
Author(s):  
A. G. Leitch ◽  
L. Clancy ◽  
D. C. Flenley
Keyword(s):  
Ventilatory Response ◽  
Normal Subjects ◽  
Co2 Response ◽  
Acute Exacerbations ◽  
Before And After ◽  
Ventilatory Failure ◽  
End Tidal ◽  
Response Line ◽  
The Right ◽  
End Tidal Co2

1. We have determined the ventilatory response to CO2 at two levels of end-tidal O2 tension in eight normal subjects before and after (1) 4 days of 0.242 mmol (80 mg) oral frusemide daily and (2) 4 days of 0.024 mmol (10 mg) bendrofluazide daily. 2. Frusemide produced no significant alkalosis, change in end-tidal CO2 tension or alteration in the CO2 response line. However, we did demonstrate a linear relationship between the change in plasma total CO2 content and the change in intercept of the CO2 response line in hyperoxia after frusemide. 3. Bendrofluazide produced a metabolic alkalosis with no significant change in end-tidal CO2 tension. The CO2 response line after the drug showed a decrease in slope in hyperoxia and a shift to the right of the intercept in hypoxia. There was no relationship between change in plasma total CO2 content and change in the intercept of the CO2 response line in hyperoxia. 4. If these results obtained on normal subjects are applicable to patients with chronic bronchitis and emphysema, frusemide might be the diuretic of choice for use with controlled oxygen therapy in the management of acute exacerbations of this disease when it is complicated by ventilatory failure.

scholarly journals ANALYSIS OF THE RESPIRATORY RESPONSE TO CARBON DIOXIDE INHALATION IN VARYING CLINICAL STATES OF HYPERCAPNIA, ANOXIA, AND ACID-BASE DERANGEMENT

1955 ◽  
Vol 34 (4) ◽  
pp. 511-532 ◽  
Author(s):  
James K. Alexander ◽  
John R. West ◽  
John A. Wood ◽  
Dickinson W. Richards
Keyword(s):  
Carbon Dioxide ◽  
Respiratory Response ◽  
Acid Base

scholarly journals Effect of growth hormone on renal and systemic acid-base homeostasis in humans

1998 ◽  
Vol 274 (4) ◽  
pp. F650-F657 ◽  
Author(s):  
Anita Sicuro ◽  
Katia Mahlbacher ◽  
Henry N. Hulter ◽  
Reto Krapf
Keyword(s):  
Growth Hormone ◽  
Metabolic Acidosis ◽  
Recombinant Human Growth Hormone ◽  
Human Growth ◽  
Normal Subjects ◽  
Acid Excretion ◽  
Bicarbonate Concentration ◽  
Acid Base ◽  
Plasma Bicarbonate ◽  
Net Acid Excretion

The effects of recombinant human growth hormone (GH, 0.1 U ⋅ kg body wt−1 ⋅ 12 h−1) on systemic and renal acid-base homeostasis were investigated in six normal subjects with preexisting sustained chronic metabolic acidosis, induced by NH4Cl administration (4.2 mmol ⋅ kg body wt−1 ⋅ day−1). GH administration increased and maintained plasma bicarbonate concentration from 14.1 ± 1.4 to 18.6 ± 1.1 mmol/l ( P < 0.001). The GH-induced increase in plasma bicarbonate concentration was the consequence of a significant increase in net acid excretion that was accounted for largely by an increase in renal [Formula: see text]excretion sufficient in magnitude to override a decrease in urinary titratable acid excretion. During GH administration, urinary pH increased and correlated directly and significantly with urinary[Formula: see text] concentration. Urinary net acid excretion rates were not different during the steady-state periods of acidosis and acidosis with GH administration. Glucocorticoid and mineralocorticoid activities increased significantly in response to acidosis and were suppressed (glucocorticoid) or decreased to control levels (mineralocorticoid) by GH. The partial correction of metabolic acidosis occurred despite GH-induced renal sodium retention (180 mmol; gain in weight of 1.8 ± 0.2 kg, P< 0.005) and decreased glucocorticoid and mineralocorticoid activities. Thus GH (and/or insulin-like growth factor I) increased plasma bicarbonate concentration and partially corrected metabolic acidosis. This effect was generated in large part by and maintained fully by a renal mechanism (i.e., increased renal NH3 production and[Formula: see text]/net acid excretion).

Chemosensitivity in normal subjects, athletes, and patients with chronic airways obstruction

1971 ◽  
Vol 30 (2) ◽  
pp. 193-199 ◽  
Author(s):  
Simon Godfrey ◽  
Richard H. T. Edwards ◽  
Grahame M. Copland ◽  
Peter L. Gross
Keyword(s):  
Normal Subjects ◽  
Response Curves ◽  
Co2 Response ◽  
Airways Obstruction ◽  
Ventilatory Capacity ◽  
The Difference ◽  
Short Time ◽  
Co2 Response Curve ◽  
Rebreathing Methods ◽  
Maximal Voluntary Ventilation

Studies of CO2 and O2 sensitivity have been made using rebreathing methods in normal subjects, athletes, and patients with and without chronic airways obstruction. The rebreathing techniques enabled isoxic CO2 response curves and isocapnic O2 response curves to be constructed from many points obtained over a short time. There was little difference in response among the groups of normal subjects but the patients with lung disease had a flatter CO2 response curve and required lower levels of Po2 to stimulate ventilation. When ventilation was expressed as a fraction of the maximal voluntary ventilation, much of the difference between normal subjects and chest patients disappeared, suggesting that the reduced ventilatory response may be of mechanical origin. There remained some patients who were truly insensitive to one or both stimuli and they appeared to be those whose clinical condition was poorest. rebreathing techniques; isoxic CO2 sensitivity; isocapnic O2 sensitivity; relation to ventilatory capacity; insensitivity of some patients

Ventilatory responses to inhaled carbon dioxide at rest and during exercise in man

1987 ◽  
Vol 73 (2) ◽  
pp. 177-182 ◽  
Author(s):  
Margaret S. Jacobi ◽  
Vincent I. Iyawe ◽  
Chandu P. Patil ◽  
Andrew R. C. Cummin ◽  
Kenneth B. Saunders
Keyword(s):  
Steady State ◽  
Time Course ◽  
Breathing Circuit ◽  
Normal Subjects ◽  
Co2 Response ◽  
Ventilatory Responses ◽  
Mixing Chamber ◽  
Inspiratory Limb ◽  
End Tidal ◽  
Mean Alveolar Pco2

1. Rapid steady-state CO2 responses were determined in six normal subjects at rest and five subjects at four different work loads up to 125 W, by injecting pure CO2 at constant flow into a small mixing chamber in the inspiratory limb of a breathing circuit. 2. The time course of the response of ventilation (V) and mean alveolar Pco2 (Paco2) was checked in separate experiments, where the flow rate of injected CO2 was changed abruptly and the effects were followed for 10 min. 3. V and Paco2 were measured every breath, and the results ensemble-averaged for each subject (two or three runs per subject) and then for the groups as a whole, in 30 s or 60 s time bins. 4. Paco2 during exercise was estimated by graphical reconstruction from the sloping alveolar plateau, and separately by the empirical equation of Jones, Robertson & Kane [1]. At rest, Paco2 was assumed equal to end-tidal Pco2 (Petco2). 5. With the constant inflow technique, 4 min was required to reach steady-state V and Paco2 during exercise, and 6 min at rest. 6. At rest, with 4 min steps (doubtful steady state) the averaged CO2 response was concave up. With 6 min steps the response was almost linear. In neither case was the deviation from linearity statistically significant. 7. During exercise, the averaged CO2 responses were essentially isocapnic at work loads greater than 75 W with either method of deriving Paco2.

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