Carbon Dioxide Titration Curve of Normal Man

Brackett, Newton C.; Cohen, Jordan J.; Schwartz, William B.

doi:10.1056/nejm196501072720102

Cited by 291 publications

(37 citation statements)

References 12 publications

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“…1. Over the range studied this relationship appears to be linear, in agreement with the observations of Barcroft, Bock, Hill, Parsons, Parsons and Shoji (1922); Cohen et al (1964) and Brackett et al (1965). For each patient Williams (1959).…”

Section: Resultssupporting

confidence: 89%

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THE IN VIVO CARBON DIOXIDE TITRATION CURVE IN MAN DURING REBREATHINC

Despas

Leigh

1970

Aust J Exp Biol Med

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Summary. The in vivo titration curve of CO, measured in five subjects during rebreathing of 7% COg in O2 for 3 minutes was not significantly different from the corresponding in vitro titration curve measured on arterial blood from each subject. The buffering of COg m vivo when measured by other methods is known to be less than it is in vitro. COj in vivo is thought to equilibrate with a well buffered compartment (intravascular) and a poorly buffered compartment (interstitial fiuid). It has been suggested that HCO3-shift takes place from the intravascular compartment. During rebreathing there may be insufficient time for HCO3-shift to occur. This would explain the identical COg titration curves in vivo and in vitro shown by this study. INTRODUGTION.The GO2 titration curve of whole blood in vivo has been obtained by exposing normal man and dogs to progressively higher levels of inspired GOî n the presence of normoxia, hyperoxia and hypoxia (Gohen, Brackett and Sehwartz, 1964; Brackett, Gohen and Schwartz, 1965; Brown and Glancy, 1965;Michel, Lloyd and Gunningham, 1966; Mithoefer, Karetzky and Porter, 1968). With these methods GO2 titration curves are constructed from measurements on blood samples after equilibration of GO2, H+ and HGOs" in intracellular, interstitial and intravascular compartments has taken place. The resulting GO2 titration curves are different from the in vitro GOo titration curves of whole blood. The HGOa" concentration is less than predicted from the in vitro GO2 curve. It is thought that loss of HGO,,-from blood to interstitial fluid takes place (Shaw and Messer, 1932;Michel et al, 1966). This paper reports the GO2 titration curve in man of whole blood in vivo obtained during rebreathing of 7% GO2 in O2 (Read, 1967). During rebreathing a rapid and progressive increase of arterial H+ and arterial PCO2 occurs. The rate of increase of arterial PCO2 is about 6 mm. Hg./min. A comparison of this in vivo curve with the corresponding in vitro GO2 titration curve enables certain inferences about the rate of HGO3"" exchange to be made. MATERIALS AND METHODS.Five male patients with obstructive lung disease (age range 15-63 years) were studied. All had been referred for assessment of respiratory function and this provided the opportunity

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Section: Resultssupporting

confidence: 89%

“…Shaw and Messer (1932) showed that the CO2 combining capacity of blood from dogs breathing GO2 enriched mixtures was lower than that observed in blood exposed to the same PCO2 in vitro. This finding has been repeatedly confirmed by similar studies in man (Brackett et al, 1965 andMichel et al, 1966).…”

Section: Resultssupporting

confidence: 82%

THE IN VIVO CARBON DIOXIDE TITRATION CURVE IN MAN DURING REBREATHINC

Despas

Leigh

1970

Aust J Exp Biol Med

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“…R e a d [18] found a range of mean slopes for normal subjects rebreathing 7 % C 0 2 between 0.55 and 0.69. These figures obtained during rebreathing are lower than those obtained by B r a ck ett et al [2] in normal subjects exposed to a constant level of C 0 2 for several minutes. The in vivo buffer lines during rebreathing are indistinguishable from those in vitro [7], probably because there is insufficient time for shifts of bicarbonate ions out of the intravascular compartment to occur.…”

Section: Discussioncontrasting

confidence: 70%

Ventilatory Responses and Acute Acid-Base Changes in Response to Inhaled Carbon Dioxide in Patients with Chronic Renal Failure on Long-Term Haemodialysis

Gibson¹,

Streeton²

1973

Respiration

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Six patients with chronic renal failure on long-term haemodialysis were studied. Measurements of acid-base status, ventilatory responses to inhaled carbon dioxide, and the ability to buffer an acute respiratory acidosis were made before and after haemodialysis The resting arterial pCO₂ values were all in the low normal range (mean 36.7, SD 1.7 mm Hg), with a mean pH of 7.37, SD 0.03. After haemodialysis, the arterial pCO⁹ values were not significantly different, despite a mean increase in pH of 0.09 units. There was no evidence of an increased sensitivity to carbon dioxide. There were no significant changes in the slopes or the intercepts of the carbon dioxide response lines following haemodialysis. After haemodialysis, the slopes of the [H⁺]/pCO₂ buffer lines were not significantly different to those obtained before haemodialysis. It would appear that the blood of these patients probably has a reduced ability to buffer an acute respiratory acidosis

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“…No discussion of acute hypercapnia studies would be complete without a brief review of some work by Bra:kett et al (4). In this study seven volunteers tolerated PIc,' of 53 mm.…”

Section: Cc~~~~imentioning

confidence: 93%

“…With one exception, no studies are reviewed with inspired Pvo. 's higher than 41 mm Hg (5.4'1), although many are available (1,2,4,8,10,53).…”

Section: Studies Symnptoms =A Poysulotagmentioning

confidence: 99%