Rate of Production of Carbon Dioxide in Patients with a Severe Degree of Metabolic Acidosis

Kamel, Kamel S.; Richardson, Robert; Goguen, Jeannette; Fine, Adrian; Levin, Adeera; Halperin, Mitchell L.

doi:10.1159/000187393

Cited by 3 publications

(3 citation statements)

References 10 publications

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“…However, several probable explanations can be offered: first, severe aci demia may lead to progressive respiratory muscle fatigue; second, maximally increased muscular activity of respira tory muscles per se may increase CO2 production [20]; and third (least likely), severe acidemia might paradoxi cally decrease respiratory drive. Certainly, it is common to observe patients with severe 'air hunger' to become fatigued.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of Ventilatory Responses in Severe Acidemia in Diabetic Ketoacidosis

Guh

Lai

et al. 1997

Am J Nephrol

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Ventilatory response in patients with severe acidemia in diabetic ketoacidosis (DKA) was unresolved. Thus, 83 patients with uncomplicated DKA were studied for the relation between arterial blood pH, calculated bicarbonate concentration (HCO3) and carbon dioxide tension (PCO₂). The equation for the PCO₂/HCO₃ pair was: PCO₂ =1.58 × HCO₃ + 7.6 (SE 2.55, r = 0.95, p < 0.01); for the PCO₂/pH pair was: PC0₂ = 43.8 × pH-293 (SE 6.23, r = 0.66, p < 0.01). The correlation coefficient for the PCO₂/HCO₃ pair was significantly greater compared to the PCCVpH pair (p < 0.001). Multiple regression analysis showed that severe acidemia (pH ≤ 7.10) per se was independently associated with PCO₂ for the PCO₂/HCO₃ pair, but not for the PCO₂/pH pair. Thus, our patients were divided into 2 groups for the PCO₂/HCO₃ pair: group 1 with pH < 7.10 (n = 25) and group 2 with pH > 7.10 (n = 58). The equations were: group 1: PCO₂ = 3.18 × HCO3 + 2.88 (SE 1.72, r = 0.87, p < 0.01); group 2: PCO₂ = 1.65 × HCO₃ + 6.6 (SE 2.6, r = 0.95, p < 0.01). There was a significant difference between these 2 equations (p < 0.01). Mathematical simulations with 10 sets of 25 or 58 random pH/PCO₂ pairs (and calculated HCO₃) for ‘group 1’ and ‘group 2’ also showed similar results, albeit with less precision. Hence, ventilatory response in DKA varies between patients with severe acidemia and those with moderate acidemia by the PCO₂/HCO₃ pair, but not by the PCO₂/pH pair.

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Section: Discussionmentioning

confidence: 99%

Evaluation of Ventilatory Responses in Severe Acidemia in Diabetic Ketoacidosis

Guh

Lai

et al. 1997

Am J Nephrol

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“…If brain work were to decline (due to a state of confusion, coma, head trauma, hypothermia, hypothyroidism, drug ingestion such as sedatives including ethanol, and during general anesthesia), the degree of ketoacidosis might become significantly more severe [22, 23]. In quantitative terms, if coma were to reduce cerebral oxygen consumption by 50% [22], the ability of the brain to remove ketoacids would fall by as much as 400 mmol/day, a value that is close to the total HCO 3 – pool size in the ECF compartment of a 70-kg normal adult.…”

Section: Concept 1: H+ Are Added To the Body When There Is A Net Incrmentioning

confidence: 99%

“…For example, hypothermia is a not an infrequent finding in this setting (lower metabolic rate). There could also be a lower rate of CO 2 production in the brain (confused mental state) [22], the kidneys (lower GFR) [16], the liver (ketogenesis, the major hepatic metabolic pathway for ATP regeneration in this setting does not produce CO 2 ) [20], and in muscle (less activity) [23]. …”

Section: Concept 2: Buffering Of H+ Is Beneficial If H+ Bind To Hco3–mentioning

confidence: 99%

A Conceptual Approach to the Patient with Metabolic Acidosis

Shafiee

Kamel²,

Halperin³

2002

Nephron

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We shall illustrate that management of patients with an acid-base disorder could be improved if the acid-base analysis was based on a better understanding of basic concepts of physiology. Three concepts of acid-base physiology and their clinical implications are emphasized in a patient with diabetic ketoacidosis. First, when an acid is produced from neutral precursors in the body, there is a net increase in the number of hydrogen ions (H⁺) and new anions. The corollary is that H⁺ will be removed when the accompanying anion is metabolized to a neutral end-product or is excreted in the urine with H⁺ or ammonium (NH₄⁺). Second, buffering of H⁺ is beneficial if H⁺ are removed by bicarbonate rather than being able to bind to proteins. This latter function depends on having a low tissue PCO₂, due to a combination of hyperventilation plus an adequate blood flow rate to vital organs. Third, the kidneys add new bicarbonate to the body when NH₄⁺ is excreted with chloride ions.

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Alcoholic ketoacidosis: Emphasis on biochemical, metabolic and quantitative aspects

Kamel

1997

Geriatric Nephrol Urol

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Rate of Production of Carbon Dioxide in Patients with a Severe Degree of Metabolic Acidosis

Cited by 3 publications

References 10 publications

Evaluation of Ventilatory Responses in Severe Acidemia in Diabetic Ketoacidosis

Evaluation of Ventilatory Responses in Severe Acidemia in Diabetic Ketoacidosis

A Conceptual Approach to the Patient with Metabolic Acidosis

Alcoholic ketoacidosis: Emphasis on biochemical, metabolic and quantitative aspects

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