Effects of bicarbonate therapy on tissue oxygenation during resuscitation of hemorrhagic shock

Mäkisalo, H.; Soini, H.; Nordin, Arno; Höckerstedt, K

doi:10.1097/00003246-198911000-00014

Cited by 20 publications

(3 citation statements)

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“…Bicarbonate therapy during resuscitation after hemorrhagic shock resulted in a delayed increase in subcutaneous oxygen tension and decreased arterial oxygen tension in a study in pigs by Mäkisalo et al [38]. Their findings, which are similar to the findings in the present study, were also attributed to the Bohr effect.…”

Section: Discussionsupporting

confidence: 91%

Evaluation of Subcutaneous Tissue Gases and pH during Induction of Acidosis and Alkalosis

Mellström

Jedlinska²,

Hartmann³

et al. 2001

Eur Surg Res

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Peripheral tissue oxygen utilization was studied during hypoxic-induced acidosis and sodium bicarbonate-induced alkalosis in 8 domestic pigs by measurements of subcutaneous oxygen tension (P_scO₂), carbon dioxide tension (P_scCO₂) and pH (pH_sc) in relation to central hemodynamic parameters and oxygenation. Hypoxic-induced acidosis resulted in a decrease in P_scCO₂ and arterial oxygen tension (P_aO₂) to one third of baseline values (p < 0.05), an increase in P_scCO₂ and arterial carbon dioxide tension (P_aCO₂) from 41 to 55 and 34 to 39 mm Hg, respectively (p < 0.05), and a decrease in pH_sc from 7.47 to 7.30 (p < 0.05). P_scO₂ and P_aO₂ increased during reversal of hypoxia and infusion of bicarbonate (p < 0.05), without reaching baseline values. In parallel P_scCO₂ decreased and pH_sc increased but changes lagged behind changes in blood gases. Alkalosis established by further infusion of bicarbonate resulted in a decrease in P_aO₂ to 62 mm Hg whereas P_scO₂ remained below baseline values (p < 0.05). Correction of oxygen utilization in the subcutaneous tissue as measured by the markers P_scCO₂ and pH_sc is slower than indicated by changes in tissue oxygen tension, blood gases and pH. Overcompensation of acidosis with bicarbonate resulting in alkalosis impairs oxygenation.

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Section: Discussionsupporting

confidence: 91%

Evaluation of Subcutaneous Tissue Gases and pH during Induction of Acidosis and Alkalosis

Mellström

Jedlinska²,

Hartmann³

et al. 2001

Eur Surg Res

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“…In a porcine model of haemorrhagic shock, bicarbonate delayed increases in tissue PO 2 , and delayed falls in plasma lactate 58. This study used small patient numbers, and repeated measures over time, but analysed differences in the data at time intervals that were not predetermined.…”

Section: Management Of Lactic Acidosismentioning

confidence: 99%

Dysoxia and lactate

Duke

1999

Archives of Disease in Childhood

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Disturbances of oxygen supply or cellular oxygen metabolism are common in critically ill patients. An understanding of dysoxia, or oxygen limited energy depletion, requires an understanding of the normal physiology of cell oxygen metabolism, and the compensatory mechanisms that supply high energy molecules under conditions of hypoxia. Understanding disorders associated with hyperlactataemia requires consideration of the cellular response in dysoxia, and pathology specific derangements in lactate metabolism. Much has recently been discovered about the causes of lactic acidosis in sepsis, and about the role of lactate in monitoring critically ill children.This review discusses how cells produce energy for metabolism under normal and hypoxic conditions; what happens to lactate produced during these processes; the clinical situations in which lactic acidosis has been described; the reasons why excess lactate may occur in sepsis; the evidence that a high lactate concentration is not simply a surrogate for tissue dysoxia; the relevance of lactate in the management of critically ill children; and suggested strategies to manage high blood lactate. Normal cellular oxygen metabolismCells require oxygen for the production of ATP, the principal energy source. ATP is hydrolysed to ADP and high energy phosphate by adenosine triphosphatases in the cytosol. Energy released is used for the maintenance of membrane integrity, ionic pumps, and other specialised functions, such as contractility of muscle cells, and impulse transmission in neurons. The body's stores of ATP will last no more than a few minutes, so it must be synthesised continuously as it is being used. Under physiological conditions, most ATP is generated from the metabolism of glucose, by the process of oxidative phosphorylation. The first stage of oxidative phosphorylation is the conversion of glucose to pyruvic acid; this occurs in the cytoplasm. The second stage, the oxidation of pyruvic acid, can only occur in the mitochondria as part of the Krebs (citric acid) cycle. Oxidative phosphorylation produces a net 36 molecules of ATP (or 1270 kJ of available energy) for every glucose molecule oxidised.Under normal conditions some tissues, such as myocytes, preferentially use free fatty acids, rather than glucose, as the substrate for ATP generation. In myocytes, palmitate forms about 60% of the total substrate metabolised, glucose 10%, and lactate 30%. During cellular hypoxia the consumption of lactate ceases, and that of glucose increases to 90% of the total substrate consumed.2 The brain, on the other hand, under any conditions can use only glucose or ketone bodies for ATP production. Thresholds of hypoxia and cell (dys)functionOxidative phosphorylation can only occur when the partial pressure of oxygen (PO 2 ) within the mitochondrion is above a critical level, thought to be in the order of 1 mm Hg (0.13 kPa).3 Although the PO 2 of dry air at sea level is 159 mm Hg, and the alveolar PO 2 is about 100 mm Hg, the mean capillary blood PO 2 is 50 mm Hg. From the capill...

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“…Others have reported similar findings. 19 Indeed, bicarbonate therapy actually delays the removal of ketone bodies from the blood.…”

Section: Diabetic Ketoacidosismentioning

confidence: 99%

Bicarbonate Therapy in Severe Metabolic Acidosis

Sabatini¹,

Kurtzman²

2009

Journal of the American Society of Nephrology

107

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The utility of bicarbonate administration to patients with severe metabolic acidosis remains controversial. Chronic bicarbonate replacement is obviously indicated for patients who continue to lose bicarbonate in the ambulatory setting, particularly patients with renal tubular acidosis syndromes or diarrhea. In patients with acute lactic acidosis and ketoacidosis, lactate and ketone bodies can be converted back to bicarbonate if the clinical situation improves. For these patients, therapy must be individualized. In general, bicarbonate should be given at an arterial blood pH of < or =7.0. The amount given should be what is calculated to bring the pH up to 7.2. The urge to give bicarbonate to a patient with severe acidemia is apt to be all but irresistible. Intervention should be restrained, however, unless the clinical situation clearly suggests benefit. Here we discuss the pros and cons of bicarbonate therapy for patients with severe metabolic acidosis.

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Effects of bicarbonate therapy on tissue oxygenation during resuscitation of hemorrhagic shock

Cited by 20 publications

References 0 publications

Evaluation of Subcutaneous Tissue Gases and pH during Induction of Acidosis and Alkalosis

Evaluation of Subcutaneous Tissue Gases and pH during Induction of Acidosis and Alkalosis

Dysoxia and lactate

Bicarbonate Therapy in Severe Metabolic Acidosis

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