Circumstances When Arterial Blood Gas Analysis Can Lead Us Astray

Albert, Tyler J.; Swenson, Erik R.

doi:10.4187/respcare.04556

Cited by 8 publications

(4 citation statements)

References 11 publications

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“…Such microenvironmental pH variation has been described in tumors, infection, and inflammation in other organs (12), but it has not been studied in the lung and in the context of ARDS pathophysiology. Furthermore, at an earlier stage of disease when local pH perturbations do not overwhelm systemic acid regulatory mechanisms, arterial blood pH, which is the only clinically available method to assess acid-base status, cannot sensitively or accurately reflect tissue level pH status (2,23).…”

Section: Introductionmentioning

confidence: 99%

Extrinsic acidosis suppresses glycolysis and migration while increasing network formation in pulmonary microvascular endothelial cells

Lee

Onanyan

Garrison

et al. 2019

American Journal of Physiology-Lung Cellular and Molecular Phys

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Acidosis is common among critically ill patients, but current approaches to correct pH do not improve disease outcomes. During systemic acidosis, cells are either passively exposed to extracellular acidosis that other cells have generated (extrinsic acidosis) or they are exposed to acid that they generate and export into the extracellular space (intrinsic acidosis). Although endothelial repair following intrinsic acidosis has been studied, the impact of extrinsic acidosis on migration and angiogenesis is unclear. We hypothesized that extrinsic acidosis inhibits metabolism and migration but promotes capillary-like network formation in pulmonary microvascular endothelial cells (PMVECs). Extrinsic acidosis was modeled by titrating media pH. Two types of intrinsic acidosis were compared, including increasing cellular metabolism by chemically inhibiting carbonic anhydrases (CAs) IX and XII (SLC-0111) and with hypoxia. PMVECs maintained baseline intracellular pH for 24 h with both extrinsic and intrinsic acidosis. Whole cell CA IX protein expression was decreased by extrinsic acidosis but not affected by hypoxia. When extracellular pH was equally acidic, extrinsic acidosis suppressed glycolysis, whereas intrinsic acidosis did not. Extrinsic acidosis suppressed migration, but increased Matrigel network master junction and total segment length. CRISPR-Cas9 CA IX knockout PMVECs revealed an independent role of CA IX in promoting glycolysis, as loss of CA IX alone was accompanied by decreased hexokinase I and pyruvate dehydrogenase E1α expression and decreasing migration. 2-deoxy-d-glucose had no effect on migration but profoundly inhibited network formation and increased N-cadherin expression. Thus, we report that while extrinsic acidosis suppresses endothelial glycolysis and migration, it promotes network formation.

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Section: Introductionmentioning

confidence: 99%

Extrinsic acidosis suppresses glycolysis and migration while increasing network formation in pulmonary microvascular endothelial cells

Lee

Onanyan

Garrison

et al. 2019

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…Hypothermic samples lead to spuriously higher PCO 2 , lower pH, and higher PO 2 . 4 The converse is true for hyperthermic samples. While it remains controversial as to whether temperature-corrected values should be used in clinical assessment of acid-base status, the calculation of the alveolar-arterial O 2 difference to assess pulmonary gas exchange efficiency is more accurate using the "in vivo" temperature-corrected values of PaO 2 and PaCO 2 .…”

Section: Arterial and Venous Blood Gas Analysismentioning

confidence: 99%

Arterial Blood Gases and Acid–Base Regulation

Sanghavi

Swenson

2023

Semin Respir Crit Care Med

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Disorders of acid-base status are common in the critically ill and prompt recognition is central to clinical decision making. The bicarbonate/carbon dioxide buffer system plays a pivotal role in maintaining acid-base homeostasis, and measurements of pH, PCO2, and HCO3 - are routinely used in the estimation of metabolic and respiratory disturbance severity. Hypoventilation and hyperventilation cause primary respiratory acidosis and primary respiratory alkalosis, respectively. Metabolic acidosis and metabolic alkalosis have numerous origins, that include alterations in acid or base intake, body fluid losses, abnormalities of intermediary metabolism, and renal, hepatic, and gastrointestinal dysfunction. The concept of the anion gap is used to categorize metabolic acidoses, and urine chloride excretion helps define metabolic alkaloses. Both the lungs and kidneys employ compensatory mechanisms to minimize changes in pH caused by various physiologic and disease disturbances. Treatment of acid-base disorders should focus primarily on correcting the underlying cause and the hemodynamic and electrolyte derangements that ensue. Specific therapies under certain conditions include renal replacement therapy, mechanical ventilation, respiratory stimulants or depressants, and inhibition of specific enzymes in intermediary metabolism disorders.

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“…Hypothermia may result in spuriously elevated pO2 and pCO2 whereas hyperthermia results in spuriously low pO2 and pCO2. 11 Since the analyzers measure at 37 • C some analyzers do temperature corrections. It is better to report both temperature corrected and temperature uncorrected values as the topic of temperature correction is controversial.…”

Section: **Patient's Body Temperaturementioning

confidence: 99%