Persistent, progressive hypophosphataemia after voluntary hyperventilation

PALEOLOGOS, M.; STONE, E.; BRAUDE, S.

doi:10.1042/cs19990172

Cited by 25 publications

(14 citation statements)

References 18 publications

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“…155 Serum phosphate falls within 20 min of hyperventilation and it persists for 90 min after the ventilation returns to normal. 156 Hypophosphataemia associated with septicaemia, severe liver disease, heat stroke, salicylate intoxication, acute gout and malignant neuroleptic syndrome are all most likely to be due to the associated hyperventilation. Carbohydrate administration has been shown to account for 40-43% of cases of hypophosphataemia.…”

Section: Causes Of Hypophosphataemiamentioning

confidence: 99%

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Phosphate homeostasis and disorders

2014

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Recent studies of inherited disorders of phosphate metabolism have shed new light on the understanding of phosphate metabolism. Phosphate has important functions in the body and several mechanisms have evolved to regulate phosphate balance including vitamin D, parathyroid hormone and phosphatonins such as fibroblast growth factor-23 (FGF23). Disorders of phosphate homeostasis leading to hypo-and hyperphosphataemia are common and have clinical and biochemical consequences. Notably, recent studies have linked hyperphosphataemia with an increased risk of cardiovascular disease. This review outlines the recent advances in the understanding of phosphate homeostasis and describes the causes, investigation and management of hypo-and hyperphosphataemia.

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Section: Causes Of Hypophosphataemiamentioning

confidence: 99%

“…157 If there is accompanying hyperventilation, the fall in serum phosphate is greater. 156 The degree of hypophosphataemia is related to the amount of carbohydrates infused. 158 Infusion of carbohydrates increase insulin release, which causes a shift of phosphate into cells.…”

Section: Causes Of Hypophosphataemiamentioning

confidence: 99%

Phosphate homeostasis and disorders

2014

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“…4,5,7,8 Alternative mechanisms leading to hypophosphatemia in acute liver failure include intracellular phosphate redistribution because of hyperventilation, dextrose infusion, or phosphate consumption. 11,14 Hypophosphatemia is frequently observed in acetaminophen-induced hepatotoxicity and is correlated to the severity of liver damage. 4,[6][7][8] If hypophosphatemia is involved in the pathogenesis of acute liver failure, then systematic measurement of serum phosphate may be of prognostic and possibly therapeutic value in acetaminophen-induced hepatic damage.…”

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confidence: 99%

Serum phosphate is an early predictor of outcome in severe acetaminophen-induced hepatotoxicity

2002

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Hypophosphatemia is frequently observed in acetaminophen-induced hepatotoxicity and may be involved in the pathogenesis of hepatic failure. The aim of the study was to evaluate the prognostic value of serial measurements of serum phosphate in patients with severe acetaminophen poisoning. Prospectively, serial measurements of serum phosphate were performed in 125 patients with severe acetaminophen poisoning. The optimum threshold value of serum phosphate to discriminate nonsurvivors was identified. Prognostic value and speed of identification were compared with those of the King's College Hospital (KCH) criteria. Phosphate concentrations were significantly higher in nonsurvivors than in survivors at 48 to 72 hours after overdose (mean 2.65 ؎ 1.18 mmol/L vs. 0.68 ؎ 0.22 mmol/L, P < .001) as well as 72 to 96 hours after overdose (2.12 ؎ 0.22 mmol/L vs. 0.59 ؎ 0.23 mmol/L, P < .001). A threshold phosphate concentration of 1.2 mmol/L at 48 to 96 hours after overdose had sensitivity 89%, specificity 100%, accuracy 98%, positive predictive value 100%, and negative predictive value 98%. The phosphate criteria had higher sensitivity, accuracy, and positive and negative predictive values than the KCH criteria, and it identified patients significantly earlier after transferal [median 1 hour (range 1-38 hours) vs. 12 hours (2-192 hours), P < .05, respectively]. In nonsurvivors, the degree of hyperphosphatemia correlated with renal dysfunction (R ‫؍‬ .55; P ‫؍‬ .02). In conclusion, hyperphosphatemia after acetaminophen overdose is seen exclusively in nonsurvivors, which makes it a highly specific as well as sensitive predictor of nonsurvival. We propose that hyperphosphatemia is caused by renal dysfunction in the absence of hepatic regeneration, as the latter appears to be associated with lowering of serum phosphate. (HEPATOLOGY 2002;36:659-665.)

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“…However, a significant response was shown to occur after 48 hours. Respiratory alkalosis induced by hyperventilation in healthy volunteers, did not exhibit deviation in the red cell 2,3-DPG concentration 15 . However, in these subjects hyperventilation was not sustained for more than twenty minutes.…”

Section: Discussionmentioning

confidence: 99%

Optimized hyperventilation preserves 2,3-diphosphoglycerate in severe traumatic brain injury

Torres¹,

Terzi

Falcão

et al. 2007

Arq. Neuro-Psiquiatr.

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ABSTRAT -Introduction:The concentration of 2,3-diphosphoglycerate (2,3-DPG/Hct) increases as a physiological occurrence to pH increase and hyperventilation. This response was tested in patients with severe traumatic brain injury (TBI). Method: The concentration of 2,3-DPG/Hct was measured daily for six days in eleven patients with severe TBI in need of optimized hyperventilation because of intracranial hypertension. Results: There was correlation between pH and the concentration of DPG/Hct. The concentration of 2,3-DPG/Hct remained predominantly within normal levels with slight increase in the sixth day of the study. The concentration of 2,3-DPG/Hct correlated significantly with measured partial pressure of oxygen that saturates 50% the hemoglobin of the blood (P50st), confirming the consistency of our data. Conclusion: The expected physiological response of a progressive increase in concentration of 2,3-DPG/Hct to hyperventilation was not observed. This fact may be explained by the intermittent and not sustained hyperventilation as dictated by the protocol of optimized ventilation.

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Persistent, progressive hypophosphataemia after voluntary hyperventilation

Cited by 25 publications

References 18 publications

Phosphate homeostasis and disorders

Phosphate homeostasis and disorders

Serum phosphate is an early predictor of outcome in severe acetaminophen-induced hepatotoxicity

Optimized hyperventilation preserves 2,3-diphosphoglycerate in severe traumatic brain injury

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