Hypophosphatemia as a cause of failed weaning

Agustí, A.; Torres, Antônio; Estopá, R; Agustí-Vidal, A

doi:10.1097/00003246-198402000-00012

Cited by 76 publications

(26 citation statements)

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“…The administration of phosphate in one study over a 4-h period was associated with an improvement in diaphragmatic function which was apparent immediately, suggesting immediate benefits with phosphate repletion. In patients with severe hypophosphataemia, failure to wean from mechanical ventilation until repletion of phosphorus has been demonstrated [46,47]. A further effect of hypophosphataemia on respiratory function is its influence on the equilibrium between oxygen and haemoglobin.…”

Section: Respiratory Effectsmentioning

confidence: 99%

HypophosphataemiaPathophysiology, effects and management on the intensive care unit

1998

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SummaryRoutine detection and treatment of hypophosphataemia on the intensive care unit is commonplace. Hypophosphataemia has been associated with a multitude of clinical effects and there are many associations between correction of hypophosphataemia and improvement in symptoms. However, there is no evidence at present to support the routine correction of hypophosphataemia in the absence of clinical symptoms or signs.

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Section: Respiratory Effectsmentioning

confidence: 99%

HypophosphataemiaPathophysiology, effects and management on the intensive care unit

1998

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“…Hipofosfateminin akut solunum yetmezliğine neden olduğu yaklaşık 30 yıldan beri bilinmektedir (11). Ancak ventilatörden ayırma başarı-sızlığını belirlemede yeri olup olmadığı konusunda yeterli çalışmalar bulunmamaktadır (12,13).…”

Section: Discussionunclassified

Effect of hypophosphatemia on weaning success from mechanical ventilation

Kara¹,

Bolayır²,

Ersoy³

et al. 2015

Tuberk Toraks

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“…Patients with significant hypoxaemia due to a variety of cardiorespiratory diseases (including acute severe asthma, pneumonia, pulmonary thromboembolism and pulmonary oedema) may hyperventilate and develop hypophosphataemic respiratory alkalosis. Respiratory muscle weakness has been demonstrated in hypophosphataemic patients [7,8], with an improvement in muscle strength once serum phosphate is restored to normal. As the duration of hyperventilation in such subjects is likely to be very much longer than in the present study, hypophosphataemia may be prolonged for many hours after therapy and resolution of the underlying disorder.…”

Section: Discussionmentioning

confidence: 99%

“…Decreases in total calcium, ionized magnesium, phosphate and potassium have been reported in association with prolonged HV [3,4,6]. Marked hypophosphataemia may cause a variety of clinical disorders, including respiratory muscle weakness [7,8], central nervous system dysfunction, rhabdomyolysis, cardiac dysfunction [7][8][9] and altered haemoglobin oxygen affinity [10].…”

Section: Introductionmentioning

confidence: 99%

Persistent, progressive hypophosphataemia after voluntary hyperventilation

PALEOLOGOS¹,

STONE²,

BRAUDE³

2000

Clinical Science

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Hyperventilation (HV) and respiratory alkalosis are associated with hypophosphataemia, although the extent and duration of HV required to produce changes in serum phosphate levels are not known. We sought to characterize the effects of HV, with or without dextrose loading, on serum phosphate levels and other biochemical parameters. HV was monitored by controlling the end-tidal partial pressure of carbon dioxide (PETCO(2)). The effect of dextrose was studied because infusion of a glucose load is known to promote a fall in serum phosphate via stimulation of glycolysis. Eight healthy volunteers were enrolled in four study protocols: (1) HV for 20 min to a PETCO(2) of 25-30 mmHg (mild); (2) HV for 20 min to a PETCO(2) of 15-20 mmHg (severe); (3) mild HV with intravenous dextrose loading, and (4) dextrose loading alone. Periodic measurements of serum phosphate, venous pH, serum 2,3-diphosphoglycerate (2,3-DPG) and other parameters were made. Serum phosphate fell during HV and continued to decline after cessation of HV. Dextrose loading alone caused a fall in serum phosphate that continued for at least 30 min after cessation of the infusion (P<0.0002). HV combined with dextrose resulted in a greater decline in serum phosphate than either variable alone (P=0.003). The maximal decline in serum phosphate occurred in severe HV, with a mean decrease of 0.38 mmol/l at 20 min after cessation of HV (P<0.0001). Serum phosphate was still significantly lowered compared with baseline at 90 min after cessation of HV (P=0.001). Other significant changes seen with HV included a decrease in serum glucose (P<0.01), a decrease in serum potassium (P<0.05) and an increase in venous pH (P<0.007). Serum 2, 3-DPG levels did not change significantly in any study protocol. Thus relatively mild acute HV produces significant changes in serum phosphate. In both mild and severe HV this effect is progressive after cessation of HV. This phenomenon has not been shown before, and may have significant clinical implications.

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Hypophosphatemia as a cause of failed weaning

Cited by 76 publications

References 0 publications

HypophosphataemiaPathophysiology, effects and management on the intensive care unit

HypophosphataemiaPathophysiology, effects and management on the intensive care unit

Effect of hypophosphatemia on weaning success from mechanical ventilation

Persistent, progressive hypophosphataemia after voluntary hyperventilation

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