Hyperventilation (HV) and respiratory alkalosis are associated with hypopho
sphataemia, although the extent and duration of HV required to produce chan
ges 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-t
idal partial pressure of carbon dioxide (PETCO2). The effect of dextrose wa
s studied because infusion of a glucose load is known to promote a fall in
serum phosphate via stimulation of glycolysis. Eight healthy volunteers wer
e enrolled in four study protocols: (1) HV for 20 min to a PETCO2 of 25-30
mmHg (mild); (2) HV for 20 min to a PETCO2 of 15-20 mmHg (severe); (3) mild
HV with intravenous dextrose loading, and (4) dextrose loading alone. Peri
odic measurements of serum phosphate, venous pH, serum 2,3-diphosphoglycera
te (2,3-DPG) and other parameters were made. Serum phosphate fell during HV
and continued to decline after cessation of HV. Dextrose loading alone cau
sed a fall in serum phosphate that continued for at least 30 min after cess
ation 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 potass
ium (P < 0.05) and an increase in venous pH (P < 0.007). Serum 2,3-DPG leve
ls did nor 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 phenomeno
n has not been shown before, and may have significant clinical implications
.