Dear Peter
There are a number of mechanisms for hyperlactataemia in alkalosis
1: increased glycolysis as you state
2: reduced O2 delivery due to shift in O2 dissociation curve
3: O2 debt leads to anaerobic respiration
......and furtehr hyperventilation
4: impaired mitochondrial respiration
5: the high lactate itself leads to vascoconstriction and exacerbates
the tissue hypoxia
BW
Julian
>>> "Galloway, Peter" <[log in to unmask]> 25 March 2013
10:46 >>>
Colleagues,
Could anyone help with the physiology –
From the history provided by others: 50 year old gentleman with
longstanding exertional pains in his muscles of uncertain aetiology,
felt increasingly tired, lightheaded with tingling in his arms and legs.
He was sweaty and felt he was going to pass out.
On admission to A+E, his blood gases showed pH 7.59, pCO2 2.25, pO2
17.4, Bic 16.1 mmol/l, BE -3 with lactate 6.1 mmol/l. This was repeated
at 6.5 mmol/l. (K 4, adj Ca 2.12, creat 87, normal LFTs)
I assume he has a partially compensated acute respiratory alkalosis.
From the Oxford Textbook, the suggestion is that alkalosis has an effect
on phosphofructokinase stimulating glycolysis. The more pyruvate formed
the more lactate. Given that alkalosis, will stop NH3 release and
stimulate bicarbonate loss, the effect will be to inhibit lactate renal
excretion. The Oxford textbook suggests that mild increase in lactate
would occur unless there was liver dysfunction – not evident in above
case.
Tietz (3rd edition) suggests that with chronic respiratory alkalosis,
lactate may increase to 2-4 mmol/l from enhanced glycolysis and lactate
with levels probably ‘owning to a decrease in hepatic blood flow’.
At review his lactate was 0.8 mmol/l. Repeat Gases weren’t undertaken
or a bicarbonate requested.
Is anyone willing to speculate whether the lactate could rise to 6.5
mmol/l in someone with normal BPand pulse during this scenario?
Thank you for your help
Peter Galloway
Glasgow
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