Download Lactic Acidosis

LACTIC ACIDOSIS
Cadel Evans, 2011 winner of the Tour de France, the oldest, most prestigious and greatest
endurance event in world sport - amoung the many great Australian sporting achievements- this
was one of the greatest! Here Cadel stands on the winner’s podium in Paris, with Ms Tina Arena
belting out a powerful and emotional rendition of the national anthem.
“For Cadel to come to Europe and spend so much time chasing his dream shows what he is
made of”
Tina Arena to the French Media, (in French)
“I think that’s the ultimate dream of a Tour rider, to stand on the Champs-Elysees with an
Australian singing the national anthem ... it’s not a dream that comes true for many
Australians…This win is for everyone in our country!”
Cadel Evans
During strenuous exercise oxygen stores are rapidly depleted and anaerobic metabolism must be
relied on for the provision of energy. This occurs however with the development of an “oxygen
debt” mainly in the form of accumulated lactic acid. It is this lactic acid, which in a large degree
accounts for the feeling of fatigue in exercise. Trained athletes such as Australia’s Tour de
France winner Cadel Evans are able to increase the oxygen consumption of their muscles to a
greater degree than untrained individuals and hence are capable of greater exertion without
depleting glycogen stores and accumulating lactic acid to the extent that occurs in an untrained
individual.
Athletes can also help minimize their lactic acid production during exercise by increasing their
glycogen stores before an event by consuming specially planned diets of large amounts of
carbohydrate and refraining from exercise 48 hours prior to the event…after the event
carbohydrate loading takes a somewhat different form …Champagne on the Champs-Elysees!
LACTIC ACIDOSIS
Introduction
Lactic acidosis is conventionally defined as the combination of an increased blood lactate
concentration and acidemia.
It is one of the causes of an increased anion gap metabolic acidosis.
Overall critically ill patients with lactic acidosis tend to have high mortality if their lactate levels
are significantly elevated (>8 mmols/L).
In each individual case however, the actual prognosis will be completely dependent on the
underlying condition, with the initial degree of lactic acidosis being a clinically useful indicator
of the severity of the shock/hypoxia.
Physiology
Under normal aerobic conditions glucose is converted to pyruvate, which is in turn converted to
acetyl-CoA. Acetyl-CoA then combines with oxaloacetate to form citrate, and so enters the
Krebs cycle. The Krebs cycle of biochemical reactions then produces water, CO2 and most
importantly, ATP, the primary cellular energy source.
Under anaerobic conditions, or when the metabolic demands of the cells exceed the oxygen
delivery capacity of the body, pyruvate is unable to enter the Krebs cycle to produce ATP for
cellular energy. Instead it is converted to lactic acid, by which some ATP is produced in
compensation, although this is of much lesser degree than that which is obtained from aerobic
metabolism, and is at the expense of an increasing lactic acidosis.
Pathology
Lactic acidosis occurs when the production of lactate exceeds the systemic metabolism of it.
Lactate is metabolized by the liver, kidneys, skeletal muscle, brain, and the red blood cells.
When the acidosis becomes severe cellular dysfunction will occur.
Classification
The Cohen and Woods 2 classification is the most commonly used.
Type A
The most common form is due to anaerobic metabolism secondary to inadequate tissue
oxygenation due to the following two causes:
1.
Shock from any cause:
●
2.
With inadequate tissue perfusion and / or abnormal oxygen utilization.
Tissue hypoxia from any cause:
●
Hypoxic hypoxia.
●
Anaemic hypoxia.
●
Stagnant hypoxia.
●
Histotoxic hypoxia.
●
Low inspired oxygen concentration
Type B
Here tissue oxygenation and perfusion is adequate but lactic acidosis is still present.
There are 3 subtypes:
B1:
Associated with “systemic” disorders that result in increased levels of lactate by mechanisms
other than tissue hypoxia or shock.
1.
Liver failure.
●
2.
A failure to metabolize lactate.
Renal failure
●
A failure to metabolize lactate and excrete
3.
Some malignant conditions (leukemia, lymphomas)
4.
Thiamine deficiency.
●
A failure of the pyruvate to oxaloacetate pathway, (hence more pyruvate is
converted to lactate).
5.
Diabetes.
6.
Sepsis.
B2:
Drugs and toxins.
1.
Biguanides.
2.
Ethanol.
3.
Methanol.
B3:
Rare inborn enzyme errors of metabolism defects.
Investigations
In cases of lactic acidosis:
1.
There will be:
●
Metabolic acidosis with increased anion gap.
●
Elevated serum lactate.
♥
●
2.
Normal value range of lactate is 0.63-2.44 mmol / L.
Absent (or minimal ketones, in pure cases of lactic acidosis).
Lactic acidosis is caused by accumulation of lactate and H+ ions.
●
It is not lactate that causes acidosis, but the attendant H+ ions, (lactate levels may
be increased without an acidosis, eg. infusion of Hartman’s solution).
●
Therefore, increased lactate is merely an indication that the observed acidosis
could be due to lactic acid production.
Interpretation:
Overall critically ill patients with lactic acidosis tend to have high mortality if their lactate levels
are significantly elevated (>8 mmols/L).
In each individual case however, the actual prognosis will be completely dependent on the
underlying condition, with the initial degree of lactic acidosis being a clinically useful indicator
of the severity of the shock/hypoxia.
Serial assessments will then allow for one way of evaluating the response to therapy.
It is also important to assess lactic acidosis in clinical context. Healthy athletes for example can
develop significant lactic acidosis during strenuous exercise, as a normal self-limited
observation.
Management
1.
2.
Treat the underlying cause:
●
The treatment of patients who have lactic acidosis, involves the treatment of the
underlying cause, not the lactic acidosis itself.
●
In type A lactic acidosis, this will mean aggressive resuscitation measures, to
improve tissue oxygenation and /or perfusion.
●
Drugs or toxins known to cause lactic acidosis (such as metformin) must be
ceased immediately, if lactic acidosis is detected.
Bicarbonate:
●
The use of bicarbonate in lactic acidosis remains uncertain and controversial
●
In practice it is often given when the acidosis is very severe or the patient is very
unstable, however its benefit has never been convincingly demonstrated. The
priority will always remain aggressive treatment of the underlying cause.
Victory!
References
1.
Cooper D. J, Nichol A.D. Lactic Acidosis, in OH. T.E, “Intensive Care Manual”, 6th ed
Butterworth Heinemann, 2009.
2.
Cohen R.D, Woods HF. Lactic acidosis revisited. Diabetes 1983; 32 181-191.
3.
Ganong, Review of Medical Physiology 17th Ed, p. 65
Dr J. Hayes
Reviewed August 2011.