Volume 6, Spring 2008 - Saddleback College

Fall 2007 Biology 3A Abstracts
During anesthesia, complications can often
occur in spite of the many precautions taken such as,
vital monitoring of blood pressure, heart rate,
electrocardiography, body temperature and entidal
CO 2 . These parameters are in addition to pre-anesthetic
and interoperative precautions such as, the evaluation
of pre-operative blood chemistries, heat support during
anesthesia and the increase of interoperative
intravenous fluid rate (intended to supplement
perfusion). Due to overall systemic depression from
anesthetic agents, such as inhalant gas anesthesia,
hypoperfusion, although in mild proportions, is often
still present (Guyton and Hall, 1996). The effects of
inadequate perfusion on cell function can be
detrimental to vital organ systems; however, if
addressed in an appropriate and timely manner, can be
reversed (Guyton and Hall, 1996). During this study,
crystalloid fluid therapy was increased to 5 ml/kg/hr
and external heat support was added while study
patients were under anesthesia in order to maintain
adequate profusion during the procedure.
Ideally, in healthy organ systems, residual
blood lactate is metabolized in part by the liver (50%)
and kidneys (20%). Liver function and liver blood flow
can influence hepatic lactate clearance. Clinically
healthy patients were utilized during the study to insure
that pre-anesthetic hypo-perfusion and systemic
compromise were not factors in the increase of lactate
intraoperatively. Pre-anesthetic blood chemistries
including lactate levels, as well as pre-operative, interoperative
and post-operative vitals were noted during
this study, however were not included as statistical
variables with respect to our results, as the specific
values were not the focus of this experiment. Further,
more specific exploration of these parameters should
be tested to establish any existing correlation with vital
signs and blood chemistries in relation to anesthesia
and the outcome of the increase in lactate.
With respect to the purpose of this study
regarding the importance of continual lactate
monitoring, Steele and Elliott (2002) conducted a
similar study examining the importance of the serial
lactate testing in humans. The study involved 137
SICU patients who had serial lactate and blood gas
measurements taken intraoperatively, 24 hours before,
and 24 hours post operatively. Patients were
categorized by absolute lactate and base deficit values
as well as time to lactate clearance. The results
indicated an initial and 24-hour lactate level that was
significantly elevated in non survivors versus
survivors. The study concluded that the elevated initial
and 24-hour lactate levels are significantly correlated
with mortality and appeared to be superior to
corresponding base deficit levels (Steele and Elliott,
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Saddleback Journal of Biology
Spring 2008
2002). Thus the significance of lactate monitoring was
supported.
The danger of increased lactate levels lies
with the causes of the decrease in clearance. The
increase in lactate level is not the cause of systemic
damage, it is the indicator of the decrease in systemic
function and a warning sign of potential damage which
may be occurring or has already occurred as a result.
An increase in lactate of greater than 5mmol/L is
classified as lactic acidosis. Furthermore lactic acidosis
is sorted into Type A and Type B lactic acidosis and
subcategorized thereafter. The principal feature of
these conditions is the incapacity to use pyruvate in
oxidative metabolic pathways. The result is the
accumulation of pyruvate, with subsequent production
of lactate (Marko et al., 2004).
Elevated lactate levels resulting from
inadequate tissue perfusion is classified as Type A
lactic acidosis (Marko et al., 2004). The accumulation
of pyruvate and hydrogen ions, along with NADH,
drives the production of lactate, however once
oxygenation is improved, aerobic metabolism should
resume and acidosis should resolve provided the organ
systems are functioning at adequate levels. The type of
lactic acidosis, in which tissue perfusion is adequate
however enzyme systems are not functioning
adequately, is classified as Type B lactic acidosis
(Guyton and Hall, 1996). While Lactate levels during
this study showed a maximum mean of 3.03 mmol/L
during the 100 minute interval, indicating moderate
Hyperlactatemia, lactic acidosis did not occur. It can
be deduced that the type of lactic acidosis that would
most likely associated with this study, had it occurred,
would be Type A lactic acidosis.
It should be noted that this study was
randomized to evaluate patients in a clinical
environment. A controlled study using a controlled test
colony would be indicated to eliminate certain random
variables. This was not the intended design of this
study, as true clinical parameters during anesthesia
were believed to be of vital importance in enhancing
future knowledge of this subject. Further studies may
be indicated in non-clinical studies that would include
non-surgical anesthetic patients without the use of fluid
therapy, or analgesia throughout the study, which may
or may not alter overall results. In this study, the
patients were limited to the standard anesthetic
protocol used during surgical procedures developed by
the board certified veterinarians at Advanced Critical
Care and Internal Medicine. Test subjects were clinical
patients and not a controlled test colony.
This study concluded that there was an
increase in lactate over time during the anesthetic
procedures; however the increase in levels during this