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Annals of Cardiac Anaesthesia 2005; 8: 39–44 ORIGINAL

Shinde et al. Blood Lactate LevelsARTICLES
during CPB 39

Blood Lactate Levels During Cardiopulmonary

Bypass for Valvular Heart Surgery
Santosh B Shinde, Kumud K Golam, Pawan Kumar, Neela D Patil
Departments of Biochemistry, Anaesthesiology, and Cardiovascular and Thoracic Surgery,
Lokmanya Tilak Municipal Medical College and Hospital, Sion, Mumbai

Cardiopulmonary bypass (CPB) is widely used to maintain systemic perfusion and oxygenation during
open-heart surgery. Tissue hypoperfusion with resultant lactic acidosis during CPB, may occur during
hypothermia, extreme haemodilution, low flow CPB, and excessive neurohormonal activation. There has
been no documentation of the correlation between blood lactate level elevations in the perioperative period,
and its relation to preoperative New York Heart Association (NYHA) classification and the use of ionotropic
support during weaning from CPB, duration of postoperative ventilatory support and perioperative
mortality. We studied the perioperative blood lactate levels in 82 patients undergoing valvular heart surgery.
Arterial blood samples were collected at different stages of CPB. The observed mean baseline lactate levels
were 1.9±0.8 mmol/L (normal range of 0.9 to 1.7 mmol/L). The mean circulating lactate levels at 15 min
and 45 min after institution of CPB increased to 7.01±2.6 mmol/L and 9.92±3.5 mmol/L. A progressive
decline in the mean lactate level, was seen during rewarming (at 35°C), immediately off-bypass, 24 hours
and 48 hours postoperatively with mean lactate levels being 7.01±3.2 mmol/L, 4.75±1.01 mmol/L, 3.06±1.1
mmol/L, and 2.10±1.05 mmol/L respectively. Comparison of mean lactate levels in NYHA class I, II, III,
and IV patients showed that in the intraoperative period and immediately after CPB, the elevation
in lactate levels were statistically significant (p< 0.001) in patients in NYHA Class IV. However the
values, in all classes, were similar at 24 and 48 hours after CPB. Also, patients with lactate levels
>4 mmol/ L required prolonged inotropic and ventilatory support. (Annals of Cardiac Anaesthesia 2005;
8: 39–44)

Key words:- Lactic acidosis, CPB, Hyperlactataemia, NYHA classification

C ardiopulmonary bypass (CPB) is instituted,

during various cardiac operations, to allow
adequate systemic perfusion. Presently there are
no definitive biochemical markers of prognostic
value in patients undergoing valvular heart
surgery under CPB.
Tissue perfusion is at risk during CPB and in
the immediate postoperative period.1 The duration
of CPB, degree of hypothermia, duration of cooling
and rewarming, pH management strategy and the
haematocrit value are all potential factors that may
contribute to tissue hypoperfusion during CPB.1 In
addition, factors like impaired venous drainage or
Address for Correspondence: Dr. K. K. Golam, D2/10 KINARA, 358,
Municipal Tenements, A.G. Road, Worli Seaface, Mumbai 400 018
Email: drkumudgolam@yahoo.com
anatomic lesions characterised by reduced
splanchnic flow or excessive systemic runoff may
limit perfusion. Finally the systemic inflammatory
response to CPB may also impair tissue
oxygenation and perhaps more specifically, tissue
oxygen extraction.1 Improvements in CPB and
overall haemodynamic management have reduced
the incidence of severe perioperative tissue
hypoperfusion.2
It is an established fact that tissue hypoperfusion
is associated with lactic acidosis secondary to
anaerobic metabolism. Measurement of blood
lactate levels can, hence be used as a marker to
assess the adequacy of tissue perfusion.2
Glycolysis is the first step of glucose metabolism
and occurs in the cytoplasm of virtually all cells.

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40 Shinde et al. Blood Lactate Levels during CPB
The end product of this pathway is pyruvate, which
can then diffuse into mitochondria and get
metabolised to carbon dioxide by the Kreb’s cycle.3
Increased blood lactate may occur with or without
concomitant metabolic acidosis. Such
hyperlactataemia is usually seen in subclinical
tissue hypoperfusion, secondary to elevated blood
catecholamine levels. This is either stress induced,
due to administration of catecholamine or due to
alkalosis where buffering systems are able to
mitigate any fall in the pH.4
This study was conducted to establish blood
lactate level, as a prognostic tool, in patients
undergoing valvular heart surgery under CPB. The
following were evaluated:
- Lactate levels and its correlation with
preoperative clinical condition (as per New York
Heart Association).
- The intra and postoperative outcomes, following
CPB for valvular heart surgery.
Methods
Eighty two consecutive patients undergoing
valvular heart surgery under CPB were included
in this study. On the basis of history, the patients
were allocated to their respective class as per the
NYHA functional classification5 (Table 1).
The departmental review board of Lokamanya
Tilak Municipal Medical College and General
Hospital approved the study. Diabetic patients on
treatment with phenformin were excluded from the
study. The reason being that in this group there is
increased peripheral extrasplanchnic glucose
utilisation by a shift from oxidative to anaerobic
metabolism. As such they have been associated
with development of lactic acidosis.
Anaesthesia Technique
On the day of surgery, the patient was
premedicated with morphine (0.2 mg/kg) and
promethazine (0.5 mg/kg) intramuscularly about
30-45 minutes prior to induction of anaesthesia.
Anaesthesia was induced with thiopentone (5 mg/
kg) and vecuronium was used to accomplish
endotracheal intubation with appropriate sized
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Annals of Cardiac Anaesthesia 2005; 8: 39–44
tube, (generally 9.0 mm for males and 7.5 mm for
females). Anaesthesia was maintained with 50%
oxygen (O2), 50% nitrous oxide (N2O) along with
halothane 0.5% to 1%.
Morphine (0.05 mg/kg) was given before
incision and 0.15 mg/kg was added to the pump
prime. Additional morphine (0.1 mg/kg) and
vecuronium (0.1 mg/kg) were administered during
rewarming. Post-CPB anaesthesia was maintained
with 50% O2, 50% N2O, halothane 0.5 to 1%, and
vecuronium (1/4th of induction dose).
The bypass circuit was primed with a mixture
of Ringer’s lactate and gelofusine to make the
priming volume 1500 ml. Standard bypass
techniques with systemic hypothermia of 28-32ºC
were employed.
Mean arterial pressure was continuously
monitored and maintained between 50 and 60 mm
Hg. The haemoglobin was maintained between 6
and 8 gm%. Urine output was monitored
throughout the procedure. Blood sugar was
monitored using a glucometer intraoperatively and
the sugar levels were maintained between 180 and
240 mg%. After surgery was completed, CPB was
discontinued and heparin was neutralised with
protamine. Patients received ionotropic support in
the form of dopamine (5-10 µg/Kg/min) and
adrenaline (0.06-0.6 µg/Kg/min) was added if
required to attain the desired haemodynamic
stability. Before shifting the patient to cardiac
intensive care unit, morphine 0.1 mg/kg was given
intravenously. In the intensive care unit the patient
was electively ventilated with continuous
monitoring of haemodynamic parameters and
arterial blood gas analysis.
Blood lactate level measurement: For measuring
lactate levels, arterial blood was collected through
the intra-arterial catheter (inserted for blood
pressure monitoring) immediately after induction
of anaesthesia. This was termed as the baseline
sample. Subsequent samples were collected at the
following intervals.
- 15 minutes after institution of CPB
- 45 minutes after institution of CPB (if any)
- Rewarming (at 35°C)
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Annals of Cardiac Anaesthesia 2005; 8: 39–44 Shinde et al. Blood Lactate Levels during CPB 41

- Immediately after terminating the CPB
- 24 hours post-surgery, and
- 48 hours post-surgery.
The blood samples were collected in a sample
tube containing 3 ml of 5% metaphosphoric acid.
Samples were stored in ice carriers and transferred
to the laboratory where they were immediately
centrifuged. The protein free filtrate was then
collected in another tube for the estimation of
lactate (using the spectrophotometer method at
340 nm). 6
NYHA class IV patients showed significant
(p<0.001) elevation in the mean lactate levels, as
compared to NYHA class I, II and III, throughout
the study period. Two patients in NYHA class IV
demonstrated abnormally high lactate levels and
were excluded. Table 5 shows the changes in
perioperative lactate levels in relation to duration
of CPB. Levels were significantly higher (p<0.05)
during rewarming at 35°C and off-bypass in
patients requiring CPB for more than one hour as
compared to those with less than 1 hour. Lactate
levels returned to normal levels in 24 and 48 hours

The endpoint of the study was predetermined Table 1. Distribution of patients according to the New York
with the last sample being collected at 48 hours Heart Association (NYHA) Classification
after termination of CPB. The one-way ANOVA NYHA class No. of patients
was used for statistical analysis. I 15
II 34
Results III 20
IV 11

Demographic data showed average age of

35±10.2 years with weight of 50±12.4 kg. There
were 43 males and 39 females. Table 1 shows Table 2. Types of surgeries performed
distribution of patients according to their NYHA Type of surgery No. of patients
class. Maximum patients (34) belonged to NYHA MVR 37
class II. Table 2 shows the distribution of various AVR 20
surgical procedures. Most patients (37) underwent DVR 13
MVR+TVR 2
mitral valve replacement. Table 3 shows mean
R. MVR 5
lactate levels during the perioperative period. Table R. AVR 1
4 shows the mean lactate levels in different NYHA R. DVR 2
class patients. No statistically significant changes MVR: mitral valve replacement, AVR: aortic valve replacement, DVR:
were seen in NYHA class I, II and III. However, double valve replacement, TVR: tricuspid valve replacement, R: redo.

Table 3. Mean lactate levels (mmol/L) during the perioperative period

N=80 Pre-op 15 min 45 min Rewarming Off- 24 Hour 48 Hour
CPB CPB 35 0C Bypass Postop Postop
Mean levels
of Lactate 1.90±0.85 7.01±2.69* 9.92±3.58* 7.01±3.20* 4.75±1.01* 3.06±1.18 2.10±1.05
The results are given as Mean±SD. * P<0.001 Values as compared to Pre-op
CPB: cardiopulmonary Bypass, Pre-op: preoperative, Postop: postoperative

Table 4. Comparison of NYHA class and their mean lactate levels (mmol/L) during preoperative period
N=80 Pre-op 15 min 45 min Rewarming Off- 24 Hour 48 Hour
35 0C Bypass
NYHA I (n=15) 1.66±0.44 4.06±2.20 5.00±2.00 5.79±2.28 5.82±2.23 3.92±1.29 2.60±0.84
NYHA II (n=34) 1.92±1.02 5.89±1.96 6.99±2.32 6.48±1.91 6.24±1.85 4.54±1.30 2.90±1.17
NYHA III (n=20) 1.93±0.85 4.94±2.70 7.55±2.87 6.51±2.40 6.03±2.40 4.21±2.37 2.63±1.16
NYHA IV (n=11) 2.22±0.64 5.67±2.22* 9.10±1.61* 7.05±2.53* 6.25±2.39* 5.00±1.74* 4.47±2.12*
The results are given as Mean±SD.
* P<0.001 Values as compared to NYHA Class I, II, III

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42 Shinde et al. Blood Lactate Levels during CPB Annals of Cardiac Anaesthesia 2005; 8: 39–44

Table 5. Comparison of duration of CPB and changes in perioperative Lactate levels

Duration Base line 15 minutes 45 minutes Rewarming Off-Bypass 24 hrs. 48 hrs.
of CPB 350C
<1 hrs. (n=40) 1.25±0.40 5.01±2.15 7.01±3.90 6.29±2.23 4.75±1.98 3.33±0.70 2.01±0.68
1-2 hrs. (n=40) 2.20±0.68 5.27±3.35 NS 7.59±2.95 NS 8.35±4.75* 5.85±3.90* 4.68±2.70 2.98±1.75
The results are given as Mean±SD.
* P<0.05 Values as compared to less than 1 hrs. duration of CPB.

after surgery. Table 6 shows the comparison of NYHA IV patients showed an increase of >4
changes in lactate levels with mean duration of mmol/L during CPB. Due to small number of
ionotropic and ventilator support. The average patients in the subgroups a statistical analysis could
duration of mechanical ventilation and duration not be performed.
of inotropic support was significantly more in the
group which demonstrated a change in lactate level Discussion
of more than 4 mmol/L (for baseline to off-bypass)
(p<0.05). Table 7 shows the relation of NYHA class CPB is used to maintain systemic perfusion and
to lactate level variations. The patients were oxygenation during open-heart operations. This is
designated to three groups. achieved by adjusting flow rate, temperature, gas
flow and haemoglobin to maintain oxygen
Group I – Patients having a change in lactate level
delivery. Tissue hypoperfusion may occur due
of < 2 mmol/L
to low flow CPB, hypothermia, extreme
Group II – Patients having a change in lactate level
haemodilution and excessive neurohormonal
of 2-4 mmol/L
activation. This leads to an anaerobic condition in
Group III – Patients having a change in lactate level
which oxidative phosphorylation is not possible
of >4 mmol/L
and adenosine triphosphate (ATP) is produced
from pyruvate, the latter being metabolised into
It reveals that 66.6% of NYHA Class I patients
lactate.7
showed a change in lactate levels of <2 mmol/L
during CPB. Fifty percent NYHA class II and 55%
An increase in lactate concentration may be the
NYHA class III patient showed increase in lactate
result of diminished tissue perfusion and oxygen
levels of 2-4 mmol/L during CPB, and 63.6% of
delivery, decreased oxygen extraction and
Table 6. Changes in lactate levels during CPB (off-Bypass- decreased hepatic lactate clearance.1 Plasma lactate
base line lactate) and duration of postoperative ionotropic concentrations reflect a balance between lactate
support and mechanical ventilation production by regional tissue beds and the ability
Change in Lactate Mean duration Mean duration of of the liver (and to a lesser extent, the heart and
mmol/ L) of inotropic mechanical renal cortex) to metabolise lactate via the Cori
Support (hours) ventilation (hours)
Cycle, gluconeogenesis, and the Krebs cycle.
<2 (n = 25) 13.12±6.68 7.35±1.65
2-4 (n = 33) 15.92±7.01 14.2±6.01
>4 (n = 22) 17.20±5.55* 15.82±5.25 * Systemic lactic acidosis has often been attributed
The results are given as Mean±SD. to the overproduction of lactic acid by hypoxic
* P<0.05 Values as compared to Less than 2 mmol/L and 2-4 mmol/L lactate.
tissues.7 The organs most likely to produce lactate,
in response to hypoperfusion or decreased oxygen
Table 7. Comparison of NYHA class to lactate level extraction, include the brain, gut, liver, kidneys and
variation skeletal muscles.8
NYHA Changes in lactate levels during CPB
Class <2 2-4 >4 Hyperlactataemia is classified as mild (lactate
(n = 27) (n = 31) (n = 22)
level 2 mmol/L), moderate (lactate level 5 mmol/L,
I 10 (66.6%) 3 (20%) 2 (13.33%)
II 11 (32.35%) 17 (50%) 6 (17.64%)
with persistent increase in blood lactate
III 2 (10 %) 11 (55%) 7 (35%) concentration without metabolic acidosis) and
IV 4 (36.36%) - 7 (63.63%) severe (characterised by persistently increased

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Annals of Cardiac Anaesthesia 2005; 8: 39–44
blood lactate levels, usually >5 mmol/L, in
association with metabolic acidosis). The
distinction between the types of lactic acidosis is
based on the presence or absence of clinical
evidence of tissue hypoperfusion.4 Cohen & Woods
have classified lactic acidosis into two categories:
Type A (lactic acidosis in association with clinical
evidence of poor tissue perfusion) and Type B
(lactic acidosis with no evidence of poor tissue
perfusion).9
Several studies have shown a strong positive
correlation between blood lactate levels and the
risk of morbidity and mortality in clinical situa-
tions such as circulatory shock, septic shock,
hypovolaemic shock, severe hypoxaemia, liver
failure, diabetes mellitus, and following exercises.4
Studies on blood lactate levels in children
undergoing cardiac surgery for congenital heart
diseases have also shown similar results.1 However,
literature on adult patients undergoing valvular
heart surgery under CPB is limited. Literature also
fails to explain the relation of elevations in serum
lactate levels during or after CPB, to definite
postoperative mortality and morbidity.
Furthermore, none of the studies have compared
the preoperative clinical condition as per the
NYHA classification to the changes in lactate levels
during CPB.
Studies performed in patients with shock
and also other critically ill patients have
demonstrated that a circulating blood lactate level
of 4 mmol/L or more predisposes to a striking
increase in morbidity and mortality rate.4 Demers
et al7 showed that blood lactate concentration of 4
mmol/L or higher during CPB identifies a
subgroup of patients with increased risk of
postoperative morbidity and mortality. In our
study, the baseline mean lactate level was 1.89±0.94
mmol/L which is similar to that shown by
Himpe.11,12
In our study, the mean lactate levels at 15 and
45 minutes on CPB increased to 7.01 mmol/L and
9.92 mmol/L respectively. The reasons for this
increase have been enlisted earlier. We also
observed a progressive decline in mean lactate
levels during rewarming (at 35°C), off bypass, 24
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Shinde et al. Blood Lactate Levels during CPB 43
hours and 48 hours postoperatively with mean
lactate levels being 7.01 mmol/L, 4.75 mmol/L, 3.06
mmol/L and 2.10 mmol/L respectively. The
elevations in mean lactate levels were significant
(p< 0.001) in patients in NYHA class IV at 15
minutes and 45 minutes on CPB, during rewarming
and 24 and 48 hours post-CPB.
Comparison of mean lactate levels with relation
to duration of CPB revealed higher levels in those
who had CPB lasting more than 1 hour (p< 0.05).
However, the levels returned to normal 48 hours
after surgery in both the groups.
An increase in the levels of circulating cate-
cholamines has been reported to cause moderate
hyperlactataemia, usually attributed to the
metabolic effects of catecholamine on glycolysis
and gluconeogenesis.4 Furthermore, an increase in
circulating catecholamines is responsible for
splanchnic vasoconstriction thereby reducing
perfusion to the gastrointestinal tract during and
after surgery. 4 However, studies done by
Shoemaker and Tuchschmidt13 have reported that
inotropic agents and vasodilators, used to achieve
specific optimised oxygen transport goal, reduce
the incidence of postoperative hyperlactataemia.4
In our study the inotropes used were dopamine
and adrenaline. Dopamine was used in doses less
than 10 µg/kg/min and hence the possibility of
dopamine-induced vasoconstriction is unlikely.
The patients with elevations in lactate levels of
more than 4 mmol/L had the longest duration of
mechanical ventilation and inotropic support while
those with lactate levels < 2 mmol/L had least
duration of postoperative mechanical ventilation
and inotropic requirement. There was no mortality.
This is in contrast to the study by Munoz et al1 who
have shown a high mortality in patients with serum
lactate levels of >4 mmol/L.
Correlation between mean lactate levels and
NYHA class shows that as the NYHA class of a
patient increases from I to IV, the extent of elevation
in lactate levels during CPB also increases.
However due to limited number of patients in each
subgroup a statistical analysis could not be
performed.
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44 Shinde et al. Blood Lactate Levels during CPB
With regards to mortality and morbidity, there
was no mortality, with morbidity occurring in 2
patients. Both these patients had elevated lactate
levels starting from baseline till 48 hours
postoperative.
References
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lactate levels during CPB for surgery for congenital
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control of glycolysis in mammalian tissues. Biochem J 1987;
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3. Boyer PD. Lipid Enzymology. In: Denmis EA, The
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Annals of Cardiac Anaesthesia 2005; 8: 39–44
We conclude that a high NYHA class and longer
duration of CPB is associated with a significant
increase in lactate levels during perioperative
period and that increased lactate levels are directly
proportional to the duration of mechanical
ventilation and inotropic support.
7. Demers P, Elkouri S, Martineau R. Outcome with high
blood lactate levels during cardiopulmonary bypass in
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