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The interpretation of perioperative lactate abnormalities in patients undergoing cardiac surgery.

Lactic acid, a hydroxyl carboxylic acid, has been recognised as a key factor in animal muscle physiology since the early 19th century and continues to inspire debate and controversy in physiology and medicine (1). Initially, lactate was seen as a "dead-end waste product", its effects deemed universally undesirable throughout the mid-late 1900s (2). In recent years, a large body of evidence has further demonstrated an association, if not causation, between elevated serum lactate and poor outcomes in critical illness (3). During and after cardiac surgery, dynamic changes in tissue and serum lactate are common and hyperlactataemia (HL) is often, but not invariably, associated with adverse surgical outcomes (4). This article aims to present an overview of lactate physiology as it pertains to the field of cardiac surgery, to demonstrate the complex relationship between time of onset of HL and patient outcomes and to summarise literature on the origin of hyperlactataemia during cardiac surgery.

CLASSIFICATION OF HYPERLACTATAEMIA

Hyperlactataemia has been defined as mild to moderate with blood lactate levels between 2 and 5 mmol/l in the absence of metabolic acidosis5. Lactic acidosis (LA) is defined as persistently elevated lactate levels (usually >5 mmol/l) with concurrent metabolic acidosis (5). Lactate is a chiral molecule; it exhibits stereo-isomerism. The D-Lactate enantiomer is produced by a number of bacterial species, some of which inhabit the human gut. It is not however produced by human cells. L-lactate is therefore the principal focus of this review.

PATHOPHYSIOLOGY OF HYPERLACTATAEMIA AND LACTIC ACIDOSIS

Lactate is a byproduct of glycolysis, whereby glucose undergoes a series of reactions to yield pyruvate and energy in the form of adenosine tri-phosphate. In turn, cytoplasmic pyruvate can undergo either: a) oxidative phosphorylation (Krebs cycle) in mitochondria in the presence of oxygen or; b) enzymatic conversion to lactate, a process which does not require oxygen. In solution, lactate is a strong anion. Therefore, it reduces the strong ion difference and the base excess and in accumulation causes a metabolic acidosis. These effects are independent of whether the lactate production occurs in a low or normal oxygen environment (6).

Under standard conditions, the ratio of serum lactate to pyruvate (the L:P ratio) approximates 10:1. This increases substantially in situations of low oxygen tension, when the majority of cellular pyruvate is converted to lactate and HL or LA occur. This has been termed a type A lactic acidosis (7,8).

However, HL can also occur in the presence of normal oxygen utilisation, whereby comparable amounts of pyruvate undergo oxidative phosphorylation and reduction to lactate. In this scenario, the serum L:P ratio remains near normal and a type B lactic acidosis occurs (8). This mechanism may explain the LA/HL seen in: a) druginduced lactic acidoses (nitroprusside, salicylates, metformin, anti-retroviral agents, adrenaline, salbutamol); b) thiamine deficiency; c) HL in malignancies with high cell turnover and; d) HL in extreme exercise (9-18). Following cardiac surgery, there is evidence that both type A and type B lactate disorders occur.

HYPERLACTATAEMIA IN CARDIAC SURGICAL PATIENTS

Hyperlactataemia is seen in a bimodal distribution during cardiac surgery and cardiopulmonary bypass (CPB). The peaks in lactate levels are seen: a) during or soon after the initiation of cardiopulmonary bypass and; b) in the subsequent 4 to 24 hours of the postoperative intensive care unit (ICU) stay (4). Table 1 summarises some of the causes of HL and LA in cardiac surgical patients.

Early-onset Hyperlactataemia

HL occurs during or soon after CPB in 10 to 21% of patients undergoing on-pump cardiac surgery and frequently persists until ICU arrival. It has been termed "immediate hyperlactaemia" (IHL) (19,20).

It is a familiar finding for cardiac anaesthetic and intensive care clinicians and commonly raises concerns about a complicated intra or postoperative course. Multiple factors contribute to the development of early hyperlactataemia and these are summarised in Table 2. With the use of tissue microdialysis, elevated levels of lactate, glycerol and an increased L:P ratio have been identified during CPB in myocardial and non-myocardial tissue (29-31); these are all indices of tissue ischaemia suggesting a type A mechanism underlying IHL.

Concerns about early-onset hyperlactataemia as a predictor of adverse postoperative complications are justified. Clinical studies in post-cardiac surgery patients have demonstrated an association between IHL during CPB or reperfusion and adverse outcomes in the postoperative period. When compared with those with a normal lactate profile, patients with IHL have an eight to tenfold increase in postoperative mortality (19,32) and have an odds ratio of death of 5.6 to 13.4 (20,33).

In a small retrospective Australian study, early lactate levels >10 mmol/l predicted postoperative death with a positive predictive value of 100% (34). In a recent prospective study by Ranucci et al, HL >3 mmol/l developing during CPB was associated with higher intra-aortic balloon pump usage (odds ratio [OR] 23[2.7-207]), and a longer duration of ICU stay (OR 4.2[1.04-17]) and mechanical ventilation (OR 4.9[1.6-15]) (35). A further study has demonstrated an association between IHL and intra-aortic balloon pump treatment failure (36). Toraman et al prospectively studied 242 patients with serum lactate >2 mmol/l within 30 minutes of completion of cardiac surgery and when compared to normolactataemic patients; they had a greater requirement for intra-aortic balloon pump therapy (OR 5.9, P=0.006) and prolonged ICU support (OR 3.4, P=0.0001) (20). Further studies confirm the association between IHL and poor outcomes (28,37). The implications of IHL in paediatric post-cardiac surgical patients seem to parallel those in adults (38-40).

More recently, a study by Perz et al demonstrated an association between "immediate and persistently increased lactate production" and mortality after cardiac surgery, with some elevated lactate levels identified during weaning from CPB (41).

Late-onset hyperlactataemia

A phenomenon of late-onset HL (LHL) has been shown to occur after cardiac surgery. Observational data describe a peak lactate 4 to 14 hours after completion of surgery, usually returning to normal within 12 to 24 hours (4,16,19,42). This occurs in 14 to 20% of adult patients following emergency and elective cardiac surgery (4,16,19).

Substantial clinical and physiological data suggest that LHL is not caused by an impairment of tissue perfusion or oxygen delivery (4,16,19,42). At least three published studies have demonstrated adequate cardiac output and oxygen delivery measured either by pulmonary artery catheterization (4,16) or by transpulmonary thermodilution42 in the setting of serum lactate levels as high as 11.9 mmol/l, with or without a high anion gap metabolic acidosis. Tissue microdialysis in patients with LHL have demonstrated a simultaneous rise in tissue lactate associated with a near normal L:P ratio; further evidence supporting a non-ischaemic aetiology (42).

While the evidence supports a separate phenomenon to IHL, the origin and significance of LHL remains unclear. In one study, despite evidence of adequate oxygen delivery, periods of maximal acidosis coincided with a peak in mixed venous oxygen saturation suggesting an underlying impairment in tissue oxygen uptake4. In addition, LHL has shown a consistent association with hyperglycaemia (4,16,19,42). The significance of this is uncertain; does hyperglycaemia provide more glucose substrate for pyruvate and lactate production, thereby increasing lactate without altering the L:P ratio or does hyperlactataemia facilitate glucose production through the Cori cycle? Current literature does not answer these questions. In addition, elevations in endogenous catecholamine levels during and following CPB may contribute to hyperlactataemia; an association has been established between these elevated levels and LHL (4) but it is not a universal phenomenon (43). Finally, a further association has been demonstrated between LHL and duration of CPB and intraoperative hypothermia, but neither causation nor mechanism has been identified (4,16,19).

There is general acceptance that type B HL has a more benign course than the type A HL; its occurrence post-cardiac surgery is not associated with increased mortality. In the three published prospective studies of 473 adult patients following elective and emergency cardiac surgery, 78 (16.5%) developed either LHL or type B LA (4,16,19). When compared to those with normal lactate, these patients had an OR of death 1.39 (95% confidence interval 0.28 to 7.04) (calculations from pooled data from two heterogenous studies reporting a mortality outcome) (4,19) .

We conducted a retrospective study of 529 patients having elective on-pump coronary artery grafting and/or valve surgery in a nine-bed tertiary cardiothoracic ICU. LHL (>2.5 mmol/l) developed in 25.1% of patients with a mean onset 649[+ or -]389 minutes after ICU admission. When compared with those with a normal postoperative lactate profile, patients with LHL had similar rates of inhospital mortality (OR 0.57 [95% confidence interval 0.07 to 5.05]) and emergency re-open surgery (OR 1.32 [95% confidence interval 0.68-2.56]) but had a significantly longer ICU length of stay (38.90[+ or -]25.64 vs 30.97[+ or -]24.42 hours, P <0.01) and duration of mechanical ventilation (14.44[+ or -]14.86 vs 11.24[+ or -]8.58 hours, P <0.05) (preliminary report) (44). A similar association between LHL and increased ICU therapies (increased volume of fluid resuscitation, greater use of inotropes and vasopressors, longer ICU stay and duration of ventilation) has been previously documented4,19. It raises the question, do patients with LHL have a favourable outcome because they receive an increased level of ICU vigilance and support, or do these ICU therapies unnecessarily prolong what would otherwise be an uncomplicated postoperative course characterised by a benign type B hyperlactataemia? This cannot be concluded from current published literature. Although some authors associate LHL with the occurrence of major postoperative outcomes (18), no study to date has been able to make reliable assertions about mortality outcomes (19).

POTENTIAL SOURCES OF LACTATE DURING CPB

Myocardium

Myocardial muscle has been shown to be a source of lactate during CPB, although tissue levels do not necessarily correlate with blood levels. Poling et al used microdialysis to measure perioperative myocardial indices of ischaemia in patients undergoing coronary artery bypass surgery with left ventricle ejection fraction <40% and normal right ventricle function (31). They showed a consistent elevation of right ventricle and left ventricle myocardial lactate levels during CPB which returned to normal within six hours of surgery. Of note, the L:P ratio was the earliest indicator of unsuccessful coronary artery revascularisation, supporting its role in the rapid detection of peri-and postoperative myocardial ischaemia.

Myocardial tissue lactate concentrations have been measured by microdialysis prior to commencing CPB by Heringlake et al (45). They demonstrated that patients with high baseline myocardial lactate were significantly more likely to manifest a low cardiac output state and to require inotropic support to successfully wean from CPB. Moreover, as myocardial lactate did not correlate with plasma lactate, the tissue lactate levels would be expected to have a higher negative predictive value for ruling out myocardial ischaemia.

A further study of 17 patients undergoing elective coronary artery grafting demonstrated marked changes in myocardial lactate, pyruvate and L:P ratio during and after CPB. The authors interpreted these changes as evidence of tissue dysoxia. That none of the patients had clinical or enzymatic features of myocardial ischaemia or abnormal plasma lactate or pyruvate makes it difficult to draw conclusions about the role of tissue lactate and pyruvate in this setting (30).

Other potential sources of lactate production

The controversy surrounding the integrity of splanchnic perfusion during CPB is not a recent one and previous work has demonstrated mucosal pH changes, altered intestinal permeability and elevated markers of ischaemia, including lactate, in splanchnic blood (46-49). More recently, two published microdialysis studies in a total of 35 patients demonstrated a significant increase in rectal lactate levels during elective coronary artery bypass surgery interpreted as metabolic dysfunction related to reduced oxygen delivery to, or utilisation by the bowel mucosa (50,51). The relationship between mucosal and arterial lactate levels was inconsistent. Notably, mucosal lactate levels were significantly lower during off-pump surgery when compared with on-pump surgery (51).

Elevated lactate levels have been demonstrated in skeletal muscle during CPB. Pojar et al used microdialysis to measure local concentrations of lactate, pyruvate and glycerol in skeletal muscle during coronary artery bypass surgery with and without CPB (29). This simple study demonstrated circumstantial evidence for muscle ischaemic injury during CPB with high L:P ratio and local elevation of glycerol. Once again, tissue lactate and L:P ratio were significantly higher during on-pump rather than off-pump surgery.

To date, studies of local pulmonary lactate production are limited to measurements from pulmonary blood lactate. Two recent studies in 56 patients confirm that the lung is a major source of lactate production following CPB and that lung lactate release may occur as late as six hours after surgery (52,53). While neither study showed correlation between duration of CPB and lung lactate release, one showed a correlation between high lung lactate and prolonged mechanical ventilation.

SUMMARY

HL occurring during or soon after CPB is most likely a manifestation of tissue ischaemia occurring during cardiopulmonary bypass. Its presence increases the risk of a complicated postoperative course and may confer an eight to tenfold increase in mortality. Therefore, it should prompt a thorough patient evaluation to identify a new shock state or potential causes of tissue hypoxia.

In contrast, late-onset HL more closely resembles a type B LA with microdialysis evidence supporting adequate oxygen delivery and uptake in the peripheral tissues. Although not an independent predictor of in-hospital mortality after cardiac surgery, it is associated with a longer intensive care unit stay and duration of ventilation. How should we respond to a new episode of late-onset HL in an otherwise stable patient several hours after completion of cardiac surgery? At the very least, this should alert the physician to the possibility of a new cardiorespiratory complication and should mandate a thorough reappraisal of the patient's condition. However, if a clinical deterioration cannot be detected, the authors suggest that extubation and weaning of support should not be delayed.

Finally, there are no published long-term outcome data on patients developing late-onset HL after cardiac surgery. Further research will evaluate long-term morbidity and mortality in such patients.

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Accepted for publication on March 27, 2012.

E. O'CONNOR *, J. F. FRASER ([dagger])

Adult Intensive Care Services, Prince Charles Hospital, Chermside, Queensland, Australia

* MB, BCh, BaO, MRCPI, FCICM, FJFICMI, PGCertMedEd, Staff Specialist in Intensive Care, Department of Intensive Care, St James' Hospital, Dublin, Ireland.

([dagger]) MB, ChB, PhD, MRCP, FRCA, FFARCSI, FCICM, Staff Specialist in Intensive Care and Director of Critical Care Research Group.

Address for correspondence: Dr E. O'Connor. Email: endamed@yahoo.com.au
Table 1

Causes of perioperative hyperlactataemia and lactic acidosis in
patients undergoing cardiac surgery

Common

Low cardiac output state

Cardiogenic shock

Distributive shock (sepsis, post-CPB shock state)

Drug-related (adrenaline, salbutamol)

Late-onset hyperlactataemia

Uncommon

Hepatic failure

Severe hypoxia

Severe anaemia

Renal failure

Severe hemolysis

Large volume blood transfusion

Excess lactate metabolism (lactate-based renal- replacement
therapy solutions)

Malignant hyperthermia

Drug-related (propofol, sodium nitroprusside)

Pancreatitis

Administration of Ringer's Lactate fluid

CPB=cardiopulmonary bypass.

Table 2

Factors implicated in the evolution of early-onset hyperlactataemia
in patients undergoing cardiac surgery

Factors

Tissue hypoxia (19)

Impaired tissue oxygen uptake due to capillary sludging
consequent to non-pulsatile flow (21)

Elevated endogenous catecholamines stimulating
gluconeogenesis and glycolysis (15)

Administration of exogenous catecholamines (4)

Activation of the hypothalamopituitary axis (22)
Hyperglycaemia (4)

Systemic inflammation and microvascular thrombosis (23)

Contents of the CPB priming fluids (24)

Lactate load from transfusion of stored packed red cells (25)

Genetic polymorphisms altering the cytokine response to the
extracorporeal circuit (26)

Low CPB rates (27)

Haemodilution (28)

Long CPB time (35)

Low oxygen delivery on CPB (35)

Elevated serum creatinine (35)

Active endocarditis at the time of surgery (35)

CPB=cardiopulmonary bypass.
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Author:O'Connor, E.; Fraser, J.F.
Publication:Anaesthesia and Intensive Care
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Date:Jul 1, 2012
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