7.3.7 Water and metabolic balance

In addition to the priming volume (800-1500 mL), ECC requires the administration of approximately 500 mL per hour. If haemofiltration is not used, the result is a very positive water balance at the end of the procedure, regardless of the diuresis. Indeed, there is an accumulation of interstitial fluid due to several phenomena: oncotic pressure is decreased, permeability of membranes is increased (inflammatory syndrome, ischaemia), venous drainage may be poor, lymphatic drainage is absent when flow is depulsed. This results in altered pulmonary gas exchange. If ventilation with PEEP is not sufficient to restore them, furosemide administration is necessary. However, this haemodilution is an aggravating factor for all organs, to the extent that a Ht of less than 23% has been shown to be an independent predictor of postoperative morbidity and mortality [7,18]. When Ht falls below 30%, haemodilution tends to increase bleeding, dilute fibrinogen and determine a hypocoagulable state on thromboelastogram [17]. Renal function worsens linearly with decreasing haemoglobin when haematocrit is below 30% [20]. Neurological sequelae clearly increase when Ht falls below 26% [6].

Three electrolytes are commonly disturbed after ECC and should be corrected if they are associated with clinical manifestations.

• Hyperkalaemia (≥ 5 mmol/L); this is related to cardioplegia and warrants Ca²⁺ administration; in the absence of renal failure, it corrects spontaneously.
• Hypocalcaemia (< 1 mmol/L); it is imperative to maintain normocalcaemia in cases of haemorrhage and administration of coagulation factors or transfusion. However, calcium has no significant inotropic effect and its administration is useless in case of normocalcaemia and normokalaemia; it may even trigger arterial spasm (mammery graft).
• Hypomagnesemia (< 0.8 mmol/L) is very common after ECC and may be associated with arrhythmias. MgCl₂ infusion is routinely prescribed for every case in some centres.

Lactate is frequently modified when weaning off ECC. Its level is related to cellular metabolism. It increases in several circumstances: reduced O₂ transport (low flow, low pressure, low Ht) or its use (sepsis, possibly bypass surgery), increased production by certain organs (digestive, hepatic, myocardial ischaemia, ischaemia of the lower limb during femoral cannulation) or certain drugs (adrenaline, stimulantsb 2), and excessive intake of lactate-containing solutions (Ringer's, Lactasol) [1]. Moderate (2-4 mmol/L) or severe (>4 mmol/L) lactate elevation is associated with the duration of ECC, surgical complexity, renal failure and acute anaemia, and is correlated with postoperative morbidity and mortality [9,12]. However, increased lactate is multifactorial in origin and has limited prognostic value, whereas its normality (< 2 mmol/L) has a strong predictive value for the absence of complication [1]. The discovery of hyperlactatemia should trigger the search for possible causes of a low DO₂ or organic ischaemia.

ECC triggers a violent stress reaction. Along with major burns, it is the situation the body experiences as the most stimulating: increase in endogenous catecholamines (4 to 15 times the norm), cortisol, ACTH, ADH, glucagon and growth hormone. The cause is hypothermia, flow depulsation, and sympathetic reflexes triggered by the exclusion of the heart from circulation. Catecholamines are normally metabolised in the lungs. During ECC, lungs are excluded from circulation, contributing to elevated serum catecholamine levels. Stimulation of the renin-angiotensin system leads to an increase in systemic arterial resistance and retention of water and sodium. It also induces a decrease in immunological defence reactions, both humoral and cellular  [5].

This metabolic stress induces pronounced hyperglycaemia. During cardiac surgery, blood glucose regulation follows a particular pattern in relation to the bypass surgery (see Chapter 21 Diabetes) [2].

• Marked hyperglycaemia (10-12 mmol/L) during normothermic (>35°C) bypass surgery; blood glucose increases almost linearly with the duration of ECC. Several phenomena are involved: hypersecretion of stress hormones, release of inflammatory activators, carbohydrate sparing created by the increase in free fatty acids linked to the administration of heparin; in fact, heparin activates lipoprotein lipases and increases the level of free fatty acids by occupying their place instead of the circulating proteins [4].
• In hypothermia (28-32°C), insulin levels are lowered compared to the normothermic period (tendency towards hyperglycaemia), but cellular metabolism is inhibited (tendency towards hypoglycaemia), so consumption is reduced, insulin requirements are lowered and apparent insulin resistance is increased. Overall, it is wise to discontinue the insulin infusion necessary to maintain normoglycaemia during the hypothermic phase : risk of hypoglycaemia.
• As the body warms up, blood glucose levels rise significantly and metabolism reactivates; although it also increases, insulin secretion remains inadequate to bring glucose back to normal values; the requirement is increased up to six times during this period. It is therefore logical to resume insulin infusion.
• Inhibition of spontaneous insulin secretion during ECC in both normothermia and hypothermia is more pronounced with non-pulsatile flow than with pulsatile flow; it diminishes progressively after bypass surgery but continues for 48 hours. In addition to inadequate insulin secretion in case of hyperglycaemia, there is an increased peripheral resistance.
• Insulin deficiency leads not only to hyperglycaemia, but also to proteolysis, lipolysis and acetonaemia characterised by acidosis (pH < 7.3), bicarbonates < 15 mmol/L and anion gap > 10 [16].
• The use of exogenous catecholamines potentiates hyperglycaemia.
• These phenomena are more pronounced when perfusates and priming solutions contain glucose or lactate.

Maintaining blood glucose levels within limits (6-10 mmol/L) is crucial, as the risk of cardiac complications after ECC increases by 17% for each unit above 6.1 mmol/L of blood glucose [13]. The risk is seven times higher in patients with inadequate intraoperative blood glucose control (blood glucose > 11 mmol/L) [15]. In both diabetic and non-diabetic patients, persistent blood glucose levels >14 mmol/L (250 mg/dL) quadruple mortality (OR 3.9), triple the incidence of MI (OR 2.7), and double the incidence of pulmonary and renal complications (OR 2.3) compared with maintaining blood glucose levels <11 mmol/L (200 mg/dL) [3] (see Chapter 21 Intraoperative Blood Glucose Control). Under general anaesthesia, however, hypoglycaemia is a greater immediate danger than hyperglycaemia, as it goes unnoticed between blood sample checks. It can only be prevented by frequent blood glucose checks (every 30-60 minutes). Based on the experience of the last ten years, the current recommendations for cardiac surgery in bypass surgery are therefore as follows [8,10,11,14,18,21].

• Diabetic patients should receive a continuous infusion of insulin based on their daily intake to maintain blood glucose levels at < 10 mmol/L permanently; the tighter the patient's blood glucose is regulated in their daily life, the tighter the control.
• In non-diabetic patients, insulin treatment becomes mandatory when blood glucose levels remain > 10 mmol/L; tolerance is lower than in a diabetic who is used to hyperglycaemic disturbances.
• In the operating room, a blood glucose level maintained between 8.0 and 10 mmol/L (140-180 mg/dL) is optimal.
• A sleeping patient who is unable to report discomfort is at high risk of dangerous hypoglycaemia as soon as blood glucose level nears 4 mmol/L.

For application, see Chapter 21 Anaesthesia for the diabetic patient.

Myocardial b receptor turnover, which is 8-12 hours, is slowed in ECC. As a result, patients are relatively devoid of b receptors during weaning, which alters the efficacy of beta catecholamines [19]. This change becomes important in patients with chronic ventricular failure, who already have a decrease in b receptor levels  compared to a . 

 © CHASSOT PG, GRONCHI F, April 2008, last update December 2019

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