Cardiovascular disease remains the most important limiting factor affecting postoperative morbidity and mortality [9]. Cardiovascular disease is the major cause of increased morbidity and mortality in dialysis patients and accounts for over 50% of deaths, while the risk of cardiovascular disease is 10–30 times higher in dialysis patients than in the normal population. Coronary artery disease impacts 25% of patients with chronic kidney disease [10]. Several factors may contribute to the development and progression of cardiovascular disease in patients on renal replacement therapy. These include both the traditional cardiovascular risk factors recognized in the general population and additional risk factors particular to chronic kidney disease. Damage starts in early stages and frequently in the form of dilated cardiomyopathy, congestive cardiac failure, left ventricular hypertrophy and pulmonary hypertension. Accelerated arteriosclerosis is promoted by diabetes and dyslipidaemias, while hypertension and cardiomyopathy is usually due to both volume and pressure overload and high levels of renin-angiotensin. Atrial fibrillation is also more prevalent in patients with ESRD than in the general population, and it is associated with increased perioperative risk for stroke and mortality. If possible, preoperative electrolyte disturbances are corrected with dialysis in order to minimize the risk of new-onset or recurrent atrial fibrillation or other cardiac dysrhythmias. An electrocardiogram (ECG) should therefore be considered as part of standard preoperative assessment.

Hypertension plays an important role in causing cardiac damage by producing left ventricular hypertrophy, which predisposes the patient to ischaemia. The prevalence of hypertension is up to 90% in patients with a glomerular filtration rate below 30 mL/min and is both a cause and a consequence of chronic kidney disease. The impairment of coronary perfusion in a hypertrophic heart results in regional impairment of left ventricular contraction and left ventricular dilatation, leading to systolic dysfunction. The risk of cardiovascular death in patients on dialysis has been reported to be 2.2 times greater in those with a pre-dialysis blood pressure of 130/80 mmHg or greater than in those with a blood pressure of less than 130/80 mmHg [11]. Foley et al. have reported that, after adjusting for age, diabetes, ischaemic heart disease, haemoglobin and serum albumin, each 10-mmHg rise in mean arterial blood pressure is associated with concentric left ventricular hypertrophy and the development of ischaemic heart disease and cardiac failure [12].

The optimal preoperative cardiac evaluation for dialysis patients is not well defined but generally depends upon the level of risk. According to the ESC/ESA guidelines on noncardiac surgery [13], effective perioperative cardiac management includes preoperative risk stratification based on preoperative assessment of functional capacity, type of surgery, cardiac risk factors and cardiovascular function. The ESC/ESA guidelines discourage indiscriminate routine preoperative cardiac testing, because it is time- and cost-consuming and resource limiting and does not improve perioperative outcome. They rather emphasize the importance of individualized preoperative cardiac evaluation and the cooperation between anaesthesiologists and cardiologists.

Patients already taking beta-blockers should continue taking their regular dose, including the morning of surgery, in order to minimize the chance of development of tachycardia or ischaemia. However, prophylactic initiation of beta-blockers prior to surgery is not recommended as this intervention may increase the risk of hypotension, stroke and death.

Diabetic nephropathy is the most common cause of ESRD in Europe. Diabetes mellitus is seen in up to 30% of patients who need renal replacement therapy and can aggravate hypertension and cardiovascular disease, resulting in a greater risk of stroke or myocardial infarction [14]. Hence, screening and treatment of coronary artery disease are essential in diabetic patients undergoing surgery. Many issues regarding the perioperative care of dialysis patients with diabetes are the same as for diabetic patients without ESRD. However, dialysis patients with type 1 diabetes may be more brittle than patients who do not have ESRD. Given the wide variations in glucose metabolism with surgery, the management of these patients may therefore be extremely difficult.

As GFR falls, phosphate excretion falls leading to reduced absorption of calcium from gastrointestinal tract and vitamin D deficiency. Hyperactivity of parathyroid glands attempts to maintain calcium. This may play a role in the pathogenesis of cardiovascular disease in CKD. A high degree of fibrosis and myocardial calcium content can lead to the development of myocardial hypertrophy and diastolic dysfunction of the left ventricle [15]. Secondary hyperparathyroidism and increased calcium phosphate product have been found to be associated with calcification of the cardiac valves and coronary arteries. It has also been suggested that hypophosphatemia is mainly responsible for cardiac valve calcification. Calcium-based chelators are widely used for phosphate control; however, high doses are required, which can lead to frequent episodes of hypercalcaemia, thus contributing further to metastatic calcification. This secondary hyperparathyroidism also leads to osteomalacia culminating into a clinical entity known widely as renal osteodystrophy. The result is bone demineralization making these patients susceptible to spontaneous pathological fractures.

Malnutrition is common in ESRD patients and its pathogenesis is complex. Under-dialysis leads to anorexia and abnormalities in taste which impact dietary nutrition intake. Increasing dialysis adequacy can improve nutritional intake. Some of the other factors involved in ESRD-related malnutrition include restrictions in diet and fluid which reduce the calories available and make food less attractive, medications which impair absorption of nutrients, bowel function and/or appetite, loss of nutrients during haemodialysis, dialysis-induced catabolism and chronic inflammation. Protein-energy wasting, inflammation and cardiovascular disease may increase mortality in the dialysis population [16]. Poor nutrition reduces tissue repair and should be corrected to minimize the risk of wound infection or dehiscence. In the case of elective surgery, there should be adequate time to involve a dietician, increase dialysis adequacy and improve nutritional intake prior to surgery.

Normochromic, normocytic anaemia is a known complication of ESRD secondary to decreased erythropoietin synthesis and release, decreased red cell life span, increased haemolysis and bleeding or repeated loss during haemodialysis. Compensatory mechanisms to overcome the decrease in oxygen carrying capacity include an increase in cardiac output and 2,3-DPG causing a right shift of oxygen dissociation curve and thus improving tissue oxygenation. Anaemia is also linked to cardiovascular morbidity and mortality. In a study by Harnett et al., the independent relative risk of mortality in dialysis patients was calculated to be 1.18 per 1.0-g/dL decrease in haemoglobin level [17]. Ideally, the preoperative haemoglobin concentration should be at the recommended target range of 11–12 g per dL (haematocrit 33–36%) in patients with CKD who receive erythropoiesis-stimulating agents [18]. The guidelines do not recommend a specific haemoglobin level at which to initiate these agents, but they are usually given when a patient’s haemoglobin level is less than 10 g per dL (100 g per L), when the rate of haemoglobin decline suggests a need for a blood transfusion and when the reduction of transfusion-related risks, such as alloimmunization, is a goal. For patients undergoing elective surgery, if the patient has haemoglobin less than target, erythropoietin-stimulating agents may be administered preoperatively. Iron studies should also be performed since iron deficiency can contribute to anaemia and erythropoietin resistance.

Inability to excrete water, electrolytes and free acids results in metabolic acidosis, hyponatraemia, hyperchloraemia and hyperkalaemia. For every 0.1 unit change in pH, potassium increases by 0.6 mEq/L. Hypermagnesaemia usually follows hyperkalaemia and can cause neuromuscular weakness, respiratory failure, bradycardia, hypotension and heart block. The potassium concentration that is acceptable for surgery depends on the urgency of the surgery. There are no guidelines that definitively state a maximum safe level of potassium prior to induction of anaesthesia but all patients with an elevated serum potassium concentration should have a 12-lead electrocardiogram. The potassium concentration that is deemed acceptable for induction of individual patients may vary depending on chronicity of hyperkalaemia and type of surgery. Surgery with anaesthesia that faces chronic hyperkalaemia (K < 6) and no ECG changes is usually well tolerated by the majority of patients. Chronic dialysis patients often have an increased tolerance for hyperkalaemia, as ECG changes are frequently not seen until the serum potassium concentration exceeds 6.0–6.5 mEq/L.

The patient’s volume status or estimated dry weight should also be appreciated preoperatively, notably by the frequency of dialysis and when it was last performed. The optimal volume status prior to surgery is based in part upon estimates of anticipated fluid to be administered and/or lost during surgery. If euvolaemia or estimated dry weight is not achieved and/or the patient receives a large volume of fluid during surgery, hypervolaemia and possibly pulmonary oedema can occur in the immediate postoperative period, thereby necessitating dialysis. On the other hand, in case of hypovolaemia, there is a risk of hypotension during anaesthesia-induced systemic vasodilatation, which can cause many significant complications, including but not limited to thrombosis of the arteriovenous access.

An increased tendency of bleeding at sites of surgery may be present in dialysis patients. Prothrombin time (PT) and activated partial thromboplastin time (aPTT) remain normal but bleeding time (BT) is prolonged. However, not all uraemic patients have a bleeding diathesis, and some are actually hypercoagulable. It is likely that multiple factors are responsible for the platelet dysfunction in uraemia. These include retention of uraemic toxins due in part to inadequate dialysis, anaemia, excess parathyroid hormone and the use of antiplatelet agents. Standard coagulation tests including prothrombin time (PT), activated partial thromboplastin time (aPTT), international normalized ratio (INR) and platelet count are usually obtained in all patients, whereas a bleeding time is not recommended as a preoperative screening test. For most patients taking aspirin for primary or secondary prevention of cardiovascular disease, the dose is held for 5–7 days before noncardiac surgery unless there are specific indications for its continuation. Aspirin is restarted after surgery, when the perioperative risk of major bleeding has passed. However, the approach to perioperative aspirin administration may differ for certain types of surgery. Clopidogrel should be stopped at least 7 days prior to surgery. The approach to patients receiving dual antiplatelet therapy after percutaneous coronary intervention should be discussed individually.