Patients with cirrhosis and portal hypertension exhibit a cardiovascular hyperdynamic syndrome characterized by increased heart rate and cardiac output and reduced systemic vascular resistance and arterial blood pressure [9]. These alterations intensify with the progression of the liver disease. Briefly, portal hypertension increased the shear stress on the splanchnic vessel walls leading to increased production of various vasodilators (such as nitric oxide), causing splanchnic vasodilation. Other factors including bacterial translocation or hyporesponsiveness of the splanchnic vessels to vasoconstrictors also contribute to the splanchnic vasodilation. The shunting of blood and the excess of vasodilators from the splanchnic to the systemic circulation following the opening of portal-systemic shunts related to increased portal pressure also leads to systemic arterial vasodilation. Altogether, these modifications lead to a reduction in the effective blood arterial volume, thereby stimulating endogenous vasoconstrictor systems (i.e., sympathetic nervous system, renin-angiotensin-aldosterone system), favoring water and salt retention, and triggering a hyperdynamic circulation in these patients [10].

In parallel, these patients can develop an authentic cirrhotic cardiomyopathy that associates impaired contractile responsiveness to stress, diastolic dysfunction, and electrophysiological abnormalities (e.g., prolonged QT interval and abnormal chronotropic response) without any other cause of cardiac disease. Thus, during the course of cirrhosis, there is a progressive deterioration of cardiac function that plays an important role in the pathogenesis of the impairment of effective arterial blood and correlates with the degree of liver failure.

Altogether, as vasodilation intensifies with disease progression, cardiac output cannot increase further, leading to arterial hypotension, activation of vasoconstrictors, and continuous renal sodium and water retention, accumulating as ascites. Refractory ascites, hyponatremia, and hepatorenal syndrome (HRS) are extreme manifestations of this process.

Often multifactorial, acute kidney injury (AKI) occurs in approximately 20% of hospitalized patients with cirrhosis and has a poor prognostic impact [11]. This prevalence may be underestimated if the diagnosis is made on serum creatinine. Indeed, muscle mass is frequently low in cirrhotic patients and the release of creatinine reduced [12]. Therefore, patients may have a normal serum creatinine in the setting of a very low glomerular filtration rate. In most of cases (70%), AKI mechanism is prerenal and results from renal hypoperfusion without glomerular or tubular lesion. Indeed, abovementioned circulatory modifications make cirrhotic patients especially susceptible to absolute or relative hypovolemia resulting from gastrointestinal bleeding, diuretic use, sepsis, or large volume paracentesis. HRS is the result of a persistent renal hypoperfusion related to systemic vasodilation in the absence of precipitating event (e.g., hypovolemia or nephrotoxic drug). It is a diagnosis of exclusion that is specific for decompensated cirrhosis and differs from other prerenal AKI because it is not volume responsive. To conclude to HRS, strict criteria should be met [13]: (1) cirrhosis with ascites, (2) serum creatinine >133 μmol/L (or 1.5 mg/dL) after at least 2 days or diuretic withdrawal and volume expansion with albumin (1 g/kg body weight), (3) absence of shock, (4) no current or recent treatment with nephrotoxic drugs, and (5) absence of parenchymal disease as indicated by proteinuria >500 mg/day, microhematuria (>50 red blood cells/high power field), and/or abnormal renal ultrasonography. Although albumin and vasoconstrictors administration can improve kidney function, the only curative treatment of HRS remains liver transplantation. Indeed, HRS occurrence represents a significant turn in the history of cirrhosis as it associated with a devastating prognosis (mortality rate up to 90%) without liver transplantation.

Regardless of the etiology, chronic liver disease has well-established effects on respiratory function. Firstly, ascites and pleural effusion can lead to a marked lung restriction and atelectasis. Hepatic hydrothorax, a pleural effusion that develops in patients with cirrhosis in the absence of substantial cardiac or pulmonary disease, may occur in as many as 10% of patients with chronic liver disease [14]. Acute pulmonary edema is favored by the high rate of cardiac diastolic dysfunction shown in these patients (48% and up to 88% in CPT classes A and C, respectively) [15]. More specifically, two distinct pulmonary vascular disorders, hepatopulmonary syndrome (HPS) and portopulmonary hypertension (POPH), may occur as a consequence of hepatic parenchymal or vascular abnormalities. HPS, which is found in approximately 20% of patients, refers to the triad of portal hypertension, hypoxemia, and intrapulmonary vascular dilations resulting in a right to left shunt. Although application of oxygen improves hypoxemia, mechanical ventilation during general anesthesia might aggravate intrapulmonary shunting [16]. POPH results from an obstruction to arterial flow in the pulmonary arterial bed. It must be screened using echocardiography in patients with liver disease and symptoms of dyspnea [17]. Portopulmonary hypertension is indistinguishable from other forms of pulmonary hypertension, and its cause is far from understood [18]. Treatment with agents approved for POPH (i.e., prostacyclin analogues, phosphodiesterase inhibitors, or endothelin receptor antagonists) for 3–6 months may be useful in improving hemodynamics and exercise capacity in patients with POPH [19].

Cirrhosis is associated with alterations of the coagulation system involving all phases of hemostasis: primary hemostasis (platelet-vessel wall interactions), coagulation (thrombin generation and inhibition), and fibrinolysis (clot dissolution) [20]. However, contrary to common belief, cirrhosis is associated with alterations of both pro- and anti-hemostatic drivers (Table 11.2) [20], and the coagulation system is in fact rebalanced. While it is important to recognize that procoagulant factors (factors II, V, VII, IX, X, and XI) are decreased in cirrhosis, one may not forget that anticoagulant factors (antithrombin and protein C) and fibrinolytic proteins produced in the liver are also reduced. Similarly, low platelet count may be counterbalanced by increased platelet aggregability caused by highly active von Willebrand multimers [21] or procoagulant changes in fibrin clot structure. Altogether, these data suggest the establishment, in cirrhotic patients, of a restored, albeit fragile, hemostasis equilibrium that can quickly move toward an acute bleeding risk. Nevertheless, to date, routine coagulation tests (such as prothrombin time) are assessing the defect in procoagulant drivers in isolation, and not the thrombotic risk of these patients [22]. Thus, there is increasing evidence that changes in both coagulation factors and platelet count regularly observed in cirrhotic patients cannot be interpreted as a reliable indicator of diffuse bleeding risk. Moreover, the increased thrombotic risk of these patients is now well documented. Cirrhosis is a risk factor for thromboembolic disease [23]. In practice, despite the lack of clear evidence, PT <30%, hypofibrinogenemia <1 g/L, and thrombopenia <50 G/L are regularly considered as threshold values that may motivate prophylactic correction of hemostasis disorders.

Patients with cirrhosis have increased risk of developing bacterial infection, sepsis, sepsis-induced organ failure, and sepsis-related death [24]. Bacterial infections increase mortality of cirrhotic patients fourfold with 30% of these deaths occurring within the year after sepsis. Furthermore, in-hospital mortality of patients with cirrhosis who have septic shock is higher than in other patients and exceeds 70% [24–26]. Such susceptibility is related to immune system alterations referred to as cirrhosis-associated immune dysfunction (CAID) that associates an immune paralysis (also called immunodeficiency) and systemic inflammation features [27]. While immune paralysis (also called immunodeficiency) is due to an impaired response to pathogen (e.g., involving reduced HLA-DR/co-stimulatory molecule expression on monocytes/macrophages or decreased phagocytosis-mediated bacterial clearance), systemic inflammation is a consequence of persistent and inadequate stimulation of cells of the immune system that may cause tissue damages and favor the development of organ failures [24].

Predisposition of cirrhotic patients to develop infections is also linked with nutritional status. Indeed, malnutrition is particularly frequent in patients with cirrhosis (up to 70% of the patients in the waiting list for liver transplantation) and especially severe in those with alcoholic liver disease. Malnutrition can be measured by anthropometric measurements (e.g., involuntary weight loss and BMI), but albuminemia and prealbuminemia are not suitable in cirrhosis as they are influenced by liver disease. In this context, measurement of muscle depletion (i.e., sarcopenia) using CT scan is particularly interesting as it is independently associated with poor outcome (see below).

Concerns related to hepatotoxicity of intravenous and even of inhaled anesthetic agents can be considered as historic. Anesthetics for which elimination primarily depends on renal clearance or redistribution (such as propofol, etomidate, fentanyl, sufentanil) are usually the first-choice drugs, However, pharmacokinetics of drugs is highly variable in severe cirrhotic patients because of major changes in distribution volumes and sodium retention, albumin plasma levels, metabolism, and elimination processes. Furthermore, hepatic perfusion is reduced and cirrhotic liver is more susceptible to hypotension and hypoxia [28]. Therefore, the effect of a bolus is unpredictable, and anesthetic agent administration should be titrated [28]. Noteworthy, intraoperative hypotension has been shown to negatively impact cirrhotic patient postoperative outcome.