The most severe form of perioperative HF with the highest mortality is cardiogenic shock. Based on European experts’ opinion, the classification of severe cardiac impairment in the perioperative period of CS should be based on the time of occurrence in relationship to the surgical intervention, and on the hemodynamic severity of the condition of the patient [132]. There are three distinct clinical scenarios of perioperative HF with cardiogenic shock —namely precardiotomy (preoperative) HF, failure to wean from CPB, and postcardiotomy (postoperative) HF – each of them requiring appropriate diagnosis, monitoring and specific management, all of which are of course also highly dependent on the hemodynamic severity of the condition. Depending on this hemodynamic severity, the cardiogenic shock patient is described as crash and burn, deteriorating fast, or stable but inotrope dependent. Crash and burn patients are in cardiac arrest or in refractory cardiogenic shock despite maximal treatment. Deteriorating fast patients require increasing dose of intravenous inotropes and/or IABP and show therefore progressive deterioration despite appropriate therapy. Finally, patients stable on inotropes are dependent on inotropes and/or IABP to maintain minimal hemodynamic goals and do not show clinical improvement; this is said with the understanding that these patients are in real need of inotropic support and fail to be weaned from inotropes, with decreasing inotropes resulting in hemodynamic compromise.

According to the STS definition of cardiogenic shock, minimal hemodynamic goals to be obtained and maintained to reverse a clinical state of hypoperfusion are commonly considered systolic BP >80 mmHg and/or CI >1.8 L/min per square meter. If intravenous inotropes and/or IABP are necessary to obtain these minimal goals cardiogenic shock is present [186]. Note that ESC hemodynamic criteria for cardiogenic shock are slightly different, including a CI <2.2 L/min per square meter and an increased PAWP of >18 mmHg, besides the necessity of inotropes or IABP to maintain a systolic BP >90 mmHg [187].

In the precardiotomy HF profile altered LV function is often primarily due to myocardial ischemia or acute MI and priorities focus on rapid diagnosis and treatment. CABG represents an important therapeutic option for revascularization in patients with cardiogenic shock, albeit in a minority of patients and particularly if the coronary anatomy is not amenable to PCI [187]. Functional MR may be present or preexistent, but conversely massive MR can be caused by an ischemic rupture of a papillary muscle. Part of the dysfunctional myocardium may not be irreversibly damaged (stunned and hibernating myocardium). An IABP is commonly inserted preoperatively and in extreme patients a mechanical device may be considered. In this clinical setting the operative morbidity and mortality is very high.

Failure to wean from CPB patients, as intended after a more than 1 h prolonged weaning time, have cardiac arrest (crash and burn), or manifest deteriorating hemodynamic instability on withdrawal of CPB and/or require increasing doses of inotropes and/or IABP to maintain minimal hemodynamic goals. They should be mechanically assisted without delay at predefined maximal level of inotropic support. Application of IABP within 30 min from the first attempt to wean from CPB and mechanical circulatory support within 1 h from the first attempts to wean from the CPB are suggested to reduce the high incidence of organ system complications that is directly related to prolonged attempted weaning without mechanical support when this is clearly needed [132, 188]. Finally there are stable but inotrope dependent patients on withdrawal from CPB, after more than 30 min weaning time. Intravenous inotropes and/or IABP are here required to maintain the minimal hemodynamic targets, without clinical improvement (failure to wean from inotropes).

IABP is the most widely used mechanical support for the treatment of cardiogenic shock, based on the beneficial effect of aortic diastolic inflation and rapid systolic deflation, improving myocardial and peripheral perfusion and reducing afterload and myocardial oxygen consumption. IABP is used on a pathophysiologic basis, because there’s no good quality evidence upon which indications for and timing of IABP in cardiac surgical patients could be based. However, timely application of effective therapies is essential if further deterioration of hemodynamics and multiple end organ failures are to be avoided.

Despite common use in clinical practice in CS, there is somewhat conflicting evidence with respect to the benefit of IABP in cardiogenic shock in a different setting: Inserting an IABP in the setting of severe perioperative HF with cardiogenic shock is clearly not the same as using an IABP in acute MI patients with cardiogenic shock. Nonetheless, some comments are in order about IABP use in cardiogenic shock after the disappointing IABP-SHOCK II trial [189] that everybody was thinking could have affirmed contemporary clinical practice and guidelines. Instead, it revealed surprising results. Use of an IABP offered no 30-day mortality benefits in this RCT that randomized to IABP or no IABP 600 acute MI patients with cardiogenic shock all scheduled for early PCI and optimal medical therapy [189]. Moreover, it did not find anything positive in the secondary end points, meaning there were no significant differences in process-of-care measures, length of stay, dose and duration of catecholamines, or renal function [189]. Importantly, no safety differences were seen either, in terms of bleeding, peripheral ischemic complications, sepsis, or stroke [189]. However, one important consideration in IABP-SHOCK II trial is the timing of pump use. It was left to the investigators when the balloon pump was inserted and, although it would have been unlikely to have a benefit after PCI, it must be pointed out that 86.6 % of IABPs were inserted only after the procedure [189], and this may as well have had a bearing on the negative results. Of note, in ESC 2012 ST elevation MI (STEMI) guidelines [187], IABP use in STEMI patients was downgraded from 1C to 2B. Certainly, IABP use in the different setting of severe perioperative HF with cardiogenic shock is still to be considered. Nonetheless, someone will now reflexively assume that we will need more and earlier LV assist devices and must avoid wasting time with IABP. There are many doubts this is the way to go. IABP is still the first choice device in intra- and perioperative cardiac dysfunction, especially with suspected coronary hypoperfusion, and if not contraindicated. Its advantages include easy insertion, the well known pathophysiologic benefits and four decades of experience resulting today in a low complication rate. Perioperative IABP insertion should therefore be considered as soon as evidence points to possible cardiac dysfunction, preferably intraoperatively to avoid the excessive need of inotropic support.

If the hemodynamics keep on being poor and a refractory perioperative cardiac failure is diagnosed as not adequately responding to advanced inotropic treatment and IABP, we must resort to ventricular assist devices, which should be considered early rather than later, before end organ dysfunction becomes evident. There are different options to mechanically assist failing ventricles. ECMO provides a low cost, short-term solution to the clinical priority of preserving end organ function while bridging the patient to further decision, or hopefully to successful recovery. Patients, whose cardiac function does not recover during the initial support and are eligible for cardiac transplantation can be switched to long-term mechanical support (bridge to transplantation, chronic mechanical support as an alternative to transplantation).

Meticulous surgical technique, contemporary coagulation management, and blood conservation strategies help to minimize postoperative bleeding in cardiac surgical patients and transfusions; these are important issues of perioperative management, as it is recognized that perioperative transfusions are associated with a worse outcome, and every attempt should be applied to limit the use of allogeneic blood products [190]. Undoubtedly, cardiovascular stability is enhanced if chest tube output is low. In addition to the other causes of acute cardiovascular dysfunction, once the chest is closed postoperative tamponade should be considered either (see Table 9.1).

Postcardiotomy (postoperative) HF patients are closed chest ICU patients who develop HF and who can be reopened quickly if needed, as in crash and burn settings like cardiac arrest or refractory cardiogenic shock (systolic BP <80 mmHg and/or CI <1.8 L/min per square meter, critical organ hypoperfusion with low SvO₂, systemic acidosis and/or increasing lactate levels despite maximal treatment, including inotropes and IABP). Patients may develop a low CO syndrome even though BP is preserved. The common initial management of postcardiotomy cardiac dysfunction is again optimization of cardiac load conditions as appropriate for rhythm and (bi)ventricular function, with the addition of support with inotropes and/or vasopressors and/or IABP as needed, and again this strategy will restore hemodynamics in most patients. Stable on inotropes patients (inotrope dependent patients) fail to decrease their inotropic support but have stable hemodynamics. Conversely, deteriorating fast patients manifest hemodynamic instability and need increasing drugs doses, shows progressive deterioration, worsening acidosis and increasing lactate levels. In these patients emergent intervention is required. In the deteriorating fast and in the refractory cardiogenic shock patient that does not deserve a reoperation, ECMO should again be early considered —on an individual basis, and taking into account the experience of the group as well as patient age and comorbidities – to preserve end organ function while bridging the patient to further decision or recovery.

Critical care of patients with RV dysfunction or RV failure and PH after CS is challenging. The appropriate treatment of such patients is based on relatively weak evidence, which has been systematically reviewed [191]. Hemodynamic management follows the same principles outlined about the postCPB phase. PAC monitoring data are extremely useful. TEE or TTE should be extensively used as well, albeit intermittently. Cardiac surgical patients with critical RV dysfunction or RV failure often require longer mechanical ventilatory support. There are no data documenting optimal ventilation strategies for these patients. In order to maintain RV output by minimizing RV afterload, it seems reasonable to limit tidal volume to a P_plat < 27 cmH₂O, with a low level of applied positive endexpiratory pressure (PEEP) <7 cmH₂O, and the avoidance of dynamic hyperinflation with intrinsic PEEP, while also avoiding hypercapnia. That is the so-called “RV protective ventilation” suggested for ARDS patients [192], and brings about the added benefit to prevent ventilation-induced lung injury [193].

As said, multimodal fast-tracking programs appear to be safe only in patients considered to be at low to moderate risk [102]. The high-risk patients, now not only defined on the basis of the preoperative data but of awareness of both intraoperative events and post-CPB status either, should be the object of special attention and care. Such patients remain sedated and ventilated in the ICU, striving for maintaining hemodynamic stability, and refraining from reducing inotropic support for 12–24 h, in the absence of obvious improvement. Later in the clinical course, as soon as conditions are sufficiently improved, extubation of these patients is to be considered.

However, more than being extubated early whatever their status, these patients need to be extubated at the right time, because discontinuing positive ventilation may exacerbate cardiac failure. In general, withdrawal of ventilatory support invariably increases intrathoracic blood volume and LV afterload and can be thought of as a type of cardiovascular stress test [194]. Full knowledge of cardiopulmonary interactions is of paramount importance in understanding the role of mechanical ventilation for treating patients with HF and, by contrast, the deleterious cardiovascular effects of respiratory weaning in patients with overt or hidden cardiac failure [195]. Weaning-induced cardiac dysfunction and acute cardiogenic pulmonary edema could explain a large amount of liberation failure from mechanical ventilation [195]. Patients with marginal cardiac function may require optimization of heart function through diuresis, afterload reduction, or inotropy before discontinuing mechanical ventilation. Moreover, low CO states directly and indirectly contribute to pulmonary dysfunction. Therefore, the timing of extubation should be carefully evaluated; and after extubation it seems also appropriate to consider preemptive use of postoperative noninvasive ventilation (NIV) or at least to have a low threshold to institute NIV to forestall untoward consequences of weaning and buy time to further improve hemodynamics with medical therapy. NIV has the potential to be an effective preemptive and therapeutic tool in the CS setting [196]. Nonetheless, it is important not to hesitate before performing reintubation when NIV is judged to be ineffective.

Anesthesia, sternotomy, surgical manipulation, and CPB create transient deleterious effects on pulmonary functions even with normal lungs. These include diminished functional residual capacity that worsens ventilation perfusion mismatch and impairs oxygenation; increased intravascular lung water with diminished lung compliance that increase the work of breathing; increased expiratory airway resistance; and reduction in the vital capacity, which favors atelectasis [197]. These changes in the mechanical properties of the respiratory system, in respiratory muscle strength, and spirometric measurements are detectable in the hours after surgery and last for many days or weeks. They can collectively be referred to as postoperative pulmonary dysfunction.

The pathophysiologic changes of the postoperative pulmonary dysfunction compound any preexisting significant underlying illnesses —which include intrinsic lung disease (e.g., COPD) as well as pulmonary dysfunction secondary to cardiac disease (e.g., congestive HF) – which increase susceptibility to postoperative respiratory problems. HF increases pulmonary capillary pressure and lung water, leading to problems ranging from mild pulmonary congestion to overt cardiogenic pulmonary edema. Furthermore, a low CO state leads to fatigue, which in turn results in weak coughing, reduced mobility, and lack of deep breathing. These conditions may exacerbate atelectasis and increase the propensity for pneumonia. Accordingly, the major cause of poor pulmonary outcome after CS is cardiac dysfunction, and the more so in patient with HF.

Indeed, we should recognize a continuum between the subclinical postoperative pulmonary dysfunction and the diagnosed postoperative pulmonary complications. It is believed that a multimodal approach consisting of careful hemodynamic and fluid balance control, coupled with intensive chest physiotherapy, semirecumbent postoperative position, early mobilization, expanded preemptive use of NIV, individualized, effective pain management, and inhaled bronchodilators might be of value, albeit not proven, to reduce the likelihood of progression from postoperative pulmonary dysfunction to overt complications. Certainly, there are some patients where the retention of secretions due to pain, weakness, dyspnea, or neurologic impairment, is very often the trigger for delayed postoperative pulmonary failure owing to atelectasis and pneumonia. It is in these patients where chest physiotherapy might be useful in mobilizing secretions, and possibly preventing atelectasis from progressing to pneumonia.

Furthermore, respiratory function after CS can be easily influenced by postoperative occurrence of extracardiac organ or systemic complications, and firstly by fluid retention secondary to low CO states and AKI [198]. Therefore, prolonged mechanical ventilation, or reintubation —either shortly after initial extubation or because of delayed respiratory failure – are not uncommon, and respiratory complications remain a leading cause of postcardiac surgical morbidity that can prolong hospital stays and increase costs. Respiratory problems are the leading reason that patients get readmitted to the ICU after CS, once again demonstrating the important nature of respiratory complications following surgery. Therefore, both early and later in the clinical course we should remain aware that the causes of postoperative dyspnea and respiratory failure after CS are manifold (see Table 9.2), in order to appropriately direct effective therapies.

One area that is often neglected is postoperative pain management, and this should not be the case in this population with sometimes tenuous hemodynamics. Patients with severely decreased ventricular function will not tolerate the stress response and tachycardia that accompany postoperative pain because of the increased MVO₂ (potentially leading to ischemia) and decreased diastolic filling time (potentially leading to decreased SV). This combination is especially deleterious in patients with poor ventricular function and will exacerbate hemodynamic instability. Obviously, inadequate analgesia also discourages deep breathing and favors atelectasis.

Nutritional support is important and must be provided via the enteral route as soon as possible. Several studies have demonstrated the beneficial effect of providing enteral versus parenteral nutrition in different conditions as soon as possible in ICU patients [199, 200]. A recent large randomized controlled trial (RCT) found that early initiation of parenteral nutrition in patients not meeting the caloric recommended intakes by enteral feeding leads to higher complication rates and longer ICU stay [201]. As parenteral feeding seems not to improve outcomes in a general ICU population, and can have untoward consequences —accumulation of uremic waste products in AKI patients, increased fluid loading – it should only be used cautiously, if at all in these HF patients.

Blood glucose control is also considered important. There is a well-performed, albeit single-centre, RCT [202] showing benefit of avoiding hyperglycemia (>210 mg/dL) in the critically ill. Tight glycemic control in the perioperative period is associated with reductions in mortality and length of critical care unit stay, as well as reductions in wound infections and complications in CS patients [203]. However, many clinicians fear the possibility of perioperative hypoglycemic events [204, 205] given the variable caloric intake and the disruption of anabolic and catabolic processes surrounding major surgery. Lowering glycemia could thus potentially be beneficial, but this small benefit is easily offset by the much higher risk of hypoglycemia [206]. In critically ill patients, it seems reasonable to use insulin therapy targeting 140–150 mg/dL to ultimately maintain plasma glucose levels between 110 and 180 mg/dL.

Another layer of perioperative pathophysiologic and clinical complexity is added by heart-kidney interactions that frequently occur and manifest in individual patients with one or more types of acute and chronic cardiorenal and/or renocardiac syndromes [207]. To avoid untoward consequences on cardiorespiratory status and on outcome, patients at increased risk for AKI and particularly those with manifest AKI require careful monitoring of their hemodynamic status, in order to balance the risk of renal hypoperfusion on the one hand and fluid overload on the other. CO and BP should be kept within optimal limits to ensure the best possible kidney perfusion. It is suggested to use protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI [208]. Such goal-directed therapy includes avoiding hypotension, optimizing oxygen delivery and careful fluid and vasopressor management when indicated [209]. However, hazardous fluid overload must be avoided, and after optimization of circulating blood volume, as renal perfusion pressure is more important than renal blood flow per se, and as the action of vasopressors is immediate and directly reversible, it is recommended using vasopressor therapy rather than extra fluid in patients with low SVR. Optimization of circulating blood volume is directed toward limiting inotropic and vasoconstrctive agents to the lower possible amount able to guarantee an adequate CO and renal perfusion pressure. Fluid intake is then commonly modulated on the basis of the urine output, and potassium intake appropriately restricted; nephrotoxic drugs are avoided or discontinued; and doses of drugs metabolized by the kidney are adjusted. Putative renal doses of dopamine are useless, and several metaanalyses have pointed out that dopamine failed to improve outcomes in patients with AKI [210, 211]. It as been suggested not using diuretics to increase urinary volume in established AKI, except for the management of volume overload [208]. Indeed, in metaanalyses, the use of furosemide was not associated with any significant clinical benefits in the prevention and treatment of AKI in adults [212, 213], Since fluid retention is one of the major consequences of impaired kidney function, initiation of continuous renal replacement therapy is common, to facilitate fluid management and nutritional support, and specifically to treat AKI early and aggressively to prevent further deterioration of the kidney function and of cardiorespiratory status.

Obviously, contemporary multimodal bundle strategies to prevent healthcare-associated infections, and optimal medical therapy are a given.

There is of course more to be said and done for the postoperative care of these challenging patients, beyond the scope of this brief overview of the main management issues. Taking an integrative approach to the heart interacting with systemic organs is of fundamental importance for improving clinical management and patient outcomes. By and large, given the limitations in physiologic reserves of patients with secondary MR and HF, perioperative clinicians should seek to accomplish a precise hemodynamic management together with aggressive, multimodal perioperative treatment strategies focused on prevention, timely recognition and early treatment of the main complications to streamline as much as possible the postoperative course, and optimize results of the patients selected for surgery.