Open access peer-reviewed chapter

Perspective Chapter: Perioperative Management in Cardiac Surgery

Written By

Maria del Carmen Renteria Arellano and Hugo de Jesus Ballesteros Loyo

Submitted: 08 November 2023 Reviewed: 06 December 2023 Published: 03 July 2024

DOI: 10.5772/intechopen.1004262

From the Edited Volume

New Insights in Perioperative Care

Nabil A. Shallik

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Abstract

The patient undergoing heart surgery must be managed differently and more intensively than the average surgical patient. These are patients with important hereditary and pathological antecedents as well as co-morbidities and chronic pathologies. For this reason, studies and compilations have been carried out in order to improve the conditions of the patients and to have a favourable evolution. Likewise, advances in technology, as well as pharmacological advances have brought new strategies for the improvement of these patients, mainly by undergoing cardiopulmonary bypass. This chapter is intended to be a guide for intensivists and the best management of patients undergoing cardiac surgery.

Keywords

  • cardiopulmonary bypass (CPB)
  • preoperative medicine
  • cardiovascular surgery
  • intensive care medicine
  • intra-aortic balloon pump (IABP)

1. Introduction

Cardiac surgery, when properly indicated, saves lives almost immediately. However, it is rarely performed in a timely manner or as a last resort in patients with significant cardiac damage.

In recent years, it has progressed exponentially, creating new expectations for patients with heart disease to recover quickly and without complications.

Different groups and/or associations have been created, such as the ERAS (Enhanced Recovery After Surgery) programme which presents a transdisciplinary enhanced care initiative to promote the recovery of patients undergoing surgery throughout their perioperative journey [1].

These programmes aim to reduce complications and promote an earlier return to normal activities for patients [2, 3]. The ERAS protocol has been associated with a reduction in all complications and length of in-hospital stay of up to 50% compared to conventional perioperative management of the non-cardiac surgery patient [4, 5, 6].

Cardiac surgery covers a wide range of surgical techniques and a variety of physiological insults that can have an impact on postoperative recovery. As in any other speciality, the patient has his or her own pre-existing comorbidities which have a major effect on the outcome. These factors range from pre-existing medical conditions to the patient’s cognitive ability or nutritional status prior to surgery.

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2. Perioperative medicine

This is a new and growing area of medicine that is of great interest in the surgical world, as it includes different specialities, in this case, cardiology, critical care medicine, anaesthesiology and cardiac surgery.

It is mainly supported by evidence-based medicine, and, as previously mentioned, by groups and/or protocols such as ERAS, which have allowed to involve patients in their care, reduce the stress response to surgical trauma and allow the patient to regain normal function more quickly after major surgery.

In recent years, cardiovascular surgery has evolved by leaps and bounds with several advances including improved myocardial protection, safer systemic perfusion during extracorporeal circulation (ECC) and cerebral protection in situations of circulatory arrest (which can occur for multiple causes, and is primarily the surgeon’s decision), as well as the implementation of safe surgery protocols during surgery; standard monitoring supported by transesophageal echocardiography of technical complications; the incorporation of minimally invasive surgical techniques, the implantation of transcatheter valves without sutures and the development of multimodal rehabilitation among many others. The aim is to improve the patient’s quality of life and return to normal life as soon as possible and with as little morbidity as possible [7].

As in all surgery, health personnel try to keep the perioperative period as short as possible, and this does not exclude cardiac surgery [8].

The perioperative period is defined as: The entire surgical process, whether urgent or scheduled, that a patient undergoes, comprising the following phases:

  • Preoperative: From the moment the patient is informed that a surgical intervention is required until his or her arrival in the operating theatre. It includes the anamnesis in the different assessments, complementary tests and pre-surgical preparation.

  • Intraoperative: Covers from the time the patient enters the operating theatre until he/she leaves.

  • Postoperative: It covers three periods:

    1. The immediate postoperative period: From the end of the surgical procedure until recovery from the effects of anaesthesia. It usually takes place in the post post-anaesthesia recovery room; in the case of cardiac surgery, it is generally in the intensive care unit. It can last between 24 and 72 hours.

    2. The mediate postoperative period: This includes recovery from the effects of anaesthesia to recovery in hospitalisation units.

    3. The late postoperative period: Includes the patient’s recovery at home until reintegration into normal life. It is considered more of an epidemiological concept.

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3. Preoperative period in cardiac surgery

3.1 Preoperative preparation

The patient should be the focus of attention [9, 10]. This implies that the physician must provide the patient with all the necessary information to obtain informed consent for surgery, as well as a detailed description of possible events and/or complications, the importance of preoperative interventions for the surgery to go well and the expectations for the postoperative period (which are mainly the improvement of the quality of life).

Generally, the definitive diagnosis is made by the clinical and/or interventional cardiologist, who must explain all the appropriate treatments according to the condition, and according to his or her experience and knowledge of medical advances, which would be ideal for the pathology to be treated.

On the other hand, the cardiologist should also be the doctor who identifies and/or manages the patient’s pre-existing diseases, such as systemic arterial hypertension, diabetes mellitus, arrhythmias, nutritional status, psychological status, anaemia, renal insufficiency, etc. However, nowadays with specialised medicine, it is preferred that it be managed by an internist or with the subspecialty that corresponds to the diagnosis.

Likewise, the treating physician must insist on changes in hygienic-dietary habits (such as giving up alcohol, smoking and drug addiction) and improving cardiopulmonary fitness [11].

3.2 Risk assessment and risk stratification

All patients undergoing cardiac surgery should be assessed for intraoperative risk. There are several scores that assess this risk, such as the EuroSCORE (European System for Cardiac Operative Risk Evaluation) or the STS (Society of Thoracic Surgeons) surgical risk. This information provides greater understanding for the patient, improves decision making, allows preoperative optimisation and enables modification of the surgical technique or procedure if necessary.

3.3 Pre-rehabilitation

It is the process of increasing the patient’s functional status and ability to cope with stress after surgery.

This includes education, correction of nutritional deficiencies, improvement of physical fitness and psychological and social support. The goal of these interventions is to reduce the patient’s anxiety, improve muscle quality and, in the background, to check that the patient has a full understanding of the surgical process, or to insist on its explanation. This stage includes:

  1. Education in cardiac surgery: This should be carried out as an individual course and teach what the surgery is based on, surgical techniques, etc., and in this way reduce and clarify doubts that the patient and/or relatives have, and, secondarily, reduce the patients’ stress. These sessions emphasise the importance of being active, living well, eating well and exercising or training to improve respiratory and muscular function before surgery.

  2. Preoperative exercise: Safe exercise programmes are available for patients with cardiorespiratory impairment, which if performed regularly improve physical and mental fitness, as it can increase the ratio of lean body mass to body fat. It also helps (although not in all patients) to decrease perioperative sympathetic dysregulation and insulin resistance [12]. Additional benefits are on the patient’s physical and psychological preparation for surgery, which helps to reduce postoperative complications, decrease the length of hospital stay and the patient has an adequate recovery before returning home [13]. This, of course, should be individualised according to each patient’s health status.

  3. Lifestyle modifications: It is common knowledge that excesses contribute to the progressive deterioration of patients, thus smoking, excessive alcohol consumption and obesity are associated with perioperative complications and poorer surgical outcomes. They can lead to serious complications, including wound infections, and only small changes in daily life, such as smoking cessation and weight loss, can significantly reduce them [14].

3.4 Minimising fasting and preoperative carbohydrate loading

Although not always accepted, mainly by anaesthesiologists, it has been shown to be safe to give clear fluids up to 2 hours before induction of anaesthesia. Several studies mention that giving the patient a carbohydrate drink (usually with 24 g of complex carbohydrates) 2 hours before surgery is a mainstay of preoperative management and is supported by most ERAS programmes. This measure is sufficiently adequate as it is associated with a reduction in insulin resistance and tissue glycosylation, stabilisation of postoperative glucose concentration and an earlier return of normal gastrointestinal function. Articles have already established that administering carbohydrate beverages prior to cardiac surgery is safe and improves cardiac function immediately after Cardiopulmonary bypass (CPB) [15].

3.5 Preoperative strategies

  1. Preoperative measurement of haemoglobin A1c for risk stratification: This simple test should be performed in practically all patients with any diagnosis. And in patients who will undergo surgery, all the more so, in order to establish optimal preoperative glycaemic control. Ideally, patients should maintain a haemoglobin A1c level of less than 6.5%; this has been associated with a significant decrease in sternal and/or mediastinal wound infections, ischaemic events and other complications [16, 17]. If the HbAc1 level is higher than 7%, significant dysglycaemia can occur, which is difficult to manage in the immediate postoperative period [18].

  2. Preoperative albumin measurement for risk stratification: It is widely known that low preoperative serum albumin in patients undergoing surgery is associated with an increased risk of morbidity and mortality after surgery. Hypoalbuminaemia is a perioperative prognostic risk factor, correlating with longer mechanical ventilation time, acute kidney injury (AKI), infections, longer hospital stay and mortality. Correction of serum albumin prior to surgery is necessary to avoid these comorbidities [19, 20, 21].

  3. Preoperative correction of nutritional deficiency: It would be great if all surgical patients were well nourished, however, this is not common. For malnourished patients, oral nutritional supplements can be given, but only have an effect if given 10 days prior to surgery. This improvement is associated with reduced prevalence of infection and improved healing. However, there is not yet a well-established programme for improving nutritional status [9, 10].

3.6 Intraoperative period

This period is characterised by the intervention of the surgeon and his skill, but just as importantly by the anaesthetic management as well as the management of the ECC by the perfusionist. However, each of these players has their own protocols depending on the type of surgery at the time and the likely complications or incidents during this period.

It should be remembered that the open heart patient requires specialised care because ECC alters physiological systems (Figures 1 and 2).

Figure 1.

Open heart surgery: Aortocoronary revascularization.

Figure 2.

Open heart surgery: Placement of valve prosthesis.

CPB (Figures 3 and 4) produces a generalised inflammatory response caused by the contact of blood with the synthetic surfaces of the bypass circuit [22]. This inflammatory response results in a series of complex reactions that activate the complement, coagulation and fibrinolytic cascade, leading to bleeding, microemboli, fluid retention and an altered hormonal response [23, 24, 25].

Figure 3.

Cardiopulmonary bypass (CPB).

Figure 4.

Cannulation for CPB.

ECC is a non-specific activator of the inflammatory system. Once ECC is discontinued, widespread complement activation occurs with elevations of anaphylatoxins C3a and C5a and this activation may result in pulmonary leukocyte sequestration and superoxide production and then further increasing leukocyte activation and leukocyte-mediated factor generation, thus further increasing the local inflammatory response [26]. Likewise, if vasoactive substances are administered during surgery, they trigger the release of platelets that also respond to ECC or protamine administration, which can lead to pulmonary hypertension and systemic hypotension [27, 28, 29].

Also, secondary to complement activation, there is an increase in vascular permeability that may predispose the patient to capillary leak syndrome with fluid sequestration in the third space, particularly in the lung.

From a clinical perspective, the generalised inflammatory response results in postoperative pulmonary dysfunction, renal dysfunction and a resetting of the hypothalamic thermoregulatory centre [26, 28, 29, 30, 31].

This inflammatory response also has direct negative cardiac effects, as the inflammation caused by CPB involves platelet-endothelial cell interactions and vasospasm leading to low flow states in the coronary circulation. Anaphylatoxin C5a is a potent spasmogenic molecule and has leukocyte-activating properties that cause degranulation and release of oxygen free radicals [32]. Leukocytes exposed to complement are attracted to adhere to vascular endothelium and aggregate, resulting in vessel margination and leukoembolisation. These inflammatory cells mediate injury by increasing their production and releasing oxygen free radicals or proteolytic enzymes, a vicious circle, increasing the inflammatory state [33].

It is this release of oxygen free radicals that is generally implicated as the cause of transient postoperative ventricular dysfunction, which manifests approximately 2 hours after cessation of CPB and worsens 4–5 hours after CPB.

Recovery of ventricular function begins within 8–10 hours and full recovery usually occurs within 24–48 hours [34].

It is now known that systemic vascular resistance (SVR) increases as ventricular function worsens. This is a compensatory mechanism to maintain systemic blood pressure and perfusion in the face of depressed ventricular contractility. Oxygen free radicals and proteolytic enzymes released by neutrophils also damage endothelial cells, which increases capillary permeability and causes capillary leakage during this period and this increase in permeability lasts 2–3 days after surgery and is proportional to the duration of CPB [35].

On the other hand, uncontrolled hypothermia is also known to cause various alterations mainly in circulatory status, predisposing to cardiac arrhythmias, increasing SVR, precipitating shivering and altering coagulation. It indirectly decreases cardiac output by increasing vasoconstriction and causing bradycardia.

The CPB circuit is not the only factor responsible for this altered physiological state. Ischaemia and reperfusion time, hypothermia, hypotension with non-pulsatile flow, impaired coagulation and administration of blood and blood products are other factors contributing to the altered postoperative physiological state [36].

But there are important points in which all participants are involved, which are as follows:

3.7 Reduction of surgical site infections

It has always been a challenge for surgeons to minimise or abolish surgical site infections. Therefore different protocols have been developed including: topical intranasal therapy to eradicate Staphylococcus aureus colonisation; depilation protocols (an important measure in the cardiac patient), preferably cutting rather than shaving, which should be performed as close as possible to the time of surgery; proper management and timing of prophylactic antibiotic administration: 1st or 2nd generation cephalosporins (Level IA) are suggested to be administered no later than 1 hour before skin incision and should be continued up to 48 hours after surgery. If surgery lasts longer than 4 hours, additional doses should be administered in the operating room.

These manoeuvres have better results if combined with other previously mentioned manoeuvres such as smoking cessation, adequate glycaemic control and promotion of postoperative normothermia during recovery [16, 37].

3.8 Avoid hyperthermia

ECC can be performed under normothermic or hypothermic conditions. The efficiency of heat exchangers means that the patient may be subjected to inadvertent hyperthermia, especially during rewarming of a hypothermic CPB. Excessive hyperthermia during rewarming is defined as a core temperature > 37.9°C and is associated with increased postoperative neurological injury, infection and renal dysfunction [38].

3.9 Rigid sternal fixation

Most cardiovascular surgeons use wire cerclage to close the sternotomy, as it has a low rate of sternal wound complications and because of the low cost of the wires. Wire cerclage joins the cut edges of the bone by wrapping a wire or band around or through them and joining the two parts together. This achieves approximation and compression, but does not eliminate side-to-side movement and therefore rigid fixation is not 100% achieved.

More recently, sternal fixation with a rigid plate has been performed, which apparently provides significantly better sternal healing, with fewer sternal complications and no additional cost compared to wire cerclage at 6 months after surgery. Improvements include significant pain reduction, improved upper extremity function and improved quality of life, with no difference in overall cost.

Also, although these studies are still limited, the findings reported a lower rate of mediastinitis, decreased painful sternal pseudarthrosis after median sternotomy and superior bone healing compared to wire cerclage [39].

However, this remains a surgeon’s decision but should be considered in special or high-risk patients, such as patients with a high body mass index, history of chest wall radiation, severe chronic obstructive pulmonary disorder or chronic steroid use.

Rigid sternal fixation may be useful to improve or accelerate sternal healing and reduce mediastinal complications [40, 41].

3.10 Management of bleeding and use of antifibrinolytics

Trans-surgical bleeding is one of the most common complications, as is bleeding greater than usual post-surgery. The range of reoperation varies from 0.69 to 7.8% and mortality increases by 15% if reoperation is performed [42, 43].

The administration of aminocaproic acid or tranexamic acid reduces the occurrence of major haemorrhage, as well as the need for less transfusion of blood products and the possibility of greater than usual bleeding or postoperative cardiac tamponade [44].

Currently, tranexamic acid is the most widely used, but it is associated with the presence of seizures, so it is recommended not to exceed a dose of 100 mg/kg body weight [45, 46, 47].

3.11 Surgical and/or haemodynamic decisions

During surgery, the big difference for an adequate recovery is the decision made for the exit of the CPB and its removal. In this area, the surgeon must decide, with the support of the anaesthesiologist, on different procedures, such as balloon counter pulsation in left ventricular failure, administration of vasoactive and/or inotropic agents or sometimes extracorporeal membrane oxygenation (ECMO).

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4. Postoperative period

This period takes place in the intensive care unit (ICU), where protocols are already established (Figure 5).

Figure 5.

Post-surgical intensive therapy unit.

Every patient admitted to the ICU has clinical problems that can change rapidly and the patient after open heart surgery is no exception [48, 49]. In fact, they are even more unpredictable. On admission, these patients are unstable and their clinical status is extremely fluid and dynamic. Care of the postoperative open heart patient requires the presence of healthcare staff at the bedside and must have knowledge of fundamental concepts of general care of the critically ill patient, as well as concepts specific to this group of patients. Initial management can set the tone for the remainder of the recovery period. Clinical errors at this time can have far-reaching implications.

Initial management should begin even before the patient arrives in the ICU. It is vital to know the medical history, previous indications for surgery, pre-operative haemodynamic data, comorbid conditions, medications and allergies [50].

Initial post-operative care in cardiac surgery requires a thorough physical examination and at least basic haemodynamic monitoring which should include: heart rate and rhythm, blood pressure, temperature, right and left heart filling pressures, haemodynamic profile, pharmacological and ventilatory support, chest drainage, assessment of neurological status, laboratory results, electrocardiogram and chest X-ray. A thorough knowledge of the specific monitoring and drug administration routes is essential, as well as having information on where the drains were placed. Once the initial assessment is complete, specific problems can be identified, prioritised and addressed [50, 51].

Subsequently, homeostasis of the internal environment should be restored, normothermia achieved, proper functioning of the epicardial pacemaker ensured and antibiotic prophylaxis continued.

It is essential to establish a multimodal analgesic strategy combining different analgesic families. This will help to reduce opioid doses, which will facilitate extubation, rehabilitation and early mobilisation of the patient.

Withdrawal of mechanical ventilation should be initiated when adequate haemodynamic stability is achieved. As in most patients, water resuscitation and actions to avoid probable acute renal failure should be administered; early initiation of thromboprophylaxis (mechanical and, when possible, pharmacological) and measures for the prevention of delirium should be given [50].

Resuscitation and haemodynamic management should be guided by objective parameters and advanced monitoring is indicated in those patients in whom there is instability, in whom it is necessary to investigate the pathophysiology of the evolution or in those patients who, due to their baseline characteristics, intraoperative evolution or the type of intervention, are considered a high surgical risk [52].

Advanced haemodynamic monitoring systems provide continuous information on more specific parameters, such as cardiac output and its determinants: preload or preload-dependence, contractility and afterload (Figure 6).

Figure 6.

Continuous haemodynamic monitoring in the ICU.

A total of 90% of all post-operative cardiac surgery patients present with transient low cardiac output (CO) related to the release of oxygen free radicals in response to the inflammatory state induced by CPB, (as explained above) or ischaemia/reperfusion injury due to cardioplegic arrest.

Low cardiac output (post-thoracotomy low cardiac output syndrome) is more common in women and when there is prolonged ECC time.

The aetiology of this syndrome may be preload, afterload, contractility or abnormal heart rate and rhythm or a combination of these.

The most common causes are related to decreased left ventricular preload caused by hypovolaemia and haemorrhage, vasodilatation, overheating, drugs, cardiac tamponade, right ventricular dysfunction, positive pressure ventilation and tension pneumothorax [50].

Increased afterload is usually the result of acute vasoconstriction, often related to vasoactive drug therapy. It may also be due to pre-existing hypertension, pain or sensitisation, fluid overload or hypothermia [50].

Decreased contractility is the main cause of low output in patients with pre-existing LV dysfunction associated with perioperative ischaemia. Perioperative ischaemia is often the consequence of poor intraoperative myocardial protection, incomplete revascularisation, coronary artery or coronary conduit spasm, coronary artery “junk” syndrome, graft closure (from any cause), acute anaemia (mainly bleeding) or the presence of hypoxia or acidosis of any aetiology [50].

Tachyarrhythmias negatively affect cardiac output by decreasing cardiac filling time and, consequently, coronary perfusion time of systolic volume. They also increase myocardial oxygen demand.

Bradyarrhythmias depress cardiac output, especially when left ventricular dysfunction limits the compensatory mechanism of increased stroke volume. Bradyarrhythmias are especially harmful in association with aortic insufficiency of any degree.

Atrial fibrillation results in loss of atrial contribution to cardiac output and a consequent fall in cardiac output.

Finally, any ventricular arrhythmia adversely affects cardiac output [50].

Contractility decreases in the immediate postoperative period of cardiac surgery compared to the preoperative period. The magnitude and duration of this phase depend on previous cardiac dysfunction, the existence of ischaemic events, preoperative complications and intraoperative evolution.

The elements that most affect cardiac dysfunction in this period are increased left ventricular mass or left ventricular dilatation, hypothermia, volume, route of cardioplegia administration and prolonged CPB time [53].

Two haemodynamic patterns may occur in the postoperative period that should be distinguished: (a) pressure overload (left hypertrophy and lusitropic dysfunction) which interferes with the assessment of filling pressures and may lead to an underestimation of volume requirements due to tachycardia intolerance; and (b) volume overload (typical in valvular regurgitation) which also alters the assessment of preload dependence and where the dynamic variables of volume response have not been validated.

Volume overload (typical in valvular regurgitation) which also alters the assessment of preload dependence and where dynamic volume response variables have not been validated.

Therefore, continuous assessment of volume response and its impact on haemodynamic parameters should be maintained to avoid inappropriate resuscitation [7].

To maintain adequate haemodynamic monitoring, there are different manoeuvres, from the placement of a flotation catheter and measurement of cardiac output and its variables to the performance of a transesophageal echocardiogram, which can be performed intraoperatively.

All these options are available in the ICU, including capillary filling, which is a validated, fast, reliable and safe technique to assess tissue perfusion in critically ill patients. As an integrator of multiple biological signals, it is a sensitive early warning system for a potentially lethal threat, activating according to the sum and intensity of the signals and turning off in the same direction.

Echocardiography has become a first-line tool in the evaluation of the postoperative patients with suspected major bleeding. As mentioned, it can be a transthoracic or transesophageal examination. Transthoracic echocardiography is of limited value in the immediate postoperative period due to the presence of wounds and their coverings and chest tubes, but it can provide some information on LV function and recognise obvious tamponade [54].

Transesophageal echocardiography is an extremely valuable tool as it provides excellent visualisation of cardiac dynamics, the pericardial space and the mediastinum. It is the best diagnostic modality for LV function, the presence of tamponade and the development of new valve abnormalities. It is also useful for the evaluation of the right ventricle [54].

Once the patient has been admitted to the unit and according to the patient’s assessment and monitoring, the relevant vasoactive substances, inotropies and, conversely, vasodilators or antihypertensives will be initiated or continued as necessary.

However, all of the above strategies should be coupled with the following strategies, which have been studied and are related to the patient’s improvement or deterioration in the postoperative period, whether or not they are implemented:

4.1 Perioperative glycaemic control

It is already well known that hyperglycaemia increases morbidity, which is multifactorial and attributed to glucose toxicity, increased oxidative stress, prothrombotic effects and pro-inflammatory effects. However, interventions to improve glycemic control are also known to improve in-hospital outcomes [55].

Preoperative carbohydrate loading has been shown to coincide with low glucose levels after a surgical procedure.

Epidural analgesia during cardiac surgery has also been shown to decrease the incidence of hyperglycaemia [56, 57, 58].

Treatment of hyperglycaemia (glucose >160–180 mg/dL) should preferably be done with post-cardiac surgery insulin infusion.

Postoperative hypoglycaemia should be avoided, especially in patients with an adjusted target blood glucose range (i.e., 80–110 mg/dL) [56, 57, 58].

4.2 Pain management

In the past, parenteral opioids were the mainstay of postoperative pain management. However, they are associated with multiple adverse effects, such as sedation, respiratory depression, nausea, vomiting and vertigo. It has now been shown that adequate pain management can be achieved through the additive or synergistic effects of different types of analgesics, allowing opioid doses to be reduced [59, 60].

NSAIDs are associated with renal dysfunction after cardiac surgery and selective COX-2 inhibition is associated with a significant risk of thromboembolic events.

The safest non-opioid analgesic is acetaminophen. When added to opioids, it has been found to produce superior analgesia, an opioid-sparing effect and independent antiemetic actions. The dose of acetaminophen is 1 g every 8 hours [61].

On the other hand, tramadol has opioid and non-opioid effects and, although it may be associated with a high risk of delirium, it decreases morphine consumption by 25%, resulting in adequate pain relief and increased postoperative patient comfort [62].

Pregabalin also reduces opioid consumption and is used in postoperative multimodal analgesia [63].

Dexmedetomidine, an intravenous α-2 agonist, reduces opioid requirements. Dexmedetomidine infusion has been shown to reduce 30-day cause-independent mortality, decrease the incidence of postoperative delirium and is associated with shorter intubation times [64].

4.3 Screening for postoperative delirium

Delirium is an acute confusional state characterised by mental status fluctuations, inattention and disorganised thinking or altered level of consciousness that occurs in approximately 50% of patients after cardiac surgery. It is associated with poorer in-hospital and long-term survival, hospital readmission and slower or reduced cognitive and functional recovery [9]. The cause is multifactorial, so early detection of delirium is critical to determine the underlying cause (pain, hypoxaemia, low cardiac output and/or sepsis) and initiate appropriate treatment [65].

Risk factors are many and include advanced age, recent alcoholism, preoperative organic brain syndrome, severe cardiac disease, multiple associated medical illnesses and prolonged time on CPB.

Common causes of delirium are drug toxicity, metabolic disorders, alcohol withdrawal, low cardiac output syndromes, periods of marginal cerebral blood flow during CPB, hypoxia, sepsis and recent stroke [9, 10].

Evaluation of delirium begins with a review of the patient’s medications and inotropic/vasoactive levels, identification of the history of recent alcoholism or substance abuse, neurological examination and determinations of arterial blood gases, electrolytes, BUN, creatinine, blood biometry, magnesium and calcium.

Treatment of delirium begins with correction of any metabolic abnormalities, discontinuation of inappropriate medication and administration of psychotropic drugs for agitation, such as haloperidol, 2.5–5 mg OV/IV every 6 hours. Treatment of suspected alcohol withdrawal includes benzodiazepines, thiamine and folate.

Due to the complexity of the pathogenesis of delirium, more than one intervention must be performed, or more than one pharmacological agent may be necessary to diminish or control it. These medications include dexmedetomidine and olanzapine. Non-pharmacological strategies are a first-line component of treatment [66, 67].

4.4 Persistent hypothermia

Postoperative hypothermia is the inability to regain or maintain normothermia (36°C or greater) for 2–5 hours after admission to the ICU following cardiac surgery. Hypothermia is associated with higher than usual bleeding, infections, prolonged hospital stay and death. Prevention of hypothermia is necessary by using forced air warming blankets, increasing the ambient room temperature and avoiding the administration of cold solutions [68, 69].

4.5 Patency of mediastinal and/or pleural catheters

All patients undergoing cardiac surgery have mediastinal and/or pleural drains placed, as the thoracic cavity must be evacuated after surgery, as most patients have some degree of bleeding [70]. However, drains used to evacuate blood from the mediastinum tend to become clogged with clotted blood in up to 36% of patients and if this happens can cause tamponade or haemothorax.

However, retained mediastinal blood haemolyses promote an oxidative inflammatory process that can cause pleural and pericardial effusions and trigger postoperative atrial fibrillation [71].

Strategies for chest tube manipulation are varied and depend on the healthcare personnel performing the manipulation. However, any strategy should fragment visible clots and/or create short periods of high negative pressure to remove clots [72, 73].

On the other hand, higher than usual bleeding may be recorded precisely because of blood drainage by the same probes, which should be quantified on an hourly basis and, according to international guidelines, acted upon, either with transfusion (plasma, cryoprecipitates) or pharmacological measures (tranexamic acid, aminocaproic acid) or surgical re-intervention.

4.6 Thromboprophylaxis

Vascular thrombotic events include both deep vein thrombosis and pulmonary embolism and represent potentially preventable diseases.

All patients benefit from mechanical thromboprophylaxis achieved with compression stockings and/or intermittent pneumatic compression during hospitalisation or until they have adequate mobility to reduce the incidence of deep vein thrombosis after surgery even in the absence of pharmacological treatment [9, 73].

After cardiac surgery, these mechanical measures should be put in place, and prophylactic pharmacological anticoagulation should be initiated in 12–24 hours. After ICU admission, as satisfactory haemostasis must first be achieved, mainly at the thoracic level, and remember that CPB produces an inflammatory response that includes the coagulation system. Once adequate haemostasis is confirmed, pharmacological prophylaxis is initiated (most commonly on postoperative day 1 until patient discharge) [73, 74].

4.7 Extubation strategies

It is recommended to try to perform extubating early, preferably within 6 hours of the patient’s arrival in the ICU. Protocols for extubating together with low-dose opioids are now available to enable such a procedure to be performed. This is safe (even in high-risk patients) and is associated with reduced ICU stay, reduced infections (pneumonia) and lower costs [9, 10, 75].

4.8 Acute kidney injury

Acute kidney injury (AKI) occurs in 22–36% of cardiac surgical procedures. Patients should be assessed on admission to identify those at risk of developing AKI, however, also the surgical procedure itself, the duration of CPB and hypotension/hypertensive events within the operating room can lead to AKI [76, 77]. Impaired renal oxygenation during CPB has been shown to improve with increased CPB flow but this may contribute to postoperative renal dysfunction and suggests the need to consider targeted perfusion strategies. It is therefore necessary to avoid nephrotoxic agents, to suspend angiotensin-converting enzyme inhibitors and angiotensin II antagonists for 48 hours, to maintain adequate blood volume and to avoid fluid overload and vasoplegic events. To avoid or prevent AKI, it is necessary to have strict control of creatinine and urine output, avoid hyperglycaemia and radiocontrast agents, as well as strict control to optimise hydration status and general haemodynamic parameters [78, 79].

When AKIN II-III acute kidney injury occurs, it is necessary to initiate renal replacement therapy, which is often with continuous slow haemodialysis (Figure 7).

Figure 7.

Continuous slow dialysis therapy in the ICU.

4.9 Fluidotherapy

This manoeuvre uses monitoring techniques to guide the administration of fluids, vasopressors and inotropes to avoid hypotension and/or low cardiac output. This manoeuvre has quantified targets including blood pressure, cardiac index, mixed venous oxygen saturation and diuresis. In addition, oxygen consumption, oxygen debt and lactate levels can augment or modify therapeutic tactics.

Adequate volemia must be maintained without overload and must not be so low as to cause AKI [80].

4.10 Other factors

There is always the possibility of anaemia in the patient following cardiac surgery. The anaesthesiologist as well as the perfusionist perform manoeuvres to avoid severe anaemia, including transfusion of red blood cell concentrates, placement of cell salvage and/or haemofiltration during CPB. However, it is recommended to maintain a minimum haemoglobin level of 10 gm/dl in mainly ischaemic patients.

During mechanical ventilation, it is preferable to manage low tidal volume, as well as to maintain positive end-expiratory pressure (PEEP) at physiological levels and maintain measures for lung protection.

Early enteral nutrition should be considered, if haemodynamics and patient conditions allow.

Early mobilisation of the patient is also recommended, according to the patient’s physical condition and possibilities [9, 19, 38].

There are also certain manoeuvres or devices that are placed in the operating room or within the ICU to maintain a better postoperative state or to improve shock, the presence of low post-thoracotomy output or immediate complications in surgical patients. This mechanical support is performed after pharmacological management either with vasoactive substances (noradrenaline, vasopressin) and/or inotropics (dobutamine, milrinone, levosimendan, etc.).

Intra-aortic balloon counterpulsation (IABP) is an effective tool for the treatment of low cardiac output states, ongoing ischaemia, valvular disease and the complications of myocardial infarction (Figure 8) [81].

Figure 8.

Intra-aortic balloon pump.

This mechanism provides haemodynamic support and ischaemia control before and after surgery. It has been shown to be effective in improving left ventricular diastolic function. IABP is highly effective in the treatment of low cardiac output states. Unlike most inotropic agents, it provides haemodynamic support to the heart when myocardial oxygen demand is decreased and improves coronary artery perfusion, stabilising the myocardial oxygen supply: demand ratio [50].

It reduces the ejection impedance of the left ventricle by rapidly deflating just before systole, thereby unloading the LV and thus decreasing myocardial oxygen demand. As it rapidly inflates just after aortic valve closure, it increases diastolic coronary perfusion and improves myocardial oxygen delivery [50].

Indications for IABP placement are perioperative ischaemia, mechanical complications of myocardial infarction (such as acute mitral regurgitation, ventricular septal defect and cardiogenic shock), presence of greater than 80% left main coronary artery lesion in the preoperative period, postoperative low cardiac output states unresponsive to moderate doses of inotropics and acute deterioration of myocardial function to provide temporary support or a bridge to transplantation. IABP is contraindicated in the presence of aortic insufficiency, aortic dissection and severe aortic and peripheral vascular disease [50].

There are also circulatory or ventricular assist devices (VADs), which can be divided into right or left ventricular assist, however, these devices are not common in patients admitted after cardiac surgery [82]. They are the definitive therapy for low cardiac output. They are usually used intraoperatively when cardiopulmonary bypass disconnection is unsuccessful but may also be a postoperative option if the patient does not respond to vasoactive agents and IABP (Figures 9 and 10).

Figure 9.

Thoratec.

Figure 10.

Chest X-ray showing placement of heart mate III.

General indications for VAD implantation include a complete and adequate cardiac surgical procedure, correction of all metabolic problems, inability to disconnect from cardiopulmonary bypass, inability to reverse haemodynamic deterioration despite maximal pharmacological therapy and IABP and a cardiac index less than 1.8–2 L/min/m2 [82, 83].

To be optimally effective, circulatory assist devices to support low output require adequate lung function and gas exchange. In circumstances of compromised cardiac and pulmonary function, support of cardiopulmonary function is also required. Cardiopulmonary support (CPS) is achieved with a portable centrifugal pump, membrane oxygenator, heat exchanger and heparin-coated tubing. This system is generally referred to as extracorporeal membrane oxygenation (ECMO) (Figure 11). The indications for ECMO or SCP are the same as those for VADs in association with impaired oxygenation [50, 84, 85].

Figure 11.

ECMO.

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5. Conclusions

Cardiovascular surgery involves multiple manoeuvres and includes virtually all systems of the human body. Optimal perioperative management of interventional patients requires a comprehensive, multidisciplinary approach that includes adequate medical-surgical training. Preoperative optimisation, minimally invasive techniques, arrhythmia and postoperative bleeding prophylaxis, goal-directed haemodynamic management and multimodal analgesia allowing early extubation and mobilisation are key elements in the recovery of these patients.

The high level of complexity for the management, treatment and recovery of these patients makes intrinsic care units the ideal place to achieve the best results.

Close communication between the intensivist and the surgeon must be maintained to reduce the possibility of complications, treat them in a timely manner and ensure that the patient has an adequate evolution and subsequently improve their quality of life.

References

  1. 1. Ljungqvist O, Scott M, Fearon KC. Enhanced recovery after surgery: A review. JAMA Surgery. 2017;152(3):292-298. DOI: 10.1001/jamasurg.2016.4952
  2. 2. Eskicioglu C, Forbes SS, Aarts MA, Okrainec A, McLeod RS. Enhanced recovery after surgery (ERAS) programs for patients having colorectal surgery: A meta analysis of randomized trials. Journal of Gastrointestinal Surgery. 2009;13(12):2321-2329. DOI: 10.1007/s11605-009-0927-2
  3. 3. Lassen K, Soop M, Nygren J, et al. Consensus review of optimal perioperative care in colorectal surgery: Enhanced recovery after surgery (ERAS) group recommendations. Archives of Surgery. 2009;144(10):961-969. DOI: 10.1001/archsurg.2009.170
  4. 4. Spanjersberg WR, Reurings J, Keus F, van Laarhoven CJ. Fast track surgery versus conventional recovery strategies for colorectal surgery. Cochrane Database of Systematic Reviews. 2011;2:CD007635
  5. 5. Stone AB, Grant MC, Pio Roda C, et al. Implementation costs of an enhanced recovery after surgery program in the United States: A financial model and sensitivity analysis based on experiences at a quaternary academic medical center. Journal of the American College of Surgeons. 2016;222(3):219-225. DOI: 10.1016/j.jamcollsurg.2015.11.021
  6. 6. Thiele RH, Rea KM, Turrentine FE, et al. Standardization of care: Impact of an enhanced recovery protocol on length of stay, complications, and direct costs after colorectal surgery. Journal of the American College of Surgeons. 2015;220(4):430-443. DOI: 10.1016/j.jamcollsurg.2014.12.042
  7. 7. Jiménez Riveraa JJ, Llanos Jorgeb C, Gudec MJL, Velad JLP. Manejo perioperatorio en cirugía cardiovascular. Medicina Intensiva. 2021;45:175-183. DOI: 10.1016/j.medin.2020.10.006
  8. 8. Grupo de trabajo de la Guía de Práctica Clínica sobre Cuidados Perioperatorios en Cirugía Mayor Abdominal. Guía de Práctica Clínica sobre Cuidados Perioperatorios en Cirugía Mayor Abdominal. Aragón, Spain: Ministerio de Sanidad, Servicios Sociales e Igualdad, Instituto Aragonés de Ciencias de la Salud (IACS); 2016. Guías de Práctica Clínica en el SNS
  9. 9. Engelman DT, Ben Ali W, Williams JB, et al. Guidelines for perioperative care in cardiac surgery enhanced recovery after surgery society recommendations. JAMA Surgery. 2019;154(8):755-766
  10. 10. Pokhrel SMD, Gregory AMD, Mellor AMD. Perioperative care in cardiac surgery. BJA Education. 2021;21(10):396-e402
  11. 11. Schonborn JL, Anderson H. Perioperative medicine: A changing model of care. British Journal of Anaesthesia. 2019;19:27e33
  12. 12. Snowden CP, Prentis J, Jacques B, et al. Cardiorespiratory fitness predicts mortality and hospital length of stay after major elective surgery in older people. Annals of Surgery. 2013;257:999-e1004
  13. 13. Waite I, Deshpande R, Baghai M, et al. Home-based preoperative rehabilitation (prehab) to improve physical function and reduce hospital length of stay for frail patients undergoing coronary artery bypass graft and valve surgery. Journal of Cardiothoracic Surgery. 2017;12:91
  14. 14. Tønnesen H, Nielsen PR, Lauritzen JB, Møller AM. Smoking and alcohol intervention before surgery: Evidence for best practice. British Journal of Anaesthesia. 2009;102:297e306
  15. 15. Brady M, Kinn S, Stuart P. Preoperative fasting for adults to prevent perioperative complications. Cochrane Database of Systematic Reviews. 2003;4:CD004423
  16. 16. Bustamante-Munguira J, Herrera-Gomez F, Ruiz-Alvarez M, Hernandez-Aceituno A, Figuerola-Tejerina A. A new surgical site infection risk score: Infection risk index in cardiac surgery. Journal of Clinical Medicine. 2019;8:480
  17. 17. Edwards FH, Engelman RM, Houck P, Shahian DM, Bridges CR, Society of Thoracic Surgeons. The Society of Thoracic Surgeons practice guideline series: Antibiotic prophylaxis in cardiac surgery: Part I. Duration. The Annals of Thoracic Surgery. 2006;81:397-e404
  18. 18. Wong J, Zoungas S, Wright C, Teede H. Evidence-based guidelines for perioperative management of diabetes in cardiac and vascular surgery. World Journal of Surgery. 2010;34(3):500-513. DOI: 10.1007/s00268-009-0380-0
  19. 19. Kudsk KA, Tolley EA, DeWitt RC, et al. Preoperative albumin and surgical site identify surgical risk for major postoperative complications. JPEN Journal of Parenteral and Enteral Nutrition. 2003;27(1):1-9. DOI: 10.1177/014860710302700101
  20. 20. Lee EH, Kim WJ, Kim JY, et al. Effect of exogenous albumin on the incidence of postoperative acute kidney injury in patients undergoing off-pump coronary artery bypass surgery with a preoperative albumin level of less than 4.0 g/dl. Anesthesiology. 2016;124(5):1001-1011. DOI: 10.1097/ALN.0000000000001051
  21. 21. Karas PL, Goh SL, Dhital K. Is low serum albumin associated with postoperative complications in patients undergoing cardiac surgery? Interactive Cardiovascular and Thoracic Surgery. 2015;21(6):777-786
  22. 22. Cameron D. Initiation of white cell activation during cardiopulmonary bypass: Cytokines and receptors. Journal of Cardiovascular Pharmacology. 1996;27(Suppl. 1):S1
  23. 23. Tulla H, Takala J, Alhava E, et al. Hypermetabolism after cardiopulmonary bypass. The Journal of Thoracic and Cardiovascular Surgery. 1991;101:598
  24. 24. Chiara O, Giomarelli PP, Biagioli B, et al. Hypermetabolic response after hypothermic cardiopulmonary bypass. Critical Care Medicine. 1987;15:995
  25. 25. Crock PA, Ley CJ, Martin IK, et al. Hormonal and metabolic changes during hypothermic coronary artery bypass surgery in diabetic and non-diabetic subjects. Diabetic Medicine. 1988;5:47
  26. 26. Chenoweth DE, Cooper SW, Hugli TE, et al. Complement activation during cardiopulmonary bypass: Evidence for generation of C3a and C5a anaphylatoxins. The New England Journal of Medicine. 1981;304:497
  27. 27. Moore FD, Warner KG, Assousa S, et al. The effects of complement activation during cardiopulmonary bypass. Attenuation by hypothermia, heparin, and hem dilution. Annals of Surgery. 1988;208:95
  28. 28. Dinarello CA. Interleukin-1 and the pathogenesis of the acute phase response. The New England Journal of Medicine. 1984;311:1413
  29. 29. McCord JM, Wong K, Stokes SH, et al. Superoxide and inflammation: A mechanism for the anti-inflammatory activity of superoxide dismutase. Acta Physiologica Scandinavica. Supplementum. 1980;492:25
  30. 30. Jastrzebski J, Sykes MK, Woods DG. Cardiorespiratory effects of protamine after cardiopulmonary bypass in man. Thorax. 1974;29:534
  31. 31. Klausner JM, Morel N, Paterson IS, et al. The rapid induction by interleukin-2 of pulmonary microvascular permeability. Annals of Surgery. 1989;209:119
  32. 32. Gold JP, Roberts AJ, Hoover EL, et al. Effects of prolonged aortic cross clamping with potassium cardioplegia on myocardial contractility in man. Surgical Forum. 1979;30:252
  33. 33. Sladen RV, Berkowitz DE. In: Gravlee GP, Gavis RF, Uhey DR, editors. Cardiopulmonary Bypass and the Lung. 1st ed. Baltimore, MD: Williams & Willkins; 1993
  34. 34. Przyklenk K, Kloner RA. “Reperfusion injury” by oxygen derived free radicals? Circulation Research. 1989;64:86
  35. 35. Spiess BD. Ischemia-a coagulation problem? Journal of Cardiovascular Pharmacology. 1996;27(Suppl. 1):538
  36. 36. Breisblatt WM, Stein KI, Wolfe CJ, et al. Acute myocardial dysfunction and recovery: A common occurrence after coronary bypass surgery. Journal of the American College of Cardiology. 1990;15:1261
  37. 37. Edwards FH, Engelman RM, Houck P, Shahian DM, Bridges CR, Society of Thoracic Surgeons. The Society of Thoracic Surgeons practice guideline series: Antibiotic prophylaxis in cardiac surgery: Part I. Duration. The Annals of Thoracic Surgery. 2006;81:397-e404
  38. 38. Engelman R, Baker RA, Likosky DS, et al. The society of thoracic surgeons, the society of cardiovascular anesthesiologists, and the American society of extra corporeal technology: Clinical practice guidelines for cardiopulmonary bypass temperature management during cardiopulmonary bypass. The Annals of Thoracic Surgery. 2015;100:748-e57
  39. 39. Allen KB, Thourani VH, Naka Y, et al. Randomized, multicenter trial comparing sternotomy closure with rigid plate fixation to wire cerclage. The Journal of Thoracic and Cardiovascular Surgery. 2017;153(4):888-896.e1. DOI: 10.1016/j.jtcvs.2016.10.093
  40. 40. Nazerali RS, Hinchcliff K, Wong MS. Rigid fixation for the prevention and treatment of sternal complications. Annals of Plastic Surgery. 2014;72(suppl. 1):S27-S30. DOI: 10.1097/SAP.0000000000000155
  41. 41. Raman J, Lehmann S, Zehr K, et al. Sternal closure with rigid plate fixation versus wire closure: A randomized controlled multicenter trial. The Annals of Thoracic Surgery. 2012;94(6):1854-1861. DOI: 10.1016/j.athoracsur.2012.07.085
  42. 42. Dyke C, Aronson S, Dietrich W, et al. Universal definition of perioperative bleeding in adult cardiac surgery. The Journal of Thoracic and Cardiovascular Surgery. 2014;147(5):1458-1463.e1. DOI: 10.1016/j.jtcvs.2013.10.070
  43. 43. Ferraris VA, Brown JR, Despotis GJ, et al. 2011 update to the Society of Thoracic Surgeons and the Society of Cardiovascular Anesthesiologists blood conservation clinical practice guidelines. The Annals of Thoracic Surgery. 2011;91(3):944-982. DOI: 10.1016/j.athoracsur.2010.11.078
  44. 44. Myles PS, Smith JA, Forbes A, et al. ATACAS investigators of the ANZCA clinical trials network. Tranexamic acid in patients undergoing coronary-artery surgery. The New England Journal of Medicine. 2017;376(2):136-148. DOI: 10.1056/NEJMoa1606424
  45. 45. Koster A, Faraoni D, Levy JH. Antifibrinolytic therapy for cardiac surgery: An update. Anesthesiology. 2015;123(1):214-221. DOI: 10.1097/ALN.0000000000068
  46. 46. Levy JH, Koster A, Quinones QJ, Milling TJ, Key NS. Antifibrinolytic therapy and perioperative considerations. Anesthesiology. 2018;128(3):657-670. DOI: 10.1097/ALN.0000000000001997
  47. 47. Carl M, Alms A, Braun J, Dongas A, Erb J, Goetz A, et al. S3-Leitlinie zur intensivmedizinischen Versorgung herzchirurgischer Patienten: Hämodynamisches Monitoring und Herz-Kreislauf-System. GMS German Medical Science [Internet]. 2010;8:1-25. Disponible en: http://www.egms.de/static/de/journals/gms/2010-8/000101.shtml
  48. 48. Pérez Vela JL, Martín Benítez JC, Carrasco González M, et al. Grupo de Trabajo de Cuidados Intensivos Cardiológicos y RCP de SEMICYUC. Clinical practice guide for the management of low cardiac output syndrome in the postoperative period of heart surgery. Medicina Intensiva. 2012;36:e1-e44. DOI: 10.1016/j.medin.2012.02.007
  49. 49. O’Donnell JM, Nácul FE, editors. Posoperative care of the cardiac surgical patient. In: Surgical Intensive Care Medicine. 2010. pp. 535-566. DOI: 10.1007/978-0-387-77893-8_47
  50. 50. Ochagavía A, Baigorri F, Mesquida J, et al. Hemodynamic monitoring in the critically patient. Recomendations of the cardiological intensive care and CPR working Group of the Spanish Society of intensive care and coronary units. Medicina Intensiva. 2014;38:154-169. DOI: 10.1016/j.medin.2013.10.006
  51. 51. Habicher M, Zajonz T, Heringlake M, et al. S3-Leitlinie zur intensivmedizinischen Versorgung herzchirurgischer Patienten. Zeitschrift für Herz- Thoraxund Gefäßchirurgie [Internet]. 2018;33:40-44. Disponible en: http://link.springer.com/10.1007/s00398-018-0242-x
  52. 52. Jiménez Rivera JJ, Llanos Jorge C, Iribarren Sarrías JL, Brouard Martín M, Lacalzada Almeida J, Pérez Vela JL, et al. Infused cardioplegia index: A new tool to improve myocardial protection. A cohort study. Medicina Intensiva. 2019;43:337-345. DOI: 10.1016/j.medin.2018.03.011
  53. 53. Geisen M, Spray D, Nicholas FS. Echocardiography-based hemodynamic management in the cardiac surgical intensive care unit. Journal of Cardiothoracic and Vascular Anesthesia. 2014;28:733-744. DOI: 10.1053/j.jvca.2013.08.006
  54. 54. Moghissi ES, Korytkowski MT, DiNardo M, et al. American association of clinical endocrinologists and American diabetes association consensus statement on inpatient glycemic control. Diabetes Care. 2009;32:1119e31
  55. 55. Lazar HL, Chipkin SR, Fitzgerald CA, Bao Y, Cabral H, Apstein CS. Tight glycemic control in diabetic coronary artery bypass graft patients improves perioperative outcomes and decreases recurrent ischemic events. Circulation. 2004;109(12):1497-1502. DOI: 10.1161/01.CIR.0000121747.71054.79
  56. 56. Chaney MA, Nikolov MP, Blakeman BP, Bakhos M. Attempting to maintain normoglycemia during cardiopulmonary bypass with insulin may initiate postoperative hypoglycemia. Anesthesia and Analgesia. 1999;89(5):1091-1095. DOI: 10.1213/00000539-199911000-00004
  57. 57. Gandhi GY, Nuttall GA, Abel MD, et al. Intensive intraoperative insulin therapy versus conventional glucose management during cardiac surgery: A randomized trial. Annals of Internal Medicine. 2007;146(4):233-243. DOI: 10.7326/0003-4819-146-4-200702200-00002
  58. 58. White PF, Kehlet H, Neal JM, Schricker T, Carr DB, Carli F, et al. The role of the anesthesiologist in fast-track surgery: From multimodal analgesia to perioperative medical care. Anesthesia and Analgesia. 2007;104(6):1380-1396. DOI: 10.1213/01.ane.0000263034.96885.e1
  59. 59. Wick EC, Grant MC, Wu CL. Postoperative multimodal analgesia pain management with nonopioid analgesics and techniques: A review. JAMA Surgery. 2017;152(7):691-697. DOI: 10.1001/jamasurg.2017.0898
  60. 60. Jelacic S, Bollag L, Bowdle A, Rivat C, Cain KC, Richebe P. Intravenous acetaminophen as an adjunct analgesic in cardiac surgery reduces opioid consumption but not opioid-related adverse effects: A randomized controlled trial. Journal of Cardiothoracic and Vascular Anesthesia. 2016;30(4):997-1004. DOI: 10.1053/j.jvca.2016.02.010
  61. 61. Radbruch L, Glaeske G, Grond S, et al. Topical review on the abuse and misuse potential of tramadol and tilidine in Germany. Substance Abuse. 2013;34(3):313-320. DOI: 10.1080/08897077.2012.735216
  62. 62. Joshi SS, Jagadeesh AM. Efficacy of perioperative pregabalin in acute and chronic post-operative pain after off-pump coronary artery bypass surgery: A randomized, double-blind placebo controlled trial. Annals of Cardiac Anaesthesia. 2013;16(3):180-185. DOI: 10.4103/0971-9784.114239
  63. 63. Ji F, Li Z, Young N, Moore P, Liu H. Perioperative dexmedetomidine improves mortality in patients undergoing coronary artery bypass surgery. Journal of Cardiothoracic and Vascular Anesthesia. 2014;28(2):267-273. DOI: 10.1053/j.jvca.2013.06.022
  64. 64. Maldonado JR. Neuropathogenesis of delirium: Review of current etiologic theories and common pathways. The American Journal of Geriatric Psychiatry. 2013;21(12):1190-1222. DOI: 10.1016/j.jagp.2013.09.0
  65. 65. Young J, Murthy L, Westby M, Akunne A, O’Mahony R, Guideline Development Group. Diagnosis, prevention, and management of delirium: Summary of NICE guidance. BMJ. 2010;341:c3704. DOI: 10.1136/bmj.c3704
  66. 66. Page VJ, Ely EW, Gates S, et al. Effect of intravenous haloperidol on the duration of delirium and coma in critically ill patients (Hope-ICU): A randomised, double-blind, placebo-controlled trial. The Lancet Respiratory Medicine. 2013;1(7):515-523. DOI: 10.1016/S2213-2600(13)70166-8
  67. 67. Karalapillai D, Story D, Hart GK, et al. Postoperative hypothermia and patient outcomes after elective cardiac surgery. Anaesthesia. 2011;66:780-784
  68. 68. Engelen S, Himpe D, Borms S, et al. An evaluation of underbody forced-air and resistive heating during hypothermic, on-pump cardiac surgery. Anaesthesia. 2011;66(2):104-110. DOI: 10.1111/j.1365-2044.2010.06609.x
  69. 69. Christensen MC, Dziewior F, Kempel A, von Heymann C. Increased chest tube drainage is independently associated with adverse outcome after cardiac surgery. Journal of Cardiothoracic and Vascular Anesthesia. 2012;26(1):46-51. DOI: 10.1053/j.jvca.2011.09.021
  70. 70. St-Onge S, Perrault LP, Demers P, et al. Pericardial blood as a trigger for postoperative atrial fibrillation after cardiac surgery. The Annals of Thoracic Surgery. 2018;105(1):321-328. DOI: 10.1016/j.athoracsur.2017.07.045
  71. 71. Day TG, Perring RR, Gofton K. Is manipulation of mediastinal chest drains useful or harmful after cardiac surgery? Interactive Cardiovascular and Thoracic Surgery. 2008;7(5):888-890. DOI: 10.1510/icvts.2008.185413 147
  72. 72. Halm MA. To strip or not to strip? Physiological effects of chest tube manipulation. American Journal of Critical Care. 2007;16(6):609-612
  73. 73. Kakkos SK, Caprini JA, Geroulakos G, et al. Combined intermittent pneumatic leg compression and pharmacological prophylaxis for prevention of venous thromboembolism. Cochrane Database of Systematic Reviews. 2016;9:CD005258
  74. 74. Sachdeva A, Dalton M, Lees T. Graduated compression stockings for prevention of deep vein thrombosis. Cochrane Database of Systematic Reviews. 2018;11:CD001484
  75. 75. Camp SL, Stamou SC, Stiegel RM, et al. Can timing of tracheal extubation predict improved outcomes after cardiac surgery? HSR Proceedings in Intensive Care and Cardiovascular Anesthesia. 2009;1(2):39-47
  76. 76. Kashani K, Al-Khafaji A, Ardiles T, et al. Discovery and validation of cell cycle arrest biomarkers in human acute kidney injury. Critical Care. 2013;17(1):R25. DOI: 10.1186/cc12503
  77. 77. Mayer T, Bolliger D, Scholz M, et al. Urine biomarkers of tubular renal cell damage for the prediction of acute kidney injury after cardiac surgery: A pilot study. Journal of Cardiothoracic and Vascular Anesthesia. 2017;31(6):2072-2079. DOI: 10.1053/j.jvca.2017.04.024
  78. 78. Vanmassenhove J, Kielstein J, Jorres A, Biesen WV. Management of patients at risk of acute kidney injury. Lancet. 2017;389(10084):2139-2151. DOI: 10.1016/S0140-6736(17)31329-6
  79. 79. Thomson R, Meeran H, Valencia O, Al-Subaie N. Goal-directed therapy after cardiac surgery and the incidence of acute kidney injury. Journal of Critical Care. 2014;29(6):997-1000. DOI: 10.1016/j.jcrc.2014.06.011
  80. 80. Osawa EA, Rhodes A, Landoni G, et al. Effect of perioperative goal-directed hemodynamic resuscitation therapy on outcomes following cardiac surgery: A randomized clinical trial and systematic review. Critical Care Medicine. 2016;44(4):724-733
  81. 81. Kantrowicz A, Tjonneland S, Freed PS, et al. Experiencia clínica inicial con bombeo intraaórtico para shock cardiogénico. Journal of the American Medical Association. 1968;203:113. DOI: 10.1001/jama.1968.03140020041011
  82. 82. Pennington DG, editor. Mechanical circulatory support. Seminars in Thoracic and Cardiovascular Surgery. 1994;6:129-194
  83. 83. Argenziano M, Oz MC, Rose EA. The continuing evolution of mechanical ventricular support. Current Problems in Surgery. 1997;34:318
  84. 84. Smedira NG, Moazami N, Golding CM, et al. Clinical experience with 202 adults receiving extracorporeal membrane oxygenation for cardiac failure: Survival at 5 years. The Journal of Thoracic and Cardiovascular Surgery. 2001;122:92
  85. 85. Smedira NG, Blackstone EH. Postcardiotomy mechanical support: Risk factors and outcomes. The Annals of Thoracic Surgery. 2001;72:S60

Written By

Maria del Carmen Renteria Arellano and Hugo de Jesus Ballesteros Loyo

Submitted: 08 November 2023 Reviewed: 06 December 2023 Published: 03 July 2024