ACA App
Annals of Cardiac Anaesthesia Annals of Cardiac Anaesthesia Annals of Cardiac Anaesthesia
Home | About us | Editorial Board | Search | Ahead of print | Current Issue | Archives | Submission | Subscribe | Advertise | Contact | Login 
Users online: 188 Small font size Default font size Increase font size Print this article Email this article Bookmark this page
 


 

 
     
    Advanced search
 

 
 
     
  
    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
    Email Alert *
    Add to My List *
* Registration required (free)  


    Abstract
   Introduction
    Organizational A...
    Hemodynamic Moni...
    Management of Hi...
   Conclusions
    The 'Difficult t...
    References
    Article Figures
    Article Tables

 Article Access Statistics
    Viewed45138    
    Printed1132    
    Emailed106    
    PDF Downloaded3446    
    Comments [Add]    
    Cited by others 9    

Recommend this journal

 


 
Table of Contents
REVIEW ARTICLE  
Year : 2012  |  Volume : 15  |  Issue : 3  |  Page : 206-223
Clinical Review: Management of weaning from cardiopulmonary bypass after cardiac surgery


1 Department of Anaesthesiology, Pharmacology and Intensive Care, University of Geneva, CH-1211 Geneva
2 Department of Cardiovascular Surgery,of the University Hospital, Faculty of Medicine, University of Geneva, CH-1211 Geneva
3 Department of Anesthesia and Intensive Care, Cardiocentro Ticino, CH-6900 Lugano

Click here for correspondence address and email

Date of Submission23-Nov-2011
Date of Acceptance01-May-2012
Date of Web Publication4-Jul-2012
 

   Abstract 

A sizable number of cardiac surgical patients are difficult to wean off cardiopulmonary bypass (CPB) as a result of structural or functional cardiac abnormalities, vasoplegic syndrome, or ventricular dysfunction. In these cases, therapeutic decisions have to be taken quickly for successful separation from CPB. Various crisis management scenarios can be anticipated which emphasizes the importance of basic knowledge in applied cardiovascular physiology, knowledge of pathophysiology of the surgical lesions as well as leadership, and communication between multiple team members in a high-stakes environment. Since the mid-90s, transoesophageal echocardiography has provided an opportunity to assess the completeness of surgery, to identify abnormal circulatory conditions, and to guide specific medical and surgical interventions. However, because of the lack of evidence-based guidelines, there is a large variability regarding the use of cardiovascular drugs and mechanical circulatory support at the time of weaning from the CPB. This review presents key features for risk stratification and risk modulation as well as a standardized physiological approach to achieve successful weaning from CPB.

Keywords: Cardiopulmonary bypass, Inotropes, Teamwork, Vasoplegic syndrome, Vasopressors, Ventricular dysfunction, Ventricular assist device

How to cite this article:
Licker M, Diaper J, Cartier V, Ellenberger C, Cikirikcioglu M, Kalangos A, Cassina T, Bendjelid K. Clinical Review: Management of weaning from cardiopulmonary bypass after cardiac surgery. Ann Card Anaesth 2012;15:206-23

How to cite this URL:
Licker M, Diaper J, Cartier V, Ellenberger C, Cikirikcioglu M, Kalangos A, Cassina T, Bendjelid K. Clinical Review: Management of weaning from cardiopulmonary bypass after cardiac surgery. Ann Card Anaesth [serial online] 2012 [cited 2018 Dec 17];15:206-23. Available from: http://www.annals.in/text.asp?2012/15/3/206/97977



   Introduction Top


Although off-pump surgery has emerged as an innovative technique, cardiopulmonary bypass (CPB) is performed in the majority of cardiac surgeries including coronary artery bypass grafting (CABG), valvular repair/replacement, congenital heart defects repair, and correction of abnormalities of great vessel. [1]

Weaning from CPB entails the progressive transition of the patient from full mechanical circulatory support to spontaneous heart activity of the patient with an aim to provide sufficient blood flow and pressure through the pulmonary and systemic circulation. The time taken for surgical verifications and hemodynamic optimization is "compressed" within the first few minutes and important information needs to be shared between surgeons, anesthesiologists, and perfusionists. Therapeutic decisions regarding pharmacological support, ventricular assistance, and additional surgical interventions have to be taken quickly to prevent myocardial damage. A scientific and individualized approach takes into account the patient's preoperative disease status and the specificities of the surgical intervention. In this context, hemodynamic monitoring and transoesophageal echocardiography (TEE) provide a snapshot of the circulatory system by assessing cardiac performances, the adequacy of surgical repair, the interdependence of both ventricles, and the coupling between the heart and the circulatory arteriovenous compartment.

Although the importance of body temperature, acid-base control, arterial inflow/venous outflow and blood pressure management during CPB have been thoroughly investigated, [2],[3],[4] the weaning procedure itself has been poorly described and most algorithms rely on empirical data and expert opinions. [5],[6] In two large surveys performed in France and North America, the use of inotropes varied between 12% and 100% and guidelines or specific algorithms were applied in less than 10% of surgical centers. [7],[8] In some institutions, inotropes were used routinely while in others inotropes were administered to reverse postischemic myocardial stunning or to normalize blood pressure values, even in the absence of clear documentation of ventricular insufficiency.

Currently, there are no specific criteria defining the "difficult-to-wean" situation. [9] Many patients come easily off CPB without requiring supportive treatments, except for minor interventions such as electrical defibrillation, temporary electrophysiological stimulation, and/or small doses of cardiovascular drugs. The purpose of this review is to provide anesthesiologists, cardiac surgeons, perfusionists, and intensive care physicians with updated guidelines regarding perioperative management and the weaning process, particularly in the high risk cases.


   Organizational Aspects and Human Factors Top


Large cohort studies have shown that better outcomes are achieved when cardiac procedures are performed by well-trained and qualified professionals in high-volume hospitals where safety practice and standardized clinical pathways have been established. [10] An extensive literature exists about ways to optimize safety and work performance in complex organizational settings such as aerospace, nuclear power, and chemical engineering. [11] With the increasing burden of patients' comorbidities, and the complexity of the surgical operations, the achievement and maintenance of clinical excellence has become increasingly challenging. Although medical errors were traditionally attributed to lack of skills, inaccurate judgement and inappropriate actions, recent work has revealed that errors may also result from poor communication and the absence of written guidelines. [12] This might also be true at the time of CPB weaning when the information flow and communication between the team members must be optimized, amid uncertainty and time pressure. In an observational study involving 102 pediatric cardiac surgical cases, an average of 16 adverse events were reported per patient, 30% occurring shortly after coming off CPB and most of them being related to communication and coordination failure. [13] Cognitive adjustment was the compensatory intervention in most of these near-misses emphasizing the importance of qualification, training, and expertise. Another study from the Mayo clinic highlighted a strong correlation between the occurrence of technical error and teamwork disruption resulting from insufficient procedural information and poor communication/coordination between the surgeon, the anesthesiologist, and the perfusionist. [14] Although many of these "sentinel events" appear inconsequential, they predispose patients to serious complications if not addressed with effective compensatory interventions. It should be noted that the operative death was highly associated with serious adverse events (1.2 per patient).

Cardiac surgical care may benefit from restructuring the team with better cohesiveness and familiarity (teamwork education), by adopting standardized communication pattern and embracing the briefing-debriefing technique as an adjunct to continuous improvement through reflective learning, deliberate practice, and immediate feedback. [15] Simulation-based training has also been shown to enhance physician's performances during weaning from CPB. Immersive training focusing on nontechnical skills are believed to be superior to passive discussion in traditional interactive teaching seminars. [16] By providing a surrounding mimicking both the standardized process and dynamic crisis, high-fidelity simulation improves active memorization and enhances appropriate behaviors in real-life while sparing patients from potential harm. [17]


   Hemodynamic Monitoring and Echocardiographic Assessment Top


The use of the pulmonary artery catheter (PAC) is no longer routinely indicated in cardiac surgery. [18] Although cardiac output (CO), pulmonary artery pressure (PAP), and mixed venous oxygen saturation offer valuable information, errors (unreliable data, false interpretation) and iatrogenic complications (arrhythmias, pulmonary embolism or hemorrhage) may negate any potential benefit. [19],[20],[21] . In a propensity-matched observational study involving 5,065 CABG patients from 70 centers, the use of a PAC during CABG surgery was associated with increased mortality and a higher risk of severe end-organ complications. [22] Failure to demonstrate improved clinical outcome with PAC may result from the lack of evidence-based treatments guided by PAC information. [23]

New hemodynamic monitors have recently emerged (e.g., Esophageal Doppler and Pulse contour analysis), providing the ability to monitor CO noninvasively and to assess patient's responsiveness to fluid loading. [24] Simple and reproducible measurements of cardiac preload, intrathoracic volume (by PiCCO® , LiDCO® systems), and tissue oxygenation (by near-infrared-spectroscopy) might be helpful to optimize the circulatory condition while getting more insight into the adequacy of tissue O 2 supply/demand. [25],[26]

Before TEE became routinely available, problems such as hypovolemia, and anatomical, or functional defects were largely overlooked, and some hypotensive conditions were erroneously attributed to myocardial stunning or heart failure which led to inappropriate use of inotropes. Although transthoracic echocardiography (TTE) is generally regarded as superior for assessing the aortic valve, some diagnosis are missed and TEE almost always gives clearer images. Before starting CPB, new diagnosis (e.g. patent foramen ovale, undiagnosed valvular dysfunction, severe atheromatosis of the ascending aorta) might be revealed by TEE that justify a modification of the surgical plan in 5-15% cases. [27],[28],[29],[30],[31] Likewise after coming off bypass or under partial CPB, TEE allows a quick assessment of the completeness of surgery, ruling out any valvular or prosthetic dysfunction, paravalvular leaks, and wall motion abnormalities. During the weaning process, TEE provides a rational basis for diagnostic and therapeutic decision making, most importantly the need for inotropes and vasopressors, intra-aortic balloon pump, and volume replacement. Although TEE measurements of cardiac performance are well validated, some measurements are tedious and impractical to be performed intraoperatively. [32],[33],[34] For cardiac preload assessment, end-diastolic areas or diameter of the LV are more reliable than filling pressures derived from PAC and/or central venous catheter. Other simple measurements such as the fractional area changes of the LV and Doppler flow measurements in addition to a "trained eye vision" are valid methods to guide fluid loading and cardiovascular drug administration. [35] Till recently, category 1 indications for intra-operative use of TEE were restricted to repair of valve(s), congenital cardiac defects, hypertrophic obstructive cardiomyopathy, valvular endocarditis, and aortic dissection. [36] Whereas coronary artery surgery for patients with poor ventricular function was a category 2b indication. Since 2010, both European and American Task Forces have recommended that TEE should be used in all elective and emergency cardiac operations unless contraindicated and the use of TEE in CABG has been upgraded as a category 2a indication. [37],[38] The risk of major complications of TEE probe insertion, notably perforation of the oesophagus, is between 1:1000 and 1:10000. No death has been reported to date. Minor complications, e.g. sore throat and odynophagia, are common but could be minimized by cautious placement of the probe with a laryngoscope. [39]


   The 'Difficult to Wean' Situations Top


Definitions

At the time of separation from bypass, underfilling of the heart is a frequent cause of hypotension that can easily be detected by TEE and by direct inspection of the right ventricle (RV) and right atrium. Optimization of cardiac preload by first reinfusing blood from the cardiotomy reservoir and then by titrating IV fluids is a simple and effective way to normalize CO and mean arterial pressure (MAP) in the majority of patients with preserved ventricular function.

In normovolemic conditions, difficulties in weaning from CPB are encountered in about 10 to 45% of patients [40] and TEE is helpful to diagnose the underlying mechanisms that can be ascribed to one of four contextual scenarios:

  1. Structural abnormalities such as intracardiac shunt, valvular regurgitation, para-prosthetic leaks, or an occluded bypass graft.
  2. Dynamic abnormalities such as left (or right) ventricular outflow tract obstruction.
  3. Ventricular systolic dysfunction characterized by depressed contractility, impairment in ventricular diastolic relaxation and restrictive filling pattern.
  4. Vasoplegic syndrome characterized by normal-to-elevated CO with preserved ventricular function and low systemic vascular resistance.


Key diagnostic features and therapeutic approaches to these pathological conditions are briefly described in [Table 1].
Table 1: Characteristics and treatment modalities of weaning difficulties

Click here to view


Mechanisms and Risk Factors of Ventricular Dysfunction and Vasoplegic Syndrome

To predict perioperative mortality, the Euroscore, the Society of Thoracic Surgeons (STS), and the Parsonnet scores have been validated in cardiac surgical patients. [41] Most items included in these scoring systems are also considered independent risk factors for vasoplegic syndrome and ventricular dysfunction.

Vasoplegic syndrome has been linked to deficient release/activity of vasopressin and angiotensin II, overexpression of inflammatory mediators, and endothelial dysfunction resulting from the activation of vascular smooth muscle ATP-sensitive potassium channels, and/or overexpression of the inducible NO synthase. [42],[43],[44] The systemic inflammatory response to CPB and surgical trauma may contribute to worsen cardiocirculatory disturbances. [45] Long-term use of certain drugs (e.g., angiotensin-converting enzyme inhibitors, calcium-channel antagonists, and heparin), patients co-morbidities (e.g., heart failure, diabetes mellitus) and procedure-related factors (e.g., prolonged CPB, residual hypothermia) have been identified as predictors of norepinephrine-resistant vasoplegia that has been associated with mortality rates as high as 25% when vasoplegia persisted for more than 36 h [Table 2]. [43],[44],[45],[46],[47],[48]
Table 2: Studies reporting the risk factors of vasoplegic syndrome after cardiac surgery

Click here to view


Ventricular function has been reported to be impaired in as much as 96% of patients following CPB with a nadir occurring between 2 and 16 h following surgery with, complete recovery being achieved 24 to 48 h after surgery. [49] In the operating room, low cardiac output syndrome (LCOS) has been defined as the inability to wean off CPB despite maximal support with a low cardiac index (<2.0-2.5 l/min/m 2 ) and evidence of end-organ dysfunction (e.g., urine output < 0.5 ml/kg/h). The prevalence of LCOS in cardiac surgical patients range from 0.2% to 6% and it is associated with increased postoperative morbidity and mortality, increasing hospital length of stay, resource utilization, and overall costs. [7],[8] The reasons for poor clinical outcome are likely related to the severity of the underlying disease and to the delay or failure to institute mechanical support.

The causes of ventricular dysfunction are multifactorial, including surgical tissue trauma, myocardial ischemia-reperfusion injuries, down-regulation of beta-adrenergic receptors, coronary embolization (e.g., air, atheroma particule), activation of inflammatory and coagulation cascades, as well as uncorrected pre-existing cardiac disease. Myocardial stunning owing to cytosolic and mitochondrial calcium overload is usually a transient phenomenon. Perioperative myocardial infarction occurs in 7% to 15% of cardiac surgical patients and has also been incriminated in causing LCOS. [49],[50] Knowledge of specific risk factors of post-CPB ventricular dysfunction is important for planning prophylactic cardioprotective interventions as well as early supportive therapy with cardiovascular drugs and eventually with mechanical circulatory devices [Table 3]. Patient-related risk factors include advanced age, decreased LV systolic function, altered LV diastolic function, chronic beta-blocker treatment, recent myocardial infarction, and other end-organ dysfunction comorbidities [renal failure, arterial disease, and pulmonary hypertension (PH)]. Among procedure-related risk factors, prolonged aortic cross-clamping and the complexity of surgery (combined procedure) have been associated with ischemic myocardial injuries. [45],[46],[47],[48],[49],[50],[51],[52],[53],[54],[55],[56],[57],[58],[59],[60] More recently, genetic variation within defined regions of the NPPA/NPPB and NPR3 natriuretic peptide system genes has been shown to be associated with post-CPB ventricular dysfunction. [61] However, in a genome-wide study of over 100 single-nucleotide polymorphisms (SNPs), no SNP was consistently associated with a strong risk [odds ratio (OR) > 2.1] of developing postoperative ventricular dysfunction. [62]
Table 3: Studies reporting the risk factors of ventricular dysfunction after cardiac surgery

Click here to view


Prognostic Implications of PH and/or Right Ventricular Dysfunction

PH is defined by a mean PAP ≥ 25 mmHg at rest (or ≥ 30 mmHg with exercise) in the presence of a pulmonary capillary wedge pressure ≤15 mmHg. [63] Although the prevalence of idiopathic PH is low (1 per 15 million), secondary forms of PH are frequently encountered in patients with HIV (0.5%), portal hypertension (2% to 6%), sickle cell disease (10% to 30%), and chronic obstructive pulmonary disease (1% to 4%). The prevalence of PH is much higher in patients with an advanced stage of LV failure (NYHA class IV, LVEF < 40%), in patients undergoing mitral valve repair (40% to 50%) and in patients undergoing aortic valve replacement for aortic stenosis (10% to 50%). [63],[64],[65] Severe PH (systolic PAP > 60 mmHg) has been included in the Euroscore and Parsonnet score for predicting 30-day operative mortality but not in the STS scoring system. [41],[66] Following valve replacement for aortic stenosis, Melby et al reported a two-fold higher operative mortality and decreased long term survival (relative risk 1.7) in patients with preoperative PH versus those with normal PAP. [67],[68] Among survivors, PAP decreased immediately by about 20% following surgery and persisted at lower levels over the 1-year follow up period. [68]

The criteria defining RV functional abnormalities are largely arbitrary and no strong consensus exists given the complex geometry of the RV with its extensive trabeculations. [69] Several observational studies indicate that various indices of RV function (RVEF < 20-40%, RV fractional area change <35%, RV myocardial performance index > 0.5) are associated with increased requirement of inotropic support, a higher incidence of postoperative heart failure, longer stay in ICU, and lower survival. [70]

A Protocol-Driven Approach for Weaning from CPB

Weaning off bypass and landing procedures in aviation share many similarities. Such procedures can be seen as models of how a multi-professional team comes together, utilizes continuously flowing information, interacts effectively and safely perform a complex task under time pressure.

Besides qualification and individual expertise, knowledge of emergency procedures, application of checklists and goal-directed protocols are key elements for successful management. Given the importance of hemodynamic and echocardiographic evaluation, the anesthesiologist should assume the leadership during this important period of weaning from CPB, albeit agreement with the surgeon is always sought for therapeutic decisions. For instance, consensus should be reached when a second pump run is justified in case of nonpatent vascular graft, persistent or new intracardiac shunt, valvular dysfunction, or ventricular outflow tract obstruction. A stepwise standardized approach for managing cpb0 weaning is summarized in [Figure 1].
Figure 1: Algorithm for weaning from cardiopulmonary bypass

Click here to view


Checklist Before Weaning Off Bypass

Before initiating the weaning procedure, several prerequisites should be routinely met:

  1. Normothermia is achieved by active rewarming by using CPB heat exchanger, by convective air circulation, and by circulating water blanket.
  2. Arterial blood analysis to ensures that oxygen content of the blood (hematocrit > 25%, PaO 2 >100 mmHg), electrolytes (K + , Ca ++ , Mg ++ ), blood sugar, and pH are within normal limits; while full anticoagulation is maintained (activated clotting time > 400 s).
  3. Lungs are manually re-inflated (FIO 2 > 0.8). Mechanical ventilation is reset, and the alarms of the cardiopulmonary monitoring are reactivated.
  4. After aortic unclamping and electrical ventricular defribillation (if required), a heart rate (HR) between 70 and 100 beats/min should be targeted. Bradycardia and atrioventricular blockade are treated with atropine, beta-adrenergic receptor agonists, or cardiac pacing.


Goal-Directed Approach for Weaning Off Bypass

While the circulatory work is shifted from the pump to the patients' heart, information on hemodynamic parameters (e.g., HR, cardiac preload indices, MAP, and functional imaging of the heart) should be shared between the cardiac surgeon, the anaesthesiologists, and the perfusionnist.

Scenario 1

During stepwise reduction of both venous return and arterial pump flow, filling of the cardiac chambers is appreciated by inspection of the RV and atrium, by TEE examination (e.g., LV end-diastolic diameter 3.5-5 cm, in transgastric short-axis view), and by central filling pressure measurement (venous or pulmonary capillary wedge pressure). Cardiac preload is considered "optimal" when further filling fails to increase blood pressure and/or CO according to the preload-recruitable stroke work concept. Indeed, progressive elongation of the sarcomeres with increasing cardiac preload enhances myocardial contraction resulting in increased stroke volume and MAP (Frank-Starling mechanism).

As soon as a critical perfusion pressure is reached (MAP > 70 mmHg), patients with normal LV function may benefit from the infusion of vasodilators (e.g., nitroglycerine, clevidipine, or nitroprussiate) which improve the efficiency of ventricular contraction and avoid hypertension during removal of the aortic cannula. Patients with arterial hypertension and hypertrophic cardiomyopathy have restrictive physiology and are at risk of ventricular outflow tract obstruction and myocardial ischemia; in these patients control of the HR, and maintenance of adequate preload and afterload is important to prevent outflow tract obstruction and to ensure adequate myocardial perfusion. Abnormal systolic motion of the anterior mitral leaflet and acceleration of the blood flow in the LV outflow tract can be detected in midesophageal aortic long axis view and in transgastric long axis view of the LV at 120°, respectively. Finally, after separation from CPB and removal of the venous cannula, transfusion of autologous blood from the cardiotomy reservoir, and cell-saver device may further enhance stroke volume by optimizing cardiac preload. During the infusion of protamine, ventilatory pressures, and hemodynamic parameters should be closely monitored since protamine may induce a bronchospastic response and severe PH with RV failure, particularly in patients with specific risk factors such as prior protamine exposure, history of PH, fish allergy, and vasectomy. [71] Slow infusion of protamine through the aortic cannula or preemptive administration of inhaled nitric oxide or prostacyclin has been recommended to mitigate or to prevent these deleterious reactions. [71],[72],[73],[74]

Scenario 2

If hypotension (MAP < 70 mmHg) persists despite adequate cardiac filling, a brief TEE examination is helpful to discriminate between a vasoplegic syndrome, LV failure, or RV failure (with or without PH). [75] In patients with vasoplegic syndrome, ventricular function is well preserved and normal levels of MAP (>70 mmHg) can be restored with incremental doses of norepinephrine or phenylephrine [Table 4]. Vasopressin receptor agonists (vasopressin 4 U/min, terlipressin 0.5-1 mg) are considered as second-line treatments. Successful management with nitric oxide inhibitors (methylene blue 1.5 mg/kg) has been reported in few cases of nonresponsive hypotension to alpha-adrenergic agonists. [76],[77]
Table 4: Recommandations for perioperative administration of inotropes and vasopressors

Click here to view


Hypotensive states resulting from ventricular dysfunction can benefit from inotropic drug support often in association with vasopressors in case of LV dysfunction and with selective pulmonary vasodilators (inhaled nitric oxide or prostacycline) in case of RV dysfunction and/or PH. [78],[79] Beta-adrenergic receptor agonists represent the first option, whereas phosphodiesterase inhibitors (PDEIs) might be preferred in patients chronically treated with β-blockers. Among β-agonists, dobutamine offers the most favorable side effects profile compared with epinephrine and dopamine [Table 4]. [80]

Tachy-arrhythmias might convert to sinus rhythm on delivering a low-intensity direct electric shock or on administration of lidocaine or amiodarone. Various modes of biventricular or atrial pacing can reduce ventricular dyssynchrony and might improve mechanical efficiency of cardiac contraction (about 14% increase in SV) without increasing myocardial oxygen consumption. [81]

Evidence of myocardial ischemia (e.g., ST segment abnormalities, new/worsening LV/RV wall motion abnormalities) may justify the need for further myocardial revascularization (ST segment elevation, transmural ischemia) or the infusion of nitroglycerine (ST segment depression, subendocardial ischemia). However, limitations in the interpretation of regional wall motion abnormalities should be considered since they have also been reported in case of hypovolemic states, conduction abnormalities (bundle branch block, ventricular pacing), and myocardial stunning. Anecdotally, transient LV dysfunction has also been attributed to Takotsubo cardiomyopathy which is characterized by ECG abnormalities (ST elevations or T wave inversion) in the absence of obstructive coronary artery disease and pathognomonic wall motion abnormalities (mid-ventricular akinesia and LV "apical ballooning"). [82],[83],[84] Excessive catecholamine stimulation, metabolic disturbances, and dysfunction of the microcirculation are thought to be the underlying mechanisms. In such cases, administration of the inotropes should be discontinued and replaced by nitroglycerin. [85]

Acute RV dysfunction after CPB can be detected by high CVP and by TEE examination which shows poor contractility and dilated RV, tricuspid regurgitation, and low tricuspid annular plane systolic excursion. [70] Ischemic causes of RV dysfunction, often missed by standard ECG, requires medical and/or surgical treatment aimed to enhance RV perfusion. If nonischemic etiologies are suspected, therapeutic options are aimed to increase contractility and to selectively reduce the afterload of the RV by inhaled NO, prostacyclin, or milrinone.

Indications and Risks of Inotropic Drugs

Based on TEE assessment and CO measurements, inotropic support is indicated in less than 50% patients following CPB. [40] Ideally, the hemodynamic response to incremental doses of inotropic agents should be tested within a short time frame of less than 5-10 min. Any delay in restoring adequate systemic oxygen delivery may aggravate ventricular dysfunction and trigger the onset of multiple organ dysfunction. Despite the wide range of available inotropes, consensus lacks regarding the optimal therapeutic regimen. [40] Conceptually, inotropes enhance postischemic recovery and facilitate weaning from CPB. The downside is that, by promoting insulin resistance and fatty acid oxidation over glucose, catecholamines increase myocardial oxygen consumption and deplete energetic substrates within the cardiomyocytes. [86] Consequently, transient hemodynamic improvement may be outweighed by adverse events related to arrhythmias, hyperglycemia, lactic acidosis and beta-adrenergic receptor desentitization. [87],[88] A mismatch between increased myocardial oxygen demand and oxygen delivery may further amplify myocardial reperfusion injuries. Increasing levels of catecholamines have also been associated with bacterial growth, increased germ virulence, and biofilm formation. [89]

Interestingly, the potential clinical impact of cardiovascular drug support in cardiac surgery has been examined in four observational studies, three of them suggest a link between the administration of catecholamines during weaning off bypass and worse clinical outcome. In a dataset of 1,471 adults undergoing elective cardiac surgical procedures, Muller et al, reported a higher 30-day mortality among patients receiving inotropes (60% of the whole cohort) compared with those untreated, although the preoperative risk profile did not differ between the two groups. [56] Likewise, in unselected consecutive cardiac cases (N=657), Fellahi et al, found that inotrope-dependent patients (13%) experienced larger release of troponin in the early postoperative period than patients nonexposed to inotropes. [90] After adjustment for confounding factors and propensity score stratification, the administration of catecholamines was highly predictive of cardiac morbidity [OR of 3.0 and 95% confidence interval (CI) between 1.2 and 7.3]. In another large cohort study (N = 1,326 patients), inotrope exposure was independently associated with increased hospital mortality (OR 2.3, 95% CI 1.2-4.5) and with renal dysfunction (OR 2.7, 95% CI 1.5-4.6). [91] In contrast to these observations, Williams et al failed to demonstrate an association between inotrope treatment and major postoperative morbidity in a retrospective analysis of 2,390 high-risk patients undergoing CABGs. [8] Given the considerable variability in inotrope use and conflicting results gathered from observational studies, randomized prospective trials are needed to evaluate specific algorithm for cardiovascular drug support in moderate-to-high-risk patients. The authors believe that the inotropes should not routinely be administered since optimization of loading conditions, fluid filling and vasodilators, may ensure adequate organ perfusion in the majority of the low risk patients.


   Management of High-Risk Patients Top


Prophylactic Interventions

Cold blood cardioplegia rather than crystalloid cardioplegia has been adopted in the majority of heart centers. In a meta-analysis of 10 randomized clinical trials (N = 879 patients), the use of blood cardioplegia (compared with crystalloid hyperkaliemic solutions) was associated with a reduced incidence of LCOS (13% vs. 16.5%) and lesser release of myocardial biomarkers. [92]

Selected patients with easily accessible coronary lesions may benefit from off-pump revascularization, avoiding ischemic cardiac arrest and its consequent postreperfusion stunning. For the majority of patients undergoing on-pump CABG, preconditioning the heart by repeated short-lasting coronary occlusion has been shown to confer cardioprotection as evidenced by a significant reduction in cardiovascular drug support and fewer episodes of ventricular arrhythmias following separation from bypass. [93] Anesthetic preconditioning is much easier to apply and affords similar cardioprotective effects compared with ischemic preconditioning. In a meta-analysis of 27 trials including 2,979 patients, lesser requirements for inotropic support, lower troponin serum concentration, and higher cardiac indexes were reported in patients pretreated with volatile anesthetic agents compared with those receiving intravenous anesthetics. [94]

Glucose-insulin-potassium infusion (GIK) is one of the oldest cardioprotective interventions. Beneficial effects have been attributed to several physiological pathways including activation of phospatidylinositol 3-kinase, hyperpolarization of cardiomyocytes, predominant glucose utilization, up-regulation of the L-arginine-nitric-oxide pathway, and anti-apoptotic effects. Administration of GIK before CPB tends to improve postoperative myocardial recovery with lesser requirement for inotropes, higher cardiac index, fewer episodes of atrial fibrillation, and shorter length of stay in ICU. [95],[96] However, in view of the deleterious consequences of hypo- and hyperglycemia, close monitoring of blood glucose levels is advocated whenever insulin treatment is initiated. [97]

Levosimendan is a novel noncatecholamine inotropic agent that binds to cardiac troponin C and enhances myofilament responsiveness to calcium, thereby increasing contractility and relaxation of the cardiomyocyte at minimal metabolic cost without promoting arrhythmias. It also increases coronary flow reserve and is thought to exert preconditioning effects by opening mitochondrial ATP-sensitive K + channels. [98] Preliminary data suggest that prophylactic administration of levosimedan in patients with severe LV dysfunction improves ventricular performance and enhances primary weaning from CPB with lesser need for additional inotropic or mechanical therapy. [99],[100],[101],[102],[103]

Phosphodiesterase inhibitors (PDEI) such as milrinone and enoxinone inhibit breakdown of cyclic adenosine monophosphate (cAMP) resulting in increased inotropy and decreased vascular tone. [104] In the PRIMACORP trial, the prophylactic administration of high-dose milrinone was associated with a 64% relative risk reduction in the development of LCOS following congenital cardiac operations. [105] Both PDEI and levosimendan are expected to be particularly efficacious in patients chronically treated with β-blockers and those with myocardial β1 -down-regulation owing to congestive heart failure. [106],[107],[108]

The insertion of an intra-aortic balloon pump (IABP) should be considered in patients with ongoing myocardial ischemia or unstable hemodynamic condition. Indeed, by reducing LV afterload and improving diastolic coronary blood flow particularly in subendocardial area, IABP exerts anti-ischemic myocardial effects and increases systemic oxygen delivery. [109] Dyub et al, performed a meta-analysis involving 2,363 high-risk patients that showed a lower mortality and shorter ICU stay in the group pretreated with IABP (4.7% vs. 8.3% in the control group). [110] Overall, one death could be prevented by treating 17 patients with an IABP. A recent cohort study including 7,440 patients confirms that preoperative IABP is associated with a strong trend toward reduced rate of operative mortality (10%) despite a higher predicted mortality based on the Parsonnet score. [111]

Ultrafiltration during CPB has been advocated in patients with congestive heart failure to remove excessive fluid volume, it eliminates inflammatory mediators, and concentrates circulating erythrocytes. [112],[113] Although this technique has been shown to reduce the need for cardiovascular drug support and blood transfusion, there are no data demonstrating an improvement in postoperative clinical outcome.

Pharmacological Treatment of Severe Ventricular Dysfunction

Patients with LCOS become (or are already) tolerant to the effects of beta-adrenergic agonists. Hence, the adjunction of non-catecholamines agents is deemed mandatory when the incremental infusion of beta-adrenergic agonists fails to enhance ventricular contractility. Both levosimendan and PDEIs (milrinone, enoximone), augment the efficiency of cardiac contraction, and increases stroke volume at a lesser metabolic cost than catecholamines, thereby facilitating the separation from CPB. Several studies including small series of patients suggest that milrinone therapy is associated with enhanced blood flow through coronary grafts, improved RV function, better LV diastolic function, attenuated release of biomarkers, and fewer myocardial infarcts. [114],[115],[116],[117] However, in the randomized controlled OPTIME-CHF trial involving patients with acute heart failure, the use of milrinone failed to produce any clinical improvement and was associated with more frequent adverse events. [106] Likewise, in patients coming off bypass, milrinone treatment was associated with a higher incidence of hypotension and atrial fibrillation (56% vs.26% in nonusers). [118] More convincing scientific data lend support to the use of levosimedan in acute heart failure and in high-risk cardiac surgery. In a meta-analysis of 19 RCTs enrolling 3,650 patients with acute heart failure, levosimendan was associated with reduced mortality and a better hemodynamic profile compared with dobutamine. [119] Likewise, in 440 cardiac surgical patients included in 10 RCTs, favorable clinical and hemodynamic effects were attributed to levosimendan compared with control patients receiving dobutamine or milrinone. [120] Interestingly, levosimendan was associated with significant reductions in perioperative mortality and in the rate of acute renal failure as well as with fewer episodes of myocardial infarction and atrial fibrillation. Although levosimendan is a promising agent, further randomized controlled clinical trials are warranted to confirm its cardioprotective effects and to assess its safety profile while optimizing the management of perioperative heart failure. However, at present the beta-adrenergic receptor agonists remain the first-line treatment of LV or RV dysfunction. Levosimendan is administered in selected high-risk patients (LV or RV EF < 30%) as a prophylactic treatment or as a rescue therapy in advanced stage of ventricular failure. [40]

Mechanical Circulatory Support

Mechanical assist devices to augment blood flow include the IABP, LV and RV assist devices, and extracorporeal membrane oxygenation (ECMO) devices [Table 5]. The decision to initiate IABP, or ECMO or implant ventricular assist device (VAD) should be made in a timely manner before the deleterious effects of increasing pharmacological therapy and multiorgan failure from persistent end-organ ischemia set in. Selecting the appropriate support device should take into account residual cardiac function, the presence of left/right or bi-ventricular failure, concomitant respiratory failure, underlying co-morbidities such as peripheral vascular disease as well as the potential of myocardial recovery [Figure 2]. [121] Once mechanical support has been instituted, efforts should be made to keep MAP above 70 mmHg and mixed venous oxygen saturation above 70%. If VAD is implanted for isolated LV or RV failure, there is a critical need to optimize preload, to maintain HR and to support the other ventricle with inotropes. Periodically, it is imperative to set goals for weaning off mechanical support based on real-time hemodynamic monitoring, echocardiographic assessment, and end-organ function.
Figure 2: Mechanical circulatory support

Click here to view
Table 5: Mechanical devices used to separate from cardiopulmonary bypass

Click here to view


Intraortic Balloon Pump (IABP)

The IABP has stood the test of time and remains the first-line device therapy of postcardiotomy LCOS due to LV failure. In RV failure, its use is more controversial. The IAPB provides a marginal increase in CO (10-15%, +0.5 L/min), alleviates ventricular work and allows a reduction in inotropic infusion. The main limitation is that IABP requires a certain level of residual LV function. The IABP is usually inserted via femoral artery, although alternative sites of insertion (ascending aorta, axillary, or brachial artery) can be considered in patients with previous vascular surgery, calcifications of the ilio-femoral arteries as well as severe atheromatous disease or tortuosity of the descending aorta. In a benchmark study including 22,663 patients treated with IABP, weaning from CPB was rated as the third most frequent indication (18%) after cardiac catheterization (19%) and cardiogenic shock (20%). [122] Procedure-related complications-leg ischemia, local infection and hemorrhage-are observed in up to 5% of patients. [123] In contrast to pre-CPB insertion, post-CPB and postoperative insertion of IABP is associated with much higher operative mortality (10% vs. 16% and 47%, respectively). [124]

Ventricular Assist Device (VAD)

From the early 1970s, mechanical circulatory support devices have evolved into advanced easy-to-implant and easy-to-use devices, capable of reversing postcardiotomy LCOS in an "exit" strategy tailored specifically for each patient ("bridge" to recovery or transplantation or as "destination" therapy). [1],[125] Overall, VADs can be divided into two main types: (1) the pulsatile pump that mimics the natural cardiac stroke volume and (2) the continuous flow devices that can be subdivided into centrifugal and axial flow pumps. In a meta-analysis including 125 patients with cardiogenic shock, Cheng et al found that, support with LVAD resulted in higher cardiac index and MAP compared with the IABP. [126] However, higher rates of bleeding and hemolysis were observed in the VAD group and 30-day mortality did not differ between the two groups.

Extracorporeal Membrane Oxygenation (ECMO)

Although initially proposed for treating the failing lungs, ECMO is also considered a suitable short-term therapy of cardiorespiratory insufficiency following cardiac surgery, particularly for patients with severe pulmonary edema, those with persistent ventricular arrhythmias due to extensive myocardial infarct and those with RV failure. [127] For initiation of ECMO right atrial blood is drained via a large cannula, pumped through an artificial lung and delivered for organ perfusion through the femoral artery. The vascular access is usually percutaneous, although direct cutdown access might be preferred in patients with profound cardiogenic shock. ECMOs with non-porous hollow fiber (polymethylpentene) lung membranes offer low resistance to blood flow and allow safe use of centrifugal pumps. Nonthrombogenic coatings of the whole circuit reduce the need for anticoagulation and the risk of bleeding.


   Conclusions Top


Knowledge of patient- and procedure-related risk factors should be integrated in the medical decision process along with the implementation of perioperative protective strategies. Team education, adoption of checklists, and simulation-based training may further enhance physician'performances during the CPB weaning process. Integration of a standardized approach for weaning off bypass focusing on simple hemodynamic targets, TEE assessment, along with a goal-directed therapy involving pharmacological agents (inotropes, vasodilators, and vasopressors) and eventually mechanical support devices can potentially improve the outcome. Large trials are warranted to assess the best cardioprotective strategies and to validate algorithms suitable for the CPB weaning process in cardiac surgery.

 
   References Top

1.Ailawadi G, Zacour RK. Cardiopulmonary bypass/extracorporeal membrane oxygenation/left heart bypass: Indications, techniques, and complications. Surg Clin North Am 2009;89:781-96, vii-viii.  Back to cited text no. 1
[PUBMED]  [FULLTEXT]  
2.Grigore AM, Murray CF, Ramakrishna H, Djaiani G. A core review of temperature regimens and neuroprotection during cardiopulmonary bypass: Does rewarming rate matter? Anesth Analg 2009;109:1741-51.  Back to cited text no. 2
[PUBMED]  [FULLTEXT]  
3.Schabel RK, Berryessa RG, Justison GA, Tyndal CM, Schumann J. Ten common perfusion problems: Prevention and treatment protocols. 1987. J Extra Corpor Technol 2007;39:203-9.  Back to cited text no. 3
[PUBMED]    
4.Murphy GS, Hessel EA 2 nd , Groom RC. Optimal perfusion during cardiopulmonary bypass: An evidence-based approach. Anesth Analg 2009;108:1394-417.  Back to cited text no. 4
    
5.Oakes DA, Mangano CT. Cardiopulmonary bypass in 2009: Achieving and circulating best practices. Anesth Analg 2009;108:1368-70.  Back to cited text no. 5
[PUBMED]  [FULLTEXT]  
6.Vakamudi M. Weaning from cardiopulmonary bypass: Problems and remedies. Ann Card Anaesth 2004;7:178-85.  Back to cited text no. 6
[PUBMED]  Medknow Journal  
7.Leone M, Vallet B, Teboul JL, Mateo J, Bastien O, Martin C. Survey of the use of catecholamines by French physicians. Intensive Care Med 2004;30:984-8.  Back to cited text no. 7
[PUBMED]  [FULLTEXT]  
8.Williams JB, Hernandez AF, Li S, Dokholyan RS, O'Brien SM, Smith PK, et al. Postoperative inotrope and vasopressor use following CABG: Outcome data from the CAPS-care study. J Card Surg 2011;26:572-8.  Back to cited text no. 8
[PUBMED]  [FULLTEXT]  
9.A V. Weaning from cardiopulmonary bypass and low cardiac output syndrome. In Perioperative care in cardiac anesthesia and surgery edited by Cheng DC, David TE; 2006. P. 135-43.  Back to cited text no. 9
    
10.Auerbach AD, Maselli J, Carter J, Pekow PS, Lindenauer PK. The relationship between case volume, care quality, and outcomes of complex cancer surgery. J Am Coll Surg 2011;211:601-8.  Back to cited text no. 10
    
11.Gore DC, Powell JM, Baer JG, Sexton KH, Richardson CJ, Marshall DR, et al. Crew resource management improved perception of patient safety in the operating room. Am J Med Qual 2011;25:60-3.  Back to cited text no. 11
    
12.Ravikumar TS, Sharma C, Marini C, Steele GDJr, Ritter G, Barrera R, et al. A validated value-based model to improve hospital-wide perioperative outcomes: Adaptability to combined medical/surgical inpatient cohorts. Ann Surg 2011;252:486-96; discussion 496-8.  Back to cited text no. 12
    
13.Barach P, Johnson JK, Ahmad A, Galvan C, Bognar A, Duncan R, et al. A prospective observational study of human factors, adverse events, and patient outcomes in surgery for pediatric cardiac disease. J Thorac Cardiovasc Surg 2008;136:1422-8.  Back to cited text no. 13
[PUBMED]  [FULLTEXT]  
14.ElBardissi AW, Wiegmann DA, Henrickson S, Wadhera R, Sundt TM 3 rd . Identifying methods to improve heart surgery: An operative approach and strategy for implementation on an organizational level. Eur J Cardiothorac Surg 2008;34:1027-33.  Back to cited text no. 14
    
15.Schraagen JM, Schouten T, Smit M, Haas F, van der Beek D, van de Ven J, et al. Assessing and improving teamwork in cardiac surgery. QualSaf Health Care 2011;19:e29.  Back to cited text no. 15
    
16.Lateef F. Simulation-based learning: Just like the real thing. J Emerg Trauma Shock 2010;3:348-52.  Back to cited text no. 16
[PUBMED]  Medknow Journal  
17.Bruppacher HR, Alam SK, LeBlanc VR, Latter D, Naik VN, Savoldelli GL, et al. Simulation-based training improves physicians' performance in patient care in high-stakes clinical setting of cardiac surgery. Anesthesiology 2011;112:985-92.  Back to cited text no. 17
    
18.Harvey S, Young D, Brampton W, Cooper AB, Doig G, Sibbald W, et al. Pulmonary artery catheters for adult patients in intensive care. Cochrane Database Syst Rev 2006;3:CD003408.  Back to cited text no. 18
[PUBMED]  [FULLTEXT]  
19.Ospina-Tascon GA, Cordioli RL, Vincent JL. What type of monitoring has been shown to improve outcomes in acutely ill patients? Intensive Care Med 2008;34:800-20.  Back to cited text no. 19
    
20.Ivanov R, Allen J, Calvin JE. The incidence of major morbidity in critically ill patients managed with pulmonary artery catheters: A meta-analysis. Crit Care Med 2000;28:615-9.  Back to cited text no. 20
[PUBMED]  [FULLTEXT]  
21.Hadian M, Pinsky MR. Evidence-based review of the use of the pulmonary artery catheter: Impact data and complications. Crit Care 2006;10(Suppl 3):S8.  Back to cited text no. 21
[PUBMED]  [FULLTEXT]  
22.Schwann NM, Hillel Z, Hoeft A, Barash P, Mohnle P, Miao Y, et al. Lack of effectiveness of the pulmonary artery catheter in cardiac surgery.Anesth Analg 2011;113:994-1002.  Back to cited text no. 22
    
23.Ranucci M. Which cardiac surgical patients can benefit from placement of a pulmonary artery catheter? Crit Care 2006;10(Suppl 3):S6.  Back to cited text no. 23
[PUBMED]  [FULLTEXT]  
24.Peyton PJ, Chong SW. Minimally invasive measurement of cardiac output during surgery and critical care: A meta-analysis of accuracy and precision. Anesthesiology 2011;113:1220-35.  Back to cited text no. 24
    
25.Hadian M, Kim HK, Severyn DA, Pinsky MR. Cross-comparison of cardiac output trending accuracy of LiDCO, PiCCO, FloTrac and pulmonary artery catheters. Crit Care 2011;14:R212.  Back to cited text no. 25
    
26.Futier E, Vallet B. Inotropes in goal-directed therapy: Do we need 'goals'? Crit Care 2010;14(5):1001.  Back to cited text no. 26
    
27.Michelena HI, Abel MD, Suri RM, Freeman WK, Click RL, Sundt TM, et al. Intraoperative echocardiography in valvular heart disease: An evidence-based appraisal. Mayo Clin Proc 2011;85:646-55.  Back to cited text no. 27
    
28.Schmid E, Nowak M, Unertl K, Rosenberger P. [Intraoperative echocardiography: Impact on surgical decision-making]. Anaesthesist 2009;58:1123-35.  Back to cited text no. 28
[PUBMED]  [FULLTEXT]  
29.Klein AA, Snell A, Nashef SA, Hall RM, Kneeshaw JD, Arrowsmith JE. The impact of intra-operative transoesophageal echocardiography on cardiac surgical practice. Anaesthesia 2009;64:947-52.  Back to cited text no. 29
[PUBMED]  [FULLTEXT]  
30.Eltzschig HK, Rosenberger P, Loffler M, Fox JA, Aranki SF, Shernan SK. Impact of intraoperative transesophageal echocardiography on surgical decisions in 12,566 patients undergoing cardiac surgery. Ann Thorac Surg 2008;85:845-52.  Back to cited text no. 30
    
31.Skinner HJ, Mahmoud A, Uddin A, Mathew T. An investigation into the causes of unexpected intra-operative transoesophageal echogardiography findings. Anaesthesia 2012;67:402-6.  Back to cited text no. 31
[PUBMED]  [FULLTEXT]  
32.Schmidlin D, Bettex D, Bernard E, Germann R, Tornic M, Jenni R, et al. Transoesophageal echocardiography in cardiac and vascular surgery: Implications and observer variability. Br J Anaesth 2001;86:497-505.  Back to cited text no. 32
[PUBMED]  [FULLTEXT]  
33.Cheung AT, Savino JS, Weiss SJ, Aukburg SJ, Berlin JA. Echocardiographic and hemodynamic indexes of left ventricular preload in patients with normal and abnormal ventricular function. Anesthesiology 1994;81:376-87.  Back to cited text no. 33
[PUBMED]  [FULLTEXT]  
34.Oh JK, Hatle L, Tajik AJ, Little WC. Diastolic heart failure can be diagnosed by comprehensive two-dimensional and Doppler echocardiography. J Am Coll Cardiol 2006;47:500-6.  Back to cited text no. 34
[PUBMED]  [FULLTEXT]  
35.Shanewise JS, Cheung AT, Aronson S, Stewart WJ, Weiss RL, Mark JB, et al. ASE/SCA guidelines for performing a comprehensive intraoperative multiplanetransesophagealechocardiography examination: Recommendations of the American Society of Echocardiography Council for Intraoperative Echocardiography and the Society of Cardiovascular Anesthesiologists Task Force for Certification in Perioperative Transesophageal Echocardiography. J Am SocEchocardiogr 1999;12:884-900.  Back to cited text no. 35
[PUBMED]  [FULLTEXT]  
36.American Society of Anesthesiologists and Society of Cardiovascular Anesthesiologists Task Force on Transesophageal Echocardiography. Practice guidelines for perioperative transesophageal echocardiography. A report by the American Society of Anesthesiologists and the Society of Cardiovascular Anesthesiologists Task Force on Transesophageal Echocardiography.Anesthesiology 1996;84:986-1006.  Back to cited text no. 36
[PUBMED]  [FULLTEXT]  
37.American Society of Anesthesiologists and Society of Cardiovascular Anesthesiologists Task Force on Transesophageal Echocardiography.Practice guidelines for perioperative transesophageal echocardiography. An updated report by the American Society of Anesthesiologists and the Society of Cardiovascular Anesthesiologists Task Force on Transesophageal Echocardiography. Anesthesiology 2010;112:1084-96.  Back to cited text no. 37
[PUBMED]  [FULLTEXT]  
38.Flachskampf FA, Badano L, Daniel WG, Feneck RO, Fox KF, Fraser AG,et al. Recommendations for transoesophageal echocardiography: Update 2010. Eur J Echocardiogr 2010;11:557-76.  Back to cited text no. 38
[PUBMED]  [FULLTEXT]  
39.Hilberath JN, Oakes DA, Shernan SK, Bulwer BE, D'Ambra MN, Eltzschig HK. Safety of transesophageal echocardiography. J Am Soc Echocardiogr 2010;23:1115-27.  Back to cited text no. 39
[PUBMED]  [FULLTEXT]  
40.Mebazaa A, Pitsis AA, Rudiger A, Toller W, Longrois D, Ricksten SE, et al. Clinical review: Practical recommendations on the management of perioperative heart failure in cardiac surgery. Crit Care 2011;14:201.  Back to cited text no. 40
    
41.Berman M, Stamler A, Sahar G, Georghiou GP, Sharoni E, Brauner R, et al. Validation of the 2000 Bernstein-Parsonnet score versus the Euroscore as a prognostic tool in cardiac surgery. Ann Thorac Surg 2006;81:537-40.  Back to cited text no. 41
[PUBMED]  [FULLTEXT]  
42.Licker M, Neidhart P, Lustenberger S, Valloton MB, Kalonji T, Fathi M, et al. Long-term angiotensin-converting enzyme inhibitor treatment attenuates adrenergic responsiveness without altering hemodynamic control in patients undergoing cardiac surgery. Anesthesiology 1996;84:789-800.  Back to cited text no. 42
[PUBMED]  [FULLTEXT]  
43.Levin MA, Lin HM, Castillo JG, Adams DH, Reich DL, Fischer GW. Early on-cardiopulmonary bypass hypotension and other factors associated with vasoplegic syndrome. Circulation 2009;120:1664-71.  Back to cited text no. 43
[PUBMED]  [FULLTEXT]  
44.Sun X, Zhang L, Hill PC, Lowery R, Lee AT, Molyneaux RE, et al. Is incidence of postoperative vasoplegic syndrome different between off-pump and on-pump coronary artery bypass grafting surgery? Eur J Cardiothorac Surg 2008;34:820-5.  Back to cited text no. 44
[PUBMED]  [FULLTEXT]  
45.Warren OJ, Smith AJ, Alexiou C, Rogers PL, Jawad N, Vincent C, et al. The inflammatory response to cardiopulmonary bypass: Part 1--mechanisms of pathogenesis. J Cardiothorac Vasc Anesth 2009;23:223-31.  Back to cited text no. 45
[PUBMED]  [FULLTEXT]  
46.Carrel T, Englberger L, Mohacsi P, Neidhart P, Schmidli J. Low systemic vascular resistance after cardiopulmonary bypass: Incidence, etiology, and clinical importance. J Card Surg 2000;15:347-53.  Back to cited text no. 46
[PUBMED]    
47.Mekontso-Dessap A, Houel R, Soustelle C, Kirsch M, Thebert D, Loisance DY. Risk factors for post-cardiopulmonary bypass vasoplegia in patients with preserved left ventricular function. Ann Thorac Surg 2001;71:1428-32.  Back to cited text no. 47
    
48.Argenziano M, Chen JM, Choudhri AF, Cullinane S, Garfein E, Weinberg AD, et al. Management of vasodilatory shock after cardiac surgery: Identification of predisposing factors and use of a novel pressor agent. J Thorac Cardiovasc Surg 1998;116:973-80.  Back to cited text no. 48
[PUBMED]  [FULLTEXT]  
49.Breisblatt WM, Stein KL, Wolfe CJ, Follansbee WP, Capozzi J, Armitage JM, et al. Acute myocardial dysfunction and recovery: A common occurrence after coronary bypass surgery. J Am Coll Cardiol 1990;15:1261-9.  Back to cited text no. 49
[PUBMED]    
50.Croal BL, Hillis GS, Gibson PH, Fazal MT, El-Shafei H, Gibson G, et al. Relationship between postoperative cardiac troponin I levels and outcome of cardiac surgery. Circulation 2006;114:1468-75.  Back to cited text no. 50
[PUBMED]  [FULLTEXT]  
51.Algarni KD, ElhenawyAM, Maganti M, Collins S, Yau TM. Decreasing prevalence but increasing importance of left ventricular dysfunction and reoperative surgery in prediction of mortality in coronary artery bypass surgery: Trends over 18 years. J Thorac Cardiovasc Surg 2011 Nov 18. [In press].  Back to cited text no. 51
    
52.Denault AY, Couture P, Buithieu J, Haddad F, Carrier M, Babin D, et al. Left and right ventricular diastolic dysfunction as predictors of difficult separation from cardiopulmonary bypass. Can J Anaesth 2006;53:1020-9.  Back to cited text no. 52
[PUBMED]  [FULLTEXT]  
53.Licker M, Cikirikcioglu M, Inan C, Cartier V, Kalangos A, Theologou T, et al. Preoperative diastolic function predicts the onset of left ventricular dysfunction following aortic valve replacement in high-risk patients with aortic stenosis. Crit Care 2011;14:R101.  Back to cited text no. 53
    
54.Ahmed I, House CM, Nelson WB. Predictors of inotrope use in patients undergoing concomitant coronary artery bypass graft (CABG) and aortic valve replacement (AVR) surgeries at separation from cardiopulmonary bypass (CPB). J Cardiothorac Surg 2009;4:24.  Back to cited text no. 54
[PUBMED]  [FULLTEXT]  
55.McKinlay KH, Schinderle DB, Swaminathan M, Podgoreanu MV, Milano CA, Messier RH, et al. Predictors of inotrope use during separation from cardiopulmonary bypass. J Cardiothorac Vasc Anesth 2004;18:404-8.  Back to cited text no. 55
[PUBMED]  [FULLTEXT]  
56.Muller M, Junger A, Brau M, Kwapisz MM, Schindler E, Akinturk H, et al. Incidence and risk calculation of inotropic support in patients undergoing cardiac surgery with cardiopulmonary bypass using an automated anaesthesia record-keeping system. Br J Anaesth 2002;89:398-404.  Back to cited text no. 56
    
57.Muehlschlegel JD, Perry TE, Liu KY, Fox AA, Collard CD, Shernan SK, et al. Heart-type fatty acid binding protein is an independent predictor of death and ventricular dysfunction after coronary artery bypass graft surgery. Anesth Analg 2011;111:1101-9.  Back to cited text no. 57
    
58.Butterworth JFt, Legault C, Royster RL, Hammon JW Jr. Factors that predict the use of positive inotropic drug support after cardiac valve surgery. Anesth Analg 1998;86:461-7.  Back to cited text no. 58
    
59.Maganti MD, Rao V, Borger MA, Ivanov J, David TE. Predictors of low cardiac output syndrome after isolated aortic valve surgery. Circulation 2005;112(9 Suppl):I448-52.  Back to cited text no. 59
    
60.Royster RL, Butterworth JFt, Prough DS, Johnston WE, Thomas JL, Hogan PE, et al. Preoperative and intraoperative predictors of inotropic support and long-term outcome in patients having coronary artery bypass grafting. Anesth Analg 1991;72:729-36.  Back to cited text no. 60
    
61.Fox AA, Collard CD, Shernan SK, Seidman CE, Seidman JG, Liu KY, et al. Natriuretic peptide system gene variants are associated with ventricular dysfunction after coronary artery bypass grafting. Anesthesiology 2009;110:738-47.  Back to cited text no. 61
[PUBMED]  [FULLTEXT]  
62.Fox AA, Pretorius M, Liu KY, Collard CD, Perry TE, Shernan SK, et al. Genome-wide assessment for genetic variants associated with ventricular dysfunction after primary coronary artery bypass graft surgery. PLoS One 2011;6:e24593.  Back to cited text no. 62
[PUBMED]  [FULLTEXT]  
63.Galie N, Hoeper MM, Humbert M, Torbicki A, Vachiery JL, Barbera JA, et al. Guidelines for the diagnosis and treatment of pulmonary hypertension: The task force for the diagnosis and treatment of pulmonary hypertension of the European Society of Cardiology (ESC) and the European Respiratory Society (ERS), endorsed by the International Society of Heart and Lung Transplantation (ISHLT). Eur Heart J 2009;30:2493-537.  Back to cited text no. 63
    
64.Kalogeropoulos AP, Vega JD, Smith AL, Georgiopoulou VV. Pulmonary hypertension and right ventricular function in advanced heart failure. Congest Heart Fail 2011;17:189-198.  Back to cited text no. 64
[PUBMED]  [FULLTEXT]  
65.Cam A, Goel SS, Agarwal S, Menon V, Svensson LG, Tuzcu EM, et al. Prognostic implications of pulmonary hypertension in patients with severe aortic stenosis. J Thorac Cardiovasc Surg 2011;142:800-8.  Back to cited text no. 65
[PUBMED]  [FULLTEXT]  
66.Shahian DM, O'Brien SM, Filardo G, Ferraris VA, Haan CK, Rich JB, et al. The Society of Thoracic Surgeons 2008 cardiac surgery risk models: Part 3-valve plus coronary artery bypass grafting surgery. Ann Thorac Surg 2009;88(1 Suppl):S43-62.  Back to cited text no. 66
    
67.Melby SJ, Moon MR, Lindman BR, Bailey MS, Hill LL, Damiano RJ Jr. Impact of pulmonary hypertension on outcomes after aortic valve replacement for aortic valve stenosis. J Thorac Cardiovasc Surg 2011:141:1424-30.  Back to cited text no. 67
[PUBMED]  [FULLTEXT]  
68.Ben-Dor I, Goldstein SA, Pichard AD, Satler LF, Maluenda G, Li Y, et al. Clinical profile, prognostic implication, and response to treatment of pulmonary hypertension in patients with severe aortic stenosis. Am J Cardiol 2011;107:1046-51.  Back to cited text no. 68
[PUBMED]  [FULLTEXT]  
69.Rudski LG, Lai WW, Afilalo J, Hua L, Handschumacher MD, Chandrasekaran K, et al. Guidelines for the echocardiographic assessment of the right heart in adults: A report from the American Society of Echocardiography endorsed by the European Association of Echocardiography, a registered branch of the European Society of Cardiology, and the Canadian Society of Echocardiography. J Am Soc Echocardiogr 2010;23:685-713.  Back to cited text no. 69
[PUBMED]  [FULLTEXT]  
70.Haddad F, Couture P, Tousignant C, Denault AY. The right ventricle in cardiac surgery, a perioperative perspective: I. Anatomy, physiology, and assessment. Anesth Analg 2009;108:407-21.  Back to cited text no. 70
[PUBMED]  [FULLTEXT]  
71.Comunale ME, Maslow A, Robertson LK, Haering JM, Mashikian JS, Lowenstein E. Effect of site of venous protamine administration, previously alleged risk factors, and preoperative use of aspirin on acute protamine-induced pulmonary vasoconstriction. J Cardiothorac Vasc Anesth 2003;17:309-13.  Back to cited text no. 71
[PUBMED]  [FULLTEXT]  
72.Despotis GJ, Levine V, Joiner-Maier D, Joist JH. A comparison between continuous infusion versus standard bolus administration of heparin based on monitoring in cardiac surgery. Blood Coagul Fibrinolysis 1997;8:419-30.  Back to cited text no. 72
[PUBMED]    
73.Fratacci MD, Frostell CG, Chen TY, Wain JC Jr, Robinson DR, Zapol WM. Inhaled nitric oxide. A selective pulmonary vasodilator of heparin-protamine vasoconstriction in sheep. Anesthesiology 1991;75:990-9.  Back to cited text no. 73
[PUBMED]  [FULLTEXT]  
74.Jerath A, Srinivas C, Vegas A, Brister S. The successful management of severe protamine-induced pulmonary hypertension using inhaled prostacyclin. Anesth Analg 2010;110(2):365-9  Back to cited text no. 74
    
75.Desjardins G, Cahalan M. The impact of routine trans-oesophageal echocardiography (TOE) in cardiacsurgery. Best Pract Res Clin Anaesthesiol 2009;23:263-71.  Back to cited text no. 75
[PUBMED]    
76.Levin RL, Degrange MA, Bruno GF, Del Mazo CD, Taborda DJ, Griotti JJ, et al. Methylene blue reduces mortality and morbidity in vasoplegic patients after cardiac surgery. Ann Thorac Surg 2004;77:496-9.  Back to cited text no. 76
[PUBMED]  [FULLTEXT]  
77.Masetti P, Murphy SF, Kouchoukos NT. Vasopressin therapy for vasoplegic syndrome following cardiopulmonary bypass. J Card Surg 2002;17:485-9.  Back to cited text no. 77
[PUBMED]    
78.Noto A, Lentini S, Versaci A, Giardina M, Risitano DC, Messina R, et al. A retrospective analysis of terlipressin in bolus for the management of refractory vasoplegic hypotension after cardiac surgery. Interact Cardiovasc Thorac Surg 2009;9:588-92.  Back to cited text no. 78
[PUBMED]  [FULLTEXT]  
79.Gillies M, Bellomo R, Doolan L, Buxton B. Bench-to-bedside review: Inotropic drug therapy after adult cardiac surgery - a systematic literature review. Crit Care 2005;9:266-79.  Back to cited text no. 79
[PUBMED]  [FULLTEXT]  
80.Winterhalter M, Simon A, Fischer S, Rahe-Meyer N, Chamtzidou N, Hecker H, et al. Comparison of inhaled iloprost and nitric oxide in patients with pulmonary hypertension during weaning from cardiopulmonary bypass in cardiac surgery: A prospective randomized trial. J Cardiothorac Vasc Anesth 2008;22:406-13.  Back to cited text no. 80
[PUBMED]  [FULLTEXT]  
81.Wang DY, Richmond ME, Quinn TA, Mirani AJ, Rusanov A, Yalamanchi V, et al. Optimized temporary biventricular pacing acutely improves intraoperative cardiac output after weaning from cardiopulmonary bypass: A substudy of a randomized clinical trial. J Thorac Cardiovasc Surg 2011;141:1002-8.  Back to cited text no. 81
[PUBMED]  [FULLTEXT]  
82.Kogan A, Ghosh P, Schwammenthal E, Raanani E. Takotsubo syndrome after cardiac surgery. Ann Thorac Surg 2008;85:1439-41.  Back to cited text no. 82
[PUBMED]  [FULLTEXT]  
83.Gariboldi V, Jop B, Grisoli D, Jaussaud N, Kerbaul F, Collart F. Takotsubo syndrome after mitral valve replacement for acute endocarditis. Ann Thorac Surg 2011;91:e31-2.  Back to cited text no. 83
[PUBMED]  [FULLTEXT]  
84.Vernick WJ, Hargrove WC, Augoustides JG, Horak J. Takotsubo cardiomyopathy associated with cardiac arrest following cardiac surgery: New variants of an unusual syndrome. J Card Surg 2010;25:679-83.  Back to cited text no. 84
[PUBMED]  [FULLTEXT]  
85.Rivera JM, Locketz AJ, Fritz KD, Horlocker TT, Lewallen DG, Prasad A, Bresnahan JF, Kinney MO. "Broken heart syndrome". Mayo Clin Proc. 2006;81:825-8.  Back to cited text no. 85
[PUBMED]  [FULLTEXT]  
86.Thackray S, Easthaugh J, Freemantle N, Cleland JG. The effectiveness and relative effectiveness of intravenous inotropic drugs acting through the adrenergic pathway in patients with heart failure-a meta-regression analysis. Eur J Heart Fail 2002;4515-29.  Back to cited text no. 86
    
87.Kogan A, Preisman S, Bar A, Sternik L, Lavee J, Malachy A, et al. The impact of hyperlactatemia on postoperative outcome after adult cardiac surgery. J Anesth 2011;[Epub ahead of print].  Back to cited text no. 87
    
88.Totaro RJ, Raper RF. Epinephrine-induced lacticacidosis followingcardiopulmonary bypass. Crit Care Med 1997;25:1693-9.  Back to cited text no. 88
[PUBMED]  [FULLTEXT]  
89.Singer M. Catecholamine treatment for shock--equally good or bad? Lancet 2007;370:636-7.  Back to cited text no. 89
    
90.Fellahi JL, Parienti JJ, Hanouz JL, Plaud B, Riou B, Ouattara A. Perioperative use of dobutamine in cardiac surgery and adverse cardiac outcome: Propensity-adjusted analyses. Anesthesiology 2008;108:979-87.  Back to cited text no. 90
[PUBMED]  [FULLTEXT]  
91.Shahin J, Devarennes B, Tse CW, Amarica DA, Dial S. The relationship between inotrope exposure, six-hour postoperative physiological variables, hospital mortality and renal dysfunction in patients undergoing cardiac surgery. Crit Care 2011;15:R162.  Back to cited text no. 91
[PUBMED]  [FULLTEXT]  
92.Guru V, Omura J, Alghamdi AA, Weisel R, Fremes SE. Is blood superior to crystalloid cardioplegia? A meta-analysis of randomized clinical trials. Circulation 2006;114(1 Suppl):I331-8.  Back to cited text no. 92
    
93.Walsh SR, Tang TY, Kullar P, Jenkins DP, Dutka DP, Gaunt ME. Ischaemic preconditioning during cardiac surgery: Systematic review and meta-analysis of perioperative outcomes in randomised clinical trials. Eur J Cardiothorac Surg 2008;34:985-94.  Back to cited text no. 93
[PUBMED]  [FULLTEXT]  
94.Symons JA, Myles PS. Myocardial protection with volatile anaesthetic agents during coronary artery bypass surgery: A meta-analysis. Br J Anaesth 2006;97:127-36.  Back to cited text no. 94
[PUBMED]  [FULLTEXT]  
95.Bothe W, Olschewski M, Beyersdorf F, Doenst T. Glucose-insulin-potassium in cardiac surgery: A meta-analysis. Ann Thorac Surg 2004;78:1650-7.  Back to cited text no. 95
[PUBMED]  [FULLTEXT]  
96.Fan Y, Zhang AM, Xiao YB, Weng YG, Hetzer R. Glucose-insulin-potassium therapy in adult patients undergoing cardiac surgery: A meta-analysis. Eur J Cardiothorac Surg 2011;40:192-9.  Back to cited text no. 96
[PUBMED]    
97.Doenst T, Bothe W, Beyersdorf F. Therapy with insulin in cardiac surgery: Controversies and possible solutions. Ann Thorac Surg 2003;75:S721-8.  Back to cited text no. 97
[PUBMED]    
98.Pollesello P, Papp Z. The cardioprotective effects of levosimendan: preclinical and clinical evidence. J Cardiovasc Pharmacol 2007;50(3):257-63.  Back to cited text no. 98
    
99.De Hert SG, Lorsomradee S, Cromheecke S, van der Linden PJ. The effects of levosimendan in cardiac surgery patients with poor left ventricular function. Anesth Analg 2007;104(4):766-73.  Back to cited text no. 99
    
100.De Hert SG, Lorsomradee S, vanden Eede H, Cromheecke S, Van der Linden PJ. A randomized trial evaluating different modalities of levosimendan administration in cardiac surgery patients with myocardial dysfunction. J Cardiothorac Vasc Anesth 2008;22(5):699-705.  Back to cited text no. 100
    
101.Tritapepe L, De Santis V, Vitale D, Guarracino F, Pellegrini F, Pietropaoli P, et al. Levosimendan pre-treatment improves outcomes in patients undergoing coronary artery bypass graft surgery. Br J Anaesth 2009;102(2):198-204.  Back to cited text no. 101
    
102.Eriksson HI, Jalonen JR, Heikkinen LO, Kivikko M, Laine M, Leino KA, et al. Levosimendan facilitates weaning from cardiopulmonary bypass in patients undergoing coronary artery bypass grafting with impaired left ventricular function. Ann Thorac Surg 2009;87(2):448-54.  Back to cited text no. 102
    
103.Kolseth SM, Nordhaug DO, Stenseth R, Sellevold O, Kirkeby-Garstad I, Wahba A. Prophylactic treatment with levosimendan: a retrospective matched-control study of patients with reduced left ventricular function. Eur J Cardiothorac Surg 2009;36(6):1024-30.  Back to cited text no. 103
    
104.Kikura M, Sato S. The efficacy of preemptive Milrinone or Amrinone therapy in patients undergoing coronary artery bypass grafting. Anesth Analg 2002;94(1):22-30  Back to cited text no. 104
    
105.Hoffman TM, Wernovsky G, Atz AM, Kulik TJ, Nelson DP, Chang AC, et al. Efficacy and safety of milrinone in preventing low cardiac output syndrome in infants and children after corrective surgery for congenital heart disease. Circulation 2003;107(7):996-1002.  Back to cited text no. 105
    
106.Cuffe MS, Califf RM, Adams KF, Jr., Benza R, Bourge R, Colucci WS, et al. Short-term intravenous milrinone for acute exacerbation of chronic heart failure: a randomized controlled trial. JAMA 2002;287(12):1541-7.  Back to cited text no. 106
    
107.Bergh CH, Andersson B, Dahlstrom U, Forfang K, Kivikko M, Sarapohja T, et al. Intravenous levosimendan vs. dobutamine in acute decompensated heart failure patients on beta-blockers. Eur J Heart Fail 2011;12(4):404-10.  Back to cited text no. 107
    
108.Sidi A, Muehlschlegel JD, Kirby DS, Lobato EB. Treatment of ischaemic left ventricular dysfunction with milrinone or dobutamine administered during coronary artery stenosis in the presence of beta blockade in pigs. Br J Anaesth 2006;97(6):799-807.  Back to cited text no. 108
    
109.Christenson JT, Licker M, Kalangos A. The role of intra-aortic counterpulsation in high-risk OPCAB surgery: a prospective randomized study. J Card Surg 2003;18(4):286-94  Back to cited text no. 109
    
110.Dyub AM, Whitlock RP, Abouzahr LL, Cina CS. Preoperative intra-aortic balloon pump in patients undergoing coronary bypass surgery: A systematic review and meta-analysis. J Card Surg 2008;23(1):79-86.  Back to cited text no. 110
    
111.Lavana JD, Fraser JF, Smith SE, Drake L, Tesar P, Mullany DV. Influence of timing of intraaortic balloon placement in cardiac surgical patients. J Thorac Cardiovasc Surg 2011;140(1):80-5.  Back to cited text no. 111
    
112.Kuratani N, Bunsangjaroen P, Srimueang T, Masaki E, Suzuki T, Katogi T Modified versus conventional ultrafiltration in pediatric cardiac surgery: a meta-analysis of randomized controlled trials comparing clinical outcome parameters. J Thorac Cardiovasc Surg. 2011;142(4):861-7  Back to cited text no. 112
    
113.Tao Zhang, Gao CQ, Li JC, Wang JL, Li LB, Xiao CS. Effect of subzero-balanced ultrafiltration on postoperative outcome of patients after cardiopulmonary bypass. Perfusion. 2009 24(6):401-8.  Back to cited text no. 113
    
114.Onorati F, Renzulli A, De Feo M, Galdieri N, Sante P, Mastroroberto P, et al. Perioperative enoximone infusion improves cardiac enzyme release after CABG. J Cardiothorac Vasc Anesth 2004;18:409-14.  Back to cited text no. 114
    
115.Jebeli M, Ghazinoor M, Mandegar MH, Rasouli MR, Eghtesadi-Araghi P, Goodarzynejad H, et al. Effect of milrinone on short-term outcome of patients with myocardial dysfunction undergoing coronary artery bypass graft: A randomized controlled trial. Cardiol J 2011;17:73-8.  Back to cited text no. 115
    
116.Arbeus M, Axelsson B, Friberg O, Magnuson A, Bodin L, Hultman J. Milrinone increases flow in coronary artery bypass grafts after cardiopulmonary bypass: A prospective, randomized, double-blind, placebo-controlled study. J Cardiothorac Vasc Anesth 2009;23:48-53.  Back to cited text no. 116
[PUBMED]  [FULLTEXT]  
117.Maslow AD, Regan MM, Schwartz C, Bert A, Singh A. Inotropes improve right heart function in patients undergoing aortic valve replacement for aortic stenosis. Anesth Analg 2004;98:891-902.  Back to cited text no. 117
[PUBMED]  [FULLTEXT]  
118.Fleming GA, Murray KT, Yu C, Byrne JG, Greelish JP, Petracek MR, et al. Milrinone use is associated with postoperative atrial fibrillation after cardiac surgery. Circulation 2008;118:1619-25.  Back to cited text no. 118
[PUBMED]    
119.Delaney A, Bradford C, McCaffrey J, Bagshaw SM, Lee R. Levosimendan for the treatment of acute severe heart failure: A meta-analysis of randomised controlled trials. Int J Cardiol 2011;138:281-9.  Back to cited text no. 119
    
120.Landoni G, Mizzi A, Biondi-Zoccai G, Bruno G, Bignami E, Corno L, et al. Reducing mortality in cardiac surgery with levosimendan: A meta-analysis of randomized controlled trials. J Cardiothorac Vasc Anesth 2011;24:51-7.  Back to cited text no. 120
    
121.Lombard FW, Grichnik KP. Update on management strategies for separation from cardiopulmonary bypass. Curr Opin Anaesthesiol 2011;24:49-57.  Back to cited text no. 121
[PUBMED]  [FULLTEXT]  
122.Ferguson JJ 3rd, Cohen M, Freedman RJJr, Stone GW, Miller MF, Joseph DL, et al. The current practice of intra-aortic balloon counterpulsation: Results from the Benchmark Registry. J Am Coll Cardiol 2001;38:1456-62.  Back to cited text no. 122
    
123.Cohen M, Urban P, Christenson JT, Joseph DL, Freedman RJJr, Miller MF, et al. Intra-aortic balloon counterpulsation in US and non-US centres: Results of the Benchmark Registry. Eur Heart J 2003;24:1763-70.  Back to cited text no. 123
    
124.Zaky SS, Hanna AH, SakrEsa WA, Xu M, Lober C, Sessler DI, et al. An 11-year, single-institution analysis of intra-aortic balloon pump use in cardiac surgery. J Cardiothorac Vasc Anesth 2009;23:479-83.  Back to cited text no. 124
    
125.Sylvin EA, Stern DR, Goldstein DJ. Mechanical support for postcardiotomy cardiogenic shock: Has progress been made? J Card Surg 2011;25:442-54.  Back to cited text no. 125
    
126.Cheng JM, den Uil CA, Hoeks SE, van der Ent M, Jewbali LS, van Domburg RT, et al. Percutaneous left ventricular assist devices vs. intra-aortic balloon pump counterpulsation for treatment of cardiogenic shock: A meta-analysis of controlled trials. Eur Heart J 2009;30:2102-8.  Back to cited text no. 126
[PUBMED]  [FULLTEXT]  
127.Bartlett RH, Gattinoni L. Current status of extracorporeal life support (ECMO) for cardiopulmonary failure. Minerva Anestesiol 2010;76:534-40.  Back to cited text no. 127
[PUBMED]  [FULLTEXT]  

Top
Correspondence Address:
Marc Licker
Department of Anesthesiology, Pharmacology & Intensive Care, University Hospital Geneva, rue Gabrielle-Perret-Gentil 4, CH-1211 Geneva 14

Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0971-9784.97977

Rights and Permissions


    Figures

  [Figure 1], [Figure 2]
 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5]

This article has been cited by
1 Spontaneous, Postpartum Coronary Artery Dissection and Cardiogenic Shock with Extracorporeal Membrane Oxygenation Assisted Recovery in a 30-Year-Old Patient
Kathleen E. Knapp,Ricardo A. Weis,Efrain I. Cubillo,Alyssa B. Chapital,Harish Ramakrishna
Case Reports in Cardiology. 2016; 2016: 1
[Pubmed] | [DOI]
2 Methylene blue treatment for cytokine release syndrome-associated vasoplegia following a renal transplant with rATG infusion: A case report and literature review
John Denny,Andrew Burr,Fred Balzer,James Tse,Julia Denny,Darrick Chyu
Experimental and Therapeutic Medicine. 2015;
[Pubmed] | [DOI]
3 Percutaneous withdrawal of HeartWare HVAD left ventricular assist device support
Stephen J. Pettit,Leonard M. Shapiro,Clive Lewis,Jayan K. Parameshwar,Steven S.L. Tsui
The Journal of Heart and Lung Transplantation. 2015;
[Pubmed] | [DOI]
4 Pharmacologic approaches to weaning from cardiopulmonary bypass and extracorporeal membrane oxygenation
Wilson W. Cui,James G. Ramsay
Best Practice & Research Clinical Anaesthesiology. 2015;
[Pubmed] | [DOI]
5 Unexpected thrombus migration obstructing the right coronary ostium after thoracic aorta graft replacement
Jae-Kwang Shim,Young Song,Taek-Yeon Lee,Yoon-Jae Kim,Young-Lan Kwak
Journal of Clinical Ultrasound. 2013; : n/a
[Pubmed] | [DOI]
6 Weaning of extracorporeal membrane oxygenation using continuous hemodynamic transesophageal echocardiography
Nicholas C. Cavarocchi,Harrison T. Pitcher,Qiong Yang,Pawel Karbowski,Joseph Miessau,Harold M. Hastings,Hitoshi Hirose
The Journal of Thoracic and Cardiovascular Surgery. 2013;
[Pubmed] | [DOI]
7 Weaning from cardiopulmonary bypass
Kim, H.
Korean Journal of Anesthesiology. 2013; 64(6): 487-488
[Pubmed]
8 Weaning from cardiopulmonary bypass
Heezoo Kim
Korean Journal of Anesthesiology. 2013; 64(6): 487
[Pubmed] | [DOI]
9 Epoetin administrated after cardiac surgery: effects on renal function and inflammation in a randomized controlled study
Sophie de Seigneux,Belen Ponte,Lucien Weiss,Jérôme Pugin,Jacques Romand,Pierre-Yves Martin,Patrick Saudan
BMC Nephrology. 2012; 13(1): 132
[Pubmed] | [DOI]



 

Top