gms | German Medical Science

Hemodynamic monitoring, adequate volume therapy and the use of positive inotropes and vasopressors are the basis of post-operative intensive care after cardiothoracic surgery.

Accordingly, the backbone of the treatment algorithm is appropriate measurement and recording of hemodynamic data. Evaluation of the measured values must occur in the context of the patient’s broader clinical picture before advanced therapeutic concepts are implemented.

The degree of diversity in available monitoring methods, positive inotropes and vasoactive substances highlights the necessity for guidelines in cardiac surgery intensive care medicine. It is not essential that all parts of the guidelines are completely implemented but rather that a local concept relevant to the local circumstances and practicalities is defined and used.

The goal of these guidelines is an appraisal of the available monitoring methods in terms of the indications, procedures, provided information, limitations, contra-indications and risks. Additionally differential therapy with various fluids versus positive inotropes and vasoactive substances, as well as differentiated catecholamine therapy including PDE III inhibitors and calcium sensitizers, and the criteria for the use of the intra-aortic counterpulsation were adressed. These guidelines are a recently updated version of previously published guidelines in German language [1].

The methodological approach for the development of the guidelines complies with the requirements of evidence-based medicine, which were defined by the Arbeitsgemeinschaft der Wissenschaftlichen Medizinischen Fachgesellschaften – AWMF (Consortium of Academic Medical Business Societies) and the Ärztliches Zentrum für Qualität – ÄZQ (Medical Centre for Quality).

The guidelines were the result of a systematic literature search and the critical appraisal of the evidence by scientific methods as well as expert discussion, the core group of whom were the authors of these guidelines.

The following steps were performed:

• Definition of the search criteria for the main topics, and definition of relevant databases.
• Systematic review of the scientific literature, as well as previously published guidelines, recommendations and expert opinions.
• Evaluation of these publications using the evidence criteria.
• Discussion of the drafts and core statements as well as integration of internal evidence (unpublished studies, experience of experts).

The presented key messages of the guidelines were approved after two consensus meetings and one Delphi round under the moderation of the Association of the Scientific Medical Societies in Germany (AWMF). In reaching consensus particular emphasis was placed on the level of evidence, ethical aspects, patient preferences, clinical relevance, risk/benefit ratios and degree of applicability.

An automated search program was used to search the Cochrane Library (Cochrane Reviews), PubMed/Medline and Embase databases. A total of 9064 articles were identified using predefined search words and the search was confined to the period from 1990 to July 2005.

After inspection of the publication titles and abstracts, and exclusion of all non English or non German publications, 655 articles were selected for further analysis.

Articles that did not have the desired themes, older work or duplicated data from the same author, articles whose main focus were pharmacological models and animal experiments were all excluded. After including literature known to the experts, 363 publications were used for the development of the guidelines.

For updating the guidelines a new literature search was performed including the period from August 2005 to October 2009. A total of 3494 articles were identified using the same search strategy as before. After inspection of the publication titles and abstracts 254 articles were selected for further analysis.

Publications were evaluated using the evidence criteria described by the Oxford Centre for Evidence Based Medicine (Levels of Evidence 2009, http://www.cebm.net/index.aspx?o=1025, 12/2009).

Recommendations for which there was not sufficient adequate external evidence available, but which were considered nonetheless indispensable to clinical practice according to experience, could, following consensus agreement, receive the highest grade of recommendation.

Recommendations for which a high grade of evidence existed, could, after consensus was reached, by reason of their marginal clinical relevance, be given a lower grade of recommendation. The recommendation levels are derived from the requirements of the Council of Europe 2001 [2].

• Grade of recommendation (GoR) – description:
  A – Strong recommendation “should“
  B – Recommendation “might“
  O – Open recommendation “can“

The critically ill patient in the intensive care unit requires adequate hemodynamic monitoring [3], [4]. Basic monitoring for a post-operative cardiac surgical intensive care patient should include ECG, pulse oximetry, invasive blood pressure measurement, central venous pressure, fluid balance (wound drainage, fluids in and out), temperature measurement and arterial and central venous blood gas analysis with a sampling frequency determined by clinical protocol.

Almost 100% of the departments who responded in a previous national census confirmed that they routinely used basic monitoring that consisted of ECG, measurement of central venous pressure (CVP), arterial saturation, fluid balance, temperature measurement and invasive blood pressure measurement [5]. These monitoring techniques can therefore be considered as standard basic monitoring for cardiac surgical patients in Germany (Attachment 1 [Attach. 1]: Table 1, Scheme 1).

Multiple studies have underlined the effectiveness of transesophageal echocardiography (TEE) for coronary as well as valvular surgery. TEE gives additional information (between 13 and 45% more) compared to other advanced monitoring methods. This additional information influences therapy in 10–52% of cases, particularly in guiding volume and catecholamine therapies, but also influenced surgical decision making [6], [7], [8]. The effect on outcome of these changes was not addressed in these studies. Compared to time needed for the primary installation of other advanced hemodynamic monitoring methods, TEE has the advantage of a relatively short period of time required to perform it. The disadvantage of TEE is not providing continuous hemodynamic monitoring, the need for expensive equipment and the dependency on operator training and availability (Attachment 1 [Attach. 1]: Table 2, Scheme 2). The data regarding the safety of this device are controversial. While earlier studies report perforation risk below 0.1%, recent publications show that TEE has a complication rate for severe gastrointestinal complications up to 1.2% [9], [10]. In a recently published observational study O’Brien et al. showed an OR of 1.47 (95% CI 1.20–1.81) for a combined end point of morbidity and mortality using TEE, but no significant difference when analyzing isolated mortality rates. While failing on specifying the indications for using TEE, associated morbidities described were renal failure, prolonged ventilator support, cardiac arrest, postoperative reintubation rate, pneumonia and GI bleeding [11].

Transpulmonary thermodilution and calibrated pulse contour analysis [12], [13], [14], [15], [16] provide a valid alternative to the pulmonary artery catheter (PAC) for the measurement of cardiac output even in hemodynamically unstable situations.

Regular (four to eight hourly) recalibration of the catheter is recommended and under some conditions, such as rapidly changing hemodynamics or after weaning from the heart-lung machine, more frequent recalibration is required [15], [17].

Pulse contour analysis is inaccurate in patients with significant aortic insufficiency and those with peripheral vascular disease. The use of an intra-aortic counterpulsation also excludes the use of this technique at present. The continuous measurement of stroke volume variation (SVV) and pulse pressure variation (PPV) is only possible under full mechanical ventilation. Application of the pulse contour analysis and the derived cardiac preload parameters are limited when cardiac arrhythmias are present (Attachment 1 [Attach. 1]: Table 3, Scheme 2).

Based on the published guidelines for pulmonary artery catheterization [18], [19], [20] the use of a PAC for diagnosis and therapy is justified in high risk patients for complex cardiac surgery interventions, in severe low cardiac output syndrome, pulmonary hypertension and for the differentiation between severe right or left ventricular dysfunction. The use of a PAC in cardiac surgery patients with a low perioperative risk is, however, not considered necessary [21], [22].

The PAC is unique in that it can be used to measure mixed venous oxygen saturation. The monitoring of mixed venous oxygen saturation (SvO₂) allows assessment of the global balance between oxygen supply and consumption. A SvO₂ orientated therapy has been shown to be relevant in regard to morbidity and hospital length of stay in post-operative cardiac surgery patients [23]. To what extent using SvO₂ to guide therapy following cardiac surgery is superior to using ScvO₂ remains unclear at the present time. It is known that ScvO₂ can be successfully used to guide sepsis therapy [24], (Attachment 1 [Attach. 1]: Table 4, Scheme 2).

The goal of fluid as well as positive inotropic and vasoactive drug management in post-operative cardiac surgery patients is sufficient tissue perfusion and a normalisation of oxidative metabolism. Cardiac output and O₂-supply are dependent on adequate intravascular volume and cardiac function.

The consensus of the expert board was that the following parameters are recommended as goals for postoperative cardiovascular therapies. The grade for these recommendations (based on the Oxford Centre for Evidence-Based Medicine) is 0:

• ScvO₂ >70% or SvO₂ >65%
• MAP (mean arterial pressure) >65 mmHg
• Cardiac Index >2.0 l/min/m²
• CVP 8–12 mmHg (dependent on ventilation mode)
• LV-EDAI 6–9 cm²/m²
• ITBVI 850–1000 ml/m²
• GEDVI 640–800 ml/m²
• PAOP 12–15 mmHg
• Diuresis >0.5 ml/kgBW/h
• Lactate <3 mmol/l

The time to initiation of interventions aimed at optimising the goal parameters is essential to the success of the intervention [23], [25].

In cardiac surgery patients it is common to have relative or absolute volume deficiency in the early post operative phase. Volume substitution should have predefined goals. Whether crystalloid or colloid solutions are preferable following cardiac surgery cannot be determined based on the existing evidence. Balanced artificial colloid and crystalloid solutions should be preferred [26], [27].

In current national practice first line treatment in cardiac surgery intensive care medicine consists in the use of artificial colloid solutions. Medium molecular weight hydroxyethylstarch derivatives are preferred. Crystalloid solutions are the second choice of volume substitution. Plasma volume substitution with human albumin is no longer used in 50% of cardiac surgery intensive care units [5]. Well performed large randomized studies investigating the role of colloids as the cause of post operative renal failure in cardiac surgery patients have not yet been performed. Nevertheless it seems prudent to avoid high molecular weight, highly substituted or hyperoncotic colloids like HAES 200/0.5 (10% and 6%), HAES 200/0.62 (10% and 6%), HAES 450/0.7 (6%) or 10% and 20% albumin, in the light recent concerns regarding hyperoncotic renal failure [28]. Additionally urea-linked gelatin solutions should be used sparingly due to their high potassium and calcium content [29] (Attachment 1 [Attach. 1]: Table 5, Scheme 3).

Causes of functional impairment include microcirculatory disturbances, hypertensive heart disease, congestive heart failure due to coronary artery disease, hypertrophic obstructive and non obstructive cardiomyopathy and dilative cardiomyopathy.

The following surrogate parameters, adapted from the criteria for low-cardiac-output-syndrome of Swan et al. [30] and El-Banayosy et al. [31], are possible indicators of a cardiocirculatory failure:

• ScvO₂ <60% with SaO₂ 98%
• Mean arterial pressure <60 mmHg
• Urine output <0.5 ml/h, existing for longer than an hour
• Plasma lactate >2.0 mmol/l
• Peripheral vasoconstriction with delayed capillary refill, respectively cool extremities corresponding to centralization.

Generally, with postoperative derangements of the cardiocirculatory sytem, optimisation of cardiac frequency and rhythm are the first-line tasks. The common cardiac rhythm disturbances following cardiopulmonary bypass are atrial fibrillation, sinus tachycardia or bradycardia, ventricular arrhythmias with ectopic excitation, ventricular tachycardia and all degrees of heart block [4].

The therapy of cardiac rhythm disturbances are described in the following guidelines:

• ACC/AHA Guideline Update for Coronary Artery Bypass Graft Surgery [32]
• ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure [33]
• ACC/AHA/ESC Guidelines for the management of patients with atrial fibrillation – Executive Summary [34]
• Guidelines on the prevention and management of de novo atrial fibrillation after cardiac and thoracic surgery [35]
• Guideline for resuscitation in cardiac arrest after cardiac surgery [36].

In case of suspected post-operative cardiovascular dysfunction, a rough initial assessment of volume status by means of central venous pressure should be performed. CVP has limitations in comparison to parameters of advanced hemodynamic monitoring and is not a suitable indicator of cardiac preload and volume responsiveness.

If there is an increase in CVP in the post operative period or in comparison to the intraoperative values, in particular an acute increase, a hemodynamically relevant pericardial effusion or a pericardial tamponade should be excluded by echocardiography.

When CVP decreases compared to intra- or post-operative reference values, an intravascular volume depletion should be excluded by evaluating the cardiovascular response to an increase in preload. The hemodynamic reaction to volume administration should first be estimated with autotransfusion by means of passive leg raising [37], [38]. Then the administration of a maximum of 10 ml/kg body weight of colloid or crystalloid solution should be performed. If a preload increase does not lead to hemodynamic stabilisation, an echocardiogram is indicated. Furthermore, in the case of unstable patients, a 12 lead ECG to rule out an acute ischemia, ScvO₂ and lactate concentration should be obtained and fluid balance should be carefully controlled (Attachment 1 [Attach. 1]: Table 6, Scheme 4).

In cases of a severe hemodynamic deterioration (as with low cardiac output syndrome LCOS), which is associated with a moderately reduced preoperative ventricular function, but not with a pre-existing cardiac failure, a normal amount and function of myocardial β-adrenoreceptors can be presumed. Therapies should focus on optimisation of the workload of the heart, with concurrent targeting of enhancement of contractility, normalisation of the preload and economizing of the afterload.

In this situation a graded approach to the choice of pharmacological inotropes should be used. Dobutamine should be regarded as being of medium efficacy, while epinephrine is highly effective.

A reduction in preload can be achieved by the administration of a venodilator such as nitroglycerin, and a combined decrease in preload and afterload can be achieved by the administration sodium nitroprusside. These therapeutic approaches are recommended in accordance with the evidence based ESC guidelines for the therapy of acute cardiac failure [33]. They can be considered to be standard clinical practice in the treatment of left ventricular failure in cardiac surgical intensive care in France and Germany [39], [5].

Following termination of the extracorporeal circulation the heart is in a particularly vulnerable state. In these circumstances an increase in cardiac pump function should not be accompanied by an increase in myocardial oxygen consumption.

In this clinical situation, the application of phosphodiesterase inhibitors (PDE-III-Inhibitor) can be beneficial. Through their receptor independent enhancement of the myocardial contractility with only a small increase in O₂ consumption because of reduction of the systolic ventricular radius, and its cAMP-mediated direct effect on vascular tone with a resulting vasodilatory component, they effectively can increase cardiac index and the stroke volume index with only moderate chronotropic effects.

Patients with an acute perioperative exacerbation or decompensation of severe chronic cardiac insufficiency due to dilatitive cardiomyopathy, ischemic cardiomyopathy or aggravation of valve defects. In these different clinical situation a different set of circumstances are to be expected.

Serious chronic cardiac failure with the various associated transformations in the neurohumoral system leads to alterations in the regulation of the cardiovascular system, which have consequences for the effects of therapeutic interventions. This principally concerns the receptor systems. Down-regulation of cardiac-β-receptors results in a reduced response to endogenous and exogenous catecholamines.

The effectiveness of catecholamine therapy can also be limited by β-blocker therapy that may have been continued to the day of operation. In this context it has been shown that catecholamines with both α- and β-mimetic effects have additional adverse qualities.

It has been shown that the use of alpha-mimetics in this situation leads to a progressive decrease in cardiac output as a result of increased peripheral vascular resistance [40]. It has to be considered, that the receptor affinity of the respective β-blockers plays a crucial role in this context [41].

As an adjunct to positive inotropic treatment levosimendan can be administered in state of severe LCOS in high risk patients. In clinical studies, levosimendan increased cardiac output and lowered cardiac filling pressures and was associated with reducing release of troponin, risk of death, and hospitalization [42], [43], [44], [45]. Unlike other positive inotropic agents, the primary actions of levosimendan are independent of interactions with adrenergic receptors. Levosimendan is not officially approved for clinical use in Germany.

The consensus belief of the expert members was that preload optimisation is the basic prerequisite for medical or mechanical management of left heart failure. Where preload optimization is not sufficient to achieve the targeted hemodynamic goals, the consensus belief of the expert board is that treatment with positive inotropes is indicated. The choice of substance is dependent on the individual patient situation.

The degree of left heart failure and its effect on the global and regional circulation will generally result in one of 4 broad clinical situations (Attachment 1 [Attach. 1]: Table 7, Scheme 5):

• Hypovolemic patients are tachycardic and show inadequate ventricular filling. In the presence of a left ventricular end diastolic area index <5 cm²/m², or a pulmonary artery occlusion pressure (PAOP) <5 mmHg or an intrathoracic blood volume index <750 ml/m², the initial therapeutic approach should be preload optimisation.

• In smaller volume deficiencies (left ventricular end diastolic area index <7 cm²/m², or pulmonary artery occlusion pressure (PAOP) <10 mmHg or an intrathoracic blood volume index <850 ml/m²) a cautious fluid challenge should be given. If a marked increase in preload parameters does not result in an adequate improvement in cardiac output or systemic blood pressure, fluid administration should be ceased. Excessive preloading bears the risk of a consecutive decrease in contractility. In addition to preload optimisation inotropic support of the left ventricle should be started. Therapy should be orientated to the mean arterial blood pressure. Dobutamine is recommended when the MAP is <60 mmHg and a PDE III inhibitor or levosimendan is recommended when the MAP is >60 mmHg. Adequate volume administration is important here as an afterload decrease can lead to a further decrease in perfusion pressure. In the case of systemic hypotension it may be essential to additionally use a vasopressor. The use of epinephrine is indicated if these therapeutic approaches fail to stabilize the hemodynamic situation or if critical hypotension is present.

• In patients with an adequate preload, a left ventricular end-diastolic area index >9 cm²/m², a pulmonary artery occlusion pressure (PAOP) >15 mmHg, or an intrathoracic blood volume index >1000 ml/m², dobutamine or a PDE III inhibitor can be used. Norepinephrine should be considered for the contra-regulation of systematic hypotension and to increase coronary perfusion. Initial treatment with epinephrine is indicated when serious hypotension is present. In cases where a LCOS does not improve significantly upon the administration of dobutamine or PDE III inhibitors, supplemental inotropic support with epinephrine is warranted. If down-regulation of β-adrenoreceptors is suspected, the combination of epinephrine and a PDE III inhibitor or levosimendan seems reasonable. If the patient has undergone a CABG operation, the implantation of an IABP is indicated.

• In a hypervolemic patient with a clearly increase in preload (left ventricular end diastolic area index >11 cm²/m², a pulmonary artery occlusion pressure (PAOP) >20 mmHg, or an intrathoracic blood volume index >1200 ml/m²) volume removal should be the primary goal and the circulation should be supported pharmacologically. Hemofiltration or hemodialysis can be used as adjuvant therapies. Hemodynamic instability should be treated with dobutamine or a PDE III inhibitor. Under certain circumstances the additional administration of epinephrine, a combination of epinephrine and a PDE III inhibitor or levosimendan may be indicated.

Once an adequate arterial pressure has been achieved and the hemodynamic situation has become stable, consideration can be given to decreasing of pre- and afterload. Total peripheral resistance should be modulated to minimize the work of the heart, while maintaining an adequate perfusion pressure at the same time. To achieve this treatment goal, vasodilators such as nitroglycerine or sodium nitroprusside and vasopressors such as norepinephrine are recommended

Clinical manifestations of right ventricular failure occur in 0.04–1% of patients after cardiac surgery [46], and are an indication for invasive monitoring. The diagnostic instrument of choice is echocardiography. The combination of a small, well contracting left ventricle and a large akinetic right ventricle is pathognomonic for acute right heart failure.

Assessment of right ventricular preload is typically made by measuring the central venous pressures (CVP) (reflects the right atrial pressure – RAP) or less frequently the right ventricular end-diastolic pressure (RVEDP). Values above 10 cmH₂0 are considered to reflect adequate ventricular filling. Many studies have shown that the CVP often does not accurately reflect end-diastolic volume and right ventricular preload. Individual volume requirements can only be evaluated by volume challenges, which should only be performed under close hemodynamic monitoring.

When volume administration increases the right atrial filling pressure without increasing the cardiac output, further volume administration is not indicated. Volume administration is indicated when the CVP is under 10 mmHg, with a CVP of up to 15 mmHg being reasonable. Volume therapy is not indicated when there is combined arterial hypotension and high right heart filling pressures (low cardiac output) [47].

There is no accepted clinical measure of right ventricular afterload. The mean pulmonary artery pressure (MPAP) most closely reflects right ventricular afterload, but it is often rendered inaccurate by variations in CO and with changes in heart size: according to La Place the afterload of a dilated right ventricle with a thin wall is higher than the afterload of a small right ventricle with a thick wall, provided that the PAP is identical. Pulmonary vascular resistance (PVR) is the next most commonly used indirect measure of right ventricular preload. The calculation requires placement of a PAC as PAP, CO, and pulmonary capillary occlusion pressure must be known. PVR cannot detect an increase in right ventricular wall tension as a result of dilation of the ventricle and can therefore underestimate changes in afterload. A further problem is that a decrease in CO caused by a decrease in contractility will result in an increase in PVR (MPAP = PVR x CO), without any change in tension in the wall of the right ventricle.

Measurement of right ventricular ejection fraction using the “fast-response” thermodilution technique is not an ideal measure of right ventricular contractility. An increase in preload commonly causes an increase in ejection fraction without any change in contractility. Conversely an increase in right ventricular afterload will result in a decreased ejection fraction. The ejection fraction only reflects right ventricular contractility under conditions of constant pre- and afterload [48].

The goal of the therapy is prevention of a LCOS. An elevated pulmonary vascular resistance should be reduced, the myocardial oxygen supply should be increased and oxygen-demand reduced. Additionally, adequate preload and coronary perfusion pressures must be ensured [47]. There is not any inotropic drug available that selectively acts on the right ventricle. To improve the contractility of a failing right heart the same substances are used as in left heart failure. Dopamine and epinephrine are known to cause pulmonary vasoconstriction in higher doses. The positive inotropic effect of these substances should always be weighed against their dose dependent vasoconstriction of the pulmonary vessels [47]. In some cases the ratio of O₂-supply and demand may actually deteriorate on administration of these substances. Nonetheless catecholamines are frequently essential in acute RV failure [48].

A reasonable adjuvant to these positive inotropes are PDE III inhibitors, which have a positive inotropic effect and additionally have a relaxing effect on the walls of vascular vessels [49], [50]. A consequent risk associated with their use is a drop in arterial blood pressure, which can be critical in patients with acute pulmonary hypertension and right heart failure associated with systemic hypotension. Thus PDE III inhibitors should only be used with caution in this situation, particularly because this effect will persist due to their long half life [47].

In contrast to inhaled vasodilators, the use of intravenous vasodilators in clinical practice is on the decline [5]. The main reason for the lack of clinical acceptance of intravenous vasodilators for the treatment of right heart failure are their potential adverse effects. None of these substances dilate the pulmonary vessels selectively. Vasodilatation in the cardiovascular system causes a decrease in blood pressure, resulting in impairment of organ perfusion. Additionally pulmonary vasodilatation can be counterproductive if it occurs in non-ventilated sections of the lung, as it can lead to hypoxic pulmonary vasoconstriction in these areas.

Inhalative administration of vasodilators increases local efficacy and minimises systemic side effects. Inhalative nitric oxide (NO) and prostanoids induce selective pulmonary vasodilatation. Several studies have shown, that both inhaled NO [51], [52], [53] and inhaled prostanoids [54], [55], [56] cause a significant decrease in MPAP and PVR, without changing systemic vascular resistance (SVR) and MAP in cardiac surgery patients.

The inhalational administration of NO has only been approved for use in newborns with primary pulmonary hypertension [57].

To summarise, it was the consensus opinion of the expert board that inhalational administration of selective pulmonary vasodilators like prostanoids or NO can be considered in prolonged right heart failure. The recommendation of the off label use of these substances is based on study data and a large body of clinical experience with these substances.

In a practical approach, the treatment of right heart failure will usually begin with three “starting points” (Attachment 1 [Attach. 1]: Table 8, Scheme 6):

• Where TEE demonstrates a low right ventricular filling volume or where the PAOP to CVP ratio is >1, cautious volume loading should be the first line treatment. If this is not successful, pharmacological treatment is then indicated. In normotensive patients, treatment with vasodilators is justified. When this therapeutic approach fails, treatment with inotropes is indicated. In hypotensive patients primary positive inotropic support is indicated.

• In normotensive patients (a MAP between 70 and 80 mmHg), where TEE shows right ventricular volume overload with signs of right ventricular dilation or where the PAOP to CVP ratio is <1, or where this ratio is rapidly increasing, dobutamine and/or a PDE III inhibitor should be used to increase inotropy. Additionally the use of a vasodilator such as nitroglycerine to decrease afterload should be considered. If the combination of dobutamine with NTG and/or a PDE III inhibitor is not effective, epinephrine should be used. Epinephrine can, if necessary, be given in combination with nitroglycerine and/or a PDE III inhibitor.
  Pre-existing pulmonary hypertension and/or therapy resistant right heart failure can be treated with inhalative prostanoids or NO in addition to positive inotropes. The treatment goal should not be to minimise PAP or PVR but rather to optimise the PVR to SVR ratio, while maintaining contractility of the right ventricle, myocardial O₂ supply blood pressure (MAP >60 mmHg).

• Hypotensive patients with a MAP <70 mmHg and high right ventricular preload are by definition in decompensated right heart failure. Here maximum inotropic stimulation is indicated. Initially therapy consists of dobutamine and a PDE III inhibitor, in combination with norepinephrine. When this approach fails to sufficiently stabilize hemodynamics, epinephrine should be used. Depending on the peripheral resistance, nitroglycerine can be additionally used. When pulmonary hypertension is present, inhalative prostacyclin or NO can be used.

The intra-aortic balloon counterpulsation is today routinely used in cardiac surgery for cardiovascular support in left ventricular failure. Its employment in post-operative low cardiac-output syndrome due to an intra- or postoperative myocardial infarction following aorto-coronary bypass operation or heart valve intervention is the classic indication in heart surgery patients. The IABP is usually implanted intraoperatively to facilitate weaning from the HLM or postoperatively in the intensive care unit when the hemodynamic situation is deteriorating, and revascularisation is not optimal [58].

The classic indications for the implantation of an IABP include a persistent or worsening LCOS, despite treatment with high dose inotropes or vasoactive substances, ST-elevation or new hypokinesia in the TEE, where surgical or interventional reversal is not possible and/or where surgical anastomoses are known to be problematic and coronary revascularisation was not complete (Attachment 1 [Attach. 1]: Table 9, Scheme 7).

It should be noted that there is no strong scientific evidence which can be used to define the indications for the use of the IABP [59], [60]. IABP should only be used after cardiac surgery when hemodynamic stabilization is not possible despite the use of high dose positive inotropic agents and catecholamines. There is no good quality evidence upon which recommendations regarding the indications for and timing of IABP in postoperative cardiac surgical patients. However, timely application is essential if multi-organ failure and related complications are to be avoided.

A systematic review [61], has demonstrated that the use of IABP improves long-term survival in cardiac surgical patients.

The detailed recommendations are listed in Attachment 1 [Attach. 1].

The long version of the guideline in German language is available from http://leitlinien.net/.

These guidelines are based on the best scientific advice currently available for each of the above topics. The Guidelines were approved by the Executive Committees of the participating scientific societies between March and April 2010. They are valid up to December 2014. The DGTHG and DGAI will nominate a project team and management for the updating of the guidelines. In the case of new relevant scientific evidence that would require a revision of the recommendations, a direct communication will follow.

The authors are members of the working group hemodynamic monitoring and cardiovascular system of the DGTHG and the DGAI. AWMF support by Prof. I. Kopp, Institute for Theoretical Medicine, Marburg.

The declarations of conflict of interest of all participants can be viewed on request, from the respective professional societies.

Five authors have received lecture fees and/or financial study support respectively exercised advisory activity. These authors specified financial competing interests for following companies: Abbott GmbH & Co KG, Aspect Medical Systems GmbH, Arrow Deutschland GmbH, Covidien GmbH, B. Braun Melsungen AG, Deltex Medical Limited, Dräger AG & Co. KGaA, Fresenius SE, GlaxoSmithKline GmbH & Co KG, Pulsion Medical Systems AG.

This guideline was funded by the DGTHG and the DGAI independent of any interest groups.