Monitoring, management, and outcome of hypotension in Intensive Care Unit patients, an international survey of the European Society of Intensive Care Medicine.

INTRODUCTION: Hypotension in the ICU is common, yet management is challenging and variable. Insight in management by ICU physicians and nurses may improve patient care and guide future hypotension treatment trials and guidelines. METHODS: We conducted an international survey among ICU personnel to provide insight in monitoring, management, and perceived consequences of hypotension. RESULTS: Out of 1464 respondents, 1197 (81.7%) were included (928 physicians (77.5%) and 269 nurses (22.5%)). The majority indicated that hypotension is underdiagnosed (55.4%) and largely preventable (58.8%). Nurses are primarily in charge of monitoring changes in blood pressure, physicians are in charge of hypotension treatment. Balanced crystalloids, dobutamine, norepinephrine, and Trendelenburg position were the most frequently reported fluid, inotrope, vasopressor, and positional maneuver used to treat hypotension. Reported complications believed to be related to hypotension were AKI and myocardial injury. Most ICUs do not have a specific hypotension treatment guideline or protocol (70.6%), but the majority would like to have one in the future (58.1%). CONCLUSIONS: Both physicians and nurses report that hypotension in ICU patients is underdiagnosed, preventable, and believe that hypotension influences morbidity. Hypotension management is generally not protocolized, but the majority of respondents would like to have a specific hypotension management protocol.

Definition and incidence of hypotension in intensive care unit patients, an international survey of the European Society of Intensive Care Medicine.

INTRODUCTION: Although hypotension in ICU patients is associated with adverse outcome, currently used definitions are unknown and no universally accepted definition exists. METHODS: We conducted an international, peer-reviewed survey among ICU physicians and nurses to provide insight in currently used definitions, estimations of incidence, and duration of hypotension. RESULTS: Out of 1394 respondents (1055 physicians (76%) and 339 nurses (24%)), 1207 (82%) completed the questionnaire. In all patient categories, hypotension definitions were predominantly based on an absolute MAP of 65 mmHg, except for the neuro(trauma) category (75 mmHg, p < 0.001), without differences between answers from physicians and nurses. Hypotension incidence was estimated at 55%, and time per day spent in hypotension at 15%, both with nurses reporting higher percentages than physicians (estimated mean difference 5%, p = 0.01; and 4%, p < 0.001). CONCLUSIONS: An absolute MAP threshold of 65 mmHg is most frequently used to define hypotension in ICU patients. In neuro(trauma) patients a higher threshold was reported. The majority of ICU patients are estimated to endure hypotension during their ICU admission for a considerable amount of time, with nurses reporting a higher estimated incidence and time spent in hypotension than physicians.

[Support of damaged heart with the Impella pump]. / Ondersteuning van beschadigd hart met Impella-pomp.

Temporary mechanical circulatory support is increasingly used, particularly in patients with cardiogenic shock or during high-risk percutaneous coronary interventions. In the last five years there have been numerous developments in this field. Experience has been gained from usage of temporary heart pumps, and new pumps have arrived on the market. Until recently, the intra-aortal balloon pump was the standard treatment for patients with cardiogenic shock; however, results from the latest research into the effectiveness of this pump have rendered it less popular. An alternative modality is the Impella system. Since 2012, usage of a heart pump in cardiogenic shock treatment is reimbursed by healthcare insurers in the Netherlands. Recently, the FDA approved the Impella system for said indication.

Plasma-derived human C1-esterase inhibitor does not prevent mechanical ventilation-induced pulmonary complement activation in a rat model of Streptococcus pneumoniae pneumonia.

Mechanical ventilation has the potential to cause lung injury, and the role of complement activation herein is uncertain. We hypothesized that inhibition of the complement cascade by administration of plasma-derived human C1-esterase inhibitor (C1-INH) prevents ventilation-induced pulmonary complement activation, and as such attenuates lung inflammation and lung injury in a rat model of Streptococcus pneumoniae pneumonia. Forty hours after intratracheal challenge with S. pneumoniae causing pneumonia rats were subjected to ventilation with lower tidal volumes and positive end-expiratory pressure (PEEP) or high tidal volumes without PEEP, after an intravenous bolus of C1-INH (200 U/kg) or placebo (saline). After 4 h of ventilation blood, broncho-alveolar lavage fluid and lung tissue were collected. Non-ventilated rats with S. pneumoniae pneumonia served as controls. While ventilation with lower tidal volumes and PEEP slightly amplified pneumonia-induced complement activation in the lungs, ventilation with higher tidal volumes without PEEP augmented local complement activation more strongly. Systemic pre-treatment with C1-INH, however, failed to alter ventilation-induced complement activation with both ventilation strategies. In accordance, lung inflammation and lung injury were not affected by pre-treatment with C1-INH, neither in rats ventilated with lower tidal volumes and PEEP, nor rats ventilated with high tidal volumes without PEEP. Ventilation augments pulmonary complement activation in a rat model of S. pneumoniae pneumonia. Systemic administration of C1-INH, however, does not attenuate ventilation-induced complement activation, lung inflammation, and lung injury.

Mechanical circulatory support with the Impella 5.0 device for postcardiotomy cardiogenic shock: a three-center experience.

AIM: Postcardiotomy cardiogenic shock (PCCS) is associated with high mortality rates, despite full conventional treatment. Although the results of treatment with surgically implantable ventricular assist devices have been encouraging, the invasiveness of this treatment limits its applicability. Several less invasive devices have been developed, including the Impella system. The objective of this study was to describe our three-center experience with the Impella 5.0 device in the setting of PCCS. METHODS: From January 2004 through December 2010, a total of 46 patients were diagnosed with treatment-refractory PCCS and treated with the Impella 5.0 percutaneous left ventricular assist device at three european heart centers. Baseline and follow-up characteristics were collected retrospectively and entered into a dedicated database. RESULTS: Within the study cohort of 46 patients, mean logistic and additive EuroSCORES were 24 ± 19 and 10 ± 4. The majority of patients underwent coronary artery bypass grafting (48%) or combined surgery (33%). Half of all patients had been treated with an intra-aortic balloon pump before 5.0-implantation, 1 patient had been treated with an Impella 2.5 device. All patients were on mechanical ventilation and intravenous inotropes. The Kaplan-Meier estimate of overall 30-day survival was 39.5%. CONCLUSION: Thirty-day survival rates for patients with PCCS, refractory to aggressive conventional treatment and treated with the Impella 5.0 device, are comparable to those reported in studies evaluating surgically implantable VADs, whereas the Impella system is much less invasive. Therefore, mechanical circulatory support with the Impella 5.0 device is a suitable treatment modality for patients with severe PCCS.

Basic concepts of fluid responsiveness.

Predicting fluid responsiveness, the response of stroke volume to fluid loading, is a relatively novel concept that aims to optimise circulation, and as such organ perfusion, while avoiding futile and potentially deleterious fluid administrations in critically ill patients. Dynamic parameters have shown to be superior in predicting the response to fluid loading compared with static cardiac filling pressures. However, in routine clinical practice the conditions necessary for dynamic parameters to predict fluid responsiveness are frequently not met. Passive leg raising as a means to alter biventricular preload in combination with subsequent measurement of the change in stroke volume can provide a fast and accurate way to guide fluid management in a broad population of critically ill patients.

Postoperative arrhythmias in adults with congenital heart disease: incidence and risk factors.

BACKGROUND: Little is known about the clinical impact of arrhythmias after surgery for congenital heart disease (CHD) in adults. Therefore, we investigated the prevalence of in-hospital arrhythmias after CHD surgery and their impact on clinical outcome. METHODS: This was a multicenter retrospective study and included adults who underwent congenital cardiac surgery between January 2009 and December 2011. Clinical events were defined as all cause mortality, heart failure (HF) requiring medical treatment, thrombo-embolic event, major infections and permanent pacemaker (PM) implantation. RESULTS: Overall, 419 patients were included (mean age 38 ± 14 years, 55% male). Arrhythmias occurred in 134 patients (32%) and included supraventricular tachycardia (SVT, n = 100), bradycardias (n = 47) and ventricular tachycardia (VT, n = 19). In multivariate analysis age ≥40 years at surgery (OR 2.48, 95% Cl 1.40-4.60, P = 0.003), NYHA class ≥ II (OR 2.42, 95% Cl 1.18-4.67, P = 0.009), significant subpulmonary AV-valve regurgitation (OR 2.84, 95% Cl 1.19-6.72, P = 0.018), coronary bypass time (OR 1.35/60 minute increase, 95% Cl 1.06-1.82, P = 0.019) and CK-MB (OR 1.05 per 10 U/L increase, 95% Cl 1.01-1.09, P = 0.021) were associated with in-hospital arrhythmias. Overall, 58 clinical events occurred in 55 patients (13%) and included in the majority of the cases permanent PM implantation (5%), HF (4%) and death (2%). In-hospital arrhythmias were independently associated with clinical events (OR 7.80, 95% CI 2.41-25.54, P = 0.001). CONCLUSION: Arrhythmias are highly prevalent after congenital heart surgery in adults and are associated with worse clinical outcome. Older and symptomatic patients with significant valvular heart disease at baseline are at risk of in-hospital arrhythmias.

Haemodynamic monitoring of morbidly obese intensive care unit patients.

Because of technical and practical difficulties in relation to increased body size, haemodynamic monitoring of morbidly obese critically ill patients (i.e. body mass index ≥40 kg÷m2) may be challenging. Obese and non-obese patients are not so different with respect to haemodynamic monitoring and goals. The critical care physician, however, should be aware of the basic principles of the monitoring tools used. The theoretical assumptions and calculations of these tools could be invalid because of the high body weight and fat distribution. Although the method of assessing haemodynamic data may be more complex in morbidly obese patients, its interpretation should not be different from that in non-obese patients. Indeed, when indexed for body surface area or (predicted) lean body mass, reliable haemodynamic data are comparable etween obese and non-obese individuals.

Cardiopulmonary interactions during mechanical ventilation in critically ill patients.

Cardiopulmonary interactions induced by mechanical ventilation are complex and only partly understood. Applied tidal volumes and/or airway pressures largely mediate changes in right ventricular preload and afterload. Effects on left ventricular function are mostly secondary to changes in right ventricular loading conditions. It is imperative to dissect the several causes of haemodynamic compromise during mechanical ventilation as undiagnosed ventricular dysfunction may contribute to morbidity and mortality.

Encouraging survival rates in patients with acute myocardial infarction treated with an intra-aortic balloon pump.

OBJECTIVE: To evaluate a 30-day and long-term outcome of patients with acute myocardial infarction (AMI) treated with intra-aortic balloon pump (IABP) counterpulsation and to identify predictors of a 30-day and long-term all-cause mortality. METHODS: Retrospective cohort study of 437 consecutive AMI patients treated with IABP between January 1990 and June 2004. A Cox proportional hazards model was used to identify predictors of a 30-day and long-term all-cause mortality. RESULTS: Mean age of the study population was 61 ± 11 years, 80% of the patients were male, and 68% had cardiogenic shock. Survival until IABP removal after successful haemodynamic stabilisation was 78% (n = 341). Cumulative 30-day survival was 68%. Median follow-up was 2.9 years (range, 6 months to 15 years). In patients who survived until IABP removal, cumulative 1-, 5-, and 10-year survival was 75%, 61%, and 39%, respectively. Independent predictors of higher long-term mortality were prior cerebrovascular accident (hazard ratio (HR), 1.8; 95% confidence interval (CI), 1.0-3.4), need for antiarrhythmic drugs (HR, 2.3; 95% CI, 1.5-3.3), and need for renal replacement therapy (HR, 2.3; 95% CI, 1.2-4.3). Independent predictors of lower long-term mortality were primary percutaneous coronary intervention (PCI; HR, 0.6; 95% CI, 0.4-1.0), failed thrombolysis with rescue PCI (HR, 0.5; 95% CI, 0.3-0.9), and coronary artery bypass grafting (HR, 0.3; 95% CI, 0.1-0.5). CONCLUSIONS: Despite high in-hospital mortality in patients with AMI treated with IABP, a favourable number of patients survived in the long-term. These results underscore the value of aggressive haemodynamic support of patients throughout the acute phase of AMI.

Left-sided native valve Staphylococcus aureus endocarditis.

Despite improved diagnostic tools and expanded treatment options, left-sided native valve endocarditis caused by Staphylococcus aureus infection remains a serious and destructive disease. The high morbidity and mortality, however, can be reduced by early recognition, correct diagnosis, and appropriate treatment. In the following article, we discuss the clinical presentation, diagnostic workup and treatment of infective endocarditis, thereby reviewing the current guidelines. Blood cultures and echocardiography are the cornerstones of diagnosis in identifying infective endocarditis but are no substitute for clinical judgement. The modified Duke criteria may facilitate the diagnostic process, but clinical evaluation remains crucial.

The microcirculation in health and critical disease.

The microcirculation is a complex system, which regulates the balance between oxygen demand and supply of parenchymal cells. In addition, the peripheral microcirculation has an important role in regulating the hemodynamics of the human body because it warrants arterial blood pressure as well as venous return to the heart. Novel techniques have made it possible that the microcirculation can be observed directly at the bedside in patients. Currently, research using these new techniques is focusing at the central role of the microcirculation in critical diseases. Experimental studies have demonstrated differences in microvascular alterations between models of septic and hypovolemic shock. In human studies, the microcirculation has most extensively been investigated in septic syndromes and has revealed highly heterogeneous alterations with clear evidence of arteriolar-venular shunting. Until now, the microcirculation in acute heart failure syndromes such as cardiogenic shock has scarcely been investigated. This review concerns the physiologic properties of the microcirculation as well as its role in pathophysiologic states such as sepsis, hypovolemic shock, and acute heart failure.

C-reactive protein and complement depositions in human infarcted myocardium are more extensive in patients with reinfarction or upon treatment with reperfusion.

BACKGROUND: Impaired perfusion of the heart induces a local inflammatory response, which involves deposition of C-reactive protein and complement activation products C3d and C5b-9. We investigated whether reperfusion or reinfarction enhances these phenomena in humans. MATERIALS AND METHODS: Depositions of C-reactive protein and complement were quantified in tissue samples of infarcted myocardium from 76 patients who had died after acute myocardial infarction. The extent of depositions in patients treated with reperfusion or suffering from reinfarction was compared with that in patients who had no reperfusion or reinfarction. RESULTS: Patients with reinfarction had significantly more extensive depositions of C-reactive protein and complement (C3d and C5b-9) in the infarcted myocardium than patients without reinfarction. Similarly, patients who received reperfusion therapy had more extensive depositions also than those who had not received this therapy. CONCLUSIONS: Both reinfarction and reperfusion therapy significantly increase the extent of C-reactive protein and complement depositions in human myocardial infarcts.

Localisation of C reactive protein in infarcted tissue sites of multiple organs during sepsis.

This report hypothesises an active role for the acute phase protein, C reactive protein (CRP), in local inflammatory reactions. This was studied in infarction sites from liver and kidney in a patient who died as a result of multiple complications after cholecystectomy. In this patient, a general acute phase protein reaction was induced, with an increase in plasma CRP. In infarction sites of kidney and liver, colocalisation of CRP and activated complement were found, whereas non-infarct sites were negative for CRP and complement. These results suggest that CRP directly participates in local inflammatory processes, possibly via complement activation, after binding of a suitable ligand.

C-reactive protein as a pro-inflammatory mediator in cardiovascular disease by its ability to activate complement: additional proof and hypothetical mechanisms.

This study was financially supported by the Netherlands Heart Foundation, grant numbers 93-119 and 97-088. Dr. Niessen is a recipient of the Dr. E. Dekker programme of the Netherlands Heart Foundation (D99025).

Granulocyte-macrophage colony-stimulating factor (GM-CSF) decreases left ventricular function. An echocardiographic study in cancer patients.

To study the effect of granulocyte-macrophage colony-stimulating factor (GM-CSF) on the heart, echocardiographic assessments of left ventricular (LV) end-diastolic and end-systolic (ES) diameters (D), ejection fraction (EF) and cardiac output (CO) were done in six male patients (28-70 years of age) with advanced sarcoma (Group 1), prior to (day -1-0), during (day 7-9) and after (day 20-21) a first course of i.v. doxorubicin (day 0) without GM-CSF and a second course (3 weeks after the first one) with GM-CSF 250 microg/m(2)subcutaneously and daily from day 1-11. A similar study was done in ten female patients with advanced breast cancer (31-58 years of age, Group 2) for a first course of doxorubicin+cyclophosphamide with GM-CSF (same schedule as in Group 1). As compared to the mean of values prior to and after the course with GM-CSF in Group 1 and 2, the LVESD during GM-CSF administration transiently increased by median 6% (range -19 to 30%, P<0.05) vs -9% (-21 to 6%, not significant) in the first course without GM-CSF in Group 1 (P<0.05 between courses). The CO and EF tended to decrease during GM-CSF. GM-CSF thus causes a small and transient decrease of LV contractility.