Search

Background: Vasopressors are administered to critically ill patients with vasodilatory shock not responsive to volume resuscitation, and less often in cardiogenic shock, and hypovolemic shock.Objectives: The objectives are to review safety and efficacy of vasopressors, pathophysiology, agents that decrease vasopressor dose, predictive biomarkers, β1-blockers, and directions for research.Methods: The quality of evidence was evaluated using Grading of Recommendations Assessment, Development, and Evaluation (GRADE).Results: Vasopressors bind adrenergic: α1, α2, β1, β2; vasopressin: AVPR1a, AVPR1B, AVPR2; angiotensin II: AG1, AG2; and dopamine: DA1, DA2 receptors inducing vasoconstriction. Vasopressor choice and dose vary because of patients and physician practice. Adverse effects include excessive vasoconstriction, organ ischemia, hyperglycemia, hyperlactatemia, tachycardia, and tachyarrhythmias. No randomized controlled trials of vasopressors showed a significant difference in 28-day mortality rate. Norepinephrine is the first-choice vasopressor in vasodilatory shock after adequate volume resuscitation. Some strategies that decrease norepinephrine dose (vasopressin, angiotensin II) have not decreased 28-day mortality while corticosteroids have decreased 28-day mortality significantly in some (two large trials) but not all trials. In norepinephrine-refractory patients, vasopressin or epinephrine may be added. A new vasopressor, angiotensin II, may be useful in profoundly hypotensive patients. Dobutamine may be added because vasopressors may decrease ventricular contractility. Dopamine is recommended only in bradycardic patients. There are potent vasopressors with limited evidence (e.g. methylene blue, metaraminol) and novel vasopressors in development (selepressin).Conclusions: Norepinephrine is first choice followed by vasopressin or epinephrine. Angiotensin II and dopamine have limited indications. In future, predictive biomarkers may guide vasopressor selection and novel vasopressors may emerge. [ABSTRACT FROM AUTHOR]

Author(s): Roeland F. Stolk [sup.1] [sup.2] [sup.3], Matthijs Kox [sup.1] [sup.2], Peter Pickkers [sup.1] [sup.2] Author Affiliations: (1) grid.10417.33, 0000 0004 0444 9382, Department of Intensive Care Medicine, Radboud University [...]

Purpose: Ventricular-arterial (V-A) decoupling decreases myocardial efficiency and is exacerbated by tachycardia that increases static arterial elastance (Ea). We thus investigated the effects of heart rate (HR) reduction on Ea in septic shock patients using the beta-blocker esmolol. We hypothesized that esmolol improves Ea by positively affecting the tone of arterial vessels and their responsiveness to HR-related changes in stroke volume (SV).Methods: After at least 24 h of hemodynamic optimization, 45 septic shock patients, with an HR ≥95 bpm and requiring norepinephrine to maintain mean arterial pressure (MAP) ≥65 mmHg, received a titrated esmolol infusion to maintain HR between 80 and 94 bpm. Ea was calculated as MAP/SV. All measurements, including data from right heart catheterization, echocardiography, arterial waveform analysis, and norepinephrine requirements, were obtained at baseline and at 4 h after commencing esmolol.Results: Esmolol reduced HR in all patients and this was associated with a decrease in Ea (2.19 ± 0.77 vs. 1.72 ± 0.52 mmHg l(-1)), arterial dP/dt max (1.08 ± 0.32 vs. 0.89 ± 0.29 mmHg ms(-1)), and a parallel increase in SV (48 ± 14 vs. 59 ± 18 ml), all p < 0.05. Cardiac output and ejection fraction remained unchanged, whereas norepinephrine requirements were reduced (0.7 ± 0.7 to 0.58 ± 0.5 µg kg(-1) min(-1), p < 0.05).Conclusions: HR reduction with esmolol effectively improved Ea while allowing adequate systemic perfusion in patients with severe septic shock who remained tachycardic despite standard volume resuscitation. As Ea is a major determinant of V-A coupling, its reduction may contribute to improving cardiovascular efficiency in septic shock. [ABSTRACT FROM AUTHOR]

Author(s): Xavier Monnet [sup.1], Paul E. Marik [sup.2] Author Affiliations: (1) grid.413784.d, 0000000121817253, Service de réanimation médicale, EA 4533 Hôpitaux Universitaires Paris-Sud, Hôpital de Bicêtre Université Paris-Sud, , 78, rue [...]

Author(s): Anthony S. McLean [sup.1], Fabio S. Taccone [sup.2], Antoine Vieillard-Baron [sup.3] [sup.4] Author Affiliations: (1) grid.1013.3, 000000041936834X, Department of Intensive Care Medicine, Nepean Hospital, University of Sydney, , Sydney, [...]

Author(s): Daniel A. Reuter [sup.1], James A. Russell [sup.2] [sup.3], Armand Mekontso Dessap [sup.4] [sup.5] Author Affiliations: (1) grid.13648.38, 0000000121803484, Department of Anesthesiology, Center of Anesthesiology and Intensive Care Medicine, [...]

Author(s): Kevin B. Laupland [sup.1], Mathieu van der Jagt [sup.2] Author Affiliations: (1) grid.416142.4, Department of Medicine, Royal Inland Hospital, , Kamloops, BC, Canada (2) grid.5645.2, 000000040459992X, Department of Intensive [...]

Purpose To test the hypothesis that a carbamylated EPO-FC fusion protein (cEPO-FC) or recombinant human erythropoietin (rhEPO) would protect against kidney ischemia/reperfusion (I/R) injury in pigs with atherosclerosis. Methods Anesthetized and mechanically ventilated animals received cEPO-FC (50 [mu]g kg.sup.-1), rhEPO (5,000 IU kg.sup.-1), or vehicle (n = 9 per group) prior to 120 min of aortic occlusion and over 4 h of reperfusion. During aortic occlusion, mean arterial pressure (MAP) was maintained at 80-120 % of baseline values by esmolol, nitroglycerin, and ATP. During reperfusion, noradrenaline was titrated to keep MAP at pre-ischemic levels. Blood creatinine and neutrophil gelatinase-associated lipocalin (NGAL) levels, creatinine clearance, fractional Na.sup.+ excretion, and HE and PAS staining were used to assess kidney function and histological damage. Plasma interleukin-6, tumor necrosis factor-[alpha], nitrate + nitrite and 8-isoprostane levels were measured to assess systemic inflammation, and nitrosative and oxidative stress. Results I/R caused acute kidney injury with reduced creatinine clearance, increased fractional Na.sup.+ excretion and NGAL levels, moderate to severe glomerular and tubular damage and apoptosis, systemic inflammation and oxidative and nitrosative stress, but there were no differences between the treatment groups. Pre-ischemia nitrate + nitrite and 8-isoprostanes levels were lower and higher, respectively, than in healthy animals of a previous study, and immune histochemistry showed higher endothelial nitric oxide synthase and lower EPO receptor expression in pre-ischemia kidney biopsies than in biopsies from healthy animals. Conclusions In swine with atherosclerosis, rhEPO and cEPO-FC failed to attenuate prolonged ischemia-induced kidney injury within an 8-h reperfusion period, possibly due to reduced EPO receptor expression resulting from pre-existing oxidative stress and/or reduced NO release., Author(s): Sárka Matejková [sup.1], Angelika Scheuerle [sup.2], Florian Wagner [sup.1], Oscar McCook [sup.1], José Matallo [sup.1], Michael Gröger [sup.1], Andrea Seifritz [sup.1], Bettina Stahl [sup.1], Brigitta Vcelar [sup.3], Enrico Calzia [...]

Author(s): Anthony C. Gordon [sup.1] Author Affiliations: (1) Critical Care Medicine, Imperial College/Charing Cross Hospital, , Fulham Palace Road, W6 8RF, London, UK Restoring and maintaining cardiac output is a [...]

Author(s): Bruno Levy [sup.1] [sup.2], Fabio S. Taccone [sup.3], Fabio Guarracino [sup.4] Author Affiliations: (1) grid.410527.5, 0000000417651301, Service de Réanimation Médicale Brabois, Pôle Cardiovasculaire et Réanimation Médicale, Hopital Brabois, CHU [...]

The article discusses a study conducted by scientists A. Morelli and coworkers on septic shock which represents maximum physical stresses to the organism and physiological response to sepsis includes increased release of cachotelamines and cardiac beta 1-adrenergic receptors. Topics discussed include hemodynamic stabilization, benefit of the combination of esmolol and milrinone in sepsis, and use of beta-blockers.

The authors present a study on cardiac assessment in the critically ill septic patient by referring to the lack of precise evaluation by practicing clinicians and discuss the cardiovascular (CV) performance or efficiency as a tool in this regards. Also discussed is the role of beta blockers such as esmolol in the improvement of cardiovascular efficiency.

Purpose: The aim of this experimental study is to investigate cardiovascular tolerance of blockade of beta-adrenergic receptors in an endotoxin model. Design: Prospective, randomized, controlled study. Setting: Animal laboratory in a university medical center. Methods: Ten anesthetized, mechanically ventilated pigs were challenged with intravenous lipopolysaccharide (LPS) to achieve a status of profound hypodynamic shock. Systemic and pulmonary hemodynamics and cardiac output were continuously monitored throughout the 5-h study period, and blood samples were taken at baseline ( T − 30 min), 1 h from the beginning of LPS infusion ( T + 60 min), and every 2 h ( T + 180 min and T + 300 min). Animals were randomly assigned to continuous intravenous esmolol infusion titrated to decrease heart rate by 20% or isotonic saline. Results: Esmolol decreased heart rate by 20%, while in the saline group, heart rate increased by 7% and 22% at T + 180 min and T + 300 min, respectively ( p < 0.001). In esmolol-treated animals, cardiac index decreased by 9% at T + 180 min and by 2% at T + 300 min, and in controls by 14% at T + 180 min and by 27% at T + 300 min ( p = 0.870). In esmolol-treated animals, median (interquartile range, IQR) stroke index was 31 (6) and 47 (11) ml/min/m at T + 180 min and T + 300 min, respectively, and decreased steadily from 45 (20) to 18 (13) ml/min/m in controls ( p = 0.030). There were no significant differences between groups for any other hemodynamics variables, except for systemic vascular resistance (SVR) ( p = 0.017). Conclusions: In large animals with endotoxemic shock, continuous infusion of esmolol, a selective beta-1 adrenergic blocker, titrated to decrease heart rate by 20%, was well tolerated and may offset LPS-induced cardiac dysfunction by a preload positive effect. [ABSTRACT FROM AUTHOR]

Author(s): Daniel De Backer [sup.1], Djillali Annane [sup.2] Author Affiliations: (1) grid.4989.c, 0000000123480746, Department of Intensive Care, CHIREC Hospitals, Université Libre de Bruxelles, , Rue Wayez 35, 1420, Braine l'Alleud, [...]

Author(s): Antoine Kimmoun [sup.1] [sup.3] [sup.4], Fabrice Vanhuyse [sup.2] [sup.4], Bruno Levy [sup.1] [sup.3] [sup.4] Author Affiliations: (1) grid.410527.5, 0000000417651301, Service de Réanimation Médicale Brabois, Pole Cardiovasculaire et Réanimation Médicale, [...]

Author(s): Mervyn Singer [sup.1], Andrew Rhodes [sup.2] Author Affiliations: (1) grid.83440.3b, 0000000121901201, Bloomsbury Institute of Intensive Care Medicine, University College London, , London, UK (2) grid.439479.4, Department of Intensive Care [...]