Sepsis is generally viewed as a disease aggravated by an inappropriate immune response encountered in the afflicted individual. As an important organ system frequently compromised by sepsis and always affected by septic shock, the cardiovascular system and its dysfunction during sepsis have been studied in clinical and basic research for more than 5 decades. Although a number of mediators and pathways have been shown to be associated with myocardial depression in sepsis, the precise cause remains unclear to date. There is currently no evidence supporting global ischemia as an underlying cause of myocardial dysfunction in sepsis; however, in septic patients with coexistent and possibly undiagnosed coronary artery disease, regional myocardial ischemia or infarction secondary to coronary artery disease may certainly occur. A circulating myocardial depressant factor in septic shock has long been proposed, and potential candidates for a myocardial depressant factor include cytokines, prostanoids, and nitric oxide, among others. Endothelial activation and induction of the coagulatory system also contribute to the pathophysiology in sepsis. Prompt and adequate antibiotic therapy accompanied by surgical removal of the infectious focus, if indicated and feasible, is the mainstay and also the only strictly causal line of therapy. In the presence of severe sepsis and septic shock, supportive treatment in addition to causal therapy is mandatory. The purpose of this review is to delineate some characteristics of septic myocardial dysfunction, to assess the most commonly cited and reported underlying mechanisms of cardiac dysfunction in sepsis, and to briefly outline current therapeutic strategies and possible future approaches.

Sepsis and the Heart

Background: The present interdisciplinary consensus review proposes clinical considerations and recommendations for anaesthetic practice in patients undergoing gastrointestinal surgery with an Enha ...

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Enhanced Recovery After Surgery (ERAS) for gastrointestinal surgery, part 2: consensus statement for anaesthesia practice

The term ''adrenergic'' originates from ''adrenaline'' and describes hormones or drugs whose effects are similar to those of epinephrine. Adrenergic stress is mediated by stimulation of adrenergic receptors and activation of post-receptor pathways. Critical illness is a potent stimulus of the sympathetic nervous system. It is undisputable that the adrenergic-driven ''fight-flight response'' is a physiologically meaningful reaction allowing humans to survive during evolution. However, in critical illness an overshooting stimulation of the sympathetic nervous system may well exceed in time and scope its beneficial effects. Comparable to the overwhelming immune response during sepsis, adrenergic stress in critical illness may get out of control and cause adverse effects. Several organ systems may be affected. The heart seems to be most susceptible to sympathetic overstimulation. Detrimental effects include impaired diastolic function, tachycardia and tachyarrhythmia, myocardial ischemia, stunning, apoptosis and necrosis. Adverse catecholamine effects have been observed in other organs such as the lungs (pulmonary edema, elevated pulmonary arterial pressures), the coagulation (hypercoagulability, thrombus formation), gastrointestinal (hypoperfusion, inhibition of peristalsis), endocrinologic (decreased prolactin, thyroid and growth hormone secretion) and immune systems (immunomodulation, stimulation of bacterial growth), and metabolism (increase in cell energy expenditure, hyperglycemia, catabolism, lipolysis, hyperlactatemia, electrolyte changes), bone marrow (anemia), and skeletal muscles (apoptosis). Potential therapeutic options to reduce excessive adrenergic stress comprise temperature and heart rate control, adequate use of sedative/analgesic drugs, and aiming for reasonable cardiovascular targets, adequate fluid therapy, use of levosimendan, hydrocortisone or supplementary arginine vasopressin.

Sympathetic Overstimulation During Critical Illness: Adverse Effects of Adrenergic Stress:

When assessing the accuracy and precision of a new technique for cardiac output measurement, the commonly quoted criterion for acceptability of agreement with a reference standard is that the percentage error (95% limits of agreement/mean cardiac output) should be 30% or less. We reviewed published data on four different minimally invasive methods adapted for use during surgery and critical care: pulse contour techniques, esophageal Doppler, partial carbon dioxide rebreathing, and transthoracic bioimpedance, to assess their bias, precision, and percentage error in agreement with thermodilution. An English language literature search identified published papers since 2000 which examined the agreement in adult patients between bolus thermodilution and each method. For each method a meta-analysis was done using studies in which the first measurement point for each patient could be identified, to obtain a pooled mean bias, precision, and percentage error weighted according to the number of measurements in each study. Forty-seven studies were identified as suitable for inclusion: N studies, n measurements: mean weighted bias [precision, percentage error] were: pulse contour N = 24, n = 714: -0.00 l/min [1.22 l/min, 41.3%]; esophageal Doppler N = 2, n = 57: -0.77 l/min [1.07 l/min, 42.1%]; partial carbon dioxide rebreathing N = 8, n = 167: -0.05 l/min [1.12 l/min, 44.5%]; transthoracic bioimpedance N = 13, n = 435: -0.10 l/min [1.14 l/min, 42.9%]. None of the four methods has achieved agreement with bolus thermodilution which meets the expected 30% limits. The relevance in clinical practice of these arbitrary limits should be reassessed.

http://www.conference.co.nz/files/docs/poster%20session%20c%20abstracts%208.pdf

Minimally invasive measurement of cardiac output during surgery and critical care: a meta-analysis of accuracy and precision.

Sepsis is aggravated by an inappropriate immune response to invading microorganisms, which occasionally leads to multiple organ failure. Several lines of evidence suggest that the ventricular myocardium is depressed during sepsis with features of diastolic dysfunction. Potential candidates responsible for septic cardiomyopathy include pathogen-associated molecular patterns (PAMPs), cytokines, and nitric oxide. Extracellular histones and high-mobility group box 1 that function as endogenous damage-associated molecular patterns (DAMPs) also contribute to the myocardial dysfunction associated with sepsis. If untreated, persistent shock causes cellular injury and the liberation of further DAMPs. Like PAMPs, DAMPs have the potential to activate inflammation, creating a vicious circle. Early infection control with adequate antibiotic care is important during septic shock to decrease PAMPs arising from invasive microorganisms. Early aggressive fluid resuscitation as well as the administration of vasopressors and inotropes is also important to reduce DAMPs generated by damaged cells although excessive volume loading, and prolonged administration of catecholamines might be harmful. This review delineates some features of septic myocardial dysfunction, assesses its most common underlying mechanisms, and briefly outlines current therapeutic strategies and potential future approaches.

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Sepsis-induced myocardial dysfunction: pathophysiology and management.

BACKGROUND:In Japan, routine clinical care does not normally involve the use of a monitoring device to guide the administration of neuromuscular blocking drugs or their antagonists. Although most previous reports demonstrate that sugammadex offers more rapid and reliable antagonism from rocuronium-i

Reversal with sugammadex in the absence of monitoring did not preclude residual neuromuscular block.

Objective:Since β-blocker therapy is known to be effective in patients with an injured heart, such as infarction, we designed the present study to examine the protective effects of infusion of the β1-selective blocker esmolol on myocardial function in peritonitis-induced septic rats using an isolate

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Infusion of the β-adrenergic blocker esmolol attenuates myocardial dysfunction in septic rats

BackgroundBecause it is postulated that gut is important via bacterial translocation in the development of the systemic inflammatory response and multiple organ dysfunction, the preservation of gut integrity is a therapeutic goal for physicians who care for critically ill patients. The aim of the cu

Epidural anesthesia retards intestinal acidosis and reduces portal vein endotoxin concentrations during progressive hypoxia in rabbits

Hypermagnesemia-induced cardiopulmonary arrest before induction of anesthesia for emergency cesarean section.

Objective
This study investigated the accuracy of the NICO monitor equipped with the newer software. Additionally, the effects of the increased dead space produced by the NICO monitor on ventilatory settings were investi- gated.

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Yoshifumi Kotake

Papers

Reversal with sugammadex in the absence of monitoring did not preclude residual neuromuscular block.

Infusion of the β-adrenergic blocker esmolol attenuates myocardial dysfunction in septic rats

Epidural anesthesia retards intestinal acidosis and reduces portal vein endotoxin concentrations during progressive hypoxia in rabbits

Hypermagnesemia-induced cardiopulmonary arrest before induction of anesthesia for emergency cesarean section.

Improved Accuracy Of Cardiac Output Estimation By The Partial CO2 Rebreathing Method