Sepsis-induced tissue hypoperfusion

Sepsis is associated with cardiovascular changes that may lead to development of tissue hypoperfusion. Early recognition of sepsis and tissue hypoperfusion is critical to implement appropriate hemodynamic support and prevent irreversible organ damage. End points for resuscitation need to be defined and invasive hemodynamic monitoring is usually required. Targets for hemodynamic optimization should include intravascular volume, blood pressure, and cardiac output. Therapeutic interventions aimed at optimizing hemodynamics in patients with sepsis include aggressive fluid resuscitation, the use of vasopressor agents, inotropic agents and in selected cases transfusions of blood products. This review will cover the most important aspects of hemodynamic optimization for treatment of sepsis induced tissue-hypoperfusion. Introduction Severe sepsis and septic shock are among the most important causes of morbidity and mortality in patients admitted to the intensive care unit. It is estimated that approximately 200,000 patients die from severe sepsis in the USA every year and more than 150,000 in Europe [1]. Sepsis is associated with a spectrum of cardiovascular derangements that may lead to development of tissue hypoperfusion [2]. Tissue hypoperfusion is an important factor in the development of multiple organ failure. Therefore, recognition of sepsisinduced tissue hypoperfusion and timely clinical intervention to prevent and correct this phenomenon are fundamental aspects of managing critically ill patients with severe sepsis. This review focuses on the pathophysiology, recognition, and management of sepsis-induced tissue hypoperfusion. For a review of other aspects of sepsis management such as antimicrobial therapy, immunomodulatory therapy, corticosteroids, and other supportive therapies, the reader is referred to other recent articles [2,3]. Sepsis-induced tissue hypoperfusion Our understanding of the pathophysiology underlying the development of sepsis, severe sepsis, and septic shock is continuously evolving [4,5]. It is important to examine the cardiovascular abnormalities that are present with sepsis and the clinical implications of these abnormalities in treating sepsis-induced tissue hypoperfusion. The hemodynamic profile of severe sepsis and septic shock is initially characterized by components of hypovolemic, cardiogenic, and distributive shock [6]. In the early phases of sepsis, increased capillary leak and increased venous capacitance will result in a decrease in venous return to the heart. Cytokines released as a result of the host response to sepsis may also cause direct myocardial depression. The end result of these changes is a decrease in stroke volume and ejection fraction, leading to a compensatory tachycardia, increased ventricular compliance, and a decrease in arteriolar resistance. Fluid therapy will modify this hemodynamic profile. Fluid administration can increase venous return, compensating for the increased capillary leak and increased venous capacitance. Compensatory changes for the decreased ejection fraction include tachycardia, increased ventricular compliance, and decreased arteriolar resistance. In the early stages of sepsis, prior to fluid therapy, patients may present with a decreased cardiac output. Fluid therapy will usually result in a hyperdynamic state with a high normal or elevated cardiac output. After adequate restoration of left ventricular preload, hypotension – if present – is dependent on the degree of decreased systemic vascular resistance and on impairment of contractility. Even with restoration of adequate blood pressure and normal or supranormal cardiac output, signs of tissue hypoperfusion may persist. This is often called ‘distributive shock’ and may be related to maldistribution of blood flow at the regional (splanchnic, mesenteric, and renal) or microvascular level and/or a cellular inability to utilize oxygen despite adequate oxygen delivery (cytotoxic hypoxia). Whether these abnormalities are present at the onset of sepsis or represent a progression of events is poorly understood. However, it is believed that early intervention with aggressive hemodynamic Review Hemodynamic optimization of sepsis-induced tissue hypoperfusion Sergio L Zanotti Cavazzoni and R Phillip Dellinger Robert Wood Johnson Medical School, University of Medicine and Dentistry of New Jersey, Camden, New Jersey, USA Corresponding author: Sergio L Zanotti Cavazzoni, [email protected] Published: 27 November 2006 Critical Care 2006, 10(Suppl 3):S2 (doi:10.1186/cc4829) This article is online at http://ccforum.com/content/10/S3/S2 © 2006 BioMed Central Ltd CO = cardiac output; CVP = central venous pressure; EGDT = early goal-directed therapy; MAP = mean arterial pressure; PAC = pulmonary artery catheter; PAOP = pulmonary artery occlusion pressure; ScvO2 = central venous oxygen saturation; SvO2 = mixed venous oxygen saturation.