الفهرس 
Incidence, Terminology and Pathophysiology of Septic ShockOnly 14 pages are availabe for public view
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Abstract
Sepsis is a clinical syndrome characterized by systemic inflammation and widespread tissue injury due to infection. There is a continuum of illness severity ranging from sepsis to severe sepsis and septic shock. When infection is absent, the clinical syndrome is termed systemic inflammatory response syndrome (SIRS).
Current theories about the onset and progression of sepsis focus on dysregulation of the inflammatory response, including the possibility that a massive and uncontrolled release of proinflammatory mediators initiates a chain of events that lead to widespread tissue injury. This response can lead to multiple organ dysfunction syndrome (MODS), which is the cause of the high mortality in these patients.
The incidence of sepsis varies among the different racial and ethnic groups, but appears to be highest among African-American males. Studies of the incidence of severe sepsis showed that incidence increased by approximately 13% each year with mortality rates ranging from 15% to 30% and more than 60% in septic shock.
Hemodynamic monitoring is a cornerstone in the care of hemodynamically unstable septic patient. Timely and adequate correction of instability and tissue hypoperfusion is essential to prevent progression to MODS. Clinical assessment and Basic monitoring,electrocardiography (ECG), arterial blood pressure (ABP) and pulse oximetry (SpO2) monitoring, of septic patients are initial steps in assessment of global perfusion.
Many methods developed for cardiac output monitoring, which are either invasive, minimally invasive or non-invasive. Thermodilution technique was used for many years for cardiac output monitoring as it is accurate and more popular since Swan and Ganz introduced the pulmonary artery catheter. However, this technique carries a lot of risks and potential for serious complications.
Many minimally invasive and non-invasive methods of cardiac output monitoring have been developed in the last few years. These methods are considered reasonably accurate and are associated with reduced risk. Most of these techniques had been discussed during the study.
During the first 6 hours of resuscitation (Crystalloids are the initial fluid of choice), the goals of initial resuscitation of sepsis- induced hypoperfusion should include all of the following as a part of a treatment protocol:
(a) CVP 8–12 mmHg
(b) MAP ≥ 65 mmHg
(c) Urine output ≥ 0.5 mL/ kg/ h
(d) Superior vena cava oxygenation saturation (ScvO2) or mixed venous oxygen saturation (SvO2) 70% or 65 %, respectively.
When resusitation fails to achieve the above goals, therapy with vasopressor agents should be initiated.
Norepinephrine is the first-choice vasopressor. It has predominant alpha-receptor agonist effects and results in potent peripheral arterial vasoconstriction without significantly increasing heart rate or cardiac output.
Norepinephrine is preferred to dopamine for managing septic shock because dopamine is known to cause unfavorable flow distribution (more arrhythmias). In this setting, norepinephrine has been shown to be both significantly safer and somewhat more effective. Dopamine should be used only in certain highly specific situations, such as when there is a low risk of tachyarrhythmias and bradycardia.
Second-line vasopressors appropriate for patients who have persistent hypotension despite maximal doses of norepinephrine or dopamine are epinephrine, phenylephrine, and vasopressin.
Dobutamine is the first choice inotropic agent if there is evidence of tissue hypoperfusion (central venous oxygen saturation [ScvO2] < 70 mm Hg) after CVP, MAP, and hematocrit goals have been met.