OverviewSepsisCardiovascular response in sepsisSevere sepsisSeptic Shock




Overview

Sepsis is a systemic inflammatory response syndrome (SIRS) where an infection is suspected or known. Other causes of SIRS include anaphylaxis, trauma and burns. Sepsis produces a profound vasodilatation and plasma leak leading to hypovolaemia and hypotension. Sepsis is classified as severe when signs of hypoperfusion and organ dysfunction are present. .Patients who do not show signs of haemodynamic recovery after fluid resuscitation are in septic shock.


Sepsis

Sepsis is a condition in which the body’s immune system overreacts to an infection and threatens the function of life-support organs such as the heart, kidneys and lungs. Infection can arise from any part of the body, and in sepsis the infection – or perhaps only some inflammatory mediators -spreads and the inflammatory response follows it. This leads to a systemic inflammatory response syndrome (SIRS). Where a SIRS is present and an infection is suspected or confirmed, a diagnosis of sepsis is appropriate. There are other possible (non-infective) triggers of a SIRS, such as anaphylaxis, severe trauma or large burns.


The cardiovascular complications of sepsis

Widespread and often profound arterial and venous vasodilation occurs in sepsis, probably due to a variety of mechanisms. There is often also a degree of endothelial dysfunction, driven by inflammatory mediators, allowing plasma to leak into tissues. This results in loss of blood volume (hypovolaemia). Both factors make it difficult for the heart to maintain organ perfusion.

It generally held that a significant component of the vasodilatation is due to excessive release of nitric oxide by immune cells such as macrophages. Nitric oxide is used by the body to kill pathogens, but is also a vasodilator. In sepsis, where the inflammatory response is systemic, nitric oxide production is similarly widespread, causing a large drop in blood pressure. Cardiovascular reflexes attempt to correct this abnormality by activating the sympathetic nervous system to cause vasoconstriction and an increase in cardiac output. For this reason, an elevated heart rate (tachycardia) is commonly seen in sepsis, and if this response is inadequate to overcome the pooling of blood in dilated blood vessels, the body goes into septic shock. This is the life-threatening side to sepsis – lack of perfusion of vital organs and subsequent organ failure and death.


Severe sepsis

In severe sepsis, vital organs begin to dysfunction due to lack of adequate perfusion. This is often evident from blood chemistry such as an elevated level of lactate (indicating excessive reliance on anaerobic metabolism by under-perfused tissues). The lungs are particularly sensitive to mediators of septic shock and/or infection and acute respiratory distress sysndrome is often an early sign of a decline into severe sepsis. Inadequate perfusion of the kidneys leads to reduced urine output (oliguria). Treatment involves fluid resuscitation to try to replace fluids lost to capillary leak and expand blood volume and blood pressure. Current guidelines recommend a fluid challenge of 30 mL/kg of cystalloid such as Hartmann’s solution or Lactated Ringer’s solution.


Septic shock

When severe sepsis-related hypotension does not respond to an appropriate fluid challenge, a patient is in septic shock. The standard initial treatment of this life-threatening condition is the use of vasopressors (typically noradrenaline) to constrict the vasculature and increase blood pressure and venous return. Current guidelines recommend aiming to restore MAP to 65 mmHg. Additional vasopressors such as vasopressin may also be required to achieve this aim in some patients.



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