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To what extent is end-tidal carbon dioxide a predictor of sepsis?

02 October 2022
Volume 14 · Issue 10

Abstract

Background:

Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection. It is a major cause of death worldwide; 245 000 cases are reported in the UK annually with a mortality rate of 20.3%. Rapid diagnosis and rapid treatment of sepsis can significantly reduce mortality but sepsis can be difficult to diagnose. End-tidal carbon dioxide (EtCO2) is the measurement of expired CO2 using capnometry and waveform capnography. For CO2 to be exhaled, it must be metabolised and transported before being exhaled by effective ventilation; EtCO2 can therefore provide an indication of metabolism, circulation and ventilation. EtCO2 has already been shown to be an indicator of other metabolic acidosis conditions so this review aims to identify the usefulness of EtCO2 in identifying sepsis.

Methods:

A systematic literature search was conducted between March and April 2021 using the CINAHL Plus and MEDLINE databases. The results were screened and evaluated.

Results:

Of the 44 papers identified in the original search, seven were included in this review.

Conclusion:

This review suggests an EtCO2 of ≤25 mmHg (3.3 kPa) in patients with a suspected infection is diagnostic of sepsis and therefore could be used to increase the speed and accuracy of diagnosis and potentially reduce sepsis mortality. It also identifies gaps in research around UK practice and in comparing EtCO2 against UK sepsis guidelines and diagnostic tools such as the UK Sepsis Trust guidelines.

The Third International Consensus defines sepsis as a ‘life-threatening organ dysfunction caused by a dysregulated host response to infection’ (Singer et al, 2016). Sepsis is a leading cause of death in the UK with 245 000 cases reported annually with a mortality rate of 20.3% (close to 50 000 deaths); globally, there are 49 million cases with 11 million deaths per year (UK Sepsis Trust, 2022).

Sepsis causes a multitude of pathological cascades, which lead to end-organ damage and homeostatic imbalances (Singer et al, 2016). These cascades lead to increased lactate production.

During the progression of sepsis, cardiovascular dysfunction because of septic shock begins to lead to systemic hypoperfusion and respiratory dysfunction (Gyawali et al, 2019). Tissue permeability caused by the cardiovascular dysfunction around the lungs leads to pulmonary oedema causing a ventilation–perfusion mismatch, resulting in hypoxia (Gotts and Matthay, 2016).

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