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. 2020;7(2):190-198.
doi: 10.31480/2330-4871/112. Epub 2020 Feb 10.

A Contemporary Approach to the Treatment of Perioperative Bronchospasm

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A Contemporary Approach to the Treatment of Perioperative Bronchospasm

Christian Bohringer et al. Transl Perioper Pain Med. 2020.

Abstract

The incidence of asthma is increasing, and the ageing of the United States population is leading to an increase in the prevalence of patients living with chronic obstructive pulmonary disease. This has led to an increased need to manage bronchospasm in the perioperative period. Very effective methods to treat bronchospasm like intravenous dexmedetomidine, lidocaine, magnesium, ketamine and steroids as well as inhalational sevoflurane are available but are currently underused. Inhaled beta-2 agonists like albuterol are instead often relied upon as the sole therapeutic agent - often with limited response. Just like with pain management, the successful treatment of perioperative bronchospasm requires a multimodal approach. The diagnosis of intraoperative bronchospasm must be rapid, and the treatment must be effective to prevent the dreaded "dynamic hyperinflation syndrome". This article reviews the diagnosis of bronchospasm and the contemporary treatment methods that should be employed to prevent bronchospasm-related morbidity and mortality during the perioperative period.

Keywords: Beta-2 agonists; Capnography; Hyperinflation; Perioperative bronchospasm.

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Figures

Figure 1:
Figure 1:
Representative capnograph trace during bronchospasm that there is an upslope during phase 3 (A). In a normal lung, there is usually a plateau during phase 3 (B). The degree of upslope is proportional to the arterial to end-tidal PaCO2 gradient and the amount of ventilation-perfusion mismatch that is present.
Figure 2:
Figure 2:
Representative chest X-ray of bronchospasm. During acute bronchospasm there is hyperinflation of the lungs with compression of the heart into a tubular shape and displacement of the diaphragm in a caudal direction. The increase in intrapulmonary pressure may lead to decreased venous return to the heart and a decrease in cardiac output.

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