Diagnosis of silent hypoxaemia
Subjective dyspnoea measurements and self-reported symptoms of shortness of breath have been used to risk stratify patients with COVID-19. However, these are insufficient to accurately detect hypoxaemia in patients who are considered high risk for severe COVID-19; thus, objective tools are required.19
Pulse oximeters, a simple and noninvasive tool, can be used to estimate arterial oxygen saturation. These tools, which are cheap and easy to use, are typically available as a device that is placed over a finger. They allow for remote monitoring of patients with COVID-19 in the community when hospitalisation is not required.19,20,21 Further information is available from the RACGP website (see https://www.racgp.org.au/clinical-resources/covid-19-resources/other-health-issues/home-care-guidelines-patients-with-mild-covid-19 and https://www.racgp.org.au/download/Documents/Standards/RACGP-Standards-for-general-practices-5th-edition.pdf).
It is crucial to recognise factors that may result in measurement error and affect pulse oximeter accuracy. Factors to consider include rapid measurement fluctuation when the arterial oxygen pressure/tension falls on the steep portion of the oxygen dissociation curve and diminished pulsatile blood flow due to hypotension, vasoconstricting medications or peripheral vascular disease.20 The increased skin pigmentation of some individuals and the use of nail polish can also affect readings.20 Additionally, the accuracy may vary depending on the type of pulse oximeter device, particularly when oxygen saturation falls below 90%.20 Issues arising from incorrect placement of the pulse oximeter over a finger can be overcome by instead using an earlobe or forehead probe; however, these devices are not readily available and are more costly than finger pulse oximeters.
Arterial blood gas (ABG) analysis is a more invasive tool that can be used to accurately detect hypoxaemia. This involves measurements of the pH and partial pressures of oxygen and carbon dioxide in arterial blood and provides information about a patient’s acid-base balance, the effectiveness of gas exchange and state of their ventilatory control. An ABG analysis requires a blood sample, usually drawn from the radial artery, and is generally not feasible to perform in the community.
How and why do patients present with silent hypoxaemia?
Hypoxaemia is often associated with dyspnoea, but the mechanisms underpinning the sensation of dyspnoea are complex and not completely understood. Factors that can contribute to dyspnoea include changes to the respiratory muscles, CO2 receptors and lung stretch receptors as well as a discord between central output and amount of airflow.22
The causes of silent hypoxaemia and underlying pathophysiological mechanisms are not clearly understood. There are limited data describing this phenomenon; however, it is thought to stem from initial insult to the lungs caused by the direct effect of the SARS-CoV-2 virus and/or secondary immune system-mediated inflammation.7 The lung insult results in alveolar epithelial and capillary endothelial damage, interstitial oedema and alveolar fluid filling, which are typical features of ARDS.
Silent hypoxaemia from COVID-19 is thought to be due to an atypical form of ARDS because autopsy findings have demonstrated typical pathological features of ARDS.23,24 However, pathophysiological differences exist between ARDS that is associated with COVID-19 and ARDS from other causes, such as the presence of more vascular abnormalities in COVID-19 lung injury.7,25 The vascular abnormalities include micro- and macro-thrombosis, vascular dilation and aberrant angiogenesis, which have also been found in other organs in patients with COVID-19.22,26,27 This supports the notion that COVID-19 is part of a systemic vascular pathological process.25
Various theories have been proposed to explain the underlying mechanisms causing silent hypoxaemia in COVID-19. These reflect changes that may occur in the lung parenchyma, blood vessels and neural centres of ventilation control, although the evidence to support them is conflicting. Due to the lack of data in this novel disease, some of this evidence is based on the pathophysiological mechanisms that are known to occur in ARDS due to other causes.7