COVID-19 patients with respiratory failure: what can we lear
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Patients with COVID-19 may present to hospitals and emergency medical services with an atypical form of ARDS. Although anecdotal, a common clinical pattern has emerged, with a remarkable discrepancy between relatively well-preserved lung compliance and a severely compromised pulmonary gas exchange, leading to grave hypoxaemia yet without proportional signs of respiratory distress.

Experiments in hypobaric chambers have revealed that hypocapnic hypoxia is not usually accompanied by air hunger; instead, a paradoxical feeling of calm and well-being may result. This phenomenon has been coined ‘silent hypoxia’.

End-tidal CO2 values in the 1.4–2.0 kPa range have been reported in COVID-19 patients, but apart from a rapid respiratory rate, the clinical presentation in these patients can be misleading. It has been observed that patients with extreme hypoxaemia showing little distress; rather they tend to be impassive, cooperative, and haemodynamically stable. However, sudden and rapid respiratory decompensation may occur.

The physiological hallmarks of hypocapnic hypoxia have been studied extensively in aviation medicine:

-- Decompression to high altitude causes severe hypoxaemia, which triggers the carotid chemoreceptors and sparks a brisk respiratory response with ensuing hypocapnia.
-- The respiratory alkalosis shifts the oxyhaemoglobin dissociation curve to the left, thereby increasing haemoglobin's oxygen affinity, evident from a decrease in the P50 value and an increase in arterial oxygen saturation (SaO2).
-- The alveolar gas equation predicts that decreased alveolar CO2 tension (PACO2) will result in a corresponding increase in alveolar oxygen tension (PAO2).
-- Combined, these two mechanisms will increase SaO2 in hypocapnic hypoxia compared with an isocapnic or hypercapnic hypoxic state.

The effects of hypocapnia on SaO2 can be illustrated with data from a recent hypobaric chamber experiment explained in the article.

Conclusively, The clinical presentation and pathophysiology of the COVID-19 patient challenge the notion of how respiratory failure in critically ill patients unfolds. Clinicians must adapt to a constantly changing situation with a rapidly expanding evidence base. Awaiting reliable data, they have to integrate experience with our understanding of physiology to make rational clinical decisions.

Source: https://bjanaesthesia.org/article/S0007-0912(20)30226-9/fulltext
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Thanks. The silent hypoxemia is sometimes called happy hypoxia as they do not seem to be in distress and are not aware of what is happening (discrepancy between normal lung compliance and impaired gas exchange). And then they suddenly collapse. At autopsy a black paint like coating is seen on their alveoli which could be due to diffuse alveolar hemorrhage (acid hematin - Hb from RBCs in acidotic environment). There is ventilation perfusion mismatch. Oxygen saturation is low. Now societies are being told to measure oxygenation of residents perhaps by using a pulse oximeter (and also their body temperature needs to be measured by an infra red thermal non contact device). The virus’ Spike S1 Protein attaches itself to ACE-2 in the vascular endothelium causing inflammation (endotheliitis) and thrombosis.... Read more
May 19, 2020Like9