Silent Hypoxemia in COVID-19 Pneumonia.

In patients suffering from Coronavirus Disease 2019 (COVID-19), dyspnoea is less likely to occur despite hypoxemia. Even if the patient develops severe hypoxemia, it cannot be detected from subjective symptoms. In other words, it becomes more serious without the person or the surroundings noticing it. Initially less talked about, hypoxemia without dyspnoea (silent hypoxemia or happy hypoxia: hypoxemia that does not coincide with dyspnoea) is now experienced in many institutions. Dyspnoea is defined as "the unpleasant sensation that accompanies breathing." Dyspnoea occurs when afferent information is transmitted to the sensory area. Receptors involved in the development of dyspnoea include central and peripheral chemoreceptors, chest wall receptors, lung receptors, upper respiratory tract receptors and corollary discharge receptors. In the present study, we considered mechanisms mediating the silent hypoxemia through three cases experienced at our hospital as a dedicated coronavirus treatment hospital. We have treated about 600 people infected with COVID-19, of which about 10% were severe cases. In the present study, the patients' condition was retrospectively extracted and analysed. We investigated three typical cases of COVID-19 pneumonia admitted to our hospital (men and women between the ages of 58 and 86 with hypoxemia and tachypnoea). Silent hypoxemia is not entirely without dyspnoea, but hypoxemia does not cause dyspnoea commensurate with its severity. The virus may have specific effects on the respiratory control system. In our cases, respiratory rate significantly increased with hypoxemia, and hyperventilation occurred. Therefore, information about hypoxemia is transmitted from the carotid body. Since hyperventilation occurs, it is suggested that information is transmitted to effectors such as respiratory muscles. The fact that these patients did not feel the unpleasant sensation indicates that information is not accurately transmitted to the sensory area of the cerebral cortex. These cases suggest that there may be a problem somewhere in the path from the respiratory centre to the sensory area.

[Severe respiratory alkalosis due to psychogenic hyperventilation. Report of one case]. / Alcalosis respiratoria grave, la transformación de un cuadro funcional en orgánico. Caso clínico.

Severe respiratory alkalosis is a life-threatening condition, as it induces hypo- calcaemia and extreme adrenergic sensitivity leading to cerebral and myocardial vasoconstriction. We report a 37-year-old woman with previous consultations for a conversion disorder. While she was infected with SARS-CoV-2 (without pulmonary involvement), she consulted in the emergency room due to panic attacks. On admission, she developed a new conversion crisis with progressive clinical deterioration, hyperventilation, and severe respiratory alkalosis (pH 7.68, Bicarbonate 11.8 mEq/L and PaCO2 10 mmHg). Clinically, she was in a coma, with respiratory and heart rates 55 and 180 per min, a blood pressure of 140/90 mmHg, impaired perfusion (generalized lividity, distal coldness, and severe skin mottling) and tetany. She also had electrocardiographic changes and high troponin levels suggestive of ischemia, and hyperlactatemia. She was managed in the hospital with intravenous benzodiazepines. The clinical and laboratory manifestations resolved quickly, without the need for invasive measures and without systemic repercussions.