Asthma is a common illness throughout the world that affects the respiratory system function, i.e., a system whose operational adequacy determines the respiratory gases exchange. It is therefore expected that acute severe asthma will be associated with respiratory acid-base disorders. In addition, the resulting hypoxemia along with the circulatory compromise due to heart–lung interactions can reduce tissue oxygenation, with a particular impact on respiratory muscles that have increased energy needs due to the increased workload. Thus, anaerobic metabolism may ensue, leading to lactic acidosis. Additionally, chronic hypocapnia in asthma can cause a compensatory drop in plasma bicarbonate concentration, resulting in non-anion gap acidosis. Indeed, studies have shown that in acute severe asthma, metabolic acid-base disorders may occur, i.e., high anion gap or non-anion gap metabolic acidosis. This review briefly presents studies that have investigated acid-base disorders in asthma, with comments on their underlying pathophysiology.

Administration of sedatives is an integral part of intensive care unit (ICU) routine practice for a plethora of reasons: reduction of patient discomfort by providing anxiolysis, treating agitation but also facilitation of care, by increasing tolerance of the ventilator and preventing accidental removal of the endotracheal tube or other instrumentation (e.g. catheters, monitors and intravenous lines). Finally, sedation reduces metabolic demands during cardiovascular and respiratory instability [1]. Agents mostly in use are benzodiazepines and other nonanalgesic sedatives such as propofol. Since these have no analgesic properties, they are often combined with parallel administration of opioids. Analgesics, at high doses, may also have a sedative effect [2]. However, because of the long half-life of the most commonly used opiates and the potentially grave side effects, such as respiratory depression, hypotension, gastrointestinal complications, urine retention and histamine secretion, administration should be rather judicious. In fact, as far as benzodiazepines are concerned, the Society of Critical Care Medicine has recommended against their use in their latest clinical practice guidelines [3].

Background/Aim: Multiple reports from all over the world link COVID-19 with endothelial/coagulation disorders as well as a dysregulated immune response. This study tested the hypothesis that immunostimulation will be greater in COVID-19 patients than in patients with H1N1 infection or bacterial sepsis. Also, whether an increase in immune stimulation will be accompanied by a more severely affected endothelium/coagulation system was examined. Patients and Methods: Twenty-three septic patients, admitted in the Intensive Care Unit (ICU), were enrolled (9 with SARS-CoV-2, 5 with H1N1 pneumonia, 9 with bacterial sepsis). Myeloperoxidase (MPO) activity along with certain endothelial/coagulation factors were assessed on admission (time point 1) and at either improvement or deterioration (time point 2). Results: MPO levels were significantly higher in COVID-19 patients compared to both other groups. Furthermore, in patients with COVID-19, vWF levels did not differ significantly, fVIII levels were lower while ADAMTS-13 activity was higher compared to patients with H1N1 pneumonia and bacterial sepsis (a trend in the latter). Conclusion: Increased immunostimulation was noted in COVID-19 patients compared to other septic patients; however, this was not accompanied by greater disturbance of the clotting system and/or more severe endothelial injury.