## 3 Results and Discussion
### Univariate Data Analysis
#### 3.1.2 Routine Blood Analyses  
From the blood analyses conducted routinely on patients admitted to the ICU, the following were considered: leukocyte profiles (neutrophils, eosinophils and lymphocytes); RBCs and ferritin; markers of the coagulation system, i.e., platelets, fibrinogen, and D-dimers; markers of the inflammatory process, i.e., procalcitonin and CRP; a general marker of tissue damage, i.e., the intracellular enzyme LDH; a marker of kidney function, i.e., creatinine; and a marker of myocardial damage, i.e., hs-cTn I. Among surviving patients, the ones requiring IVM (Group B) presented significantly higher CRP (\(p\) = 0.028) and significantly lower RBCs (\(p\) = 0.028) in comparison to less severely ill patients, i.e., patients not requiring IMV (Group A) (Table 3). Accordingly, CRP, a known marker of systemic inflammation, has been independently associated with respiratory impairment, need for IMV in patients with acute respiratory distress syndrome, and lower mortality [38; 39]. It was observed that deceased patients (Group C) presented significantly lower RBCs in comparison to all discharged patients (Groups A + B) (\(p\) = 0.028). These results could be linked to the fact that, when infected by SARS-CoV-2, RBCs are affected by the virus and the complex inflammatory process that results from the disease, altering their function and capacity for oxygen transportation and contributing to the development of hypoxia [40; 41] and the need for IMV [40]. Lymphocyte counts were solely below normality cutoffs for deceased patients (Group C), being significantly decreased when compared to those from Group B (\(p\) = 0.015) and from Group A + B (\(p\) = 0.003). This is in accordance with studies that considered lymphopenia as a marker of disease severity and mortality [42], including in COVID-19 patients [43]. Notably, interferences that occur in the IL-2/IL-2R pathway due to SARS-CoV-2 infection lead to lower levels of lymphocytes, especially in critical COVID-19 patients [32]. The levels of hs-cTn I were way above normality cutoffs for deceased patients, leading to significant difference when compared to those from Group A (\(p\) = 0.026) and Group A + B (\(p\) = 0.037). This may be associated to myocardial ischemia/injury (recognized as one of the leading causes of death in SARS-CoV-2 infected patients), which is a result from the hyperinflammatory state triggered by the cytokine storm, subsequently causing vascular inflammation and hypercoagulability [44; 45]. Regarding the remaining biomarkers, neutrophil counts, procalcitonin, and LDH were above normality cutoffs for all groups, despite not demonstrating significant differences among them. As in any viral infection, neutrophil levels tend to increase, even leading to neutrophil, as described for COVID-19 [46]. On the other hand, in the same context, procalcitonin production can be downregulated by mediators like IFN-\(\gamma\). However, the current patients presented high levels of this biomarker, whose production can be stimulated by TNF-\(\alpha\) and IL-6 [47]. LDH, besides being considered an independent predictor of myocardial injury, is also associated with disease severity in COVID-19. Its increases have been related to multiorgan dysfunction, with systemic inflammation and tissue damage/necrosis [48]. Biomarkers related to the coagulation process were not significantly different among groups, although the ferritin, fibrinogen and D-dimer results were above normality cutoffs, a finding which has been systematically reported in COVID-19 patients [49]. High levels of ferritin may be related to the impact of SARS-CoV-2 on hemoglobin, resulting in the release of iron into the bloodstream. This can contribute to complications such as impaired oxygen binding and oxidative damage to organs. Additionally, the excess of iron, stored in proteins like ferritin, increases the blood's viscosity, contributing to thrombotic mechanisms and increasing the risk of mortality [50; 51]. Another