Intensive care management of patients with COVID-19: a practical approach

Abstract

SARS-CoV-2, the causative agent of coronavirus disease 2019 (COVID-19), is responsible for the largest pandemic facing humanity since the Spanish flu pandemic in the early twentieth century. Since there is no specific antiviral treatment, optimized support is the most relevant factor in the patient's prognosis. In the hospital setting, the identification of high-risk patients for clinical deterioration is essential to ensure access to intensive treatment of severe conditions in a timely manner. The initial management of hypoxemia includes conventional oxygen therapy, high-flow nasal canula oxygen, and non-invasive ventilation. For patients requiring invasive mechanical ventilation, lung-protective ventilation with low tidal volumes and plateau pressure is recommended. Cardiovascular complications are frequent and include myocardial injury, thrombotic events, myocarditis, and cardiogenic shock. Acute renal failure is a common complication and is a marker of poor prognosis, with significant impact in costs and resources allocation. Regarding promising therapies for COVID-19, the most promising drugs until now are remdesivir and corticosteroids although further studies may be needed to confirm their effectiveness. Other therapies such as, tocilizumab, anakinra, other anti-cytokine drugs, and heparin are being tested in clinical trials. Thousands of physicians are living a scenario that none of us have ever seen: demand for hospital exceed capacity in most countries. Until now, the certainty we have is that we should try to decrease the number of infected patients and that an optimized critical care support is the best strategy to improve patient's survival.

Keywords: COVID-19; Circulatory support and invasive ventilation; Intensive care unit.

Fig. 1

The pathophysiology of SARS-CoV-2 infection. SARS-CoV-2, via its surface spike protein, binds to the human ACE2 receptor after spike protein activation by TMPRSS2. This results in down-regulation of ACE2 and increased angiotensin II levels and consequently increased plasminogen activator inhibitor C-1 expression and reduced fibrinolysis. The disease it causes is associated with an increase in inflammatory cytokines and coagulation disorders, with predisposition to thrombus formation. Mononuclear cells interact with activated platelets and the coagulation cascade, which activate 1 inflammatory cells by binding thrombin and tissue factor with specific protease activated receptors and by binding fibrin to Toll-like receptor 4. The activation of inflammatory cells results in the release of pro-inflammatory cytokines, leading to impairment of the natural coagulation pathways and shut down of fibrinolysis. This state of hyper inflammation and hypercoagulability leads to multiple organ dysfunction, most commonly affecting the lungs, heart and kidneys. ACE2 angiotensin-converting enzyme-2, aPTT activated partial thromboplastin time, ARDS acute respiratory distress syndrome, COVID-19 coronavirus disease 2019, HFpEF heart failure preserved ejection fraction, HFrEF, heart failure reduced ejection fraction, IL interleukin, PAR protease-activated receptor, PT prothrombin time, SARS-COV-2severe acute respiratory syndrome coronavirus 2, TMPRSS2 transmembrane protease serine, TLR4 Toll-like receptor 4, TNFα tumor necrosis factor-α

Fig. 2

Ventilatory support in COVID-19 patients. PBW predicted body weight, ARDS acute respiratory distress syndrome, BNP brain natriuretic peptide, CPAP continuous positive airways pressure, CT computerized tomography, CVVH continuous venovenous hemofiltration, CRP C-reactive protein, ECMO extracorporeal membrane oxygenation, LDH lactic dehydrogenase, PEEP positive end-expiratory pressure, PPlat plateau pressure, HNFC high-flow nasal cannulas, NIV non-invasive ventilation, PEEP positive end-expiratory pressure, SpO2 peripheral O2 saturation, PaO2 partial pressure of oxygen, Vt tidal volume, V-V venovenous, V-A venous-arterial

Fig. 3

Cardiovascular involvement in patients with COVID-19; pathophysiology, diagnostic findings, most common clinical findings and proposed management. IL-6 interleukine-6, FDPs fibrin degradation product, PT prothrombin time, ACS acute coronary syndrome, NSTEMI non-ST elevation myocardial infarction, STEMI ST elevation myocardial infarction, VTE venous thromboembolism, RV right ventricle, LV left ventricle, Hb hemoglobin, V-A venous-arterial, Echo echocardiography, ECG electrocardiogram

Fig. 4

Algorithm proposed for the management of antithrombotic therapy in patients with COVID-19