Assuntos
Angiotensina I/fisiologia , Betacoronavirus , Infecções por Coronavirus/prevenção & controle , Lesão Pulmonar/prevenção & controle , Pandemias/prevenção & controle , Fragmentos de Peptídeos/fisiologia , Pneumonia Viral/prevenção & controle , Enzima de Conversão de Angiotensina 2 , COVID-19 , Humanos , Pulmão/virologia , Peptidil Dipeptidase A/fisiologia , SARS-CoV-2RESUMO
Avoiding pain, agitation and delirium as well as avoiding unnecessary deep sedation is a powerful yet challenging strategy in critical care medicine. A number of interactions between cerebral function and respiratory function should be regarded in patients with respiratory failure and mechanical ventilation. A cooperative sedation strategy (i.e. patient is awake and free of pain and delirium) is feasible in many patients requiring invasive mechanical ventilation. Especially patients with mild acute respiratory distress syndrome (ARDS) seem to benefit from preserved spontaneous breathing. While completely disabling spontaneous ventilation with or without neuromuscular blockade is not a standard strategy in ARDS, it might be temporarily required in patients with severe ARDS, who have substantial dyssynchrony or persistent hypoxaemia. Since pain, agitation and delirium compromise respiratory function they should also be regarded during noninvasive ventilation and during ventilator weaning. Pharmacological sedation can have favourable effects in these situations, but should not be given routinely or uncritically.
Assuntos
Cuidados Críticos/métodos , Delírio/terapia , Manejo da Dor/métodos , Agitação Psicomotora/terapia , Síndrome do Desconforto Respiratório/terapia , Terapia Combinada/métodos , Sedação Consciente/métodos , Humanos , Bloqueio Neuromuscular/métodos , Respiração Artificial/métodos , Desmame do Respirador/métodosRESUMO
BACKGROUND: The lungs and kidneys represent the most often affected organs (acute respiratory distress syndrome, ARDS or kidney failure) in multiple organ failure (MOF) due to shock, trauma, or sepsis with a still unacceptable high mortality for both organ failures. PATHOGENESIS AND INTERACTIONS: Although the exact pathophysiological mechanisms of MOF are not completely elucidated, it appears that the lungs and kidneys share several pathophysiologic pathways and have the potential to further harm each other (kidney-lung crosstalk). Inflammatory signals in both directions and volume overload with consecutive edema formation in both organs may play a key role in this crosstalk. TREATMENT: The organ replacement therapies used in both organ failures have the potential to further injure the other organ (ventilator trauma, dialyte trauma). On the other hand, renal replacement therapy can have positive effects on lung injury by restoring volume and acid-base homeostasis. The new development of "low-flow" extracorporeal CO2 removal on renal replacement therapy platforms may further help to decrease ventilator trauma in the future.