As we learn more about the pathophysiology of COVID-19, alternative treatments are being explored for the severe sequelae of this disease. SARS-CoV-2 enters human cells via the ACE2 receptor, located in many organs, including the heart, vascular endothelium, and alveolar epithelium causing an inflammatory cascade that can lead to ARDS, vasodilatory shock, myocarditis, acute kidney injury and capillary leak. Given the relationship between SARS-CoV-2 and the RAAS, is there a role for angiotensin II in vasodilatory shock caused by COVID-19?
A 36-year-old woman presented to urgent care with cough, dyspnea and hypoxemia. She was transported to the ED where she rapidly progressed to severe ARDS despite lung protective ventilation, paralysis and inhaled epoprostenol. Post-intubation, it was determined that she was pregnant with ultrasound revealing a fetus at 23 weeks, 6 days gestational age. She underwent cannulation for venovenous ECMO. What is the role of ECMO in the pregnant patient? A recently published analysis of the ELSO registry for peripartum patients supported with ECMO demonstrates a 70 percent survival rate.
Over the last three decades since the introduction of the term ventilator-induced lung injury (VILI), we have recognized that positive pressure mechanical ventilation can injure the lungs. It is widely recognized that the cornerstone of lung protective ventilation requires control of tidal volume and transpulmonary pressure. On the other hand, there has been considerably less focus on the impact of respiratory rate and flow on VILI. Mechanical power unites the causes of ventilator-induced lung injury in a single variable that incorporates both the elastic and resistive load of the positive pressure breath.6 In other words, mechanical power quantifies the energy delivered to the lung during each positive pressure breath by assessing the relative contribution of pressure, volume, flow and respiratory rate.
Venous thromboembolism is considered one of the most preventable causes of in-hospital death. Venovenous extracorporeal membrane oxygenation (VV ECMO) utilization for severe respiratory failure has increased in the decade following the 2009 influenza A H1N1 pandemic and the publication of the CESAR trial.1 The interaction between a patient’s blood and the ECMO circuit produces an inflammatory response that can provoke both thrombotic and bleeding complications. In a systematic review of patients with H1N1 treated with VV ECMO published in 2013, the incidence of cannula-associated deep venous thrombosis (CaDVT) was estimated to be as low as 10 percent; however, more recent data suggests the incidence of venous thrombosis after decannulation is much higher. Additionally, a significant proportion of CaDVT are distal thrombi located in the vena cava, which would be missed with a traditional ultrasound diagnostic approach after decannulation from VV ECMO.
Lung-protective mechanical ventilation with low tidal volume and restricted plateau pressure improves survival in ARDS. However, the optimal approach to PEEP titration to minimize VILI is still debated. Should oxygenation, lung compliance, driving pressure or transpulmonary pressure guide adjustment of PEEP in ARDS?