One out of ten critically ill patients in the intensive care unit (ICU) will develop acute respiratory distress syndrome (ARDS). In addition to low tidal volume ventilation, prone positioning and neuromuscular blockade, adjusting the mechanical ventilation mode may be another strategy to implement early in a patient’s clinical course when faced with ARDS complicated by refractory hypoxemia. 

Several drugs have been investigated in patients with ARDS, including epoprostenol, nitric oxide, statins, and methylprednisolone, but have not improved survival. Meduri et al. performed an RCT demonstrating that methylprednisolone was associated with a reduction in lung injury score and duration of mechanical ventilation. While not powered to evaluate mortality, this trial raised interest in the use of corticosteroid to mitigate inflammatory lung injury. The 2017 Guidelines from the Society of Critical Care Medicine (SCCM) and the European Society of Intensive Care Medicine (ESICM) recommend steroids for treatment of ARDS based on a meta-analysis of nine randomized controlled trials demonstrating reduction in markers of inflammation and duration of mechanical ventilation, although many of the trials had a small sample size and some were performed without lung protective ventilation. In March 2020, Villar et al. published the largest randomized control trial of corticosteroid therapy for moderate to severe ARDS investigating the impact of dexamethasone on survival and duration of mechanical ventilation.  

A 34-year-old woman at 32 weeks gestation presents to the emergency department with cough, dyspnea and hypoxemia. She rapidly progresses to severe ARDS despite lung protective ventilation, paralysis and inhaled epoprostenol. P/F ratio is 99 mm Hg. Is prone positioning safe to perform in pregnant patients with severe ARDS? If so, are modifications necessary to offload the abdomen and monitor the fetus? A recently published review in Obstetrics and Gynecology discusses this important topic. 

A 52-year-old man with a history significant for hypertension presented to the emergency department with cough, dyspnea and fever. He progressed to severe acute respiratory distress syndrome (ARDS) secondary to COVID-19 pneumonia. He developed refractory hypoxemia with P/F < 60 mm Hg despite low tidal volume ventilation, paralysis, inhaled epoprostenol and prone positioning. Is this patient a candidate for venovenous ECMO and, if so, who should guide initiation and management of ECMO? The Society of Critical Care Medicine (SCCM) and Extracorporeal Life Support Organization (ELSO) recently published a position paper on the role of the intensivist in the initiation and management of ECMO. 

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?

What is airway pressure release ventilation (APRV)? Here is a simplified breakdown of the ventilator settings, pressure and flow waveforms. 

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. 

Prone positioning was discovered by a woman. 

She was a nurse. 

This should surprise no one. 

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.