ABSTRACT
Acute respiratory distress syndrome is characterized by non-cardiogenic pulmonary edema, decreased pulmonary compliance, and abnormalities in gas exchange, especially hypoxemia. Patients with acute respiratory distress syndrome (ARDS) who receive support with venovenous (V-V) extracorporeal membrane oxygenation (ECMO) usually have severe lung disease. Many patients with ARDS have associated pulmonary vascular injury which can result in elevated pulmonary vascular resistance and right heart dysfunction. Since V-V ECMO relies upon preserved cardiac function, right heart failure has important implications for patient evaluation, management, and outcomes. Worsening right heart function complicates ARDS and disease processes. Given the increasing use of ECMO to support patients with ARDS, an understanding of right ventricular-ECMO and cardiopulmonary interactions is essential for the clinician. A narrative review of the manifestations of right heart dysfunction, as well as diagnosis and management strategies for the patient with ARDS on ECMO, is provided.
ABSTRACT
Background: It is known that acute cor pulmonale (ACP) worsens the prognosis of non-coronavirus disease 2019 (COVID-19) acute respiratory distress syndrome (NC-ARDS). The ACP risk score evaluates the risk of ACP occurrence in mechanically ventilated patients with NC-ARDS. There is less data on the risk factors and prognosis of ACP induced by COVID-19-related pneumonia. Objective: The objective of this study was to evaluate the prognostic value of ACP, assessed by transthoracic echocardiography (TTE) and clinical factors associated with ACP in a cohort of patients with COVID-19-related pneumonia. Materials and methods: Between February 2020 and June 2021, patients admitted to intensive care unit (ICU) at Amiens University Hospital for COVID-19-related pneumonia were assessed by TTE within 48 h of admission. ACP was defined as a right ventricle/left ventricle area ratio of >0.6 associated with septal dyskinesia. The primary outcome was mortality at 30 days. Results: Among 146 patients included, 36% (n = 52/156) developed ACP of which 38% (n = 20/52) were non-intubated patients. The classical risk factors of ACP (found in NC-ARDS) such as PaCO2 >48 mmHg, driving pressure >18 mmHg, and PaO2/FiO2 < 150 mmHg were not associated with ACP (all P-values > 0.1). The primary outcome occurred in 32 (22%) patients. More patients died in the ACP group (n = 20/52 (38%) vs. n = 12/94 (13%), P = 0.001). ACP [hazards ratio (HR) = 3.35, 95%CI [1.56-7.18], P = 0.002] and age >65 years (HR = 2.92, 95%CI [1.50-5.66], P = 0.002) were independent risk factors of 30-day mortality. Conclusion: ACP was a frequent complication in ICU patients admitted for COVID-19-related pneumonia. The 30-day-mortality was 38% in these patients. In COVID-19-related pneumonia, the classical risk factors of ACP did not seem relevant. These results need confirmation in further studies.
ABSTRACT
Acute respiratory distress syndrome (ARDS) is characterized by protein-rich alveolar edema, reduced lung compliance and severe hypoxemia. Despite some evidence of improvements in mortality over recent decades, ARDS remains a major public health problem with 30% 28-day mortality in recent cohorts. Pulmonary vascular dysfunction is one of the pivot points of the pathophysiology of ARDS, resulting in a certain degree of pulmonary hypertension, higher levels of which are associated with morbidity and mortality. Pulmonary hypertension develops as a result of endothelial dysfunction, pulmonary vascular occlusion, increased vascular tone, extrinsic vessel occlusion, and vascular remodeling. This increase in right ventricular (RV) afterload causes uncoupling between the pulmonary circulation and RV function. Without any contractile reserve, the right ventricle has no adaptive reserve mechanism other than dilatation, which is responsible for left ventricular compression, leading to circulatory failure and worsening of oxygen delivery. This state, also called severe acute cor pulmonale (ACP), is responsible for excess mortality. Strategies designed to protect the pulmonary circulation and the right ventricle in ARDS should be the cornerstones of the care and support of patients with the severest disease, in order to improve prognosis, pending stronger evidence. Acute cor pulmonale is associated with higher driving pressure (≥18 cmH2O), hypercapnia (PaCO2 ≥ 48 mmHg), and hypoxemia (PaO2/FiO2 < 150 mmHg). RV protection should focus on these three preventable factors identified in the last decade. Prone positioning, the setting of positive end-expiratory pressure, and inhaled nitric oxide (INO) can also unload the right ventricle, restore better coupling between the right ventricle and the pulmonary circulation, and correct circulatory failure. When all these strategies are insufficient, extracorporeal membrane oxygenation (ECMO), which improves decarboxylation and oxygenation and enables ultra-protective ventilation by decreasing driving pressure, should be discussed in seeking better control of RV afterload. This review reports the pathophysiology of pulmonary hypertension in ARDS, describes right heart function, and proposes an RV protective approach, ranging from ventilatory settings and prone positioning to INO and selection of patients potentially eligible for veno-venous extracorporeal membrane oxygenation (VV ECMO).
ABSTRACT
Acute respiratory distress syndrome (ARDS) is burdened with significant mortality, mainly in connection with circulatory failure. The right ventricle (RV) is the weak link of hemodynamic stability among ARDS patients and its failure, also named "severe" acute cor pulmonale (ACP), is responsible for excess mortality. Driving pressure ≥18 cmH2O, PaCO2 ≥48 mmHg and PaO2/FiO2 <150 mmHg are three preventable factors recently identified as independently associated with ACP, on which ventilator strategy designed to protect the RV has to focus. This is largely achieved by the use of early and extended sessions of prone positioning (PP) and by daily monitoring of the RV by echocardiography.