Acute cor pulmonale and the acute respiratory distress syndrome

Abstract

Acute respiratory distress syndrome (ARDS) is characterized by arterial hypoxemia secondary to protein-rich pulmonary edema associated with acute inflammation and loss of aerated lung volume [1,2]. ARDS also involves injury to the pulmonary circulation that is associated with pulmonary hypertension and an elevation in pulmonary dead space [1,2]. The pulmonary circulation is involved at different stages of ARDS with progression of the clinical syndrome. First, injury to the lung microcirculation causes an increase in lung vascular permeability which initiates the accumulation of pulmonary edema. Second, intravascular microthrombi can develop from an imbalance between procoagulant and fibrinolytic activity in the presence of acute inflammation and endothelial injury. Third, the marked reduction in functional residual capacity (FRC) can increase pulmonary vascular resistance (PVR). Fourth, positive pressure ventilation can induce high lung volume in some lung regions and compress alveolar vessels, resulting in increased PVR. The resulting higher regional FRC can also increase PVR. Fifth, hypoxic pulmonary vasoconstriction can further increase PVR. All these of mechanisms can contribute to an elevation in PVR that can occur within 48 h after the onset of ARDS, as demonstrated many years ago [3] and also more recently [4,5]. The elevation in PVR may also be exacerbated by hypercapnia and acidosis. These mechanisms are summarized in Fig. 1.An elevation in PVR has long been recognized as a predictor of poor prognosis in ARDS. Under normal conditions, the right ventricle (RV) pumps against a low resistance pulmonary circulation, but in the presence of an acute increase in afterload from a rise in PVR, the RV attempts to compensate by increasing end-systolic and end-diastolic volumes. If the increase in afterload is substantial, impairment of RV systolic function and interventricular septal kinetics results in a reduction in cardiac output and acute core pulmonale (ACP) with RV failure and shock. Before the era of lung protective ventilation, the incidence of ACP from elevated PVR in ARDS was as high as 60 % [6].In a recent article in Intensive Care Medicine, Mekontso-Dessap and colleagues [7] report the results of a study of 752 moderate to severe ARDS patients (ratio of partial pressure arterial oxygen and fraction of inspired oxygen: PaO 2 /FiO 2 \200 mmHg) designed (1) to determine the incidence of ACP, (2) to test a clinical score to predict the presence of ACP and (3) to determine the association of ACP with mortality. The diagnosis of ACP was determined by transesophageal echocardiography (TEE) and defined by septal dyskinesia with a dilated RV, end-diastolic RV/left ventricle area ratio of [0.6, and a score of [1 for severe ACP. Overall, ACP developed in Intensive Care Med (2016) 42:934-936

The pathophysiology of ‘happy’ hypoxemia in COVID-19

“…Endothelial injury is emerging as a central hallmark of COVID-19 pathogenesis, and the cytopathic virus can directly infect lung capillary endothelial cells that express ACE2 [54,56]. Intravascular microthrombi are the net result of an imbalance between procoagulant and fibrinolytic activity in the presence of acute inflammation and endothelial injury [45,[57][58][59]. The pro-coagulant activity might result from complement system-mediated activation of clotting, similar to some forms of thrombotic microangiopathy (TMA), or could be due to inhibition of plasminogen activation and fibrinolysis via increased activity of plasminogen activator inhibitor (PAI-1 and -2) which are induced as acute-phase proteins under the influence of IL-6.…”

Correlations of IL-17 and NF-κB gene polymorphisms with susceptibility and prognosis in acute respiratory distress syndrome in a chinese population

“…Acute respiratory distress syndrome (ARDS) is a devastating clinical syndrome which is most commonly a manifestation of sepsis-induced organ dysfunction, characterized by disruption of endothelial barrier integrity and diffuse lung damage [1]. This can result in increased vascular permeability of alveolar-capillary membrane, acute onset of pulmonary edema, along with bilateral pulmonary infiltrates and decreased lung compliance that patients with ARDS need supportive care in the intensive care unit (ICU) to maintain oxygenation and prevent adverse outcomes [2,3]. Despite various therapeutic strategies, the mortality of ARDS remain as high as 40%.…”

Frequency and prognostic impact of basic critical care echocardiography abnormalities in patients with acute respiratory distress syndrome

“…Such strategies include targeting plateau pressures below 27 cm H 2 O, maintaining adequate oxygenation and avoiding hypercarbia beyond 60 mmHg [ 2 , 5 ]. Prone positioning to off-load the right ventricle and extracorporeal carbon dioxide removal to allow tidal volume (and hence plateau pressure) reduction could also be considered [ 5 , 6 ]. However, while we encourage BCCE, it should only be done if frontline physicians are competent in its use and interpretation [ 25 ].…”

“…In particular, patients with ARDS may develop right ventricular overload and acute cor pulmonale (ACP) [ 2 – 4 ]. The pathophysiology of ACP is complex and is related to pulmonary vasoconstriction, permissive hypercapnia, intrapulmonary microthrombi and positive pressure mechanical ventilation [ 4 – 6 ].…”