Acute cor pulmonale in ARDS

Excerpt

In 1977, Zapol and colleagues [1] reported that the pulmonary circulation was injured in patients with ARDS, leading to elevated pulmonary vascular resistance and pulmonary hypertension. The investigators suggested that the pathogenesis was related to competition between alveolar distending pressure and blood flow in these patients who were ventilated with high airway pressure [2], as proposed by West et al. [3]. Pulmonary vascular remodeling also occurs with muscularization of normally non-muscularized arteries. Subsequently, using transesophageal echocardiography (TEE), 24 years later Vieillard-Baron et al. [4] reported an incidence of acute cor pulmonale (ACP) of 25 % during the first 3 days in 75 ARDS patients treated with lung protective ventilation. A few years later, the same group reported a much higher incidence of 50 % in more severe patients, all exhibiting a PaO₂/FiO₂ <100 mmHg [5]. The same group studied 352 patients and found that the incidence of ACP was related to elevated plateau airway pressure (Pplat) with a safe limit for the right ventricle of 27 cmH₂O [6]. Since then, several questions are still unresolved, including: What is the actual incidence of ACP in a larger population? Which are the main variables associated with ACP? What is the impact of ACP on prognosis, if any? Should RV function be monitored, and, if so, how? Should clinicians adjust the ventilatory strategy to RV function? Recently published clinical studies provide answers to some of these questions. …