[Physiopathology of pulmonary arterial hypertension and gas exchange in acute pulmonary embolism].

Pulmonary embolism alters the distribution of ventilation/perfusion relationships, and increases pulmonary vascular resistance. These changes lead to hypoxemia and hypocapnia, and eventually, to right heart failure. The thin-walled and compliant right ventricle adapts to any increase in afterload by dilatation and decreased stroke volume, but this is largely prevented or delayed by the pulmonary circulation being a low resistance, recruitable and distensible circuit. Pulmonary embolism cannot be associated with a mean pulmonary artery pressure higher than 40 mmHg. More severe pulmonary hypertension indicates the presence of a hypertrophied right ventricle in the context of preexistent cardiac or pulmonary disease. Gas exchange is initially affected because of increased ventilation/perfusion ratios in embolized lung areas, and decreased ventilation/perfusion ratios in remaining non embolized lung areas. Both physiologic shunt and physiologic dead space increase accordingly, resulting in hypoxemia and hypocapnia. However, these changes are rapidly affected by an increase in ventilation, and by a "pneumoconstriction" which decreases physiologic dead space in embolized areas. In addition, a series of secondary alterations contribute to increase perfusion to lung units with low ventilation/perfusion ratios, thereby aggravating hypoxemia, while hypocapnia persists.