Pulmonary emboli can cause severe hemodynamic and respiratory disorders whose physiopathologic mechanisms need to be well understood to ensure appropriate treatment. In previously healthy subjects only massive obstructions (greater than 50%) have dangerous effects due to the very large functional reserve of the pulmonary vascular bed. The same is not always true where there are previous anomalies of pulmonary circulation. In man, vascular obstruction appears to be primarily mechanical, although the presence of emboli may also trigger the release of vasoconstrictor mediators. In the animal it is accepted that these mediators may play an important role, in particular by increasing the critical closing pressure in pulmonary microcirculation. Apart from resistance to continuous bloodflow, the vascular obstruction may accentuate a number of dynamic phenomena specifically obstructing the passage of a pulsatile flow. The aggregate obstacles to right ventricular ejection are known by the term pulmonary artery impedance. Gas exchanges can be disturbed by a wide variety of mechanisms. Arterial hypoxemia chiefly results from maldistribution of the ventilation/perfusion ratio and, in severe forms associated with a fall in cardiac output, from diminution of the partial oxygen pressure of mixed venous blood. The right auricular pressure increase may sometimes contribute to hypoxemia by causing reopening of a permeable ductus Botalli with onset of right-left shunt. This possibility should be considered if oxygen administration does not correct hypoxemia. The dead space effect is not always in relation to the size of the vascular obstruction due to hypocapnic bronchoconstriction in the hypoperfused areas.(ABSTRACT TRUNCATED AT 250 WORDS)