HEMODYNAMICS AND GAS-EXCHANGE IN PULMONARY-EMBOLISM - PHYSIOPATHOLOGY AND TREATMENT

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 (> 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 veinous 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 broncho-constriction in the hypoperfused areas. The normal right ventricle (RV) is not a very effective pressure generator, which is the reason why an embolus occurring in a previously healthy subject never causes major pulmonary hypertension (average pulmonary artery pressure < 40 mm Hg). In the event of massive vascular obstruction, the RV reacts by diminishing its systolic ejection volume and raising its telediastolic volume. Acute RV dilatation may compromise filling of the left ventricle (ventricular interference). In the final stages the fall in average aortic pressure and the rise in average RV pressure cause ischemia of the RV through a critical reduction of right coronary perfusion pressure. In the treatment of low output syndrome due to pulmonary embolism it is important to avoid any measure which may lower blood pressure and thus be likely to cause or aggravate RV ischemia. Preference should therefore be given to sympathicomimetic amines devoid of marked beta-2 effect (dopamine or dobutamine); also, any attempt to influence pulmonary artery impedance by pharmacologic means must be avoided due to their foreseeable effects on systemic arterial pressure. Vascular filling is potentially dangerous since it may aggravate ventricular interference effects; it should be reserved for clearcut hypovolemic conditions.