13 When a vessel is occluded by an embolus and forward blood flow through the vessel stops, perfusion of pulmonary capillaries normally supplied by that vessel ceases. If ventilation to the corresponding alveoli continues, it is wasted and the region of lung serves as dead space. As discussed in Chapter 1, assuming that minute ventilation remains constant, increasing the dead space automatically decreases alveolar ventilation and hence CO2 excretion. However, despite the potential for CO2 retention in pulmonary embolic disease, hypercapnia is an unusual consequence of pulmonary embolism, mainly because patients routinely increase their minute ventilation after an embolism occurs and more than compensate for the increase in dead space. In fact, the usual consequence of a pulmonary embolus is hyperventilation and hypocapnia, not hypercapnia. However, if minute ventilation is fixed (e.g., in an unconscious or anesthetized patient whose ventilation is controlled by a mechanical ventilator), a PCO2 rise may result from the increase in dead space caused by a relatively large pulmonary embolus. In addition to creating an area of dead space, another potential consequence of mechanical occlusion of one or more vessels is an increase in pulmonary vascular resistance. As discussed in Chapter 12, the pulmonary vascular bed is capable of recruitment and distention of vessels. Not surprisingly, experimental evidence indicates no increase in resistance or pressure in the pulmonary vasculature until approximately 50% to 70% of the vascular bed is occluded. The experimental model is somewhat different from the clinical setting, however, because release of chemical mediators may cause vasoconstriction and additional compromise of the pulmonary vasculature.
Pulmonary Embolism
Pathophysiology
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree