The pathophysiologic consequences of pulmonary thromboembolism depend largely on the size of the embolus, which in turn dictates the size of the occluded pulmonary artery, and the cardiopulmonary status of the patient. There are two important consequences of pulmonary arterial occlusion: (1) an increase in pulmonary artery pressure from blockage of flow and, possibly, vasospasm caused by neurogenic mechanisms and/or release of mediators (e.g., thromboxane A2, serotonin); and (2) ischemia of the downstream pulmonary parenchyma. Thus, occlusion of a major vessel results in an abrupt increase in pulmonary artery pressure, diminished cardiac output, right-sided heart failure (acute cor pulmonale), and sometimes sudden death. If smaller vessels are occluded, the result is less catastrophic and may even be clinically silent. Hypoxemia develops as a result of multiple mechanisms:
Perfusion of atelectatic lung zones. Alveolar collapse occurs in ischemic areas because of a reduction in surfactant production and because pain associated with embolism leads to reduced movement of the chest wall.
The decrease in cardiac output causes a widening of the difference in arterial-venous oxygen saturation.
Right-to-left shunting of blood may occur through a patent foramen ovale, present in 30% of normal individuals.
Recall that the lungs are oxygenated not only by the pulmonary arteries but also by bronchial arteries and directly from air in the alveoli. Thus, ischemic necrosis (infarction) is the exception rather than the rule, occurring in as few as 10% of patients with thromboemboli. It occurs only if there is compromise in cardiac function or bronchial circulation, or if the region of the lung at risk is underventilated as a result of underlying pulmonary disease.
MORPHOLOGYTheconsequencesofpulmonaryembolism,asnoted,dependonthesizeoftheembolicmassandthegeneralstateofthecirculation.Alargeembolusmayembedinthemainpulmonaryarteryoritsmajorbranchesorlodgeastridethebifurcationasasaddle embolus (
Fig.13.24 ).Deathusuallyfollowssosuddenlyfromhypoxiaoracutefailureoftherightsideoftheheart(acutecorpulmonale)thatthereisnotimeformorphologicalterationsinthelung.Smallerembolibecomeimpactedinmedium-sizedandsmall-sizedpulmonaryarteries.Withadequatecirculationandbronchialarterialflow,thevitalityofthelungparenchymaismaintained,butalveolarhemorrhagemayoccurasaresultofischemicdamagetotheendothelialcells.
Withcompromisedcardiovascularstatus,asmayoccurwithcongestiveheartfailure,infarction results.Themoreperipheraltheembolicocclusion,thehighertheriskforinfarction.Aboutthree-fourthsofallinfarctsaffectthelowerlobes,andmorethanone-halfaremultiple.Characteristically,theyarewedge-shaped,withtheirbaseatthepleuralsurfaceandtheapexpointingtowardthehilusofthelung.Pulmonaryinfarctstypicallyarehemorrhagicandappearasraised,red-blueareasofcoagulativenecrosisintheearlystages(
Fig.13.25 ).Theadjacentpleuralsurfaceofteniscoveredbyafibrinousexudate.Theoccludedvesselisusuallylocatedneartheapexoftheinfarctedarea.Theredcellsbegintolysewithin48hours,andtheinfarctgraduallybecomesred-brownashemosiderinisproduced.Intime,fibrousreplacementbeginsatthemarginsasagray-whiteperipheralzoneandeventuallyconvertstheinfarctintoascar.