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The Quarterly Journal of Nuclear Medicine 2001 December;45(4):281-6

Copyright © 2009 EDIZIONI MINERVA MEDICA

lingua: Inglese

Ventilation/perfusion scan and dead space in pulmonary embolism: are they useful for the diagnosis?

Giuntini C.

From the Cardiac and Thoracic Department University of Pisa, Pisa, Italy Institute of Clinical Physiology National Research Council, Pisa, Italy


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The diag­nostic ­strategy for pul­mo­nary embo­lism, ­based on the mis­match of the ven­ti­la­tion/per­fu­sion ­scan, was devel­oped ­some 30 ­years ago on the fol­lowing assump­tion: ­since the dis­order ­involves the pul­mo­nary ves­sels, it was sur­mised ­that in the embol­ized ­regions ­lung ­alveoli are unper­fused or ­poorly per­fused but ­well ven­ti­lated. ­Hence, it was ­inferred ­that ­this dis­order was char­ac­ter­ized, ­unlike paren­chymal dis­ease, by ven­ti­la­tion/per­fu­sion mis­match in the ­affected ­lung ­zones and by an ­obvious ­increase of ­wasted ven­ti­la­tion, i.e., ­dead ­space. As ­matter of ­fact, experi­mental evi­dence on the redis­tri­bu­tion of ven­ti­la­tion ­away ­from the vas­cular ­occluded ­lung had ­been ­already ­obtained in the ­early 60s of the ­last cen­tury. ­More ­recently, the ­behavior of ­regional pul­mo­nary ven­ti­la­tion (V.A) and ­blood ­flow (Q.) in ­patients ­with ­acute pul­mo­nary embo­lism (APE) has ­been ­studied by ­applying the mul­tiple ­inert gas elim­i­na­tion tech­nique (­MIGET). It has ­been ­shown ­that the devel­op­ment of ­lung ­units ­with ­high V.A/Q. ­ratio (­those ­with rel­a­tive prev­a­lence of per­fu­sion obstruc­tion) is accom­pa­nied by sub­stan­tial redis­tri­bu­tion of ven­ti­la­tion ­away ­from ­these ­units. Fur­ther­more, radio­iso­topic tech­niques, ­used to vis­u­alize the top­o­graphic dis­tri­bu­tions of V.A and Q. in the ­same ­patients ­studied by ­MIGET, ­have ­shown ­reduced or ­absent V.A in the embol­ized ­regions. ­This may ­occur by dif­ferent mech­a­nisms in the var­ious ­stages of APE: bron­choc­on­stric­tion medi­ated by ­local hypo­capnia, ate­lec­tasis (occa­sion­ally hemor­rhagic) ­related to alter­a­tion of sur­fac­tant pro­duc­tion, bron­chi­olar obstruc­tion and pul­mo­nary infarc­tion ­ascribed to degen­er­a­tive and/or ­necrotic ­changes sec­on­dary to insuf­fi­cient ­blood ­flow. In ­dogs and ­humans ­alike, the ­dead ­space meas­ured by ­MIGET ­does not ­increase and ­that ­obtained ­from CO2 ­increases far ­less ­than the ­amount of unper­fused ­lung in APE ­thus con­firming a sub­stan­tial redis­tri­bu­tion of ven­ti­la­tion ­away ­from the embol­ized ­lung ­zones. ­Taken ­together, all ­these obser­va­tions pro­vide the path­o­phy­sio­log­ical expla­na­tion of the unac­cept­edly low ­level of sen­si­tivity for the diag­nostic ­strategy of APE ­based on the mis­match of the ven­ti­la­tion/per­fu­sion ­scan.

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