I meccanismi dell'ipossiemia nell'embolia polmonare acuta

Very fcw studies reportcd suecessful investigation of acute pulrnonary cmbolism in humans (PE) by using the multiple inert gas clirnination technique (MIGET) to identily and quantitate thc physiologic mcchanisms or hypoxernia in this disorder, because of its acute nature which makes it very difficult to study in mano We studied lO patients spontaneously breathing room air, using MIGET in the very acute phase of PE, demonstrated by perfusion lung scintigraphy (PLS), and for some of them by angiography, and confirmed after one week of appropriate therapy by evaluating the presence of a substantial recovery of perfusion at PLS. PE was severe as demonstrated by the average number of unperfused lung segments visible at PLS (12.1±2.6) showing that more than 60% of the vascular bed was obstructed. In 6 out lO patients MIGET was also repeated after a peri od of treatment. AH patients were hypoxernic (Pa02 = 63±11 mmHg, PaC02 = 30±4 mmHg), mean Ppa was 38±17.4 mmHg. Cardiac index (CI) was reduced (2.2±0.5 J/min/m2) and Pv02 was 31±4 mmHg. MIGET revealed ventilation-perfusion inhomogeneity CVA/QJ,as documented by the increase of the second moment of VA and Q distributions (log SO VA = 0.88±0.35, log SO Q = 0.96±0.39, upper limit of normals = 0.6), shunt 4.6±4.8% of cardiac output, dead space 34±15%. A 'Yidel!ed unimodal VA/Q distribution was present in 4 out of lO patients, low VA/Q «0.1) regions in 3 patients, hig? VA/Q (>10) regions in 5 patients in which VE was markedly increased. Mean Pa02 predicted from VA/Q distributions larger by 6 mmHg than that measured value. Log SO Q correlated poorly with the magnitude of vascular obstruction at PLS, whereas it correlated roughly with CI (r = 0.64, p<0.05). After treatment patients showed reduced hypoxemia (Pa~)2 ~ 74 mmHg, PaC02 = 36 mmHg), correspondingly VA/Q inequality decreased in ali patients. We conclude that VA/Q mismatch appears an important mechanism responsible for the impairment of gas exch.ang~ in PE and that different factors could explain hypoxemia (shunt, low Pv02, low CI, redistribution of Q in low VA/Q units, diffusion limitation). However, other confounding factors (time elapsed after ernbolization, preexisting cardiopulmonary diseaes, variability in the amount of embolism, ventilatory response, humoral activity at the time of the study) may have had effects on the mentioned mechanisms and consequently on the shape of VA/Q distribution.