1985. Chest. Hipoxemia in Acute Pulmonary Embolism

HypoxemiaYann Huet, M.D.;* Christian Bernard Didier in Acute Pulmonary Francots Lemaire, Embolism M.D.;* A. Knaus, M.D.;*t M.D.;* and Brun-Buisson, M.D.;* Teisseire, Ph.D.;1: Didier Mathieu, M.D. William Payen, Most have roles patients arterial with severe, acute pulmonary embolism (PE) hypoxemia. of ventilation shunt in the mechanism of hypoxemia, we used both right heart catheterization and the six inert gas elimination technique in seven patients with severe, acute PE (mean vascular obstruction, 55 percent) and hypoxemia (mean Pa08, 67±11 mm Hg). None had previous cardiopulmonary disease, and all were studied within the first ten days of initial symptoms. Increased calculated venous admixture (mean QVt/QT 16.6 ± 5.1 percent) was present in all patients. The relative contributions of VA/() mismatching and shunt to this venous admixture varied, however, according to pulmonary radiographic abnormalities and the time elapsed from initial symptoms to the gas exchange study, trapulmonary To further define the respective to perfusion (VA/Q) mismatch and in- all patients had some degree of VA/(I mismatch, the two patients studied early (ie, <48 hours following acute FE) had normal chest x-ray film findings and no significant shunt; VA/ mismatching accounted for most of the hypoxemia. In the others a shunt (3 to 17 percent of cardiac output) was recorded along with radiographic evidence of atelectasis or infiltrates and accounted for most of the venous admixture in one. In all patients, a low mixed venous oxygen tension (27 ± 5 mm Hg) additionally contributed to the hypoxemia. Our findings suggest that the initial hypoxemia of acute FE is caused by an altered distribution of ventilation to perfusion. Intrapulmonary shunting contributes significantly to hypoxemia only when atelectasis or another cause of lung volume loss develops. Although cute pulmonary common embolism diagnoses (PE) of remains acutely frequent for one ill, of the hospi- after the PE. In one of these, Wilson et al’#{176} suggested for most of the the major role to the investigators relative contributimes oxygen of ininferred gives an cardiac by of VA/ oxygen to the more talized patients tions to occur ders.’2 clinical feature and one of the more during hospitalization is of PE significance established. impaired as well been unclear. a Its consistent complicaother disorimportant and pre- Hypoxemia and that atelectasis and shunt accounted hypoxemia, whereas Kafer2 attributed VA/Q mismatching. In these studies were unable to examine directly the tions after method trapulmonary of the “A/a pathophysiology cise clinical been clearly abnormalities,45 ary shunting, remains shunts,4’6’7 of each Although in man, however, have not Ventilation/perfusion (VA/a) diffusion,3 and intrapulmonas right-to-left but related intracardiac the exact role implicated, mismatching embolus. Both shunting vs shunt at different studies also used the and not the degree but was measured to assess hypoxemia, all have hypoxemia using the alveolar-arterial oxygen difference. Today, bedside right heart catheterization accurate evaluation of the contribution factors Wagner technique distributions method In this to the et hypoxemia.” al’2 of the The multiple precise possible these recent, aim was recent inert gas of has been to the degree introduction elimination of pulmonary vascular obstruction reports of massive PE with normal tension (Pa02).#{176}No clear relationship clinical characteristics and the PaO, Variations in the timing and methods hypoxemia in previous studies may gas long, this confusion. humans were *SeMce de (PVO),8 there are arterial oxygen between other allows a more than was alone. study, evaluation using the has been used found. to assess to we combined patients with acute PE. Our two techniques angiographically to determine the chest gas have contributed The major performed exchange frequently studies in months, Mondor and study seven documented Reanimation M#{233}dicale, H#{244}pital Henri mechanism of their of our investigation abnormalities study. to the hypoxemia and each results by relating patient’s of their timing x-ray Universit#{233} Paris-Val de Mane, France. tICU Research Unit, The George Washington University Medical Center, Washington, DC. Laboratoire des echanges gazeux (INSERM U 138), H#{244}pitalHenri Mondor and Universit#{233} Paris-Val de Mane. §Service de Radiologie, H#{244}pital Henri Mondor and Universit#{233} Paris-Val de Marne. This work was supported in part by a grant from the D#{233}partement de Pharmacologie Clinique, H#{244}pital Henri Mondor, Creteil. Presented at the Annual Meeting of the American Thoracic Society, Anaheim, Calif, May, 1985. Manuscript received April 2; revision accepted July 15. exchange PATIENTS AND METHODS Patients Seven (ICU) studied. had any consecutive for hemodynamic Their individual significant patients clinical admitted and to our treatment Intensive of acute Care Unit monitoring preexisting PE were 1. None One pa- characteristics cardiopulmonary are in Table disease. CHEST / 88 / 6 I DECEMBER, 1985 829 Downloaded From: http://journal.publications.chestnet.org/ on 08/10/2013 because admixture of extensive (QVAJQT) pulmonary using and PaO. blender. were intravenously simultaneous last by Evans gases and Wagner. by ratios PaCO. (8) assessed by the Bohr dead space for carbon expired) from body as (arterial-mixed was assumed space divided weight of”. equilibrated cyclopropane.#{176} changes. (Statham index (CI).. a 5 percent rate samples (IV) at a constant dextrose of 5 mI/mm were drawn of the gas was in a and infused for 25 minutes. solution hexafluoride and acetone) Then. ie.3 percent. The blood solubility coefficient of each gas was determined for each patient.JQ <0. approximately two hours after the pulmonary angiogram. je. (1) minute Wright gas and in the the following ventilation inspiratory arterial recorder). (9) distribution technique.) (SaC).’4 ing ram VA/Q 1. high VA/Q. VA/Q<100.publications. and dead space (Vu/VT). After the study. sum distribution analysis were made: calibrated sampling pulmonary.S curves of the the was curves of the ridge and the were ventilationregression then measurements WE) and volume calculations (VT) using 0. The delay between the first symptom of PE (acute chest pain and/or dyspnea) and the inert gas study was carefully determined and ranged between one and nine days (Table 1). ducer cardiac perfurmed and tidal of the spirometer. absent. perfusion technique.Table 1-Clinical Features Clinical and Features . plus using (1 mI/Ib) (80 ml). % of pulmonary as follows: bed. ethane. The patients were receiving only heparin therapy at the time of the study.) atrial. oxygen (ABL tension 30. ie.org/ on 08/10/2013 . systemic (CO) (2) fraction line pressures (4) cardiac by computer of inspired circuit. The diagnosis of PE was made on clinical history and the results of a pulmonary angiogram perfurmed within a few hours of ICU admission.chestnet.) (OSMII. low VA/Q. The error of measurement of SF6 determined in our laboratory was 1. were the five equilibrated expired detector other gases artery for analysis 50 ml of expired with nitrogen were 429. ventilation which The the is taken ventilation mixed venous distribution calculated to as an index of blood the and in abcissa combined were determined. Six inert halopropane. The mean peak values flow and (log ventilation. a humidifier. Fi ndings at Time . A. we gave urokinase to all except patient 5. obstruction). The gas exchange study was perfbrmed on the first day in the ICU. who was recovering from recent neurosurgery. venous PaCO. The relative concentrations of the inert gases in arterial and mixed venous samples were derived from the equilibrated samples and the measured solubilities.8 percent and these. All were breathing spontaneously via a face mask with humidified room air or supplemental oxygen (patients 3 and 7) as required to maintain an adequate oxygen arterial partial pressure. was for the the residual the best other five gases. thermodilution 9520. The degree of PVO was determined using the index described by Tibutt et al. Y. nary capillary two patients. Radi(TPR) calculated as mean by cardiac were index possible the (pulmoonly arterial oxygen SD of the distribution with a natural of dispersion perfusion for the flow were VE. No vasoactive drug was used.2 ± 2.. cardiac model’4 to predict the arterial 830 Hypoxemla In Acute Pulmonary Embolism (Huet of a!) Downloaded From: http://journal. Chest X-ray Findings in 7 Patients with Acute Pulmonary Embolism - . (Flo. 10<VA/Q <100. blood gases.. Edwards (3) right derived The mean between 3. ie. estimated + Notation minimal changes. technique in 15-mI blood multiple gas elimination of this [SF61. tient had suffered a pulmonary embolism five yeas before but had no residual effects.0. gas samples (Packard by analyzed Packard ionization electron for capture a flame (Packard).&/( as described follows. distribution indicatinert gas of the and output P23 DB transfrom compatibility data. 0. Methods The gas exchange study was done with patients in a semirecumposition. ie.1.’4 A brief summary (sulfur ether. Retention-solubility a by From distributions excretion-solubility approximation using of square determined. The expiratory tubing was also heated to prevent condensation and extraction of the more soluble gas.. 0. saturation the technique Laborato- ries). from the pulmonary inert gas concentrations. samples blood and the bath for 45 minutes. sampled. X-ray . heated The for SF6 Instrument detector The equilibrated by an Co) and blood artery and a systemic At the same time.#{176} A Swan-Ganz catheter and radial artery line were already in place. as Copenhagen) ometer).005<VA/Q<0.005. dioxide (5) arterial tension and (6) total arterial wedge most (7) and (PaO. and a specially designed heated mixing box via a one-way valve. and less than constructed.’4 Honeywell in triplicate A computer-assisted measured (CO mixed PO. and carbon Radiometer ratios allowed the determination of shunt (Qs/Qt). described marked and/or by Tibutt multiple et al. method physiologic dioxide Anatomic instrumental the and computed dead space calculated dead inert space dead with the standard equation of Berggren. 1 2 3 4 5 6 7 * Since Precipitating Cause Immobilization Pelvic surgery limb Lower fracture Pulmonary Vascular Obstructiont 58 60 65 cancer limb 56 35 65 surgery 50 Age. of Studyl Hours Patient No. partial 50-compartment of oxygen. log scale distributions as well of blood output. Patients breathed through a circuit consisting of an 0. yr/Sex 4IJF 41/M 40/F 69/F Occurrence of PE 24 48 84 102 128 192 216 Elevated Diaphragm + 0 + + 0 + + Platelike Atelectasis 0 0 + + Infiltrates 0 0 0 + + + Immobilization Hepatic Lower fracture + + 50/M 61/M Immobilization Neurosurgery Immobilization Abdominal Lower fracture limb + + ++ + + + + 50/M according to time vascular 0 sign ++ ++ *Numbering tIn elapsed since initial according symptoms to index + + of embolism. bent In each patient. with in the pressure SD). The masks were tightly fitted to the patient’s face so that no air leaks occurred. acetone. pulmonary pulmonary pressure pressure likely venous resistance (PAP) divided measurements and SO. 84 0.6 ± studied parenchymal within two days of initial symptoms no in radiographic abnormalities.5 11.54 2.5) with a calculated mean oxygen consumption of 165±39 mllminm’. saturation. Cardiac index was abnormalities. 1 2 3 4 5 6 7 Mean ±SD *HR cardiac = Data* SAP CI. of oxygen. mm VD/VT (Bohr).51 7. 7.Table 2-Hemodynamic Patient No.6 10.30).47 P(A-a)0. ranging from 44 to 75 percent of minute ventilation. ie. - No. Mean pulmonary arterial pressure was only moderately increased (24 ± 5 mm Hg).5 92.3 15. 103 106 86 18 arterial 2. difference.. 1 2 3 4 5 6 7 Mean ±SD *4.1 of oxygen.9 9. multiple observers expressed for opacities.25 2.* Gas Exchange SaO.96 L/minm’) and notably study. and each areas emphasis present opacities.2 mmHg/L. mm 66 60 90 62 65 57 70 67 11 except = Hg % 94 93. 831 CHEST I 88 I 6 I DECEMBER. Analysis of the films was who did not know the patient’s Fleischner.40 7. (oxygen 93.1). pressure cm 162 180 170 157 180 170 171 170 8 room air. CI = TPR chest pulmonary was also resistance.ll patients kg 45 73 71 62 68 72 80 67.91 L/min#{149}m’). VD/VT dead space (Bohr). All of the patients had an arterial hypocarbia. monary venous patient..2 3.min.94 = XP = = total mean right atrial mean pulmonary pressure. 27 ± 5 mm Hg and 52 ± 10 percent. between data geographic relationship and site of embolus.m’).. Height.04). Right atrial pressure ranged from 2 to 15 mm Hg. Hg 42 55 88 53 43 44 112 - There was radiologic no are shown in Table 2. The inert gas study revealed different patterns of VA/Q distribution in relation to the timing of the study and the with presence Acute of x-ray Pulmonary PO.6 66 75 62 47 62 44 59 10 SaO. observers According on the followor absent.91 mm TPR. Table 3-Standard Patient Weight.5 5.5 93 2 3 and 7 (FIo. mm 34 27 29 26 31 37 26 30 4 Hg pH 7. The Bohr dead space was markedly high. obtained on the day of the to (2) were + + A standard x-ray film moderately low (2. mean systemic pressure.52 7.58 2.3 10 breathing saturation. ± RESULTS Standard gas exchanges mild hypoxemia (mean 67 patients are listed from 1 all patients.5 15. as mean agreement All the oxygen difference (mean 5.3 15.5 89.65 3.2 2. as could be expected from the decreased cardiac index. of the obvious findings The pulmonary arterial vascular bed).7 7. The enlarged. Mixed oxyhemoglobin venous method).2 ± 3.76 1.49 7.2 12. Calculated admixture (0.5 mm 34 25 25 21 25 29 32 27 5 Hg mm % 25. 57.8 Shunt.chestnet.8 10. beats/mm 105 110 RAP mm 2 12 15 10 2 3 3 7 5 Hg PAP mm 20 24 29 32 24 20 19 24 5 pressure. alveolar-arterial QVA/QT mixed Sco. (>VA/(>r.5 95 92.47±0. had a systolic blood pressure less than 90 mm Hg. and respiratory alkalosis was noted in five of seven patients (mean pH. from 10. The hemodynamic impact of PE was further evidenced by the increased arteriovenous of consolidation + for (“infiltrates”) scored marked between abnormality. PaO.45 7..5 to 25. Mixed venous oxygen partial atelectasis and/or small infiltrates were patients studied later. method) was elevated in each and ranged (mean.04 Abbreviations: P(A-a)O. The chest recorded in Table 1. Total pulmonary resistance was markedly elevated (9.” ing: (1) elevated atelectasis 0 for and/or the data two are no platelike they described hemidiaphragm and made by two independent clinical characteristics.6 18. Hgfmin/m’/L 4.6 percent of cardiac 5..publications. output are presented in Table 11mm Hg) was recorded 02 difference 3.org/ on 08/10/2013 .. Hg 65 45 43 44 45 57 65 52 10 % 19. film were with marked slight There ± SD. in 7 Patients PaCO.3 arterial HR.7 ± 1. 0.2 12. PaO. No patient. = Hg mm 100 70 60 87 76 145 90 103 84 110 107 20 heat index. however. respectively).. PO. = = arterial partial oxygen = pressure tension admixture arterial = oxyhemoglobin venous partial arterial = dioxide venous tension. standard hemodynamic pressure and saturation were low (mean. rate.49 7. 1985 Downloaded From: http://journal. Pulmonary arterial was substantial in all patients (mean value. PaCO.6 5. Hg Limin#{149}m’ 4.84±0. A in In all tables and figures the alveolar-arterial was to 7 corresponding symptoms of PE x-ray findings are to the time elapsed from initial to the gas exchange study. on all films. 16.42 7.= carbon 0. was close depressed in patient 2 (1.5 16. The two patients had Localized common obstruction 55 percent but did not correlate to the degree of pulvascular obstruction or to the PaO. Embolism SO. 89 1.838 Log SD of Ventilation Distribution 1. Figure 1 correlates the shunt ties.4 5. Thus. values were closely related to the values predicted from the PiIO.4 35.3 3 4. ventilation the The PaO.58 1.4 24.4 55.26 0.fl I I I I I F I 0 FIGURE 1 2 3 4 5 6 7 8 9 Days 1.fl.58 5. to 6. despite absence of a definite zone of very low VAJQ ratios.20 0.5 23.65 1.163 1. perfusion patients part to the unventilated 1 and 2 but accounted output (3. ‘A/() 100.210 0.031 CO. In all patients. areas Atelectasis a Sc o Infiltrat#{149}s 0 0 ++ + + ++ ++ ++ 1+ o 0 + ++ .8 percent) in patients in 3 each patient not and shows a normal that control. It is clear that a significant shunt is present only when chest x-ray is abnormal.8 10.1 Meas/Pred.4 51.5 31. to Ventilation to Unperfused Lung.005.8 16.5 30. .4 6.21).8 53 63.235 1.950 0.01 2. Conversely.9 5.83 0.95 ± 0. the mean different Analysis peak from 1 (1. There was no relationship venous admixture measured with the Qs/t (six inert gases method). VE.877 0.4). when output in between a large dispersion of perfusion was (0.691 1.129 0.org/ on 08/10/2013 .4 5. VA/ and shows that a significant infiltrates the 2 shows occurred seen distribution only radiofor atelectasis Figure and/or were VAJQ graphically.2 4.2 of the of blood ± \TA/ distribution flow. had part “A/( of cardiac although markedly 0. + + = marked and/or multiple opacities.723 0.1).39 1. 832 Hypoxemla In Acute Pulmonary Embolism (Huot of a!) Downloaded From: http://journal.03 0. §Anatomic dead space assumed from weight (1 ml/lb) plus instrumental dead space. CO 1. 58. measured PaO.2 0. %CO Perfusion Pa02/PaO. 0.publications.1 % Anatomic Dead Space. Limn 1 2 3 4 5 6 7 11 20 31 21 14 13 17 18 7 VT.8 24.2 1.Table 4-Inert Gas Data#{176} Perfusion Distribution.15 [ .96 1.676 57/66 70/66 67/71 11/15 ventilation.40 2. mm Hg ml 730 910 910 820 700 650 770 784 101 iTE 66/72 60/56 90/106 62168 65/63 56.1 5. %VE . was negligible for a low but significant to 8. L/mn 5.22 1. .142 0.8 32.22 #{176}Abbreviations: t’7A/( = expired = = cardiac output.2 lung. normal chest films were obtained in patients with no detectable shunt and studied within 48 hours after embolism.842 0.ii. Ventilation Distribution.494 0.9 VT Log SD of Blood Flow Mean Ratio 1.877 1.66 1.1 tidal volume.1 40.2 8. and to as much as 17 percent of cardiac patient 7 (Table 4).t % 0 0.68 2.7 6. X-ray changes scored as: 0 = no abnormality.3 24.88 1. to the and unperfused the distributions (Table 4). distributed to lung a significant units with 02 method x-ray abnormali- and to the shunt ratios lower than 1 (between 1 and 0.19 VA/Q Distribution 0.6 3.3 5. Association between shunt measured with the six inert gas technique and x-ray findings in relation to time elapsed since the occurrence of PE.45 5.815 0.* % Mean Ratio VAJQ Unventilated Lung.10 - I .3 4. + = slight opacities.chestnet.67 Mean ±SD 0.. 4 C03 SHUNT 0.0 DEAD SPACE 58.org/ on 08/10/2013 . Normally.0% DEAD 56.5% 21 SPACE SHUNT 4. with tall and narrow unique peak.2 1/ ii” 001 0.4 © YE DEAD 74 SPACE 1.01 0 z 4 1. with a narrowed perfusion peak around 1 and a shunt of 9 and 17 percent.1 1 1O tOO 10 500 VENTILATION CO 3i% - PERFUSION 1. perfusion and ventilation are distributed to VA1Q around 1.chestnet.1 I 1 ‘I 10 I 100 0.6% 0.7 () VE DEAD 55.I.6 0 0 0 0. Distribution of ventilation and perfusion.2 0. The ventilation peak is shifted to the right.2 0.4 SHUNT 1. have a normal mode of VAJQ ratio distribution.4 0. VE = minute ventilation (Limmn).5% CO 5.8 0. patients 1 and 2.3 DEAD YE I? SPACE SHUNT 8.01 0. Patients 6 and 7.2 0:01 100 VENTILATION-PERFUSION RATIO i#{243}o FIGURE 2 (A.4 © 1.__J 10 100 VE DEAD 31 SPACE 63. minute CHEST I 88 I 6 I DECEMBER. and B.0 16. a significant part of perfusion is distributed to VA/Q between land 0.1% 26. respectively).4 SPACE 53. Co = cardiac output (Llmin).3 YE SHuNT 0.8 CO 4.2 0. Dead space is markedly increased.2% DEAD SHUNT 40.0 VE DEAD I’ 20 CO 4. have no shunt but a marked enlargement of the perfusion peak. As a conseventilation 1985 833 Downloaded From: http://journal. lower). By contrast.‘.01 01 10 IA I 1.1 / / \\.4% 1.4 YE CO 13 SHUNT 6.publications.6 08 I S 0 0 0 0 0.2 W.e / ‘OI OI’ 1 0.‘ 0.9% 35.5% 1.0 to E 0.1.4 PATIO YE 14 SPACE 5. quence of the increased dead space.8% 11 SPACE C E 1.4% A 0.4 CO 5.3% 1. respectively.2 0 001 0.0 SHUNT 4. Anatomic dead space assumed from body weight was markedly smaller than inert gas dead space (27 percent vs 52 percent. studied within the 48 first hours. studied later. upper.4 1.6 o -V #{149}#{149}‘t I 0. Thus. according to the ventilation! perfusion ratios in a normal subject (0) and 7 patients with acute PE (ito 7).6 o. 0 I 0.0 I S 0 /.1 I II 1/ 10 0. (dead space) was markedly high (52±10 percent) and accounted for as much as 63 percent of YE in patient 3 (Table 4). No shunt exists.4% 0 z 4 1.8% 1.0% 1. VA/Q distribution. VA/Q diagrams in Figure these different compare them 1. hours film patterns of to normal. and each had moderate sion from vasoactive zation nique shunt. in whom a venous admixture inert The of the 16 percent of cardiac increased zone may output. who event was and had 2 make VA/ it possible distribution example.A/ x-ray peak the there is substantial dispersion of the perfusion but no shunt. eg. approximately chest x-ray film. and venous addition. drugs. DIscUssIoN we found however. hemodynamic depresbut right none heart required catheteri- overperfusion.46 intracardiac membrane. mismatch in perpneumoconstriction lung that remain in experimental is attributed to reflex Bronshown in with the multiple to determine the ‘s’A/Q gas elimination techimpact of pulmonary and their cardiac hypox- demonstrated thromboembolism has mismatch. studied normal within chest level. and impaired In this study. The low the basis of an lung. patients or in the severity of the embolism long delay between initial symptoms investigation.9 such or pneumoconstricsubsequent volume loss loss occurs. a mean 1.5 In terpreted hypoxemia P(A-a)0.” In each of these patients the analysis showed emboli perfusion It has could areas fused.3’8 (2) ventilation and (3) shunting of blood. of lung units mismatching). perfusion shunting contributor (Fig of lung was mainly to perfusion from ie.’#{176} The clinical signifi- perfusion from of these measurements are since they are influenced diffusion. values predicted This suggests for hypoxemia several For 24 of the find- transit time of blood vascular bed.’” with value centered ratio of In contrast. VAJ of patients percent) shortly with but automated mismatching. Pulmonary al’#{176} found patients’ in Acute they could if they the pulmonary contribution to the Embolism (Huet Downloaded From: http://journal.22). factors the acute embolism.’4 also been consistently emia was depending elapsed caused by different on chest x-ray since the PE. early. contribution lung became if atelectasis In may then be responsible volume in the embolic data suggest that when of blood unventilated Shunt only loss units. 1 and volume mechanisms.” tion lung Our This bronchoconstriction for lung. experimental was in and infiltrates percent. on the time early followVA/ In patients low VA/C a significant human pulmonary embolism. in most of our patients an increased venous admixture (0. usually autopsy. difficulty in in discovering the selection and variations in We its of to the clinical inin tial portion in patients no shunt and confirmed documenting out a definite VA/ ratios increased the conclusion This was most 1 and 2.’#{176} In experimental PE is at temwere of a!) causes developed. a large of the The contrast and to patient embolic ings.7’#{176} An embolus could theoretically decrease in diffusing capacity by reducing area of the alveolar capillary membrane gas exchange flow through the measured PaO. diffusing capac- and was above 20 IJmin in patient ventilation was also consistently VA/ 2.’7 a group difficult to deterby shunt. values distributions.org/ on 08/10/2013 . of ratios (ie. porarily clinical picture.chestnet.. method) in the absence of a parallel increase in Qs/t (inert gases method) indicated that VAIQ of their studied was the found VA/ mismatching hypoxemia. 2. a significant or other our studied proposed hypoxemia series 48 to to hypoxemia shunt enters the discoid atelectasis has already been studies.88 ± 1. The high incidence of in patients with measurable shunts emphasized. studied one week after onset of symptoms and presenting with atelectasis a shunt of 9 is close to VA/Q were nearly from the that in our recent impaired patients. artery.83 ± . we examined analysis of ventilation-perfusion lung scans in II patients with acute pulmonary emboli and normal chest x-ray findings. In patient 6.345’#{176}but its believed cause was that part related to consistently demonstrated etiology remains unclear.publications. on a agreement with cal studies. His normal. hypoxemia with without through 2). in regard past studies to associated and mismatching dispersion in these patients by of perfusion.” canine lung areas remote that had an abnormal with also be caused contiguous This has relative been suggested by selective to the embolic been and from those matching that this affected by the of ventilation to \TA/ large (mean vascular obstruction 55 nonlethal acute pulmonary embolism their first symptoms. or the intrapulmonary cause a the surface available for ratios (mean.(‘‘E) was consistently increased (mean VE 17±7 L/min) following ity across to perfusion at to in either acute the the PE: (1) a decreased 0. despite accounted for a substanapparent virtually of 19 gas study Hypoxemia has been acute PE. We combined inert relative after hypoxemic (mean PaO.4 and a shift of ventilation away from the unperfused lung has been demonstrated in man after the temporary occlusion of one pulmonary ing embolism. cance mine. distribution (. We found that pulmonary findings and studied due bronchoconstriction choconstriction or pneumoconstriction. The shifted with mean peak of to the high dispersion pulmonary mismatching. But identical actual diffusion a finding and clinito the ‘. not a cause or by decreasing the a reduced pulmonary PaO.67). impaired diffusion. All were 67 ± II). these characteristics were found in patients hours or more after the initial symptoms. on the hypoxemia. Three major mechanisms have been explain 834 shunt as a major reported when Wilson lower et their Hypoxemla contributor to hypoxemia alveolar collapse is seen that P(A-a)O. withon (Fig 2).” This computer was have changes of very low be explained to the nonembolic a recent admixture. Dependsupport part of initial capacity. with VA/Q ratios (Fig 2). and Alpert JS. Tremblay thromboem- up to 31 L in patient pulmonary CHEST I 88 I 6 I DECEMBER. Pulmonary obstruction produced pulmonary Measured space. As already A/ of lung volume attributed to therefore increasing ing on the should the loss develop should the hypoxemia be shunting.” be a critical or in recent experimenwas found between the moderate magnitude and of V dispro- clinical circumstances. but their right atrial pressures were in the normal range. ated with their acute PE. Cardiovasc 2 Moser 115:829-52 3 Robin Alveolar Med 4 Sasahara Clinical Pulmonary Forkner 262:283-87 embolism. in the areas of for right-to-left shunts from the consolidation. and shunt however. they had low PO. Morse studies pulmonary RL. of cardiac function further intrapulmonary until atelectasis develop. however. 1985 835 Downloaded From: http://journal. Similarly. shifted 59 ± to the dead 10 right.3 The patent foramen ovale cannot be entirely our patients.’6 distributions remain changed. suffered from of hypoxemia recorded in our that an additional factor may Except patient 1. with VA/Q the early between occurrence 10 and 100.encouraged to breathe 80 to ifi percent of their ventilation 2. reperfusion edema alveolar-capillary permeability flow to the still-perfused lung tion for shunting in acute PE.” in patients None or from increased blood is an alternative explanaand animal reports free of our alveolar edema has experiments. no shunt was demonstrated in the study by Caldini6 when mechanical ventilation with periodic sighs was used. edly increased. depression tributor of cardiovascular to the hypoxemia function is a major in acute PE. all of our hemodynamic changes associBecause of their low cardiac (27 ± 5 mm Hg). We are indebted to Robert Herigault and her excellent technical assistance. to 40mm Hg. with using and a mean both the the value expired of of predicted inspiratory capacity. Fiorella Delcampe manuscript. Dis Natural 1975. consistently minute in all pawas markthe peak of gas exchange AA. J JJ. increased ventilation 3. doubt role recently Assuming contributed of a low PO. Neverthein these individuals are an acutely ill patient is caused by VA/Q or other indications when patent foramen ovale6’7 or intrapulmonary the opening of precapillary shunts. The major limitation to our findings number of patients studied and that. 52±10 percent) anatomic dead space to the to the ventilation of dead space. within shunt have the inert gas study could not individuals over time.88. calculated that a marked inwould result from an increase REFERENCES 1 Dalen Prog of PiO. initial Only when has acute mismatch. in Sidd embolism. percent) excretion soluble gases (inert gas dead was higher than the predicted (27 ± 4 percent). pulmonary are distinctly been shown in convincing clinical edema rare. DM.’6’7 of PE with acute of left heart patients had disease x-ray disappeared after a few hours. we believe that firm enough to suggest PE. shunting opening shunts opening ruled in of a from of a out in excluded explanations are intracardiac observations made less. individuals. and to and Maryse Gu#{233}rinfor preparation of the Bower. the same evidence of acute lung. In addition space. corresponding unperfused lung. Rev Croteau Respir embolism. The opening of precapillary shunts never has been demonstrated in patients tal studies. N EngI GM. Therefore.org/ on 08/10/2013 . Initial therapeutic measures be aimed functional function at preserving residual may also rapid or. these authors crease in predicted PaO. ED. repeatedly However. mentioned. In dog experiments. CO. 1960. permitted the Repeated patient the is the small for practical be repeated to document changes in VA/Q and A larger number of patients would use of stronger statistical testing to and in the relationship determinations would have between the results that hypoxemia atelectasis between further atelectasis of gas exchange supported demonstrate shunting. Travis Dead space was tients. history 17:259-70 of pulmonary Am PA. Cannilla physiologic in clinical JE. PE high et al of that patients studied within the first 48 hours following had a supplemental mode of ventilation.chestnet. and con- JE. were mismatching CONCLUSION portionate patients. of shunt Dantzker would by The or low and potential VA/ The pulmonary tern sion primary cause embolism of the appears initial hypoxemia a disturbed Simultaneous contributes in acute patdepresto hypoxbecome of lung to be of ventilation to perfusion. but important volume loss shunting does not or another cause for any level emphasized VA/ has unACKNOWLEDGMENT: Francoise Veyssi#{232}re for Mrs. if possible. Bromberg Jr. thus decreasing the amount of focal alveolar collapse. worsen patients to the degree This suggests the hypoxemia. This explains why PaO. especially in those with the largest shunts. and this no hypoxemia. been that to their emia. Consequently. CE. KM. Dantzker have such already demonstrated a high mode.” and no relationship shunt and PAP in our patients. (Bohr. It may be that significant loss of lung volume and alveolar early collapse to those developed of pulmonary in lung vascular of these from alteration zones of areas corresponding and that shunting. clinically significant shunting was found only in those with atelectasis and infiltrates (Fig 1). output. values in this study were significantly reduced despite relatively mild degrees of’/ mismatch and shunt. Subclinical cannot be Remaining acute PE edema in nonembolic areas of the focal pulmonary edema.publications. In the patients we studied. Dis 1977. of cardiovascular management. reasons. chestnet. GE. 20:10-20 in pulmonary and AppI Ann arterial 1965. 3:77-80 Wings a clinical A. Rev Harf Wagner after 42:92-103 Bower gas Respir A. Lemaire gas elimination. exchange (vol M. Desfonds factors influencing with RB. 75:473-77 Dantzker DR. 1975. Duroux P. Physiol West J 7 Gazzanica and Dalen Sasahara in JE. Sanchez pulmonary Care AK. distribubreathing GC. West ratios Invest Thomas embolism. ed. 5 Kafer disease. J Appl F JB. vs reflex dogs. Bourdarias without ER. 22 D’Alonzo nisms embolism. of alveolar in D.publications. SE. obliterative 59:20316 of gas exchange pulmonary Ventilation-perfusion Pulmonary J Clin 1980:219-62 836 Hypoxemia in Acute Pulmonary Embolism (Huef of a!) Downloaded From: http://journal. in pulmonary 50:481-91 P. Fevens BS. Paradoxical AA. New In: York: in pulAA. H. 16 Fleischner monary Observations Sasahara York: on the Crone gas microembolism 30 on arterio venous J Thorac embolism. Continuous subjects 54:54-68 Sutton the 1974. Gurdjian embolism PD. exchange 1978. Evaluation of major JW. Physiopathol Identification embolization. 1969. the Duroux constriction mechaBr Med ventilation dog. Allen shunt D. Observations pulmonary in acute DH. 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