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Some patients with chronic pulmonary embolism causing severely symptomatic pulmonary hypertension have been managed by heart-lung transplantation with an associated hospital mortality of 24%. To allow comparison with pulmonary thromboendarterectomy (PTE), we have reviewed the hospital morbidity and mortality in 149 consecutive patients. From 1 October 1984 to 18 September 1989, these patients underwent PTE utilizing a standardized procedure consisting of median sternotomy, cardiopulmonary bypass, deep hypothermia and circulatory arrest for bilateral PTE in 91% (136/149) of the procedures with 7.4% (11/149) and 1.3% (2/149) undergoing right or left PTE, respectively. Ventilator dependency (greater than or equal to 5 days on respirator) occurred in 28.3% (41/146). Hospital mortality (death within 30 days or in hospital) was 11.4% (17/149). The most common causes of death were respiratory and multiorgan failure, 10 (59% of deaths) and acute pulmonary hemorrhage, 3 (17% of deaths). We conclude that PTE with an operative mortality of half that of heart-lung transplantation (11.4% vs. 24%) should be the procedure of choice for significantly symptomatic chronic pulmonary embolism. Furthermore, the hazards of immunosuppression and chronic graft rejection are avoided.

Objective. —To determine the frequency of pulmonary embolism in patients admitted for treatment of deep venous thrombosis. Design. —An open, multicenter, dose-ranging study to assess the safety and pharmacokinetic characteristics of tissue-type plasminogen activator in deep venous thrombosis and pulmonary embolism. Perfusion and ventilation lung scans, chest roentgenograms, and venograms (in deep venous thrombosis) or pulmonary angiograms (in pulmonary embolism) were obtained before and 24 hours after inception of therapy. Heparin therapy was then administered. Settings. —Five tertiary-care hospitals. Patients. —All patients with suspected deep venous thrombosis or pulmonary embolism seen from August 1987 through November 1988 entered the study if they met inclusion criteria and if the diagnosis was confirmed by venogram (deep venous thrombosis) or pulmonary angiogram (pulmonary embolism). Interventions. —All patients received tissue-type plasminogen activator followed by intravenous heparin therapy. Main Outcome Measures. —The primary measure was the frequency of pulmonary embolism in patients with deep venous thrombosis who had no symptoms of pulmonary embolism. This was not the original purpose of the study but emerged as an important finding as the data were analyzed. Results. —Nearly 40% of patients with deep venous thrombosis who had no symptoms of pulmonary embolism had evidence of pulmonary embolism based on ventilation-perfusion scan and chest roentgenogram findings. Conclusions. —Because all of those considered to have embolism had so-called high-probability scan results, the frequency of embolism reported likely represents the minimum incidence of pulmonary embolism in patients with deep venous thrombosis who have no embolic symptoms. These data emphasize that venous thromboembolism is one disorder. ( JAMA . 1994;271:223-225)

Excerpt To the Editors:The meta-analysis reported by Hommes and colleagues (1) is likely to rekindle a long-simmering controversy about the relative safety and efficacy of subcutaneous compared wit...

There is widespread acceptance of the thesis that in a patient with suspected embolism, a normal perfusion lung scan excludes the diagnosis of acute pulmonary embolism. However, limited published data exist which validate this thesis. We have explored this question by longitudinal follow-up of 68 patients who were referred for lung scanning to rule out embolism and proved to have normal perfusion lung scans. Risk factors for venous thromboembolism among these patients were similar to those reported in prior series of patients with pulmonary embolism. Our data support the widely-held views that: 1) a normal perfusion lung scan excludes the diagnosis of clinically significant pulmonary emboli; 2) the diagnostic work-up for suspected pulmonary embolism need not extend beyond a normal perfusion scan; 3) anticoagulant therapy can be discontinued after a normal perfusion scan, except in the presence of documented venous thrombosis; and 4) a normal lung scan has the same value in ruling out embolism in man as does a normal pulmonary angiogram.

Nine patients with moderate pulmonary emphysema, six of PiZ phenotype and three of PiM phenotype, have received a single intravenous infusion of alpha-1-proteinase inhibitor (human) (A1PI), in a dose of 60 mg/kg over a 30-minute period. They also received a tracer dose (300 μCi) of 131I-labeled A1PI. No active or passive immunization against hepatitis was given. No acute toxicity was observed. Compared with baseline data, significant elevations of serum A1PI (measured both antigenically and as anti-elastase activity) occurred, with a serum half-life approximating 110 hours. Bronchoalveolar lavage fluid, obtained 48 hours after infusion, reflected a significant increase in A1PI concentration versus baseline bronchoalveolar lavage fluid values. Serial gamma camera images of the lungs confirmed persistence of enhanced lung radioactivity for several days. Urinary desmosine excretion did not change following A1PI infusion. During the period of follow-up thus far, no patient has had chronic toxicity, results of liver function tests have been stable, and there has been no development of hepatitis B antigen or antibodies to hepatitis B surface or core antigens.

Lavage limited to an isolated lobe was performed on multiple occasions using a cuffed fiberoptic bronchoscope in a patient with alveolar proteinosis. Sequential ventilation-perfusion scintiphotoscans were used to preselect and follow the functional behavior of the lavaged lobe. Lavage led to functional improvement. The technique of fiberoptic bronchoscopic lobar lavage is simple and may find application in patients in whom lavage of an entire lung may be hazardous.

Pulmonary thromboendarterectomy is an innovative surgical technique for treating pulmonary hypertension caused by chronic thromboembolism. The procedure uses cardiopulmonary bypass but necessitates dramatically longer bypass times than coronary artery bypass grafting or valve operations. We prospectively evaluated 22 patients undergoing pulmonary thromboendarterectomy to determine the incidence of delirium and its relationship to certain preoperative and postoperative medical variables as well as to duration of cardiopulmonary bypass, deep hypothermia, and circulatory arrest. Delirium occurred in 77% of patients with a peak incidence around 72 hours postoperatively. No preoperative or postoperative medical variable distinguished delirious from nondelirious patients. Total bypass time was not associated with delirium, but deep hypothermia time and total circulatory arrest time were both strongly associated. Overall prediction of delirium was 81% when total circulatory arrest time was considered. Further analysis suggested that a total circulatory arrest time greater than 55 minutes was both sensitive to (82%) and specific for (80%) delirium. Implications for the mechanism of postcardiotomy delirium and future research directions are discussed.

To assess the response of the right and left ventricles to the subcutaneous administration of terbutaline sulfate, a beta-2 selective agonist, we evaluated 14 patients with chronic obstructive pulmonary disease (COPD) with equilibrium radionuclide angiography (RNA). Prior to injection, eight patients (57%) had an abnormal right ventricular ejection fraction (RVEF), four (29%) had a low left ventricular ejection fraction (LVEF), and three (21%) had low ejection fractions of both ventricles. After terbutaline injection, RVEF increased in 13 of 14 patients (93%) by 17 +/- 8% (p less than 0.001) while LVEF increased in all patients by 15 +/- 7% (p less than 0.001). Both left and right ventricular end-diastolic volumes decreased (p less than 0.01), while stroke volume was unchanged. Cardiac output rose by 0.8 +/- 1.3 L/min (p less than 0.05), primarily due to the increase in heart rate (10 bpm, p less than 0.001), since stroke volume did not significantly change. We conclude that in patients with COPD subcutaneous terbutaline has significant beta-1 cardiac effects; it increases the heart rate and decreases cardiac size.

In 1980 we described bilateral pulmonary thromboendarterectomy with median sternotomy, cardiopulmonary bypass, deep hypothermia, and circulatory arrest for the relief of pulmonary hypertension caused by chronic pulmonary embolism. In our subsequent experience, which totals 41 patients, we have identified three groups of patients characterized by differences of intraoperative management In Group A (N = 16) myocardial protection consisted of single-dose crystalloid cardioplegia followed by pericardial irrigation with cold saline. Extrapericardial dissection of the pulmonary arteries was performed. Group B (N = 7) was treated the same as Group A except for the substitution of saline slush contained in a laparotomy pad for iced saline. In Group C (N = 18) myocardial protection was single-dose blood cardioplegia followed by the application of a specially designed cooling jacket to the right and left ventricles. Another modification was that of intrapericardial dissection of the pulmonary arteries with extension of the dissection into the hilar tissues without entrance into the pleural spaces. The hospital mortalities of Groups A, B, and C were 18.7%, 14.3%, and 5.5%, respectively (not statistically significant differences). However, other statistically significant differences (p

To study the penetration of alpha 1-proteinase inhibitor (A1Pl) into the lungs of healthy dogs, 83 mg/kg of active A1Pl was administered intravenously over 30 min followed by a bolus of 131I-A1Pl. Animals were lavaged 2 to 72 h after infusion, sequential gamma camera scans were acquired, and urine was analyzed for the excretion of desmosine. After a distribution phase, infused A1Pl left the bloodstream with a half-life of 103 +/- 24 h. Analysis of plasma antiprotease activity demonstrated preservation of function of the infused A1Pl. Lavage fluid A1Pl concentration and activity were significantly increased 24 h after infusion. Gamma camera scans demonstrated that lung, liver, and spleen acquired 131I-A1Pl similarly; radioactivities per gram of tissue of these organs were similar at autopsy. Excretion of desmosine did not decrease from a baseline of 157 +/- 59 nmol/24 h after A1Pl infusion, indicating no effect of A1Pl infusion on background elastolysis. These data suggest that intravenous administration of A1Pl can raise lung antiproteinase levels within 24 h despite the absence of preferential uptake by the lung of the infused protein.

To determine whether postural changes in ratio of upper to lower (U:L) zone pulmonary blood flow reflect pulmonary arterial pressures, we used pulmonary perfusion photoscintigraphy to study 12 normal subjects and 10 patients with precapillary pulmonary hypertension (eight classified as "primary" and two as thromboembolic). All patients underwent right-heart catheterization and measurement of pulmonary arterial systolic, diastolic, mean and capillary (wedge) pressures. The distribution of perfusion was then assessed in the supine and erect positions after i.v. injection of technetium-99m-labeled, macroaggregated albumin. Perfusion distribution was corrected for lung volume by xenon-133 equilibrium ventilation scans. In normal subjects, the U:L lung zone perfusion ratio decreased by 70.7 +/- 12.2% with the change in position. The patient group differed (p less than 0.0001) from normal subjects in that there was only a 19 +/- 17.4% shift of U:L ratio with the postural change. The mean pulmonary arterial pressure in the patient groups was 50 +/- 24.2 mm Hg. The postural change in U:L zone ratio correlated significantly with the mean pulmonary arterial pressure (r = -0.84, p less than 0.01) pulmonary arterial systolic (r = -0.83, p less than 0.01) and diastolic pressures (r = -0.72, p less than 0.05) and with the pulmonary vascular resistance (r = -0.74, p less than 0.02). No correlation was found with other hemodynamic, spirometric or blood gas data. We conclude that the postural shift in U:L ratio warrants further exploration as a noninvasive approach for detecting and quantifying pulmonary hypertension.

Major vessel chronic thromboembolic pulmonary hypertension is potentially remediable by thromboendarterectomy. The diagnosis often has been delayed because a lung perfusion scan demonstrated modest defects thought to be incompatible with severe vascular obstruction. To define the relationships between perfusion scan abnormalities, angiographic findings, and hemodynamic data, we analyzed 25 consecutive patients with chronic major vessel thromboembolic pulmonary hypertension who subsequently underwent thromboendarterectomy. We found that the perfusion lung scan consistently caused us to underestimate the severity of pulmonary arterial obstruction as defined by pulmonary angiography. Furthermore, there was no significant correlation between the severity of hemodynamic compromise and the extent of obstruction defined by perfusion scan or angiogram. These findings suggest that, when pulmonary hypertension is known or suspected, the diagnosis of correctable, chronic major vessel obstruction should be pursued by angiography and hemodynamic assessment even though the perfusion scan may demonstrate only two segmental defects.

To evaluate the utility of transthoracic needle aspiration biopsy (TTNAB) following negative fiberoptic bronchoscopy (FOB) in a patient with a solitary pulmonary nodule (SPN), we reviewed the records from 262 patients who had undergone TTNAB over an eight-year period. Fifty-eight patients had a SPN and met the criteria for inclusion in this series. Twenty-five of these (43 percent) were diagnosed by TTNAB; 24 had malignant lesions; one had M tuberculosis. Of the remaining 33 patients, 18 went on to definitive diagnostic procedures (surgery, repeat FOB or TTNAB). Nine of these patients had a malignancy. Fifteen patients were followed long-term; one was diagnosed with carcinoma two years after the initial work-up. Carcinoma was not found in any patient under 40 years of age. A benign lesion was diagnosed by TTNAB in only two patients. We conclude that TTNAB is a valuable procedure in the evaluation of patients with a SPN and negative FOB. While a negative FOB and TTNAB do not assure that the lesion is benign, a complex of variables influences the decision regarding thoracotomy vs careful follow-up.

The goal of heparin therapy in deep vein thrombosis is to prevent thrombus extension. The relationship between thrombus extension and the results of coagulation tests used to monitor heparin therapy is unclear. To explore this relationship, we studied the effect of several heparin regimens on the accretion of indium-111-labeled platelets on fresh venous thrombi, as detected by gamma imaging, and monitored the activated partial thromboplastin time (APTT). Six dogs were treated with a 300-U/kg bolus of heparin followed by a 90-U/kg/hour heparin infusion, a dose of heparin sufficient to increase the APTT to levels greater than eight times baseline (APTT ratio); platelet accretion (thrombus imaging) occurred only after the heparin effect was reversed with protamine sulfate. Nineteen dogs were treated with a 150-U/kg bolus of heparin followed by a 4-hour, 45-U/kg/hour heparin infusion; a thrombus was demonstrated only after protamine injection in 12 (mean APTT ratio 1.3 +/- 0.19) and before protamine injection in seven. In thirteen of these 19 dogs, 30 minutes separated the platelet injection from heparin therapy, while in six this duration was less than 30 minutes. In four of these six dogs, thrombi were demonstrated before protamine therapy and at APTT ratios greater than 3.0. Finally, 10 dogs were treated with a 100-U/kg bolus followed by a 3-hour, 50-U/kg/hour heparin infusion, after which the APTT was allowed to return to baseline values spontaneously. In all 10 dogs, a thrombus was demonstrated only after cessation of the heparin infusion, and at a mean APTT ratio of 1.4 +/- 0.15 times baseline. These results suggest that, except with very early platelet injection, platelet accretion by thrombi is consistently inhibited by heparin at APTT ratios greater than 2.5. Platelet accretion by venous thrombi occurs within narrow limits of heparin effect as reflected by the APTT.

The time course and locus of radiolabelled fibrinogen (RLF) incorporation into venous thrombi were studied in dogs. Incorporation of radiolabelled fibrinogen (RLF) into fresh venous thrombi induced in vivo was studied by serial autoradiography, well-counting and surface counting. Autoradiographs disclosed diffuse incorporation of RLF into thrombi formed before and after RLF injection. Well-counting data also reflected thrombus RLF accumulation in both instances, although this accumulation was discernible earlier in thrombi induced in the presence of circulating RLF. Thrombi induced prior to RLF injection were detectable by surface counting after six hours. These studies support the potential value of RLF in detecting human venous thrombosis but also point out the limitations of the technique as well as questions which require clarification.

Patients with fibrosing mediastinitis causing obstruction of pulmonary veins and arteries may present with many of the historic, physical, and laboratory findings of patients with pulmonary hypertension due to chronic thrombotic obstruction of major pulmonary arteries. Because the latter is subject to surgical correction, and the former is not, it is important to differentiate between the two and to be aware of the similarities in presentation. Three patients with pulmonary hypertension due to compression of pulmonary veins and the right pulmonary artery by fibrosing medias tinitis are presented who illustrate these points. A review of the literature documents other instances in which vascular involvement due to fibrosing mediastinitis has mimicked other types of pulmonary hypertension.

To assess the value of fiberoptic bronchoscopy and transbronchial biopsy for evaluating patients suspected of having tuberculosis, we reviewed the records of 56 patients (1974–1980). All patients (1) were clinically suspected of having active tuberculosis; (2) had an abnormality on chest roentgenogram consistent with tuberculosis; (3) had an absence of acid-fast bacilli on three sputum smears or an inability to produce sputum; (4) had undergone fiberoptic bronchoscopy and transbronchial biopsy. The evaluations included fiberoptic bronchoscopy with collection of bronchial washings and brushings, and transbronchial biopsy and postbronchoscopy sputum specimens. Thirteen patients subsequently underwent percutaneous needle aspiration and one underwent thoracotomy. Evaluations were diagnostic in 29 of the 56 patients (52 percent). Diagnoses were mycobacterial infection in 22 (39 percent) and other disease processes in seven (13 percent). Fiberoptic bronchoscopy and transbronchial biopsy provided a diagnosis when sputum cultures obtained before bronchoscopy were negative for Mycobacteria in 11 (20 percent) patients. Immediate diagnoses were made from microscopic specimens obtained from 11 of 23 (48 percent) fiberoptic bronchoscopy and transbronchial biopsy procedures on patients with previously undiagnosed mycobacterial infection. Transbronchial biopsy had the best yield for a microscopic diagnosis. On culture, bronchoscopy specimens had a lower yield (10 of 23 or 44 percent) than sputum specimens obtained before bronchoscopy (14 of 21 or 67 percent) probably due to the inhibition of mycobacterial growth by tetracaine. Of the patients in whom evaluation proved nondiagnostic, 17 of 27 were lost to follow-up; therefore, a definitive statement regarding the number of false negative evaluations is not possible. Fiberoptic bronchoscopy and transbronchial biopsy (FFB/TBB) is a useful procedure in evaluating patients with negative smears who are clinically suspected of having tuberculosis. It can improve the ability to document active tuberculosis, provide a sensitive means of making an immediate diagnosis, and uncover other disease processes presenting like tuberculosis.

Fourteen patients with adult respiratory distress syndrome were admitted to the medical intensive care unit and received bedside heart catheterization with the use of a balloon-tipped, flow directed catheter. Four of the 14 (29 percent) were found to have left ventricular failure (LVF), defined as a pulmonary artery wedge pressure greater than 12 mm Hg. Analysis of the standard clinical and laboratory data demonstrated no criteria which could differentiate those patients with LVF from those without. Three of the four patients indentified as having LVF responded to therapy directed toward LVF with substantial clinical improvement.

Fifteen dogs were studied by perfusion scan, angioscopy and autopsy. In 10, emboli were formed in leg veins and released before study; five dogs were not embolized and served as controls. In controls, angioscopy disclosed no emboli, perfusion scans were normal after angioscopy and autopsy disclosed no emboli. Among the embolized dogs, 23 emboli were identified at autopsy. Perfusion scans disclosed 23 defects, but in three dogs there was a disparity between scan and autopsy localization. Angioscopy identified 21 of the 23 autopsy-defined emboli and localized them correctly; two emboli in vessels less than 1 mm in diameter were not visualized. Angioscopy may provide a useful new approach in animal investigations of pulmonary embolism and perhaps, after additional study, in selected patients.

The purpose of this study was to evaluate a number of equilibrium radionulide methods for analyzing right ventricular size and function, in an attempt to determine if any of a variety of approaches could accurately characterize right ventricular hemodynamics. Fourteen patients being clinically evaluated for coronary artery disease (N = 9), congestive cardiomyopathy (N = 2), valvular disease (N = 2), or intracardiac shunts (N = 1) underwent biplane contrast right ventriculography following gated blood pool imaging. Four radionuclide techniques were examined and included: (1) a semiautomatic edge-detection algorithm using a variable right ventricular region-of-interest and a right ventricular apical end diastolic background; (2) a fixed right ventricular end-diastolic region-of-interest with a C-shaped background; (3) the same fixed end-diastolic right ventricular region-interest with a right ventricular end-diastolic apical background; and (4) both right ventricular end-diastolic and end-systolic regions-of-Interest with a background chosen lateral to the left ventricle. Right ventricular end-diastolic volume was obtained by correcting end-diastolic counts by frame time, the number of processed heart beats, and blood radioactivity. The results illustrate the wide discrepancy among these methods. The correlation coefficients comparing right ventricular ejection fractions by radlonuclide methods 1 to 4 with contrast ventriculography were 0.23, 0.74, 0.40, and 0.42, respectively. For right ventricular end-diastolic volumes, the correlation coefficients were 0.90, 0.72, 0.90, and 0.92, respectively. While these techniques may be useful for analyzing serial changes in right heart function and size, further investigation is needed before right ventricular equilibrium radionuclide techniques can be acceptably utilized in clinical practice, particularly in individual subjects.

Failure of pulmonary emboli to undergo fibrinolytic resolution generates a small but significant patient population progressively disabled by hypoxemia, chronic pulmonary hypertension, and eventual right heart failure. Medical management of these patients has not been effective. In the few patients treated surgically, no clear picture has emerged regarding the most effective surgical approach or the late results. Four male patients with chronic pulmonary embolism were managed operatively. Extrapericardial dissection, cardiopulmonary bypass, deep hypothermia, and intermittent circulatory arrest were utilized to perform pulmonary thromboendarterectomy. All patients, ages 30 to 65 years, had had severe dyspnea with minimal exertion for 1 to 20 years. Angiograms showed 50% to 75% of the pulmonary vasculature to be occluded, with frequent involvement of the segmental arteries. Preoperative pulmonary pressures varied from 60/33 to 74/24 mm Hg. Pulmonary vascular resistance values ranged from 450 to 750 dynes-sec-cm-5. All patients survived the operative procedure. The eldest patient died 3 weeks postoperatively following an acute posteroseptal myocardial infarction. The remaining patients had a 20 to 50 mm Hg decrease in pulmonary systolic pressure with a 50% to 75% reduction in pulmonary vascular resistance. Neither static nor dynamic lung volumes were changed appreciably. Follow-up angiograms in all patients confirmed significant increase in pulmonary perfusion. Each patient had improvement in functional capacity; one is completely asymptomatic. The primary advantage of the surgical approach described is the more complete removal of distally located thrombofibrotic material. The late results suggest that this surgical approach should be considered in the management of patients disabled by chronic pulmonary embolism.

To evaluate the relationship between right and left ventricular function in patients with obstructive lung disease, we studied 10 normal subjects (group 1) and 37 patients with chronic obstructive pulmonary disease by first pass radionuclide angiography. These 37 patients were divided into three groups: nine with mild chronic obstructive pulmonary disease (group 2), 20 with severe chronic obstructive pulmonary disease (group 3) and eight with severe chronic obstructive pulmonary disease and primary left ventricular disease (group 4). In each subject right ventricular ejection fraction (RVEF), left ventricular ejection fraction (LVEF) and ejection fraction during first third of systole (first third LVEF) were calculated. LVEF RVEF First-Third LVEF Group 1 0.60 ± 0.05 0.52 ± 0.03 0.29 ± 0.04 Group 2 0.61 ± 0.08 0.52 ± 0.03 0.29 ± 0.02 Group 3 0.58 ± 0.09 0.46 ± 0.09∗ 0.24 ± 0.06∗ Group 4 0.51 ± 0.06∗ 0.44 ± 0.09∗ 0.20 ± 0.03∗ ∗ p

Tracheal injury continues to be a major complication of the use of cuffed endotracheal/tracheostomy tubes. To assess the determinants of such injury, 22 dogs were studied. It was found that the degree of tracheal injury induced by high compliance-low pressure tracheal cuffs was substantially less than that provoked by low compliance-high pressure cuffs. Marked compromise of tracheal arterial circulation by the high pressure cuffs was demonstrated by vascular injection studies. Tantalum tracheography was useful in assessing the presence of cuff-induced mucosal injury and in delineating tracheal distortion induced by the cuffs. Comparing the cuff compliance (pressure-volume) curve obtained outside the trachea with that obtained inside the trachea can provide a reasonable guide to cuff suitability in terms of the pressure it will apply to the trachea waff. Intercurrent hypotension or the use of positive-pressure ventilation had no discernible influence on extent of tracheal injury. It is cmicluded that high compliance-low pressure cuffs should be used exclusively in clinical practice.

To assess left ventricular (LV) response to supine bicycle exercise, we studied 10 normals (group 1), 10 patients with coronary artery disease (CAD) (group 2), 12 patients with severe obstructive lung disease (COPD) (group 3), and eight patients with both CAD and COPD (group 4) by gated equilibrium radionuclide angiography. Most individuals in all groups also had pulmonary catheter-obtained measurements of LV filling pressures during exercise. Normal individuals increased their ejection traction (EF) during exercise by increasing stroke volume (SV) and reducing end-systolic volume (ESV) without changing end-diastolic volume (EDV); pulmonary artery (PAP) and wedge (PAW) pressures were unaltered. CAD patients (group 2) showed no change in EF with increased EDV, ESV, SV, and PAW. COPD patients (group 3) exhibited decreases in EDV, ESV, and SV, accounting for abnormal EF responses in 6 of 12; PAW was unchanged and the marked elevation of PAP correlated with reduced EDV. Group 4 patients (CAD plus COPD) had abnormal EF responses with increased EDV and ESV without change in SV. Thus an abnormal LV function response to exercise in COPD patients may be multifactorial, thereby indicating the possible need for therapeutic modalities in addition to those employed in alleviating pulmonary parenchymal disease.

Eighteen COPD patients enrolled in a comprehensive, multidisciplinary pulmonary rehabilitation program were randomly assigned to perform either: 1) walking, or 2) ventilatory muscle exercise training (VMT) using a prototype, portable device for isocapnic hyperventilation training. Both groups performed exercise training at home. Twelve patients completed the study and follow-up evaluation (five VMT, seven walkers). Pulmonary function did not change in either group. For the VMT patients, there were modest increases in ventilatory muscle endurance and exercise performance. V ˙ o 2 max and V ˙ Emax increased significantly. For the walkers, only walking endurance time increased significantly. These results indicate that isocapnic hyperventilation exercise training can be performed successfully by COPD patients in an unsupervised home setting and can lead to improvement in both ventilatory muscle endurance and exercise performance. Walking exercise training did not improve ventilatory muscle endurance.

SUMMARY There is no question that a substantial risk of venous thrombosis, pulmonary embolism, and lethal pulmonary embolism exists among patients undergoing urologic surgery. Available prophylactic strategies should sharply reduce this risk. Acceptable treatment options exist for patients who develop thromboembolism despite, or in the absence of, prophylaxis. Accurate diagnosis, however, is essential in order to select the most appropriate option. Finally, it should be noted that in making judgments, the comments provided can offer only general guidelines for patients undergoing urologic surgery. Individual patients may have a particular constellation of circumstances that dictates a rational deviation in decision-making from these general guidelines. However, one pivotal decision from which there should be no deviation without extraordinarily special justification is that some form of prophylaxis for deep venous thrombosis should be offered to all patients undergoing major urologic surgical procedures.

Autopsy findings suggest that lung surfactant is damaged in the adult respiratory distress syndrome. In the present study 225 bronchoalveolar lavage specimens (78 from 36 patients, 1-78 yr old with respiratory failure, 135 from another 128 patients with other respiratory disease, and 12 from healthy controls) were assayed for the lung profile [lecithin/sphingomyelin (L/S) ratio, saturated lecithin, phosphatidylinositol, and phosphatidylglycerol]. Bronchoalveolar lavage fluid was further analyzed for phospholipids and for phosphatidic acid phosphohydrolase, phospholipase A2, and phosphatidylinositol phosphodiesterase activities. A lipid-protein complex was isolated and analyzed for surface activity, and plasma was measured for myoinositol. There were only small differences seen in the recovery of total phospholipid between respiratory failure patients and normal controls. However, in respiratory failure, phospholipids in bronchoalveolar lavage were qualitatively different from those recovered either from normal controls or from patients with other lung disease: the LO/S ratio, phosphatidylglycerol, and disaturated lecithin were low, whereas sphingomyelin and phosphatidylserine were prominent. These abnormalities were present early in respiratory failure and tended to normalize during recovery. Low L/S ratio (less than 2), and low phosphatidylglycerol (1% or less of glycerophospholipids) in bronchoalveolar lavage was always associated with respiratory failure. Abnormal lavage phospholipids were not due to plasma contamination. The phospholipase studies revealed little evidence of increased catabolism of phospholipids. In respiratory failure, the lipid-protein complexes from lung lavage were not surface active, whereas that from healthy controls had surface properties similar to lung surfactant. Phospholipids from patients with respiratory failure were similar to those from respiratory distress syndrome in the newborn. However, the latter condition is characterized by fast recovery of surfactant deficiency and by high plasma myoinositol that suppresses the synthesis of surfactant phosphatidylglycerol and increases phosphatidylinositol (Pediatr. Res. 1981. 15: 720). On the other hand, in adult respiratory distress syndrome, the abnormality in surfactant phospholipids may last for weeks and in most cases is associated with low phosphatidylinositol, low phosphatidylglycerol, and low plasma myoinositol.

Trauma patients are at exceedingly high risk for the development of deep venous thrombosis and pulmo nary embolism. The incidence, pathophysiology, diag nosis, prophylaxis, and therapy of deep venous throm bosis and pulmonary embolism in the trauma patient are reviewed. The type of injury, systemic pertubations, and enforced immobility are important factors in pathogenesis. Patients with lower extremity injuries and spine fractures with paraplegia appear to be at highest risk. Orthopedic devices used to treat these injuries of ten preclude the conventional noninvasive diagnostic modalities. Further, hemorrhagic risk often impacts the judgment regarding the use of prophylactic measures as well as the therapy once deep venous thrombosis is diagnosed. Better data regarding the incidence of ve nous thromboembolism and the applicability of existing diagnostic, prophylactic, and treatment approaches in this population are needed. Accidents are responsible for over 140,000 deaths and approximately 70 million nonfatal injuries an nually in the United States [1]. Most of the fatalities occur within hours of injury as a result of exsangui nation or a lethal head injury, but approximately 20% survive for days or weeks [2], usually in the intensive care unit. The primary causes of late death are sepsis and multiple-organ failure [2]. Increasing evidence, however, suggests that pulmonary embo lism (PE) is now becoming a leading cause of late death, especially in some high-risk groups [3-5]. The increase in the incidence of PE is due in part to improvements in trauma care, which have lowered the early mortality rate [6-8], leaving more patients at risk for late death. In addition, autopsy examina tions, used more frequently to audit trauma care systems [6,9], have documented an increase in clini cally unsuspected deep venous thrombosis (DVT) and PE. This review was prompted because of the appar ent increase in DVT and PE in the trauma popula tion, and because the trauma patient presents very difficult and unique problems compared with the nontrauma patient with regard to the diagnosis, prophylaxis, and treatment of these disorders. In this review, we address the incidence, pathophys iology, diagnosis, treatment, and prophylaxis of DVT and PE in the trauma patient. We do not con sider the entities of fat embolism or pulmonary microemboli as a cause of late pulmonary failure.

A retrospective review of 15 patients with angiographically- or biopsy-documented primary pulmonary hypertension was performed to assess the value of pulmonary perfusion scanning in noninvasively differentiating these patients from those with potentially operable, chronic (large-vessel) thromboembolic pulmonary hypertension. None of the 15 patients with primary pulmonary hypertension demonstrated a segmental or larger perfusion defect whereas such defects have been uniformly present in previous reports of patients with large-vessel thromboembolic pulmonary hypertension. While perfusion scans in primary pulmonary hypertension may show certain abnormalities, the presence of segmental or larger perfusion defects should suggest the diagnosis of potentially correctable, large-vessel thromboembolic pulmonary hypertension rather than small-vessel, obliterative (primary, idiopathic) pulmonary hypertension.

A case is reported of chronic massive thromboembolic occlusion of major pulmonary arterial branches successfully treated with embolectomy and endarterectomy. The historic features, physical signs and pathophysiologic alterations which form the basis for the diagnosis of this disorder are reviewed.

In ten patients with stenosis of the pulmonary arteries, the relative distribution of right and left pulmonary blood flow was related to the localization of the coarctation by angiography and the degree of stenosis. To evaluate the distribution of pulmonary blood flow, the scintillation lung scan after injection of 131 I macroaggregated albumin (MAA) was utilized. Scintillation scanning of the lungs after inhalation of xenon-133 gas was also performed to assess the distribution of ventilation. The relative right to left pulmonary arterial blood flow distribution showed a good correlation with the catheterization pressure gradients and the angiographic findings. The distribution of ventilation was relatively unaffected. In a patient with a precordial murmur that exhibits disproportionate radiation to the axilla and back, an altered distribution of right to left perfusion helps to substantiate the diagnosis of stenosis of the pulmonary arteries. However, if the obstruction is bilateral and of equal degree, the distribution of blood flow may be normal. In patients with isolated acyanotic left to right shunts, the right to left distribution of pulmonary blood flow is apparently unaltered so that a lateral shift from the normal pattern raises the question of stenosis of the pulmonary arteries as an additional lesion. The finding of patchy areas of decreased radioactivity in both perfusion and ventilation lung scans in four of ten patients suggest that there may be a high incidence of emphysema or other lung disease in these patients.

This rather exhaustive review of pulmonary involvement in angiokeratoma corporis diffusum universale, as reported in the literature and as reflected in our three patients, was undertaken to determine whether persistent suggestions of substantial pulmonary parenchymal and vascular involvement were justified. If they were, this would be of substantial interest to all those concerned with the pathogenesis of the chronic obstructive pulmonary diseases and so-called primary pulmonary hypertension. If they were not, the record should be set straight. Our review indicates that the bulk of evidence favors the second conclusion. Pathologic evidence does exist for both pulmonary parenchymal and vascular involvement of some degree, and there is at least a suggestion that the latter may cause pulmonary arterial obstruction in some patients. Further, the possibility that hemoptysis may occasionally result from such direct vascular involvement or from angiectatic lesions in bronchi merits notation and future inspection. But beyond these limited points of interest, the available data would indicate that pulmonary involvement has little clinical or functional impact upon patients with Fabry's disease.

The therapeutic goal in thromboembolism includes not only clot dissolution but also the maintenance of vascular patency. Clinical and experimental evidence, as well as theoretic considerations, suggest that a sequence of clot dissolution followed by a recurrence of thrombosis may occur when fibrinolytic therapy is relied upon exclusively. Concomitant use of anticoagulant drugs appears to offer the best current method for avoiding this sequence. Heparin, because of its mechanism of action, prompt onset of effect and easy reversibility, seems to provide the most desirable anticoagulant supplement to fibrinolytic therapy. To insure that no increased hemorrhagic risk attends this combined thrombolytic-anticoagulant program, the dosage-response characteristics of each type of fibrinolytic agent should be accurately defined. Evidence suggesting antagonism between thrombolytic and anticoagulant agents in vivo has not been encountered but several aspects of this problem require further study. Failure to provide protection against a recurrence of thrombosis after initial fibrinolytic therapy can not only lead to misinterpretation of experimental data regarding the efficacy of fibrinolytic drugs but also may prevent attainment of optimum clinical results in man. While further development of fibrinolytic agents may obviate or alter the need for combination therapy, the concurrent use of fibrinolytic and anticoagulant drugs appears to provide the optimum therapeutic approach to thromboembolism at the present time.

Ten patients with clinical-laboratory evidence suggesting extensive acute or chronic pulmonary thromoboembolism were studied by pulmonary photoscan and by utilizing radiolabeled macroaggregates of human serum albumin (R-MAA) and by angiographic technics. A high degree of correlation between the inactive areas of the radioscan and the nonperfused areas of the angiogram was noted. The radioscan accurately reflected the pattern of arteriolarcapillary blood flow, whereas the angiogram provided precise information regarding the pulmonary vascular anatomy. The two procedures should be considered complementary rather than competitive. Lung radioscanning was found to offer a readily available, safe, rapid and reliable screening technic for definition of nonperfused pulmonary areas. Problems in radioscan interpretation, including “false positives,” lack of anatomic precision and limitations of resolution are discussed. Such problems underscore the basic tenet that accurate evaluation of the radioscan requires that it be viewed in proper clinical context.

The regional distribution of pulmonary ventilation is nonuniform in health and disease. Single and multiple breath techniques have been developed to assess this nonuniformity. Limitations of these expired gas techniques include: identification of only several of the component washout exponentials and preferential representation in this single curve of the better ventilated spaces. In ten normal persons and eight patients we assessed the washout of ventilation by three simultaneous techniques and obtained three clearance curves: nitrogen washout with 100 percent O2; washout of 133Xe at the mouth with 100 percent O2; clearance of 133Xe from the patients' lung fields. A scintillation camera/computer system was utilized to provide clearance curves for 133Xe from selected zones of interest varying from both lungs to sublobar regions. In normal persons all three curves were superimposable. In patients with diffuse lung disease the expired curve for N2 and 133Xe at the mouth were abnormal but superimposable, while the xenon clearance over the lung fields revealed slower and more abnormal clearances. These latter curves provided an appreciation of the presence, localization, and extent of both slow and fast spaces.

1.1. Cases are presented to illustrate sickle cell anemia and sickle variants complicated by pulmonary infarction which could not be explained on an embolic basis. Pulmonary thrombosis is postulated. 2.2. Physiologic mechanisms through which the sickling process may be intensified within the venous blood are discussed. 3.3. It is indicated that the pulmonary vascular bed, aside from being the passive receptor of intensely sickled venous blood, may be subject to intrapulmonary influences which tend to promote the development of thrombosis in situ and infarction. 4.4. Pathologic evidence regarding the occurrence of pulmonary thrombosis and infarction in sickle subjects is reviewed. 5.5. Cor pulmonale may be an ultimate consequence of such multiple recurrent infarctions. The necessity for increased cardiac output may be a contributory factor. 6.6. The importance of maintaining a high index of suspicion regarding this association between pulmonary infarction, cor pulmonale and the sickle states is stressed.