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We conducted a retrospective statistical analysis of the Heyman, Saltzman, Whalen 1966 study of 22 stroke patients treated with hyperbaric oxygen (HBO2)--13 of them one to five hours post-stroke. We examined patients who received HBO2 treatment within seven hours post-stroke. An exploratory logistic regression analysis examining the influence of time post-stroke, time in chamber and dose of HBO2, range 2.02 atmospheres absolute (ATA) to 3.04 ATA, was conducted. Only time post-stroke was a significant influence for recovery, with each passing hour decreasing the chance of at least partial transient recovery by 62% - odds ratio: 0.38 (95% CI: 0.15 -0.95), p = 0.039. In the one- to five-hour group of 13 patients, nine (41% of 22) had recovery or recovery with relapse. This represented 69% (+/- 25% SE) of this time frame. Only two of the nine had permanent recovery. Past six hours poststroke, only one patient (11% +/- 21% SE) had partial recovery with relapse. The other eight past six hours had no recovery at all. The first three hours post-stroke HBO2 administration has the most promise for efficacy and improvement of rtPA therapy. HBO2 may also prove to be a useful challenge pre-rtPA administration to assess the risk-benefit ratio for giving rtPA.

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Seventy-five patients (41 women and 34 men, 20-85 years old) with clinically suspected deep venous thrombosis (DVT) were examined with MR imaging and sonography. In 26 patients, the final diagnosis was acute femoropopliteal DVT. The sensitivity of MR imaging for detecting this disease was 100% with a 95% confidence interval (CI) of 87-100%; the specificity was 100% with a CI of 92-100%; and the accuracy was 96% with a CI of 89-99%. The correspond-ing sensitivity of sonography was 77% with a CI of 53-92%; the specificity was 98% with a CI of 89-100%; and the accuracy was 83% with a CI of 72-90%. In four of the 75 patients, MR images revealed thrombus of the pelvis (n = 1) or calf (n = 3) without femoropopliteal involvement. The estimated prevalence of isolated calf and/or pelvic DVT was 5% with a CI of 1-13%. MR imaging is significantly more sensitive (P = .02) and accurate (P < .01) than sonography in the detection of lower extremity DVT, but there was no difference in the specificity of MR imaging and that of sonography (P = .31).

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The diagnosis and management of acute pulmonary embolism continues to evolve as new diagnostic modalities develop and become refined and as experience is gained with prevention and therapy. This article describes some of the milestones in the development of diagnostic modalities and some useful diagnostic and therapeutic techniques that may become practical in the future.

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PURPOSE: To study the accuracy of magnetic resonance (MR) pulmonary angiography in 20 patients in whom pulmonary embolism (PE) was clinically suspected. MATERIALS AND METHODS: Fourteen patients (group 1) were recruited for the MR pulmonary angiography study before they underwent conventional pulmonary angiography (CPA) based on clinical findings. Six patients (group 2) did not undergo CPA but were considered to have PE on the basis of findings in other studies. MR venography was performed at the time of MR pulmonary angiography in 13 patients. RESULTS: MR pulmonary angiography had a sensitivity of 92%-100% and specificity of 62% for detection of PE. Performance of MR pulmonary arteriography and MR venography in a single examination to demonstrate thrombus in both the arterial and deep venous systems was proved feasible. CONCLUSION: This report describes an early clinical implementation of new MR pulmonary angiographic techniques. Further advances to improve specificity by enhancing sensitivity to slow flow and increasing spatial resolution are necessary before routine clinical use of MR pulmonary angiography is justified.

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STUDY PROTOCOL: Two separate groups of clinical investigators have provided new information and divergent approaches to the management of acute pulmonary embolism (PE). In this position paper, investigators from both groups (Prospective Investigation of Pulmonary Embolism Diagnosis [PIOPED] and Canadian study groups) have utilized the combined scientific database in order to rationalize seemingly polarized diagnostic recommendations into a single practical algorithm. METHODS: An in-depth review established the relative risks of deep venous thrombosis (DVT) and the related accuracy of diagnostic tests. In PIOPED, 640 of 887 patients at risk for PE had either an intermediate probability ventilation/perfusion (V/Q) scan or a V/Q scan probability that was discordant with the prior estimate of probability by clinical assessment. The risk of PE in these patients was 16 to 88 percent (average, 34 percent). In this group, we calculated the probability of PE assuming that tests for DVT had been performed and that 50 percent of patients with PE have detectable proximal DVT. By calculation, 108 in 640 patients of whom the diagnosis of PE was uncertain, would have shown proximal DVT. In 239 of these 640 patients, tests for DVT would have been negative and the risks of PE in these patients is calculated to be less than 10 percent. RESULTS: Therefore, we calculate that in 347 of 640 patients, confident recommendations for treatment or no treatment could have been given without pulmonary angiography. Accordingly, in the PIOPED study group of 887 patients, the need for pulmonary angiography would have been reduced from 640 (72 percent) to 293 patients (33 percent). CONCLUSION: In conclusion, a diagnostic strategy that includes the clinical evaluation, V/Q scan, and evaluation for DVT would decrease the number of patients who require pulmonary angiography from 72 to 33 percent.

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The clinical features and noninvasive tests, including ventilation perfusion (V/Q) lung scans, were assessed in 108 patients with chronic obstructive pulmonary disease (COPD) suspected of having pulmonary embolism (PE). Twenty-one (19 percent) of 108 patients had PE. In the majority of patients, it was impossible to distinguish between patients with and without PE by clinical assessment alone. However, when a high clinical index of suspicion was present, PE was confirmed by angiography in three of three patients, but the V/Q scan was of intermediate probability. No roentgenographic abnormalities distinguished between PE and no PE. There was no difference between the alveolar-arterial oxygen gradients in either group, nor was there evidence of a reduction in the PaCO2 in patients with PE who had prior hypercapnia. Among the 108 patients with COPD, high, intermediate, low, and normal/near normal probability scans were present in 5 percent, 60 percent, 30 percent, and 5 percent, respectively. The frequency of PE in these V/Q scan categories was five (100 percent) of five, 14 (22 percent) of 65, two (6 percent) of 33, and zero (0 percent) of five, respectively. In conclusion, in the majority of patients, the V/Q scan diagnosis is usually intermediate and such patients require further investigational studies, including angiography. However, among the few patients who demonstrated a high probability lung scan, there was a high positive predictive value for PE effectively avoiding the need for further studies. In those patients with low probability or near normal/normal V/Q scans, the negative predictive value was not lower than the general hospital population.

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BACKGROUND: The Prospective Investigation of Pulmonary Embolism Diagnosis (PIOPED) addressed the value of ventilation/perfusion scans in acute pulmonary embolism (PE). The present study evaluates the risks and diagnostic validity of pulmonary angiography in 1,111 patients who underwent angiography in PIOPED: METHODS AND RESULTS: Complications were death in five (0.5%), major nonfatal complications in nine (1%), and less significant or minor in 60 (5%). More fatal or major nonfatal complications occurred in patients from the medical intensive care unit than elsewhere: five of 122 (4%) versus nine of 989 (1%) (p less than 0.02). Pulmonary artery pressure, volume of contrast material, and presence of PE did not significantly affect the frequency of complications. Renal dysfunction, either major (requiring dialysis) or less severe, occurred in 13 of 1,111 (1%). Patients who developed renal dysfunction after angiography were older than those who did not have renal dysfunction: 74 +/- 13 years versus 57 +/- 17 years (p less than 0.001). Angiograms were nondiagnostic in 35 of 1,111 (3%), and studies were incomplete in 12 of 1,111 (1%), usually because of a complication. Surveillance after negative angiograms showed PE in four of 675 (0.6%). Angiograms, interpreted on the basis of consensus readings, resulted in an unchallenged diagnosis in 96%. CONCLUSIONS: The risks of pulmonary angiography were sufficiently low to justify it as a diagnostic tool in the appropriate clinical setting. Clinical judgment is probably the most important consideration in the assessment of risk.

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The diagnostic features of acute pulmonary embolism among 72 patients greater than or equal to 70 years old were evaluated and compared with characteristics of pulmonary embolism among 144 patients 40 to 69 years and 44 patients less than 40 years old. Syndromes characterized by either 1) pleuritic pain or hemoptysis, 2) isolated dyspnea, or 3) circulatory collapse were observed with comparable frequency among patients greater than or equal to 70 years old and younger patients. One of these presenting syndromes occurred in 64 (89%) of the 72 patients greater than or equal to 70 years old. Those who did not show these syndromes were identified on the basis of unexpected radiographic abnormalities, which may have been accompanied by tachypnea or a history of thrombophlebitis. Among the 72 patients greater than or equal to 70 years with pulmonary embolism, dyspnea or tachypnea (respirations greater than or equal to 20/min) occurred in 66 (92%), dyspnea or tachypnea or pleuritic pain in 68 (94%) and dyspnea or tachypnea or radiographic evidence of atelectasis or a parenchymal abnormality in 72 (100%). Complications of angiography were evaluated among patients with and without pulmonary embolism. Major complications of pulmonary angiography among patients greater than or equal to 70 years old (2 [1%] of 200) were not more frequent than among younger patients (6 [1.1%] of 562) (p = NS). However, renal failure (major or minor) was more frequent in patients greater than or equal to 70 years old than in younger patients (6 [3%] of 200 versus 4 [0.7%] of 562) (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

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The purpose of this study was to assess the impact of prior cardiac or pulmonary disease upon the utility of ventilation/perfusion (V/Q) scans in the diagnosis of acute pulmonary embolism (PE). Ventilation/perfusion scans were evaluated among 365 patients with no prior cardiac or pulmonary disease and compared to V/Q scans in 526 patients with prior cardiac or pulmonary disease. Among patients with no prior cardiac or pulmonary disease, PE was present in 117 and PE was excluded in 248. Among patients with prior cardiac or pulmonary disease, PE was present in 140 and excluded in 386. The positive predictive value for PE of high probability V/Q scans among patients with prior cardiac or pulmonary disease, 55 of 66 (83 percent), was not significantly lower than among patients without prior cardiac or pulmonary disease, 50 of 54 (93 percent) (NS). The positive predictive value of low probability V/Q scans was similar with prior cardiac or pulmonary disease, 25 of 182 (14 percent), and without prior cardiac or pulmonary disease, 17 of 113 (15 percent) (NS), as was the predictive value of near normal/normal V/Q scans, 2 of 51 (4 percent), vs 3 of 79 (4 percent) (NS). The sensitivity of high probability V/Q scans, with pre-existing cardiac or pulmonary disease and without, 55 of 140 (39 percent) vs 50 of 117 (43 percent), did not differ significantly. The specificity of high probability V/Q scans with prior cardiac or pulmonary disease and without, 375 of 386 (97 percent) vs 244 of 248 (98 percent) was also similar (NS). In conclusion, the diagnostic utility of V/Q scans for acute PE was not impaired by the presence of pre-existing cardiac or pulmonary disease. Fewer patients, however, with no prior cardiac or pulmonary disease, had intermediate (indeterminate) V/Q scans.

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The history, physical examination, chest radiograph, electrocardiogram and blood gases were evaluated in patients with suspected acute pulmonary embolism (PE) and no history or evidence of pre-existing cardiac or pulmonary disease. The investigation focused upon patients with no previous cardiac or pulmonary disease in order to evaluate the clinical characteristics that were due only to PE. Acute PE was present in 117 patients and PE was excluded in 248 patients. Among the patients with PE, dyspnea or tachypnea (greater than or equal to 20/min) was present in 105 of 117 (90 percent). Dyspnea, hemoptysis, or pleuritic pain was present in 107 of 117 (91 percent). The partial pressure of oxygen in arterial blood on room air was less than 80 mm Hg in 65 of 88 (74 percent). The alveolar-arterial oxygen gradient was greater than 20 mm Hg in 76 of 88 (86 percent). The chest radiograph was abnormal in 98 of 117 (84 percent). Atelectasis and/or pulmonary parenchymal abnormalities were most common, 79 of 117 (68 percent). Nonspecific ST segment or T wave change was the most common electrocardiographic abnormality, in 44 of 89 (49 percent). Dyspnea, tachypnea, or signs of deep venous thrombosis was present in 107 of 117 (91 percent). Dyspnea or tachypnea or pleuritic pain was present in 113 of 117 (97 percent). Dyspnea or tachypnea or pleuritic pain was present in 113 of 117 (97 percent). Dyspnea or tachypnea or pleuritic pain or atelectasis or a parenchymal abnormality on the chest radiograph was present in 115 of 117 (98 percent). In conclusion, among the patients with pulmonary embolism that were identified, only a small percentage did not have these important manifestations or combinations of manifestations. Clinical evaluation, though nonspecific, is of considerable value in the selection of patients in whom there is a need for further diagnostic studies.

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The value of bedside examination and noninvasive tests in the diagnosis of acute pulmonary embolism (PE) among patients with a normal chest radiograph was investigated. Normal chest radiographs were present in 20 of 260 patients (8%) with acute PE and in 113 of 642 (18%) with suspected acute PE, in whom the diagnosis was excluded. A partial pressure of oxygen in arterial blood less than or equal to 70 mm Hg in a dyspneic patient with a normal chest radiograph was more often seen among patients with PE (9 of 17, 53%) than among patients in whom PE was excluded (18 of 93, 19%; p less than 0.01). However, no combinations of blood gases, signs and symptoms were strictly diagnostic. High probability ventilation/perfusion scans among patients with a normal chest radiograph were indicative of PE in only 6 of 9 patients (67%). Among patients with low-probability ventilation/perfusion scans, 8 of 47 (17%) had PE. This study showed that the combination of dyspnea and hypoxia in a patient with a normal chest radiograph is a useful clue to the diagnosis of PE. Although intuition suggested that ventilation/perfusion scans would yield better results in patients with a normal chest radiograph, the ability to diagnose PE by ventilation/perfusion scans in this subset of patients was not enhanced, except by a reduction of the percentage of patients with intermediate probability scans.

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In a previous study of normal subjects exercising at sea level and simulated altitude, ventilation-perfusion (VA/Q) inequality and alveolar-end-capillary O2 diffusion limitation (DIFF) were found to increase on exercise at altitude, but at sea level the changes did not reach statistical significance. This paper reports additional measurements of VA/Q inequality and DIFF (at sea level and altitude) and also of pulmonary arterial pressure. This was to examine the hypothesis that VA/Q inequality is related to increased pulmonary arterial pressure. In a hypobaric chamber, eight normal subjects were exposed to barometric pressures of 752, 523, and 429 Torr (sea level, 10,000 ft, and 15,000 ft) in random order. At each altitude, inert and respiratory gas exchange and hemodynamic variables were studied at rest and during several levels of steady-state bicycle exercise. Multiple inert gas data from the previous and current studies were combined (after demonstrating no statistical difference between them) and showed increasing VA/Q inequality with sea level exercise (P = 0.02). Breathing 100% O2 did not reverse this increase. When O2 consumption exceeded about 2.7 1/min, evidence for DIFF at sea level was present (P = 0.01). VA/Q inequality and DIFF increased with exercise at altitude as found previously and was reversed by 100% O2 breathing. Indexes of VA/Q dispersion correlated well with mean pulmonary arterial pressure and also with minute ventilation. This study confirms the development of both VA/Q mismatch and DIFF in normal subjects during heavy exercise at sea level. However, the mechanism of increased VA/Q mismatch on exercise remains unclear due to the correlation with both ventilatory and circulatory variables and will require further study.

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An accurate diagnosis of pulmonary embolism is essential to prevent excessive morbidity and mortality from lack of therapy or inappropriate anticoagulation. Clinical signs and symptoms are reported to be nonspecific, although published studies do not allow calculation of true specificity. Since certain clinical characteristics or groups of findings may be sensitive enough for pulmonary embolism, the diagnosis is unlikely in their absence. Ventilation-perfusion lung scanning has high sensitivity but variable specificity for pulmonary embolism. Patients with scans showing multiple segmental or lobar perfusion defects with normal ventilation have a high probability of pulmonary embolism. Scans with less extensive perfusion abnormalities or matching ventilation defects do not reliably exclude pulmonary embolism. Pulmonary angiography is the most definitive procedure for diagnosing pulmonary embolism. Digital subtraction pulmonary angiography and radiolabeled platelet scanning are promising but require more extensive validation before routine use.

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To investigate the effects of both exercise and acute exposure to high altitude on ventilation-perfusion (VA/Q) relationships in the lungs, nine young men were studied at rest and at up to three different levels of exercise on a bicycle ergometer. Altitude was simulated in a hypobaric chamber with measurements made at sea level (mean barometric pressure = 755 Torr) and at simulated altitudes of 5,000 (632 Torr), 10,000 (523 Torr), and 15,000 ft (429 Torr). VA/Q distributions were estimated using the multiple inert gas elimination technique. Dispersion of the distributions of blood flow and ventilation were evaluated by both loge standard deviations (derived from the VA/Q 50-compartment lung model) and three new indices of dispersion that are derived directly from inert gas data. Both methods indicated a broadening of the distributions of blood flow and ventilation with increasing exercise at sea level, but the trend was of borderline statistical significance. There was no change in the resting distributions with altitude. However, with exercise at high altitude (10,000 and 15,000 ft) there was a significant increase in dispersion of blood flow (P less than 0.05) which implies an increase in intraregional inhomogeneity that more than counteracts the more uniform topographical distribution that occurs. Since breathing 100% O2 at 15,000 ft abolished the increased dispersion, the greater VA/Q mismatching seen during exercise at altitude may be related to pulmonary hypertension.

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The relative roles of ventilation-perfusion (VA/Q) inequality, alveolar-capillary diffusion resistance, postpulmonary shunt, and gas phase diffusion limitation in determining arterial PO2 (PaO2) were assessed in nine normal unacclimatized men at rest and during bicycle exercise at sea level and three simulated altitudes (5,000, 10,000, and 15,000 ft; barometric pressures = 632, 523, and 429 Torr). We measured mixed expired and arterial inert and respiratory gases, minute ventilation, and cardiac output. Using the multiple inert gas elimination technique, PaO2 and the arterial O2 concentration expected from VA/Q inequality alone were compared with actual values, lower measured PaO2 indicating alveolar-capillary diffusion disequilibrium for O2. At sea level, alveolar-arterial PO2 differences were approximately 10 Torr at rest, increasing to approximately 20 Torr at a metabolic consumption of O2 (VO2) of 3 l/min. There was no evidence for diffusion disequilibrium, similar results being obtained at 5,000 ft. At 10 and 15,000 ft, resting alveolar-arterial PO2 difference was less than at sea level with no diffusion disequilibrium. During exercise, alveolar-arterial PO2 difference increased considerably more than expected from VA/Q mismatch alone. For example, at VO2 of 2.5 l/min at 10,000 ft, total alveolar-arterial PO2 difference was 30 Torr and that due to VA/Q mismatch alone was 15 Torr. At 15,000 ft and VO2 of 1.5 l/min, these values were 25 and 10 Torr, respectively. Expected and actual PaO2 agreed during 100% O2 breathing at 15,000 ft, excluding postpulmonary shunt as a cause of the larger alveolar-arterial O2 difference than accountable by inert gas exchange.(ABSTRACT TRUNCATED AT 250 WORDS)

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Reflectance spectrophotometry through the skull was used to investigate carbon monoxide (CO) binding by tissue hemoproteins in the brains of barbiturate-anesthetized Sprague-Dawley rats. After splenectomy and extensive perfluorotributylamine exchange transfusion, steady-state spectral scans were obtained in Soret and visible wave-length regions during O2 ventilation, during subsequent exposure to O2-enriched gases containing 1, 3, or 5% CO, and finally after N2 anoxia. These CO exposures were well-tolerated and electroencephalograph (EEG) activity continued to be present. Initial difference spectra were influenced by CO binding to residual hemoglobin, but spectral evidence of CO-mediated b-type cytochrome reduction was obtained in the visible region as CO concentration was increased to 3 or 5%. This was associated with Soret spectra compatible with formation of the reduced cytochrome a3-CO complex. Reduction of cytochrome a at 605 nm and cytochrome c + c1 at 550 nm was absent. These findings may indicate respiratory chain branching through b cytochromes, either to a separate a3-like oxidase independent of the classical cytochrome aa3 or to an unidentified alternative CO-sensitive oxidase.

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To assess the metabolic recovery of mitochondria after injury, we have monitored, in vivo and noninvasively, changes in the redox state of cytochrome (cyt) a,a3 in 35 rats after tissue hypoxia induced by rapid exsanguination to a mean arterial pressure of 30-35 mmHg. This level of mean arterial pressure was maintained for a shorter period of time in group I (n = 17) and a longer period of time in group II (n = 18), then the shed blood was returned by infusion. The surviving animals were observed for 2 more h before terminating the experiments. During exsanguination, reinfusion and recovery intervals brain tissue parameters of blood oxygenation, relative blood volume, and cyt a,a3 redox state were monitored continuously by spectrophotometry through the closed skull and intact skin. Group I had a high survival rate while group II had a very low survival rate. In both groups, with the onset of hypotension, there was a prompt rapid shift, followed by a slow continued progressive shift, of cyt a,a3 toward a more reduced state. The extent of recovery of cyt a,a3 following reinfusion was different in each group. In group I there was a rapid reoxidation of cyt a,a3 to a level above the base line (16 +/- 12%, mean +/- SEM). In contrast, the extent of reoxidation of cyt a,a3 in group II was significantly lower and stayed 31 +/- 6% below the base-line level. To further evaluate the mechanisms responsible for these observations, another related experiment was performed. 12 rats were subjected to shock and resuscitation as outlined for groups I and II. After death or killing of the animal, we measured, in vitro, oxygen consumption of cerebral cortical slices. Oxygen consumption of cortical tissue slices in subgroup I was significantly higher than in subgroup II. We conclude that, under these experimental conditions, the oxidative response of cyt a,a3 correlates closely with survival or death in the two groups. If in group I animals the greater oxidation of cyt a,a3, in vivo after resuscitation, reflects greater oxygen utilization, as is suggested by the in vitro observations in subgroup I, then we may be observing a useful adaptive response to tissue injury leading to preserved organ function and enhanced survival. Therefore, noninvasively measured cyt a,a3 redox state, reflecting intracellular metabolic activity, seems to indicate both the overall cerebral cellular response to injury and the likelihood of survival.

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