99mTc technegas ventilation and perfusion lung scintigraphy for the diagnosis of pulmonary embolus.
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Lung scintigraphy is used widely for diagnosis of pulmonary embolus (PE). Technegas ventilation imaging has many advantages over other methods, but little outcome data exists on this technique. The aims of this study were to better define the role of lung scintigraphy in the management of patients with suspected PE and to evaluate technegas ventilation imaging by following patient outcomes. METHODS: A group of 717 out of 834 consecutive patients, referred to a university teaching hospital for lung scintigraphy to confirm or refute the diagnosis of PE, was followed for 18-30 mo to determine clinical outcome. The follow-up endpoints were death as a result of PE, death as a result of hemorrhage after treatment for PE, uncomplicated survival, survival with subsequent PE, nonfatal hemorrhage after treatment for PE and recurrence of PE in treated patients. Ventilation imaging was performed using technegas, and perfusion imaging was performed using intravenous 99mTc macroaggregated albumin. The modified PIOPED (Prospective Investigation of Pulmonary Embolism Diagnosis) diagnostic criterion was used for interpretation of lung scintigraphy. RESULTS: Diagnostic results included 3.5% normal studies, 67.4% assessed as low probability for PE, 10% as moderate probability for PE and 19.1% as high probability for PE. A total of 231 patents received therapy with heparin, followed by warfarin, including those receiving anticoagulation therapy for other conditions. Ninety-six percent of patients with normal and low probability studies (n = 508) had good outcomes, 6 patients died as a result of PE and 12 subsequently developed PE. The odds ratio for death by PE in this group was 0.2. Of the 72 moderate probability studies, 39 patients were untreated. In this group there was 1 death due to PE, and PE subsequently developed in 2 patients. None of the remaining 33 treated patients died, but 4 patients experienced bleeding complications. The odds ratio for death by PE in the moderate probability group was 0.7. In those patients with high-probability studies, there were 8 deaths by PE, 6 deaths by hemorrhage, 11 nonfatal hemorrhages and 7 patients who experienced recurrences of PE. The odds ratios in this group were 6 and 10 for death by PE, or death by PE and the treatment of PE, respectively. CONCLUSION: The use of the modified PIOPED diagnostic classification is valid for technegas lung scintigraphy. Using technegas, normal/low-probability and high-probability results are highly predictive of respective outcomes. Technegas lung scintigraphy reduces the number of indeterminate studies. (+info)
Mechanisms of improvement in pulmonary gas exchange during isovolemic hemodilution.
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Severe anemia is associated with remarkable stability of pulmonary gas exchange (S. Deem, M. K. Alberts, M. J. Bishop, A. Bidani, and E. R. Swenson. J. Appl. Physiol. 83: 240-246, 1997), although the factors that contribute to this stability have not been studied in detail. In the present study, 10 Flemish Giant rabbits were anesthetized, paralyzed, and mechanically ventilated at a fixed minute ventilation. Serial hemodilution was performed in five rabbits by simultaneous withdrawal of blood and infusion of an equal volume of 6% hetastarch; five rabbits were followed over a comparable time. Ventilation-perfusion (VA/Q) relationships were studied by using the multiple inert-gas-elimination technique, and pulmonary blood flow distribution was assessed by using fluorescent microspheres. Expired nitric oxide (NO) was measured by chemiluminescence. Hemodilution resulted in a linear fall in hematocrit over time, from 30 +/- 1.6 to 11 +/- 1%. Anemia was associated with an increase in arterial PO(2) in comparison with controls (P < 0.01 between groups). The improvement in O(2) exchange was associated with reduced VA/Q heterogeneity, a reduction in the fractal dimension of pulmonary blood flow (P = 0.04), and a relative increase in the spatial correlation of pulmonary blood flow (P = 0. 04). Expired NO increased with anemia, whereas it remained stable in control animals (P < 0.0001 between groups). Anemia results in improved gas exchange in the normal lung as a result of an improvement in overall VA/Q matching. In turn, this may be a result of favorable changes in pulmonary blood flow distribution, as assessed by the fractal dimension and spatial correlation of blood flow and as a result of increased NO availability. (+info)
A tidal breathing model for the multiple inert gas elimination technique.
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The tidal breathing lung model described for the sine-wave technique (D. J. Gavaghan and C. E. W. Hahn. Respir. Physiol. 106: 209-221, 1996) is generalized to continuous ventilation-perfusion and ventilation-volume distributions. This tidal breathing model is then applied to the multiple inert gas elimination technique (P. D. Wagner, H. A. Saltzman, and J. B. West. J. Appl. Physiol. 36: 588-599, 1974). The conservation of mass equations are solved, and it is shown that 1) retentions vary considerably over the course of a breath, 2) the retentions are dependent on alveolar volume, and 3) the retentions depend only weakly on the width of the ventilation-volume distribution. Simulated experimental data with a unimodal ventilation-perfusion distribution are inserted into the parameter recovery model for a lung with 1 or 2 alveolar compartments and for a lung with 50 compartments. The parameters recovered using both models are dependent on the time interval over which the blood sample is taken. For best results, the blood sample should be drawn over several breath cycles. (+info)
Gas exchange response to a PAF receptor antagonist, SR 27417A, in acute asthma: a pilot study.
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The pathogenic role of platelet-activating factor (PAF) in asthma has been questioned due to the limited or negative efficacy of PAF antagonists; however, in acute asthma (AA), where the endogenous release of PAF may be enhanced, the effects of PAF antagonist receptors have not been investigated. It was postulated that inhaled PAF provokes gas exchange defects in mild asthma likely to be related to airway vascular leakage. The response to a potent, selective PAF receptor antagonist, SR 27471A, on pulmonary gas exchange was studied, more specifically ventilation-perfusion (VA'/Q') distributions, in patients with AA within 48 h of hospitalization. A randomized, double-blind, placebo-controlled, parallel group (n=6, each) design was used. After baseline measurements, either placebo or SR 27417A (20 mg, orally) was administered and measurements were repeated 3 h later. Conventional anti-asthma medication was not interrupted. Despite a near-complete inhibition of the in vitro, platelet aggregation tests by 40 nM PAF (mean+/-SEM from 72+/-9 to 6+/-2%) and 80 nM PAF (from 81+/-7 to 6+/-3% both p<0.01) by SR 27471A indicating a good bioactivity of the compound, no significant changes in baseline forced expiratory volume in one second, (40+/-6%), respiratory system resistance (6.2+/-0.7 cmH2O x L(-1) x s), alveolar-arterial pressure difference for oxygen (5.2+/-0.4 kPa), arterial oxygen tension (9.0+/-0.5 kPa) or VA'/Q' distributions, as expressed by the dispersion of pulmonary blood flow (LogSD Q, 1.07+/-0.09; normal values <0.60), were observed. It is concluded that SR 27417A has limited value when added to the conventional treatment of acute asthma. These findings minimize the potential pathogenic role of endogenous platelet-activating factor as a relevant mediator of airway inflammation during acute asthma. (+info)
Pulmonary gas exchange in cystic fibrosis: basal status and the effect of i.v. antibiotics and inhaled amiloride.
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In order to evaluate the degree and type of gas exchange impairment in cystic fibrosis, ventilation/perfusion relationships in ten patients (mean age 26 yrs, mean Shwachman score 86) were examined. Pulmonary gas exchange was studied using the multiple inert gas elimination technique. High-resolution computed tomography (HRCT) and spirometry, including diffusing capacity, were performed after each gas exchange study for comparison. Examinations were done before and after home i.v. antibiotic treatment (HIVAT, 14 days) and after inhaled amiloride and placebo (14 days), in crossover fashion, clinical status after HIVAT serving as the baseline for the crossover study. Before HIVAT, the mean residual volume was 182% of the predicted value, the mean vital capacity 72% pred and the mean forced expiratory volume in one second 53% pred (p<0.001). The dispersion of pulmonary blood flow at different ventilation/perfusion ratios (V'/Q') ((logarithmic SD of the perfusion distribution (log SDQ)), used as an index for gas exchange impairment, was increased to a mean of 0.72. No linear correlation was seen between ventilation/perfusion inequality, spirometry and HRCT (p>0.05). After HIVAT, log SDQ was significantly improved to 0.66 (p<0.05). After placebo, but not after amiloride, log SDQ, arterial oxygen tension, alveolar-arterial oxygen tension difference and maximal expiratory flows when 50% and 25% of the forced vital capacity tension remain to be exhaled were significantly worse (p<0.05, respectively). Areas with a low V'/Q' were significantly lower after amiloride compared to after the placebo period (p<0.05). Moderate ventilation/perfusion inequality was present in the majority of the studied cystic fibrosis patients. The degree of ventilation/perfusion inequality cannot be estimated from spirometry or high-resolution computed tomography. The low proportion of low ventilation/perfusion ratios indicates that the regular treatment directed towards mucus plugging of small airways is beneficial. An improvement in the ventilation/perfusion relationship was seen after home i.v. antibiotic treatment and inhaled amiloride may possibly have a further positive effect on gas exchange. (+info)
Pulmonary gas exchange during exercise in highly trained cyclists with arterial hypoxemia.
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The causes of exercise-induced hypoxemia (EIH) remain unclear. We studied the mechanisms of EIH in highly trained cyclists. Five subjects had no significant change from resting arterial PO(2) (Pa(O(2)); 92.1 +/- 2.6 Torr) during maximal exercise (C), and seven subjects (E) had a >10-Torr reduction in Pa(O(2)) (81.7 +/- 4.5 Torr). Later, they were studied at rest and during various exercise intensities by using the multiple inert gas elimination technique in normoxia and hypoxia (13.2% O(2)). During normoxia at 90% peak O(2) consumption, Pa(O(2)) was lower in E compared with C (87 +/- 4 vs. 97 +/- 6 Torr, P < 0.001) and alveolar-to-arterial O(2) tension difference (A-aDO(2)) was greater (33 +/- 4 vs. 23 +/- 1 Torr, P < 0. 001). Diffusion limitation accounted for 23 (E) and 13 Torr (C) of the A-aDO(2) (P < 0.01). There were no significant differences between groups in arterial PCO(2) (Pa(CO(2))) or ventilation-perfusion (VA/Q) inequality as measured by the log SD of the perfusion distribution (logSD(Q)). Stepwise multiple linear regression revealed that lung O(2) diffusing capacity (DL(O(2))), logSD(Q), and Pa(CO(2)) each accounted for approximately 30% of the variance in Pa(O(2)) (r = 0.95, P < 0.001). These data suggest that EIH has a multifactorial etiology related to DL(O(2)), VA/Q inequality, and ventilation. (+info)
Controversies in pulmonary embolism and deep venous thrombosis.
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The diagnosis of venous thromboembolic disease, and pulmonary embolism in particular, remains problematic. Physicians should strongly consider empiric anticoagulation if the best available diagnostic tests are inconclusive, because treatment is usually safe and successful. Twice-daily subcutaneous low-molecular-weight heparin, dosed without monitoring, may eventually replace standard heparin for most treatment of venous thromboembolism, but it is not yet labeled for the treatment of pulmonary embolism. Deep venous thromboembolism and pulmonary embolism should be treated with anticoagulants rather than inferior vena cava filters, even in oncology patients, unless anticoagulation is contraindicated; if so, when the contraindication remits, anticoagulation should be employed. The most effective prophylaxis of venous thromboembolism in at-risk patients should be used, with prolonged duration if evidence from clinical trials supports efficacy and safety. Low-dose warfarin should be used to prevent venous thrombosis and indwelling central venous catheter thrombosis in patients with cancer. (+info)
Hemodilution during venous gas embolization improves gas exchange, without altering V(A)/Q or pulmonary blood flow distributions.
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BACKGROUND: Isovolemic anemia results in improved gas exchange in rabbits with normal lungs but in relatively poorer gas exchange in rabbits with whole-lung atelectasis. In the current study, the authors characterized the effects of hemodilution on gas exchange in a distinct model of diffuse lung injury: venous gas embolization. METHODS: Twelve anesthetized rabbits were mechanically ventilated at a fixed rate and volume. Gas embolization was induced by continuous infusion of nitrogen via an internal jugular venous catheter. Serial hemodilution was performed in six rabbits by simultaneous withdrawal of blood and infusion of an equal volume of 6% hetastarch; six rabbits were followed as controls over time. Measurements included hemodynamic parameters and blood gases, ventilation-perfusion (V(A)/Q) distribution (multiple inert gas elimination technique), pulmonary blood flow distribution (fluorescent microspheres), and expired nitric oxide (NO; chemoluminescence). RESULTS: Venous gas embolization resulted in a decrease in partial pressure of arterial oxygen (PaO2) and an increase in partial pressure of arterial carbon dioxide (PaCO2), with markedly abnormal overall V(A)/Q distribution and a predominance of high V(A)/Q areas. Pulmonary blood flow distribution was markedly left-skewed, with low-flow areas predominating. Hematocrit decreased from 30+/-1% to 11+/-1% (mean +/- SE) with hemodilution. The alveolar-arterial PO2 (A-aPO2) difference decreased from 375+/-61 mmHg at 30% hematocrit to 218+/-12.8 mmHg at 15% hematocrit, but increased again (301+/-33 mmHg) at 11% hematocrit. In contrast, the A-aPO2 difference increased over time in the control group (P < 0.05 between groups over time). Changes in PaO2 in both groups could be explained in large part by variations in intrapulmonary shunt and mixed venous oxygen saturation (SvO2); however, the improvement in gas exchange with hemodilution was not fully explained by significant changes in V(A)/Q or pulmonary blood flow distributions, as quantitated by the coefficient of variation (CV), fractal dimension, and spatial correlation of blood flow. Expired NO increased with with gas embolization but did not change significantly with time or hemodilution. CONCLUSIONS: Isovolemic hemodilution results in improved oxygen exchange in rabbits with lung injury induced by gas embolization. The mechanism for this improvement is not clear. (+info)