A simple method for the differential characterization of alveoli and alveolar ducts in injured lungs.

RATIONALE AND HYPOTHESIS: Previous studies evaluating the histoarchitecture of distal airspaces have been shown to be limited by the difficulty in adequately differentiating alveoli and alveolar ducts. This limitation has been specially noticed in studies addressing lung recruitment and in situations of diffuse alveolar damage (DAD), where generic nominations for distal airspaces had to be created, such as "peripheral airspaces" (PAS) and "large-volume gas-exchanging airspaces" (LVGEA). Elastic stains have been largely used to describe normal lung structures. Weigert's resorcin-fuchsin staining (WRF) demarcates the thickened free portions of the ductal septum facilitating its recognition. We hypothesized that this staining could help in differentiating alveoli from alveolar ducts in distorted lung parenchyma. MATERIAL AND METHODS: Samples of control lungs and of DAD lungs induced by mechanical ventilation (VILI) were stained with hematoxylin-eosin (HE) and with WRF. Using morphometry we assessed the volume proportion of alveoli, alveolar ducts and LVGEA in control and VILI lungs. RESULTS: WRF stained VILI lungs showed a significant decrease in the volume proportion of LVGEA and alveoli and a significant increase in the volume proportion of alveolar ducts when compared to HE stained samples. CONCLUSION: We conclude that WRF staining is useful to distinguish alveolar ducts from alveoli in a DAD model, and suggest that it should be routinely used when morphometric studies of lung parenchyma are performed.

Pulmonary and extrapulmonary acute respiratory distress syndrome are different.

Acute respiratory distress syndrome (ARDS) can be derived from two pathogenetic pathways: a direct insult on lung cells (pulmonary ARDS (ARDSp)) or indirectly (extrapulmonary ARDS (ARDSexp)). This review reports and discusses differences in biochemical activation, histology, morphological aspects, respiratory mechanics and response to different ventilatory strategies between ARDSp and ARDSexp. In ARDSp the direct insult primarily affects the alveolar epithelium with a local alveolar inflammatory response while in ARDSexp the indirect insult affects the vascular endothelium by inflammatory mediators through the bloodstream. Radiological pattern in ARDSp is characterised by a prevalent alveolar consolidation while the ARDSexp by a prevalent ground-glass opacification. In ARDSp the lung elastance, while in ARDSexp the chest wall and intra-abdominal chest elastance are increased. The effects of positive end-expiratory pressure, recruitment manoeuvres and prone position are clearly greater in ARDSexp. Although these two types of acute respiratory distress syndrome have different pathogenic pathways, morphological aspects, respiratory mechanics, and different response to ventilatory strategies, at the present, is still not clear, if this distinction can really ameliorate the outcome.

Morphometric differences in pulmonary lesions in primary and secondary ARDS. A preliminary study in autopsies.

The present study was undertaken in order to describe the morphological differences between pulmonary lesions in acute respiratory distress syndrome originating from direct pulmonary injury (ARDSp) and those originating from extrapulmonary injury (ARDSexp). We investigated a total of 38 ARDS-patients (27 males) ranging in age from 19 to 75 years, classified according to underlying disease in pulmonary (ARDSp) and extrapulmonary disease (ARDSexp). The extent of acute diffuse alveolar damage was assessed morphometrically on histologic gross sections in the upper and lower lobes of one lung. The lesions showed quantitative differences in extent and distribution according to underlying disease (primary pulmonary or secondary involvement). In pulmonary ARDS, a predominance of alveolar collapse (16.6%+/-12.3% versus 10.3%+/-11.9%, p = 0,03), fibrinous exudate (1.7%+/-3.2% versus 0.4%+/-1.1%, p = 0.01) and alveolar wall edema (11.2%+/-7.4% versus 6.6%+/-4.4%, p = 0,05) were found compared to extrapulmonary ARDS. We conclude that the morphology of acute diffuse alveolar damage (DAD) is mainly determined by underlying disease (pulmonary ARDS or extrapulmonary ARDS) differing in quantitative terms within the lung. Physiological, radiographic and respiratory system mechanics differences described in ARDSp and ARDSexp may therefore be due to morphometric differences in pulmonary lesions.

Different low constant flows can equally determine the lower inflection point in acute respiratory distress syndrome patients.

Among the possible techniques to obtain the pressure-volume (P x V) curve at the bedside the low constant flow (CF) is the easiest and quickest one. However, the best value for CF to perform a good semi-static P x V curve is still to be determined. The purpose of this study was to evaluate the influence of 4 different CFs (1, 2, 5, and 10 L/min) on determination of lower inflection point of the P x V curve (L-Pflex) and upper inflection point of the P x V curve (U-Pflex) on the maximum slope and on the inspiratory work of breathing (up to volume of 1.35 L; inspiratory work L/cm H2O), comparing the volume estimated from the CF with the measured volume obtained by the respiratory inductive plethysmograph. The design was a prospective study, and the setting was an adult medical intensive care unit of a university hospital. There were 7 acute respiratory distress syndrome (ARDS) patients, less than 5 days of installation, after the standardization of lung volume history received sequentially from 4 different low inspiratory CFs in 2 trials. The P x V curve lasted from 73 +/- 1.6 s (1 L/min) to 8.8 +/- 0.69 s (10 L/min). The L-Pflex differed in the 2 performed trials (p = 0.04). There was no difference of L-Pflex among the 4 CFs comparing the 3 methods (p = 0.072) used for its calculation as well as comparing the estimated and the measured volume (p = 0.456). The maximum slope decreased significantly while increasing the flow from 1 to 10 L/min just in the estimated volume (p = 0.03). The inspiratory work did not increase with the increment of the flow either in the estimated volume (p = 0.217) or in the measured volume (p = 0.149). The U-Pflex differed among the trials (p = 0.003) and the methods used for its calculation (p < 0.01). Constant flows from 1 to 10 L/min can equally determine L-Pflex in ARDS patients and is an easy and quick way to obtain the L-Pflex in order to optimize positive end expiratory pressure (PEEP) in ARDS patients.

Mask mechanics and leak dynamics during noninvasive pressure support ventilation: a bench study.

OBJECTIVE: To study the mask mechanics and air leak dynamics during noninvasive pressure support ventilation. SETTING: Laboratory of a university hospital. DESIGN: A facial mask was connected to a mannequin head that was part of a mechanical respiratory system model. The mask fit pressure (P(mask-fit)) measured inside the mask's pneumatic cushion was adjusted to 25 cmH(2)O using elastic straps. Pressure support (PS) was set to ensure a maximal tidal volume distal to the mask (VT(distal)) but avoiding failure to cycle to exhalation. MEASUREMENTS: Airway pressure (P(aw)), P(mask-fit), mask occlusion pressure (P(mask-occl)=P(mask-fit)-P(aw)), VT proximal (VT(prox)), distal to the mask (VT(distal)), air leak volume ( Leak=VT(prox)-VT(distal)), and inspiratory air leak flow rate (difference between inspiratory flow proximal and distal to the mask) were recorded. RESULTS: PS 15 cmH(2)O was the highest level that could be used without failure to cycle to exhalation (VT(distal) of 585+/-4 ml, leak of 32+/-1 ml or 5.2+/-0.2% of VT(prox), and a minimum P(mask-occl) of 1.7+/-0.1 cmH(2)O). During PS 16 cmH(2)O the P(mask-occl) dropped to 1.1+/-0.1 cmH(2)O, and at this point all flow delivered by the ventilator leaked around the mask, preventing the inspiratory flow delivered by the ventilator from reaching the expiratory trigger threshold. CONCLUSION: P(mask-fit) and P(mask-occl) can be easily measured in pneumatic cushioned masks and the data obtained may be useful to guide mask fit and inspiratory pressure set during noninvasive positive pressure ventilation.

Interação cardiopulmonar durante a ventilação mecânica / Cardiopulmonary interaction during mechanical ventilation

As interaçöes cardiopulmonares durante a ventilação mecânica são complexas e dependem do estado volêmico do paciente (hipovolemia, normovolemia e hipervolemia), das funçöes dos ventrículos direito e esquerdo, assim como de sua pós-carga, do estado funcional dos pulmöes (normal, restritivo, ou obstrutivo) e da complacência do sistema toracoabdominal. Nos estados hipovolêmicos, a adição de pressão positiva intratorácica prporciona diminuição do retorno venoso e conseqüente dominuição do débito cardíaco. Esse efeito encontr-se exacerbado nas disfunçöes do ventrículo direito presentes no tromboembolismo pulmonar e na doença pulmonar obstrutiva crônica e, em menor grau, do ventrículo esquerdo. Nos estados de hipervolemia, a pré-carga de ambos os ventrículos está aumentada. Quando a pressão capilar pulmonar ultrapassa 18 mmHg em pulmöes normais ocorre o extravasamento de líquido para o interstício pulmonar e interior dos alvéolos. Esse efeito está exacerbado nas alteraçöes de permeabilidade da membrana alveolocapilar (síndrome do desconforto respiratório agudo). Nos estados hipervolêmicos, a adição de pressão intratorácica positiva não costuma ocasionar a diminuição do débito cardíaco. Nas disfunçöes de ventrículo esquerdo com pressão capilar acima de 18 mmHg, a adição de pressão intratorácica positiva mantém os alvéolos abertos, melhorando a oxigenação e diminuição a pós-carga do ventrículo esquerdo, o que proporciona a melhora do desempenho ventricular. Assim observando-se e compreendendo-se essas complexas interaçöes cardiopulmonares, poderemos otimizar as condiçöes cardiorrespiratórias nas diferentes situaçöes clínicas.

Effect of a protective-ventilation strategy on mortality in the acute respiratory distress syndrome.

BACKGROUND: In patients with the acute respiratory distress syndrome, massive alveolar collapse and cyclic lung reopening and overdistention during mechanical ventilation may perpetuate alveolar injury. We determined whether a ventilatory strategy designed to minimize such lung injuries could reduce not only pulmonary complications but also mortality at 28 days in patients with the acute respiratory distress syndrome. METHODS: We randomly assigned 53 patients with early acute respiratory distress syndrome (including 28 described previously), all of whom were receiving identical hemodynamic and general support, to conventional or protective mechanical ventilation. Conventional ventilation was based on the strategy of maintaining the lowest positive end-expiratory pressure (PEEP) for acceptable oxygenation, with a tidal volume of 12 ml per kilogram of body weight and normal arterial carbon dioxide levels (35 to 38 mm Hg). Protective ventilation involved end-expiratory pressures above the lower inflection point on the static pressure-volume curve, a tidal volume of less than 6 ml per kilogram, driving pressures of less than 20 cm of water above the PEEP value, permissive hypercapnia, and preferential use of pressure-limited ventilatory modes. RESULTS: After 28 days, 11 of 29 patients (38 percent) in the protective-ventilation group had died, as compared with 17 of 24 (71 percent) in the conventional-ventilation group (P<0.001). The rates of weaning from mechanical ventilation were 66 percent in the protective-ventilation group and 29 percent in the conventional-ventilation group (P=0.005): the rates of clinical barotrauma were 7 percent and 42 percent, respectively (P=0.02), despite the use of higher PEEP and mean airway pressures in the protective-ventilation group. The difference in survival to hospital discharge was not significant; 13 of 29 patients (45 percent) in the protective-ventilation group died in the hospital, as compared with 17 of 24 in the conventional-ventilation group (71 percent, P=0.37). CONCLUSIONS: As compared with conventional ventilation, the protective strategy was associated with improved survival at 28 days, a higher rate of weaning from mechanical ventilation, and a lower rate of barotrauma in patients with the acute respiratory distress syndrome. Protective ventilation was not associated with a higher rate of survival to hospital discharge.

Temporal hemodynamic effects of permissive hypercapnia associated with ideal PEEP in ARDS.

The associated use of permissive hypercapnia (PHY) and high PEEP levels (PEEP(IDEAL)) has been recently indicated as part of a lung-protective-approach (LPA) in acute respiratory distress syndrome (ARDS). However, the net hemodynamic effect produced by this association is not known. We analyzed the temporal hemodynamic effects of this combined strategy in 48 patients (mean age 34 +/- 13 yr) with ARDS, focusing on its immediate (after 1 h), early (first 36 h), and late (2nd-7th d) consequences. Twenty-five patients were submitted to LPA--with the combined use of permissive hypercapnia (PHY), VT < 6 ml/kg, distending pressures above PEEP < 20 cm H2O, and PEEP 2 cm H2O above the lower inflection point on the static inspiratory P-V curve (P(FLEX))- and 23 control patients were submitted to conventional mechanical ventilation. LPA was initiated at once, resulting in an immediate increase in heart rate (p = 0.0002), cardiac output (p = 0.0002), oxygen delivery (DO2l, p = 0.0003), and mixed venous Po2 (p = 0.0006), with a maintained systemic oxygen consumption (p = 0.52). The mean pulmonary arterial pressure markedly increased (mean increment 8.8 mm Hg; p < 0.0001), but the pulmonary vascular resistance did not change (p = 0.32). Cardiac filling pressures increased (p < 0.001) and the systemic vascular resistance fell (p = 0.003). All these alterations were progressively attenuated in the course of the first 36 h, despite persisting hypercapnia. Plasma lactate suffered a progressive decrement along the early period in LPA but not in control patients (p < 0.0001). No hemodynamic consequences of LPA were noticed in the late period and renal function was preserved. A multivariate analysis suggested that these acute hyperdynamic effects were related to respiratory acidosis, with no depressant effects ascribed to high PEEP levels. In contrast, high plateau pressures were associated with cardiovascular depression. Thus, as long as sufficiently low distending pressures are concomitantly applied, the sudden installation of PHY plus PEEP(IDEAL) induces a transitory hyperdynamic state and pulmonary hypertension without harmful consequences to this young ARDS population.

Human pulmonary dirofilariasis: analysis of 24 cases from São Paulo, Brazil.

STUDY OBJECTIVE: To present the clinical, radiologic, and pathologic aspects of 24 cases of human pulmonary dirofilariasis (HPD) from São Paulo, Brazil. DESIGN: Retrospective study of 24 patients with a confirmed diagnosis of HPD over a 14-year period (from February 1982 to June 1996). SETTING: Thoracic Surgery and Pulmonary Division, University of São Paulo and Hospital Albert Einstein, São Paulo, Brazil. RESULTS: Seventeen patients were male (70.1%) and seven were female (29.9%). Their mean age was 51.4 years. Fifty-four percent of the patients were asymptomatic and 75% had a well-circumscribed noncalcified peripheral subpleural pulmonary nodule on the chest radiograph and thoracic CT scan, located preferentially in the lower lobes. The diagnosis was made after thoracotomy and wedge resections in 16 patients, by videothoracoscopy in six, after a pleural biopsy in one, and after necropsy in one. The pathologic examination of all the nodules revealed a central zone of necrosis, surrounded by a narrow granulomatous zone and peripherally by fibrous tissue. Pulmonary vessels exhibit varying degrees of endarteritis. In all cases, a dead worm, usually necrotic and fragmented, was found. CONCLUSIONS: A subpleural, noncalcified pulmonary nodule in the appropriate clinical and epidemiologic setting should alert the clinician, radiologist, or pathologist to the possibility of Dirofilaria. HPD should be considered in the differential diagnosis of pulmonary nodules.

Primary malignant fibrous histiocytoma of the lung. Report of a case with bronchial brushing cytologic features.

BACKGROUND: Malignant fibrous histiocytoma (MFH) arising primarily in the lungs is rare, and a preoperative diagnosis, as well as a surgical planning, is very important because of the tumor's propensity for vascular invasion and its low incidence of lymph node metastasis. The correct preoperative diagnosis of thoracic MFH is not easy to establish because the small fragments from needle and transbronchial biopsies are often inadequate for a conclusive histologic analysis. A preoperative bronchial brushing cytology suggestion of the diagnosis of primary MFH of the lungs may be helpful in such cases. CASE: A 37-year-old male presented with a large, irregular mass in the inferior and middle lobes on chest roentgenography as well as on computed tomography. Two bronchoscopies were performed, with the diagnosis of undifferentiated large cell carcinoma. After surgical resection a more sophisticated pathologic analysis, including immunohistochemical and ultrastructural studies, revealed a primary MFH of the lungs. Revision of the bronchial brushing cytology disclosed many spindle-shaped cells with a "comet" configuration, strongly suggestive of MFH. CONCLUSION: The bronchial brushing cytology features of spindle-shaped and bizarre, multinucleated giant cells with a comet appearance may be the key to the cytomorphologic diagnosis of MFH.

Noncardiogenic pulmonary edema complicating diabetic ketoacidosis.

OBJECTIVE: To alert physicians to the possibility of pulmonary edema as a complication of diabetic ketoacidosis. METHODS: We report a case of adult respiratory distress syndrome after resuscitative efforts to compensate the first episode of diabetic ketoacidosis in a previously healthy young woman. RESULTS: In a 26-year-old woman with a 3-day history of malaise, polyuria, nausea, and vomiting, severe hypoxia and rales developed, and intubation and mechanical ventilation became necessary. Hemodynamic evaluation and striking electron microscopic findings on open-lung biopsy confirmed the diagnosis of adult respiratory distress syndrome. Despite adequate ventilatory support and hemodynamic management, death ensued and was attributed to irresponsive and progressive acute respiratory failure due to increased pulmonary capillary permeability edema. CONCLUSION: Clinicians should be aware of this possibly fatal pulmonary complication of diabetic ketoacidosis.

Beneficial effects of the "open lung approach" with low distending pressures in acute respiratory distress syndrome. A prospective randomized study on mechanical ventilation.

Alveolar overdistention and cyclic reopening of collapsed alveoli have been implicated in the lung damage found in animals submitted to artificial ventilation. To test whether these phenomena are impairing the recovery of patients with acute respiratory distress syndrome (ARDS) submitted to conventional mechanical ventilation (MV), we evaluated the impact of a new ventilatory strategy directed at minimizing "cyclic parenchymal stretch." After receiving pre-established levels of hemodynamic, infectious, and general care, 28 patients with early ARDS were randomly assigned to receive either MV based on a new approach (NA, consisting of maintenance of end-expiratory pressures above the lower inflection point of the P x V curve, VT < 6 ml/kg, peak pressures < 40 cm H2O, permissive hypercapnia, and stepwise utilization of pressure-limited modes) or a conventional approach (C = conventional volume-cycled ventilation, VT = 12 ml/kg, minimum PEEP guided by FIO2 and hemodynamics and normal PaCO2 levels). Fifteen patients were selected to receive NA, exhibiting a better evolution of the PaO2/FIO2 ratio (p < 0.0001) and of compliance (p = 0.0018), requiring shorter periods under FIO2 > 50% (p = 0.001) and a lower FIO2 at the day of death (p = 0.0002). After correcting for baseline imbalances in APACHE II, we observed a higher weaning rate in NA (p = 0.014) but not a significantly improved survival (overall mortality: 5/15 in NA versus 7/13 in C, p = 0.45). We concluded that the NA ventilatory strategy can markedly improve the lung function in patients with ARDS, increasing the chances of early weaning and lung recovery during mechanical ventilation.

[Hemodynamic impact of thrombolytic therapy in acute pulmonary thromboembolism]. / Repercussões hemodinâmicas da terapia trombolítica no tromboembolismo pulmonar agudo.

PURPOSE: To evaluate pre and post-hemodynamic changes after thrombolytic therapy in patients with acute pulmonary embolism with multiple pulmonary segments compromised. METHODS: Nine patients, 5 females, aged between 27 and 83 (mean 62 +/- 16) years, with the onset of symptoms preceding 7 days, were submitted to thrombolytic therapy, administered after baseline perfusion-ventilation lung scan, echodopplercardiography (ECO) and hemodynamic measurements with a Swan-Ganz thermodilution catheter. The same procedures were done after the thrombolytic infusion. Streptokinase (SK) was used in 7 (78%) cases and recombinant human tissue-type plasminogen activator (rt-PA, alteplase) in 2 with the following doses: SK-250,000 i.u. infusion over 30 min, then 100,000 i.v/h over 24 to 72 h and rt-PA-20 mg in bolus infusion, then 80 mg over 6 h. Thrombolytic was infused in pulmonary artery trunk in 8 (88%) cases and a peripheral vein in 1 (12%) case, until mean pulmonary artery pressure (PAP) reached 20 mmHg. All patients received i.v. heparin and oral anticoagulation after thrombolytic therapy. RESULTS: A significant (p < 0.05) decrease in right atrial pressure (12 +/- 3 vs 8 +/- 2 mmHg), PAP (32 +/- 5 vs 19 +/- 2 mmHg), pulmonary vascular resistance (397 +/- 125 vs 87 +/- 24 dyne.s/cm5) and increase in cardiac output (3.4 +/- 0.5 vs 5.5 +/- 1.0 l/min) and stroke volume (30 +/- 5 vs 57 +/- 10 ml/beat) were observed after thrombolytic infusion. Two patients died as a result of pulmonary infection unrelated to the embolic event or thrombolysis. Minor bleeding complications occurred in two cases and major in one patient with orthopedic prosthesis. CONCLUSION: Thrombolytic therapy exert desirable effects on hemodynamic abnormalities, achieving lungs scan and ECO improvement in patients with acute pulmonary embolism.

Volume-assured pressure support ventilation (VAPSV). A new approach for reducing muscle workload during acute respiratory failure.

This study reports the preliminary clinical evaluation of a new mode of ventilation--volume-assured pressure support ventilation (VAPSV)--which incorporates inspiratory pressure support (PSV) with conventional volume-assisted cycles (VAV). This combination optimizes the inspiratory flow during assisted/controlled cycles, reducing the patient's respiratory burden commonly observed during VAV. Different from conventional PSV, VAPSV assures precise control of tidal volume (VT) in unstable patients. Eight patients with acute respiratory failure (ARF) were submitted to assisted ventilation under VAV and VAPSV. Patient's ventilatory workload (evaluated through the pressure-time product, mechanical work per liter of ventilation, and work per minute) and patient's ventilatory drive (occlusion pressure--P0.1) were significantly reduced during VAPSV. This "relief" was more evident among the most distressed patients (p < 0.001), allowing a reduction of more than 60 percent in muscle load, without the need of increasing peak tracheal pressure. Mean inspiratory flow (VT/TI), VT, and effective dynamic compliance were significantly increased during VAPSV, whereas the effective inspiratory impedance decreased. These mechanical advantages of VAPSV allowed a reduction of intrinsic PEEP, whenever it was present. Blood gas values were similar in both periods. We concluded that VAPSV is a promising form of ventilatory support. At the same time that it was able to safely assure a minimum preset VT, VAPSV reduced patient workload and improved synchrony between the patient and the ventilator during ARF.

The relationship between pleural fluid findings and the development of pleural thickening in patients with pleural tuberculosis.

The objective of the study was to determine if residual pleural thickening after treatment for pleural tuberculosis could be predicted from the pleural fluid findings at the time of the initial thoracentesis. Forty-four patients initially diagnosed as having pleural tuberculosis between January 1986 and January 1988 were separated into two groups: the 23 patients in group 1 had residual pleural disease, while the 21 patients in group 2 had no residual pleural disease after treatment for their pleural tuberculosis was completed. The clinical characteristics of the two different groups did not differ significantly, but the patients in group 1 tended to be a little sicker in that the duration of their symptoms was longer, their hemoglobin values were lower, and weight loss and cough were more frequent. There were no significant differences in the pleural fluid findings in the two different groups. The mean pleural fluid protein level was 5.40 +/- 0.58 g/dl for group 1 and 5.17 +/- 0.80 g/dl for group 2, while the mean pleural fluid glucose level was 78.6 +/- 19.5 mg/dl for group 1 and 79.5 +/- 20.1 mg/dl for group 2. The mean pleural fluid lactate dehydrogenase (LDH) level in group 1 was 593 +/- 498 IU/L, while the mean level for group 2 was 491 +/- 198 IU/L. The presence of residual pleural thickening was not related to the chemotherapeutic regimen or the performance of a therapeutic thoracentesis. From this study we conclude that approximately 50 percent of patients with pleural tuberculosis will have residual pleural thickening when their therapy is completed, but that one cannot predict which patients will have residual pleural thickening from either their clinical characteristics or their pleural fluid findings.

Resposta a administracao de corticosteroide em pacientes portadores de doenca pulmonar obstrutiva cronica e asma / Response to administration of corticosteroids in patients with chronic obstructive lung disease and asthma

Realizamos estudo espirometrico avaliando a resposta a adminisatracao de 200 mcg de salbutamol via inalatoria, antes e apos a administracao diaria de 8 mg de triancinolona, via oral, por um periodo de em media duas semanas, em 21 pacientes portadores de doenca pulmonar obstrutiva cronica (DPOC) ou asma. Onze pacientes responderam com aumento significante da CVF ou "VEF IND. 1" ou "FEF IND. 25-75 por cento", apos o uso de corticosteroides. Dez pacientes nao responderam. Houve em media aumento significante da CVF e "VEF IND. 1" (p < 0,01) e do "FEF IND. 25-75 por cento" (p < 0,05), apos o uso de corticosteroide. Nao houve diferenca significante entre os respondedores e nao respondedores ao uso de corticosteroide quanto a idade, a CVF, "VEF IND. 1" e "FEF IND. 25-75 por cento" iniciais (percentagem do predito). O grupo dos pacientes respondedores ao uso de corticosteroide, tambem respondeu ao uso do broncodilatador, quanto ao "FEF IND. 25-75 por cento", deferindo significativamente do grupo dos nao respondedores (p < 0,02). Houve correlacao negativa significante entre a intensidade da resposta ao corticosteroide e ao broncodilatador, avaliada pelo delta "FEF IND. 25-75 por cento" (p < 0,05). A administracao do corticoide nao modificou a resposta ao broncodilatador.

A resposta do fluxo aereo a administracao de broncodilatadores em pacientes portadores de doenca pulmonar obstrutiva cronica ou asma / Response of airflow to administration of bronchodilator agents in patients with chronic obstructive lung disease or asthma

Analisamos as espirometrias de 30 pacientes portadores de DPOC ou asma antes e apos a administracao de 200 mcg de salbutamol, via inalatoria. Todos os pacientes apresentaram resposta significante quanto ao fluxo. Quinze pacientes responderam com aumento do "VEF IND. 1" maior que 13 por cento (grupo I) e quinze com aumento exclusivo do"FEF IND. 25-75 por cento" (porcentagem do predito) iniciais, cujos valores foram significantemente menores (p < 0.01) no grupo I. Nao houve diferenca significante quanto a idade, sexo e CVF (porcentagem do predito) iniciais.