Biomedical subjects
R K Albert
Publications and source records attributed to R K Albert.
Non-drug issues related to the treatment of tuberculosis.
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Bronchiolitis obliterans caused by Legionella pneumophila.
A diabetic patient presented with symptoms and laboratory findings compatible with atypical pneumonia. Despite appropriate antibiotic therapy, his dyspnea, arterial oxygenation, and chest roentgenographic findings worsened. Because the patient had a history of homosexual contact, an open lung biopsy was obtained to morphologically define the tissue reaction and to search for a specific etiology. Histologic examination showed bronchiolitis obliterans but did not demonstrate a cause. Legionnaires' disease was subsequently diagnosed on the basis of a fourfold rise in indirect fluorescent antibody titer. This case report demonstrates that Legionella pneumophila may induce lung injury with bronchiolitis obliterans. Such patients may benefit from corticosteroid treatment.
Positive end-expiratory pressure decreases bronchial blood flow in the dog.
Positive end-expiratory pressure (PEEP) increases pulmonary vascular resistance, but its effect on the bronchial circulation is unknown. We have compared two techniques for measuring bronchial blood flow in anesthetized, open-chest, ventilated dogs at varying levels of PEEP. Bronchial blood flow ( Qbr ) to the left lower lobe (LLL) and trachea was measured with radiolabeled microspheres. Total Qbr was partitioned into tracheal, bronchial, and parenchymal fractions. We also measured the bronchopulmonary anastomotic flow ( Qbra ) by attaching cannulas from the lobar pulmonary artery and vein to reservoirs, interrupting the LLL pulmonary blood flow and collecting the flow going into the reservoirs. We measured Qbr and Qbra in 10 animals ventilated with varying levels of PEEP (3, 10, and 15 cmH2O) applied randomly. Pulmonary venous pressure was kept at 0 cmH2O. There was no difference observed between Qbr and Qbra at PEEP 3 and 10 cmH2O, but at PEEP 15 cmH2O, Qbr was greater than Qbra , suggesting that at low left atrial pressures bronchial blood flow drains mainly to the left atrium, whereas at elevated alveolar pressures a larger fraction empties into the right side of the heart. PEEP decreased LLL Qbr and Qbra (P less than 0.01). That fraction of Qbr going to the trachea did not change with PEEP. However, the bronchial and parenchymal fractions decreased.
Leukotriene B4 production by the human alveolar macrophage: a potential mechanism for amplifying inflammation in the lung.
Leukotriene B4 (LTB4) is a lipoxygenase product of arachidonic acid that has potent chemotactic activity for blood leukocytes. To assess the potential role of LTB4 in lung inflammatory responses, we investigated the production of LTB4 by human alveolar macrophages and determined its chemotactic activity for lung and blood phagocytes in vitro and in vivo. Human alveolar macrophages were stimulated with the calcium ionophore A23187 (10 micrograms/ml), and lipoxygenase products in the supernatants were isolated by high-performance liquid chromatography. Leukotriene B4 was the predominant arachidonate lipoxygenase product from the alveolar macrophages of 2 nonsmokers (17.3 +/- 2.7 ng/10(6) cells) and 3 of 4 smokers (23.4 +/- 14.8 ng/10(6) cells). Alveolar macrophages produced more LTB4 than did similarly treated peripheral blood neutrophils. Stimulated alveolar macrophages also produced 5-hydroxyeicosatetraenoic acid (HETE) and 2 isomers of LTB4: 5-(S),12-(R)-6-trans-LTB4 and 5-(S),12-(S)-6-trans-LTB4. Leukotriene B4 showed little chemotactic activity for alveolar macrophages in vitro and was a more potent chemoattractant for peripheral blood neutrophils than for monocytes (p less than 0.05). When instilled into the airways of anesthetized rats, LTB4 was less potent as an attractant for neutrophils and mononuclear cells than either zymosan-activated serum or bacterial-derived chemotactic factors. Leukotriene B4 production by alveolar macrophages may provide a mechanism by which phagocytes are recruited to the human lung during inflammatory processes.
Predictors of drug-resistant Mycobacterium tuberculosis.
Drug susceptibility testing is usually performed when Mycobacterium tuberculosis organisms are recovered from Asian immigrants or from patients whose sputum remains culture positive despite several months of antituberculosis medication. Alcoholism, previous antituberculosis treatment, history of adverse reactions to previous treatment, and patient unreliability have also been suggested as risk factors, but the ability of these factors to predict the presence of drug-resistant organisms has not been assessed. Starting in January 1980, the Washington State Tuberculosis Laboratory began testing every positive M. tuberculosis culture for drug resistance. This enabled us to prospectively evaluate the sensitivity and specificity of 7 risk factors for drug resistance in consecutive patients. From January 1, 1980, through December 31, 1982, cultures from 803 patients were positive for M. tuberculosis; 766 of these (95%) were tested for drug resistance. The incidence of resistance was 13% (101/766). Of the 101 patients with drug-resistant organisms, 61 (60%) were Asian, supporting the need to routinely test Asian immigrants for drug-resistant disease. The ability of the other risk factors to separate the 40 non-Asians (40%) with drug-resistant disease from the group of 513 non-Asians with drug-sensitive organisms was poor. All risk factors were insensitive and had a high false positive rate. These results demonstrate that the presence of drug-resistant disease in non-Asians cannot accurately be predicted. This finding suggests that all cultures of M. tuberculosis should be tested for drug sensitivity, and that in areas where the incidence of drug resistance is sufficiently high, initial treatment should be with 3 drugs until drug susceptibility is known.
Extra-alveolar vessel contribution to hydrostatic pulmonary edema in in situ dog lungs.
We determined the relative contribution of larger extra-alveolar arteries and veins to hydrostatic edema in in situ dog lungs. Left lower lobe alveolar and vascular pressures were controlled in 24 open-chest, anesthetized, heparinized dogs. Zero pressure was at the lobe base. Normal blood gases were maintained by ventilating the right lung. The left lower lobe was inflated with 5% CO2 and air to an alveolar pressure of 10 or 25 cmH2O and suspended from a strain gauge, which allowed continual weight recording. Vascular pressures were raised to alveolar pressure plus lung height (zone III) before and after pulmonary arterial or venous embolization with 37- to 74-microns polystyrene beads, which isolated the larger extra-alveolar arteries or veins from alveolar vessels. The weight change occurring during the last 3 min of the 5-min hydrostatic stress was taken to represent transvascular fluid flux. At an alveolar pressure of 25 cmH2O (estimated transmural pressure 40 cmH2O), leakage from the larger extra-alveolar arteries and veins accounted for 41 and 32%, respectively, of the total transvascular fluid flux occurring after embolization. At an alveolar pressure of 10 cmH2O (estimated transmural pressure 22 cmH2O), no extra-alveolar vessel leakage occurred. However, when vascular pressures were raised to provide a transmural pressure similar to that present at the higher alveolar pressure, the same contribution from larger extra-alveolar vessels was observed.
Mechanisms of physiological dead space response to PEEP after acute oleic acid lung injury.
In acute increased-permeability edema, the Bohr physiological dead space (VD/VTCO2) can be influenced by changes in anatomic dead space, ventilation-perfusion (VA/Q) heterogeneity, shunt, and the Haldane effect. We used the multiple inert gas elimination technique to assess the effect of positive end-expiratory pressure (PEEP) on each of these components of VD/VTCO2 in 14 pentobarbital-anesthetized dogs with increased permeability edema induced by infused oleic acid. PEEP of 5, 10, 15, and 20 cmH2O was applied in random sequence. Following injury VD/VTCO2 increased. It decreased with 5 or 10 cmH2O PEEP but increased progressively at higher PEEP levels. The decrease in VD/VTCO2 at 5 or 10 cmH2O PEEP was due to reductions in shunt and midrange VA/Q heterogeneity. The increase in VD/VTCO2 that occurred with higher PEEP levels was due to increased ventilation to high VA/Q regions and a larger anatomic dead space. Haldane effect magnified the shunt component of VD/VTCO2 but reduced the influence of midrange VA/Q heterogeneity.
Noninvasive monitoring of arterial blood gases. A report of the ACCP section on respiratory pathophysiology.
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Leukotriene C4 and D4 increase pulmonary vascular permeability in excised rabbit lungs.
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The prognosis of patients with chronic obstructive pulmonary disease after hospitalization for acute respiratory failure.
We followed the course of 36 consecutive patients hospitalized with chronic obstructive pulmonary disease and acute respiratory failure due to exacerbation of chronic bronchitis in order to clarify the prognosis in this common group of patients. All of the patients had spirometric evidence of severe, poorly reversible airflow limitation and all had a similar cause of acute respiratory failure. In addition, all received similar treatment during hospitalization and follow-up. Patients wtih asthma and pneumonia were excluded by clinical, spirometric, and roentgenographic criteria. Hospital survival was 94 percent, and only one patient required intubation. Two-year survival was 72 percent, and none of the patients died during a readmission for acute respiratory failure. This prognosis is much better than commonly recognized and compares favorably to that of stable outpatients with similar degrees of airflow limitation. An episode of acute respiratory failure, triggered by an exacerbation of chronic bronchitis, does not necessarily alter the prognosis of patients with COPD.
Hand-washing patterns in medical intensive-care units.
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Lung inflation can cause pulmonary edema in zone I of in situ dog lungs.
We investigated whether increases in lung water can occur due to lung inflation in zone I when alveolar vessels are collapsed. Static left lower lobe alveolar pressure, pulmonary arterial pressure, and pulmonary venous pressure were controlled in living, anesthetized, open-chested dogs. The lobe was inflated with 6% CO2 in air and suspended from a strain gauge, which allowed continual weight recording. The lung was held in zone I conditions. Arterial and venous pressures were equal at either 1 or 5 cmH2O, relative to the base of the 10- to 14-cm-high lobes. Weight changes were measured for 5 min after 5-cmH2O increments of alveolar pressure from 0 or 5 to 30 cmH2O. Lung weight gain due to edema occurred with inflation to alveolar pressures above 10 cmH2O. Greater lung distension resulted in greater rates of weight gain. Weight loss occurred on deflation. The fluid may have leaked from distended extra-alveolar vessels. This mechanism could explain the increased lung water seen with mechanical ventilation and/or positive end-expiratory pressure breathing.
Controlled clinical trial of methylprednisolone in patients with chronic bronchitis and acute respiratory insufficiency.
To evaluate the role of corticosteroids as treatment for acute exacerbations of chronic obstructive pulmonary disease, we conducted a double-blind, randomized, placebo-controlled trial in 44 consecutive patients with chronic bronchitis and severe airflow obstruction. All were hospitalized with acute respiratory insufficiency from acute bronchitis. Patients with asthma, atopy, or pneumonia were excluded. Treatment consisted of intravenous aminophylline, inhaled isoproterenol, antibiotics, and either methylprednisolone, 0.5 mg/kg of body weight, or placebo every 6 h intravenously for 72 h. Bedside spirometry was done before and after bronchodilator inhalation three times daily. The methylprednisolone-treated group had a greater improvement in both prebronchodilator and postbronchodilator forced expiratory volume in 1 second (P less than 0.001). More patients with large improvements in their prebronchodilator or postbronchodilator flow rates, or both (greater than or equal to 40% by 72 h), received methylprednisolone (P less than 0.01). Methylprednisolone improved airflow more than placebo when added to standard therapy in patients with chronic bronchitis and acute respiratory insufficiency.
Upper intestinal endoscopy induces hypoxemia in patients with obstructive pulmonary disease.
We studied the effects of fiberoptic upper intestinal endoscopy on blood oxygenation and cardiac rhythm in 13 patients. Six patients had normal pulmonary function or mild obstruction to air flow. None of these developed arterial oxygen desaturation during endoscopy. Seven patients had moderate to severe airflow obstruction. Six of these desaturated to less than 90%; the mean +/- SEM arterial oxygen tension changed from a baseline of 75 +/- 2 mm Hg to 54 +/- 2 mm Hg during endoscopy (P less than 0.01). Electrocardiographic changes during endoscopy occurred in 5 patients, 4 of whom had moderate to severe airflow obstruction. In 3 of these patients, the ECG changes were concurrent with desaturation. Patients with moderate to severe airflow obstruction frequently become hypoxemic and may develop cardiac arrhythmias during upper gastrointestinal endoscopy.
Increased surface tension favors pulmonary edema formation in anesthetized dogs' lungs.
The possibility that surface tension may affect the hydrostatic transmural pressure of pulmonary vessels and the development of pulmonary edema was studied in anesthetized, open-chested dogs. Isogravimetric pressure (the static intravascular pressure at which transmural osmotic and hydrostatic pressures are balanced such that net fluid flux is zero and lung weight is constant) was measured in nine animals under three conditions: (a) control, normal surface tension, at an alveolar pressure of 30 cm H2O with the apenic lung at room temperature; (b) after increasing surface tension by cooling and ventilating at a low functional residual capacity, at an alveolar pressure sufficient to produce the same lung volume present during control measurements; and (c) after restoring surface tension by rewarming while holding the lung at a high inflation volume, again at the control lung volume. Lung volumes were established from external dimensions and confirmed +/- 10% by deflation spirometry. The isogravimetric pressure (relative to alveolar pressure) was significantly less with increased surface tension than during either the initial control condition (P less than 0.01), or when the surface tension has been restored (P less than 0.01). Similar changes occurred in each of three additional studies performed with control alveolar pressures of 10 cm H2O. Thus, increased surface tension favors fluid leakage presumably because it increases the microvascular transmural pressure.
Fluid leaks from extra-alveolar vessels in living dog lungs.
Edema transudation from extra-alveolar vessels was investigated in anesthetized, open-chested dogs. Fluid accumulation at different alveolar and extra-alveolar vascular pressures was assessed by continuous lung weighing and microscopy. The left (experimental) lung was distended with 6% CO2 and air while normal arterial blood gases were maintained by separately ventilating the right lung. Extra-alveolar vessels were isolated by compressing alveolar vessels with alveolar pressures high enough to stop blood flow. Weight increased steadily (edemogenesis) when pulmonary arterial and/or pulmonary venous pressure was 1 cmH2O below this pressure. Because some alveolar vessels at the lung base could have remained open and leaked, extra-alveolar vessels were also separated from alveolar vessels by glass bead embolization sufficient to stop perfusion. Lung weight gains followed selective pulmonary arterial or venous pressure elevations. Electron microscopy demonstrated edema in experimental lobes which was not present in control lobes with undistended extra-alveolar vessels at the same alveolar pressure. Thus pulmonary edema can be caused by fluid leaking from extra-alveolar vessels.
Flexible fiberoptic bronchoscopy in the teaching hospital. Yield and complications.
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