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Biomedical subjects

J E Heffner

Publications and source records attributed to J E Heffner.

At least 91 records · Page 5Linked to original sources
PubMed1990

Acid-base disturbances in acute asthma.

The clinical features, arterial blood gases, and acid-base profile were examined in 229 consecutive episodes of acute asthma in 170 patients who required hospitalization. A simple respiratory alkalosis was the most common acid-base disturbance, occurring in 48 percent of the episodes. Metabolic acidosis, either alone or as part of a mixed disturbance, was noted in 28 percent. Of 60 episodes presenting with respiratory acidosis, 37 (62 percent) had a coexistent metabolic acidosis. Metabolic acidosis was more likely to occur in male subjects and in patients with evidence of more severe airflow obstruction. Patients with metabolic acidosis had an average anion gap of 15.8 mEq/L; these patients were more hypoxemic than those without metabolic acidosis and there was a significant inverse correlation between the anion gap and the degree of hypoxemia. We conclude that metabolic acidosis is a common finding in acute, severe asthma and suggest that the pathogenesis of lactic acidosis is multifactorial and includes contributions from lactate production by respiratory muscles, tissue hypoxia, and intracellular alkalosis.

Acid-Base Equilibrium↗
PubMed1990

Pulmonary reactions from illicit substance abuse.

The epidemic spread of illicit substance abuse in the United States and the adaptation of novel modes of drug delivery have increased the incidence of pulmonary complications of drug addiction. Chest manifestations of drug abuse relate not only to the particular substance used, but also to the route of administration, the presence of contaminating foreign material or microbiologic pathogens host response, and the practice of sharing drug paraphernalia. This article outlines the important lung disorders linked to drug addiction and discusses pathophysiologic mechanisms, diagnosis, and management.

Cannabis↗
PubMed1990

Airway management in the critically ill patient.

Decisions regarding the application and care of airways in respiratory failure are important determinants of outcome in critically ill patients. Specialized procedures for institution of translaryngeal intubation in difficult circumstances, such as fiberoptic intubation, and provision of immediate surgical airway access, such as cricothyroidotomy, are requisite skills for the intensivist. The evolving application of standard techniques and advent of newer procedures for airway cannulation require extensive experience and cognitive skills in the management of tracheal intubation to enhance patient benefit and limit adverse effects from tracheal intubation.

Critical Care↗
PubMed1990

The effect of theophylline on respiratory muscle contractility and fatigue.

The traditional role of theophylline as a bronchodilator has been expanded by recent findings that suggest this drug has more than smooth muscle relaxant properties. Several investigators indicate that theophylline has an inotropic effect on respiratory muscle, causing enhanced muscular contraction and prevention of muscle fatigue. In animal studies, the drug enhanced respiratory muscle contraction by 15-20%, with levels in the upper end of the therapeutic range (15-20 mg/L). Results of studies in healthy volunteers and patients with lung disease, however, are conflicting. Five clinical trials demonstrated increased diaphragmatic contractility, whereas seven trials showed no effect, with five referring to the diaphragm and the remaining two to the sternomastoid muscle. Disparity in outcomes may be attributed to differences in patient populations, study designs, and techniques used to determine diaphragmatic contractility. Few long-term trials exist that document significant clinical benefit. Theophylline may prove to be of value in selected populations, such as adults with hypercapnic obstructive lung disease.

Animals↗
PubMed1990

Effects of prostaglandin E1 on platelet attenuation of oxidant-induced edema in isolated rabbit lungs.

Numerous studies suggest that platelets may contribute to preservation of normal endothelial cell permeability in models of lung injury. We have previously shown that washed human platelets prevent xanthine oxidase-induced edema in the isolated perfused lung and that protective mechanisms depend on the platelet glutathione redox cycle. It is uncertain, however, whether platelets preserve endothelial function by reducing toxic oxygen metabolites or by aggregating and releasing endothelial cell supportive factors-an activity that may require the glutathione redox cycle. In this study, we present data demonstrating that platelet prevention of oxidant lung injury occurs independent of platelet aggregation and release. Isolated rabbit lungs perfused with a cell-free medium were instilled with purine (2 mmol/L) and xanthine oxidase (0.003 U/ml) to generate oxidant lung edema. The infusion of washed human platelets (1 x 10(10) cells) prevented lung edema formation as measured by lung weight gain, wet-to-dry lung weight ratios, and lung histology. Incubation of platelets with prostaglandin E1 (PGE1), a potent inhibitor of platelet aggregation and release, did not inhibit platelet attenuation of lung edema. Additionally, with the instillation of PGE1 into the perfusate to further inhibit platelet aggregation, no prevention of lung protection by PGE1-treated platelets was seen when these results were compared with those from studies in which lungs were infused with xanthine oxidase and PGE1. Aggregometry studies documented that the inhibitory effect of PGE1 on platelet aggregation persisted for up to 60 minutes, which was the duration of the isolated lung protocol. We conclude that platelet aggregation and release of platelet factors is not required for platelet attenuation of oxidant lung edema.

Alprostadil↗
PubMed1989

Human platelets modulate edema formation in isolated rabbit lungs.

The role of platelet glucose-6-phosphate dehydrogenase (G-6-PD) in mediating the effects of human platelets on oxidant-induced edema in the isolated perfused rabbit lung was investigated using dehydroepiandrosterone, a specific steroidal inhibitor of G-6-PD. Xanthine oxidase (0.003 and 0.012 U/ml) caused lung edema that was attenuated by coinfusion of washed human platelets. Platelets that were incubated with DEA to inhibit G-6-PD activity augmented xanthine oxidase-induced lung edema and pulmonary hypertension at both doses of xanthine oxidase. Infusion of papaverine to maintain stable pulmonary artery (PA) pressures, incubation of G-6-PD-inhibited platelets with acetylsalicylate, or infusion of a thromboxane-prostaglandin endoperoxide receptor site antagonist, SQ 29548, into the lung perfusate prevented augmentation of lung edema and the PA pressor response by G-6-PD-inhibited platelets. It was concluded that antioxidant-intact platelets attenuate oxidant-induced lung edema by preventing increased membrane permeability, and that G-6-PD-inhibited platelets augment lung edema through hydrostatic mechanisms mediated by release of platelet cyclooxygenase products.

Animals↗
PubMed1989

Bilateral vocal cord paralysis with respiratory failure. A presenting manifestation of bronchogenic carcinoma.

A patient with lung cancer presented with upper airway obstruction and hypercapnic respiratory failure resulting from bilateral vocal cord paralysis. Computed tomography demonstrated tumor extension into the superior mediastinum, with probable disruption of both recurrent laryngeal nerves. Unlike the more common unilateral cord paralysis, bilateral cord dysfunction is often associated with preservation of voice and varying degrees of stridor that may lead to potentially life-threatening delays in diagnosis and treatment. Proper management requires urgent translaryngeal intubation if airway obstruction is high grade, with subsequent consideration of laryngeal surgical procedures for long-term care.

Airway Obstruction↗
PubMed1988

Pocket computer for interpretation of office spirometry.

Office spirometry is an integral part of the evaluation of any patient with known or suspected lung disease. Though accurate and affordable bellows-type spirometers are available to clinicians, the available microprocessors that calculate test results markedly increase the cost of the equipment. I have successfully used an inexpensive pocket computer programmed to provide predicted values and interpretation of test results, printing this information in a format suitable for mounting in the office chart. The reliability of the results and interpretations permits convenient and low-cost pulmonary function testing in office patients when clinically warranted.

Adult↗
PubMed1988

Human platelets attenuate oxidant injury in isolated rabbit lungs.

Because platelets contain active antioxidant systems, the capacity of platelets to attenuate oxidant lung injury was investigated. Purine and xanthine oxidase were infused into isolated perfused rabbit lungs (IPL) to generate H2O2, thereby causing increased membrane permeability edema. The coinfusion of washed human platelets (1.20 +/- 0.07 x 10(10) cells) attenuated the degree of edema formation as measured by lung weight gain and lung lavage albumin concentration. Electron microscopy of lung preparations demonstrated platelet adherence to capillary endothelial luminal surfaces of oxidant-injured lungs, but there was no evidence of vascular plugging with platelet macroaggregates. The platelet glutathione redox cycle or platelet catalase were inhibited before infusion of platelets into the IPL with purine and xanthine oxidase. Inhibition of the glutathione redox cycle with 1,3-bis(2-chloroethyl)-1-nitrosourea, 1-chloro-2,4-dinitrobenzene, or buthionine sulfoximine prevented platelet attenuation of lung injury. Inactivation of platelet catalase with 3-amino-1,2,4-triazole, however, did not significantly reduce the platelet-induced lung protection. We conclude that the platelet glutathione redox cycle plays a major role in reducing enzymatically generated toxic O2 metabolites and attenuating lung injury.

Animals↗
PubMed1988

Catalase pretreatment attenuates oleic acid-induced edema in isolated rabbit lung.

Because reactive O2 metabolites have been demonstrated to be potent mediators of vascular dysfunction and are synthesized by lung tissue, their involvement as mediators of oleic acid (OA)-induced pulmonary edema in the isolated Krebs-perfused rabbit lung was assessed. Injection of OA (0.1 ml) into the pulmonary artery after vehicle pretreatment induced marked increases in lung weight [50.4 +/- 13.9 vs. 4.2 +/- 2.0 (SE) g 45 min after OA or vehicle, respectively, P less than 0.05], an index of pulmonary edema, and airway pressure. OA also caused a significant though minimal increase in pulmonary arterial pressure. Pretreatment with catalase (1,000 U/ml), a scavenger of H2O2, significantly (P less than 0.05, Friedman's) attenuated the increases in lung weight (50.4 +/- 13.9 vs. 15.1 +/- 4.9 g), airway pressure, and pulmonary arterial pressure. In contrast to catalase, pretreatment with Cu-tryptophan (40 microM), a lipid-soluble scavenger of superoxide, provided no protective effect by itself, nor was there any potentiation of protection when combined with catalase. Further evidence implicating O2 metabolites in OA-induced edema was obtained by electron paramagnetic resonance (EPR) spectroscopy of perfusate samples to which the spin trap, sodium 3,5-dibromo-4-nitrosobenzenesulfonate (10 mM), was added. Analysis of these samples revealed the presence of free radicals after OA. Pretreatment with catalase (1,000 U/ml) and superoxide dismutase (250 U/ml) attenuated the EPR signal, indicating that proximal formation of O2 free radicals was in part responsible for the signal. These results suggest that reactive O2 metabolites are mediators of OA-induced pulmonary edema in the isolated perfused rabbit lung.

Animals↗
PubMed1988

Lidocaine concentrations in bronchoscopic specimens.

We measured lidocaine concentrations in bronchoscopic specimens and found that bronchoalveolar lavage (BAL) concentrations (16 +/- 7 micrograms/ml) were lower than those in bronchial washings (967 +/- 379 micrograms/ml [p less than 0.001]). Lidocaine concentrations in bronchial washings obtained "early" (991 +/- 505 micrograms/ml) compared with "late" (943 +/- 580 micrograms/ml) in the procedure did not differ (p = NS). High lidocaine concentrations sufficient to inhibit growth in culture of mycobacterial and fungal pathogens (greater than 5,000 micrograms/ml) occurred in one early and two late bronchial washings but no BAL specimens. No correlation between lidocaine dose and measured concentrations was noted in any specimen category; however, highest bronchial washing concentrations occurred with the use of greater than 250 mg of lidocaine. We conclude that BAL specimens are suitable for culturing pathogens that may be inhibited by lidocaine. Furthermore, collecting bronchial washings late in the procedure or limiting the lidocaine dosage do not reliably decrease measured lidocaine concentrations.

Bronchoalveolar Lavage Fluid↗
PubMed1988

Pleuropulmonary manifestations of actinomycosis and nocardiosis.

Actinomycosis and nocardiosis are uncommon pulmonary infections that share a similar predisposition to involve the pleural space. After establishment of an initial pneumonitis, infection spreads across lung fissures causing pleural thickening, pleural effusions, and empyema. Although less common in the antibiotic era, associated sinus tracts or subcutaneous abscesses may develop adjacent to pleural abnormalities. Both disorders most commonly present as chronic, debilitating illnesses with radiographic manifestations simulating lung cancer or tuberculosis; however, immunocompromised hosts may develop fulminant disease resembling acute bacterial pneumonia. Diagnosis depends on a high degree of suspicion so as to alert the microbiology and pathology laboratories to employ special methods to identify the organisms. The presence of pleural abnormalities in a chronic pulmonary condition is a diagnostic clue, and pleural fluid analysis may occasionally be the only means of confirming the diagnosis.

Actinomycosis↗
PubMed1988

The impact of respiratory failure on the diagnosis of tuberculosis.

Six patients with hypoxic respiratory failure (arterial PO2/alveolar PO2 less than 0.50) resulting from active tuberculosis were evaluated to assess the impact of respiratory failure on the diagnosis of the underlying tuberculosis. All patients demonstrated anemia (hematocrit [mean +/- SEM], 0.29 +/- 0.01 [29.0% +/- 1.0%]) and hypoalbuminemia (serum albumin, 22 +/- 2 g/L [2.2 +/- 0.2 g/dL]) and noted an illness longer than one week. Findings on chest roentgenograms varied from a miliary pattern, misinterpreted as congestive heart failure, to cavitary and noncavitary alveolar infiltrates, misdiagnosed as bacterial pneumonia. Tuberculosis was not considered as a diagnostic possibility on admission in any patient. The mean time from admission until consideration of tuberculosis was 4.7 +/- 1.0 days and the time to diagnosis was 7.2 +/- 1.7 days. In contrast, tuberculosis was considered on admission in 12 patients presenting with undiagnosed active tuberculosis without respiratory failure. We conclude that respiratory failure delays the diagnosis of active tuberculosis by suggesting nontuberculous pneumonia.

Adult↗
PubMed1988

Tracheal intubation in mechanically ventilated patients.

Airway management is an important skill in the care of patients undergoing mechanical ventilation. This article reviews the available techniques of tracheal cannulation and describes common complications, preferred routes of intubation, and approaches to weaning.

Humans↗