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Biomedical subjects

R A Matthay

Publications and source records attributed to R A Matthay.

At least 37 records · Page 2Linked to original sources
PubMed1990

Malignancies metastatic to the pleura.

In patients over 50 years of age, neoplasms of the pleura are probably the second most common cause of a pleural effusion after congestive heart failure. Lung cancer, breast cancer, lymphoma, ovarian carcinoma, and stomach cancer are the leading causes of malignant pleural disease, and adenocarcinoma is the most common cell type. This review discusses in detail the etiology and incidence, pathogenesis, clinical manifestations, diagnosis, prognosis, and treatment of neoplasms that involve the pleura with special reference to malignant and paramalignant pleural effusions.

Humans↗
PubMed1990

Imaging techniques for assessing pulmonary artery hypertension and right ventricular performance with special reference to COPD.

Several imaging techniques, both noninvasive and minimally invasive, have now been applied widely for determining cardiovascular performance in patients with chronic respiratory disease, particularly COPD. Moreover, some of these techniques are useful for evaluating response to therapeutic intervention in these patients. The plain chest radiograph is useful primarily for detecting the presence of pulmonary artery hypertension in patients with COPD. Radionuclide angiocardiography, using either first-pass techniques or the gated equilibrium technique, is particularly useful for determining right and left ventricular ejection fraction. Echocardiography has evolved as a technique for assessing right ventricular size and function and, in some cases, the degree of pulmonary artery hypertension.

Echocardiography↗
PubMed1990

Pulmonary effects of cytotoxic agents other than bleomycin.

Multiple chemotherapeutic agents have been reported to cause pulmonary injury, usually manifested as interstitial pneumonitis and fibrosis. Several unique presentations have been described for mitomycin, methotrexate, and the combinations of mitomycin and vinca alkaloids. Mechanisms of lung injury remain mostly speculative, although ongoing investigations may someday elucidate such pathways of injury. With a greater understanding of how these agents damage lung tissue, physicians may be able to more safely administer these drugs to patients. The drugs which have been shown to cause pulmonary injury most frequently are BCNU, mitomycin (with and without vinca alkaloids), and methotrexate. All physicians using cytotoxic drugs must be aware of the potential for lung injury with these agents.

Antineoplastic Agents↗
PubMed1990

Cor pulmonale in chronic obstructive pulmonary disease. Circulatory pathophysiology and management.

The development of pulmonary hypertension and right ventricular failure in COPD patients signals a poor prognosis. In hypoxic patients, long-term oxygen therapy prolongs life and appears to prevent or lessen the progression of pulmonary hypertension. However, oxygen therapy does not benefit and is not indicated for all COPD patients, and even in those patients who improve with oxygen, there remains a need to further improve survival. Therefore, there continues to be active investigations into pharmacologic agents that might reduce pulmonary hypertension or improve right ventricular function. Although many agents appear to have salutary acute effects, it has been more difficult to establish evidence for sustained hemodynamic benefits from chronic drug therapy. Furthermore, some effective agents may not provide additive benefit when combined with standard supplemental oxygen use, although the available data are limited. Clearly, further research is necessary to identify which COPD patients, if any, may benefit from either beta-agonists or vasodilators for the treatment or prevention of cor pulmonale at some time during the natural history of their disease.

Adrenergic beta-Agonists↗
PubMed1990

Mechanical heart-lung interaction in the adult respiratory distress syndrome.

We have discussed the complex hemodynamic changes that occur throughout the respiratory cycle during spontaneous and mechanical ventilation. In patients, many cumulative factors account for the total hemodynamic burden of inspiration and expiration. Thus, the change in pleural pressure, ventilation rate, mode of ventilation, amount of spontaneous ventilation, underlying lung and cardiac disease, and intravascular volume status all affect cardiocirculatory equilibrium. In addition, in the patient with ARDS, various immune mediators that are released into the circulation will affect LV function. Knowledge of the effects discussed in this article will aid the physician in choosing therapeutic options for patients with ARDS.

Animals↗
PubMed1989

Differing responses in right and left ventricular filling, loading and volumes during positive end-expiratory pressure.

Using a combined hemodynamic and radionuclide technique, 20 patients with varied ventricular function were evaluated during positive end-expiratory pressure (PEEP) application. Left ventricular (LV) and right ventricular (RV) ejection fractions and cardiac output were measured, and ventricular volumes were derived. Seven patients (group 1) who had an increase in LV end-diastolic volume with PEEP and 13 patients (group 2) who had the more typical response, a decrease in LV end-diastolic volume with PEEP, were identified. Compared with group 2, group 1 patients had a higher incidence of coronary artery disease (5 of 7 vs 1 of 13, p less than 0.005) and lower cardiac output (3.9 +/- 1.6 vs 9.1 +/- 3.2 liters/min, p less than 0.005), LV ejection fraction (27 +/- 13 vs 51 +/- 21%, p less than 0.05), RV ejection fraction (15 +/- 6 vs 32 +/- 8%, p less than 0.005) and peak filling rate (1.32 +/- 0.43 vs 3.51 +/- 1.70 end-diastolic volumes/s, p less than 0.05). LV and RV volumes increased and peak filling rate decreased with PEEP in group 1, whereas in group 2 LV volume decreased and RV volume and peak filling rate remained unchanged. Using stepwise regression analysis, the change in LV volume with PEEP was related directly to baseline systemic vascular resistance and inversely to baseline blood pressure. Similarly, the change in peak filling rate with PEEP was inversely related to the change in RV end-diastolic volume. Thus, the hemodynamic response to PEEP is heterogeneous and may be related to LV ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Pulmonary manifestations of gastrointestinal disease.

The respiratory and gastrointestinal systems share several functional similarities. In health, the two systems remain structurally distinct and functionally integrated, so as to maintain physiologic homeostasis. However, in the setting of disease, pathophysiologic alterations in one system may be reflected in the other. This article focuses upon the nonmalignant gastrointestinal causes of respiratory illness. Using an anatomic approach, the pulmonary manifestations of selected gastrointestinal diseases are outlined. Emphasis is placed on the distinguishing features, pathophysiology, and therapy of the pulmonary sequelae of digestive diseases.

Esophageal Diseases↗
PubMed1989

Pulmonary manifestations of the collagen vascular diseases.

The collagen vascular diseases are a heterogeneous group of immunologically mediated inflammatory disorders. The organs and tissues that compose the respiratory system are frequently affected by these diseases. Potential targets of the inflammation and injury include the lung parenchyma, tracheobronchial tree, pulmonary vasculature, pleura, larynx, and respiratory muscles. In this article, the spectrum of respiratory disease caused by systemic lupus erythematosus, rheumatoid arthritis, scleroderma, polymyositis/dermatomyositis, mixed connective tissue disease, ankylosing spondylitis, relapsing polychondritis, and Sjögren's syndrome is reviewed. Where appropriate, therapeutic options are discussed.

Arthritis, Rheumatoid↗
PubMed1989

Pulmonary and pleural manifestations of extrathoracic malignancies.

Metastatic spread of nonpulmonary malignancies to the lung is a common clinical problem. However, the evaluation and treatment of metastatic lung disease may be confusing. This article considers both pulmonary and pleural metastases. The basic biology of the metastatic process is discussed, together with the pathologic, clinical, radiologic, diagnostic, and therapeutic features of pulmonary metastases. Metastatic disease to the pleura is reviewed in detail, including etiology and incidence, pathogenesis, clinical manifestations, diagnosis, prognosis, and treatment.

Bone Neoplasms↗
PubMed1988

Effect of positive end-expiratory pressure on right ventricular performance. Importance of baseline right ventricular function.

Thirty-six patients with diverse baseline right ventricular function were evaluated during incremental positive end-expiratory pressure (PEEP) application. Right heart pressures, cardiac output, right ventricular ejection fractions, and ventricular volumes were obtained at each PEEP level. Right ventricular peak systolic pressure-end-systolic volume relations were analyzed as an index of contractile function. Patients with severely depressed baseline right ventricular ejection fractions (30 percent or less) had an increase in end-diastolic (270 +/- 74 to 391 +/- 76 ml, 0 to 20 cm water (H2O) PEEP, p less than 0.05) and end-systolic volumes (210 +/- 70 to 321 +/- 70 ml, 0 to 20 cm H2O PEEP, p less than 0.05). These patients also had a decline in estimated right ventricular contractile function at 20 cm H2O PEEP as estimated by the slope of systolic pressure-volume relations (0.12 to 0.04 mm Hg/ml, 0 to 15 and 15 to 20 cm H2O PEEP, respectively, p less than 0.05). Patients with normal (40 percent or more) or moderately depressed (31 to 40 percent) baseline right ventricular ejection fractions had no change in right ventricular volumes or estimated contractile function. Therefore, the effect of PEEP on right ventricular function differs depending on the baseline right ventricular ejection fraction.

Adult↗
PubMed1988

Terbutaline and diaphragm function in chronic obstructive pulmonary disease: a double-blind randomized clinical trial.

We conducted a double-blind, randomized crossover trial to evaluate whether oral terbutaline (2.5 mg orally three times daily for a week) increased the force of diaphragmatic contraction in normocapnic patients with chronic obstructive pulmonary disease. Ten patients with moderate to severe airway obstruction completed the trail. Compared with placebo, terbutaline produced a mean increase of 5.8 cmH2O in peak inspiratory mouth pressure and a mean increase of 5.0 cmH2O in transdiaphragmatic pressure during a maximal inspiratory manoeuvre. These small changes with terbutaline failed to achieve statistical significance. Also, terbutaline failed to alter flow rates (FEV1, Vmax50) or patients' dyspnoea ratings using two separate clinical scales (Pneumoconiosis Research Unit Score and the Modified Dyspnoea Index). Because all observed changes in respiratory muscle strength were small and because the trial had power to detect small changes in inspiratory mouth pressures, we suggest that oral terbutaline at the dose administered in this study has little noteworthy effect on respiratory muscle strength in normocapnic patients with chronic obstructive pulmonary disease.

Aged↗
PubMed1988

Oral terbutaline augments cardiac performance in chronic obstructive pulmonary disease.

In previous research, we have demonstrated that parenterally administered terbutaline can augment resting cardiac function in patients with chronic obstructive pulmonary disease (COPD). Because the oral form of terbutaline is more widely utilized, a double-blind, randomized, crossover, placebo-controlled trial of the cardiopulmonary effects of oral terbutaline was conducted in ten patients with COPD. Right and left ventricular ejection fractions (RVEF and LVEF) were determined by first pass radionuclide angiography. There were no differences in spirometry and hemodynamic measurements between treatment and placebo days. Following 5 mg of oral terbutaline, there was a small but statistically significant increase in forced expiratory volume in 1 second and in heart rate, but no significant change in forced vital capacity or blood pressure. LVEF improved significantly with terbutaline both at rest (62% +/- 6% vs. 67% +/- 9%, mean +/- SD) and during submaximal steady state exercise (61% +/- 5% vs. 67% +/- 10%). RVEF improved significantly at rest (64% +/- 6% vs. 69% +/- 5%), but not during submaximal steady state exercise (65% +/- 6% vs. 68% +/- 7%). Thus, oral terbutaline produces significant improvement in biventricular systolic pump performance at rest, and increases left ventricular ejection fraction during submaximal exercise in patients with moderate to severe COPD.

Administration, Oral↗
PubMed1988

Mechanisms of drug-induced pulmonary disease.

Administration of a number of therapeutic agents is associated with respiratory alterations. Mechanisms of these alterations are unclear but may include both direct toxic effects of the drugs and indirect effects through actions of the drugs on inflammatory cells. This review discusses mechanisms of the varied patterns of drug-induced pulmonary disease.

Alveolitis, Extrinsic Allergic↗
PubMed1988

The effect of incremental positive end-expiratory pressure on right ventricular hemodynamics and ejection fraction.

The effects of incremental positive end-expiratory pressure (PEEP) on right ventricular (RV) function were evaluated in 36 (n = 36) ventilated patients. Positive end-expiratory pressure was increased from 0 (baseline) to 20 cm H2O in 5-cm H2O increments and RV hemodynamics and thermally derived right ventricular ejection fraction (RVEF), right ventricular end-diastolic volume index (RVEDVI), and right ventricular end-systolic volume index (RVESVI) were computed. Right ventricular contractility was determined from the analysis of RV systolic pressure-volume relations. Right ventricular ejection fraction declined from 42 +/- 8% at baseline to 30 +/- 9% at 20 cm H2O PEEP. Right ventricular end-diastolic volume index declined between 0 and 5 cm H2O PEEP (103 +/- 42 to 92 +/- 34 ml.m-2) and then increased to 113 +/- 40 at 20 cm H2O PEEP. Right ventricular end-systolic volume index increased from 60 +/- 31 ml.m-2 at baseline to 79 +/- 34 ml.m-2 at 20 cm H2O PEEP. The slope (E) of the relation of RV peak systolic pressure to RV end-systolic volume index decreased from 0.26 mm Hg.m2.ml-1 between PEEP of 0-15 cm H2O to 0.05 mm Hg.m2.m-1 at PEEP greater than 15 cm H2O. It is concluded that low levels of PEEP have a predominant preload reducing effect on the RV. Above 15 cm H2O PEEP, RV volumes increase and E decreases, consistent with increased RV afterload and a decline in RV contractility.

Adult↗
PubMed1988

Effects of mechanical ventilation on right and left ventricular function.

We have discussed the complex hemodynamic changes that occur throughout the respiratory cycle during mechanical ventilation and have reviewed the physiologic changes associated with spontaneous respiration. In patients, many cumulative factors account for the total hemodynamic burden of mechanical inspiration and expiration. Thus, the change in pleural pressure, respiratory rate, mode of ventilation, amount of spontaneous ventilation, underlying lung and cardiac disease, and intravascular volume status all affect cardiocirculatory equilibrium during the respiratory cycle. Knowledge of the effects presented in this article will aid the physician in choosing the therapeutic options in instrumented, mechanically ventilated patients.

Cardiac Output↗
PubMed1987

Drug-induced pulmonary disease.

Administration of more than 40 separate pharmacologic agents has been associated with some form of pulmonary toxicity. This problem is becoming more significant every year. Occasionally, effective modes of therapy must be withdrawn because of undesirable pulmonary side effects, putting patients at risk for potentially lethal diseases. Pulmonary parenchymal damage due to drugs is an especially troublesome problem because irreversible pulmonary disease may occur. Mechanisms of pulmonary parenchymal tissue damage by drugs are unclear. It appears that some drugs induce direct tissue injury in addition to indirect tissue damage through amplification of pulmonary inflammation; other drugs cause pulmonary alterations solely through indirect mechanisms. Common clinical syndromes associated with drug-induced pulmonary parenchymal disease include pneumonitis/fibrosis, hypersensitivity lung disease, and noncardiogenic pulmonary edema. Less common patterns of pulmonary parenchymal injury by drugs include bronchiolitis obliterans and a pulmonary renal syndrome. Risk factors for pulmonary injury due to pharmacologic agents are partially defined but not entirely understood. To date, there are no adequate tests for early detection of pulmonary damage by drugs, although research into this area is active. This review discusses mechanisms and clinical features of drug-induced pulmonary parenchymal injury to aid the clinician in recognizing and understanding these syndromes.

Anti-Arrhythmia Agents↗
PubMed1987

Favorable cardiovascular effects of theophylline in COPD.

Theophylline has been utilized widely as a bronchodilator. However, recent studies have shown the potential for administering this drug to enhance cardiovascular performance in patients with chronic obstructive pulmonary disease (COPD). Administered to COPD patients orally as a sustained-action preparation or intravenously as aminophylline, theophylline enhances both right and left heart systolic pump function and lowers both pulmonary artery pressure and pulmonary vascular resistance. These favorable cardiovascular actions suggest an additional use for theophylline in COPD beyond its effects as a bronchodilator.

Administration, Oral↗