Traditionally, ventilatory limitation (constraint) during exercise has been determined by measuring the ventilatory reserve or how close the minute ventilation (VE) achieved during exercise (i.e., ventilatory demand) approaches the maximal voluntary ventilation (MVV) or some estimate of the MVV (i.e., ventilatory capacity). More recently, it has become clear that rarely is the MVV breathing pattern adopted during exercise and that the VE/MVV relationship tells little about the specific reason(s) for ventilatory constraint. Although it is not a new concept, by measuring the tidal exercise flow-volume (FV) loops (extFVLs) obtained during exercise and plotting them according to a measured end-expiratory lung volume (EELV) within the maximal FV envelope (MFVL), more specific information is provided on the sources (and degree) of ventilatory constraint. This includes the extent of expiratory flow limitation, inspiratory flow reserve, alterations in the regulation of EELV (dynamic hyperinflation), end-inspiratory lung volume relative to total lung capacity (or tidal volume/inspiratory capacity), and a proposed estimate of ventilatory capacity based on the shape of the MFVL and the breathing pattern adopted during exercise. By assessing these types of changes, the degree of ventilatory constraint can be quantified and a more thorough interpretation of the cardiopulmonary exercise response is possible. This review will focus on the potential role of plotting the extFVL within the MFVL for determination of ventilatory constraint during exercise in the clinical setting. Important physiologic concepts, measurements, and limitations obtained from this type of analysis will be defined and discussed.

To review the literature to determine the benefits of corticosteroids (CCSs) (oral, IM, IV, or inhaled) in the treatment of adult patients with acute asthma presenting at an acute-care setting.

A 29-year-old woman with an unusual form of pulmonary metastasis from epithelioid sarcoma of the right forearm is presented. Since she manifested left pneumothorax due to metastatic pulmonary cyst 7 years ago, the only metastatic manifestation has been the presence of bilateral multiple thin-walled pulmonary cysts; no other types of pulmonary lesions, such as nodules, cavitary lesions with thick or irregular walls, or extrapulmonary metastases, have been found. Pathologic studies revealed metastatic proliferation of sarcoma cells in the wall of the pulmonary cysts and infiltration of malignant cells inside the microscopic cavitary metastases surrounded by normal lung parenchyma.

Ticks are capable of transmitting viruses, bacteria, protozoa, and rickettsiae to man. Several of these tick-borne pathogens can lead to pulmonary disease. Characteristic clinical features, such as erythema migrans in Lyme disease, or spotted rash in a spotted fever group disease, may serve as important diagnostic clues. Successful management of tick-borne diseases depends on a high index of suspicion and recognition of their clinical features. Patients at risk for tick bites may be coinfected with two or more tick-borne pathogens. A Lyme vaccine has recently become available for use in the United States. Disease prevention depends on the avoidance of tick bites. When patients present with respiratory symptoms and a history of a recent tick bite or a characteristic skin rash, a differential diagnosis of a tick-borne pulmonary disease should be considered. Early diagnosis and appropriate antibiotic therapy for these disorders lead to greatly improved outcomes.

To identify the drugs associated with pleural disease and to review the clinical, radiographic, and pleural fluid findings that occur, the natural history of the pleural reaction, and the response to therapy.

Pulmonary hypertension (PH) is a chronic and disabling condition that affects the pulmonary vasculature. Once PH is diagnosed, the prognosis is generally poor with a rapid downhill course. PH management is largely empirical because the underlying pathophysiologic mechanisms that are responsible for the excessive vasoconstrictor and vascular smooth muscle proliferative responses are poorly understood. Based on new information concerning the role of adrenergic receptors in regulating various cellular functions, a new perspective on the genesis of PH has emerged, along with a unifying hypothesis for the role of alpha1-adrenergic receptors present in the pulmonary vasculature as the major contributor to the pathophysiologic changes associated with PH. Adrenergic receptors that are present on vascular smooth muscle cells regulate vascular tone and growth. The alpha1-adrenergic receptors that are present on the small- and medium-sized pulmonary arteries have a unique and greatly enhanced affinity and activity to alpha1-adrenergic agonists. Under physiologic conditions, this helps in regulating vascular tone and maintains an adequate ventilation/perfusion matching. However, the excessive stimulation of alpha1-adrenergic receptors produces not only smooth muscle contraction but also proliferation and growth. The conditions that produce an increase in alpha1-adrenoreceptor gene synthesis, density, and activity (such as hypoxia or changes in vessel wall pressure) or increase the levels of its agonists (such as norepinephrine, appetite suppressants, or cocaine) greatly enhance pulmonary vascular smooth muscle contractile and proliferative responses and lead to the development of PH. An understanding of the role played by these receptors in the pathophysiology of PH would not only help to avoid the use of alpha1-agonists for appetite suppression and other disease states, but also would help in developing new drugs to block these receptors. A further understanding of the alpha1-adrenoreceptor subtypes present in the pulmonary vasculature, the factors that regulate their expression, and their intracellular signaling pathways would help researchers to devise newer therapeutic strategies and, hopefully, to find a cure for this crippling condition.

Pulmonary embolism (PE) is a common disorder that is accompanied by significant morbidity and mortality. Although anticoagulation is the standard treatment for PE, thrombolytic therapy, with its ability to produce rapid clot lysis, has long been considered an attractive alternative. Although many studies have been performed over the past three decades, however, the indications for the use of thrombolytic agents in patients with PE remain controversial. In this article, we review the medical literature and provide evidence-based guidelines for the use of thrombolytic therapy. We will also discuss the practical aspects of PE thrombolysis.

Like 201Tl imaging, technetium Tc 99m sestamibi (MIBI) myocardial imaging can be used with exercise and pharmacologic testing to assess the presence of coronary artery disease. An increasing body of literature indicates that MIBI can also be used to assess risk of future cardiac events such as myocardial infarction or death. This article summarizes the current status of MIBI imaging for evaluating prognosis in patients with known or suspected coronary artery disease.