Pulmonary hypertension may be primary (idiopathic) or secondary. While the etiologies for secondary pulmonary hypertension are diverse, infection with the human immunodeficiency virus (HIV) has not been included. To date there have been 16 reported cases of pulmonary hypertension in the HIV-infected population. Plexogenic arteriopathy was the most common pathologic finding. We report two HIV-infected patients who were concomitantly found to have pulmonary hypertension with plexogenic arteriopathy. One patient had lymphocytic interstitial pneumonitis, an entity not previously associated with pulmonary hypertension. We review the 16 previous cases of pulmonary hypertension and HIV infection and discuss this association.

The purpose of this article is to assess critically the evidence for a causal relationship between gastric colonization by Gram-negative bacilli and nosocomial pneumonia in the intensive care unit. Articles were found using MEDLINE search and citations in relevant articles. Nine diagnostic tests of causation were applied and analysis showed that the major tests were satisfied. The strongest evidence comes from randomized controlled trials of selective gut decontamination and stress ulcer prophylaxis in intensive care units. These studies confirm that the incidence of nosocomial pneumonia correlates directly with the rate of gastric colonization by Gram-negative bacilli. Further support comes from other tests of causation such as strength and consistency of association, temporal relationship, and dose-response gradient. The data reviewed suggest that gastric colonization with Gram-negative bacilli plays a causal role in the development of nosocomial pneumonia in the intensive care unit patient. This relationship impacts on future studies of pathogenesis and prevention of this potentially lethal infection.

The major determinants of VO2 resp and, thus, diaphragmatic endurance are the tension-time index, work rate and lung volume. Changes in breathing pattern that adversely affect any of these factors can impair diaphragmatic endurance. A TTdi above 0.15-0.18 indicates a potentially fatiguing pattern of contraction. However, fatigue may occur at a TTdi below 0.15 if the work rate is sufficiently high or the Pdimax is not measured at the prevailing lung volume. Inspiratory muscle fatigue usually elicits an increase in minute ventilation and respiratory rate and to a lesser degree a reduction in tidal volume. However, fatigue may not always be accompanied by changes in breathing pattern. Furthermore, fatigue may sometimes result in a reduction rather than an increase in motor outflow to the respiratory muscles. Finally, abdominal paradox initially considered to be characteristic clinical sign of inspiratory muscle fatigue appears to be due to increases in respiratory load rather than to muscle fatigue.

Pulmonary embolus-in-transit represents an important cause of morbidity and mortality in the critically ill patient. Unexplained shock and acute pulmonary hypertension were evaluated with echocardiography. Standard transthoracic echocardiography failed to identify a large embolism-in-transit that was easily visualized by transesophageal imaging. A review of the literature involving emboli-in-transit suggests that early intervention in these patients may be beneficial.

The adult respiratory distress syndrome (ARDS) continues to demonstrate high mortality. This syndrome is frequently observed as a remote complication of another disease process and is characterized by a significant inflammatory component. The purpose of this review is to compare and contrast published research on the use of anti-inflammatory agents, steroidal and nonsteroidal, in animal models of acute lung injury. Emphasis is given to the nature of the experimental pulmonary injury, infusion (ie, oleic acid and zymosan-activated plasma) or bacteriologically (ie, endotoxin and live bacteria) induced and the timing of drug administration relative to induction of the insult. The clinical data available on the use of these drugs in ARDS are discussed, and a rationale is presented for future clinical trials in these patients.

Gram-negative sepsis remains an urgent medical problem, with more than 200,000 cases occurring each year in the United States and an associated mortality rate of 20 to 50 percent. Since the onset of shock greatly worsens prognosis and to encourage early intervention, the term sepsis syndrome was developed to describe the features of a preshock septic state. Early clinical and metabolic indicators are discussed, and current therapy is reviewed. Better understanding of the pathophysiology of endotoxin release from Gram-negative bacteria and advances in biotechnology have led to the development of potential new treatments for sepsis. One such development--monoclonal antibodies to endotoxin--has shown great promise in the effort to block the progression to septic shock, reduce mortality, and decrease the overall costs of sepsis to the patient and to the national economy.