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Purpose Central vein point-of-care ultrasonography must be reproducible to detect intravascular volume changes. We sought to determine which measurement step, image acquisition or interpretation, could be more compromising for reproducibility. Methods Three investigators each acquired inferior vena cava (IVC) and internal jugular (IJV) vein ultrasonographic sequences (US) from a convenience sample of 21 hospitalized general medicine participants and then interpreted each US three separate times. We partitioned the random errors of acquisition and interpretation, attributing wider dispersions of each to larger reductions in reproducibility. Results We analyzed 351 interpretations of 39 IVC and 432 interpretations of 48 IJV US. Reproducibility of the maximum (standard error of measurement 3.3 mm [95% confidence interval, CI 2.7–4.2 mm]) and minimum (4.8 mm [3.9–6.3 mm]) IVC diameter measurements were worse than that of the mediolateral (2.5 mm [2.0–3.2 mm]) and anteroposterior (2.5 mm [2.0–3.1 mm]) IJV diameters. The dispersions of random measurement errors were wider among acquisitions than interpretations. Conclusions Among our investigators, central vein diameter measurements obtained by point-of-care ultrasonography are not sufficiently reproducible to distinguish clinically meaningful intravascular volume changes from measurement errors. Reproducibility could be most effectively improved by reducing the random measurement errors of acquisition. © 2017 Wiley Periodicals, Inc. J Clin Ultrasound, 2017

OBJECTIVE Plots of blood volume measurements over time (profiles) may identify euvolemia during fluid removal for acute heart failure. We assessed agreement between two noninvasive measurements of blood volume profiles during mechanical fluid removal, which exemplifies the interstitial fluid shifts that occur during diuretic-induced fluid removal. APPROACH During hemodialysis we compared change in maximum diameter of the inferior vena cava by ultrasound ([Formula: see text]) to change in relative blood volume derived from capillary hemoglobin concentration from finger-clip spectrophotometry (RBVSpHb). We grouped profiles of these measurements into three distinct shapes using an unbiased, data-driven modeling technique. METHODS Fifty patients who were not in acute heart failure underwent a mean of five paired measurements while an average of 1.3 liters of fluid was removed over 2 h during single hemodialysis sessions. [Formula: see text] changed -1.0 mm (95% CI -1.9 to -0.2 mm) and the RBVSpHb changed -1.1% (95% CI -2.7 to +0.5%), but these changes were not correlated (r -0.04, 95% CI -0.32 to +0.24). Nor was there agreement between categorization of profiles of change in the two measurements (kappa -0.1, 95% CI -0.3 to +0.1). SIGNIFICANCE [Formula: see text] and RBVSpHb estimates of blood volume do not agree during mechanical fluid removal, likely because regional changes in blood flow and pressure modify IVC dimensions as well as changes total blood volume.

Central airway stenosis is extremely rare in pregnancy and could lead to respiratory and cardiovascular embarrassment, especially at the time of delivery. Initially, patients may not show obvious signs of respiratory difficulty. Early recognition of the disease and anticipatory management of a complicated delivery are very important. We present a pregnant patient with tuberculosis-induced severe tracheobronchial stenosis and discuss the management challenges of her delivery.

A 62-year-old woman presented with a 3-month history of abdominal distension and decreased exercise tolerance. A chest radiograph showed a probable left pleural effusion (Fig 1). A CT scan of the abdomen revealed a solid ovarian mass with omental caking and a large volume of ascites; there was also confirmation of a left pleural effusion. Three days before surgery a CT pulmonary angiogram (CTPA) showed no evidence of pulmonary thromboembolism (PTE). The patient had some improvement in her symptoms after paracentesis and thoracentesis with drainage of 2,000 mL and 250 mL of fluid, respectively. She underwent total abdominal hysterectomy, bilateral oophorectomy, and partial sigmoid resection with an estimated blood loss of 850 mL. During the operation, she received 5 L of crystalloid and required phenylephrine at 40 to 80 μg/min to maintain a mean arterial pressuregt; 65 mm Hg. She was extubated after surgery, but immediately after extubation, she became markedly hypotensive and hypoxemic with a BP of 50/20 mm Hg and an oxygen saturation of 70%. An ECG showed T-wave inversions from V1 to V5 and an S1Q3T3 pattern (Fig 2). A bedside echocardiogram showed an enlarged right ventricle (RV), septal dyskinesia, and obliteration of the left ventricle, all consistent with systolic and diastolic RV overload (Fig 3).

Imperceptible levels of proportional assist ventilation applied throughout inspiration reduced inspiratory time (Ti) in awake humans. More recently, the reduction in Ti was associated with flow assist, but flow assist also reaches a maximum value early during inspiration. To test the separate effects of flow assist and timing of assist, we applied a pseudorandom binary sequence of flow-assisted breaths during early, late, or throughout inspiration in eight normal subjects. We hypothesized that imperceptible flow assist would shorten Ti most effectively when applied during early inspiration. Tidal volume, integrated respiratory muscle pressure per breath, Ti, and Te were recorded. All stimuli (early, late, or flow assist applied throughout inspiration) resulted in a significant increase in inspiratory flow; however, only when the flow assist was applied during early inspiration was there a significant reduction in Tiand the integrated respiratory muscle pressure per breath. These results provide further evidence that vagal feedback modulates breathing on a breath-by-breath basis in conscious humans within a physiological range of breath sizes.

A direct relationship exists within subjects between midlatency features (

In 2009, the American Thoracic Society (ATS) funded an assembly project, Palliative Management of Dyspnea Crisis, to focus on identification, management, and optimal resource utilization for effective palliation of acute episodes of dyspnea. We conducted a comprehensive search of the medical literature and evaluated available evidence from systematic evidence-based reviews (SEBRs) using a modified AMSTAR approach and then summarized the palliative management knowledge base for participants to use in discourse at a 2009 ATS workshop. We used an informal consensus process to develop a working definition of this novel entity and established an Ad Hoc Committee on Palliative Management of Dyspnea Crisis to further develop an official ATS document on the topic. The Ad Hoc Committee members defined dyspnea crisis as "sustained and severe resting breathing discomfort that occurs in patients with advanced, often life-limiting illness and overwhelms the patient and caregivers' ability to achieve symptom relief." Dyspnea crisis can occur suddenly and is characteristically without a reversible etiology. The workshop participants focused on dyspnea crisis management for patients in whom the goals of care are focused on palliation and for whom endotracheal intubation and mechanical ventilation are not consistent with articulated preferences. However, approaches to dyspnea crisis may also be appropriate for patients electing life-sustaining treatment. The Ad Hoc Committee developed a Workshop Report concerning assessment of dyspnea crisis; ethical and professional considerations; efficient utilization, communication, and care coordination; clinical management of dyspnea crisis; development of patient education and provider aid products; and enhancing implementation with audit and quality improvement.

Dyspnea may be defined as an uncomfortable sensation of breathing. The sense of respiratory effort, chemoreceptor stimulation, mechanical stimuli arising in lung and chest wall receptors, and neuroventilatory dissociation may all contribute to the sensation of dyspnea. Different mechanisms likely give rise to qualitatively different sensations of dyspnea. In most patients, dyspnea is probably due to a combination of mechanisms. For example, in asthma, a heightened sense of effort, neuroventilatory dissociation, and vagal stimuli arising from bronchoconstriction and airway inflammation may all play a role. Patients with different disorders and different mechanisms of dyspnea use different phrases to describe their breathing discomfort. Hence, the language patients use to describe their dyspnea may provide clues to the etiology of their symptoms.

IMPLICATIONS We report a case of toxicity from the drug solvent propylene glycol resulting from prolonged, large-dose lorazepam infusion. The case is unusual in that toxicity developed during continuous veno-venous hemofiltration with dialysis, a renal replacement therapy that should been have been effective at eliminating the chemical and its metabolites.

Background This consensus statement was developed based on the understanding that patients with advanced lung or heart disease are not being treated consistently and effectively for relief of dyspnea. Methods A panel of experts was convened. After a literature review, the panel developed 23 statements covering five domains that were considered relevant to the topic condition. Endorsement of these statements was assessed by levels of agreement or disagreement on a five-point Likert scale using two rounds of the Delphi method. Results The panel defined the topic condition as "dyspnea that persists at rest or with minimal activity and is distressful despite optimal therapy of advanced lung or heart disease." The five domains were: measurement of patient-reported dyspnea, oxygen therapy, other therapies, opioid medications, and ethical issues. In the second round of the Delphi method, 34 of 56 individuals (61%) responded, and agreement of at least 70% was achieved for 20 of the 23 statements. Conclusions For patients with advanced lung or heart disease, we suggest that: health-care professionals are ethically obligated to treat dyspnea, patients should be asked to rate the intensity of their breathlessness as part of a comprehensive care plan, opioids should be dosed and titrated for relief of dyspnea in the individual patient, both the patient and clinician should reassess whether specific treatments are serving the goal of palliating dyspnea without causing adverse effects, and it is important for clinicians to communicate about palliative and end-of-life care with their patients.

Breathlessness induced by hypercapnia may be related to the sensation of respiratory effort or to the central or peripheral effects of CO2. To examine the relationship among breathlessness, respiratory effort, and hypercapnia, we studied eight normal naive subjects. By using a visual feedback system, subjects maintained a constant ventilation of 50-60 L/min. PETCO2 was held at 40 mm Hg during the first 2 min of each trial (control period), then for 4 min (test period) was either kept at 40 mm Hg or elevated to 50 mm Hg. At the end of each control and test period, subjects were asked to give separate ratings for dyspnea (an unpleasant urge to breathe) and for the sense of respiratory effort (analogous to lifting a weight) on a 50-cm visual analog scale. Hypercapnia was associated with a significant reduction in effort ratings (-7.3 +/- 6.4, mean +/- SD, p0.05) and a concomitant increase in dyspnea (+6.6 +/- 6.0, p0.05). We conclude that dyspnea associated with hypercapnia is dissociated from changes in respiratory effort, and that CO2 has a direct central effect that leads to breathlessness. Our data also suggest that the sense of effort at a given level of ventilation is less when the ventilation is the result of "reflex" stimuli to breathe rather than "voluntary" signals to the respiratory muscles.

Unlike individuals with comparable degrees of respiratory muscle weakness from other causes, quadriplegic patients have a blunted ventilatory and P0.1 response to hypercapnia. This suggests that the diminished response in quadriplegia is due, in part, to an alteration in respiratory drive. We measured the hypercapnic response in 9 subjects with chronic quadriplegia (Q) and 8 normal controls (N). Ventilatory muscle strength, maximum voluntary ventilation (MVV), and lung volumes were measured in all subjects. The ventilatory response (HCVR) in Q was significantly less than in N (0.73 ± 0.37 vs 2.95 ± 0.4 L·min −1 · mmHg −1 ; P , even when normalized for indices of respiratory muscle performance (e.g., vital capacity, MVV). There was no significant change in the HCVR in Q after the administration of naloxone. We also serially studied 2 subjects with acute quadriplegia, and found that despite progressive improvement in respiratory muscle performance, there was no accompanying increase in the response to hypercapnia. These data suggest that muscle weakness alone cannot explain the blunted hypercapnic response in quadriplegia, and are consistent with the hypothesis that these subjects have a reduced ventilatory drive.

Limited information is available about current practice patterns involving the use of antibiotics in the inpatient management of acute exacerbations of chronic obstructive pulmonary disease (AECOPD). We sought to characterize current patterns of antibiotic use and to compare them to evidence-based guidelines. This study is a retrospective case series of patients at a regional tertiary care medical center. Charts were reviewed to identify patients admitted between January 2006 and 2008 with an initial diagnosis of AECOPD who had no evidence of another infectious process and who were not immunocompromised. Relevant data extracted from charts included initial clinical presentation, antibiotic administration, microbiological studies, and hospital course. One hundred sixteen admissions meeting inclusion criteria were identified. There was no statistically significant relationship between the presence of an established indication for antibiotic administration and the use of antibiotics, with roughly 75% of patients in all groups receiving therapy. A significant fraction of patients received combination therapy that was more appropriate for the management of pneumonia than for AECOPD. There were significant deviations between practice patterns and guidelines regarding the use and selection of antibiotics. Some of these may reflect areas of uncertainty in the primary literature and varying sets of guidelines.

A recent randomized trial of mechanical ventilation in acute lung injury (ALI)/adult respiratory distress syndrome (ARDS) demonstrated a 22% relative reduction in mortality rate using 6 mL/kg predicted body weight tidal volume vs. 12 mL/kg predicted body weight tidal volume. We determined whether publication of these findings changed clinical practice.Retrospective cohort, 12 months before (Pre) and 12 months after publication (Post) of a randomized trial supporting the use of a 6 mL/kg predicted body weight tidal volume strategy.Three tertiary care hospitals in northern New England.From a sample of 943 patients receiving prolonged mechanical ventilation between 1998 and 1999 (Pre) and between 2000 and 2001 (Post), 300 patients meeting the American-European Consensus Conference definition of ALI or ARDS were selected for analysis.The tidal volume, tidal volume/kg predicted body weight, and proportion receiving tidal volume/kgor =6 mL/kg andor =12 mL/kg predicted body weight were recorded at noon the first day after the diagnosis of ALI or ARDS was established.Pre and Post mean tidal volume (+/- sd) size and tidal volume size/kg predicted body weight were 759 +/- 158 mL (median 750 mL) vs. 639 +/- 138 mL (median 600 mL, p.001) and 12.3 +/- 2.7 mL/kg (median 11.7 mL/kg) vs. 10.6 +/- 2.4 mL/kg (median 10.7 mL/kg, p.001) respectively. Pre and Post plateau pressures and peak airway pressures were similar.Publication of a trial demonstrating large mortality reductions using small tidal volume was associated with significant reductions in tidal volume delivered to patients with ALI/ARDS. However, wide variation in practice persists, and the proportion of patients receiving tidal volumes within recommended limits (or =8 mL/kg) remains modest.

Acute respiratory distress syndrome is the clinical manifestation of severe, acute lung injury. It is characterized by the acute onset of diffuse, bilateral pulmonary infiltrates secondary to noncardiogenic pulmonary edema, refractory hypoxia, and decreased lung compliance. Acute respiratory distress syndrome occurs most frequently in the setting of sepsis, aspiration of gastric contents, trauma, or multiple transfusions. Its complex pathophysiology involves an inciting local or systemic event that initiates pulmonary endothelial and epithelial damage and subsequent increased permeability. Tachypnea, hypoxia, and respiratory alkalosis are typical early clinical manifestations, and they are usually followed by the appearance of diffuse pulmonary infiltrates and respiratory failure within 48 hours. Early identification and treatment of the underlying disorder, along with aggressive supportive care, are essential. Experimental therapies, including those using nitric oxide and surfactant, have not been shown to improve mortality in patients with ARDS, but new therapeutic approaches such as low-volume ventilation have been shown to decrease mortality. Many patients who survive ARDS have permanent, mild to moderate impairment of lung function. Quality of life after hospitalization with ARDS may be poorer than that in similar patients without ARDS.

Instillation into the urinary tract of the bacillus Calmette-Guérin (BCG), a strain of Mycobacterium bovis, is associated only rarely with severe side effects. We report here two cases of culture-proven pulmonary infection due to therapy with BCG. The first patient, who was seropositive for the human immunodeficiency virus, developed bilateral interstitial pneumonitis after instillation of BCG into the bladder. The second patient developed a right-lower-lobe infiltrate and empyema after instillation of BCG into the right renal pelvis. The clinical isolates from these two patients and from a third patient with a psoas abscess following intravesical instillation were analyzed with use of pulsed field gel electrophoresis (PFGE) to resolve chromosomal restriction fragment polymorphisms. The clinical isolates were confirmed to be BCG by comparison with known vaccine strains that differed from M. bovis isolates. We conclude that the potential for subsequent dissemination be considered prior to the intravesical administration of BCG. Analysis with PFGE may be useful for identifying species of the Mycobacterium tuberculosis complex.

Dyspnea is a cardinal symptom of asthma and may arise from several pathophysiological mechanisms, including pulmonary hyperinflation, stimulation of vagal receptors, and, rarely, chemoreceptor stimulation. The language that patients use to describe their breathlessness may provide important clues about the physiology underlying symptoms in a particular patient. Several physiological derangements may contribute to dyspnea in a given individual. The variability in the severity of breathlessness for any given degree of airflow obstruction may relate to differences in the relative importance of these physiological changes and/or to a range of perceptual abilities in asthmatic patients. One hypothesis that is under current investigation is that defective perception of asthma symptoms may lead to undertreatment and the potential for greater morbidity and mortality from asthma.

Objective: To examine the phenomenon of inappropriate triggering caused by an in-line suction catheter. Design: We used a test lung to assess inappropriate triggering in four ventilators with both pressure and flow triggering. Results: With pressure triggering, inappropriate triggering occurred only in the presence of PEEP. However, with flow triggering, inappropriate triggering occurred both with and without PEEP. Inappropriate triggering did not occur in a model of severe airflow obstruction. Conclusion: In-line suction catheters may lead to inappropriate triggering and potentially dangerous increases in delivered ventilation.

Evidence of the Hering-Breuer reflex has been found in humans during anesthesia and sleep but not during wakefulness. Cortical influences, present during wakefulness, may mask the effects of this reflex in awake humans. We hypothesized that, if lung volume were increased in awake subjects unaware of the stimulus, vagal feedback would modulate breathing on a breath-to-breath basis. To test this hypothesis, we employed proportional assist ventilation in a pseudorandom sequence to unload the respiratory system above and below the perceptual threshold in 17 normal subjects. Tidal volume, integrated respiratory muscle pressure per breath, and inspiratory time were recorded. Both sub- and suprathreshold stimulation evoked a significant increase in tidal volume and inspiratory flow rate, but a significant decrease in inspiratory time was present only during the application of a subthreshold stimulus. We conclude that vagal feedback modulates respiratory timing on a breath-by-breath basis in awake humans, as long as there is no awareness of the stimulus.

We encountered a young woman with severe central sleep apnea caused by a medullary glioma located slightly dorsal to and to the right of the midline, a region not generally associated with CO(2) chemosensitivity. The patient had normal spirometric readings, lung volumes, diffusing capacity, maximal inspiratory pressure, and alveolar-arterial oxygen difference. While awake, she displayed marked irregularity in her breathing pattern; her end-tidal CO(2) (FET(CO(2))) ranged from 5.3 to 10.9%. During voluntary hyperpnea, she could quickly reduce her FET(CO(2)) to 4.2%, but her PCO(2) did not change after administration of acetazolamide or progesterone. Like patients with congenital central hypoventilation syndrome (CCHS), our patient had a relatively intact ventilatory response to exercise; her PCO(2) was high at the start of exercise and increased slightly thereafter. In contrast to CCHS patients, however, our patient had an intact hypoxic ventilatory response (DeltaVE/ DeltaSa(O(2)) = -0.37 L/min/Sa(O(2))). In further contrast to CCHS patients, our patient had a very short breathholding time and described a sensation of air hunger as the factor limiting her breathholding ability. Her heart rate and blood pressure responses to the Valsalva maneuver were normal.

This paper reviews new developments in bronchodilator therapy for chronic obstructive pulmonary disease (COPD). Most patients with COPD respond to bronchodilators, but we have no reliable way to predict which patients will respond. When responsiveness is assessed, changes in lung volume as well as improvements in FEV1 should be considered. The combination of a beta-agonist and an anticholinergic agent produces greater improvement than either agent alone. Anticholinergic agents have few adverse side effects in patients with COPD, but concern remains about the possible cardiac side effects of beta-agonists. No clear answer exists about whether new, long-acting beta-agonists, such as salmeterol, should supplant anticholinergic agents as "first-line" therapy in COPD.

We used the global field power (GFP) to estimate the magnitude and timing of activation of the somatosensory cortex by respiratory mechanoreceptor afferents in normal humans in response to brief, negative oral pressure pulses applied at the onset of inspiration. We compared responses before (test) and after insertion of a laryngeal mask airway (LMA) that prevented supraglottal airway receptors from sensing the applied stimulus. Evoked potential responses without supraglottic stimulation were smaller, with delayed or missing features, than those with all receptors stimulated. Supraglottic receptors contribute about one-half of the GFP summed over the 100 ms poststimulus, and subglottal receptors, including those in the larynx, provide a GFP response ∼38% above baseline. The most obvious difference between test and LMA responses occurred at 55 ms on average, when the LMA GFP lacked activation features seen in the test condition. We conclude that mechanoreceptors above the larynx are responsible for a major portion of the midlatency afferent information arriving at the somatosensory cortex in response to applied pressure pulses.

We examined the effect of inspiratory flow rate (IFR) on respiratory sensation during mechanical ventilation in 10 normal subjects. We adjusted the ventilator tidal volume (VT), frequency, and IFR until subjects indicated that they were maximally comfortable ("comfort IFR"). Subjects then rated breathing discomfort on a visual analog scale (VAS) while IFR was varied among four levels: 70%, 100%, 200%, and 300% of the comfort IFR. When compared with VAS ratings at the comfort IFR (4.4 +/- 1.2, mean +/- SEM), VAS ratings were significantly greater at the lowest (i.e., 70% comfort; 12.1 +/- 2.1) and highest (300% comfort; 8.2 +/- 0.9) IFR; there was no difference in ratings between the comfort IFR and 200% comfort IFR. At the lowest IFR, the breathing discomfort arose in the chest and had an air hunger-like quality; at high IFR, the discomfort arose in the upper airway. In the second portion of the study, subjects used open magnitude estimation to rate breaths of five different sizes at three different IFR (70%, 100%, and 200% of comfort rate). Neither the exponent nor intercept for VT perception differed among the three IFR. Our results demonstrate that although IFR does not alter magnitude estimation of breath size, deviations of IFR from that desired by the subject may greatly affect respiratory comfort.

We examined the relationship between tidal volume (VT) perception and level of CO2. Ten normal subjects were connected to a volume-cycled ventilator set in control mode, and VT and respiratory rate were adjusted until subjects were comfortable. At 2 levels of CO2 which differed by 6-8 mmHg, subjects rated ten different ventilator tidal volumes which ranged from 40-200% of the VT that made them comfortable at the lower CO2. Despite large differences in inspiratory muscle activity, there was no significant difference between the two levels of CO2 for either the exponent [1.39 +/- 0.35 vs 1.36 +/- 0.49 (low CO2 vs high CO2, mean +/- SD), P0.5] or constant (-0.09 +/- 0.12 vs -0.14 +/- 0.17, P0.1) for VT perception. For the group, there was no correlation between the hypercapnic ventilatory response (HCVR) measured by rebreathing and the exponent for VT perception. We conclude that: (1) the level of CO2 does not influence magnitude estimation of VT; (2) respiratory muscle activity is not essential to VT perception; and (3) there is no correlation between the HCVR and magnitude estimation of VT.

The preponderance of evidence indicates that high airway pressure is not by itself injurious to the lung. Rather, overdistention of the lung appears to be the fundamental mechanism underlying VALI. The physician must bear in mind the factors (ie, flow-resistive pressure losses, respiratory muscle activity, and abnormalities in rib cage or abdominal compliance) that may alter the relationship between PAP and lung volume. Under some circumstances, high PAP may, in fact, reflect lung overdistention, and maneuvers that minimize overdistention may also reduce PAP. Similarly, the goal of improving oxygenation may sometimes entail strategies (such as prolonging inspiratory time) that lower PAP. In these settings, however, the reduction in PAP should be regarded as a by-product of achieving another therapeutic goal and not an end point in and of itself. In other settings, such as the mechanically ventilated patient with severe airflow obstruction, measures that lower PAP by reducing inspiratory flow rate may worsen pulmonary hyperinflation, and thereby increase the risk of complications.

The act of breathing diminishes the discomfort associated with hypercapnia and breath-holding. To investigate the mechanisms involved in this effect, we studied the effect of tidal volume (V T ) on CO 2 -evoked air hunger in 5 high-level quadriplegic subjects whose ventilatory capacity was negligible, and who lacked sensory information from the chest wall. Subjects were ventilated at constant frequency with a hyperoxic gas mixture, and end-tidal P CO 2 was maintained at a constant but elevated level. V T was varied between the subjects' normal V T and a smaller V T . Subjects used a category scale to rate their respiratory discomfort or ‘air hunger’ at 30–40 sec intervals. In 4 of 5 subjects there was a strong inverse relationship between breath size and air hunger ratings. The quality of the sensation associated with reduced V T was nearly identical to that previously experienced with CO 2 alone. We conclude that afferent information from the lungs and upper airways is sufficient to modify the sensation of air hunger.

In patients with obstructive sleep apnea (OSA), substantial elevations of systemic blood pressure (BP) and depressions of oxyhemoglobin saturation (SaO2) accompany apnea termination. The causes of the BP elevations, which contribute significantly to nocturnal hypertension in OSA, have not been defined precisely. To assess the relative contribution of arterial hypoxemia, we observed mean arterial pressure (MAP) changes following obstructive apneas in 11 OSA patients during non-rapid-eye-movement (NREM) sleep and then under three experimental conditions: 1) apnea with O2 supplementation; 2) hypoxemia (SaO2 80%) without apnea; and 3) arousal from sleep with neither hypoxemia nor apnea. We found that apneas recorded during O2 supplementation (SaO2 nadir 93.6% +/- 2.4; mean +/- SD) in six subjects were associated with equivalent postapneic MAP elevations compared with unsupplemented apneas (SaO2 nadir 79-82%): 18.8 +/- 7.1 vs. 21.3 +/- 9.2 mmHg (mean change MAP +/- SD); in the absence of respiratory and sleep disruption in eight subjects, hypoxemia was not associated with the BP elevations observed following apneas: -5.4 +/- 19 vs. 19.1 +/- 7.8 mmHg (P less than 0.01); and in five subjects, auditory arousal alone was associated with MAP elevation similar to that observed following apneas: 24.0 +/- 8.1 vs. 22.0 +/- 6.9 mmHg. We conclude that in NREM sleep postapneic BP elevations are not primarily attributable to arterial hypoxemia. Other factors associated with apnea termination, including arousal from sleep, reinflation of the lungs, and changes of intrathoracic pressure, may be responsible for these elevations.

over the past 20-30 years, substantial progress has been made in our understanding of dyspnea. We have come to the realization that dyspnea encompasses a number of distinct sensations ([16][1]) and that a diverse array of receptors in the chest wall, lungs, airways, and central nervous system may

Severe ethylene glycol toxicity can cause profound morbidity and is almost universally fatal if untreated. Central nervous system depression with intoxication, pulmonary edema, and acute oliguric renal failure with crystalluria are among the most commonly encountered complications of ingestion. The previously reported gastrointestinal side effects of ethylene glycol toxicity are mostly nonspecific, including nausea, abdominal pain, and cramping. In addition, hepatic damage due to calcium oxalate deposition has been reported. We describe a patient who developed acute colonic ischemia following ethylene glycol intoxication. Three months after the ingestion, the patient presented with severe abdominal pain secondary to a colonic stricture and perforation, necessitating emergent colectomy. Histology of the resected colon revealed polarizable polyhedral crystals suggestive of oxalate deposition. The pathophysiology underlying ethylene glycol intoxication, treatment strategies, and gastrointestinal toxicity are discussed.