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Introduction: Lactate clearance has been implicated as a predictor of mortality among emergency department (ED) patients with severe sepsis or septic shock. We aimed to validate prior studies showing that lactate clearance during the ED stay is associated with decreased mortality. Methods: Retrospective dual-centered cross-sectional study using patients identified in the Yale-New Haven Hospital Emergency Medicine sepsis registry with severe sepsis or septic shock who had initial lactate levels measured in the ED and upon arrival (

Oxygen is standard therapy for acute cardiopulmonary diseases, and long-term oxygen therapy is common in the outpatient setting. In part I of a two-part review, Wemple and colleagues discuss the physiology of tissue hypoxia, mechanisms of hypoxemia, and its clinical assessment. [ABSTRACT FROM AUTHOR]

The article presents a case study of a 60-year-old male with upper lobe predominant heterogeneous emphysema. Topics include Health-related quality of life (HRQOL) and respiratory symptoms being assessed using the SGRQ; and initial workup showing a pulmonary function test exhibiting a forced expiratory volume in 1 second.

The article focuses on the need for improved diagnostic sampling methods for lung cancer lesions, including bronchoscopic and percutaneous approaches. It discusses recent studies on image-guided techniques like electromagnetic navigation bronchoscopy (ENB) and the use of fluoroscopic correction to enhance diagnostic yield, showing promising results but highlighting the need for further research to determine their best applications and cost-effectiveness.

Acetazolamide prevents acute mountain sickness (AMS) by inhibition of carbonic anhydrase. Since it also reduces acute hypoxic pulmonary vasoconstriction (HPV), it may also prevent high-altitude pulmonary edema (HAPE) by lowering pulmonary artery pressure. We tested this hypothesis in a randomized, placebo-controlled, double-blind study. Thirteen healthy, nonacclimatized lowlanders with a history of HAPE ascended (<22 h) from 1,130 to 4,559 m with one overnight stay at 3,611 m. Medications were started 48 h before ascent (acetazolamide: n = 7, 250 mg 3 times/day; placebo: n = 6, 3 times/day). HAPE was diagnosed by chest radiography and pulmonary artery pressure by measurement of right ventricular to atrial pressure gradient (RVPG) by transthoracic echocardiography. AMS was evaluated with the Lake Louise Score (LLS) and AMS-C score. The incidence of HAPE was 43% versus 67% (acetazolamide vs. placebo, P = 0.39). Ascent to altitude increased RVPG from 20±5 to 43±10 mmHg (P < 0.001) without a group difference (P = 0.68). Arterial Po2 fell to 36±9 mmHg (P < 0.001) and was 8.5 mmHg higher with acetazolamide at high altitude (P = 0.025). At high altitude, the LLS and AMS-C score remained lower in those taking acetazolamide (both P < 0.05). Although acetazolamide reduced HAPE incidence by 35%, this effect was not statistically significant, and was considerably less than reductions of about 70%-100% with prophylactic dexamethasone, tadalafil, and nifedipine performed with the same ascent profile at the same location. We could not demonstrate a reduction in RVPG compared with placebo treatment despite reductions in AMS severity and better arterial oxygenation. Limited by small sample size, our data do not support recommending acetazolamide for the prevention of HAPE in mountaineers ascending rapidly to over 4,500 m. NEW & NOTEWORTHY This randomized, placebo-controlled, double-blind study is the first to investigate whether acetazolamide, which reduces acute mountain sickness (AMS), inhibits short-term hypoxic pulmonary vasoconstriction, and also prevents high-altitude pulmonary edema (HAPE) in a fast-climbing ascent to 4,559 m. We found no statistically significant reduction in HAPE incidence or differences in hypoxic pulmonary artery pressures compared with placebo despite reductions in AMS and greater ventilation-induced arterial oxygenation. Our data do not support recommending acetazolamide for HAPE prevention. [ABSTRACT FROM AUTHOR]

The ongoing coronavirus disease (COVID-19) pandemic has been unprecedented on many levels, not least of which are the challenges in understanding the pathophysiology of these new critically ill patients. One widely reported phenomenon is that of a profoundly hypoxemic patient with minimal to no dyspnea out of proportion to the extent of radiographic abnormality and change in lung compliance. This apparently unique presentation, sometimes called "happy hypoxemia or hypoxia" but better described as "silent hypoxemia," has led to the speculation of underlying pathophysiological differences between COVID-19 lung injury and acute respiratory distress syndrome (ARDS) from other causes. We explore three proposed distinctive features of COVID-19 that likely bear on the genesis of silent hypoxemia, including differences in lung compliance, pulmonary vascular responses to hypoxia, and nervous system sensing and response to hypoxemia. In the context of known principles of respiratory physiology and neurobiology, we discuss whether these particular findings are due to direct viral effects or, equally plausible, are within the spectrum of typical ARDS pathophysiology and the wide range of hypoxic ventilatory and pulmonary vascular responses and dyspnea perception in healthy people. Comparisons between lung injury patterns in COVID-19 and other causes of ARDS are clouded by the extent and severity of this pandemic, which may underlie the description of "new" phenotypes, although our ability to confirm these phenotypes by more invasive and longitudinal studies is limited. However, given the uncertainty about anything unique in the pathophysiology of COVID-19 lung injury, there are no compelling pathophysiological reasons at present to support a therapeutic approach for these patients that is different from the proven standards of care in ARDS. [ABSTRACT FROM AUTHOR]

The creation of dedicated sepsis guidelines and their broad dissemination over the past 2 decades have contributed to significant improvements in sepsis care. These successes have spurred the creation of bundled care mandates by major healthcare payers, such as the Center for Medicare and Medicaid Services. However, despite the likely benefits of guideline-directed sepsis bundles, mandated treatments in sepsis may lead to unintended consequences as the standard of care in sepsis improves. In particular, the heterogeneous spectrum of presentation and disease severity in sepsis, as well as the complexity surrounding the benefits of specific interventions in sepsis, argues for an individualized and titrated approach to interventions: an approach generally not afforded by care mandates. In this review, we review the risks and benefits of mandated care for sepsis, with particular emphasis on the potential adverse consequences of common bundle components such as early empiric antibiotics, weight-based fluid administration, and serum lactate monitoring. Unlike guideline-directed care, mandated care in sepsis precludes providers from tailoring treatments to heterogeneous clinical scenarios and may lead to unintended harms for individual patients. [ABSTRACT FROM AUTHOR]

The authors discuss a study of exercise-induced desaturation and functional limitation in survivors of COVID-19. During acute illness, majority of the survivors required supplemental oxygenation and 35% needed intubation. They emphasize the need to explore the role of the respiratory system in the exercise limitation in post-COVID-19 patients. They suggest the importance of screening such patients for exertional hypoxemia.

The first part of this article1 discusses the history, physiology, and evaluation for oxygen therapy. In this second part, we discuss the acute and chronic indications for oxygen, the delivery of supplemental oxygen (outside of invasive and noninvasive positive-pressure ventilation), and its potential adverse effects and toxicity. [ABSTRACT FROM AUTHOR]

The article presents a case study of a 61-year-old woman presented with three weeks of dyspnea cough, and fevers. Topics include examines the nasopharyngeal RT-PCR for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and common respiratory pathogens was negative; and reports that patient had no signs or symptoms of an underlying rheumatologic condition and took no medications.

Decreased oxygen saturation (SO2) at high altitude is associated with potentially life-threatening diseases, e.g., high-altitude pulmonary edema. Wearable devices that allow continuous monitoring of peripheral oxygen saturation (SpO2), such as the Garmin Fēnix® 5X Plus (GAR), might provide early detection to prevent hypoxia-induced diseases. We therefore aimed to validate GAR-derived SpO2 readings at 4559 m. SpO2 was measured with GAR and the medically certified Covidien Nellcor SpO2 monitor (COV) at six time points in 13 healthy lowlanders after a rapid ascent from 1130 m to 4559 m. Arterial blood gas (ABG) analysis served as the criterion measure and was conducted at four of the six time points with the Radiometer ABL 90 Flex. Validity was assessed by intraclass correlation coefficients (ICCs), mean absolute percentage error (MAPE), and Bland–Altman plots. Mean (±SD) SO2, including all time points at 4559 m, was 85.2 ± 6.2% with GAR, 81.0 ± 9.4% with COV, and 75.0 ± 9.5% with ABG. Validity of GAR was low, as indicated by the ICC (0.549), the MAPE (9.77%), the mean SO2 difference (7.0%), and the wide limits of agreement (−6.5; 20.5%) vs. ABG. Validity of COV was good, as indicated by the ICC (0.883), the MAPE (6.15%), and the mean SO2 difference (0.1%) vs. ABG. The GAR device demonstrated poor validity and cannot be recommended for monitoring SpO2 at high altitude. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented that responds to the article "The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3)" by M. Singer, C. S. Deutschman, C. W. Seymour, et al.

Patients suffering from chronic mountain sickness (CMS) have excessive erythrocytosis. Low −level cobalt toxicity as a likely contributor has been demonstrated in some subjects. We performed a randomized, placebo controlled clinical trial in Cerro de Pasco, Peru (4380 m), where 84 participants with a hematocrit (HCT) ≥65% and CMS score > 6, were assigned to four treatment groups of placebo, acetazolamide (ACZ, which stimulates respiration), N -acetylcysteine (NAC, an antioxidant that chelates cobalt) and combination of ACZ and NAC for 6 weeks. The primary outcome was change in hematocrit and secondary outcomes were changes in PaO 2 , PaCO 2 , CMS score, and serum and urine cobalt concentrations. The mean (±SD) hematocrit, CMS score and serum cobalt concentrations were 69 ± 4%, 9.8 ± 2.4 and 0.24 ± 0.15 μg/l, respectively for the 66 participants. The ACZ arm had a relative reduction in HCT of 6.6% vs. 2.7% (p = 0.048) and the CMS score fell by 34.9% vs. 14.8% (p = 0.014) compared to placebo, while the reduction in PaCO 2 was 10.5% vs. an increase of 0.6% (p = 0.003), with a relative increase in PaO 2 of 13.6% vs. 3.0%. NAC reduced CMS score compared to placebo (relative reduction of 34.0% vs. 14.8%, p = 0.017), while changes in other parameters failed to reach statistical significance. The combination of ACZ and NAC was no better than ACZ alone. No changes in serum and urine cobalt concentrations were seen within any treatment arms. ACZ reduced polycythemia and CMS score, while NAC improved CMS score without significantly lowering hematocrit. Only a small proportion of subjects had cobalt toxicity, which may relate to the closing of contaminated water sources and several other environmental protection measures. [ABSTRACT FROM AUTHOR]

Background: Small cohort studies have shown rapid pleurodesis protocol's (RPP) effectiveness and capacity to expedite pleurodesis for malignant pleural effusion (MPE). This study intends to evaluate the effectiveness of the RPP in inducing pleurodesis in patients with pleural effusions from either malignant or benign etiologies., Methods: In this single-center, retrospective cohort study spanning 2 decades, we assessed patients with recurrent symptomatic chronic noninfectious pleural effusion, both benign and malignant. Post-RPP, chest tubes were removed when fluid output dropped below 150 mL/d, and patients were discharged with daily indwelling pleural catheter (IPC) drainage. Exclusion criteria included nonexpandable lung and active pleural infection. Treatment success was defined as IPC removal on reduced output (<50 mL) on 3 consecutive drainages and radiologic effusion resolution. Recurrence was defined as the occurrence of pleural effusion requiring additional pleural procedures postsuccess. Duration outcome was expressed as median with IPC placement as time zero., Results: Of the 210 patients studied, 72% had MPE, and 28% had benign effusions. The median hospital stay was 4 days post-RPP. Treatment was successful in 177 (84%) patients within a median of 12 days, with no significant differences between MPE and benign cases. Nine patients (5%) experienced recurrence within a median of 152 days. Complications included hemothorax in 4 (1.9%) and empyema in 2 (1%). The thirty-day mortality rate was 9%, with a median survival time of 245 days postprocedure., Conclusion: The RPP combines the benefit of chemical pleurodesis and IPC and appears to be a reasonable option for patients with recurrent and symptomatic pleural effusion., Competing Interests: Disclosure: There is no conflict of interest or other disclosures., (Copyright © 2024 Wolters Kluwer Health, Inc. All rights reserved.)

Background: Short-term airway stent placement (stent evaluation) has been employed to evaluate whether patients with excessive central airway collapse (ECAC) will benefit from tracheobronchoplasty. Although retrospective studies have explored the impact of stent placement on ECAC, prospective randomized controlled trials are absent., Methods: This was a randomized open-label trial comparing patients receiving airway stent placement and standard medical treatment (intervention group) versus standard medical treatment alone (control group) for ECAC. At baseline, patients' respiratory symptoms, self-reported measures, and functional capabilities were assessed. Follow-up evaluations occurred 7 to 14 days postintervention, with an option for the control group to crossover to stent placement. Follow-up evaluations were repeated in the crossover patients., Results: The study enrolled 17 patients in the control group [medical management (MM)] and 14 patients in the intervention group. At follow-up, 15 patients in the MM crossed over to the stent group, resulting in a total of 29 patients in the combined stent group (CSG). Subjectively (shortness of breath and cough), 45% of the CSG exhibited improvement with the intervention compared with just 12% in the MM. The modified St. George Respiratory Questionnaire score in the CSG improved significantly from 61.2 at baseline to 52.5 after stent placement (-8.7, P = 0.04). With intervention, the 6-minute walk test in CSG improved significantly from 364 meters to 398 meters (34 m, P < 0.01). The MM did not show a significant change in the St. George Respiratory Questionnaire score or 6-minute walk test distance., Conclusion: Short-term airway stent placement in patients with ECAC significantly improves respiratory symptoms, quality of life, and exercise capacity., Competing Interests: Disclosure: There is no conflict of interest or other disclosures., (Copyright © 2024 Wolters Kluwer Health, Inc. All rights reserved.)

Oxygen Therapy Part 2: Indications and ToxicityWemple et al. continue their review of oxygen therapy, discussing the acute and chronic indications for oxygen and the delivery of supplemental oxygen (and its potential adverse effects and toxicity).

Purpose: To evaluate findings after transbronchial lung cryobiopsy (TBLC) using intraprocedural cone-beam CT (CBCT) and follow-up chest CT examinations., Materials and Methods: A single-center, prospective cohort study was performed with 14 participants (mean age, 65 years ± 13 [SD]; eight male participants) undergoing CBCT-guided TBLC between August 2020 and February 2021 who underwent follow-up chest CT imaging. Intraprocedural CBCT and follow-up chest CT images were interpreted for changes compared with baseline CT images. Statistical analyses were performed using independent samples t test and analysis of variance., Results: A total of 62 biopsies were performed, with 48 in the field of view of CBCT immediately after biopsy. All 48 biopsy sites had evidence of postprocedural hemorrhage, and 17 (35%) had pneumatoceles at the biopsy site. Follow-up CT images showed resolution of these findings. Solid nodules developed at 18 of the 62 (29%) biopsy sites., Conclusion: Postbiopsy hemorrhage and pneumatoceles on intraprocedural CBCT images (which were clinically occult and resolved spontaneously) and new solid nodules on follow-up chest CT images were commonly observed after TBLC. These findings may help alleviate unnecessary follow-up imaging and tissue sampling. Keywords: Biopsy/Needle Aspiration, CT, Lungs, Lung Biopsy, Interventional Bronchoscopy© RSNA, 2023., Competing Interests: Disclosures of conflicts of interest: B.P.P. No relevant relationships. K.E.S. No relevant relationships. D.K.D. No relevant relationships. B.S. No relevant relationships. H.B. No relevant relationships. H.H.G. No relevant relationships., (© 2023 by the Radiological Society of North America, Inc.)

Background: Systemic arterial gas embolism (SAGE) is a rare yet serious and underrecognized complication of bronchoscopic procedures. A recent case of presumed SAGE after transbronchial needle aspiration prompted a systematic literature review of SAGE after biopsy procedures during flexible bronchoscopy., Methods: We performed a systematic database search for case reports and case series pertaining to SAGE after bronchoscopic lung biopsy; reports or series involving only bronchoscopic laser therapy or argon plasma coagulation (APC) were excluded. Patient data were extracted directly from published reports., Results: A total of 29 unique patient reports were assessed for patient demographics, specifics of the procedure, clinical manifestations, diagnostic findings, and clinical outcomes. Cases of SAGE occurred after multiple types of bronchoscopic biopsy and under both positive and negative pressure ventilation. The most common clinical findings were neurologic, followed by cardiac manifestations; temporal patterns included acute onset of cardiac or neurologic emergencies immediately after biopsy, or delayed awakening post-procedure. There was a high mortality rate among cases (28%), with residual neurologic deficits also common (24%)., Discussion: SAGE is an underrecognized but severe adverse effect of bronchoscopic lung biopsy, which often presents with acute coronary or cerebral ischemia or delayed awakening from sedation. It is important for all physicians who perform bronchoscopic biopsies to be aware of the clinical manifestations and therapeutic management of SAGE in order to mitigate morbidity and mortality among patients undergoing these procedures., Competing Interests: Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://dx.doi.org/10.21037/jtd-21-717). The authors have no conflicts of interest to declare., (2021 Journal of Thoracic Disease. All rights reserved.)

Nitric oxide (NO) is a potent vasodilator in terrestrial vertebrates, but whether vascular endothelial-derived NO plays a role in vascular regulation in fish remains controversial. To explore this issue, a study was made of spiny dogfish sharks (Squalus acanthias) in normoxia and acute hypoxia (60 min exposure to seawater equilibrated with 3% oxygen) with various agents known to alter NO metabolism or availability. In normoxia, nitroprusside (a NO donor) reduced blood pressure by 20%, establishing that vascular smooth muscle responds to NO. L-arginine, the substrate for NO synthase, had no hemodynamic effect. Acetylcholine, which stimulates endothelial NO and prostaglandin production in mammals, reduced blood pressure, but also caused marked bradycardia. L-NAME, an inhibitor of all NO synthases, caused a small 10% rise in blood pressure, but cell-free hemoglobin (a potent NO scavenger and hypertensive agent in mammals) had no effect. Acute hypoxia caused a 15% fall in blood pressure, which was blocked by L-NAME and cell-free hemoglobin. Serum nitrite, a marker of NO production, rose with hypoxia, but not with L-NAME. Results suggest that NO is not an endothelial-derived vasodilator in the normoxic elasmobranch. The hypertensive effect of L-NAME may represent inhibition of NO production in the CNS and nerves regulating blood pressure. In acute hypoxia, there is a rapid up-regulation of vascular NO production that appears to be responsible for hypoxic vasodilation.