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.
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.
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.
9 August 2024 in Journal of Bronchology & Interventional Pulmonology
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.