Publications by authors named "Brian C Harvey"

Measuring continuous changes in maternal ventilation during labor neuraxial analgesia is technically difficult. Consequently, the magnitude of pulmonary minute ventilation (MV) alterations following labor analgesia remains unknown. We hypothesized that a novel, bio-impedance based non-invasive respiratory monitor would provide this information.

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Background: Pediatric patients following surgery are at risk for respiratory compromise such as hypoventilation and hypoxemia depending on their age, comorbidities, and type of surgery. Quantitative measurement of ventilation in nonintubated infants/children is a difficult and inexact undertaking. Current respiratory assessment in nonintubated patients relies on oximetry data, respiratory rate (RR) monitors, and subjective clinical assessment, but there is no objective measure of respiratory parameters that could be utilized to predict early respiratory compromise.

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Background: Monitoring respiratory status using end tidal CO2 (EtCO2), which reliably reflects arterial PaCO2 in intubated patients under general anesthesia, has often proven both inaccurate and inadequate when monitoring non-intubated and spontaneously breathing patients. This is particularly important in patients undergoing procedural sedation (e.g.

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In this study, we modeled concentrations of fine particulate matter (PM) and ozone (O) attributable to precursor emissions from individual airports in the United States, developing airport-specific health damage functions (deaths per 1000t of precursor emissions) and physically-interpretable regression models to explain variability in these functions. We applied the Community Multiscale Air Quality model using the Decoupled Direct Method to isolate PM- or O-related contributions from precursor pollutants emitted by 66 individual airports. We linked airport- and pollutant-specific concentrations with population data and literature-based concentration-response functions to create health damage functions.

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With every breath, the airways within the lungs are strained. This periodic stretching is thought to play an important role in determining airway caliber in health and disease. Particularly, deep breaths can mitigate excessive airway narrowing in healthy subjects, but this beneficial effect is absent in asthmatics, perhaps due to an inability to stretch the airway smooth muscle (ASM) embedded within an airway wall.

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Background: Current respiratory monitoring technologies such as pulse oximetry and capnography have been insufficient to identify early signs of respiratory compromise in nonintubated patients. Pulse oximetry, when used appropriately, will alert the caregiver to an episode of dangerous hypoxemia. However, desaturation lags significantly behind hypoventilation and alarm fatigue due to false alarms poses an additional problem.

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Periodic length fluctuations of airway smooth muscle during breathing are thought to modulate airway responsiveness in vivo. Recent animal and human intact airway studies have shown that pressure fluctuations simulating breathing can only marginally reverse airway narrowing and are ineffective at protecting against future narrowing. However, these previous studies were performed on relatively large (>5 mm diameter) airways, which are inherently stiffer than smaller airways for which a preponderance of airway constriction in asthma likely occurs.

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Recent reports suggest that tidal stretches do not cause significant and sustainable dilation of constricted intact airways ex vivo. To better understand the underlying mechanisms, we aimed to map the physiological stretch-induced molecular changes related to cytoskeletal (CSK) structure and contractile force generation through integrin receptors. Using ultrasound, we measured airway constriction in isolated intact airways during 90 minutes of static transmural pressure (Ptm) of 7.

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Fluctuating forces imposed on the airway smooth muscle due to breathing are believed to regulate hyperresponsiveness in vivo. However, recent animal and human isolated airway studies have shown that typical breathing-sized transmural pressure (Ptm) oscillations around a fixed mean are ineffective at mitigating airway constriction. To help understand this discrepancy, we hypothesized that Ptm oscillations capable of producing the same degree of bronchodilation as observed in airway smooth muscle strip studies requires imposition of strains larger than those expected to occur in vivo.

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Airway hyperresponsiveness is a hallmark of asthma in which airways narrow excessively in response to an agonist, resulting in difficulty in breathing. Constriction of the smooth muscle that spirals around the airways is the principle cause of airway narrowing during an asthma attack. It is likely that several mechanisms are involved in the development of a hyperresponsive airway in asthma.

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