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Trauma Anaesthesia
Published in Kenneth D Boffard, Manual of Definitive Surgical Trauma Care: Incorporating Definitive Anaesthetic Trauma Care, 2019
Besides the standard anaesthesia monitoring, a five-lead ECG in case of thoracic injury is advisable. Blunt cardiac injury can be detected by changes in ECG and treated with supportive therapy. Ventilation should be monitored with pulse oximetry for adequate oxygenation and end-tidal (ET) CO2 for assuring adequate respiratory minute volume. ETCO2 further informs us about cardiac output decreasing in case of circulatory collapse.
Screening Smokes: Applications, Toxicology, Clinical Considerations, and Medical Management *
Published in Brian J. Lukey, James A. Romano, Salem Harry, Chemical Warfare Agents, 2019
Lawrence A. Bickford, Harry Salem
The likelihood for the development of symptoms following inhalation exposure and the nature and severity of respiratory tract injury depend on a number of factors, which include the chemical nature of the smoke, concentration and toxic potency of inhaled materials, particle size and vapor proportion, duration of exposure, water solubility, respiratory minute volume, and personal characteristics (e.g., differential susceptibility or exertion). During training and operational use, exercise will result in an increased respiratory minute volume (effect of tachypnea and increased tidal volume) and thus, a greater inhalation exposure dose. Most of the more soluble inhaled material will tend to predominantly affect the upper airways, and the less soluble materials affect mainly the peripheral airways and alveoli.
Diagnostic tests in respiratory medicine
Published in Vibeke Backer, Peter G. Gibson, Ian D. Pavord, The Asthmas, 2023
Vibeke Backer, Peter G. Gibson, Ian D. Pavord
After a 10-minute warm-up on the treadmill, to test oxygen uptake, participants perform a maximal run. The constant speed is set individually so that all subjects finish in 4–6 minutes (14–16 km h−1). After 2 minutes, the treadmill incline is adjusted to 2%; it is then increased by a further 2% every 90 s until exhaustion. Respiratory variables are measured continuously (AMIS 2001 automated metabolic cart, INNOVISION, Odense, Denmark) and averaged for each 15-s period, and the mean of the three highest VO2 15-s values is recorded as the maximal oxygen uptake (VO2max). The main objective of ergometric stress testing, aside from diagnostic evaluation of clinical manifestations (dyspnea, dizziness, exhaustion, pain, etc.), is to measure the parameters relating to exercise physiology for the assessment of performance capacity. The main parameters to be measured and monitored include the performance achieved (in watts or km/h), heart rate (HR), ECG, arterial blood pressure (BP), lactate concentration (Lac), the spiro-ergometric parameters oxygen uptake (VO2), carbon dioxide release (VCO2), respiratory quotient (RQ = VO2/VCO2), respiratory rate (RR), respiratory minute volume (VE) and respiratory equivalent (RE = VE/VO2). Cardiovascular fitness can be measured as peak oxygen uptake (absolute and relative VO2peak) or peak power output (Wpeak). When tested according to the guidelines, these measures show few variations and can be used to evaluate change over time, such as from baseline to follow-up. In asthmatic people, testing might be done after inhalation of bronchodilator, although effect of this is questioned.
Numerical modeling of nanoparticle deposition in realistic monkey airway and human airway models: a comparative study
Published in Inhalation Toxicology, 2020
Nguyen Dang Khoa, Nguyen Lu Phuong, Kazuhide Ito
In order to calculate the minute volume under rest conditions, the Guyton’s formula (Guyton 1947) was applied to estimate the respiratory minute volume of the monkey airway. The equation (1) is stated as follows: MV is the minute volume (mL/min), 2.35 is a constant value obtained from six monkey subjects, and BW is the bodyweight (g) of the monkey. In a monkey with a bodyweight of 1200 g, the MV was estimated to be 480 mL/min (0.48 L/min), under the specified inhalation conditions. Assuming an equal duration of the inhalation and exhalation processes, the inspiratory flow rate of 0.96 L/min was selected corresponding to twice the minute volume. Inhalation airflow simulations were conducted at the flow rates of 0.96 L/min and 1.92 L/min, in order to span a range of physiologic breathing rates in both monkey and human models, as listed in Table 1. Table 2 summarizes the numerical and boundary conditions of the two upper airway models. In this study, all the predictions for airflow patterns as well as particle transportation and depositions were conducted for inhalation process only.
Bridging inhaled aerosol dosimetry to physiologically based pharmacokinetic modeling for toxicological assessment: nicotine delivery systems and beyond
Published in Critical Reviews in Toxicology, 2019
A. R. Kolli, A. K. Kuczaj, F. Martin, A. W. Hayes, M. C. Peitsch, J. Hoeng
A similar PBPK model, but with 4 lung regions, was developed by Sarangapani et al. with special emphasis on characterizing the transitional bronchiolar compartment for inhaled gases (Sarangapani, Teeguarden, et al. 2002). This model assumed that the air flow rate in the upper and conducting airways was equal to the respiratory minute volume and that the flow rate in the transitional and pulmonary airways was equal to the alveolar ventilation. A fraction of inhaled chemical was absorbed in the nasal cavity, conducting airways, and transitional airways. The dominant process that delivered the substance to epithelial tissues in the nose was airflow. By developing a more complete description of the regions of the lungs, it now has become possible to assess the role of airway equilibration in controlling dose-response curves for metabolism in tissues all along the airways of the RT.
Influence of aerodynamic particle size on botulinum neurotoxin potency in mice
Published in Inhalation Toxicology, 2021
Jeremy A. Boydston, John J. Yeager, Jill R. Taylor, Paul A. Dabisch
Final mortality data was utilized to estimate the dilution of the liquid from the aerosol sampler that resulted in 50% mortality and the MIPLD50 was determined using probit analysis in JMP (v. 11.2.0, SAS Institute Inc., Cary, NC). The total number of MIPLD50s present in a sample were utilized to calculate the inhaled dose for each group. The inhaled dose (Dinh), in MIPLD50 was defined as the amount of BoNT inhaled per mouse and was calculated as the product of the BoNT aerosol concentration in the breathing zone of the subject during the exposure period (Ca) and the respiratory volume (Vr), defined as the volume of air inhaled over the course of the exposure period (Equation 1). The average aerosol concentration in the breathing zone of the subject during the exposure period (Ca) was calculated as the ratio of the product of the BoNT concentration recovered from the gelatin filter utilized during the exposure (Cs; in MIPLD50/mL) and the dissolution volume (Vs; in mL) to the product of the sampler flow (Qs; in mL/min) and the sampling time (t; in min) (Equation 2). Two previously published studies provide significantly different estimates of the mouse respiratory volume (Guyton 1947; Flandre 2003). While the study by Flandre et al. (2003) is more recent and utilized modern real-time plethysmography methodologies, the study by Guyton (1947) is still utilized in much of the biodefense community. Therefore, two different estimates of inhaled dose are presented, with each one utilizing a different estimate for the mouse respiratory minute volume (Vr).