Respiratory minute volume

Subsequently, individual data on exposure are converted to dose by using conversion factors (OECD/NEA, 1983). The choice of the appropriate numerical value depends on physiological parameters (e.g. respiratory minute volume) as well as physical characteristics of the inhaled aerosol (e.g. particle size). Mean values range typically from about 5 mSv/WLM (non-occupational exposure) to about 10 mSv/WLM (occupational exposure). 

The absorption of inhaled -hexane has been investigated in six healthy male volunteers (Veulemans et al. 1982). Three different trials were performed on each volunteer 4-hour exposure at 102 ppm -hexane 4-hour exposure at 204 ppm, and exposure during exercise on a stationary bicycle ergometer at 102 ppm. Each trial was done at least two weeks apart. Lung clearance (from alveolar air to blood) and retention were calculated from -hexane concentrations in inhaled and expired air. After exposure, /7-hcxane in exhaled air was measured for up to 4 hours to determine respiratory elimination. Retention of -hexane (calculated from lung clearance and respiratory minute volume) was approximately 20-25%... 

Recent multiservice (Army, Marine Corps, Navy, and Air Force) guidance on agent-specific exposure limits estimates the VX EC/50 for mild toxicity in humans (miosis, rhinorrhea) to be 0.10 mg VX-min/m for 2-360 min exposures (DA, 2005). The inhalation/ocular ECtso for severe effects in humans (i.e. muscular weakness, tremors, breathing difficulty, convulsions, paralysis) was estimated to be 10 mg-min/m for 2-360 min exposures for a respiratory minute volume of 15 1/min (DA, 2005). 

Following inhalation of sarin, the median lethal dosage (LCt5o) in humans has been estimated to be 70mgminm at a respiratory minute volume (RMV) of 15lmin, lOOmgminm at an RMV of lOlmin (resting) for a duration of 0.5-2 min. 

The likelihood for the development of symptoms following inhalation exposure and the nature and severity of respiratoiy tiact injuiy depends on a number of factors, which include the chemical namre 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, 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. 

As in the case of s.c. toxicokinetics, the kinetics of C(+)P(-)- and C(—)P(—)-soman were described mathematically as a discontinuous process, with an equation for the exposure period and an equation for the post-exposure period. In view of the limited number of data points during exposure, the absorption phase was described with a mono-exponential function. In order to describe the exposure phase of C(+)P(-)-soman, lag times of 2 and 4 min were selected for the 8-min exposures to 0.8 and 0.4 LCtjo, respectively. These lag times correspond with the earliest time points at which this stereoisomer could be detected. Toxicokinetic parameters derived from the various calculated concentration-time curves are given in Table 2.6. There were no measurable effects of the exposures on the respiratory minute volume (RMV) and respiratory frequency (RF). 

Meperidine crosses the placental barrier and, even in reasonable analgesic doses, causes a significant increase in the percentage of babies who show delayed respiration, decreased respiratory minute volume, or decreased oxygen saturation, or who require resuscitation. Fetal and maternal respiratory depression induced by meperidine can be treated with naloxone. The fraction of drug that is bound to protein is lower in the fetus concentrations of free drug thus may be considerably higher than in the mother. Nevertheless,... 

Maximal respiratory depression occur more rapidly with more lipid-soluble agents. After therapeutic doses, respiratory minute volume may be reduced for as long as 4-5 hours. The respiratory depression by opioids involves a reduction in the responsiveness of the brainstem respiratory centers to COj. Opioids also depress the pontine and medullary centers involved in regulating respiratory rhythmicity. 

However, there are some facts which are difficult to explain on the basis of a depressed respiratory center, and there are other facts which suggest a different explanation. In the first place the decreased oxygen consumption after morphine and the quieting effect indicate a decreased respiratory minute volume requirement. But the decrease in respiratory minute volume can be interpreted as greater than the decrease for which these two components might account. Yet the subcutaneous administration of 5 mg. of morphine cuts the normal minute volume of the rabbit in half, while the oxygen content of the expired air is not reduced below 17.8%. 

The second fact which suggests that the respiratory center is not depressed is the consideration that, if a dose of morphine is given and a marked depression of respiratory minute volume is obtained, further doses of morphine lead to a respiratory stimulation. It is difficult to imagine how the capabilities of a cell can be depressed almost to zero, and then be resuscitated by still more of the depressing agent. Further, the administration of morphine leads to increased respiratory minute volume in the midbrain rabbit, that is, in a rabbit whose cerebral lobes and thalamus have been removed but whose medulla and respiratory center in the medulla are still reasonably intact (1). 

It remains to be seen if the evidence in favor of depressed neurons need necessarily be interpreted in that light. The reduction of respiratory minute volume and the increase in alveolar carbon dioxide may be explained on the basis of a decreased oxygen consumption and of an increased alkaline reserve. The greater increase in respiratory minute volume by low concentrations of carbon dioxide in the inspired air in normal animals can also be explained by the fact that a 1 % increase in carbon dioxide concentration in the inspired air does not increase alveolar carbon dioxide tension to the same relative or absolute extent in the normal and mor-phinized animals. 

In man the respiratory factors are usually not markedly changed by morphine. In resting healthy individuals minute volume may be decreased 10-15% and respiratory rate may be unmodified or increased. Oxygen consumption decreases 8-10%. Alveolar carbon dioxide tension increases 2-3 mm. and the blood carbon dioxide capacity remains within 4 vol. % of the control value. The response to carbon dioxide in the inspired air is decreased and the blood remains neutral or shifts 0.05 pH toward the acid side, but experiments are recorded also where respiratory minute volume and oxygen consumption increase and all authors are concordant with respect to a low respiratory quotient after morphine. 

Respiratory rate is the number of breathing cycles in one minute. A normal rate would be between 10-20 cpm. Respiratory minute volume (RMV) is the total volume of air moved in and out of the lungs in one minute. It is computed by multiplying the tidal volume by the respiratory rate, RMV ranges from about 6 1/min to more than 100 1/min. 

The panic evacuation increased the toxic dose of minimum inhibitory concentration (MIC) to the casualties by increasing their respiratory minute volume while mnning. There was effectively an enhancement of the Haber effect... 

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