The Historical Development of AMA Guides Impairment Ratings for Asthma

In 1956, the Board of Trustees of the American Medical Association convened an ad hoc Committee on Medical Rating of Physical Impairment that published thirteen articles in JAMA between 1958 and 1970, including one on pulmonary impairment rating on November 22, 1965. That article rated pulmonary impairment by radiographic abnormalities, the historical description of the degree of shortness of breath, the results of at least two of three spirometric tests (forced vital capacity, forced expiratory flow in one second, and the maximal ventilatory volume), the maximal ventilatory volume, and oxygen saturation (if performed). Use of the examinee's history has come full circle from being part of the impairment rating process to being excluded to being reintroduced in the AMA Guides to the Evaluation of Permanent Impairment, Sixth Edition. The concept that asthma is not easily rated using methods applicable to other pulmonary diseases was introduced in the fifth edition and was modified for use in the sixth edition. Since the publication of the fifth edition, several medications have been approved for treatment of asthma. Future editions likely will refine the medication usage table to reflect medications in clinical use at the time and, one hopes, also will eliminate the clumsy reference to “beclomethasone equivalents” and are likely instead to reference low, medium, and high doses of the inhaled corticosteroids.

Compensatory airway dilation and additive ventilatory augmentation mediated by dorsomedial medullary 5-hydroxytryptamine 2 receptor activity and hypercapnia

5-HT2 receptor activity in the hypoglossal nucleus and hypercapnia is associated with airway dilation. 5-HT neurons in the medullary raphe and hypercapnia are responsible for tidal volume change. In this study, the effects of 5-HT2 receptors in the dorsomedial medulla oblongata (DMM), which receives projections from the medullary raphe, and hypercapnia on airway resistance and respiratory variables were studied in mice while monitoring 5-HT release in the DMM. A microdialysis probe was inserted into the DMM of anesthetized adult mice. Each mouse was placed in a double-chamber plethysmograph. After recovery from anesthesia, the mice were exposed to stepwise increases in CO2 inhalation (5%, 7%, and 9% CO2 in O2) at 8-min intervals with a selective serotonin reuptake inhibitor, fluoxetine, or fluoxetine plus a 5-HT2 receptor antagonist, LY-53857 in the DMM. In response to fluoxetine plus LY-53857 coperfusion, specific airway resistance was increased, and tidal volume and minute ventilation were decreased. CO2 inhalation with fluoxetine plus LY-53857 coperfusion in the DMM largely decreased airway resistance and additively increased minute ventilation. Thus, 5-HT2 receptor activity in the DMM increases basal levels of airway dilation and ventilatory volume, dependent on central inspiratory activity and the volume threshold of the inspiratory off-switch mechanism. Hypercapnia with low 5-HT2 receptor activity in the DMM largely recovers airway dilation and additively increases ventilatory volume. Interaction between 5-HT2 receptor activity in the DMM and CO2 drive may elicit a cycle of hyperventilation with airway dilation and hypoventilation with airway narrowing.

Thermoregulation and ventilation in the tawny frogmouth, Podargus strigoides: a low-metabolic avian species

Oxygen consumption (VO2) and body temperature (Tb) were measured during daytime (corresponding to the normal resting phase) in the tawny frogmouth (Podargus strigoides, mean body mass of 341 g) at ambient temperatures (Ta) between -1ºC and 30ºC. Mean body temperature (over this range of Ta) was 37.8ºC and there was only a small (0.4ºC), and insignificant, day-night variation in Tb. Mean VO2 within thermoneutrality (25-30ºC) was 0.59 mL O2 g-1 h-1 , corresponding to a basal metabolic rate (BMR) of 3.32 W kg-1 . This value is only 61% of the predicted value for a non-passeriform bird. The minimal thermal conductance attained at Ta below thermoneutrality was 0.156 W kg-1 ºC-1, a value which is very close to the allometrically predicted value. The relatively low VO2 was paralleled by a low total ventilatory volume. This, in turn, was mainly the result of a low respiratory frequency (10.2 breaths min-1, only 52% of that expected for a similar-sized bird) whereas tidal volume (6.6 mL [BTPS]) was 107% of the expected value. Thus, our results suggest that the changing ventilatory needs during the evolution of the low VO2 in the tawny frogmouth have been met primarily by changes in respiratory frequency.

Effects of pyridostigmine bromide on human thermoregulation during cold water immersion

This study examined the effects of an oral 30-mg dose of pyridostigmine bromide (PYR) on thermoregulatory and physiological responses of men undergoing cold stress. Six men were immersed in cold water (20 degrees C) for up to 180 min on two occasions, once each 2 h after ingestion of PYR and 2 h after ingestion of a placebo. With PRY, erythrocyte cholinesterase inhibition was 33 +/- 12% (SD) 110 min postingestion (10 min preimmersion) and 30 +/- 7% at termination of exposure (mean 117 min). Percent cholinesterase inhibition was significantly related to lean body mass (r = -0.91, P less than 0.01). Abdominal discomfort caused termination in three of six PYR experiments but in none of the control experiments (mean exposure time 142 min). During immersion, metabolic rate, ventilatory volume, and respiratory rate increased significantly (P less than 0.05) over preimmersion levels and metabolic rate increased with duration of immersion (P less than 0.01) in both treatment but did not differ between conditions. PYR had no significant effect on rectal temperature, mean body temperature, thermal sensations, heart rate, plasma cortisol, or change in plasma volume. It was concluded that a 30-mg dose of PYR does not increase an individual's susceptibility to hypothermia during cold water immersion; however, in combination with cold stress, PYR may result in marked abdominal cramping and limit cold tolerance.

Respiratory and cardiac function during exercise in squid

We investigated the cardiorespiratory performance of the squid Loligo opalescens at rest and during jet locomotion while tethered in an aquarium or while swimming in a Brett respirometer at speeds ranging from 0.05 to 0.6 m∙s−1. Simultaneous records of systemic heart rate and ventilatory frequency at each swimming speed were used with data for oxygen consumption to calculate the cardiac output and stroke volume. For a squid of mean weight 0.03 kg and length 0.18 m the resting heart rate averaged 60/min, the ventilatory rate was 26/min, and the calculated stroke volume was 0.05 mL (0.9 mL∙g heart−1) at 12 °C. During exercise the increased oxygen demand was accommodated by increases in both heart rate and stroke volume of almost 100% at the critical swimming speed of about 0.34 m∙s−1. Concomitant increases in the ventilation rate (350%) and ventilatory volume (500%) due to the requirements of jet locomotion were much greater than needed to deliver oxygen to the gills. At rest the oxygen extraction from the respiratory stream was 11%, and this declined to 5% at the critical swimming speed. The possibility that mechanical coupling of the circulatory and respiratory pumps may occur during jet swimming is examined.