Dyspnea

Dyspnea, an unpleasant sensation of difficulty in breathing, is a common accompaniment of cardiopulmonary disease. The underlying mechanisms generating this sensation are not clearly understood. There does not appear to be any one specific site or specific receptor(s) involved in this sensation; however, reflex increase in central respiratory motor "command," as well as activity of the respiratory muscles, appear to be necessary for the genesis of the sensation. Whether there is a direct dyspnogenic effect of changes in chemical drive (increased arterial PCO2 or decreased arterial PO2) is unclear. Several methods to quantify dyspnea for clinical purposes have been described; techniques using exercise as the stimulus and expressing the response on a visual analogue or Borg category scale appear to be clinically applicable. The specific treatment of dyspnea remains in the experimental stage. The direct effects of exercise conditioning are unclear. A number of drugs (mainly central nervous system depressants) have been examined; preliminary work holds promise, but no particular drug can as yet be recommended for routine clinical use.     

Effects of bronchodilation on magnitude estimation of added resistive loads in asthmatic subjects

The magnitude estimation of 6 added resistive loads (delta R), ranging from 2.7 to 22.5 cmH2O/L/s, was studied in 7 normal and 6 stable asthmatic subjects. Each subject squeezed a handgrip dynamometer to indicate load magnitude. The magnitude estimation of a range of 5 weights, from 0.1 to 1.0 kg, placed on the hand was also assessed by dynamometry and numerical estimation. Airways resistance and spirometry were measured in each group. Metaproterenol, 0.13 mg, was then given by inhalation; after 15 min, the complete study was repeated. There was a significant bronchodilation in the asthmatic subjects, with a subjective decrease in chest "tightness," but no significant change in the normal subjects. In the control state, the perceived magnitude (psi) of delta R could be expressed by the relationship: psi = K. delta R beta, in accordance with Stevens' law. There was no significant difference (p greater than 0.05) in the value of beta between the normal and asthmatic group (0.55 and 0.67, respectively). However, the y-intercept in the control state was significantly greater in the asthmatics; when the perceived magnitude was expressed in terms of the mouth pressure (Pm) during the loaded breath in the control state, i.e., psi = K.Pm beta, there was no significant difference, either in beta or in the y-intercept. These results suggest that psi is related to Pm and is greater for any delta R in asthmatics because Pm is increased.(ABSTRACT TRUNCATED AT 250 WORDS)