TACHYPNEA (tachypnoe; Greek tachys bystry, fast + pnoe breath) — increase in a respiration rate over 40 in 1 min.; the respiration rate can reach 100 and more in 1 min.
In the mechanism of development of T. are important stimulation of a respiratory center afferent impulses from carotid, aortal and other hemoretseptorny reflexogenic zones, neurogenic stimulation of a respiratory center impulses from thermoreceptors, irritantny, or epithelial, receptors of easy, various receptors of a musculoskeletal system (tendinous, joint, muscular), and also the incentives coming to a respiratory center from overlying departments of a brain. T. it can be caused by direct influence of humoral shifts on a respiratory center.
As fiziol. phenomenon of T. arises during muscular work and promotes increase in minute volume of alveolar ventilation according to the increased requirement of an organism in gas exchange (see). At the animals deprived of sweat glands, sharply expressed to T. with increase of breath in 10 and more times (so-called thermoregulatory, or thermal, a polypnea) represents reaction to exogenous overheating, being the major mechanism in these conditions thermolyses (see).
T. is adaptive reaction of system of external respiration to the hypoxia (see) caused by decrease in contents 02 in inhaled air (e.g., at a hypobaropathy), at sharply expressed anemias (see), a collapse (see), deterioration in cordial activity (see. Heart failure), etc. T. often develops at pneumonia (see), atelectases (see), developments of stagnation in lungs (see). Consider that in the mechanism of development of T. at the same time the exciting afferentation with irritantny and J-receptors of lungs is of great importance. Reason of T. there can be a pain at injuries of a thorax, pleura, a peritoneum leading to restriction of depth of breath and compensatory increase in its frequency (the so-called sparing breath).
T. the central origin can arise at functional (e.g., hysteria) or organic (tumors of a brain, meningitis, encephalitis, a craniocereberal injury, etc.) damages of a brain. Increase of breath can be observed at a thyrotoxicosis, nek-ry intoxications (e.g., at overdose of analeptical means), at fervescence.
T. can be followed both by increase, and reduction of respiratory volume. When the changes of minute volume of breath accompanying T., T are inadequate to the needs of an organism for gas exchange. gains independent pathogenic value. Frequent and deep breath quite often leads to a hyperventilation. At frequent and shallow breathing there can be alveolar hypoventilation owing to increase in functional dead space (see. Harmful space ).
Bibliography: Breslav XI. Page and Glebovsky V. D. Regulation of breath, JI., 1981; Marshak M. E. Regulation of breath at the person, M., 1961; The Guide to clinical physiology of breath, under the editorship of JI. L. Shika and H. N. Kanayeva, L., 1980; F r and N to sh t e y S. I. and Sergeyev's N 3. H. Self-control of breath is normal also of pathology, M., 1966.
N. I. Losev.