Upper airway anesthesia induces airflow limitation in awake humans.

Upper airway receptors are thought to contribute to upper airway stability by reducing collapsing forces. Their activity can be abolished by topical anesthesia. We have measured in 16 healthy volunteers (mean +/- SD age, 23.7 +/- 1.6 yr) specific airway conductance (SGaw), maximal inspiratory (MIFR) and expiratory (MEFR) flow rates before and 15, 35, and 45 min after extensive upper airway anesthesia (UAA) with 10% lidocaine. Average values of MIFR decreased (p less than 0.01) 15 min after UAA, but they returned to or near to control values at 45 min: MIF25 (4.8 versus 6.0 L/s); MIF50 (5.1 versus 6.2 L/s); MIF75 (4.4 versus 5.3 L/s). Transient decreases in flow (V) rates, reaching zero flow in some subjects, were observed in 13 subjects during forced inspiratory vital capacity (FIVC) maneuvers and in seven subjects during forced expiratory vital capacity (FEVC) maneuvers. MEFR at 25, 50, and 75% FVC, SGaw, and FVC did not change after anesthesia. Simultaneous measurements of supraglottic pressure, V, and lung volume in 12 of the 16 subjects showed that the site of flow limitation was localized at the level of the glottis in all except one subject in whom there was both a glottic and a supraglottic obstruction. We conclude that extensive upper airway anesthesia induced a profound but transitory upper airway obstruction during FIVC and FEVC maneuvers. These findings are compatible with the concept of reflex regulation of upper airway caliber.

Pattern of breathing and ventilatory response to CO2 in subjects practicing hatha-yoga.

WE studied eight Belgian subjects well advanced in the practice of hatha-yoga and compared them with eight sex-, age-, and height-matched control subjects. Practice of yoga (range 4-12 yr) involves control of posture and manipulation of breathing, including slow near-vital capacity maneuvers accompanied by apnea at end inspiration and end expiration. Average values for the yoga and the control group (in parentheses) are as follows: ventilation (VE) 5.53 1 X min-1 (7.07); tidal volume (VT), 1.03 liters (0.56); rate of breathing, 5.5 min-1 (13.4); end-tidal PCO2, 39.0 Torr (35.3). All differences are significant (P less than 0.05). Ventilatory response to CO2 (rebreathing technique) was significantly lower in the yoga group (P less than 0.01). The regression relating VE to VT during rebreathing of CO2 was VE = 8.1 (VT - 0.23) for the yoga group and VE = 15.8 (VT - 0.16) for the control group (P less than 0.005). We attribute these changes to chronic manipulation of respiration.

Impaired early left ventricular relaxation in coronary artery disease: effects of intracornary nifedipine.

It has been shown that the maximal rate of left ventricular (LV) relaxation is impaired in patients with coronary artery disease (CAD) under basal conditions. To test the hypothesis that this impaired LV relaxation could be related to viable but metabolically abnormal myocardium, we studied the time course of isovolumic LV pressure fall in 21 patients with CAD and in 13 control subjects under basal conditions. This study was repeated after intracoronary injection of the calcium antagonist nifedipine (N) in 11 patients with CAD and in eight controls. Our data showed that isovolumic pressure fall was biexponential in 20 of 21 CAD patients and in six of 13 controls. Moreover, the time constant of isovolumic pressure fall during the first 40 msec after peak (negative) dP/dt (T1) was significantly greater in CAD patients than in controls (62 +/- 3 vs 44 +/- 1 msec, p < 0.002); the time constant of pressure fall during the 40-80 msec after peak (negative) dP/dt (T2) was similar in both groups ( 42 +/- 2 vs 39 +/- 2 msec, NS). Thirty seconds after injection of nifedipine, T1 and T2, were significantly prolonged in patients with CAD (14 msec and 16 msec, respectively, p < 0.005) and in controls 12 msec and 14 msec, respectively, p < 0.05), and a negative inotropic effect was observed in both groups (peak (positive) dP/dt - 16% in controls and -23% in CAD patients, p < 0.01). At rest, impairment of isovolumic relaxation in CAD patients is mainly limited to the first 40 msec after peak (negative) dP/dt, suggesting a dyssynchronous wall motion. This impairment of LV relaxation is better identified by T1 than by peak (negative) dP/dt in individual patients, and cannot be improved by administration of a calcium antagonist.