Jörg Vettermann

Position and motion of the human diaphragm during anesthesia-paralysis

Regional motion of the human diaphragm was determined by high-speed, three-dimensional x-ray computed tomography. Six healthy volunteers were studied first while awake and breathing spontaneously and again while anesthetized-paralyzed and their lungs ventilated mechanically. Tidal volume (VT) and respiratory frequency were similar during both conditions. Three subjects were studied while they were supine and three while they were prone. During spontaneous breathing, movement of dependent diaphragm regions was greater than that of nondependent regions in four of six subjects. In five of the six subjects, dorsal diaphragm movement exceeded ventral movement regardless of body position. The volume displaced by the diaphragm (delta Vdi) was similar to VT in supine subjects but tended to be less than VT in prone subjects. After induction of anesthesia-paralysis, the end-expiratory position of the diaphragm did not change consistently in supine subjects, whereas a consistent cephalad volume shift occurred in prone subjects. During anesthesia-paralysis and mechanical ventilation, delta Vdi was reduced to approximately 50% of VT in both body positions. In the supine position, the pattern of diaphragm motion during mechanical inflation was nearly uniform. By contrast, in the prone position, the motion was nonuniform, with most motion occurring in the dorsal (nondependent) regions. It is concluded that the dominant influence on diaphragm motion may be some anatomical difference between the crural and costal diaphragm regions rather than the abdominal hydrostatic pressure gradient.

Direct and Neurally Mediated Effects of Halothane on Pulmonary Resistance In Vivo

It has been suggested that halothane inhibits contraction of airway smooth muscle in vivo mainly by reducing reflex activity in nerves innervating the muscle with only minimal direct effects on the muscle itself. To examine possible mechanisms of action of halothane at clinically relevant concentrations the authors studied the effect of halothane on increases in pulmonary resistance (RL) produced by either vagus nerve stimulation (VNS, which caused neurally mediated constriction) or the inhalation of nebulized acetylcholine (ACh, which directly stimulated the smooth muscle cell) in nine mongrel dogs. The frequency of bilateral VNS and the dose of nebulized ACh were adjusted to produce approximately equal increases in RL. Halothane reduced the response to both types of stimulation in a dose-dependent fashion. At halothane concentrations greater than or equal to 0.4 MAC, the VNS response was significantly less than the ACh response. When tetrodotoxin was given to block neural activity, the ACh response was unchanged, confirming that neural activation did not contribute significantly to smooth muscle contraction in response to ACh. The authors conclude that in addition to neurally mediated effects, halothane at clinically used concentrations has significant direct effects on airway smooth muscle stimulated by ACh. The relative importance of each factor in vivo should depend on the stimulus that causes contraction of airway smooth muscle.

Pulmonary resistance during halothane anesthesia is not determined only by airway caliber.

Studies of the effect of halothane on airway smooth muscle have used pulmonary resistance as an index of airway caliber. However, pulmonary resistance (RL) is the sum of airway resistance (Raw), which changes with airway caliber, and of tissue resistance (Rti), which depends on the pressure-volume hysteresis of the lung. To separate the effects of halothane on airway caliber from its possible effects on tissue pressure-volume hysteresis in the unstimulated lung and during bronchoconstriction, the authors measured both components of RL before and during vagus nerve stimulation in 12 dogs before and during halothane administration. Rti was always the major component of RL, constituting 77 +/- 14% (mean +/- SD) of RL before vagus nerve stimulation and 64 +/- 21% of RL during stimulation in the absence of halothane. Vagus nerve stimulation caused approximately equal increases in both Rti and Raw. Halothane attenuated the response of both Rti and Raw to vagus nerve stimulation in a dose-dependent fashion. At 1 MAC, the Rti response was 44 +/- 13% of its value before halothane administration and the Raw response was 32 +/- 12% of its value before halothane administration; these responses were not significantly different. The authors conclude that changes in RL during halothane administration are caused not only by changes in airway caliber, as previously assumed, but also reflect a significant effect of halothane on lung tissue pressure-volume hysteresis.