Inhibition of phrenic nerve activity during positive‐pressure ventilation at high and low frequencies

A study was made to determine whether the ventilatory pattern, in terms of ventilatory frrqurnry, insufllation period and end‐expiratory pressure, influences the arterial blood gas level at which central inspiratory activity is inhibited, and whether further expansion of the lung changes this activity. This was accomplished by measuring arterial pH and blood gases, and intratracheal, intrapleural and transpulmonary pressurrs, at the setting of positive‐pressure ventilation causing inhibition of phrenic nerve activity in chloralose‐anaesthetized cats. Spontaneous breathing movements were prevented by muscle relaxation. Ventilatory frequencies of 15–120 breaths per minute (b.p.m.) were studied at at least two different insumation times. A volume‐controlled ventilator with a large compressible volume was used in the frequency range 15–45 b.p.m. and a constant flow respirator with a low‐compressible volume in the range 45–120 b.p.m. A much lower Pco2 was needed for phrenic nerve activity to be inhibited at a ventilatory frequency of 15 b.p.m. than at higher frequencies. At ventilatory frequencies between 30 and 120 b.p.m. inhibition ronld be achieved at a higher Pco2, within the normal range. The inhibition of phrenic nerve activity tended to he less stable when PEEP was added during ventilation with a long insumation period, but PEEP did not influence the arterial blood gas level at which inhibition occurred. In the lower frequency range of 15–30 b.p.m., inspiratory activity was observed with bursts at the same rate as the insumations given by the ventilator. The intratracheal peak pressures at ventilation causing inhibition of phrenic nerve activity decreased with increasing ventilatory frequencies. The intratracheal peak pressure was always highest at 15 b.p.m., and at each ventilatory frequency it was higher when PEEP was used.