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Background: Inspiratory activity is a prerequisite for successful application of patient triggered ventilation such as proportional assist ventilation (PAV). It has recently been reported that surfactant instillation increases the activity of slowly adapting pulmonary stretch receptors (PSRs) followed by a shorter inspiratory time (Sindelar et al, J Appl Physiol, 2005 [Epub ahead of print]). Changes in lung mechanics, as observed in preterm infants with respiratory distress syndrome and after surfactant treatment, might therefore influence the inspiratory activity when applying PAV early after surfactant treatment., Objective: To investigate the regulation of breathing and ventilatory response in surfactant-depleted young cats during PAV and during continuous positive airway pressure (CPAP) early after surfactant instillation in relation to phrenic nerve activity (PNA) and the activity of PSRs., Methods: Seven anesthetized, endotracheally intubated young cats were exposed to periods of CPAP and PAV with the same end-expiratory pressure (0.2-0.5 kPa) before and after lung lavage and after surfactant instillation. PAV was set to compensate for 75% of the lung elastic recoil., Results: Tidal volume and respiratory rate were higher with lower PaCO2 and higher PaO2 during PAV than during CPAP both before and after surfactant instillation (p < 0.05; both conditions). As an indicator of breathing effort, esophageal deflection pressure and PNA were lower during PAV than during CPAP in both conditions (p < 0.02). Peak PSR activity was higher and occurred earlier during PAV than during CPAP (p < 0.01), and correlated linearly with PNA duration in all conditions studied (p < 0.001). The inspiratory time decreased as tidal volume increased when CPAP was changed to PAV, with the highest correlation observed after surfactant instillation (r = -0.769). No apneic periods could be observed., Conclusion: PSR activity and the control of breathing are maintained during PAV in surfactant-depleted cats early after surfactant instillation, with a higher ventilatory response and a lower breathing effort than during CPAP.

The functional residual capacity (FRC) was measured in cats by the nitrogen washout technique during positive-pressure ventilation. Frequencies of 60 and 100 b.p.m. were used with insufflation periods of 20% and 35% of the ventilatory cycle, without and with a positive end-expiratory pressure. The higher frequency combined with the shorter insufflation period gave FRC close to that obtained during spontaneous breathing. The lower frequency and the longer insufflation period always gave greater FRC values. A further increase in FRC of about 23-27% was obtained after application of a positive end-expiratory pressure of 0.5 kPa. Adequate ventilation was achieved with small intratracheal and intrapleural pressures at all settings used.

In 24 seriously ill newborn infants with respiratory distress syndrome (IRDS) and ensuing respiratory failure, high-frequency positive-pressure ventilation was administered. The mean gestational age of the infants was 32 +/- 3 weeks. In the infant ventilator employed, the compressible volume had been reduced in order to give higher flow rates but lower intratracheal pressures. The ventilation frequency was kept constant at 60-66 per min and the insufflation period at 32-35% of the ventilatory cycle. A positive end-expiratory pressure (PEEP) of 0.2-0.6 kPa was used. Arterial PCO2 was maintained at 4.0-5.3 kPa and PO2 at 8.5-10.5 kPa by adjusting the gas flow through the patient circuit, the peak tubing pressure, the PEEP and the oxygen concentration in inspired gas. High-frequency positive-pressure ventilation improved oxygenation and gave adequate alveolar ventilation in all infants, in most cases at a low peak pressure. Only one infant developed pneumothorax during intermittent positive pressure ventilation, and in no infant did bronchopulmonary dysplasia or retrolental fibroplasia occur. One infant died from intracranial hemorrhage during the ventilation period, giving a survival rate of 96%.

To investigate how continuous positive airway pressure (CPAP) changes the vagal nerve activity and whether CPAP alters the efferent phrenic nerve activity or the breathing pattern similarly before and after vagotomy, a study was made of vagal and phrenic nerve activity in chloralose-anaesthetized cats. In the vagal nerve, CPAP increased the mean impulse frequency during expiratory rest. The breath-related impulse frequency also increased with CPAP. With higher CPAP (greater than or equal to 0.5 kPa), the peak of breath-induced activity in the vagal nerve lasted longer than inspiration. In the phrenic nerve, the impulse frequency in the bursts increased almost linearly with CPAP irrespective of whether the vagal nerves were intact or not. The duration of the phrenic nerve bursts decreased with increasing CPAP when the vagal nerves were intact. When the vagal nerves were cut, the burst duration did not change. The rate of breathing was almost unchanged by CPAP regardless of whether the vagal nerves were cut or not. The inspiration/expiration ratio decreased with increasing CPAP when the vagal nerves were intact, but not when they were cut.

To determine the lowest continuous positive airway pressure (CPAP) at which breathing becomes regular and to determine whether the phrenic nerve activity changes simultaneously, breathing pattern and phrenic nerve activity were studied in spontaneously breathing newborn lambs at various levels of CPAP. A CPAP of 0.25 kPa decreased the variability of phrenic burst interval, i.e. made the breathing regular. This CPAP also increased the mean impulse frequency within the phrenic nerve bursts, indicating greater inspiratory activity. A high CPAP did not offer any further advantages to the breathing pattern or to the inspiratory activity.

High intrapulmonary pressure is probably an important factor in the development of extra-alveolar air leaks and bronchopulmonary dysplasia during neonatal intermittent positive pressure ventilation (IPPV). Spontaneous breathing, which may be asynchronous with the ventilator as a result of hypoventilation or sometimes of the ventilatory pattern of the ventilator, can be prevented by neuromuscular blockade. During neuromuscular blockade with pancuronium bromide the central inspiratory (phrenic nerve activity) activity could be inhibited during IPPV at all ventilatory frequencies tested, but a lower arterial PCO2 and a higher pH were needed to achieve inhibition at a low frequency (15 bpm). In the present study it was observed that central inspiratory activity in cats was stimulated by intravenous injection of pancuronium bromide. In cats not subjected to neuromuscular blockade the inspiratory activity was inhibited during IPPV at all ventilatory frequencies studied. At the onset of inhibition of this activity, the arterial blood gases and pH in these animals were almost the same at all ventilatory frequencies. When ventilation was administered at a low frequency, higher peak intratracheal pressures were needed to obtain inhibition of central inspiratory activity than when high frequencies were used, both before and after neuromuscular blockade.

Pulmonary gas exchange was studied in association with high frequency ventilation and its relation to the duration of insufflation and end-expiratory pressure investigated. Alveolar deadspace, alveolar ventilation and the alveolar-arterial oxygen difference were obtained in cats receiving a constant minute ventilation. Alveolar deadspace increased with ventilatory frequency when a long insufflation time was used. A positive end-expiratory pressure (PEEP) decreased the alveolar deadspace in high frequency ventilation. Thus, with the low compressible volume ventilator, more efficient high frequency ventilation can be achieved with a short period of insufflation plus low PEEP.

A study was made to determine whether the ventilatory pattern, in terms of ventilatory frequency, insufflation 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 pressures, 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 insufflation 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 could be achieved at a higher PCO2, within the normal range. The inhibition of phrenic nerve activity tended to be less stable when PEEP was added during ventilation with a long insufflation 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 insufflations given by the ventilator. The intratracheal peak pressures at ventilation causing inhibition of phrenic nerve activity decreased with increasing ventilatory frequencies.(ABSTRACT TRUNCATED AT 250 WORDS)