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Suppression of Spontaneous Breathing During High-Frequency Jet Ventilation Separate Effects of Lung Volume and Jet Frequency

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Suppression of Spontaneous Breathing During High-Frequency Jet Ventilation Separate Effects of Lung Volume and Jet Frequency Intensive Care Med (1987) 13:315-322 Intensive Care Medicine © Springer-Verlag 1987 Suppression of spontaneous breathing during high-frequency jet ventilation Separate effects of lung volume and jet frequency A. J. van Vught 1'2, A. Versprille 1 and J. R. C. Jansen 1 1Pathophysiological Laboratory, Department of Pulmonary Diseases, Erasmus University, Rotterdam, and 2Pediatric Intensive Care Unit, University Children's Hospital "Het Wilhelmina Kinderziekenhuis",Utrecht, The Netherlands Received: 15 October 1986; accepted: 2 December 1986 Abstract. The effect of ventilatory frequency of high- High-frequency ventilation can suppress central frequency jet ventilation (HFJV) from 1 to 5 Hz, apart respiratory activity in animals [2, 7, 10, 12, 15, 23, 24] from changes in thoracic volume, on spontaneous as well as in humans [6]. Although the exact mecha- breathing activity was studied in Yorkshire piglets nism is unknown the phenomenon has been attributed under pentobarbital anesthesia. The highest PaCO 2 at mainly to afferent inhibiting signals from pulmonary which the animals did not breathe against the ven- [2, 3, 10, 12, 15, 23], thoracic [10, 15, 23, 26] and tilator (apnea point) was established either by chang- laryngo-tracheal [8] mechano-receptors. ing minute volume of ventilation or by adding CO2 to Four different kinds of mechanical receptor activa- the respiratory gas. The higher the apnea point, the tion in the respiratory system can be postulated during higher the suppression of spontaneous breathing ac- high-frequency ventilation: (a) the static component tivity was assumed to be. If the apnea point was sear- of the stretch stimulus depending on the level of tissue ched for by changing minute volume a progressive in- stretch at end-expiration, (b) the change in stretch crease of suppression of spontaneous respiratory ac- stimulus depending on tidal volume, (c) the velocity of tivity was found at ventilatory rates of 3 Hz or more, stretch depending on the flow of insufflation and (d) concomitantly with a rise in end-expiratory pressure the repetitive activation of stretch receptors depending (PEE). In case the tidal volume was kept constant, in- on ventilatory frequency. crease of ventilatory rate resulted in a tremendous in- From previous experiments [24] we concluded that crease of lung volume, together with considerably suppression of breathing activity during high-fre- higher levels of PEE. When under these conditions the quency jet ventilation (HFJV) in piglets was positively apnea point was searched for by adding CO 2 to the related to jet frequency as well as to end-expiratory in- respiratory gas a much higher CO2-drive was needed tratracheal pressure, increasing lung volume and thus for spontaneous breathing and therefore a much the basic level of tissue stretch. Neither the change in stronger inhibition of spontaneous breathing was con- stretch nor the velocity of stretch of pulmonary or cluded. By placing the animals in a body box in which thoracic mechano-receptors seemed to be a mecha- pressure could be varied, thoracic volume could be nism for the suppression of spontaneous breathing. In kept constant during HFJV. When thoracic volume an attempt to differentiate between jet frequency and was kept constant in this way a constant tidal volume end-expiratory lung volume, we have examined the ef- at increasing jet frequencies resulted in only a slight fect of repetitive activation of stretch receptors on increase in suppression of spontaneous breathing. breathing activity during HFJV by studying the rela- We conclude that the increase in lung volume is a tionship between ventilatory frequency and the major factor in suppressing central respiratory activity PaCO2 necessary to provoke spontaneous breathing during HFJV. Jet frequency by itself might be an addi- movements, with and without concomitant changes in tional suppressive factor. Airway CO2 did not seem to lung volume. Because CO 2 is a potent drive for respir- have an important effect. atory activity, a higher PaCO 2 level without spontane- ous breathing indicates a higher degree of suppression. Key words: PEEP - Lung stretch - Respiratory drive The highest PaCO 2 at which the animals did not - Carbon dioxide - Piglets breathe against the ventilator was denoted as the apnea point (PaCOz-apnea). In addition, based on ex- 316 A.J. van Vught et al.: HFJV and spontaneous breathing perimental evidence [4, 16, 17], that airway CO2 tions in mixed expiratory air were measured by a mass could act upon pulmonary stretch receptors we have spectrometer (Perkin-Elmer MGAll00) from the tried to analyse the effect of mixed expiratory CO 2 mixing box. PO2, PCO 2 and acid-base variables in (FECO2) in suppressing respiratory activity during blood were determined by means of an automatic HFJV. blood gas analyser (Radiometer ABL3) and oxygen saturation and hemoglobin with an oxymeter (Radiometer OSM2). Methods In six piglets changes in thoracic volume were esti- mated from changes in resistance of a mercury strain The methods have been previously described [24]. gauge. Within certain limits the electrical resistance of Therefore, only the essentials of the technique and its a mercury strain gauge has a linear relationship to its modifications will be given here. The experimental set- stretch; more stretch will give a higher resistance when up is shown in Figure 1. the mercury filled column becomes longer and thinner Yorkshire piglets (5-7 weeks old, 7-10 kg) were [5, 21]. The frequency response is linear up to 30 Hz anesthetized with pentobarbital sodium (30 mg.kg -1 [14]. The resistance range of the mercury strain gauge i.p.). Anesthesia was maintained by a continuous infu- in our experiments was between 700 and 800 m~ with sion of pentobarbital (7.5-10 mg. kg- 1. h-l), suffi- a temperature dependence of 1 mQ-°C-1 which was cient to eliminate pain reflexes, but allowing the neglected. animals to breathe spontaneously. Central tempera- The strain gauge was calibrated and checked on ture was kept at approximately 39 °C. linearity at the end of the experiment by stepwise in- After tracheostomy and connection via a Y-can- flation of air with a syringe after paralysing the nula to inspiratory and expiratory tubes, catheters animals with d-tubocurarine hydrochloride were inserted into the right common carotid artery, the (0.1mg.kg-1). Changes in thoracic volume of superior caval vein and the pulmonary artery for 4-8 ml could so be detected. No absolute values of blood pressure monitoring, blood sampling and infu- lung volume were measured. However, the strain gauge sions. During venous cannulation the animals were was primarily used as a zero-method, which means ventilated in order to prevent air embolism. Tracheal that its length and the corresponding thoracic volume pressure was measured deep in the trachea with a fluid were restored to its initial values. For such a method filled catheter provided with side holes at the tip. linearity is not relevant and frequency response less Blood pressures and tracheal pressure were measured critical. with Statham transducers P23De. Blood pressures Experimental procedures were measured relative to atmospheric pressure at manubrium level. For intratracheal measurement end- The animals were ventilated with frequencies from 1 to expiratory pressure during spontaneous breathing was 5 Hz using a high-frequency jet ventilator. Inspiratory taken as zero-reference. Heparin was administered in- time was kept constant at 0.1 s. The inspiratory gas termittently (250 IU" kg-l-h- l). The electrocardio- contained 40% oxygen, the fraction of inspired carbon gram was monitored continuously. dioxide could be varied from 0-0.20 as indicated in Ventilatory (tidal) volume was calculated by in- Figure 1. Spontaneous breathing was allowed via an tegration of mean airway flow, measured with a Fleish inlet valve in the inspiratory tube. During HFJV this pneumotachograph (type 0 Godart) behind a mixing valve was clamped off in order to prevent entrainment box in the expiratory tube. CO 2 and 0 2 concentra- of air. PaCO2 could be varied either by changing the airflow O2-N 2 CL,MP ./I ~ 40-60°~ Fig. 1. Experimental set-up. During ventilation with ventilator the CO2-O2-N2 / I I the jet 20-40-40% expiratory valve is closed at each insufflation. Changes in thoracic volume were measured with a mer- 1. MIXING BOX MASS SPECTROMETER cury strain gauge. Thoracic volume 2. FLOW METER was varied by varying pressure in the EXP. VALVE body box, using a water seal and a r::£7 ,uoE pbox continuous air flow, in order to eliminate effects of slight air leakages TRACHEAL PRESSURE under pressure A. J. van Vught et al.: HFJV and spontaneous breathing 317 minute volume or by adding CO 2 to the inspiratory PaCO2-apnea at 1 Hz (41.6___3.7 mmHg, mean_+ 1 SD) gas. Spontaneous inspiratory activity during HFJV as a reference point. These animals breathed was detected by concomitant decreases in intra- spontaneously at a PaCO 2 of 44.2_+3.2 mmHg (mean tracheal, central venous and pulmonary artery pres- _+ 1 SD). PaCO2-apnea, searched for by changing sures. minute volume of ventilation, increased with increas- In a first group of five piglets (group I) the apnea ing ventilatory frequency. As we reported previously point for five successive jet frequencies was searched [24] tidal volume under these conditions has been for by changing tidal volume. Thereafter, in a second decreased to find the apnea point. Concomitantly series of observations in the same group, tidal volume end-expiratory intratracheal pressure rose (Fig. 2b). (VT) was kept constant for all frequencies and was However, when tidal volume was kept constant at a equal to V T at the apnea point at 1 Hz. This implied level just sufficient to get apnea at 1 Hz a linear increase of minute volume with frequency.
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