High-frequency ventilation lengthens expiration in the anesthetized dog

1983 ◽  
Vol 55 (2) ◽  
pp. 329-334 ◽  
Author(s):  
R. Banzett ◽  
J. Lehr ◽  
B. Geffroy

We tested the response of nine barbiturate-anesthetized dogs to high-frequency ventilation (HFV) (40-55 ml tidal volumes at 15 Hz) while measuring and controlling lung volume and blood gases. When lung volume and PCO2 were held constant, six of the nine responded to HFV by lengthening expiration. In each of these six dogs the maximal response was apnea. The response was immediate. In submaximal responses only expiration was changed; inspiratory time and peak diaphragmatic electrical activity were unaffected. There was a variable effect on abdominal muscle activity. If mean expiratory lung volume was allowed to increase at the onset of HFV, the Hering-Breuer inflation reflex added to the response. The strength of the response depended on level of anesthesia and arterial PO2. Vagotomy abolished the response in all cases. We conclude that oscillation of the respiratory system reflexly prolongs expiration via mechanoreceptors, perhaps those in the lungs.

1986 ◽  
Vol 61 (5) ◽  
pp. 1896-1902 ◽  
Author(s):  
Y. Yamada ◽  
J. G. Venegas ◽  
D. J. Strieder ◽  
C. A. Hales

In 10 anesthetized, paralyzed, supine dogs, arterial blood gases and CO2 production (VCO2) were measured after 10-min runs of high-frequency ventilation (HFV) at three levels of mean airway pressure (Paw) (0, 5, and 10 cmH2O). HFV was delivered at frequencies (f) of 3, 6, and 9 Hz with a ventilator that generated known tidal volumes (VT) independent of respiratory system impedance. At each f, VT was adjusted at Paw of 0 cmH2O to obtain a eucapnia. As Paw was increased to 5 and 10 cmH2O, arterial PCO2 (PaCO2) increased and arterial PO2 (PaO2) decreased monotonically and significantly. The effect of Paw on PaCO2 and PaO2 was the same at 3, 6, and 9 Hz. Alveolar ventilation (VA), calculated from VCO2 and PaCO2, significantly decreased by 22.7 +/- 2.6 and 40.1 +/- 2.6% after Paw was increased to 5 and 10 cmH2O, respectively. By taking into account the changes in anatomic dead space (VD) with lung volume, VA at different levels of Paw fits the gas transport relationship for HFV derived previously: VA = 0.13 (VT/VD)1.2 VTf (J. Appl. Physiol. 60: 1025–1030, 1986). We conclude that increasing Paw and lung volume significantly decreases gas transport during HFV and that this effect is due to the concomitant increase of the volume of conducting airways.


1991 ◽  
Vol 70 (5) ◽  
pp. 2188-2192 ◽  
Author(s):  
M. J. Jaeger

Dogs were ventilated with a high-frequency oscillation device varying the frequency (5-15 Hz), the tidal volume (25-100 ml), and the resident gas (He, N2, SF6). Tidal volume was measured with a body plethysmograph. Blood gases were measured after a quasi-steady state was established. The kinematic viscosity of the breathing gas mixture, which changed by 1,700%, was found to have little effect on arterial PO2 and PCO2. The results are consistent with findings in a branched model that consisted of tubes with a diameter of 1 cm and with the theory of Taylor-type diffusion in turbulent flow. In addition, experiments were performed reducing and increasing the equipment dead space. This resulted in changes of PO2 and PCO2 that were appreciably less than those resulting from variations of tidal volume of the same magnitude.


1984 ◽  
Vol 56 (2) ◽  
pp. 454-458 ◽  
Author(s):  
V. Brusasco ◽  
T. J. Knopp ◽  
E. R. Schmid ◽  
K. Rehder

The efficiency of oxygenation and the uniformity of the distribution of regional ventilation (Vr) to regional perfusion (Qr) along the vertical and horizontal axes was compared in anesthetized dogs between conventional mechanical ventilation (CMV) and high-frequency ventilation (HFV) at 5.8, 15.0, and 29.8 Hz. Both CMV and HFV were adjusted to result in similar arterial CO2 tensions. The distribution of Vr/Qr during HFV at 5.8 Hz tended to be more uniform than during HFV at 15.0 or 29.8 Hz or during CMV. Consistent with this observation, arterial O2 tension (PaO2) tended to be higher during HFV at 5.8 Hz (means +/- SD, 90 +/- 9 Torr) than during HFV at 15.0 Hz (83 +/- 9 Torr) or 29.8 Hz (78 +/- 10 Torr); PaO2 was significantly higher during HFV at 5.8 Hz than during CMV (83 +/- 7 Torr).


1988 ◽  
Vol 32 (2) ◽  
pp. 140-146 ◽  
Author(s):  
T. Haghenberg ◽  
M. Wendt ◽  
J. Meyer ◽  
K. Wrenger ◽  
P. Lawin

1986 ◽  
Vol 60 (3) ◽  
pp. 885-892 ◽  
Author(s):  
V. Brusasco ◽  
K. C. Beck ◽  
M. Crawford ◽  
K. Rehder

The volume of gas delivered from a high-frequency ventilation (HFV) circuit was measured with an ultrasonic flowmeter. The measurements were done in vitro (20-liter air-filled glass bottle) and in vivo (9 anesthetized dogs lying supine) at oscillation frequencies ranging from 4 to 23 Hz and stroke volumes of the pump ranging from 36 to 150 ml. We varied the length and diameter of the tube connecting the pump with the endotracheal tube, the length and diameter of the bias outflow tube, the diameter of the endotracheal tube, and the stroke volume of the pump. Both in vitro and in vivo, there was resonant amplification of the delivered gas volume; i.e., the delivered gas volume exceeded the stroke volume at certain frequencies. Altering the dimensions of connecting tube, endotracheal tube, bias outflow tube, or stroke volume, i.e., changing the resistance to gas flow, gas compliance, and/or gas inertance in these elements, altered the ratio of gas delivered to stroke volume that could be predicted by an electric analog. These data indicate that the delivered gas volume during HFV depends critically on the configuration of the HFV circuit, the size of the endotracheal tube, the oscillation frequency, and the pump stroke volume. Knowledge of the delivered gas volume during HFV and appreciation of the phenomenon of resonant amplification of the delivered gas volume will permit a more accurate description of factors contributing to gas transport during HFV.


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