Intermittent high frequency ventilation: a new mode to measure changes in lung volume and alveolar gas concentration, enhance CO2elimination and reduce intrapulmonary pressures

1988 ◽  
Vol 32 (4) ◽  
pp. 295-303 ◽  
Author(s):  
M. K. Chakrabarti ◽  
G. O. Swenzen ◽  
J. G. Whitwam
Keyword(s):  
Lung Volume ◽  
High Frequency ◽  
High Frequency Ventilation ◽  
Gas Concentration ◽  
Frequency Ventilation

High-frequency ventilation lengthens expiration in the anesthetized dog

1983 ◽  
Vol 55 (2) ◽  
pp. 329-334 ◽  
Author(s):  
R. Banzett ◽  
J. Lehr ◽  
B. Geffroy
Keyword(s):  
Lung Volume ◽  
High Frequency ◽  
Blood Gases ◽  
Abdominal Muscle ◽  
High Frequency Ventilation ◽  
Maximal Response ◽  
Variable Effect ◽  
Frequency Ventilation ◽  
Anesthetized Dogs ◽  
Arterial Po2

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.

Effects of mean airway pressure on gas transport during high-frequency ventilation in dogs

1986 ◽  
Vol 61 (5) ◽  
pp. 1896-1902 ◽  
Author(s):  
Y. Yamada ◽  
J. G. Venegas ◽  
D. J. Strieder ◽  
C. A. Hales
Keyword(s):  
Lung Volume ◽  
High Frequency ◽  
Airway Pressure ◽  
Gas Transport ◽  
Blood Gases ◽  
Co2 Production ◽  
High Frequency Ventilation ◽  
Mean Airway Pressure ◽  
Arterial Blood ◽  
Frequency Ventilation

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.

Relationship for gas transport during high-frequency ventilation in dogs

1985 ◽  
Vol 59 (5) ◽  
pp. 1539-1547 ◽  
Author(s):  
J. G. Venegas ◽  
J. Custer ◽  
R. D. Kamm ◽  
C. A. Hales
Keyword(s):  
Body Weight ◽  
Functional Residual Capacity ◽  
Lung Volume ◽  
High Frequency ◽  
Alveolar Ventilation ◽  
High Frequency Ventilation ◽  
Arterial Pco2 ◽  
Expiration Time ◽  
Residual Capacity ◽  
Frequency Ventilation

Alveolar ventilation during high-frequency ventilation (HFV) was estimated from the washout of the positron-emitting isotope (nitrogen-13-labeled N2) from the lungs of anesthetized paralyzed supine dogs by use of a positron camera. HFV was delivered at a mean lung volume (VL) equal to the resting functional residual capacity with a ventilator that generated tidal volumes (VT) between 30 and 120 ml, independent of the animal's lung impedance, at frequencies (f) from 2 to 25 Hz, with constant inspiratory and expiratory flows and an inspiration-to-expiration time ratio of unity. Specific ventilation (SPV), which is equivalent to ventilation per unit of compartment volume, was found to follow closely the relation: SPV = 1.9(VT/VL)2.1 X f. From this relation and from arterial PCO2 measurements we found an expression for the normocapnic settings of VT and f, given VL and body weight (W). We found that the VL was an important normalizing parameter in the sense that VT/VL yielded a better correlation (r = 0.91) with SPV/f than VT/W (r = 0.62) or VT alone (r = 0.8).

Mean airway pressure and alveolar pressure during high-frequency ventilation

1984 ◽  
Vol 57 (4) ◽  
pp. 1069-1078 ◽  
Author(s):  
B. A. Simon ◽  
G. G. Weinmann ◽  
W. Mitzner
Keyword(s):  
Tidal Volume ◽  
Lung Volume ◽  
High Frequency ◽  
Airway Pressure ◽  
High Frequency Ventilation ◽  
Alveolar Pressure ◽  
Mean Flow ◽  
Mean Airway Pressure ◽  
Expiratory Flow Limitation ◽  
Frequency Ventilation

Studies and applications of high-frequency ventilation (HFV) are often performed under conditions of controlled mean airway pressure (Paw). In the present study we tested the assumption that controlling Paw adequately controls lung volume during HFV by investigating the relationship between a reliably measured Paw and the mean alveolar pressure (Palv) of the lungs during HFV of healthy dogs. We minimized the errors of Paw measurement due to the Bernoulli effect and various technical factors by appropriate choice of transducers, amplifiers, and measurement site. Palv was estimated by clamping the ventilator tube during oscillation and measuring the equilibration pressure of the lung and airways. Paw and Palv were determined as functions of frequency (8–25 Hz), tidal volume (60–90 ml), Paw (-5 to 12 cmH2O), and position of the animal (supine vs. lateral). We found that Paw could significantly underestimate Palv and that the degree of underestimation increased at higher frequencies, larger tidal volumes, and lower Paw. Shifting the animal from the supine to the lateral position greatly accentuated this effect. The elevation of Palv above Paw was seen to be a function of mean flow and largely independent of the frequency-tidal volume combination which produced the flow. A possible explanation of this pressure difference is that it results from differences in inspiratory and expiratory airway impedances, which in turn depend on airway geometry, compliance, lung volume, and expiratory flow limitation.

Pulmonary afferent activity during high-frequency ventilation at constant mean lung volume

1986 ◽  
Vol 61 (1) ◽  
pp. 192-197 ◽  
Author(s):  
G. M. Barnas ◽  
R. B. Banzett ◽  
M. B. Reid ◽  
J. Lehr
Keyword(s):  
Lung Volume ◽  
High Frequency ◽  
High Frequency Ventilation ◽  
Afferent Activity ◽  
Stretch Receptors ◽  
Pulmonary Stretch Receptors ◽  
Normal Frequency ◽  
Residual Capacity ◽  
Frequency Ventilation ◽  
End Tidal

We recorded the responses of 21 slowly adapting pulmonary stretch receptors (PSRs) and 8 rapidly adapting pulmonary stretch receptors (RARs) from the vagi of anesthetized open-chest dogs to high-frequency ventilation (HFV) at 15 Hz, at constant mean end-expiratory lung volume, and constant end-tidal PCO2. HFV applied in this way has been shown to prolong expiration. The responses of pulmonary afferents during HFV at constant mean volume have not been described. In the present experiments, receptor discharge during HFV was compared with that during the end-expiratory pause of normal-frequency ventilation. Average PSR discharge increased when HFV was applied, although not all PSRs exhibited increases. RARs were generally silent during normal and high-frequency ventilation at functional residual capacity and above. However, at low lung volumes, RAR discharge increased greatly when HFV was applied. We conclude that PSR discharge is increased during HFV in the absence of increased lung volume and that increases in PSR discharge during HFV are sufficient to explain the reflex that prolongs expiration in dogs.

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