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.

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).

High-frequency ventilation-induced apnea: interaction of frequency, volume, FRC, and CO2

1989 ◽  
Vol 66 (5) ◽  
pp. 2462-2467 ◽  
Author(s):  
P. W. Davenport ◽  
D. J. Dalziel
Keyword(s):  
High Frequency ◽  
Blood Gas Analysis ◽  
Gas Analysis ◽  
High Frequency Ventilation ◽  
Emg Activity ◽  
Bipolar Electrodes ◽  
Residual Capacity ◽  
Frequency Ventilation ◽  
Anesthetized Dogs ◽  
End Tidal

Apnea is often observed during high-frequency oscillatory ventilation (HFOV). This study on anesthetized dogs varied the oscillator frequency (f) and determined the stroke volume (SV) at which apnea occurred. Relaxation functional residual capacity (FRC) and the eupneic breathing end-tidal CO2 level were held constant. Airway pressure and CO2 were measured from a side port of the tracheostomy cannula. An arterial cannula was inserted for blood gas analysis. Diaphragm electromyogram (EMG) was recorded with bipolar electrodes. Apnea was defined as the absence of phasic diaphragm EMG activity for a minimum of 60 s. During HFOV, SV was increased at each f (5–40 Hz) until apnea occurred. The apnea inducing SV decreased as f increased. SV was minimal at 25–30 Hz. Frequencies greater than 30 Hz required increased SV to produce apnea. The f-SV curve was defined as the apneic threshold. Increased FRC resulted in a downward shift (less SV at the same f) in the apneic threshold. Elevated CO2 caused an upward shift (more SV at the same f) in the apneic threshold. These results demonstrate that the apnea elicited by HFOV is dependent on the interaction of oscillator f and SV, the FRC, and CO2.

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.

Responses of pulmonary vagal mechanoreceptors to high-frequency oscillatory ventilation

1988 ◽  
Vol 65 (2) ◽  
pp. 633-639 ◽  
Author(s):  
J. A. Wozniak ◽  
P. W. Davenport ◽  
P. C. Kosch
Keyword(s):  
High Frequency ◽  
Spontaneous Breathing ◽  
High Frequency Oscillatory Ventilation ◽  
Oscillatory Ventilation ◽  
Stretch Receptors ◽  
Pulmonary Stretch Receptors ◽  
Residual Capacity ◽  
Anesthetized Dogs ◽  
Increased Activity ◽  
High Frequency Oscillatory

The discharge of 57 slowly adapting pulmonary stretch receptors (PSR's) and 16 rapidly adapting receptors (RAR's) was recorded from thin vagal filaments in anesthetized dogs. The receptors were localized and separated into three groups: extrathoracic tracheal, intrathoracic tracheal, and intrapulmonary receptors. The influence of high-frequency oscillatory ventilation (HFO) at 29 Hz on receptor discharge was analyzed by separating the response to the associated shift in functional residual capacity (FRC) from the oscillatory component of the response. PSR activity during HFO was increased from spontaneous breathing (49%) and from the static FRC shift (25%). PSR activity during the static inflation was increased 19% over spontaneous breathing. RAR activity was also increased with HFO. These results demonstrate that 1) the increased activity of PSR and RAR during HFO is due primarily to the oscillating action of the ventilator and secondarily to the shift in FRC associated with HFO, 2) the increased PSR activity during HFO may account for the observed apneic response, and 3) PSR response generally decreases with increasing distance from the tracheal opening.

Characteristics of sustained graded inspiratory inhibition by phasic lung volume changes

1980 ◽  
Vol 48 (2) ◽  
pp. 302-307 ◽  
Author(s):  
J. P. Baker ◽  
J. E. Remmers
Keyword(s):  
Lung Volume ◽  
Dynamic Properties ◽  
Constant Flow ◽  
Afferent Activity ◽  
Volume Changes ◽  
Lung Inflation ◽  
Stretch Receptors ◽  
Pulmonary Stretch Receptors ◽  
Integrative Processing ◽  
Inhibitory Threshold

The dynamic characteristics of graded reversible inspiratory inhibition by vagal feedback were investigated in pentobarbital-anesthetized paralyzed cats, ventilated with a servo respirator. The volume and time associated with various levels of graded inhibition were determined by using a series of constant-flow lung inflations. Protracted phrenic inhibition was produced by lung inflation, which was arrested when the phrenic discharge was partially inhibited. Thereafter, the volume was withdrawn along a trajectory that approximately paralleled the fall in inhibitory threshold. This volume-withdrawal trajectory would be expected to produce a sustained nearly constant level of inhibition based on the results determined from the constant-flow inflations. However, the observed inhibition exceeded that expected, increasing to a maximum and then decreasing to expected values over a period ranging from 1 to 2 s in most animals. This excess inhibition cannot be attributed to the known dynamic properties of pulmonary stretch receptors; their activity should be reduced, for any particular lung volume, during the volume withdrawal maneuver. These results suggest a central integrative processing of vagal afferent activity that causes inhibition to lag volume. This delay acts to promote inspiratory off-switching because it prevents the development of a protracted period of reversible inhibition.

Expiratory flow limitation and dynamic pulmonary hyperinflation during high-frequency ventilation

1986 ◽  
Vol 60 (6) ◽  
pp. 2071-2078 ◽  
Author(s):  
J. Solway ◽  
T. H. Rossing ◽  
A. F. Saari ◽  
J. M. Drazen
Keyword(s):  
High Frequency ◽  
Progressive Increase ◽  
High Frequency Ventilation ◽  
Dynamic Hyperinflation ◽  
Flow Limitation ◽  
Expiratory Flow Limitation ◽  
Pulmonary Hyperinflation ◽  
Residual Capacity ◽  
Frequency Ventilation ◽  
Expiratory Flow

Dynamic hyperinflation of the lungs occurs during high-frequency oscillatory ventilation (HFOV) and has been attributed to asymmetry of inspiratory and expiratory impedances. To identify the nature of this asymmetry, we compared changes in lung volume (VL) observed during HFOV in ventilator-dependent patients with predictions of VL changes from electrical analogs of three potential modes of impedance asymmetry. In the patients, when a fixed oscillatory tidal volume was applied at a low mean airway opening pressure (Pao), which resulted in little increase in functional residual capacity, progressively greater dynamic hyperinflation was observed as HFOV frequency, (f) was increased. When mean Pao was raised so that resting VL increased, VL remained at this level during HFOV as f was increased until a critical f was reached; above this value, VL increased further with f in a fashion nearly parallel to that observed when low mean Pao was used. Three modes of asymmetric inspiratory and expiratory impedance were modeled as electrical circuits: 1) fixed asymmetric resistance [Rexp greater than Rinsp]; 2) variable asymmetric resistance [Rexp(VL) greater than Rinsp, with Rexp(VL) decreasing as VL increased]; and 3) equal Rinsp and Rexp, but with superimposed expiratory flow limitation, the latter simulated using a bipolar transistor as a descriptive model of this phenomenon. The fixed and the variable asymmetric resistance models displayed a progressive increase of mean VL with f at either low or high mean Pao. Only the expiratory flow limitation model displayed a dependence of dynamic hyperinflation on mean Pao and f similar to that observed in our patients. We conclude that expiratory flow limitation can account for dynamic pulmonary hyperinflation during HFOV.

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