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).

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.

Inspiratory-to-expiratory time ratio and alveolar ventilation during high-frequency ventilation in dogs

1986 ◽  
Vol 61 (5) ◽  
pp. 1903-1907 ◽  
Author(s):  
Y. Yamada ◽  
C. A. Hales ◽  
J. G. Venegas
Keyword(s):  
Steady State ◽  
Arterial Pressure ◽  
High Frequency ◽  
Alveolar Ventilation ◽  
High Frequency Ventilation ◽  
Flow Rates ◽  
Expiratory Time ◽  
Time Ratio ◽  
Frequency Ventilation ◽  
Expiratory Flow Rates

It has been suggested that the increase in inspiratory flow rate caused by a decrease in the inspiratory-to-expiratory time ratio (I:E) at a constant tidal volume (VT) could increase the efficiency of ventilation in high-frequency ventilation (HFV). To test this hypothesis, we studied the effect of changing I:E from 1:1 to 1:4 on steady-state alveolar ventilation (VA) at a given VT and frequency (f) and at a constant mean lung volume (VL). In nine anesthetized, paralyzed, supine dogs, HFV was performed at 3, 6, and 9 Hz with a ventilator that delivered constant inspiratory and expiratory flow rates. Mean airway pressure was adjusted so that VL was maintained at a level equivalent to that of resting FRC. At each f and one of the I:E chosen at random, VT was adjusted to obtain a eucapnic steady state [arterial pressure of CO2 (PaCO2) = 37 +/- 3 Torr]. After 10 min of each HFV, PaCO2, arterial pressure of O2 (PaO2), and CO2 production (VCO2) were measured, and I:E was changed before repeating the run with the same f and VT. VA was calculated from the ratio of VCO2 and PaCO2. We found that the change of I:E from 1:1 to 1:4 had no significant effects on PaCO2, PaO2, and VA at any of the frequencies studied. We conclude, therefore, that the mechanism or mechanisms responsible for gas transport during HFV must be insensitive to the changes in inspiratory and expiratory flow rates over the VT-f range covered in our experiments.

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.

Physiological dead space during high-frequency ventilation in dogs

1984 ◽  
Vol 57 (3) ◽  
pp. 881-887 ◽  
Author(s):  
G. G. Weinmann ◽  
W. Mitzner ◽  
S. Permutt
Keyword(s):  
Gas Exchange ◽  
Tidal Volume ◽  
Dead Space ◽  
High Frequency ◽  
Minute Ventilation ◽  
Alveolar Ventilation ◽  
High Frequency Ventilation ◽  
Physiological Dead Space ◽  
Frequency Ventilation ◽  
Normal Ventilation

Tidal volumes used in high-frequency ventilation (HFV) may be smaller than anatomic dead space, but since gas exchange does take place, physiological dead space (VD) must be smaller than tidal volume (VT). We quantified changes in VD in three dogs at constant alveolar ventilation using the Bohr equation as VT was varied from 3 to 15 ml/kg and frequency (f) from 0.2 to 8 Hz, ranges that include normal as well as HFV. We found that VD was relatively constant at tidal volumes associated with normal ventilation (7–15 ml/kg) but fell sharply as VT was reduced further to tidal volumes associated with HFV (less than 7 ml/kg). The frequency required to maintain constant alveolar ventilation increased slowly as tidal volume was decreased from 15 to 7 ml/kg but rose sharply with attendant rapid increases in minute ventilation as tidal volumes were decreased to less than 7 ml/kg. At tidal volumes less than 7 ml/kg, the data deviated substantially from the conventional alveolar ventilation equation [f(VT - VD) = constant] but fit well a model derived previously for HFV. This model predicts that gas exchange with volumes smaller than dead space should vary approximately as the product of f and VT2.

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.

Chemical and mechanical determinants of apnea during high-frequency ventilation

1988 ◽  
Vol 65 (1) ◽  
pp. 179-186 ◽  
Author(s):  
S. L. Thompson-Gorman ◽  
R. S. Fitzgerald ◽  
W. Mitzner
Keyword(s):  
High Frequency ◽  
Important Determinant ◽  
Multiple Logistic Regression Analysis ◽  
High Frequency Ventilation ◽  
Multiple Logistic Regression ◽  
Mean Airway Pressure ◽  
Arterial Pco2 ◽  
Frequency Ventilation ◽  
Respiratory Centers ◽  
Respiratory Variables

The factors responsible for the apnea observed during high-frequency ventilation (HFV) were evaluated in 14 pentobarbital sodium-anesthetized cats. A multiple logistic regression analysis provided an estimate of the probability of apnea during HFV as a function of four respiratory variables: mean airway pressure (Paw), tidal volume (VT), frequency, and arterial PCO2 (PaCO2). When mean Paw was 2 cmH2O, PaCO2, VT, and their interaction contributed significantly to the probability of apnea during HFV. At a low value of PaCO2 (25 Torr), the probability of apnea had a minimum value of 0.19 and gradually increased toward 1.0 as VT increased from 0.5 to 7 ml/kg. At higher levels of PaCO2 (30 and 35 Torr) the probability of apnea was zero in the low range of VT but sharply approached 1.0 above a VT of approximately 2.0 ml/kg. However, when Paw was increased to 6 cmH2O, only PaCO2 was an important determinant of apnea. In this case, the probability of apnea was 0.51 when PaCO2 was 25 Torr but decreased to 0.22 when PaCO2 was raised to 25 Torr. At neither Paw was the probability of apnea dependent on frequency. These results suggest that chemoreceptor inputs, in addition to both static and dynamic lung mechanoreceptor afferents, are responsible for determining the output of the central respiratory centers during HFV.

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