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

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.

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Physiological dead space during high-frequency ventilation in dogs

Journal of Applied Physiology ◽

10.1152/jappl.1984.57.3.881 ◽

1984 ◽

Vol 57 (3) ◽

pp. 881-887 ◽

Cited By ~ 24

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.

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A general dimensionless equation of gas transport by high-frequency ventilation

Journal of Applied Physiology ◽

10.1152/jappl.1986.60.3.1025 ◽

1986 ◽

Vol 60 (3) ◽

pp. 1025-1030 ◽

Cited By ~ 20

Author(s):

J. G. Venegas ◽

C. A. Hales ◽

D. J. Strieder

Keyword(s):

High Frequency ◽

Oscillatory Flow ◽

Mammalian Species ◽

Alveolar Ventilation ◽

High Frequency Ventilation ◽

Linear Regression Equation ◽

Dimensionless Equation ◽

Frequency Ventilation ◽

Dimensionless Variables ◽

Conducting Airways

To identify a general relationship between eucapnic oscillatory flow (Vosc) and frequency (f) in high-frequency ventilation (HFV), we searched the literature for eucapnic HFV data in different mammalian species. We found suitable results for rat, rabbit, monkey, dog, human, and horse, which we expressed in terms of two dimensionless variables, Q = Vosc/Va and F = f/(VA/VD), with VA the alveolar ventilation and VD the volume of the conducting airways. The experimental HFV data define the linear regression equation in Q = 0.54 In F + 0.92 (R = 0.94). Krogh's equation for conventional ventilation (CV), Vosc = VA + fVD, in dimensionless terms becomes Q = 1 + F, which is valid for low F. The intersection of the CV and HFV equations at F = 5.0 defines a transition frequency, ft = 5.0 (VA/VD). At that point the alveolar ventilation per breath, VA/f, represents 20% of VD, and tidal volume (VT) equals 1.20 VD. For eucapnia ft ranges from 5.9 Hz in the rat to 0.9 Hz in the dog. The dimensional form of our HFV equation, VA = 0.13 (VT/VD)1.2 (VTf) is very similar to other empirical equations reported for dogs in noneucapnic settings. Therefore the dimensionless equation should also be valid within a species at noneucapnic settings.

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ASSESSMENT OF LOCAL ALVEOLAR VENTILATION IN INTERMITTENT POSITIVE PRESSURE VENTILATION AND HIGH FREQUENCY VENTILATION WITH A PET SCANNER

Anesthesiology ◽

10.1097/00000542-198609001-00483 ◽

1986 ◽

Vol 65 (Supplement 3A) ◽

pp. A485

Author(s):

Y. Yamada ◽

J. G. Venegas ◽

C. A. Burnham ◽

C. A. Hales

Keyword(s):

High Frequency ◽

Positive Pressure Ventilation ◽

Intermittent Positive Pressure Ventilation ◽

Alveolar Ventilation ◽

Positive Pressure ◽

High Frequency Ventilation ◽

Frequency Ventilation

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Relationship for gas transport during high-frequency ventilation in dogs

Journal of Applied Physiology ◽

10.1152/jappl.1985.59.5.1539 ◽

1985 ◽

Vol 59 (5) ◽

pp. 1539-1547 ◽

Cited By ~ 10

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).

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Ventilatory response to CO2 and O2 near eupnea in awake dogs

Journal of Applied Physiology ◽

10.1152/jappl.1988.65.2.788 ◽

1988 ◽

Vol 65 (2) ◽

pp. 788-796 ◽

Cited By ~ 1

Author(s):

W. W. Hwang ◽

S. M. Yamashiro ◽

D. Sedlock ◽

F. S. Grodins

Keyword(s):

Steady State ◽

High Frequency ◽

Ventilatory Response ◽

Nonlinear Behavior ◽

High Frequency Ventilation ◽

Frequency Ventilation ◽

Extracorporeal Circuits ◽

The Subject ◽

Ventilatory Response To Co2 ◽

Mild Hypoxia

The problem faced in determining the ventilatory response to CO2 near eupnea has been the difficulty of unloading metabolically produced CO2 from the subject in the steady state. Previous methods using extracorporeal circuits to unload CO2 are technically difficult and provide a limited number of experimental states per experiment. Using the method of high-frequency ventilation to unload CO2, we were able to obtain a large number of determinations in the same subject under conditions of hypoxia, normoxia, and hyperoxia. Data collected in five awake dogs show that the ventilatory response to CO2 is linear down to apnea during normoxic conditions but exhibits nonlinear behavior dependent on the level of arterial O2 tension. During hyperoxic conditions, the response was concave curvilinear, with a statistically significant decrease in slope near apnea. In contrast, mild hypoxia led to a convex curvilinear response with an increased slope near apnea.

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