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

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.

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.


2014 ◽  
Vol 2 (1) ◽  
Author(s):  
Ricardo Luiz Cordioli ◽  
Marcelo Park ◽  
Eduardo Leite Vieira Costa ◽  
Susimeire Gomes ◽  
Laurent Brochard ◽  
...  

1984 ◽  
Vol 56 (1) ◽  
pp. 31-34 ◽  
Author(s):  
S. J. England ◽  
A. Onayemi ◽  
A. C. Bryan

Phrenic nerve activity was monitored in anesthetized cats during high-frequency ventilation (HFV). Rhythmic phrenic discharge disappeared during HFV in all animals at normal arterial PCO2 levels. Rhythmic activity returned after neuromuscular blockade in the vagally intact animal. Although vagotomy alone also restored phrenic discharge, this activity was further enhanced by subsequent neuromuscular blockade. Therefore we suggest that apnea during HFV results from inspiratory inhibition mediated by both chest wall and vagal afferent mechanisms.


1985 ◽  
Vol 58 (3) ◽  
pp. 996-1004 ◽  
Author(s):  
K. G. Kaiser ◽  
N. J. Davies ◽  
R. Rodriguez-Roisin ◽  
H. Z. Bencowitz ◽  
P. D. Wagner

Ten anesthetized normal dogs were each given two methacholine inhalational challenges to produce large amounts of low ventilation-perfusion (VA/Q) regions but little shunt. After one challenge, high-frequency ventilation (HFV) was applied, whereas after the other conventional mechanical ventilation (MV) was used, the order being randomized. Levels of both ventilatory modes were selected prior to challenge so as to result in similar and normal mean airway pressures and arterial PCO2 levels during control conditions. Gas exchange was assessed by both respiratory and multiple inert-gas transfer. Comparing the effect of HFV and MV, no statistically significant differences were found for lung resistance, pulmonary hemodynamic indices, arterial and mixed venous PO2, expired-arterial PO2 differences, or inert-gas data expressed as retention-excretion differences. The only variables that were different were mean airway pressure (2 cm higher during HFV, P less than 0.04) and arterial PCO2 (10 Torr higher during HFV, P less than 0.002). These results suggest that in this canine model of lung disease characterized by large amounts of low VA/Q regions, HFV is no more effective in delivering fresh gas to such regions than is MV.


1985 ◽  
Vol 59 (5) ◽  
pp. 1539-1547 ◽  
Author(s):  
J. G. Venegas ◽  
J. Custer ◽  
R. D. Kamm ◽  
C. A. Hales

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).


1984 ◽  
Vol 57 (4) ◽  
pp. 1069-1078 ◽  
Author(s):  
B. A. Simon ◽  
G. G. Weinmann ◽  
W. Mitzner

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.


1987 ◽  
Vol 63 (1) ◽  
pp. 413-417 ◽  
Author(s):  
R. H. Hastings ◽  
F. L. Powell

We studied gas exchange in anesthetized ducks and geese artificially ventilated at normal tidal volumes (VT) and respiratory frequencies (fR) with a Harvard respirator (control ventilation, CV) or at low VT-high fR using an oscillating pump across a bias flow with mean airway opening pressure regulated at 0 cmH2O (high-frequency ventilation, HFV). VT was normalized to anatomic plus instrument dead space (VT/VD) for analysis. Arterial PCO2 was maintained at or below CV levels by HFV with VT/VD less than 0.5 and fR = 9 and 12 s-1 but not at fR = 6 s-1. For 0.4 less than or equal to VT/VD less than or equal to 0.85 and 3 s-1. less than or equal to fR less than or equal to 12 s-1, increased VT/VD was twice as effective as increased fR at decreasing arterial PCO2, consistent with oscillatory dispersion in a branching network being an important gas transport mechanism in birds on HFV. Ventilation of proximal exchange units with fresh gas due to laminar flow is not the necessary mechanism supporting gas exchange in HFV, since exchange could be maintained with VT/VD less than 0.5. Interclavicular and posterior thoracic air sac ventilation measured by helium washout did not change as much as expired minute ventilation during HFV. PCO2 was equal in both air sacs during HFV. These results could be explained by alterations in aerodynamic valving and flow patterns with HFV. Ventilation-perfusion distributions measured by the multiple inert gas elimination technique show increased inhomogeneity with HFV. Elimination of soluble gases was also enhanced in HFV as reported for mammals.(ABSTRACT TRUNCATED AT 250 WORDS)


1982 ◽  
Vol 53 (6) ◽  
pp. 1638-1642 ◽  
Author(s):  
Y. K. Ngeow ◽  
W. Mitzner

We describe simple high-frequency oscillation systems that incorporate a CO2 absorber and supply O2 on a need basis. These systems have the advantage of easy control of mean airway pressure and airway hydration and negligible loss of oscillatory tidal volume. Experiments done at constant tidal volume showed that as frequency (and hence total ventilation) increased, arterial CO2 tension (PaCO2) decreased. The fall in PaCO2 occurred until frequency reached approximately 20 Hz; above 20 Hz further increases in frequency had little or no effect on PaCO2. Because of their practical advantages the techniques described here may be quite useful in a clinical setting where an oscillator, rather than jet-type high-frequency, ventilation system is desired.


1998 ◽  
Vol 74 (5) ◽  
pp. 411-5 ◽  
Author(s):  
Marcus A.J. Oliveira ◽  
Antônio C. P. Ferreira ◽  
João S. Oliveira ◽  
José S. Oliveira ◽  
Yara G. Silva

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