Costal and crural diaphragm function during panting in awake canines

During natural panting for thermal regulation, the pattern of activation of the major respiratory muscles, including costal and crural diaphragm segments, is not known. We measured diaphragm segmental length, shortening, and electromyographic (EMG) activity in five chronically implanted canines awake and breathing spontaneously at rest and during a mild dry heat stress. During panting, minute ventilation increased fourfold from 5.07 l/min and respiratory rate increased from 16.9 to 192.8 breaths/min or 3.2 Hz. During panting, end-expiratory length of both costal and crural segments decreased, concurrent with significant increases in end-expiratory EMG. With the onset of panting, tidal costal shortening decreased significantly from 6.29% of end-expiratory length to 3.54%, whereas crural shortening decreased from 6.04 to 2.46%. Meanwhile, segmental EMG tended to increase during panting. During panting, intrabreath costal and crural segmental function revealed differential activation; the costal segment shortened in concert with inspiratory flow, whereas peak crural shortening occurred in expiration, almost 180 degrees out of phase with costal. The divergence in segmental shortening during panting was accompanied by a lesser shift in timing of segmental EMG. In the awake spontaneously panting canine, asynchronous costal and crural shortening may enhance gas mixing in a manner analogous to high-frequency ventilation.

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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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Effect of oral high frequency ventilation by jet or oscillator on minute ventilation in normal subjects.

Thorax ◽

10.1136/thx.40.10.749 ◽

1985 ◽

Vol 40 (10) ◽

pp. 749-755 ◽

Cited By ~ 3

Author(s):

R J George ◽

R J Winter ◽

M A Johnson ◽

I P Slee ◽

D M Geddes

Keyword(s):

High Frequency ◽

Minute Ventilation ◽

Normal Subjects ◽

High Frequency Ventilation ◽

Frequency Ventilation

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

Journal of Applied Physiology ◽

10.1152/jappl.1989.66.5.2462 ◽

1989 ◽

Vol 66 (5) ◽

pp. 2462-2467 ◽

Cited By ~ 4

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.

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High-frequency ventilation of ducks and geese

Journal of Applied Physiology ◽

10.1152/jappl.1987.63.1.413 ◽

1987 ◽

Vol 63 (1) ◽

pp. 413-417 ◽

Cited By ~ 6

Author(s):

R. H. Hastings ◽

F. L. Powell

Keyword(s):

Gas Exchange ◽

High Frequency ◽

Minute Ventilation ◽

Control Ventilation ◽

High Frequency Ventilation ◽

Opening Pressure ◽

Arterial Pco2 ◽

Bias Flow ◽

Airway Opening ◽

Frequency Ventilation

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)

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Augmented diffusion in the airways can support pulmonary gas exchange

Journal of Applied Physiology ◽

10.1152/jappl.1980.49.2.232 ◽

1980 ◽

Vol 49 (2) ◽

pp. 232-238 ◽

Cited By ~ 119

Author(s):

J. J. Fredberg

Keyword(s):

Gas Exchange ◽

Tidal Volume ◽

High Frequency ◽

Molecular Diffusion ◽

Minute Ventilation ◽

Turbulent Dispersion ◽

High Frequency Ventilation ◽

Ventilation Efficiency ◽

Airway Opening ◽

Frequency Ventilation

Bohn et al. (J Appl. Physiol.: Respirat. Environ. Exercise Physiol, 48: 710-716, 1980) reported that paralyzed beagle dogs maintained normal gas exchange for 6 h or more when small tidal volumes at high breathing rates were maintained at the airway opening (15 ml tidal volume at 15 breaths/s). These tidal volumes were 25% of dead space and thereby were too small to permit convective gas exchange with pulmonary air spaces. I have used a semiempirical analysis to show that augmented diffusion in the central airways, akin to Taylor's turbulent dispersion (Proc. R. Soc. Ser. A 223: 446-468, 1954) combined with molecular diffusion in the periphery of the lung, can account for most if not all of the observed gas transport during small tidal volume, high-frequency ventilation. Ventilation efficiency (alveolar ventilation/minute ventilation) is approximately 2-5% and is insensitive to the combination of frequency and tidal volume giving rise to the minute ventilation.

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