Effects of altering ventilation on steady-state diffusing capacity for carbon monoxide

1963 ◽  
Vol 18 (1) ◽  
pp. 89-96 ◽  
Author(s):  
Kaye H. Kilburn ◽  
Harry A. Miller ◽  
John E. Burton ◽  
Ronald Rhodes

Alterations in the steady-state diffusing capacity for carbon monoxide (Dco) by the method of Filley, MacIntosh, and Wright, produced by sequential changes in the pattern of breathing were studied in anesthetized, paralyzed, artificially ventilated dogs. The Dco of paralyzed, artificially ventilated control dogs did not differ significantly during 3 hr from values found in conscious and anesthetized controls. A fivefold increase in tidal volume without changing frequency of breathing raised alveolar ventilation and CO uptake 500% and Dco 186%. A high correlation between tidal volume and Dco was noted during reciprocal alterations of tidal volume and rate which maintained minute volume. The Dco appeared to fall when alveolar ventilation was tripled by increments of rate with a fixed-tidal volume, despite a 63% increase in CO uptake. Doubling end-expiratory lung volume by positive pressure breathing without altering tidal volume or rate did not affect Dco. The addition of 100 ml of external dead space with rate and tidal volume constant decreased Dco to 42% of control level, however, stepwise reduction of dead space from 100 ml to 0 in two dogs failed to change Dco. Added dead space equal to frac12 tidal volume (170 ml) reduced Dco to 25% of control in two dogs with a return to control with removal of dead space. Thus, in paralyzed artificially ventilated dogs, tidal volume appears to be the principal ventilatory determinant of steady-state Dco. Dco is minimally affected by increases in alveolar ventilation with a constant tidal volume effected by increasing the frequency of breathing. Prolonged ventilation, at fixed rate and volume, and increased dead space either did not effect, or they reduced Dco, perhaps by rendering less uniform the distribution of gas, and blood in the lungs. Although lung volume was doubled by positive-pressure breathing, pulmonary capillary blood volume was probably reduced to produce opposing effects on diffusing capacity and no net change. Submitted on March 14, 1962

1964 ◽  
Vol 19 (1) ◽  
pp. 59-74 ◽  
Author(s):  
Paul S⊘lvsteen

A method of measuring the lung diffusing capacity (Dl) with radioactive carbon monoxide (C14O) and nonuniformity of ventilation with nonabsorbable gas in a closed system is described. Treating ventilation as a continuous phenomenon and disregarding dead space, the mathematical equations for uniform and nonuniform ventilation (two lung regions ventilated in parallel) are derived. It is proved that sooner or later the curve for carbon monoxide, plotted on semilogarithmic paper, will be rectilinear. Experiments in six normal subjects and eight patients with chronic lung disease are described. Determinations of the distribution of the ventilation and the Dl are made in separate experiments. Since the method is unreliable at high Dl values, many of the Dl estimations are performed at high oxygen tension, which reduces the apparent Dl. It is shown that the assumption of a uniform distribution of Dl to lung volume explains the experimental findings better than the assumption of a uniform distribution of Dl to alveolar ventilation. Dl was decreased in four of the eight patients. mathematics of uniform and nonuniform ventilation; distribution of lung diffusing capacity in relation to lung volume and alveolar ventilation; N2 curve for use in calculating alveolar ventilation and regional lung volumes; CO curve for use in calculating lung diffusing capacity; diffusing capacity of lung determined with a closed system Submitted on October 15, 1962


1988 ◽  
Vol 64 (5) ◽  
pp. 2240-2244 ◽  
Author(s):  
J. Ampil ◽  
J. I. Carlin ◽  
R. L. Johnson

To develop a rebreathing method for lung volumes, cardiac output with acetylene, and CO diffusing capacity in awake exercising dogs, we have modified and adapted the low-dead-space mask of Montefusco et al. (Angiology 34: 340–354, 1983). We have simplified the fabrication procedure, allowing the physiologist to make the device from parts that can be prefabricated before each dog is custom fitted with the mouthpiece. This decreases the anesthesia time required to custom fit the mouthpiece to each dog. We have also reduced the weight of the mask, making it more tolerable during exercise. We have validated that the mask is leak-free by having the dog rebreathe an inert insoluble gas, He, until equilibration is achieved between the bag and lung. Preliminary measurements of lung volume, cardiac output with acetylene, and CO diffusing capacity have been made during exercise.


1963 ◽  
Vol 18 (3) ◽  
pp. 447-456 ◽  
Author(s):  
G. M. Turino ◽  
E. H. Bergofsky ◽  
R. M. Goldring ◽  
A. P. Fishman

The effect of graded exercise on the pulmonary diffusing capacity for both oxygen and carbon monoxide measured simultaneously was studied in healthy young adults by steady-state methods. Pulmonary diffusing capacity for oxygen increases progressively with increasing severity of exercise; it exceeds the DlCO at high levels of exercise by amounts greater than can be accounted for by the difference in diffusivity of the test gases. Diffusing capacity for carbon monoxide increases less than DlOO2 for comparable grades of exercise but no definite plateau value could be established. The supine or upright body position does not influence the values of either DlOO2 or DlCO during exercise. Diffusing capacity of the lung for oxygen does not limit the maximum levels of exercise which may be achieved by normal man. Submitted on August 6, 1962


1984 ◽  
Vol 57 (3) ◽  
pp. 881-887 ◽  
Author(s):  
G. G. Weinmann ◽  
W. Mitzner ◽  
S. Permutt

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.


1989 ◽  
Vol 64 (1) ◽  
pp. 51-59 ◽  
Author(s):  
KENNETH C. BECK ◽  
ROBERT E. HYATT ◽  
BRUCE A. STAATS ◽  
PAUL L. ENRIGHT ◽  
JOSEPH R. RODARTE

1962 ◽  
Vol 17 (5) ◽  
pp. 805-811 ◽  
Author(s):  
Joseph A. Lipsky ◽  
Joseph F. Tomashefski ◽  
Earl T. Carter

Fourteen male subjects were mechanically hyperventilated by intermittent positive pressure breathing. Tidal volume and respiratory frequency were increased approximately three times and one and one-half times control, respectively. Breath-by-breath analyses of CO2 output indicate a loss of approximately 2.5 liters of CO2 from the body stores in 12 min. Only one-third of that volume was restored during the ensuing 12-min recovery period, mostly as a result of hypoventilation rather than apnea. Over the entire recovery period, the volume of CO2 regained by the blood store approximated 75% of the CO2 content lost during hyperventilation. Under the conditions of these experiments, tissues regained less than 20% of the depleted CO2 store. CO2 retention patterns may be more effective than arterial blood or alveolar air analyses in determining a return to a steady state when tissue stores have been considerably reduced. Submitted on August 24, 1961


2011 ◽  
pp. 101-107
Author(s):  
James R. Munis

The sine qua non of ventilation is arterial carbon dioxide. If you want to know about ventilation, just check the PaCO2. If it is low or normal, ventilation is fine, regardless of any other parameter, including respiratory rate, tidal volume, or dead space ratio. However, if PaCO2 is high, then alveolar ventilation (VA) is impaired (relative to the carbon dioxide load being presented to the lungs). In a conventional breathing circuit, dead space ends at the Y-shaped junction of the inspiratory and expiratory arms of the circuit and the endotracheal tube. On the machine side of that junction, the inspiratory and expiratory limbs see only fresh inspired or expired gas, respectively, but not both. You should know 2 other things about ventilation. One is the Bohr equation, which estimates the ratio of dead space to tidal volume. The anatomic dead space is estimated as the expired volume that coincides with half maximal nitrogen content. The second thing is the effect of gravity on the distribution of ventilation within the lung.


1971 ◽  
Vol 31 (6) ◽  
pp. 847-852 ◽  
Author(s):  
P. D. Wagner ◽  
R. W. Mazzone ◽  
J. B. West

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