Gas-Mixing Dead Space Measurement with Paired Tracers1

Author(s):  
N. B. Kindig ◽  
M. E. Perry ◽  
G. F. Filley
1976 ◽  
Vol 41 (1) ◽  
pp. 115-119 ◽  
Author(s):  
M. Paiva ◽  
L. M. Lacquet ◽  
L. P. van der Linden

The anatomical data of the human lung published by Hansen and Ampaya are used in a model of gas transport in the lung. The Bohr dead space is calculated from solutions of a transport equation where diffusivity is given by an empirical formula obtained by Sherer et al. A satisfactory agreement is found with experimental data obtained from simultaneous washouts of H2 and SF6 for respiratory frequencies ranging between 15 and 60 min-1 and tidal volumes between 200 and 1,800 ml. The results support the idea that molecular diffusion is the main but not the only physical phenomenom which intervenes in gas mixing during breathing.


1982 ◽  
Vol 53 (4) ◽  
pp. 930-939 ◽  
Author(s):  
M. F. Petrini ◽  
B. T. Peterson ◽  
R. W. Hyde ◽  
V. Lam ◽  
M. J. Utell ◽  
...  

To evaluate the rate of gas mixing in human lungs during rebreathing maneuvers used to measure pulmonary tissue volume (Vt) and pulmonary capillary blood flow (Qc), we devised a method to determine the dead space during rebreathing (VRD). Required measurements are initial concentration of a foreign inert insoluble gas in the rebreathing bag, first mixed expired concentration, equilibrated concentration, volume inspired, and volume of the first expired breath. In subjects breathing rapidly at 30 breaths/min with inspired volumes in excess of 2 liters, VRD had values three or more times greater than the predicted anatomical dead space (VD). Breath holding after the first inspiration progressively diminished VRD so that after 10–15 s, it approximately equaled predicted VD. VRD measured with helium was smaller than VRD measured with sulfur hexafluoride. The reported degree of uneven ventilation from gravitational forces in normal humans can account for only about one-third of the difference between VRD and VD. These findings support the concept that mixing by diffusion between peripheral parallel airways is incomplete at normal breathing rates in humans and can result in errors as high as 25% in Vt and Qc.


2014 ◽  
Vol 45 (6) ◽  
pp. 1704-1716 ◽  
Author(s):  
H. Thomas Robertson

An elevated physiological dead space, calculated from measurements of arterial CO2 and mixed expired CO2, has proven to be a useful clinical marker of prognosis both for patients with acute respiratory distress syndrome and for patients with severe heart failure. Although a frequently cited explanation for an elevated dead space measurement has been the development of alveolar regions receiving no perfusion, evidence for this mechanism is lacking in both of these disease settings. For the range of physiological abnormalities associated with an increased physiological dead space measurement, increased alveolar ventilation/perfusion ratio (V′A/Q′) heterogeneity has been the most important pathophysiological mechanism. Depending on the disease condition, additional mechanisms that can contribute to an elevated physiological dead space measurement include shunt, a substantial increase in overall V′A/Q′ ratio, diffusion impairment, and ventilation delivered to unperfused alveolar spaces.


1993 ◽  
Vol 74 (1) ◽  
pp. 470-475 ◽  
Author(s):  
I. T. Merth ◽  
G. J. Verschragen ◽  
I. C. Olievier ◽  
P. J. De Winter ◽  
P. H. Quanjer

Details are given of two spirometers for use in neonates and infants < 12 mo old. The minimum volumes are 520 and 670 ml, respectively. The maximum volume changes that can be recorded are 250 and 450 ml, respectively. The minimal detectable volume changes are 0.4 and 0.6 ml, respectively. Rebreathing of dead space gas is prevented by a fan producing a flow of 6.2 and 10.2 l/min, respectively; 100% gas mixing after injecting a gas bolus in the two spirometers is achieved in 5.7 and 6.6 s, respectively. Resistance to airflow is 0.2 kPa.l-1.s (2 cmH2O.l-1.s) at 150 ml/s in both spirometers. The frequency response of both instruments is flat to 6 cycles/s. The instruments can be easily cleaned and are suitable for bedside measurements.


1995 ◽  
Vol 430 (5) ◽  
pp. 862-870 ◽  
Author(s):  
A. C. M. Schrikker ◽  
H. Wesenhagen ◽  
S. C. M. Luijendijk
Keyword(s):  

CHEST Journal ◽  
2005 ◽  
Vol 128 (4) ◽  
pp. 2195-2202 ◽  
Author(s):  
Kerstin Hogg ◽  
Deborah Dawson ◽  
Ted Tabor ◽  
Beverly Tabor ◽  
Kevin Mackway-Jones

1982 ◽  
Vol 62 (5) ◽  
pp. 549-551 ◽  
Author(s):  
W. Kox ◽  
F. Langley ◽  
K. Horsfield ◽  
G. Cumming

1. Atropine is known to diminish broncho-motor tone. In order to investigate the acute effect of atropine on respiration and alveolar gas mixing, a dose of 2.4 mg was given intravenously. 2. Ten normal male volunteers were each studied three times with a nitrogen washout method, once before administration of atropine and then 20 min and 60 min thereafter. 3. After the administration of atropine there was a reduction in tidal volume, a slight increase in frequency of respiration and an increase in series dead space. The tidal mixing volume showed a fall of 25%. In spite of the reduced alveolar dead space the effective mixing volume fell by 29%. Multi-breath alveolar mixing efficiency fell by 3.5%. 4. Multi-breath alveolar mixing efficiency was found to be less with smaller tidal mixing volumes, a fall of 518 ml in the latter causing a reduction of 17.2% in mixing efficiency. 5. A reduction of 100 ml in tidal volume in normal subjects was associated with a decrease of 6.9% in alveolar mixing efficiency. In the subjects receiving atropine tidal volume reduced by 96 ml, but the observed fall in alveolar mixing efficiency was only 3.5%, This suggests an improvement in alveolar mixing of 3.4% due to the administration of atropine. Despite this small improvement, the mixing efficiency is still only 66%. The residual inefficiency of 34% cannot therefore be explained on the basis of broncho-motor tone.


2012 ◽  
Vol 114 (4) ◽  
pp. 866-874 ◽  
Author(s):  
Gerardo Tusman ◽  
Fernando Suarez Sipmann ◽  
Stephan H. Bohm

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