Effect of common dead space on VA/Q distribution in the dog

1990 ◽  
Vol 68 (6) ◽  
pp. 2488-2493 ◽  
Author(s):  
K. Tsukimoto ◽  
J. P. Arcos ◽  
W. Schaffartzik ◽  
P. D. Wagner ◽  
J. B. West

Several previous studies have shown worsening ventilation-perfusion (VA/Q) relationships in humans during heavy exercise at sea level. However, the mechanism of this deterioration remains unclear because of the correlation with ventilatory and circulatory variables. Our hypothesis was that the decrease in the series dead space-to-tidal volume ratio during exercise might be partly responsible because mixing in the common dead space can reduce apparent inequality. We tested this notion in 10 resting anesthetized normocapnic dogs passively hyperventilated by increase tidal volume and a) inspired CO2 or b) external dead space. We predicted less apparent VA/Q inequality in condition b because of mixing in the added dead space. After base-line measurements, conditions a and b were randomly assigned, and after a second set of base-line measurements they were repeated in the reverse order in each dog. VA/Q inequality was measured by the multiple inert gas elimination technique. Comparison of conditions a and b demonstrated that additional external dead space improved (P less than 0.001) the blood flow distributions as hypothesized [log standard deviation of perfusion = 0.49 +/- 0.02 (SE) in condition b and 0.61 +/- 0.03 in condition a with respect to 0.52 +/- 0.03 at base line]. This study suggests that the increased tidal volume during exercise could uncover VA/Q inequality not evident at rest because of the higher ratio of common dead space to tidal volume at rest.

1976 ◽  
Vol 4 (3) ◽  
pp. 203-204 ◽  
Author(s):  
A. Morton ◽  
P. Mahoney ◽  
P. Hansen ◽  
M. McBride ◽  
A. B. Baker

Many studies have shown that after uncomplicated abdominal surgery arterial hypoxaemia frequently occurs because of regional underventilation in relation to perfusion. This paper produces evidence that shows a small increase in physiological dead space to tidal volume ratio following general anaesthesia for abdominal surgery. This increase is thought to be due to tachypnoea rather than alteration in pulmonary blood flow.


1983 ◽  
Vol 54 (4) ◽  
pp. 1131-1140 ◽  
Author(s):  
N. B. Robinson ◽  
E. Y. Chi ◽  
H. T. Robertson

Previous investigations suggest that ventilation-perfusion (VA/Q) relationships after hemorrhagic shock are primarily dependent on regional distribution of pulmonary blood flow and implicated early VA/Q heterogeneity secondary to disproportionate redistribution of pulmonary blood flow to dependent lung regions. Multiple inert gas elimination analysis, as described by Wagner et al. (J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 36: 588–599, 1974), was applied to a standard hemorrhagic shock preparation to test this hypothesis. Soon after hemorrhage, VA/Q distributions shifted homogeneously into high VA/Q compartments, preserving base-line VA/Q relationships around a new mean VA/Q ratio. Although the mean VA/Q and VA/Q distribution returned to base line after resuscitation with autologous blood, absolute dead space ventilation persisted. Gas exchange defects included increased Bohr dead space ventilation, which could be attributed to 1) a homogeneous shift of VA/Q distributions into high VA/Q compartments, and 2) new absolute dead space ventilation associated with observed intravascular leukostasis and vascular occlusion. In contrast to previous investigations, these data suggest that VA/Q heterogeneity does not occur after hemorrhage, but rather pulmonary blood flow decreases proportionately throughout all lung regions, preserving base-line VA/Q patterns around a new mean VA/Q ratio.


1980 ◽  
Vol 49 (3) ◽  
pp. 528-532 ◽  
Author(s):  
P. W. Bradley ◽  
M. Younes

We measured the "effective" dead space of five commonly used respiratory valves: Hans Rudolph valve, two-way J valve, triple-J valve, and modified Otis-McKerrow valves without and with vane. The dead space was measured using a technique that mimicked the operation of valves during ordinary laboratory procedures. The valves were ventilated with tidal volumes ranging from 0.35-3.00 liters and at different frequencies. With all valves, there was a marked tendency for "effective" dead space to be tidal volume dependent. The measured dead space approached the water-displacement volume of the common chamber of the valve only at tidal volumes in excess of 2.0 liters. The relation between valve dead space and tidal volume was independent of frequency.


Burns ◽  
1995 ◽  
Vol 21 (5) ◽  
pp. 337-339 ◽  
Author(s):  
R.P. Mlcak ◽  
M.H. Desai ◽  
E. Robinson ◽  
R.L. McCauley ◽  
J. Richardson ◽  
...  

1984 ◽  
Vol 57 (6) ◽  
pp. 1704-1709 ◽  
Author(s):  
C. J. Allen ◽  
N. L. Jones ◽  
K. J. Killian

Changes in expired alveolar O2 and CO2 were measured breath-by-breath in six healthy male subjects (mean age 30 yr, mean weight 80 kg) at rest, 600 kpm/min, and 1,200 kpm/min. Changes were expressed in relation to expired volume (liters) and time (s) and separated into an initial dead-space component using the Fowler method applied to expired CO2 and O2, and alveolar slope. The alveolar slopes with respect to time (dPACO2, dPAO2, Torr/s) increased in relation to CO2 output (VCO2, 1/min, STPD) and O2 intake (VO2, 1/min, STPD) but were reduced by increasing tidal volume (VT, liters, BTPS): dPACO2 = 2.7 + 4.6(VCO2) - 1.9(VT) (r = 0.97); and dPAO2 = 2.3 + 5.5(VO2) - 1.9(VT) (r = 0.96). From the alveolar slopes, tidal volume, and airway dead-space volume, mean expired alveolar PO2 and PCO2 (PAO2, PACO2) were calculated. There was no change in arterialized capillary PCO2 (PaCO2) between rest (38.9 +/- 0.66 Torr) and heavy exercise (38.2 +/- 2.18 Torr), but mean PACO2 rose from 36.7 +/- 0.55 to 40.8 +/- 1.67 Torr during heavy exercise. There was no change in arterialized capillary (mean = 84.3 +/- 0.7 Torr) or alveolar (mean = 107.2 +/- 1.03 Torr) PO2. Exercise increases the fluctuations in alveolar gas composition leading to discrepancies between the PCO2 in mean alveolar gas and arterial blood to an extent that is dependent on VCO2 and VT.


1982 ◽  
Vol 52 (5) ◽  
pp. 1138-1146 ◽  
Author(s):  
M. A. Baker ◽  
M. J. Hawkins ◽  
R. D. Rader

Common carotid blood flow (CCBF) and respiratory water loss (RWL) were measured in dogs resting at ambient temperatures between 25 and 50 degrees C, during hypothalamic heating, and during light and heavy exercise at ambient temperatures of 25 and 35 degrees C. In resting dogs, CCBF varied with the level of RWL. Elevations in CCBF and RWL occurred within seconds of each other during bursts of panting. Mean unilateral CCBF increased from 6.2 ml . min-1 . kg-1 at 25 degrees C to 16.8 ml . min-1 . kg-1 at 45 degrees C, in parallel with increasing RWL. Hypothalamic heating elicited simultaneous elevations in CCBF and RWL, and the level of CCBF was strongly correlated with the hypothalamic temperature. Both CCBF and RWL increased rapidly at the onset of exercise and continued to rise during a 15-min run. Highest rates of blood flow and evaporation occurred during heavy exercise at 35 degrees C. It is concluded that the rate of blood flow through the common carotid arteries in the dog is related to the thermoregulatory needs of the animal, and most of the increased flow occurring during heat stress is destined for evaporative surfaces of the nose, mouth, and tongue.


1986 ◽  
Vol 60 (1) ◽  
pp. 295-298 ◽  
Author(s):  
T. V. Santiago ◽  
J. A. Neubauer ◽  
N. H. Edelman

Ventilation and brain blood flow (BBF) were simultaneously measured during carbon monoxide (CO) inhalation in awake and sleeping goats up to HbCO levels of 40%. Unilateral BBF, which was continuously measured with an electromagnetic flow probe placed around the internal maxillary artery, progressively increased with CO inhalation in the awake and both sleep stages. The increase in BBF with CO inhalation during rapid-eye-movement (REM) sleep (delta BBF/delta arterial O2 saturation = 1.34 +/- 0.27 ml X min-1 X %-1) was significantly greater than that manifested during wakefulness (0.87 +/- 0.14) or slow-wave sleep (0.92 +/- 0.13). Ventilation was depressed by CO inhalation during both sleep stages but was unchanged from base-line values in awake goats. In contrast to slow-wave (non-REM) sleep, the ventilatory depression of REM sleep was primarily due to a reduction in tidal volume. Since tidal volume is more closely linked to central chemoreceptor function, we believe that these data suggest a possible role of the increased cerebral perfusion during hypoxic REM sleep. Induction of relative tissue alkalosis at the vicinity of the medullary chemoreceptor may contribute to the ventilatory depression exhibited during this sleep period.


1995 ◽  
Vol 1 (5) ◽  
pp. 401-408 ◽  
Author(s):  
Marco Guazzi ◽  
Giancarlo Marenzi ◽  
Emilio Assanelli ◽  
Giovanni B. Perego ◽  
Gaia Cattadori ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document