scholarly journals Dead space: the physiology of wasted ventilation

2014 ◽  
Vol 45 (6) ◽  
pp. 1704-1716 ◽  
Author(s):  
H. Thomas Robertson
Keyword(s):  
Dead Space ◽  
Distress Syndrome ◽  
Severe Heart Failure ◽  
Alveolar Ventilation ◽  
Pathophysiological Mechanism ◽  
Physiological Dead Space ◽  
Disease Condition ◽  
Physiological Abnormalities ◽  
Ventilation Perfusion Ratio ◽  
Space Measurement

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.

Physiological dead space during high-frequency ventilation in dogs

1984 ◽  
Vol 57 (3) ◽  
pp. 881-887 ◽  
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.

Measurement of dead space ventilation using a pHa servo-controlled ventilator

1981 ◽  
Vol 51 (1) ◽  
pp. 154-159 ◽  
Author(s):  
R. L. Coon ◽  
E. J. Zuperku ◽  
J. P. Kampine
Keyword(s):  
Dead Space ◽  
Close Agreement ◽  
Minute Volume ◽  
Alveolar Ventilation ◽  
Independent Method ◽  
Servo Control ◽  
Physiological Dead Space ◽  
Arterial Ph ◽  
Before And After ◽  
Dead Space Ventilation

A control system for the systemic arterial pH (pHa) servo control of mechanical ventilation has recently been developed. If pHa is maintained constant by the change, separation of minute volume into alveolar ventilation and physiological dead space ventilation (VE = fVA VDp) can be manipulated to show that VDp = (VE1 - VE 2)/(f1 - fe) where f1 and f2 are different ventilator frequencies and VE1 and VE2 are expired minute volumes at these frequencies. Also, added dead space can be measured. VDadded = (VE2 - VE1)/f where VE1 and VE2 are the minute volumes before and after the dead space was added. The validity of these equations was tested in the anesthetized dog. The measured added dead space was in close agreement with the volume of dead space which was added and with that measured by another independent method. The measurement of VDp, probably as a result of tidal volume-related changes in VDp, did not agree as well with VDp measured by an independent method.

Pulmonary gas exchange and its determinants during sustained microgravity on Spacelabs SLS-1 and SLS-2

1995 ◽  
Vol 79 (4) ◽  
pp. 1290-1298 ◽  
Author(s):  
G. K. Prisk ◽  
A. R. Elliott ◽  
H. J. Guy ◽  
J. M. Kosonen ◽  
J. B. West
Keyword(s):  
Gas Exchange ◽  
Dead Space ◽  
Pulmonary Gas Exchange ◽  
Phase Iii ◽  
Physiological Dead Space ◽  
Co2 Output ◽  
Residual Capacity ◽  
End Tidal ◽  
Ventilation Perfusion Ratio ◽  
Topographic Distribution

We measured resting pulmonary gas exchange in eight subjects exposed to 9 or 14 days of microgravity (microG) during two Spacelab flights. Compared with preflight standing measurements, microG resulted in a significant reduction in tidal volume (15%) but an increase in respiratory frequency (9%). The increased frequency was caused chiefly by a reduction in expiratory time (10%), with a smaller decrease in inspiratory time (4%). Anatomic dead space (VDa) in microG was between preflight standing and supine values, consistent with the known changes in functional residual capacity. Physiological dead space (VDB) decreased in microG, and alveolar dead space (VDB-VDa) was significantly less in microG than in preflight standing (-30%) or supine (-15%), consistent with a more uniform topographic distribution of blood flow. The net result was that, although total ventilation fell, alveolar ventilation was unchanged in microG compared with standing in normal gravity (1 G). Expired vital capacity was increased (6%) compared with standing but only after the first few days of exposure to microG. There were no significant changes in O2 uptake, CO2 output, or end-tidal PO2 in microG compared with standing in 1 G. End-tidal PCO2 was unchanged on the 9-day flight but increased by 4.5 Torr on the 14-day flight where the PCO2 of the spacecraft atmosphere increased by 1–3 Torr. Cardiogenic oscillations in expired O2 and CO2 demonstrated the presence of residual ventilation-perfusion ratio (VA/Q) inequality. In addition, the change in intrabreath VA/Q during phase III of a long expiration was the same in microG as in preflight standing, indicating persisting VA/Q inequality and suggesting that during this portion of a prolonged exhalation the inequality in 1 G was not predominantly on a gravitationally induced topographic basis. However, the changes in PCO2 and VA/Q at the end of expiration after airway closure were consistent with a more uniform topographic distribution of gas exchange.

Lung cytokinetics after exposure to hypobaria and/or hypoxia and undernutrition in growing rats

1995 ◽  
Vol 79 (4) ◽  
pp. 1299-1309 ◽  
Author(s):  
H. S. Sekhon ◽  
W. M. Thurlbeck
Keyword(s):  
Gas Exchange ◽  
Dead Space ◽  
Normal Gravity ◽  
Phase Iii ◽  
Physiological Dead Space ◽  
Co2 Output ◽  
Residual Capacity ◽  
End Tidal ◽  
Ventilation Perfusion Ratio ◽  
Topographic Distribution

We measured resting pulmonary gas exchange in eight subjects exposed to 9 or 14 days of microgravity (microG) during two Spacelab flights. Compared with preflight standing measurements, microG resulted in a significant reduction in tidal volume (15%) but an increase in respiratory frequency (9%). The increased frequency was caused chiefly by a reduction in expiratory time (10%), with a smaller decrease in inspiratory time (4%). Anatomic dead space (VDa) in microG was between preflight standing and supine values, consistent with the known changes in functional residual capacity. Physiological dead space (VDB) decreased in microG, and alveolar dead space (VDB-VDa) was significantly less in microG than in preflight standing (-30%) or supine (-15%), consistent with a more uniform topographic distribution of blood flow. The net result was that, although total ventilation fell, alveolar ventilation was unchanged in microG compared with standing in normal gravity (1 G). Expired vital capacity was increased (6%) compared with standing but only after the first few days of exposure to microG. There were no significant changes in O2 uptake, CO2 output, or end-tidal PO2 in microG compared with standing in 1 G. End-tidal PCO2 was unchanged on the 9-day flight but increased by 4.5 Torr on the 14-day flight where the PCO2 of the spacecraft atmosphere increased by 1–3 Torr. Cardiogenic oscillations in expired O2 and CO2 demonstrated the presence of residual ventilation-perfusion ratio (VA/Q) inequality. In addition, the change in intrabreath VA/Q during phase III of a long expiration was the same in microG as in preflight standing, indicating persisting VA/Q inequality and suggesting that during this portion of a prolonged exhalation the inequality in 1 G was not predominantly on a gravitationally induced topographic basis. However, the changes in PCO2 and VA/Q at the end of expiration after airway closure were consistent with a more uniform topographic distribution of gas exchange.

scholarly journals Correction to: Physiological dead space and alveolar ventilation in ventilated infants

2021 ◽  
Author(s):  
Emma Williams ◽  
Theodore Dassios ◽  
Paul Dixon ◽  
Anne Greenough
Keyword(s):  
Dead Space ◽  
Alveolar Ventilation ◽  
Physiological Dead Space

scholarly journals Potential Effects of Corticosteroids on Physiological Dead-Space Fraction in Acute Respiratory Distress Syndrome

2012 ◽  
Vol 57 (3) ◽  
pp. 377-383 ◽  
Author(s):  
J. M. Raurich ◽  
M. Ferreruela ◽  
J. A. Llompart-Pou ◽  
M. Vilar ◽  
A. Colomar ◽  
...  
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Dead Space ◽  
Distress Syndrome ◽  
Physiological Dead Space

"Murder mystery" for student practice of pulmonary physiology calculations.

1991 ◽  
Vol 261 (6) ◽  
pp. S3
Author(s):  
M B Maron ◽  
F J Bosso
Keyword(s):  
Partial Pressure ◽  
Dead Space ◽  
Alveolar Ventilation ◽  
Physiological Dead Space ◽  
Pulmonary Physiology ◽  
Student Practice ◽  
O2 Delivery

We have developed an exercise designed to give students practice calculating arterial O2 content, O2 delivery, physiological dead space, dead space and alveolar ventilation, and alveolar partial pressure of O2 and CO2. The exercise is in the form of a "murder mystery" in which students are required to make these calculations to identify the murderer.

Dead-space ventilation as a determinant in the ventilation-perfusion concept

1960 ◽  
Vol 15 (3) ◽  
pp. 363-371 ◽  
Author(s):  
Benjamin B. Ross ◽  
Leon E. Farhi
Keyword(s):  
Dead Space ◽  
Alveolar Ventilation ◽  
Gas Composition ◽  
New Concepts ◽  
Straight Line ◽  
Variable Quantity ◽  
Line Passing ◽  
Ventilation Perfusion Ratio ◽  
Actual Ratio ◽  
Additional Area

Gas exchange in an alveolus is affected by the redistribution of dead-space gas during inspiration. Theoretical analysis of the total ventilation of an alveolus permits the description of several new concepts. a) The gas inspired by an alveolus may be identified on a PCO2-PO2 diagram as any point within an area formed by the alveolar ventilation-perfusion curve and a straight line drawn through the environmental and mixed venous points. b) The composition of gas in an alveolus may lie anywhere within this area and an additional area above the conventional curve. c) The actual ratio of exchange in an alveolus is identified by the blood R line passing through the alveolar point. The ratio of exchange between alveolus and environment is not necessarily the same as the blood R. d) The total ventilation-perfusion ratio compatible with a given alveolar gas composition is a variable quantity. e) The rebreathing of dead-space gas has a buffering action in limiting the range of gas compositions possible in alveoli. Submitted on November 30, 1959

scholarly journals Physiological dead space and alveolar ventilation in ventilated infants

2021 ◽  
Author(s):  
Emma Williams ◽  
Theodore Dassios ◽  
Paul Dixon ◽  
Anne Greenough
Keyword(s):  
Dead Space ◽  
Alveolar Ventilation ◽  
Physiological Dead Space
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