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.

scholarly journals Reductions in dead space ventilation with nasal high flow depend on physiological dead space volume: metabolic hood measurements during sleep in patients with COPD and controls

2018 ◽  
Vol 51 (5) ◽  
pp. 1702251 ◽  
Author(s):  
Paolo Biselli ◽  
Kathrin Fricke ◽  
Ludger Grote ◽  
Andrew T. Braun ◽  
Jason Kirkness ◽  
...  
Keyword(s):  
Respiratory Rate ◽  
Dead Space ◽  
Minute Ventilation ◽  
High Flow ◽  
Physiological Dead Space ◽  
Copd Patients ◽  
Dead Space Volume ◽  
Anatomical Dead Space ◽  
Dead Space Ventilation ◽  
Space Volume

Nasal high flow (NHF) reduces minute ventilation and ventilatory loads during sleep but the mechanisms are not clear. We hypothesised NHF reduces ventilation in proportion to physiological but not anatomical dead space.11 subjects (five controls and six chronic obstructive pulmonary disease (COPD) patients) underwent polysomnography with transcutaneous carbon dioxide (CO2) monitoring under a metabolic hood. During stable non-rapid eye movement stage 2 sleep, subjects received NHF (20 L·min−1) intermittently for periods of 5–10 min. We measured CO2 production and calculated dead space ventilation.Controls and COPD patients responded similarly to NHF. NHF reduced minute ventilation (from 5.6±0.4 to 4.8±0.4 L·min−1; p<0.05) and tidal volume (from 0.34±0.03 to 0.3±0.03 L; p<0.05) without a change in energy expenditure, transcutaneous CO2 or alveolar ventilation. There was a significant decrease in dead space ventilation (from 2.5±0.4 to 1.6±0.4 L·min−1; p<0.05), but not in respiratory rate. The reduction in dead space ventilation correlated with baseline physiological dead space fraction (r2=0.36; p<0.05), but not with respiratory rate or anatomical dead space volume.During sleep, NHF decreases minute ventilation due to an overall reduction in dead space ventilation in proportion to the extent of baseline physiological dead space fraction.

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.

scholarly journals Changes in respiratory function following the intramuscular administration of etorphine to boer goats (Capra hircus)

2001 ◽  
Vol 72 (3) ◽  
Author(s):  
P.E. Buss ◽  
D.G.A. Meltzer
Keyword(s):  
Respiratory Function ◽  
Minute Ventilation ◽  
Minute Volume ◽  
Capra Hircus ◽  
Physiological Effects ◽  
Physiological Changes ◽  
Respiratory Effects ◽  
Physiological Dead Space ◽  
Boer Goats ◽  
Dead Space Ventilation

The physiological effects on respiratory function of etorphine (M99, Logos Agvet) (30 µg/kg) administered intramuscularly were determined in boer goats. The goats were habituated to the experimental procedures so that respiratory function could be determined while the animals stood quietly at rest. This enabled the physiological changes induced by etorphine to be measured and compared with those obtained before administration of the immobilising drug. The effectiveness of diprenorphine (M5050, Logos Agvet) (3 mg/1 mg etorphine) as an antagonist of the physiological changes induced by the etorphine treatment was also determined. Etorphine depressed respiratory function, which resulted in a decrease in PaO2 and an increase in PaCO2. These changes were limited and occurred as a result of decreases in respiratory minute volume and alveolar minute ventilation caused by a decrease in respiratory rate. The physiological shunt fraction did not change significantly but there was a significant decrease in percentage physiological dead space ventilation. It was not possible to determine how effectively diprenorphine reversed the respiratory effects due to etorphine.

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.

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

"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.

Comparison of Ventilation/Perfusion Lung-Imaging and Dead-Space Measurements in Airway Disease

1981 ◽  
Vol 60 (1) ◽  
pp. 17-23 ◽  
Author(s):  
M. I. M. Noble ◽  
F. Langley ◽  
M. Buckman ◽  
P. Vernon ◽  
A. Seed ◽  
...  
Keyword(s):  
Dead Space ◽  
Total Lung Capacity ◽  
Pulmonary Function Tests ◽  
Airway Disease ◽  
Alveolar Ventilation ◽  
Lung Imaging ◽  
Residual Volume ◽  
Alveolar Dead Space ◽  
Lung Capacity ◽  
Dead Space Ventilation

1. Nineteen patients (three normal subjects, and 16 patients with chronic airway disease) were investigated with radionuclide lung-imaging and pulmonary function tests. 2. There was a statistically significant correlation between the ratio of residual volume to total lung capacity and alveolar dead-space ventilation for nitrogen as a percentage of alveolar ventilation (an index of gas mixing inefficiency); rS = 0.54, P < 0.05. 3. There were statistically significant associations between an abnormal ventilation or perfusion radionuclide lung image and (a) the ratio of residual volume to total lung capacity and (b) the alveolar dead-space ventilation for nitrogen as a percentage of alveolar ventilation. 4. The radionuclide counts from the posterior images were normalized for lung size and injected dose; perfusion counts were then subtracted from ventilation counts at locations from the top to the bottom of the lungs. 5. There was a statistically significant association between low ventilation minus perfusion areas and arterial hypoxia. 6. There was a statistically significant association between high ventilation minus perfusion areas and an increased alveolar dead-space ventilation for carbon dioxide as a percentage of alveolar ventilation.

Dead space ventilation promotes alveolar hypocapnia reducing surfactant secretion by altering mitochondrial function

Thorax ◽  
2019 ◽  
Vol 74 (3) ◽  
pp. 219-228 ◽  
Author(s):  
Martina Kiefmann ◽  
Sascha Tank ◽  
Marc-Oliver Tritt ◽  
Paula Keller ◽  
Kai Heckel ◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Dead Space ◽  
Lung Compliance ◽  
Alveolar Ventilation ◽  
Alveolar Epithelial Cells ◽  
Perfusion Failure ◽  
Physiologic Dead Space ◽  
Surfactant Secretion ◽  
Dead Space Ventilation

BackgroundIn acute respiratory distress syndrome (ARDS), pulmonary perfusion failure increases physiologic dead space ventilation (VD/VT), leading to a decline of the alveolar CO2 concentration [CO2]iA. Although it has been shown that alveolar hypocapnia contributes to formation of atelectasis and surfactant depletion, a typical complication in ARDS, the underlying mechanism has not been elucidated so far.MethodsIn isolated perfused rat lungs, cytosolic or mitochondrial Ca2+ concentrations ([Ca2+]cyt or [Ca2+]mito, respectively) of alveolar epithelial cells (AECs), surfactant secretion and the projected area of alveoli were quantified by real-time fluorescence or bright-field imaging (n=3–7 per group). In ventilated White New Zealand rabbits, the left pulmonary artery was ligated and the size of subpleural alveoli was measured by intravital microscopy (n=4 per group). Surfactant secretion was determined in the bronchoalveolar lavage (BAL) by western blot.ResultsLow [CO2]iA decreased [Ca2+]cyt and increased [Ca2+]mito in AECs, leading to reduction of Ca2+-dependent surfactant secretion, and alveolar ventilation in situ. Mitochondrial inhibition by ruthenium red or rotenone blocked these responses indicating that mitochondria are key players in CO2 sensing. Furthermore, ligature of the pulmonary artery of rabbits decreased alveolar ventilation, surfactant secretion and lung compliance in vivo. Addition of 5% CO2 to the inspiratory gas inhibited these responses.ConclusionsAccordingly, we provide evidence that alveolar hypocapnia leads to a Ca2+ shift from the cytosol into mitochondria. The subsequent decline of [Ca2+]cyt reduces surfactant secretion and thus regional ventilation in lung regions with high VD/VT. Additionally, the regional hypoventilation provoked by perfusion failure can be inhibited by inspiratory CO2 application.

Unanesthetized dogs with increased respiratory dead space

1960 ◽  
Vol 15 (5) ◽  
pp. 838-842 ◽  
Author(s):  
Thomas B. Barnett ◽  
Richard M. Peters
Keyword(s):  
Tidal Volume ◽  
Respiratory Rate ◽  
Dead Space ◽  
Minute Volume ◽  
Alveolar Ventilation ◽  
Physiologic Dead Space ◽  
Consistent Change ◽  
The Dead ◽  
Animal Preparation ◽  
Respiratory Dead Space

A method is described for maintaining a permanent tracheostomy in dogs. This animal preparation has been used to study the effects of artificially increased respiratory dead space. Trained dogs with tracheostomies have made possible measurements of ventilation without anesthesia. It has been found that additions to the respiratory dead space in the form of tubing of frac34 in. i.d. result in an increase in physiologic dead space of the same magnitude as the volume of tubing added. Increasing the dead space in this manner resulted in an increased minute volume which was accomplished principally by an increase in tidal volume without a significant or consistent change in respiratory rate. Alveolar ventilation remained unchanged even with large additions to the dead space (20–30 cc/kg of animal wt.). Arterial pCO2 was significantly higher in these animals than in the controls. The CO2 tension was similarly elevated when extra dead space of lesser volume (5–20 cc/kg) was allowed to remain on the dogs for more than 48 hours. Submitted on April 13, 1960

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