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

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.

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.

scholarly journals Respiratory mechanics and gas exchanges in the early course of COVID-19 ARDS: a hypothesis-generating study

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
J.-L. Diehl ◽  
N. Peron ◽  
R. Chocron ◽  
B. Debuc ◽  
E. Guerot ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Dead Space ◽  
Respiratory Mechanics ◽  
Invasive Mechanical Ventilation ◽  
Endothelial Damage ◽  
Circulating Endothelial Cells ◽  
Pulmonary Mechanics ◽  
High Peep ◽  
Gas Exchanges ◽  
Physiological Dead Space

Abstract Rationale COVID-19 ARDS could differ from typical forms of the syndrome. Objective Pulmonary microvascular injury and thrombosis are increasingly reported as constitutive features of COVID-19 respiratory failure. Our aim was to study pulmonary mechanics and gas exchanges in COVID-2019 ARDS patients studied early after initiating protective invasive mechanical ventilation, seeking after corresponding pathophysiological and biological characteristics. Methods Between March 22 and March 30, 2020 respiratory mechanics, gas exchanges, circulating endothelial cells (CEC) as markers of endothelial damage, and D-dimers were studied in 22 moderate-to-severe COVID-19 ARDS patients, 1 [1–4] day after intubation (median [IQR]). Measurements and main results Thirteen moderate and 9 severe COVID-19 ARDS patients were studied after initiation of high PEEP protective mechanical ventilation. We observed moderately decreased respiratory system compliance: 39.5 [33.1–44.7] mL/cmH2O and end-expiratory lung volume: 2100 [1721–2434] mL. Gas exchanges were characterized by hypercapnia 55 [44–62] mmHg, high physiological dead-space (VD/VT): 75 [69–85.5] % and ventilatory ratio (VR): 2.9 [2.2–3.4]. VD/VT and VR were significantly correlated: r2 = 0.24, p = 0.014. No pulmonary embolism was suspected at the time of measurements. CECs and D-dimers were elevated as compared to normal values: 24 [12–46] cells per mL and 1483 [999–2217] ng/mL, respectively. Conclusions We observed early in the course of COVID-19 ARDS high VD/VT in association with biological markers of endothelial damage and thrombosis. High VD/VT can be explained by high PEEP settings and added instrumental dead space, with a possible associated role of COVID-19-triggered pulmonary microvascular endothelial damage and microthrombotic process.

PULMONARY FUNCTION IN THE NEWBORN INFANT

PEDIATRICS ◽  
1962 ◽  
Vol 30 (6) ◽  
pp. 975-989
Author(s):  
N. M. Nelson ◽  
L. S. Prod'hom ◽  
R. B. Cherry ◽  
P. J. Lipsitz ◽  
C. A. Smith
Keyword(s):  
Pulmonary Function ◽  
Respiratory Distress ◽  
Newborn Infant ◽  
Dead Space ◽  
Clinical Course ◽  
Average Difference ◽  
Alveolar Dead Space ◽  
Physiological Dead Space ◽  
New Born ◽  
Pulmonary Capillary

The arterial-alveolar tension gradient for CO2 has been investigated in 17 normal new born infants and in 15 with some degree of respiratory distress. Whereas the normal infants had virtually no Pco2 gradient from pulmonary capillary to alveolus, an average difference of 13.9 mm Hg was detected in sick infants. This gradient for Pco2 is caused by increased alveolar (and total physiological dead space, the relative amount of which closely parallels the clinical course of the disease. The data obtained indicate the increase in alveolar dead space to be largely due to poor perfusion of ventilated alveoli. In severely ill infants more than 60% of ventilated alveoli appear to be under-perfused.

Ventilation standards for small mammals

1964 ◽  
Vol 19 (2) ◽  
pp. 360-362 ◽  
Author(s):  
Leonard I. Kleinman ◽  
Edward P. Radford
Keyword(s):  
Body Weight ◽  
Tidal Volume ◽  
Small Mammals ◽  
Artificial Respiration ◽  
Alveolar Ventilation ◽  
Breathing Frequency ◽  
Slide Rule ◽  
Physiological Dead Space ◽  
The Relationship ◽  
Tidal Volume Breathing

Ventilation standards for small mammals have been prepared on the basis of the relationship between alveolar ventilation and metabolism. On the assumptions of an average respiratory quotient of 0.85 and physiological dead space directly proportional to tidal volume, the relationship between tidal volume, breathing frequency, and body weight has been derived. The standards are presented in a graphic form and as a slide rule. animal ventilation; artificial respiration; tidal volume, breathing frequency and body weight relationship Submitted on August 15, 1963

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.

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