"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.

Expiratory and arterial partial pressure relations under different ventilation-perfusion conditions

1983 ◽  
Vol 54 (6) ◽  
pp. 1745-1753 ◽  
Author(s):  
A. Zwart ◽  
S. C. Luijendijk ◽  
W. R. de Vries
Keyword(s):  
Partial Pressure ◽  
Dead Space ◽  
Gas Analysis ◽  
Lung Model ◽  
Breathing Patterns ◽  
Tracer Gas ◽  
Physiological Dead Space ◽  
Arterial Partial Pressure ◽  
The Difference ◽  
End Tidal

Inert tracer gas exchange across the human respiratory system is simulated in an asymmetric lung model for different oscillatory breathing patterns. The momentary volume-averaged alveolar partial pressure (PA), the expiratory partial pressure (PE), the mixed expiratory partial pressure (PE), the end-tidal partial pressure (PET), and the mean arterial partial pressure (Pa), are calculated as functions of the blood-gas partition coefficient (lambda) and the diffusion coefficient (D) of the tracer gas. The lambda values vary from 0.01 to 330.0 inclusive, and four values of D are used (0.5, 0.22, 0.1, and 0.01). Three ventilation-perfusion conditions corresponding to rest and mild and moderate exercise are simulated. Under simulated exercise conditions, we compute a reversed difference between PET and Pa compared with the rest condition. This reversal is directly reflected in the relation between the physiological dead space fraction (1--PE/Pa) and the Bohr dead space fraction (1--PE/PET). It is argued that the difference (PET--Pa) depends on the lambda of the tracer gas, the buffering capacity of lung tissue, and the stratification caused by diffusion-limited gas transport in the gas phase. Finally some determinants for the reversed difference (PET--Pa) and the significance for conventional gas analysis are discussed.

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

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 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.

Interaction of hypoxia and hypercapnia on cerebral hemodynamics and brain electrical activity in dogs

1987 ◽  
Vol 253 (4) ◽  
pp. H890-H897 ◽  
Author(s):  
R. W. McPherson ◽  
D. Eimerl ◽  
R. J. Traystman
Keyword(s):  
Partial Pressure ◽  
Elevated Level ◽  
Severe Hypoxia ◽  
O2 Uptake ◽  
Animal Group ◽  
Moderate Hypoxia ◽  
Co2 Partial Pressure ◽  
Arterial Blood ◽  
O2 Partial Pressure ◽  
O2 Delivery

The interaction of hypoxic hypoxia, hypercapnia, and mean arterial blood pressure (MABP) was studied in 15 pentobarbital-anesthetized ventilated dogs. In one group of animals (n = 5) hypercapnia [arterial CO2 partial pressure (PaCO2) approximately 50 Torr] was added to both moderate hypoxia and severe hypoxia. Moderate hypoxia [arterial O2 partial pressure (PaO2) = 36 mmHg] increased MABP and cerebral blood flow (CBF) without changes in cerebral O2 uptake (CMRO2). Superimposed hypercapnia increased CBF and MABP further with no change in CMRO2. In another group of animals (n = 5), a MABP increase of approximately 40 mmHg during moderate hypoxia without hypercapnia did not further increase CBF, suggesting intact autoregulation. Thus, during moderate hypoxia, hypercapnia is capable of increasing CBF. Severe hypoxia (PaO2 = 22 mmHg) increased CBF, but MABP and CMRO2 declined. Superimposed hypercapnia further decreased MABP and decreased CBF from its elevated level and further decreased CMRO2. Raising MABP under these circumstances in another animal group (n = 5) increased CBF above the level present during severe hypoxia alone and increased CMRO2. The change in CBF and CMRO2 during severe hypoxia plus hypercapnia with MABP elevation were not different from that severe hypoxia alone. We conclude that, during hypoxia sufficiently severe to impair CMRO2, superimposed hypercapnia has a detrimental influence due to decreased MABP, which causes a decrease in CBF and cerebral O2 delivery.

PULMONARY FUNCTION, DEDUCED FROM URINARY NITROGEN TENSIONS

PEDIATRICS ◽  
1967 ◽  
Vol 40 (6) ◽  
pp. 937-938
Author(s):  
M. E. A.
Keyword(s):  
Carbon Dioxide ◽  
Blood Flow ◽  
Pulmonary Function ◽  
Partial Pressure ◽  
Urine Sample ◽  
Pulmonary Blood Flow ◽  
Lung Perfusion ◽  
Alveolar Ventilation ◽  
Arterial Oxygen ◽  
Urinary Nitrogen

THE elegant studies reported by Led-better, Homma, and Farhi in this issue are entitled `'Readjustment in Distribution of Alveolar Ventilation and Lung Perfusion in the Newborn." It must come as a great surprise to the reader to discover that the only measurement actually made was the partial pressure of nitrogen in the infants' urine. How could one conclude that there were significant imbalances between the distribution of alveolar ventilation and pulmonary blood flow (VA/Q) in the first days of life in normal infants from a urine sample? It is all the more astounding in the light of previous (and seemingly more direct) studies of alveolar-arterial oxygen and carbon dioxide differences which led others to consider the differences largely explained by anatomical right-to-left shunts.

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.

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