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

A Breath of Fresh Air—Ventilation

2011 ◽  
pp. 101-107
Author(s):  
James R. Munis
Keyword(s):  
Carbon Dioxide ◽  
Tidal Volume ◽  
Respiratory Rate ◽  
Dead Space ◽  
Breathing Circuit ◽  
Alveolar Ventilation ◽  
Air Ventilation ◽  
Expired Gas ◽  
Space Ratio ◽  
Normal Ventilation

The sine qua non of ventilation is arterial carbon dioxide. If you want to know about ventilation, just check the PaCO2. If it is low or normal, ventilation is fine, regardless of any other parameter, including respiratory rate, tidal volume, or dead space ratio. However, if PaCO2 is high, then alveolar ventilation (VA) is impaired (relative to the carbon dioxide load being presented to the lungs). In a conventional breathing circuit, dead space ends at the Y-shaped junction of the inspiratory and expiratory arms of the circuit and the endotracheal tube. On the machine side of that junction, the inspiratory and expiratory limbs see only fresh inspired or expired gas, respectively, but not both. You should know 2 other things about ventilation. One is the Bohr equation, which estimates the ratio of dead space to tidal volume. The anatomic dead space is estimated as the expired volume that coincides with half maximal nitrogen content. The second thing is the effect of gravity on the distribution of ventilation within the lung.

Alveolar ventilation during high-frequency oscillation: core dead space concept

1984 ◽  
Vol 56 (3) ◽  
pp. 700-707 ◽  
Author(s):  
D. Isabey ◽  
A. Harf ◽  
H. K. Chang
Keyword(s):  
Tidal Volume ◽  
Dead Space ◽  
High Frequency ◽  
Alveolar Ventilation ◽  
High Frequency Oscillation ◽  
High Frequency Ventilation ◽  
Frequency Oscillation ◽  
Simple Physical Model ◽  
Small Tube ◽  
The Dead

To assess the role of direct alveolar ventilation during high-frequency ventilation, we studied convective gas mixing during high-frequency oscillation with tidal volumes close to the dead space volume in a simple physical model. A main conduit representing a large airway was connected with a rigid sphere (V = 77, 517, and 1,719 cm3) by a small circular tube (d = 0.3 and 0.5 cm; L = 5, 10, and 20 cm). The efficiency of sinusoidal oscillations (f = 5, 20, and 40 Hz) applied at one end of the main conduit was assessed from the washout of a CO2 mixture from the sphere; to flush CO2 from the main fluid line, a constant flow of air was used. The decay in CO2 concentration measured in the sphere was exponential and therefore characterized by a measured time constant (tau m). Taking the small tube volume as the ventilatory dead space (VD), an effective tidal volume (VT*) was computed from tau m and compared with the tidal volume (VT) obtained separately from the pressure variation in the sphere. The discrepancy between these two tidal volumes has been found to be uniquely dependent on the ratio VT/VD within the range of VT/VD studied (0.5–2.2). For VT/VD less than 1.2, VT* was larger than VT, indicating that the conventional concept of alveolar ventilation does not apply. From the partition of the oscillatory flow in the small tube into two regions, the core and the unsteady boundary layer, we theoretically computed the proportions of the sinusoidal flow (or tidal volume) and the dead space for each region.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of altering ventilation on steady-state diffusing capacity for carbon monoxide

1963 ◽  
Vol 18 (1) ◽  
pp. 89-96 ◽  
Author(s):  
Kaye H. Kilburn ◽  
Harry A. Miller ◽  
John E. Burton ◽  
Ronald Rhodes
Keyword(s):  
Carbon Monoxide ◽  
Steady State ◽  
Tidal Volume ◽  
Lung Volume ◽  
Dead Space ◽  
Control Level ◽  
Alveolar Ventilation ◽  
Positive Pressure ◽  
Diffusing Capacity ◽  
Fixed Rate

Alterations in the steady-state diffusing capacity for carbon monoxide (Dco) by the method of Filley, MacIntosh, and Wright, produced by sequential changes in the pattern of breathing were studied in anesthetized, paralyzed, artificially ventilated dogs. The Dco of paralyzed, artificially ventilated control dogs did not differ significantly during 3 hr from values found in conscious and anesthetized controls. A fivefold increase in tidal volume without changing frequency of breathing raised alveolar ventilation and CO uptake 500% and Dco 186%. A high correlation between tidal volume and Dco was noted during reciprocal alterations of tidal volume and rate which maintained minute volume. The Dco appeared to fall when alveolar ventilation was tripled by increments of rate with a fixed-tidal volume, despite a 63% increase in CO uptake. Doubling end-expiratory lung volume by positive pressure breathing without altering tidal volume or rate did not affect Dco. The addition of 100 ml of external dead space with rate and tidal volume constant decreased Dco to 42% of control level, however, stepwise reduction of dead space from 100 ml to 0 in two dogs failed to change Dco. Added dead space equal to frac12 tidal volume (170 ml) reduced Dco to 25% of control in two dogs with a return to control with removal of dead space. Thus, in paralyzed artificially ventilated dogs, tidal volume appears to be the principal ventilatory determinant of steady-state Dco. Dco is minimally affected by increases in alveolar ventilation with a constant tidal volume effected by increasing the frequency of breathing. Prolonged ventilation, at fixed rate and volume, and increased dead space either did not effect, or they reduced Dco, perhaps by rendering less uniform the distribution of gas, and blood in the lungs. Although lung volume was doubled by positive-pressure breathing, pulmonary capillary blood volume was probably reduced to produce opposing effects on diffusing capacity and no net change. Submitted on March 14, 1962

Relation between respiratory valve dead space and tidal volume

1980 ◽  
Vol 49 (3) ◽  
pp. 528-532 ◽  
Author(s):  
P. W. Bradley ◽  
M. Younes
Keyword(s):  
Tidal Volume ◽  
Dead Space ◽  
Water Displacement ◽  
Respiratory Valve ◽  
Laboratory Procedures ◽  
The Common ◽  
The Dead ◽  
Marked Tendency

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.

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 Physiological respiratory parameters in pre-hospital patients with suspected COVID-19: A prospective cohort study

PLoS ONE ◽  
2021 ◽  
Vol 16 (9) ◽  
pp. e0257018
Author(s):  
Johan Mälberg ◽  
Nermin Hadziosmanovic ◽  
David Smekal
Keyword(s):  
Logistic Regression ◽  
Hospital Admission ◽  
Tidal Volume ◽  
Respiratory Rate ◽  
Dead Space ◽  
Hospital Admissions ◽  
Rapid Shallow Breathing Index ◽  
Respiratory Parameters ◽  
Hospital Patients ◽  
Adjusted Logistic Regression

Background The COVID-19 pandemic has presented emergency medical services (EMS) worldwide with the difficult task of identifying patients with COVID-19 and predicting the severity of their illness. The aim of this study was to investigate whether physiological respiratory parameters in pre-hospital patients with COVID-19 differed from those without COVID-19 and if they could be used to aid EMS personnel in the prediction of illness severity. Methods Patients with suspected COVID-19 were included by EMS personnel in Uppsala, Sweden. A portable respiratory monitor based on pneumotachography was used to sample the included patient’s physiological respiratory parameters. A questionnaire with information about present symptoms and background data was completed. COVID-19 diagnoses and hospital admissions were gathered from the electronic medical record system. The physiological respiratory parameters of patients with and without COVID-19 were then analyzed using descriptive statistical analysis and logistic regression. Results Between May 2020 and January 2021, 95 patients were included, and their physiological respiratory parameters analyzed. Of these patients, 53 had COVID-19. Using adjusted logistic regression, the odds of having COVID-19 increased with respiratory rate (95% CI 1.000–1.118), tidal volume (95% CI 0.996–0.999) and negative inspiratory pressure (95% CI 1.017–1.152). Patients admitted to hospital had higher respiratory rates (p<0.001) and lower tidal volume (p = 0.010) compared to the patients who were not admitted. Using adjusted logistic regression, the odds of hospital admission increased with respiratory rate (95% CI 1.081–1.324), rapid shallow breathing index (95% CI 1.006–1.040) and dead space percentage of tidal volume (95% CI 1.027–1.159). Conclusion Patients taking smaller, faster breaths with less pressure had higher odds of having COVID-19 in this study. Smaller, faster breaths and higher dead space percentage also increased the odds of hospital admission. Physiological respiratory parameters could be a useful tool in detecting COVID-19 and predicting hospital admissions, although more research is needed.

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 Nasal high flow reduces minute ventilation during sleep through a decrease of carbon dioxide rebreathing

2019 ◽  
Vol 126 (4) ◽  
pp. 863-869 ◽  
Author(s):  
Maximilian Pinkham ◽  
Russel Burgess ◽  
Toby Mündel ◽  
Stanislav Tatkov
Keyword(s):  
Carbon Dioxide ◽  
Gas Exchange ◽  
Tidal Volume ◽  
Respiratory Rate ◽  
Dead Space ◽  
Minute Ventilation ◽  
Control Ventilation ◽  
High Flow ◽  
Carbon Dioxide Rebreathing ◽  
Anatomical Dead Space

Nasal high flow (NHF) is an emerging therapy for respiratory support, but knowledge of the mechanisms and applications is limited. It was previously observed that NHF reduces the tidal volume but does not affect the respiratory rate during sleep. The authors hypothesized that the decrease in tidal volume during NHF is due to a reduction in carbon dioxide (CO2) rebreathing from dead space. In nine healthy males, ventilation was measured during sleep using calibrated respiratory inductance plethysmography (RIP). Carbogen gas mixture was entrained into 30 l/min of NHF to obtain three levels of inspired CO2: 0.04% (room air), 1%, and 3%. NHF with room air reduced tidal volume by 81 ml, SD 25 ( P < 0.0001) from a baseline of 415 ml, SD 114, but did not change respiratory rate; tissue CO2 and O2 remained stable, indicating that gas exchange had been maintained. CO2 entrainment increased tidal volume close to baseline with 1% CO2 and greater than baseline with 3% CO2 by 155 ml, SD 79 ( P = 0.0004), without affecting the respiratory rate. It was calculated that 30 l/min of NHF reduced the rebreathing of CO2 from anatomical dead space by 45%, which is equivalent to the 20% reduction in tidal volume that was observed. The study proves that the reduction in tidal volume in response to NHF during sleep is due to the reduced rebreathing of CO2. Entrainment of CO2 into the NHF can be used to control ventilation during sleep. NEW & NOTEWORTHY The findings in healthy volunteers during sleep show that nasal high flow (NHF) with a rate of 30 l/min reduces the rebreathing of CO2 from anatomical dead space by 45%, resulting in a reduced minute ventilation, while gas exchange is maintained. Entrainment of CO2 into the NHF can be used to control ventilation during sleep.

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