Control of expiratory time in conscious humans

1995 ◽  
Vol 78 (5) ◽  
pp. 1910-1920 ◽  
Author(s):  
G. F. Rafferty ◽  
J. Evans ◽  
W. N. Gardner
Keyword(s):  
Auditory Feedback ◽  
Respiratory Control ◽  
Open Circuit ◽  
Respiratory Pattern ◽  
Control Mechanisms ◽  
Inspiratory Time ◽  
Expiratory Time ◽  
Small Influence ◽  
Computer Controlled ◽  
End Tidal

Combinations of 17 normal awake humans breathed mildly hyperoxic and hypercapnic gas mixtures via a pneumotachograph into an open circuit. Respiratory pattern was measured for each breath in real time by computer. Use of computer-controlled auditory feedback at a constant end-tidal PCO2 (PETCO2) allowed prolonged changes of 1) inspiratory time (TI) at constant inspired tidal volume (VTI), 2) VTI up and down in repeated steps at constant TI, and 3) expiratory time (TE) at constant VTI. The remaining variables were free to be determined by the subjects' automatic respiratory control mechanisms. We showed that TE changed in parallel with the change in TI despite constant VTI, TE did not change in response to step changes in VTI at constant TI, and large changes in TE had no influence on the subsequent TI, but VTI increased slightly as TE lengthened despite clamping. Time for expiratory flow (TE--end-expiratory pause) changed in parallel with TE in all protocols. Thus, in conscious humans, inspiratory timing has a direct influence on expiratory timing, independent of volume change and chemical drive, but expiratory timing has no influence on the inspiratory timing of the subsequent breath but has a small influence on volume.

Control of the respiratory cycle in conscious humans

1996 ◽  
Vol 81 (4) ◽  
pp. 1744-1753 ◽  
Author(s):  
G. F. Rafferty ◽  
W. N. Gardner
Keyword(s):  
Tidal Volume ◽  
Auditory Feedback ◽  
Free Breathing ◽  
Relative Strength ◽  
Open Circuit ◽  
The Body ◽  
Respiratory Cycle ◽  
Inspiratory Time ◽  
Wide Range ◽  
End Tidal

Rafferty, G. F., and W. N. Gardner. Control of the respiratory cycle in conscious humans. J. Appl. Physiol. 81(4): 1744–1753, 1996.—We studied in conscious humans the relative strength of mechanisms controlling timing and drive components of the respiratory cycle around their resting set points. A system of auditory feedback with end-tidal[Formula: see text] held constant in mild hyperoxia via an open circuit was used to induce subjects independently to change inspiratory time (Ti) and tidal volume (Vt I) over a wide range above and below the resting values for every breath for up to 1 h. Four protocols were studied in various levels of hypercapnia (1–5% inspired CO2). We found that Ti (and expiratory time) could be changed over a wide range (1.17–2.86 s, P < 0.01 for Ti) and Vt Iincreased by ≥500 ml ( P < 0.01) without difficulty. However, in no protocol was it possible to decrease Vt I below the free-breathing resting value in response to reduction of auditory feedback thresholds by up to 600 ml. This applied at all levels of chemical drive studied, with resting Vt I values varying from 1.06 to 1.74 liters. When reduction in Vt I was forced by the more “programmed” procedure of isocapnic panting, end-expiratory volume was sacrificed to ensure that peak tidal volume reached a fixed absolute lung volume. These results suggest that the imperative for control of resting breathing is to prevent reduction of Vt I below the level dictated by the prevailing chemical drive, presumably to sustain metabolic requirements of the body, whereas respiratory timing is weakly controlled consistent with the needs for speech and other nonmetabolic functions of breathing.

A fast gas-mixing system for breath-to-breath respiratory control studies

1982 ◽  
Vol 52 (5) ◽  
pp. 1358-1362 ◽  
Author(s):  
P. A. Robbins ◽  
G. D. Swanson ◽  
A. J. Micco ◽  
W. P. Schubert
Keyword(s):  
High Voltage ◽  
Special Form ◽  
Low Voltage ◽  
Respiratory Control ◽  
Gas Mixing ◽  
Tidal Forcing ◽  
Mixing Chamber ◽  
Computer Controlled ◽  
End Tidal ◽  
Gas Fractions

A computer-controlled gas-mixing system that manipulates inspired CO2 and O2 on a breath-to-breath basis has been developed. The system uses pairs of solenoid valves, one pair for each gas. These valves can either be fully shut when a low voltage is applied, or fully open when a high voltage is applied. The valves cycle open and shut every 1/12 s. A circuit converts signals from the computer, which dictates the flows of the gases, into a special form for driving the valve pairs. These signals determine the percentage of time within the 1/12-s cycle each valve spends in a open state and the percentage of time it spends shut, which, in effect, set the average flows of the various gases to the mixing chamber. The delay for response of the system to commanded CO2 or O2 changes is less than 200 ms. The system has application for the manipulation of inspired gas fractions so as to achieve desired end-tidal forcing functions.

Hypercapnic vs. hypoxic control of cardiovascular, cardiovagal, and sympathetic function

2009 ◽  
Vol 296 (2) ◽  
pp. R402-R410 ◽  
Author(s):  
Craig D. Steinback ◽  
Deborah Salzer ◽  
Philip J. Medeiros ◽  
J. Kowalchuk ◽  
J. Kevin Shoemaker
Keyword(s):  
Muscle Sympathetic Nerve Activity ◽  
Venous Pressure ◽  
Peripheral Resistance ◽  
Respiratory Pattern ◽  
Inspiratory Time ◽  
Burst Frequency ◽  
Set Point ◽  
Sympathetic Function ◽  
Chemoreflex Sensitivity ◽  
End Tidal

We compared the integrated cardiovascular and autonomic responses to hypercapnia and hypoxia to test the hypothesis that these stimuli differentially affect muscle sympathetic nerve activity (MSNA) discharge patterns and cardiovagal and sympathetic baroreflex function in a manner related to ventilatory chemoreflex sensitivity. Six males and six females underwent 5 min of hypoxia (end-tidal Po2 = 45 Torr) and 5 min of hypercapnia (end-tidal Pco2 = +8 Torr from baseline), causing similar ventilatory responses. A downward right shift in cardiovagal set point was observed during both conditions, which was strongly related to the change in inspiratory time (Ti) from baseline to hypercapnia ( r2 = 0.67, P = 0.007) and hypoxia ( r2 = 0.79, P < 0.001). Cardiovagal baroreflex gain was decreased during hypoxia (20.1 ± 6.9 vs. 8.9 ± 5.1 ms/mmHg, P < 0.001) but not hypercapnia (26.7 ± 12.7 vs. 23.0 ± 9.1 ms/mmHg). Both hypoxia and hypercapnia increased MSNA burst amplitude, whereas hypoxia, but not hypercapnia, also increased in MSNA burst frequency (21 ± 9 vs. 28 ± 7 bursts/min, P = 0.03) and total MSNA (4.56 ± 3.07 vs. 7.37 ± 3.26 mV/min, P = 0.002). However, neither hypercapnia nor hypoxia affected sympathetic burst probability or baroreflex gain. Hypoxia also caused a greater reduction in total peripheral resistance ( P = 0.04), a greater increase in heart rate ( P = 0.002), and a trend for a greater cardiac output response ( P = 0.06) compared with hypercapnia. Nonetheless, central venous pressure remained unchanged during either condition. These results suggest that hypercapnia and hypoxia exert differential effects on cardiovagal, but not sympathetic, baroreflex gain and set point in a manner not related to ventilatory chemoreflex sensitivity. Furthermore, the data suggest that the individual's respiratory pattern to hypoxia or hypercapnia, as reflected in the inspiratory time, was a strong determinant of cardiovagal baroreflex set- point rather than the total ventilatory chemoreflex gain per se.

Phrenic neural output during hypoxia in dogs: constant-flow ventilation vs. spontaneous breathing

1991 ◽  
Vol 70 (5) ◽  
pp. 2045-2051 ◽  
Author(s):  
S. S. Naqvi ◽  
A. S. Menon ◽  
B. E. Shykoff ◽  
A. S. Rebuck ◽  
A. S. Slutsky
Keyword(s):  
Spontaneous Breathing ◽  
Pattern Generation ◽  
Afferent Feedback ◽  
Respiratory Pattern ◽  
Constant Flow ◽  
Inspiratory Time ◽  
Amplitude Response ◽  
Expiratory Time ◽  
Neural Information ◽  
Anesthetized Dogs

We studied the effects of removing cyclic pulmonary afferent neural information on respiratory pattern generation in anesthetized dogs. Phrenic neural output during spontaneous breathing (SB) was compared with that occurring during constant-flow ventilation (CFV) at several levels of eucapnic hypoxemia. Hypoxia caused an increase in both the frequency and the amplitude of the moving time average (MTA) phrenic neurogram during both SB and CFV. The change in frequency as arterial saturation was reduced from 90 to 60% during SB was significantly higher than that during CFV [SB, 32.3 +/- 10.9 (SD) breaths/min; CFV, 10.3 +/- 5.8 breaths/min; P = 0.001]. By contrast, the increase in the amplitude of the MTA phrenic neurogram was smaller (SB, 0.62 +/- 0.68 units; CFV, 1.35 +/- 0.81 units; P = 0.01). The changes in frequency with hypoxia during both modes of ventilation resulted primarily from a shortening of expiratory time. Both inspiratory time and expiratory time were greater during CFV than during SB, but their change in response to hypoxia was not significantly different. We conclude that the amplitude response of the MTA phrenic neurogram to hypoxia is similar to that seen during hypercapnia; in the presence of phasic afferent feedback the MTA amplitude response is decreased and the frequency response is increased relative to the response observed in the absence of phasic afferents.

Effects of thoracic dorsal rhizotomies on the respiratory pattern in anesthetized cats

1977 ◽  
Vol 43 (1) ◽  
pp. 20-26 ◽  
Author(s):  
R. Shannon
Keyword(s):  
Tidal Volume ◽  
Respiratory Activity ◽  
Respiratory Rhythm ◽  
Respiratory Pattern ◽  
Thoracic Wall ◽  
Intercostal Muscle ◽  
Inspiratory Time ◽  
Expiratory Time ◽  
Intercostal Muscles ◽  
Dorsal Roots

Experiments were conducted to determine if thoracic wall proprioceptor afferents are involved in the modulation of respiratory activity during eupnea. The effects of elimination of thoracic wall afferents (thoracic dorsal rhizotomies (TDR) on tidal volume (VT), frequency (f), inspiratory time (ti) and expiratory time (te) were studied in vagotomized cats anesthetized with diallylbarbituric acid (Dial). Dorsal rhizotomies 1–12 resulted primarily in a decreased VT and ti, and an increased f. Further experiments were performed to determine if these changes in respiratory pattern could be correlated with known reflexes from the middle and lower intercostal muscles, or lungs, via thoracic dorsal roots. Afferents from these sources were eliminated by TDR 5–9, 10–13, and 1–4. TDR 1–4 had no significant effect on the respiratory pattern. TDR 5–9 and TDR 10–13 produced changes similar in direction to TDR 1–12. The results indicate that: a) afferents 1–4 from the upper intercostal muscles and lungs (sympathetic afferents) do not contribute significantly to the control of the spontaneous respiratory rhythm, and b) afferents via the middle thoracic roots, 5–9, and the lower thoracic roots, 10–13, contribute significantly to the rhythm. The results do not completely correlate with known intercostal reflexes, but it is suggested that elimination of intercostal muscle proprioceptor afferents is responsible for the observed effects of thoracic dorsal rhizotomies.

Effects of inspiratory resistive load on respiratory control in hypercapnia and exercise

1989 ◽  
Vol 66 (5) ◽  
pp. 2391-2399 ◽  
Author(s):  
C. S. Poon
Keyword(s):  
Steady State ◽  
Breathing Pattern ◽  
Ventilatory Response ◽  
Respiratory Control ◽  
Resistive Load ◽  
Occlusion Pressure ◽  
Inspiratory Time ◽  
Co2 Output ◽  
End Tidal ◽  
Inspiratory Load

Eight healthy young men underwent two separate steady-state incremental exercise runs within the aerobic range on a treadmill with alternating periods of breathing with no load (NL) and with an inspiratory resistive load (IRL) of approximately 12 cmH2O.1–1.s. End-tidal PCO2 was maintained constant throughout each run at the eucapnic or a constant hypercapnic level by adding 0–5% CO2 to the inspired O2. Hypercapnia caused a steepening, as well as upward shift, relative to the corresponding eucapnic ventilation-CO2 output (VE - VCO2) relationship in NL and IRL. Compared with NL, the VE - VCO2 slope was depressed by IRL, more so in hypercapnic [-19.0 +/- 3.4 (SE) %] than in eucapnic exercise (-6.0 +/- 2.0%), despite a similar increase in the slope of the occlusion pressure at 100 ms - VCO2 (P100 - VCO2) relationship under both conditions. The steady-state hypercapnic ventilatory response at rest was markedly depressed by IRL (-22.6 +/- 7.5%), with little increase in P100 response. For a given inspiratory load, breathing pattern responses to separate or combined hypercapnia and exercise were similar. During IRL, VE was achieved by a greater tidal volume (VT) and inspiratory duty cycle (TI/TT) along with a lower mean inspiratory flow (VT/TI). The increase in TI/TT was solely because of a prolongation of inspiratory time (TI) with little change in expiratory duration for any given VT. The ventilatory and breathing pattern responses to IRL during CO2 inhalation and exercise are in favor of conservation of respiratory work.(ABSTRACT TRUNCATED AT 250 WORDS)

Central origin of biphasic breathing pattern during hypoxia in newborns

1983 ◽  
Vol 55 (2) ◽  
pp. 483-488 ◽  
Author(s):  
E. E. Lawson ◽  
W. A. Long
Keyword(s):  
Control Level ◽  
Respiratory Control ◽  
Co2 Flux ◽  
Pulmonary Mechanics ◽  
Continuous Exposure ◽  
Control Mechanisms ◽  
Vagus Nerves ◽  
Mechanically Ventilated ◽  
Control Value ◽  
End Tidal

The ventilatory response to moderate hypoxia of both animal and human newborns differs significantly from that of adults. The newborn response is characterized by transient hyperpnea followed by return of ventilation toward or below the control level and even apnea. To determine whether central respiratory control mechanisms are affected by hypoxia in newborns, we used an anesthetized, paralyzed, mechanically ventilated piglet model in which the vagus nerves were cut. Respiratory activity was determined by measuring electrical activity of a cut phrenic nerve. During a 6-min continuous exposure to 15% O2 as the inspired gas, 11 piglets increased their respiratory output to 181 +/- 38% of the control value within 2.5 min. However, by the 6th min the average respiratory output had declined to 104 +/- 25% of the control. During the exposure to hypoxia, the servo-controlled ventilator frequency (an index of CO2 flux to the lungs) was persistently greater than control (28.0 +/- 1.0 vs. 30.5 +/- 1.4 cycles/min; P less than 0.01). These data indicate that the newborn's characteristic breathing response to hypoxia is due to failure of central neural respiratory control mechanisms. Paralysis, constant end-tidal PCO2, and increased ventilator rate during hypoxia exclude changes in pulmonary mechanics or decreased metabolic rate as explanations of the paradoxical decline in respiratory output.

scholarly journals End-Tidal Carbon Dioxide Pressure Measurement after Prolonged Inspiratory Time Gives a Good Estimation of the Arterial Carbon Dioxide Pressure in Mechanically Ventilated Patients

Diagnostics ◽  
2021 ◽  
Vol 11 (12) ◽  
pp. 2219
Author(s):  
Arthur Salomé ◽  
Annabelle Stoclin ◽  
Cyrus Motamed ◽  
Philippe Sitbon ◽  
Jean-Louis Bourgain
Keyword(s):  
Carbon Dioxide ◽  
Distress Syndrome ◽  
Inspiratory Time ◽  
Arterial Blood Gas ◽  
Mechanically Ventilated ◽  
Expiratory Time ◽  
Arterial Blood ◽  
End Tidal Carbon Dioxide ◽  
Carbon Dioxide Pressure ◽  
End Tidal

Background: End-tidal carbon dioxide pressure (PetCO2) is unreliable for monitoring PaCO2 in several conditions because of the unpredictable value of the PaCO2–PetCO2 gradient. We hypothesised that increasing both the end-inspiratory pause and the expiratory time would reduce this gradient in patients ventilated for COVID-19 with Acute Respiratory Distress Syndrome and in patients anaesthetised for surgery. Methods: On the occasion of an arterial blood gas sample, an extension in inspiratory pause was carried out either by recruitment manoeuvre or by extending the end-inspiratory pause to 10 s. The end-expired PCO2 was measured (expiratory time: 4 s) after this manoeuvre (PACO2) in comparison with the PetCO2 measured by the monitor. We analysed 67 Δ(a-et)CO2, Δ(a-A)CO2 pairs for 7 patients in the COVID group and for 27 patients in the anaesthesia group. Results are expressed as mean ± standard deviation. Results: Prolongation of the inspiratory pause significantly reduced PaCO2–PetCO2 gradients from 11 ± 5.7 and 5.7 ± 3.4 mm Hg (p < 0.001) to PaCO2–PACO2 gradients of −1.2 ± 3.3 (p = 0.043) and −1.9 ± 3.3 mm Hg (p < 0.003) in the COVID and anaesthesia groups, respectively. In the COVID group, PACO2 showed the lowest dispersion (−7 to +6 mm Hg) and better correlation with PaCO2 (R2 = 0.92). The PACO2 had a sensitivity of 0.81 and a specificity of 0.93 for identifying hypercapnic patients (PaCO2 > 50 mm Hg). Conclusions: Measuring end-tidal PCO2 after prolonged inspiratory time reduced the PaCO2–PetCO2 gradient to the point of obtaining values close to PaCO2. This measure identified hypercapnic patients in both intensive care and during anaesthesia.

END-TIDAL CO2 AFFECTED BY INSPIRATORY TIME AND FLOW WAVEFORM–TIME FOR A CHANGE

1986 ◽  
Vol 14 (4) ◽  
pp. 374 ◽  
Author(s):  
Michael J. Banner ◽  
Philip G. Boysen ◽  
Samsun Lampotang ◽  
Marc J. Jaeger
Keyword(s):  
Flow Waveform ◽  
Inspiratory Time ◽  
End Tidal ◽  
End Tidal Co2

Effect of transcendental meditation on breathing and respiratory control

1984 ◽  
Vol 56 (3) ◽  
pp. 607-612 ◽  
Author(s):  
N. Wolkove ◽  
H. Kreisman ◽  
D. Darragh ◽  
C. Cohen ◽  
H. Frank
Keyword(s):  
Transcendental Meditation ◽  
Minute Ventilation ◽  
Respiratory Control ◽  
Respiratory Pattern ◽  
Quiet Breathing ◽  
The Unconscious ◽  
Eyes Closed ◽  
Significant Difference ◽  
Regulation Of Breathing ◽  
Eyes Open

We studied the effect of transcendental meditation (TM) on breathing using 16 experienced meditators and 16 control subjects. In controls, there was no significant difference in minute ventilation (VE), respiratory pattern, or hypercapnic response, whether breathing with eyes open-awake (CA), or with eyes closed-relaxing (CR). In meditators, VE decreased significantly during quiet breathing from 14.0 +/- 0.7 1/min with eyes open-awake (MA) to 12.4 +/- 0.6 1/min during meditation (MM) (P less than 0.02). The change in VE during meditation was due to a decrease in tidal volume (VT) resulting from a shortened inspiratory time (TI). Meditation was associated with a decreased response to progressive hypercapnia from 3.7 +/- 0.4 to 2.5 +/- 0.21 X min-1 X Torr-1 during MA and MM trials, respectively (P less than 0.01). During meditation VT was smaller at a given alveolar PCO2 than during MA studies because of a decrease in mean inspiratory flow rate (VT/TI). These observations suggest that an alteration in wakefulness, more subtle than sleep or the unconscious state, can significantly affect the chemical and neural regulation of breathing.

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