scholarly journals Effect of Work Intensity on Time Delay in Mediation of Ventilation by Arterial Carbon Dioxide During Recovery From Impulse Exercise

2014 ◽  
pp. 457-463
Author(s):  
R. AFROUNDEH ◽  
T. ARIMITSU ◽  
R. YAMANAKA ◽  
C. S. LIAN ◽  
K. SHIRAKAWA ◽  
...  

Time delay in the mediation of ventilation (VE) by arterial CO2 pressure (PaCO2) was studied during recovery from short impulse-like exercises with different work loads of recovery. Subjects performed two tests including 10-s impulse like exercise with work load of 200 watts and 15-min recovery with 25 watts in test one and 50 watts in test two. VE, end tidal CO2 pressure (PETCO2) and heart rate (HR) were measured continuously during rest, warming up, exercise and recovery. PaCO2 was estimated from PETCO2 and tidal volume (VT). Results showed that predicted arterial CO2 pressure (PaCO2 pre) increased during recovery in both tests. In both tests, VE increased and peaked at the end of exercise. VE decreased in the first few seconds of recovery but started to increase again. The highest correlation coefficient between PaCO2 pre and VE was obtained in the time delay of 7 s (r=0.854) in test one and in time delays of 6 s (r=0.451) and 31 s (r=0.567) in test two. HR was significantly higher in test two than in test one. These results indicate that PaCO2 pre drives VE with a time delay and that higher work intensity induces a shorter time delay.

1982 ◽  
Vol 52 (5) ◽  
pp. 1198-1208 ◽  
Author(s):  
Y. Miyamoto ◽  
T. Hiura ◽  
T. Tamura ◽  
T. Nakamura ◽  
J. Higuchi ◽  
...  

Stroke volume, heart rate, cardiac output, tidal volume, respiratory frequency, minute ventilation, end-tidal tensions of O2 and CO2, O2 uptake, CO2 output, and respiratory exchange ratio were measured simultaneously in healthy male volunteers before, during, and after upright bicycle exercise from 0 to 360 and 720 kpm/min. The circulatory variables were determined continuously once per 20 cardiac cycles and the respiratory variables breath by breath using separate computer-based systems in which an impedance pneumograph and an impedance cardiograph were incorporated. Stroke volume, heart rate, and cardiac output started to increase without measurable delay at the onset of exercise. Stroke volume increased by 20% from resting control value in response to the mildest exercise and essentially leveled off with a further increase in work load. Time constant for cardiac output increased with the increasing work load. Time constant for minute ventilation was much longer than that for cardiac output and independent of work intensity. A good synchronization between the ventilation and cardiac output responses at an initial period of transitions from rest to exercise and from exercise to rest seems to support the concept of cardiodynamic hyperpnea.


2007 ◽  
Vol 32 (4) ◽  
pp. 721-732 ◽  
Author(s):  
Andrew N. Curtis ◽  
Michael L. Walsh ◽  
Matthew D. White

The purpose of this study was to examine the potential interaction of core temperature and isocapnic hypoxia on human ventilation and heart rate (HR). In 2 resting head-out water-immersion trials, 8 males first breathed air and then 12% O2 in N2 while the end-tidal partial pressure of carbon dioxide was kept 0.98 (0.66) mmHg (mean (SD)) above normothermic resting levels. The first immersion trial was with a normothermic esophageal temperature (Tes) of ~36.7 °C, and for the second trial, 1 h later, water temperature was increased to give a hyperthermic Tes of ~38.2 °C. Isocapnic hypoxia increased normothermic ventilation by 4 L·min–1 (p = 0.01) from 10.12 (1.07) to 14.20 (3.21) L·min–1, and hyperthermic ventiliation by 7 L·min–1 (p = 0.002) from 13.58 (2.58) to 20.79 (3.73) L·min–1. Ventilation increases during hyperthermia were mediated by breathing frequency and, during isocapnic hypoxia, by tidal volume. Unexpectedly, there was an absence of any hypoxic ventilatory decline that could be attributed to a hydrostatic effect of immersion. Isocapnic hypoxia increased the HR by similar amounts of ~10 and ~11 beats·min–1 in normothermia and hyperthermia, respectively. In conclusion, it appears that hyperthermia increases human ventilatory but not heart rate responses to isocapnic hypoxia.


Author(s):  
Valarmathi Marimuthu ◽  
Bhuvaneswari Murugan

Background: A pneumoperitoneum is created by insufflating a gas (usually carbon dioxide) into the peritoneal cavity during laparoscopic surgery. Intra-abdominal pressure (IAP) rises as a result of this. At a rate of 4–6 liter min-1, carbon dioxide is insufflated into the peritoneal cavity at a pressure of 10–20 mm Hg. Aim of the research was to compare the hemodynamic effects and the level of post-operative symptoms due to high pressure and low-pressure pneumoperitoneum in patients undergoing laparoscopic cholecystectomy.Methods: 60 patients fulfilling inclusion criteria who were posted for elective cholecystectomy under general anaesthesia were divided into two groups, 30 patients in each group. Group L included pneumoperitoneum created with intra-abdominal pressure of 7-10 mmHg, and group H included pneumoperitoneum created with intra-abdominal pressure of 12-14 mmHg. Variables such as the systolic blood pressure, diastolic blood pressure, heart rate, end-tidal CO2, the level of post-operative abdominal pain, shoulder-tip pain, nausea and vomiting, and the liver function test were compared between the two groups.Results: Between groups, no statistical difference has been noted in the demographic characters of the patient. There was a statistical difference of intraoperative and post-operative systolic blood pressure (SBP), diastolic blood pressure (DBP) and heart rate (HR) between groups. End-tidal CO2 was compared between the two groups during the surgery and a significant difference regarding EtCO2. Liver function tests showed a significant difference in all measured factors after surgery between the two groups.Conclusions: Low-pressure pneumoperitoneum decreases hemodynamic complications. Post-operative abdominal pain, shoulder tip pain, nausea and vomiting are reduced.


PEDIATRICS ◽  
1995 ◽  
Vol 95 (6) ◽  
pp. 864-867
Author(s):  
Janet G. Wingkun ◽  
Janet S. Knisely ◽  
Sidney H. Schnoll ◽  
Gary R. Gutcher

Objective. To determine whether there is a demonstrable abnormality in control of breathing in infants of substance-abusing mothers during the first few days of life. Methods. We enrolled 12 drug-free control infants and 12 infants of substance abusing mothers (ISAMs). These infants experienced otherwise uncomplicated term pregnancies and deliveries. The infants were assigned to a group based on the results of maternal histories and maternal and infant urine toxicology screens. Studies were performed during quiet sleep during the first few days of life. We measured heart rate, oxygen saturations via a pulse oximeter, end-tidal carbon dioxide (ET-CO2) level, respiratory rate, tidal volume, and airflow. The chemoreceptor response was assessed by measuring minute ventilation and the ET-CO2 level after 5 minutes of breathing either room air or 4% carbon dioxide. Results. The gestational ages by obstetrical dating and examination of the infants were not different, although birth weights and birth lengths were lower in the group of ISAMs. Other demographic data were not different, and there were no differences in the infants' median ages at the time of study or in maternal use of tobacco and alcohol. The two groups had comparable baseline (room air) ET-CO2 levels, respiratory rates, tidal volumes, and minute ventilation. When compared with the group of ISAMs, the drug-free group had markedly increased tidal volume and minute ventilation on exposure to 4% carbon dioxide. These increases accounted for the difference in sensitivity to carbon dioxide, calculated as the change in minute ventilation per unit change in ET-CO2 (milliliters per kg/min per mm Hg). The sensitivity to carbon dioxide of control infants was 48.66 ± 7.14 (mean ± SE), whereas that of ISAMs was 16.28 ± 3.14. Conclusions. These data suggest that ISAMs are relatively insensitive to challenge by carbon dioxide during the first few days of life. We speculate that this reflects an impairment of the chemoreceptor response.


1980 ◽  
Vol 48 (6) ◽  
pp. 1083-1091 ◽  
Author(s):  
R. Casaburi ◽  
R. W. Stremel ◽  
B. J. Whipp ◽  
W. L. Beaver ◽  
K. Wasserman

The effects of hyperoxia on ventilatory and gas exchange dynamics were studied utilizing sinusoidal work rate forcings. Five subjects exercised on 14 occasions on a cycle ergometer for 30 min with a sinusoidally varying work load. Tests were performed at seven frequencies of work load during air or 100% O2 inspiration. From the breath-by-breath responses to these tests, dynamic characteristics were analyzed by extracting the mean level, amplitude of oscillation, and phase lag for each six variables with digital computer techniques. Calculation of the time constant (tau) of the ventilatory responses demonstrated that ventilatory kinetics were slower during hyperoxia than during normoxia (P less than 0.025; avg 1.56 and 1.13 min, respectively). Further, for identical work rate fluctuations, end-tidal CO2 tension fluctuations were increased by hyperpoxia. Ventilation during hyperoxia is slower to respond to variations in the level of metabolically produced CO2, presumably because hyperoxia attenuates carotid body output; the arterial CO2 tension is consequently less tightly regulated.


Heliyon ◽  
2019 ◽  
Vol 5 (6) ◽  
pp. e01871 ◽  
Author(s):  
Christina N. Stine ◽  
Josh Koch ◽  
L. Steven Brown ◽  
Lina Chalak ◽  
Vishal Kapadia ◽  
...  

1989 ◽  
Vol 17 (4) ◽  
pp. 482-486 ◽  
Author(s):  
M. A. Stockwell ◽  
W. Bruce ◽  
N. Soni

A mechanical lung model was used to investigate the effect of varying carbon dioxide production and deadspace on the end-tidal carbon dioxide levels achieved during mechanical ventilation when using the Bain, Humphrey ADE, and circle systems. Both factors had significant influence on end-tidal cardon dioxide concentration and could result in values in excess of those considered acceptable in clinical practice. The implications of the results are discussed.


1981 ◽  
Vol 51 (3) ◽  
pp. 654-659 ◽  
Author(s):  
R. B. Banzett ◽  
G. F. Inbar ◽  
R. Brown ◽  
M. Goldman ◽  
A. Rossier ◽  
...  

We recorded the diaphragm electromyogram (EMG) of quadriplegic men before and during exposure of the lower torso to continuous negative pressure, which caused shortening of the inspiratory muscles by expanding the respiratory system by one tidal volume. The moving-time-averaged diaphragm EMG was larger during expansion of the respiratory system. When we repeated the experiment with subjects who breathed through a mouthpiece, we found qualitatively similar EMG changes and little or no change in tidal volume or end-tidal CO2 partial pressure. When the pressure was applied or removed rapidly, changes in EMG occurred within one or two breaths. Because end-tidal CO2 partial pressure did not increase, and because the response was rapid, we suggest that the response results from proprioceptive, rather than chemoreceptive, reflexes. As most of these men had complete spinal lesions at C6 or C7 the afferent pathways are likely to be vagal or phrenic.


1977 ◽  
Vol 42 (6) ◽  
pp. 968-975 ◽  
Author(s):  
D. H. Pearce ◽  
H. T. Milhorn ◽  
G. H. Holloman ◽  
W. J. Reynolds

A computer-based system for the determination of tidal volume, respiratory frequency, minute ventilation, oxygen transfer, carbon dioxide transfer, respiratory exchange ratio, end-tidal oxygen, end-tidal carbon dioxide, and heart rate is presented. These variables are first determined on a breath-by-breath basis from data (expired carbon dioxide and oxygen fractions, airflow, and ECG) prerecorded on an FM magnetic type system. The breath-by-breath data are then averaged for each experimental run in 5-s increments. The 5-s increment data from a group of subjects can then be averaged and the SEM determined at prescribed periods of time. For the study of individual respiratory transient we found the 5-s increment data to be more useful than the breath-by-breath data because it has a lesser degree of fluctuation. The system is especially adapted to careful observation of the responses within the first few seconds of a change in work load. Appropriate computer programs are discussed. The results of several experiments are compared with data from other sources and found to be in good agreement.


1996 ◽  
Vol 6 (2) ◽  
pp. 136-142 ◽  
Author(s):  
Luc Mertens ◽  
Ralph Rogers ◽  
Tony Reybrouck ◽  
Monique Dumoulin ◽  
Luc Vanhees ◽  
...  

AbstractThe purpose of this study was to assess cardiorespiratory responses to submaximal exercise in patients with univentricular atrioventricular connection after the Fontan operation, and to evaluate whether changes occur during medium-term follow-up. Eighteen patients (age 12.1±5.5 years) underwent graded exercise test on a treadmill 2.3±1.4 year after the Fontan repair. Ventilatory gases were measured using breath-by-breath analysis. Results were compared to gender/age-matched controls. Twelve patients (age 14.2±5.4 years) were reevaluated 2.4±2.1 years after the first test. Aerobic exercise performance was subnormal in all patients during the first test. At the lowest level of exercise, the ventilatory threshold was already surpassed in 6/18 patients, while it was reduced in all other patients (p<0.001). All patients were in stable sinus rhythm throughout the test. Heart rate at all exercise levels was ±10% below normal (p<0.05). The respiratory frequency was increased at all exercise levels (p<0.001). The ventilatory equivalent for oxygen was increased (p<0.001), and the end-tidal tension of carbon dioxide was decreased (p<0.001). The ratio of physiological dead space/tidal volume was increased in all patients (p<0.001), while the normal decrease of this ratio during exercise was not observed. Upon reevaluation heart rate, respiratory rate, oxygen uptake, venti latory equivalent for oxygen, end-tidal carbon dioxide tension and physiological dead space did not change signifi cantly. Only a slight further decrease in ventilatory threshold was observed. Aerobic performance after the Fontan procedure ranges widely from just above resting metabolic rate to the lower limit of normal. Dyspnea during exercise is exacerbated by a decreased ventilatory threshold, increased physiological dead space, and decreased respir-atory efficiency. Cardiorespiratory response to exercise, nonetheless, remains relatively stable during medium-term follow-up.


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