scholarly journals Clinical course, heart rate and pulmonal function during thoracoscopy in the standing sedated horse – part 2: respiratory rate, expiratory tidal volume, expiratory minute ventilation and end-expiratory carbon dioxide level

2013 ◽  
Vol 29 (1) ◽  
pp. 14-20
Author(s):  
D Scharner ◽  
J Theißen ◽  
J-C Ionita
Keyword(s):  
Carbon Dioxide ◽  
Heart Rate ◽  
Tidal Volume ◽  
Respiratory Rate ◽  
Clinical Course ◽  
Minute Ventilation ◽  
Carbon Dioxide Level

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.

The effect of carbon dioxide, respiratory rate and tidal volume on human heart rate variability

2003 ◽  
Vol 48 (1) ◽  
pp. 93-101 ◽  
Author(s):  
M. Pöyhönen ◽  
S. Syväoja ◽  
J. Hartikainen ◽  
E. Ruokonen ◽  
J. Takala
Keyword(s):  
Carbon Dioxide ◽  
Heart Rate ◽  
Heart Rate Variability ◽  
Tidal Volume ◽  
Respiratory Rate ◽  
Human Heart

Decreased Carbon Dioxide Sensitivity in Infants of Substance-Abusing Mothers

PEDIATRICS ◽  
1995 ◽  
Vol 95 (6) ◽  
pp. 864-867
Author(s):  
Janet G. Wingkun ◽  
Janet S. Knisely ◽  
Sidney H. Schnoll ◽  
Gary R. Gutcher
Keyword(s):  
Carbon Dioxide ◽  
Tidal Volume ◽  
Minute Ventilation ◽  
Demographic Data ◽  
Substance Abusing ◽  
Quiet Sleep ◽  
Co2 Level ◽  
The Difference ◽  
End Tidal ◽  
Drug Free

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.

scholarly journals Deep-breath frequency in bronchoconstricted monkeys (Macaca fascicularis)

2006 ◽  
Vol 100 (3) ◽  
pp. 786-791 ◽  
Author(s):  
Joseph M. Dybas ◽  
Catharine J. Andresen ◽  
Edward S. Schelegle ◽  
Ryan W. McCue ◽  
Natasha N. Callender ◽  
...  
Keyword(s):  
Tidal Volume ◽  
Respiratory Rate ◽  
Macaca Fascicularis ◽  
Minute Ventilation ◽  
Mechanical Resistance ◽  
External Resistance ◽  
Deep Breath ◽  
Ventilatory Parameters ◽  
Tissue Compliance ◽  
Airway Opening

Deep-breath frequency has been shown to increase in spontaneously obstructed asthmatic subjects. Furthermore, deep breaths are known to be regulated by lung rapidly adapting receptors, yet the mechanism by which these receptors are stimulated is unclear. This study tested the hypothesis that deep-breath frequency increases during experimentally induced bronchoconstriction, and the magnitude of the increased deep-breath frequency is dependent on the method by which bronchoconstriction is induced. Nine cynomolgus monkeys ( Macaca fascicularis) were challenged with methacholine (MCh), Ascaris suum (AS), histamine, or an external mechanical resistance. Baseline (BL) and challenge deep-breath frequency were calculated from the number of deep breaths per trial period. Airway resistance (Raw) and tissue compliance (Cti), as well as tidal volume, respiratory rate, and minute ventilation, were analyzed for BL and challenged conditions. Transfer impedance measurements were fit with the DuBois model to determine the respiratory parameters (Raw and Cti). The flow at the airway opening was measured and analyzed on a breath-by-breath basis to obtain the ventilatory parameters (tidal volume, respiratory rate, and minute ventilation). Deep-breath frequency resulting from AS and histamine challenges [0.370 (SD 0.186) and 0.467 breaths/min (SD 0.216), respectively] was significantly increased compared with BL, MCh, or external resistance challenges [0.61 (SD 0.046), 0.156 (SD 0.173), and 0.117 breaths/min (SD 0.082), respectively]. MCh and external resistance challenges resulted in insignificant changes in deep-breath frequency compared with BL. All four modalities produced similar levels of bronchoconstriction, as assessed through changes in Raw and Cti, and had similar effects on the ventilatory parameters except that non-deep-breath tidal volume was decreased in AS and histamine. We propose that increased deep-breath frequency during AS and histamine challenge is the result of increased vascular permeability, which acts to increase rapidly adapting receptor activity.

scholarly journals Hypoxia-induced vagal withdrawal is independent of the hypoxic ventilatory response in men

2019 ◽  
Vol 126 (1) ◽  
pp. 124-131 ◽  
Author(s):  
Christoph Siebenmann ◽  
Camilla K. Ryrsø ◽  
Laura Oberholzer ◽  
James P. Fisher ◽  
Linda M. Hilsted ◽  
...  
Keyword(s):  
Heart Rate ◽  
Tidal Volume ◽  
Respiratory Rate ◽  
Spontaneous Breathing ◽  
Animal Studies ◽  
Pulmonary Ventilation ◽  
Vagal Activity ◽  
Adrenergic Blockade ◽  
Controlled Breathing ◽  
Vagal Withdrawal

Hypoxia increases heart rate (HR) in humans by sympathetic activation and vagal withdrawal. However, in anaesthetized dogs hypoxia increases vagal activity and reduces HR if pulmonary ventilation does not increase and we evaluated whether that observation applies to awake humans. Ten healthy males were exposed to 15 min of normoxia and hypoxia (10.5% O2), while respiratory rate and tidal volume were volitionally controlled at values identified during spontaneous breathing in hypoxia. End-tidal CO2 tension was clamped at 40 mmHg by CO2 supplementation. β-Adrenergic blockade by intravenous propranolol isolated vagal regulation of HR. During spontaneous breathing, hypoxia increased ventilation by 3.2 ± 2.1 l/min ( P = 0.0033) and HR by 8.9 ± 5.5 beats/min ( P < 0.001). During controlled breathing, respiratory rate (16.3 ± 3.2 vs. 16.4 ± 3.3 breaths/min) and tidal volume (1.05 ± 0.27 vs. 1.06 ± 0.24 l) were similar for normoxia and hypoxia, whereas the HR increase in hypoxia persisted without (8.6 ± 10.2 beats/min) and with (6.6 ± 5.6 beats/min) propranolol. Neither controlled breathing ( P = 0.80), propranolol ( P = 0.64), nor their combination ( P = 0.89) affected the HR increase in hypoxia. Arterial pressure was unaffected ( P = 0.48) by hypoxia across conditions. The hypoxia-induced increase in HR during controlled breathing and β-adrenergic blockade indicates that hypoxia reduces vagal activity in humans even when ventilation does not increase. Vagal withdrawal in hypoxia seems to be governed by the arterial chemoreflex rather than a pulmonary inflation reflex in humans. NEW & NOTEWORTHY Hypoxia accelerates the heart rate of humans by increasing sympathetic activity and reducing vagal activity. Animal studies have indicated that hypoxia-induced vagal withdrawal is governed by a pulmonary inflation reflex that is activated by the increased pulmonary ventilation in hypoxia. The present findings, however, indicate that humans experience vagal withdrawal in hypoxia even if ventilation does not increase, indicating that vagal withdrawal is governed by the arterial chemoreflex rather than a pulmonary inflation reflex.

Ventilatory Responses to Exercise and to Carbon Dioxide in Mitral Stenosis before and after Valvulotomy: Causes of Tachypnoea

1978 ◽  
Vol 54 (1) ◽  
pp. 9-16 ◽  
Author(s):  
J. W. Reed ◽  
M. Ablett ◽  
J. E. Cotes
Keyword(s):  
Carbon Dioxide ◽  
Tidal Volume ◽  
Mitral Stenosis ◽  
Vital Capacity ◽  
Minute Ventilation ◽  
Residual Effect ◽  
Minute Volume ◽  
Cardiac Frequency ◽  
Control Subjects ◽  
Exercise Ventilation

1. The ventilation and cardiac frequency during progressive exercise and the respiratory responses to breathing carbon dioxide have been measured in 33 female patients with mitral stenosis and in 31 control subjects. Compared with the control subjects, the patients' exercise ventilation and cardiac frequency were increased; the exercise tidal volume at standard minute volume, the vital capacity and the ventilatory response to carbon dioxide were reduced. The extent to which the standardized tidal volume was lower during exercise than during breathing carbon dioxide was correlated with the severity of the stenosis, as gauged by the increase in exercise cardiac frequency above the level predicted from anthropometric measurements. 2. Twenty patients were studied postoperatively. In the 12 who showed clinical improvement the exercise ventilation and cardiac frequency were reduced and the exercise tidal volume at a given minute ventilation was increased. The latter change occurred despite a reduction in vital capacity, which was probably a residual effect of thoractomy. There was no significant change in the response to breathing carbon dioxide. No material change in function was observed in the patients whose condition was not improved by the operation. 3. It is suggested that in mitral stenosis the tachypnoea which occurs during exercise, whilst mainly a mechanical consequence of the reduced vital, capacity, is also partly due to pulmonary congestion stimulating intrapulmonary receptors.

scholarly journals Effects of Mentha Piperita Essential Oil Uptake or Inhalation on Heart Rate Variability and Cardiopulmonary Regulation during Exercise

2021 ◽  
Vol 10 (2) ◽  
pp. 65-72
Author(s):  
Tso-Yen Mao ◽  
◽  
Chun-Feng Huang ◽  
De-Yen Liu ◽  
Chien-Ting Chen ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Heart Rate ◽  
Heart Rate Variability ◽  
Essential Oil ◽  
Respiratory Rate ◽  
Low Frequency ◽  
Carbon Dioxide Production ◽  
Mentha Piperita ◽  
Control Group ◽  
Frequency Area

This study compares the effects of the uptake or inhalation of 50uL Mentha piperita (MP) essential oil for 10 days on heart rate variability (HRV) and cardiopulmonary regulation during various exercise intensities. Forty-eight healthy male subjects were randomly assigned to MP uptake (MPU; n=16), MP inhalation (MPI; n=16), and control group (C; n=16). All participants were measured resting HRV, respiratory, cardiovascular, and metabolic parameters during aerobic, anaero- bic, and graded exercise tests (GXT) before and after treatment. There were significant increases in the low-frequency area (LFa; 1.8±0.1 vs 2.2±0.2 ms²), the ratio of low frequency to respiration frequency area (LFa/RFa; 0.9±0.1 vs 1.3±0.1) at resting and carbon dioxide production (VCO 2 ; 41.2±4.0 vs 49.2±6.8 mL/min -1 /kg -1 ), ventilation per minute (V E ; 80.2±4.3 vs 97.5±5.5 L/min -1 ), and respiratory rate (RR; 38.2±1.9 to 44.3±2.1 breath/min -1 ) in an anaerobic test following MPU inter- vention. In GXT, maximal carbon dioxide production (VCO 2max; 51.9±3.5 to 59.1±6.4 mL/min -1 /kg -1 ), maximal ventilation per minute (V Emax ; 126.4±6.5 to 138.4±5.4 L/min -1 ) and maximal respiratory rate (RR max ; 52.7±3.6 to 60.1±2.3 breath/min -1 ) significantly increased in MPU. The correlations of ΔLFa with ΔVCO 2max , ΔV Emax , and ΔRR max in the MPU group were signifi- cant. Continuous uptake or inhalation of 50uL MP oil for 10 days does not improve aerobic capacity and maximal exercise performance, but 10 days’ uptake of MP essential oil increased sympathetic activity at rest and may relate to respiratory regulation under high-intensity exercise.

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.

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