The Pattern of Breathing Following a 10-Breath Voluntary Hyperventilation During Hyperoxic Rebreathing

1997 ◽  
Vol 22 (3) ◽  
pp. 256-267 ◽  
Author(s):  
Deep Chatha ◽  
James Duffin
Keyword(s):  
Carbon Dioxide ◽  
Carbon Dioxide Tension ◽  
Short Term ◽  
Voluntary Hyperventilation ◽  
Partial Pressures ◽  
Term Potentiation ◽  
Respiratory Chemoreflex ◽  
End Tidal ◽  
Peripheral Chemoreflex ◽  
Female Responses

The pattern of breathing following a 10-breath voluntary hyperventilation period during hyperoxic rebreathing was compared to that without hyperventilation in 6 subjects (3 male and 3 female). The aim was to measure the posthyperventilation short-term potentiation of ventilation without changes in respiratory chemoreflex drives induced by the voluntary hyperventilation. Hyperoxia was used to reduce the peripheral chemoreflex drive, and rebreathing to prevent the decrease in arterial carbon dioxide tension normally produced by hyperventilation. There were significant differences between the male and female responses. However, in all subjects, ventilation and heart rate were increased during hyperventilation but end-tidal partial pressures of carbon dioxide and oxygen were unchanged. Following hyperventilation, ventilation immediately returned to the values observed when hyperventilation was omitted. Hyperventilation did not induce a short-term potentiation of ventilation under these conditions: changes in chemoreflex stimuli brought about by cardiovascular changes induced by hyperventilation may play a role in the short-term potentiation observed under other circumstances. Key words: rebreathing, hyperventilation, short-term potentiation

The Ventilatory Response to Hypoxia Below the Carbon Dioxide Threshold

1997 ◽  
Vol 22 (1) ◽  
pp. 23-36 ◽  
Author(s):  
Theodore Rapanos ◽  
James Duffin
Keyword(s):  
Carbon Dioxide ◽  
Partial Pressure ◽  
Ventilatory Response ◽  
Pressure Threshold ◽  
Partial Pressures ◽  
Progressive Hypoxia ◽  
End Tidal ◽  
Peripheral Chemoreflex ◽  
Ventilatory Response To Hypoxia ◽  
Lower Carbon

The ventilatory response to acute progressive hypoxia below the carbon dioxide threshold using rebreathing was investigated. Nine subjects rebreathed after 5 min of hyperventilation to lower carbon dioxide stores. The rebreathing bag initially contained enough carbon dioxide to equilibrate alveolar and arterial partial pressures of carbon dioxide to the lowered mixed venous partial pressure (≈ 30 mmHg), and enough oxygen to establish a chosen end-tidal partial pressure (50-70 mmHg), within one circulation time. During rebreathing, end-tidal partial pressure of carbon dioxide increased while end-tidal partial pressure of oxygen fell. Ventilation increased linearly with end-tidal carbon dioxide above a mean end-tidal partial pressure threshold of 39 ± 2.7 mmHg. Below this peripheral-chemoreflex threshold, ventilation did not increase, despite a progressive fall in end-tidal oxygen partial pressure to a mean of 37 ± 4.1 mmHg. In Conclusion, hypoxia does not stimulate ventilation when carbon dioxide is below its peripheral-chemoreflex threshold. Key words: peripheral chemoreflex, rebreathing technique, hyperventilation

Sex Differences in Morphine-induced Ventilatory Depression Reside within the Peripheral Chemoreflex Loop 

1999 ◽  
Vol 90 (5) ◽  
pp. 1329-1338 ◽  
Author(s):  
Elise Sarton ◽  
Luc Teppema ◽  
Albert Dahan
Keyword(s):  
Carbon Dioxide ◽  
Sex Differences ◽  
Minute Ventilation ◽  
Carbon Dioxide Tension ◽  
Central Component ◽  
Men And Women ◽  
Ventilatory Depression ◽  
End Tidal ◽  
Peripheral Chemoreflex ◽  
Sustained Hypoxia

Background This study gathers information in humans on the sites of sex-related differences in ventilatory depression caused by the mu-opioid receptor agonist morphine. Methods Experiments were performed in healthy young men (n = 9) and women (n = 7). Dynamic ventilatory responses to square-wave changes in end-tidal carbon dioxide tension (7.5-15 mmHg) and step decreases in end-tidal oxygen tension (step from 110 to 50 mmHg, duration of hypoxia 15 min) were obtained before and during morphine infusion (intravenous bolus dose 100 microg/kg, followed by 30 microg x kg(-1) x h(-1)). Each hypercapnic response was separated into a fast peripheral and slow central component, which yield central (Gc) and peripheral (Gp) carbon dioxide sensitivities. Values are mean +/- SD. Results In carbon dioxide studies in men, morphine reduced Gc from 1.61 +/- 0.33 to 1.23 +/- 0.12 l x min(-1) x mmHg(-1) (P < 0.05) without affecting Gp (control, 0.41 +/- 0.16 and morphine, 0.49 +/- 0.12 l x min(-1) x mmHg(-1), not significant). In carbon dioxide studies in women, morphine reduced Gc, from 1.51 +/- 0.74 to 1.17 +/- 0.52 l x min(-1) x mmHg(-1) (P < 0.05), and Gp, from 0.54 +/- 0.19 to 0.39 +/- 0.22 l x min(-1) x mmHg(-1) (P < 0.05). Morphine-induced changes in Gc were equal in men and women; changes in Gp were greater in women. In hypoxic studies, morphine depressed the hyperventilatory response at the initiation of hypoxia more in women than in men (0.54 +/- 0.23 vs. 0.26 +/- 0.34 l x min(-1) x %(-1), respectively; P < 0.05). The ventilatory response to sustained hypoxia (i/e., 15 min) did not differ between men and women. Conclusions The data indicate the existence of sex differences in morphine-induced depression of responses mediated via the peripheral chemoreflex pathway, with more depression in women, but not of responses mediated via the central chemoreflex pathway. In men and women, morphine did not change the translation of the initial hyperventilatory response to short-term hypoxia into the secondary decrease in inspired minute ventilation (Vi) caused by sustained hypoxia.

Influences of Subanesthetic Isoflurane on Ventilatory Control in Humans

1995 ◽  
Vol 83 (3) ◽  
pp. 478-490. ◽  
Author(s):  
Maarten van den Elsen ◽  
Albert Dahan ◽  
Jacob DeGoede ◽  
Aad Berkenbosch ◽  
Jack van Kleef
Keyword(s):  
Carbon Dioxide ◽  
Healthy Volunteers ◽  
Ventilatory Response ◽  
Carbon Dioxide Tension ◽  
Central Component ◽  
Ventilatory Control ◽  
Ventilatory Responses ◽  
End Tidal ◽  
Peripheral Chemoreflex ◽  
Ventilatory Response To Hypoxia

Background The purpose of this study was to quantify in humans the effects of subanesthetic isoflurane on the ventilatory control system, in particular on the peripheral chemoreflex loop. Therefore we studied the dynamic ventilatory response to carbon dioxide, the effect of isoflurane wash-in upon sustained hypoxic steady-state ventilation, and the ventilatory response at the onset of 20 min of isocapnic hypoxia. Methods Study 1: Square-wave changes in end-tidal carbon dioxide tension (7.5-11.5 mmHg) were performed in eight healthy volunteers at 0 and 0.1 minimum alveolar concentration (MAC) isoflurane. Each hypercapnic response was separated into a fast, peripheral component and a slow, central component, characterized by a time constant, carbon dioxide sensitivity, time delay, and off-set (apneic threshold). Study 2: The ventilatory changes due to the wash-in of 0.1 MAC isoflurane, 15 min after the induction of isocapnic hypoxia, were studied in 11 healthy volunteers. Study 3: The ventilatory responses to a step decrease in end-tidal oxygen (end-tidal oxygen tension from 110 to 44 mmHg within 3-4 breaths; duration of hypoxia 20 min) were assessed in eight healthy volunteers at 0, 0.1, and 0.2 MAC isoflurane. Results Values are reported as means +/- SF. Study 1: The peripheral carbon dioxide sensitivities averaged 0.50 +/- 0.08 (control) and 0.28 +/- 0.05 l.min-1.mmHg-1 (isoflurane; P < 0.01). The central carbon dioxide sensitivities (control 1.20 +/- 0.12 vs. isoflurane 1.04 +/- 0.11 l.min-1.mmHg-1) and off-sets (control 36.0 +/- 0.1 mmHg vs. isoflurane 34.5 +/- 0.2 mmHg) did not differ between treatments. Study 2: Within 30 s of exposure to 0.1 MAC isoflurane, ventilation decreased significantly, from 17.7 +/- 1.6 (hypoxia, awake) to 15.0 +/- 1.5 l.min-1 (hypoxia, isoflurane). Study 3: At the initiation of hypoxia ventilation increased by 7.7 +/- 1.4 (control), 4.1 +/- 0.8 (0.1 MAC; P < 0.05 vs. control), and 2.8 +/- 0.6 (0.2 MAC; P < 0.05 vs. control) l.min-1. The subsequent ventilatory decrease averaged 4.9 +/- 0.8 (control), 3.4 +/- 0.5 (0.1 MAC; difference not statistically significant), and 2.0 +/- 0.4 (0.2 MAC; P < 0.05 vs. control) l.min-1. There was a good correlation between the acute hypoxic response and the hypoxic ventilatory decrease (r = 0.9; P < 0.001). Conclusions The results of all three studies indicate a selective and profound effect of subanesthetic isoflurane on the peripheral chemoreflex loop at the site of the peripheral chemoreceptors. We relate the reduction of the ventilatory decrease of sustained hypoxia to the decrease of the initial ventilatory response to hypoxia.

Inhibitory effect of an intellectual task on breathing after voluntary hyperventilation

1996 ◽  
Vol 81 (3) ◽  
pp. 1379-1387 ◽  
Author(s):  
K. Chin ◽  
M. Ohi ◽  
M. Fukui ◽  
H. Kita ◽  
T. Tsuboi ◽  
...  
Keyword(s):  
Video Game ◽  
Minute Ventilation ◽  
Normal Subjects ◽  
Inhibitory Effect ◽  
Inspiratory Flow Rate ◽  
Short Term ◽  
Voluntary Hyperventilation ◽  
Term Potentiation ◽  
The Central Nervous System ◽  
Increased Activity

We investigated the effects of an intellectual task on posthyperventilation (PHV) breathing by using a video game. Eight normal subjects were placed in a supine positions. The game task by itself led to increase ventilation compared with the control tasks via an increase in the average inspiratory flow rate (P < 0.01) and the respiratory frequency (P < 0.001). After hypocapnic voluntary hyperventilation (VHV), the task led to a decrease in the 1-min PHV breathing level compared with the control tasks after VHV [after VHV, first 60 s average minute ventilation while watching television and while playing a video game are 5.54 +/- 2.91 (SD) and 2.05 +/- 1.40 l/min, respectively; P < 0.01]. Only one subject showed PHV apnea for at least 10 s during the control protocol, whereas seven of the same eight subjects showed PHV apnea while performing the task. After isocapnic VHV, the task still led to a decrease in PHV breathing compared with the control tasks. However, this decrease was smaller than in the hypocapnic studies and was only significant during the first 15 s of recovery. These results suggest that increased activity in the higher centers of the central nervous system has an inhibitory effect on PHV breathing at a time when the effects of short-term potentiation after VHV, hypocapnia, and perhaps other mechanisms would be expected to be acting on breathing.

Effect of intravenous dopamine on hypercapnic ventilatory response in humans

1983 ◽  
Vol 55 (5) ◽  
pp. 1418-1425 ◽  
Author(s):  
D. S. Ward ◽  
J. W. Bellville
Keyword(s):  
Carbon Dioxide ◽  
Ventilatory Response ◽  
Carbon Dioxide Concentration ◽  
Carbon Dioxide Tension ◽  
Model Parameters ◽  
Loop Gain ◽  
Loop Contribution ◽  
Dopamine Infusion ◽  
Hypercapnic Ventilatory Response ◽  
End Tidal

This study assessed the effect of low-dose intravenous dopamine (3 micrograms X kg-1 X min-1) on the hypercapnic ventilatory response in humans. Six normal healthy subjects were studied. By manipulating the inspired carbon dioxide concentration, the end-tidal carbon dioxide tension was raised in a stepwise fashion from 41 to 49 Torr and held at this level for 4 min. The end-tidal CO2 tension was then lowered back to 41 Torr in a stepwise fashion. The end-tidal O2 tension was held constant at 106 Torr throughout the experiment. The ventilatory response to this normoxic hypercapnic stimulus was analyzed by fitting two exponential functions, allowing the response to be separated into slow and fast chemoreflex loops. Each loop is described by a gain, time constant, and time delay. A single eupneic threshold was used for both loops. Nine control experiments and eight experiments performed during dopamine infusion were analyzed. The dopamine infusion caused the fast loop gain to be significantly (P less than 0.05) reduced from 0.64 to 0.19 l X min-1 X Torr-1, while the slow loop gain was unchanged. The fast loop contribution was reduced from 28 to 11% of the total ventilatory response. None of the other model parameters were significantly affected by the dopamine infusion. Exogenously administered dopamine substantially reduces the sensitivity of the fast chemoreflex loop to carbon dioxide.

scholarly journals Dynamic Forcing of End-Tidal Carbon Dioxide and Oxygen Applied to Functional Magnetic Resonance Imaging

2007 ◽  
Vol 27 (8) ◽  
pp. 1521-1532 ◽  
Author(s):  
Richard G Wise ◽  
Kyle TS Pattinson ◽  
Daniel P Bulte ◽  
Peter A Chiarelli ◽  
Stephen D Mayhew ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Blood Oxygenation ◽  
Dynamic Responses ◽  
Bold Signal ◽  
Tidal Forcing ◽  
Partial Pressures ◽  
Oxygenation Level ◽  
Mri Environment ◽  
Dynamic Forcing ◽  
End Tidal

Investigations into the blood oxygenation level-dependent (BOLD) functional MRI signal have used respiratory challenges with the aim of probing cerebrovascular physiology. Such challenges have altered the inspired partial pressures of either carbon dioxide or oxygen, typically to a fixed and constant level (fixed inspired challenge (FIC)). The resulting end-tidal gas partial pressures then depend on the subject's metabolism and ventilatory responses. In contrast, dynamic end-tidal forcing (DEF) rapidly and independently sets end-tidal oxygen and carbon dioxide to desired levels by altering the inspired gas partial pressures on a breath-by-breath basis using computer-controlled feedback. This study implements DEF in the MRI environment to map BOLD signal reactivity to CO2. We performed BOLD (T2*) contrast FMRI in four healthy male volunteers, while using DEF to provide a cyclic normocapnichypercapnic challenge, with each cycle lasting 4 mins (PetCO2 mean±s.d., from 40.9 ± 1.8 to 46.4 ± 1.6 mm Hg). This was compared with a traditional fixed-inspired (FiCO2 = 5%) hypercapnic challenge (PetCO2 mean±s.d., from 38.2 ± 2.1 to 45.6 ± 1.4 mm Hg). Dynamic end-tidal forcing achieved the desired target PetCO2 for each subject while maintaining PetCO2 constant. As a result of CO2-induced increases in ventilation, the FIC showed a greater cyclic fluctuation in PetCO2. These were associated with spatially widespread fluctuations in BOLD signal that were eliminated largely by the control of PetCO2 during DEF. The DEF system can provide flexible, convenient, and physiologically well-controlled respiratory challenges in the MRI environment for mapping dynamic responses of the cerebrovasculature.

Carbon dioxide narcosis due to human error in a dog

2020 ◽  
Vol 8 (2) ◽  
pp. e001053
Author(s):  
Victoria Phillips ◽  
Alessandra Mathis
Keyword(s):  
Carbon Dioxide ◽  
Human Error ◽  
Visual Inspection ◽  
Carbon Dioxide Tension ◽  
Breathing System ◽  
Normal Limits ◽  
Inhalational Anaesthesia ◽  
Prolonged Recovery ◽  
End Tidal ◽  
Circle Breathing System

Incorrect assembly of a parallel Lack (Mapleson A) breathing system resulted in carbon dioxide narcosis in a dog due to rebreathing of expiratory gases. A seven-year-old, male neutered Rottweiler, weighing 49 kg, failed to recover after discontinuation of inhalational anaesthesia following a forequarter amputation for osteosarcoma. During recovery, the endotracheal tube had been connected to a parallel Lack anaesthetic breathing system delivering 100 per cent oxygen at 5 l/minute. Although a prolonged recovery, 30 minutes, all vital parameters were considered within normal limits until a severe increase in respiratory effort was noted. Capnography revealed rebreathing with an end-tidal carbon dioxide tension of >150 mm Hg (>19.9 kPa). The dog was transferred to a circle breathing system, and with normalisation of the capnogram, recovery proceeded without further complications. Visual inspection of the parallel Lack breathing system revealed misassembly which had resulted in rebreathing of expiratory gases, extreme hypercapnia causing prolonged recovery due to narcosis.

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