Relationship Between Heart Rate and Minute Ventilation, Tidal Volume and Respiratory Rate During Brief and Low Level Exercise

1988 ◽  
Vol 11 (11) ◽  
pp. 1860-1865 ◽  
Author(s):  
F. VAI ◽  
J.L. BONNET ◽  
PH. RITTER ◽  
G. PIOGER
2006 ◽  
Vol 100 (3) ◽  
pp. 786-791 ◽  
Author(s):  
Joseph M. Dybas ◽  
Catharine J. Andresen ◽  
Edward S. Schelegle ◽  
Ryan W. McCue ◽  
Natasha N. Callender ◽  
...  

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.


2019 ◽  
Vol 126 (1) ◽  
pp. 124-131 ◽  
Author(s):  
Christoph Siebenmann ◽  
Camilla K. Ryrsø ◽  
Laura Oberholzer ◽  
James P. Fisher ◽  
Linda M. Hilsted ◽  
...  

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.


2019 ◽  
Vol 126 (4) ◽  
pp. 863-869 ◽  
Author(s):  
Maximilian Pinkham ◽  
Russel Burgess ◽  
Toby Mündel ◽  
Stanislav Tatkov

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.


2003 ◽  
Vol 48 (1) ◽  
pp. 93-101 ◽  
Author(s):  
M. Pöyhönen ◽  
S. Syväoja ◽  
J. Hartikainen ◽  
E. Ruokonen ◽  
J. Takala

Author(s):  
Amelia A. Lowell

The main goal of mechanical ventilation is to unload the respiratory muscles to facilitate oxygenation and ventilation. This is accomplished by providing a minute ventilation (VE) (respiratory rate × tidal volume [VT]) that will result in adequate alveolar ventilation coupled with supplemental oxygen and a mean airway pressure that will result in adequate arterial oxygenation.


1993 ◽  
Vol 75 (6) ◽  
pp. 2425-2428 ◽  
Author(s):  
M. S. Fairbarn ◽  
S. P. Blackie ◽  
R. L. Pardy ◽  
J. C. Hogg

The circulating leukocyte (WBC) count increases with exercise, because WBCs enter the circulation from the marginated pool. The lung is a major source of the demarginating cells, but it is unclear whether this occurs because of increased ventilatory movements, increased cardiac output, or both. The present study examined the mechanical effect of ventilation (VE) in six healthy men with three different protocols on three separate occasions. First, the subjects cycled for 5-min intervals at 50, 100, 150, and 200 W, and we measured heart rate (HR), minute ventilation (VE), tidal volume (VT), respiratory rate, and end-tidal CO2. Second, each subject reproduced his exercise VE by matching VT, respiratory rate, and end-tidal CO2 on a circuit designed for isocapnic hyperpnea (matched VE). The subjects then performed a hyperventilation (hyper-VE) protocol with a minimum VT of 1.5 liters and a respiratory rate of 20 breaths/min. Blood samples were drawn at rest and throughout each protocol for measurement of WBCs, hematocrit, and band cells. During cycling, VE increased (9 +/- 1 to 66 +/- 7 l/min), HR increased (71 +/- 7 to 172 +/- 10 beats/min), and WBCs increased (5.5 +/- 0.9 to 7.8 +/- 1.3 x 10(9)/l). During matched VE, VE increased (11 +/- 2 to 69 +/- 11 l/min), but neither HR nor WBCs increased (67 +/- 13 to 78 +/- 12 beats/min and 5.3 +/- 1.6 to 5.7 +/- 1.5 x 10(9)/l, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)


2021 ◽  
Vol 11 (7) ◽  
pp. 265-271
Author(s):  
Abhinav Salve ◽  
Sachin Maghade ◽  
Sneha Katke

Background: Respiratory PNF technique is a proprioceptive and tactile stimulus that alters the depth and rate of breathing. Intercostal stretch enhances the chest wall elevation and increase chest expansion and diaphragm excursion to improve intra-thoracic lung volume which contributes to improvement in flow rate percentage. Vertebral pressure is another respiratory PNF where there is increased epigastric abdominal excursion over T2-T4. Objective: To find out the effect of Vertebral pressure and Intercostal stretch technique on respiratory rate, tidal volume, SpO2 & heart rate among organophosphorus poisoning patients Method: Data was collected from 24 ICU patients who were on mechanical ventilator. Subjects were divided in two groups. Intercostal stretch technique was given to group A and vertebral pressure technique was given to group B, changes HR, RR, SpO2, tidal volume was noted and data analysis was done. Result: There was significant difference between pre intervention and post intervention readings for both the groups A and B at heart rate, respiratory rate, SpO2 and tidal volume related (p<0.001). It thus proved that respiratory stimulation improves TV, Decrease in RR and HR and increase in SpO2 for both groups. Conclusion: Proprioceptive Neuromuscular Facilitation techniques are effective in improving HR, RR, lung capacity and Oxygen saturation in patients with OP poisoning. There was significant difference between pre intervention and post intervention readings for both the groups A and B at heart rate, respiratory rate, SpO2 and tidal volume. Key words: Organophosphorus poisoning, Mechanical ventilator, intercostal stretch, Vertebral pressure, Respiratory PNF.


1995 ◽  
Vol 78 (4) ◽  
pp. 1374-1381 ◽  
Author(s):  
D. Gozal ◽  
J. H. Ben-Ari ◽  
R. M. Harper ◽  
T. G. Keens

In early phases of respiratory disease, patients are more likely to experience intermittent hypercapnia than a continuous increase in PCO2. The effect of intermittent arterial PCO2 elevation on subsequent breathing patterns is unclear. To examine this issue, a series of six ventilatory challenges (CH1-CH6), consisting of 2 min of breathing 5% CO2 in O2, followed by 5 min in room air (RA) were performed in 10 naive healthy subjects (age 12–39 yr). Minute ventilation (VE) increased from 11.9 +/- 1.0 (SE) l/min in RA to 27.6 +/- 3.0 l/min in 5% CO2 (P < 0.0005) in each of the six hypercapnic challenges. Respiratory rate increased from 21.3 +/- 2.6 breaths/min on RA to 29.6 +/- 3.9 breaths/min during CH1 (P < 0.05). However, respiratory rate consistently decreased with successive CO2 challenges (CH6: 21.5 +/- 2.6 breaths/min; P < 0.02). Thus, maintenance of VE was achieved by gradual increases in tidal volume with each of the first four consecutive CO2 challenges (CH1: 1.05 +/- 0.09 liters; CH4: 1.44 +/- 0.13 liters; P < 0.002). Similarly, the ratio of tidal volume to inspiratory time increased from CH1 (1.16 +/- 0.16 l/s) to CH6 (1.57 +/- 0.21 l/s; P < 0.001). These changes in ventilatory strategy were not observed when RA recovery periods were extended to 15 min in five subjects. We conclude that during repeated short hypercapnic challenges similar levels of VE are achieved. However, increased mean inspiratory flows are generated to maintain VE. We speculate that intermittent hypercapnia either modifies central controller gain or induces a long-term modulatory effect to account for the progressive changes in ventilatory components.


1985 ◽  
Vol 59 (3) ◽  
pp. 869-874 ◽  
Author(s):  
M. A. Bureau ◽  
J. Lamarche ◽  
P. Foulon ◽  
D. Dalle

The contribution of the carotid body chemoreceptor to postnatal maturation of breathing was evaluated in lambs from 7 to 70 days of age. The study was conducted by comparing the eupneic ventilation and resting pneumograms in intact conscious lambs with those of lambs that were carotid body chemodenervated (CBD) at birth. In comparison to the 1-wk-old intact lambs, the CBD lambs had significant decreases in minute ventilation (VE, 313 vs. 517 ml/kg), tidal volume (VT, 7.2 vs. 10.5 ml/kg), respiratory rate (f, 44 vs. 51 breaths/min), and occlusion pressure (P0.1, 2.8 vs. 7.2 cmH2O). Arterial PO2's were 59 vs. 75 Torr (P less than 0.05) and arterial PCO2's 47 vs. 36 Torr (P less than 0.05), respectively, in CBD and intact lambs. In intact lambs from 7 to 70 days, resting VE decreased progressively from 517 to 274 ml/kg (P less than 0.01) due to a fall in VT, mean inspiratory flow (VT/TI), and f, whereas the ratio of inspiratory time to total breath duration remained constant. P0.1 decreased from 7.2 to 3.9 cmH2O from 7 to 42 days. In contrast the CBD lambs experienced only minimal changes in VE, VT, VT/TI, and f during the same period. VE only decreased from 313 to 218 and P0.1 from 2.8 to 2.4 cmH2O. In contrast to that of intact lambs the resting pneumogram of CBD lambs remained relatively fixed from 7 to 70 days. Three CBD lambs died unexpectedly, without apparent cause, in the 4th and 5th wk of life.


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