Step changes in end-tidal CO2: methods and implications

Swanson, George D.; Bellville, J. Weldon

doi:10.1152/jappl.1975.39.3.377

Cited by 100 publications

(60 citation statements)

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“…Hypoxia also tends to increase cardiac output, which could shorten the transport time by as much as half (37). Added CO 2 produced a larger and faster response at the carotid body during hypoxia compared with normoxia (29,50). In addition, as we discussed above, the influence of neuromechanical inhibition may be exaggerated by hypoxia (45).…”

Section: Discussionmentioning

confidence: 94%

“…When a normoxia trial immediately followed a hyperoxia or hypoxia trial, the pressure support protocol was not initiated until the PETCO 2 and SaO 2 both returned to the normoxic baseline level. In hypoxia or hyperoxia trials, the pressure support protocol was not initiated until the SaO 2 stabilized at 78 -80% or FIO 2 stabilized at 50 -53% for at least 5 min to allow subjects to approach a steady state (50).…”

Section: Methodsmentioning

confidence: 99%

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Influence of arterial O₂ on the susceptibility to posthyperventilation apnea during sleep

Xie¹,

Skatrud²,

Puleo³

et al. 2006

Journal of Applied Physiology

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Xie, Ailiang, James B. Skatrud, Dominic S. Puleo, and Jerome A. Dempsey. Influence of arterial O2 on the susceptibility to posthyperventilation apnea during sleep. J Appl Physiol 100: 171-177, 2006. First published September 22, 2005 doi:10.1152/japplphysiol.00440.2005.-To investigate the contribution of the peripheral chemoreceptors to the susceptibility to posthyperventilation apnea, we evaluated the time course and magnitude of hypocapnia required to produce apnea at different levels of peripheral chemoreceptor activation produced by exposure to three levels of inspired PO 2. We measured the apneic threshold and the apnea latency in nine normal sleeping subjects in response to augmented breaths during normoxia (room air), hypoxia (arterial O 2 saturation ϭ 78 -80%), and hyperoxia (inspired O2 fraction ϭ 50 -52%). Pressure support mechanical ventilation in the assist mode was employed to introduce a single or multiple numbers of consecutive, sighlike breaths to cause apnea. The apnea latency was measured from the end inspiration of the first augmented breath to the onset of apnea. It was 12.2 Ϯ 1.1 s during normoxia, which was similar to the lung-to-ear circulation delay of 11.7 s in these subjects. Hypoxia shortened the apnea latency (6.3 Ϯ 0.8 s; P Ͻ 0.05), whereas hyperoxia prolonged it (71.5 Ϯ 13.8 s; P Ͻ 0.01). The apneic threshold end-tidal PCO 2 (PETCO 2 ) was defined as the PETCO 2 at the onset of apnea. During hypoxia, the apneic threshold PET CO 2 was higher (38.9 Ϯ 1.7 Torr; P Ͻ 0.01) compared with normoxia (35.8 Ϯ 1.1; Torr); during hyperoxia, it was lower (33.0 Ϯ 0.8 Torr; P Ͻ 0.05). Furthermore, the difference between the eupneic PET CO 2 and apneic threshold PET CO 2 was smaller during hypoxia (3.0 Ϯ 1.0 Torr P Ͻ 001) and greater during hyperoxia (10.6 Ϯ 0.8 Torr; P Ͻ 0.05) compared with normoxia (8.0 Ϯ 0.6 Torr). Correspondingly, the hypocapnic ventilatory response to CO 2 below the eupneic PETCO 2 was increased by hypoxia (3.44 Ϯ 0.63 l ⅐ min Ϫ1 ⅐ Torr Ϫ1 ; P Ͻ 0.05) and decreased by hyperoxia (0.63 Ϯ 0.04 l ⅐ min Ϫ1 ⅐ Torr Ϫ1 ; P Ͻ 0.05) compared with normoxia (0.79 Ϯ 0.05 l ⅐ min Ϫ1 ⅐ Torr Ϫ1 ). These findings indicate that posthyperventilation apnea is initiated by the peripheral chemoreceptors and that the varying susceptibility to apnea during hypoxia vs. hyperoxia is influenced by the relative activity of these receptors. apnea threshold THE RELATIVE CONTRIBUTION of peripheral vs. central chemoreception in initiating the posthyperventilation apneas remains an unresolved question. The importance of peripheral chemoreception in mediating the rapid ventilatory response to hypocapnia has been supported using animal models. Carotid body denervation either eliminated or prolonged the time course for the development of apnea after the administration of augmented breaths (6, 39). However, carotid body denervation profoundly alters central chemoreception as indicated by the substantial CO 2 retention after denervation. Our laboratory has previously demonstrated the complex effect of hypoxia in t...

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Section: Discussionmentioning

confidence: 94%

Section: Methodsmentioning

confidence: 99%

Influence of arterial O₂ on the susceptibility to posthyperventilation apnea during sleep

Xie¹,

Skatrud²,

Puleo³

et al. 2006

Journal of Applied Physiology

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“…We, therefore, defined hyperventilation by an upright ETCO 2 consistently <30 Torr that persisted during the tilt test. Patients who hyperventilated received supplemental CO 2 near the end of tilt using the “dynamic end tidal forcing” technique,20 to return their ETCO 2 to eucapnic levels. This allowed for the manipulation of the end‐tidal concentration of one gas while maintaining the end‐tidal concentration of the other gases constant.…”

Section: Methodsmentioning

confidence: 99%

Postural Hyperventilation as a Cause of Postural Tachycardia Syndrome: Increased Systemic Vascular Resistance and Decreased Cardiac Output When Upright in All Postural Tachycardia Syndrome Variants

Stewart

Pianosi

Shaban

et al. 2018

JAHA

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BackgroundPostural tachycardia syndrome (POTS) is a heterogeneous condition. We stratified patients previously evaluated for POTS on the basis of supine resting cardiac output (CO) or with the complaint of platypnea or “shortness of breath” during orthostasis. We hypothesize that postural hyperventilation is one cause of POTS and that hyperventilation‐associated POTS occurs when initial reduction in CO is sufficiently large. We also propose that circulatory abnormalities normalize with restoration of CO 2.Methods and ResultsFifty‐eight enrollees with POTS were compared with 16 healthy volunteer controls. Low CO in POTS was defined by a resting supine CO <4 L/min. Patients with shortness of breath had hyperventilation with end tidal CO 2 <30 Torr during head‐up tilt table testing. There were no differences in height or weight between control patients and patients with POTS or differences between the POTS groups. Beat‐to‐beat blood pressure was measured by photoplethysmography, and CO was measured by ModelFlow. Systemic vascular resistance was defined as mean arterial blood pressure/CO. End tidal CO 2 and cerebral blood flow velocity of the middle cerebral artery were only reduced during head‐up tilt in the hyperventilation group, whereas blood pressure was increased compared with control. We corrected the reduced end tidal CO 2 in hyperventilation by addition of exogenous CO 2 into a rebreathing apparatus. With added CO 2, heart rate, blood pressure, CO, and systemic vascular resistance in hyperventilation became similar to control.ConclusionsWe conclude that all POTS is related to decreased CO, decreased central blood volume, and increased systemic vascular resistance and that a variant of POTS is consequent to postural hyperventilation.

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“…Mean Tp for the various kinds of steps used were fairly uniform, though two of the differences were marginally significant (CO2 steps, Table 1, A to B shorter than C to B; and Table 2, the steps out of hypoxia B to D and C to E and Table 3, A to D were together shorter than the steps into hypoxia, (Bellville et al 1979) and 120 s (Gardner, 1980) for background hypoxia at rest, and than the 98 s (Swanson & Bellville, 1975) and 180 s (Bellville et al 1979) for euoxia at rest. If the time constant of the central chemoreceptors is dependent upon cerebral perfusion, as assumed by Bellville et al (1979), then the hyperkinetic effect of hypoxic exercise may have been responsible for our short values of T,.…”

Section: Peripheral Time Constants Tpmentioning

confidence: 95%

Dynamics of the ventilatory response in man to step changes of end‐tidal carbon dioxide and of hypoxia during exercise.

Macfarlane¹,

Cunningham²

1992

The Journal of Physiology

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SUMMARY1. Four human subjects exercised in hypoxia (end-tidal partial pressure Of 02 (PET, 02) ca 55 Torr; heart rate ca 100-130 beats min-), and the contribution to the respiratory drive of the peripheral and central chemoreflex pathways have been separated on the basis of the latencies and the time courses of the responses to sudden changes of stimulus.2. The subjects were exposed to repeated end-tidal step changes in PCO2 of ca 3-3 5 Torr (at nearly constant PET, 02 ) and P02 (between ca 55 and 230 Torr) at three regions along the expiratory ventilation VE-PET°2 response line (hypocapnia, eucapnia, hypercapnia). The dynamics of the ventilatory responses were calculated using a two-compartment non-linear least-squares optimization method.3. The component of the response attributable to the peripheral chemoreflex loop may in some subjects contribute up to 75% of the ventilatory drive during mild hypocapnic hypoxic exercise and ca 72 % of the total gain following steps Of PET, CO, during hypoxic exercise. These data support the notion that the effectiveness of the peripheral chemoreceptor pathway is enhanced in moderate exercise.4. During hypoxic exercise, the time delays and time constants attributed to the peripheral chemoreflex pathways (ca 3-5 and 9 s respectively) and to the central chemoreflex pathways (ca 9-5 and 47 s respectively) are some of the shortest reported.5. The dynamics of the peripheral and central chemoreflex pathways appeared to be largely independent of each other.6. There was a notable absence of systematic change of inspiratory and expiratory durations during the step-induced transients.

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Step changes in end-tidal CO2: methods and implications

Cited by 100 publications

References 0 publications

Influence of arterial O₂ on the susceptibility to posthyperventilation apnea during sleep

Influence of arterial O₂ on the susceptibility to posthyperventilation apnea during sleep

Postural Hyperventilation as a Cause of Postural Tachycardia Syndrome: Increased Systemic Vascular Resistance and Decreased Cardiac Output When Upright in All Postural Tachycardia Syndrome Variants

Dynamics of the ventilatory response in man to step changes of end‐tidal carbon dioxide and of hypoxia during exercise.

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