Apnea following hyper ventilation in man

doi:10.1016/0022-510X(82)90111-3

Journal of the Neurological Sciences

Volume 57, Issue 1, November–December 1982, Pages 67-82

https://doi.org/10.1016/0022-510X(82)90111-3 Get rights and content

Abstract

To assess the incidence of posthyperventilation apnea (PHA), breathing patterns after active voluntary hyperventilation were determined during EEG recording by means of: (1) a thermocouple in 1060 patients; (2) a pneumotachograph coupled with a capnograph in 100 further patients. All the patients were randomly chosen. PHA of 12.6 ± 0.48 occurred in only 18% of awake subjects and was not related to the magnitude of the lowering of end-tidal F_ECO₂ during the test. PHA frequency increased when sleep followed hyperventilation and in patients with clinical or EEG evidence of cerebral pathology and seemed to be age-related.

This study supports the hypothesis that in man a central neural mechanism closely linked to vigilance and connected with active breathing supplies sufficient neural facilitation to prevent the apnea consequent on the decrease in chemical humoral stimulation. Posthyperventilation sleep reduces this neural facilitation, allowing the lack of chemical stimulation to induce apnea. The high incidence of PHA reported in some studies might be due to a decrease in vigilance which was not detected by the usual behavioral or electroencephalographic tests.

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With the rapid somatic growth and development in infants, simultaneous accurate measurements of lung volume and airway function are essential. Raised volume rapid thoracoabdominal compression (RTC) is widely used to generate forced expiration from an airway opening pressure of 30 cmH₂O (V₃₀). The (dynamic) functional residual capacity (FRC_dyn) remains the lung volume most routinely measured. The aim of this study was to develop comprehensive integrated spirometry that included all subdivisions of lung volume at V₃₀ or total lung capacity (TLC₃₀). Measurements were performed on 17 healthy infants aged 8.6–119.7 weeks. A commercial system for multiple-breath nitrogen washout (MBNW) to measure lung volumes and a custom made system to perform RTC were used in unison. A refined automated raised volume RTC and the following two novel single maneuvers with dual volume measurements were performed from V₃₀ during a brief post-hyperventilation apneic pause: (1) the passive expiratory flow was integrated to produce the inspiratory capacity (IC) and the static (passive) FRC (FRC_st) was estimated by initiating MBNW after end-passive expiration; (2) RTC was initiated late during passive expiration, flow was integrated to produce the slow vital capacity (_jSVC) and the residual volume (RV) was measured by initiating MBNW after end-expiration while the jacket (j) was inflated. Intrasubject FRC_dyn and FRC_st measurements overlapped (p = 0.6420) but neither did with the RV (p < 0.0001). Means (95% confidence interval) of FRC_dyn, IC, FRC_st, _jSVC, RV, forced vital capacity and tidal volume were 21.2 (19.7–22.7), 36.7 (33.0–40.4), 21.2 (19.6–22.8), 40.7 (37.2–44.2), 18.1 (16.6–19.7), 40.7 (37.1–44.2) and 10.2 (9.6–10.7) ml/kg, respectively. Static lung volumes and capacities at V₃₀ and variables from the best forced expiratory flow-volume curve were dependent on age, body length and weight. In conclusion, we developed a comprehensive physiologically integrated approach for in-depth investigation of lung function at V₃₀ in infants.
Apnea while awake
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Hyperventilation and attention: Effects of hypocapnia on performance in a Stroop task
2000, Biological Psychology
This study aimed to investigate the effect of hypocapnia on attentional performance. Hyperventilation, producing hypocapnia, is associated with physiological changes in the brain and with subjective symptoms of dizziness, concentration problems and derealization. In this study (N=42), we examined cognitive performance on a Stroop-like task, following either 3 min of hypocapnic or normocapnic overbreathing. Both overbreathing trials were run on separate days, each preceded by a baseline trial with the same task during normal breathing. More and other symptoms were reported after hypocapnia compared to normocapnia. Also, more errors were made and progressively slower reaction times (RT's) were observed during recovery from hypocapnia. These performance deficits were only found in participants characterized by apneas. The number of symptoms did not correlate with RT's or errors. The pattern of data suggested that hypoxia, as a result of apneas during recovery from hypocapnia, caused the cognitive performance deficit.
Polysomnographic characteristics of patients with Rett syndrome
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During wakefulness, patients with Rett syndrome have disordered breathing. To understand further this ventilatory control disorder, we performed polysomnography in 30 patients with Rett syndrome and 30 control subjects (female subjects with primary snoring). The median age was 7 years (range, 1 to 32 years) for Rett syndrome and 6 years (range, 1 to 17 years) for control subjects. During periods of wakefulness, 67% of patients with Rett syndrome had the characteristic pattern of disordered breathing (i.e., episodes of hyperventilation followed by central apnea and desaturation). No such events occurred during sleep. Sleep efficiency and sleep architecture were similar for both groups. During sleep, there was no difference in duration of periodic breathing, number of episodes of central apnea with desaturation, or number of episodes of obstructive apnea or end-tidal carbon dioxide tension between the two groups. Although arterial oxygen saturation during rapid eye movement (REM) sleep was slightly lower in patients with Rett syndrome (nadir, 94% ± 2% vs 96% ± 2%), it remained within the normal range. Parental history reflected the awake respiratory findings in most cases. We conclude that patients with Rett syndrome have normal breathing during non-rapid eye movement (NREM) sleep. We speculate that patients with Rett syndrome have normal brain-stem control of ventilation, and that the disordered breathing seen during wakefulness is due to an abnormality of the cortical influence on ventilation. (J PEDIATR 1994;125:218-24)
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Research reportApnea following hyper ventilation in man

Abstract

The absence of posthyperventilation apnea in the wakeful state

J. Physiol. (Lond.)

Posthyperventilation apnea in awake man

J. appl. Physiol.

Absence of apnoea after forced breathing

J. Physiol. (Lond.)

La respiration

The causes of periodic or Cheyne-Stokes breathing

J. Physiol. (Lond.)

Posthyperventilation breathing — different effects of active and passive hyperventilation

J. appl. Physiol.

Central neural respiratory stimulatory effect of active respiration

J. appl. Physiol.

Maintenance of respiration by central neural feedback mechanisms

Influence of cerebral activity in wakefulness on regulation of breathing

J. appl. Physiol.

Monitoring of ventilation by integrated diaphragmatic electromyogram — Determination of carbon dioxide (CO2) threshold in anesthetized man

J. Amer. med. Ass.

Central regulation of respiration during anesthesia and wakefulness

Ann. N.Y. Acad. Sci.

Sur la cause de l'apnée

Arch. Biol. (Paris)

Etude polygraphique des manifestations épisodiques (hypniques et respiratoires) du syndrome de Pickwick

Rev. neurol. (Paris)

The regulation of the lung-ventilation

J. Physiol. (Lond.)

Research report
Apnea following hyper ventilation in man

Monitoring of ventilation by integrated diaphragmatic electromyogram — Determination of carbon dioxide (CO₂) threshold in anesthetized man