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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is well accepted that hyperventilation before breath hold swimming and diving makes it possible for a person to extend the time under water. Less well known is the fact that this maneuver can cause loss of consciousness due to hypoxia. This accident happens almost exclusively to males (56 cases). The most common age group was 16-20 years (range 12-33 years). All were known to be good swimmers or divers. Approximately 80% of the cases occurred in guarded pools. Thirty-five subjects survived the accident and of the twenty-three fatalities, there was only one good autopsy report. In this instance the findings were those associated with classical drowning preceded by hypoxia and hypercapnia. Breath holding experiments indicated that the times between loss of consciousness and death may be no longer than 2.5 minutes. The patterns associated with these cases suggest that those who are responsible for aquatic safety as supervisors or guards of pools could prevent most accidents by watching for young male swimmers who are practicing hyperventilation and underwater swimming in competition with themselves or with others.
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PMID:Summary of 58 cases of loss of consciousness during underwater swimming and diving. 97 64

Breath holding was used as the basis of a simple test of respiratory chemosensitivity. Breath holding was begun at selected degrees of hypercapnia produced by CO2 rebreathing. In 16 healthy control subjects there was a linear regression of the log of breath-holding time on the PCO2 at the start of breath holding. Breath-holding time (BHT) and the slope of a log BHT/Pco2 plot were closely correlated with the ventilatory response to CO2. In five cases of the idiopathic hypoventilation syndrome, CO2 retention and reduced ventilatory response to CO2 were accompanied by prolonged breath-holding time and the regression of log BHT on Pco2 was abnormally flat. However, in 17 patients with chronic airways obstruction, breath-holding time was never prolonged and the log BHT/Pco2 relationship was normal, even though 13 had a diminished ventilatory response to CO2 and four had chronic CO2 retention. It is concluded that the BHT/Pco2 relationship provides a useful index of respiratory chemosensitivity which is not influenced by airways obstruction. This may be helpful in the detection of impaired chemosensitivity as a cause of CO2 retention even when the ventilation CO2 response is reduced non-specifically by coexisting airways obstruction.
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PMID:Evaluation of breath holding in hypercapnia as a simple clinical test of respiratory chemosensitivity. 114 39

The authors examine the respiratory tests performed during a two years-period in 676 pneumoconiotic miners. Spirography was normal in 8% of the cases; a mixed ventilatory impairment, with an obstructive prevalence of variable extent, was present in 2/3 of the cases. Pharmacodynamic tests in 353 subjects showed a frequent non-specific bronchial sensitivity (34.2% of the whole group). Hypoxaemia (PaO2 below 75 mmHg) with normo- or hypocapnia was observed in 379 patients; hypercapnia was relatively uncommon (9.9%) and occurred mainly in bronchitic patients. The breath holding CO lung transfer test was very often disturbed, as the diffusing capacity (DLCO) was below the predicted value in about 80% of the population. Radiofunctional comparisons were carried out in an homogeneous group of 212 subjects. The data clearly demonstrate that functional abnormalities were not exclusively seen in extensive radiological forms. As far as it goes beyond a simple ventilatory study, the measurement of the breath holding lung transfer factor for CO has proved to be a valuable element in the functional statement of anthracosilicosis. The polymorphism of the pulmonary repercussions of dust exposure explains individual differences between the results of the main investigations, and this emphasizes the need for a series of diversified tests.
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PMID:[Respiratory parameters in pneumoconiotic miners in the north French coal district (author's transl)]. 121 56

The tolerance of totally curarized subjects for prolonged breath hold is viewed by many as evidence that respiratory muscle contraction is essential to generate the sensation of breathlessness. Although conflicting evidence exists, none of it was obtained during total neuromuscular block. We completely paralyzed four normal, unsedated subjects with vecuronium (a non-depolarizing neuromuscular blocker). Subjects were mechanically ventilated with hyperoxic gas mixtures at fixed rate and tidal volume. End-expiratory PCO2 (PETCO2) was varied surreptitiously by changing inspired PCO2. Subjects rated their respiratory discomfort or 'air hunger' every 45 sec. At low PETCO2 (median 35 Torr) they felt little or no air hunger. When PETCO2 was raised (median 44 Torr) all subjects reported severe air hunger. They had reported the same degree of air hunger at essentially the same PETCO2 before paralysis. When questioned afterwards all subjects said the sensation could be described by the terms 'air hunger', 'urge to breathe', and 'shortness of breath', and that is was like breath holding. They reported no fundamental difference in the sensation before and after paralysis. We conclude that respiratory muscle contraction is not important in the genesis of air hunger evoked by hypercapnia.
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PMID:'Air hunger' from increased PCO2 persists after complete neuromuscular block in humans. 212 Jul 57

Changes in common carotid blood flow (CCF) and resistance index (RI), calculated from velocity waveforms by a noninvasive pulsed Doppler technique, were measured during apneic episodes and voluntary breath holding in five sleep apnea patients (SA) and during breath holding in five normal subjects (N). During apneic episodes averaging 27 s, CCF was reduced by 9% and RI increased by 4%, both trends being related to apneic duration. Internal carotid artery measurements in one SA indicated more dramatic changes in blood flow and RI than noted in CCF. During breath holding, CCF decreased significantly in SA but not in N, and RI showed a smaller reduction in SA. These changes in CCF and RI during sleep apnea are similar to those noted in anesthetized dogs where vasomotor waves and associated apneas were induced by elevating intracranial pressure. Previously reported recordings of ventilatory and systemic cardiovascular responses in SA are similar to these recordings in dogs, and it is therefore proposed that vasomotor responses to intermittent cerebral ischemia and hypercapnia may be the principle event in SA and periodic breathing only a secondary consequence of the prevailing autonomic dysfunction.
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PMID:Sleep apnea and autonomic cerebrovascular dysfunction. 310 21

To determine the characteristics of and mechanisms causing the bradycardia during sleep apnea (SA), both patients with SA and normals were studied. Evaluation of six consecutive SA patients demonstrated that bradycardia occurred during 95% of all apneas (central, obstructive, and mixed) and became marked with increased apnea length (P less than 0.01) and increased oxyhemoglobin desaturation (P less than 0.01). Heart rate slowed 9.5 beats per minute (bpm) during apneas of 10-19 s in duration, 11.4 bpm during 20-39s apneas, and 16.6 bpm during 40-59-s apneas. Sleep stage had no effect unexplained by apnea length or degree of desaturation. Oxygen administration to four SA patients completely prevented the bradycardia although apneas lengthened (P less than 0.05) in three. Sleeping normal subjects did not develop bradycardia during hypoxic hyperpnea but, instead, HR increased with hypoxia in all sleep stages, although the increase in HR was not as great as that which occurred while awake. Breath holding in awake normals did not result in bradycardia during hyperoxia (SaO2 = 99%), but was consistently (P less than 0.01) associated with heart rate slowing during room air breath-holds (-6 bpm) at SaO2 = 93%, with more striking slowing (-20 bpm) during hypoxic breath-holds (P less than 0.01) at SaO2 = 78%. Breath holding during hyperoxic hypercapnia had no significant effect on rate. Breath holding in awake SA subjects demonstrated similar findings. We conclude that the bradycardia of SA is a consistent feature of apnea and results from the combined effect of cessation of breathing plus hypoxemia.
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PMID:Bradycardia during sleep apnea. Characteristics and mechanism. 708 75

The normal role of the carotid bodies in ventilatory dynamics in man has been inferred from studies comparing the responses of a group of control subjects to: a) hypoxic-hyperoxic transitions, b) steady-state hypercapnia, c) constant-load and incremental exercise, and d) breath holding with various inspired O2 levels, with the responses of subjects who had had both carotid bodies surgically resected (CBR). Ventilation, metabolic rate, and alveolar gas tensions were computed breath by breath and blood was sampled from a brachial artery catheter. With eucapnia, hypoxic ventilatory drive is subserved entirely by the carotid bodies, both at rest and during exercise, whereas only approximatly equal to 30% of the hyercapnic response in euoxia is attributable to these structures. CBR resulted in appreciable slowing of the ventilatory dynamics during exercise, causing a transient respiratory acidosis. In the steady state of moderate exercise, ventilation was normal in the CBR group, as other receptors provide the approximately equal to 15% of the drive attributable to the carotid bodies. The respiratory compensation for the acute metabolic acidosis of exercise appears to be exclusively mediated by the carotid bodies. Breath-holding time is significantly prolonged following CBR, especially under hypoxic conditions. The carotid bodies therefore provide important information to respiratory control in man, most notably under hypoxia, metabolic acidosis, and dynamic states of muscular exercise.
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PMID:Carotid bodies and ventilatory control dynamics in man. 739 96

The normal breathing pattern of the turtle, Chrysemys picta (Schneider), consists of periods of continuous breathing interspersed with periods of breath holding. During each ventilatory period respiratory frequency and tidal volume are controlled independently. There is a large variability in inspiratory and expiratory gas-flow rates yet tidal volumes are maintained within narrow limits by adjustments of the lengths of the active inspiratory and expiratory intervals. Lung volume information carried within the vagus nerve is responsible for the careful regulation of tidal volume as well as for modulation of the air flow rates and lowering of the threshold of the mechanism initiating expiration following breath holding. Increases in pulmonary minute ventilation during hypercapnia are caused by increases in respiratory frequency due solely to a shortening of the periods of breath holding. There is some increase in tidal volume but the breath length remains constant and thus the frequency of breathing within each ventilatory period also remains constant. After vagotomy, changes in minute ventilation due to hypercapnia stem primarily from changes in tidal volume while changes in respiratory frequency are greatly reduced.
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PMID:The role of vagal afferent information and hypercapnia in control of the breathing pattern in chelonia. 742 20

1. To determine whether discomfort associated with breathing (dyspnoea) is related to the chemical drive to breath, three subjects were totally paralysed while fully conscious. Subjective responses to a rising CO2 stimulus were obtained during rebreathing, rebreathing with CO2 added, and breath holding. Dyspnoea was measured with a 10-point Borg scale. 2. Following nasotracheal intubation and ventilation (oxygen saturation, O2,Sat, 98-100% and end-tidal CO2, PET,CO2, 30-40 mmHg), total neuromuscular blockade was induced by a rapid injection of atracurium (> 2.5 mg kg-1) and complete paralysis was maintained with an infusion (5 mg (kg h)-1). Paralysis was confirmed by abolition of the compound muscle action potentials of both the diaphragm and abductor hallucis evoked by supramaximal electrical stimulation of the relevant nerves. Communication via finger movement was preserved for the first 20-30 min following paralysis by inflation of a sphygmomanometer cuff on one arm. 3. Before and during complete paralysis, dyspnoea increased progressively during hypercapnia produced by rebreathing (with or without CO2 added to the circuit at 250 ml min-1). The mean PET,CO2 eliciting 'severe' dyspnoea was 46 mmHg during rebreathing, 42 mmHg during 'breath holding', and 52 mmHg during rebreathing with added CO2. There were no significant differences between the values obtained during paralysis and in the control study immediately before paralysis. The duration of breath holding was not prolonged by paralysis and the PET,CO2 at the 'break point' was not altered by paralysis. 4. Thus, dyspnoea is preserved following total neuromuscular blockade. This suggests that chemoreceptor activity, via the central neuronal activity which it evokes, can lead to discomfort in the absence of any contraction of respiratory muscles. 5. During paralysis, attempted contraction of arm, leg and trunk muscles increased heart rate and blood pressure. For attempted handgrip contractions, the increases in heart rate (range, 7-15 beats min-1) and mean arterial pressure (range, 20-32 mmHg) were similar to those recorded with actual contractions in trials immediately before paralysis. In one subject, graded increases in heart rate and blood pressure occurred for attempted contractions of 45 s duration over a range of intensities (0-100% maximal effort). 6. During complete paralysis, transcranial electromagnetic stimulation of the motor cortex produced illusory twitch-like movements of the wrist and digits. This also occurred in separate studies during complete ischaemic paralysis and anaesthesia of the forearm and hand.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Respiratory sensations, cardiovascular control, kinaesthesia and transcranial stimulation during paralysis in humans. 830 55

Several studies have demonstrated a clear association between snoring, sleep apnoea and increased risk of stroke. However, the possible role of sleep apnoea in the pathophysiogenetic mechanisms of cerebrovascular disease is still unknown. Our aim in this study was to investigate cerebral haemodynamic changes during the waking state in eight patients with sleep apnoea syndrome (OSAS) by means of transcranial Doppler (TCD). In particular, we studied cerebral vascular reactivity (CVR) to hypercapnia calculated by means of the breath holding index (BHI). The investigation was performed in the early morning, soon after awakening, and in the late afternoon. Data were compared with those of eight healthy subjects matched for age and vascular risk factors. OSAS patients showed significantly lower BHI values with respect to controls both in the morning (0.56 vs. 1.36; P < 0.0001) and in the afternoon (1.12 vs. 1.53; P < 0.0001). In patients, BHI values in the afternoon were significantly higher than in the morning (P < 0.0001). These data demonstrate a diminished vasodilator reserve in OSAS patients, particularly evident in the morning. This reduction of the possibility of cerebral vessels to adapt functionally in response to stimulation could be linked to hyposensitivity of cerebrovascular chemoreceptors after the continuous stress caused by nocturnal hypercapnia.
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PMID:Impairment of daytime cerebrovascular reactivity in patients with obstructive sleep apnoea syndrome. 984 56


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