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

Maintenance of eucapnia during sleep in obstructive sleep apnea (OSA) requires a balance between CO(2) loading during apnea and CO(2) elimination. This study examines individual respiratory events and relates magnitude of postevent ventilation to CO(2) load during the preceding respiratory event in 14 patients with OSA (arterial PCO(2) 42-56 Torr). Ventilation and expiratory CO(2) and O(2) fractions were measured on a breath-by-breath basis during daytime sleep. Calculations included CO(2) load during each event (metabolic CO(2) production - exhaled CO(2)) and postevent ventilation in the 10 s after an event. In 12 of 14 patients, a direct relationship existed between postevent ventilation and CO(2) load during the preceding event (P < 0.05); the slope of this relationship varied across subjects. Thus the postevent ventilation is tightly linked to CO(2) loading during each respiratory event and may be an important mechanism that defends against development of acute hypercapnia in OSA. An inverse relationship was noted between this postevent ventilatory response slope and the chronic awake arterial PCO(2) (r = 0.90, P < 0.001), suggesting that this mechanism is impaired in patients with chronic hypercapnia. The link between development of acute hypercapnia during respiratory events asleep and maintenance of chronic awake hypercapnia in OSA remains to be further investigated.
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PMID:Postevent ventilation as a function of CO(2) load during respiratory events in obstructive sleep apnea. 1218 86

The cardiorespiratory responses were examined in yellowtail, Seriola quinqueradiata exposed to two levels of hypercapnia (seawater equilibrated with a gas mixture containing 1% CO(2) (water PCO(2) = 7 mmHg) or 5% CO(2) (38 mmHg)) for 72 hr at 20 degrees C. Mortality was 100% within 8 hr at 5% CO(2), while no fish died at 1% CO(2). No cardiovascular variables (cardiac output, Q; heart rate, HR; stroke volume, SV and arterial blood pressure, BP) significantly changed from pre-exposure values during exposure to 1% CO(2). Arterial CO(2) partial pressure (PaCO(2)) significantly increased (P < 0.05), reaching a new steady-state level after 3 hr. Arterial blood pH (pHa) decreased initially (P < 0.05), but was subsequently restored by elevation of plasma bicarbonate ([HCO(3)(-)]). Arterial O(2) partial pressure (PaO(2)), oxygen content (CaO(2)), and hematocrit (Hct) were maintained throughout the exposure period. In contrast, exposure to 5% CO(2) dramatically reduced Q (P < 0.05) through decreasing SV (P < 0.05), although HR did not change. BP was transiently elevated (P < 0.05), followed by a precipitous fall before death. The pHa was restored incompletely despite a significant increase in [HCO(3)(-)]. PaO(2) decreased only shortly before death, whereas CaO(2) kept elevated due to a large increase in Hct (P < 0.05). We tentatively conclude that cardiac failure is a primary physiological disorder that would lead to death of fish subjected to high environmental CO(2) pressures.
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PMID:Effects of lethal levels of environmental hypercapnia on cardiovascular and blood-gas status in yellowtail, Seriola quinqueradiata. 1271 43

There are currently three surgical treatments for emphysema: bullectomy, lung transplantation, and lung volume reduction surgery (LVRS). Unfortunately, most emphysema patients are poor candidates for any surgical intervention. A meticulous selection process is favoured in which indications and contraindications are considered and the best solution is devised for each patient. Patients with giant bullae filling half the thoracic volume and compressing relatively normal adjacent parenchyma are offered bullectomy; those with hyperinflation, heterogeneous distribution of destruction, forced expiratory volume in 1 second (FEV(1)) >20%, and a normal carbon dioxide tension (PCO(2)) are offered LVRS; and patients with diffuse disease, lower FEV(1), hypercapnia, and associated pulmonary hypertension are directed towards transplantation. Using these criteria, few patients are serious candidates for surgical procedures. Combinations of LVRS and lung transplantation, either simultaneously or sequentially, are possible but rarely necessary.
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PMID:Chronic obstructive pulmonary disease. 10: Bullectomy, lung volume reduction surgery, and transplantation for patients with chronic obstructive pulmonary disease. 1283 85

Callinectes sapidus, the Atlantic blue crab, encounters hypoxia, hypercapnia (elevated CO(2)), and bacterial pathogens in its natural environment. We tested the hypothesis that acute exposure to hypercapnic hypoxia (HH) alters the crab's ability to clear a pathogenic bacterium, Vibrio campbellii 90-69B3, from the hemolymph. Adult male crabs were held in normoxia (well-aerated seawater) or HH (seawater with PO(2) = 4 kPa; PCO(2) = 1.8 kPa; and pH = 6.7-7.1) and were injected with 2.5 x 10(4) Vibrio g(-1) body weight. The animals were held in normoxia or in HH for 45, 75, or 210-240 min before being injected with Vibrio, and were maintained in their respective treatment conditions for the 120-min duration of the experiment. Vibrio colony-forming units (CFU) ml(-1) hemolymph were quantified before injection, and at 10, 20, and 40 min afterward. Total hemocytes (THC) ml(-1) of hemolymph were counted 24 h before (-24 h), and at 10 and 120 min after injection. Sham injections of saline produced no change in the bacterial or hemocyte counts in any treatment group. Among the groups that received bacterial injections, Vibrio was almost completely cleared within 1 h, but at 10-min postinjection, Vibrio CFU ml(-1) hemolymph was significantly higher in animals held in HH for 75 and 210-240 min than in those held in normoxia. Within 10 min after crabs were injected with bacteria, THC ml(-1) significantly decreased in control and HH45 treatments, but not in the HH75 and HH210-240 treatments. By 120 min after injection of bacteria, hemocyte counts decreased in all but the HH45 group. These data demonstrate that HH significantly impairs the ability of blue crabs to clear Vibrio from the hemolymph. These results also suggest that HH alters the normal role of circulating hemocytes in the removal of an invading pathogen.
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PMID:Effects of hypercapnic hypoxia on the clearance of Vibrio campbellii in the Atlantic blue crab, Callinectes sapidus Rathbun. 1519 44

Ventilatory responses to progressive hypercapnia were analyzed in the normocapnic and hypercapnic obstructive sleep apnea patients (OSA). The rebreathing hypercapnic and hypoxic tests were performed using the computerized equipment (Lungtest, MES), according to Read's method. The ventilatory response to hypoxia was impaired in all OSA patients. Concerning the hypercapnic ventilatory response, there were no differences between the OSA patients with normal end-tidal PCO(2) and controls. Nine moderately hypercapnic OSA patients showed a right shift with a normal slope of the regression curve describing the relationship between the end-tidal PCO(2) and minute ventilation. In contrast, three severely hypercapnic OSA patients showed a right shift with a decreased slope of this regression curve. We conclude that awake OSA patients who developed hypercapnic ventilatory insufficiency showed an impaired hypercapnic defense reaction.
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PMID:Reflex respiratory responses to progressive hyperoxic hypercapnia and normocapnic hypoxia in normocapnic and hypercapnic obstructive sleep apnea patients. 1561 5

Time-dependent ventilatory responses to hypoxic and hypercapnic challenges, such as posthypoxic frequency decline (PHxFD) and posthypercapnic frequency decline (PHcFD), could profoundly affect breathing stability. However, little is known about the mechanisms that mediate these phenomena. To determine the contribution of specific carotid body chemostimuli to PHxFD and PHcFD, we developed a novel in situ arterially perfused, vagotomized, decerebrate rat preparation in which central and peripheral chemoreceptors are perfused separately (i.e., a nonanesthetized in situ dual perfused preparation). We confirmed that 1) the perfusion of central and peripheral chemoreceptor compartments was independent by applying specific carotid body hypoxia and hypercapnia before and after carotid sinus nerve transection, 2) the PCO(2) chemoresponse of the dual perfused preparation was similar to other decerebrate preparations, and 3) the phrenic output was stable enough to allow investigation of time-dependent phenomena. We then applied four 5-min bouts (separated by 5 min) of specific carotid body hypoxia (40 Torr PO(2) and 40 Torr PCO(2)) or hypercapnia (100 Torr PO(2) and 60 Torr PCO(2)) while holding the brain stem PO(2) and PCO(2) constant. We report the novel finding that specific carotid body chemostimuli were sufficient to elicit several phrenic time-dependent phenomena in the rat. Hypoxic challenges elicited PHxFD that increased with bout, leading to progressive augmentation of the phrenic response. Conversely, hypercapnia elicited short-term depression and PHcFD, neither of which was bout dependent. These results, placed in the context of previous findings, suggest multiple physiological mechanisms are responsible for PHxFD and PHcFD, a redundancy that may illustrate that these phenomena have significant adaptive advantages.
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PMID:Specific carotid body chemostimulation is sufficient to elicit phrenic poststimulus frequency decline in a novel in situ dual-perfused rat preparation. 1580 55

The physiopathology of obstructive sleep apnea syndrome is multifactorial. Gender and obesity status, as well as genetic, anatomic, and hormonal factors, together with ventilatory drive, interact in a diverse manner in the physiopathology and clinical expression of the disease. Obesity is the main risk factor, since increases in body mass index, visceral fat, and neck circumference are strong predictors of the disease. Progesterone increases the activity of the upper airway dilator muscles and therefore plays a protective role in premenopausal women. This explains the fact that the prevalence of the disease is higher in postmenopausal patients, in patients with polycystic ovary syndrome, as well as in males. Evidence supports the fact that, as individuals grow older, there is a decrease in muscle tonus, with a consequent reduction in the dimensions of the upper airway lumen. Craniofacial anomalies, such as in retrognathia or micrognathia, are accompanied by posterior positioning of the tongue and can result in narrowing of the upper airway lumen. Finally, decreased ventilatory drive has been detected in patients with obstructive sleep apnea syndrome and hypercapnia.
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PMID:Physiopathology of obstructive sleep apnea-hypopnea syndrome. 1756 74

The authors tested the hypothesis that in the high-altitude acclimatized fetus, hypercapnia has a significantly less effect on cerebral blood flow (CBF) and cerebral oxygenation than that in normoxic sea level controls. In the high-altitude acclimatized fetus (3801 m; maintained from day 30 of gestation to near term; n = 6), by use of a laser Doppler flowmeter with a fluorescent O (2) probe, the authors measured relative CBF (laser Doppler CBF [LD-CBF]), cortical tissue PO(2) (tPO(2)), and sagittal sinus oxyhemoglobin saturation (HbO(2)) in response to 20-minute hypercapnia. They also calculated cerebral O(2)delivery and cerebral fractional O(2) extraction. The authors compared these results to those obtained in near-sea-level control animals (low-altitude group). In response to hypercapnia (arterial PCO(2) = 63+/- 2 torr vs 42+/- 1 torr baseline), high-altitude fetuses showed similar increases in LD-CBF, cortical tPO(2), and sagittal sinus (HbO(2)) as compared with those responses seen in the fetus at low altitude. Nonetheless, these fetuses showed a significantly smaller decrease in cerebral fractional O(2) extraction compared to low-altitude fetuses. In response to hypercapnia in high-altitude, acclimatized, long-term hypoxic fetal sheep, the response of CBF and cerebral oxygenation did not differ significantly from that of low-altitude controls.
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PMID:Fetal hypercapnia in high-altitude acclimatized sheep: cerebral blood flow and cerebral oxygenation. 1763 16

CO(2) is an important metabolic product whose concentrations are constantly monitored by CO(2) chemoreceptors. However, the high systemic CO(2) sensitivity may not be achieved by the CO(2) chemoreceptors without neuronal network processes. To show modulation of network properties during hypercapnia, we studied brainstem neurons dissociated from embryonic rats (P17-19) in multielectrode arrays (MEA) after initial period (3 weeks) of culture. Spike trains of 33,622 pairs of units were analyzed using peri-event histograms (PEH). The amplitude of peri-central peaks between two CO(2)-stimulated units increased and the peak latency decreased during hypercapnia. Similar enhancement of synaptic strength was observed in those sharing a common input. These phenomena were not seen in CO(2)-unresponsive neurons. The amplitude of peri-central peaks between two CO(2) inhibited units also increased without changing latency. Over 60% CO(2)-stimulated neurons studied received mono-/oligosynaptic inputs from other CO(2)-stimulated cells, whereas only approximately 10% CO(2)-unresponsive neurons had such synaptic inputs. A small number of brainstem neurons showed electrical couplings. The coupling efficiency of CO(2)-stimulated but not CO(2)-unresponsive units was suppressed by approximately 50% with high PCO(2). Inhibitory synaptic projections were also found, which was barely affected by hypercapnia. Consistent with the strengthening of excitatory synaptic connections, CO(2) sensitivity of post-synaptic neurons was significantly higher than presynaptic neurons. The difference was eliminated with blockade of presynaptic input. Based on these indirect assessments of synaptic interaction, our PEH analysis suggests that hypercapnia appears to modulate excitatory synaptic transmissions, especially those between CO(2)-stimulated neurons.
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PMID:Hypercapnia modulates synaptic interaction of cultured brainstem neurons. 1796 65

Hypercapnic respiratory failure is usually caused by an overload of the respiratory muscles (respiratory pump). After treatment of the underlying disease, mechanical ventilation will achieve optimal treatment success and higher degrees of respiratory muscle unloading will improve the outcome in terms of lower PaCO (2) levels and improved exercise performance. Routinely assisted modes are being used for ventilation, where the patient has to trigger the ventilator with his effort. Controlled ventilation is usually applied in sedated patients lacking spontaneous breathing efforts that are necessary to trigger the ventilator. Controlled ventilation, however, is feasible in awake patients but requires operator expertise. In this process, the respiratory pattern of the ventilator has to be adapted to the patient's own respiratory pattern. Changing conditions require a re-adaptation of parameters. In order to automatise this complex and time-consuming operation, a time-adaptive mode (TA-mode) has been developed. This programmed mode incorporates a self-learning algorithm, primarily detecting the patient's respiratory pattern. The software then calculates a matching flow profile using a motion equation that gives consideration to resistance and compliance. The operator has to pre-select allowed ranges of parameters (especially in- and expiratory pressures, IPAP and EPAP). After detection of a stable respiratory pattern (usually after 10 - 20 breaths), the ventilator will slowly increase the calculated flow profile and achieve controlled ventilation without irritating respiratory centres of the brain. Respiratory drive will cease usually within three to five minutes. Restart of the respiratory drive, for example, after coughing or during REM sleep with an altered respiratory pattern will be detected as ventilator fighting and the programme will return to the analysis algorithm again. After the respiratory pattern has become stable, the ventilator will take over ventilation again. The new mode has been validated in an accreditation study. For this purpose we selected 21 patients with stable hypercapnic respiratory failure, most of whom (20) had previously been ventilated with a controlled T-mode and only one patient had previously been ventilated with an assisted mode and adapted them to the new ventilator under polygraphic surveillance. Each time seven patients were adapted to a T-, ST- and TA-mode, respectively. Two patients, however, could not be adapted to ST-mode ventilation and were switched to TA-mode. PCO (2) values before and after ventilation were not significantly different between modes. Patient satisfaction was rated very good in 34 %, good in 45 % and non-gratifying in 21 % of cases ventilated with TA-mode. Consideration has to be given to the fact that patients previously had been receiving optimal ventilator treatment. The TA-mode is a self-learning system, capable of copying the patients own breathing pattern while awake, in order to achieve complete unloading of the respiratory muscles through controlled ventilation during a circumscribed period.
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PMID:[Time-adaptive mode, a new ventilation form for the treatment of respiratory insufficiency--a self-learning system]. 1843 1


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