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

The effects of hypercapnia and hypocapnia on respiratory resistance were studied in 15 healthy subjects and 30 asthmatic subjects. Respiratory resistance (impedance) was measured with the pseudo-random noise forced oscillation technique while the subjects rebreathed from a wet spirometer in a closed respiratory circuit in which end tidal carbon dioxide tension (PCO2) could be controlled. Hypercapnia was induced by partially short circuiting the carbon dioxide absorber, and hypocapnia by voluntary hyperventilation. The circulating air was saturated with water vapour and kept at body temperature and ambient pressure. A rise of end tidal PCO2 of 1 kPa caused a significant fall in respiratory resistance in both normal and asthmatic subjects (15% and 9% respectively). A fall of PCO2 of 1 kPa did not cause any significant change in impedance in the control group. In the asthmatic patients resistance increased by 13%, reactance fell by 45%, and the frequency dependence of resistance rose 240%. These findings confirm that hypocapnia may contribute to airway obstruction in asthmatic patients, even when water and heat loss are prevented.
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PMID:Effects of hypercapnia and hypocapnia on respiratory resistance in normal and asthmatic subjects. 190 37

We studied the breathing pattern and pulmonary function at rest, and ventilatory responses to progressive hypoxia and hypercapnia in 7 awake patients who had undergone esophageal-carcinoma resection with sectioning of the right pulmonary vagal branch by lymphadenectomy. Twelve control patients, who had received the same surgery without vagotomy, were also studied by the same protocol. Two months after the operation, both patient groups demonstrated substantial depressions in FVC and FEV1.0, and slight augmentations in breathing frequency, minute ventilation, and occlusion pressure at 0.2s (P0.2) at rest. In the vagotomized group, the occlusion pressure responses to hypercapnia (delta P0.2/delta PaCO2) and hypoxia (delta P0.2/delta SaO2) in terms of response curve slope increased from 1.3 +/- 1.2 to 1.9 +/- 1.1 cm H2O/Torr and from 0.29 +/- 0.19 to 0.88 +/- 0.53 cm H2O/% (p less than 0.05), respectively. Contrary to the vagotomized patients, the nonvagotomized control group exhibited no significant changes in ventilatory chemosensitivities. Furthermore, when comparing the control and vagotomized groups, postoperative ventilatory chemosensitivity responses in terms of both hypercapnic and hypoxic occlusion pressure responses were significantly higher in the latter. We suggest that (1) due to the development of the substantial mechanical limitation in pulmonary functions, the Hering-Breuer inflation reflex became activated after surgery, and (2) a diminished Hering-Breuer reflex effect to inhibit the respiratory centers by unilateral vagotomy may have resulted in augmented ventilatory chemosensitivities.
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PMID:Effect of unilateral pulmonary vagotomy on respiratory control in man. 212 37

Animal studies have demonstrated that mechanical ventilation with high peak inspiratory pressure (PIP) results in acute lung injury characterised by hyaline membranes, granulocyte infiltration and increased pulmonary and systemic vascular permeability. This can result in progressive respiratory failure and death. In surfactant deficient lungs this occurs with tidal volumes (Vt) as low as 12 ml/kg, and PIP as low as 25 cm H2O, values which are frequently used clinically. The mechanisms resulting in this form of ventilator induced lung injury are not clear, but it appears to result from global or regional overdistension of the lung or terminal airways. It can be prevented or reduced in severity in some animal models by the use of PEEP. It is suggested that the use of high PIP in some patients may result in progressive deterioration of their ARDS, possibly contributing to mortality both from respiratory failure and other causes. It may be very important to limit PIP by reducing Vt even if this results in hypercapnia and a deterioration of oxygenation in the short term.
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PMID:Ventilatory management of ARDS: can it affect the outcome? 219 41

Both hypercapnia and tracheal irritation are known to constrict the airways in animals. To see whether similar responses occur in humans, we investigated tracheal smooth muscle (TSM) responses to hypercapnia and tracheal irritation with water in 14 paralyzed and anesthetized humans. TSM tone was monitored by measuring the pressure in the saline-filled cuff of the endotracheal tube. Although, tracheal irritation caused TSM constriction in 10 of 14 patients, 4 patients showed no TSM response. Administration of intravenous atropine attenuated the TSM constriction response. Hypercapnia did not cause any change in TSM tone in any of the 14 patients. These results indicate that in paralyzed and anesthetized humans, there exist interindividual differences in the TSM responses to tracheal irritation and that hypercapnia cannot be an effective stimulus for the TSM constriction.
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PMID:Effects of tracheal irritation and hypercapnia on tracheal smooth muscle in humans. 222 49

Using awake, chronically catheterized newborn pigs, we measured cerebral blood flow (CBF), net cerebral vascular 6-keto-prostaglandin F1 alpha production, and cerebral metabolic rate of oxygen (CMRO2) during hypercapnia and during hypercapnia at increased mean airway pressure (Paw), both before and after treatment with indomethacin. CBF nearly doubled during hypercapnia. The hypercapnia-induced cerebral hyperemia was maintained when Paw was increased from 3 +/- 2 to 16 +/- 4 cm H2O during hypercapnia. Sagittal sinus pressure increased in proportion to the increase in Paw, and cardiac output was unchanged. Net cerebral production of 6-keto-prostaglandin F1 alpha increased from 9 +/- 1 to 15 +/- 1 ng/min/100 g tissue during hypercapnia and increased dramatically to 57 +/- 1 ng/min/100 g when hypercapnia was coupled with an increase in Paw. CMRO2 was not changed by either hypercapnia or increased Paw. After indomethacin, CBF decreased and cerebral vasodilation to hypercapnia did not occur. After indomethacin, adding increased Paw during hypercapnia dropped CBF below baseline, adversely affecting CMRO2. These results suggest that cerebral hypercapnia hyperemia requires brain prostanoid production and that when Paw is increased during hypercapnia, the contribution of prostanoids to maintaining CBF is increased. Increasing ventilation pressure during hypercapnia in piglets pretreated with indomethacin compromises CBF sufficiently to reduce CMRO2.
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PMID:Pressure ventilation increases brain vascular prostacyclin production in newborn pigs. 228 59

During wet dives in a hyperbaric chamber to 6.8 atm abs (690 kPa), air breathing subjects were experimentally exposed to external breathing resistance. Two of them were, unbeknownst to themselves, severely incapacitated. In the first incident the subject had been exercising for 25 min (end-tidal PCO2 60-65 mmHg, 7.3-8.0 kPa) when the breathing resistance was rapidly increased from low to very high (requiring pressure swings of 80 cmH2O, 8 kPa, peak to peak). He functioned normally (end-tidal PCO2 72 mmHg, 9.6 kPa) for about 100 s but 20 s later he was confused and irrational. After being extracted from the water (end-tidal PCO2 above 90 mmHg, 12 kPa), he lost consciousness for about 60 s. In the second incident the subject was exercising and breathing against a high resistance (pressure swings of 50-55 cmH2O, 5.0-5.6 kPa). His end-tidal PCO2 was high (65-68 mmHg, 8.7-9.3 kPa) throughout the exercise period, and after 24 min he reported mild dyspnea. A few seconds later he became confused. In other experiments both subjects voluntarily terminated experiments when the breathing resistance became overwhelming. These 2 subjects generally had high end-tidal PCO2 levels, but 1 other subject with end-tidal PCO2 levels in the same range never experienced any problems. These incidents indicate that severe hypercapnia does not necessarily correlate with dyspnea and that severe disturbances in mental function due to hypercapnia can develop suddenly when high breathing resistance is encountered in diving.
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PMID:CO2 retention with minimal symptoms but severe dysfunction during wet simulated dives to 6.8 atm abs. 228 42

Between October 6, 1986 and September 17, 1987, 11 patients underwent insertion of mandibular dental prostheses by the same oral surgeon. Three patients suffered cardiac arrest during surgery and subsequently died. Two of the patients who died had received general anaesthetics and the other had intravenous sedation given by three different anaesthetists. All three patients arrested suddenly, developing profound cyanosis and electrical mechanical dissociation, underwent prolonged resuscitative efforts, and had marked hypoxaemia and hypercapnia, despite cardiopulmonary resuscitation. Two other patients had signs of injection of air but survived, one suffering cardiac collapse and the other sustaining massive subcutaneous emphysema. Air embolism was produced by inadvertent injection of a mixture of air and water, passing through the hollow dental drill, directly into the mandible to the facial and pterygoid plexus veins and thence to the superior vena cava and right atrium.
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PMID:Fatal air embolism during dental implant surgery: a report of three cases. 227 34

Respiratory arrests occur in the clinical setting of respiratory failure, but the mechanism is unclear. We used a dog model with increased inspiratory resistance and hypoxemia to explore the cause. We hypothesized that respiratory muscle fatigue (RMF) played a role in these respiratory arrests, and that the combination of hypoxia and resistive loading would produce respiratory arrest by the mechanism of RMF. Our preparation had transdiaphragmatic pressures that were 40% of maximum (Pdimax = 46.3 +/- 10.0 cm H2O) and progressive hypoxia resulting in a final arterial PO2 of 38 +/- 9 mm Hg and a phrenic vein O2 content of 1.8 +/- 1.1 mg/dl. Instead of failure associated with carbon dioxide retention and RMF, we saw a rapid decrease in tidal volume and respiratory rate, leading to apnea over 30 to 60 s while the diaphragm still responded with significant pressure generation when externally stimulated. These results suggest that respiratory muscle fatigue may not be a major factor in respiratory arrests associated with inspiratory loading and hypoxia, but that suppression of central drive, induced by the combination of inspiratory loading and hypoxemia, may be important.
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PMID:The mechanism of respiratory arrest in inspiratory loading and hypoxemia. 232 56

Arousal from sleep in response to asphyxia can be a lifesaving event. However, the mechanisms responsible for this important arousal response are uncertain. A unifying hypothesis is that arousal results from the increased respiratory effort that occurs as a result of ventilatory stimulation. If this is true, the magnitude of this effort during the breaths immediately preceding arousal from sleep should be similar regardless of the stimulus. Therefore, the negative inspiratory pleural pressure during the breaths preceding arousal would be similar, whether stimulated by added inspiratory resistive load, hypoxia, or hypercapnia. To test this hypothesis, we studied eight young, healthy men during full-night sleep studies. We measured their electroencephalography (EEG), electromyography (EMG), electrooculography (EOG), inspired ventilation (VI), end tidal PCO2 (PETCO2), O2 saturation, and esophageal pressure (esophageal balloon) while inducing arousal from non-REM sleep using (1) a 30-cm H2O/L/s added resistive load, (2) progressive hypoxia, and (3) progressive hyperoxic hypercapnia. All subjects were eventually aroused following the addition of the 30-cm H2O/L/s added load and during progressive hypercapnia. However, only six of the eight men were aroused when the O2 saturation was reduced to a minimum of 70%. For each stimulus, arousal occurred at very different levels of ventilation and arterial chemistry (SaO2 and CO2). However, ventilatory effort for each subject was similar at the point of arousal regardless of the stimulus. The peak-negative esophageal pressure for the single inspiration preceding arousal (for the six subjects arousing with all three stimuli) was 16.8 +/- 1.4 cm H2O for added resistive load, 15.0 +/- 2.4 cm H2O for hypoxia, and 14.7 +/- 2.1 cm H2O for hypercapnia. We conclude that increasing ventilatory effort may be the stimulus to arousal from sleep independent of the source of this rising drive to breathe.
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PMID:The influence of increasing ventilatory effort on arousal from sleep. 238 92

The right ventricular responses to mild hypocarbia and hypercarbia were studied in 18 anesthetized and paralyzed patients following coronary artery bypass surgery. Maintaining constant tidal volume (8 ml.kg-1), FIO2 (0.5), and PEEP (5 cm H2O), the ventilator rate was varied to sequentially produce: 1) normocarbia (PaCO2, 38.3 +/- 2.5 mmHg; mean +/- SD), 2) hypocarbia (PaCO2, 33.2 +/- 2.8 mmHg), 3) hypercarbia (PaCO2, 49.8 +/- 2.9 mmHg) and 4) normocarbia (PaCO2, 38.8 +/- 3.6 mmHg). Pulmonary and right ventricular hemodynamics were assessed using a rapid-response pulmonary artery catheter after 10 min of stabilization at each PaCO2. Pulmonary and right ventricular hemodynamics remained unaffected by slight hypocarbia. In contrast, hypercarbia increased pulmonary vascular resistance by 54% (P less than 0.001) and mean pulmonary artery pressure by 34% (P less than 0.001). This was accompanied by a 24% (P less than 0.001) increase in right ventricular end-diastolic volume, a 38% (P less than 0.001) increase in right ventricular end-systolic volume, and a 20% decrease (P less than 0.001) in right ventricular ejection fraction. Despite an increase in right ventricular afterload, stroke volume was maintained unchanged because of a 45% (P less than 0.001) increase in right ventricular stroke work index. Although the patients maintained pulmonary blood flow during hypercarbia using preload augmentation, compensatory reserve might be exceeded in patients with more compromised right ventricular function.
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PMID:Right ventricular response to hypercarbia after cardiac surgery. 239 25


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