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

The airway pressure 100 msec after the onset of an inspiratory effort against a closed airway (P100, occlusion pressure) is theoretically a more accurate index of respiratory neuron motor output than ventilation. Occlusion pressure and ventilation responses to hypercapnia were compared in repeated trials in 10 normal subjects while in the seated and supine positions. During progressive hypercapnia changes in P100 were also compared to changes in tidal volume and inspiratory airflow. These studies show that occlusion pressure increases linearly with hypercapnia in both sitting and supine subjects. Changing from the seated to the supine position, or vice versa, had no significant effect on either ventilation or occlusion pressure responses to CO2. Correlations between P100 and ventilation or airflow rate were significantly higher than correlations between P100 and tidal volume or breathing frequency. Intermittent random airway occlusion had no effect on either ventilation or pattern of breathing during hypercapnia. Occlusion pressure responses were no less variable than ventilation responses in groups of subjects whether studied seated or supine. However, maintenance of a constant moderate breathing frequency (20 breaths per minute) reduced the interindividual variability in ventilation and occlusion pressure responses to hypercapnia.
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PMID:Comparison of occlusion pressure and ventilatory responses. 86 36

The effects of hypercapnia and inspiratory flow-resistive loading on mouth pressure during periods of arrested airflow were studied in conscious human subjects to determine the usefulness of inspiratory muscle force in the assessment of respiratory neural efferent activity. Hypercapnia increased the peak end-inspiratory mouth pressure (Ppeak) during complete airway occlusion and the pressures at 100, 200, and 300 ms after the onset of inspiration (P100, P200, P300). During rebreathing without added mechanical loads, P100 and Ppeak increased linearly with the electrical activity of the diaphragm and changes in P100 and Ppeak during hypercapnia correlated well with ventilatory responses to PCO2 (DELTA V/DELTA PCO2) suggesting that occluded mouth pressures are reliable measures of respiratory activity. In individuals with the greatest reduction in delta V/DELTA PCO2 during inspiratory flow-resistive loading, changes in P100 and Ppeak with PCO2 increased only minimally. In contrast, there was a much greater increase in occluded mouth pressures with hypercapnia in the presence of mechanical loading when inspiratory flow-resistive loading failed to depress delta V/DELTA PCO2. In all subjects, occluded mouth pressures were greater at any given PCO2 during mechanical loading than during free breathing. Mechanical loading resulted in augmented respiratory neural efferent activity unexplained by alterations in chemical stimulation.
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PMID:Effects of hypercapnia on mouth pressure during airway occlusion in conscious man. 93 47

Measurement of occlusion pressure in the airways within the first 100 msec of the inspiration (P100) is a simple noninvasive test for estimating the central inspiratory activity in patients. This test does not require any sophisticated diagnostic equipment, it is not burdensome and does not demand the patient's cooperation. The P100 criterion noticeably varies in healthy subjects, in patients with exacerbation of chronic respiratory failure, and in the immediate postoperative period. The use of the test has additional advantages in patients in critical conditions where the carrying out of different tests (hypoxia, hypercapnia) to estimate the central inspiratory activity is not feasible or unsafe for the patient.
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PMID:[Occlusion pressure P100 as a criterion of the central regulation of respiration in respiratory insufficiency and anesthesiological care]. 178 Dec 18

Eight healthy young men underwent two separate steady-state incremental exercise runs within the aerobic range on a treadmill with alternating periods of breathing with no load (NL) and with an inspiratory resistive load (IRL) of approximately 12 cmH2O.1-1.s. End-tidal PCO2 was maintained constant throughout each run at the eucapnic or a constant hypercapnic level by adding 0-5% CO2 to the inspired O2. Hypercapnia caused a steepening, as well as upward shift, relative to the corresponding eucapnic ventilation-CO2 output (VE - VCO2) relationship in NL and IRL. Compared with NL, the VE - VCO2 slope was depressed by IRL, more so in hypercapnic [-19.0 +/- 3.4 (SE) %] than in eucapnic exercise (-6.0 +/- 2.0%), despite a similar increase in the slope of the occlusion pressure at 100 ms - VCO2 (P100 - VCO2) relationship under both conditions. The steady-state hypercapnic ventilatory response at rest was markedly depressed by IRL (-22.6 +/- 7.5%), with little increase in P100 response. For a given inspiratory load, breathing pattern responses to separate or combined hypercapnia and exercise were similar. During IRL, VE was achieved by a greater tidal volume (VT) and inspiratory duty cycle (TI/TT) along with a lower mean inspiratory flow (VT/TI). The increase in TI/TT was solely because of a prolongation of inspiratory time (TI) with little change in expiratory duration for any given VT. The ventilatory and breathing pattern responses to IRL during CO2 inhalation and exercise are in favor of conservation of respiratory work.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of inspiratory resistive load on respiratory control in hypercapnia and exercise. 250 Dec 81

Hypercapnia in patients with pulmonary disease is believed to result from an interaction between mechanical lung impairment and intrinsic chemical respiratory drive. We tested this hypothesis in this study by examining the ventilatory (delta VE/delta PCO2) and occlusion pressure (delta P100/delta PCO2) responses to CO2 in 12 obese patients with no history of alveolar hypoventilation and correlating these with their ventilatory responses to abdominal surgery. Preoperatively the mean vital capacity (VC) was 78% +/- 6% standard error of the mean predicted, the delta VE/delta PCO2 was 1.56 +/- 0.26 L/min/torr, delta P100/delta PCO2 was 0.25 +/- 0.08 cm H2O/torr, the mean PaCO2 37.9 +/- 1.1 mm Hg, and mean PO2 77.6 +/- 3.7 mm Hg. Postoperatively the VC decreased to 56% +/- 6% of the preoperative value. PCO2 values at 24 hours increased in six patients, were unchanged in three, and decreased in three patients. However, over the entire spectrum of PCO2 change, both indexes of CO2 chemosensitivity correlated strongly with the postoperative change in PCO2 (r = -0.86 for delta VE/delta PCO2 and r = -0.66 for delta P100/delta PCO2). All six patients with a delta VE/delta PCO2 of 1.5 L/min/torr or less manifested postoperative increases in PCO2, while those with greater values did not (p = 0.005). In contrast, neither preoperative nor postoperative VC showed high correlations with postoperative PCO2 (r = -0.56 and -0.43, respectively). Thus ventilatory responses to CO2 predicted postoperative PCO2 at both ends of the spectrum; low responders hypoventilated while high responders hyperventilated. We conclude that in obese subjects, CO2 chemosensitivity plays a permissive role in determining the net ventilatory responses to situations that either mechanically load the respiratory system or modulate ventilation such as postoperative pain or analgesia.
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PMID:Chemical respiratory drive as a determinant of postoperative ventilation in the non-Pickwickian obese patient. 310 48

To evaluate the role of the cerebral cortex in the response to externally added inspiratory flow-resistive load, we studied 7 patients manifesting clinical presenile dementia of the Alzheimer's type. All subjects exhibited diffuse cerebral cortical atrophy on computerized tomography of the brain. The mean age of the group was 45.6 yr. The rebreathing technique was used to assess minute ventilation (VE) and occlusion pressure (P100) responses to progressive hypercapnia. Rebreathing runs were performed before and during the addition of an inspiratory flow-resistive load of 18 cm H2O.L-1.s. The respiratory control data of these patients were compared with data obtained by similar techniques in a matched normal volunteer control group. In the patient group, with the addition of load, the VE/PCO2 response slope decreased (p less than 0.005), whereas the P100/PCO2 response slope did not significantly change. In the control group, P100/PCO2 response slope increased with load to maintain ventilation. These results suggest that in presenile dementia, during added inspiratory load, the drop in VE is associated with an inadequate increase in respiratory neuromuscular output. This lack of load compensation in patients with presenile dementia suggests a role for the cerebral cortex in the response to externally added load.
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PMID:Respiratory control in presenile dementia. 333 57

This paper describes a system that was designed to evaluate ventilatory responses to hypercapnia, airway occlusion pressure (P100), as well as measuring ventilatory drive and timing. Parameters measured include minute ventilation (VE), breathing rate (f), tidal volume (VT), inspiratory time (TI), fractional inspiratory time (TI/TTot), mean inspiratory flow (VT/TI), and end tidal partial pressure of carbon dioxide (PETCO2). These measurements allow for a thorough analysis of abnormalities of neural and neuromuscular ventilatory drive. The system's architecture was based primarily on currently available microcomputer components designed for the IEEE 696 bus.
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PMID:Evaluating control of breathing utilizing an on-line microcomputer. 372 83

The ventilatory effects of inspiratory flow-resistive loading and increased chemical drive were measured in ten neonates during progressive hypercapnia in control and loaded states. Hypercapnia (mean increase PCO2 = 15-20) resulted from inspiring 8% CO2 in room air and inspiratory loading by a flow-resistive load = 100 cmH2O X l-1) X s. Hypercapnia produced an increase in group minute ventilation secondary to increasing tidal volumes and breathing frequencies. Loading shifted the minute ventilation-CO2 response to the right, and slopes decreased significantly (P less than 0.05) consequent to a significant decrease in the frequency-CO2 slopes (P less than 0.05), which became negative in four of the ten subjects. Mouth pressure measured at 100 ms after onset of inspiratory effort (P100) occlusion pressure-CO2 slopes measured in five subjects showed no significant increase with load application. Resistive loading produced significant increases in inspiratory time (P less than 0.02) and the inspiratory time/total breath time ratio (P less than 0.01). Airway occlusion elicited the Hering-Breuer reflex, with a significant increase in inspiratory time-to-total breath time ratio (P less than 0.01). The results show that the inspiratory resistive load produced ventilatory compromise in newborns and insufficient compensatory augmentation of central drive.
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PMID:Preterm infants: ventilation and P100 changes with CO2 and inspiratory resistive loading. 392 86

The ventilatory and occlusion pressure (P100) responses to hypercapnia, maximal inspiratory airway and transdiaphragmatic pressures, and the separate volume contributions of the rib cage and abdomen to tidal breathing were evaluated in 16 patients with chronic stable interstitial lung disease. Compared with those in the normal subjects, ventilation and P100 at a PCO2 = 55 mmHg were significantly higher (p less than 0.05 and p less than 0.01, respectively) in the patients with interstitial lung disease. However, the ventilatory and occlusion pressure responses to hypercapnia (delta VE/delta PCO2 and delta P 100/delta PCO2, respectively) were not significantly different between the groups. Maximal inspiratory airway pressure was significantly reduced in the patient group (p less than 0.05); maximal transdiaphragmatic pressure was also reduced but not significantly. At any given level of ventilation, tidal volume was decreased and breathing frequency increased in the patients with interstitial lung disease (p less than 0.05). The greater respiratory frequency was caused by reductions in both expiratory and inspiratory time. Because of smaller tidal volumes, rib cage expansion was reduced in the group of patients when compared with that in normal subjects during both spontaneous breathing and when compared at the same level of hypercapnia; abdomen volume was reduced to a lesser extent. We conclude that in patients with interstitial lung disease, non-chemical, presumably neural, mechanisms, increase respiratory drive and alter the breathing pattern. We speculate that both vagal mechanisms and mechanoreceptors in the chest wall sensitive to rib cage expansion contribute to these responses.
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PMID:Occlusion pressure and breathing pattern in patients with interstitial lung disease. 640 5

We studied the responses of ventilation and occlusion pressure (P100) to hypercapnia, with and without the application of an inspiratory flow-resistive load (12 cm H2O/L/sec), in eight control subjects and in eight subjects with obstructive sleep apnea who did not retain carbon dioxide while awake. The hypercapnic response was assessed by a modification of the Read rebreathing technique. For a given endtidal carbon dioxide, ventilation in control subjects was the same with or without load, and P100 was increased with loading. In contrast, the subjects with sleep apnea decreased their ventilation during loading and did not increase their P100 in response to loading. Relationships between ventilation and P100 were similar in the two groups both with and without load. We conclude that patients with occlusive sleep apnea do not exhibit the normal increase in neural drive to compensate for inspiratory flow-resistive loading.
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PMID:Control of breathing in obstructive sleep apnea. 669 97


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