Acid-base response to acute carbon dioxide changes in chronic obstructive pulmonary disease.

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The influence of the chronic arterial carbon dioxide tension on the acid-base response to acute change in arterial carbon dioxide tension was studied in patients with chronic obstructive pulmonary disease. Acute changes in arterial carbon dioxide tension were produced experimentally by having the patients breathe various mixtures of carbon dioxide in air and by hyperventilation. Acute changes in arterial carbon dioxide tension occurred clinically during oxygen-induced hypoventilation, followed by ventilator therapy. The acute acid-base response was expressed as the ratio of change in arterial hydrogen ion concentration to change in arterial carbon dioxide tension. This ratio was inversely and linearly related to chronic values of arterial carbon dioxide tension and plasma bicarbonate concentration. The more efficient buffering of acute changes in carbon dioxide tension in patients with chronic obstructive pulmonary disease with hypercapnia was attributed both to high chronic bicarbonate concentrations and...

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New FindingsWhat is the central question of this study?The relationship between changes in cerebral blood flow and arterial carbon dioxide tension is used to assess cerebrovascular function. Hypercapnia is generally evoked by two methods, i.e. steady-state and transient increases in carbon dioxide tension. In some cases, the hypercapnia is immediately preceded by a period of hypocapnia. It is unknown whether the cerebrovascular response differs between these methods and whether a period of hypocapnia blunts the subsequent response to hypercapnia.What is the main finding and its importance?The cerebrovascular response is similar between steady-state and transient hypercapnia. However, hyperventilation-induced hypocapnia attenuates the cerebral vasodilatory responses during a subsequent period of rebreathing-induced hypercapnia.Cerebral vasomotor reactivity (CVMR) to changes in arterial carbon dioxide tension () is assessed during steady-state or transient changes in . This study tested the following two hypotheses: (i) that CVMR during steady-state changes differs from that during transient changes in ; and (ii) that CVMR during rebreathing-induced hypercapnia would be blunted when preceded by a period of hyperventilation. For each hypothesis, end-tidal carbon dioxide tension () middle cerebral artery blood velocity (CBFV), cerebrovascular conductance index (CVCI; CBFV/mean arterial pressure) and CVMR (slope of the linear regression between changes in CBFV and CVCI versus) were assessed in eight individuals. To address the first hypothesis, measurements were made during the following two conditions (randomized): (i) steady-state increases in of 5 and 10 Torr above baseline; and (ii) rebreathing-induced transient breath-by-breath increases in . The linear regression for CBFV versus (P = 0.65) and CVCI versus (P = 0.44) was similar between methods; however, individual variability in CBFV or CVCI responses existed among subjects. To address the second hypothesis, the same measurements were made during the following two conditions (randomized): (i) immediately following a brief period of hypocapnia induced by hyperventilation for 1 min followed by rebreathing; and (ii) during rebreathing only. The slope of the linear regression for CBFV versus (P < 0.01) and CVCI versus (P < 0.01) was reduced during hyperventilation plus rebreathing relative to rebreathing only. These results indicate that cerebral vasomotor reactivity to changes in is similar regardless of the employed methodology to induce changes in and that hyperventilation-induced hypocapnia attenuates the cerebral vasodilatory responses during a subsequent period of rebreathing-induced hypercapnia.

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  • 10.1164/arrd.1970.102.6.921
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In contrast to previous studies in which arterial hypoxia in patients with chronic obstructive pulmonary disease did not appear to be a major factor influencing their subsequent ventilatory response to an oxygen test, the degree of pre-existing hypoxia in this study of 151 patients was significantly correlated with the amount of ventilatory depression observed during subsequent oxygen administration. On the other hand, arterial pH, which was of high significance in other studies, had the lowest correlation in this study. The variability of ventilatory responses observed by others in smaller groups of patients has been confirmed, and no combination of factors related to arterial carbon dioxide tension, arterial oxygen tension, or pH could be identified to account for this variability. Patients who manifested a priority for diminution of dyspnea rather than a constancy of arterial carbon dioxide tension did not correspond to the bronchitic type B patients of Burrows and associates, because in this study, pa...

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The effect of endotracheal suctioning on cerebral haemodynamics was investigated in 29 newborn infants with a mean gestational age of 31 weeks (range 25-40 weeks). Prior to one of two suctioning procedures, the inspiratory fraction of oxygen was increased by 10%. Brain oxygenation and total haemoglobin concentration were estimated continuously by near infrared spectroscopy. Mean arterial blood pressure, arterial blood oxygen saturation and carbon dioxide tension were recorded simultaneously. Brain oxygenation decreased in parallel with arterial oxygen saturation during suctioning. Preoxygenation ameliorated the decrease in brain oxygenation and arterial oxygen saturation whereas there was no benefit with regard to the changes in total haemoglobin concentration, carbon dioxide tension or mean arterial pressure. Changes in total haemoglobin concentration were related closely to concomitant changes in carbon dioxide tension (p less than 0.0001) but unrelated to changes in mean arterial pressure or arterial oxygen saturation. Our findings suggest that cerebral blood volume may react to changes in carbon dioxide tension during endotracheal suctioning in mechanically ventilated neonates. Apparently, preoxygenation prior to suctioning does not ameliorate the stress in normoxic infants.

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The influence of changes in pH and the partial pressure of carbon dioxide in arterial blood on the neuromuscular blocking effect of a single dose of tubocurarine or dimethyl tubocurarine was investigated in rabbits. The sciatic nerve was stimulated supramaximally at a rate of 3 per second and the electrical response of the gastrocnemius muscle was recorded; the amplitude of the first and fourth response was measured. During the period of spontaneously subsiding block after a single injection of the blocking agent, a shift in the arterial pH was produced either with or without a change in carbon dioxide tension. An increase of the block during this period was always considered significant but a decrease of the block only if it was followed by a spontaenous increase. The action of tubocurarine increased during acidosis and diminished during alkalosis. This effect was greater during metabolic alkalosis and acidosis, corresponding to a more rapid shift in pH, than during respiratory alkalosis and acidosis, but no qualitative difference was observed. The effect of a shift in pH is explained by changes in the potency of tubocurarine. The action of dimethyl tubocurarine was not influenced by changes in pH or carbon dioxide tension.

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The results of pulmonary function tests in 663 patients and pulmonary vascular resistance in 136 patients were evaluated in relation to prognosis. The studies included spirogram, lung volumes, arterial blood gases, nitrogen washout, lung recoil at total lung capacity, airway resistance, diffusing capacity, and pulmonary vascular resistance. Forced expired volume in 1 second contributed significantly to predicting survival. Other tests probably contributed to predicting survival independent of 1-second forced expiratory volume. These tests were diffusing capacity for carbon monoxide, recoil pressure at total lung capacity, radiographic emphysema, arterial carbon dioxide tension, and single breath nitrogen washout. Decrease in 1-second forced expiratory volume averaged 52 ml per year. Changes from one follow-up period to another in any 1 patient showed considerable variability.

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  • Jan 1, 1994
  • European Journal of Cardio-Thoracic Surgery
  • P Fallon + 5 more

Neurological impairment may occur following cardiopulmonary bypass (CPB) and the effect of CPB on cerebrovascular control may be important in the mechanism of cerebral injury. We have used near infrared spectroscopy (NIRS) to observe cerebral haemodynamics non-invasively before and during CPB. We measured the change in cerebral blood volume (CBV) associated with changing PaCO2 (CBVR). Patients (n = 19) were aged from 1 to 135 (median 14) months. The cerebral blood volume response was determined pre-operatively at normothermia under the influence of standardised anaesthesia employing isoflurane (up to ET conc 0.5%) and during steady-state hypothermic bypass (22-32 degrees C) at an arterial pump flow rate of 1.9-2.4 lm-2.min-1. Complete data was available for 10 patients. The relation between CBV, arterial carbon dioxide tension (PaCO2), mean arterial pressure (MAP) and central venous pressure (CVP) was examined using analysis of covariance (P < or = 0.05) was accepted as significant). The change in CBV associated with changing PaCO2 was corrected for the effects of MAP and CVP. Preoperatively the median CBVR was 0.130 (25th-75th percentile 0.079-0.243) ml.100 g-1.kPa-1 and during hypothermic bypass the median CBVR was 0.093 (25th-75th percentile 0.026-0.255) ml.100 g-1.kPa-1. These values were compared with our reference range derived for normal conscious children using the Kruskal-Wallis test. There was not statistically significant difference between the three groups (P = 0.35). These results, indicating preservation of CBVR during the conditions of anaesthesia and bypass used, are consistent with the observations of previous authors who measured cerebral blood flow response to carbon dioxide by a variety of other methods. Near infrared spectroscopy is proving to be a reliable, non-invasive technique for the investigation of cerebral haemodynamics during CPB.

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