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

We investigated the relative contribution of peripheral and central chemosensory mechanisms to ventilatory responses to metabolic alkalosis in anesthetized cats by simultaneously measuring steady-state carotid body chemosensory activity and ventilation. The effects of graded steady-state levels of metabolic alkalosis at constant levels of arterial O2 and CO2 partial pressure (PaO2 and PaCO2, respectively) were studied first. Then the responses to isocapnic hypoxia and hyperoxic hypercapnia before and after the induction of a given level of metabolic alkalosis were studied. From the relationship between the carotid chemosensory activity and ventilation, the contribution of the two chemosensory mechanisms was estimated. The depression of ventilation that could not be accounted for by a decrease in the carotid chemosensory activity is attributed to the central effect. We found that metabolic alkalosis decreased both carotid chemosensory activity and ventilation at all levels of PaO2 or PaCO2. The ventilatory effect of alkalosis increased during hypoxia due to suppression of both peripheral chemosensory input and its interaction with the central CO2-H+ drive. During hyperoxia the central effect of alkalosis was predominant, although the peripheral effect increased with hypercapnia. We conclude that acute metabolic alkalosis suppresses both peripheral and central chemosensory drives, and its ventilatory effect grows larger with decreasing PaO2.
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PMID:Relative peripheral and central chemosensory responses to metabolic alkalosis. 631 76

This study examined urinary acidification shortly after recovery from chronic hypocapnia induced by hypoxemia. Distal acidification was evaluated by measuring the urinary PCO2 and urine-blood PCO2 difference (U-B PCO2) when blood PCO2 had returned to normal. In posthypocapnic rats, maximal alkalinization of the urine by acute sodium bicarbonate loading failed to increase urine PCO2 and U-B PCO2 to the level of posthypoxemic control rats and normal control rats with comparable blood pH and urine bicarbonate concentration. To test the hypothesis that decreased distal hydrogen ion secretion in posthypocapnic rats resulted from intracellular alkalosis secondary to protracted hypocarbia, posthypocapnic rats were exposed to hypercapnia of brief duration (30 min) and prolonged duration (120 min) in an attempt to restore distal acidification to normal. In posthypocapnic rats, hypercapnia of brief duration was associated with a significant increase in urine PCO2 and a fall in urine pH. Prolonged hypercapnia resulted in a marked increase in urine PCO2 and a further fall in urine pH. At any urinary bicarbonate concentration, however, the urine PCO2 and U-B PCO2 posthypocapnic rats exposed to hypercapnia were still significantly lower than in normal control rats identically subjected to prolonged hypercapnia and with comparable blood PCO2 and blood pH. Our findings indicate that distal acidification after abrupt recovery from chronic hypocapnia is decreased as if the kidneys were still under the influence of sustained hypocapnia. These findings could not be ascribed to extracellular alkalemia but could be explained by postulating that decreased urinary acidification resulted from persistence of cell alkalinity secondary to the accumulation of non-CO2 buffers generated during protracted hypocarbia. Alternatively, factors other than cell pH could mediate the adaptive decrease in distal hydrogen ion secretion of posthypocapnic rats.
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PMID:Suppression of distal urinary acidification after recovery from chronic hypocapnia. 641 9

The infrared CO2 analyzer continuously monitors the CO2 tension in exhaled air at end-tidal expiration. In experimental animals, we found a consistent relationship between PaCO2 and end-tidal CO2 (ET.CO2) in the normal steady state, and in acid-base disturbances (respiratory acidosis and alkalosis, and hypoperfusion acidosis). Paired data analyses of PaCO2 (X) and ET.CO2 (Y) yielded correlation coefficients of r = 0.98 (Y = 0.96X + 4.43) during progressive hypercarbia (PaCO2: 32----110 torr), and r = 0.93 (Y = 0.89X + 0.93) during hyperventilation hypocapnia (PaCO2: 41----14 torr). The relationship between PaCO2 and ET.CO2 was seen during hypovolemic shock if pulmonary perfusion was maintained uniform in all areas of lung. The ability of the ET.CO2 sensor to predict instantaneously the PaCO2 makes it attractive enough to be used in conjunction with the subcutaneous tissue pH(pHe) sensor in the management of acid-base disturbances. After hypercarbia (FiCO2 0.15 X 40 min; PaCO2/ET.CO2: 100/101 torr), when the dogs were returned to room air, abruptly both the ET.CO2 and pHe sensors were sensitive to the changes in Fi.CO2. But the response of the ET.CO2 was swifter. The advent of transcutaneous gas monitors has shown that intermittent blood gas analyses, however frequent, are inadequate for the monitoring of the rapidly altering blood gas status in the acutely ill. The ability of the pHe sensor to identify whole-body acidosis and alkalosis combined with the speed and ease of the ET.CO2 monitor in pinpointing hypercarbic and hypocarbic states makes this two-parameter system suitable for the continuous, noninvasive monitoring of the critically ill.
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PMID:End-tidal CO2 and tissue pH in the monitoring of acid-base changes: a composite technique for continuous, minimally invasive monitoring. 644 Sep 69

In order to determine the relative roles of O2 tension and content, CO2 tension, hydrogen ion concentration, arterial blood pressure, and cardiac output in the regulation of fetal cerebral blood flow (CBF), we used radioactively labeled microspheres to measure flow to 20 major brain regions in 24 chronically catheterized fetal lambs. We continually monitored fetal heart rate and blood pressure, and periodically measured arterial PO2, PCO2, pH, and hematocrit. In addition to CBF measurements during control periods, we measured CBF during: 1) hypoxia (O2 content less than 6 ml X dl-1; O2 tension less than 15 torr) induced by having the ewe breathe a gas mixture with low O2 concentration, 2) hypercapnia (PCO2 greater than 50 torr) induced by increasing the maternal inspired CO2, 3) acidosis and alkalosis (7.60 greater than pH greater than 6.60) induced by infusing lactic acid or bicarbonate into the fetus, and 4) hypotension (blood pressure less than 35 mm Hg) and hypertension (blood pressure greater than 55 mm Hg) induced by rapidly phlebotomizing or transfusing the fetus. We used multiple regression analysis and analysis of covariance to examine the dependence of total cerebral blood flow on arterial O2 tension and content, CO2 tension, pH, blood pressure, and cardiac output.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regional cerebral blood flow: studies in the fetal lamb during hypoxia, hypercapnia, acidosis, and hypotension. 644 Nov 42

Ventilatory regulation of intact, unrestrained lugworms Arenicola marina living in glass-tube artificial burrows was examined for values of inspired seawater PO2, PIO2, from 20 to 700 torr, at constant ambient pH and PCO2 values. The water ventilation rate and the respiratory characteristics of the ventilated seawater were measured. The water convection requirement and the corresponding specific rates of O2 uptake and CO2 production were calculated. The mean ventilatory water flow was a complex function of PIO2: decrease in hyperoxia, increase in hypoxia, decrease in extreme hypoxia. Compared to the normoxic responses, hyperoxia led to a hypercapnia (and acidosis) and moderate hypoxia to a hypocapnia (and alkalosis) in the expired water, variations which presumably reflect blood acid-base balance changes. Thus, as in other water breathers, the regulation of the organism's oxygenation may override the regulation of its acid-base balance. The lugworm's oxygen exchanger is highly efficient. However, below a critical partial pressure, PIO2 ca 120 torr, values of O2 consumption and ventilation decreased. A second critical O2 partial pressure appeared at PIO2 values between 80 and 40 torr; a 'switch-on' of anaerobic metabolism. These phenomena may be viewed as features of an adaptative respiratory strategy selected for in relation with the lugworm's particular peristaltic ventilatory mechanism and its intertidal mode of life.
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PMID:Ventilation and respiratory gas exchanges of the lugworm Arenicola marina (L.) as functions of ambient PO2 (20-700 torr). 644 Dec 15

On day 16 of the chick embryo, a catheter was implanted in the allantoic vein carrying arterialized blood, and a syringe was attached to the blunt end of the shell connecting to the air cell. This technique allowed for repetitive sampling and analysis of air cell gas and arterialized blood when these eggs were exposed to a He-O2 or SF6-O2 atmosphere. Exposure to He-O2 reduced the arterial CO2 tension(PaCO2) from 36 to 17 Torr and increased pH by 0.17 units; exposure to SF6-O2 increased PaCO2 from 37 to 62 Torr and reduced the pH by 0.14 units. These responses were brought about by changes in the gas conductance of the shell, resulting in a diffusive hypocapnia and respiratory alkalosis in He-O2 and a diffusive hypercapnia and respiratory acidosis in SF6-O2. During a 4-h exposure to these foreign gases the observed pH changes were smaller than predicted because of marked shifts of HCO3- into the blood (SF6-O2) or out of the blood (He-O2).
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PMID:Changes in acid-base balance of chick embryos exposed to a He or SF6 atmosphere. 679 Apr 88

In acute experiments on cats responses of the lung vessels to hypoxic and hypercapnic stimuli and the latters effect on minor circle hemodynamics were studied as well as the role of changes of the blood acid-alkaline balance and volume of ventilation in potentiation and blocking of the above responses. The alveolar hypoxia and hypercapnia being induced a reversed dependence between the relative mass of the lung area and reduction of its blood flow vasdseined Hyperventilation with hypoxic gas mixture inhibited the hypoxic vasoconstriction in respective lung area which seems to suggest a shift towards alkalosis of the blood in the area of gases respiratory diffusion. The autoregulation of the lung gas exchange is supposed to be the function of the respiratory dead space.
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PMID:[Analysis of pulmonary vasomotor responses to alveolar hypoxia and hypercapnia]. 679 10

Asystole can be the presenting ECG finding of accidental hypothermia when the core temperature is less than 28 degrees C. Even two hours of persistent asystole does not represent irreversible cardiac compromise. With cardiopulmonary support and active rewarming, resuscitation and survival without serious sequelae can be achieved. Case reports and electrophysiology studies suggest that asystole is a primary manifestation of hypothermia potentiated by carbon dioxide retention. However, ventricular fibrillation in this setting is probably a secondary complication of resuscitation efforts, being precipitated by hypocapnic alkalosis, physical manipulation of the heart, and rewarming.
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PMID:Recovery after prolonged asystolic cardiac arrest in profound hypothermia. A case report and literature review. 698 23

Pathophysiologic ecologic and therapeutic study was made on respiratory disturbances, especially on hypercapnia in patients with lung tuberculosis. 1) Of all in-patients (497 cases), 192 (38.6%) had respiratory disturbances, among which 70 cases (14.1%) exhibited hypercapnia. 2) Of these hypercapnic patients, about one-third (31.4%) were after thoracoplastic surgery, the main disturbances being restrictive in nature. In the half of non-operative cases, obstruction and inadequate gas mixing were the main cause for hypercapnia. 3) Critical values for inducing hypercapnia were % VC 45 for patients with restrictive disturbances and FEV1-0%/expected VC 40 for hypercapnic patients. 4) Significant band in the PaCO2 similar to (HCO-3) regression chart in patients (20 cases) with chronic stable hypercapnia showed a linear relationship with an increasing PaCO2, given by an equation, (HCO-3)p = 7.7 + 0.43 PaCO2 (PaCO2 45 -- 113 mmHg, SD = +/- 1.2, r = 0.99). Twelve percent of the unstable patients (100 cases) showed an alkalosis (pH greater than 7.45) over the range above 45 mmHg of PaCO2. 5) Even in patients with normal pH values, administered HCO-3 was estimated to move into the intracellular or interstitial fluid. 6) Increase in oxygen consumption was greater with increasing ventilation volume in hypercapneic patients. Even in these patients, voluntary or drug-induced hyperventilation caused a decrease in PaCO2, resulting in an amelioration of suppressed respiration under oxygen or even pethidine HCl administration. Discussion was made on the usefulness of these therapies on patients with hypercapnia.
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PMID:[Studies on hypercapnia in patients with lung tuberculosis (author's transl)]. 723 19

The role of the carotid body chemoreflex in the ventilatory acclimatization to chronic hypoxia was studied in the unanesthetized goat and sheep. The time-cours of changes in ventilation, PCO2, pH and PO2 of arterial blood and cisternal fluid (CF) were measured before and following exposure to a simulated altitude of 3660-5000 m, with and without intact carotid sinus nerves. At sea level, after section of carotid sinus nerves most animals hypoventilated chronically, and developed mild arterial hypoxemia and hypercapnia. Upon exposure to acute hypoxia, all of the intact animals hyperventilated and CF pH increased from 7.310 to 7.380 whereas after chemodenervation, the increase in ventilation was small and delayed, and CF pH decreased from 7.285 to 7.143. During exposure of the intact animals to chronic hypoxia, hyperventilation accompanied by decreases in arterial and CF P CO2 reached its peak in two days; these changes partially subsided during the next few days. Partial compensation of respiratory alkalosis occurred during the first day. In contrast, several chemodenervated animals died during chronic hypoxia; the survivors showed either a small decrease or an increase in Pa CO2. Thus, an intact peripheral chemoreflex drive during hypoxia is necessary for ventilatory acclimatization which raises the arterial and presumably tissue PO2 in spite of alkalosis. The new proposal is that a central tissue metabolic acidosis resulting from a direct effect of acute hypoxia is partly compensated as hypoxia is prolonged. This central compensation decreases ventilatory drive and hence opposes the ventilatory acclimatization during chronic hypoxia initiated by the peripheral chemoreflexes.
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PMID:Role of carotid chemoreflex in respiratory acclimatization to hypoxemia in goat and sheep. 732 94


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