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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using the intra-arterial 133xenon (133Xe) method, the cerebrovascular response to acute Paco2 reduction was studied in 26 unconscious, brain-injured patients subjected to controlled ventilation. The CO2 reactivity was calculated as delta in CBF/delta Paco2. The perfusion pressure was defined as the difference between mean arterial pressure and mean intraventricular pressure. Although the CO2 reactivities did not differ significantly from that in awake, normocapnic subjects, it was low in the acute phase of injury, especially in those patients with severe outcome in whom the brain-stem reflexes were often affected. An increase of the CO2 reactivity with time was observed, indicating normal response after 1-2 weeks. Chronic hypocapnia in six unconscious patients resulted in sustained CSF pH adaptation. The question whether a delay in CSF pH adapation exerts an influence on the CO2 reactivity, and the influence of cerebral lactacidosis on the CO2 response are discussed.
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PMID:The cerebrovascular CO2 reactivity during the acute phase of brain injury. 1 91

Acid-base derangements are encountered frequently in clinical practice and many have life-threatening implications. Treatment is dependent on correctly identifying the acid-base disorder and, whenever possible, repairing the underlying causal process. Bicarbonate is the agent of choice for the treatment of acute metabolic acidosis. Controversy surrounds the use of alkali therapy in lactic acidosis and diabetic ketoacidosis, but bicarbonate should clearly be administered for severe acidosis. In most patients with mild to moderate chloride-responsive metabolic alkalosis, providing an adequate amount of a chloride salt will restore acid-base balance to normal over a matter of days. In contrast, therapy of the chloride-resistant metabolic alkalosis is best directed at the underlying disease. When alkalemia is severe, administering hydrochloric acid or a hydrochloric acid precursor may be necessary. Treatment of respiratory acidosis should be targeted at restoring ventilation; alkali should be administered only for superimposed metabolic acidosis. The therapy of respiratory alkalosis is centred on reversal of the root cause; short of this goal, there is no effective treatment of primary hypocapnia. The coexistence of more than one acid-base disorder (i.e. a mixed disorder) is not uncommon. When plasma bicarbonate concentration and arterial carbon dioxide tension (paCO2) are altered in opposite directions, extreme shifts in pH may occur. In such cases, it is imperative that the nature of the disturbance is identified early and therapy directed at both disorders.
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PMID:Rational treatment of acid-base disorders. 219 65

It is well known that brain pH changes rapidly in acute hypercapnia or hypocapnia. The effect of acute isocapnic metabolic acid-base change on brain pH is less certain. To study this problem, acute isocapnic metabolic acidosis was induced by HCl or lactic acid infusions in rats, and recovery from acidosis was accomplished by NaHCO3 infusion. Brain pH was measured by 31P-nuclear magnetic resonance. Despite decreases in blood pH of 0.34 and 0.36 units, respectively, in less than 1 h of acid infusion and rapid recovery during bicarbonate infusion, brain pH was unaffected (ranging between 7.08 and 7.11) and was uncorrelated with blood pH. The blood pH minus brain pH gradient was eliminated by the acidosis. By contrast, hypoxia-induced endogenous lactic acidosis lowered blood and brain pH equivalently, but the fall in brain pH preceded that in blood. During normoxic recovery, brain pH overshot and became alkaline when blood pH was still significantly reduced and blood lactate levels were markedly elevated. Presumably, this is due to stimulated active H+ transport. The results demonstrate that brain pH is affected differently in metabolic, respiratory, and endogenous acid-base disturbances. Thus brain pH cannot be predicted solely from blood pH values.
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PMID:Brain pH in acute isocapnic metabolic acidosis and hypoxia: a 31P-nuclear magnetic resonance study. 230 94

Cerebrospinal fluid (CSF) lactate and pyruvate concentrations were determined in 16 patients with hepatic encephalopathy before and/or after treatment. CSF lactate was significantly increased to 1.92 +/- 0.11 mmol/l in hepatic encephalopathy before the treatment in comparison to 1.40 +/- 0.05 mmol/l in control subjects. In 9 of 11 patients with moderate or stage 2 encephalopathy, CSF lactate levels were below 2 mmol/l. In contrast, in 4 of 5 patients with stage 3-4 encephalopathy, CSF lactate levels were higher than 2 mmol/l. CSF lactate was decreased with the recovery of neurological symptoms by the treatment. These findings indicate that CSF lactate levels reflect the severity of metabolic impairment of the brain. Hypocapnia was frequently observed in these encephalopathic patients, and arterial PCO2 correlated inversely with CSF lactate and linearly with CSF HCO3-, suggesting that CSF lactic acidosis contributes to hyperventilation in hepatic encephalopathy. It is concluded from present results that metabolic disorder of neuronal cells might be one of the important factors for the development of hepatic encephalopathy.
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PMID:Cerebrospinal fluid lactate in patients with hepatic encephalopathy. 311 61

In humans alveolar ventilation (VA) is adjusted almost perfectly to the metabolic demands of mild and moderate exercise. For example, in exercise transitions and in the steady state, PaCO2 rarely deviates by more than 1 to 3 mmHg from the value at rest. This near-homeostasis contrasts to most other mammalian species; equines for example, demonstrate a progressive hypocapnia and alkalosis as exercise intensity is increased to moderate levels. In equines, the control systems seem programmed for a specific hyperventilation that contributes to maintenance of PaO2 homeostasis. Generally, during heavy exercise all species hyperventilate creating hypocapnia, increased PAO2, widened A-a O2 gradient, and PaO2 homeostasis. The origin of the metabolic ventilatory stimulus remains controversial. Evidence exists for: a) "neural" mediation, either central command or peripheral afferent in nature; and b) "humoral" mediation with an intra-thoracic metabolite receptor being a possibility. The mechanism of the species differences in hyperventilation during exercise does not appear to be due to species variation in chemoreceptor "fine tuning". Contrary to traditional thinking, recent findings suggest that the hyperventilation during heavy exercise might not be mediated by lactacidosis stimulation of chemoreceptors. The increase in VA during exercise is achieved efficiently in that airway diameter is modulated and the pattern of breathing and the recruitment of respiratory muscles are set to minimize the O2 cost of breathing. It has been postulated that mechanoreceptors in airways, lung parenchyma and the chest wall are important to efficient breathing. Their role and contribution to the exercise hyperpnea has been shown by reductions in respiratory neural output within breath when respiratory impedance is reduced via helium breathing. Hilar nerve afferents do not appear to be critical to this response. However, carotid chemoreceptors appear essential for "fine tuning" of VA when respiratory impedance is reduced. In most healthy exercising mammals, the efficiency component of the exercise stimulus does not compromise VA. There are two known major exceptions. One is the extremely fit human athlete during very high workloads when atypically there is minimal or no hyperventilation resulting in arterial hypoxemia. That indeed the high O2 cost of breathing compromises VA is indicated by hyperventilation and alleviation of hypoxemia with resistance unloading through helium breathing. A second example of a compromise of VA is that of a galloping racehorse at very high workloads.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Breathing during exercise: demands, regulation, limitations. 328 19

The cerebral vasomotor reactivity to arterial hypotension and hypocapnia was studied in 34 patients between the 3rd and 13th day after rupture of an intracranial saccular aneurysm. Using the intra-arterial xenon-133 injection method, regional cerebral blood flow (rCBF) and cerebral metabolic rate of oxygen (CMRO2) were measured. The intraventricular pressure and cerebrospinal fluid (CSF) lactate and pH levels were determined. The degree of vasospasm was measured on angiograms taken immediately following the rCBF study. The patients were graded clinically according to the system of Hunt and Hess. Cerebral autoregulation was intact in patients in good clinical condition, but was impaired in patients in poor clinical condition. There was a close correlation between the degree of vasospasm and the degree of autoregulatory impairment, which varied from focal disturbances to global impairment. Intracranial hypertension and CSF lactic acidosis were commonly found in association with vasoparalysis. Cerebrovascular response to hyperventilation was generally preserved, although often reduced. During hyperventilation, the cerebral perfusion pressure became elevated, and increases in CMRO2 were often found, even in patients with severe diffuse spasm and cerebral ischemia. The clinical significance of the results in relation to the treatment of delayed cerebral ischemia and to the use of intraoperative induced hypotension is discussed.
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PMID:Cerebrovascular reactivity in patients with ruptured intracranial aneurysms. 391 94

Five asthmatics aged 25-30 were studied during bicycle ergometer and treadmill exercise. Metabolic and ventilatory changes during exercise were compared with the degree of bronchoconstriction which followed exercise. In all patients bronchoconstriction was greater after treadmill exercise. Contrary to previous suggestions, exercise-induced bronchoconstriction did not seem to be caused by lactic acidosis, increase in minute ventilation, acidaemia, hypocapnia, or change in arterial Po(2)
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PMID:Metabolic changes preceding exercise-induced bronchoconstriction. 505 31

We hypothesized that part of the newborn tolerance of asphyxia involves strong ion changes that minimize the cerebral acidosis and hasten its correction in recovery. After exposure of newborn puppies to 15 or 30 min experimental asphyxia (inhalation of gas with fractional concentration of CO2 and of O2 in inspired gas = 0.07-0.08 and 0.02-0.03, respectively), blood lactate increased to 13.2 and 23.4 mmol/l, respectively, brain tissue lactate increased to 14.4 and 19.7 mmol/kg, and cerebrospinal fluid (CSF) lactate increased to 7.6 and 14.4 mmol/l. We presume that the tissue lactate increase reflects increases in brain cell and extracellular fluid lactate concentration. The lactate increase, a change that will decrease the strong ion difference (SID), [HCO3-], and pH, was accompanied by increases in Na+ (plasma, CSF, brain), K+ (plasma, CSF), and osmolality without change in Cl-. After 60-min recovery, plasma and brain lactate decreased significantly, but CSF lactate remained unchanged. [H+] recovery was more complete than that of the strong ions due to hyperventilation-induced hypocapnia. We conclude that during asphyxia-induced lactic acidosis, changes in strong ions occur that lessen the decrease in SID and minimize the acidosis in plasma and CSF. To the extent that the increase in brain tissue sodium reflects increases in intra-and extracellular fluid sodium concentration, the decrease in SID will be less in these compartments as well. In recovery, CSF ionic values change little; plasma and brain tissue lactate decrease with a similar time course, and the [H+] is rapidly returned toward normal by hypocapnia even while the SID is below normal.
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PMID:Newborn puppy cerebral acid-base regulation in experimental asphyxia and recovery. 632 80

In order to determine the influence of hyperthermia on respiratory, blood gas and acid-base changes in exercising birds, we exercised domestic fowl on a treadmill at ambient temperatures of 5, 20, 30 and 35 degrees C for 10 min at graded running speeds up to 4.3 km.h-1. Ventilation and gas exchange were measured continuously and arterial blood gases, pH and the concentration of lactic acid in arterial blood were measured in samples taken during the last minute of each run. During exercise at 5 degrees C rectal temperature did not change significantly from rest (isothermic condition) and there was no sign of thermal influence on respiratory pattern, such as was observed at higher ambient temperatures. At any given running speed, increased ambient temperature caused increased ventilation by an increase in respiratory frequency (f) together with a decrease in tidal volume (VT). Under isothermic conditions, at low running speeds, birds maintained an isocapnic hyperpnoea: arterial PCO2, PO2 and pH and oxygen extraction were unchanged. However at higher speeds (ca. greater than 2.5 km.h-1) some hyperventilation occurred with subsequent falls in arterial PCO2 and oxygen extraction. Arterial pH also fell significantly (P less than 0.01). During hyperthermic exercise, oxygen extraction, arterial PCO2 and bicarbonate concentration all fell significantly (P less than 0.01) and progressively with increasing work load, and birds hyperventilated at all running speeds. This produced a significant arterial hypocapnia and alkalosis at the lower speeds (P less than 0.05) but this was replaced by a hypocapnic metabolic acidosis at the higher running speeds. Blood lactate concentration rose steeply at speeds above ca. 2.5 km.h-1 but arterial pH fell by only 0.1 units or less partly as a result of buffering by blood bicarbonate. It is concluded that both hyperthermia and lactacidosis are causes of hyperventilation and arterial hypocapnia during heavy running exercise in birds. However, ventilatory adjustments similar to those observed in resting hyperthermic birds, viz. increased f and reduced VT prevent severe arterial hypocapnia from occurring in hyperthermic exercising birds.
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PMID:Effects of body temperature on ventilation, blood gases and acid-base balance in exercising fowl. 642 18

High frequency of bronchilitis, 70% of 1117 infants with respiratory infections, and clinical, radiological and laboratory features concerning partial tension of haematic gases, haematic lactate, enzymic activities of serum (CK, GPT, GOT) in 31 infants hospitalized with symptoms of shock in course of respiratory infections apparently affecting the upper respiratory tracts, are reported. This minimal respiratory pathology, evidenced in 3% of 1117 infants, defined as "minimal" viral pneumopathy, can be brought out trough a shock: lactacidosis, combined in half the cases with an increase of serum levels of CK and GPT and with normal PaO2 was ascertained in 87% of the cases. Three groups of bronchiolitis can be differentiated by haemogasanalytic monitoring: 1st group with a "serious" respiratory functional damage (hipercapnia hypoxemia), 14%. 2nd group with a "moderate" damage (normocapnia-hypoxemia), 20%. 3rd group with a "sligth" damage (hypocapnia-normoxemia), 66%. Decompensated shock is considered as a frequent occurrence and it is referred to the widespread involvement of the pulmonary circulation caused by the immunity-flogistic process.
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PMID:["Minimal" viral pneumopathies and respiratory virosis in Campagna in 1978: pathology for research]. 653 98


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