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At least 19 recordsLinked to original sources
PubMed1975

[Artificial hyperventilation in head injury. I. Spontaneous hyperventilation and assisted ventilation (author's transl)].

The present study was desined to clarify the roles of artificial hyperventilation in management of the patients with cerebral injury. Here reported is the first part of the serial studies and concerned with general informations about hyperventilation. The measurements of PaCO2, minute ventilation volume (VE), dead space (VD), tidal volume (VT), cardiac output (by dye dilution method), oxygen consumption (by Fick' principle) and oxygen equilibrium were performed in the patients suffering from acute, severe head injury. And the effect of assisted ventilation on them were investigated (using pressure-limited respirator). 1. There was a common finding that marked and sustained increase in VE, VA (alveolar ventilation), and decrease in PaCO2 existed during the first week of injury. 97% of both VE and VA were above normal and mean value of PaCO2 was 29-33 mmHg. The syndrome of spontaneous hyperventilation was evidently more prominent in the nonsurvived group of patients. It was noteworthy that increased VE (or VA) was dependent neither on VD or pulmonary dysfunction nor on metabolic acidosis of arterial blood. The relation of VA to base excess in head injury was well contrasted to that of acute CO poisoning. 2. Assisted ventilation resulted in increased VT and decreased respiratory rate, and little change in VE. Consequently, PaCO2 changed only from 33.0 to 29.4 mmHg as a mean of entire series of patients. But when the influence affected by hypoxemic drive was subsided, a significant reduction of PaCO2 was disclosed following assisted ventilation. The assisted ventilation with pure oxygen was also associated with reduced cardiac output (from 6.0l/min to 5.3l/min), though the oxygen consumption changed variedly among the patients. 3. The fact was confirmed that both hypocapnea and alkalosis produced the left-sised shift of oxygen dissociation curve, decrease in P50 (P02 at 50% saturation of oxygen), and in addition, narrowed arterio-mixed venous oxygen difference. The changes of artero-mixed venous oxygen saturation difference which were calculated at 100 mmHg of PaO2 and 40mmHg of mixed venous PO2 were in a linear fashion with those of P50. Apart from the problems on injured brain, the beneficial and non-beneficial effects of hyperventilation were further discussed. The availability and inidcation of artificial hyperventilation should be precisely evaluated later, in a comprehensive manner with the subsequent studies (Part 2 and 3) on cerebral metabolism and intracranial pressure.

Brain Injuries↗
PubMed1979

[Hyperventilation and airway resistance. Bronchial spasms after hyperventilation].

Airway resistance, FEV1.0 and lung volume were measured by body plethysmography before and after voluntary hyperventilation. In normal subjects, resistance increased to 130--140% of the initial value measured before hyperventilation. The same increase was observed in silicosis patients without chronic obstructive bronchitis. Asthmatic patients in an asymptomatic phase showed a rise in airway resistance to an average of 255% of the nearly normal initial values, and also a reduction in FEV1.0. In normal subjects and asthmatic patients, the administration of bronchodilators inhibits the rise in airway resistance induced by hyperventilation. The hyperventilation test can be used to identify increased susceptibility to bronchoconstriction.

Asthma↗
PubMed1975

Physiologic effects of hyperventilation and phlebotomy in baboons: systemic and cerebral oxygen extraction.

Eighteen anesthetized baboons were studied to determine the effects of passive hyperventilation and phlebotomy on oxygen transport. After 1 hour of hyperventilation a significant increase in the red cell affinity for oxygen occurred in vivo. This was not associated with any significant changes in cardiac output, oxygen consumption, or in lactic acid production. There was a 40% decrease in cerebral blood flow, a 10 mm Hg decrease in the pulmonary artery Po2 level, and a 17 mm Hg decrease in the jugular venous Po2 level. After 1 hour of hyperventilation, the plasma inorganic phosphorus level decreased significantly, the red cell ATP level decreased slightly, and the red cell 2. 3 DPG level increased significantly, indicating that inorganic phosphorus had been removed from the blood during hyperventilation. Passive hyperventilation was maintained, and the baboons were bled 32% of their red cell volume. The blood volume was partially restored with nonbuffered isotonic saline. One hour after the phlebotomy and volume restoration (2 hours of hyperventilation) there were no changes in oxygen consumption, cardiac output, cerebral blood flow, or blood lactate levels, but the pulmonary artery Po2 level was decreased by 15 mm Hg, and the jugular venous Po2 level was decreased by 20 mm Hg. Systemic oxygen consumption was not affected by the significant decrease in pulmonary artery Po2.

Animals↗
PubMed1978

The role of hyperventilation in exercise-induced bronchoconstriction.

Significant bronchoconstriction, comparable in severity to that observed after moderate treadmill exercise, was induced in asthmatic children by voluntary isocapnic hyperventilation of 3-min and 10-min duration. In both hyperventilation and exercise, nasal breathing inhibited the bronchoconstrictive responses, whereas mouth breathing potentiated the bronchoconstrictive response. In the asthmatic children, 10 min of voluntary isocapnic hyperventilation did not represent a greater bronchoconstrictive stimulus than did 10 min of exercise or 3 min of isocapnic hyperventilation. This study also showed that in normal children there was no measurable airway response after either voluntary isocapnic hyperventilation or moderate exercise. Finally, this study indicates that it is the stimulation of upper airway receptors by relatively cold and dry air, rather than hyperventilation per se, that provokes exercise-induced bronchoconstriction.

Adolescent↗
PubMed1975

[Energy state of the cerebral cortex of the cat during hyperventilation (author's transl)].

Average Po2 and Pco2, local blood flow and pH values in the cerebral cortex of the cat were measured during passive hyperventilation (arterial Pco2 below 19 mm Hg). At defined intervals tissue samples were taken for metabolite analysis. The object of the study was to correlate the data obtained on the brain surface with metabolic responses. Immediately after the start of hyperventilation blood flow decreased, average cortical tissue pressures of O2 and CO2 fell, and there was a simultaneous rise in cortical pH. At a later stage in the experiment the local blood supply reverted to its resting level. Despite a fivefold rise in tissue lactate level during hyperventilation and a decrease in local O2 pressure on the brain surface to 5-10 mm Hg the degree of phosphorylation of energy rich phosphates was not less than under normal conditions of oxygenation. Our investigations showed no evidence of energy lack in cerebral cortex cells during hyperventilation. Cellular hypoxia and its characteristics are defined. The possible causes of raised tissue lactate levels during hyperventilation despite the lack of evidence of cellular hypoxia are discussed.

Adenosine Diphosphate↗
PubMed1975

Surfactant inactivation by hyperventilation: conservation by end-expiratory pressure.

Hyperventilation, defined as repeated hyperinflations, for three hours in open-chested anesthetized cats increased elastic recoil and elevated minimum surface tension of lung extracts as measured on a surface film balance. Equivalent hyperventilation from an elevated lung volume did not alter the pressure-volume relationships. When a mixture of [3H]glycerol and [14C]palmitate had been injected 17 h before the three hour period of phyerventilation, an increase in the ratio of specific activity in wash to tissue lecithin occurred in the hyperventilated cats compared to controls. These findings suggest that hyperventilation promotes release of surface active material from tissue to alveolus, but the released material is inactivated. The application of 2.5 cmH2O positive end-expiratory pressure prevented the adverse effects of hyperventilation. The same increase in wash to tissue lecithin occurred during this study; since the material was appropriately surface active, we conclude that the positive end-expiratory pressure prevented its inactivation.

Animals↗
PubMed1978

Sympathetic influence on alveolar surface activity in hyperventilated dog.

Hyperventilating IPPB, defined as intermittent positive-pressure breathing with a frequency of 32 beats/min and inspiratory pressure of 30 cmH2O, was administered for 14 h to open-chested anesthetized dogs in which nerves to one bronchus were operatively blocked. In the nerve-intact lungs, the lung stability index calculated from the pressure-volume relationship decreased with the duration of the hyperventilating IPPB (correlation coefficient r = -0.66, P less than 0.001), and atelectasis and hemorrhage appeared. In the nerve-blocked lungs, the index did not decrease during the 14 h of hyperventilating IPPB, and the appearance was almost normal. After pharmacologic sympathetic block with phenoxybenzamine, the lung stability index of both the operatively nerve-blocked lung and the nerve-intact lung was not decreased by hyperventilating IPPB. From these findings, we conclude that sympathetic block can protect pulmonary surface activity from the adverse effects of hyperventilating IPPB.

Animals↗
PubMed1978

The aetiology of the hyperventilation syndrome. A review of the literature.

The aetiology of the hyperventilation syndrome is reviewed with special emphasis on psychological aspects. Early reports linking overbreathing and the emotions can be found as far back as the 16th century. During the last 50 years research has been carried out into respiration in psychiatric disorders but as far as the hyperventilation syndrome is concerned there have been few psychiatric studies. Though many people believe that hyperventilation occurs as a response to anxiety, it has recently been suggested that it is due to a bad breathing habit. Whichever view should prove to be correct, most people would agree that the distressing symptoms produced by hyperventilation may themselves cause anxiety and exacerbate the hyperventilation, thus setting up a vicious circle. By the time the patient presents, this vicious circle has usually become established.

Emotions↗
PubMed1976

The effect of hyperventilation on distal nephron hydrogen ion secretion.

This study was designed to determine the effect of acute hyperventilation on distal nephron hydrogen ion secretion. The blood PCO2 declined and stabilized rapidly when bicarbonate loaded rats were hyperventilated. In contrast, the urine PCO2 declined slowly, resulting in an early increase in the urine minus blood (U-B) PCO2 which could not be obliterated by carbonic anhydrase infusion. Within approximately 50 min, the U-B PCO2 in the hyperventilated and carbonic anhydrase infused rats approached zero. Consequently, equilibrium between collecting duct urine and arterial blood PCO2 was then presumed to exist. This provided the basis for the subsequent studies on a series of rats. The U-B PCO2 decreased from a control of 22+/-1 mm Hg (mean+/-SEM) to 11+/-2 mm Hg (mean+/-SEM) with hypocapnia, and rose again to its control value when the blood PCO2 returned to prehyperventilation values. This decline in U-B PCO2 with acute hyperventilation could not be attributed to changes in urine flow, phosphate, or bicarbonate excretion, suggesting, therefore, a decrease in distal nephron (probably collecting duct) hydrogen ion secretion with acute hyperventilation. Possible pitfalls in the interpretation of the UB PCO2 are illustrated.

Acute Disease↗
PubMedDate not supplied

Hyperventilation in neurosurgery.

An outline of the nature and varieties of hyperventilation is presented together with a discussion on the role of artificial hyperventilation in the management of neurosurgical patients. Attention is called to the value of gasometric investigations in the ventricular cerebrospinal fluid for evaluation of disturbances in pH of the intracranial environment and possible effectiveness of hyperventilation. The results of our measurements of cerebrospinal fluid pressure are presented in 21 cases of supratentorial cerebral tumours in which controlled ventilation with hyperventilation was conducted. In 19 cases, the cerebrospinal fluid pressure fell by a mean of 44.3% with a simultaneous fall of PaCO2 by 29.3%. In the conclusions the authors stress the role of hyperventilation in the lowering of raised cerebrospinal fluid pressure and prevention of cerebral oedema.

Acid-Base Imbalance↗
PubMed1976

The effects of carbon dioxide on pulmonary mechanics in hyperventilating, normal volunteers.

Transpulmonary pressure, air flow, and end-tidal carbon dioxide levels were measured in normal human volunteers during hypocapnic, eucapnic, and hypercapnic hyperventilation. Respiratory rate and tidal volumes were well matched at a minute ventilation of 52 L. on three inspired gas mixtures: 21 per cent oxygen and 79 per cent nitrogen; 5 per cent carbon dioxide, 21 per cent oxygen and 74 per cent nitrogen; and 12 per cent carbon dioxide, 21 per cent oxygen and 67 per cent nitrogen. Respiratory rate, tidal volume, lung compliance, resistance, and resistive work per liter were calculated with a digital computer. In 13 experiments in 7 normal volunteers, no net bronchoconstriction or bronchodilatation was observed when eucapnic hyperventilation was compared to hypocapnic or hypercapnic hyperventilation. During hyperventilation of this degree, a change in bronchomotor tone owing to alteration in arterial or alveolar PCO2 either does not occur or else is masked by other reflexes or mechanical factors acting on the bronchi.

Adult↗
PubMed1979

Investigation of a simple, retrospective test for in-flight hyperventilation.

The experiment was designed to study the feasibility of using a single rebreathing estimate of mixed venous carbon dioxide tension (PvCO2) was a simple field test for hyperventilation in pilots. The results confirmed that the fall of end tidal carbon dioxide tension (P(ET)CO2) during hyperventilation and rise during recovery was exponential. The results also showed that the relationships between PvCO2 and P(ET)CO2 values during the unsteady states of carbon dioxide washout and accumulation may be described as a loop which encloses the theoretically derived line for the steady-state relationships. The deviation from the steady-state line appears on theoretical consideration to be directly proportional to carbon dioxide elimination rate, and indirectly proportional to cardiac output. Because of the exponential recovery, and because one value of PvCO2 could correspond to a range of values of P(ET)CO2, it is concluded that a field test for hyperventilation based on a single rebreathing estimate of PvCO2 would not be of value. The finding of a low value of PvCO2 would, however, be an indication that hyperventilation had taken place.

Aerospace Medicine↗
PubMedDate not supplied

[Hyperventilation and mannitol administration during surgery in patients with space-occupying intracranial lesions].

The aim of this work was to evaluate the effect of hyperventilation and mannitol on brain volume during neurosurgical operations. The material comprises 30 cases of supratentorial tumours. pO2, pCO2, pH and lactate concentration were determined in the arterial blood and in 7 cases also in the CSF. It was established that hyperventilation sometimes fails to decrease ICP; it was observed that hyperventilation was more effective in decreasing brain volume of the pCO2 level decreased by 14,6 mm Hg on the average. The joint use of hyperventilation and hypertonic mannitol was found to be more effective. Neither of the above methods was effective in the case of cystic tumors.

Adolescent↗
PubMed1977

Activation of partial complex seizures by hyperventilation.

Hyperventilation evoked abnormal EEG discharges or discharges and clinical seizures in 11% our patients with partial complex seizures. Hyperventilation is useful in the diagnosis of this kind of epilepsy, but may need to be pursed more vigorously and for a longer duration than is usual practice. The vigorous use of hyperventilation in selected patients with partial seizures should be employed before the use of other more complicated, expensive, and potentially harmful activating procedures.

Adolescent↗
PubMed1979

Dibutyryl cyclic GMP and hyperventilation promote rat lung phospholipid release.

Ventilation of rats at high inspiratory pressures raises lung tissue content of guanosine 3',5'-cyclic monophosphate (cGMP). Hyperventilation in rabbits augments release of phospholipid into lavage fluid. Can cGMP, in the absence of hyperventilation, increase lung phospholipid release? Sprague-Dawley rats are injected with [14C]palmitate, and after 1.5 h are anesthetized and ventilated for 20 min. Three groups are ventilated at peak inspiratory pressures (PIP) of 10 cmH2O, while saline, dibutyryl adenosine 3',5'-cyclic monophosphate (DBcAMP), or dibutyryl cGMP (DBcGMP) is infused into the pulmonary artery. In a fourth group, saline is infused into the pulmonary artery, but ventilation is performed with PIP of 25 cmH2O. Lung tissue and lavage fluid are then analyzed for phospholipid (PL) content and for incorporation of [14C]palmitate into lavage and tissue PL fractions. Ventilation at increased pressure and infusion of DBcGMP are associated with increases in release of labeled PL into lavage fraction. The findings suggest that the increase in lavage PL release associated with hyperventilation is, at least in part, mediated by cGMP.

Animals↗
PubMed1979

Effects on fetal breathing movements of maternal challenges. Cross-over study on dynamic work, static work, passive movements, hyperventilation and hyperoxygenation.

Ten women in the last trimester of a normal pregnancy were subjected to five different loads in a cross-over study. Fetal breathing movements (FBM), fetal heart rate (FHR), maternal heart rate (MHR), and mean arterial pressure (MAP), maternal transcutaneously measured pO2 (Tc-pO2), and the energy supply to the Tc-pO2 electrode were recorded continuously before, during, and after the load. Maternal capillary pH and pCO2 were measured at three representative time points. The immediate responses of the incidence of FBM to the different challenges were: increase after dynamic work (bicycle test); no change after static work (isometric muscle contraction) and passive movements; decrease after hyperventilation and hyperoxygenation. FHR was unaffected by all challenges. The FBM incidence varied in parallel with pCO2 after dynamic work and hyperventilation and inversely with the Tc-pO2 rise caused by hyperoxygenation. Maternal pH was increased after passive movements (no change in FBM) and after hyperventilation (decreased incidence of FBM), FBM seem to be more sensitive to environmental changes than is the FHR. Mechanical stimuli to the uterus were not responsible for the augmentation of FMB seen after the bicycle test. The present observations reveal the multifactorial nature of the regulation of FBM, and support the role of CO2 as a major stimulator of breathing movements also in prenatal life.

Adult↗
PubMed1978

[Hyperventilation test in coronary disease: a comparison with a bicycle ergometer exercise test. Report of 100 cases].

A hundred cases have been studied and divided into three categories:--60 normal subjects;--30 coronary subjects with a positive exercise test;--10 subjects with defective nervous control of the circulation; using the exercise test, we studied the effects of hyperventilation on repolarisation of the ventricle. In the normal subjects there was no ischaemic depression of the ST segment, but there were minor changes in repolarisation which affected the T wave in 73% of subjects and were essentially posterior in distribution. In the coronary subjects, we found three with ischaemic depression of the ST segment and one with ST elevation of 2.5 mm (6.7% of the coronary subjects). This last finding is evidence against the commonly held hypothesis that reproduction of ST depression by hyperventilation during the exercise test indicates a false positive test. In the patients with defective nervous control of the circulation, 9 had an ischaemic type of ST depression, either as a new feature or as a more severe one compared with that found at rest. The mechanism by which these depressions are produced has not been totally explained:--in the cases with defective nervous control of the circulation, it appears that latent increased sympathetic activity is increased by the hyperventilation;--in the coronary subjects, it may be caused by true ischaemia or by an associated defect in nervous control of the circulation.

Adult↗
PubMed1979

[Hyperventilation and oxygen supply of the myocardium. II. Effect of nitroglycerin and dipyridamole].

1. Voluntary hyperventilation during rest in the recumbent position induces a fall in H+ concentration, PCO2 and PO2 in mixed venous blood and in the blood of the coronary sinus. 2. If the breathing volume is increased during voluntary hyperventilation between 2- and 2.5 fold above the volume at rest, O2 uptake increases by only 6% but CO2 excretion rises by 66%. 3. Cardiac output decreases by 8% and the O2 extraction of the myocard increases by 12%. There is a quantitative relationship between arterial pH or PCO2 and changes in the systemic and coronary circulation. Blood pressure decreases in the pulmonary circulation. 4. Nitroglycerin during hyperventilation produces an additional reduction in cardiac output but no effect on the O2 extractions of the myocard. 5. With dipyridamol, the O2 extraction of the myocard is reduced and the PO2 in the blood of the coronary sinus increases. 6. In the case of severe coronary obstruction, the effect of dipyridamol can cause acute angina pectoris and left heart insufficiency due to poststenotic ischemis (steal syndrome).

Adult↗