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PubMed1999

Regional cerebral blood flow during mechanical hyperventilation in patients with fulminant hepatic failure.

Hyperventilation is frequently used to prevent or postpone the development of cerebral edema and intracranial hypertension in patients with fulminant hepatic failure (FHF). The influence of such therapy on regional cerebral blood flow (rCBF) remains, however, unknown. In this study the CBF-distribution pattern was determined within the first 12 hours after development of hepatic encephalopathy (HE) stage 4 before and during hyperventilation. Ten consecutive patients (median age 48 [range 33-57] years) with FHF and 9 healthy controls (median age 54 [24-58] years) had rCBF determined by single photon emission computed tomography (SPECT) using intravenous injection of 133Xenon. For determination of high resolution CBF pattern, the patients were also studied with 99mTc-hexa-methylpropyleneamine oxime (HMPAO) in the hyperventilation condition. There was no significant difference in the rCBF distribution pattern during normoventilation as compared with hyperventilation. The anterior to posterior (AP) ratio was significantly lower in patients as compared with healthy controls. After hepatic recovery and disappearance of HE, 3 patients had restored normal rCBF distribution pattern as compared with healthy controls. We conclude that in sedated patients with FHF, a relatively lower rCBF is found in the frontal regions and in the basal ganglia as compared with posterior regions. This rCBF-distribution pattern was not aggravated during hyperventilation. It is speculated that this change of rCBF in patients with FHF may render the frontal brain regions more susceptible to hypoxia. The relative frontal rCBF decrease was shown to be reversible with hepatic recovery and alleviation of HE.

Adult↗
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↗
PubMed1998

Cerebral blood flow changes in the primary motor and premotor cortices during hyperventilation.

The aim of this study was to clarify the regional differences in cerebral blood flow (CBF) change during hyperventilation by using H2(15)O and positron emission tomography (PET). Eight healthy volunteers (age: 63.0 +/- 8.9 yr.) were studied. Regional CBF was measured by the H2(15)O autoradiographic method and PET. Statistical parametric maps (SPM) and conventional regions of interest (ROI) analysis were used for estimating regional CBF differences in the normocapnic state with normal breathing and the hypocapnic state induced by hyperventilation. Total CBF decreased during the hypocapnic state. The SPM revealed that primary motor and premotor cortices were significantly activated by hyperventilation. In these areas absolute CBF values were significantly higher than those in the temporal, occipital and parietal lobes in the hypocapnic state, but there were no significant regional differences in the normocapnic state. In the hypocapnic state induced by hyperventilation, the primary motor and premotor CBF shows combined changes with vasoreaction to hypocapnia and increase in activation due to hyperventilation.

Aged↗
PubMed2001

Intracranial pressure, brain PCO2, PO2, and pH during hypo- and hyperventilation at constant mean airway pressure in pigs.

OBJECTIVE: To evaluate in healthy, non-brain-traumatized animals the effects of hypo- and hyperventilation on intracranial pressure (ICP) and brain carbon dioxide, oxygen, and pH during the use of a ventilatory mode at constant mean airway pressure (MAwP). DESIGN AND SETTING: Prospective animal study in a university laboratory. SUBJECTS: Eight crossbred Landrace/Yorkshire pigs. INTERVENTIONS: The animals were ventilated in a pressure-controlled mode according to the open lung concept with an inspired oxygen fraction of 1.0. Starting at normoventilation, a stepwise hypo- and hyperventilation was performed to PaCO2 values of 90.4+/-10.4 and 26.9+/-4.1 mmHg, respectively. The ICP and brain parenchyma values [carbon dioxide (PbrCO2), oxygen (PbrO2), and pH (brpH)] measured by multiparameter sensors were recorded continuously during these maneuvres. RESULTS: During hypoventilation there was a significant increase in PbrCO2 tension, PbrO2 tension, and ICP. During hyperventilation there was a significant decrease in PbrCO2 tension and ICP while the change in PbrO2 was not significant. MAwP was kept stable during the stepwise hypo- and hyperventilation, and this resulted in a constant mean arterial pressure. CONCLUSIONS: Controlled hypo- and hyperventilation at constant MAwP in non-brain-traumatized pigs appears to induce changes in ICP and cerebral perfusion pressure which, however, do not necessarily lead to cerebral ischemia. To achieve adequate cerebral perfusion at an increased ICP level due to hypoventilation one must maintain sufficient arterial blood pressure. Hypercapnia resulted in a significant increase in brain oxygenation; however, this does not necessarily mean that permissive hypercapnia is neuroprotective.

Animals↗
PubMed2003

Effects of hydration and hyperventilation on cortical complexity.

The effects of hydration and hyperventilation on cortical complexity were investigated in a sample of 19 healthy volunteers in a double-blind placebo design using magnetoencephalographic recordings. The subjects were asked to abstain from the intake of liquids 18 h before the study. Spontaneous magnetoencephalograms (MEG) were recorded before and after drinking 750 ml water (WAT group: nine subjects) or saline solution (SAL group: ten subjects) with eyes closed and open and during hyperventilation (HV) with eyes open. The MEG data were analysed using both linear (spectral power) and non-linear (pointwise dimension and largest Lyapunov exponent) algorithms. The prediction that intake of water, because of induced cell swelling, will lead to an increased synchronization and a decreased complexity of the spontaneous MEG during hyperventilation was confirmed. Hyperventilation following the drinking condition produced an increase in all power spectra with a stronger increase of delta and theta power after drinking of water. This synchronization of spontaneous MEG is accompanied by a general significant decrease of cortical complexity, especially after water drinking. Moreover, cortical complexity was inversely related to delta and theta power and partly also to alpha power. The SAL and WAT groups showed different relations between alpha power and dimensional complexity during HV: whereas in the SAL group the correlations between these measures became more negative during HV, they reversed in the WAT group to become positive. The synchronizing effect of hyperventilation, leading to a decrease of cortical complexity, is related in the SAL group to delta, theta and alpha power, whereas in the WAT group only delta and theta activity contribute to a reduction of cortical complexity.

Adult↗
PubMed1994

Suppression of hyperventilation-induced attacks with infusion of B-type (brain) natriuretic peptide in patients with variant angina.

B-type (brain) natriuretic peptide (BNP) forms a peptide family with A-type (atrial) natriuretic peptide (ANP), which is involved in the regulation of blood pressure and fluid volume. We have demonstrated that BNP is a novel cardiac hormone secreted predominantly from the ventricle and that plasma levels of BNP markedly increase in proportion to the severity of congestive heart failure. Spasm of a major coronary artery (coronary spasm) is the cause of variant angina and can be induced by hyperventilation. We examined whether BNP infusion suppresses coronary spasm in patients with variant angina. The effect of BNP infusion on anginal attacks induced by hyperventilation was studied in 11 patients with variant angina in whom the attacks were reproducibly induced by hyperventilation. This study was performed in the early morning on 3 consecutive days. Fourteen minutes after infusion of BNP was begun (day 2, 0.05 micrograms/kg/min) or saline (days 1 and 3), hyperventilation was started and continued for 6 minutes. Anginal attacks were induced in all 11 patients by hyperventilation on days 1 and 3, respectively. Anginal attacks were not induced in any patient on day 2 (BNP infusion). Fourteen minutes after BNP infusion was begun, plasma BNP levels increased from 23.7 +/- 6.7 pg/ml to peak levels of 2591 +/- 255 pg/ml (p < 0.01) and plasma ANP levels increased from 28.9 +/- 7.5 pg/ml to peak levels of 69.2 +/- 13.2 pg/ml. Five minutes after BNP infusion was finished, plasma levels of cyclic guanosine monophosphate (cGMP) increased from 20.3 +/- 7.4 pg/ml to peak levels of 63.5 +/- 13.7 pg/ml (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1980

Pseudoischemic "false positive" S-T segment changes induced by hyperventilation in patients with mitral valve prolapse.

Hyperventilation-induced S-T segment changes that simulate myocardial ischemia have previously been noted, but the origin of this electrocardiographic finding has never been defined. To investigate further the basis for this response, the records were reviewed of 1,678 consecutive patients who underwent forced hyperventilation for 90 seconds and treadmill exercise testing. Twenty-eight patients (1.7 percent) were identified in whom hyperventilation resulted in ischemic-appearing S-T segment changes, and follow-up was possible in 21 (17 women, 4 men). Of the 21 patients, 16 (76 percent), including 15 (88 percent) of the 17 women, had evidence of mitral valve prolapse, 6 on auscultation alone, 2 on echocardiography alone and 6 with a combination of studies. Ten of the 21 patients had a negative exercise test; of the 11 patients who had a positive exercise test, only 1 had angiographic evidence of coronary arterial narrowing. The finding of ischemic-appearing S-T segment changes in response to forced hyperventilation has a high predictive value for the presence of mitral valve prolapse, particularly in women. The possible association of autonomic factors and mitral valve prolapse in the pathogenesis of an abnormal response to hyperventilation is discussed.

Adult↗
PubMed1986

Hyperventilation syndrome and asthma.

Hyperventilation syndrome is a common and often disabling condition. Traditional treatment consists of reassurance and anxiolytic drugs. Hyperventilation is known to precipitate an asthmatic reaction. A retrospective review of patients with hyperventilation syndrome was performed to ascertain the frequency of asthma as well as the response to bronchodilator medication. Forty-seven patients were seen. Thirty-eight were tested, and asthma was proved in 36. Two additional patients had positive clinical responses with bronchodilators. Thus, asthma was identified in 38 of 47 consecutive patients seen for hyperventilation syndrome (80 percent), and asthma was proved in 36 of 38 of patients tested (95 percent). Hyperventilation syndrome was eliminated in 29 of 35 patients (90 percent) treated with a combination of explanation and bronchodilator treatment.

Adult↗
PubMed1987

Hyperventilation and panic disorder.

Hyperventilation syndrome and panic disorder are both common, serious, and easily treatable disorders. The similarity of their symptoms and physiology, the demonstration of hyperventilation during spontaneous and laboratory-induced panic episodes, provocation of panic-like symptoms in some patients with panic disorder using hyperventilation, the importance of psychologic factors in producing hyperventilation, and successful treatment of panic disorder with breathing retraining all indicate a strong association between these two conditions. About 50 percent of patients in each group show evidence of both disorders. It is suggested that many patients in each group show evidence of both disorders. It is suggested that many patients with either diagnosis have the same disorder and share a biologically and often genetically determined hypersensitivity of a central "alarm" system. Panic and hyperventilation provoked by inappropriate activation of this system are postulated to reinforce each other by a positive feedback loop. Treatments directed at any part of this loop are likely to be successful. Clinical implications of the link between these conditions are discussed.

Anti-Anxiety Agents↗
PubMed1989

Anxiety sensitivity and history of panic as predictors of response to hyperventilation.

In this study, we examined the effects of anxiety sensitivity on the response to hyperventilation in college students with and without a history of spontaneous panic attacks. Reiss et al.'s (Behav. Res. Ther. 24, 1-8, 1986) Anxiety Sensitivity Index and Norton et al.'s (Behav. Ther. 17, 239-252, 1986) Panic Attack Questionnaire were used to select Ss. Following five min of voluntary hyperventilation, high anxiety sensitivity Ss reported more anxiety and more hyperventilation sensations than did low anxiety sensitivity Ss. A history of panic was only associated with enhanced responding to hyperventilation in Ss with high anxiety sensitivity; low anxiety sensitivity Ss who had experience with panic were no more responsive than low anxiety sensitivity Ss who had never had a panic attack. These findings suggest that high anxiety sensitivity may be a crucial determinant of panic attacks provoked by biological challenges (e.g. hyperventilation, sodium lactate infusion).

Adult↗
PubMed1991

The effects of voluntary hyperventilation on patients with chest pain without coronary artery disease.

The present investigation was designed to examine panic symptom experience in patients with chest pain of nonorganic etiology, using a hyperventilation provocation procedure. Given the recent focus on panic disorder in patients with nonorganic chest pain, we assessed three indices of physiological arousal, subjective anxiety, and endorsement of DSM-III-R panic symptomatology in response to 3 min of voluntary hyperventilation. Subjects included 23 patients with nonorganic chest pain (CP sample) and matched normal controls (NC sample). The results indicate that hyperventilation produced significant increases in skin conductance, heart rate, and upper trapezious EMG in both CP and NC samples. Despite equivalent levels of physiological arousal and subjective anxiety, the CP sample endorsed a greater number of DSM-III-R panic symptoms relative to the NC sample. Examination of post-hyperventilation symptoms indicated that a greater percentage of the CP sample reported palpitations, nausea, and chest pain when compared with normals. Comparison of CP patients with and without Panic Disorder revealed no significant differences on any measure. The results suggests that hyperventilation plays a role in symptom experience in patients with nonorganic chest pain, although anxiety does not appear central in moderating this effect.

Adult↗
PubMed1995

Physiological, subjective and behavioral responses to hyperventilation in clinical and infrequent panic.

This study investigated the physiological, subjective and behavioral responses to hyperventilation of four groups of Ss with: (1) clinical panic disorder (n = 13); (2) infrequent panic (n = 16); (3) no panic and high trait anxiety (n = 16); and (4) no panic and low trait anxiety. After completing a number of anxiety-related questionnaires, Ss participated in 2 min of hyperventilation during which heart rate and electrodermal activity were recorded continuously. Subjective sensations and cognitions during hyperventilation were assessed immediately following the task. After recovery, Ss could participate in a second, optional hyperventilation from which they could escape at any time. Analyses revealed no group differences in physiological responses to the hyperventilation, although group differences in subjective sensations and cognitions were found. Data are discussed with regards to the role of physiological processes vs subjective responses to anxiety-provoking stimuli in the psychopathology of clinical panic disorder.

Adult↗
PubMed1980

EEG and end-tidal carbon dioxide concentration in the hyperventilation syndrome.

The hyperventilation syndrome (HVS) is a functional disorder with repeated involuntary hyperventilation attacks together with symptoms of respiratory alkalosis. We have studied the EEG and end-tibial pCO2 in the resting state and during hyperventilation activation in 12 HVS patients in order to find out whether there is a greater susceptibility to cerebral vasoconstriction in HVS patients than in controls, as indicated by slowing of the EEG. A surprisingly high proportion (58%) of abnormal resting EEGs was found in HVS patients, although the patients were neurologically normal. More theta and beta background activity was usually revealed in a quantitative computer analysis, especially frontally. Although the hyperventilation activation caused the same degree of hypocapnia in HVS patients and in controls, peripheral symptoms like tingling and numbness of fingers, as well as carpopedal spasms, occurred much more often in HVS patients. However, the EEG changes due to hyperventilation were similar in both HVS patients and normal controls, and it thus seems that the reason for cerebral symptoms in HVS patients is not a greater susceptibility to cerebral vasoconstriction.

Adult↗
PubMed1991

Quantitative EEG during progressive hypocarbia and hypoxia. Hyperventilation-induced EEG changes reconsidered.

To investigate the role of cerebral hypoxia as a causative factor in the alteration of the qEEG during hyperventilation, qEEG changes caused by progressive hypocapnia were compared with qEEG changes due to progressive normobaric hypoxia in two parallel groups of 12 and 10 healthy male subjects (age 20-27 years), respectively. In the first group, qEEG records were obtained before and during hyperventilation to pCO2 levels of 4.0, 3.0 and 2.0 kPa. In the second group, the qEEG samples were taken before and during hypoxia with hemoglobin oxygen saturations of 80, 70 and 60%. In both groups, blood flow velocity in the middle cerebral artery was also recorded. Hyperventilation caused an exponential increase in slow activity and a decrease in alpha power. No shift in the alpha mean frequency and alpha peak frequency was observed, except with the pCO2 level of 4.0 kPa, which caused an increase in both variables. Hypoxia with a hemoglobin oxygen saturation of 60% caused a much less pronounced increase in slow activity. No change in total power in the alpha band was found, but both the alpha peak frequency and alpha mean frequency decreased. Lesser degrees of hypoxia caused only minimal EEG changes. Blood flow velocity was decreased by hyperventilation but increased by hypoxia. It is concluded that the EEG changes observed during hyperventilation must mainly or totally be attributed to factors other than cerebral hypoxia.

Adult↗
PubMed1992

Quantitative EEG changes due to cerebral vasoconstriction. Indomethacin versus hyperventilation-induced reduction in cerebral blood flow in normal subjects.

Hyperventilation leads to an increase in slow EEG activity as well as to a decrease in alpha activity. These effects may be considered a result of reduction in cerebral blood flow due to vasoconstriction, but metabolic factors, such as alkalosis and the increased formation of cerebral lactate, may also have to be taken into account. As indomethacin decreases cerebral blood flow it is possible to study cerebral vasoconstriction, without concomitant metabolic alkalosis or cerebral lactate formation. Two parallel groups of 12 healthy male subjects (age 20-25) were studied with quantitative EEG (qEEG) and cerebral blood flow velocity as parameters. In the first group the effect of 100 mg indomethacin was studied. In the parallel group a standardized hyperventilation procedure was performed. In the indomethacin group the blood flow velocity decreased to 60% of the initial value; the qEEG showed a 0.5 Hz slowing of the alpha peak frequency (P less than 0.01) and a decrease in the power of the alpha band without any change in the delta or theta band. In the hyperventilation group the blood flow velocity decreased to 63% of the initial value and the qEEG showed a marked increase in delta and theta activity (P less than 0.01), but a non-significant change in alpha peak frequency. Indomethacin and hyperventilation caused similar degrees of vasoconstriction; however, the increase in qEEG slow wave activity, which was observed only in the hyperventilation group, is apparently related to metabolic rather than haemodynamic factors.

Adult↗
PubMed1988

Hyperventilation syndrome and muscle fatigue.

Fatigue is a frequent complaint from patients suffering from the hyperventilation syndrome. Fatigue was quantified in terms of the endurance time that a certain force can be generated in a sustained handgrip contraction, and in terms of the time course of changes in certain parameters of the EMG-power spectrum of the contracting muscles. This was done in a group of 25 normal subjects and a group of 30 patients suffering from the hyperventilation syndrome. No difference in endurance times was found. The EMG-fatiguability in the hyperventilation group developed even slower than in the normal group. In three normals the fatigue parameters were also measured in three conditions of normo-, hypo-, and hyper-capnia. No intraindividual correlations were found between fatigue parameters and CO2-levels. Neither were such correlations found between individuals in the hyperventilation group and the normal group. It is concluded that the subjective feelings of fatigue in the hyperventilation patients cannot be corroborated by the objective measurements used in this study. Thus their fatigue is not of a peripheral type. The levels of CO2 do not have an effect on objectively measured fatigue parameters. The hypothesis that lactate accumulation in contracting muscles mediates EMG-fatiguability, cannot explain the present results, and therefore is not supported by results from this study.

Adult↗
PubMed1989

Alveolar phospholipids, hyperventilation and temperature of conservation of rat lungs.

Hyperventilation has been found to increase the phospholipid content of broncho-alveolar lavage fluids. Had the temperature of conservation of the lungs an influence? Two groups of rats were allowed to ventilate normally (NV), and two groups (HV) were induced to hyperventilate for 1 h by addition of a dead space. After sacrifice, the isolated lungs were kept for 25 min at 37 degrees C (NV37 and HV37), or 10 degrees C (NV10 and HV10), and then washed at the same temperatures. The phospholipid content of lavage fluid was only found to be increased in the HV37 group (P less than 0.05). Neither hyperventilation followed by conservation of lungs at 10 degrees C nor normal ventilation followed by conservation of lungs at 37 degrees C led to an increase in phospholipid content. It was the association of hyperventilation and conservation of lungs at 37 degrees C that led to the increase. In vivo hyperventilation is thought to lead to an equal increase in secretion and reabsorption of alveolar phospholipids, and conservation of the lungs at 37 degrees C was thought to lead to an imbalance between these two processes.

Animals↗
PubMed1991

Hypoxia following voluntary hyperventilation during exercise in man.

The importance of carbon dioxide in the control of ventilation during exercise was tested by emptying CO2 stores by voluntary hyperventilation. Healthy subjects were studied after 3 min hyperventilation down to an end-tidal PCO2 of about 20 mmHg on a background of steady exercise at 75 W. Control runs were performed when the hyperventilation was made isocapnic by the addition of CO2. Following hypocapnic hyperventilation, there was a period when ventilation fell below control and this was accompanied by a fall in end-tidal PO2 (minimum 48 mmHg) and oximeter reading (minimum 73%). Ventilation rapidly returned to baseline following isocapnic hyperventilation and hypoxia was not seen. A mathematical simulation suggested that brain PCO2 recovered more slowly than arterial PCO2 and that at the times that ventilation was depressed central chemoreceptor PCO2 would have been low. We conclude that CO2 provides a crucial drive for maintaining adequate ventilation during steady exercise and that the central chemoreceptor may be involved.

Adolescent↗