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PubMed1993

Hyperventilation and panic attacks in general hospital patients.

The 2-week prevalence of panic attacks according to DSM-III-R criteria was assessed in 102 general hospital patients with unexplained somatic symptoms suggestive of the hyperventilation syndrome (HVS). Thirty-six patients were classified as panickers. In comparison to nonpanickers, panickers reported more severe panic and hyperventilation symptoms and state anxiety during anxiety episodes in daily life and also obtained higher scores on measures for depression, generalized anxiety, agoraphobic anxiety, and agoraphobic avoidance. During the Hyperventilation Provocation Test, panickers reported more panic and hyperventilation symptoms and state anxiety and also rated their symptoms to be more similar to those occurring in daily life than nonpanickers. However, no differences were observed between panickers and nonpanickers in base excess values or in minute respiratory volume, respiratory rate, or fraction of end-tidal carbon dioxide during the resting, hyperventilation, and recovery phase. It is concluded that the prevalence of panic attacks in this group of patients is relatively high and that medical specialists must be more attentive to the occurrence of panic attacks or panic disorder in general hospital patients with unexplained somatic symptoms suggestive of HVS.

Adult↗
PubMed1998

Hyperventilation restores cerebral blood flow autoregulation in patients with acute liver failure.

BACKGROUND/AIMS: In patients with acute liver failure loss of cerebral blood flow autoregulation may result from cerebral vasodilatation. Since arterial hypocapnia induces cerebral vasoconstriction, we investigated whether cerebral blood flow autoregulation could be reestablished by mechanical hyperventilation. METHODS: Seven consecutive patients (median age 45, range 30-50 years) with acute liver failure and hepatic encephalopathy stage IV entered the study. They were all maintained on mechanical ventilation. Cerebral blood flow autoregulation was evaluated by using transcranial Doppler sonography to assess mean flow velocity (Vmean) in the middle cerebral artery, during a rise in mean arterial pressure by norepinephrine infusion (0.5-10 microg/h). The patients were subsequently hyperventilated for 15 min before cerebral blood flow autoregulation was re-evaluated in the same mean arterial pressure range. RESULTS: At baseline PaCO2 (4.0 (3.5-4.9)kPa), all patients had impaired cerebral blood flow autoregulation as Vmean increased from 47 (30-78) to 68 (49-107) cm x s(-1) (p<0.05), as MAP was raised from 82 (60-88) to 106 (89-123) mmHg. During hyperventilation, five of seven patients restored cerebral autoregulation as Vmean remained unchanged at 51 (45-70) cm x s(-1) during a rise in MAP from 84 (65-94) to 110 (89-130) mmHg. Cerebral blood flow autoregulation was not restored in two patients, but hyperventilation reduced the slope of the mean arterial pressure-Vmean correlation. These two patients had renal failure and were treated with intermittent hemodialysis. CONCLUSIONS: Cerebral blood flow autoregulation was restored by hyperventilation in five of seven patients with acute liver failure, indicating that cerebral vasodilatation is of pathophysiological importance in dysregulation of cerebral circulation in acute liver failure.

Adult↗
PubMedDate not supplied

Hyperventilation, anxiety, craving for alcohol: a subacute alcohol withdrawal syndrome.

Hyperventilation leading to respiratory alkalosis is part of the acute alcohol withdrawal syndrome On the basis of clinical observations and a literature review on withdrawal symptoms the following was hypothesized: (a) hyperventilation is also part of a subacute alcohol withdrawal syndrome and (b) hyperventilation appears together with anxiety and craving for alcohol. These hypotheses were tested in a sample of 37 male alcoholic inpatients, abstinent for periods from several weeks to 9 months. Subjects were administered a questionnaire dealing with drinking history and craving for alcohol during abstinence, the Spielberger Anxiety Inventory and a hyperventilation complaint checklist. Subjects' disposition to hyperventilation was assessed during a physiological measurement session. Results show that hyperventilatory symptoms, anxiety and craving for alcohol appear together. Moreover, the severity of hyperventilatory and anxiety symptomatology is positively correlated with the duration of physically dependent alcohol use but not with the duration of excessive drinking per se, irrespective of age. These results corroborate the hypotheses outlined before.

Adolescent↗
PubMed1995

Hyperventilation activation on EEG recording in children with epilepsy.

In 20 patients with epilepsy, electroencephalography (EEG) slowing was quantitatively characterized during standardized hyperventilation activation (respiratory rate: 30/min, threefold elevation of total expiratory volume, duration: 4 min) and changes in cerebral blood flow and velocity in the right common carotid artery were monitored with the Doppler ultrasonic method. Thirteen age-matched normal children served as controls. The results were as follows: (1) EEG slowing in the epilepsy group was greater compared with controls. (2) There was a significant decrease in mean frequency (decrease in alpha power and increase in delta power) during hyperventilation in the epilepsy group, but no significant change in the controls. (3) The decrease in cerebral blood flow (CBF) was greater in the epilepsy group at the beginning of hyperventilation, possibly related to the greater EEG slowing. (4) The percentage of CBF at the end of hyperventilation was similar in the epilepsy and control groups. The difference in EEG response to hyperventilation between the 2 groups may be due to differences in the decrease in CBF volume and the sensitivity of the change in CBF.

Blood Flow Velocity↗
PubMed1993

Short chain fatty acid-induced hyperventilation is due to PGF2-alpha.

While studying the significance of the short chain fatty acids (SCFAs) in the pathogenesis of hyperventilation, we have found that experimental rabbits injected with SCFA sodium salt (4 mmol/kg b.wt) develop hyperventilation 20 min later. This hyperventilation results in a decrease of PCO2 in the arterial blood from 32.05 +/- 1.18 to 24.55 +/- 0.83 (p < 0.001). The SCFAs also bring about pronounced mixed alkalosis. The prostaglandin F2-alpha (PGF2-alpha) in both the arterial and venous blood of rabbits increased significantly after treatment with SCFAs salts. If the rabbits are pretreated with indomethacin (10 mg/kg), the SCFAs do not cause hyperventilation. Therefore we can conclude, that the SCFAs bring about hyperventilation through an increase in the PGF2-alpha synthesis.

Alkalosis↗
PubMed2006

Parietal lobe source localization and sensitivity to hyperventilation in a patient with subclinical rhythmic electrographic discharges of adults (SREDA).

OBJECTIVE: Subclinical rhythmic electrographic discharges of adults (SREDA) is currently considered a benign EEG pattern of uncertain significance. The underlying cortical sources and generating mechanisms are unknown. We performed a source localization analysis of SREDA with the aim of better understanding this unusual EEG pattern. METHODS: Multiple spontaneous episodes of typical SREDA were recorded in a patient during continuous EEG monitoring. Additional SREDA episodes were induced by hyperventilation. Source localization was carried out using statistical non-parametric mapping (SNPM) of low resolution electromagnetic tomography (LORETA). RESULTS: SNPM of both time- and frequency-domain LORETA revealed a widespread biparietal cortical origin of SREDA, the anatomical distribution of which included the parietal operculum and the known vascular watershed areas between anterior, middle and posterior cerebral arteries. Vigorous deep hyperventilation induced SREDA on three of four attempts. Mean duration of the hyperventilation-induced SREDA was approximately three times longer than spontaneous events. CONCLUSIONS: Investigations in this patient with typical SREDA revealed hyperventilation sensitivity and a posterior hemispheric source localization maximal in the parietal cortex bilaterally, in large part overlying the anatomical distribution of the vascular watershed areas. SIGNIFICANCE: The source localization results and sensitivity to hyperventilation suggest some sort of association between cerebral vascular supply and SREDA, as originally proposed by Naquet et al. [Naquet R, Louard C, Rhodes J, Vigouroux M. A propos de certaines décharges paroxystiques du carrefour temporo-pariéto-occipital. Leur activation par l'hypoxie. Rev Neurol 1961;105:203-207.].

Aged↗
PubMed2006

Symptoms of premenstrual syndrome may be caused by hyperventilation.

OBJECTIVE: To determine whether women with premenstrual syndrome (PMS) differ from healthy women in the extent of hyperventilation during the luteal phase of the cycle. DESIGN: Case report. SETTING: Medical university. PATIENT(S): Three reproductive-age women with severe symptoms of PMS in whom dramatic decline in end-tidal PCO2 (PETCO2) occurred during the luteal phase of the cycle. INTERVENTION(S): Measurements of PETCO2, administration of GnRH agonist triptorelin. MAIN OUTCOME MEASURE(S): PETCO2 was determined daily by sidestream capnometry. RESULT(S): The decline in PETCO2 in women with PMS was 12-18 mm Hg, on the average. This was significantly more pronounced than the decline of PETCO2 that was observed in healthy women. With the decline of PETCO2 the symptoms of PMS appeared. Symptoms disappeared at the end of the luteal phase when PETCO2 was increasing again. During treatment with the GnRH agonist, PETCO2 did not decline, and all women were free of symptoms. CONCLUSION(S): The symptoms of PMS observed in our patients were associated with a pronounced decline of PETCO2 that occurred during the luteal phase of the cycle. Because the symptoms were similar to symptoms observed in the chronic hyperventilation syndrome it is suggested that some symptoms of PMS may be caused by chronic hyperventilation. It appears that in women with PMS the sensitivity of the respiratory center to CO2 is increased more than normal by P or some other secretory product of the corpus luteum, resulting in pronounced hyperventilation with the associated clinical signs and symptoms of a chronic hyperventilation syndrome.

Adult↗
PubMed2004

Effects of hyperventilation on heart rate and QT variability in panic disorder pre- and post-treatment.

Panic disorder is associated with an elevated risk of cardiovascular disease and sudden death. Individuals with panic disorder have been shown to have reduced variability in heart rate and increased variability in the QT interval on electrocardiogram (ECG), patterns predictive of sudden cardiac death in certain forms of cardiomyopathy. Given that panic disorder patients often hyperventilate during a panic attack, we assessed the effects of voluntary hyperventilation on the ECG utilizing linear analyses of heart rate and QT interval variability. Sixteen symptomatic, medication-free patients underwent hyperventilation challenge. A small subgroup of eight subjects underwent re-challenge after treatment. Pre-treatment, hyperventilation resulted in a decrease in a measure of heart rate variability and an increase in the QT variability index (QTVI; QT variance normalized for mean QT, divided by heart rate variance normalized for mean heart rate). In a remitted state, the QTVI was reduced both during rest and during hyperventilation compared with the respective pre-treatment levels. These findings suggest a possible mechanism explaining increased rates of cardiovascular morbidity and mortality in panic disorder. Moreover, the reduction in QTVI observed post-treatment raises the question of whether treatment might have cardioprotective effects, at least in panic disorder patients who have particular types of co-morbid cardiac disease. Yet these results must be interpreted cautiously; they are preliminary, exploratory and observed in a very small sample without a healthy comparison group.

Adult↗
PubMed2005

Response of laryngeal motoneurons to hyperventilation induced apnea in the rat.

Central apnea is common in the premature newborn. To explain the upper airway findings in different clinical conditions characterized by central apnea, we made single unit recordings from laryngeal motoneurons during normal and hyperventilation. Posterior cricoarytenoid (n = 4) and cricothyroid (n = 4) motoneurons displayed an inspiratory pattern during normal ventilation and remained synchronous with phrenic nerve discharge (PND) during hyperventilation. Laryngeal constrictor motoneurons (LCon) displayed a post-inspiratory pattern during normal ventilation, but lost phasic activity during early hyperventilation (the period after the onset of hyperventilation but before cessation of PND; n = 12). There was a nearly linear relationship between the post-inspiratory activity and strength of PND. Six LCon motoneurons remained silent throughout hyperventilation, while the other six developed a tonic activity during cessation of PND. Further analysis suggested that the silent and tonic LCon motoneurons are likely to share a similar mechanism in their post-inspiratory pattern generation, but differ from each other in their responses to CO2 inputs. In addition, strong inhibition of the LCon tonic activity by the early return of PND could be an important factor in recovery following a period of apnea. Failure of this inspiratory inhibition to occur might explain certain clinical situations, where obstructive apnea supervenes following a period of central apnea.

Action Potentials↗
PubMed1996

Influence of breathing therapy on complaints, anxiety and breathing pattern in patients with hyperventilation syndrome and anxiety disorders.

The effect of breathing therapy was evaluated in patients with hyperventilation syndrome (HVS). The diagnosis of HVS was based on the presence of several suggestive complaints occurring in the context of stress, and reproduced by voluntary hyperventilation. Organic diseases as a cause of the symptoms were excluded. Most of these patients met the criteria for an anxiety disorder. The therapy was conducted in the following sequence: (1) brief, voluntary hyperventilation to reproduce the complaints in daily life: (2) reattribution of the cause of the symptoms to hyperventilation: (3) explaining the rationale of therapy-reduction of hyperventilation by acquiring an abdominal breathing pattern, with slowing down of expiration: and (4) breathing retraining for 2 to 3 months by a physiotherapist. After breathing therapy, the sum scores of the Nijmegen Questionnaire were markedly reduced. Improvements were registered in 10 of the 16 complaints of the questionnaire. The level of anxiety evaluated by means of the State-Trait Anxiety Inventory (STAI) decreased slightly. The breathing pattern was modified significantly after breathing retraining. Mean values of inspiration and expiration time and tidal volume increased, but end-tidal CO2 concentration (FETCO2) was not significantly modified except in the group of younger women (< or = 28 years). A canonical correlation analysis relating the changes of the various complaints to the modifications of breathing variables showed that the improvement of the complaints was correlated mainly with the slowing down of breathing frequency. The favorable influence of breathing retraining on complaints thus appeared to be a consequence of its influence primarily on breathing frequency, rather than on FETCO2.

Adolescent↗
PubMed2002

beta-Endorphin modulation of pressor response to hyperventilation in hypertensive patients.

After hyperventilation, systolic and diastolic blood pressure (BP) significantly decreased in 14 hypertensive patients (group 1), did not change in 9 (group 2) and increased in 8 (group 3). Basal BP, norepinephrine and dynorphin B levels were higher in group 1 than in groups 2 and 3. The decrease in BP after hyperventilation was associated with a decrease in plasma norepinephrine, Met-enkephalin and dynorphin B and an increase in beta-endorphin. Naloxone abolished the hyperventilation-induced BP and norepinephrine decreases. Our findings indicate that hyperventilation may select hypertensive patients with different sympatho-adrenergic activity and that the increase in beta-endorphin reduces BP response to hyperventilation in patients with high sympatho-adrenergic tone.

Aged↗
PubMed2000

Panic, hyperventilation and perpetuation of anxiety.

1. Studies on the pathogenesis of panic disorder (PD) have concentrated on panic attacks. However, PD runs a chronic or episodic course and panic patients remain clinically unwell between attacks. Panic patients chronically hyperventilate, but the implications of this are unclear. 2. Provocation of panic experimentally has indicated that several biological mechanisms may be involved in the onset of panic symptoms. Evidence from provocation studies using lactate, but particularly carbon dioxide (CO2) mixtures, suggests that panic patients may have hypersensitive CO2 chemoreceptors. Klein proposed that PD may be due to a dysfunctional brain's suffocation alarm and that panic patients hyperventilate to keep pCO2 low. 3. Studies of panic patients in the non-panic state have shown EEG abnormalities in this patient group, as well as abnormalities in cerebral blood flow and cerebral glucose metabolism. These abnormalities can be interpreted as signs of cerebral hypoxia that may have resulted from hyperventilation. 4. Cerebral hypoxia is probably involved in the causation of symptoms of anxiety in sufferers of chronic obstructive pulmonary diseases. By chronically hyperventilating, panic patients may likewise be at risk of exposure to prolonged periods of cerebral hypoxia which, in turn, may contribute to the chronicity of their panic and anxiety symptoms. 5. Chronic hyperventilation may engender a self-perpetuating mechanism within the pathophysiology of PD, a hypothesis which warrants further studies of panic patients in the non-panic state.

Carbon Dioxide↗
PubMed1997

Hyperventilation syndrome: an elegant but scientifically untenable concept.

The concept of hyperventilation and the principle of a vicious circle provide an elegant explanation for the development of a wide range of somatic and psychological symptoms, the so-called hyperventilation syndrome (HVS). The model has a high degree of credibility and has led to the development of therapeutic interventions that appeared beneficial. However, recent investigations dismiss hyperventilation as an important symptom-producing mechanism. First, the hyperventilation provocation test appears to be invalid as a diagnostic test. Second, studies using ambulant monitoring of pCO2 demonstrate that the vast majority of real-life attacks are not attended by decreases in pCO2. Third, the evaluation of therapy outcome studies indicate that the beneficial effect of breathing retraining is probably not mediated by reducing the tendency to hyperventilate. We conclude that a diagnosis of HVS should be avoided.

Humans↗
PubMed2003

On the function of groaning and hyperventilation during sexual intercourse: intensification of sexual experience by altering brain metabolism through hypocapnia.

Sexual arousal is accompanied by some typical physiological reaction patterns. Another typical feature of sexual intercourse is involuntary sound production implying in its more intense forms acceleration of breathing (hyperventilation). Up to now no study examined spCO2 during intense sexual intercourse, but there is evidence that some degree of hyperventilation with its physiological consequences may often be induced during sexual intercourse. This article discusses implications of hyperventilation during sexual intercourse for alterations of consciousness and subjective experience in the light of recent studies of brain metabolic changes during states of hyperventilation. Groaning and hyperventilation are interpreted in this context as a psychophysiological mechanism to deepen states of sexual trance.

Brain↗
PubMed2006

Prevalence of hyperventilation syndrome in an allergy clinic, compared with a routine ENT clinic.

OBJECTIVES: A high prevalence of chronic hyperventilation syndrome in patients with asthma has been reported. We examined whether this phenomenon extended to allergy clinic patients in general and whether the prevalence was higher in patients attending a general allergy clinic compared with those attending a routine ENT clinic in our hospital. METHODS: We examined the prevalence of hyperventilation syndrome in unselected, consecutive patients (n = 100) seen in an allergy clinic. The validated Nijmegen questionnaire was completed by patients in the waiting room. We also administered the questionnaire to unselected, consecutive patients (n = 100) in a routine ENT clinic. RESULTS: There was no significant difference in prevalence of hyperventilation between allergy clinic and routine ENT clinic patients (25/100 vs 23/100). CONCLUSION: The result indicates a high prevalence of hyperventilation amongst hospital attendees in general. Consideration should perhaps be given to the possible role of hyperventilation in symptomatology.

Adolescent↗
PubMed2003

Hyperoxia and the cerebral hemodynamic responses to moderate hyperventilation.

BACKGROUND: A reduction in the arterial partial pressure of CO2 (PaCO2) leads to a rapid reduction in cerebral blood flow (CBF). However, despite continuing hypocapnia there is secondary recovery of CBF over time as a result of increases in lactic acid production. Hyperoxia is thought to modulate the production of lactic acid. This study examined the kinetics of middle cerebral artery flow velocity (MCA FV) reduction during hyperventilation, and its modulation by hyperoxia. METHODS: Cerebral blood flow was assessed using transcranial Doppler ultrasound in nine healthy, awake human volunteers. Subjects were ventilated, via a mouthpiece, to achieve a stable end-tidal CO2 (PETCO2). After a 20-min baseline period the minute volume on the ventilator was passively increased by approximately 20% to reduce PETCO2 by 0.75-1 kPa. After a 10-min stabilization period the new PETCO2 level was maintained at a constant level for 20 min, and MCA FV recovery was measured during this 20-min period. Subjects undertook the protocol breathing air and breathing 100% oxygen. RESULTS: The PETCO2 level was (mean +/- SD) 4.9 +/- 0.4 kPa (normoxia baseline), 4.0 +/- 0.3 kPa (normoxia hyperventilation), 4.6 +/- 0.4 kPa (hyperoxia baseline) and 3.9 +/- 0.4 kPa (hyperoxia hyperventilation). CO2 reactivity was significantly lower with normoxia than hyperoxia (16.5 +/- 3.8 vs. 21.2 +/- 4.6 % kPa-1; P< 0.05). Middle cerebral artery FV recovery was significantly more rapid with normoxia than hyperoxia (0.23 +/- 0.17 vs. 0.08 +/- 0.1 % baseline min-1; P< 0.01). CONCLUSIONS: Our results suggest that cerebral hemodynamic responses to moderate hyperventilation are different in normoxic and hyperoxic conditions. Clinical assessment of CO2 reactivity and CBF recovery during hyperventilation should take the degree of arterial oxygenation into account.

Adult↗
PubMed2001

Effects of hyperventilation on fast goal-directed limb movements in spinocerebellar ataxia type 6.

It has been shown previously that hyperventilation modifies the features of the nystagmus in cerebellar patients (Walker and Zee, 1999). It has been hypothesized that hyperventilation influences the oculomotor control through a metabolic effect on cerebellar calcium channels, which play a critical role in the firing behaviour of neuronal populations in the cerebellum. This hypothesis has been tested here by analysing fast goal-directed limb movements before and after hyperventilation in spinocerebellar ataxia type 6 (SCA-6), a disease associated with a polyglutamine expansion in the alpha 1-A voltage-dependent calcium channel. Cerebellar hypermetria associated with fast distal single-joint movements was found to be increased following hyperventilation in patients presenting SCA-6 but remained unchanged in patients with idiopathic late-onset cerebellar degeneration (ILOCA). This is a new provocative test to enhance distal dysmetria in SCA-6. The present results strengthen the hypothesis of Walker and Zee. It is suggested that hyperventilation enhances the defective calcium transfers in SCA-6, resulting in an impairment of the calcium influx in particular into Purkinje cells involved in the control of fast goal-directed voluntary movements.

Biomechanical Phenomena↗
PubMed1997

[The effect of short-term hyperventilation on the concentration of ionized serum calcium].

BACKGROUND AND OBJECTIVE: Paraesthesias and carpopedal spasms on hyperventilation are explained by a reduction in ionised serum calcium (ISC). We tested whether 5-minute hyperventilation changes the concentration of ISC. SUBJECTS AND METHOD: Arterial blood samples were obtained via a small plastic catheter introduced into the femoral artery of ten healthy male volunteers (mean age 33 years) before, during and after 5 minutes of hyperventilation, which was achieved by deep and rapid breathing and considered adequate when the end-expiratory pCO2 had fallen to 2.5 kPA within the first minute and remained below this level during the remaining 4 minutes. These criteria were met in nine of the ten patients. The ISC concentration was measured with an ion-selective electrode, the pH, paCO2 and bicarbonate levels with an autoanalyser. RESULTS: Paraesthesias of the fingers and hand occurred in nine of the volunteers, carpopedal spasms in seven. Despite a definite rise in pH from 7.39 +/- 0.02 to 7.75 +/- 0.045, the concentration of ISC did not change significantly during the hyperventilation. CONCLUSION: Paraesthesias and carpopedal spasms which occur during hyperventilation are not caused by a fall in ionised serum calcium in arterial blood.

Adult↗