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PubMed1989

Hyperventilation and anxiety in panic disorder, social phobia, GAD and normal controls.

Patients with DSM-III Agoraphobia, Panic Disorder, GAD, Social Phobia and normal controls underwent a series of experimental procedures and measures to determine whether panic attack patients show a greater tendency towards hyperventilation that is independent from their anxiety levels. Contrary to expectations, the Agoraphobia and Panic Disorder patients did not show significantly lower levels of expired pCO2 at rest than the other anxious or non-anxious groups. However, the panic attack patients did show significantly higher levels of anxiety and hyperventilatory symptoms during a hyperventilation test and during breathing 5% CO2 in air. A strong relationship was found between hyperventilatory symptoms and anxiety in all groups of patients and in the controls. On the basis of these results it was concluded that Agoraphobia and Panic Disorder patients do not show a unique tendency toward hyperventilation, but rather that their hyperventilatory symptoms and perhaps intermittent overbreathing episodes are a function of the high levels of anxiety they experience.

Agoraphobia↗
PubMed1992

The role of hyperventilation in panic disorder: a response to Ley (1991)

Ley (Behaviour Research and Therapy, 29, 301-304, 1991) provided a reinterpretation of experimental findings on the efficacy of breathing retraining plus cognitive restructuring in reducing the symptomatology of patients with panic disorder with agoraphobia which were presented in a 1989 article in this journal. On the basis of his reinterpretation, they concluded that our findings supported the central role of hyperventilation in panic attacks. Ley's arguments are discussed and we conclude that his reinterpretation provides new arguments against a hyperventilation theory of panic. Furthermore, recent evidence from empirical studies does not support a central role for hyperventilation in panic attacks.

Arousal↗
PubMed1986

EEG and spectral analysis in acute hyperventilation.

Acute hypocapnia decreases CBF, increases hemoglobin affinity for oxygen and causes cerebral tissue hypoxia. This tissue hypoxia is reversed with inhalation of 100% O2 in dogs. EEG slowing produced by hyperventilation is considered a manifestation of cerebral hypoxia due to decreased CBF and is thought to be reversed with hyperoxia. This study evaluated the effects of 3 gas mixtures (16% O2, 21% O2, 100% O2) on posterior frequencies of the resting and hyperventilatory EEG in normal subjects aged 23-37. Hypocapnia was maintained to an end-tidal pCO2 of 21 mm Hg for 3 min. Respiratory measures, heart rate, saO2, minute ventilation and side effects were recorded. EEG was analyzed by visual inspection and by spectral analysis. Spectral analysis evaluated total amplitude, percentile frequencies, and peak frequencies. There were significant changes from eucapnia to hypocapnia for the group in all physiologic parameters, total amplitude by spectral analysis, and posterior frequencies by visual analysis. There were no significant differences among the gases. We conclude that the EEG changes of hyperventilation are independent of the concentration of inspired oxygen over the range studied in our subjects. Symptoms of hyperventilation are likewise independent of the inspired oxygen concentration for the range studied.

Acute Disease↗
PubMed1986

Heart rate response, emotional disturbance and hyperventilation.

The heart rate and electrocardiographic responses were documented in 40 subjects undergoing hyperventilation provocation tests. Forced overbreathing produced a similar mean heart rate increase in all subjects, regardless of whether the result of the provocation tests suggested the hyperventilation syndrome. In contrast subjects diagnosed as hyperventilators by virtue of prolonged hypocapnia in response to psychological provocation showed significant increased heart rate responses compared to the remaining subjects (p less than 0.001). Significant electrocardiographic abnormalities were also produced. The view is presented that the hypocapnia may allow persistence of the cardiovascular responses in the presence of emotional challenge.

Adult↗
PubMed1991

Hyperventilation provocation in patients with chest pain and a negative treadmill exercise test.

Seventeen (39%) of 44 patients with chest pain but without significant ST depression on treadmill exercise had their usual chest pain reproduced during or after 3 min of voluntary hyperventilation (VHV) at rest. These patients with hyperventilation positive tests had not only significantly more hyperventilation-related symptoms and respiratory complaints but also shorter breath-holding times, lower mean resting end-tidal pCO2 and higher mean respiratory rates than those with negative tests and normal controls. Of the psychological variables, only phobic avoidance scores for agoraphobia were higher in patients with positive tests. These findings suggest that in two fifths of patients with exercise tests negative for ischaemia, chest pain is associated with HV, but abnormalities of breath control and relative hypocapnia are present even in the absence of chest pain. It is possible that a chronic abnormality of respiratory control may interact with attitudinal factors in the experience of non-cardiac chest pain.

Adult↗
PubMed1991

The test-retest reliability of the hyperventilation provocation test.

The hyperventilation provocation test (HPT) has been widely used for reproducing symptoms of panics. It is assumed that subjects experience similar symptoms on consecutive occasions of hyperventilation. Fourteen subjects with a history of panics and fourteen without such a history underwent the HPT on two occasions one week apart. In the group of 28 subjects as a whole, there were moderate similarities between the HPTs in both the choice and severity of symptoms reported, even when pre-existing symptoms were controlled statistically. Nevertheless, in the subject-by-subject analysis, many subjects showed no resemblance between the two HPTs in the choice of symptoms. This suggests that many subjects would not show any resemblance between the symptoms experienced in an HPT and those of their latest panic even if hyperventilation occurred in that panic.

Adult↗
PubMed1993

Discordance between symptom and physiological criteria for the hyperventilation syndrome.

Hyperventilation is assumed to produce a set of somatic and psychological symptoms, the so-called Hyperventilation Syndrome (HVS). Recognition of symptoms during the hyperventilation provocation test (HVPT) is the most widely used criterion for diagnosing HVS, but additional physiological and symptom criteria have been proposed. The concordance of various diagnostic criteria for HVS is investigated in the present study. Forty-eight psychiatric patients with panic disorder and 90 somatic patients with symptoms suspective of HVS performed a HVPT. There was a strong interrelationship between the various symptom criteria as well as the physiological criteria. However, almost no association between symptom and physiological HVS criteria were found. Symptom recognition was significantly related to trait anxiety, agoraphobia and depression. These data do not only question the validity of the HVPT, but also of the concept of HVS. The results are more consistent with a cognitive approach to anxiety in which the HVPT is seen as an aspecific stressor during which more anxious patients anticipate an anxiety attack.

Acid-Base Equilibrium↗
PubMed1995

Treatment of the hyperventilation syndrome with bisoprolol: a placebo-controlled clinical trial.

The hyperventilation syndrome (HVS) can be regarded as a form of panic disorder associated with a relative increase in sympathomimetic tone, the effects of which can be counterbalanced by beta-adrenoceptor blockade. The efficacy of the beta-blocker bisoprolol was investigated in a double-blind placebo-controlled randomised crossover trial involving 60 patients from 17 general practices. Following a single-blind placebo prephase, patients who met the inclusion criteria were randomised to treatment with either 5 mg bisoprolol or an identical-looking placebo tablet once daily for three weeks. They were then crossed over to the other treatment arm. At the end of each treatment phase the number of hyperventilation attacks and the severity of symptoms were assessed and side effects recorded. The number of attacks decreased from 4.04 per week at baseline to 3.52 with placebo and to 1.26 with bisoprolol. The decrease of attacks with bisoprolol was significant (p < 0.05) compared to baseline and placebo. The severity of the complaints improved from 29 (scale 0 to 64) at baseline not significantly to 26 with placebo and significantly (p < 0.05) to 15 with bisoprolol. No serious side effects were reported. Five milligrams of bisoprolol once daily is effective and safe in the maintenance of symptom reduction in patients with the hyperventilation syndrome.

Adult↗
PubMed1984

Human vocal cord movements during voluntary hyperventilation.

Using a fiberoptic laryngoscope and video equipment, we studied the respiratory movements of the vocal cords during sustained hyperventilation in 4 normal human subjects. The expiratory narrowing of the glottic airway that occurs in quiet breathing was attenuated during hyperventilation in 7 of 8 experiments, and the pattern of vocal cord movements throughout the breathing cycle closely resembled the patterns previously found in exercise and hypercapnia. These responses were similar during normocapnic and hypocapnic hyperventilation. The similarity of laryngeal movements in voluntary and involuntary hyperpneic states suggests that common brain stem mechanisms may be entrained by both 'behavioral' and 'automatic' ventilatory control systems.

Adult↗
PubMed1988

The effect on airway function of inspired air conditions after isocapnic hyperventilation with dry air.

The magnitude of postexercise or posthyperventilation bronchoconstriction in patients with asthma is related to the temperature and the water content of the inspired air during the exercise or hyperventilation period. Recent studies have suggested that the inspired air conditions during recovery from exercise may also be important in determining the magnitude of postexercise airway narrowing. In the present study, normal subjects (n = 8) and patients with asthma (n = 12) were studied on separate days. On day 1 the subjects performed isocapnic hyperventilation with warm dry air and recovered breathing warm dry air. On the second day, an identical warm dry air challenge was administered, but recovery occurred while they were breathing warm humid air. There was no significant bronchoconstriction in the normal subjects, irrespective of the inspired air conditions during recovery. The patients with asthma showed greater bronchoconstriction during recovery in warm, humid air (maximal decrease in FEV1 31% +/- 17%) than in dry air (maximal decrease in FEV1 19% +/- 20%; p less than 0.05). These results suggest that the inspired air condition during recovery from isocapnic hyperventilation of dry air is also a determinant of the magnitude of the bronchoconstrictor response.

Adult↗
PubMed1985

Is hyperventilation a physiologically significant stimulus for prostaglandin release in the human pulmonary vascular bed?

The influence of hyperventilation on the pulmonary prostaglandin (PG) release was studied in healthy volunteers. Hyperventilation was forced by adding 8% CO2 to the inhaled air and arterial and mixed venous blood was sampled for radioimmunoassays of 6-keto-PGF1 alpha and PGE2. The increased ventilation did not alter the arterio-venous PG concentration differences suggesting that hyperventilation accompanying the activation of chemoreceptors is not a physiologically significant stimulus for the pulmonary PG release in man.

6-Ketoprostaglandin F1 alpha↗
PubMed1987

Pharmacological analysis of hyperventilation in arthritic rats.

The study examined the validity of increased minute volume of ventilation as a measurement of chronic pain in arthritic rats. The opiates morphine and R 62 818 attenuated arthritic hyperventilation, but only at doses which also reduced the ventilatory response to CO2 in normal rats. The non-steroidal anti-inflammatory drugs (NSAIDs), indomethacin and suprofen, the corticosteroids, cortisone and dexamethasone, and the tranquillizers, haloperidol and chlordiazepoxide, were essentially ineffective except at doses that also produced anti-inflammatory and/or toxic effects. A combination of an in itself ineffective dose of R 62 818 with an ineffective dose of suprofen did attenuate arthritic hyperventilation, and the combination constituted the only pharmacological treatment that did so in the absence of anti-inflammatory, toxic or intrinsic respiratory effects. The data are consistent with the hypothesis that pain rather than acidosis mediates arthritic hyperventilation. They also suggest that combinations of an opiate with an NSAID may perhaps be effective in alleviating this pain.

Analgesics↗
PubMed2004

Prefrontal hemodynamic response to verbal-fluency task and hyperventilation in bipolar disorder measured by multi-channel near-infrared spectroscopy.

BACKGROUND: Many neuroimaging studies of patients with bipolar disorder have demonstrated functional hypofrontality (reduced activation of the frontal cortex), although this finding is still controversial. We previously found hypoactivation of the left prefrontal region in remitted subjects with bipolar disorder measured by one-channel near-infrared spectroscopy (NIRS). The aim of the present study was to clarify whether or not this finding was due to altered cerebral lateralization or caused by reduced cerebrovascular reactivity. METHODS: We enrolled nine remitted patients with bipolar disorder and nine normal controls. Hemodynamic responses in the prefrontal cortex during the verbal-fluency and hyperventilation tasks were monitored by 24-channel NIRS, which can measure oxygenated hemoglobin (OxyHb), deoxygenated hemoglobin, and total hemoglobin (TotalHb). RESULTS: The increases of OxyHb and TotalHb in the bipolar group were significantly smaller than that in the controls during the verbal-fluency task. The response of TotalHb during hyperventilation in the bipolar group was weaker than that in the controls. LIMITATIONS: The sample size was small. CONCLUSIONS: These findings suggest that the bilateral hypofrontality to a cognitive task is seen in remitted subjects with bipolar disorder, which may be related to vascular function as measured by the response to hyperventilation.

Adult↗
PubMed2006

Comparison between hyperventilation and breath-holding in panic disorder: patients responsive and non-responsive to both tests.

Our aim was to compare the demographic and psychopathological features of panic disorder (PD) patients who underwent hyperventilation and breath-holding challenge tests, and to describe the features of patients who had a panic attack after both tests versus those patients who did not experience panic after either test. Eighty-five PD patients were induced to hyperventilate (30 breaths/min) for 4 min, and a week later to hold their breath for as long as possible four times with a 2-min interval in between. Anxiety scales were applied before and after the tests. Patients who responded with a panic attack to both tests (BPA, n = 25) were compared with patients who experienced spontaneous panic attacks but did not panic in response to the two tests (NPA, n = 16). The BPA group had a significantly higher presence of respiratory symptoms during a panic attack. The criteria for the respiratory PD subtype were fulfilled in 18 (72.0%) BPA patients and in 6 (37.5%) NPA patients. The BPA patients had a later onset of panic disorder and a higher familial prevalence of PD. Our data suggest that there is a distinction between PD patients who were sensitive to both hyperventilation and breath-holding tests and PD patients who were not affected by the challenge tests. The panic attack may be a final common pathway for different types of stimuli, and respiratory tests may characterize different PD subgroups.

Adult↗
PubMed2006

Lactic acid buffering, nonmetabolic CO2 and exercise hyperventilation: a critical reappraisal.

It has been suggested that hyperventilation and the disproportionate increase in VCO2 versus VO2 above the ventilatory threshold (V(TH)) in ramp exercise are due to the production of nonmetabolic CO2 in muscle because of lactic acid buffering by plasma bicarbonate entering the cell in exchange with lactate [Wasserman, K., 1982. Dyspnea on exertion. Is it the heart or the lungs? JAMA 248, 2039-2043]. According to this model, plasma standard bicarbonate concentration decreases in a approximately 1:1 ratio with the increase in plasma lactate concentration, 1 mmol of CO2 is generated above that produced by aerobic metabolism for each mmol of lactic acid buffered, and nonmetabolic CO2 produced in the muscle is partly responsible for hyperventilation because of the resulting increase in the CO2 flow to the lungs. The present report shows that this model is not consistent with experimental data: (1) bicarbonate is not the main buffer in the muscle; (2) the decrease in standard bicarbonate concentration is not the mirror image of the increase in lactate concentration; (3) buffering by bicarbonate does not increase CO2 production in muscle (no nonmetabolic CO2 is produced in tissues); (4) the CO2 flow to the lungs, which should not be confused with VCO2 at the mouth, does not increase at a faster rate above than below V(TH). The disproportionate increase in VCO2 at the mouth above V(TH) is due to hyperventilation (not the reverse) and to the low plasma pH which both reduce the pool of bicarbonate readily available in the body.

Acid-Base Equilibrium↗
PubMed2005

Two-rescuer CPR results in hyperventilation in the ventilating rescuer.

The "Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care--International Consensus on Science" recommend a tidal ventilation volume of 10 ml/kg body-weight without the use of supplemental oxygen during two-rescuer adult cardiopulmonary resuscitation (CPR). This relates to a ventilation volume of about 6.4 l/min. Additionally, the first aid provider ventilating the victim will breathe for him/herself during the external chest compression period adding another 3.2 l/min of ventilation. Finally, a deep breath is recommended before each ventilation to increase the end-expiratory oxygen concentration of the air exhaled. To investigate the effects of these recommendations, 20 healthy volunteers were asked to perform two-rescuer CPR in a lung model connected to a BLS-manikin. End-tidal carbon dioxide, oxygen saturation, and heart rate were recorded continuously. Capillary blood gas samples were collected and non-invasive blood pressure was recorded prior to the start of external chest compressions and immediately after the end of each measurement period. Furthermore, hyperventilation related symptoms reported by the volunteers were also recorded. The data reveal a significant decrease in capillary and end-tidal carbon dioxide pressure in the volunteers (P < 0.001). Additionally, in 75% of test persons multiple hyperventilation associated symptoms occurred. Ventilation during two-rescuer CPR performed according to the Guidelines 2000 may cause injury to the health of first aid providers. To minimize hyperventilation, both rescuers should exchange their positions at intervals of 3-5 min. These data challenge the recommendation to take a deep breath prior to each ventilation.

Adult↗
PubMed2003

Emotional responding to hyperventilation as a predictor of agoraphobia status among individuals suffering from panic disorder.

Some data suggest that panic patients with extensive agoraphobia (PDA) display more intense respiratory distress during their panic attacks than Panic disorder (PD) patients. However, no studies have determined if PDA patients also show heightened sensitivity to a respiratory challenge compared to PD patients. The current study examined the differential emotional responding to hyperventilation among PDA patients, PD patients, and a non-clinical group with a history of panic attacks. Response to hyperventilation challenge did not distinguish non-clinical panickers from panic patients; however, behavioral tolerance to hyperventilation challenge significantly predicted agoraphobia status among panic disorder patients, even after controlling for demographic and clinical status variables.

Adolescent↗
PubMed1984

Response to cold air hyperventilation in normal and in asthmatic children.

To assess the sensitivity of isocapnic hyperventilation with cold air in detecting airway hyperreactivity in asthmatic children, we studied 13 asthmatic patients (mean age 11.1 years) and 10 normal children. Cold air challenge consisted of 4 minutes of moderate hyperventilation plus another 4 minutes of maximal hyperventilation, both with subfreezing air (-16 degrees to -18 degrees C). Exercise and IHCA tests were done within 5 days and in random sequence. Mean (+/- SE) maximal % delta FEV1 after IHCA was 27 +/- 5.1% in the asthmatic children vs 4.5 +/- 1.2% in the normal subjects (P less than 0.01), even though there were no significant differences in the maximal minute ventilation equivalent between the two groups. Mean maximal % delta FEV1 after exercise was 31.7 +/- 5.6 in the asthmatic group. There was no difference in the sensitivity of the exercise and IHCA tests to detect bronchospasm in asthmatic children. Airway obstruction after IHCA was sharp and brief: maximal at 3 minutes after challenge, and back to 10% of baseline after 11 minutes. In seven asthmatic children the refractoriness to cold air and exercise was studied by repeating each test within 30 minutes; all seven showed significant refractoriness to exercise, and six showed no refractoriness to IHCA. We conclude that exercise and cold air-induced bronchospasm have different physiologic mechanisms, and that cold air testing can be used as a routine challenge to identify airway hyperreactivity in children.

Adolescent↗