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PubMedDate not supplied

Hyperventilation in panic disorder and social phobia.

The aim of our study was to observe the induction of panic attacks by hyperventilation in a group of panic disorder and social phobia patients (DSM-IV). We randomly selected 26 panic disorder patients, 22 social phobics and 25 normal volunteers. They were drug-free for 1 week. Hyperventilation (30 breaths/min) was induced for 3 min. Anxiety scales were taken before and after the test. 61.5% (n = 16) of panic disorder patients, 22.7% (n = 5) of social phobics and 4.0% (n = 1) of control subjects had a panic attack after hyperventilating (p < 0.01, panic disorder vs. control; p < 0.05, panic disorder vs. social phobia; p = n.s., social phobia vs. control). Both anxiety disorder groups were more sensitive to hyperventilation than normal volunteers. The induction of panic attacks by voluntary hyperventilation may be an easy and useful test for validating the diagnosis in some specific panic disorder patients.

Adolescent↗

PubMed2004

Psychopathological description of hyperventilation-induced panic attacks: a comparison with spontaneous panic attacks.

Our aim was to describe the clinical features of hyperventilation-induced panic attacks (HPA) in panic disorder patients - DSM-IV - and to compare them with their spontaneous panic attacks and with spontaneous panic attacks in panic disorder (PD) patients not sensible to the hyperventilation challenge test. We reexamined 88 previously studied PD patients when they were submitted to a hyperventilation challenge test. They were induced to hyperventilate (30 breaths/min) for 4 min and anxiety scales were applied before and after the test. A total of 51.1% (n = 45) PD patients had a panic attack after hyperventilating - HPA (chi(2) = 13.11, d.f. = 1, p = 0.017). The clinical symptoms of the most severe panic attack were recorded by the HPA patient and by the PD patients not sensible to this test (non-HPA; n = 43, 48.9%) in a diary during a 1-week period and then compared. The HPA group had more respiratory symptoms (chi(2) = 15.26, d.f. = 1, p < 0.001), fulfilling the criteria for the respiratory PD subtype (75.6%), the disorder started later (Mann-Whitney, p < 0.001), had a higher familial prevalence of PD (chi(2) = 19.45, d.f. = 1, p = 0.036), and had more previous depressive episodes (chi(2) = 18.74, d.f. = 1, p < 0.001). The HPA group had similar symptomatology in spontaneous attacks and HPA. The HPA group may be regarded as a subgroup of the respiratory panic disorder subtype with diagnostic and therapeutic implications.

Adult↗

PubMed1997

Changes in arterial and transcutaneous oxygen and carbon dioxide tensions during and after voluntary hyperventilation.

The purposes of our study were (1) to investigate whether a 3-min short-term hyperventilation leads to posthyperventilatory hypoxemia and (2) to assess the role of transcutaneous blood gas measurements for monitoring oxygen and carbon dioxide changes during the after the test. In 10 male volunteers arterial and transcutaneous blood gases were measured simultaneously before, during and after a 3-min voluntary hyperventilation maneuver. Baseline arterial PO2 increased from 13.7 +/- 0.4 kPa (103 +/- 3 mm Hg) to 18.6 +/- 0.3 kPa (139 +/- 2.3 mm Hg; p < 0.005 compared to baseline) during hyperventilation. After the provocation test posthyperventilatory hypoxemia occurred with a minimal mean value of 7.8 +/- 1.3 kPa (58.5 +/- 9.8 mm Hg; p < 0.05 compared to baseline). Whereas close agreement between arterial and transcutaneous measurements was obtained for carbon dioxide values before hyperventilation, transcutaneous O2 consistently underestimated arterial O2. A short-term over-breathing of 3 min causes a significant posthyperventilatory hypoxemia. We hypothesize that posthyperventilatory hypoxemia is caused by hypopnea as a result of depleted CO2 body stores. Noninvasive transcutaneous blood gas measurements are not reliable for monitoring blood gas changes during and after hyperventilation, most probably because of the slow response time of the electrodes and the reflex vasoconstriction of the skin vessels.

Adult↗

PubMed1991

Effect of hyperventilation on distal colonic motility and rectal sensitivity in irritable bowel syndrome.

Hyperventilation is associated with some symptoms suggestive of irritable bowel syndrome and has been implicated in provoking excessive oesophageal contractility. Sixteen patients with irritable bowel syndrome were therefore studied in order to assess the effect of hyperventilation on distal colonic motility and rectal sensitivity. No significant change in either the amplitude or frequency of colonic contractile activity was noted following hyperventilation, nor was any alteration in rectal sensitivity observed. This study shows that acute hyperventilation does not affect colonic motor activity or visceral sensitivity and suggests that hyperventilation and irritable bowel syndrome are not causally related.

Adult↗

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↗

PubMed1994

Refractoriness of eucapnic hyperventilation-induced bronchoconstriction in rabbits.

The mechanism of refractoriness in bronchoconstriction after repeated hyperventilation was investigated in 18 sensitized rabbits. Rabbits were separated into three groups: an untreated control group (n = 7), a cimetidine-treated group (n = 6), and an indomethacin-treated group (n = 5). After anesthetization, hyperventilation was performed for 15 min (120 breaths/min, 7 ml/kg tidal volume) with dry air containing 5% CO2. Total lung resistance (RL) and dynamic compliance (Cdyn) were measured before (baseline) and after hyperventilation challenge. After RL and Cdyn had returned to baseline values, the hyperventilation challenge was repeated. In the control group maximal increase in percent RL (max %RL) was 49 +/- 9% after the first challenge, but 16 +/- 4% after the second challenge, indicating refractoriness. A similar tendency was observed in percent Cdyn. In the cimetidine- and indomethacin-treated groups, max %RL were 42 +/- 3% and 60 +/- 15% after the first challenge, and 35 +/- 8% and 60 +/- 7% after the second challenge, respectively, indicating no refractoriness. These results suggest that the H2-receptor and bronchodilating prostanoids play an important role in producing the refractoriness to bronchoconstriction observed in sensitized rabbits after repeated hyperventilation.

Airway Resistance↗

PubMed1999

Hyperventilation with dry air increases airway surface fluid osmolality in canine peripheral airways.

Hyperventilation-induced bronchoconstriction (HIB) is a component of exercise-induced asthma (EIA) believed to result from the penetration of unconditioned air into the lung periphery. We used a canine model of EIA to examine the effect of hyperventilation on airway surface fluid (ASF) volume and osmolality, and to determine if the observed kinetics support the hypothesis that hyperventilation-induced changes in ASF osmolality initiate bronchoconstriction. Exposure of sublobar airways to dry air at baseline insufflation resulted in stable measurements of ASF volume, ASF osmolality, and peripheral airway resistance (Rp). Baseline insufflation of warm humidified air increased ASF volume, but did not alter ASF osmolality. Hyperventilation challenge with warm humidified air (WAC) increased Rp and ASF volume, but decreased ASF osmolality. Dry air challenge (DAC) increased Rp, ASF volume, and ASF osmolality. ASF osmolality during DAC was markedly higher when compared with posthyperventilation values. Post-DAC changes in (Delta) ASF volume and osmolality were poorly correlated with the development of HIB. In contrast to Delta ASF after DAC, Delta ASF osmolality during DAC was strongly correlated with HIB, and tended to be inversely related to Delta ASF volume. These observations are consistent with the hypothesis that changes in airway osmolality during hyperventilation initiate peripheral airway constriction.

Air↗

PubMed1990

Formoterol, a new inhaled beta-2 adrenergic agonist, has a longer blocking effect than albuterol on hyperventilation-induced bronchoconstriction.

The duration of effect of inhaled formoterol (24 micrograms) was compared with that of a placebo and that of inhaled albuterol (200 micrograms) in 12 adult asthmatic subjects who underwent hyperventilation tests with cold dry air (-20 degrees C) on 4 study days. On the control day, they were subjected to four hyperventilation tests to ensure functional stability. On the 3 remaining days, after a first hyperventilation test, they inhaled placebo, albuterol, or formoterol in randomized, double-blind fashion. The hyperventilation test was repeated 1, 4, and 8 h and, if the blocking effect was still present, 12 and 24 h after the drug had been administered. The dose of hyperventilation of cold air causing a 20% fall in FEV1 (PD20) was interpolated on the dose-response curve. The magnitude of the blocking effect at each time interval on each study day was assessed by comparing the changes in PD20 from baseline with the within-day variability of PD20 (standardized change in PD20). The acute bronchodilator effect was not significantly different as assessed 15 min (21 +/- 14% for albuterol and 18 +/- 18% for formoterol) and 1 h (20 +/- 13% for albuterol and 18 +/- 17% for formoterol) after administering the medication. The duration of the blocking effect, defined as the return to 2 SD from the standardized change in PD20, was significantly more prolonged for formoterol (8.0 +/- 3.4 h) than for albuterol (3.0 +/- 1.7 h) (t = 4.2, p less than 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Inhalation↗

PubMed2003

Neurokinins modulate hyperventilation-induced bronchoconstriction in canine peripheral airways.

This study was designed to test the hypotheses that (1) neurokinin (NK) receptor activity modulates hyperventilation-induced bronchoconstriction (HIB) in canine peripheral airways and (2) NK receptor activity is stimulated via hyperventilation-induced eicosanoid production and release. A bronchoscope was used in anesthetized dogs to record peripheral airway resistance (Rp); to test airway reactivity to NK A (NKA), substance P, and hypertonic saline; and to examine HIB before and after combined treatment with NK-1 (CP 99,994) and NK-2 (SR 48,968) receptor antagonists. Bronchoalveolar lavage fluid cells, prostaglandin D2, and cysteinyl leukotrienes from hyperventilated airways pretreated with either vehicle or NK antagonists were also measured. Pretreatment with NK-1 and NK-2 antagonists significantly attenuated HIB and the response to substance P, virtually abolished the response to NKA, and had little effect on the response to HS. Blockade of NK-1 and NK-2 receptors did not affect either the cell profiles or the mediator concentrations recovered in bronchoalveolar lavage fluid after hyperventilation. We conclude that NKs modulate the development of HIB and appear to do so via hyperventilation-induced eicosanoid production and release.

Animals↗

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↗

PubMed1994

Anxiogenic effects of CO2 and hyperventilation in patients with panic disorder.

OBJECTIVE: Previous studies have indicated that patients with panic disorder are more likely than normal subjects to have acute panic attacks during inhalation of CO2, but methodological objections have been raised. In this study the authors attempted to address three of these methodological problems by ensuring that raters who assessed whether panic attacks occurred were blind to subjects' diagnoses, by randomizing the order of administration of 5% CO2 and hyperventilation, and by challenging a greater number of subjects with 7% CO2. METHOD: Patients with panic disorder and normal subjects underwent 20-minute inhalations of 5% CO2 and 7% CO2 and 15 minutes of room-air hyperventilation. Ratings of panic/no panic during each condition were made separately by an assessor blind to diagnosis and by the subject. Scores on four panic rating scales were also recorded before and after each intervention. RESULTS: Room-air hyperventilation caused panic attacks in a small number of patients; the difference in panic rate between patients and comparison subjects was statistically significant by the subjects' but not by the raters' assessment. Panic rates during 5% CO2 and 7% CO2 were significantly greater among the patients by both assessments; the panic rate was greatest during 7% CO2. Order of administration did not significantly affect panic rates for hyperventilation and 5% CO2. CONCLUSIONS: Panic patients were clearly more sensitive to the anxiogenic effects of CO2 than comparison subjects, and CO2 was a more potent anxiogenic stimulus than room-air hyperventilation. Seven percent CO2 discriminated best between patients and comparison subjects and should be the focus of further research.

Administration, Inhalation↗

PubMed1990

Hyperventilation-induced reduction in cerebral blood flow: assessment by positron emission tomography.

The use of positron emission tomography (PET) has been well documented as a relatively noninvasive method of measuring cerebral blood flow (CBF), both globally and regionally. The utility of readily detecting alterations in CBF is apparent, particularly when applied to the evaluation of therapeutic interventions thought to influence CBF. We report the effects of hypocapnia, an experimental condition of known cerebral vasoconstriction, in ten normal volunteers. Subjects had brain blood flow evaluated utilizing H215O as the positron emitter before and after approximately five minutes of hyperventilation. Baseline CBF was measured as a mean +/- SD of 61.2 +/- 16.3 mL/min/100 g of tissue. Mean baseline arterial blood gas values were PaO2 107.4 +/- 14 mm Hg, PaCO2 37.7 +/- 0.89 mm Hg, and pH 7.39 (calculated from mean [H+]). Post hyperventilation, global CBF was measured as 31.1 +/- 10.8 mL/min/100 g. Mean arterial blood gas values were PaO2 141.7 +/- 21 mm Hg, PaCO2 19.7 +/- 5 mm Hg, and pH 7.63 (calculated from mean [H+]). CBF decreased by a mean of 49.5 +/- 11 percent. Data analysis using the Student's t-test showed a significant change over baseline in PaCO2 (p less than 0.001) and CBF (p less than 0.001), in the hyperventilated state. Correlations were noted between the decrease in CBF and change in PaCO2 (r = 0.81) as well as between hyperventilation PaCO2 and the change in CBF (r = 0.97). We conclude that, as measured by PET, CBF decreases significantly during a state of artificial hyperventilation to a degree consistent with results seen using other methods. PET appears to be a valuable tool in the assessment of interventions that could influence CBF.

Cerebrovascular Circulation↗

PubMedDate not supplied

Hyperventilation following a large-scale hazardous-materials incident.

Actual or perceived exposure to hazardous materials may result in physiologic and psychological effects. However, hyperventilation following such exposures has not previously been reported. After a large-scale industrial release of oxides of nitrogen, five (29%) of 17 patients evaluated at a major trauma center were hyperventilating, as defined by arterial PCO2 <33 mm Hg, and nine patients (53%) had arterial PCO2 <37 mm Hg. First responders (rescue team members and paramedics) had a higher rate of hyperventilation than other occupational groups. Age, gender, marital status, decontamination, and mode of arrival were not significantly associated with hyperventilation, although marital status approached significance. This study suggests that hyperventilation may be a common reaction after hazardous-materials incidents, and that certain populations may be at increased risk for this condition.

Adolescent↗

PubMed2005

The effects of sevoflurane and hyperventilation on electrocorticogram spike activity in patients with refractory epilepsy.

UNLABELLED: We investigated the effects of sevoflurane and hyperventilation on intraoperative electrocorticogram (ECoG) spike activity in 13 patients with intractable epilepsy. Grid electrodes were placed on the brain surface and ECoG was recorded under the following conditions: 1) 0.5 minimal alveolar anesthetic concentration (MAC) sevoflurane, 2) 1.5 MAC sevoflurane, and 3) 1.5 MAC sevoflurane with hyperventilation. The number of spikes per 5 min and the percentage of leads with spikes were assessed in each condition. In 4 patients with chronically implanted-subdural electrodes, the leads with seizure onset and with spikes during the interictal periods in the awake state were compared with those during sevoflurane anesthesia at 0.5 MAC and 1.5 MAC. The number of spikes and the percentage of leads with spikes were significantly more under 1.5 MAC sevoflurane anesthesia compared with those under 0.5 MAC sevoflurane (P < 0.05). The induction of hyperventilation significantly increased the number of spikes and percentage of leads with spikes (P < 0.05). With 0.5 MAC sevoflurane, the leads with spikes were similar to those at seizure onset in the awake state, whereas with 1.5 MAC sevoflurane, spikes were similar to those occurring during interictal periods in the awake state. These results indicate that sevoflurane and hyperventilation can affect the frequency and extent of ECoG spike activity in patients with intractable epilepsy. Careful attention should be paid to the concentration of sevoflurane used and ventilatory status when intraoperative EcoG is used to localize epileptic lesions. IMPLICATIONS: Electrocorticogram can be used to define the location and extent of epileptic foci during epilepsy surgery. However, electrocorticogram can be affected by anesthetic technique. The present study found that sevoflurane concentration and hyperventilation affected the frequency and the extent of electrocorticogram spike activity in epileptic patients.

Adult↗

PubMed2003

A case of adversive seizures induced by hyperventilation.

We report a case of adversive seizures featuring neck rotation and conjugate deviation induced by the hyperventilation maneuver. At the age of 6 years the patient suffered from conjugate deviation to the left. She herself felt no symptoms other than oculomotor symptoms. Hyperventilation induced an adversive seizure and ictal EEG showed sharp waves in the right frontal, central, and parietal areas. No brain image showed abnormal findings. Zonisamide completely attenuated her attacks. It is well known that hyperventilation induces absence seizures, and it has been reported that hyperventilation can induce complex partial seizures. However, no previous reports have described patients diagnosed as having adversive seizures with conjugate deviation induced by hyperventilation. We report the present case because, although its epileptogenesis is unknown, the patient is a rare case not only clinically but also electrophysiologically.

Child↗

PubMed1975

Hyperventilation-induced T-wave changes in the limb lead electrocardiogram.

Seventy-two healthy young individuals were subjected to controlled, moderate hyperventilation with room air and with 4.9 percent CO2 in air, and monitored electrocardiographically. Significant summed frontal T-wave changes with hyperventilation (sigmaT1,2,3 larger than or equal to 1.5 mm) were observed in 12 patients. Six subjects (8.3 percent) showed T-wave depression. It was reversed in five patients by hyperventilation with 4.9 percent CO2 in air. T-wave elevation, observed in six subjects, was reversed in four patients by hyperventilation with 4.9 percent CO2. A short period of hyperventilation with an air mixture containing 4-5 percent CO2 is suggested as a means of screening patients under suspicion of ischemic heart disease exclusively on the basis of ECG changes.

Adolescent↗

PubMed1999

Panic disorder and hyperventilation.

UNLABELLED: Respiratory abnormalities are associated with anxiety, particularly with panic attacks. Symptoms such as shortness of breath, "empty-head" feeling, dizziness, paresthesias and tachypnea have been described in the psychiatric and respiratory physiology related to panic disorder. Panic disorder patients exhibit both behaviorally and physiologically abnormal responses to respiratory challenges tests. OBJECTIVE: We aim to observe the induction of panic attacks by hyperventilation in a group of panic disorder patients (DSM-IV). METHOD: 13 panic disorder patients and 11 normal volunteers were randomly selected. They were drug free for a week. They were induced to hyperventilate (30 breaths/min) for 3 minutes. Anxiety scales were taken before and after the test. RESULTS: 9 (69.2%) panic disorder patients and one (9.1%) of control subjects had a panic attack after hyperventilating (p < 0.05). CONCLUSION: The panic disorder group was more sensitive to hyperventilation than normal volunteers. The induction of panic attacks by voluntary hyperventilation may be a useful and simple test for validating the diagnosis in some specific panic disorder patients.

Adult↗

PubMed1992

Eucapnic hyperventilation-induced bronchoconstriction in rabbits.

We examined whether eucapnic hyperventilation with dry air produces the bronchoconstriction in anesthetized, non-sensitized rabbits and in ovalbumin sensitized rabbits. Eucapnic hyperventilation challenge with dry air containing 5% CO2 at room temperature was performed with 4 non-sensitized and 7 sensitized rabbits by mechanical ventilation for 15 min (120 breaths/min, 7 ml tidal volume/kg body weight). Total lung resistance (RL) and dynamic compliance (Cdyn) were measured before and 0, 5, 15, and 30 min after hyperventilation. In non-sensitized rabbits, RL and Cdyn did not change significantly. However, in sensitized rabbits, RL increased maximally by 48.9% +/- 9.0% at 5 min, and then decreased to the baseline level at 30 min after challenge. Cdyn decreased maximally by 12.5% +/- 3.5% at 15 min after challenge. These changes were significantly different from the baselines (p < 0.05). Furthermore, to investigate the role of histamine on hyperventilation-induced bronchoconstriction (HIB) in sensitized rabbits, we performed the hyperventilation challenges in 5 sensitized rabbits with the pretreatment of H1-receptor antagonist (chlorpheniramine, 1 mg/kg, i.v.) and found that the maximum increment of RL was suppressed to 24.2% +/- 7.4% of the control, which was significantly lower than the maximal RL in nontreated sensitized rabbits (p < 0.05). We concluded that HIB occurs only in sensitized rabbits and that histamine may play an important role in the development of HIB in sensitized rabbits.

Airway Resistance↗