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PubMed1998

Increased excitability of the human corticospinal system with hyperventilation.

OBJECTIVES: Hyperventilation is effective in inducing generalized spike-wave discharges in patients with absence seizures and improves visual function and normalizes visual function in patients with multiple sclerosis. Hyperventilation increases the excitability of cutaneous and motor axons. In experimental animals, hyperventilation increases excitability of hippocampal neurons. There is however no direct evidence of a hyperventilation-induced increase in neuronal excitability within the central nervous system in humans. In this study we determined the effects of hyperventilation on the human corticospinal system. METHODS: We studied the effects of hyperventilation on (1) motor evoked potentials (MEPs) induced by transcranial magnetic pulse stimulation of the motor cortex and (2) F-wave responses. Six subjects were studied. RESULTS: Hyperventilation resulting in an end-tidal pCO2 of 15 mm Hg or less enhanced the amplitude of the MEP and resulted in a shortened onset latency. F-wave amplitudes were enhanced without any change in onset latency. CONCLUSIONS: These findings indicate that hyperventilation increases the excitability of the human corticospinal system. A hyperventilation-induced increase in excitability within the central nervous system may account for clinical phenomena such as facilitation of spike-wave discharges.

Adult↗

PubMed1996

Hyperventilation alters colonic motor and sensory function: effects and mechanisms in humans.

UNLABELLED: BACKGROUND & AIMS. Hyperventilation-induced hypocapnia affects hemodynamic function and enhances colonic motility. The aims of this study were to determine the effects of hypocapnic hyperventilation on colonic motility and sensation in health and to explore the putative neurohumoral mechanisms. METHODS: In experiment 1, colonic tone, sensation, plasma levels of cortisol, beta-endorphin, selected gut neuropeptides, norepinephrine, epinephrine, and splanchnic blood volume were measured during two sequences of hypocapnic hyperventilation. In experiment 2, colonic tone and sensation were assessed during eucapnic hyperventilation and abdominal compression. RESULTS: Hypocapnic hyperventilation, but not eucapnic hyperventilation or abdominal compression, significantly increased colonic tone and sensitivity to balloon distention (P = 0.017) without altering humoral mediators or splanchnic blood volume. Plasma norepinephrine level increased (P = 0.017) and splanchnic blood volume decreased (P = 0.028) during 5 minutes after hyperventilation, consistent with homeostatic responses. CONCLUSIONS: Increased colonic tone and sensation during hypocapnic hyperventilation are not caused by colonic compression. These effects of hyperventilation are not mediated humorally but may result from direct metabolic effects of hypocapnia on colonic muscle or from changes in central autonomic control of colonic smooth muscle.

Adult↗

PubMed1997

Excitability changes in human sensory and motor axons during hyperventilation and ischaemia.

This study was undertaken to compare the excitability changes of sensory and motor axons during hyperventilation and ischaemia, and to determine why ectopic impulse activity develops more readily during hyperventilation, and in sensory fibres. During hyperventilation for 20 min, all six subjects reported paraesthesiae in the hand and face, and four out of the six developed muscle twitching and cramps, associated with significant decreases of 20-30% in the threshold current required to produce sensory and motor potentials of constant size. During ischaemia four out of the six subjects reported paraesthesiae, but none reported muscle twitching. There were significant decreases of 15-20% in threshold for sensory and motor fibres. Ischaemia produced a marked decrease in supernormality, an increase in refractoriness and an increase in latency of the test compound sensory or motor potential, changes that were not seen with hyperventilation. The decrease in threshold during these manoeuvres was associated with a significant increase in strength--duration time constant (tau SD), indicating a relatively greater decrease in rheobase current. Using the technique of latent addition, we found that the changes in tau SD were consistent with a recently proposed model in which non-inactivating, voltage-dependent 'threshold channels' (presumably persistent Na+ channels) are active at resting potential. The failure of hyperventilation to alter conduction velocity, refractoriness or supernormality appreciably indicates that, unlike ischaemic depolarization, hyperventilation does not increase inactivation of conventional Na+ channels or activation of K+ channels, and this implies that the hyperventilation-induced increase in excitability is not the result of conventional depolarization, as seems to occur during ischaemia. These results suggest that hyperventilation has a rather selective action on the threshold channels, and they help to explain its greater effectiveness compared with ischaemia in provoking ectopic discharges. The greater expression of threshold channels in sensory than in motor fibres can explain why hyperventilation induces paraesthesiae before fasciculation and why only paraesthesiae occur during ischaemia.

Action Potentials↗

PubMed1988

Hyperventilation in the awake state: potentially treatable component of Rett syndrome.

Hyperventilation, which occurs in some patients with severe mental handicap, is a prominent feature in the histories of most girls with Rett syndrome but its mechanism and effects have not been established. Respiratory function was therefore studied in 18 patients with Rett syndrome and 23 healthy controls. Ten of the patients (56%), but none of the controls, hyperventilated only when awake, and began doing so after a period of normal breathing without hypoxaemia. After hyperventilation was established it was interspersed with prolonged periods of apnoea (over 19 seconds) accompanied by Valsalva manoeuvres. Hypoxaemia (less than 90%) occurred in 47% of these periods of apnoea and five (50%) of the patients had oxygen saturation values of under 50%. During hyperventilation severe hypocapnia developed in every patient, and recorded arterial pH measurements ranged from 7.47 to 7.60. A further four patients (22%) did not hyperventilate, but had clear histories of hyperventilation when younger. All had frequent apnoeic pauses accompanied by Valsalva manoeuvres. The remaining four girls (22%) neither hyperventilated nor gave a clear history of doing so. Three had occasional apnoeic pauses associated with the Valsalva manoeuvres. All but one of the 18 patients had increased quantities of periodic apnoea compared with the control subjects. The hypocapnic alkalaemia and hypoxaemia resulting from hyperventilation may contribute to the cerebral impairment in Rett syndrome. Since the hyperventilation is 'primary', and not secondary to preceding apnoea, it is potentially treatable. Further studies will determine if treatment is practical and of benefit.

Adolescent↗

PubMed1993

Effect of hyperventilation and mental stress on coronary blood flow in syndrome X.

OBJECTIVES: To assess the effect of hyperventilation and mental stress on coronary blood flow and symptom production in patients with syndrome X. DESIGN: A prospective study. Hyperventilation and mental stress tests were performed on the ward and were repeated in the cardiac catheter laboratory where coronary blood flow velocity was also measured with an intracoronary Doppler catheter in the left anterior descending coronary artery. Oesophageal manometry studies were also performed. PATIENTS: 29 patients with syndrome X (typical anginal chest pain, a positive exercise test, and normal coronary angiogram). SETTING: A regional cardiothoracic centre. RESULTS: Hyperventilation produced typical chest pain in 16 patients on the ward. 13 patients experienced their typical chest pain with mental stress test 5. Ten patients experienced chest pain with both hyperventilation and mental stress tests. This pattern was reproduced exactly when the tests were repeated in the cardiac catheter laboratory. Hyperventilation produced a significant increase in the rate-pressure product during ward and laboratory testing. There was, however, no significant change in the rate-pressure product on mental stress tests. The mean (SEM) coronary flow velocity decreased significantly on hyperventilation in the catheter laboratory from 10.0 (0.92) cm/s to 5.9 (0.72) cm/s (p < 0.001). There was also a significant reduction in the mean (SEM) coronary blood flow velocity on mental stress tests from 9.8 (0.86) cm/s to 7.4 (0.6) cm/s (p < 0.001). This reduction in flow velocity occurred in the absence of any changes in diameter of the left anterior descending artery. Further analysis showed that the coronary flow velocity was reduced significantly in only that group of patients in which hyperventilation and mental stress provoked chest pain. There was a significant increase in the arterial concentrations of noradrenaline on both hyperventilation and mental stress testing. Oesophageal manometry showed abnormalities in 17% of patients. CONCLUSIONS: Both hyperventilation and mental stress can produce chest pain in patients with syndrome X and this is associated with a reduction in coronary blood flow velocity. The results of this study suggests that this reduction in coronary flow occurs as a result of increased microvascular resistance.

Adult↗

PubMed1997

The pattern of breathing following a 10-breath voluntary hyperventilation during hyperoxic rebreathing.

The pattern of breathing following a 10-breath voluntary hyperventilation period during hyperoxic rebreathing was compared to that without hyperventilation in 6 subjects (3 male and 3 female). The aim was to measure the posthyperventilation short-term potentiation of ventilation without changes in respiratory chemoreflex drives induced by the voluntary hyperventilation. Hyperoxia was used to reduce the peripheral chemoreflex drive, and rebreathing to prevent the decrease in arterial carbon dioxide tension normally produced by hyperventilation. There were significant differences between the male and female responses. However, in all subjects, ventilation and heart rate were increased during hyperventilation but end-tidal partial pressures of carbon dioxide and oxygen were unchanged. Following hyperventilation, ventilation immediately returned to the values observed when hyperventilation was omitted. Hyperventilation did not induce a short-term potentiation of ventilation under these conditions; changes in chemoreflex stimuli brought about by cardiovascular changes induced by hyperventilation may play a role in the short-term potentiation observed under other circumstances.

Adult↗

PubMed1997

Alpha 2-adrenergic modulation of colonic tone during hyperventilation.

Our aims were to assess the role of adrenergic modulation in the hyperventilation-induced increase in colonic tone. Of 40 healthy volunteers, 12 received placebo (saline) and the remaining 28 received either clonidine, yohimbine, phenylephrine, or ritodrine. Time-frequency mapping of heart rate based on Wigner distribution assessed variations in parasympathetic and sympathetic activity during hyperventilation. Tone in the descending colon was recorded by a barostat balloon before, during, and after 5 min of hyperventilation. Heart rate spectral analysis suggested diminished sympathetic and vagal activity during hyperventilation and increased sympathetic and vagal activity after hyperventilation. Adrenergic agents influenced (P = 0.01) the tonic response after, but not during, hyperventilation. Yohimbine reduced the increment in colonic tone after hyperventilation compared with saline (P < 0.05) and clonidine (P = 0.002); phenylephrine and ritodrine had no effects. Different mechanisms modulate the increase in colonic tone during and after hyperventilation. Yohimbine attenuates the increase in colonic tone after hyperventilation probably by enhancing inhibitory sympathetic input to the colon.

Adrenergic alpha-Agonists↗

PubMed1993

Ventilatory work and oxygen consumption during exercise and hyperventilation.

The work of breathing (WB), and thus the energy requirement of the respiratory muscles, is increased any time minute ventilation (VE) is elevated, by either exercise or voluntary hyperventilation. Respiratory muscle O2 consumption (VRMO2) in humans has generally been estimated by having subjects breathe at a level comparable to that during exercise while the change in O2 consumption (VO2) is measured. The difference between VO2 at rest and during hyperventilation is attributed to the respiratory muscles and is assumed to be similar to VRMO2 during exercise at the same VE. However, it has been suggested that WB differs between exercise and hyperventilation and that WB during exercise is lower than during hyperventilation at the same VE. In this study we measured WB during exercise and hyperventilation and from these measurements estimated VRMO2. WB, VE, and VO2 were measured in five male subjects during rest and during exercise or hyperventilation at levels of VE ranging from 30 to 130 l/min. VE/WB relationship was determined for both hyperventilation and exercise. Multiple regression analysis showed that the shape of the two curves was different (P < 0.0001), with WB at high levels of VE being < or = 25% higher in hyperventilation than in exercise. In a second study in which frequency, tidal volume, and duty cycle were controlled as well as VE, there was no difference in WB between exercise and hyperventilation. VO2 was significantly correlated with WB, and the estimated VRMO2 did not increase as a fraction of total VO2 as exercise intensity rose.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1989

Effect of magnesium on anginal attack induced by hyperventilation in patients with variant angina.

To examine whether or not magnesium suppresses coronary spasm, the effect of magnesium infusion on anginal attacks induced by hyperventilation was studied in 20 patients with variant angina. In all patients, anginal attacks associated with ischemic ST segment changes on the electrocardiogram were repeatedly induced by hyperventilation. The study was performed in the early morning successively for 3 days. On days 1 and 3 (control studies), 50 minutes before the hyperventilation test, a 5% glucose solution was infused as a placebo. On day 2 (magnesium study), 50 minutes before the hyperventilation test, magnesium sulfate (0.27 mM/kg body wt) was infused during a 20-minute period. During the control studies, anginal attack was induced by hyperventilation in all 20 patients, whereas during the magnesium study, anginal attack was induced by hyperventilation in only six (30%) of the 20 patients (p less than 0.001 vs. control studies). The changes in arterial blood pH and PCO2 caused by hyperventilation were not significant between the control study and the magnesium study. Mean serum magnesium concentration increased from 2.2 +/- 0.2 to 6.0 +/- 0.5 mg/dl immediately after infusing magnesium and was 4.5 +/- 0.6 mg/dl before the hyperventilation test during the magnesium study. We conclude that magnesium suppresses anginal attacks induced by hyperventilation in patients with variant angina.

Aged↗

PubMed1997

Unsteadiness of breathing in patients with hyperventilation syndrome and anxiety disorders.

The breathing pattern of 399 patients with hyperventilation syndrome (HVS) and/or with anxiety disorders and that of 347 normal controls was investigated during a 5 min period of quiet breathing and after a 3 min period of voluntary hyperventilation. 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. The anxiety disorders were diagnosed by means of an abbreviated version of the Anxiety Disorders Interview Schedule (ADIS). There was a large overlap between the two diagnoses. Simply breathing via a mouthpiece and pneumotachograph made end-tidal CO2 fractional concentration (FET,CO2) decrease progressively both in hyperventilators and in patients with anxiety disorders, but not in normals. At the start of the measurement the FET,CO2 was not different between patients and healthy subjects. In patients < or = 28 yrs, the decrease of FET,CO2 resulted from a higher tidal volume, and in patients > or = 29 years from an increase in frequency. After voluntary hyperventilation, the recovery of FET,CO2, was delayed in patients, due to a slower normalization of respiratory frequency in females and in older males, and of tidal volume in younger males, and also due to less frequent end-expiratory pauses. When breathing was recorded first by means of inductive plethysmography (Respitrace), the progressive decline of FET,CO2 seen in patients was not observed: from the onset of the recording, FET,CO2 was reduced in patients. It did not change further when, immediately afterwards, the subject switched to mouthpiece breathing. The finding that breathing through a mouthpiece induces hyperventilation in patients and that recovery of FET,CO2 is delayed after voluntary hyperventilation, suggests that the respiratory control system is less resistant to challenges (mouthpiece or voluntary hyperventilation) in those patients. On the other hand, the lower values of FET,CO2 measured during recording by means of a Respitrace probably result from a challenge, prior to the recordings, induced by the fitting of the measuring device to the patient. This unsteadiness of breathing characterizes patients with hyperventilation syndrome and those with anxiety disorders, but is not sufficiently sensitive to be used for individual diagnosis.

Adult↗

PubMed1985

[Cerebral angiography following hyperventilation in moyamoya disease--in reference to the "re-build up" phenomenon on EEG].

It is a well known fact that ischemic symptoms are apt to be induced after hyperventilation in child case of Moyamoya disease. We have previously noted that characteristic EEG findings are seen after hyperventilation in this disease. Among these findings, characteristic slow waves which appear after the disappearance or attenuation of ordinary build up have been labelled as "re-build up". Since this phenomenon is highly pathognomonic, we have been evaluating EEG records as an important screening test for childhood Moyamoya disease. Sequential angiograms were taken to understand the nature and pathophysiology of the "re-build up" phenomenon. We now report some interesting findings thought to be related to the particular hemodynamics and pathology of childhood Moyamoya disease. Hyperventilation angiography was performed in 17 patients with Moyamoya disease (7 children, 5 adults whose onset was in childhood and 5 adults). A control study was performed in 5 patients (one child and 4 adults) who were angiographically normal. In each patient, the presence or absence of the "re-build up" phenomenon in the EEG was determined within 1 month prior to the angiographical examination. Angiography was performed prior to 3 minutes of hyperventilation and in the period of "re-build up" under the same conditions with respect to position, site of the catheter tip, volume and the rate of injected contrast media and timing of angiography. In control cases and those cases which did not show "re-build up," angiography was performed 1 minute after termination of hyperventilation. During examination, serial arterial blood sampling was carried out for blood gas analysis. In two cases of Moyamoya disease, hyperventilation under inhalation of 8% CO2 was also performed. In patients with Moyamoya disease who showed the "re-build up" phenomenon, angiographical vascular changes such as decrease in the size of basal Moyamoya and decrease in the diameter of cortical arteries appeared together with "re-building up." These vascular changes are thought to be closely related to the "re-build up" phenomenon. In control cases and adult patients, these findings were not observed. Since these vascular changes did not occur in patients with the "re-build up" phenomenon after hyperventilation of 8% CO2, this phenomenon is thought to be initiated as a direct result of decreased arterial CO2 tension. Although during hyperventilation PaO2 increased, after hyperventilation it decreased significantly while the EEG showed "re-build up".(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗

PubMedDate not supplied

[Induction of coronary artery spasm by combined cold pressor and hyperventilation test in patients with variant angina].

To examine whether or not a combination of nonpharmacologic provocative tests potentiated the occurrence of coronary spasm, the cold pressor test combined with hyperventilation was studied in 22 consecutive patients with variant angina admitted to our hospital. After a 12-lead electrocardiogram and blood pressure were recorded, the patient was asked to hyperventilate vigorously at a rate of 30 respirations per min for 6 min under continuous electrocardiographic monitoring. Immediately after hyperventilation, the cold pressor test was performed with the patient's right hand submerged in ice water for 2 min. In some patients who showed a positive response to the combined test, a hyperventilation and cold pressor test was performed on another day. Positive response (ST segment elevation > or = 0.1 mV) to the combination test was seen in 18 of 22 patients (82%). Positive response to the hyperventilation test was seen in seven of 11 patients (64%). The response to cold pressor test was all negative in seven patients. The onset of electrocardiographic changes by the combined test occurred an average of 120 sec (30-240 sec) after the end of hyperventilation, whereas the onset by hyperventilation test occurred an average of 210 sec later (60-370 sec). These results suggest the combination of the cold pressor test and hyperventilation test potentiated the occurrence of coronary spasm. The combined cold pressor and hyperventilation test is a powerful and useful nonpharmacologic provocative test for coronary artery spasm in patients with variant angina.

Adult↗

PubMed1995

[Simultaneous measurement of arterial and end-expiratory carbon dioxide before, during and after voluntary hyperventilation].

Hyperventilation syndrome is considered an established diagnosis if it is confirmed that the patient's complaints correlate with arterial hypocapnia. In the diagnostic criteria set up by a group in Nijmegen, paCO2 is determined indirectly by measuring the end tidal CO2. Values below 4 kPa measured at rest and 10 or more minutes after deliberate hyperventilation are classified positive diagnostic criteria for hyperventilation syndrome. However, it has not been proven that end tidal pCO2 agrees well with paCO2 during the entire manoeuvre. We performed simultaneous measurements of both parameters in 10 healthy non-smokers, before, during and after 3 minutes of deliberate hyperventilation. A comparison of the values employed for diagnosing a hyperventilation syndrome (during normal respiration before and 10 and more minutes after hyperventilation) yields a mean difference of 0.39 kPa according to the statistical computation described by Bland and Altman (limits of the range of agreement between 0.98 and -0.18). The end tidal CO2 values measured during the normal respiratory phase as well as 10 and more minutes after hyperventilation, agree well with the arterial values (the arterial values being slightly higher). During and shortly after hyperventilation the values obtained by both methods differ from one another, so that the exact degree of hypocapnia during a hyperventilation period cannot be assessed by measuring the end tidal CO2.

Adult↗

PubMed1998

Hyperventilation impairs oxygenation after bidirectional superior cavopulmonary connection.

BACKGROUND: Bidirectional superior cavopulmonary connection (BSCC) may be complicated by systemic hypoxemia. Hyperventilation, which is standard therapy for postoperative hypoxemia, has opposing effects on the pulmonary and cerebral vascular beds, which are connected after BSCC. It is unknown which of these effects predominates and, therefore, whether hyperventilation improves or impairs systemic oxygenation after BSCC. METHODS AND RESULTS: Twelve consecutive patients (median age, 6.4 months; age range, 6.0 to 32.0, months) undergoing BSCC were studied prospectively. Patients were studied in the intensive care unit within 6 hours of surgery and while sedated, paralyzed, and mechanically ventilated. Inotropes were not altered, and no transfusions were given. FIO2 was set at 100%, and peak end-expiratory pressure was set at 0. Each patient was studied first during normal ventilation, then during hyperventilation, and finally again during normal ventilation. Hyperventilation resulted in significant decreases in arterial PO2, systemic oxygen saturation, and transpulmonary gradient. Cerebral blood flow velocity was measured in 6 patients through transcranial Doppler sonography of the middle cerebral artery. Mean cerebral flow velocity decreased significantly during hyperventilation. CONCLUSIONS: Hyperventilation significantly impairs systemic oxygenation after BSCC. This fall in oxygenation occurs despite a decrease in transpulmonary gradient. A possible mechanism for this effect is that hyperventilation lowers arterial PCO2, raising cerebral vascular resistance, and lowering cerebral, superior vena caval, and pulmonary blood flows. Supportive evidence for this mechanism is the decrease in cerebral flow velocity that occurs during hyperventilation. After BSCC, normal ventilation rather than hyperventilation should be used to improve systemic oxygen levels.

Adolescent↗

PubMed1985

The effect of verapamil and inspired CO2 on the bronchoconstriction provoked by hyperventilation in normal humans.

Two groups of eight normal subjects were investigated in separate studies to demonstrate the effects of changes in end-tidal PCO2, and of pretreatment with the calcium antagonist drug verapamil, on bronchoconstriction provoked by voluntary hyperventilation. Total respiratory resistance (Ros) was measured by the forced oscillation technique before and after 90 s voluntary hyperventilation. End-tidal PCO2 during hyperventilation was varied by altering inspired CO2 concentration. When end-tidal PCO2 fell during hyperventilation, there was a rise in Ros. This did not occur if end-tidal PCO2 was controlled at a normal resting level during hyperventilation. Specific conductance (sGaw) was measured before and after 90 s voluntary hyperventilation of air. Subjects were treated with oral verapamil or placebo for 2 1/2 days and the effect of hyperventilation on sGaw was reassessed. Verapamil reduced significantly the fall in sGaw caused by hyperventilation. Placebo had no effect. In normal humans, bronchoconstriction provoked by hyperventilating air at ambient temperature and humidity is mediated by the fall in PCO2, and is also reduced by verapamil.

Adult↗

PubMed1988

Mechanisms of the haematological changes induced by hyperventilation.

During voluntary hyperventilation an increase in the lymphocyte and thrombocyte counts occurs, paralleled by an increase in plasma epinephrine and norepinephrine. All these changes are rapidly reversible after hyperventilation and are followed by an increase in the neutrophil granulocyte count. The pathophysiological mechanisms of these changes were investigated by comparison of the hyperventilation-induced changes of the blood picture in 11 normal, 9 splenectomized and 12 beta-blocked volunteers. Splenectomy did not affect the hyperventilation-induced mobilization of lymphocytes and neutrophils but totally suppressed the change in the thrombocyte count. beta-blockade by 80 mg propranolol did not suppress the hyperventilation-induced increase in neutrophils. It reduced the absolute increase of lymphocytes and thrombocytes by half, but it also increased the baseline counts of these cells. The study shows that hyperventilation mobilizes thrombocytes from the spleen but not from extralienal pools, and that lymphocytes and neutrophils are mobilized from extralienal pools. Whereas neutrophil mobilization is not suppressed by beta-blockade, the reduction of hyperventilation-induced mobilization of lymphocytes and thrombocytes may be due to a reduction in the size of the mobilizable cell pools, and therefore cannot be interpreted as a sure indication that adrenergic mechanisms are involved in their hyperventilation-induced mobilization.

Adult↗

PubMed1989

The hyperventilation syndrome in panic disorder, agoraphobia and generalized anxiety disorder.

The symptom complex of panic disorder and generalized anxiety disorder suggests an etiological role for hyperventilation. The present study investigates the overlap between DSM-III-R panic disorder, panic disorder with agoraphobia and generalized anxiety disorder with hyperventilation syndrome (HVS). The anxiety disorder diagnoses were based on a structured interview, and HVS syndrome (HVS). The anxiety disorder diagnoses were based on a structured interview, and HVS determined by the so-called hyperventilation provocation test (a brief period of voluntary hyperventilation with recognition of symptoms). The overlap rates with HVS were: 48% for panic disorder, 83% for panic disorder with agoraphobia and 82% for generalized anxiety disorder. However, a pilot study on transcutaneous monitoring of carbon dioxide tension leads us to question the validity of the voluntary hyperventilation method that we used to determine HVS-status. It is unclear whether hyperventilation plays an important role in panic and general anxiety, as our overlap findings suggest. For patients who recognize the symptoms induced by voluntary hyperventilation, the hyperventilation provocation procedure provides a therapeutic means of exposure to feared bodily sensations.

Adult↗

PubMed1997

Hyperventilation as a specific test for diagnosis of coronary artery spasm.

The hyperventilation test has been used as a clinical tool to induce coronary spasm. However, its diagnostic and prognostic values have not been fully elucidated. This study was designed to establish the sensitivity and specificity of the hyperventilation test and to clarify the characteristics of hyperventilation test-positive patients. We examined 206 patients in whom coronary spasm was documented by angiography (spasm group), and 183 patients without angina at rest in whom acetylcholine failed to induce spasm (nonspasm group). All patients performed vigorous hyperventilation for 6 minutes in the early morning. Of the spasm group patients, 127 showed positive responses to the test, including ST elevation (n = 111), ST depression (n = 15) and negative U wave (n = 1). None in the nonspasm group showed any ischemic electrocardiographic change. Thus, the sensitivity and specificity of this test for diagnosis of coronary spasm were 62% and 100%, respectively. In the spasm group, there were no significant differences between hyperventilation test-positive and test-negative patients in age, sex, the prevalence of hypertension, diabetes mellitus, obesity, smoking, and the number of diseased vessels. When clinical characteristics were compared, the proportions of the patients with high disease activity (> or =5 attacks a week), with severe arrhythmias (second- or third-degree atrioventricular block and/or ventricular tachycardia) during attacks, and with multivessel spasm were significantly higher in the hyperventilation test-positive patients than in the negative patients (69% vs 20%, p <0.0001; 31% vs 11%, p <0.005; and 58% vs 34%, p <0.01, respectively). These findings imply that hyperventilation is a highly specific test for the diagnosis of coronary artery spasm, and that hyperventilation test-positive patients are likely to have life-threatening arrhythmias during attacks and multivessel spasm.

Adult↗