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PubMed2001

Role of nitric oxide during hyperventilation-induced bronchoconstriction in the guinea pig.

Airway function is largely preserved during exercise or isocapnic hyperventilation in humans and guinea pigs despite likely changes in airway milieu during hyperpnea. It is only on cessation of a hyperpneic challenge that airway function deteriorates significantly. We tested the hypothesis that nitric oxide, a known bronchodilator that is produced in the lungs and bronchi, might be responsible for the relative bronchodilation observed during hyperventilation (HV) in guinea pigs. Three groups of anesthetized guinea pigs were given saline and three groups given 50 mg/kg N(G)-monomethyl-L-arginine (L-NMMA), a potent nitric oxide synthase inhibitor. Three isocapnic ventilation groups included normal ventilation [40 breaths/min, 6 ml/kg tidal volume (VT)], increased respiratory rate only (150 breaths/min, 6 ml/kg VT), and increased respiratory rate and increased volume (100 breaths/min, 8 ml/kg VT). L-NMMA reduced expired nitric oxide in all groups. Expired nitric oxide was slightly but significantly increased by HV in the saline groups. However, inhibition of nitric oxide production had no significant effect on rate of rise of respiratory system resistance (Rrs) during HV or on the larger rise in Rrs seen 6 min after HV. We conclude that nitric oxide synthase inhibition has no effect on changes in Rrs, either during or after HV in guinea pigs.

Airway Resistance↗

PubMed1992

Widespread reduction of regional cerebral blood flow during hyperventilation-induced EEG slowing ('buildup'). Observation from subtraction of brain imaging with single photon emission computed tomography using technetium-99m hexamethyl-propyleneamine oxime.

To study the pathophysiological mechanisms of hyperventilation-induced EEG showing, i.e., the so-called 'buildup' phenomenon, changes in regional cerebral blood flow (rCBF) were investigated before and during the phenomenon in a 16-year-old woman with headache, thought to be of neurotic origin, by subtraction technique of brain images with single photon emission computed tomography using technetium-99m hexamethyl-propyleneamine oxime (99mTc-HMPAO). The tracer uptake during buildup decreased by 31-42% as compared to baseline values at rest before buildup in all of the measured regions, reflecting a widespread reduction in rCBF. Gas analyses of arterial blood collected during buildup showed a decrease in PaCO2, and increases in PaO2 and pH with a slight decrease in blood pressure and an increase in pulse rate. These results directly demonstrate a close correlation between the hyperventilation-induced EEG and rCBF changes, suggesting that the buildup phenomenon results from cerebral ischemic change, presumably due to cerebral vasoconstriction caused by the PaCO2 decrease.

Adolescent↗

PubMed1983

Beta-blockade in the hyperventilation syndrome. A retrospective assessment of symptoms and complaints.

The effect of beta-adrenergic blockade on ventilatory parameters and on subjective complaints was studied in 73 patients suffering from hyperventilation syndrome. The beta-blockade made the PA,CO2 increase as much as tranquillizer therapy. No effect of any kind of therapy was found on the subjective complaints. A remarkable dissociation was found between the measured ventilatory parameters and the quantified subjective complaints. It is concluded that beta-blockade is an effective therapy for the basic problem of hypocapnia in the hyperventilation syndrome; in this respect it is to be preferred over other therapies such as tranquillizers.

Adult↗

PubMed1993

Elevated ventilatory equivalents during exercise in patients with hyperventilation syndrome.

In hyperventilation syndrome (HVS), hyperventilation is often provoked by exercise. This study was undertaken to investigate gas exchange parameters and their correlation to arterial blood gas values in HVS patients during exercise. Ventilatory equivalents for oxygen (VE/VO2) and carbon dioxide (VE/VCO2) were significantly higher in HVS patients than in the controls. (VE/VO2) during light exercise (40-50 W) was 23.1 +/- 2.7 (n = 10) in the controls and 35.2 +/- 8.2 (n = 10) in the HVS group (p < 0.01). VE/VCO2 during light exercise was 30.0 +/- 3.3 in the controls and 41.8 +/- 6.0 in the HVS group (p < 0.01). In HVS, significantly correlations were observed between VE/VCO2 and PaCO2, and between VE/VO2 and PaCO2 during both light and maximal exercise (p < 0.02). The findings suggest that exercise testing can be used to aid HVS diagnosis without invasive arterial cannulation.

Adult↗

PubMed1980

Role of stress in the development of the hyperventilation syndrome.

The occurrence of the hyperventilation syndrome (HVS) has often been associated with stress. In this experiment with normal subjects responses of PACO2, respiration rate, heart rate and checklist measures were registered in a stressful, real-life situation, namely waiting for an examination. Heart rate and one checklist measure showed a significant arousal response. There was a small but significant decrease in PACO2 from a precontrol session to the stress session, but PACO2 had not returned to base level on a postcontrol session. Respiration rate did not change at all. Similar results in other experiments led to the conclusion that stress brings about only a mild degree of hyperventilation in normal subjects. The discrepancy with results found in HSV patients has been discussed.

Adult↗

PubMed1975

Impairment of myocardial O2 supply due to hyperventilation.

Thirteen patients with ischemic coronary heart disease purposely hyperventilated for seven minutes in order to induce hypocapnic alkalosis. One patient experienced chest pain, and one exhibited chemical signs of myocardial hypoxia. Heart rate, blood pressure and myocardial O2 consumption did not change significantly. Coronary blood flow decreased and coronary (a-v)O2 difference widened. Since the alkalosis increased the blood O2 affinity, the fall in PO2 in coronary venous blood was proportionately even greater than the fall in O2 concentration. Thus, hypocapnic alkalosis due to hyperventilation interferes with myocardial O2 supply by 1) coronary vasoconstriction and 2) increased O2 affinity of blood.

Coronary Circulation↗

PubMed1978

Coronary arterial spasm and Prinzmetal's variant form of angina induced by hyperventilation and Tris-buffer infusion.

Vigorous hyperventilation was induced for five minutes immediately after a five-minute infusion of 100 ml of Tris-buffer (pH 10) in nine patients with Prinzmetal's variant angina. In eight of the patients, chest pain with ischemic changes in the electrocardiogram occurred during this procedure or within five minutes after it ended. Coronary arterial spasm appeared after the procedure and disappeared after the administration of nitroglycerin in all four patients in whom coronary cinearteriography was performed. This was evident both before and after the procedure and after sublingual administration of nitroglycerin (0.6 mg). The oral administration of 90 mg of diltiazem, a calcium antagonistic drug, two hours before, completely suppressed the attack induced by the procedure in all of the five patients who received this drug. We conclude that hyperventilation plus Tris-buffer infusion induces coronary arterial spasm and anginal attack in patients with Prinzmetal's variant angina and that diltiazem suppresses these reactions.

Angina Pectoris↗

PubMed1989

Effect of nimodipine on cerebral blood flow and metabolism in rats during hyperventilation.

Nimodipine shws promise in the prevention and treatment of brain ischemia. We examined the interaction of nimodipine pretreatment in a dose sufficient to prevent postischemic hypoperfusion and hyperventilation. We studied four groups of rats: normocarbia plus vehicle (Group 1, n = 5), hypocarbia plus vehicle (Group 2, n = 4), normocarbia plus nimodipine (Group 3, n = 7), and hypocarbia plus nimodipine (Group 4, n = 6). Groups 3 and 4 received 1 mg/kg i.p. nimodipine, and Groups 1 and 2 received an equivalent amount of vehicle. Ventilation was left unaltered in Groups 1 and 3 or increased to lower PaCO2 to 21-24 mm Hg in Groups 2 and 4. Determination of regional cerebral glucose utilization (rCGU) was carried out using the [3H]2-deoxyglucose method, and regional cerebral blood flow (rCBF) was determined by the indicator fractionation method using [14C]iodoantipyrine. The brain regions studied were the cerebral hemispheres, the diencephalon, the cerebellum, and the brainstem. Hyperventilation in Groups 2 and 4 from approximately 38 to 22 mm Hg reduced rCBF to 60% of normocarbic levels (p less than 0.05). The slope and intercept of this response were similar in vehicle- and nimodipine-pretreated rats. Nimodipine modestly decreased mean arterial blood pressure by 20% and increased plasma glucose concentration by 60% (p less than 0.05). Although nimodipine tended to increase rCBF and decrease regional cerebrovascular resistance (rCVR), this was significant only for hemispheric rCVR (p less than 0.05). There was a borderline effect for nimodipine to increase rCGU, especially during hypocarbia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

Refractory period during provocation with eucapnic hyperventilation and methacholine.

Eucapnic voluntary hyperventilation (EVH) and methacholine inhalation challenge (MIC) both cause bronchoconstriction in asthmatics. A refractory period, or time when the response to bronchoprovocation in a series of challenges is diminished, has been found after hyperventilation or exercise but not after MIC. We investigated whether EVH or MIC blunted the response to the other test. Sixteen asthmatics were studied on 2 d, taking both tests each day. They were randomized to either EVH or MIC first on Day 1, then the opposite order on Day 2, 6 to 14 d apart. After EVH as a first test, the mean decline in FEV1 from baseline was 18.66 +/- 4.76% (mean +/- SEM), but when EVH followed MIC, the response to EVH was reduced by 30%, to a decline in FEV1 of only 13.02 +/- 3.75% (p = 0.0026). During MIC, the mean provocation dose to cause 20% decrease in FEV1 (PD20) given as the initial challenge was 54.77 +/- 21.60 breath units, compared with 46.94 +/- 19.55 breath units when MIC followed EVH (p = 0.54). However, the subset of patients most sensitive to methacholine (PD20 < 0.1 breath unit) had changes suggestive of a refractory period after EVH, with a mean increase in the PD20 from 0.06 +/- 0.01 to 3.35 +/- 1.43 (p = 0.069). Our data show that MIC attenuates the response to subsequent challenge with EVH. Conversely, EVH may only affect subsequent MIC in those most sensitive to methacholine.

Adult↗

PubMed1994

A case of pulmonary AV fistula. Possible involvement of adenosine in hyperventilation.

A 21-yr-old man with multiple pulmonary AV fistulae presented with moderate hypoxemia with chronic hyperventilation, which continued even after sufficient oxygenation by 100% O2 inhalation. The infusion of aminophylline, an adenosine receptor blocker, not only increased PaCO2 from 35 to 39 mm Hg but also depressed the magnitude of hypoxic ventilatory response (HVR). After a surgical removal of the major fistulae, PaCO2 increased to 42 mm Hg. At this time, aminophylline increased the resting ventilation and slightly augmented the HVR value, which was opposite to the findings of preoperation. Dipyridamole, which potentiates endogenous adenosine by inhibiting its cellular uptake, increased the magnitude of HVR both before and after the operation. We propose that the hyperventilation observed in this case can at least in part be attributed to the ventilatory stimulation by endogenous adenosine, which presumably passed through the fistulae without being metabolized in the pulmonary circulation.

Adenosine↗

PubMed1990

Analysis of refractory period after exercise and eucapnic voluntary hyperventilation challenge.

We compared specific airway conductance (SGaw) and the FEV1 after repetitive exercise or repetitive eucapnic voluntary hyperventilation (EVH) challenges. Replicate challenges were matched in terms of inspired air conditions and minute ventilations (VE) in order to determine the degree of refractoriness after each type of challenge in patients with exercise-induced asthma. Ten patients exercised or hyperventilated dry, room temperature air at matched VE on two study days. When the patients FEV1 had returned to 90% of baseline or better, or at 3.75 h if FEV, had not returned to 90% of baseline, patients repeated the identical exercise or the EVH challenge. Minimum FEV1 values expressed as a percent of predicted FEV1 after the first and second exercise challenges were 52 +/- 16 and 58 +/- 17, respectively, which were statistically different (p less than 0.001; paired t test). Minimum FEV1 values after the first and second EVH challenges were 52 +/- 13 and 59 +/- 9% of predicted, respectively, which were also statistically different (p less than 0.01; paired t test). Seven of 10 subjects demonstrated higher SGaw values after the second exercise challenge compared with the first challenge, whereas eight of 10 subjects showed higher SGaw values after the second EVH challenge compared with the first challenge. Paired t test analysis indicated that percent protection, measured by FEV1, was similar after either type of challenge. We conclude that replicate exercise or EVH challenges with similarly matched inspired air conditions and VE induce similar degrees of refractoriness.(ABSTRACT TRUNCATED AT 250 WORDS)

Airway Resistance↗

PubMed1986

Intraesophageal perfusion of acid increases the bronchomotor response to methacholine and to isocapnic hyperventilation in asthmatic subjects.

Gastroesophageal reflux (GER) has been shown to be more frequent in people with asthma, but the mechanism by which it might aggravate asthmatic symptoms remains unclear. We compared the effects on maximal expiratory flow at 50% of VC (MEF50) of esophageal perfusion of hydrochloric acid (HCl) and of normal saline (NaCl) in 12 asthmatic subjects chosen at random. In all subjects, HCl perfusion did not change MEF50 but potentiated the bronchoconstriction induced by isocapnic hyperventilation of dry air (maximal decrease in MEF50 = 44 +/- 7% with HCl versus 22 +/- 5% with NaCl; p less than 0.001) or methacholine (provocative dose producing a 20% decrease in FEV1 = 349 +/- 99 micrograms with HCl versus 496 +/- 119 micrograms with NaCl; p less than 0.01). Seven of the asthmatic subjects were found to have GER on esophageal pH monitoring. In these subjects, HCl alone decreased MEF50 slightly but significantly (-17.5 +/- 5.5%; p less than 0.05), possibly reflecting the higher degree of basal bronchial hyperreactivity observed in this group. Thus, perfusion of acid into the distal esophagus caused slight but significant bronchoconstriction in asthmatic subjects with GER and increased the bronchoconstriction produced by isocapnic hyperventilation and by methacholine in asthmatic subjects without regard for the presence of GER.

Adolescent↗

PubMed1984

Response to hyperventilation in a group of patients with panic disorder.

Twelve patients with DSM-III diagnoses of panic disorder and four normal volunteers were studied during hyperventilation of room air and increased ventilation stimulated by 5% CO2. Patients also underwent sodium lactate infusion. Eight of the patients had a panic attack during sodium lactate infusion, seven during CO2 inhalation, and three during room-air hyperventilation. Since CO2 increases the firing of the locus ceruleus, and since sodium lactate infusion is known to increase cerebral CO2, these findings are consistent with other evidence implicating the locus ceruleus in panic anxiety.

Adult↗

PubMed1992

Hyperventilation-induced cerebral ischemia in panic disorder and effect of nimodipine.

Basilar artery blood flow was measured by transcranial Doppler ultrasonography before and during hyperventilation in nine patients with panic disorder and nine normal comparison subjects. The hyperventilation-induced decrease in basilar artery blood flow was significantly greater in patients with panic attacks than in comparison subjects. Two patients with decreases in basilar flow greater than 80% were successfully treated with nimodipine, a centrally active calcium channel blocker.

Adult↗

PubMed1997

Response to hyperventilation and 5.5% CO2 inhalation of subjects with types of specific phobia, panic disorder, or no mental disorder.

OBJECTIVE: This study tested the hypothesis that compared to other DSM-IV specific phobia types, situational specific phobias have more in common with panic disorder and agoraphobia. METHOD: Responses to hyperventilation and CO2 inhalation were compared across groups of patients with the four main DSM-IV specific phobia types, a group with panic disorder, and a group of comparison subjects with no anxiety disorder (N = 15 per group). RESULTS: Although these challenges have been shown previously to distinguish patients with panic disorder from other groups, no groups differed significantly in their responses to hyperventilation. In addition, whereas the patients with panic disorder responded more to the CO2 challenge than did the normal subjects, the specific phobia groups did not differ from one another or from the other groups on most measures. For the few CO2 measures on which specific phobia groups differed, patients with situational and natural environment phobias showed the greatest response. CONCLUSIONS: Overall, these findings provided only limited support for the hypothesis that situational specific phobias are related to panic disorder.

Adolescent↗

PubMed1986

Neurological manifestations of the hyperventilation syndrome.

Seventy-eight patients with the hyperventilation syndrome are described, none of whom had been diagnosed prior to referral for neurological assessment. There is a constellation of symptoms associated with this condition, and attacks need to be reproduced by hyperventilation in order for the diagnosis to be established. Loss of consciousness and paraesthesiae were more frequent than in previously published series.

Adolescent↗

PubMed1987

Role of the nurse counsellor in managing patients with the hyperventilation syndrome.

A hyperventilation clinic was established specifically to deal with patients referred from the accident and emergency department with the hyperventilation syndrome. This was run by a staff nurse, who counselled the patients and taught abdominal breathing techniques and relaxation. In 30 patients so managed, 63% said their symptoms were much better or had completely gone and in only 6% was there no improvement; 43% had previously had more than one attendance at the A&E department, but following treatment only 2 patients represented during 5 months of follow up. The use of a nurse counsellor seems to be a simple and effective approach to managing these patients and considerably reduces both casualty and outpatient physician time.

Adolescent↗

PubMed2001

Critical conditions for hyperventilation responses. The role of autonomic response propositions during emotional imagery.

Hyperventilation is often conceived of as part of a fight-or-flight response, triggered by situations with high arousal and negative valence. However, a previous study using emotional imagery found hyperventilation responses during imagery of high-arousal scenes regardless of their valence. Those imagery scripts contained suggestions of autonomic activity, which may have partly induced or enhanced the hyperventilatory responsivity. The present study used four emotional scripts--depicting relaxing, fearful, depressive, and pleasant situations--without suggestions of autonomic or respiratory responses. After each imagery trial, participants rated their imagery for valence, arousal, and vividness. Fractional end-tidal carbon dioxide (FetCO2), inspiratory and expiratory time, tidal volume, and pulse rate were measured in a non-intrusive way. Results showed significant FetCO2 drops during the fearful and pleasant scripts. However, this effect was much smaller compared to imagery scripts with autonomic response propositions. Participants imagining scripts without autonomic response information found it harder to imagine the scripts vividly and reported lower levels of subjective arousal.

Adolescent↗