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PubMed1996

Patients with acute hyperventilation presenting to an inner-city emergency department.

We studied 23 consecutive patients with acute hyperventilation presenting to an inner-city emergency department, diagnosed on clinical grounds by the attending physician and confirmed by arterial blood gas values in 5 patients. An organic basis for the presenting complaints was excluded and chest radiograph, serum biochemistry, blood cell count, and thyroid function test results were normal. The male to female ratio was 12:11. Presenting complaints were dyspnea (61%), paresthesia (35%), chest pain or tightness (43%), muscle spasm (9%), dizziness (13%), palpitations (13%), and panic (30%). Similar previous episodes were reported in 74%. Misattribution of the presenting complaints to a cardiac or other life-threatening disorder was reported in 20 patients (87%) and was the main reason for their presentation to the hospital. Although no patients presented with clinical features of asthma, 7 (30%) were known asthmatics receiving treatment and another 10 (44%) had a history and investigation results suggestive of asthma. Only 2 had a history of anxiety or depression, but 17 (78%) patients exceeded the threshold for anxiety or panic on Clinical Interview Schedule (CIS-R) interview (score > or = 12). Marihuana or alcohol abuse were involved in 17% with a history of past abuse in 26%. When assessed 2 months after the attack, 13 (57%) had resting or stressor-induced hyperventilation with a significant (p < 0.05) association with asthma but not with a positive CIS-R score. These results illustrate the multifactorial basis of acute hyperventilation, the importance of misattribution, and the danger of using the term "hyperventilation syndrome" in the emergency department.

Acute Disease↗
PubMed1988

Hyperventilation and myocardial infarction.

Chest pain that is associated with hyperventilation is often considered to be benign and noncardiac in nature. While not commonly recognized, hyperventilation can provoke coronary vasospasm. We report a man who presented with hyperventilation and developed myocardial infarction. In the setting of hyperventilation, chest pain and ST segment elevation, coronary vasospasm must be considered.

Coronary Angiography↗
PubMed2004

Clinical features of panic patients sensitive to hyperventilation or breath-holding methods for inducing panic attacks.

Our aim was to compare the clinical features of panic disorder (PD) patients sensitive to hyperventilation or breath-holding methods of inducing panic attacks. Eighty-five PD patients were submitted to both a hyperventilation challenge test and a breath-holding test. They were asked 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. Anxiety scales were applied before and after the tests. We selected the patients who responded with a panic attack to just one of the tests, i.e., those who had a panic attack after hyperventilating (HPA, N = 24, 16 females, 8 males, mean age +/- SD = 38.5 +/- 12.7 years) and those who had a panic attack after breath holding (BHPA, N = 20, 11 females, 9 males, mean age +/- SD = 42.1 +/- 10.6 years). Both groups had similar (chi(2) = 1.28, d.f. = 1, P = 0.672) respiratory symptoms (fear of dying, chest/pain discomfort, shortness of breath, paresthesias, and feelings of choking) during a panic attack. The criteria of Briggs et al. [British Journal of Psychiatry, 1993; 163: 201-209] for respiratory PD subtype were fulfilled by 18 (75.0%) HPA patients and by 14 (70.0%) BHPA patients. The HPA group had a later onset of the disease compared to BHPA patients (37.9 +/- 11.0 vs 21.3 +/- 12.9 years old, Mann-Whitney, P < 0.001), and had a higher family prevalence of PD (70.8 vs 25.0%, chi(2) = 19.65, d.f. = 1, P = 0.041). Our data suggest that these two groups--HPA and BHPA patients--may be specific subtypes of PD.

Adolescent↗
PubMed1990

Hyperventilation and panic attacks.

The role of hyperventilation in the aetiology of panic attacks is still unclear. This paper briefly reviews the role of hyperventilation and abnormal respiration to panic attacks and examines the experimental evidence. Evidence has been found that physiological variables such as paCO2 and pH are involved in the aetiology of panic attacks and panic disorder but the extent and the nature of the involvement of cognitive variables is undetermined. Based on current evidence, there is a need to integrate cognitive variables with the physiological framework proposed by the hyperventilation theory. Until clear experimental evidence is produced about the relationships between cognitive and physiological factors, the applicability of hyperventilation in the aetiology and treatment of panic attacks remains in question.

Agoraphobia↗
PubMed1988

Pial arteriolar vessel diameter and CO2 reactivity during prolonged hyperventilation in the rabbit.

Hyperventilation reduces intracranial pressure (ICP) acutely through vasoconstriction, but its long-term effect on vessel diameter is unknown. In seven rabbits with a cranial window implanted 3 weeks earlier, the effect of prolonged hyperventilation on vessel diameter was studied. Anesthesia was maintained for 54 hours with a pentobarbital drip (1 mg/kg/hr). The pH, CO2, and HCO3- levels were measured in arterial blood and cisterna magna cerebrospinal fluid (CSF). The diameter of 31 pial arterioles was measured with an image splitter. After baseline measurements, pCO2 was reduced from 38 to 25 mm Hg and allowed to return to 38 mm Hg for 10 minutes every 4 hours. There was an initial vasoconstriction of 13%, which progressively diminished by 3% every 4 hours. Thus, by the 20th hour, vessel diameters at a pCO2 of 25 mm Hg had returned to slightly above baseline values obtained at a pCO2 of 38 mm Hg. The temporary return of pCO2 to 38 mm Hg every 4 hours caused vasodilation: 12% at 4 hours, gradually increasing to 16% at 52 hours. Thus, at 52 hours, the vessel diameters were 105% of baseline at a pCO2 of 25 mm Hg and increased to 122% at a pCO2 of 38 mm Hg. Arterial pH had returned to baseline at 20 hours, and CSF pH had returned at 24 hours. Bicarbonate in blood and CSF remained decreased throughout the experiments. In three control experiments during which normocapnia was maintained, vessel diameter and pH and bicarbonate levels remained unaltered over the same period. The CO2 reactivity, tested by brief periods of hyperventilation every 4 hours, also did not change. These results indicate that hyperventilation is effective in reducing cerebral blood volume for less than 24 hours and that it should be used only during actual ICP elevations. If used preventively, its effect may have worn off by the time ICP starts to rise for other reasons, and further decreases in pCO2 cannot be obtained. Moreover, the reduction in buffer capacity with lower bicarbonate renders the vessels more sensitive to changes in PaCO2. This could lead to more pronounced elevations in ICP during transient rises in PaCO2, such as during endotracheal suctioning in head-injured patients.

Animals↗
PubMed1990

Cerebral venous oxygen content as a measure of brain energy metabolism with increased intracranial pressure and hyperventilation.

In order to test the hypothesis that the cerebral arteriovenous oxygen difference (AVDO2) and venous oxygen content (VO2) could be used to monitor brain energy metabolism in the setting of increased intracranial pressure (ICP). 12 cats were studied with 31P-magnetic resonance spectroscopy. six cats were subjected to intracranial hypertension by cisternal infusion of saline. Energy failure occurred at an average AVDO2 of 8.4 +/- 3.2 vol% (+/- standard deviation) (range 4.7 to 14.7 vol%). The VO2 at the point of metabolic failure averaged 1.45 +/- 0.6 vol% and extended over a narrower range (1.0 to 2.9 vol%). In an additional six cats, ICP was raised to the threshold of metabolic failure and hyperventilation was then instituted (pCO2 10 to 18 torr). Five of the six cats experienced a drop in VO2 with hyperventilation. In two of these animals, hyperventilation resulted in a VO2 of 1.1 vol% or less and in metabolic failure as evidenced by a fall in phosphocreatine. It is concluded that a VO2 of less than 2 vol% is correlated with brain ischemia and that the safety of hyperventilation in the setting of increased ICP can be monitored by the use of VO2.

Animals↗
PubMed1986

Hyperventilation syndrome.

Hyperventilation is a common, though often unrecognized, disorder of adolescents. While relatively benign, the lack of recognition may lead to extensive, expensive, and unnecessary medical work-ups. The single most important factor in making the diagnosis of HVS lies in the awareness of the disorder's existence. HVS may be diagnosed through a positive response to the provocation test. Patients are asked to hyperventilate and questioned as to whether they experience the symptoms of which they have complained. Successful treatment involves reassurance, education, and giving the patient a strategy for controlling the hyperventilation. If treatment is not successful in a short period, patients should be referred to a qualified mental health professional. While the relationship between hyperventilation and anxiety disorders is unclear, some correlation between them does appear to exist.

Adolescent↗
PubMed1976

The effects of carbon dioxide on pulmonary mechanics in hyperventilating, normal volunteers.

Transpulmonary pressure, air flow, and end-tidal carbon dioxide levels were measured in normal human volunteers during hypocapnic, eucapnic, and hypercapnic hyperventilation. Respiratory rate and tidal volumes were well matched at a minute ventilation of 52 L. on three inspired gas mixtures: 21 per cent oxygen and 79 per cent nitrogen; 5 per cent carbon dioxide, 21 per cent oxygen and 74 per cent nitrogen; and 12 per cent carbon dioxide, 21 per cent oxygen and 67 per cent nitrogen. Respiratory rate, tidal volume, lung compliance, resistance, and resistive work per liter were calculated with a digital computer. In 13 experiments in 7 normal volunteers, no net bronchoconstriction or bronchodilatation was observed when eucapnic hyperventilation was compared to hypocapnic or hypercapnic hyperventilation. During hyperventilation of this degree, a change in bronchomotor tone owing to alteration in arterial or alveolar PCO2 either does not occur or else is masked by other reflexes or mechanical factors acting on the bronchi.

Adult↗
PubMed1992

[Duration of bronchial protective effect of salmeterol in asthma induced by hyperventilation with dry cold air].

The duration of the blocking effect of salmeterol (50 micrograms), albuterol (200 micrograms) and placebo was compared in a double-blind study carried out in 12 adult asthmatic subjects who underwent hyperventilation tests with cold dry air on 4 study days. On the first day, the hyperventilation test was carried out at various time intervals with spontaneous functional recovery between each test. The response was assessed by interpolating the dose of cold dry air causing a 20% fall in FEV1 (PD20). On the three other days, the active or placebo medications were administered. Spirometry was assessed 15 minutes and 1 hour later. The hyperventilation test was then performed and repeated at various time intervals after administering the drug. The mean duration of the blocking effect was 0.25 hour for placebo, 3.5 hours for albuterol, and of 15.9 hours for salmeterol. Eight of the 12 subjects still showed some blocking effect eight hours after salmeterol by comparison with only one subject after albuterol. The authors conclude that salmeterol has a significantly longer effect than albuterol on bronchoconstriction induced by hyperventilation.

Adrenergic beta-Agonists↗
PubMedDate not supplied

Hyperventilation in children with dengue hemorrhagic fever (DHF).

Many studies of Dengue Hemorrhagic Fever (DHF) have been done but only a few revealed the respiratory status. Respiratory problems arise because of plasma leakage through the damaged capillaries, causing lung edema and in turn result in hypoxemia. This later on will be compensated by a hyperventilation state. During a 6-month-period (May to September 1988), two aspects were studied in 85 patients hospitalized with DHF. First, the ventilatory pattern and second, the result of giving oxygen support in improving the respiratory disturbance, in this case alveolar hyperventilation. The incidence of alveolar hyperventilation in DHF grade II (DHF II) and Dengue Shock Syndrome (DSS) differed significantly. Hypoxemia occurred in DHF II and DSS with no significant differences. The difference of the incidence of metabolic acidosis in DHF II and DSS were significant. In DHF II patients having had hyperventilation state, oxygen therapy decreased respiration rate significantly and increased the PaCO2 though not significantly.

Acidosis, Respiratory↗
PubMed1991

[The breathing casette; a useful aide in hyperventilation].

The breathing cassette (Hyperfree) was tested on 10 persons suffering from hyperventilation syndrome. Each subject performed a hyperventilation provocation of two minutes on three separate occasions. Immediately after the hyperventilation provocation the subject was asked to terminate the hyperventilation, firstly with no aid at all, later using a plastic bag or the breathing cassette. The %vol. CO2 in the exhaled air was recorded with a capnograph. The use of the plastic bag and the breathing cassette resulted in an equal restoration of the %vol. CO2. After using the cassette for six weeks the patients completed a questionnaire. All patients stated that they intended to continue using the breathing cassette, and that it was easy and handy to use. Most patients carried the cassette always with them, since it made them feel comfortable.

Adult↗
PubMed1991

[Echocardiographic assessment of segmental kinetic changes of the left ventricle during ischemic attacks induced by slow hyperventilation].

UNLABELLED: The detection of stress-induced wall motion abnormalities by means of 2D Echo represents a reliable marker of ischemia. Few reports about two-dimensional echocardiography and provocative tests in patients suffering from primary angina are available in the literature. Twenty patients with electrocardiographically documented ischemic transitory attacks at rest underwent hyperventilation test 2-15 days after a spontaneous episode. A new wall motion abnormality and/or a worsening of an asynergy already present at rest occurred in ten patients; eight of them also showed diagnostic ECG changes. Wall motion abnormalities arose significantly earlier (from the end of hyperventilation: 1.7 +/- .84 vs 2.16 +/- 1.15 min, p less than .05). Three patients had angina, which, in all patients started after echocardiographic and ECG changes. All patients experienced paresthesia, and two patients tinnitus due to blood alkalosis. No clinical adverse reaction resulted from the test. Only one patient had ventricular arrhythmias in the recovery phase of the ischemia. IN CONCLUSION: As concerns hyperventilation test, echocardiography has proven useful in identifying myocardial ischemia, comparable to electrocardiography. Moreover, in this study some patients had echocardiographic but not electrocardiographic changes as ischemic manifestations. Events after induction of ischemia with hyperventilation seem to follow the same sequence already observed in spontaneous attacks.

Adult↗
PubMed1987

Hyperventilation and panic attacks.

The symptoms of hyperventilation syndrome and panic disorder are very similar. A questionnaire was used to assess the incidence of panic disorder in 274 patients; 35% of the patients with hyperventilation and only 5% of the non-hyperventilating patients showed panic disorder. The authors conclude that hyperventilation plays an important role in panic disorder and in generalized anxiety disorder.

Adult↗
PubMed1986

Conditioned hyperventilation as a factor in animal, infant, and adult apnea: a theoretical analysis of experimental and clinical data.

An apnea hypothesis is proposed termed Conditioned Hyperventilation. An organism (animal, infant, or adult) can become conditioned to anticipate traumatic terminal breathing. The resulting hyperventilation produces excessive oxygen, which triggers apnea, allowing an increase in carbon dioxide. This apnea serves as an additional unconditioned stimulus (UCS) causing the hyperventilation (apnea) to increase. Organic blockage can also serve as the UCS. Apnea may be reduced or prevented by monitoring and extinguishing hyperventilation through the use of behavioral modification techniques, or biofeedback. Infant lung collapse during the first six months is suggested as one UCS in infants.

Adult↗
PubMed1979

Investigation of a simple, retrospective test for in-flight hyperventilation.

The experiment was designed to study the feasibility of using a single rebreathing estimate of mixed venous carbon dioxide tension (PvCO2) was a simple field test for hyperventilation in pilots. The results confirmed that the fall of end tidal carbon dioxide tension (P(ET)CO2) during hyperventilation and rise during recovery was exponential. The results also showed that the relationships between PvCO2 and P(ET)CO2 values during the unsteady states of carbon dioxide washout and accumulation may be described as a loop which encloses the theoretically derived line for the steady-state relationships. The deviation from the steady-state line appears on theoretical consideration to be directly proportional to carbon dioxide elimination rate, and indirectly proportional to cardiac output. Because of the exponential recovery, and because one value of PvCO2 could correspond to a range of values of P(ET)CO2, it is concluded that a field test for hyperventilation based on a single rebreathing estimate of PvCO2 would not be of value. The finding of a low value of PvCO2 would, however, be an indication that hyperventilation had taken place.

Aerospace Medicine↗
PubMed1984

Relation between efficacy of sodium cromoglycate and baseline lung function in exercise- and hyperventilation-induced asthma.

The protective effect of sodium cromoglycate (SCG) against exercise- and hyperventilation-induced asthma with respect to basal lung function was investigated in young asthmatics. The subjects performed standardized exercise or isocapnic hyperventilation challenge tests breathing cold dry air; in each case the effect of SCG was compared with that of a placebo in a double-blind fashion. With exercise as the challenge in 24 subjects, there was a strong positive correlation between the protective effect of SCG and the basal level of lung function. Using hyperventilation as the challenge in 11 subjects, there was no such correlation, but excluding two known placebo responders, there was a negative correlation between the protective effect of SCG and basal lung function. There findings suggest that exercise and hyperventilation operate differently in inducing asthma.

Adolescent↗
PubMed1983

Two types of responses to exercise and isocapnic hyperventilation in asthmatics.

Seven young adult asthmatics (17-35 years old) with an established diagnosis of mild to severe bronchial asthma were tested twice per day on six different days. On these days, all of the subjects undertook the treadmill exercise test of varying intensity for a duration of 6 minutes. Four hours later a voluntary isocapnic hyperventilation challenge of 6 minutes duration was done with essentially the same level of minute ventilation as achieved during and immediately after the exercise. During exercise and voluntary isocapnic hyperventilation tested patients inhaled dry compressed air of 23 degrees C. Heart rate, minute ventilation and end tidal pCO2 were monitored before, during and after each test. Pulmonary functions were measured before and after each procedure including: spirometry, measurement of airway resistance (Raw) and thoracic gas volume (Tgv). We found that five out of seven patients showed a dose-response-like relationship between a change in pulmonary function (FEF25-75% and FEV1) and total ventilation as measured during treadmill exercise or isocapnic hyperventilation challenge. In two patients we failed to establish this relationship. In these two patients different levels of ventilation (as measured during exercise or isocapnic hyperventilation) induced a similar degree of bronchoconstriction. These two patients had the lowest baseline pulmonary function of the whole group and by definition they had the most reactive airways.

Adolescent↗
PubMed1983

Comparison of isocapnic hyperventilation and treadmill exercise in children with exercise-induced asthma.

The degree of post-exercise airway obstruction (Exercise-Induced Asthma (EIA] in 14 children was compared to the degree of airway obstruction following isocapnic hyperventilation. EIA was provoked by 6 min of treadmill running. Isocapnic hyperventilation was performed sitting during 6 min. The total ventilation (Vtot) during the two provocations was identical. The temperature of the inspired air was also identical during the two provocations, and the relative humidity was 40% during treadmill-running and 15% during hyperventilation. The decrease in peak expiratory flow after treadmill-running was 29%. After hyperventilation a fall on 19% was seen. These figures are statistically different. It is concluded that although there is a significant difference in airway obstruction after the two provocations the ventilation is greater importance for EIA than is the work load.

Adolescent↗