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PubMed1994

Infrequent panic: physiological and subjective reactions to hyperventilation.

Forty-eight females were evaluated to detect differences in panic-related symptomatology and physiological responses to 2 min of hyperventilation. Ss were divided into 3 groups: infrequent panickers; no panic/high trait anxiety; and no panic/low trait anxiety. The low trait anxiety group scored significantly lower on various self-report measures of anxiety-related symptomatology compared to Ss with infrequent panic and high trait anxiety. Hyperventilation produced no significant group differences in physiological reactivity or recovery. However, Ss with low trait anxiety reported significantly less severe sensations and a significantly lower incidence of panic during hyperventilation than the infrequent panickers and the high trait anxiety group. Ss who panicked during hyperventilation reported more intense sensations and negative cognitions than those who did not panic. Thus, Ss were distinguished by their subjective, but not their physiological responses.

Adult↗
PubMed1994

Subjective symptoms and cardiac reactivity to brief hyperventilation in individuals with high anxiety sensitivity.

Cognitive models maintain that panic attacks may be initiated by fear resulting from the interpretation of somatic sensations as personally threatening or harmful. Similarly, several researchers have proposed that the enhanced response of panickers to biological challenge may result from the fear of induced anxiety sensations rather than from direct stimulation of aberrant biochemical systems. The present study examined the effects of both panic history and fear of anxiety sensations on subjective and cardiac responses to biological challenge. Eighty nonclinical subjects were chosen on the basis of level of anxiety sensitivity and history of previous panic attacks. High and low anxiety-sensitive panickers and nonpanickers (four groups of 20 subjects) were subjected to a 90 sec period of voluntary hyperventilation, during which heart rate was assessed. Regardless of panic history, total symptom scores did not differ between high and low anxiety-sensitive subjects at baseline or pre-hyperventilation, but did differ at post-hyperventilation. There were, however, no significant differences in post-hyperventilation measures of heart rate. The apparent mismatch of subjective and physiological responsivity to the challenge in high anxiety-sensitive individuals (i.e. more severe symptom self-reports in the absence of increased cardiac activation) provides support for the hypothesis that high anxiety sensitivity is associated with an enhanced tendency to panic in response to biological challenge.

Adult↗
PubMed1984

Diagnosis of hyperventilation syndrome on the basis of reported complaints.

Four hundred consecutive patients referred for diagnosis of hyperventilation syndrome were studied to assess the utility of self-reported complaints for making primary diagnoses of the syndrome. One-half of the subjects were unequivocally diagnosed as positive for the disorder, the other half as negative. This diagnosis was determined by the presence or absence of two criteria with established validity: (a) recognition of major presenting symptoms during a period of voluntary hyperventilation, and (b) slow return of end-tidal CO2 levels to pre-hyperventilation baseline values after the voluntary period of overbreathing. Analyses focused on differences in presenting symptoms between those patients with and those without the syndrome. Results revealed many significant differences in frequency of specific complaints between groups. However, there was much overlap between groups with regard to all complaints. A discriminant analysis of the complaint items led to a correct classification of 66 per cent of the subjects. Our findings thus indicate that the risks of misclassification of hyperventilation syndrome are relatively large when diagnosis is solely based on presenting complaints. Consequently, reported symptoms characteristic of the disorder should be used as preliminary indications requiring further evaluation.

Adolescent↗
PubMed1987

Effects of induced hyperventilation on electrodermal response habituation to agoraphobia-relevant stimuli.

The role of hyperventilation in the aetiology of anxiety disorders was investigated in an analogue study. It was hypothesised that induced hyperventilation would alter subsequent subjective and physiological responses to visually presented agoraphobic material. Three groups (N = 16) of students were used and each was divided into two sub-groups which were presented with slides of either potentially agoraphobic or neutral content. During the first phase of the experiment, subjects were exposed to 10 slides whilst their breathing rate was manipulated. Group FB was instructed to hyperventilate by asking the subjects to breathe fast and deeply, Group SB was instructed to breathe at a slow rate and Group NB breathed normally. After a recovery phase, subjects were re-exposed to the same visual stimuli as used in the first phase of the experiment. Measures of skin conductance response amplitude were obtained for each stimulus in the series. In addition, heart rate and respiration were monitored, and subjective measures of somatic and affective states were obtained. Subjects also rated the pleasantness of the stimuli. The hyperventilation instructions resulted in delayed electrodermal habituation relative to the other groups. This finding could not be accounted for in terms of group differences in either physiological or subjective 'arousal'.

Adult↗
PubMed1995

Hypoxic response is inversely related to degree of exercise hyperventilation.

The Dejours hyperoxic test has been used to quantitate peripheral chemoreceptor contribution to the hyperpnea of exercise. The strength of this drive, measured by the percent reduction in ventilation, varies among individuals and is lacking in chemodenervated humans, who also fail to manifest a hyperventilatory response in heavy exercise. We reasoned that greater hyperventilation in exercise above the anaerobic threshold ought to be associated with greater hypoxic (carotid body) drive. The present study tested this hypothesis. In 17 naive subjects, carotid body O2 chemosensitivity was tested repeatedly during exercise above the ventilatory anaerobic threshold (VAT) using 2 breaths of O2. The response to these transients was quantitated by the percentage change in ventilation, and exercise hyperventilation was quantitated by VE in excess of VCO2 predicted from the slope of delta VE/delta VCO2 below VAT in incremental exercise. Contrary to expectations, there was an inverse relation between the degree of exercise hyperventilation and the percentage reduction in exercise ventilation in response to O2. The significance of this observation and its integration with current thinking of the role of the peripheral chemoreceptor in mediating hyperventilation of heavy exercise is discussed.

Adult↗
PubMed1996

Post-hyperventilation hypopnea in humans during NREM sleep.

We wished to determine if mild hypocapnia above the "apneic threshold" would result in apnea or hypopnea during NREM sleep. Hypocapnia was induced by nasal mechanical hyperventilation for 1 min either under normoxia (51 trials, n = 7) or hyperoxia (43 trials, n = 5). Cessation of mechanical ventilation resulted in hypopnea due to reduced VT without a change in f. Central apnea occurred mostly under hyperoxic conditions (9/43 versus 2/51 trials under normoxic conditions), and only when complete inhibition of ventilatory motor output occurred during mechanical ventilation. Significant correlation between the magnitude of hypocapnia and nadir VE was noted under both normoxic and hyperoxic conditions. However, nadir VE was variable when hypocapnia was modest (-2 mmHg); further hypocapnia (-4 mmHg) was associated with consistent reduction in nadir VE below 30% of control under normoxic conditions, and central apnea under hyperoxic conditions. We conclude that: (1) Brief hyperventilation during NREM sleep is followed by hypocapnic hypopnea due to reduced VT and not breathing frequency; (2) Hypocapnia due to brief mild hyperventilation does not cause central apnea unless peripheral chemoreceptors are also inhibited; (3) Sustained hyperventilation or more severe hypocapnia may be required for the development of hypocapnic central apnea during NREM sleep.

Adult↗
PubMed1988

Attenuation of hyperventilation-induced bronchospasm by terfenadine: a new antihistamine.

The effect of terfenadine, a selective H1-receptor antagonist devoid of central nervous system side effects, was evaluated on hyperventilation-induced bronchospasm in 11 adult subjects with asthma in a double-blind, placebo-controlled, crossover study. Increases in specific airway resistance (SRaw) were induced by isocapnic hyperventilation with dry air on two occasions, 7 days apart. Before the tests, the subjects received oral terfenadine (120 mg, twice daily) or placebo for 3 days with the last dose administered 3 hours before the test. Baseline SRaw and spirometric values (vital capacity and FEV1) were similar for the two tests. Terfenadine yielded a significant (p less than 0.001) parallel shift to the right of the stimulus (hyperventilation)-response (SRaw) curve; 100% increases in SRaw occurred at ventilation rates of 44 L/min after placebo treatment and 64 L/min after terfenadine treatment. These data suggest that histamine release plays a role in hyperventilation-induced bronchospasm despite the fact that increase in plasma histamine has not been found in this situation, in contrast to exercise-induced bronchospasm.

Adolescent↗
PubMed1992

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

The duration of the blocking effect of salmeterol (50 micrograms), albuterol (200 micrograms), and a placebo were compared in a double-blind study in 12 adult subjects with asthma who underwent hyperventilation tests with cold dry air (-20 degrees C) on 4 study days. On the first day, the hyperventilation test was performed at various time intervals (baseline, 1, 4, 6, 8, 12, and 24 hours) with spontaneous functional recovery between each test to determine the within-day within-subject variability of the response. The response was assessed by interpolating the dose of cold dry air causing a 20% fall in FEV1. On the 3 remaining days, separated by an interval of at least 5 days, the active or placebo medication was administered after spontaneous recovery from the first hyperventilation test. Spirometry was assessed 15 minutes and 1 hour later. The hyperventilation test was then performed and repeated 4 hours after administration of the drug. The test was repeated 6, 8, 12, and 24 hours later to detect any significant blocking effect. The improvement in FEV1 15 minutes and 1 hour after the drug was administered was 19.8% and 20.4%, as compared to baseline for albuterol, and 16.3% and 16.8% for salmeterol (not significant). The mean duration of the blocking effect was 0.25 hour for the placebo, 3.5 hours for albuterol, and 15.9 hours for salmeterol (F = 24.5; p less than 0.001; Newman-Keul's test was significant for every contrast). Eight of the 12 subjects still demonstrated some blocking effect 8 hours after taking salmeterol; this was true for only one subject receiving albuterol.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1991

Elevated serum lactate associated with panic attacks induced by hyperventilation.

Several lines of evidence suggest that lactate metabolism may be altered in panic disorder. We recently reported exaggerated increases in serum lactate in panic patients following hyperventilation during glucose infusion. In the current study, lactate metabolism was stimulated by hyperventilation following glucose ingestion in 12 panic patients and 12 controls. The seven patients who panicked during hyperventilation exhibited larger increases in serum lactate levels than nonpanicking patients or controls. The lactate response was significantly correlated with peak ratings of anxiety and panic symptoms, but not correlated with insulin or cortisol levels, heart rate, pCO2, adiposity, exercise habits, or diet. Hyperventilation-induced panic appears to be associated with metabolic changes leading to elevated serum lactate.

Adult↗
PubMed1989

Transcranial pulsed Doppler measurements of blood velocity in the middle cerebral artery: reference values at rest and during hyperventilation in healthy volunteers in relation to age and sex.

Transcranial pulsed Doppler analysis of blood velocity in the middle cerebral artery was performed in 120 healthy volunteers (age 20-70 y, 12 male and 12 female subjects per decade), meeting strict selection criteria. The intention was to create normative reference data, both at rest and during hyperventilation, for the assessment of abnormality in patients with cerebral vascular disorders. The measured blood velocity at rest decreased significantly with increasing age. Females up to 50 years of age had significantly higher blood velocity values than males. Blood velocity diminution was induced by means of voluntary hyperventilation, under capnographic control. An age related decline of blood velocity as present at rest was not found during hyperventilation, thus the relative value of hyperventilation induced changes diminished with increasing age. The pCO2 related change in the blood velocity index appeared not to be a constant value, as suggested by previous authors. The blood velocity index was largest in the change from resting condition to 4 kPa pCO2, and smallest in the change 3 kPa pCO2 to 2 kPa pCO2. When examining the blood velocity in the MCA, the age, sex and end-tidal pCO2 pressure have to be taken into account for a correct interpretation of the data obtained.

Adult↗
PubMed1989

Increased plasma fibrinopeptide A levels during attacks induced by hyperventilation in patients with coronary vasospastic angina.

Plasma fibrinopeptide A levels, beta-thromboglobulin levels and platelet factor 4 levels were estimated by enzyme-linked immunosorbent assay before and after hyperventilation in 12 patients with coronary vasospastic angina and in 12 control subjects matched for age and gender. In all 12 study patients, anginal attacks accompanied by electrocardiographic (ECG) changes (ST elevation in 11 patients and ST depression in 1 patient) were induced by hyperventilation. Coronary angiography was performed on 11 of the 12 patients, and coronary artery spasm with the same ECG changes was induced by intracoronary injection of acetylcholine in all 11. The plasma fibrinopeptide A levels increased significantly from 2.0 +/- 0.4 to 10.0 +/- 2.4 ng/ml during the attack (p less than 0.001) in the study patients, but remained unchanged before and after hyperventilation in the control subjects. The plasma levels of beta-thromboglobulin and platelet factor 4 remained unchanged after hyperventilation in both groups. Our data indicate that coronary artery spasm may induce thrombin generation and trigger thrombus formation in the coronary artery.

Aged↗
PubMed1995

The effect of hyperventilation on motor cortical inhibition in humans: a study of the electromyographic silent period evoked by transcranial brain stimulation.

We studied the effects of hyperventilation under control of the end-tidal PCO2, on the electromyographic silent period evoked by transcranial magnetic brain stimulation and by peripheral nerve stimulation. We also studied the effects of hyperventilation on the threshold, latency and amplitude of motor potentials. Hyperventilation significantly reduced the duration of the cortical silent period, but did not affect the length of the peripheral silent period. Neither did it alter the latency, amplitude or threshold of the motor potentials. These findings suggest that hyperventilation selectively depresses motor cortical inhibition in humans.

Adult↗
PubMed2005

[Hyperventilation syndrome in children].

Hyperventilation syndrome is frequent in adults. There are only very few and very ancient publications in children. Diagnosis is sometimes difficult, because the symptoms often mimic those of organic diseases. Hyperventilation syndrome and organic diseases, especially asthma, often coincide. Intensive efforts should be made to diagnose hyperventilation syndrome at an early stage because this will prevent stigmatization and fixation of symptoms and disease, and also prevent children from undergoing unnecessary medical examinations and therapies. The authors review the literature about hyperventilation syndrome in children.

Asthma↗
PubMed2004

Redefining the impact of oxygen and hyperventilation after the Norwood procedure.

OBJECTIVE: Postoperative management after the Norwood procedure is aimed at optimizing systemic oxygen delivery and mixed venous oxygen saturation. High levels of fraction of inspired oxygen and hyperventilation may increase pulmonary blood flow at the expense of systemic flow. This study determines the effects of these interventions on mixed venous saturation and systemic oxygen delivery in postoperative neonates. METHODS: We prospectively studied the effects of 100% fraction of inspired oxygen and hyperventilation in 14 neonates (median age 8 days) 1 to 3 days after the Norwood procedure, while they were sedated, paralyzed, and mechanically ventilated. After establishment of baseline conditions (fraction of inspired oxygen = 29% +/- 2%, normal ventilation), patients were exposed to each of the 2 interventions in random order. Mixed venous saturation was measured through a transthoracic line in the superior vena cava. Oxygen excess factor (Omega = systemic oxygen delivery/oxygen consumption) was used as an indicator of systemic oxygen delivery. RESULTS: High levels of fraction of inspired oxygen produced significant increases from baseline in systemic saturation (90% +/- 1% vs 80% +/- 1%, P <.01), mixed venous saturation (54% +/- 3% vs 44% +/- 2%, P <.01), and oxygen excess factor (2.6% +/- 0.2% vs 2.3 +/- 0.2%, P <.01), but there was no change in arteriovenous saturation difference or blood pressure. Hyperventilation resulted in no changes in systemic or mixed venous saturation, arteriovenous saturation difference, oxygen excess factor, or blood pressure. CONCLUSIONS: High levels of fraction of inspired oxygen can improve mixed venous oxygen saturation and systemic oxygen delivery after the Norwood procedure. Hyperventilation does not change either mixed venous saturation or oxygen delivery. Management protocols aimed at minimizing the fraction of inspired oxygen and carefully controlling ventilation may not be warranted.

Blood Pressure↗
PubMed1980

Use of heart rate responses to standing and hyperventilation at rest to detect coronary artery disease: correlation with the S-T response to exercise.

The heart rate responses to standing and to hyperventilation, expressed as a percent change over the sitting heart rate value, were measured in 48 patients with angiographic coronary artery disease (less than or equal to 70 percent luminal narrowing) and 50 young, healthy asymptomatic individuals. When an abnormal response suggesting coronary artery disease was defined as an increase in the heart rate of < 15% over the sitting value and < 20% increase in the heart rate to hyperventilation relative to the sitting value, the sensitivity of such a criterion was 56%, the specificity was 92% and the predictive value was 87%. These values were not significantly different (P > 0.05) from those for the S-T response to exercise, which were 77%, 98%, and 97% respectively. When either a positive S-T response to exercise or a positive response for control heart rate changes to standing and hyperventilation were used as criteria for a positive test, the sensitivity significantly increased to 98% (P < 0.01), while specificity and predictive value remained significantly unchanged (P > 0.05) at 90% for each. The use of the heart rate response to standing and hyperventilation may be a useful test in detecting coronary artery disease in patients unable to undergo stress testing. The use of such heart rate responses in addition to S-T depression with exercise results in a highly sensitive and specific test with great predictive value.

Adult↗
PubMed1997

Hyperventilation syndrome: a chimera?

There is now an impressive body of research to suggest that the concept of a discrete hyperventilation syndrome is no longer tenable. The evidence for this has been carefully gathered and the scientific studies have employed innovative methodological techniques and have introduced a key psychological dimension. Both have led to a greater understanding of the respiratory correlates of anxiety, but in the process have revealed the "hyperventilation syndrome" to be a chimera. Furthermore, there is no evidence to support the view that panic attacks and hyperventilation are synonymous: on the contrary, hyperventilation rarely accompanies panic and, when it does, it is more likely to be a consequence than a cause of the panic. Finally, there is no evidence that "breathing therapy" works by normalizing pCO2; its nonspecific effects on anxiety appear to be mediated in part by slowing respiratory rate. Further research in this field might be more profitably focused on the nature of the association between anxiety disorders and organic lung disease, especially asthma.

Breathing Exercises↗
PubMed1990

Comparison of the effects of inhaled corticosteroids on the airway response to histamine, methacholine, hyperventilation, and sulfur dioxide in subjects with asthma.

To investigate whether inhaled steroids modulate the airway response to different bronchoconstrictive stimuli, we studied 25 subjects with mild asthma with a double-blind, noncrossover design to compare the effect of a 3-week treatment with salbutamol (0.2 mg, four times a day [q.i.d.]) and placebo (N = 11) to the effect of salbutamol (0.2 mg q.i.d.) and inhaled beclomethasone dipropionate (BDP, 0.5 mg q.i.d.) (N = 14). Airway response to histamine and methacholine was assessed as the provocative concentration (in milligrams per milliliter) necessary to increase the specific airway resistance (SRaw) (in centimeters of H2O times second) by 100% (PC100 SRaw). Airway response to hyperventilation of air and to hyperventilation of 0.75 ppm of sulfur dioxide (SO2) was determined as the provocative ventilation (in liters per minute) necessary to increase SRaw by 75% (PV75 SRaw). Challenges were performed on separate days before and after treatment, and salbutamol inhalation was withheld at least 6 hours before each challenge. Salbutamol and placebo did not change perchallenge baseline SRaw nor did they have any significant effect on the airway response to the stimuli. Salbutamol and BDP decreased the mean prechallenge baseline SRaw (SEM) from 7.7 (0.37) to 5.9 (0.28) (p less than 0.01) and significantly (p less than 0.01) increased geometric mean (SEM) PC100 SRaw for histamine from 0.5 (1.42) to 0.9 (1.53) mg/ml; for methacholine, from 0.2 (1.47) to 0.5 (1.51) mg/ml; and mean (SEM) PV75 SRaw for hyperventilation of air from 51.8 (2.32) to 58.4 (1.86) L/min. In contrast, the change of PV75 SRaw during hyperventilation of SO2 from 26.2 (2.29) to 31.4 (3.30) L/min was not significant.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Inhalation↗
PubMed2003

Artificial ventilation for basic life support leads to hyperventilation in first aid providers.

The 'Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care - International Consensus on Science' recommend an artificial ventilation volume of 10 ml/kg bodyweight (equivalent to a tidal volume of 700-1000 ml) without the use of supplemental oxygen in adults with respiratory arrest. For first aid providers using the mouth-to-mouth or mouth-to-nose-ventilation technique, respectively, a ventilation volume of approximately 9.6 l/min results. Additionally, a deep breath is recommended before each ventilation to increase the end-expiratory oxygen concentration of the air exhaled by the first aid provider. To investigate the effects of these recommendations in healthy volunteers, test persons were asked to ventilate an artificial lung model for a period of up to 10 min. The tidal volume was set at 800 ml at a breathing rate of 12/min. End-tidal carbon dioxide, oxygen saturation (measured by pulse oximetry), and heart rate were measured continuously. Capillary blood gas samples were collected and non-invasive blood pressure readings were recorded prior to the start of ventilation and immediately after the end of the measuring period. The data reveal a statistically significant and clinically relevant decrease in end-tidal carbon dioxide pressure (P<0.001, median decrease 14 mmHg), and the occurrence of hyperventilation-associated symptoms such as paraesthesia, dizziness, and carpopedal spasms in more than 75% of the participants. Clinically and statistically significant hyperventilation results in first aid providers performing artificial ventilation according to the guidelines. This artificial ventilation is associated with a significant decrease in capillary and end-tidal carbon dioxide pressure as well as with multiple symptoms of an acute hyperventilation syndrome. Ventilation performed according to these guidelines may cause injury to the health of the first aid provider. Rescuers ventilating the victim should be replaced at regular intervals and the recommendation to take a deep breath before each ventilation should not be upheld in order to minimise the risk of hyperventilation.

Adult↗