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PubMed2004

The use of quantitative end-tidal capnometry to avoid inadvertent severe hyperventilation in patients with head injury after paramedic rapid sequence intubation.

BACKGROUND: This study aimed to determine whether field end-tidal carbon dioxide CO2 (ETCO2) monitoring decreases inadvertent severe hyperventilation after paramedic rapid sequence intubation. METHODS: Data were collected prospectively as part of the San Diego Paramedic Rapid Sequence Intubation Trial, which enrolled adults with severe head injuries (Glasgow Coma Score, 3-8) that could not be intubated without neuromuscular blockade. After preoxygenation, the patients underwent rapid sequence intubation using midazolam and succinylcholine. A maximum of three intubation attempts were allowed before Combitube insertion was mandated. Tube confirmation was accomplished by physical examination, qualitative capnometry, pulse oximetry, and syringe aspiration. Standard ventilation parameters (tidal volume, 800 mL; 12 breaths/minute) were taught. One agency used portable ETCO2 monitors, with ventilation modified to target ETCO2 values of 30 to 35 mm Hg. Trial patients transported by aeromedical crews also underwent ETCO2 monitoring. The primary outcome measure was the incidence of inadvertent severe hyperventilation, defined as arterial blood gas partial pressure of CO2 (pCO2) of less than 25 mm Hg at arrival, for patients with and those without ETCO2 monitoring. These groups also were compared in terms of age, gender, clinical presentation, Abbreviated Injury Score, Injury Severity Score, arrival arterial blood gas data, and survival. RESULTS: The study enrolled 426 patients and administered neuromuscular blocking agents to 418 patients. Endotracheal intubation was successful for 355 of these patients (85.2%). Another 58 patients (13.6%) underwent Combitube insertion. For 291 successfully intubated patients, arrival pCO2 values were documented, with continuous ETCO2 monitoring performed for 144 of these patients (49.4%). Patients with ETCO2 monitoring had a lower incidence of inadvertent severe hyperventilation than those without ETCO2 monitoring (5.6% vs. 13.4%; odds ratio, 2.64; 95% confidence interval, 1.12-6.20; p = 0.035). There were no significant differences in terms of age, gender, clinical presentation, Abbreviated Injury Score, Injury Severity Score, arrival partial pressure of oxygen (PO2) and pH, or survival. The patients in both groups with severe hyperventilation had a significantly higher mortality rate than the patients without hyperventilation (56 vs. 30%; odds ratio, 2.9; 95% confidence interval, 1.3-6.6; p = 0.016), which could not be explained solely on the basis of their injuries. CONCLUSIONS: The use of ETCO2 monitoring is associated with a decrease in inadvertent severe hyperventilation.

Abbreviated Injury Scale↗

PubMed2004

Does hyperventilation elicit epileptic seizures?

PURPOSE: Voluntary hyperventilation has been advocated for many decades as an "activating" procedure to provoke clinical seizures and epileptiform discharges in subjects with suspected epilepsy who undergo standard EEG recordings. This study was undertaken to determine the effects of hyperventilation in patients with proven epilepsy. METHODS: We examined the records of 433 consecutive patients with proven epilepsy, as documented by long-term video-EEG studies. The patients underwent 5 min of voluntary hyperventilation during standard EEG recordings. All EEGs were interpreted by board-certified electroencephalographers. The patients ranged in age from 10 to 64 years; 384 (88.7%) had localization-related and 48 (11.3%) generalized epilepsy syndromes. RESULTS: Hyperventilation was associated with a clinical seizure in two (0.46%) of the subjects (partial seizures in both cases). Interictal epileptiform discharges were interpreted as showing in increase in frequency during hyperventilation in 19 (4.4%) patients, when compared with the baseline EEG. CONCLUSIONS: Voluntary hyperventilation in patients with unequivocal epilepsy is rarely associated with either clinical seizures or an increase in frequency of epileptiform discharges.

Adolescent↗

PubMed1990

Acute chest pain without obvious organic cause before the age of 40 years: response to forced hyperventilation.

A hyperventilation provocation test (HVPT) was performed on a group (n = 63) of consecutive patients, below the age of 40 years, attending an emergency care unit complaining of chest pain without obvious organic cause. The results were compared with those for a control group (n = 32). There was no tendency to hyperventilate in the patient group, either after discontinuing hyperventilation or during the ensuing relaxation period. PETCO2 measurements during this time thus showed no significant differences between the patient group and the control group. During the HVPT, 44% of patients reported three or more listed symptoms familiar to them from earlier occasions and regarded as typical of hyperventilation, compared to 23% of the controls (P less than 0.05). In a previously reported study, 38% of the patients were found to have similar symptoms during standardized mental stress, despite lack of hypocapnia. It is concluded that, on the basis of PETCO2 measurements, there were no signs of abnormal hyperventilation in the patient group. Moreover, the HVPT did not appear to be specific for diagnosis of hyperventilation syndrome, since mental stress itself was able to reproduce symptoms without concomitant hypocapnia, and since the provocation test was 'positive' in many control subjects.

Adult↗

PubMed1995

Lactate metabolism and hypocarbic hyperventilation. An experimental study in piglets.

Hyperventilation has been reported to increase blood lactate levels. Uncertainty exists as to whether high lactate levels are caused by increased peripheral release or decreased hepatic uptake. Seven piglets were investigated during controlled normoventilation and 13 piglets during controlled hyperventilation. Blood was drawn from catheters in the femoral artery and vein and in the hepatic vein. Blood flow was measured in the femoral artery by an electromagnetic flow meter and in the splanchnic area by indocyanine green extraction. In addition, repeated muscle biopsies from the hind limb and back muscles were taken. The mean PaCo2 was 5.4 in the normoventilated and 3.5 kPa in the hyperventilated group. The average hind limb oxygen uptake was the same in both groups. The arterial blood lactate concentration was significantly higher (P = 0.03) in the hyperventilated group (2.6 mmol.l-1) as compared to the normoventilated group (1.5 mmol.l-1). However, the release of lactate from the hind limb, and the muscular content of lactate were the same in both groups. Similar and unchanged skeletal muscle contents of glucose-6-phosphate, fructose-1,6-diphosphate, alpha-glycerophosphate, pyruvate, citrate and ATP were recorded in both groups. The splanchnic region did not take up or release lactate at normal PaCO2, but released lactate after 120 minutes of hyperventilation. The results indicate that the increased concentration of lactate during hypocarbic hyperventilation was not caused by an increased peripheral release from the skeletal muscles of the pig but could be caused by an altered splanchnic turn-over of lactate.

Adenosine Triphosphate↗

PubMed1995

Changes in cerebral blood flow as monitored by transcranial Doppler during voluntary hyperventilation and their effect on the electroencephalogram.

Hyperventilation results in a fall in carbon dioxide concentration, a fall in cerebral blood flow, and slowing of activity on the electroencephalogram. The temporal relationship and duration of these responses are uncertain, and were investigated using simultaneous monitoring of cerebral blood flow velocity and of the electroencephalograph, with end-tidal carbon dioxide monitoring. Sixteen patients and 9 normal volunteers were studied. Cerebral blood flow velocity in the middle cerebral artery was measured using transcranial Doppler sonography during 3 minutes of hyperventilation and during a 3-minute recovery period. Electroencephalographic recordings were rated by both visual score and measurement of the dominant posterior frequency. End-tidal expired carbon dioxide tension was monitored during the same hyperventilation protocol in the volunteers. Flow velocity fell rapidly during active hyperventilation. Electroencephalographic slowing closely correlated with the decrease in flow velocity (r = 0.86), but lagged behind it. In healthy volunteers capnographic records showed a very tight coupling between end-tidal carbon dioxide concentration and flow velocity (r = 0.94). Three minutes after hyperventilation, carbon dioxide concentration, cerebral blood flow velocity, and electroencephalographic activity were still not back to the resting state. The fall in both cerebral blood flow velocity and carbon dioxide concentration are related to but precede electroencephalographic slowing. The abnormalities persist for at least 3 minutes after hyperventilation and this must be taken into account in clinical electroencephalography. Transcranial Doppler sonography is well suited to monitoring short-term changes in the cerebral circulation.

Adult↗

PubMed1985

Are coronary artery spasm and progressive damage to the heart associated with the hyperventilation syndrome?

A case of coronary artery vasospasm was studied in a man with a four year history of angina. He had evidence of symptomatic hyperventilation during a spontaneous episode of chest pain. When asked to hyperventilate the pain in his chest and ST elevation were reproduced in the same leads as occurred during the spontaneous attack. This may be the first reported case of spontaneous hyperventilation producing vasoconstriction, and the patient's previous admissions to the coronary care unit may have been associated with coronary vasospasm induced by hyperventilation. When patients with variant angina report pains in the chest in association with dizziness and breathlessness hyperventilation should be considered to be a possible cause of the symptoms. As coronary vasospasm is increasingly implicated in angina after myocardial infarction the role of hyperventilation should be considered more often.

Angina, Unstable↗

PubMed1982

Exercise hyperventilation in patients with McArdle's disease.

This study was undertaken to determine if patients who lack muscle phosphorylase (i.e., McArdle's disease), and therefore the ability to produce lactic acid during exercise, demonstrate a normal hyperventilatory response during progressive incremental exercise. As expected these patients did not increase their blood lactate above resting levels, whereas the blood lactate levels of normal subjects increased 8- to 10-fold during maximal exercise. The venous pH of the normal subjects decreased markedly during exercise that resulted in hyperventilation. The patients demonstrated a distinct increase in ventilation with respect to O2 consumption similar to that seen in normal individuals during submaximal exercise. However their hyperventilation resulted in an increase in pH because there was no underlying metabolic acidosis. End-tidal partial pressures of O2 and CO2 also reflected a distinct hyperventilation in both groups at approximately 70-85% maximal O2 consumption. These data show that hyperventilation occurs during intense exercise, even when there is no increase in plasma [H+]. Since arterial CO2 levels were decreasing and O2 levels were increasing during the hyperventilation, it is possible that nonhumoral stimuli originating in the active muscles or in the brain elicit the hyperventilation observed during intense exercise.

Adult↗

PubMed1986

Hyperventilation, alkalosis, prostaglandins, and pulmonary circulation of the newborn.

This study was designed to determine whether the effects of hyperventilation on the pulmonary circulation of the newborn lamb were 1) due to mechanical factors or to respiratory alkalosis; and 2) mediated by prostaglandins. Six control lambs were studied during normal ventilation and during hyperventilation with, and without, decreased carbon dioxide (CO2). Five lambs were given indomethacin and studied similarly. In control lambs, hyperventilation with decreased CO2 decreased pulmonary arterial pressure from 26 +/- 2.2 to 18 +/- 1.0 (SE) Torr (P less than or equal to 0.005) and pulmonary vascular resistance from 0.099 +/- 0.035 to 0.070 +/- 0.011 Torr X kg-1 X min-1 (P less than or equal to 0.015). Hyperventilation with normal CO2 did not affect the pulmonary circulation. Hyperventilation with decreased CO2 increased pulmonary arterial concentrations of 6-ketoprostaglandin F1 alpha, a major metabolite of prostacyclin, in control lambs but not in the indomethacin-treated lambs. However, it affected the pulmonary circulation of the control- and indomethacin-treated lambs similarly. In conclusion, hyperventilation affected the pulmonary circulation by respiratory alkalosis not by mechanical factors and prostaglandins did not mediate its effects.

6-Ketoprostaglandin F1 alpha↗

PubMed1987

Voluntary hyperventilation changes recruitment order of parasternal intercostal motor units.

The order of recruitment of single-motor units in parasternal intercostal muscles during inspiration was studied in normal human subjects during quiet breathing and voluntary hyperventilation. Electromyograms were recorded from the second and third intercostal spaces by means of bipolar fine wire electrodes. Flow at the mouth, volume, end-expired CO2, and rib cage and abdominal anterior-posterior diameters were monitored. Single-motor units were identified using criteria of amplitude and shape, and the time of first appearance of each unit in each inspiration was noted. Hyperventilation was performed with visual feedback of the display of rib cage and abdomen excursions, keeping the ratio of rib cage to abdominal expansion. Subjects were normocapnic in quiet breathing and developed hypocapnia during hyperventilation. Recruitment order was stable in quiet breathing, but in some cases was altered during voluntary hyperventilation. Some low threshold units that fired early in the breath in quiet breathing fired earlier at the beginning of a period of voluntary hyperventilation but progressively later in the breath as hyperventilation went on, whereas later firing units moved progressively toward the early part of inspiration. This suggests that different groups of motoneurons in the pool supplying parasternal intercostal muscles receive different patterns of synaptic input.

Action Potentials↗

PubMed1989

Airway blood flow response to eucapnic dry air hyperventilation in sheep.

Eucapnic hyperventilation, breathing dry air, produces a two- to fivefold increase in airway blood flow in the dog. To determine whether airway blood flow responds similarly in the sheep we studied 16 anesthetized sheep. Seven sheep (1-7) were subjected to two 30-min periods of eucapnic hyperventilation breathing 1) warm humid air [100% relative humidity (rh)] followed by 2) warm dry air [0% rh] at 40 breaths/min. To determine whether there was a dose-response effect on blood flow of increasing levels of hyperventilation of dry air, another nine sheep (8-16) were subjected to four 30-min periods of eucapnic hyperventilation breathing warm humid O2 followed by warm dry O2 at 20 or 40 breaths/min in random sequence. Five minutes before the end of each period of hyperventilation, hemodynamics, blood gases, and tracheal mucosal temperature were measured, and tracheal and bronchial blood flows were determined by injection of 15- or 50-micron-diam radiolabeled microspheres. After the last measurements had been made, all sheep were killed, and the lungs and trachea were removed for determination of blood flow to trachea, bronchi, and parenchyma. In sheep 1-7, warm dry air hyperventilation at 40 breaths/min produced an increase in blood flow to trachea (7.6 +/- 3.5 to 17.0 +/- 6.2 ml/min, P less than 0.05) and bronchi (9.0 +/- 5.4 to 18.2 +/- 8.2 ml/min, P less than 0.05) but not to the parenchyma. When blood flow was compared with the two ventilatory rates (sheep 8-16), tracheal blood flow increased (9.1 +/- 3.3 to 18.2 +/- 6.1 ml/min, P less than 0.05) at a rate of 40 breaths/min but not at 20 breaths/min.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1999

Mucosal injury and eicosanoid kinetics during hyperventilation-induced bronchoconstriction.

Bronchoalveolar lavage (BAL) of canine peripheral airways was performed at various times after hyperventilation, and BAL fluid (BALF) cell and mediator data were used to evaluate two hypotheses: 1) hyperventilation-induced mucosal injury stimulates mediator production, and 2) mucosal damage is correlated with the magnitude of hyperventilation-induced bronchoconstriction. We found that epithelial cells increased in BALF immediately after a 2- and a 5-min dry air challenge (DAC). Prostaglandins D(2) and F(2alpha) and thromboxane B(2) were unchanged immediately after a 2-min DAC but were significantly increased after a 5-min DAC. Leukotriene C(4), D(4), and E(4) did not increase until 5 min after DAC. Hyperventilation with warm moist air did not alter BALF cells or mediators and caused less airway obstruction that occurred earlier than DAC. BALF epithelial cells were correlated with mediator release, and mediator release and epithelial cells were correlated with hyperventilation-induced bronchoconstriction. These observations are consistent with the hypothesis that hyperventilation-induced mucosal damage initiates peripheral airway constriction via the release of biochemical mediators.

Airway Resistance↗

PubMed2003

Blood pressure response to hyperventilation test reflects daytime pressor profile.

Recent studies show that healthy subjects and patients with moderate hypertension have different pressor responses to hyperventilation, depending on their sympathoadrenergic reactivity. In the present study, we investigated whether a different response to the hyperventilation test is related to differences in the daily blood pressure profiles recorded with noninvasive ambulatory monitoring. Forty-five healthy subjects and 67 patients with essential hypertension of grades 1 and 2 (Joint National Committee VI and World Health Organization) were investigated. Healthy subjects and hypertensive patients responding to hyperventilation with an increase in systolic blood pressure had, during daytime ambulatory blood pressure assessment, peak systolic blood pressure values (146.0+/-5.0 mm Hg, 182.2+/-9.0 mm Hg, respectively) similar to the hyperventilation peak systolic blood pressure values (147.2+/-3.5 mm Hg, 183.0+/-4.7 mm Hg, respectively). Hypertensive patients responding to hyperventilation with a decrease in blood pressure showed clinic systolic blood pressure values (178.4+/-3.2 mm Hg) higher than daytime average ambulatory systolic blood pressure (155.2+/-7.1 mm Hg; P<0.01). Our results indicate that a hyperventilation test yields information on daily peak blood pressure values in healthy subjects and hypertensive patients when it induces a pressor increase and can identify hypertensive patients with the so-called "white coat effect" when it induces a pressor decrease.

Adult↗

PubMed2000

Effect of short-term hyperventilation on cerebral blood flow autoregulation in patients with acute bacterial meningitis.

BACKGROUND AND PURPOSE: Cerebral blood flow (CBF) autoregulation is impaired in patients with acute bacterial meningitis: this may be caused by cerebral arteriolar dilatation. We tested the hypothesis that CBF autoregulation is recovered by acute mechanical hyperventilation in 9 adult patients with acute bacterial meningitis. METHODS: Norepinephrine was infused to increase mean arterial pressure (MAP) 30 mm Hg from baseline. Relative changes in CBF were concomitantly recorded by transcranial Doppler ultrasonography of the middle cerebral artery, measuring mean flow velocity (V(mean)), and by measurement of arterial to jugular oxygen content difference (a-v DO(2)). The slope of the regression line between MAP and V(mean) was calculated. Measurements were performed during normoventilation and repeated after 30 minutes of mechanical hyperventilation. RESULTS: At normoventilation (median PaCO(2) 4.4 kPa, range 3.5 to 4.9), MAP was increased from 68 mm Hg (60 to 101) to 109 mm Hg (95 to 126). V(mean) increased with MAP from 48 cm/s (30 to 61) to 65 cm/s(33 to 86) (P<0.01), and a-v DO(2) decreased from 2.2 mmol/L (1.0 to 2.7) to 1.4 mmol/L (0.8 to 1.8) (P<0.05). During hyperventilation (PaCO(2) 3.5 kPa, range 3.3 to 4.1), MAP was increased from 76 mm Hg (58 to 92) to 109 mm Hg (95 to 121). V(mean) increased from 45 cm/s (29 to 55) to 53 cm/s (33 to 78) (P<0.01), and a-v DO(2) decreased from 2.5 mmol/L (1.8 to 3.0) to 1.8 mmol/L (1.2 to 2.4) (P<0.05). Four patients recovered autoregulation completely during hyperventilation. The slope of the autoregulation curve decreased during hyperventilation compared with normoventilation (P<0.05). CONCLUSIONS: CBF autoregulation is partially recovered during short-term mechanical hyperventilation in patients with acute bacterial meningitis, indicating that cerebral arteriolar dilation in part accounts for the regulatory impairment of CBF in these patients.

Adult↗

PubMed1996

Effect of hyperventilation on airway mucosal blood flow in normal subjects.

The purpose of this study was to determine the effect of hyperventilation (40 L/min) with room air (25 degrees C; 70% relative humidity) and frigid air (-10 degrees C; 0% relative humidity) on airway mucosal blood flow (Qaw) in normal subjects (n = 7; 26 to 54 yr of age). Qaw was measured with the dimethyl ether uptake technique, which reflects blood flow in the mucosa of large airways corresponding to a 50-ml anatomic dead space segment extending distally from the trachea. Mean (+/- SE) baseline Qaw during quiet (room air) breathing was 6.6 +/- 0.6 ml/min (range, 3.9 to 10.9). Qaw failed to change significantly during and after eucapnic hyperventilation with room air (thermal stress, 224 cal/min). In contrast, eucapnic hyperventilation with frigid air (thermal stress, 720 cal/min) increased Qaw in every subject, with the peak value occurring either during or over a 30-min period after hyperventilation; by 60 min, Qaw had returned toward baseline. The mean maximal Qaw was 310 +/- 49% of baseline (p < 0.05). Neither type of hyperventilation had an effect on airway resistance. We conclude that in normal subjects, Qaw increases during and/or after eucapnic hyperventilation with frigid air, and that this response is related to the magnitude of the thermal stress rather than to the level of ventilation.

Adult↗

PubMed1978

The role of hyperventilation in exercise-induced bronchoconstriction.

Significant bronchoconstriction, comparable in severity to that observed after moderate treadmill exercise, was induced in asthmatic children by voluntary isocapnic hyperventilation of 3-min and 10-min duration. In both hyperventilation and exercise, nasal breathing inhibited the bronchoconstrictive responses, whereas mouth breathing potentiated the bronchoconstrictive response. In the asthmatic children, 10 min of voluntary isocapnic hyperventilation did not represent a greater bronchoconstrictive stimulus than did 10 min of exercise or 3 min of isocapnic hyperventilation. This study also showed that in normal children there was no measurable airway response after either voluntary isocapnic hyperventilation or moderate exercise. Finally, this study indicates that it is the stimulation of upper airway receptors by relatively cold and dry air, rather than hyperventilation per se, that provokes exercise-induced bronchoconstriction.

Adolescent↗

PubMed1983

Refractory period after hyperventilation-induced asthma.

Nine young asthmatic subjects undertook isocapnic hyperventilation while breathing air under different conditions. Each subject undertook 2 pairs of tests. Pair A consisted of 2 hyperventilation challenges performed while breathing cold (2.8 +/- 1.4 degrees C) dry (2.3 +/- 0.05 mg H2O/L) air. Pair B consisted of an initial warm (38.0 +/- 0.9 degrees C) saturated air challenge followed by a cold dry challenge. Tests were closely matched in terms of ventilation and respiratory heat loss in the cold dry tests. The subjects were rendered refractory by the first cold dry hyperventilation challenge, the fall in forced expiratory volume in one second (FEV1) after hyperventilation in the first test (delta FEV1 = 39 +/- 5%) being significantly greater than that after the second challenge of Pair A (delta FEV1 = 21 +/- 5%, p less than 0.005). In test Pair B, the warm humid hyperventilation challenge neither caused significant asthma (delta FEV1 6 +/- 3%) nor rendered the subjects refractory to the subsequent cold dry test (delta FEV1 38 +/- 4%). Because in a previous study it was shown that exercise while breathing warm humid air could induce a refractory period without itself causing asthma, we conclude that hyperventilation-induced asthma is not the same as exercise-induced asthma in most subjects.

Adolescent↗

PubMed2004

Ventilatory responses to inhaled carbon dioxide, hypoxia, and exercise in idiopathic hyperventilation.

Idiopathic hyperventilation (IH) is a poorly understood condition of sustained hypocapnia and controversial etiology. Although behavioral/emotional factors may contribute, it is uncertain whether chemosensitivity is altered, hyperventilation is maintained during exercise, and the associated breathlessness reflects the hyperventilation. In 39 patients with IH and 23 control subjects, we described ventilatory responses to isocapnic-hypoxia, hyperoxic-hypercapnia, and exercise; breath-hold tolerance; breathlessness; and psychologic status. Patients demonstrated hyperventilation at rest, with hypocapnia (28 +/- 3.8 mm Hg), a normal (slightly alkaline) arterial pH and [H(+)]a, and a significant base excess (-4.5 +/- 2.7 mEq/L), consistent with compensated respiratory alkalosis. Hyperventilation was sustained during exercise, despite hyperoxic-hypercapnic ventilatory responsiveness being normal and isocapnic-hypoxic ventilatory responsiveness being low relative to control (but exceeding control [2.4 +/- 1.0 vs. 1.6 +/- 0.5 L/min/%, p < 0.05] with acute restoration to normocapnia). Hyperventilation was maintained during exercise, at the resting CO(2) "setpoint." Relative to control, the breath-hold tolerance was attenuated, and dyspnea during exercise was significantly greater and not simply ascribable to the high ventilation. These observations suggest that patients with IH have a sustained hyperventilatory and dyspneic drive that, although not attributable to central chemosensitivity, may possibly have peripheral chemoreflex contributions. The nature and etiology of this chronic hyperventilatory drive remain unclear.

Administration, Inhalation↗

PubMed1996

Hyperventilation and panic attacks.

OBJECTIVE: Hyperventilation has been posed as an important symptom-producing mechanism in panic attacks. Some arguments and experimental findings, such as the possibility of inducing panic symptoms by voluntary hyperventilation in panic disorder patients, seem to favor this suggestion. This study was undertaken to clarify the role of hyperventilation in panic disorder. Long-term ambulatory measurement of transcutaneous arterial CO2 pressure (PCO2) offers an opportunity to test directly the co-occurrence of panic and hyperventilation under natural conditions. METHOD: Transcutaneous PCO2 was measured during three to four sessions of approximately 7 hours each in 28 panic disorder patients. Patients were instructed to expose themselves to fear-provoking situations and to press a button as soon as they experienced panic. One-half of the patients experienced one or more panic attacks during these sessions. RESULTS: A decrease in PCO2 was observed during only one of the 24 registered panic attacks that lasted at least 3 minutes. Even during this particular attack, the degree of hyperventilation was not impressive. CONCLUSIONS: These findings indicate that the hypothesis that hyperventilation is an important symptom-producing mechanism in panic may be dismissed.

Adult↗