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PubMed1994

Monitoring of the intracranial hemodynamics and oxygenation during and after hyperventilation in newborn rabbits with near-infrared spectroscopy.

Oxyhemoglobin, deoxyhemoglobin, total hemoglobin, and oxidized cytochrome aa3 were monitored, blood pressure and heart rate were continuously recorded, and cerebral hemodynamic changes were analyzed during and after hyperventilation (arterial CO2 tension < 2.67 kPa) and/or hyperoxemia (100% O2 inhalation) in 11- to 12-d-old rabbits. Oxyhemoglobin, deoxyhemoglobin, total hemoglobin, and oxidized cytochrome aa3 were monitored by means of near-infrared spectroscopy. Near-infrared spectroscopy ideally demonstrated decreases in oxyhemoglobin and total hemoglobin and an increase in deoxyhemoglobin during hyperventilation and a return to the previous values after hyperventilation. Cytochrome aa3 decreased during hyperventilation. On hyperventilation with 100% O2 inhalation, however, cytochrome aa3 was not reduced, although the changes in oxyhemoglobin and total hemoglobin were more significant. This reduction of cerebral oxygenation during hyperventilation without the administration of oxygen may induce hypoxic-ischemic brain damage. Noninvasive monitoring of cerebral oxygenation and hemodynamics, for which near-infrared spectroscopy is useful, is a requisite for the prevention of brain injury caused by severe hypocarbia in hyperventilation therapy.

Animals↗

PubMed1999

Hyperventilation-induced nystagmus in patients with vestibular schwannoma.

OBJECTIVE: To analyze the nystagmus evoked by hyperventilation in patients with unilateral vestibular schwannoma and to use this information to predict the effects of hyperventilation on individual ampullary nerves. METHODS: Three-dimensional scleral search coil eye movement recording techniques were used to record the magnitude and time course of eye movements in six patients with unilateral vestibular schwannoma and hyperventilation-induced nystagmus. The presenting complaints in five of these patients were vertigo or dysequilibrium. RESULTS: The eye movement response to hyperventilation was a "recovery" nystagmus with slow-phase components corresponding to excitation of the affected vestibular nerve. Projection of the eye velocity vector into the plane of the semicircular canals revealed that fibers arising from the ampulla of the horizontal canal were most affected by hyperventilation with lesser activation of fibers to the superior canal and smaller, more variable responses from posterior canal fibers. CONCLUSIONS: The three-dimensional characteristics of the nystagmus evoked by hyperventilation in patients with vestibular schwannoma provide insight into the vestibular end organs affected by the tumor and the mechanism responsible for the nystagmus. This finding indicates that hyperventilation resulted in a transient increase in activity from these partially demyelinated axons.

Adult↗

PubMed1999

Role of nitric oxide in hypoxia-induced hyperventilation and hypothermia: participation of the locus coeruleus.

Hypoxia elicits hyperventilation and hypothermia, but the mechanisms involved are not well understood. The nitric oxide (NO) pathway is involved in hypoxia-induced hypothermia and hyperventilation, and works as a neuromodulator in the central nervous system, including the locus coeruleus (LC), which is a noradrenergic nucleus in the pons. The LC plays a role in a number of stress-induced responses, but its participation in the control of breathing and thermoregulation is unclear. Thus, in the present study, we tested the hypothesis that LC plays a role in the hypoxia-induced hypothermia and hyperventilation, and that NO is involved in these responses. Electrolytic lesions were performed bilaterally within the LC in awake unrestrained adult male Wistar rats weighing 250-350 g. Body temperature and pulmonary ventilation (V E) were measured. The rats were divided into 3 groups: control (N = 16), sham operated (N = 7) and LC lesioned (N = 19), and each group received a saline or an N G-nitro-L-arginine methyl ester (L-NAME, 250 microg/microl) intracerebroventricular (icv) injection. No significant difference was observed between control and sham-operated rats. Hypoxia (7% inspired O2) caused hyperventilation and hypothermia in both control (from 541.62 +/- 35.02 to 1816.18 +/- 170.7 and 36.3 +/- 0.12 to 34. 4 +/- 0.09, respectively) and LC-lesioned rats (LCLR) (from 694.65 +/- 63.17 to 2670.29 +/- 471.33 and 36 +/- 0.12 to 35.3 +/- 0.12, respectively), but the increase in V E was higher (P<0.05) and hypothermia was reduced (P<0.05) in LCLR. L-NAME caused no significant change in V E or in body temperature under normoxia, but abolished both the hypoxia-induced hyperventilation and hypothermia. Hypoxia-induced hyperventilation was reduced in LCLR treated with L-NAME. L-NAME also abolished the hypoxia-induced hypothermia in LCLR. The present data indicate that hypoxia-induced hyperventilation and hypothermia may be related to the LC, and that NO is involved in these responses.

Animals↗

PubMed2000

Hyperventilation in panic disorder patients and healthy first-degree relatives.

Our aim was to observe the induction of panic attacks by a hyperventilation challenge test in panic disorder patients (DSM-IV) and their healthy first-degree relatives. We randomly selected 25 panic disorder patients, 31 healthy first-degree relatives of probands with panic disorder and 26 normal volunteers with no family history of panic disorder. All patients had no psychotropic drugs for at least one week. They were induced to hyperventilate (30 breaths/min) for 4 min and anxiety scales were applied before and after the test. A total of 44.0% (N = 11) panic disorder patients, 16.1% (N = 5) of first-degree relatives and 11.5% (N = 3) of control subjects had a panic attack after hyperventilating (chi(2) = 8.93, d.f. = 2, P = 0.011). In this challenge test the panic disorder patients were more sensitive to hyperventilation than first-degree relatives and normal volunteers. Although the hyperventilation test has a low sensitivity, our data suggest that there is no association between a family history of panic disorder and hyperreactivity to an acute hyperventilation challenge test. Perhaps cognitive variables should be considered to play a specific role in this association since symptoms of a panic attack and acute hyperventilation overlap.

Adult↗

PubMed1989

Effects of heavy hyperventilation on transcutaneous and arterial oxygen tensions in healthy adults.

Transcutaneous pO2 on thorax and the volar part of the forearm was measured in six healthy volunteers during heavy hyperventilation, and the values compared with simultaneously measured arterial blood pO2. We found a significant rise in arterial pO2 during hyperventilation with a lesser increase in thoracic transcutaneous pO2. When measured on arm the transcutaneous pO2 did not even rise significantly. After hyperventilation pO2 fell to values below the resting level. The transcutaneous/arterial pO2 index, fell significantly during hyperventilation with the greatest reduction in the arm index. After hyperventilation the arm index returned to the control values, whereas the thoracic index remained low. We suggest, that the significant fall in transcutaneous/arterial blood pO2 index during hyperventilation is caused primarily by skin vasoconstriction, whereas the fall in pO2 after hyperventilation is caused by hypoxia. When measured on areas with increased muscular activity transcutaneous pO2 might depend on the local blood flow and skin oxygen consumption also, causing problems in interpretation with certain patient groups.

Adult↗

PubMed2001

Will prior hyperventilation reduce cerebral blood flow during escape from a submarine?

This study was undertaken to determine if hyperventilation would reduce cerebral blood velocity (CBV) and thereby the risk of decompression illness (DCI) during escape from a submarine and increase the depth from which escape can be made. CBV was measured in eight subjects using Doppler ultrasound as they completed a mock submarine escape exercise. The exercise involved climbing a ladder followed by immersion in cold water-in a real escape the escapee would be exposed to increased pressure and at risk of DCI during the immersion phase. Immediately before the escape exercise the seated subjects either rested or hyperventilated at a controlled rate for2 min. There was a third condition in which the subjects hyperventilated for 2 min and then sat and rested. The three conditions were each undertaken twice. Hyperventilation reduced mean CBV by 45%. In the first session during the first 90s of immersion, CBV was 10% lower (P < 0.05) when the escape procedure followed hyperventilation than when following rest. In the second session CBV was similar for the two escape conditions. Following hyperventilation the restoration of CBV was more rapid during the escape condition than when the subjects rested--the reasons for this are unclear. It is concluded that, although hyperventilation effectively reduces CBV, the reduction is neither sustained during the escape procedure nor sufficiently consistent to recommend that it should be used before escape from a submarine.

Adult↗

PubMed2003

Echocardiographic monitoring of left ventricular regional motion during hyperventilation and intravenous infusion of trometamol (tris) for detection of variant angina.

BACKGROUND: In spite of constant progress and development of new diagnostic tests, the detection of variant angina, which occurs in approximately 30% of patients with ischaemic heart disease (IHD), remains challenging. AIM: To assess the sensitivity and specificity of echocardiographically monitored transient abnormalities of regional wall motion of left ventricle (LV) during hyperventilation after intravenous infusion of trometamol (TRIS-buffer) for the detection of coronary artery spasm. METHODS: The study group consisted of 72 patients (14 women and 58 men, aged from 32 to 69 years) with IHD. A control group was composed of 20 healthy men. Patients with IHD were divided into two groups. Group I consisted of 46 patients with Prinzmetal's angina whereas group II was composed of 26 patients with exertional angina and a history of myocardial infarction. Two-dimensional echocardiographic monitoring of LV contractility was carried out during hyperventilation after an intravenous infusion of 100 ml of trometamol. RESULTS: Transient abnormalities of regional LV wall motion during infusion of trometamol and hyperventilation occurred in 91% of patients from group I and in 8% of patients from group II (p<0.00001). Electrocardiographic ST-segment changes during hyperventilation-trometamol test were observed in 63% of patients from group I and in 23% of patients from group II (p<0.0001). No transient regional dyssynergy of LV nor ST-segment changes during hyperventilation-trometamol test in the control group were observed. The sensitivity and specificity of regional LV wall motion during hyperventilation-trometamol test in the identification of patients with variant angina were 91% and 92%, respectively, and the sensitivity and specificity of ST-segment changes - 63% and 76%, respectively. CONCLUSIONS: Echocardiographic monitoring of regional LV wall motion during hyperventilation after intravenous infusion of trometamol is a sensitive and specific test for detection of variant angina.

Adult↗

PubMedDate not supplied

Definition of the hyperventilation syndrome.

Delegates attending the Fourth International Symposium on Respiratory Psychophysiology indicated on a questionnaire those features of personality and mental disorders, symptoms, signs and measurements which they felt to be essential, closely associated, occasionally associated or irrelevant in the diagnosis of the hyperventilation syndrome (HVS). They also supplied their own definition of the HVS. Anxiety, symptoms reproduced in whole or in part by voluntary hyperventilation, breathlessness, hyperventilation and low CO2 were the features from the questionnaire most commonly considered to be essential in the diagnosis of the HVS. Delegates used the following phrases most frequently in their own definitions: "a variety of somatic symptoms", "hyperventilation", "associated low PCO2", "no organic disease" and "physiologically inappropriate". A consensus definition might read "the hyperventilation syndrome is a syndrome characterized by a variety of somatic symptoms induced by physiologically inappropriate hyperventilation and usually reproduced in whole or in part by voluntary hyperventilation". But for practical use, the nature of the symptoms and any other relevant features need to be clearly identified if this diagnosis is to be entertained in the course of a clinical consultation. This definition still lacks the qualities which are essential for an operational definition.

Health Occupations↗

PubMed1998

[Tetany, spasmophilia, hyperventilation syndrome: theoretical and therapeutic synthesis].

The hyperventilation syndrome (HVS), characterised by multiple somatic symptoms induced by inappropriate hyperventilation, constitutes the physiopathological manifestation of a common disorder in general medicine. As a synonym of spasmophilia or tetany, it has the advantage of offering diagnostic criteria, even though the latter are still vaguely defined. But its definition allows for objective measurements: indeed, a decrease in PCO2 during a hyperventilation provoking test and an abnormally low PCO2 rate at rest can be easily quantified. Moreover, the HVS concept offers a treatment which is both structured (respiratory reeducation, psychotherapy and pharmacology) and efficient. Yet, a number of scientific uncertainties still exist. There is no general agreement regarding the criteria which should be taken into account in a hyperventilation provoking test in order to diagnose an hyperventilation syndrome; the specificity of such a test is weak and a placebo can induce as many symptoms as can a HVS. Respiratory reeducation has good results but does not necessarily have an effect on PCO2. Some therapists see in it no more than a mechanism of relaxation and a rational explanation of frightening symptoms. This has led some authors to reject the term "hyperventilation syndrome" and to prefer the expression "chronic hyperventilation of unknown origin".

Carbon Dioxide↗

PubMed2005

Effects of moderate hyperventilation on cerebrovascular pressure-reactivity after head injury.

In volunteers, hyperventilation improves autoregulation. However, in head-injured patients, hyperventilation-induced deterioration and improvement of autoregulation have been reported. We have re-examined this question using an index of pressure reactivity. Thirty patients with severe or moderate head-injury were studied. Arterial blood pressure, cerebral perfusion pressure (CPP), and intracranial pressure (ICP) were recorded over 20 minute epochs separated by ten minutes of equilibration at baseline and during moderate (>3.5 kPa) hyperventilation. End-tidal CO2 was constant during each phase of data acquisition. Pressure reactivity was assessed using an index 'PRx' based on the response of ICP to spontaneous blood pressure changes. Hyperventilation decreased PaCO2 from 5.1 +/- 0.4 to 4.4 +/- 0.4 kPa (p < 0.0001). ICP decreased by 3.7 +/- 2.2 mmHg (p < 0.001). CPP increased by 5.9 +/- 8.2 mmHg (p < 0.001). Overall, PRx did not change significantly with hyperventilation. However, there was a significant negative correlation between baseline PRx and the change in PRx (r = -0.71, p < 0.0001). This suggests that patients with disturbed pressure-reactivity may improve, whereas patients with intact pressure reactivity remain largely unchanged. Our data suggest that the response of pressure reactivity to hyperventilation is heterogeneous. This could be due to hyperventilation-induced changes in cerebral metabolism, or the change in CPP.

Adult↗

PubMed1987

Can eucapnic hyperventilation prolong a subsequent breath-hold?

Previous studies have shown that, upon breaking a maximal breath-hold (BH), reinhalation of the expired gas allows an additional period of breath-holding. This indicates that mere ventilatory movements can diminish the urge to breathe. We sought to determine if vigorous ventilations, performed immediately prior to a maximal BH and in such a way that CO2 stores are not changed, can prolong a subsequent BH. Maximal BHs were accomplished with and without a preceding period of hyperventilation. The gas breathed during hyperventilation was air with 4.37% CO2, or oxygen containing either 0.04% CO2 (hypocapnic hyperventilation) or 4.37% CO2 (eucapnic hyperventilation). During hyperventilation, expired minute volume and frequency were clamped at 60 L/min and 30 breaths/min, respectively. End-tidal and transcutaneous CO2 tensions were monitored. Eucapnic hyperventilation did not prolong maximal BHs. Therefore, the ventilatory movements of hyperventilation do not appear to affect the duration of a subsequent maximal BH if these movements are not accompanied by changes in CO2 stores.

Adult↗

PubMed2000

Effects of graded hyperventilation on cerebral blood flow autoregulation in experimental subarachnoid hemorrhage.

An impaired CBF autoregulation can be restored by hyperventilation at a PaCO2 level of about 2.9 to 4.1 kPa (22 to 31 mm Hg). However, it is uncertain whether the restoring effect can take place at lesser degrees of hypocapnia. In the current study, CBF autoregulation was studied at four PaCO2 levels: 5.33 kPa (40 mm Hg, normoventilation), 4.67 kPa (35 mm Hg, slight hyperventilation), 4.00 kPa (30 mm Hg, moderate hyperventilation), and 3.33 kPa (25 mm Hg, profound hyperventilation). At each PaCO2 level, eight rats 2 days after experimental subarachnoid hemorrhage (SAH) and eight sham-operated controls were studied. The CBF was measured by the intracarotid 133Xe method. The CBF autoregulation was found to be intact in all controls but completely disturbed in the normoventilated SAH rats. However, by slight hyperventilation, CBF autoregulation was restored in seven of eight SAH rats with a decline in CBF of 10%. The CBF autoregulation was found intact in all of the moderately or profoundly hyperventilated SAH rats, whereas the decline in CBF was 21% and 28%, respectively. In conclusion, hyperventilation to a PaCO2 level between 4.00 and 4.67 kPa (30 to 35 mm Hg) appears to be sufficient for reestablishing an impaired autoregulation after SAH.

Animals↗

PubMed1982

Effect of hyperventilation and starvation on rat lung mechanics and surfactant.

We studied the effects of hyperventilation and starvation on rat lung mechanics and surfactant. We hyperventilated lungs by excising and ventilating them at 3 times the normal tidal volume. Three days starvation reduced the alveolar pool of disaturated phosphatidyl choline by about 20% but did not significantly reduce the functional residual capacity. Air and saline deflation pressure-volume curves were performed in 4 groups: control lungs, lungs from starved rats, hyperventilated lungs, and hyperventilated lungs from starved rats. The area under each curve was calculated; this indicated the relative position of the curve in the pressure-volume diagram. We found that starvation did not change recoil, that hyperventilation increased surface recoil, and that combined starvation and hyperventilation increased it even more. We conclude that hyperventilation-induced dysfunction of surfactant is greater when the alveolar pool of surfactant is reduced by starvation. This effect might also occur clinically in the intensive care setting.

Air Pressure↗

PubMed1991

Adverse effects of prolonged hyperventilation in patients with severe head injury: a randomized clinical trial.

There is still controversy over whether or not patients should be hyperventilated after traumatic brain injury, and a randomized trial has never been conducted. The theoretical advantages of hyperventilation are cerebral vasoconstriction for intracranial pressure (ICP) control and reversal of brain and cerebrospinal fluid (CSF) acidosis. Possible disadvantages include cerebral vasoconstriction to such an extent that cerebral ischemia ensues, and only a short-lived effect on CSF pH with a loss of HCO3-buffer from CSF. The latter disadvantage might be overcome by the addition of the buffer tromethamine (THAM), which has shown some promise in experimental and clinical use. Accordingly, a trial was performed with patients randomly assigned to receive normal ventilation (PaCO2 35 +/- 2 mm Hg (mean +/- standard deviation): control group), hyperventilation (PaCO2 25 +/- 2 mm Hg: HV group), or hyperventilation plus THAM (PaCO2 25 +/- 2 mm Hg: HV + THAM group). Stratification into subgroups of patients with motor scores of 1-3 and 4-5 took place. Outcome was assessed according to the Glasgow Outcome Scale at 3, 6, and 12 months. There were 41 patients in the control group, 36 in the HV group, and 36 in the HV + THAM group. The mean Glasgow Coma Scale score for each group was 5.7 +/- 1.7, 5.6 +/- 1.7, and 5.9 +/- 1.7, respectively; this score and other indicators of severity of injury were not significantly different. A 100% follow-up review was obtained. At 3 and 6 months after injury the number of patients with a favorable outcome (good or moderately disabled) was significantly (p less than 0.05) lower in the hyperventilated patients than in the control and HV + THAM groups. This occurred only in patients with a motor score of 4-5. At 12 months posttrauma this difference was not significant (p = 0.13). Biochemical data indicated that hyperventilation could not sustain alkalinization in the CSF, although THAM could. Accordingly, cerebral blood flow (CBF) was lower in the HV + THAM group than in the control and HV groups, but neither CBF nor arteriovenous difference of oxygen data indicated the occurrence of cerebral ischemia in any of the three groups. Although mean ICP could be kept well below 25 mm Hg in all three groups, the course of ICP was most stable in the HV + THAM group. It is concluded that prophylactic hyperventilation is deleterious in head-injured patients with motor scores of 4-5.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗

PubMed2002

Cerebral tissue PO2 and SjvO2 changes during moderate hyperventilation in patients with severe traumatic brain injury.

OBJECT: The aim of this study was to investigate the effects of moderate hyperventilation on intracranial pressure (ICP), jugular venous oxygen saturation ([SjvO2], an index of global cerebral perfusion), and brain tissue PO2 (an index of local cerebral perfusion). METHODS: Ninety-four tests consisting of 20-minute periods of moderate hyperventilation (27-32 mm Hg) were performed on different days in 36 patients with severe traumatic brain injury (Glasgow Coma Scale score < or = 8). Moderate hyperventilation resulted in a significant reduction in average ICP, but in seven tests performed in five patients it was ineffective. The response of SjvO2 and brain tissue PO2 to CO2 changes was widely variable and unpredictable. After 20 minutes of moderate hyperventilation in most tests (79.8%), both SjvO2 and brain tissue PO2 values remained above the lower limits of normality (50% and 10 mm Hg, respectively). In contrast, in 15 tests performed in six patients (16.6% of the studied population) brain tissue PO2 decreased below 10 mm Hg although the corresponding SjvO2 values were greater than 50%. The reduction of brain tissue PO2 below 10 mm Hg was favored by the low prehyperventilation values (10 tests), higher CO2 reactivity, and, possibly, by lower prehyperventilation values of cerebral perfusion pressure. In five of those 15 tests, the prehyperventilation values of SjvO2 were greater than 70%, a condition of relative hyperemia. The SjvO2 decreased below 50% in four tests; the corresponding brain tissue PO2 values were less than 10 mm Hg in three of those tests, whereas in the fourth, the jugular venous O2 desaturation was not detected by brain tissue PO2. The analysis of the simultaneous relative changes (prehyperventilation - posthyperventilation) of SjvO2 and brain tissue PO2 showed that in most tests (75.5%) there was a reduction of both SjvO2 and brain tissue PO2. In two tests moderate hyperventilation resulted in an increase of both SjvO2 and brain tissue PO2. In the remaining 17 tests a redistribution of the cerebral blood flow was observed, leading to changes in SjvO2 and brain tissue PO2 in opposite directions. CCONCLUSIONS. Hyperventilation, even if moderate, can frequently result in harmful local reductions of cerebral perfusion that cannot be detected by assessing SjvO2. Therefore, hyperventilation should be used with caution and should not be considered safe. This study confirms that SjvO2 and brain tissue PO2 are two parameters that provide complementary information on brain oxygenation that is useful to reduce the risk of secondary damage. Changes in SjvO2 and brain tissue PO2 in opposite directions indicate that data obtained from brain tissue PO2 monitoring cannot be extrapolated to evaluate the global cerebral perfusion.

Adolescent↗

PubMed1990

[Bronchoconstriction in isocapnic hyperventilation-induced asthma].

It is well known that some asthmatic patients develop bronchoconstriction after exercise challenge (exercise-induced asthma, EIA). Recently, it has been pointed out that isocapnic hyperventilation also induces similar bronchoconstriction (hyperventilation-induced asthma, HIA) in the same asthmatic subjects. However, the mechanism of HIA has not yet been determined. In the present study, we performed exercise and hyperventilation challenge in the same patients and pulmonary function data and neutrophil chemotactic factor (NCF) in peripheral blood were examined before and after both challenges. Twelve asthmatic patients with normal pulmonary function data on testing days were subjected to exercise test on a bicycle ergometer and then isocapnic hyperventilation tests in subsequent days. Subjects breathed dry air from the cylinder. Isocapnic hyperventilation was performed by monitoring minute ventilation and each patient followed the same minute ventilation exercise. The reduction of FEV1.0 and time course of airway obstruction were almost the same after exercise and hyperventilation testing. All patients who developed EIA also developed HIA and other patients did not develop both EIA and HIA. Changes of Rrs, V50 and V25 and their time course after each test were also similar in EIA(+) and HIA(+), and in EIA(-) and HIA(-). NCF increased significantly after both challenges in EIA(+) and HIA(+) patient, although increment of NCF was much less these the increases of HIA(+). These data may suggest that the development of bronchoconstriction was compatible after exercise and hyperventilation in each asthmatic patient, however, the mechanism of HIA may differ from EIA, although NCF slightly but significantly increased in HIA, suggesting the possible role of a chemical mediator.

Adolescent↗

PubMed2002

Can hyperventilation improve cerebral microcirculation in patients with high ICP?

Gosling's pulsatility index (PI) is generally thought to reflect cerebrovascular resistance. Hyperventilation and increased intracranial pressure (ICP) usually increase PI. In this study, the effect of hyperventilation on PI was assessed in head injured patients with and without elevated ICP. A total of 73 hyperventilation studies were conducted on 20 intubated TBI patients. EtCO2, ICP, MCA flow velocity and MCA PI bilaterally were recorded simultaneously. Hemispheric CO2-Reactivity (hCO2R) was calculated. Only studies with a baseline ICP < 15 or > 30 mm Hg were included for analysis. With hyperventilation pCO2 decreased on average from 33.54.2 to 26.84.8 mmHg. PI increased significantly in patients with baseline ICP < 15 mmHg (11.8%; p < 0.0001) but decreased significantly if baseline ICP was > 30 mm Hg (12.21%; p = 0.0013). High baseline ICP, low initial GCS and impaired hCO2R were associated with the decrease of PI. Hyperventilation unexpectedly reduced PI in patients with high ICP. Because decreased PI suggests decreased CVR, it is postulated that hyperventilation in the setting of raised ICP improves cerebral microcirculation.

Adult↗

PubMed1991

Comparison of refractoriness after exercise- and hyperventilation-induced asthma.

To study the relationship of bronchoconstriction and refractoriness we performed pairs of exercise and hyperventilation tests in 15 patients (mean [SEM] age 28.5 [2.8] years) with a history of exercise-induced asthma. Mean (SEM) maximum specific airway resistance (SRaw) increased during the first exercise test to 33.9 (4.5) and during the second exercise test to 29.8 (5.2) cmH2O x s (n.s.). Mean (SEM) maximum specific airway resistance (SRaw) increased during the first hyperventilation test to 44.0 (5.9) and during the second hyperventilation test to 27.4 (3.3) cmH2O x s (p less than 0.01). Mean maximum bronchoconstriction after corresponding exercise and hyperventilation tests did not differ statistically. There was a significantly larger inter-individual variability in the airway response to hyperventilation (p less than 0.001). From these data we suggest that similar refractoriness can be observed after both exercise and hyperventilation.

Adolescent↗