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PubMed1987

Gravity-induced hyperventilation is caused by a reduced brain perfusion.

The suggestion that hyperventilation caused by increased gravity is mediated by a decrease in brain perfusion has led us to propose a mathematical model based on: (1) the CO2 balance equation for the respiratory center (RC), and (2) the relationship between RC blood flow (QRC), foot-to-head acceleration (Gz) and PRCCO2, namely, QRC = [1 - a(Gz - 1)](b X PRCCO2 + c), where the coefficients a, b and c can be calculated from data in the literature. QRC is significantly affected by + GZ only at high PaCO2. The model can be used to calculate oxygen pressure in the RC; the numbers so obtained are in good agreement with measurements of jugular vein PO2 obtained by others.

Blood Flow Velocity↗
PubMed1983

Relationship between bronchial responsiveness to hyperventilation with cold and methacholine in asthma.

Twenty-seven subjects with asthma and normal baseline lung function were challenged with aerosols of methacholine (M) and by isocapnic hyperventilation with cold air (HV). Stimulus-effect relationships were determined for each provocational technique on separate days and were expressed as the dose required to produce a 20% fall in forced expired volume in 1 sec (FEV1) obtained by linear interpolation from log stimulus vs. response curves (PD20). Each stimulus was applied with a sufficient intensity to produce a 20% or greater fall in FEV1 in each subject. The PD20 for M correlated significantly with the PD20 for HV (p less than 0.001) when the latter was expressed in liters per minute. The correlation between cumulative M PD20 and HV PD20 expressed as a percent of maximal voluntary ventilation was significant but less strong. We conclude that the airway response to HV reflects nonspecific bronchial hyperresponsiveness and that the dose of HV is best determined as the absolute level of ventilation.

Adolescent↗
PubMed1986

Hyperosmolarity as the stimulus to asthma induced by hyperventilation?

Hyperosmolarity of the epithelial fluid of the large airways caused by evaporative water loss (wloss) has been proposed as the stimulus to exercise-induced asthma. The aim of this study was to compare the wloss during hyperpnea with a theoretical wloss from a known hypertonic stimulus in order to determine whether comparable volumes of wloss will induce the same response. Since wloss also occurs during isocapnic hyperventilation (ISH), we decided to compare the airway response to ISH with the response obtained after inhaling 4.5% NaCl aerosol. Changes in FEV1 were measured in 17 subjects with asthma in response to increasing rates of ventilation (ISH) and increasing doses of 4.5% NaCl aerosol. For ISH, wloss was calculated at 29 mg/L of expired air and for 4.5% NaCl, at 4.0 ml/l ml of aerosol inhaled, as this is the volume of water that will bring the periciliary fluid to normal tonicity. Two dose-response curves were drawn for each subject. These curves were similar both in position (PD20) and in shape (i.e., the slope of the curve as estimated by the ratio of wloss for maximum recorded percent fall in FEV1 [PDmax] to PD20). There was no significant difference in the PD20 (ISH, 10.3 ml, 95% confidence limits 7.5 and 13.9; 4.5% NaCl, 12.3 ml, 95% confidence limits 8.9 and 17.1) or between the ratio of log PDmax:log PD20 (ISH, 1.19 +/- 1 SD, 0.14; 4.5% NaCl, 1.17 +/- 1 SD, 1.17; p = not significant). These findings support the concept that airway hyperosmolarity may be the mechanism for ISH and exercise-induced asthma.

Adolescent↗
PubMed1993

No chronic hyperventilation in panic disorder patients.

Arterial blood gases were measured and base excess calculated in 18 nonpanicking panic disorder (PD) patients, 12 subjects suffering from other anxiety disorders, and 18 normal control subjects. There was neither chronic nor clinically significant acute hyperventilation in either group.

Acid-Base Equilibrium↗
PubMed1984

Vasogenic edema with intraparenchymatous expanding mass lesions: a theory on its pathophysiology and mode of action of hyperventilation and corticosteroids.

Vasogenic edema with expanding mass brain lesions is hypothesized to be due to an increased intracapillary pressure. The latter may be due to preferential occlusion of the venous system by the growth of the lesion but endothelila proliferation and biogenic amines may also play a part. Endocytosis appears to be a mechanical response to the increased intraluminal pressure. This is a poorly selective process which can explain the proteinaceous nature of vasogenic edema. Steroids may act by forming hydrophobic bonds in the endothelial cell membrane and making it more difficult for any membrane fission to occur. Hyperventilation can be of use in vasogenic edema by decreasing intracranial pressure, providing better oxygenation and also by diminishing the capillary head pressure.

Adrenal Cortex Hormones↗
PubMed1992

Profound alkalemia during treatment of tricyclic antidepressant overdose: a potential hazard of combined hyperventilation and intravenous bicarbonate.

Two patients with cardiovascular and neurologic toxicity from intentional tricyclic antidepressant overdose received bicarbonate infusions in association with hyperventilation for alkalinization. Both patients developed profound alkalemia. One patient died, and the other patient's alkalemia resolved prior to her death. Bicarbonate infusions have become the standard of care for symptomatic tricyclic antidepressant toxicity. Severe alkalemia (pH greater than 7.60) in other settings has been reported to correlate with higher rates of mortality. Careful monitoring of the pH is imperative when bicarbonate therapy is used. It is probably prudent to keep the pH level in the range 7.45 to 7.60. Capnography may also be useful in monitoring patients during alkalinization.

Adult↗
PubMed1995

Hyperventilation in normal subjects. A clinical, gas-analytic and EMG study.

Clinical (paresthesiae and Trousseau's sign), EMG, blood biochemical (lactic acid and total Ca2+) and gas-analytic (pH, PCO2, PO2, HCO3) changes were studied during and after 5 min voluntary hyperventilation (HV) in 15 normal subjects. Paresthesiae and spontaneous motor activity were common manifestations (87% and 67% respectively) in our test. They were significantly related only to changes in pH, PCO2 and PO2, with paresthesiae arising earlier and at milder gas-analytic changes than motor activity. Paresthesiae and motor activity induced by HV cannot be used as reliable indicators of pathology. Their presence simply reflects the degree of the blood gas-analytic changes (pH, PCO2 and PO2) which therefore should be carefully monitored before drawing any conclusion from an HV test.

Adolescent↗
PubMed2006

An examination of worry in relation to anxious responding to voluntary hyperventilation among adolescents.

This study examined the association between worry and fearful responding to a 3-min voluntary hyperventilation procedure. Participants were 160 adolescents (71 females) between the ages of 12 and 17 years (M=14.92 years). After accounting for the significant effects of state anxiety and anxiety sensitivity, results indicated that pre-challenge levels of worry indexed by the Penn State Worry Questionnaire-Child Version predicted post-challenge anxiety and intensity of panic symptoms. Results are discussed in terms of the role of worry in relation to panic-relevant emotional vulnerability among youth.

Adolescent↗
PubMed2005

Exercise hyperventilation in chronic heart failure is not caused by systemic lactic acidosis.

BACKGROUND: Patients with heart failure have an abnormally high ventilatory response to exercise associated with gas exchange defects and reduced arterial pCO(2). AIMS: We examined the possibility of lactic acidosis as the stimulus to this increased ventilation that abnormally depresses pCO(2) during exercise in heart failure. METHOD AND RESULTS: We studied 18 patients with chronic heart failure. We measured VE/VCO(2) slope during exercise, arterial blood gases and lactate concentrations during cardiopulmonary exercise testing (rest, peak exercise and one minute after the end of exercise). Neither VE/VCO(2) slope nor arterial pCO(2) were related to arterial lactate concentrations at peak exercise (r = -0.16, p = 0.65 and r = -0.15, p = 0.6). During early recovery, patients with a high VE/VCO(2) slope had a particularly pronounced rise in arterial lactate and hydrogen ion concentrations (r = 0.57, p < 0.05 and r = 0.84, p < 0.0001) and yet their arterial pCO(2) rose rather than fell (r = 0.79, p < 0.001). The rise in arterial pCO(2) correlated with the increase in arterial hydrogen concentration (r = 0.78, p < 0.001) and with arterial pCO(2) at peak exercise (r = -0.76, p < 0.001). CONCLUSIONS: In heart failure VE/VCO(2) slope and low arterial pCO(2) at peak exercise are not related to the degree of systemic lactic acidosis. Lactic acidosis is therefore not a plausible mechanism of exercise induced hyperventilation.

Acidosis, Lactic↗
PubMed2003

Sleep but not hyperventilation increases the sensitivity of the EEG in patients with temporal lobe epilepsy.

PURPOSE: To evaluate the relative impact of 3 and 5 min of hyperventilation (HV) and different sleep stages on the sensitivity of the interictal EEG in focal epilepsy. METHODS: We examined 20 patients with temporal lobe epilepsy (TLE, 85%) or extratemporal epilepsy during EEG-monitoring. We compared 6 min EEG (12 epochs of 30s) during/after each: (a) waking; (b) 5 or 3 min of HV; (c) sleep stages 1, 2, 3/4 and REM regarding the frequency of epileptiform discharges (ED). The Wilcoxon matched pairs signed rank test was used. The main endpoint was the comparison of 5 min of HV with sleep stage 2. RESULTS: During sleep stage 2, ED were more frequent than during/after 5 min of HV (P=0.002). Compared to the waking EEG, all NREM-sleep stages activated ED. Sleep stage 2 was associated with the strongest activation. There was no difference between the waking state and REM-sleep. Compared to the waking EEG, neither 3 nor 5 min of HV showed an activation of ED. CONCLUSION: In patients with TLE, sleep stage 2 shows a significantly higher sensitivity for ED than 5 min of HV. Compared to the waking EEG, HV showed no activating effect on ED. These results suggest that in patients with the clinical diagnosis of TLE (and possibly other focal epilepsies) measures to record sleep stage 2 (such as sleep deprivation) should be increased whereas HV appears to be dispensable in this setting.

Adult↗
PubMed2005

Hyperventilation-induced tetany associated with epidural analgesia for labor.

We report a case of painful carpo-pedal spasm associated with the initiation of epidural analgesia for labor. The patient, an otherwise healthy primigravida in early labor at term, was experiencing severe hyperventilation as a result of inappropriate use of the Lamaze breathing technique. Bilateral carpo-pedal spasm occurred, and produced severe pain. Resolution of symptoms coincided with onset of effective epidural labor pain relief. A diagnostic challenge was presented to the anesthesiologist, as the symptoms could have been consistent with subdural block, local anesthetic toxicity, high sensory level of analgesia or eclamptic neuro-excitation activity.

Adult↗
PubMed2005

Central neurogenic hyperventilation in a conscious man with CSF dissemination from a pineal glioblastoma.

A 40-year old conscious man developed central neurogenic hyperventilation (CNH). He had tumor dissemination to the brainstem 10 months after undergoing partial removal of a pineal glioblastoma. To the best of our knowledge, this is the first report of CNH caused by the cerebrospinal fluid dissemination of a tumor. The authors suggest that multiple lesions from an infiltrative tumor in the brainstem may give rise to CNH and further our understanding of the pathogenesis of CNH.

Adult↗
PubMed1997

Hyperventilation effect on postural sway.

OBJECTIVE: To examine the effect of voluntary hyperventilation (HV) on postural sway. DESIGN: Crossover controlled, experimental study. SETTING: Human movement and balance clinical research unit. SUBJECTS: Four different groups of normal subjects (n = 6, 6, 7, and 9) and patients with bilateral absence of vestibular function (n = 9). INTERVENTION: Partial carbon dioxide pressure (tc-PCO2) was measured transcutaneously with surface electrodes. Body sway was measured with a force platform immediately after maximal voluntary HV for 30 to 90 seconds. Recordings were obtained with eyes open and eyes closed, standing on the platform and on foam-rubber, and after head or body movements. MAIN OUTCOME MEASURE: Postural sway. RESULTS: HV increased body sway in all conditions, but the effects were more intense when subjects were standing directly on the platform surface with their eyes closed. Recordings after HV of 30, 60, and 90 sec in normal subjects showed that although CO2 levels were inversely related to the duration of HV, body sway did not increase further. HV also increased sway after active movements by the subjects. The main sway increase was in sway area and mean and maximal deviations but less for mean sway velocity. HV preferentially increased low-frequency sway oscillations. These effects were also present in labyrinthine-defective subjects. CONCLUSIONS: HV increases body sway, but the relationship between CO2 levels and degree of unsteadiness is not linear. The dizziness reported by patients with HV syndrome may be partly caused by objective unsteadiness. The presence of HV-induced unsteadiness in patients with absent vestibular function indicates that the effects of HV are not mediated by the labyrinth.

Adult↗
PubMed1981

The independent effects of hyperventilation, tolazoline, and dopamine on infants with persistent pulmonary hypertension.

We studied the separate and combined effects of hyperventilation and administration of dopamine and tolazoline in five infants with pulmonary hypertension managed with indwelling pulmonary artery catheters. In five infants the right-to-left shunt reversed during ventilator-induced respiratory alkalosis (pH greater than 7.6). Response to drugs was variable and unpredictable. One infant could be oxygenated at normal pH during combined dopamine and tolazoline infusion. Other infants showed no response to drugs, or became worse during infusion. The ratio of pulmonary artery to systemic artery pressure averaged 1.14 with standard therapy, but decreased to 0.98 following respiratory alkalosis alone, to 0.87 following drug infusions, and to 0.70 following the combination of alkalosis and drug infusion. These changes were significant by analysis of variance at P less than 0.02, P less 0.001, and P less than 0.001, respectively. Systemic oxygenation was satisfactory in all cases when the pulmonary to systemic pressure ratio was less than 1.0.

Alkalosis, Respiratory↗
PubMedDate not supplied

Epinephrine-induced panic attacks and hyperventilation.

To assess the effects of epinephrine on ventilation in patients with panic disorder and in social phobics, analyses were performed on pooled data from two previous infusion studies. Throughout the infusion, changes in transcutaneous PCO2 (tcPCO2), subjective anxiety, heart rate and blood pressure were recorded continuously. Twenty-nine patients received epinephrine, ten patients received placebo. Thirteen patients (45%) had a panic attack during epinephrine. The fall in tcPCO2 and the cardiovascular response was greater in panicking patients than patients who did not panic. Although the fall in tcPCO2 associated with panic was not substantial and did not indicate clinically significant acute hyperventilation, it appears to be a sensitive index for epinephrine-induced panic. The fall in tcPCO2 was predicted rather by the frequency of occurrence of anxiety-related somatic symptoms than by the fear of these symptoms. These findings further reduce a role for fear of bodily sensations in epinephrine-induced panic attacks and favor a biological sensitivity to sympathetic stimulation.

Adult↗
PubMed1977

Hyperventilation: An important cause of pseudoangina.

50 patients initially referred to a cardiac clinic for confirmation or exclusion of angina were found to be habitual hyperventilators. 13 of them also had some organic heart disease. Simple physiotherapy aimed at restoring a normal breathing pattern proved an effective treatment, 76% of those followed for 11-68 months being symptom-free.

Adult↗
PubMed2003

Recovery function of and effects of hyperventilation on somatosensory evoked high-frequency oscillation in Parkinson's disease and myoclonus epilepsy.

To evaluate recovery function of and effects of hyperventilation (HV) on high-frequency oscillations (HFOs) of median nerve somatosensory evoked potential (SEP), we recorded SEPs in 8 Parkinson's disease (PD) patients with enlarged HFOs, 4 myoclonus epilepsy (ME) patients and 10 healthy volunteers (N). SEP was recorded from the hand sensory area contralateral to the median nerve stimulated at the wrist. Responses were amplified with filters set at 0.5 and 3000 Hz. HFOs were obtained by digitally filtering raw SEPs from 500 to 1000 Hz. We measured amplitudes of the N20 onset-peak (N20o-p), N20 peak-P25 peak (N20p-P25p), P25 peak-N33 peak (P25p-N33p), the early (1st-2nd) and late (3rd) HFOs. For the recovery function study, paired-pulse stimuli at various interstimulus intervals (20, 50, 100, 150, 200 and 300 ms) were given. To investigate effects of HV, amplitudes of several components of SEPs recorded after HV were compared with those before HV. In PD and ME, the N20o-p recovery curve showed significantly less suppression as compared with those of N. The P25p-N33p recovery curve of ME showed longer suppression than those of N and PD. There were no significant differences in the early or late HFOs recovery curves among three groups. At the dysinhibited state after HV, the late HFO was reduced in association with a significant enlargement of the N20p-P25p amplitude in normal subjects. This suggests that the late HFOs should reflect bursts of inhibitory interneurons. In the ME patients, the early HFOs significantly decreased by HV. The pattern in ME patients may be explained by a kind of compensation for already enhanced SEPs (giant SEP) in the dysinhibited situation. We conclude that (1) Giant HFOs are normally regulated by inhibitory neuronal systems involving in paired stimulation SEP. (2) The late HFOs must reflect bursts of GABAergic inhibitory interneurons.

Adult↗
PubMed1990

Thalamic hemorrhage imitating hyperventilation.

A 52-year-old woman developed subjective right hemiparesthesias over a two-day period. Because of a paucity of physical findings, apparent anxiety with tachypnea, and a respiratory alkalosis with hypocapnia, a diagnosis of hyperventilation syndrome was considered. However, because of the unilateral symptoms, a computed tomography scan was performed, demonstrating a left posterior thalamic infarct. Most reports of thalamic infarct indicate altered mental status, vertical gaze palsies, or sensorimotor hemiparesis with sensory involvement predominant. The case of a patient with thalamic hemorrhage who presented with only hemiparesthesia is reported to heighten clinicians' awareness of this diagnosis.

Cerebral Hemorrhage↗