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PubMed1991

Paraesthesiae and tetany induced by voluntary hyperventilation. Increased excitability of human cutaneous and motor axons.

Anxiety can induce hyperventilation, and the resultant hypocapnia and hypocalcaemia can lead to paraesthesiae and tetany. To define the nature of the disturbance created in peripheral nerve, the excitability of cutaneous and motor axons was monitored in 6 normal subjects requested to hyperventilate until paraesthesiae developed in the hands, face and trunk. This occurred when alveolar PCO2 (PACO2) had declined on average by 20 mmHg. Spontaneous EMG activity developed when PACO2 had declined by a further 4 mmHg. Changes in the excitability of cutaneous and motor axons were measured from changes in the compound action potentials evoked by stimulation of the median nerve at the wrist and recorded over the digital nerves of the index finger and over the thenar muscles, respectively. As PACO2 declined, the size of the compound sensory and muscle potentials evoked by a constant stimulus progressively increased, indicating an increase in axonal excitability. These changes occurred before paraesthesiae or tetany developed. In each subject there was a statistically significant inverse correlation between PACO2 and axonal excitability. Independent of this increase in axonal excitability, there was no significant change in the supernormal phase of the recovery cycle of cutaneous axons. Microneurographic recordings from the median nerve in 2 subjects revealed spontaneous bursting activity of cutaneous axons, perceived as paraesthesiae. It is concluded that the paraesthesiae and tetany induced by hyperventilation result solely from changes in the excitability of cutaneous and motor axons in the peripheral nerve, presumably due to an alteration in the electrical properties of the axonal membrane resulting from a reduced plasma [Ca2+]. The supernormal phase may entrain the ectopic discharge and thereby determine the maximal discharge frequency of impulses in ectopically generated trains, but does not otherwise contribute to the physiological disturbance.

Action Potentials↗
PubMed2002

Cerebral blood volume and blood flow responses to hyperventilation in brain tumors during isoflurane or propofol anesthesia.

UNLABELLED: Using computerized tomography, we measured absolute cerebral blood flow (CBF) and cerebral blood volume (CBV) in tumor, peri-tumor, and contralateral normal regions, at normocapnia and hypocapnia, in 16 rabbits with brain tumors (VX2 carcinoma), under isoflurane or propofol anesthesia. In both anesthetic groups, CBV and CBF were highest in the tumor region and lowest in the contralateral normal tissue. For isoflurane, a significant decrease in both CBV and CBF was observed in all tissue regions with hyperventilation (P < 0.05), but without accompanying changes in intracranial pressure. However, the percent reduction in regional CBF with hypocapnia was two times larger than that observed in the CBV response (P < 0.01). In contrast, there were no significant changes in CBV and CBF in the Propofol group with hyperventilation for all regions (P > 0.10). In addition, there were no differences between CBV values for isoflurane at hypocapnia when compared with CBV values for propofol at normo- or hypocapnia (P > 0.34 and P > 0.35, respectively, in the tumor regions). Our results indicate that propofol increases cerebral vascular tone in both neoplastic and normal tissue vessels compared with isoflurane. CBV and CBF during normocapnia were significantly greater in all regions (tumor, peri-tumor, and contralateral normal tissue) with isoflurane than with propofol. CBV and CBF remained responsive to hyperventilation only with isoflurane. IMPLICATIONS: In rabbits with brain tumors, brain blood flow and volume were significantly larger in all regions (tumor, peri-tumor, and contralateral normal tissue) with isoflurane than with propofol during normocapnia, and remained responsive to a reduction in PaCO(2). Consequently, during hypocapnia, brain blood flow and volume values with isoflurane were similar to values with propofol.

Anesthesia↗
PubMed1984

Effect of hyperventilation on total calcium, ionized calcium, and serum phosphorus in neonates.

The effect of alkalosis (pH greater than 7.55) on total calcium, ionized calcium, and serum phosphorus was studied in seven infants with persistent pulmonary hypertension (PPH) before, during, and after hyperventilation. Hyperventilation-induced alkalosis resulted in marked decreases in total calcium, phosphorus, and ionized calcium. There was an inverse correlation between plasma Ca+2 and pH; a 0.1-unit increase in blood pH decreased Ca+2 by 0.42 mg/dl. Two of the study infants had ionized calcium concentrations less than 2.5 mg/dl during hyperventilation. These disturbing changes in total calcium, ionized calcium, and serum phosphorus could have potentially detrimental effects on neonates with PPH.

Alkalosis↗
PubMed1998

Peripheral neural modulation of endotoxin-induced hyperventilation.

OBJECTIVE: To delineate the role of the peripheral neural reflexes involved in modulating hyperventilation during endotoxemia. DESIGN: A prospective, randomized, controlled, multigroup study. SETTING: Research animal laboratory. SUBJECTS: Adult Sprague-Dawley rats (n=43; 354+/-24 g) of either gender. INTERVENTIONS: Eight rats received a sham operation on their vagus, carotid sinus, and aortic nerves before the administration of a saline vehicle to serve as the time control. In the endotoxin group, 11 rats received a sham operation before endotoxin challenge. The remaining 24 rats received bilateral vagotomy (n=8), perivagal capsaicin treatment (n=8), or denervation of peripheral chemoreceptors (n=8) before endotoxin challenge. After the breathing pattern returned to a steady state, endotoxin (L-4130, serotype 0111, B4 lipopolysaccharide; 50 mg/kg) was injected into the vein. The rat's respiration was then monitored continuously for 5 hrs or until the animal died. MEASUREMENTS AND MAIN RESULTS: The respiratory rate and tidal volume did not change over the 5-hr observation period in the time control group. In the endotoxin group, the respiratory rate increased significantly from baseline (135.4%) 2 hrs after endotoxin challenge and increased persistently until the rats died. The tidal volume increased gradually to < or =132.8% of baseline 4 hrs after endotoxin challenge. Bilateral cervical vagotomy and perineural capsaicin treatment of the vagus nerves eliminated the tachypnea response to endotoxin injection. Denervation of the peripheral chemoreceptor accentuated the hyperventilation response to endotoxin, and resulted in the shortest survival time. CONCLUSIONS: Both lung vagal C-fiber afferents and peripheral chemoreceptors are involved in modulating the hyperventilation response after endotoxin challenge in rat models. Stimulation of vagal C-fiber afferents increased the respiratory rate. Conversely, the role of peripheral chemoreceptors was to restrain the hyperventilatory response and these receptors may play a protective role during endotoxemia.

Animals↗
PubMedDate not supplied

Hyperventilation is not diagnostically specific to panic patients.

It has been claimed that hyperventilation is a cause of panic attacks in patients suffering from panic disorder (PD), and various studies have, in fact, documented low resting CO2 in PD patients. However, most comparisons have been made using non-psychiatric controls. Since increased ventilation is a common concomitant of distress, the relevance of using healthy/non-anxious control groups may be questioned. Respiratory peculiarities of PD patients may actually just reflect background anxiety rather than a diagnostically specific feature. In order to explore the possible diagnostic specificity of hyperventilation, as well as increased respiratory rate and respiratory variability, to PD patients, capnographic patterns were analyzed from PD patients, non-panic disorder anxiety patients, and healthy controls. Capnographic data were obtained while subjects were resting, watching an exciting film, relaxing, and being exposed to idiosyncratically relevant fearful imagery. Findings were robust. As found in most studies, PD patients had lower resting CO2 than healthy controls; however, that of non-panic disorder anxiety patients was just as low as PD patients. The exciting film and fearful imagery produced consistent increases in distress and concomitant increases in respiratory rate, variability of end-tidal CO2, and decreases in end-tidal CO2. However, this was similar in all three groups. Data suggest that hyperventilation is not specific to PD patients.

Adult↗
PubMedDate not supplied

Slow recovery from voluntary hyperventilation in panic disorder.

OBJECTIVE: Because hyperventilation has figured prominently in theories of panic disorder (PD) but not of social phobia (SP), we compared predictions regarding diagnosis-specific differences in psychological and physiological measures before, during, and after voluntary hyperventilation. METHOD: Physiological responses were recorded in 14 patients with PD, 24 patients with SP, and 24 controls during six cycles of 1-minute of fast breathing alternating with 1 minute of recovery, followed by 3 minutes of fast breathing and 10 minutes of recovery. Speed of fast breathing was paced by a tone modulated at 18 cycles/minute, and depth by feedback aimed at achieving an end-tidal pCO2 of 20 mm Hg. These values were reached equally by all groups. RESULTS: During fast breathing, PD and SP patients reported more anxiety than controls, and their feelings of dyspnea and suffocation increased more from baseline. Skin conductance declined more slowly in PD over the six 1-minute fast breathing periods. At the end of the final 10-minute recovery, PD patients reported more awareness of breathing, dyspnea, and fear of being short of breath, and their pCO2s, heart rates, and skin conductance levels had returned less toward normal levels than in other groups. Their lower pCO2s were associated with a higher frequency of sigh breaths. CONCLUSIONS: PD and SP patients report more distress than controls to equal amounts of hypocapnia, but PD differ from SP patients and controls in having slower symptomatic and physiological recovery. This finding was not specifically predicted by hyperventilation, cognitive-behavioral, or suffocation alarm theories of PD.

Adult↗
PubMed2000

The use of hyperventilation in the treatment of plateau waves in two patients with severe traumatic brain injury: contrasting effects on cerebral oxygenation.

We present the case reports of two patients with severe traumatic brain injury who, in the absence of external stimuli, developed episodes of acute elevation of intracranial pressure (plateau waves) associated with jugular bulb oxyhemoglobin (SjO2) desaturation, severe reduction of cerebral tissue PO2 (PbrO2), and deterioration of neurological status. In all of these episodes hyperventilation was successful in extinguishing plateau waves, but in one patient it was associated with an improvement of both the global (increased SjO2) and local (increased PbrO2) cerebral perfusion, while in the other patient it was associated with a reduction of both SjO2 and PbrO2. In both patients the effects of hyperventilation (and other pharmacological treatments) were short-lived; plateau waves reappeared and the patients had to be submitted to decompressive craniotomy (first patient) and cerebrospinal fluid (CSF) drainage (second patient). We conclude that hyperventilation can be useful as a temporary measure to treat plateau waves, but cerebral oxygenation should always be monitored to avoid iatrogenic cerebral ischemia.

Accidents, Traffic↗
PubMedDate not supplied

Acquired lightheadedness in response to odors after hyperventilation.

OBJECTIVE: This study aimed to investigate whether lightheadedness in response to odors could be acquired through previous associations with hyperventilation-induced hypocapnia. METHODS: Diluted ammonia and acetic acid served as conditional odor cues (CSs) in a differential associative learning paradigm. Hyperventilation-induced hypocapnia (unconditional stimulus [US]) was used to induce lightheadedness. In a training phase, participants (n = 28) performed three hypocapnic and three normocapnic overbreathing trials of 60 seconds each. One odor was consistently paired with the hypocapnic overbreathing (CS+); the other (control) odor was paired with normocapnic overbreathing (CS-). In the test phase, each odor was presented once during spontaneous breathing and once during normocapnic overventilation. Lightheadedness was assessed online during each breathing trial, which was followed by an extensive hyperventilation symptom checklist. Fractional end-tidal CO2, breathing frequency, and inspiratory volume were measured throughout the experiment. RESULTS: In the test phase, participants experienced lightheadedness more quickly in response to the odor that had been paired with hypocapnic overbreathing compared with the control odor. They also scored higher on the symptom "feeling unreal." CONCLUSION: Lightheadedness in response to odors can be acquired easily. The present results may help to elucidate the paradox that both avoidance and exposure to chemicals seem to be effective in reducing symptoms in idiopathic environmental illness.

Adult↗
PubMed1985

Vasospastic ischaemia induced by the hyperventilation test in patients with a negative response to ergometrine.

We present the case histories of two patients with angina pectoris who developed coronary artery spasm in response to provocation with prolonged hyperventilation (verified by ST segment elevation in both and coronary angiography in one) despite a negative ECG response to intravenous injection of 0.4 mg ergometrine. This new observation, which is in conflict with recent publications stating that ergot provocation is more sensitive than hyperventilation, suggests that in some patients diagnostic provocation with hyperventilation may be an alternative to the widely used ergot provocation.

Adult↗
PubMed1987

Vasospastic angina: control of disease activity and efficacy of drug treatment using the prolonged hyperventilation test.

Sixteen consecutive patients with vasospastic angina underwent a control provocation test in the coronary care unit or the cardiac catheterization laboratory in order to evaluate the disease activity and the efficacy of long-term calcium antagonist treatment. In patients without angina at rest, the prolonged hyperventilation test was negative in 10/10 patients on calcium antagonist treatment (group A + B) and in 4/5 patients without medication (group C). The test was positive in 1/1 patient with angina at rest without medication (group D). However, the test provoked vasospastic angina in 1/5 patients who were asymptomatic without medication. In both the latter patients the prolonged hyperventilation test became negative after the restart of calcium antagonist treatment. During a mean follow-up period of 18 months (range 16-19) after the control hyperventilation test, no relapse of angina at rest, arrhythmias, syncopes, deaths or myocardial infarctions were registered. Thus, a negative test is compatible with low disease activity and/or efficacy of calcium antagonist treatment. Further, the test may reveal a subclinical tendency to coronary artery spasm.

Adult↗
PubMed1987

Airway constriction by isocapnic hyperventilation of cold, dry air: comparison of magnitude and duration of protection by nedocromil sodium and sodium cromoglycate.

The protective effect of 1, 2 and 4 mg of nedocromil sodium against airway constriction induced by hyperventilation of cold, dry air was compared with 10 mg sodium cromoglycate and placebo in a double-blind randomized trial. On 5 days, twelve asthmatic subjects received one of the trial medications from a metered dose inhaler. Twenty minutes, 2.5 and 5 hr later, airway responsiveness to hyperventilation of cold, dry air was measured. At 20 min, there was significant protection by all four active medications when compared to placebo, with a trend towards a nedocromil dose relationship but there was no statistical difference between the four active medications. All four showed a similar progressive decrease in protection over 5 hr. The results of this study suggest that nedocromil gives protection against hyperventilation-stimulated airway constriction and that the magnitude and duration of effect for all three doses is similar to 10 mg of cromoglycate.

Air↗
PubMed1989

Inhaled lignocaine does not alter bronchial hyperresponsiveness to hyperventilation of dry cold air in asthmatic subjects.

It has been hypothesized that bronchoconstriction due to exercise and hyperventilation is caused by the stimulation of irritant receptors in the upper airways. However, controversial results have been reported on the effect of lignocaine, which can inhibit the stimulation of these receptors. The aim of this study was to investigate the effect of inhaled lignocaine on bronchial responsiveness to hyperventilation of cold dry air in asthmatic subjects. Eight adult asthmatic subjects in a clinical steady state came on four different days (two placebo and two active days in random order) with a maximum interval of 3 weeks. After assessment of forced expiratory flow rates, inhalation of either phosphate-buffered saline (placebo) or lignocaine solution (40 mg) was carried out in a single-blind fashion. The technician was not aware which medication was being inhaled, but the asthmatic subject knew which drug it was by the sensation in his or her throat. Forced expiratory flow rates were reassessed 15 min after the nebulization; then, the subjects were asked to inhale cold dry air (-20 degrees C) in progressively increasing levels of ventilation (7.5, 15, 30 and 60 l/min and maximum voluntary ventilation). PD20 was interpolated from the dose-response curve, relating the dose of cold air on a non-cumulative logarithmic scale on the abscissa and the percentage change in FEV1 on the ordinate. There were no significant changes in FEV1 and PD20 after inhalation of lignocaine as compared to the placebo. We conclude that inhaled lignocaine does not significantly alter bronchial hyperresponsiveness to hyperventilation of cold air in asthmatic subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Inhalation↗
PubMed2004

Hyperventilation in the vestibular clinic: use of the Nijmegen Questionnaire.

The objective of the present study was to determine the prevalence of hyperventilation syndrome in patients seen for vestibular assessment and to assess the clinical utility of the Nijmegen Questionnaire in this group. The Nijmegen Questionnaire and Dizziness Handicap Inventory (DHI) were administered prospectively to a consecutive series of 100 patients identified as candidates for vestibular assessment within the University Hospital Neuro-otology practice. Twenty-three per cent of patients seen for vestibular assessment were diagnosed with hyperventilation syndrome using the Nijmegen Questionnaire. Seventeen of these (74%) would have remained undetected had the Nijmegen questionnaire not been used. No relationship was found between vestibular assessment results and either Nijmegen or DHI scores. A significant correlation was found between DHI scores and Nijmegen Questionnaire scores (rho = 0.348, P = 0.0005). In conclusion, the Nijmegen Questionnaire is a quick, easy to administer and low-impact assessment tool for hyperventilation syndrome and is a useful adjunct to the otological consultation. Diagnosed patients can then be offered breathing control exercises as part of a vestibular rehabilitation programme.

Anxiety↗
PubMed1985

Hypoxic pulmonary vasoconstriction in man: effects of hyperventilation.

The pulmonary vasoconstriction response to hypoxia was studied in eight anaesthetized supine subjects. One lung was made hypoxic while the other was ventilated with 100% oxygen. This was achieved by separating the tidal gas-distribution to the lungs by means of a double-lumen tracheal catheter. The hypoxic pulmonary vasoconstriction (HPV) response was estimated from the blood flow diversion away from the hypoxic lung. Blood flow distribution between the lungs was calculated from the regional expired carbon dioxide production, assuming regional carbon dioxide production to be proportional to blood flow. The subjects were studied during six different conditions. Firstly, when ventilated with 100% oxygen to both lungs at a PaCO2 of about 6 kPa. Secondly, with 100% oxygen to the left lung and 5% oxygen in nitrogen to the right (test) lung. The ratio between carbon dioxide output from right and left lung was calculated. These measurements were repeated during two states of hyperventilation (PaCO2 of about 4.5 kPa and 3.5 kPa, respectively) with and without hypoxia (conditions 3-6). During normoventilation, blood flow distribution between the lungs was equal. During hypoxia, blood flow distribution to the hypoxic lung decreased by 35% of the pre-hypoxic value. Furthermore, a decrease in arterial oxygen tension from 51.5 +/- 4.5 to 11.5 +/- 2.1 kPa was observed. During excessive hyperventilation (PaCO2 3.2 +/- 0.2 kPa), blood flow distribution to the hypoxic right lung decreased by only 10% of its pre-hypoxic value. A further decrease in arterial oxygen tension to 8.5 +/- 1.8 kPa was observed. This decrease in PaO2 was possibly due to an increased venous admixture caused by an abolished HPV response. It is concluded that hyperventilation counteracts hypoxic pulmonary vasoconstriction in man.

Adult↗
PubMed1990

Cardiovascular responses to verapamil and nifedipine in hypoventilated and hyperventilated rats.

1. The influence of hypoventilation or hyperventilation on blood pressure and pulse rate responses to verapamil and nifedipine was studied in chloralose-anaesthetized rats. 2. Artificial ventilation with room air at a fixed volume of 10 ml kg-1 successfully induced combinations of hypoxaemia, hypercarbia and acidosis at a ventilator rate of 37 strokes min-1 and of hyperoxaemia, hypocarbia and alkalosis at 160 strokes min-1. 3. Hypoventilation caused significant decreases in both the blood pressure and pulse rate, whereas hyperventilation produced significant increases in these parameters. 4. In the controls, intravenous injections of graded doses of either verapamil or nifedipine caused dose-dependent decreases in mean blood pressure. The effects on pulse rate were not marked. 5. The hypotensive effects of verapamil were significantly more intense in hyperventilated rats, whereas those of nifedipine were significantly less pronounced in hypoventilated animals. The hypoventilated rats exhibited a significant dose-dependent decrease in pulse rate in response to verapamil administration. 6. It is concluded that cardiovascular responses to verapamil, nifedipine and probably other calcium antagonists are altered in the presence of blood gas abnormalities.

Animals↗
PubMed1996

Will a critical level of hyperventilation-induced hypocapnia always induce an absence seizure?

We wished to determine if the degree of hypocapnia correlates with increased frequency of absence seizures and if there is a critical pCO2 at which absence seizures are reliably provoked. Twelve untreated children with newly diagnosed absence epilepsy were continuously monitored by EEG and end-expiratory CO2 recording during quiet respiration and hyperventilation (to absence seizure or exhaustion) while breathing four gas mixtures: (a) room air, (b) 100% O2, (c) 4% CO2 in room air, or (d) 4% CO2 + 96% O2). In quiet respiration, a reduction in number of spike and wave bursts and total seconds of spike and wave was noted in children breathing supplemental CO2 (gases c and d vs. gases a and b), p < 0.05. Supplemental O2 had no effect. Eight subjects had absence seizures elicited with each trial of hyperventilation. All subjects had their own critical pCO2, ranging from 19 to 28 mmHg. Three children had no seizures, two despite hypocapnia to pCO2 of 19 and 21 and 1 who achieved a pCO2 of only 25. In 1, absence seizures were provoked in only six of nine hyperventilation trials to pCO2 of 17-23. In 67% of subjects, absence seizures were reliably provoked by hypocapnia. Critical pCO2 varied among children with absence. Determination of whether variation in sensitivity to hypocapnia may be helpful in determining response to antiepileptic drugs (AEDs) or remission of seizures will require further study.

Air↗
PubMedDate not supplied

Effects of acute hyperventilation on serum potassium in the dog.

The effects of increasing respiratory rates on arterial pH, PaCO2, HCO3, and potassium (K) were measured in normal anesthetized dogs. Hyperventilation resulted in increased pH, decreased PaCO2, decreased HCO3, and decreased K compared with those parameters in spontaneously breathing dogs. The changes were related quantitatively: each 10 mmHg decrease in PaCO2 was associated with a pH increase of 0.1, a HCO3 decrease of 2.0 mEq/L, and a K decrease of 0.4 mEq/L. There were no cardiac arrhythmias or clinical signs of hypokalemia. After termination of hyperventilation, serum K was slower to return to control values than PaCO2. The ratio of the duration of hyperventilation to the time required for return of serum K to control was 0.67.

Acid-Base Imbalance↗
PubMed1990

Hyperventilation syndrome: clinical, ventilatory, and personality characteristics as observed in neurological practice.

The symptoms of the hyperventilation syndrome (HVS) are sometimes diffuse, and HVS may resemble other clinical conditions. A diagnosis of HVS was made in 25 patients referred for neurological assessment because of atypical, shortlasting, episodic complaints. The referral diagnoses varied within a wide range. A need for more indepth knowledge about this group of patients thus arose. During a provocation test with forced respiration, all patients reported symptoms similar to those during attacks. Eight patients described numbness or paraesthesias with unilateral predominance. End-tidal pCO2 levels were monitored prior to and during a forced hyperventilation test. Compared with controls, the patients had significantly decreased end-tidal pCO2 even during symptom free periods. After hyperventilation, hypocapnia followed a protracted course in the patient group. Sensory symptoms may be asymmetric and mimic focal cerebral disease. Strained respiration may be denied during spontaneous attacks. Personality characteristics were evaluated with the Minnesota Multiphasic Personality Inventory (MMPI). A mean group profile very similar to profiles reported on "pseudoepileptic" patients was found. The profile indicates a neurotic pattern where patients tend to respond to psychological stress with somatic symptoms.

Adolescent↗