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PubMed2000

Caffeine can affect velocity in the middle cerebral artery during hyperventilation, hypoventilation, and thinking: a transcranial Doppler study.

This study examined possible caffeine-mediated changes in blood flow velocity in the middle cerebral artery (VMCA) induced by tests of cerebrovascular responsiveness. Transcranial Doppler (TCD) sonography provided simultaneous bilateral VMCA measures while healthy college students hypoventilated, hyperventilated, and performed cognitive activities (short-term remembering, generating an autobiographical image, solving problems), each in 31-second tests. VMCA measures were obtained from the same persons, in separate testing sessions, when they were noncaffeinated and under two levels of caffeine: a smaller amount (from a cola, 45 mg/12 oz) and a larger amount (from coffee, 117 mg/8 oz). Compared with the no-caffeine control condition, a smaller amount of caffeine had no significant effects on global VMCA, but a larger amount suppressed VMCA by 5.8%. Time-course analyses showed that VMCA (1) followed a triphasic pattern to increase over baselines during hypoventilation regardless of caffeine condition, (2) slowed below baselines during hyperventilation (with the degree of slowing attenuated under caffeine), and (3) increased over baselines during all cognitive activities (ranges 3.8-6.9%). It is concluded that a large amount of caffeine can suppress VMCA, and this possibility should be anticipated when TCD is used to assess cerebral hemovelocity.

Adult↗
PubMed1986

Ventilation and cardiac output during the onset of exercise, and during voluntary hyperventilation, in humans.

Three normal subjects performed rest--exercise transitions on a cycle ergometer, from rest to unloaded pedalling (0 W), 50, 100 and 150 W. Each experiment was performed in triplicate, with randomized work load order, in two sessions. Ventilation was obtained breath-to-breath by integration of a pneumotachygraph signal, and cardiac output beat-to-beat by a new development of the Doppler technique. Results were bin-averaged in 4 s bins over the first 20 s, and compared to resting values. Both ventilation and cardiac output increased significantly in the first 2 s. This initial rise in ventilation was due entirely to an increase in rate, the subsequent rise mainly to increase in tidal volume. Cardiac output increased predominantly through change in rate with smaller increases in stroke volume. A striking feature was a tendency for ventilation and cardiac output responses to be biphasic with an initial rise followed by a slight fall at the 14 s mark, and a subsequent rise, at all work loads. Overall correlation between ventilation and cardiac output was therefore high (r = 0.92). Six normal subjects hyperventilated for 45 s voluntarily, (a) at rate 24/min and normal tidal volume; (b) at normal rate and tidal volume of 1.5 l; (c) at rate 24/min and tidal volume of 1.5 l. Cardiac output, averaged over 10-45 s, rose by 0.4, 0.5, and 1.0 l min-1 respectively, with falls in end-tidal PCO2 of 4, 6, and 8 mmHg. Six normal subjects hyperventilated for 60 s with rate 24/min and tidal volume of 1.4 l, and end-tidal PCO2 maintained at 38 +/-2 mm Hg. Cardiac output, averaged from 10-60 s, rose by 1.0 l min-1. With increased rate and tidal volume, whether isocapnic or hypocapnic, cardiac output responses showed an overshoot with a peak value at about 30 s. The hypothesis of 'cardiodynamic hyperpnoea' considers a possible effect of increasing cardiac output on ventilation. The effects of ventilation on cardiac output must also be considered. We propose an extended hypothesis involving stable positive feed-back.

Adult↗
PubMed1980

Effect of hypercapnea and hyperventilation on human intraocular pressure general anaesthesia following acetazolamide administration.

The changes in intraocular pressure due to blood pH, PCO2, and PO2 alterations induced by hyperventilation and hypercapnea in man undergoing routine general anaesthesia were studied. It was shown that hypercapnea produces elevation of intraocular pressure, while hyperventilation lowers it. Acetazolamide pretreatment did not alter these IOP responses to PCO2, PO2, and blood pH changes.

Acetazolamide↗
PubMed1985

Respiratory and psychiatric abnormalities in chronic symptomatic hyperventilation.

Many physicians believe that the hyperventilation syndrome is invariably associated with anxiety or undiagnosed organic disease such as asthma and pulmonary embolus, or both. Twenty one patients referred by specialist physicians with unexplained somatic symptoms and unequivocal chronic hypocapnia (resting end tidal Pco2 less than or equal to 4 kPa (30 mm Hg) on repeated occasions during prolonged measurement) were investigated. All but one complained of inability to take a satisfying breath. Standard lung function test results and chest radiographs were normal in all patients, but histamine challenge showed bronchial hyper-reactivity in two of 20 patients tested, and skin tests to common allergens were positive in three of 18. Ventilation-perfusion scanning was abnormal in a further three of 15 patients studied, with unmatched perfusion defects in two and isolated ventilation defects in one. None of the 21 had thyrotoxicosis, severe coronary heart disease, or other relevant cardiovascular abnormalities. Ten of the 21 patients were neurotic and suffered from chronic psychiatric disturbance characterised by anxiety, panic, and phobic symptoms. The remainder had no detectable psychiatric disorders but reported proportionately more somatic than anxiety symptoms. Severe hyperventilation can occur in the absence of formal psychiatric or detectable respiratory or other organic abnormalities. Asthma and pulmonary embolus must be specifically excluded.

Adult↗
PubMed2002

Widespread cardiovascular autonomic dysfunction in primary amyloidosis: does spontaneous hyperventilation have a compensatory role against postural hypotension?

OBJECTIVE: To investigate the possible causes of abnormal blood pressure control in light chain related (primary, AL) amyloidosis. DESIGN: Cardiovascular, autonomic, and respiratory response to passive tilting were investigated in 51 patients with primary amyloidosis (mean (SEM) age 56 (2) years) and in 20 age matched controls. Spontaneous fluctuations in RR interval, respiration, end tidal carbon dioxide, blood pressure, and skin microcirculation were recorded during supine rest and with tilting. The values were subjected to spectral analysis to assess baroreflex sensitivity and the autonomic modulation of cardiac and vascular responses. SETTING: Tertiary referral centre. RESULTS: Autonomic modulation of the heart and blood pressure was nearly absent in the patients with amyloidosis: thus baroreflex sensitivity and the low frequency (0.1 Hz) fluctuations in all cardiovascular signals were severely reduced (p < 0.01 or more), as were respiratory fluctuations in the RR interval, and no change was observed upon tilting. Despite reduced autonomic modulation, blood pressure remained relatively stable in the amyloid group from supine to tilting. End tidal carbon dioxide was reduced in the amyloid patients (p < 0.001) indicating persistent hyperventilation; the breathing rate correlated inversely with the fall in blood pressure on tilting (p < 0.05). CONCLUSIONS: In primary amyloidosis, pronounced abnormalities in arterial baroreflexes and cardiovascular autonomic modulation to the heart and the vessels may be partly compensated for by hyperventilation at a slow breathing rate.

Amyloidosis↗
PubMed1989

Value of hyperventilation in pattern-reversal visual evoked potentials.

The effects of a standard 3 minutes' hyperventilation on the full-field pattern-reversal visual evoked potential (VEP) were studied in 33 normal subjects, 30 definite multiple sclerosis patients and in twenty-five patients with abnormal VEPs due to either tumourous compression of the anterior visual pathways or optic atrophy of other origin. Significantly greater reductions in P100 latency occurred in multiple sclerosis patients in comparison with controls (p less than 0.05). This change appeared to be specific for demyelinative type of lesion, for it was not found in cases with other types of pathology. Hyperventilation also increased the sensitivity of visual pathway impairment detection in multiple sclerosis.

Adult↗
PubMed1991

Syncope or seizure? The diagnostic value of the EEG and hyperventilation test in transient loss of consciousness.

In a prospective study of consecutive patients (age 15 or over) with transient loss of consciousness 45 patients had a history of seizure and 74 patients had a history of syncope. All patients had an EEG, ECG, laboratory tests and a hyperventilation test and were followed for an average of 14.5 months. Epileptiform activity in the interictal EEG had a sensitivity of 0.40 and a specificity of 0.95 for the diagnosis of a seizure. Epileptiform activity nearly doubled the probability of a seizure in doubtful cases. If no epileptiform activity was found, this probability remained substantially the same. The hyperventilation test had a sensitivity of 0.57 and a specificity of 0.84 for the diagnosis of syncope. A positive test increased the probability of syncope half as much in doubtful cases. A negative test did not exclude syncope. Laboratory tests were not helpful except for an ECG which was helpful in elderly patients.

Adolescent↗
PubMed1987

Hyperventilation and Raynaud's disease.

A 42 year old woman with long standing Raynaud's disease, unresponsive to medical and surgical treatment, was noted to have a typical history of the hyperventilation syndrome. Rewarming of the hands following cold challenge was markedly prolonged in the presence of hypocapnia. It is suggested that hyperventilation may have an aetiological role in maintaining digital artery spasm in Raynaud's disease, which would benefit from recognition and treatment.

Adult↗
PubMed2000

Orthostatic increase of respiratory gas exchange in hyperventilation syndrome.

BACKGROUND: Hyperventilation syndrome (HVS) is a common disorder which is difficult to diagnose because of somatic symptoms and its episodic nature. In previous studies respiratory alkalosis in arterial blood was often found during orthostatic tests in patients with HVS. The purpose of this study was to assess these orthostatic changes by non-invasive pulmonary gas exchange measurements and to evaluate whether these responses discriminate patients with HVS from healthy subjects. METHODS: Respiratory gases were collected with a face mask and pulmonary gas exchange was measured after 10 minutes at rest and after eight minutes standing upright in 16 patients with HVS and 13 healthy control subjects. In patients with HVS arterial blood samples were also drawn at rest and in the standing position. RESULTS: At rest the variables of respiratory gas exchange did not differ significantly between the groups. As a response to standing, minute ventilation increased in both study groups but significantly more in the patients with HVS (mean difference 5.4 l/min (95% CI 1.1 to 9.6)). The changes in end tidal CO(2) fraction (FETCO(2)) and in ventilatory equivalents for oxygen (VE/VO(2)) and for CO(2) (VE/VCO(2)) during the orthostatic test were also significantly larger in patients with HVS than in healthy controls. During standing FETCO(2) was significantly lower (mean difference -1.1 kPa; 95% CI -1.5 to -0.6) and VE/VO(2) (mean difference 18.4; 95% CI 7.7 to 29.0) and VE/VCO(2) (mean difference 11.7; 95% CI 4.8 to 18.6) were significantly higher in HVS patients than in healthy controls. By using the cut off level of 4% for FETCO(2) the sensitivity and specificity of the test to discriminate HVS were 87% and 77%, respectively, and by using the cut off level of 37 for VE/VO(2) they were 93% and 100%, respectively. In the HVS patients arterial PCO(2) and FETCO(2) were closely correlated during the orthostatic test (r = 0.93, p<0.0001). CONCLUSIONS: As a response to change in body position from supine to standing, patients with HVS have an accentuated increase in ventilation which distinguishes them from healthy subjects. These findings suggest that non-invasive measurements of pulmonary gas exchange during orthostatic tests are useful in the clinical evaluation of patients with hyperventilation disorders.

Adult↗
PubMed1981

Circulating catecholamines in exercise and hyperventilation induced asthma.

Plasma noradrenaline, adrenaline, and cyclic 3'5' AMP (cAMP) were measured in seven asthmatic patients with known exercise-induced bronchospasm and six matched non-atopic control subjects during a standard treadmill exercise test and then during matched isocapnic hyperventilation. Normal subjects showed a 5.5 fold rise in noradrenaline and a 3.2 fold rise in adrenaline during exercise compared with a 2.1 fold rise in noradrenaline and no significant rise in adrenaline in asthmatics who all developed bronchoconstriction after exercise (mean fall in peak flow rate 28.4 +/- 5.8%). Plasma cAMP rose 1.4 fold in controls but showed no significant rise in asthmatics. This reduced sympatho-adrenal response to exercise in asthmatics is difficult to explain. The failure of circulating catecholamines to rise and stimulate beta adrenoceptors on the mast cell may facilitate the release of bronchoconstrictor mediators. Matched hyperventilation produced bronchospasm in asthmatics (mean fall in peak flow rate 29.0 +/- 4.4%) but no change in catecholamines in either group suggesting that circulating catecholamines have no direct role in exercise-induced bronchospasm but may play a permissive role via the mast cell.

Adolescent↗
PubMed1975

Effect of hyperventilation on dynamics of cerebral energy metabolism.

Hypocapnia of moderate and extreme degree (Paco2 21.1 and 13.5 torr, respectively)was induced by hyperventilation in rats subjected to the closed system of Lowry inorder to evaluate the effects on utilization rate of cerebral energy metabolites. The tissue levels of high-energy phosphates and calculated intracellular pH did not change, whereas glucose, pyruvate, and lactate increased significantly. The La/Pyratio and NADH/NAD-+ RATIO BOTH INCREASED IN PROPORTION TO THE DEGREE OF HYPOCAPNIA. Utilization rates of glucose, glycogen, and ATP were all significantly reduced by hypocapnia, whereas the utilization rate of phosphocreatine was increased. The rate oftotal high-energy phosphate use was also diminished in proportion to the degree of hypocapnia. The constant value of the energy charge (0.94 plus or minus 0.01) indicates that the energy production rate might also be reduced by hyperventilation; thus the intermediate metabolics and substrates increased. It is concluded that extreme hypocapnia reduces the rate of cerebral energy metabolism significantly.

Adenosine Triphosphate↗
PubMed2003

SP-A is necessary for increased clearance of alveolar DPPC with hyperventilation or secretagogues.

The role of surfactant protein-A (SP-A) in pulmonary uptake and metabolism of [(3)H]dipalmitoylphosphatidylcholine ([(3)H]DPPC) was studied in SP-A gene-targeted mice (SP-A -/-). Unilamellar liposomes were instilled into the trachea of anesthetized mice. Uptake was measured as dpm in lungs plus liver and kidney for in vivo experiments and in lungs and perfusate for isolated lung experiments. [(3)H]DPPC uptake increased with CO(2)-induced hyperventilation in wild-type mice (SP-A +/+) but was unchanged in SP-A -/-. Secretagogue treatment approximately doubled the uptake of [(3)H]DPPC in isolated lungs from SP-A +/+ but had no effect in SP-A -/-. Lungs degraded 23 +/- 1.2% of internalized [(3)H]DPPC in SP-A +/+ and 36 +/- 0.6% in SP-A -/-; degradation increased with 8-bromoadenosine 3',5'-cyclic monophosphate in SP-A +/+ but was unchanged in SP-A -/-. Activity of lysosomal-type phospholipase A(2) (PLA(2)) was significantly greater in lungs from SP-A -/- compared with SP-A +/+. Thus SP-A is necessary for lungs to respond to hyperventilation or secretagogues with increased DPPC uptake and also modulates the PLA(2)-mediated degradation of internalized DPPC.

1,2-Dipalmitoylphosphatidylcholine↗
PubMed1991

Posterior cricoarytenoid activity in normal adults during involuntary and voluntary hyperventilation.

The effect of isocapnic hypoxia and hyperoxic hypercapnia on the electrical activity of the posterior cricoarytenoid (PCA) muscle was determined in eight normal adult humans by use of standard rebreathing techniques and was compared with PCA activity during voluntary hyperventilation performed under isocapnic and hypocapnic conditions. PCA activity was recorded with intramuscular hooked-wire electrodes implanted through a fiberoptic nasopharyngoscope. During quiet breathing in all subjects, the PCA was phasically active on inspiration and tonically active throughout the respiratory cycle. At comparable increments in respiratory output, hypercapnia, hypoxia, and voluntary hyperventilation appeared to be associated with similar increases in phasic or tonic PCA activity. During quiet breathing, the onset of phasic PCA activity usually occurred before inspiratory airflow and extended beyond the start of expiratory airflow. The duration of phasic PCA preactivation and postinspiratory phasic PCA activity remained unchanged during progressive hypercapnia and progressive hypoxia. The results, in combination with recent findings for vocal cord adductors, suggest that vocal cord position throughout the respiratory cycle during hyperpnea is actively controlled by simultaneously acting and antagonistic intrinsic laryngeal muscles.

Adult↗
PubMed1991

Effect of hyperventilation on oxygenation of the brain cortex of newborn piglets.

A new phosphorescence imaging method (Rumsey et al. Science Wash. DC 241: 1649-1651, 1988) has been used to continuously monitor the PO2 in the blood of the cerebral cortex of newborn pigs. A window was prepared in the skull and the brain superfused with artificial cerebrospinal fluid. The phosphorescent probe for PO2, Pd-meso-tetra(4-carboxyphenyl)porphine, was injected directly into the systemic blood. The phosphorescence of the probe was imaged, and the lifetimes were measured using flash illumination and a gated video camera. The PO2 in the blood of the veins and capillary beds of the cortex was calculated from the lifetimes. Systemic blood pressure was continuously monitored while the systemic arterial PCO2, PO2, and blood pH were measured periodically. The PO2 in the blood was quantitated for 60- to 200 microns2 regions within the image (from a total field of approximately 3 mm diam). The PO2 in the microvasculature was not uniform across the viewing field but increased or decreased in each region independently of the other regions. Thus at any point in time the PO2 in a region could be substantially above or below the average value. During hyperventilation, which lowered arterial PCO2 and increased pH of the blood, the average PO2 decreased in proportion to the decrease in arterial PCO2. For example, hyperventilation, which decreased arterial PCO2 from its normal value of 40 Torr to 10 Torr, caused a rapid (within 5 min) decrease in PO2 in the blood of capillaries and veins to approximately one-third of normal.

Animals↗
PubMed1995

Low chemoresponsiveness and inadequate hyperventilation contribute to exercise-induced hypoxemia.

Is inadequate hyperventilation a cause of the exercise-induced hypoxemia observed in some athletes during intense exercise? If so, is this related to low chemoresponsiveness? To test the hypothesis that exercise-induced hypoxemia, inadequate hyperventilation, and chemoresponsiveness are related, 36 nonsmoking healthy men were divided into hypoxemic (Hyp; n = 13) or normoxemic (Nor; n = 15) groups based on arterial oxygen saturation (SaO2; Hyp < or = 90%, Nor > 92%) observed during maximum O2 uptake (VO2max). Men with intermediate SaO2 values (n = 8) were only included in correlation analysis. Ventilatory parameters were collected at rest, during a treadmill maximal oxygen consumption (VO2max) test, and during a 5-min run at 90% VO2max. Chemoresponsiveness at rest was assessed via hypoxic ventilatory response (HVR) and hypercapnic ventilatory response (HCVR). VO2max was not significantly different between Nor and Hyp. SaO2 was 93.8 +/- 0.9% (Nor) and 87.7 +/- 2.0% (Hyp) at VO2max. End-tidal PO2 and the ratio of minute ventilation to oxygen consumption (VE/VO2) were lower while PETCO2 was higher for Hyp (P < or = 0.01). End-tidal PO2, end-tidal PCO2, and VE/VO2 correlated (P < or = 0.05) to SaO2 (r = 0.84, r = -0.70, r = 0.72, respectively), suggesting that differences in oxygenation were due to differences in ventilation. HVR and HCVR were significantly lower for Hyp. HVR was related to VE/VO2 (r = 0.43), and HCVR was related to the ratio of VE to CO2 production at VO2max (r = 0.61).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1997

Hyperventilation-induced airway injury and vascular leakage in dogs: effects of alpha1-adrenergic agonists.

alpha1-Adrenergic agonists inhibit hyperventilation-induced bronchoconstriction (HIB) in dogs. We tested the hypothesis that alpha-agonists inhibit HIB by reducing bronchovascular leakage and edema that theoretically could cause airway obstruction. Peripheral airways were isolated by using a bronchoscope; pretreated with either methoxamine (Mx), norepinephrine (NE), or saline aerosol; and then exposed to a 2,000 ml/min dry-air challenge (DAC) for 2 min. Colloidal carbon was injected before DAC and used to quantify bronchovascular permeability. Mx-, NE-, and vehicle-treated airways were prepared for morphometric analysis within 1 h after DAC. Light microscopy revealed that the 2-min DAC produced minimal bronchovascular leakage and little epithelial damage. However, pretreatment with either Mx or NE significantly enhanced dry air-induced bronchovascular hyperpermeability and mucosal injury. The increased damage associated with these alpha1-agonists implicates a protective role for the bronchial circulation. The fact that alpha1-agonists inhibit HIB suggests that neither dry air-induced leakage nor injury directly contributes to the development of airway obstruction. In addition, our data suggest that alpha-agonists attenuate HIB in part by augmenting hyperventilation-induced bronchovascular leakage and by replacing airway water lost during a DAC.

Administration, Inhalation↗
PubMed1998

Thermal drive contributes to hyperventilation during exercise in sheep.

The etiology of exercise hypocapnia is unknown. The contributions of exercise intensity (ExInt), lactic acid, environmental temperature, rectal temperature (Tre), and physical conditioning to the variance in arterial CO2 tension (PaCO2) in the exercising sheep were quantified. We hypothesized that thermal drive contributes to hyperventilation. Four unshorn sheep were exercised at approximately 30, 50, and 70% of maximal O2 consumption for 30 min, or until exhaustion, both before and after 5 wk of physical conditioning. In addition, two of the sheep were shorn and exercised at each intensity in a cold (<15 degrees C) environment. Tre and O2 consumption were measured continuously. Lactic acid and PaCO2 were measured at 5- to 10-min intervals. Data were analyzed by multiple regression on PaCO2. During exercise, Tre rose and PaCO2 fell, except at the lowest ExInt in the cold environment. Tre explained 77% of the variance in PaCO2, and ExInt explained 5%. All other variables were insignificant. We conclude that, in sheep, thermal drive contributes to hyperventilation during exercise.

Animals↗
PubMed1998

Effect of nitric oxide synthase inhibition on hypercapnia-induced hypothermia and hyperventilation.

Hypercapnia elicits hypothermia in a number of vertebrates, but the mechanisms involved are not well understood. In the present study, we assessed the participation of the nitric oxide (NO) pathway in hypercapnia-induced hypothermia and hyperventilation by means of NO synthase inhibition by using Nomega-nitro-L-arginine (L-NNA). Measurements of ventilation, body temperature, and oxygen consumption were performed in awake unrestrained rats before and after L-NNA injection (intraperitoneally) and L-NNA injection followed by hypercapnia (5% CO2). Control animals received saline injections. L-NNA altered the breathing pattern during the control situation but not during hypercapnia. A significant (P < 0.05) drop in body temperature was measured after both L-NNA (40 mg/kg) and 5% inspired CO2, with a drop in oxygen consumption in the first situation but not in the second. Hypercapnia had no effect on L-NNA-induced hypothermia. The ventilatory response to hypercapnia was not changed by L-NNA, even though L-NNA caused a drop in body temperature. The present data indicate that the two responses elicited by hypercapnia, i.e., hyperventilation and hypothermia, do not share NO as a common mediator. However, the L-arginine-NO pathway participates, although in an unrelated way, in respiratory function and thermoregulation.

Animals↗