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We have shown in this study of 20 patients that the frequency of Rolandic spikes was significantly lower during hyperventilation and the 2 minutes following hyperventilation than during normal wakefulness.
The aim of the study was to discover the relative effectiveness of four methods of treating patients suffering from hyperventilation attacks. The methods used were: breathing and relaxation therapy, hyperventilation provocation training, treatment based on influencing the factors which lead to the development of the syndrome, and drug treatment. The first three methods were demonstrated to be effective, whilst the fourth showed no signs of effectiveness. The condition of patients in the control group remained the same or deteriorated.
Prostacyclin is released during hyperventilation (HV); however, its role as mediator of HV-induced pulmonary vasodilation remains controversial. We have investigated this by studying the effects of HV on pulmonary artery pressure (PAP) in otherwise normal lungs versus lungs vasoconstricted with group B streptococci (GBS), with and without prior prostacyclin synthesis inhibition. Two- to 3-wk-old piglets were given tranylcypromine, a prostacyclin synthetase inhibitor (n = 6), or placebo (n = 6). Animals were mechanically ventilated normally, then hyperventilated (PCO2 1.5 +/- 0.2 kPa) and then returned to normal ventilation. After each 30-min segment, plasma 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) (prostacyclin hydrolysis product) levels and PAP were measured. Then GBS infusions were administered to both groups to induce pulmonary hypertension. With GBS, the normal ventilation/hyperventilation/normal ventilation protocol was repeated as above.(ABSTRACT TRUNCATED AT 250 WORDS)
In the perinatal period, glucocorticoids are frequently administered to enhance pulmonary maturity or prevent chronic lung disease of prematurity. Recently, it has been suggested that the perinatal exposure to glucocorticoids can be associated with unfavorable neurologic development. We studied the hypothesis that 24-h pretreatment with glucocorticoid might modify cerebrovascular responses to high and low partial arterial CO(2) tension in newborn animals in vivo. A closed cranial window was implanted over the left parietal cortex of 20 anesthetized ventilated newborn (<3 d old) pigs. The actual experiments were carried out in 15 pigs: eight pretreated with a total dose of 6 mg/kg of dexamethasone and seven controls. Five pigs were used for preliminary experiments as described in the text. Pial arteriolar diameters were measured during 1) baseline conditions (normocapnia), 2) hypercapnia induced by ventilating the animals with a gas mixture containing 10% CO(2), or 3) hyperventilation with resultant hypocapnia. Under these conditions, the concentrations of 6-keto-PGF(1alpha) in the CSF were measured in five experimental animals and six controls. In summary, the dexamethasone pretreatment 1) attenuated the hypercapnia-induced dilator responses of pial arterioles and prevented the hypercapnia-associated fall in mean arterial blood pressure; 2) caused moderate, although not statistically significant, diminution in 6-keto-PGF(1alpha) levels in the CSF during baseline; 3) blocked hypercapnia-induced elevation of 6-keto-PGF(1alpha); and 4) enhanced vasoconstrictive arteriolar responses to hyperventilation. We speculate that in the clinical setting, the dexamethasone effects may compromise the adjustments of global or regional cerebral blood flow to changing physiologic states in neonates.
The short chain fatty acid sodium octanoate was infused into rabbits as an 0.2 M solution over 4 hours, resulting in blood and brain levels of 200 to 700 mumoles per liter. During the infusion, animals exhibited marked hyperventilation, resulting in a mild respiratory alkalosis. Octanoate infusion also resulted in significant hyperammonemia and lactic acidemia. Saline-treated control animals demonstrated no clinical or chemical abnormalities. Several short chain fatty acids, including octanoate, are increased in the plasma of patients with hepatic encephalopathies and Reye syndrome. The present study suggests that short chain fatty acids may be endogenous toxins in these clinical disorders. In particular, the central hyperventilation in these conditions may be due to the neurotoxic effect of short chain fatty acids.
A 57-year-old awake man developed central neurogenic hyperventilation associated with a pontine mass. Serum pH reached as high as 7.72 with serum carbon dioxide of 6 torr. Examination of CSF during overbreathing showed that CSF pH was markedly alkaline. Pathologic study showed a well-differentiated pontine astrocytoma. The combination of alkaline CSF and an infiltrating pontine lesion supports a structural, rather than chemical, mechanism for central hyperventilation.
We report the case of a head-injured patient with spontaneous hyperventilation who had recurrent episodes of relative hypoventilation associated with increases in intracranial pressure. Detailed ventilatory studies were performed during the 2nd week after injury. Our findings in this patient prompted us to review the possible mechanisms underlying the observed changes. We suggest that spontaneous hyperventilation in head injury is secondary to a decrease in cortical inhibitory influences on respiratory control mechanisms and that the transient episodes of relative hypoventilation observed in our patient may reflect modified ventilatory responses dependent on the altered state of consciousness. (Neurosurgery, 5: 701--707, 1979).
Methacholine inhalation challenge (MIC) is probably the most widely used and best standardized test for nonspecific bronchoprovocation challenge (BPC). There has been increasing interest in developing "physical" stimuli such as eucapnic voluntary hyperventilation (EVH) with dry gas to assess airway hyperreactivity (AHR), because of inherent problems with using a pharmacologic agent in epidemiologic surveys. To our knowledge, no studies exist that compare MIC with EVH in known asthmatics. We conducted a prospective, randomized, crossover trial with a group of subjects (n = 16) who met the American Thoracic Society definition of asthma with these objectives: (1) to compare the sensitivity of EVH with MIC; (2) to compare the quantitative response of one test with the response to the other challenge; and (3) to correlate the response of both tests with symptoms, serum IgE levels, and serum eosinophil counts. We found that (1) EVH was positive in 75 percent of cases and MIC was positive in 81 percent of cases; one subject reacted to EVH but not to MIC and vice-versa. (2) The quantitative response to one test correlated with the response to the other test (r = -0.60, p = 0.01). (3) There was a correlation between severity of asthma symptoms and the response to EVH (r = 0.62; p = 0.01), but not to MIC. (4) Response to MIC (log PD20), but not EVH, correlated with serum IgE level (r = -0.53, p = 0.04). We suggest that EVH may be used for the initial assessment of AHR in the evaluation of asthma. Eucapnic voluntary hyperventilation is a sensitive measure of AHR and it correlates well with symptoms. Furthermore, though these points were not addressed in our study, it is more physiologic than MIC, and it is easy and less expensive to perform.
Eucapnic voluntary hyperventilation (EVH) of dry gas is a physiologic bronchoprovocation challenge useful in the diagnosis of asthma. To determine the best parameter and threshold for diagnosis and the proper timing of postchallenge measurements, we reviewed 120 challenges, comparing the decrement from baseline in FVC, FEV1, mean forced expiratory flow during the middle half of the FVC (FEF25-75%), and peak expiratory flow rate (PEFR) each at 0, 5, 10, and 20 min postchallenge. After adjustment to a standard minute ventilation of 30 times the baseline FEV1 for 6 min, the mean response by 90 mild asthmatics differed from 30 normal subjects in all four parameters (p < 0.0001). In asthmatics, maximum decline from baseline (mean +/- SEM) was as follows: FVC, 12.1 +/- 1.2%; FEV1, 19.7 +/- 1.7%; FEF 25-75%, 33.5 +/- 2.5%; and PEFR, 29.0 +/- 1.9%. Normal subjects had a maximum fall as follows: FVC, 2.9 +/- 0.7%; FEV1, 3.8 +/- 0.7%; FEF25-75%, 11.8 +/- 2.0%; and PEFR, 11.5 +/- 1.0%. Based on comparison of receiver operator characteristic curves, FEV1 was more accurate than FEF25-75% and equivalent to FVC and PEFR. A threshold of 10% change or greater in FEV1 had a specificity of 90%, with a sensitivity of 63.3%. A threshold of 15% or greater had a specificity of 100%, with a sensitivity of 53.3%. The FEV1 fell by 10% or more in 55 of 90 asthmatics at 5 or 10 min after hyperventilation. Measurements at 0 or 20 min added two additional positive responses. We conclude that in the proper clinical setting, subjects whose FEV1 declines by 10% or more at 5 or 10 min after EVH should be diagnosed as having asthma.
STUDY OBJECTIVE: Inhalation of dust in a swine confinement building causes an intense airway inflammatory reaction in the airways and increased bronchial responsiveness to methacholine. The aims of the present study were to investigate whether exposure to organic dust also influences bronchial responsiveness to an indirect stimulus, and to assess the duration of increased postexposure bronchial responsiveness. DESIGN: Twenty-two healthy nonatopic, nonsmoking subjects were exposed to dust for 3 h in a swine confinement building. Lung function was assessed, and either a methacholine bronchial provocation (n = 11) or a challenge with eucapnic hyperventilation of dry air (n = 11) was performed before exposure and at 7 h, 1 week, 2 weeks, and 4 weeks after exposure. RESULTS: Vital capacity and FEV(1) decreased 3% and 6%, respectively (p < 0.001), and airway resistance increased 15% (p < 0.05) after exposure. The median provocative dose of methacholine causing a 20% decline in FEV(1) fell from 1.38 mg (25th to 75th percentiles, 0.75 to 7.20 mg) before exposure to 0.18 mg (0.11 to 0.30 mg) after exposure (p = 0.004). Corresponding values for the dose-response slope were 15.3%/mg (2.88 to 25.3%/mg) and 100.2%/mg (2.1 to 27.3%/mg), respectively (p = 0.01). Bronchial responsiveness to eucapnic hyperventilation was not affected by the exposure: FEV(1) fell 4.3% (- 7.2 to - 1.8%) before and 4.8% (- 6.7 to - 1.6%) after exposure (p = 0.72). One week after exposure, the bronchial responsiveness to methacholine was normalized. CONCLUSIONS: The bronchial responsiveness to methacholine but not to dry air increases after exposure to swine house dust. Thus, exposure to organic dust induces increased bronchial responsiveness with different characteristics from that frequently found in asthma.
Chest pain is frequently a prominent symptom of the hyperventilation syndrome (HVS) and must be distinguished from angina pectoris due to coronary atherosclerotic heart disease (CAHD). The association between hyperventilation and chest pain may be apparent if psychoneurotic traits or anxiety are present. Many patients with HVS are not overtly anxious or neurotic, but in the great majority, a careful history and physical examination will indicate whether chest pain is due to HVS or CAHD. The failure to make this clinical differential diagnosis, which often leads to unnecessary coronary angiography, should not be as frequent as generally experienced. Fifteen of 95 consecutive patients had chest pain and additional typical HVS symptoms. Reassurance and detailed explanation about the cause of the chest pain gave significant relief, so that all patients were less symptomatic 24 to 44 months later, and none had developed new signs or symptoms to suggest that symptomatic CAHD had been overlooked. The risk and expense of coronary angiography was avoided.
A patient with lymphomatoid granulomatosis and focal transformation to lymphoma limited to the central nervous system presented with severe central neurogenic hyperventilation. The hyperventilation resolved as the underlying pathologic condition was treated with prednisone and cyclophosphamide.
To establish a safe and sensitive diagnostic procedure for detecting coronary vasospasm, we utilized 201-thallium myocardial SPECT combined with hyperventilation (HV-SPECT) in 29 patients with vasospastic angina (VAP) and 11 controls. Twenty-five of 29 patients with VAP and 5 of 11 controls developed transient perfusion defects on HV-SPECT, resulting in a sensitivity and specificity calculated at 86% and 55%, respectively. Overall accuracy in identifying corresponding vessels with coronary vasospasm, respectively. Coronary vasospasm tended to be identified more accurately in the left anterior descending branch and the right coronary artery than in the circumflex branch (75%, 71% and 50%, respectively). The hyperventilation test induced ischemic ECG changes in 11 of 29 patients with VAP, yielding a sensitivity of 38%. Analyzing the washout rate of HV-SPECT in patients with VAP, both the extent and severity scores of patients with ischemic ECG changes were larger than those of patients without. No serious complications occurred during HV-SPECT. In conclusion, HV-SPECT was a safe and sensitive procedure as a primary diagnostic approach for VAP. From the results of washout analysis, HV-SPECT could detect more mild myocardial ischemia than could the ECG, and seemed quite useful especially for detecting coronary vasospasm accompanied by minimal ischemic ECG changes.
The acid-base and oxygen status were assessed in patients undergoing abdominal surgery. We determined the measured and calculated parameters described by Siggaard-Andersen in arterial and mixed venous blood before, during and after a controlled hyperventilation. In these dynamic conditions, the mixed venous calculated p50 showed the most interesting variations. Derived values in arterial blood were unreliable since: 1) fitting to hyperbolic tangent function is not possible when SaO2 greater than 0.98; 2) in these patients, the arterio-venous difference in CtO2 is different from 2.3 mmol/L. The acute changes in calculated p50 are in agreement with the effect of hyperventilation on oxygen status.
We have studied the effects of positive expiratory pressure (PEP), continuous positive airway pressure (CPAP) and hyperventilation on 9 hypoxemic and hypercapnic chronic obstructive pulmonary disease (COPD) patients. All the patients were in a stable condition and received continuous oxygen. PEP and nasal CPAP were each given for 3 days in random order once every hour during the day and 3 times overnight. The effects of treatment were compared with a 3-day period in which the patients had no treatment for CO2 elimination. The effects were based on transcutaneous measurements of PO2 (PtcO2), PCO2 (PtcCO2) and SO2 (SpO2) and arterial blood gas measurements. The transcutaneous measurements showed that the PEP treatment reduced the PtcCO2 in COPD patients by 0.5 kPa and the CPAP treatment reduced it by 0.1 kPa (p < 0.05). The hyperventilation maneuver caused a decrease in the PtcCO2 of 0.7 kPa. The nocturnal treatments and measurements were all similar to the daytime measurements; the PtcCO2 decreased by 0.6 kPa using PEP and by 0.3 kPa using CPAP (p < 0.01). This indicated that all 3 methods reduced the PtcCO2, but only in the short term as the effects lasted for less than 4 min. COPD patients had no "late response" after any form of treatment. Arterial blood gases in COPD patients showed an elevation in PaCO2 (1.2 kPa) and a decrease in PaO2 and SaO2 during the night (11 pm to 7 am) without treatment. After 3 days of treatment with PEP and CPAP, the same pattern was noticed. The PaCO2 increased with both therapies, 1.3 kPa with PEP and 0.6 kPa with CPAP. Our data indicate that the effects were not of clinical significance and there is no justification for treating stable hypercapnic COPD patients with these methods.
Three patients wtih severe cardiotoxicity secondary to tricyclic antidepressant (TCA) overdosage were treated with induced mechanical hyperventilation. All three demonstrated marked QRS narrowing, reflecting improved intracardiac conduction, after hyperventilation therapy. Such therapy may help to prevent or abolish ventricular dysrhythmias, often a feature of life-threatening TCA overdoses.
A 92-year-old woman was admitted to our hospital due to hypertension, nausea, pain in the anterior part of the chest, epigastralgia, and tachypnea. During the initial examination of the patient in the emergency ward, she was very excited, howled, and both her hands were numb. Arterial blood gas analysis revealed a marked alkalemia (pH greater than 7.55) and hypocapnia (Pco2 24.1 mmHg). After paper bag re-breathing, the pH and Pco2 were within normal limits. Because there was no lesion in the lungs or the brain that would account for hyperventilation and convulsions, the attack was considered to be a manifestation of hyperventilation syndrome should be carefully considered in the differential diagnosis of disturbance of consciousness even in elderly patients.
The combined effect upon cerebral blood flow (CBF) of an elevation of cerebrospinal fluid pressure (CSFP) and changes in respiratory CO2 was studied in nine baboons under chloralose anesthesia. The animals were mildly hyperventilated and provided with increasing amounts of CO2 in O2-air. Arterial CO2 tensions (PaCO2) increased from 17 to 58 mm Hg. Internal carotid blood flow (ICBF) was measured at normal CSFP and at hydrostatically maintained 50 mm Hg CSFP. It was found that: 1) end-tidal CO2 may be used as a substitute for arterial PaCO2 determinations; 2) this elevation of CSFP has little effect on ICBF during hypercapnia and normocapnia; however, 3) during hypocapnia the ICBF is reduced an additional 20% when CSFP is elevated; that is, ICBF is reduced 50% from normal when end-tidal CO2 is reduced to 2% at this elevated level of CSFP. Caution should be exercised during hyperventilation therapy particularly if the elevated CSFP or intracranial pressure (ICP) is not reduced to approach normal levels; in these conditions, the combination of decreasing PaCO2 and elevated ICP may reduce CBF below critical levels and thus lead to cerebral hypoxia.