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PubMed1979

[Effect of hyperventilation on the vestibular system].

Nineteen normal subjects with no past history of hearing or balance impairment have undergone an electronystagmogram (E.N.G.), according to the usual technique in our laboratory. About one month or more after this first test, they underwent a second E.N.G. but this time with periods of hyperventilation distributed at certain precise moments of the test. Our analyses have not demonstrated that hyperventilation causes nystagmus or enhances in preexisting nystagmus in normal subjects, although the changes in the positional test were close to being significant.

Adult↗
PubMed1988

[Changes in the EEG background rhythm and in the hyperventilation effect at different stages of HIV infection].

The visual evaluation of 370 clinical EEGs of 125 patients in different stages of the HIV-infection as well as 42 HIV-seronegative volunteers of the same high risk population (male homosexuals) proved the increasing appearance of CNS dysfunction with progression of the disease. An especially established hyperventilation-index for a semiquantitative evaluation of hyperventilation response showed an increase of slow-wave activity in the course of the infection. The appearance of slow-waves as well as a significant slowing of background activity in advanced stages of the HIV-infection can be regarded as unspecific signs of a beginning diffuse functional CNS disorder caused by a direct affection of the CNS through the Human Immunodeficiency Virus (HIV). The EEG changes in early stages are not specific as to their causative agent and do not allow the distinction between primary and secondary CNS involvement. The changes may precede clinical-neurological alterations.

AIDS-Related Complex↗
PubMed1988

[Hyperventilation syndrome and its clinico-pathogenetic importance in autonomic disorders of a psychogenic nature].

The role of hyperventilation-induced shifts in the pathogenesis of different kinds of autonomic disorders (autonomic paroxysms, syncopal states, allergic signs) was investigated in 156 patients. This role should be considered in therapeutic interventions, especially in respiratory training aimed at correcting the respiratory pattern in order to achieve psychoautonomic stabilization. Distinct pathogenic mechanisms of combined hyperventilation and autonomic disorders are discussed.

Autonomic Nervous System Diseases↗
PubMed1986

[Hemodynamic changes in healthy persons and in patients with arterial hypertension during hyperventilation].

Hemodynamic changes in response to the hyperventilation test were examined in normal males and females of varying age, and in patients with first- and second-stage essential hypertension, renal arterial hypertension and hypertensive neurocirculatory dystonia. Normal subjects showed increased heart rate (HR) and cardiac index (CI), and lowered specific peripheral resistance in response to hyperventilation, the magnitude of HR and CI changes declining with age. The increase in HR and CI during the test was somewhat more pronounced in patients with essential hypertension as compared to normal subjects, whereas in hypertensive neurocirculatory dystonia hemodynamic shifts were similar to those of normal subjects.

Adolescent↗
PubMed1979

[Change of intracranial pressure in neurosurgical patients by hyperventilation, positive negative pressure ventilation and PEEP (author's transl)].

The effects of a hyperventilation, positive negative pressure ventilation (PNPV) and ventilation using positive endexpiratory pressure (PEEP), on intracranial pressure (ICP) was measured in 24 patients suffering from different neurosurgical disorders. The patients were given a basic anaesthesia including muscle relaxation. The investigations showed, that hyperventilation, followed by a PCO2 of 26 and 30 torr, clearly lowered the intracranial pressure. The pressure drop was much more pronounced when the preexisting ICP was high than when it was low, due to the form of the compliance curve of the brain. PNPV also lowered intracranial pressure, but a harmful effect of this technique on lung function and structure is known. Its use is justified only for short periods and in addition to other measures for lowering ICP. The results also demonstrated that PNPV possesses limited beneficial properties with regard to the subject discussed here. Ventilation by PEEP significantly increased ICP. This technique is to be employed with caution in neurosurgery. Arterial pressure (radial artery) and central venous pressure (subclavian vein) were also recorded.

Adolescent↗
PubMed1985

[Controlled hyperventilation in the therapy of acute myocardial infarction].

Two patients with anterior wall infarction were hyperventilated under control with the aim of the induction of an inverse steal-phenomenon. Simultaneously the registration of the ST-dynamics was performed by means of precordial mapping. In a region of an arterial carbon dioxide partial pressure up to about 20 mm Hg the increasing hypocapnia causes a rapid and clear reduction of the sum of ST segment elevations. The optimization of the myocardial oxygen balance caused by an inverse steal-phenomenon can be made evident by the increase of the left-ventricular compliance and might be favoured by the decrease of the left-ventricular filling pressure caused by the positive respiration pressure. The parameters of the global haemodynamics remain in the region of their initial values. With the controlled hyperventilation a new myocardium-protective therapy principle for patients with infarction is demonstrated, which is to be involved into their therapy regime.

Carbon Dioxide↗
PubMed1979

Hyperventilation in aircrew: a review.

The causes and effects of hyperventilation, relevant to the flight environment, have been reviewed and one case history is presented. Methods of investigating in-flight hyperventilation are discussed.

Aerospace Medicine↗
PubMed1978

Aspirin, hyperventilation, and cerebellar infarction in sickle cell disease.

Aspirin ingestion was followed by hyperventilation, cerebellar signs, and fatal brain stem dysfunction in a patient with sickle cell disease. Autopsy showed a swollen, recently infarcted cerebellum with tonsillar herniation compressing the medulla. We propose that hypocapnea from aspirin-induced hyperventilation caused carotid artery constriction and focal cerebral hypoxia, resulting in cerebellar sickling nad infarction. Hypocapnea should be treated promptly to prevent brain damage in patients with sickle cell disease.

Adult↗
PubMed1984

Changes in the vulnerable period of the rat myocardium during hypoxia, hyperventilation and heart failure.

Changes in the duration and size of the vulnerable period of the myocardium in the presence of respiratory changes were studied in acute experiments on rats. The limits of the vulnerable period were determined by directly stimulating the heart during ventilation via the enlarged respiratory dead space, during hyperventilation and during heart failure. In the control group (normal ventilation without enlargement of the dead space), the vulnerable period lasted 5.7 +/- 0.76 ms. During ventilation via the enlarged dead space, hypercapnic hypoxaemia developed and the vulnerable period was markedly prolonged (18.55 +/- 5.29 ms) by a shift of its inner limit to the left. Hyperventilation caused normoxic to hyperoxic hypocapnia and markedly reduced the duration of the vulnerable period (8.17 +/- 2.21 and 9.31 +/- 2.38 ms respectively). The vulnerable period lengthened the most in heart failure (25.46 +/- 3.93), mainly as a result of a shift of its outer limit. In all the experimental groups there was a shift of the vulnerable period to the right, which was fastest in hypercapnic hypoxaemia and slowest in hyperoxic hypocapnia. The administration of Inderal (3 mg/kg i.p.) or Arfonad (50 mg/kg i.p.) markedly shortened the vulnerable period during hypercapnic hypoxaemia (9.87 +/- 2.78 and 9.32 +/- 2.16 ms respectively), but did not block the shift. Lengthening of the vulnerable period during hypercapnic hypoxaemia was probably due to activation of sympathetic nerves via beta-adrenergic receptors.

Animals↗
PubMed1978

[Hyperventilation and oxygen supply to the myocardium].

1. Voluntary hyperventilation during rest and in the recumbent position induces a fall in H+ concentration, PCO2 and PO2 in mixed venous blood and in the blood of the coronary sinus. 2. In 7 of 12 patients the arterio-venous O2 difference increased by more than 10% of the control value (mean increase 21%). At the same time the O2 extraction of the myocard increased (mean increase 17%) in these subjects. Blood pressure and pulse rate varied only slightly in these experiments. 3. Chest pain and angina pectoris due to hyperventilation are the result of impaired myocardial O2 supply, a finding which is valid for subjects with and without coronary heart disease.

Angina Pectoris↗
PubMed1982

The protective effect of ipratropium bromide aerosol against bronchospasm induced by hyperventilation and the inhalation of allergen, methacholine and histamine.

The ability of the anticholinergic agent, ipratropium bromide, Atrovent, (40 mcg from a metered dose inhaler) to prevent bronchoconstriction produced by four different provocation tests was compared with placebo in 12 asthmatic patients. The provocation tests used were hyperventilation and inhalations of histamine, methacholine and an allergen to which the subject was known to be sensitive. The order in which each patient received the tests was determined according to a Latin-square design and remained the same on both test days. Pretreatment with ipratropium bromide and placebo was allocated randomly and administered in double-blind fashion. Ipratropium bromide provided significant protection at the 5% level against all four types of challenge. The average number of breaths required to produce a fall of at least 20% in FEV1 (forced expiratory volume in one second) was doubled for both histamine and allergen and increased by a factor of six for methacholine. The fall in FEV1 induced by hyperventilation was approximately halved. No side effects were noted with ipratropium bromide.

Adolescent↗
PubMed1984

[The hyperventilation syndrome].

Acute hyperventilation (HV) rarely poses diagnostic or therapeutic problems. Chronic hyperventilation, however, with vague and multiple symptomatology due to respiratory alkalosis and increased breathing work, is often overlooked or misinterpreted, though it is a very common disorder of the general patient population. Chronic HV is frequently associated with emotional disturbances such as anxiety, panic and depression, or with psychosomatic disorders such as irritable bowel, effort syndrome and chronic pain. The diagnosis of chronic HV relies primarily on taking of a thorough history and is confirmed by an HV provocation test and arterial or cutaneous measurements of pCO2. Therapeutic measurements include psychotherapy, psychoactive drugs (antidepressants and benzodiazepines), beta-blockers and modification of abnormal breathing patterns.

Humans↗
PubMed1983

[Pseudo-ischemic changes in the ECG caused by hyperventilation].

Exercise was found to produce pseudoischemic changes of ST segment in 6% of patients with neurocirculatory dystonia, and T-wave inversion in 15-16%, which may be due to hyperventilation. It was demonstrated that T-wave inversion could not be a reliable indicator of coronary insufficiency, nor could respiratory alkalosis, hypocapnia, tachycardia, increased work of respiratory muscles, hypoxemia be immediate causes of hyperventilation changes. It is suggested that the changes in question are related to disrupted vegetative control of the cardiovascular system.

Adolescent↗
PubMedDate not supplied

Isocapnic hyperventilation with cold air in healthy non-smokers, smokers and asthmatic subjects.

Isocapnic hyperventilation with subfreezing air was performed by 15 healthy non-smokers, 10 asymptomatic smokers and 9 asthmatics. All subjects had normal ventilatory function and airway resistance (Raw) before challenge. The hyperventilation was performed twice. In one session, total respiratory resistance (Rrs) and reactance (Xrs) were measured at various frequencies, using a forced oscillation technique; in another session, vital capacity (VC), forced expiratory volume in 1 s (FEV1), maximal expiratory flow rates (FEF) and Raw were determined. In non-smokers, no changes in FEV1, FEF nor Raw were observed, whereas Rrs increased significantly (+ 20% of the prechallenge value), without change in resonant frequency nor in the Rrs-frequency relationship. This suggests a constrictory effect on central airways (possibly a narrowing of the glottis) only. In smokers, Rrs showed a similar, though longer lasting, increase than in non-smokers. Besides, a significant change of the Rrs-frequency relationship and a reduction in FEF at 50% of VC was found, suggesting an involvement of peripheral airways also. In asthmatics, bronchial reactivity was more pronounced, resulting in significant changes in all parameters: Rrs increased by about 100% of the prechallenge value, and became highly frequency dependent; Xrs decreased markedly, resulting in an increase in resonant frequency of the respiratory system. Similarly, VC, FEV1 and FEF decreased. These alterations are compatible with a more generalized constriction of the peripheral as well as central airways.

Airway Obstruction↗
PubMed1980

Influence of 1% enflurane (Ethrane) anesthesia on regional cerebral blood flow repartition under normo-and hyperventilation.

This study is based on the same group of neurosurgical patients as our previous publication. All, except one, had suffered from head injury. We made a first measurement of rCBF under N2O anesthesia, a second under N2O + 1% enflurane anesthesia, both at a PaCO2 of 40 Torr. A third measurement was performed under N2O + 1% enflurane but at a PaCO2 of 30 Torr. The method we used consists of the intracarotid injection of 133Xe and recording of the radioactivity by a gammacamera. Mean arterial pressure was maintained constant by an intravenous phenylephrine drip. For each measurement of each patient, a map was drawn, representing the distribution of the regional cerebral blood flows (rCBF), compared to the mean value of the hemisphere. We have studied rCBF in one case of normal hemisphere, and in cases of traumtic lesions in acute and chronic states, taking into account that the normal brain exhibits areas with higher flow in the frontoparietal and insular regions. In the normal brain, introduction of 1% enflurane decreases uniformally mean CBF, rCBF repartition not being changed. Hyperventilation to 30 Torr shows that regions with previously higher flow react more to hypocapnia by a slightly more decreased flow. In severe brain trauma, mean CBF is generally low, and it is difficult to visualize the lesions under N2O and N2O + 1% enflurane anesthesia. Neither mean CBF, nor rCBF repartition are significantly modified. On the other hand, in the acute phase, hypocapnia causes a more decreased flow in the previously well irrigated areas, and shows a lack of vascular reactivity in the damaged region. Passing to the chronic state, the patient clinically recovering, the rCBF repartition is normalized and the contused area becomes agains vasoactive. Severe losses of neuronal tissue are characterized by definitive low flows without reactivity by hyperventilation.

Adolescent↗
PubMed1981

Hyperventilation as a variant of tardive dyskinesia.

Respiratory dyskinesia, a variant of tardive dyskinesia, may mimic chronic psychogenic hyperventilation syndrome, hence pseudopsychogenic hyperventilation. Respiratory alkalosis and sympathetic discharge may occur in both conditions. Neurological symptoms, dyspnea, chest pain, muscle spasms may also occur. Ventilation increases with stress and disappears with sleep in both conditions. However, respiratory dyskinesia has been seen in association with other choreiform movement disorders. Speech is interrupted by breathing and breathing is interrupted by grunts and groans. Respiratory dyskinesia is under partial voluntary control and is not due to a "psychological problems."

Aged↗
PubMed1981

[Effects and dangers of hyperventilation].

As the notable danger of diving in breath-holding is mostly rapported to the preventive hyperventilation and the effects of such technique of breath, practically applied, are scarcely studied and known, the Author examines the effects of hyperventilation and its consequences on the next breath-holdings in surface and in depth.

Blood Pressure↗