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PubMed1984

Hyperventilation in flight.

Hyperventilation in flight may be caused by environmental, psychological, pharmacological, and pathological factors. The effects are discussed and two case histories are presented, illustrating the development and effect of hyperventilation in training or aircrew under stress. Investigation of in-flight hyperventilation is technically very difficult, but positive acceleration, hypoglycaemia, and anxiety are important contributory factors. The incidence of hyperventilation must be reduced by educating aircrew in its aetiology, early recognition, and treatment.

Aerospace Medicine↗

PubMed1980

[Thromboelastographic patterns in patients suffering from chronic obstructive lung disease after hyperventilation].

In an our previous study we studied the influence of O2 therapy administration on the thromboelastographic pattern of patients suffering from chronic obstructive lung disease. We showed that basal hypocoagulability of our patients became normal after O2 administration. In this study we refer the thromboelastographic pattern observed in patients suffering from the same disease before and after hyperventilation. We don't find any changes about total coagulability either in patients or in healthy subjects after hyperventilation. Therefore we suggest that the absence of any changes is due to PCO2 and pH variations that occur at the same time of PO2 modification during hyperventilation; PCO2 and pH variations may influence the haemoglobin oxygen affinity and annul the effect of the increase PO2 on the tissue oxygenation. We suppose that the increase of patients suffering from chronic obstructive lung disease, is due to decreased fibrinolysis or to increased production of prostacycline induced by hyperventilation.

Adult↗

PubMed1995

Effect of prolonged hyperventilation on ischemic injury of neurons after global brain ischemia in the dog.

The influence of prolonged postischemic hyperventilation was studied in the model of global brain ischemia produced by 15 min cardiac arrest in dogs with 8 h recirculation. Histopathological examination of neuronal damage using silver impregnation showed the presence of numerous heavy argyrophylic neurons in the striatum and CA2 hippocampal subfield after 8 h of normoxic reperfusion. In dogs with prolonged 8 h postischemic hyperventilation a reduction in the occurrence of argyrophylic neurons in the striatum and their significant decrease in the hippocampal area were found. Electron microscopic study was performed to characterize the effect of respiratory alkalosis on the ultrastructural changes in neurons and correlate them with the results of silver impregnation. Ultrastructural analysis after the cardiac arrest without recirculation did not reveal the presence of dark neurons within the striatal and hippocampal areas. Neuronal alterations included a decrease in endoplasmic reticulum, mitochondrial swelling and a mild chromatin clumping. After 8 h of normoxic reperfusion many dark, shrinked neurons containing perinuclear clusters of clear vesicles were found. In hyperventilated animals the occurrence of dark neurons with extensive perineuronal edema was substantially reduced in the CA2 subfield. The effect of hyperventilation on postischemic calcium overload is discussed.

Animals↗

PubMed1996

Hyperventilation and esophageal dysmotility in patients with noncardiac chest pain.

OBJECTIVES: Hyperventilation is known to cause esophageal spasm, but the importance of this interaction in clinical practice is unknown. In the present study, we report the effects of hyperventilation provocation on esophageal motility in a consecutive series of patients with noncardiac chest pain. METHODS: In a prospective observational study design, 46 consecutive patients with normal coronary angiograms were studied. Esophageal motility was recorded at rest and after voluntary over-breathing at 40 breaths/min for 3 min. RESULTS: Hyperventilation was associated with a significant fall in mean distal peristaltic amplitude [66 (SD 28) to 55 (SD 24) mm Hg, p <0.001] and mean duration [2.9 (SD 0.7) to 2.6 (SD 0.9) s,p = 0.02]. It induced diffuse spasm in two (4%) patients, and nonspecific motility disorders in 10 (22%). Chest pain was reproduced in seven (15%) patients, but in none did this coincide with an important change in peristaltic amplitude, duration, or frequency. CONCLUSION: Hyperventilation has important effects on esophageal motility, and manometrists should be aware of these before recommending that anxious patients overbreathe to help relaxation during clinical studies. Although overbreathing is a common source of dysmotility, it rarely produces chest pain via its effects on the esophagus.

Breath Tests↗

PubMed1997

Regional dynamic signal changes during controlled hyperventilation assessed with blood oxygen level-dependent functional MR imaging.

PURPOSE: To quantitate the amplitude changes and temporal dynamics of regional functional MR imaging signals during voluntary hyperventilation using blood oxygen level-dependent contrast echo-planar imaging. METHODS: Seven male subjects were studied during voluntary hyperventilation (PetCO2 = 20 mm Hg) regulated by capnometry. Measurements were made on multisection echo-planar MR images obtained with parameters of 1000/66 (repetition time/echo time), flip angle of 30 degrees, and voxel size of 3 x 3 x 5 mm3. Sensitivity of the functional MR imaging signal to changes in PetCO2, time delays in relation to PetCO2 changes, and time constants of functional MR imaging signal changes were assessed on a region-by-region basis. RESULTS: Within 20 seconds of starting hyperventilation, rapid and substantial decreases in the functional MR imaging signal (by as much as 10%) were measured in areas of gray matter, which were significantly greater than the modest changes observed in white matter. Regional-specific effects in areas of the frontal, occipital, and parietooccipital cortex were stronger than in subcortical regions or in the cerebellum. Signal decreases measured with functional MR imaging were significantly delayed with respect to the reduction in PetCO2. Apparent differences between regional time constants did not reach statistical significance. CONCLUSION: Regional and gray-white matter differences in functional MR imaging signal changes during controlled hyperventilation may reflect differences in metabolic activity, vascular regulation, and/or capillary density. When measuring brain activation with functional MR imaging, arterial PCO2 differences due to unregulated respiration may confound interpretation of activation-related functional MR imaging signal changes.

Adult↗

PubMedDate not supplied

Changes in blood flow velocity and diameter of the middle cerebral artery during hyperventilation: assessment with MR and transcranial Doppler sonography.

PURPOSE: To compare blood flow velocity changes within the middle cerebral artery (MCA) during hyperventilation, as measured with by both transcranial Doppler sonography and MR imaging, with the diameter of the MCA as measured with MR imaging alone. METHODS: The studies were performed in six healthy volunteers ranging in age from 22 to 31 years (mean, 27 years). Transcranial Doppler sonography was carried out with a range-gated 2-MHz transducer. MR examinations were done on a 1.5-T imaging unit. MR angiography was performed using the time-of-flight technique. MR flow measurements were carried out by using the phase-mapping technique with an ECG-triggered phase-contrast sequence. RESULTS: During hyperventilation, the mean blood flow velocity of the proximal MCA declined by 49.6% +/- 5.7 (mean +/- standard deviation) as measured with Doppler sonography, and by 47% +/- 4.6 as measured with MR flow calculation. The diameter of the MCA (3.4 +/- 0.3 mm) remained unchanged on MR imaging studies (3.3 +/- 0.3 mm). CONCLUSION: We found a good correlation between relative flow velocity changes measured by transcranial Doppler sonography and MR techniques. MR imaging revealed no significant changes in the diameter of the proximal MCA during normal versus hyperventilation. Relative changes in flow velocity in the MCA would thereby reflect relative changes in cerebral blood flow, at least during hyperventilation.

Adult↗

PubMedDate not supplied

[Hyperventilation and mannitol administration during surgery in patients with space-occupying intracranial lesions].

The aim of this work was to evaluate the effect of hyperventilation and mannitol on brain volume during neurosurgical operations. The material comprises 30 cases of supratentorial tumours. pO2, pCO2, pH and lactate concentration were determined in the arterial blood and in 7 cases also in the CSF. It was established that hyperventilation sometimes fails to decrease ICP; it was observed that hyperventilation was more effective in decreasing brain volume of the pCO2 level decreased by 14,6 mm Hg on the average. The joint use of hyperventilation and hypertonic mannitol was found to be more effective. Neither of the above methods was effective in the case of cystic tumors.

Adolescent↗

PubMed1984

Metabolic and hemodynamic response to hyperventilation in patients with head injuries.

The effects of controlled moderate hyperventilation (paCo2 approximately 31 mmHg) on cardiovascular parameters and whole-body-oxygen-uptake (VO2) was studied in 10 patients with head injuries, who were unconscious and artificially ventilated at the time of the investigation. VO2 was measured with the Beckmann Metabolic Measurement Cart and also calculated from cardiac output and arterio-mixed venous oxygen content difference. A mean increase in VO2 (+ 19.6% of control) was observed after 2 h of hyperventilation. Cardiac output remained unchanged. This resulted in a decrease of venous oxygen content and impaired full oxygenation of the blood. Our results indicate that hyperventilation should not be a routine procedure. Close monitoring of arterial and venous blood gases is recommended, when hyperventilation is applied.

Adult↗

PubMed2006

Carvedilol reduces exercise-induced hyperventilation: A benefit in normoxia and a problem with hypoxia.

AIMS: To evaluate whether carvedilol influences exercise hyperventilation and the ventilatory response to hypoxia in heart failure (HF). METHODS AND RESULTS: Fifteen HF patients participated to this double blind, randomised, placebo controlled, cross-over study. Patients were evaluated by quality of life questionnaire, echocardiography, pulmonary function and cardiopulmonary exercise tests (ramp and constant workload) both in normoxia (FiO2 = 21%) and hypoxia (FiO2 = 16%, equivalent to a simulated altitude of 2000 m). Carvedilol improved clinical condition and reduced left ventricle size, but had no effect on lung mechanics. In normoxia during exercise, ventilation was lower, V(CO2) unchanged and PaCO2 (constant workload) or PetCO2 (ramp) higher with carvedilol, exercise capacity was unchanged (peak workload 92+/-22 and 90+/-22W for placebo and carvedilol, respectively). Abnormal V(E)/V(CO2) slope was reduced by carvedilol. Hypoxia increased ventilation but less with carvedilol; exercise capacity decreased to 87+/-21W (placebo) and to 80+/-11 W (carvedilol, p < 0.01). With hypoxia, carvedilol decreased V(E)/V(CO2) slope. At constant workload exercise with hypoxia, PaO2 decreased to 69+/-6 mm Hg (placebo) and to 64+/-5 (carvedilol, p < 0.01). CONCLUSION: Carvedilol reduced hyperventilation possibly by reducing peripheral chemoreflex sensitivity as suggested by PaCO2 increase with normoxia and PaO2 decrease with hypoxia without V(CO2) and V(D)/V(T) changes. Lessening hyperventilation is beneficial when breathing normally, but detrimental when hyperventilation is needed for exercise at high altitude.

Adrenergic beta-Antagonists↗

PubMed1996

A look at recent hyperventilation studies: outcomes and recommendations for early use in the head-injured patient.

During the past decade, mounting controversy surrounding the use of hyperventilation for the treatment of head injury has raised concerns about its safety and therapeutic benefits. A recent investigation of the medical literature was conducted to determine if outcomes for the head-injured patient continued to support the use of indiscriminate, and often unmonitored, hyperventilation in the pre-hospital and early hospital phases of care, and to determine if current investigators are recommending the use of hyperventilation for the initial treatment of all unconscious head-injured patients. Findings suggest that head-injured patients in the pre-hospital and early phases of care are at increased risk for suffering hyperventilation-induced secondary brain injury. Current researchers are now recommending a highly monitored, cautions and selective approach to care; this approach calls our current practice into question.

Brain↗

PubMed1996

Hyperventilation and head injury: controversies and concerns.

The use of hyperventilation for the treatment of severe head injuries has been the standard of care for more than two decades in the prehospital, emergency department and critical care settings. Controversy has surrounded its use, even when advocates recommended use for all unconscious, head-injured patients. Autoregulation, cerebral acidosis control, reduction of elevated intracranial pressure and the "steal phenomenon" were thought to be beneficial effects of hyperventilation therapy. Current researchers and developments in technology, however, have provided controversial information which suggests that hyperventilation therapy can be harmful, warranting the need for careful monitoring and selective treatment. This information calls into question the use of unmonitored hyperventilation therapy in the prehospital and early hospital settings.

Brain↗

PubMed1985

Effects of hyperventilation and hypoventilation on stress-induced intestinal vasoconstriction.

The combined effects of defined changes in ventilation and stress-induced vasoconstriction were studied in the intestinal vascular bed in cats (n = 20) anaesthetized with fentanyl, nitrous oxide and diazepam. Intestinal reflex vasoconstriction was induced by stimulation either of the hypothalamic defence-alarm area or of somatic and visceral pain afferents. The volume-controlled ventilation was changed by altering the tidal volume, and stimulations were performed during either control conditions (Paco2 4.5-5.0 kPa), hyperventilation (Paco2 3.0-3.5 kPa) or hypoventilation (Paco2 6.5-7.5 kPa). The increase in intestinal vascular resistance (IVR) elicited by defence-alarm area stimulation was potentiated during hyperventilation (306 +/- 83% vs 198 +/- 62%; P less than 0.01) and attenuated during hypoventilation (176 +/- 62% vs 240 +/- 44%; P less than 0.05). The increase in IVR elicited by pain fibre stimulation was potentiated during hyperventilation (73 +/- 21% vs 54 +/- 19%; P less than 0.01), but not significantly changed during hypoventilation (47 +/- 19% vs 68 +/- 34% during control ventilation). Our data indicate that the ventilatory pattern can be decisive for the vasoconstrictor response during experimental stress. We suggest that remote neurogenic mechanisms account for the increased responsiveness during hyperventilation. The decreased responsiveness during hypoventilation, on the other hand, seems to correlate with the local vasodilator effects of carbon dioxide.

Animals↗

PubMed1982

Hyperventilation-induced asthma: evidence for two mechanisms.

The mechanism by which airway cooling induces airflow obstruction in asthmatic subjects has not yet been established. Using a pair of isocapnic hyperventilation challenges, with a 40-minute interval, we looked for the presence of a refractory period in 19 asthmatic patients (aged 9-18 years). The subjects fell into two groups. The eight in the "non-refractory" group showed less than a 25% reduction in response to the second challenge, but the 11 in the "refractory" group showed at least a 35% reduction. Twelve subjects also performed a hyperventilation challenge after cholinergic blockade with inhaled ipratropium bromide. In five, in whom no refractoriness after hyperventilation was seen, there was a significant protection from cholinergic blockade (p less than 0.05). In these a vagal (cholinergic) reflex seems likely. The remaining seven, who had a refractory period, received no significant protection from cholinergic blockade and therefore no evidence for the presence of any cholinergic mechanism. We conclude that two mechanisms are responsible for hyperventilation-induced asthma, one of which is a vagal reflex while mediator release may be the other.

Adolescent↗

PubMed1986

Oral progesterone treatment in chronic obstructive lung disease: failure of voluntary hyperventilation to predict response.

Previous studies have shown that some patients with chronic obstructive lung disease and hypercapnia will respond to medroxyprogesterone with improvement in arterial blood gases. The exact mechanism of this effect is unclear but it is presumed to be a result of ventilatory stimulation. To determine whether the ability to correct arterial blood gas abnormalities by voluntary hyperventilation would predict a subsequent favourable response to progesterone, we studied 11 subjects with chronic obstructive lung disease and chronic hypercapnia. Five subjects had chronic obstructive lung disease of moderate severity with mean (SE) FEV1 1.8 (0.34) 1 maximum voluntary ventilation (MVV) 40.4 (7.16) 1/min-1, arterial oxygen tension (Pao2) 53.8 (2.40 mm Hg, and arterial carbon dioxide tension Paco2) 49.6 (3.91) mm Hg, and were able to normalise their blood gas tensions during voluntary hyperventilation (Pao2 85.4 (8.01) mm Hg; Paco2 32.8 (3.43) mm Hg). Six subjects had severe chronic obstructive lung disease with FEV1 0.77 (0.12) 1, MVV 19 (3.09) 1/min-1, Pao2 60.0 (2.89) mm Hg and Paco2 50.5 (1.38) mm Hg, and they could not significantly alter their blood gases with voluntary hyperventilation (Pao2 62.5 (3.19) mm Hg, Paco2 49.7 (1.84) mm Hg). The groups were similar in age, height, weight, and resting Pao2 and Paco2. Each subject received one month of oral placebo and one month of medroxyprogesterone acetate (Provera). 20 mg orally thrice daily, given in a randomised, double blind fashion. The groups responded similarly with a significantly higher Pao2 and lower Paco2 while having medroxyprogesterone acetate than while having placebo. Two patients with polycythaemia showed a reduction in haemoglobin concentration while taking progesterone. It is concluded that the response to medroxyprogesterone is not predictable from spirometric or blood gas changes after voluntary hyperventilation.

Blood Gas Analysis↗

PubMed1998

Hyperventilation induces release of cytokines from perfused mouse lung.

Artificial mechanical ventilation represents a major cause of iatrogenic lung damage in intensive care. It is largely unknown which mediators, if any, contribute to the onset of such complications. We investigated whether stress caused by artificial mechanical ventilation leads to induction, synthesis, and release of cytokines or eicosanoids from lung tissue. We used the isolated perfused and ventilated mouse lung where frequent perfusate sampling allows determination of mediator release into the perfusate. Hyperventilation was executed with either negative (NPV) or positive pressure ventilation (PPV) at a transpulmonary pressure that was increased 2.5-fold above normal. Both modes of hyperventilation resulted in an approximately 1.75-fold increased expression of tumor necrosis factor alpha (TNFalpha) and interleukin-6 (IL-6) mRNA, but not of cyclooxygenase-2 mRNA. After switching to hyperventilation, prostacyclin release into the perfusate increased almost instantaneously from 19 +/- 17 pg/min to 230 +/- 160 pg/min (PPV) or 115 +/- 87 pg/min (NPV). The enhancement in TNFalpha and IL-6 production developed more slowly. In control lungs after 150 min of perfusion and ventilation, TNFalpha and IL-6 production was 23 +/- 20 pg/min and 330 +/- 210 pg/min, respectively. In lungs hyperventilated for 150 min, TNFalpha and IL-6 production were increased to 287 +/- 180 pg/min and more than 1,000 pg/min, respectively. We conclude that artificial ventilation might cause pulmonary and systemic adverse reactions by inducing the release of mediators into the circulation.

Animals↗

PubMed2000

[Uses and abuses of hyperventilation in severe traumatic brain injury].

A critical evaluation was done about the guidelines and effects of the hyperventilation maneuver on prevention and treatment of increased intracranial pressure (ICP) that follows severe traumatic brain injury (TBI). The prophylactic use of hyperventilation should be avoided after severe TBI acute phase, unless high venous O2 values are recorded at jugular bulb blood (SjO2), or to allow time when there are evidences of neurologic deterioration with posturing. The lack of cerebrovascular response to hyperventilation to low the ICP means that the blood brain barrier (BBB) function is extensively impaired. Then, hyperventilation may be used as a screening therapeutic test in acute severe TBI, since BBB impairment is the pointer that other available clinical procedures for high ICP control (sedation, paralysis and osmotic diuretics) are not workable. A new pathogenetic hypothesis about traumatic brain edema and its therapeutic approach is presented.

Acute Disease↗

PubMed2000

[Is the combination of nitrous oxide and hyperventilation in elective neurosurgical operations useful?].

The use of nitrous oxide (N2O) and hyperventilation (HV) in elective neurosurgery is controversially discussed. The emphasis of the study was to show the effects of N2O and/or moderate hyperventilation (paCO2 31.0 +/- 1.2 mmHg) on parameters of cerebral metabolism: jugularvenous oxygen saturation (SjVO2), cerebral extraction of oxygen (CEO2), arterial jugularvenous difference of oxygen contents (AJDO2), arterial jugularvenous difference of lactate (AJDL) and glucose (AJDGL) and lactate-oxygen index (LOI). The study was approved by the Ethics Committee of the University of Leipzig. Forty patients undergoing an elective craniotomy for brain tumour resection were divided into four groups: group 1: n = 10, N2O + normoventilation (NV), group 2: n = 10, N2O + hyperventilation (HV), group 3: n = 10, O2/air + NV, group 4: n = 10, O2/air + HV. N2O + HV led to a significant decrease in SjVO2 from 68.1 +/- 10.7% to 49.7 +/- 5.6%. O2/Air + HV produced a drop from 67.1 +/- 11.1% to 49.8 +/- 7.7%. CEO2 increased significantly in the group N2O + HV from 30.6 +/- 10.6% to 49.6 +/- 5.5% and in the group O2/Air + HV from 31.7 +/- 11.1% to 50.0 +/- 7.8%. AJDO2 increased significantly in the group N2O + HV from 5.79 +/- 1.54 ml% to maximal 8.49 +/- 1.10 ml% and in the group O2/Air + HV from 5.29 +/- 1.76 ml% to maximal 8.03 +/- 1.76 ml%. In the normoventilation-groups 1 and 3, no significant changes in SjVO2, CEO2 and AJDO2 were observed between MP2 and 4. The parameters AJDL, AJDGL and LOI did not show any significant changes in any of the four groups. The described data represent a reduction of cerebral oxygenation, but deleterious effects caused by cerebral ischaemia could not be observed. Based on our data, hyperventilation and its combination with N2O should not be used routinely in neuroanaesthesia.

Adult↗

PubMed1990

[The effect of quiet breathing of nitrogen dioxide and sulfur dioxide on the sensitivity of the respiratory tract to hyperventilation of sulfur dioxide].

In 14 patients with an oversensitive bronchial system (non-smokers), we investigated the question as to whether quiet breathing in a nitrogen dioxide or sulphur dioxide atmosphere would modify the sensitivity of the airways to sulphur dioxide. On three consecutive days, over a period of 30 minutes at rest, the patients breathed either filtered air or an atmosphere containing 0.25 ppm nitrogen dioxide, or 0.5 ppm sulphur dioxide. There then followed isocapnic hyperventilation of 0.75 ppm sulphur dioxide in increasing ventilation steps of 3 minutes duration each. On three other experimental days, in 7 patients, a stepwise hyperventilation of filtered air was carried out. Quiet breathing of nitrogen dioxide or sulphur dioxide resulted in no obstruction of the airways. The ventilation required to achieve a doubling of the specific airway resistance (PV100SRaw) during hyperventilation of sulphur dioxide was, on average, 46.5, 37.7 and 45.4 l/min after inhalation of filtered air, nitrogen dioxide and sulphur dioxide, respectively. Following nitrogen dioxide, PV100SRaw was significantly smaller (p less than 0.01 than following filtered air or sulphur dioxide. During hyperventilation of filtered air, the average PV100SRaw was 58.2, 51.8 and 55.7 l/min, respectively. We conclude that in non-smokers with an hypersensitive bronchial system, the inhalation of nitrogen dioxide can bring about an increase in the obstructive reaction to sulphur dioxide, without itself leading to an obstruction of the airways; in contrast, sulphur dioxide does not modify the degree of sensitivity.

Adult↗