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PubMed1972

The effect of hyperventilation on maternal placental blood flow in pregnant rabbits.

1. In anaesthetized pregnant rabbits near term, cardiac output and its distribution were measured by injection of isotope-labelled microspheres. Hypocapnia (mean arterial P(CO) (2) 18 mm Hg), induced by intermittent positive pressure hyperventilation, caused a 43% reduction in maternal placental blood flow, attributed mainly to vasoconstriction. Myometrial flow was not significantly changed.2. Moderate hypercapnia (mean arterial P(CO) (2) 46 mm Hg) caused no change in placental flow, compared with observations made while breathing air spontaneously (P(CO) (2) 31 mm Hg).3. Intravenous infusions of adrenaline or noradrenaline 1 mug/kg. min caused maternal placental vasoconstriction.4. During the especially warm summer of 1969, there was a mean 46% reduction in maternal placental blood flow in pregnant rabbits near term, breathing room air spontaneously with normal blood gas values and rectal temperatures. This was associated with an increase in the number of runts and dead foetuses.

Animals↗
PubMed2002

No effect of chinese acupuncture on isocapnic hyperventilation with cold air in asthmatics, measured with impulse oscillometry.

The cost to society and the individual of treating asthma has been increasing in developed countries. This has given rise to studies of the efficacy of complementary treatments. The aim of this study was to evaluate the efficacy of traditional Chinese Acupuncture in patients with mild asthma. The method used for evaluation of efficacy was total airway resistance at 5Hz (R5) as measured by impulse oscillometry (IOS)--a forced oscillation technique, at baseline and after a bronchial challenge with voluntary isocapnic hyperventilation of cold air (IHCA). The study was a parallel group randomised placebo controlled trial with evaluator blinding. Twenty-seven asthmatics were recruited and 24 completed the study, 10 of them received acupuncture and 14 received a placebo treatment (mock-TENS). Treatment continued for 15 weeks, and efficacy was tested two weeks following the last treatment. Randomisation resulted in female over representation in the acupuncture group, but lung-function and bronchial responsiveness to IHCA were comparable in the two populations before the start of treatment (p>0.05 vs. p > 0.05). There were no statistically significant effects of the treatment before (p > 0.05) or after IHCA (p > 0.05) in either of the groups. The statistical power of the study to show a clinically relevant difference in bronchial responsiveness to IHCA after treatment was near 80%. We conclude that there were no significant effects of traditional Chinese Acupuncture on airway status in our patients with asthma.

Acupuncture Therapy↗
PubMed2005

Effects of montelukast on airway narrowing from eucapnic voluntary hyperventilation and cold air exercise.

BACKGROUND: Exercise induced bronchoconstriction (EIB) is common in elite athletes. Eucapnic voluntary hyperventilation (EVH) is a laboratory test recommended for the identification of EIB in athletes, secondary to a field exercise challenge. Montelukast attenuates EIB, but its protective effect against airway narrowing from EVH has not been investigated. OBJECTIVE: To examine the effectiveness of montelukast after exercise and after EVH. METHODS: A randomised, placebo controlled, double blind, crossover study was performed with 11 physically active EIB positive subjects (eight men, three women; mean (SD) age 22.8 (6.8) years). Six hours before each of the following challenges 10 mg montelukast or placebo was ingested: (a) a six minute, cold air (-3 degrees C) maximal effort work accumulation cycle ergometer exercise; (b) EVH, breathing 5% CO(2) compressed air at 85% maximal voluntary ventilation for six minutes. Spirometry was performed before and 5, 10, and 15 minutes after the challenge. At least 48 hours was observed between challenges. RESULTS: No differences in forced expiratory volume in one second (FEV(1)) were found after the two challenges. Exercise and EVH resulted in falls in FEV(1) of 22.4 (18.0) and 25.6 (16.8) respectively. Falls in FEV(1) after montelukast were less than after placebo (10.6 (10.6) and 14.3 (11.3) after exercise and EVH respectively; p<0.05). Montelukast provided protection against bronchoconstriction (59% and 53%; p<0.05) for eight exercising subjects and 10 EVH subjects; no protection was afforded for three exercising and one EVH challenged subject. CONCLUSIONS: Both exercise and EVH were potent stimuli of airway narrowing. A single dose of montelukast provided reasonable protection in attenuating bronchoconstriction from either exercise or EVH. The similar protection by montelukast suggests that EVH is a suitable laboratory surrogate for EIB evaluation.

Acetates↗
PubMed1971

Mechanism of hyperventilation in acute cerebrovascular accidents.

Lumbar cerebrospinal fluid and arterial blood acid-base state were assessed in 19 patients within 24 hours of an acute cerebrovascular accident. Those with haemorrhage into the C.S.F. showed a lower C.S.F. pH and higher C.S.F. lactate than those without haemorrhage but the Pco(2), was similar in the two groups, suggesting that this greater C.S.F. acidity was not responsible for a greater degree of hyperventilation. In those without haemorrhage an inverse relation was found between C.S.F. pH and arterial Pco(2), suggesting that a non-chemical ventilatory drive-for example, due to central neurological damage-was responsible for the acid-base changes observed.

Acidosis↗
PubMed2000

Hyperventilation: cause or effect?

A young person presenting with shortness of breath is common to the accident and emergency department. Usually this hyperventilation is anxiety related or a panic attack, but sometimes it can be caused by a serious underlying condition like pulmonary embolus. Acute shortness of breath in any patient should never be dismissed lightly. It is important to realise that pulmonary embolus can present without chest pain and with shortness of breath as the major symptom. Such patients can be distinguished by close attention to history and examination, risk factors for thromboembolic disease and the use of basic investigations (electrocardiogram, chest radiography and arterial blood gas analysis). A serious cause for shortness of breath must be excluded before labelling it as "hysteria" or "panic".

Acute Disease↗
PubMed2003

Attenuation of hypercapnic carbon dioxide chemosensitivity after postinfarction exercise training: possible contribution to the improvement in exercise hyperventilation.

OBJECTIVE: To elucidate the responsible mechanisms of increased slope of minute ventilation relative to carbon dioxide production (VE/VCO(2)) during exercise after acute myocardial infarction without overt signs of heart failure, patients who had an acute myocardial infarction were examined after participating in a three month supervised exercise training programme. DESIGN: Exercise testing, hypercapnic CO(2) chemosensitivity measurement (rebreathing method), and pulmonary function test were repeated at entry and after three months in 50 acute myocardial infarction patients with neither symptoms nor signs of heart failure who completed the training programme. Ten patients who performed initial inhospital training served as controls. RESULTS: Age, peak oxygen uptake, left ventricular ejection fraction, CO(2) chemosensitivity, respiratory parameters (percentage of predicted normal vital capacity (%VC), forced expiratory volume in one second, and carbon monoxide transfer factor (%TLCO)) were all significantly correlated with VE/VCO(2) slope. Multivariate regression analysis showed that age (beta = 0.29, p = 0.01), %TLCO (beta = -0.27, p = 0.01), and CO(2) chemosensitivity (beta = 0.49, p < 0.001) were independent determinants of VE/VCO(2) slope. After three months, there was no significant change in these parameters in the control group. Peak oxygen uptake, %TLCO, and %VC and attenuation in CO(2) chemosensitivity increased significantly in the training group. The VE/VCO(2) slope decreased marginally (p = 0.11). The changes in VE/VCO(2) slope were correlated only with those in CO(2) chemosensitivity (r = 0.50, p < 0.001). CONCLUSION: After acute myocardial infarction, exercise hyperventilation is seen in association with aging, enhanced hypercapnic CO(2) chemosensitivity, and reduced TLCO, even in the absence of overt heart failure. The correlation of VE/VCO(2) attenuation after training with the reduction in CO(2) chemosensitivity suggests that exercise training may reduce increased VE/VCO(2) slope, at least partially by reducing CO(2) chemosensitivity.

Breath Tests↗
PubMed1988

Possible role of coronary spasm in acute myocardial infarction precipitated by hyperventilation.

Acute myocardial infarction was precipitated by hyperventilation in a 65 year old man. His coronary arteriogram in the chronic phase showed almost normal coronary arteries. Injection of acetylcholine (50 micrograms) into the left coronary artery induced spasm of the circumflex artery with chest pain in association with ST-segment elevation in the inferior leads and ST-segment depression in the precordial leads. In this patient there may have been atherosclerosis of the coronary arteries with absent or dysfunctional endothelium, despite an almost normal angiographic appearance. In the absence of endothelium the response of the smooth muscle to acetylcholine is constriction.

Acetylcholine↗
PubMed1974

Post-hyperventilation apnoea in patients with brain damage.

A study of 100 subjects has confirmed that brief voluntary hyperventilation commonly causes apnoea in patients with supramedullary lesions, but not in healthy people. Apnoea was related to drowsiness rather than to the extent of the lesion; it was unrelated to the measured reduction in end-tidal carbon dioxide tension.

Adolescent↗
PubMed1988

Abolition of methacholine induced bronchoconstriction by the hyperventilation of exercise or volition.

Total pulmonary resistance was measured from continuous records of flow and oesophageal pressure in five normal subjects on three separate days before and after inhalation of methacholine. The dose of methacholine produced, on average, a fivefold increase in airway resistance. Immediately after methacholine inhalation the subjects underwent a progressive exercise test on a cycle ergometer (day 1) or voluntary hyperventilation (day 2) or remained resting (day 3). On the first day during exercise pulmonary resistance fell rapidly to baseline levels within two to three minutes and remained there for the 10 minute duration of the exercise. On day 2 voluntary reproduction of the same level and pattern of ventilation as during exercise resulted in a similar fall of resistance. On the third day, when the subjects remained at rest, pulmonary resistance remained raised for 10 minutes. It is concluded that the bronchodilator effects of exercise can be explained by the increased ventilation rather than the exercise itself, but with much smaller tidal volumes than have previously been thought necessary to reduce drug induced bronchoconstriction.

Adult↗
PubMed1994

Excitability of human motor cortex during hyperventilation and hypercapnia.

We tested the hypothesis that the excitability of corticospinal neurons was altered by changes in PCO2. Magnetic stimulation was used to excite the neurons in the human motor cortex that give rise to the fast-conducting corticospinal pathway. The characteristics of the composite excitatory postsynaptic potentials (EPSPs) produced in individual spinal motoneurons by cortical stimulation were derived from changes in the firing probability of voluntarily activated motor units. The amplitudes of these composite EPSPs in response to a constant cortical stimulus were assumed to reflect the excitability of cortical neurons. In 10 healthy subjects, we found no statistically significant changes in the excitability of the cortical neurons during normocapnic conditions (mean end-tidal PCO2 5.1 kPa), during hyperventilation-induced hypocapnia (mean end-tidal PCO2 2.9 kPa), and during hyperoxic hypercapnia induced by a rebreathing technique (mean end-tidal PCO2 6.9 kPa). We conclude that the excitability of corticospinal neurons activated by magnetic stimulation is not significantly affected by changes in PCO2.

Adult↗
PubMed2006

Postural hypocapnic hyperventilation is associated with enhanced peripheral vasoconstriction in postural tachycardia syndrome with normal supine blood flow.

Previous investigations have demonstrated a subset of postural tachycardia syndrome (POTS) patients characterized by normal peripheral resistance and blood volume while supine but thoracic hypovolemia and splanchnic blood pooling while upright secondary to splanchnic hyperemia. Such "normal-flow" POTS patients often demonstrate hypocapnia during orthostatic stress. We studied 20 POTS patients (14-23 yr of age) and compared them with 10 comparably aged healthy volunteers. We measured changes in heart rate, blood pressure, heart rate and blood pressure variability, arm and leg strain-gauge occlusion plethysmography, respiratory impedance plethysmography calibrated against pneumotachography, end-tidal partial pressure of carbon dioxide (Pet(CO2)), and impedance plethysmographic indexes of blood volume and blood flow within the thoracic, splanchnic, pelvic (upper leg), and lower leg regional circulations while supine and during upright tilt to 70 degrees. Ten POTS patients demonstrated significant hyperventilation and hypocapnia (POTS(HC)) while 10 were normocapnic with minimal increase in postural ventilation, comparable to control. While relative splanchnic hypervolemia and hyperemia occurred in both POTS groups compared with controls, marked enhancement in peripheral vasoconstriction occurred only in POTS(HC) and was related to thoracic blood flow. Variability indexes suggested enhanced sympathetic activation in POTS(HC) compared with other subjects. The data suggest enhanced cardiac and peripheral sympathetic excitation in POTS(HC).

Adolescent↗
PubMed1982

Maternal hyperventilation helps preserve arterial oxygenation during high-altitude pregnancy.

We examined arterial oxygenation during pregnancy and 3 mo postpartum in 35 nonsmoking residents of Leadville, CO (elevation 3,100 m) to determine how well and by what mechanisms maternal arterial oxygenation was maintained during pregnancy at high altitude. Hyperventilation raised arterial O2 saturation above that in the nonpregnant state. Respiratory alkalosis persisted throughout pregnancy, shifting the O2-hemoglobin dissociation curve to the left, further facilitating O2 loading in the lung. However, a decrease in blood hemoglobin concentration and a slight increase in the alveolar-arterial O2 gradient in the late pregnancy caused the arterial O2 content to fall below that in the nonpregnant state. Compared to published sea level values, the Leadville women had higher ventilation and hemoglobin values, yielding arterial O2 contents as high as in pregnant women at sea level. Thus, ventilation and hemoglobin concentration were important variables contributing to O2 ttransport during pregnancy at high altitude.

Adult↗
PubMed1983

Effect of beta-adrenergic blockade on hyperventilation and exercise tolerance in emphysema.

Ventilation, heart rate, and arterial blood gas tensions were measured at rest and during incremental exercise in 10 patients with emphysema after intravenous placebo or 7 mg metoprolol. Metoprolol reduced heart rate by 14% (P less than 0.001) and ventilation by 11% (P less than 0.01), but there was no significant difference in arterial O2 or CO2 tension (Pao2 and PaCO2, respectively). Metoprolol increased the time to exhaustion on a cycle ergometer (P less than 0.05) but did not improve the 12-min walking distance. A double-blind randomized crossover comparison of 4 wk treatment with atenolol (100 mg/day), metoprolol (100 mg/day), or matched placebo was performed in 12 patients with emphysema. Both beta-adrenoceptor antagonists reduced resting heart rate by 33% (P less than 0.001) and resting minute ventilation by 11% (P less than 0.025). There was no change in resting or exercise Pao2 or Paco2. During steady-state exercise on a cycle ergometer, atenolol and metoprolol reduced ventilation by 14 and 4%, respectively. This was accompanied by 11 and 5% reductions in O2 consumption (P less than 0.05) and 13 and 6% falls in CO2 production (P less than 0.05). There were no significant changes in tests of exercise tolerance, but forced expiratory volume in 1 s and forced vital capacity were reduced during beta 1-adrenergic blockade. beta 1-Blocking drugs reduce hyperventilation in emphysema by reducing pulmonary gas exchange without a change in arterial blood gas tensions. Increased airflow obstruction prevents this reduction being of therapeutic value.

Administration, Oral↗
PubMed1983

Hyperventilation in ponies at the onset of and during steady-state exercise.

We studied blood gases in ponies to assess the relationship of alveolar ventilation (VA) to pulmonary CO2 delivery during moderate treadmill exercise. In normal ponies for 1.8, 3, or 6 mph, respectively, partial pressure of CO2 in arterial blood (PaCO2) decreased maximally by 3.1, 4.4, and 5.7 Torr at 30-90 s of exercise and remained below rest by 1.4, 2.3, and 4.5 Torr during steady-state (4-8 min) exercise (P less than 0.01). Partial pressure of O2 in arterial blood (PaO2) and arterial pH, (pHa) also reflected hyperventilation. Mixed venus CO2 partial pressure (PVCO2) decreased 2.3 and 2.9 Torr by 30 s for 3 and 6 mph, respectively (P less than 0.05). In work transitions either from 1.8 to 6 mph or from 6 mph to 1.8 mph, respectively, PaCO2 either decreased 3.8 Torr or increased 3.3 Torr by 45 s of the second work load (P less than 0.01). During exercise in acute (2-4 wk) carotid body denervated (CBD) ponies at 1.8, 3, or 6 mph, respectively, PaCO2 decreased maximally below rest by 9.0, 7.6, and 13.2 Torr at 30-45 s of exercise and remained below rest by 1.3, 2.3, and 7.8 Torr during steady-state (4-8 min) exercise (P less than 0.1). In the chronic (1-2 yr) CBD ponies, the hypocapnia was generally greater than normal but less than in the acute CBD ponies. We conclude that in the pony 1) VA is not tightly matched to pulmonary CO2 delivery during exercise, particularly during transitional states, 2) the exercise hyperpnea is not mediated by PaCO2 or PVCO2, and 3) during transitional states in the normal pony, the carotid bodies attenuate VA drive thereby reducing arterial hypocapnia.

Animals↗
PubMed1986

Plasma volume and proteins in voluntary hyperventilation.

In a controlled study the changes of the plasma volume and plasma proteins induced by voluntary hyperventilation (HV) were investigated in nine splenectomized volunteers. The plasma volume changes were calculated from the changes of the hemoglobin and hematocrit. After 20 min of HV in supine position, which lead to a decrease of the venous CO2 partial pressure by 19 Torr and to an increase of plasma epinephrine and norepinephrine levels, the plasma volume was reduced by 12.9%. The intravascular masses of total protein, albumin, and several other proteins decreased during HV but a similar decrease of these proteins was also observed during the control study (C), i.e., rest in supine position without HV. The differences between changes during HV and C were not significant, indicating that the loss of protein was not due to HV. It is concluded that acute HV leads to a rapidly reversible loss of a virtually protein-free solution from the vascular space. The red cell compartment participated in fluid shifts in that the mean red cell volume decreased by 2.2% (P less than 0.02 compared with C). Comparison with earlier work shows that addition of erythrocytes from the normal spleen does not play a part in the HV-induced increase of hemoglobin and hematocrit.

Adolescent↗
PubMed1990

Sensation of dyspnea during hypercapnia, exercise, and voluntary hyperventilation.

To determine whether the intensity of dyspnea at a given level of respiratory motor output depends on the nature of the stimulus to ventilation, we compared the sensation of difficulty in breathing during progressive hypercapnia (HC) induced by rebreathing, during incremental exercise (E) on a cycle ergometer, and during isocapnic voluntary hyperventilation (IVH) in 16 normal subjects. The sensation of difficulty in breathing was rated at 30-s intervals by use of a visual analog scale. There were no differences in the level of ventilation or the base-line intensity of dyspnea before any of the interventions. The intensity of dyspnea grew linearly with increases in ventilation during HC [r = 0.98 +/- 0.02 (SD)], E (0.95 +/- 0.03), and IVH (0.95 +/- 0.06). The change in intensity of dyspnea produced by a given change in ventilation was significantly greater during HC [0.27 +/- 0.04 (SE)] than during E (0.12 +/- 0.02, P less than 0.01) and during HC (0.30 +/- 0.04) than during IVH (0.16 +/- 0.03, P less than 0.01). The difference in intensity of dyspnea between HC and E or HC and IVH increased as the difference in end-tidal PCO2 widened, even though the time course of the increase in ventilation was similar. No significant differences were measured in the intensity of dyspnea that occurred with changes in ventilation between E and IVH. These results indicate that under nearisocapnic conditions the sensation of dyspnea produced by a given level of ventilation seems not to depend on the method used to produce that level of ventilation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Comparison of effects of exercise and hyperventilation on leukocyte kinetics in humans.

The circulating leukocyte (WBC) count increases with exercise, because WBCs enter the circulation from the marginated pool. The lung is a major source of the demarginating cells, but it is unclear whether this occurs because of increased ventilatory movements, increased cardiac output, or both. The present study examined the mechanical effect of ventilation (VE) in six healthy men with three different protocols on three separate occasions. First, the subjects cycled for 5-min intervals at 50, 100, 150, and 200 W, and we measured heart rate (HR), minute ventilation (VE), tidal volume (VT), respiratory rate, and end-tidal CO2. Second, each subject reproduced his exercise VE by matching VT, respiratory rate, and end-tidal CO2 on a circuit designed for isocapnic hyperpnea (matched VE). The subjects then performed a hyperventilation (hyper-VE) protocol with a minimum VT of 1.5 liters and a respiratory rate of 20 breaths/min. Blood samples were drawn at rest and throughout each protocol for measurement of WBCs, hematocrit, and band cells. During cycling, VE increased (9 +/- 1 to 66 +/- 7 l/min), HR increased (71 +/- 7 to 172 +/- 10 beats/min), and WBCs increased (5.5 +/- 0.9 to 7.8 +/- 1.3 x 10(9)/l). During matched VE, VE increased (11 +/- 2 to 69 +/- 11 l/min), but neither HR nor WBCs increased (67 +/- 13 to 78 +/- 12 beats/min and 5.3 +/- 1.6 to 5.7 +/- 1.5 x 10(9)/l, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Effects of nasal positive-pressure hyperventilation on the glottis in normal sleeping subjects.

We have previously observed that, in normal awake subjects passively hyperventilated with intermittent positive-pressure ventilation delivered through nasal access (nIPPV), the glottis could interfere with the ventilation. We report on data obtained in the same subjects during stable sleep. In all cases, the glottis was continuously observed through a fiber-optic bronchoscope, and other indexes were also continuously recorded. Mechanical ventilation was progressively increased up to 30 l/min. We have observed during passive nIPPV in stable sleep that increases in delivered minute ventilation (VEd) resulted in progressive narrowing of the glottic aperture, with increases in inspiratory resistance and progressive reductions in the percentage of the delivered tidal volume effectively reaching the lungs. For a given level of VEd, comparisons showed that the glottis was significantly narrower during sleep than during wakefulness and that the glottis was significantly narrower during stage 2 than during stages 3/4 non-rapid-eye-movement sleep. Moreover, when CO2 is added to the inspired air, glottic aperture increased in five of nine trials without changes in sleep stage. We also observed a significant negative correlation between glottic width and the VED, independent of the CO2 level. We conclude that during nIPPV glottis narrowing results in a decrease in the proportion of the delivered tidal volume reaching the lungs.

Adult↗