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PubMedDate not supplied

Hyperventilation, anxiety sensitivity, and the expectations for alcohol use: subjective and physiological reactivity to alcohol cues.

The present study examined the relation between alcohol-related expectancies, body sensation fear and reactions to cues for alcohol following a hyperventilation task. Forty-two undergraduate students participated for course credit. Each student hyperventilated for 5 min, paced at a rate of 30 breaths per minute. Following hyperventilation, each student was exposed to containers with alcohol (beer and wine coolers), with subjective urge to consume and heart rate measures taken. Path analysis supported models associated with tension reduction and self-focused attention expectancies as significant contributors to increased urge to consume alcohol and lowered heart rate following hyperventilation. However, social-anxiety-related expectancies failed to demonstrate a relationship. These results suggest that additional work on the tension reduction model of alcohol use should examine physiological stressors in association with subject characteristics such as proneness to experience panic symptoms.

Adolescent↗
PubMed1987

The standardization of hyperventilation on EEG recording in childhood. II. The quantitative analysis of build-up.

In thirty-seven children free of neurological symptoms, we attempted the quantitative analysis of EEG slowing during standarized hyperventilation activation, respiration rate of 30/min, a three-fold elevation of VE and duration of 4 minutes. The degree of build-up gradually became mild with increasing age and no build-up was observed in the subjects older than 14 years old. Fast Fourier Transform analysis of the build-up showed that a big build-up was due to both increasing delta and theta power, and markedly decreasing alpha power with markedly increasing total power, and the mild build-up was due predominantly to increasing theta power. These changes disappeared, the levels before the activation being attained again, within one minute after the hyperventilation in almost all subjects. As to age differences in EEG slowing during hyperventilation, an increase in both delta and theta activity was observed in the younger subjects (6-9 years old), and a mild increase in theta activity was predominantly observed in adolescents. On topographic analysis of EEG slowing, the delta power was found to have expanded to the posterior area and the theta power to have expanded to become diffuse. The standardization of hyperventilation in childhood is important for judgement of the build up because of these age differences, and also may be useful for understanding the development of the central nervous system.

Adolescent↗
PubMedDate not supplied

The utility of the ASI factors in predicting response to voluntary hyperventilation among nonclinical participants.

Empirical research has demonstrated that the Anxiety Sensitivity Index (ASI) contains three separable factors and that ASI total scores are useful in predicting response to physiological challenge procedures. Little is known, however, of the predictive capability of the ASI factors. This study investigated the utility of the three factors of the ASI compared to ASI total scores and the STAI-T, a more general measure of trait anxiety, in predicting response to hyperventilation. As expected, the ASI total score was a significant predictor of response to hyperventilation, while the STAI-T was not. Using multiple regression, when the physical concerns factor was entered first, the social concerns and mental incapacitation factors of the ASI were not significant predictors of response to hyperventilation. Furthermore, when the physical concerns factor was entered into a regression equation followed by the remainder of the ASI items, only the physical concerns factor remained a significant predictor of response to hyperventilation. These results suggest that while response to physiological challenge procedures is predicted by ASI total scores, it may be best predicted by the physical concerns factor, and that the mental incapacitation and social concerns subscales do not play key roles in predicting response to physiological challenge procedures.

Adult↗
PubMedDate not supplied

Relationships between anxiety sensitivity, hyperventilation, and emotional reactivity to displays of facial emotions.

Undergraduate women who scored in the top (n = 24) and bottom 15% (n = 24) on the Anxiety Sensitivity Index viewed randomly counterbalanced sets of three neutral and three dysphoric faces after having either hyperventilated or relaxed. Participants rated the amount of change they experienced in Happiness, Sadness, Fear, Anger, Surprise, Disgust, and Contempt after viewing each face. High Anxiety Sensitive (AS) women reported significantly greater changes on six of the seven emotions, even though pretreatment differences in somatically experienced anxiety were covaried out. Significant three-way interactions were found for participants self-rated changes in Fear and Surprise, with tendencies toward significance (p < .10) also emerging for Anger and Disgust. The pattern of interactions was identical for all four variables. Low AS women manifested greater reductions in these four emotions when viewing neutral as opposed to dysphoric faces, regardless of whether they hyperventilated or relaxed. High AS women who relaxed manifested similar discriminative abilities. High AS women who hyperventilated, however, reported no relative changes in emotional arousal to both dysphoric and neutral faces. The blunted discrimination shown by high AS women who hyperventilated suggests that, when these individuals are in a physiologically challenged state, they may be less responsive to "early warning" indicators of social distress displayed by others which may, in turn, cause them to experience subsequent interpersonal difficulties.

Adult↗
PubMed1998

Effects of hyperventilation and hypoventilation on PaCO2 and intracranial pressure during acute elevations of intraabdominal pressure with CO2 pneumoperitoneum: large animal observations.

BACKGROUND: The side effects of acute elevations in intraabdominal pressure (IAP) are related to a multifactorial etiology. Previous studies have reported that acute elevations in IAP produce an immediate increase in intracranial pressure (ICP). This study was designed to analyze the reasons for increased ICP during acute elevations of IAP and to determine the combined effects of IAP and changes in ventilation indices on ICP and hemodynamic indices. STUDY DESIGN: Five pigs were studied. A subarachnoid screw was placed for ICP monitoring. The jugular vein, femoral vein, and femoral artery were cannulated. Mean arterial pressure (MAP), central venous pressure (CVP), ICP, and arterial pressure of carbon dioxide (PaCO2) were monitored before and after carbon dioxide pneumoperitoneum was established at 0, 10, and 20 mmHg of IAP Effects of hyperventilation and hypoventilation were recorded and compared with baseline ventilation. Cavography was performed to evaluate the morphology of the inferior vena cava (IVC) at different levels of IAP. Multiple regression and Student's t-test were used to examine the effects of IAP and ventilation on dependent variables. RESULTS: The IVC showed a progressive narrowing at the level of the diaphragm as IAP was increased. There was a simultaneous increase in CVP, MAP, and ICP. The mean changes in ICP with hypoventilation were significantly larger than with hyperventilation. CONCLUSIONS: Acutely increased IAP displaces the diaphragm cranially, narrowing the IVC and increasing intrathoracic pressure. This increases CVP and increases ICP by venous stasis and increased pressure in the sagittal sinus with decreased resorption of cerebrospinal fluid. Hemodynamic changes are directly related to the rise in ICP. Hypoventilation and hypercarbia significantly increase ICP when compared with hyperventilation and hypocarbia. Hyperventilation does not significantly decrease ICP during acute elevations of IAP.

Abdomen↗
PubMed1999

Splanchnic circulation is maintained during passive hyperventilation in orthotopic liver recipients.

BACKGROUND: Mechanical hyperventilation is an established treatment to reduce brain edema and intracranial pressure in patients with encephalopathia caused by acute liver failure. Hyperventilation and ensuing hypocarbia may also affect central and systemic circulation and thereby influence graft performance in patients following orthotopic liver transplantation (OLT). METHODS: We measured the effects of normocapnia and hypocapnia on systemic hemodynamics, gastric tonometry, as a marker of splanchnic oxygenation, and the indocyanine green kinetic, as a global marker of graft function, in humans post OLT. RESULTS: Hyperventilation was performed to a PaCO2 of 4.2 +/- 0.4 kPa (31 +/- 3.4 mm Hg) for about 1 h in 14 liver transplant recipients. Systemic hemodynamics as well as indices of splanchnic oxygenation and indocyanine green kinetics remained statistically unchanged. CONCLUSION: We did not observe any statistically significant circulatory effects or changes in indocyanine green kinetics in liver transplant recipients in the immediate OLT postoperative period caused by short-term mechanical hyperventilation.

Blood Pressure↗
PubMed1981

Venous plasma histamine in exercise- and hyperventilation-induced asthma in man.

1. Venous plasma histamine was measured by a specific and sensitive radioenzymatic assay in seven male extrinsic asthmatic and six age-matched non-atopic non-asthmatic male subjects during exercise and voluntary isocapnic hyperventilation. 2. There was no change in peak expiratory flow in normal subjects with exercise or hyperventilation, but asthmatic subjects showed a 29.4 +/- SEM 5.8% fall after exercise and a 29.0 +/- 5.4% fall after matched hyperventilation. 3. Plasma histamine was significantly higher (P less than 0.05) in asthmatic (6.2 +/- 0.95 nmol/l) than that in normal subjects (3.4 +/- 0.61 mol/l) and showed a significant (P less than 0.01) rise (to 14.4 +/- 1.83 nmol/l) during exercise in asthmatic, but not in normal subjects. This suggests that discharge of mast-cell mediators may occur during exercise in asthmatic subjects who develop exercise-induced asthma. 4. With hyperventilation there was no change in plasma histamine in either asthmatic or normal subjects, but this does not exclude the possibility that mediators may be released locally in the airways.

Adolescent↗
PubMed1996

Plasma ionized magnesium during acute hyperventilation in humans.

1. Respiratory alkalosis accompanies the clinical syndrome of tetany, precipitates cardiac arrhythmias and predisposes to coronary vasoconstriction. Magnesium plays a critical role in the maintenance of membrane function, and magnesium depletion is often associated with cardiac arrhythmias or vasoconstriction. 2. As technology for detecting circulating ionized magnesium (the most interesting form with respect to physiological and biological properties) is now available in the form of new magnesium-selective electrodes, the effect of respiratory alkalosis induced by voluntary overbreathing for 30 min on circulating ionized magnesium was studied in eight healthy subjects. 3. The total plasma magnesium concentration was not modified by hyperventilation. On the contrary, hyperventilation was associated with a significant reduction in the ionized magnesium concentration of 0.05 (0.02-0.15) mmol/l (median and range) and in the free magnesium fraction of 0.06 (0.01-0.19). During hyperventilation the relative intravascular magnesium mass, calculated from changes in total plasma magnesium concentration and haematocrit, decreased significantly. 4. It is concluded that acute overbreathing reduces the circulating ionized magnesium concentration and the intravascular magnesium mass. It is therefore conceivable that extracellular magnesium deficiency is at least a subsidiary cause of the syndrome of tetany and the cardiac complications that are precipitated by hyperventilation.

Acute Disease↗
PubMed1986

Human growth hormone, cortisol, and acid-base balance changes after hyperventilation and breath-holding.

The purpose of this study was to investigate the effects of hyperventilation and breath-holding on hormonal activity and the acid-base balance in men. Three different experimental procedures were carried out with 11 trained subjects aged 24.5 years. In experiment I, all subjects performed hyperventilation for 3 min maintaining a paced ventilation of 47 l X min-1. In experiment II, they performed a threefold maximal voluntary breath-holding, separated by 1-min periods of normal breathing. Experiment III consisted of a combination of hyperventilation immediately followed by maximal voluntary breath-holding. Capillary blood samples were taken for determination of pO2, pCO2, and pH. Venous blood samples were drawn before and at the 5th and 30th min after the cessation of the applied procedure for RIA determination of human growth hormone (HGH) and cortisol. During the last 15 s of hyperventilation, pO2 increased to 89.4 +/- 16.2 mm Hg, pCO2 decreased to 19.6 +/- 1.6 mm Hg, and pH increased to 7.652 +/- 0.041. During the last 15 s of the third breath-holding, the results were pO2 = 58.0 +/- 5.1, pCO2 = 45.7 +/- 3.7, and pH = 7.367 +/- 0.053. In experiment III, the mean values were pO2 = 42.6 +/- 7.9 mmHg, pCO2 = 39.2 +/- 4.6 mmHg, and pH = 7.320 +/- 0.024. A significant hormonal response after the applied experimental procedures was found for HGH (1.5- to 5.56-fold increase) and cortisol (1.5- to 2.2-fold increase).(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1983

Hyperventilation syndrome: a review.

This article has dealt with the psychophysiological phenomenon known as "hyperventilation syndrome." Published research on this syndrome dates back at least a century to Da Costa's classic investigation involving "soldier's heart". Various labels such as "effort syndrome," "anxiety neurosis," "neurocirculatory asthenia," "vasoregulatory asthenia," and "irritable heart," have been employed over the past century to describe this syndrome. The use of different labels to describe this syndrome seems to be inappropriate. While the symptoms associated with these diagnostic labels appear to be remarkably similar, the treatment for the syndrome often differs as a function of the diagnostic label. Symptoms include breathlessness or dyspnea with effort, parathesia, trembling, tachycardia, tetany, carpopedal spasms, and convulsions in the case of a full-blown attack. Hyperventilation, a normal consequence of vigorous exercise and/or high temperatures, can often occur in some individuals for no apparent reason. Hyperventilation, and the resulting physiological changes, are often associated with decrements in psychomotor performance along with increased error rates. The symptoms which characterize the hyperventilation syndrome can be readily produced in certain "types" of individuals within minutes by requiring the individual to overbreathe or through introduction of a CO2 challenge. The symptoms, once produced, can be quickly reversed by placing a paper sack over the subject's head and requiring him/her to rebreathe expired air. Overbreathing and CO2 challenges do not, however, produce full-blown hyperventilatory attacks in most individuals. That is, some individuals or "types" appear to be especially sensitive to the effects of overbreathing and/or CO2 loading.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Nitrous oxide sedation causes post-hyperventilation apnoea.

We have studied, in six normal subjects, the effect of nitrous oxide sedation on the ventilatory pattern and oxygen saturation using pulse oximetry (SpO2) after hyperventilation to an end-tidal carbon dioxide partial pressure (PE'CO2) of 3 kPa. This value of PE'CO2 was shown to be less than the apnoeic threshold of all these subjects when their ventilation vs PE'CO2 response curves were plotted. All subjects became apnoeic when told to relax following hyperventilation while breathing 75% nitrous oxide for 90 s. Apnoea was defined as cessation of breathing for 20 s or more. The mean duration of apnoea was 78 s (range 29-130 s). All subjects demonstrated arterial desaturation (mean SpO2 75%, range 44-87%). In contrast, following hyperventilation with air, no apnoea was seen in any subject, although there was some evidence of desaturation (mean SpO2 92.5%, range 88-98%). It was concluded that subjects who are sedated with nitrous oxide behave similarly to those who are anaesthetized rather than to those who were fully conscious, in that they become apnoeic below the apnoeic threshold point. The reduction in SpO2 after hyperventilation was explained almost entirely by apnoea and may explain abnormalities of respiratory control and hypoxaemia in patients recovering from general anaesthesia or sedation accompanied by hypocapnia. This mechanism may be of importance in obstetric patients after breathing Entonox, when apnoea and hypoxaemia may reduce oxygen delivery to the fetus.

Adult↗
PubMed1994

Effects of hyperventilation on the inspiratory to end-tidal oxygen difference.

We assessed the inspiratory to end-tidal oxygen difference (PIO2-PE'O2) during voluntary hyperventilation in 10 healthy male volunteers. The oxygen difference was measured with a fast-response paramagnetic differential oxygen sensor. As simultaneous changes in metabolism and cardiac output also influence (PIO2-PE'O2), oxygen uptake was measured with indirect calorimetry and non-invasive transthoracic electrical bioimpedance was used for measurement of cardiac output. After a rest period, subjects were instructed to double their minute ventilation volume (VE) and after 5 min triple their resting VE for another 5 min. (PIO2-PE'O2) decreased from a zero value of 6.4 kPa to 3.9 kPa at 5 min (P < 0.01) and 2.9 kPa at 10 min (P < 0.01). At 15 min (i.e. 5 min after the end of hyperventilation) there was an increase in (PIO2-PE'O2) to 8.3 kPa (P < 0.05). Regression analysis between (PIO2-PE'O2) (kPa) and VE (litre m-2 min-1) gave the formula: (PIO2-PE'O2) = 1/(0.059 + 0.034 VE), r = -0.92, n = 158. Oxygen uptake and cardiac output did not change significantly during hyperventilation, but decreased in the post-hyperventilation period. An oxygen difference of more than 8 kPa was associated with significant arterial desaturation.

Adult↗
PubMed1997

The capnography-tilt test for the diagnosis of hyperventilation syncope.

We describe the capnography tilt test (CTT) for the diagnosis of hyperventilation syncope. The CTT is a 10-min supine, 30-min head-up tilt test with simultaneous monitoring of end-tidal PCO2 (ETPCO2). Hyperventilation (HV) was defined as ETPCO2 < or = 25 mmHg. Hyperventilation syncope (HV syncope) was defined as loss of consciousness with ETPCO2 < or = 25 mmHg and no significant drop in blood pressure. Four groups of patients had the CTT: group I (n = 14), patients presenting with syncope who during a prior tilt test had lost consciousness without concomitant fall in blood pressure; group II (n = 50), syncope, primary evaluation, no prior tilt test done; group III (n = 20), generalized anxiety disorder, no syncope; group IV (n = 80), arterial hypertension, no syncope. Hyperventilation was found in 11/14 patients in group I, 5/50 in group II, 7/20 in group III, and none in group IV; HV syncope was diagnosed in seven patients, all in group I. None of the parameters measured in the evaluation, including ETPCO2, predicted HV syncope on tilting. The mechanisms of resting HV and HV during tilt are not well understood. We confirm the existence of HV syncope. The tilt test should probably be used to screen patients presenting with syncope, with the CTT reserved for patients who lose consciousness during the tilt test without an associated fall in blood pressure, as HV is not always clinically obvious.

Adolescent↗
PubMed1991

The response of the canine cerebral circulation to hyperventilation during anesthesia with desflurane.

Arterial CO2 tension (PaCO2) is an important factor controlling cerebral blood flow (CBF) and cerebral vascular resistance (CVR) in animals and humans. The normal responsiveness of the cerebral vasculature to PaCO2 is approximately 2 ml.min-1.100 g-1.mmHg-1. This study examined the effect of desflurane, a new volatile anesthetic, on the responsiveness of the cerebral vasculature to changes in PaCO2. Mean arterial pressure (MAP), CBF, CVR, intracranial pressure (ICP), and cerebral metabolic rate for O2 (CMRO2) were measured in five dogs anesthetized with desflurane (0.5-1.5 MAC) at normocapnia (PaCO2 = 40 mmHg) and at two levels of hypocapnia (PaCO2 = approximately 30 and approximately 20 mmHg). Under desflurane anesthesia, similar changes in CBF and CVR occurred with hyperventilation at all MAC levels of desflurane. At 0.5 MAC, CBF decreased significantly, from 81 +/- 6 to 40 +/- 3 ml.min-1.100 g-1 (P less than 0.05, mean +/- SE) when PaCO2 was decreased from 40 to 24 mmHg; i.e., the CBF decreased approximately 2.6 ml.min-1.100 g-1.mmHg-1. At 1.0 MAC desflurane, CBF decreased significantly, from 79 +/- 10 to 43 +/- 5 ml.min-1.100 g-1 with hyperventilation (2.0 ml.min-1.100 g-1.mmHg-1); at 1.5 MAC desflurane, CBF decreased from 65 +/- 6 to 38 +/- 2 ml.min-1.100 g-1 with hyperventilation (1.6 ml.min-1.100 g-1.mmHg-1). Despite the significant decreases in CBF with hyperventilation, there was no significant change in ICP. Dose-dependent decreases in MAP were observed with increasing concentrations of desflurane but were not significantly affected by ventilation.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗
PubMed2004

Death by hyperventilation: a common and life-threatening problem during cardiopulmonary resuscitation.

CONTEXT: This translational research initiative focused on the physiology of cardiopulmonary resuscitation (CPR) initiated by a clinical observation of consistent hyperventilation by professional rescuers in out-of-hospital cardiac arrest. This observation generated scientific hypotheses that could only ethically be tested in the animal laboratory. OBJECTIVE: To examine the hypothesis that excessive ventilation rates during performance of CPR by overzealous but well-trained rescue personnel causes a significant decrease in coronary perfusion pressure and an increased likelihood of death. DESIGN AND SETTING: In the in vivo human aspect of the study, we set out to objectively and electronically record rate and duration of ventilation during performance of CPR by trained professional rescue personnel in a prospective clinical trial in intubated, adult patients with out-of-hospital cardiac arrest. In the in vivo animal aspect of the study, to simulate the clinically observed hyperventilation, nine pigs in cardiac arrest were ventilated in a random order with 12, 20, or 30 breaths/min, and physiologic variables were assessed. Next, three groups of seven pigs in cardiac arrest were ventilated at 12 breaths/min with 100% oxygen, 30 breaths/min with 100% oxygen, or 30 breaths/min with 5% CO2/95% oxygen, and survival was assessed. MAIN OUTCOME MEASURES: Ventilation rate and duration in humans; mean intratracheal pressure, coronary perfusion pressure, and survival rates in animals. RESULTS: In 13 consecutive adults (average age, 63 +/- 5.8 yrs) receiving CPR (seven men) the average ventilation rate was 30 +/- 3.2 breaths/min (range, 15 to 49 breaths/min) and the average duration of each breath was 1.0 +/- 0.07 sec. The average percentage of time in which a positive pressure was recorded in the lungs was 47.3 +/- 4.3%. No patient survived. In animals treated with 12, 20, and 30 breaths/min, the mean intratracheal pressures and coronary perfusion pressures were 7.1 +/- 0.7, 11.6 +/- 0.7, 17.5 +/- 1.0 mm Hg/min (p < .0001) and 23.4 +/- 1.0, 19.5 +/- 1.8, 16.9 +/- 1.8 mm Hg (p = .03) with each of the different ventilation rates, respectively (p = comparison of 12 breaths/min vs. 30 breaths/min for mean intratracheal pressure and coronary perfusion pressure). Survival rates were six of seven, one of seven, and one of seven with 12, 30, and 30 + CO2 breaths/min, respectively (p = .006). CONCLUSIONS: Despite seemingly adequate training, professional rescuers consistently hyperventilated patients during out-of-hospital CPR. Subsequent hemodynamic and survival studies in pigs demonstrated that excessive ventilation rates significantly decreased coronary perfusion pressures and survival rates, despite supplemental CO2 to prevent hypocapnia. This translational research initiative demonstrates an inversely proportional relationship between mean intratracheal pressure and coronary perfusion pressure during CPR. Additional education of CPR providers is urgently needed to reduce these newly identified and deadly consequences of hyperventilation during CPR. These findings also have significant implications for interpretation and design of resuscitation research, CPR guidelines, education, the development of biomedical devices, emergency medical services quality assurance, and clinical practice.

Adult↗
PubMed2005

Hyperventilation at referring hospitals is common before transport in intubated children with neurological diseases.

OBJECTIVE: To assess if cardiopulmonary complications and abnormal carbon dioxide tension are more likely in intubated children with neurological diseases undergoing transport. METHODS: We reviewed the transport records of all ventilated children retrieved to a pediatric teaching hospital in the United States within a 12-month period. RESULTS: Twenty-seven children were transported by ground (n = 11), helicopter (n = 10), and fixed-wing aircraft (n = 6). Adjustments of ventilator settings were made in 17 (63%). There were no pneumothoraces, endotracheal tube complications, arrhythmias, or cardiopulmonary resuscitation en route. Twelve patients (44%) had a primary neurological condition. In the neurological category, the pretransport blood gases revealed 7 patients with hyperventilation (Pco2, 20-29 mm Hg), and the posttransport blood gases showed 4 patients with hyperventilation (Pco2, 15-28 mm Hg). In the nonneurological category, hyperventilation occurred only in one patient before and another after transport. No significant difference between the mode of transport, stabilization time, return time, and the occurrence of hypercapnia and hypocapnia was identified. Patients who had a neurological condition were more likely to be hyperventilated at the referring hospitals (P = 0.007). Additional maneuvers were considered necessary in 3 of the 6 neurological patients and 2 of the 5 nonneurological patients with DeltapH greater than +/-0.1, whereas the management of all but one patient with DeltapH less than +/-0.1 was considered appropriate (DeltapH defined as the difference between posttransport and pretransport pH values). CONCLUSION: There is no cardiopulmonary disaster in the various modes of pediatric transport. When compared with ground transport, there is no significant increase in the risk for cardiopulmonary complications or abnormal CO2 tension in air transport of intubated children. DeltapH, in conjunction with clinical data and PCO2 values, may be a simple index for evaluation of cardiopulmonary management during transport.

Adolescent↗
PubMed1981

Prinzmetal's variant angina)(PVA). Circadian variation in response to hyperventilation.

The study reports on the outcome of hyperventilation tests in a 57-year-old male with Prinzmetal's variant angina, formerly often complicated by ventricular fibrillation. It was found that hyperventilation for a period of 6 min after a delay of 4 to 6 min was followed by the development of ST-elevation and pain, but only when the test was performed in the morning, whereas the outcome of tests performed later in the day were negative. Pretreatment with calcium blockers, nifedipine or verapamil proved effective in preventing the anginal response to the test, also when it was performed in the morning. It is concluded that hyperventilation performed in the early morning, but not later in the day, may prove to be an effective and safe procedure for provoking Prinzmetal's variant angina, and that hyperventilation may be useful in the evaluation of the efficacy of drug therapy.

Angina Pectoris↗
PubMed1997

Paradoxical effect of oxygen administration on breathing stability following post-hyperventilation apnoea in lambs.

1. Oxygen administration is thought to suppress periodic breathing (PB) by reducing carotid body activity, and yet earlier experiments in neonates have shown that PB incidence may be increased following the application of hyperoxia. To clarify this paradox, we studied the changes in the pattern of PB that occur following administration of oxygen in a lamb model of PB. 2. PB was induced in eleven of seventeen anaesthetized lambs following passive hyperventilation with air. When oxygen was administered during PB, the pattern was first enhanced, as evidenced by a sudden decrease in the ratio of the ventilatory duration to the apnoeic pause duration, and then suppressed, as evidenced by a progressive return to stable breathing which was associated with an increase in minute ventilation. 3. Five of the six lambs that did not show PB following passive hyperventilation with air could be made to do so if oxygen was substituted for air as the inspired gas following passive hyperventilation. 4. Five of the eleven lambs that showed PB following hyperventilation with air responded to the application of oxygen during PB by switching to a gross form of episodic breathing consisting of long apnoeic pauses followed by equally long periods of breathing during which minute ventilation fell progressively with time. 5. We conclude that when applied against a background of arterial hypoxaemia, oxygen has a destabilizing influence on ventilation in that (a) it accentuates the unstable breathing that occurs during PB, (b) it induces PB in lambs that exhibited stable breathing in air, and (c) it may precipitate episodic breathing.

Animals↗