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PubMed2004

Post-hyperventilation hypoxaemia is due to alteration of ventilation and perfusion matching.

OBJECTIVE: The aim of this study was to investigate the mechanisms of post-hyperventilation hypoxia. METHODOLOGY: Seven healthy male volunteers, aged 29.1 +/- 1.4 years, underwent two 10-min periods of voluntary hyperventilation to pulmonary end tidal CO2 values of 20 mmHg (severe hyperventilation), or 30 mmHg (moderate hyperventilation). Post-hyperventilation, the arterial oxygen saturation, VE and arterial blood gas values were measured. Sleep was excluded by EEG monitoring. RESULTS: Maximal hypoxaemia occurred in proportion to severity of hyperventilation; at approximately 5 min post-hyperventilation Pao2 fell to 64 +/- 7 mmHg (severe hyperventilation) and 72 +/- 6 mmHg (moderate hyperventilation) from 97 +/- 3 mmHg at baseline. Hypoxaemia persisted beyond the time of normalization of Paco2 and HCO3. On another occasion, a N2 washout test was performed after severe hyperventilation, which excluded bronchoconstriction. CONCLUSION: Relative hypoventilation may partly explain post-hyperventilation hypoxaemia, but by excluding bronchoconstriction and periodic breathing, we have demonstrated that most of the hypoxaemia must have been due to alteration of pulmonary blood flow distribution causing a fall in V/Q ratio.

Adult↗

PubMed1998

Augmented neuronal death in CA3 hippocampus following hyperventilation early after controlled cortical impact.

UNLABELLED: Minimizing secondary injury after severe traumatic brain injury (TBI) is the primary goal of cerebral resuscitation. For more than two decades, hyperventilation has been one of the most often used strategies in the management of TBI. Laboratory and clinical studies, however, have verified a post-TBI state of reduced cerebral perfusion that may increase the brain's vulnerability to secondary injury. In addition, it has been suggested in a clinical study that hyperventilation may worsen outcome after TBI. OBJECT: Using the controlled cortical impact model in rats, the authors tested the hypothesis that aggressive hyperventilation applied immediately after TBI would worsen functional outcome, expand the contusion, and promote neuronal death in selectively vulnerable hippocampal neurons. METHODS: Twenty-six intubated, mechanically ventilated, isoflurane-anesthetized male Sprague-Dawley rats were subjected to controlled cortical impact (4 m/second, 2.5-mm depth of deformation) and randomized after 10 minutes to either hyperventilation (PaCO2 = 20.3 +/- 0.7 mm Hg) or normal ventilation groups (PaCO2 = 34.9 +/- 0.3 mm Hg) containing 13 rats apiece and were treated for 5 hours. Beam balance and Morris water maze (MWM) performance latencies were measured in eight rats from each group on Days 1 to 5 and 7 to 11, respectively, after controlled cortical impact. The rats were killed at 14 days postinjury, and serial coronal sections of their brains were studied for contusion volume and hippocampal neuron counting (CA1, CA3) by an observer who was blinded to their treatment group. Mortality rates were similar in both groups (two of 13 in the normal ventilation compared with three of 13 in the hyperventilation group, not significant [NS]). There were no differences between the groups in mean arterial blood pressure, brain temperature, and serum glucose concentration. There were no differences between groups in performance latencies for both beam balance and MWM or contusion volume (27.8 +/- 5.1 mm3 compared with 27.8 +/- 3.3 mm3, NS) in the normal ventilation compared with the hyperventilation groups, respectively. In brain sections cut from the center of the contusion, hippocampal neuronal survival in the CA1 region was similar in both groups; however, hyperventilation reduced the number of surviving hippocampal CA3 neurons (29.7 cells/hpf, range 24.2-31.7 in the normal ventilation group compared with 19.9 cells/hpf, range 17-23.7 in the hyperventilation group [25th-75th percentiles]; *p < 0.05, Mann-Whitney rank-sum test). CONCLUSIONS: Aggressive hyperventilation early after TBI augments CA3 hippocampal neuronal death; however, it did not impair functional outcome or expand the contusion. These data indicate that CA3 hippocampal neurons are selectively vulnerable to the effects of hyperventilation after TBI. Further studies delineating the mechanisms underlying these effects are needed, because the injudicious application of hyperventilation early after TBI may contribute to secondary neuronal injury.

Anesthetics, Inhalation↗

PubMed2000

Hyperventilation therapy for acute traumatic brain injury.

BACKGROUND: Because hyperventilation is often associated with a rapid fall in intracranial pressure, it has been assumed to be effective in the treatment of severe head injury. Hyperventilation reduces raised intracranial pressure by causing cerebral vasoconstriction and a reduction in cerebral blood flow. Whether reduced cerebral blood flow improves neurological outcome however, is unclear. OBJECTIVES: To quantify the effect of hyperventilation on death and neurological disability following head injury. SEARCH STRATEGY: The search strategy drew on that of the Injuries Group as a whole. The reference lists of all relevant articles identified were checked and the first author of reports was contacted to ask for assistance in identifying any further trials. Most recent search was done in September 1999. SELECTION CRITERIA: All randomised trials of hyperventilation, in which study participants had a clinically defined acute traumatic head injury of any severity. There were no language restrictions. DATA COLLECTION AND ANALYSIS: We collected data on the participants, the timing and duration of the intervention, duration of follow up, neurological disability and death. Relative risks (RR) and 95% confidence intervals were calculated for each trial on an intention to treat basis. Timing, degree and duration of hyperventilation were identified a-priori as potential sources of heterogeneity between trials. MAIN RESULTS: One trial of 113 participants was identified. Hyperventilation alone, as well as in conjunction with the buffer THAM showed a beneficial effect on mortality at one year after injury, although the effect measure was imprecise (RR=0.73; 95% CI 0.36;1.49 and RR=0.89; 95% CI 0.47;1.72 respectively). This improvement in outcome was not supported by an improvement in neurological recovery. For hyperventilation alone, the RR for death or severe disability was 1. 14 (95% CI 0.82;1.58). The RR for death or severe disability in the hyperventilation plus THAM group, was 0.87 (95% CI 0.58;1.28). REVIEWER'S CONCLUSIONS: The data available are inadequate to assess any potential benefit or harm that might result from hyperventilation in severe head injury. Randomised controlled trials to assess the effectiveness of hyperventilation therapy following severe head injury are needed.

Brain Injuries↗

PubMed1991

Effects of tromethamine and hyperventilation on brain injury in the cat.

The metabolic brain acidosis after trauma has been thought to be harmful and to contribute to neurological deterioration. Amelioration of the brain acidosis either by systemic buffering agents or by hyperventilation has been proposed as a method of treatment. The objective of this study was to explore with magnetic resonance (MR) spectroscopy the metabolic changes in brain that occur with the use of hyperventilation, THAM (tromethamine; tris[hydroxymethyl]aminomethane), and a combination (THAM and hyperventilation) therapy in experimental fluid-percussion injury. Brain lactate, brain pH, inorganic phosphate (Pi), and adenosine triphosphate levels were measured by 1H and 31P MR spectroscopy. Arterial and cerebrovenous lactate and water content in brain tissue was determined in 29 cats using the specific gravimetric technique. Following injury, the phosphocreatine (PCr)/Pi ratio, which is an index of cerebral energy depletion, decreased to 76% in four untreated animals, to 79% in 11 THAM-treated animals, to 68% in seven animals receiving hyperventilation, and to 66% in seven animals with combination THAM and hyperventilation therapy. The PCr/Pi ratio returned to a normal level in 8 hours in animals treated with THAM and THAM in combination with hyperventilation. The brain lactate index increased to 157% in the hyperventilation group after trauma. In cats receiving THAM plus hyperventilation, the brain lactate index was reduced to 142%, while the minimum rise of 126% was associated with treatment of THAM alone. In the THAM-treatment and combination-treatment groups, the water content of the white and gray matter was significantly decreased compared with that in untreated cat brains. Prolonged hyperventilation provided relative ischemia in brain tissue and promoted more production of brain lactate, no recovery of the PCr/Pi ratio, and no decrease in brain edema. On the other hand, administration of THAM decreased production of brain lactate and brain edema and promoted the recovery of cerebral energy dysfunction. It was found that THAM ameliorates the deleterious effects of hyperventilation by minimizing energy disturbance and that it also decreases brain edema. The authors conclude that THAM may be effective in reducing brain tissue acidosis and helpful as a metabolic stabilizing agent following severe head injury.

Acidosis, Lactic↗

PubMed1999

The pathophysiology of hyperventilation syndrome.

Hyperventilation is defined as breathing in excess of the metabolic needs of the body, eliminating more carbon dioxide than is produced, and, consequently, resulting in respiratory alkalosis and an elevated blood pH. The traditional definition of hyperventilation syndrome describes "a syndrome, characterized by a variety of somatic symptoms induced by physiologically inappropriate hyperventilation and usually reproduced by voluntary hyperventilation". The spectrum of symptoms ascribed to hyperventilation syndrome is extremely broad, aspecific and varying. They stem from virtually every tract, and can be caused by physiological mechanisms such as low Pa,CO2, or the increased sympathetic adrenergic tone. Psychological mechanisms also contribute to the symptomatology, or even generate some of the symptoms. Taking the traditional definition of hyperventilation syndrome as a starting point, there should be three elements to the diagnostic criterion: 1) the patient should hyperventilate and have low Pa,CO2, 2) somatic diseases causing hyperventilation should have been excluded, and 3) the patient should have a number of complaints which are, or have been, related to the hypocapnia. Recent studies have questioned the tight relationship between hypocapnia and complaints. However, the latter can be maintained and/or elicited when situations in the absence of hypocapnia in which the first hyperventilation and hypocapnia was present recur. Thus, the main approach to diagnosis is the detection of signs of (possible) dysregulation of breathing leading to hypocapnia. The therapeutic approach to hyperventilation syndrome has several stages and/or degrees of intervention: psychological counselling, physiotherapy and relaxation, and finally drug therapy. Depending on the severity of the problem, one or more therapeutic strategies can be chosen.

Breathing Exercises↗

PubMed1994

Hyperventilation and chronic fatigue syndrome.

We studied the link between chronic fatigue syndrome (CFS) and hyperventilation in 31 consecutive attenders at a chronic fatigue clinic (19 females, 12 males) who fulfilled criteria for CFS based on both Oxford and Joint CDC/NIH criteria. All experienced profound fatigue and fatigability associated with minimal exertion, in 66% developing after an infective episode. Alternative causes of fatigue were excluded. Hyperventilation was studied during a 43-min protocol in which end-tidal PCO2 (PETCO2) was measured non-invasively by capnograph or mass spectrometer via a fine catheter taped in a nostril at rest, during and after exercise (10-50 W) and for 10 min during recovery from voluntary overbreathing to approximately 2.7 kPa (20 mmHg). PETCO2 < 4 kPa (30 mmHg) at rest, during or after exercise, or at 5 min after the end of voluntary overbreathing, suggested either hyperventilation or a tendency to hyperventilate. Most patients were able voluntarily to overbreathe, but not all were able to exercise. Twenty-two patients (71%) had no evidence of hyperventilation during any aspect of the test. Only four patients had unequivocal hyperventilation, in one associated with asthma and in three with panic. Only one patient with severe functional disability and agoraphobia had hyperventilation with no other obvious cause. A further five patients had borderline hyperventilation, in which PETCO2 was < 4 kPa (30 mmHg) for no more than 2 min, when we would have expected it to be normal. There was no association between level of functional impairment and degree of hyperventilation. There is only a weak association between hyperventilation and chronic fatigue syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1998

Influence of hyperventilation on brain tissue-PO2, PCO2, and pH in patients with intracranial hypertension.

A harmful effect of prolonged hyperventilation on outcome has been shown in comatose patients after severe head injury. The purpose of this study was to assess the acute effect of moderate hyperventilation for treatment of intracranial hypertension (ICP < 20 mmHg) on invasively measured brain tissue-PO2 (PtiO2), PCO2 (PtiCO2) and pH (tipH) in severely head injured patients. 15 severely head injured patients (GCS < or = 8) were prospectively studied. Intracranial pressure (ICP), mean arterial blood pressure (MABP), cerebral perfusion pressure (CPP), endtidal CO2 (ETCO2), PtiO2, PtiCO2 and tipH (Paratrend or Licox microsensors) were continuously recorded using multimodal monitoring. Following a baseline period of 15 minutes, patients were hyperventilated for 10 minutes. Arterial blood gas analysis was done before, during and after hyperventilation. At least three hyperventilation maneuvers were performed per patient. For statistical analysis the Friedman test was used. Hyperventilation (paCO2: 32.4 +/- 0.6 to 27.7 +/- 0.5 mmHg) significantly reduced ICP from 25.3 +/- 1.5 to 14.2 +/- 1.9 mmHg (p < 0.01). As a consequence, CPP increased by 9.6 +/- 3.4 mmHg to 76.8 +/- 3.2 mmHg. Brain tissue PCO2 decreased from 37.5 +/- 1.3 to 34.6 +/- 1.2 while tipH increased from 7.13 to 7.16. In all patients, hyperventilation led to a reduction of brain tissue PO2 (PtiO2/Licox: 24.6 +/- 1.4 to 21.9 +/- 1.7 mmHg, n.s.; PtiO2/Paratrend: 35.8 +/- 4.3 to 31.9 +/- 4.0 mmHg, n.s.). In one case hyperventilation even had to be stopped after 7 min because the drop in brain tissue PO2 below 10 mmHg signalized imminent hypoxia. As well known, hyperventilation improves CPP due to a reduction in ICP. However, this does not ameliorate cerebral oxygenation as demonstrated by the decrease in PtiO2. This underlines that hyperventilation should only be used with caution in the treatment of intracranial hypertension.

Acid-Base Equilibrium↗

PubMed1989

Hyperventilation and ergonovine tests in Prinzmetal's variant angina pectoris in men.

Hyperventilation and ergonovine tests were carried out in a group of 30 patients with variant angina to assess the sensitivity of the 2 tests and to correlate the response with spontaneous disease activity. Hyperventilation produced a positive response in 83% (25 of 30) and ergonovine in 93% (28 of 30) of the patients. After hyperventilation 22 of 25 showed ST-segment elevation, 2 ST depression and 1 T-wave pseudonormalization; after ergonovine ST-segment elevation developed in 23 patients, ST depression in 4 and T-wave pseudonormalization in 1. In all cases the electrocardiographic changes occurred in the same leads as during the spontaneous attacks. The incidence of chest pain and ventricular arrhythmias was similar during both tests; spontaneous remission of ischemia, however, was more frequent (48 vs 14%) after hyperventilation than after ergonovine. Acute ischemia developed at a mean of 218 +/- 112 seconds after the end of hyperventilation in 19 of 25 positive tests; at that time double product was not significantly different from basal values. The sensitivity of hyperventilation was similar (95 vs 100%) to ergonovine in the patients with greater than or equal to 1 daily attack, while in those with less than 1 daily attack the sensitivity of hyperventilation decreased to 55% compared to 77% with ergonovine. Thus, in variant angina the sensitivity of both tests correlates with disease activity. Hyperventilation is a safe provocative test with a sensitivity similar to ergonovine in patients with active disease; however, in patients with sporadic attacks hyperventilation has a lower sensitivity than ergonovine and therefore a limited diagnostic value.

Adult↗

PubMed1990

Waning of panic sensations during prolonged hyperventilation.

Recent theories about panic emphasize that a hyperventilatory positive feedback loop is involved in panic: catastrophic misinterpretation of bodily sensations may trigger anxiety, anxiety may stimulate hyperventilation, hyperventilation may promote the salience of feared sensations etc. Such models leave unexplained how and when panics come to an end. It was hypothesised that panic with hyperventilation may end because pronounced hyperventilation becomes, in the course of time, less powerful in generating perceivable bodily sensations. Twenty healthy subjects hyperventilated forcefully and experienced clear panic symptoms as defined by DSM IIIR. When pCO2 was kept 55% below base line for 90 min, panic symptoms waned. The mean intensity of the symptoms declined as did the number of symptoms occurring. No panic symptoms were observed in the control group (n = 20) who ventilated normally. In so far as hyperventilation is involved in the positive feedback loops that characterize panic, panic attacks may be time-limited because sensations induced by hyperventilation become less salient even if massive hyperventilation continues. As to the explanation of the reported phenomenon, it is suggested that, apart from habituation, local physiological changes due to prolonged hyperventilation may produce a decrease in interoceptive input.

Adult↗

PubMed1991

Hyperventilation-induced panic attacks in panic disorder with agoraphobia.

Eight minutes of hyperventilation to an end-tidal PCO2 of less than 20 mmHg led to a panic attack in 7 of 12 patients with panic disorder with agoraphobia and only 1 of 12 normal controls. Patients experienced greater increases in panic symptoms than controls during hyperventilation. Patients who reported more distress from somatic symptoms of hyperventilation during the preceding week were more likely to panic during hyperventilation. Patients who panicked during hyperventilation exhibited a delayed recovery of normocapnia following hyperventilation. Hyperventilation by this protocol is an effective means of inducing panic attacks in the laboratory. A hyperventilation challenge may identify a subgroup of patients for whom hyperventilation symptoms are frequently associated with panic.

Adult↗

PubMed1987

Provocative testing with prolonged hyperventilation and ergometrine in patients suspected of coronary artery spasm: a comparative study.

We induced coronary vasoconstriction by hyperventilation for 6 minutes (arterial pH = 7.6 +/- 0.06) and ergometrine (0.4 mg) in 24 patients suspected of coronary vasospasm. ST deviation greater than or equal to 1 mm was induced in 12 patients by hyperventilation and in 10 by ergometrine. Using spontaneous ST deviation as the independent reference the sensitivity of hyperventilation was 86% and the sensitivity of ergometrine 77%. Ergometrine caused sinus bradycardia and hypotension in 3 patients; hyperventilation caused no untoward reactions. In 12 of the patients coronary angiogram and wedge pressure were obtained during provocative testing. A computer-assisted analysis of coronary diameters in 43 arterial segments (3-4 per patient) showed a 16 +/- 12.6% and 14 +/- 16.7% reduction after hyperventilation and ergometrine, respectively. The maximal coronary diameter reduction induced by hyperventilation and ergometrine was 26 +/- 13.9% and 28 +/- 15.0%, respectively, and showed a significant correlation between the two tests (r = 0.77, N = 12, P less than 0.01). The wedge pressure increase induced by hyperventilation correlated to the maximal coronary diameter reduction (r = 0.63, N = 12, P less than 0.05), while no such correlation was found by ergometrine testing. We conclude that hyperventilation leading to arterial pH about 7.6 has essentially the same potency as 0.4 mg ergometrine, but the hyperventilation test appears to be safer.

Angiography↗

PubMed1990

Hyperventilation-induced EEG changes in humans and their modulation by an anticonvulsant drug.

Surface-negative DC shifts, arising from depolarization of apical dendrites of cortical pyramidal cells, represent excitability of cortical neuronal networks. Hyperventilation, used in epilepsy diagnosis to provoke epileptiform discharges, is thought to increase excitability of neuronal tissue; correspondingly, hyperventilation produces negative DC shifts. Extreme negative DC shifts, accompanying epileptiform EEG patterns, have been observed in epileptic patients during hyperventilation. Anticonvulsants, supposed to dampen cortical excitability, should inhibit the development of overexcitability and, hence, also of pronounced negative DC shifts. The present study examined DC shifts induced by hyperventilation in healthy human subjects under the influence of the benzodiazepine, clonazepam, which is used as anticonvulsant. In a double-blind setting, 36 male student volunteers received 4.5 mg clonazepam or the equivalent amount of placebo. DC-EEG and respiration rate were measured during 3 periods each of 3 min: baseline, hyperventilation, and recovery. Compared to baseline, hyperventilation produced a negative DC shift of an average 36 +/- 8 microV under placebo conditions. Clonazepam reduced the hyperventilation-induced negativity to 13 +/- 5 microV. Negativity suppression became weakened with increasing blood plasma levels of the drug. Respiration depth and frequency, increasing under hyperventilation, did not differ among the groups. Clonazepam treatment gave rise to beta-waves and prevented the increase in alpha and theta activity that was found in placebo subjects during the recording period; this was only true, however, for low to moderate plasma concentrations of clonazepam. Results are consistent with the notion that a hyperventilation-induced increase in neuronal excitability can be measured by cortical DC shifts. The reduction of negative shifts under anticonvulsants might indicate dampening of cortical neuronal excitability which is intended by antiepileptic drugs.

Adult↗

PubMed2004

Cardio-respiratory measures following isocapnic voluntary hyperventilation.

In some individuals, breathing is greater than at rest following voluntary hyperventilation. Most previous investigations have employed short hyperventilation periods; here we examine the time course of cardio-respiratory measures before, during, and after a 5-min voluntary hyperventilation, maintaining isocapnia throughout. We examined the possible co-involvement of the cardiovascular system; hypothesising that post-hyperventilation hyperpnoea results from an increase in autonomic arousal. In four subjects (two males, two females) of 18 (nine males, nine females) we observed a post-hyperventilation hyperpnoea, characterised by a slow decline of ventilation toward resting levels with a time constant of 109.0 +/- 16.1s. By contrast, heart rate, and systolic and diastolic blood pressure were unchanged from rest during and after voluntary hyperventilation for all subjects. We concluded that males and females were equally likely to exhibit post-hyperventilation hyperpnoea, and suggest that they may be characterised by an increased resting heart rate and the choice of breathing frequency to increase ventilation during the voluntary hyperventilation. We further concluded that post-hyperventilation hyperpnoea is rare, but when present is a strong and lasting phenomenon, and that it is not the result of an increased autonomic arousal.

Adult↗

PubMed1997

The chronic fatigue syndrome and hyperventilation.

Chronic fatigue syndrome (CFS) is characterized by severe fatigue, lasting for at least 6 months, for which no somatic explanation can be found. Because hyperventilation can produce substantial fatigue, it seems worthwhile to investigate the relationship between it and CFS. It might be hypothesized that hyperventilation plays a causal or perpetuating role in CFS. CFS patients, non-CFS patients known to experience hyperventilation, and healthy controls were compared on complaints of fatigue and hyperventilation. CFS patients and non-CFS patients known to experience hyperventilation offered substantial complaints of fatigue and hyperventilation, both to a similar degree. Physiological evidence of hyperventilation was found significantly more often in CFS patients than in healthy controls. However, no significant differences between CFS patients with and CFS patients without hyperventilation were found on severity of fatigue, impairment, number of complaints, activity level, psychopathology, and depression. It is concluded that hyperventilation in CFS should probably be regarded as an epiphenomenon.

Adult↗

PubMed1998

Increased excitability of the human corticospinal system with hyperventilation.

OBJECTIVES: Hyperventilation is effective in inducing generalized spike-wave discharges in patients with absence seizures and improves visual function and normalizes visual function in patients with multiple sclerosis. Hyperventilation increases the excitability of cutaneous and motor axons. In experimental animals, hyperventilation increases excitability of hippocampal neurons. There is however no direct evidence of a hyperventilation-induced increase in neuronal excitability within the central nervous system in humans. In this study we determined the effects of hyperventilation on the human corticospinal system. METHODS: We studied the effects of hyperventilation on (1) motor evoked potentials (MEPs) induced by transcranial magnetic pulse stimulation of the motor cortex and (2) F-wave responses. Six subjects were studied. RESULTS: Hyperventilation resulting in an end-tidal pCO2 of 15 mm Hg or less enhanced the amplitude of the MEP and resulted in a shortened onset latency. F-wave amplitudes were enhanced without any change in onset latency. CONCLUSIONS: These findings indicate that hyperventilation increases the excitability of the human corticospinal system. A hyperventilation-induced increase in excitability within the central nervous system may account for clinical phenomena such as facilitation of spike-wave discharges.

Adult↗

PubMed1996

Hyperventilation alters colonic motor and sensory function: effects and mechanisms in humans.

UNLABELLED: BACKGROUND & AIMS. Hyperventilation-induced hypocapnia affects hemodynamic function and enhances colonic motility. The aims of this study were to determine the effects of hypocapnic hyperventilation on colonic motility and sensation in health and to explore the putative neurohumoral mechanisms. METHODS: In experiment 1, colonic tone, sensation, plasma levels of cortisol, beta-endorphin, selected gut neuropeptides, norepinephrine, epinephrine, and splanchnic blood volume were measured during two sequences of hypocapnic hyperventilation. In experiment 2, colonic tone and sensation were assessed during eucapnic hyperventilation and abdominal compression. RESULTS: Hypocapnic hyperventilation, but not eucapnic hyperventilation or abdominal compression, significantly increased colonic tone and sensitivity to balloon distention (P = 0.017) without altering humoral mediators or splanchnic blood volume. Plasma norepinephrine level increased (P = 0.017) and splanchnic blood volume decreased (P = 0.028) during 5 minutes after hyperventilation, consistent with homeostatic responses. CONCLUSIONS: Increased colonic tone and sensation during hypocapnic hyperventilation are not caused by colonic compression. These effects of hyperventilation are not mediated humorally but may result from direct metabolic effects of hypocapnia on colonic muscle or from changes in central autonomic control of colonic smooth muscle.

Adult↗

PubMed1997

Excitability changes in human sensory and motor axons during hyperventilation and ischaemia.

This study was undertaken to compare the excitability changes of sensory and motor axons during hyperventilation and ischaemia, and to determine why ectopic impulse activity develops more readily during hyperventilation, and in sensory fibres. During hyperventilation for 20 min, all six subjects reported paraesthesiae in the hand and face, and four out of the six developed muscle twitching and cramps, associated with significant decreases of 20-30% in the threshold current required to produce sensory and motor potentials of constant size. During ischaemia four out of the six subjects reported paraesthesiae, but none reported muscle twitching. There were significant decreases of 15-20% in threshold for sensory and motor fibres. Ischaemia produced a marked decrease in supernormality, an increase in refractoriness and an increase in latency of the test compound sensory or motor potential, changes that were not seen with hyperventilation. The decrease in threshold during these manoeuvres was associated with a significant increase in strength--duration time constant (tau SD), indicating a relatively greater decrease in rheobase current. Using the technique of latent addition, we found that the changes in tau SD were consistent with a recently proposed model in which non-inactivating, voltage-dependent 'threshold channels' (presumably persistent Na+ channels) are active at resting potential. The failure of hyperventilation to alter conduction velocity, refractoriness or supernormality appreciably indicates that, unlike ischaemic depolarization, hyperventilation does not increase inactivation of conventional Na+ channels or activation of K+ channels, and this implies that the hyperventilation-induced increase in excitability is not the result of conventional depolarization, as seems to occur during ischaemia. These results suggest that hyperventilation has a rather selective action on the threshold channels, and they help to explain its greater effectiveness compared with ischaemia in provoking ectopic discharges. The greater expression of threshold channels in sensory than in motor fibres can explain why hyperventilation induces paraesthesiae before fasciculation and why only paraesthesiae occur during ischaemia.

Action Potentials↗

PubMed2001

Voluntary hyperventilation before a rapid-sequence induction of anesthesia does not decrease postintubation PaCO2.

UNLABELLED: To prevent hypercapnia, voluntary hyperventilation is recommended for patients with increased intracranial pressure before the induction of general anesthesia. We sought to determine whether this maneuver results in a lower PaCO2 than breathing 3 min of oxygen 100% by face mask (preoxygenation) after intubation. Thirty patients requiring general anesthesia were randomly assigned to breathe either 3 min of oxygen 100% by face mask (Group P) or 1 min of oxygen 100% followed by 2 min of voluntary hyperventilation with oxygen 100% (Group H). All patients received a standard rapid-sequence induction of anesthesia followed by a 90-s period of apnea. Patients were then tracheally intubated and mechanically ventilated. Five arterial blood gas samples were taken: with room air, after preoxygenation or hyperventilation, after 60 and 90 s of apnea, and after tracheal intubation. Voluntary hyperventilation decreased PaCO2 before rapid-sequence induction (hyperventilation, 30.0 +/- 3.5 mm Hg versus preoxygenation, 37.9 +/- 5.2 mm Hg; P < 0.0001), but after 60 s of apnea, both groups had similar PaCO2 (hyperventilation, 36.1 +/- 3.3 mm Hg versus preoxygenation, 35.6 +/- 3.4 mm Hg; P = 0.673), and no benefit was found after intubation (hyperventilation, 40.5 +/- 3.9 mm Hg versus preoxygenation, 41.4 +/- 2.7 mm Hg; P = 0.603). We conclude that voluntary hyperventilation before rapid-sequence induction does not provide protection against potential hypercapnia during intubation. IMPLICATIONS: Voluntary hyperventilation before anesthesia induction is recommended for patients with increased intracranial pressure to prevent hypercapnia. This randomized, prospective study demonstrated that this maneuver does not result in a lower postintubation PaCO2 than standard preoxygenation.

Adult↗