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At least 631 records · Page 35Linked to original sources
PubMed1992

Retraction brain ischaemia: cerebral blood flow, evoked potentials, hypotension and hyperventilation in a new animal model.

Undue intraoperative brain retraction can cause significant neurosurgical morbidity. By combining brain retractor blade pressure measurement with monitoring of brain electrical activity, one can determine the limits of safe brain retraction and then test systematically various therapeutic interventions. Cortical evoked potential (EP) mapping and laser-Doppler cerebral blood flow (CBF) measurement were undertaken during brain retraction in the miniature swine (Sus scrofa). Forelimb somatosensory EP recording during subtemporal retraction simulated the pterional and subtemporal approaches, respectively. Retraction pressure of 30 mmHg usually resulted in a 50% decrement in EP amplitude after 10 to 20 minutes in normotensive, normocapnic adult animals. Recovery of EP occurred within 5 to 10 minutes of retraction release. The effects of animal age, induced hypotension (nitroprusside, MAP approximately 40), and induced hypocapnia (hyperventilation, PaCO2 approximately 28) on EP preservation during retraction were then investigated, with data reported here from 23 animals (8 to 35 kg). By Spearman rank correlation coefficients, early loss of EP was associated with the following: lower MAP (p approximately 0.0001), lower CBF (p approximately 0.0005), lower PaCO2 (p less than 0.001), and older age (p approximately 0.01). These results indicate (1) retractors should be relaxed every 10-15 minutes whenever possible (for at least 5 minutes), and (2) hypotension, in particular, but also hypocapnia (hyperventilation) should not be used indiscriminately. Details of this new model of retraction ischaemia are presented.

Aging↗
PubMed1995

Neuroanesthesia adjunct therapy (mannitol and hyperventilation) is as effective as cerebrospinal fluid drainage for prevention of paraplegia after descending thoracic aortic cross-clamping in the dog.

We compared cerebrospinal fluid (CSF) drainage (Group D; n = 8) to neuroanesthesia adjunct therapy (hyperventilation and mannitol administration; Group N; n = 8) for the prevention of paraplegia using a canine model of descending thoracic aortic cross-clamping (AXC; 2.5 mm distal to the left subclavian artery for 30 min). We expected no difference in neurologic outcome between groups. After surgical preparation and a 30-min stabilization period, dogs in Group D had CSF drained prior to application of the AXC. During the period of AXC, CSF was allowed to drain freely in an attempt to have cerebrospinal fluid pressure (CSFP) no greater than central venous pressure (CVP). Dogs in Group N were hyperventilated (PaCO2 28-32 mm Hg) and received 2 g/kg of mannitol prior to AXC and then 1 g.kg-1.hr-1 during clamping. Systemic hemodynamics, CSFP, and arterial blood gases were measured at 1) baseline, 2) 2 min after AXC, 3) 20 min after AXC, 4) 5 min after AXC release, and 5) 30 min after resuscitation. With release of the AXC, PaCO2 was not controlled in Group D; in Group N the minute ventilation was further increased to maintain PaCO2 constant. At precisely 24 h after AXC, the animals were assessed for incidence and severity of paraplegia, using the Tarlov score, by an observer unaware of the experimental protocol. The animals were then killed, and the entire spinal cord was removed for histologic assessment. Multiple sections of the lumbar spinal cord were processed and stained with hematoxylin and eosin, then examined by light microscopy for nonviable neurons in the anterior spinal cord.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗
PubMed1998

The effect of hyperventilation and hyperoxia on cerebral venous oxygen saturation in patients with traumatic brain injury.

UNLABELLED: Eighteen head-injured patients undergoing hyperventilation were studied for changes in jugular venous oxygen saturation (SjvO2) and arteriovenous oxygen content difference (AVDO2) in response to changes in PaO2 and PaCO2. SjvO2 decreased significantly from 66% +/- 3% to 56% +/- 3% (mean +/- SD) when PaCO2 decreased from 30 to 25 mm Hg at a PaO2 of 100-150 mm Hg. SjvO2 values returned to baseline (66% +/- 2%) when PaCO2 was restored to 30 mm Hg. Repetition of the study at a PaO2 of 200-250 mm Hg produced a similar pattern. However, SjvO2 values were significantly greater with PaO2 within the range of 200-250 mm Hg (77% +/- 4% and 64% +/- 3%) than SjvO2 measured at a PaO2 of 100-150 mm Hg at PaCO2 values of both 30 and 25 mm Hg. AVDO2 also improved with a PaO2 of 200-250 mm Hg at each PaCO2 (P < 0.001). In conclusion, decreases in SjvO2 associated with decreases in PaCO2 may be offset by increasing PaO2. IMPLICATIONS: The adequacy of cerebral oxygenation can be estimated in head-injured patients by monitoring jugular bulb oxygen saturation and the arteriovenous oxygenation content difference. Increasing the partial pressure of arterial oxygen above normal offset deleterious effects of hyperventilation on jugular bulb oxygen saturation and arteriovenous oxygenation content difference in head-injured patients.

Adolescent↗
PubMed1991

Hyperventilation reduces transcutaneous oxygen tension and skin blood flow.

Transcutaneous oxygen tension (PtcO2) is often used to monitor neonates and infants in special care units and the operating room. The transcutaneous index (TCI = PtcO2/arterial oxygen tension [PaO2]) is known to depend both on age and on cardiac index but is assumed to be independent of other physiologic variables. In this study we have shown that TCI also depends upon arterial carbon dioxide tension (PaCO2). Five young pigs were anesthetized and paralyzed and their lungs mechanically ventilated while they were monitored with PtcO2 electrodes and serial arterial blood gas analyses. For a 45 degrees C PtcO2 sensor, the mean TCI during normocapnia was 0.78, whereas during hyperventilation (PaCO2 = 20 mmHg) the mean TCI was reduced 65%, to 0.27. The corresponding TCI values for a 43 degrees C sensor were 0.33 and 0.065, representing an 80% decrease in TCI during hyperventilation. Hypoventilation had little effect upon TCI as long as hypoxemia was avoided. Twelve awake adult volunteers with radial artery cannulas were monitored with PtcO2 sensors at several body sites and two sensor temperatures. For a 44 degrees C sensor on the chest, the mean TCI decreased from 0.77 at normocapnia to 0.60 at a PaCO2 of 17 mmHg, a 22% change. For the same sensor on the foot, TCI decreased from 0.63 to 0.32, a 49% change. For a 42 degrees C sensor under the same conditions, the corresponding TCI decreases were 51 and 64%. Six of the volunteers were also monitored with laser-Doppler skin blood flow probes located on the chest, hand, and foot.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2000

Role of nitric oxide in rat locus coeruleus in hypoxia-induced hyperventilation and hypothermia.

The locus coeruleus modulates the ventilatory and thermoregulatory response to hypoxia and contains nitric oxide synthase. Therefore, we examined the effects of L-NAME unilaterally microinjected into the locus coeruleus on hypoxic hyperventilation and hypothermia. Ventilation and body temperature were measured before and after microinjection of L-NAME (100 nmol/0.5 microl) into the locus coeruleus, followed by hypoxia. Control rats received microinjection of D-NAME (an inactive enantiomer of L-NAME). Under normoxia, L-NAME treatment did not affect ventilation or body temperature. D-NAME did not affect hypoxia-induced hyperventilation and hypothermia. L-NAME treatment reduced the ventilatory response to hypoxia but did not affect hypoxia-induced hypothermia. These data suggest that nitric oxide in the locus coeruleus is involved in the ventilatory response to hypoxia, exercising an inhibitory modulation on the locus coeruleus neurons, but plays no role in hypoxia-induced hypothermia.

Animals↗
PubMed2000

Comparison of hyperventilation and inhaled nitric oxide for pulmonary hypertension after repair of congenital heart disease.

BACKGROUND: Pulmonary hypertension is associated with congenital heart lesions with increased pulmonary blood flow. Acute increases in pulmonary vascular resistance (PVR) occur in the postoperative period after repair of these defects. These increases in PVR can be ablated by inducing an alkalosis with hyperventilation (HV) or bicarbonate therapy. Studies have shown that these patients also respond to inhaled nitric oxide (iNO), but uncertainty exists over the relative merits and undesirable effects of HV and iNO. HYPOTHESIS: Alkalosis and iNO are equally effective in reducing PVR and pulmonary artery pressure (PAP) in children with pulmonary hypertension after open heart surgery. SETTING: Critical care unit of a tertiary care pediatric hospital. DESIGN: Prospective, randomized, crossover design. PATIENTS: Twelve children with a mean PAP > 25 mm Hg at normal pH after biventricular repair of congenital heart disease. INTERVENTIONS: Patients were assigned to receive iNO or HV (pH > 7.5) in random order, and the effect on hemodynamics was measured. Each treatment was administered for 30 mins with a 30-min washout period between treatments. Finally, both treatments were administered together to look for a possible additive effect. MEASUREMENTS AND MAIN RESULTS: Cardiac output and derived hemodynamic parameters using the dye dilution technique. Hyperventilation, achieved by an increase in ventilator rate without a change in mean airway pressure, decreased Pa(CO2) from a mean (SD) of 43.7+/-5.3 to 32.3+/-5.4 mm Hg and increased pH from 7.40+/-0.04 to 7.50+/-0.03. This significantly altered both pulmonary and systemic hemodynamics with a reduction in PAP, PVR, central venous pressure, and cardiac output and an increase in systemic vascular resistance. In comparison, iNO selectively reduced PAP and PVR only. The reduction in PVR was comparable between treatments, although addition of iNO to HV resulted in a small additional reduction in PVR. An additional decrease in PAP was seen when HV was added to iNO, attributable to a reduction in cardiac output rather than a further decrease in PVR. CONCLUSIONS: Inhaled NO and HV are both effective at lowering PAP and PVR in children with pulmonary hypertension after repair of congenital heart disease. The selective action of iNO on the pulmonary circulation offers advantages over HV because a decrease in cardiac output and an increase in SVR are undesirable in the postoperative period.

Administration, Inhalation↗
PubMed1993

Transcranial Doppler monitoring during induction of anesthesia: effects of propofol, thiopental, and hyperventilation in patients with large malignant brain tumors.

Disturbed autoregulation and CO2 reactivity have been reported in patients with brain tumors. Therefore, we decided to monitor the cerebrovascular effects of anesthetic drugs and hyperventilation. Transcranial Doppler sonography (TCD) can measure noninvasively alterations of flow velocities (v) and cross-sectional vessel area (VA) in large brain arteries. Twenty-eight patients with large malignant brain tumors in the territory of the middle cerebral artery (MCA) randomly received propofol or thiopental for induction and maintenance of anesthesia. Mean arterial pressure (MAP), heart rate (HR), and TCD parameters (vMCA and VA of the tumor or nontumor side) were determined at six data points (DP). The first measurements (MAP, HR, and TCD of the nontumor side) were performed before (DP I) and 60 s after (DP II) induction of anesthesia with either 2 mg/kg propofol or 4 mg/kg thiopental. After intubation and normoventilation (50% O2 in air), 0.05-0.1 mg/kg midazolam and an alfentanil infusion (100 micrograms/kg x h) were initiated. Then MAP, HR, vMCA, and VA of the tumor side were analyzed before (DP III) and 60 s after (DP IV) either propofol (1 mg/kg) or thiopental (2 mg/kg) were given. Finally, the effects of hyperventilation on HR, MAP, vMCA, and VA (tumor side) were determined (DP V and VI). Mean +/- SD, thiopental or propofol reactivity (non-tumor and tumor side) and CO2 reactivity (tumor side) were calculated; statistical comparison between DP I and II, III and IV, and V and VI was performed by paired t tests (p < 0.05). Unpaired t tests were used to evaluate differences between groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2005

Hyperventilation in severe diabetic ketoacidosis.

OBJECTIVE: To explore whether the carbon dioxide-bicarbonate (P(CO(2))-HCO(3)) buffering system in blood and cerebrospinal fluid (CSF) in diabetic ketoacidosis should influence the approach to ventilation in patients at risk of cerebral edema. DATA SOURCE: Medline search, manual search of references in articles found in Medline search, and use of historical literature from 1933 to 1967. DESIGN: A clinical vignette is used--a child with severe diabetic ketoacidosis who presented with profound hypocapnia and then deteriorated--as a basis for discussion of integrative metabolic and vascular physiology. STUDY SELECTION: Studies included reports in diabetic ketoacidosis where arterial and CSF acid-base data have been presented. Studies where simultaneous acid-base, ventilation, respiratory quotient, and cerebral blood flow data are available. DATA EXTRACTION AND SYNTHESIS: We revisit a hypothesis and, by reassessing data, put forward an argument based on the significance of low [HCO(3)](CSF) and rising Pa(CO(2))- hyperventilation in diabetic ketoacidosis and the limit in biology of survival; repair of severe diabetic ketoacidosis and Pa(CO(2))-and mechanical ventilation. CONCLUSION: The review highlights a potential problem with mechanical ventilation in severe diabetic ketoacidosis and suggests that the P(CO(2))--HCO(3) hypothesis is consistent with data on cerebral edema in diabetic ketoacidosis. It also indicates that the recommendation to avoid induced hyperventilation early in the course of intensive care may be counter to the logic of adaptive physiology.

Acid-Base Equilibrium↗
PubMedDate not supplied

Imagined risk of suffocation as a trigger for hyperventilation.

OBJECTIVE: Although hyperventilation has been hypothesized to play a role in many pathologies, its critical triggers remain poorly understood. The present experiment aimed to test whether stronger hyperventilation responses occur in response to suggested risk of suffocation compared with other fearful situations in high- and low-trait anxious women. METHODS: Fractional end-tidal CO2-concentration (FetCO2), respiratory frequency, and inspiratory volume were measured nonintrusively in high- (n = 24) and low- (n = 24) trait anxious women during imagery of 3 fear, 1 tension, 1 depressive, and 3 relaxation scripts. The fear scripts were equal in ratings of unpleasantness and arousal but differed regarding the inclusion of suggested risk of suffocation and entrapment. After each imagery trial, participants rated the emotional dimensions of pleasantness, arousal, and dominance and the vividness of their imagery. RESULTS: Decreases in FetCO2 occurred in all fear scripts. High-trait anxious women showed a stronger reduction in FetCO2 compared with low-trait anxious women during the fear script suggesting risk of suffocation but not during the other fear scripts. This effect was unrelated to any of the self-reported fear ratings. Self-reported fear of entrapment was associated with an overall lower FetCO2 but not with enhanced reactivity to imagined entrapment. CONCLUSION: High-trait anxiety is associated with stronger respiratory responsivity to imagined risk of suffocation and may constitute a specific vulnerability factor for the development of panic disorder and claustrophobia.

Adolescent↗
PubMed2004

The impact of hypoxia and hyperventilation on outcome after paramedic rapid sequence intubation of severely head-injured patients.

BACKGROUND: An increase in mortality has been documented in association with paramedic rapid sequence intubation (RSI) of severely head-injured patients. This analysis explores the impact of hypoxia and hyperventilation on outcome. METHODS: Adult severely head-injured patients (Glasgow Coma Scale score of 3-8) unable to be intubated without neuromuscular blockade underwent paramedic RSI using midazolam and succinylcholine; rocuronium was administered after confirmation of tube position. Standard ventilation parameters were used for most patients; however, one agency instituted use of digital end-tidal carbon dioxide (ETCO2) and oxygen saturation (Spo2) monitoring during the trial. Each patient undergoing digital ETCO2/Spo2 monitoring was matched to three historical nonintubated controls on the basis of age, gender, mechanism, and Abbreviated Injury Scale scores for each of six body regions. Logistic regression was used to explore the impact of oxygen desaturation during laryngoscopy and postintubation hypocapnia and hypoxia on outcome. The relationship between hypocapnia and ventilatory rate was explored using linear regression and univariate analysis. In addition, trial patients and controls were compared with regard to mortality and the incidence of "good outcomes" using an odds ratio analysis. RESULTS: Of the 426 trial patients, a total of 59 had complete ETCO2/Spo2 monitoring data; these were matched to 177 controls. Logistic regression revealed an association between the lowest ETCO2 value and final ETCO2 value and mortality. Matched-controls analysis confirmed an association between hypocapnia and mortality. A statistically significant association between ventilatory rate and ETCO2 value was observed (r = -0.13, p < 0.0001); the median ventilatory rate associated with the lowest recorded ETCO2 value was significantly higher than for all other ETCO2 values (27 mm Hg vs. 19 mm Hg, p < 0.0001). In addition, profound desaturations during RSI and hypoxia after intubation were associated with higher mortality than matched controls. Overall mortality was 41% for trial patients versus 22% for matched controls (odds ratio, 2.51; 95% confidence interval, 1.33-4.72; p = 0.004). CONCLUSIONS: Hyperventilation and severe hypoxia during paramedic RSI are associated with an increase in mortality.

Adult↗
PubMed2001

Hyperventilation beyond fight/flight: respiratory responses during emotional imagery.

Hyperventilation (HV) is often considered part of a defense response, implying an unpleasant emotion (negative valence) combined with a strong action tendency (high arousal). In this study, we investigated the importance of arousal and valence as triggers for HV responses. Forty women imagined eight different scripts varying along the arousal and valence dimensions. The scripts depicted relaxation, fear, depressive, action, and desire situations. After each trial, the imagery was rated for valence, arousal, and vividness. FetCO2, inspiratory and expiratory time, tidal volume, and pulse rate were measured in a nonintrusive way. FetCO2 drops and decreases in inspiratory and expiratory time occurred in all but the depressive and the relaxation scripts, suggesting that a defense conceptualization of hyperventilation is not always appropriate.

Adolescent↗
PubMed2005

Hyperventilation revisited: physiological effects and efficacy on focal seizure activation in the era of video-EEG monitoring.

PURPOSE: Hyperventilation is an activation method that provokes physiological slowing of brain rhythms, interictal discharges, and seizures, especially in generalized idiopathic epilepsies. In this study we assessed its effectiveness in inducing focal seizures during video-EEG monitoring. METHODS: We analyzed the effects of hyperventilation (HV) during video-EEG monitoring (video-EEG) of patients with medically intractable focal epilepsies. We excluded children younger than 10 years, mentally retarded patients, and individuals with frequent seizures. RESULTS: We analyzed 97 patients; 24 had positive seizure activation (PSA), and 73 had negative seizure activation (NSA). No differences were found between groups regarding sex, age, age at epilepsy onset, duration of epilepsy, frequency of seizures, and etiology. Temporal lobe epilepsies were significantly more activated than frontal lobe epilepsies. Spontaneous and activated seizures did not differ in terms of their clinical characteristics, and the activation did not affect the performance of ictal single-photon emission computed tomography (SPECT). CONCLUSIONS: HV is a safe and effective method of seizure activation during monitoring. It does not modify any of the characteristics of the seizures and allows the obtaining of valuable ictal SPECTs. This observation is clinically relevant and suggests the effectiveness and the potential of HV in shortening the presurgical evaluation, especially of temporal lobe epilepsy patients, consequently reducing its costs and increasing the number of candidates for epilepsy surgery.

Adolescent↗
PubMed1993

Episodic central neurogenic hyperventilation in an awake child with systemic histiocytosis.

A 3 year old boy with systemic histiocytosis, diabetes insipidus and a lytic parietal bone lesion experienced episodes of central neurogenic hyperventilation 3 weeks after radiation to the head but was conscious and alert at presentation. At admission, the PaO2 was 133 mmHg, PaCO2 was 8 mmHg and pH 7.65. Magnetic resonance imaging revealed a pontomedullary lesion that resolved during the ensuring year. Central neurogenic hyperventilation has not been described previously as a complication of systemic histiocytosis.

Brain Diseases↗
PubMed1986

Reproducibility of hyperventilation of cold dry air in children with cystic fibrosis.

Wheezing is a significant problem in some patients with cystic fibrosis. Currently available tests are not reliable at determining whether this wheezing is due to co-existent asthma or to the underlying pulmonary disease. The reproducibility of hyperventilation of cold dry air (HVCDA) was studied over eight days in 11 children with cystic fibrosis. A group with mild lung disease were selected to minimize the variability due to underlying pulmonary disease. Fifty-six per cent of subjects had consistent responses to HVCDA. A test of reproducibility was performed on the respiratory heat exchange, the percentage fall in FEV1 after HVCDA and the ratio of these two (R). Respiratory heat exchange was found to be highly reproducible with a reproducibility co-efficient of 0.97. The percentage fall in FEV1 after HVCDA and R were not reproducible over the eight-day period. Hyperventilation of cold dry air did not give reproducible results in children with cystic fibrosis, suggesting that a single test may not be suitable for judging bronchial liability.

Adolescent↗
PubMed1989

Hyperventilation or hypoglycaemia?

Two women with insulin-treated diabetes who presented with hyperventilation in the setting of generalized anxiety disorder and panic disorder, respectively, are reported. The symptoms of hyperventilation and hypoglycaemia proved indistinguishable even after successful treatment with a behavioural approach including explanation, breathing retraining, and relaxation. With diabetic patients a cognitive strategy is complicated by conditioning to think in terms of diabetic control and an inability to safely reattribute symptoms to faulty breathing habit because of the risk of ignoring hypoglycaemia.

Adult↗
PubMed1981

Enuresis and hyperventilation response in the EEG.

A total of 420 enuretic children aged between four and 15 years and 100 controls were examined by EEG in order to determine their hyperventilation response, which is considered to be a non-specific sign of brain dysfunction or of cortical instability as a result of delayed maturation. It was found that an increased hyperventilation response occurred mainly among children with primary enuresis (bed-wetters from birth). This was true even if the children had a 'uropathy'. It was also commoner among the children with pathological EEGs at rest. The results for those with secondary enuresis (later onset) were similar to the controls. These findings indicate that disturbed cerebral control of the bladder is an important factor in primary enuresis. Psychological factors are thought to account for the occurrence of secondary enuresis.

Adolescent↗
PubMed1991

The effect of hyperventilation in cluster headache patients.

The effect of voluntary hyperventilation was assessed in 22 cluster headache patients (8 in a cluster period and 14 in a remission) and 19 healthy individuals. Using an ear oximeter and a capnograph with a nasal probe, the oxygen saturation (SaO2) and the end-tidal CO2 were monitored continuously. During the hyperventilation per se, cluster headache patients and controls showed absolute values of end-tidal CO2 and of SaO2 of the same order of magnitude. In the posthyperventilation phase, however, the average of the lowest SaO2 levels was lower in controls than in cluster headache patients. In the posthyperventilation phase, headache patients outside the cluster period showed a trend more similar to that of the controls with respect to SaO2 than did those inside the cluster period. The observed discrepancy might, if reproducible, be a consequence of an altered chemoreceptor sensitivity in cluster headache patients during the bout.

Adult↗
PubMed1989

Asystole with syncope secondary to hyperventilation in three young athletes.

We describe three athletes who had syncope after (case 1) or during (cases 2, 3) hyperventilation. During the episode, ECG showed prolonged sinus arrest. Clinical data and noninvasive investigations were normal and the phenomenon was not reproducible. Electrophysiological study after autonomic blockade allowed a prolonged intrinsic heart rate in case 1, and abnormal corrected sinus node recovery time in cases 1 and 2. During follow-up, symptomatic sinus arrest provoked by deep inspiration occurred in case 3. These cases document prolonged asystole of unknown etiology, secondary to hyperventilation, and probably caused by different vagally-mediated mechanisms.

Adolescent↗