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PubMed1997

Hyperventilation technetium-99m-HMPAO brain SPECT in moyamoya disease to assess risk of natural childbirth.

We report a pregnant 19-yr-old patient with moyamoya disease who had undergone bilateral superficial temporal artery to middle cerebral artery anastomosis and encephalomyosynangiosis at 8 yr with an uneventful postoperative course and who desired natural delivery after becoming pregnant at 18 yr. We determined her cerebral vascular reserve since natural delivery can result in decreased cerebral blood flow during labor. Technetium-99m-HMPAO brain SPECT, with hyperventilation challenge, was performed to assess cerebral vascular reserve since the stress of hyperventilation was thought likely to rehearse that of labor. The brain SPECT images, obtained using 333 MBq 99mTc-HMPAO, revealed maintenance of cerebral vascular reserve. In addition, whole-body images including the 27-wk-old fetus were obtained. These images demonstrated accumulation in the fetal liver. Natural delivery was, thus, considered indicated for this patient, who subsequently delivered a healthy baby girl. Technetium-99m-HMPAO brain SPECT with hyperventilation challenge was useful for estimating cerebral vascular reserve and for determining whether natural delivery was indicated for this patient with moyamoya disease.

Adult↗
PubMed1998

Cerebral hemodynamic changes during sustained hypocapnia in severe head injury: can hyperventilation cause cerebral ischemia?

Hyperventilation (HV) is routinely used in the management of increased intracranial pressure (ICP) in severe head injury. However, this treatment continues to be controversial because it has been reported that long-lasting reduced cerebral blood flow (CBF) due to profound sustained hypocapnia may contribute to the development or deterioration of ischemic lesions. Our goal in this study was to analyze the effects of sustained hyperventilation on cerebral hemodynamics (CBF, ICP) and metabolism (arterio jugular differences of lactates = AVDL). CO2-reactivity and CBF was estimated using AVDO2 (arteriojugular differences of oxygen content). Global cerebral ischemia and increased anaerobic metabolism were considered according to AVDO2 and AVDL respectively. Thirty-three patients with severe and moderate head injury and increased ICP were included. Within 72 hours after accident, patients were hyperventilated for a period of 4 hours. During this time jugular oxygen saturation (SjO2), arterial oxygen saturation (SaO2), ICP, mean arterial blood pressure (MABP), AVDO2 and AVDL were recorded. In our study, most patients preserved CO2-reactivity (88.2%). In these cases HV was very effective in lowering ICP. Our findings showed that this reduction was due to a CBF decrease. According to basal AVDO2 twenty-five patients (75.7%) were considered as hyperemic and eight (24.2%) as not hyperemic. Global ischemia and increased anaerobic metabolism were detected in one case in the non-hyperemic group. According to AVDO2 and AVDL, no adverse effects were found during four hours of HV in hyperemic patients. Nevertheless, AVDO2 and AVDL are global measurements and might not detect regional ischemia surrounding focal lesions such as contusions and haematomas. We suggest that monitoring of AVDO2 or other haemometabolic variables should be mandatory when sustained HV is used in the management of head injury patients.

Adolescent↗
PubMed1988

Acute trichloroethylene poisoning with additional ingestion of ethanol--concentrations of trichloroethylene and its metabolites during hyperventilation therapy.

One hour after suicidal ingestion of about 150 g of trichloroethylene, a 32-year-old male was admitted to hospital. On admission, the patient's state of consciousness deteriorated from somnolence to coma. Based on blood level data, an absorbed trichloroethylene dose of at least 35 g was estimated. Additionally, ethanol, which is a strong inhibitor of trichloroethylene metabolism, had been ingested. With respect to the high dose of trichloroethylene, hyperventilation therapy was performed for 28 h. Concentrations of trichloroethylene and its metabolites in blood and urine were determined by gas chromatography. Due to hyperventilation and inhibition of trichloroethylene metabolism, not more than 30% of the absorbed dose was metabolized and excreted via kidneys. Under normal respiratory conditions and in the absence of ethanol, this fraction amounts to about 75%. Obviously, hyperventilation and ethanol-induced inhibition of metabolism led to considerably enforced pulmonary elimination of the absorbed trichloroethylene.

Adult↗
PubMed1999

Transcutaneous PCO2 monitoring in the evaluation of hyperventilation of patients with recurrent nerve paralysis.

Hyperventilation during phonation is one of the causes of fatigue in patients with vocal cord disorders. Transcutaneous (TC) PCO2 and PO2 were analyzed during phonation in patients with known recurrent nerve paralyses (RNP). There was no significant change in TCPCO2 in eight normal subjects. In cases with unilateral RNP and incomplete glottic closure, TCPCO2 decreased during phonation. This decrease in TCPCO2 resulted from hyperventilation during phonation. The TCPCO2 did not decrease in one case with RNP and complete glottic closure. In one case with incomplete glottic closure, the decrease in TCPCO2 and fatigue disappeared after treatment. These results suggest that hyperventilation is one of the causes for easy fatiguability during phonation in patients with RNP, Findings also show that measurements of TCPCO2 during phonation are useful for evaluating the cause of fatigue in patients with vocal disorders.

Adult↗
PubMed1990

The changes in brain surface, intracerebral tissue, and transconjunctival oxygen tension during hypo- and hyperventilation.

To evaluate the validity of organ surface oxygen tension monitoring for assessment of cerebral perfusion, the oxygen tension in brain surface (Pbs(O)(2)), intracerebral tissue (Pic(O)(2)), and conjunctiva (Pcj(O)(2)) were measured simultaneously during hypo- and hyperventilation in dogs, and the comparative study was done. Pbs(O)(2) and Pic(O)(2) significantly increased during hypoventilation and decreased during hyperventilation. And the values of Pbs(O)(2) and Pic(O)(2) were correlated to the corresponding Pa(CO)(2) values significantly ( P << 0.001 in each case). On the contrary, Pcj(O)(2) did not change significantly during hypo- and hyperventilation. These findings indicate that Pbs(O)(2) as well as Pic(O)(2) could reflect the changes in cerebral perfusion caused by induced hyper- and hypocapnia but that Pcj(O)(2) could not.

Journal Article↗
PubMed1998

Experimental tricyclic antidepressant toxicity: a randomized, controlled comparison of hypertonic saline solution, sodium bicarbonate, and hyperventilation.

STUDY OBJECTIVE: We sought to compare the effects of hypertonic sodium chloride solution (HTS), sodium bicarbonate solution, and hyperventilation (HV) on severe tricyclic antidepressant (TCA) toxicity in a swine model. METHODS: Twenty-four mixed-breed, domestic swine of either sex were given an intravenous infusion of nortriptyline (NT) until development of both a QRS duration longer than 120 ms and a systolic blood pressure (SBP) less than or equal to 50 mm Hg. Animals were randomly assigned to 1 of 4 groups. On reaching toxicity, the control group received 10 mL/kg of 5% dextrose in water (D5W); the HTS group received 10 mL/kg of 7.5% NaCl solution (15 mEq Na+/kg); the NaHCO3 group received 3 mEq/kg of 8.4% sodium bicarbonate solution followed by enough D5W solution to equal 10 mL/kg of total volume; and the HV group was mechanically hyperventilated to maintain arterial pH between 7.50 and 7.60 and given 10 mL/kg of D5W. RESULTS: The mean SBP 10 minutes after treatment was 54+/-18 mm Hg in the control group, 134+/-21 mm Hg in the HTS group, 85+/-19 mm Hg in the NaHCO3 group, and 60+/-12 mm Hg in the HV group (P<.05). Mean QRS duration 10 minutes after treatment was 144+/-38 ms in the control group, 80+/-14 ms in the HTS group, 105+/-38 ms in the NaHCO3 group, and 125+/-46 ms in the HV group (P<.05). CONCLUSION: In this model of TCA, toxicity HTS was more effective than sodium bicarbonate. Hyperventilation had little effect. Sodium loading may be the most important factor in reversing TCA toxicity.

Animals↗
PubMed1997

The use of hyperventilation and its impact on cerebral ischemia in the treatment of traumatic brain injury.

Traumatic brain injury is a common occurrence in the United States, leading to approximately 190,000 deaths or long-term disabilities. Following the primary insult, secondary disturbances in cerebral blood flow (CBF) and metabolism may have deleterious effects on potentially viable neurons. Recent studies evaluating CBF immediately following head injury have revealed flows low enough to produce cerebral ischemia. Hyperventilation is used routinely to lower suspected increased intracranial pressure (ICP). Aggressive hyperventilation produces a marked reduction in CBF, which may give rise to or exacerbate cerebral ischemia, thus enhancing rather than reducing secondary injury. This article reviews the role of hyperventilation in the treatment of increased ICP and its impact on cerebral ischemia following traumatic brain injury.

Animals↗
PubMed1998

Propofol and hyperventilation for the treatment of increased intracranial pressure in rabbits.

UNLABELLED: Using a rabbit model of intracranial hypertension, we studied (a) the additive effect of propofol and hyperventilation (HV) on increased intracranial pressure (ICP), (b) the ICP-lowering effect of additive therapy (i.e., propofol plus HV versus HV plus propofol), and (c) whether combined therapy induced cerebral ischemia. Twenty-three New Zealand White rabbits were studied, of which seven were control animals. The animals were anesthetized with midazolam and fentanyl. An extradural balloon was used to increase ICP to 26+/-2 mm Hg. Elevation of ICP resulted in a >50% reduction in ipsilateral somatosensory evoked potential (SEP) amplitude. The rabbits were then randomized to be treated with propofol followed by HV (Group 1, n = 8) or HV then propofol (Group 2, n = 8). With HV, PaCO2 was reduced from 41+/-2 mm Hg to 27+/-3 mm Hg. In Group 1 rabbits, the ICP decreased with treatment (from 26+/-2 to 12+/-2 mm Hg). The reduction in ICP was significantly greater (P = 0.008) than that in Group 2 rabbits (from 26+/-2 to 16+/-5 mm Hg). In both groups, propofol and HV had an additive effect in reducing ICP. Further, when propofol was used as the initial treatment, there was a significant increase in SEP amplitude that was not apparent in Group 2 rabbits. In conclusion, we found propofol and HV to be additive in the treatment of increased ICP. In animals treated with propofol followed by HV, there was a greater decrease in ICP than in rabbits treated initially with HV and then propofol. IMPLICATIONS: We have demonstrated that propofol has a greater effect on increased intracranial pressure than hyperventilation when used as the initial treatment and that the two treatments are additive. Should control of intracranial pressure be required after the administration of propofol, then hyperventilation may be added to the treatment.

Anesthesia↗
PubMed1984

Prolonged hyperventilation and intracranial pressure.

The effects of PaCO2 changes on intracranial pressure (ICP) often remain even after prolonged hyperventilation. Two representative cases are described where PaCO2 rises were directly related to serious rises in ICP after 4, 6, and 14 days of hyperventilation. This is common in head injuries and suggests that where hyperventilation is used to reduce ICP in the presence of brain swelling, withdrawal of the technique should be cautious.

Adolescent↗
PubMed1985

Transition phase during hyperventilation therapy for persistent pulmonary hypertension of the neonate.

It is important for the clinician who is hyperventilating infants with persistent pulmonary hypertension (PPHN) to recognize a transition phase during therapy when pulmonary hypertension is no longer the primary cause of hypoxemia, because infants who are hyperventilated develop parenchymal lung disease after 2 to 3 days. This study reports ten infants who showed PaO2 lability early in the course of PPHN, with an inverse relationship between PaO2 and PaCO2. At a mean age of 79 +/- 14 (SEM) there was a transition phase, after which PaO2 lability decreased and the infants did not require hyperventilation. The mean change in PaO2 per change in PaCO2 was significantly (p less than .05) higher pretransition (22.4 +/- 5.2) compared to during transition (5.1 +/- 1.4) or post-transition (1.9 +/- 1.2). Mean alveolar-arterial oxygen gradient was higher (p less than .05) pretransition (495 +/- 36) vs. post-transition (405 +/- 52) and was more labile relative to PaCO2 change pretransition (20.3 +/- 5.9) compared to post-transition (.3 +/- 2.4). When ventilator settings were reduced after the transition phase, PaCO2 rose by 12.2 torr.

Carbon Dioxide↗
PubMed1985

Pulmonary complications of hyperventilation therapy for persistent pulmonary hypertension.

Hyperventilation has become a primary therapeutic modality in the management of neonates with persistent pulmonary hypertension (PPH). Of 51 PPH infants undergoing hyperventilation therapy, 45% developed pneumothorax. The subgroup which developed pneumothorax was exposed to assisted ventilation for significantly longer time periods and at higher peak inspiratory pressures. They were also exposed to longer periods of oxygen therapy at higher oxygen concentrations. Survival in the pneumothorax group was significantly lower. The incidence of bronchopulmonary dysplasia (BPD) in the 35 survivors was only 6%. These data indicate that the use of hyperventilation to treat PPH is associated with a significant incidence of pneumothorax but a low incidence of BPD.

Bronchopulmonary Dysplasia↗
PubMed1986

Effects of hyperventilation on pattern-reversal visual evoked potentials in patients with demyelination.

The effects of hyperventilation on the pattern-reversal visual evoked potential (VEP) were studied in seven normal subjects and 13 multiple sclerosis patients with visual pathway involvement. Significantly greater reductions in P100 latency occurred in the multiple sclerosis patients than in controls and normalisation of the half-field response topography occurred in one patient after hyperventilation. The VEP changes are attributed to improved impulse transmission in demyelinated fibres in the visual pathway as a result of the alkalosis and changes in ionised calcium levels induced by hyperventilation.

Adult↗
PubMed1979

Running, walking, and hyperventilation causing asthma in children.

To examine further the relation between type of exercise, workload, ventilation, and exercise-induced asthma, we compared treadmill walking with treadmill running and treadmill running with isocapnic hyperventilation in separate studies in children and adolescents. Inspired air conditions were identical during each pair of tests. Walking and running with similar minute ventilation and oxygen consumption were followed by similar falls in peak expiratory flow rate as were running and hyperventilation with similar minute ventilation and end-tidal carbon dioxide tension. This study supports the concept that hyperventilation is a central mechanism in exercise-induced asthma.

Adolescent↗
PubMed1975

Splanchnic hemodynamic response to passive hyperventilation.

Two groups of anesthetized, splenectomized, and paralyzed dogs were hyperventilated (Vt 40 ml/kg). Normocapnia was maintained in one group (mean Paco2 37.6 mm"h'g, mean p"h '7.41) and respiratory alkalosis (mean Paco2 8 mmHg, mean pH 7.75) in the other. Splanchnic hemodynamic responses were similar in both groups. Average hepatic venous pressure increased from 3.2 to 6.4 mmHg in the normocapnic group and from 3.8 to 7.7 mmHg in the hypocapnic group. Average portal venous pressure increased from 10.7 to 12.0 mmHg and 10.8 to 12.7 mmHg in the normocapnic and hypocapnic groups, respectively. Mesenteric vascular resistance increased in 93 per cent of dogs. A decrease in functional intestinal capillary surface area during hyperventilation was indicated by a significant reduction in mesenteric Vo2 (from 15 to 11 ml/min, average 30 per cent), and a concomitant reduction in mesenteric O2 extraction ratio. Changes in mesenteric Vo2 were reflected in calculated splanchinic Vo2. Hepatic O2 uptake was essentially unchanged by tidal hyperventilation with or without hypocapnia.

Alkalosis, Respiratory↗
PubMed1989

Surfactant metabolism during hyperventilation of newborn lambs with atrial right to left shunts.

We studied the effect on surfactant metabolism of 8 h of mechanical ventilation at tidal volumes of 13 +/- 0.3 ml/kg and very high tidal volumes of 28 +/- 1.5 ml/kg, with and without added CO2, in the presence of an atrial right to left shunt in 4- to 8-day-old lambs. Similarly aged, spontaneously breathing lambs were used as controls. Right to left atrial shunts were created by inflating a balloon in the right atrium after a Rashkind atrial septostomy, thus creating a stable, easily controlled atrial shunt. Radiolabeled surfactant phospholipid precursors were used to probe incorporation into and secretion of surfactant phosphatidylcholine, whereas intratracheally administered labeled natural surfactant was used to evaluate alveolar clearance. Protein leak from the vascular space to the lungs was measured using radioactive iodine-labeled albumins. At the end of the 8-h study period, tissue association of alveolar surfactant was significantly increased to 63% in the mechanically hyperventilated lambs as compared to 44% in those lambs mechanically ventilated but not hyperventilated (p less than 0.05) and to 39% in the spontaneously breathing control animals (p less than 0.05). No increased surfactant secretion or decreased compliance was detected with hyperventilation. However, the lambs had very large surfactant-saturated phosphatidylcholine pool sizes, and a large portion (50%) was already in the alveolar pool, even in the spontaneously breathing lambs. Precursor incorporation into saturated phosphatidylcholine was similar in all groups, and very low and comparable protein leaks were seen in the different groups of lambs.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Acute tetrachloroethylene poisoning--blood elimination kinetics during hyperventilation therapy.

After ingestion of 12-16 g tetrachloroethylene, a 6-year-old boy was admitted to the clinic in coma. In view of the high initial tetrachloroethylene blood level, hyperventilation therapy was performed. Under this therapeutic regimen, the clinical condition of the patient improved considerably. The tetrachloroethylene blood level profile which was determined under hyperventilation therapy could be computer-fitted to a two-compartment model. Elimination of tetrachloroethylene from the blood compartment occurred via a rapid and a slow process with half-lives of 30 min and 36 hours, respectively. These values compared favourably with the half-lives of 160 min and 33 hours under normal respiratory conditions. During hyperventilation therapy, the relative contribution to the fast elimination process increased from 70% for physiological minute volume to 99.9%. A minor fraction of the ingested dose was excreted with the urine (integral of 1% during the first 3 days). In contrast to previous results, trace amounts of unchanged tetrachloroethylene were detected in the urine besides trichloroacetic acid and trichloroethanol.

Acute Disease↗
PubMed1995

An additional therapeutic effect of adequate hyperventilation in severe acute brain trauma: normalization of cerebral glucose uptake.

In a total of 309 frequent serial studies, arteriojugular differences in glucose and oxygen levels were concurrently evaluated in 33 adult patients who were experiencing the most acute phase of severe brain trauma. Hyperventilation therapy was optimized to maintain both normalized intracranial pressure and cerebral extraction of oxygen. Under these circumstances, global cerebral glucose extraction was found to be closest to normal during profound optimized hyperventilation, with PaCO2 levels below 25 mm Hg. In contrast, during normocapnia global cerebral glucose extraction dropped below normal range, indicating impairment of cerebral glucose uptake. Findings from this study show that in severe acute brain injury, optimized hyperventilation exerts an additional metabolic effect with respect to cerebral glucose uptake.

Adolescent↗
PubMed2000

Effect of hyperventilation on brain tissue oxygen pressure, carbon dioxide pressure, pH value and intracranial pressure during intracranial hypertension in pigs.

OBJECTIVE: To study the effect of hyperventilat ion on brain tissue oxygen pressure (P(ti)O(2)), brain tissue carbon dio xide pressure (P(ti)O(2)), pH value and intracranial pressure (ICP) dur ing intracranial hypertension in pigs. METHODS: Autologous arterial blood (5.5 mlplus minus0.5 ml) was injected into the left frontal lobe by micropump to establish the model of intr acerebral hematoma in pigs. After blood injection, the animals were hyperventila ted for 15 minutes to decrease the pressure of carbon dioxide in arterial blood (P(a)CO(2)) to 27.35 mm Hgplus minus11.97 mm Hg (1 mm Hg=0.133 kPa). The mean arterial pressure (MAP), intracranial pressure (ICP), cerebral perfusion pressure (CPP), P(ti)O(2), (P(ti)CO(2)), pH value and [HCO(3)(-)] were continuously monitored and the blood gas was analyzed. RESULTS: After hyperventilation, the ICP significantly decr eased (P<0.01), the CPP significantly increased (P<0.05), while the P(ti)O(2) greatly decreased to t he ischemic level (8.20 mm Hgplus minus2.50 mm Hg) (P<0.01), the P(ti)CO(2) decreased (P<0.01) and the pH value increased (P<0.01). At the same time, bl ood gas analysis showed that the P(a)CO(2) greatly decreased and the pH valu e increased. CONCLUSIONS: Hyperventilation can decrease the ICP and the P(ti)O(2) significantly. Therefore, hyperventilation should be avoided earl y after brain injury. The P(ti)O(2) monitoring will be helpful for detec ting cerebral ischemia early.

Journal Article↗