Cases reported "Hyperventilation"

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1/16. Correlation between jugular bulb oxygen saturation and partial pressure of brain tissue oxygen during CO2 and O2 reactivity tests in severely head-injured patients.

    PURPOSE: To correlate the jugular bulb oxygen saturation (SjvO2) and brain tissue oxygen pressure (PbtO2) during carbon dioxide (CO2) and oxygen (O2) reactivity tests in severely head-injured patients. methods AND RESULTS: In nine patients (7 men, 2 women, age: 26 /- 6.5 years, GCS of 6.5 /- 2.9), a polarographic microcatheter (Clark-type) was inserted into nonlesioned white matter (frontal lobe). PbtO2 and SjvO2 were monitored simultaneously and cerebral vasoreactivity to CO2 and O2 was tested on days three, five and seven after injury. Simultaneous measurements of vasoreactivity by transcranial Doppler (TCD) were undertaken. A total of twenty-one CO2 and O2 reactivity tests were performed. Critical values of PbtO2 (< 15 mm Hg) during induced hyperventilation could be observed four times in two patients. High PbtO2 values up to 80 mm Hg were observed during hyperoxygenation (FiO2 100%). CO2 vasoreactivity by means of PbtO2 was absent in four tests in which measurements by TCD showed intact responses. A stronger correlation between SjvO2 and PbtO2 during the O2 reactivity tests was observed (r = 0.6, p < 0.001), in comparison to values obtained during the CO2 reactivity tests (r = 0.33, p < 0.001). In addition, there was no statistically significant correlation (r = 0.22, p = 0.26) between CO2 reactivity values measured by TCD (4.5 /- 5.7%) and PbtO2 (3 /- 2.8%). CONCLUSIONS: Correlation between SjvO2 and PbtO2 during CO2 reactivity test is low, even if significant differences between normo- and hyperventilation values are present. In comparison to SjvO2, monitoring of PbtO2 might more accurately detect possible focal ischaemic events during rapidly induced hyperventilation in severely head-injured patients. The CO2 vasoreactivity by means of changes in Vm MCA seems to be higher in comparison to changes of PbtO2. These observations lead to the hypothesis that vasoreactivity measured by TCD overestimates the cerebrovascular response to CO2.
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2/16. Continuous monitoring of cerebrospinal fluid acid-base balance and oxygen metabolism in patients with severe head injury: pathophysiology and treatments for cerebral acidosis and ischemia.

    INTRODUCTION: Continuous monitoring of cerebral acid-base balance and oxygen metabolism has been introduced in neurointensive care settings. The hypothesis of this study utilizing multimodal neuromonitoring modalities is that hyperventilation and hypothermia improve cerebral acidosis through prevention of cerebral ischemia aggravation in patients with severe head injury. patients AND methods: Continuous monitoring of cerebrospinal fluid (CSF) pH, PCO2, HCO3-, base excess (BE), PO2, SO2, temperature, lactate and pyruvate (La and Py) measurements were conducted in 8 patients with severe head injury. temperature-corrected CSF parameters were correlated with those in the jugular blood including oxygen saturation (SjO2), regional oxygen saturation (rSO2), intracranial pressure (ICP) and cerebral perfusion pressure (CPP), jugular blood temperature (Tjb), and endtidal PCO2 (PetCO2). Therapeutic significance of hyperventilation and hypothermia was evaluated. RESULTS: 1) CSF acidosis was observed in all cases (minimum pH 6.59-7.17) due to increased CSF PCO2 and/or decreased CSF HCO3- and tended to associate with abnormal ICP and/or CPP or ischemic episodes indicated by CSF PO2 and SO2, rSO2, and/or SjO2 during monitoring. 2) It was more obvious in CSF than in jugular blood that increased PCO2, La and Py, and/or decreased HCO3- resulted in decreased BE and pH. 3) Decreased CSF PO2 and SO2 only correlated with severe CSF acidosis. 4) hyperventilation: Decreased PetCO2 did not always closely correlate with CSF PCO2 decrease and CSFpH increase. 5) hypothermia: There were negative correlations of Tjb with CSF pH and SO2 in all cases, though correlation coefficients were not always high. CONCLUSIONS: CSF acidosis caused by increased CSF PCO2, La and Py, and/or decreased HCO3- tended to associate with abnormal ICP and CPP, and desaturation indicated by CSF SO2, rSO2, and/or SjO2. hypothermia rather than hyperventilation tends to improve cerebral acidosis and ischemia.
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3/16. Central neurogenic hyperventilation with primary cerebral lymphoma: a case report.

    We report a case of a bright, alert patient with central neurogenic hyperventilation (CNH) associated with cerebral malignant lymphoma. CNH is a syndrome comprising normal or elevated arterial oxygen tension, decreased arterial carbon dioxide tension, and respiratory alkalosis in the absence of cardiac or pulmonary disease that stimulates a compensatory hyperpnea. A-72-year-old man with recurrent central nervous system lymphoma presented with hyperpnea. showing a respiratory rate over 30 per minute. He was fully awake and conscious. Routine laboratory studies and chest X-ray were normal, but arterial blood gas examination on room air showed respiratory alkalosis, regardless of wakefulness or sleep. pulmonary infarction was denied by pulmonary flow scintigram. Rebreathing from a paper bag, intravenous administration of diazepam, and oxygen inhalation failed to alter the respiratory pattern. Brain MRI demonstrated two mildly enhanced lesions within the left side of the medulla oblongata and right side of the pons. CNH is rare in patients with normal consciousness. It seems to be caused by brainstem injury that includes the respiratory center.
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4/16. Positional hyperventilation-induced hypoxaemia in pectus excavatum.

    The presented case is of a young male (aged 19 yrs) with a pectus excavatum who showed significant exercise intolerance, despite normal pulmonary function at rest, including carbon monoxide diffusing capacity. Clinical exercise testing led to a strong suspicion of a right-to-left shunt due to an abnormally wide alveolo-arterial oxygen gradient (26.4 kPa) at peak oxygen uptake, with severe arterial hypoxaemia (arterial oxygen tension 12.54 kPa). A right-to-left shunt was confirmed by transoesophageal echocardiography demonstrating a permeable foramen ovale, despite normal right heart pressures. The right-to-left venous flow was mainly dependent on the upright body position and the deep inspiration. Indeed, i.v. dobutamine infusion to selectively affect cardiac output and hyperventilation induced by tidal volume expansion at constant breathing rate in the supine position did not result in arterial oxygen desaturation or shunting. Closure of the foramen ovale through atrial umbrella placement dramatically improved clinical and physiological abnormalities. This observation demonstrates that a hyperventilatory manoeuvre in the upright position is able to detect a permeable foramen ovale favouring flow in the inferior vena cava in the direction of the abnormal pre-existing atrial channel in a patient with a pectus excavatum.
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5/16. Cyanotic episodes in a male child with fragile x syndrome.

    A 9-year-old male with a diagnosis of fragile x syndrome (FXS) was evaluated for cyanotic episodes of unknown etiology. Clinical observation revealed frequent episodes of hyperventilation lasting several minutes, only while the patient was awake. This was followed by apnea associated with cyanosis and oxygen desaturation. Polysomnogram confirmed episodic central apnea temporally associated with hypocapnia, only during the awake state. Extensive evaluation failed to reveal other neurological, cardiac, gastrointestinal, or pulmonary etiologies for the events. The clinical observations and investigations allowed us to conclude that the patient's cyanotic episodes were caused by primary behavioral hyperventilation in the awake state. Similar behaviors have been reported in children with a variety of diagnoses but to our knowledge have not been previously reported in children with FXS. Treatment for this unusual behavior in FXS consists of reassurance and behavior modification to decrease the frequency and severity of the cyanotic episodes.
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6/16. Hypoxic hazards of traditional paper bag rebreathing in hyperventilating patients.

    It is traditional practice to treat acute hyperventilation (thought to be due to anxiety) by having patients rebreathe into a brown paper bag. The author reports three cases in which this treatment, erroneously applied to patients who were hypoxemic or had myocardial ischemia, resulted in death. This clinical experience motivated a study of the effects of paper bag rebreathing in normal volunteers. Subjects deliberately hyperventilated to an average end-tidal CO2 concentration of 21.6 (SD, 3.2) mm Hg and then continued to hyperventilate into a no. 4 Kraft brown paper bag containing the calibrated sensors for a Hewlett-Packard 47210A capnograph and a Teledyne TED 60J digital oxygen monitor. Fourteen men and six women with an average age of 36 years (SD, 6.1) were tested. Results are reported as mm Hg. After 30 seconds of rebreathing, mean change in O2 from room air was -15.9 (SD, 4.6) and mean CO2 was 38.7 (SD, 6.2); at 60 seconds, -20.5 (6.0) and 40.2 (6.4); at 90 seconds -22 (6.8) and 40.5 (6.4); at 120 seconds -23.6 (6.8) and 40.7 (6.5); at 150 seconds -25.1 (1.2) and 41 (7.3); and at 180 seconds -26.6 (8.4) and 41.3 (7.5). A few subjects achieved CO2 levels as high as 50, but many never reached 40. The mean maximal drop in O2 was 26 (8.8); seven subjects had drops in oxygen of 26 mm Hg at three minutes, four had drops of 34 mm Hg, and one had a drop of 42 mm Hg.(ABSTRACT TRUNCATED AT 250 WORDS)
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7/16. Cardiovascular response to acute airway obstruction and hypoxia.

    We wished to evaluate the role of hypoxia in the production of cardiovascular manifestations of acute airway obstruction. We monitored blood pressure, electrocardiogram, and radionuclide ejection fraction in 14 healthy volunteers on exposure to four experimental conditions: expiratory resistive loading while breathing room air (RAL), expiratory resistive loading while hypoxic (HL), hypoxia alone (H), and expiratory resistive loading while voluntarily hyperventilating in a pattern similar to HL trials (VL). Mean respiratory-related oscillation in systolic blood pressure (pulsus paradoxus) increased significantly under each experimental condition compared with those at baseline (2 /- 2.3 mm Hg): for RAL, 21 /- 8.4 mm Hg; for HL, 34 /- 16.3 mm Hg; for H, 10 /- 5.4 mm Hg; for VL 26 /- 13.4 mm Hg. Pulsus paradoxus was significantly greater under conditions of moderate hypoxia (saturation, 80%) than of mild hypoxia (saturation, 90%). Electrocardiographic changes were more marked under HL and H conditions than under RAL and VL conditions. HL induced changes in blood pressure and frontal QRS axis that were qualitatively similar to those seen in naturally occurring asthma. Radionuclide ejection fraction showed no dramatic change with any experimental condition. We conclude that hypoxia magnifies the cardiovascular changes induced by acute expiratory resistive loads and may contribute to the degree of pulsus paradoxus seen in severe asthma.
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keywords = hypoxia
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8/16. hyperventilation in the awake state: potentially treatable component of rett syndrome.

    hyperventilation, which occurs in some patients with severe mental handicap, is a prominent feature in the histories of most girls with rett syndrome but its mechanism and effects have not been established. Respiratory function was therefore studied in 18 patients with rett syndrome and 23 healthy controls. Ten of the patients (56%), but none of the controls, hyperventilated only when awake, and began doing so after a period of normal breathing without hypoxaemia. After hyperventilation was established it was interspersed with prolonged periods of apnoea (over 19 seconds) accompanied by Valsalva manoeuvres. Hypoxaemia (less than 90%) occurred in 47% of these periods of apnoea and five (50%) of the patients had oxygen saturation values of under 50%. During hyperventilation severe hypocapnia developed in every patient, and recorded arterial pH measurements ranged from 7.47 to 7.60. A further four patients (22%) did not hyperventilate, but had clear histories of hyperventilation when younger. All had frequent apnoeic pauses accompanied by Valsalva manoeuvres. The remaining four girls (22%) neither hyperventilated nor gave a clear history of doing so. Three had occasional apnoeic pauses associated with the Valsalva manoeuvres. All but one of the 18 patients had increased quantities of periodic apnoea compared with the control subjects. The hypocapnic alkalaemia and hypoxaemia resulting from hyperventilation may contribute to the cerebral impairment in rett syndrome. Since the hyperventilation is 'primary', and not secondary to preceding apnoea, it is potentially treatable. Further studies will determine if treatment is practical and of benefit.
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9/16. diagnosis and management of postoperative pulmonary hypertensive crisis.

    In this paper we discuss two infants and one child who experienced a previously unreported complication after complete correction of a large, unrestrictive ventricular septal defect. Two patients had documented pulmonary hypertensive crises and severe right-heart failure secondary to hypoxia and pulmonary vasoconstriction. These crises were associated with significantly increased right ventricular (RV) peak systolic and end-diastolic pressures and right-to-left shunting via a foramen ovale which, in turn, exaggerated the hypoxis. The crises were treated successfully with tolazoline in the second and third patients. RV pressure returned to normal values and have remained normal up to 12 months postoperatively in the second patient. Although the RV pressures decreased with tolazoline in the third patient, they never reached normal values. Postoperative monitoring of pulmonary artery and RV pressures in infants with large ventricular septal defects is essential when unexplained complications are encountered. tolazoline proved to be very effective in the treatment of two patients with pulmonary vasoconstriction secondary to hypoxia.
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10/16. aspirin, hyperventilation, and cerebellar infarction in sickle cell disease.

    aspirin ingestion was followed by hyperventilation, cerebellar signs, and fatal brain stem dysfunction in a patient with sickle cell disease. autopsy showed a swollen, recently infarcted cerebellum with tonsillar herniation compressing the medulla. We propose that hypocapnea from aspirin-induced hyperventilation caused carotid artery constriction and focal cerebral hypoxia, resulting in cerebellar sickling nad infarction. Hypocapnea should be treated promptly to prevent brain damage in patients with sickle cell disease.
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