Cases reported "Hyperventilation"

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1/22. 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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2/22. 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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3/22. Psychosomatic disorders in pediatrics.

    Psychosomatic symptoms are by definition clinical symptoms with no underlying organic pathology. Common symptoms seen in pediatric age group include abdominal pain, headaches, chest pain, fatigue, limb pain, back pain, worry about health and difficulty breathing. These, more frequently seen symptoms should be differentiated from somatoform or neurotic disorders seen mainly in adults. The prevalence of psychosomatic complaints in children and adolescents has been reported to be between 10 and 25%. These symptoms are theorized to be a response to stress. Potential sources of stress in children and adolescents include schoolwork, family problems, peer pressure, chronic disease or disability in parents, family moves, psychiatric disorder in parents and poor coping abilities. Characteristics that favour psychosomatic basis for symptoms include vagueness of symptoms, varying intensity, inconsistent nature and pattern of symptoms, presence of multiple symptoms at the same time, chronic course with apparent good health, delay in seeking medical care, and lack of concern on the part of the patient. A thorough medical and psychosocial history and physical examination are the most valuable aspects of diagnostic evaluation. Organic etiology for the symptoms must be ruled out. Appropriate mental health consultation should be considered for further evaluation and treatment.
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4/22. Widespread reduction of regional cerebral blood flow during hyperventilation-induced EEG slowing ('buildup'). observation from subtraction of brain imaging with single photon emission computed tomography using technetium-99m hexamethyl-propyleneamine oxime.

    To study the pathophysiological mechanisms of hyperventilation-induced EEG showing, i.e., the so-called 'buildup' phenomenon, changes in regional cerebral blood flow (rCBF) were investigated before and during the phenomenon in a 16-year-old woman with headache, thought to be of neurotic origin, by subtraction technique of brain images with single photon emission computed tomography using technetium-99m hexamethyl-propyleneamine oxime (99mTc-HMPAO). The tracer uptake during buildup decreased by 31-42% as compared to baseline values at rest before buildup in all of the measured regions, reflecting a widespread reduction in rCBF. Gas analyses of arterial blood collected during buildup showed a decrease in PaCO2, and increases in PaO2 and pH with a slight decrease in blood pressure and an increase in pulse rate. These results directly demonstrate a close correlation between the hyperventilation-induced EEG and rCBF changes, suggesting that the buildup phenomenon results from cerebral ischemic change, presumably due to cerebral vasoconstriction caused by the PaCO2 decrease.
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5/22. Dynamic changes in regional CBF, intraventricular pressure, CSF pH and lactate levels during the acute phase of head injury.

    The authors measured regional cerebral 133xenon (133Xe) blood flow (rCBF), intraventricular pressure (IVP), cerebrospinal fluid (CSF) pH and lactate, systemic arterial blood pressure (SAP), and arterial blood gases during the acute phase in 23 comatose patients with severe head injuries. The IVP was kept below 45 mm Hg. The rCBF was measured repeatedly, and the response to induced hypertension and hyperventilation was tested. Most patients had reduced rCBF. No correlation was found between average CBF and clinical condition, and neither global nor regional ischemia contributed significantly to the reduced brain function. No correlation was found between CBF and IVP or CBF and cerebral perfusion pressure (CPP). The CSF lactate was elevated significantly in patients with brain-stem lesions, but not in patients with "pure" cortical lesiosn. The 133Xe clearance curves from areas of severe cortical lesions had very fast initial components called tissue peaks. The tissue peak areas correlated with areas of early veins in the angiograms, indicating a state of relative hyperemia, referred to as tissue-peak hyperemia. Tissue-peak hyperemia was found in all patients with cortical laceration or severe contusion but not in patients with brain-stem lesions without such cortical lesions. The peaks increased in number during clinical deterioration and disappeared during improvement. They could be provoked by induced hypertension and disappeared during hyperventilation. The changes in the tissue-peak areas appeared to be related to the clinical course of the cortical lesion.
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6/22. Breath-holding spells in somatoform disorder.

    Breath-holding spells (BHS) are commonly seen in childhood. However, there are no case reports of BHS occurring in adolescents or young adults. We report two young adult cases and discuss the pathogensis, both physically and psychologically. BHS occurred for 1-2 minutes after hyperventilation accompanied by cyanosis in both cases. oxygen saturation was markedly decreased. Each patient had shown distress and a regressed state psychologically. These cyanotic BHS occurred after hyperventilation, and we considered that a complex interplay of hyperventilation followed by expiratory apnea increased intrathoracic pressure and respiratory spasm. Breath-holding spells can occur beyond childhood.
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7/22. Pulmonary hyperinflation and respiratory distress following solvent aspiration in a patient with asthma: expectoration of bronchial casts and clinical improvement with high-frequency chest wall oscillation.

    An 18-year-old student with a history of asthma accidentally inhaled organic solvent during a class, with immediate cough and dyspnea that worsened over several hours. He presented in severe respiratory distress, with hypoxemia and marked pulmonary hyperinflation. Administration of inhaled bronchodilator was ineffective because of agitation, and the patient could not be positioned for chest physiotherapy to treat presumed widespread mucus plugging. High-frequency chest wall oscillation (HFCWO) in the sitting position initially caused increased distress but was subsequently tolerated when noninvasive positive-pressure ventilation (NPPV) via nasal mask was initiated. Almost immediately, the patient began expectorating bronchial mucus casts, with concomitant clinical improvement. Endotracheal intubation was avoided, and with aggressive pharmacologic treatment for acute severe asthma and continuation of intermittent HFCWO-NPPV, the patient made a full recovery over the next several days. This case suggests that the combination of HFCWO and NPPV may be helpful in the presence of mucus plugging as a complication of acute inhalation injury or acute severe asthma.
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8/22. 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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9/22. Self-administered hyperventilation cardiopulmonary resuscitation for 100 s of cardiac arrest during Holter monitoring.

    An 80-year-old man remained conscious due to vigorous deep breathing during 100 s of ventricular arrest which was recorded on a Holter ECG. Arterial blood flow is considered to have been maintained by changes in intrathoracic pressure produced by deep respiratory movements. This case may represent a pure model of the "thoracic pump" mechanism.
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10/22. Central neurogenic hyperventilation: pharmacologic intervention with morphine sulfate and correlative analysis of respiratory, sleep, and ocular motor dysfunction.

    Central neurogenic hyperventilation (CNH), for which there is no effective therapy, can eventually result in respiratory fatigue and death. This report describes a patient with CNH due to a brainstem anaplastic astrocytoma who also exhibited disturbances of sleep and ocular motor function. The CNH responded clinically to morphine sulfate and methadone. Analysis of ventilatory response to CO2 before and after morphine demonstrated a depression of ventilatory response (49 to 53% of baseline) and occlusion pressure response (35 to 50% of baseline) to CO2, with a requirement for high doses of naloxone (10 mg IV) to reverse the effect. polysomnography revealed sustained hyperventilation, elevated O2 saturation, and low end-tidal CO2 throughout all stages of non-rapid eye movement (NREM) sleep, and absence of rapid eye movement (REM) sleep. Ocular motor evaluation disclosed absence of horizontal and reflexive saccades with compensatory head thrusts. Correlation of the clinical and physiologic data with the MRI abnormalities suggested that the lesion responsible for CNH in this patient might reside in the medial tegmental parapontine reticular formation. Since recurrent episodes of hyperventilation responded in a sustained fashion to IV and oral opiates, this treatment may warrant consideration in other patients with CNH.
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