61/147. Flexible bronchoscopic removal of radioccult polyurethane foam, with pneumonitis in a hyperventilated lobe. An intellectually delayed adult ingested and aspirated a large quantity of polyurethane foam, developing acute respiratory failure in association with partial airway obstruction. The foam was identified by flexible bronchoscopy and successfully removed from the bronchus intermedius and left mainstem bronchus with a retrieval basket. This facilitated normalization of blood gases and eventual recovery. However, the unobstructed right upper lobe became infiltrated radiographically, presumably resulting from regional hyperinflation and/or occult focal aspiration. ( info) |
| A 52-year-old woman developed subjective right hemiparesthesias over a two-day period. Because of a paucity of physical findings, apparent anxiety with tachypnea, and a respiratory alkalosis with hypocapnia, a diagnosis of hyperventilation syndrome was considered. However, because of the unilateral symptoms, a computed tomography scan was performed, demonstrating a left posterior thalamic infarct. Most reports of thalamic infarct indicate altered mental status, vertical gaze palsies, or sensorimotor hemiparesis with sensory involvement predominant. The case of a patient with thalamic hemorrhage who presented with only hemiparesthesia is reported to heighten clinicians' awareness of this diagnosis. ( info) |
63/147. Integrating music in breathing training and relaxation: II. Applications. Psychophysiological observations, especially PETCO2 and EEG, during relaxation training with deep-diaphragmatic breathing and mental imagery, suggest that the addition of certain types of music "deepens" breathing and quickens relaxation: PETCO2 "normalizes" with decreased respiration rate, and EEG shows decreased average theta and increased alpha. The combined psychophysiological indices suggest that music potentiates the hypometabolic counterarousal state. And clients unanimously report that they enjoy it. ( info) |
| 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. ( info) |
65/147. 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) ( info) |
66/147. Dual-respiratory rhythms. A key to diagnosis of diaphragmatic flutter in patients with HVS. We discuss three cases of diaphragmatic flutter in patients with extreme polypnea and symptoms of respiratory alkalosis. Initially, the diagnosis for each case was HVS. However, analysis of the respiratory pattern during attacks revealed two frequencies. A fast respiratory rhythm (230 to 250 breaths per minute) was superimposed on a slow rhythm (15 to 30 breaths per minute). The fast rhythm maintained blood gases at normal limits or hypocapnic levels. The dual respiratory rhythms, which do not occur with HVS, indicated diaphragmatic flutter. In addition, the usual treatment for HVS-breathing CO2 mixed air-did not influence the attacks. For two of the three patients, an intravenous dose of DPH suppressed the abnormal respiratory patterns immediately and completely. The third patient responded to an intramuscular injection of haloperidol. For these cases, the dual respiratory rhythms were the key to diagnosis of diaphragmatic flutter which accompanied hyperventilation. ( info) |
| 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. ( info) |
| We report a case of acute myocardial infarction following a hyperventilation test performed at coronary angiography. The potential pathophysiological mechanisms and clinical implications are discussed. ( info) |
| There is uncertainty about the diagnosis and definition of the hyperventilation syndrome. We prefer to regard hyperventilation (or hypocapnia with which it is synonymous) as a physiological response to abnormally increased respiratory "drive", which can be caused by a wide range of organic, psychiatric and physiological disorders, or a combination of these. This review outlines a clinical scheme for the diagnosis and assessment of hyperventilation and its causes. ( info) |
70/147. High incidence of primary cerebral lymphoma in tumor-induced central neurogenic hyperventilation. An awake patient presented with central neurogenic hyperventilation induced by a cerebral tumor. Corticosteroid therapy and brain irradiation while the patient was anesthetized and respiration controlled under pancuronium-induced respiratory paralysis were followed by tumor regression and resolution of hyperventilation. recurrence of tumor 6 weeks later was not accompanied by recurrence of hyperventilation. Cytologic study of cerebrospinal fluid revealed B-cell lymphoma. This patient brings to 10 the number of cases recorded with tumor-induced central neurogenic hyperventilation. Five of the eight patients with known tumor histology had a primary cerebral lymphoma, a rare neoplasm that comprises only 1% of all intracranial neoplasms. The disproportionately high frequency of central neurogenic hyperventilation in patients with cerebral lymphoma has therapeutic implications that are briefly reviewed. ( info) |