1/32. Acute respiratory alkalosis associated with low minute ventilation in a patient with severe hypothyroidism. PURPOSE: patients with severe hypothyroidism present unique challenges to anesthesiologists and demonstrate much increased perioperative risks. overall, they display increased sensitivity to anesthetics, higher incidence of perioperative cardiovascular morbidity, increased risks for postoperative ventilatory failure and other physiological derangements. The previously described physiological basis for the increased incidence of postoperative ventilatory failure in hypothyroid patients includes decreased central and peripheral ventilatory responses to hypercarbia and hypoxia, muscle weakness, depressed central respiratory drive, and resultant alveolar hypoventilation. These ventilatory failures are associated most frequently with severe hypoxia and carbon dioxide (CO2) retention. The purpose of this clinical report is to discuss an interesting and unique anesthetic presentation of a patient with severe hypothyroidism. CLINICAL FEATURES: We describe an unique presentation of ventilatory failure in a 58 yr old man with severe hypothyroidism. He had exceedingly low perioperative respiratory rate (3-4 bpm) and minute ventilation volume, and at the same time developed primary acute respiratory alkalosis and associated hypocarbia (P(ET)CO2 approximately 320-22 mmHg). CONCLUSION: Our patient's ventilatory failure was based on unacceptably low minute ventilation and respiratory rate that was unable to sustain adequate oxygenation. His profoundly lowered basal metabolic rate and decreased CO2 production, resulting probably from severe hypothyroidism, may have resulted in development of acute respiratory alkalosis in spite of concurrently diminished minute ventilation. ( info) |
2/32. hyperventilation associated with quetiapine. OBJECTIVE: To describe a case of hyperventilation associated with the administration of quetiapine. CASE SUMMARY: A 69-year-old African-American woman admitted to a psychiatric hospital for treatment of major depression with psychotic features was treated and successfully discharged with quetiapine, along with metronidazole and miconazole to treat bacterial/monilial vaginitis. Three days after discharge, the patient presented to a community hospital with shortness of breath and hyperventilation. The patient was admitted and treated for tachypnea and acute respiratory alkalosis. During this hospitalization, the patient was noted to have increased respiratory rate following the administration of quetiapine. DISCUSSION: hyperventilation was reported during the clinical trials of quetiapine; however, this is the first published report to date. serotonin is involved both centrally and peripherally in the regulation of respiration. A contributing factor in this case may have been the concomitant administration of metronidazole, which inhibits the cytochrome P450 enzyme (CYP3A4) also responsible for the metabolism of quetiapine. CONCLUSIONS: The development of hyperventilation and respiratory alkalosis was associated with the administration of quetiapine. ( info) |
3/32. 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. ( info) |
4/32. Central neurogenic hyperventilation in a conscious child associated with glioblastoma multiforme. Central neurogenic hyperventilation refers to progressive tachypnea leading to hypocarbia and respiratory alkalosis caused by cortical disorders, initially reported in comatose patients with mainly pontine infarction. Central neurogenic hyperventilation in conscious patients is even rarer, numbering around 30 reported cases including seven children, mainly associated with infiltrative gliomas and lymphomas of the brainstem and pons. We report the evolution of central neurogenic hyperventilation in a conscious child associated with an infiltrative glioblastoma multiforme diagnosed 1 year before admission. He presented with progressive tachypnea and dyspnea of 1 week duration. On examination he was fully alert and aware of his respiratory disorder. respiratory rate was 56 breaths per minute using accessory respiratory muscles. hyperventilation was unchanged during sleep. Arterial blood gases disclosed marked hypocarbia: Pco(2) of 8 mm Hg resulting in severe respiratory alkalosis at pH of 7.8. Central neurogenic hyperventilation was therefore suggested after exclusion of other respiratory or cardiac disorders. The exaggerated tachypnea persisted along with respiratory alkalosis. Over a period of 2 months his overall state markedly deteriorated; he lapsed into coma, and finally succumbed after involvement of medullary cardiovascular centers. Although extremely rare in the pediatric age group, central neurogenic hyperventilation should be suspected in any alert child presenting with unexplained increasing tachypnea and hypocarbia leading to respiratory alkalosis. The evolution of such a disorder may be an alarming sign of ensuing deterioration in patients with tumors of the brainstem and medulla before cardiovascular derangement. ( info) |
| We present an 84-year-old man with a history of chronic obstructive pulmonary disease, type 2 diabetes, hypertension, glaucoma, and bladder cancer who presented to the emergency department after the police found him disoriented and confused. metformin therapy began 3 days before, and he denied any overdose or suicidal ideation. Other daily medications included glipizide, fluticasone, prednisone, aspirin, furosemide, insulin, and potassium supplements. In the emergency department, his vital signs were significant for hypertension (168/90), tachycardia (120 bpm), and Kussmaul respirations at 24 breaths per minute. oxygen saturation was 99% on room air, and a fingerstick glucose was 307 mg/dL. He was disoriented to time and answered questions slowly. metformin was discontinued, and by day 3, the patient's vital signs and laboratory test results normalized. He has been asymptomatic at subsequent follow-up visits. metformin-associated lactic acidosis is a well-known phenomenon. Respiratory alkalosis may be an early adverse event induced by metformin prior to the development of lactic acidosis. ( info) |
6/32. Seizure-like movements during induction of anaesthesia with sevoflurane. Clonic and tonic seizure-like movements of the extremities were observed during induction of anaesthesia with sevoflurane in a 9-yr-old girl. The tonic movements were associated with respiratory alkalosis and were not abolished by an i.v. injection of thiamylal 75 mg. arterial pressure, heart rate and body temperature remained normal during the episode. Ventilation was assisted easily and then controlled via a face mask. No neurological abnormalities were obvious after the anaesthesia. The movements may have been the result of seizure activity in the central nervous system, or myoclonus of the extremities. ( info) |
7/32. An unusual cause of respiratory alkalosis. A 56-year-old man with a longstanding tracheostomy presented to the hospital with upper GI bleeding and was found to have a profound respiratory alkalosis. The cause of this patient's involuntary hyperventilation was hiccuping complicated by the absence of glottic closure. ( info) |
| We describe a patient with central neurogenic hyperventilation secondary to extension of a laryngeal tumor into the base of the brain, resulting in extrinsic compression of the medulla. Such an association has not been previously described. Unique features which distinguish this patient from previously reported cases are emphasized. Possible mechanisms involved in pathogenesis, as well as types of therapy, are outlined. ( info) |
9/32. Stridor in an adult. An unusual presentation of functional origin. A 34-year-old woman with a recent history of a influenza-like illness and signs of bronchopneumonia presented with many of the features of acute epiglottitis, a condition which still carries a high mortality in adults. Urgent laryngoscopy and bronchoscopy under inhalational anaesthesia were negative. The results of arterial blood gases, taken when stridor was at its worst, revealed marked hypocapnia and respiratory alkalosis. We conclude that the resultant acute reduction of serum ionised calcium produced stridor as a result of tetany of the vocal cords. Similar cases from the literature and the role of emotional factors in the aetiology are discussed. ( info) |
10/32. Is maternal alkalosis harmful to the fetus? Normal pregnancy is characterized by a compensated respiratory alkalosis. The effect of maternal alkalosis on the fetus is less well understood than the more common problem of maternal acidosis. We present a case of maternal alkalosis, complicated by bronchial asthma, in which the fetus was stillborn. The pathophysiology of this condition is discussed with data to support the potential harm of maternal alkalosis in pregnancies complicated by a fetus with borderline reserve. In such instances, the fetus should be carefully monitored and consideration might be given to therapy such as the use of acetozolomide, discouraging hyperventilation by the mother and even early delivery of the fetus. ( info) |