Cases reported "Hypercapnia"

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1/17. subarachnoid hemorrhage following permissive hypercapnia in a patient with severe acute asthma.

    In this article, we describe a case of a subarachnoid hemorrhage (SAH) in an acute severe asthma patient following mechanical hypoventilation. A 49-year-old man was admitted to an intensive care Unit with an acute exacerbation of asthma. After 3 days of mechanical ventilation (hypercapnia and normoxaemia), it was noted that his right pupil was fixed, dilated, and unreactive to light. Computed tomography (CT) scan showed localized SAH within the basilar cisterns and diffuse cerebral swelling. On the fourth day, a new CT scan showed hemorrhage resorption and a cerebral swelling decrease. In the following days, the patient's condition continued improving with no detectable neurological deficits. A review of similar published reports showed that all patients performed respiratory acidosis, normoxaemia, and hypercapnia. The most frequent neurological sign was mydriasis, and all subjects showed cerebral edema. Since normoxaemic hypercapnia has been associated with absence, or less cerebral edema, we considered additional factors to explain cerebral edema and intracranial hypertension causes. Thus, intrathoracic pressures due to patient's efforts by forcibly exhaling, or during mechanical ventilation, would further increase intracranial pressure by limiting cerebral venous drainage. This case emphasizes the fact that patients with acute severe asthma who have developed profoundly hypercarbic without hypoxia before or during mechanical ventilation, may have raised critical intracranial pressure.
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keywords = hypoventilation
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2/17. An unusual cause of tracheal stenosis.

    PURPOSE: To report a large chronic tracheal foreign body, causing tracheal stenosis in an 11-yr-old girl. CLINICAL FEATURES: The history was suggestive of obstructive airways disease with secondary bronchiectasis. Physical findings were crepitations and rhonchi all over the chest. Blood gases were normal. Chest X-ray showed bronchiectasis and a ventilation perfusion scan identified a tracheo-esophageal fistula. During anesthesia to confirm this, intubation and ventilation were difficult because of tracheal stenosis. The hypoventilation resulted in severe hypercarbia and acidosis. A subsequent CT scan showed a stenosis of 2 mm diameter and 1 cm length in the middle third of trachea, bronchiectasis, and an air filled pocket between the trachea and esophagus. PFT showed a severe obstruction. Antitubercular treatment which was started on the presumptive diagnosis of tuberculous stenosis and tracheoesophageal fistula caused a delay with deterioration of patient from intermittent dyspnea to orthopnea with severe hypecarbia and acidosis. The anesthetic management of the tracheal reconstruction was difficult due to her moribund condition even after medical treatment, the short length of the trachea above the obstruction, its severity and lack of resources for alternative techniques. A large foreign body was found lying obliquely in the trachea dividing it into an anterior narrow airway mimicking a stenosed trachea, and a wider posterior blind passage. CONCLUSION: The anesthetic consequences were peculiar to the unexpected etiology of the stenosis and poor general condition of the patient. Minor details like the tracheal tube bevel and ventilatory pattern became vitally important.
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keywords = hypoventilation
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3/17. Uncontrollable high-frequency tachypnea in a case of unilateral medial medullary infarct.

    BACKGROUND: Medullary infarcts can be associated with breathing disorders that usually consist in central hypoventilation. PATIENT: We describe the case of a 54-year-old man, fully conscious, presenting with an uncontrollable high frequency and shallow tachypnea (95/min) at the onset of a unilateral medial medullary infarct. This disorder disappeared under inspiratory pressure support mechanical ventilation. MEASUREMENTS AND RESULTS: Respiratory drive (respiratory rate, occlusion pressure, and mean inspiratory flow), efferent pathway (transcranial and cervical magnetic stimulation), and afferent pathway (response to CO(2) and to lung inflation) were investigated. The respiratory drive was increased. The phrenic nerve conduction time was normal. The sensitivity of the central pattern generator to lung inflation and to CO(2) was preserved. The territory of the infarct was supplied by the spinal anterior artery. CONCLUSIONS: An extremely rapid and shallow tachypnea due to the increase in respiratory drive can be associated with unilateral medullary infarction.
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keywords = hypoventilation
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4/17. Acute respiratory failure and sleep-disordered breathing in arnold-chiari malformation.

    We report on the case of a 32-year-old man who was admitted after an episode of acute respiratory failure. Clinical and laboratory investigations revealed nocturnal hypoventilation with predominately obstructive sleep apneas accompanied by lower cranial nerve palsies, cerebellar and mild pyramidal signs. magnetic resonance imaging disclosed Arnold-Chiari type I malformation with syringomyelia. transcranial magnetic stimulation demonstrated the integrity of the corticodiaphragmatic pathway and it was postulated that the respiratory disorder was mainly due to the severe and irreversible lower cranial nerve palsies. Two years after decompressive craniectomy, sleep disordered-breathing persisted despite no radiological evidence of brain stem compression. Nevertheless, non-invasive positive pressure ventilation (NIPPV) during sleep proved to be quite effective in the management of the patient's refractory respiratory insufficiency. In conclusion, Arnold-Chiari type I may rarely present with acute respiratory failure and sleep apneas. An electrophysiological investigation into the mechanism of the respiratory dysfunction is presented.
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keywords = hypoventilation
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5/17. Nonrecurring transient cortical blindness after coronary angiography: a role for hypoventilation and hypercarbia?

    A 73-year-old morbidly obese patient suffered cortical blindness following coronary angiography. Symptoms rapidly resolved and did not recur following a repeated procedure. hypoventilation due to narcotics with subsequent hypercarbia and blood-brain barrier breaching may be implicated in the pathogenesis of this complication.
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ranking = 4
keywords = hypoventilation
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6/17. Severe hypercapnia associated with a non-respiratory alkalosis.

    A case of hypoventilation in response to a non-respiratory alkalosis is presented. It is postulated that the degree of hypoventilation encountered was a normal response and that a fall in intracellular hydrogen ion concentration was responsible for the hypoventilation. This explains why the alkalosis associated with potassium deficiency is not associated with hypoventilation since the intracellular hydrogen ion concentration then remains constant. The renal response in this condition is responsible for maintaining the alkalosis and seems to be aimed at sodium conservation and hence plasma volume control rather than defence of acid-base balance.
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ranking = 4
keywords = hypoventilation
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7/17. Central hypoventilation in a seven year old child following pertussis treated with negative pressure ventilation.

    We report the case of a 7 year old girl who developed central hypoventilation following pertussis and who was treated by negative pressure ventilation using a new portable tank respirator. We believe this is the first reported case of central hypoventilation following pertussis successfully treated by intermittent negative pressure ventilation.
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ranking = 6
keywords = hypoventilation
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8/17. Treatment of alveolar hypoventilation in a six-year-old girl with intermittent positive pressure ventilation through a nose mask.

    persons with alveolar hypoventilation have abnormal daytime arterial blood gases and abnormal responses to hypercapnia and hypoxia in the absence of any identifiable lung or neuromuscular disease. The underlying defect in the control of breathing has not, however, been confirmed. We studied a 6-yr-old girl who was admitted in respiratory failure after a long history of disturbed breathing awake and asleep, which had been diagnosed as primary alveolar hypoventilation, (PaCO2 = 120). After several days of endotracheal intubation and assisted ventilation, her condition improved and she was extubated. At this time her ventilatory response to hypoxia was absent (VE/SaO2:0.1 l/min/% at a CO2 of 45) and there was a right-shifted response to hypercapnia (VE/PaCO2:2.6 l/min/mmHg). As obstructive sleep apnea was suspected, nocturnal nasal continuous positive airway pressure (CPAP) was tried; however, it was not effective in maintaining arterial oxyhemoglobin saturation. Definite central apneas were observed during sleep both with and without nasal CPAP, and there was an absence of snoring. Her condition deteriorated, and there was a progressive increase in her awake arterial CO2 levels for a period of 4 wk. The IPPV with 5 cm H2O of PEEP was administered through a nose mask during sleep and this maintained both oxygen saturation and transcutaneous CO2 levels within the normal range. After 10 days of nocturnal assisted ventilation, the hypercapnic response returned to the normal position (VE/CO2:2.1 l/min/mmHg).(ABSTRACT TRUNCATED AT 250 WORDS)
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ranking = 6
keywords = hypoventilation
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9/17. Marked hypochloremic metabolic alkalosis with severe compensatory hypoventilation.

    In metabolic alkalosis, a compensatory decrease in alveolar ventilation with hypercapnia has been noted only rarely. We recently managed a patient with gastric outlet obstruction from a duodenal ulcer who survived after arriving in the emergency room comatose with severe hypochloremic metabolic alkalosis, compensatory hypoventilation, and hypercapnia. We know of no report in the English literature of a patient with gastric outlet obstruction having a respiratory acidosis or hypochloremia as severe as that in our patient. Proper understanding of the pathophysiology of primary metabolic alkalosis due to gastric losses is necessary to correct the acid-base abnormalities quickly and to restore normal alveolar ventilation.
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ranking = 5
keywords = hypoventilation
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10/17. Reversible hypercapnic respiratory insufficiency in scleroderma caused by respiratory muscle weakness.

    A patient with scleroderma presented with hypercapnic respiratory failure. Evaluation of pulmonary mechanics revealed severe restriction caused in part by respiratory muscle weakness. Treatment with prednisone corrected hypoventilation, improved symptoms, increased lung volumes, returned respiratory muscle strength to normal range, but did not change the degree of lung stiffness. This case demonstrates that restrictive patterns in scleroderma can be due to either lung or chest wall disease and that the latter may be reversible. If respiratory muscle weakness is present with restrictive ventilatory patterns in patients with scleroderma, a therapeutic trial of corticosteroid is warranted.
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ranking = 1
keywords = hypoventilation
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