1/4. Hypercapnic respiratory failure and partial upper airway obstruction during high frequency oscillatory ventilation in an adult burn patient.PURPOSE: To present a case of severe hypercapnic respiratory failure in an adult burn patient and to describe our clinical problem solving approach during support with an unconventional mode of mechanical ventilation. CLINICAL FEATURES: A 19-yr-old male with smoke inhalation and flame burns to 50% total body surface area was admitted to the Ross Tilley Burn Centre. High frequency oscillatory ventilation (HFOV) was initiated on day three for treatment of severe hypoxemia. By day four, the patient met consensus criteria for acute respiratory distress syndrome. On day nine, alveolar ventilation was severely compromised and was characterized by hypercapnea (PaCO(2) 136 mmHg) and acidosis (pH 7.10). Attempts to improve CO(2) elimination by a decrease in the HFOV oscillatory frequency and an increase in the amplitude pressure failed. An intentional orotracheal tube cuff leak was also ineffective. A 6.0-mm nasotracheal tube was inserted into the supraglottic hypopharynx to palliate presumed expiratory upper airway obstruction. After nasotracheal tube placement, an intentional cuff leak of the orotracheal tube improved ventilation (PaCO(2) 81 mmHg) and relieved the acidosis (pH 7.30). The improvement in ventilation (with normal oxygen saturation) was sustained until the patient's death from multiple organ dysfunction four days later. CONCLUSION: During HFOV in burn patients, postresuscitation edema of the supraglottic upper airway may cause expiratory upper airway obstruction. The insertion of a nasotracheal tube, combined with an intentional orotracheal cuff leak may improve alveolar ventilation during HFOV in such patients.- - - - - - - - - - ranking = 1keywords = alveolar (Clic here for more details about this article) |
2/4. 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)- - - - - - - - - - ranking = 3keywords = alveolar (Clic here for more details about this article) |
3/4. 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.- - - - - - - - - - ranking = 1keywords = alveolar (Clic here for more details about this article) |
4/4. Longitudinal assessment of hypercapnic ventilatory drive after tracheotomy in a patient with the prader-willi syndrome.The clinical course and changes in hypercapnic ventilatory drive over time were serially assessed before and after tracheostomy placement in a 14 year old, morbidly obese female patient with prader-willi syndrome, severe obstructive sleep apnoea, and obesity-hypoventilation syndrome. A tracheostomy became necessary after supplemental oxygen and continuous positive airway pressure (CPAP) had failed to improve the severity of nocturnal hypoventilation. Continued improvement in the slope to rebreathing hyperoxic hypercapnia occurred from 2-10 weeks after tracheotomy in conjunction with night-time bilevel pressure ventilation, and remained unchanged thereafter. In contrast, increases in mean resting minute ventilation at an end-tidal carbon dioxide tension (PET,CO2) of 8 kPa (60 mmHg) were documented even after 30 weeks. This case study illustrates the time-frame of dynamic ventilatory changes occurring after removal of upper airway resistance and normalization of nocturnal alveolar ventilation.- - - - - - - - - - ranking = 0.5keywords = alveolar (Clic here for more details about this article) |