Management of post-hyperventilation apnea during dental treatment under monitored anesthesia care with propofol

Although hyperventilation syndrome generally carries a good prognosis, it is associated with the risk of developing severe symptoms, such as post-hyperventilation apnea with hypoxemia and loss of consciousness. We experienced a patient who suffered from post hyperventilation apnea. A 17-year-old female who suffered from hyperventilation syndrome for several years developed post-hyperventilation apnea after treatment using the paper bag rebreathing method and sedative administration during a dental procedure. We subsequently successfully provided her with monitored anesthesia care with propofol. Monitored anesthesia care with propofol may be effective for the general management of patients who have severe hyperventilation attacks and post-hyperventilation apnea. This case demonstrates that appropriate emergency treatment should be available for patients with hyperventilation attacks who are at risk of developing post-hyperventilation apnea associated with hypoxemia and loss of consciousness

Endotoxic shock alters distribution of blood flow within the intestinal wall.

OBJECTIVE: To investigate whether a redistribution of blood flow from the mucosa to the muscular layer of the intestinal wall contributes to the observed increased arterial-mucosal Pco2 gradient and the decreased mucosal tonometric pH during endotoxic shock. DESIGN: A prospective, controlled, animal study. SETTING: Animal laboratory in a university medical center. SUBJECTS: Ten domestic pigs. INTERVENTIONS: Pigs were anesthetized with ketamine and pentobarbital, mechanically ventilated, hemodynamically monitored, and then challenged with Escherichia coli endotoxin (10 micrograms/ kg i.v.). MEASUREMENTS AND MAIN RESULTS: Cardiac output, mesenteric artery blood flow, and systemic, pulmonary, and portal pressures were measured. Intestinal mucosa tonometric Pco2 and pH were determined with saline-filled balloon tonometers. The tissue blood flow to the mucosa and the muscular layer were independently measured with colored microspheres, using the arterial reference sample method. Thus, total intestinal blood flow was evaluated with respect to its transmural (mucosa vs. muscularis) and geographical (proximal jejunum, mid-small intestine, and terminal ileum) distribution. Endotoxin administration with fluid resuscitation induced a distributive shock with a decrease in intestinal mucosa tonometric pH. Under endotoxemic conditions, the mucosal flow increased in each geographical area, with the increase being larger proximally in the jejunum than distally in the ileum. The mucosal tonometric pH was found to correlate inversely with mucosal blood flow. The increase in blood flow to the mucosa was balanced by a decrease in blood flow to the muscularis, with total mesenteric flow remaining unchanged. CONCLUSIONS: Mucosal hypoperfusion does not account for the acidotic mucosal tonometric pH in endotoxic shock. The results suggest either a primary cytotoxic effect or an enhanced counter-current-mediated hypoxic insult in the apical villus. The decrease in blood flow to the muscularis may contribute to loss of intestinal wall peristaltic activity and structural wall integrity

Effects of PEEP on liver arterial and venous blood flows

Total venous return decreases with positive end-expiratory pressure (PEEP). It is likely that the liver plays an important role in this response, either through the development of an increase in venous resistance or through an increase in the venous backpressure at the outflow end of the liver. In addition, hepatic arterial flow is reported to be selectively decreased by the application of PEEP. Therefore, to clarify the effects of PEEP on liver hemodynamics, we generated pressure-flow (P-Q) relationships in both liver vascular beds of anesthetized, mechanically ventilated pigs at PEEP of 0, 5, 10, and 15 cm H2O to obtain values of backpressure (Pback, mm Hg) from linear extrapolation of the P-Q relationships and resistance (mm Hg/ml/min/kg) from its slope. PEEP decreased portal vein flow (Qpv) and caused an increase in the liver venous resistance (from 0.08 +/- 0.01 to 0.16 +/- 0.02 mm Hg/ml/min/kg; p < 0.05). Ppvback and right atrial pressure (Pra) increased equally (from 5.1 +/- 0.3 to 9.9 +/- 0.4 mm Hg, p < 0.05, and from 4.0 +/- 0.2 to 8.6 +/- 0.5 mm Hg, p < 0.05, respectively, at PEEP 15). The reduction in portal venous flow was related to an increase in the backpressure to flow (as a result of an increase in Pra) and to an increase in liver venous resistances that may cause blood pooling in the splanchnic compartment and decrease venous return through the liver. PEEP increased Phaback (from 11.2 +/- 0.9 to 14.5 +/- 0.7 mm Hg at PEEP 15, p < 0.05) but did not change hepatic arterial resistance.(ABSTRACT TRUNCATED AT 250 WORDS