Ron Somogyi

MRI mapping of cerebrovascular reactivity using square wave changes in end-tidal PCO2.

Cerebrovascular reactivity can be quantified by correlating blood oxygen level dependent (BOLD) signal intensity with changes in end‐tidal partial pressure of carbon dioxide (PCO2). Four 3‐min cycles of high and low PCO2 were induced in three subjects, each cycle containing a steady PCO2 level lasting at least 60 sec. The BOLD signal closely followed the end‐tidal PCO2. The mean MRI signal intensity difference between high and low PCO2 (i.e., cerebrovascular reactivity) was 4.0 ± 3.4% for gray matter and 0.0 ± 2.0% for white matter. This is the first demonstration of the application of a controlled reproducible physiologic stimulus, i.e., alternating steady state levels of PCO2, to the quantification of cerebrovascular reactivity. Magn Reson Med 45:1011–1013, 2001.

Dispersal of Respiratory Droplets With Open vs Closed Oxygen Delivery Masks: Implications for the Transmission of Severe Acute Respiratory Syndrome

Nosocomial transmission of droplet-borne respiratory infections such as severe acute respiratory syndrome (SARS) may be influenced by the choice of oxygen face mask. A subject inhaled saline mist and exhaled through three oxygen masks to illustrate the pattern of dispersal of pulmonary gas. In two commonly used masks, exhaled gas formed a plume emanating from the side vents, while a third mask with a valved manifold, which was modified by adding a respiratory filter, retained the droplets. Maintaining respiratory isolation during the administration of oxygen may reduce the risk of the nosocomial transmission of respiratory infections such as SARS.

Calculation Of O2 Consumption During Low-Flow Anesthesia from Tidal Gas Concentrations, Flowmeter, and Minute Ventilation

We present the principles of a new method to calculate O2 consumption (VO2) during low-flow anesthesia with a circle circuit when the source gas flows, end-tidal O2 concentrations and patient inspired minute ventilation are known. This method was tested in a model with simulated O2 uptake and CO2 production. The difference between calculated VO2 and simulated VO2 was 0.01 ± 0.02 L/min. A similar approach can be used to calculate uptake of inhaled anesthetics. At present, with this method, the limiting factor in precision of measurement of VO2 and uptake of anesthetic is the precision of measurement of gas flow and gas concentration (especially O2 concentration in end-tidal gas, FETO2) available in clinical anesthetic units.