Gaseous Emboli Research Articles

Gaseous Emboli Removal Efficiency in Arterial Screen Filters: A Comparative Study

Seven commercially available arterial filters were evaluated for their effectiveness in removing gaseous emboli produced by various sources. All filters were of the screen type and ranged from 20–40 micron pore size. The first phase of the study consisted of an appraisal of carbon dioxide flushing to facilitate priming. Two filters of each type were used. The first filter was primed without a carbon dioxide flush. The second filter was flushed with carbon dioxide. Immediately after priming, microemboli were monitored distal to the filters for 10 minutes at 6 L/Min. In the second phase each filter’s capability of removing gaseous emboli when used in conjunction with a bubble oxygenator was evaluated. Microemboli were alternately monitored pre and post filter at fluid flow rates ranging from I to 6 L/Min. At each liter of fluid flow rate the gas:fluid ratio was varied from 1:1 to 3:1. In the third phase of the study, the efficacy of each filter in removing varying amounts of room air was evaluated. Boluses of room air ranging from 1 to 50 cc. were injected proximal to the filter with microembolism monitoring distally. Injections were made at flow rates ranging from 1 to 6 L/Min. Although carbon dioxide flushing does facilitate priming the filters, it does not reduce microemboli counts distally. Gaseous emboli removal rates ranged from 69.6 to 100% when used in conjunction with a bubble oxygenator. Air emboli activity distal to the filter after air injections ranged from 0 to 91,000 counts/L of fluid flow.

Histopathology of oxygen intoxication in the juvenile red abalone, Haliotis rufescens Swainson

. Juvenile abalone were exposed to supersaturated oxygen conditions (about 150–200% of saturation) in order to reproduce similar conditions encountered in intensive husbandry systems and to then study the resultant lesions. Depigmentation, lethargy and swelling of tissues were observed clinically. Histopathology showed that the cytoplasmic vacuoles of large haemocytes were enlarged. Oxygen emboli were observed throughout the muscular tissue and connective tissue but separation of fibrous neural sheath from nerve cell bodies and surrounding tissue was the predominant lesion. Chromatin of the nuclei of nerve cells became marginated. Gaseous emboli were observed at various other locations in the vascular system. At termination of the experiment all animals sampled bacteriologically showed systemic infection with Vibrio alginolyticus. The clinical signs appeared to result from mechanical interference caused by the accumulation of oxygen and from dysfunction of neural structures. The predominant histopathological changes occurred after only 3 h or less exposure time. Normal histology of the haemocytes and nerve structures is described.

Pathophysiology of Bends and Decompression Sickness

Current concepts in the pathophysiology of decompression sickness are reviewed. Mild, moderate, and severe forms of this syndrome resulting from gaseous and lipid emboli are described. Therapy is aimed at restoring or specifically treating each alteration. Plasma volume deficit is restored by colloidal re-expansion. Decompression sickness is partially treated when recompression alone is used. Blood lipid alterations are managed by use of antilipemic agents. Dextran is mentioned. Divers at depths of 61 m display changes in hematocrit, platelet, and blood lipid profiles. Cord paralysis may occur from bubbles in the vena cava. Retrograde migration blocks the venous circulation of the spinal cord. Ultrasonic devices can detect "silent" bubbles during decompression. Recompression, when available, is a lifesaving treatment for diving accidents involving saturation diving. Air embolism is discussed. Monitoring emboli by EEG and fundoscopy are reported.

Ultrasonic identification of sources of gaseous microemboli during open heart surgery.

An ultrasonic transducer was used to detect gaseous microemboli during open heart surgery. When placed over the carotid artery of patients during surgery it was recognized that gaseous emboli were released into the systemic circulation following recognizable surgical procedures and from the oxygenator during bypass. Fixation of the transducer on the arterial return from the oxygenator demonstrated that the two types of disposable bubble oxygenators and disc oxygenators tested delivered microbubbles in the arterial blood. Some factors affecting the number of bubbles released were recognized and are discussed. Case reports of two patients who received large volumes of gaseous microemboli from different sources are presented.

The passage of gaseous emboli through the pulmonary circulation

Rats were exposed to pressures of air and oxy-helium varying between 100 and 130 pounds per square inch for 1 hour. Decompression to atmospheric pressure generated gaseous emboli in the circulatory system, and 37% of the animals died within 1 hour of reaching atmospheric pressure. Post mortem examination revealed that only the highest pressure used gave bubbles in the pulmonary vein or left auricle. Air injected intravenously failed to appear in the arterial system, but air injected intra-arterially did appear intravenously. It is concluded that it is difficult, if not impossible, under normal physiological conditions for gaseous emboli to pass through the pulmonary circulation. Bubbles were seen to grow, and move, back up the arterial circulation, following decompression. This only seemed to occur when the animal was near to death from decompression sickness.

Results of quantitative and qualitative analysis of gaseous emboli of the heart

Results of quantitative and qualitative analysis of gaseous emboli of the heart