Search PubMed⌕ Search

Biomedical subjects

B D Butler

Publications and source records attributed to B D Butler.

At least 37 records · Page 2Linked to original sources
PubMed1995

Patent foramen ovale and hypobaric decompression.

Gas microbubbles were detected in the left ventricle of a supine subject being screened for an atrial septal defect as a participant of a hypobaric decompression study. This determination was made using the saline echocontrast procedure. We found provocation by a Valsalva maneuver not to be necessary in this individual for right-to-left passage of contrast microbubbles into the left heart and middle cerebral artery. When this same individual underwent hypobaric decompression to a simulated altitude of 21,000 ft, numerous gas microbubbles were detected in the right heart, but no gas bubbles were detected in either the left ventricular outflow tract or in the middle cerebral artery. This observation appears to be a novel finding, not previously reported.

Cerebral Arteries↗
PubMed1994

Body position does not affect the hemodynamic response to venous air embolism in dogs.

Current therapy for massive venous air embolism (VAE) includes the use of the left lateral recumbent (LLR) position. This recommendation is based on animal studies, conducted 50 yr ago, which looked primarily at survival. Little is known, however, about the concomitant hemodynamic response after VAE in various body positions. The purpose of this study was to investigate the hemodynamic and cardiovascular changes in various body positions after VAE. Twenty-two mechanically ventilated supine mongrel dogs received a venous air infusion of 2.5 mL/kg at a rate of 5 mL/s. One minute after the infusion, 100% oxygen ventilation was commenced and the body position of the dogs was changed to either the LLR (n = 6), the LLR with the head 10 degrees down (LLR-10 degrees; n = 6) or the right lateral recumbent (RLR; n = 5) position. Five dogs were maintained in the supine position (SUP; n = 5). One dog died in every group except in the SUP group, where all the dogs recovered. There were no significant differences among the various body positions in terms of heart rate, mean arterial pressure, pulmonary artery pressure, central venous pressure, left ventricular end-diastolic pressure, or cardiac output. The acute hemodynamic changes occurring during the first 5-15 min after VAE recovered to 80% of control within 60 min. Our data suggest that body repositioning does not influence the cardiovascular response to VAE. Specifically, our data do not support the recommendation of repositioning into the LLR position for the treatment of VAE.

Animals↗
PubMed1993

Continuous venous air embolism in patients receiving positive end-expiratory pressure.

The occurrence of venous air embolism in critically ill patients can cause profound cardiopulmonary compromise. Recognized causes include aspiration through an indwelling catheter and pneumothorax. We report three patients in whom we found continuous air embolism in the inferior vena cava that persisted for days. The bubbles appeared to arise from splanchnic veins, and they were associated with barotrauma and positive airway pressure. In the two survivors, the bubbling ceased when the ARDS resolved and airway pressures were decreased. We suspect that venous air embolism is not an uncommon occurrence in critically ill patients receiving high positive airway pressure.

Adolescent↗
PubMed1993

Use of a disposable carbon dioxide detector with emergency intubation in a hyperbaric chamber.

Emergency intubation in a hyperbaric chamber can be complicated by the confined space, inadequate lighting and high levels of background noise. Inadvertent esophageal intubation may be difficult to recognize in these conditions. In more controlled settings such as the operating room, the detection of end-tidal carbon dioxide is the standard procedure for verifying proper placement of the endotracheal tube. Within a hyperbaric chamber, a capnograph may not be readily available for this purpose. We present a case report describing the use of a simple disposable colorimetric carbon dioxide detector for rapid verification of endotracheal tube position following emergency intubation in a hyperbaric chamber.

Adult↗
PubMed1991

Magnetic resonance imaging of hyperbaric oxygen treated rats with spinal cord injury: preliminary studies.

Magnetic resonance imaging (MRI) has been performed to assess the efficacy of hyperbaric oxygen (HBO) treatment on experimental spinal cord injury in a rat animal model. A moderately severe injury, similar to Type III injury seen in humans (Kulkarni et al. Radiology 164:837;1987) has been chosen for these studies. An improvement in the neurologic recovery (based on Tarlov scale) has been observed following HBO treatment over a period of 72 hr. Based on MRI, HBO treatment appears to arrest the spread of hemorrhage and resolve edema.

Animals↗
PubMed1991

Doppler detection of decompression bubbles with computer assisted digitization of ultrasonic signals.

Precordial Doppler ultrasonic monitoring is routinely used for detection of venous gas bubbles resulting from decompression in hypobaric or hyperbaric applications. Bubble scoring codes have been devised in an attempt to quantify the number of audible bubble signals heard over the background sounds of the cardiac cycle. The audio interpretation of these ultrasonic backscatter signals remains the most common method for decompression evaluation. We report on the use of an inexpensive, commercially available audio digitizer in conjunction with a personal computer to digitize Doppler bubble signals for visual and electronic evaluation. This device can be operated simultaneously with Doppler audio monitoring. Precordial and arterial Doppler recordings of gas bubbles were obtained from anesthetized dogs after intravascular infusion or following decompression. Additional evaluations were conducted on Doppler bubble recordings obtained from human decompression studies. The device can be used in real-time or for later signal analysis. Accompanying menu-driven software provides for numerous signal modification options and visual displays. This device can provide a simultaneous visual display of Doppler signals normally only available for audio evaluation.

Animals↗
PubMed1990

Loss of resistance technique for locating the epidural space: evaluation of glass and plastic syringes.

Location of the epidural space in epidural anaesthesia usually involves the measurement of loss of resistance using glass or plastic syringes. In the present study two varieties of glass syringe and one plastic type were evaluated to determine the resistive forces associated with plunger movement. The mean static (fs) and dynamic (fd) forces for polished glass syringes having a ground plunger only were fs = 0.47 X 10(-3) +/- 0.22 X 10(-3) N and fd = 0.37 X 10(-3) +/- 0.19 X 10(-3) N and for polished glass syringes having a ground barrel and plunger were fs = 0.43 X 10(-3) +/- 0.16 X 10(-3) N and fd = 0.38 X 10(-3) +/- 0.15 X 10(-3) N. Each of these values was significantly lower (P less than 0.5) than those for plastic syringes fs = 2.22 X 10(-3) +/- 0.48 X 10(-3) N and fd = 1.46 X 10(-3) +/- 0.37 X 10(-3) N. It is concluded that glass syringes are favoured over plastic for locating the epidural space because frictional forces developed with glass syringes were significantly lower than with plastic.

Anesthesia, Epidural↗
PubMed1990

Changes in microvascular permeability with acceleration of edema in dog lungs.

Elevation of left atrial pressure to 25-40 mmHg causes continuous pulmonary edema formation in dog lungs. However, after 5-120 min, the rate of edema formation often increases (acceleration of edema). Acceleration of edema could be associated with an increase in microvascular membrane permeability because an increase in permeability would cause fluid to filter through the microvascular membrane more rapidly. To test the hypothesis that acceleration is associated with increased permeability, we used the continuous weight-gain technique to estimate the pulmonary microvascular membrane filtration coefficient (Kf) before and after acceleration of edema in 10 dogs. Acceleration occurred 36 +/- 38 (SD) min after elevation of left atrial pressure to 35.2 +/- 5.4 mmHg. Rate of weight gain increased from 0.47 +/- 0.17 g/min before acceleration to 0.88 +/- 0.26 g/min (P less than 0.05) after acceleration of pulmonary edema. Kf was increased from initial values of 0.058 +/- 0.027 to 0.075 +/- 0.029 ml.min-1.mmHg-1 (P less than 0.05) after acceleration. In five additional dogs we cannulated lung lymphatics and determined the lymph to plasma protein concentration ratio (CL/CP) before and after acceleration. CL/CP increased from base-line values of 0.37 +/- 0.07 to 0.44 +/- 0.06 (P less than 0.05) after acceleration. Both the increase in Kf and CL/CP data support the hypothesis that acceleration of edema is due, in part, to a slight increase in microvascular membrane permeability. However, the findings could also have been caused by an increase in interstitial conductance, washout of interstitial proteins, or alveolar flooding.

Animals↗
PubMed1990

Surface tension effects of heparin coating on arterial line filters.

An investigation was conducted to determine the effects that heparin-coated screen arterial line filters have on the surface tension of cardiopulmonary bypass (CPB) priming solution. Five brands of non-heparin coated arterial line filters (Bard H625, Bentley AF1040, Intersept 40mum, Pall EC3840 and Pall SP3840) and four brands of heparin-coated filters (Bard H640, Bentley AF1040C and AF1040D and Intersept 40mum) were tested in a closed-loop circuit containing two litres of Plasma-Lyte A and pumped at a rate of five litres per minute. Samples were collected at 0.5, 20, 60 and 120 minutes to determine the surface tension of the recirculated solution. The non-heparin coated arterial line filters showed no significant changes in surface tension, either between the individual groups or over time. The benzalkonium-heparin coated filters (Bard H640, Bentley AF1040C and Intersept 40mum) all showed significant decreases in surface tension when compared to zero circulation time or to the noncoated groups. The largest drop in surface tension occurred within the first five minutes of recirculation. The circuit with a Bentley AF 1040D (a new nonbenzalkonium process) coated filter showed no significant change in surface tension.

Benzalkonium Compounds↗
PubMed1989

Effect of lysophosphatidylcholine on the filtration coefficient in intact dog lungs.

Lysophosphatidylcholine (lyso-Pc) is a lysophospholipid normally found in low concentrations in the lung. At high concentrations lyso-Pc, instilled into the airways, causes pulmonary edema. We tested the hypothesis that the edema caused by lyso-Pc was due to an increase in pulmonary microvascular membrane permeability. In 11 anesthetized dogs we continuously weighed the left lower lobes (LLL) while instilling lyso-Pc (20 mM) into the LLL airways. After 30 min we determined the microvascular membrane fluid filtration coefficient (Kf) from the relationship between the rate of LLL weight gain and the pulmonary microvascular pressure. Kf was not significantly different between the lyso-Pc-treated lobes (0.048 +/- 0.018 ml.min-1.mmHg-1) vs. control lobes (0.067 +/- 0.031 ml.min-1.mmHg-1). Our data do not support the hypothesis that lyso-Pc, instilled into the airways, causes an increase in pulmonary microvascular permeability.

Animals↗
PubMed1989

Pulmonary hemodynamics, extravascular lung water and residual gas bubbles following low dose venous gas embolism in dogs.

Pulmonary hemodynamic responses, extravascular lung water and bubble longevity times were studied in halothane anesthetized dogs receiving low dose venous gas infusions. Dogs in one group (23.3 +/- 4.3 kg, n = 6) were embolized with air (0.05 ml.kg-1.min -1) for 60 min followed by a recovery period lasting 70 min. During the recovery the ventilatory gases were intermittently switched from nitrogen (68-69%)/oxygen (30%) to nitrous oxide (68-69%)/oxygen (30%) to expand any residual pulmonary vascular bubbles. Subsequent changes in pulmonary artery pressure, pulmonary vascular resistance, end-tidal carbon dioxide and arterial carbon dioxide tensions were used to indicate the presence of remaining bubbles that would have expanded in volume with the nitrous oxide ventilation. This embolization sequence was repeated three times to simulate repetitive exposure of the pulmonary circulation to venous gas emboli. In a second group of dogs (20.2 +/- 2.7 kg, n = 8) the venous gas infusions (0.05 ml.kg-1.min-1) were continuous for 180 min, followed by recovery with intermittent nitrous oxide/oxygen challenges to determine bubble longevity. Pulmonary hemodynamic and carbon dioxide data were significantly changed from baseline following each embolization. These differences as well as the development of extravascular lung water (edema formulation) were not significant when comparisons were made between the Repetitive gas embolism group after 180 min. Residual pulmonary vascular bubbles were indicated (mean +/- S.E.M.) 26.9 +/- 2.3 min following the 180 min Continuous venous gas infusion and 39.5 +/- 5.3, 46.4 +/- 5.0 and 55.5 +/- 4.4 min, respectively, following the three 60 min Repetitive venous gas infusions.

Animals↗
PubMed1989

Venous gas embolism: time course of residual pulmonary intravascular bubbles.

The time course of pulmonary intravascular air emboli was studied in anesthetized dogs. In one series of experiments air was infused into the right atrium at 0.10 ml.kg-1.min-1 or 0.25 ml.kg-1.min-1 for 15 min or given as a bolus injection of 2 ml/kg at 2 ml/sec. In a second series of series of experiments venous air was infused into dogs (0.25 ml.kg-1.min-1, 15 min) ventilated with 100% oxygen for 0, 30, or 210 min before the embolization. After the air infusions the animals were allowed to recover, breathing 70% nitrogen:30% oxygen. At 10-min intervals during recovery, the nitrogen was replaced with nitrous oxide (N2O) for 5 min to expand any residual pulmonary vascular bubbles. Subsequent changes in pulmonary artery pressure (Ppa) and end-tidal carbon dioxide (PETCO2) concentrations, pulmonary vascular resistance (PVR) and carbon dioxide tensions (PaCO2) as a result of the N2O challenges indicated the presence of residual gas bubbles in the pulmonary arterial system. Residual times of the pulmonary bubbles were 24.5 +/- 12.3 min (0.10 ml.kg-1.min-1 air dose), 43 +/- 10.8 min (0.25 ml.kg-1.min-1 air dose), and 17.8 +/- 2.5 min (bolus). The latter two were significantly different from each other. With 100% oxygen breathing the residual times were 19 +/- 2.2 (0 min), 22 +/- 6.7 min (30 min), and 17 +/- 4.0 (210 min). These values were reduced significantly when compared to the dogs ventilated with 30% oxygen.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Effect of the Trendelenburg position on the distribution of arterial air emboli in dogs.

We examined the effects of buoyancy on the distribution of arterial gas bubbles using in vitro and in vivo techniques in dogs. A simulated carotid artery preparation was used to determine the effects of bubble size and vessel angle on the velocity and direction of bubble movement in flowing blood. Because buoyancy tends to float bubbles away from dependent areas, bubble velocity would be expected to decrease as the vessel angle increased. We found that larger bubbles increased in velocity in the same direction as the blood flow at 0-, 10-, and 30-degree vessel angles and decreased when the vessel was positioned at 90 degrees. Smaller bubbles did not change velocity from 0 to 30 degrees and increased in velocity in the same direction as blood flow at 90 degrees. In 10 anesthetized dogs, we studied the effects of 0-, 10-, 15-, and 30-degree Trendelenburg's position on carotid artery distribution of gas bubbles injected into the left ventricle or ascending aorta. Regardless of the degree of the Trendelenburg position, the bubbles passed into the carotid artery simultaneously with passage into the abdominal aorta. We conclude that the forces of buoyancy do not overcome the force of arterial blood flow and that the Trendelenburg position does not prevent arterial bubbles from reaching the brain.

Animals↗
PubMed1988

Effects of inhalation anaesthetics on filtration of venous gas emboli by the pulmonary vasculature.

Venous gas emboli are prevented from reaching the systemic circulation by filtration in the pulmonary vasculature. This filtration can be overwhelmed by exceeding certain critical rates of venous air infusion. To characterize further these filtration phenomena, the effects of pentobarbitone, isoflurane and halothane anaesthesia on the incidence of spillover of venous bubbles into the arteries were studied in groups of nine dogs. Venous air was infused at rates of 0.25, 0.30, and 0.35 ml kg-1 min-1. Spillover of venous bubbles into the arteries was detected with a Doppler ultrasonic probe located over the suprarenal aorta. At the lowest venous air dose (0.25 ml kg-1 min-1), no bubbles were detected in the systemic circulation in the pentobarbitone- or halothane-anaesthetized dogs, while arterial bubbles were detected in two with isoflurane anaesthesia. At 0.30 ml kg-1 min-1 air, one, four and two dogs had arterial bubbles detected with pentobarbitone, halothane or isoflurane anaesthesia, respectively, while at 0.35 ml kg-1 min-1 spillover of bubbles occurred in four, five and three, respectively. The spillover of venous bubbles into the arteries was dose-related for the pentobarbitone- and halothane-anaesthetized dogs.

Anesthesia, Inhalation↗