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Biomedical subjects

M T Snider

Publications and source records attributed to M T Snider.

At least 19 recordsLinked to original sources
PubMed1996

Precise control of nitric oxide concentration in the inspired gas of continuous flow respiratory devices.

Inhaled NO has become widely used for diagnosis and therapy of pulmonary hypertension. The potential hazards of NO inhalation include the formation of methemoglobin, formation of NO2, and generation of free radicals in the presence of humidity and oxygen. Careful monitoring of NO and NO2 concentration, and titration of the dose according to a patient's clinical response is essential to minimize toxicity. This paper describes a formula and method that permits calculation and precise control of NO concentration in the inspired gas. The accuracy of the delivery system was assessed by a comparison of calculated and measured NO and NO2 concentrations in a continuous flow ventilator circuit. A comparison of electrochemical detector (ECD) versus chemiluminescence detector (CLD) monitoring techniques showed agreement between the instruments within approximately 2 ppm, with the ECD averaging a higher reading than the calculated or CLD measured values. We deemed a 2 ppm discrepancy between instruments clinically acceptable, and concluded that the instruments could be used interchangeably for clinical purposes to measure NO1 and that the ECD was preferable to CLD for measuring NO2. Details about the equipment are given and techniques are discussed to avoid the risk of inhalation of toxic concentrations of NO and NO2. This method provides the possibility of using inhaled NO with appropriate safety precautions in the range 0-60 ppm in a variety of continuous flow respiratory devices.

Electrochemistry↗
PubMed1993

Radiologic evaluation of the intravenous oxygenator.

This report describes the radiologic appearance of the intravenous oxygenator (IVOX), an intracorporeal CO2-O2 exchanger for use in patients with severe respiratory deficiency, and the extensive radiographic and sonographic support required for its use. Six patients aged 19-39 years who had severe adult respiratory distress syndrome (ARDS) and who were not expected to survive were selected for IVOX placement; ARDS was caused by trauma (four patients), severe pneumonia (one patient), or a fat embolus from a tibial fracture (one patient). Before insertion of the IVOX, all patients underwent evaluation of their right internal jugular vein, right common femoral vein, and inferior vena cava with real-time ultrasound (US) to ascertain vascular size. The IVOX improved oxygenation in all patients; because of such improvement, one patient survived. Use of the IVOX may become common; hence, radiologists should understand how the IVOX functions and its appropriate placement, be able to identify it on chest and abdominal radiographs, and appreciate the importance of US in placement of this device and follow-up.

Adult↗
PubMed1992

Clinical trials of an intravenous oxygenator in patients with adult respiratory distress syndrome.

In patients with severe adult respiratory distress syndrome, mechanical ventilation may not be able to ensure gas exchange sufficient to sustain life. We report the use of an intravenous oxygenator (IVOX) in five patients who were suffering from severe adult respiratory distress syndrome as a result of aspiration, fat embolism, or pneumonia. IVOX was used in an attempt to provide supplemental transfer of CO2 and O2 and thereby reduce O2 toxicity and barotrauma. All patients were tracheally intubated, sedated, and chemically paralyzed and had a PaO2 < 60 mmHg when the lungs were ventilated with an FIO2 = 1.0 and a positive end expiratory pressure of > or = 5 cmH2O. The right common femoral vein was located surgically, and the patient was systemically anticoagulated with heparin. A hollow introducer tube was inserted into the right common femoral vein, and the furled IVOX was passed into the inferior vena cava and advanced until the tip was in the lower portion of the superior vena cava. IVOX use ranged from 2 h to 4 days. In this group of patients, IVOX gas exchange ranged from 21 to 87 ml x min-1 of CO2 and from 28 to 85 ml x min-1 of O2. One of the five patients survived and was discharged from the hospital. The IVOX transferred up to 28% of metabolic gas-exchange requirements. One patient with a small vena cava showed signs of caval obstruction. Three other patients demonstrated signs of a septic syndrome after the device was inserted.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Detection of venous air embolism by continuous mixed venous oximetry in dogs.

Continuous mixed venous oxygen saturation (SvO 2) was evaluated as a monitor of venous air embolism in a canine model. Nineteen dogs were anesthetized, paralyzed, and mechanically ventilated. Invasive monitoring included SvO 2, systemic and pulmonary artery blood pressures, and thermodilution cardiac outputs. Air boluses of 0.25 and 0.5 ml/kg were injected in six dogs and 1 ml/kg in all. All 1 ml/kg emboli were detected by greater than or equal to 5% decreases in the SvO 2. The SvO 2 decreased from 82 +/- 8% to 72 +/- 11% (mean +/- SD), an average decrease of 9 +/- 5% (p = 0.004). Time to the SvO 2 nadir was 2.6 +/- 2.5 min. Of the 0.5 and 0.25 ml/kg emboli, 50% and 17% were detected, respectively. Cardiac output decreased from 2.9 +/- 0.8 to 2.1 +/- 0.8 L/min after the 1 ml/kg emboli (p = 0.02). The 1 ml/kg emboli increased pulmonary artery pressures and decreased systemic blood pressure in 100% and 75% of animals, respectively. Peak changes in pulmonary artery pressure occurred at 1.2 +/- 0.8 min. In the present study, time to maximum change was greater for SvO 2 than for pulmonary artery pressure changes. Use of fiberoptic pulmonary artery catheters for continuous measurement of SvO 2 can add a new diagnostic modality to venous air embolism detection in patients who require a pulmonary artery catheter for other medical indications.

Animals↗
PubMed1991

Detection of arterial gas embolism by increased end-tidal nitrogen in dogs.

Increased end-tidal (ET) nitrogen in a patient being ventilated with a nitrogen-free gas mixture through a leak-free circuit has been considered a specific sign of venous air embolism. We hypothesized that increased ETN2 would occur after arterial air emboli, just as following venous air emboli, and that clinically relevant arterial air emboli could be detected with respiratory gas monitoring by mass spectrometry. After approval from the institutional Animal Utilization Committee, eight mongrel dogs were studied. All were anesthetized with pentobarbital and ventilated with room air by a volume ventilator. Each animal was monitored by a femoral artery and a pulmonary artery catheter for systemic and pulmonary blood pressures, respectively, an electrocardiograph, pulse oximetry, and inspired and expired respiratory gas measurements by mass spectrometry. Arterial blood gas analysis was undertaken after one series of air emboli. Air boluses (containing the nonradioactive nitrogen isotope N2) of 50, 100, 200, and 500 mul/kg were injected slowly into the distal aorta through a second arterial catheter advanced 35 cm above the inguinal ligament. All emboli >/=100 mul/kg and 60% of the 50 mul/kg emboli were detected by increased ETN2 within 30 s, reaching peak levels in <2.75 min. The washout time for the N2 was longer for larger emboli, ranging from 2.9 +/- 2.8 min for 50 mul/kg emboli to 17.3 +/- 3.2 min for the 500 mug/kg emboli. There were no significant changes in end-tidal carbon dioxide, pulmonary or systemic blood pressures, or arterial blood gases. Increased ETN2 can no longer be considered pathognomonic for venous air embolism; arterial air embolism may have occurred.

Journal Article↗
PubMed1991

Venous air emboli with 15N2: pulmonary excretion and physiologic responses in dogs.

Venous air embolism occurs with decompression sickness as well as during a wide variety of surgical procedures in hospitalized patients. We developed a canine model to allow documentation and quantitation of pulmonary excretion of intravascular air emboli both in a control air breathing state and during treatment. We utilized 15N2 (a stable, nonradioactive isotope of room air nitrogen, 14N2) as the nitrogen component of venous air emboli (1 ml.kg-1) given to 27 anesthetized mongrel dogs ventilated with room air (tidal volume = 15 ml.kg-1). End-tidal 15N2 was measured and the embolism diagnosed by increased levels in exhaled gases. Exhaled gases were also collected in Douglas bags and the 15N2 recovered was quantitated by a helium dilution technique. Systemic and pulmonary artery pressure changes and quantitation of excreted 15N2 were documented after embolism during a control state with continued room air (21% oxygen) ventilation, and after treatments with either a) 100% oxygen ventilation; b) compression to 2128 mmHg, or 2.8 atm abs, and room air ventilation; or c) a combination of 100% oxygen ventilation and 2.8 atm abs compression. Increased end-tidal 15N2 was characteristic of all emboli, and use of 15N2 allowed accurate measurement of excreted gas during both room air and 100% oxygen ventilation. Embolic gas recoveries were not increased significantly by any of the treatments.

Animals↗
PubMed1991

Breath-by-breath monitoring of respiratory gas concentrations during compression and decompression.

We compared six systems for sampling respiratory gases from within a hyperbaric chamber to provide online gas concentrations by a mass spectrometer (MS) outside the chamber. Gas at hyperbaric pressure was sampled through either a capillary and mass flow controller (system 1), a capillary and micrometering manual valve (system 2), or a capillary alone (system 3) by a vacuum pump outside the chamber. In each system, a small amount of decompressed gas was drawn into the MS for analysis while the balance vented into the room. Systems 4-6 were constructed from systems 1-3, respectively, by eliminating the vacuum pump. Using a square wave respiratory simulator, which generated known gas concentration profiles within the chamber, MS analyses were recorded from each sampling system at compression and decompression rates of 20 meters of sea water.min(-1) and chamber pressures from 1.0 to 6.0 atm abs. Inspiratory and end-expiratory concentrations of nitrogen (0.0 and 1.0%, respectively) and carbon dioxide (0.0 and 4.2%, respectively) were accurately determined at respiratory rates of up to 70 breaths.min(-1) with a sensitivity of 0.05% and without pressure artifact.

Blood Gas Analysis↗
PubMed1990

Detection of venous air embolism in dogs by emission spectrometry.

Emission spectrometers provide alternative, relatively inexpensive methods for detecting the concentration of respiratory gas nitrogen. Mass spectrometers are accepted as reliable monitors of end-tidal nitrogen for detection of venous air embolisms. We evaluated an inexpensive emission spectrometer for detecting changes in nitrogen levels and compared it with a mass spectrometer for detecting increased end-tidal nitrogen levels in dogs with venous air embolisms. During in vitro gas flow studies (helium; oxygen; helium/oxygen mixtures; or 70% nitrous oxide/30% oxygen with 0, 1, 2, or 3% isoflurane), air boluses (0.01 to 5.0 ml) were injected into a gas flow circuit and outlet nitrogen levels were measured by a Collins 21232 emission spectrometer. Responses were greater after each bolus when helium rather than oxygen was the major diluent gas. During in vivo studies, 5 dogs were anesthetized, ventilated, denitrogenated, and given venous air embolisms (0.1, 0.5, and 1.0 ml.kg-1) during oxygen and then during Heliox (20% oxygen:80% helium) breathing. End-tidal nitrogen increased approximately two-fold after venous air embolisms given during Heliox as compared with oxygen ventilation. In all 0.1-ml.kg-1 venous air embolisms end-tidal nitrogen increased when the emission spectrometer was used, but venous air embolisms less than 1.0 ml.kg-1 were not consistently detected by mass spectrometry. Emission spectrometry can be used to detect increased end-tidal nitrogen levels indicative of venous air embolism and may be a more sensitive detector than mass spectrometry.

Animals↗
PubMed1990

Hyperbaric nitrous oxide as a sole anesthetic agent in humans.

Nitrous oxide (N2O) has been used to produce analgesia and anesthesia for more than 100 yr. However, because of its high MAC value (1.04), general anesthesia with N2O can usually be attained only in a hyperbaric environment. Because of the sparsity of documentation for human physiologic responses to hyperbaric N2O, we studied eight male volunteers at 2 ATA (1520 mm Hg) anesthetized with N2O only for periods of 2-4 h. N2O partial pressures ranged from 836 to 1368 mm Hg. The anesthetic state was associated with tachypnea, tachycardia, increases in systemic blood pressure, mydriasis, diaphoresis, and at times, clonus and opisthotonus. A stable level of physiologic activity was difficult to maintain.

Adult↗
PubMed1990

Adult respiratory distress syndrome in the trauma patient.

A high mortality rate still exists for the patient with ARDS 20 years after the severe syndrome was first formally defined. Hypoxia and hypercarbia remain major clinical challenges requiring mechanical ventilation. The pulmonary vascular bed has been identified as a prime site of injury. The major working hypothesis is that cellular injury is caused by oxyradicals produced by activated neutrophils. There is no present pharmacologic therapy based on this hypothesis. Steroids have no demonstrable effect on outcome. Major advances have been made in the use of extracorporeal membrane lungs to relieve hypercarbia and hypoxia while minimizing pulmonary oxygen toxicity and barotrauma. The most promising current technique is extracorporeal CO2 removal during venovenous perfusion. Further advances must await definition of the early stages of the ARDS.

Critical Care↗
PubMed1989

An evaluation of intra-cage ventilation in three animal caging systems.

Although temperature and relative humidity have been quantitated and their effects on research data studied, few studies have measured the air turnover rates at cage level. We evaluated the air distribution and air turnover rates in unoccupied shoe-box mouse cages, filter-top covered cages and shoe-box mouse cages housed in a flexible film isolator by using discontinuous gas chromatography/mass spectrometry and smoke. Results showed that air turnover was most rapid in the unoccupied shoe-box mouse cage and slowest in the filter-top covered cage. Placing mice in the filter-top covered cage did not significantly improve the air turnover rate. Although filter-top covered cages reduce cage-to-cage transmission of disease, the poor airflow observed within these cages could lead to a buildup of gaseous pollutants that may adversely affect the animal's health.

Air Conditioning↗
PubMed1988

Carbon dioxide elimination during total cardiopulmonary bypass in infants and children.

The authors measured the rate of carbon dioxide elimination (VCO2) in 25 pediatric patients (age 2 days to 9 yr) during total cardiopulmonary bypass at average venous blood temperatures ranging from 19.5 to 35.9 degrees C. A multiplexed mass spectrometer was connected to the gas inlet and exhaust ports of the bubble oxygenator, and the gas-phase Fick principle was used to determine VCO2. A curvilinear relationship was found between log VCO2 and venous blood temperature, and a quadratic regression equation (r2 = 0.74) was fit to the data. Q10 (the ratio of VCO2 before and after a 10 degree C temperature change) was estimated to be 2.7 or 3.0, depending on the analytic method used. Venous blood temperature as a predictor variable explained a greater proportion of the variability of log VCO2 than did nasopharyngeal or rectal temperatures. Analysis of covariance revealed that total circulatory arrest during bypass (utilized in 10 patients for 34 +/- 4 min, mean +/- SEM) affected the relationship of venous blood temperature with log VCO2, by increasing the y-intercept (P = .008) but not the slope. These data, with associated 95% prediction intervals, define the expected CO2 elimination rates at various temperatures during standard bypass conditions in our patients. Real-time measurement of VCO2 using mass spectrometry can be a useful routine monitor during CPB that may help to assess patient metabolic function, adequacy of perfusion, and oxygenator performance.

Blood Physiological Phenomena↗
PubMed1987

The accuracy and precision of an open-circuit system to measure oxygen consumption and carbon dioxide production in neonates.

We measured the oxygen consumption, carbon dioxide production, and respiratory quotient during the combustion of a known mass of anhydrous ethanol and methanol to assess the accuracy of an open-circuit flow-through system. Continuous measurements were made of the mass of alcohol burned, the velocity of gas flow through the apparatus, and simultaneous measurements of the fractional concentration of oxygen, carbon dioxide and nitrogen of the inlet and outlet gas using paramagnetic oxygen analyzer, infrared carbon dioxide meter, and mass spectrometer. Standard respiratory and stoichiometric equations were used to calculate the oxygen consumption, carbon dioxide production and RQ for the mass of absolute alcohol combustion per unit time. In a series of 12 consecutive laboratory experiments (on 7 days), the measured values of gas exchange (similar to the rate of respiratory gas exchange by an infant of 1-4 kg) were in agreement within 5% of the true values for ethanol and methanol combustion, confirming the validity of the open-circuit method. The paramagnetic oxygen analyzer and the mass spectrometer gave similar oxygen consumption results and differed very little when the rate of absolute alcohol combustion was used to quantify the accuracy of the complete measurement system. A positive measurement error was observed for the carbon dioxide production results from both the IR meter and mass spectrometer, with the result that the respiratory quotient measurements were 3.4-4.7% higher than the true value. The mass spectrometer gave more precise oxygen consumption results, whereas smaller variance of carbon dioxide production measurements was observed using the infrared CO2 meter.(ABSTRACT TRUNCATED AT 250 WORDS)

Carbon Dioxide↗
PubMed1986

Increased N-pentane excretion in humans: a consequence of pulmonary oxygen exposure.

Lipid peroxidation by free radicals has been suggested as a mechanism of a lung injury caused by breathing higher than normal concentrations of oxygen. The appearance of hydrocarbons such as n-pentane in the expired gas of mammals has been proposed as in vivo evidence of lipid peroxidation. The excretion of n-pentane was studied in 15 healthy volunteers in whom excretion of exogenous n-pentane was determined over a 60- to 90-min period while breathing hydrocarbon-free gases. N-pentane elimination rates (mean +/- SEM) in the expired gas at 0, 30, 60, 90, and 120 min were 10.2 +/- 1.5, 1.6 +/- 0.2, 1.2 +/- 0.9, 1.3 +/- 0.4, and 1.3 +/- 0.3 (pmol X kg-1 X min-1), respectively. Using a specially assembled circuit, a 2-h oxygen exposure study was performed on six healthy volunteers, in whom basal n-pentane excretion varied ten-fold among individuals, from 0.25 to 2.25 pmol X kg-1 X min-1. After breathing 100% oxygen, n-pentane excretion was augmented 62-420% within 30 to 120 min. The authors conclude that lipid peroxidation may occur in humans within 30 min of breathing 100% oxygen.

Adult↗
PubMed1985

Rapid induction of halothane anaesthesia in man.

The cardiopulmonary and anaesthetic responses of nine healthy volunteers, breathing concentrations of 1-4% halothane in oxygen, were studied. Supine fasting subjects breathing room air exhaled to residual volume and then inhaled a vital capacity breath of 1, 2, 3 or 4% halothane in oxygen. After a breath-hold of 30-90 s they exhaled and then breathed spontaneously the same anaesthetic mixture for up to 2 min. The electrocardiogram, arterial pressure, heart sounds and arterial oxygen saturation, were monitored, and respiratory gases were analysed by mass spectrometry. The maximum effect was seen after breathing 4% halothane. All volunteers were amnesic after the first breath and unresponsive to command after 2 min. Little or no excitement occurred. A maximum decrease of 12 mm Hg in systolic pressure was seen while breathing 4% halothane. Bradycardia, hypoxia and clinically important hypercarbia did not occur. At all inspired concentrations of halothane, the end-tidal halothane concentration increased rapidly and was 30% of the inspired value after 1 min. No volunteer found this technique to be unpleasant. Rapid induction of general anaesthesia with 2-4% halothane in oxygen is effective, safe and well accepted by healthy young adults.

Adult↗