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Biomedical subjects

G Volgyesi

Publications and source records attributed to G Volgyesi.

18 recordsLinked to original sources
PubMed2005

Precise control of end-tidal carbon dioxide levels using sequential rebreathing circuits.

Anaesthesiologists have traditionally been consulted to help design breathing circuits to attain and maintain target end-tidal carbon dioxide (P(ET)CO2). The methodology has recently been simplified by breathing circuits that sequentially deliver fresh gas (not containing carbon dioxide (CO2)) and reserve gas (containing CO2). Our aim was to determine the roles of fresh gas flow, reserve gas PCO2 and minute ventilation in the determination of P(ET)CO2. We first used a computer model of a non-rebreathing sequential breathing circuit to determine these relationships. We then tested our model by monitoring P(ET)CO2 in human volunteers who increased their minute ventilation from resting to five times resting levels. The optimal settings to maintain P(ET)CO2 independently of minute ventilation are 1) fresh gas flow equal to minute ventilation minus anatomical deadspace ventilation, and 2) reserve gas PCO2 equal to alveolar PCO2. We provide an equation to assist in identifying gas settings to attain a target PCO2. The ability to precisely attain and maintain a target PCO2 (isocapnia) using a sequential gas delivery circuit has multiple therapeutic and scientific applications.

Anesthesia, Closed-Circuit↗
PubMed2001

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.

Adult↗
PubMed2000

Tracheal constrictor drive above the apneic threshold in anesthetized dogs.

We have previously shown that raising arterial PCO(2) (Pa(CO(2))) by small increments in dogs ventilated below the apneic threshold (AT) results in almost complete tracheal constriction before the return of phrenic activity (Dickstein JA, Greenberg A, Kruger J, Robicsek A, Silverman J, Sommer L, Sommer D, Volgyesi G, Iscoe S, and Fisher JA. J Appl Physiol 81: 1844-1849, 1996). We hypothesized that, if increasing chemical drive above the AT mediates increasing constrictor drive to tracheal smooth muscle, then pulmonary slowly adapting receptor input should elicit more tracheal dilation below the AT than above. In six methohexital sodium-anesthetized, paralyzed, and ventilated dogs, we measured changes in tracheal diameter in response to step increases in tidal volume (VT) or respiratory frequency (f) below and above the AT at constant Pa(CO(2)) ( approximately 40 and 67 Torr, respectively). Increases in VT (400-1,200 ml) caused significantly more (P = 0.005) tracheal dilation below than above AT (7.0 +/- 2.2 vs. 2.8 +/- 1.0 mm, respectively). In contrast, increases in f (14-22 breaths/min) caused similar (P = 0.93) tracheal dilations below and above (1.0 +/- 1.3 and 1.0 +/- 0.8 mm, respectively) AT. The greater effectiveness of dilator stimuli below compared with above the AT is consistent with the hypothesis that drive to tracheal smooth muscle increases even after attainment of maximal constriction. Our results emphasize the importance of controlling PCO(2) with respect to the AT when tracheal smooth muscle tone is experimentally altered.

Animals↗
PubMed2000

A simple "new" method to accelerate clearance of carbon monoxide.

The currently recommended prehospital treatment for carbon monoxide (CO) poisoning is administration of 100% O(2). We have shown in dogs that normocapnic hyperpnea with O(2) further accelerates CO elimination. The purpose of this study was to examine the relation between minute ventilation (V E) and the rate of elimination of CO in humans. Seven healthy male volunteers were exposed to CO (400 to 1,000 ppm) in air until their carboxyhemoglobin (COHb) levels reached 10 to 12%. They then breathed either 100% O(2) at resting V E (4.3 to 9.0 L min) for 60 min or O(2) containing 4.5 to 4.8% CO(2) (to maintain normocapnia) at two to six times resting V E for 90 min. The half-time of the decrease in COHb fell from 78 +/- 24 min (mean +/- SD) during resting V E with 100% O(2) to 31 +/- 6 min (p < 0. 001) during normocapnic hyperpnea with O(2). The relation between V E and the half-time of COHb reduction approximated a rectangular hyperbola. Because both the method and circuit are simple, this approach may enhance the first-aid treatment of CO poisoning.

Adult↗
PubMed1999

Isocapnic hyperpnea accelerates carbon monoxide elimination.

A major impediment to the use of hyperpnea in the treatment of CO poisoning is the development of hypocapnia or discomfort of CO2 inhalation. We examined the effect of nonrebreathing isocapnic hyperpnea on the rate of decrease of carboxyhemoglobin levels (COHb) in five pentobarbital-anesthetized ventilated dogs first exposed to CO and then ventilated with room air at normocapnia (control). They were then ventilated with 100% O2 at control ventilation, and at six times control ventilation without hypocapnia ("isocapnic hyperpnea") for at least 42 min at each ventilator setting. We measured blood gases and COHb. At control ventilation, the half-time for elimination of COHb (t1/2) was 212 +/- 17 min (mean +/- SD) on room air and 42 +/- 3 min on 100% O2. The t1/2 decreased to 18 +/- 2 min (p < 0.0005) during isocapnic hyperpnea. In two similarly prepared dogs treated with hyperbaric O2, the t1/2 were 20 and 28 min. We conclude that isocapnic hyperpnea more than doubles the rate of COHb elimination induced by normal ventilation with 100% O2. Isocapnic hyperpnea could improve the efficacy of the standard treatment of CO poisoning, 100% O2 at atmospheric or increased pressures.

Animals↗
PubMed1998

Inhibition of exhaled nitric oxide production during sepsis does not prevent lung inflammation.

OBJECTIVES: Increases in exhaled nitric oxide have been demonstrated to originate from the lungs of rats after septic lung injury. The aim of this study was to investigate whether treatment with the nitric oxide synthase inhibitor N-nitro-L-arginine methyl ester (L-NAME) would prevent lipopolysaccharide (LPS)-induced increases in exhaled nitric oxide and whether this would have an effect on septic lung inflammation. DESIGN: Prospective, randomized, placebo-controlled animal laboratory investigation. SETTING: University laboratory. SUBJECTS: Male, anesthetized, paralyzed, and mechanically ventilated Sprague-Dawley rats (n = 27). INTERVENTIONS: Rats were mechanically ventilated with air filtered to remove nitric oxide (expiratory rate 40 breaths/min, tidal volume 3 mL, positive end-expiratory pressure 0, FIO2 0.21). They were then randomized to receive intravenous injections of either L-NAME (25 mg/kg/hr x 4 hrs) (n = 11) or saline (n = 10). Both groups were again randomized to receive either LPS (Salmonella typhosa: 20 mg/kg i.v. x 1 dose) or an equal volume of saline 5 mins later. Thereafter, exhaled gas was collected in polyethylene bags for measurements of nitric oxide concentration. After 4 hrs, the rats were killed and the lungs were preserved and examined histologically. To examine the effect of L-NAME and LPS on mean arterial blood pressure, six additional rats underwent the same ventilation protocol with cannulation of the right internal carotid artery so that systemic arterial pressures could be measured. MEASUREMENTS AND MAIN RESULTS: Exhaled gas was collected and measurements of NO concentrations were made using chemiluminescence every 20 mins for 240 mins during ventilation. A total lung injury score was calculated by determining the extent of cellular infiltrate, exudate and hemorrhage. Mean arterial pressure was recorded every 5 mins for 20 mins and then at 20-min periods for 120 mins. Exhaled nitric oxide concentrations increased in all the LPS-treated rats that did not receive L-NAME by 120 mins; a plateau was reached by 190 mins that was approximately 4 times greater than control rats not treated with LPS (p < .001). In contrast, rats treated with L-NAME and LPS did not show an increase in exhaled NO. Administration of L-NAME induced a 10-min nonsustained increase in mean arterial pressure in two rats treated with L-NAME followed by LPS. This increase in mean arterial pressure was not seen in two placebo and two LPS-treated rats that did not receive L-NAME. Lung inflammation was significantly worse in the two groups of rats which received LPS compared with the two that did not. L-NAME did not cause lung inflammation in rats that did not receive LPS; however, LPS-treated rats that received L-NAME had more inflammatory interstitial infiltrate (p < .05) and a trend toward worse lung injury than did LPS-treated rats that did not receive L-NAME. CONCLUSION: We conclude that L-NAME can inhibit the increase in exhaled NO from the lungs of septic rats, but that this inhibition does not reduce lung inflammation, and may worsen it.

Analysis of Variance↗
PubMed1995

Dynamic measurement of tracheal diameter in dogs.

We describe and validate a new minimally invasive method for continuous measurement of tracheal diameter in anesthetized dogs. The method is based on measuring displacement of water into and out of a modified endotracheal tube cuff placed in the trachea. The system was calibrated to allow tracheal diameter to be calculated from known cuff volume. The resolution of the method in measuring changes in tracheal diameter is 0.1 mm over a range of approximately 10-25 mm. The apparatus was tested in five dogs by observing the response of the trachea to four stimuli previously shown to alter tracheal tone: stimulation of nasal mucosa, hyperinflation of the lungs, induction of hypocapnea, and infusion of atropine. The observed changes in tracheal diameter were generally consistent with those of previous studies. The direction and extent of changes in tracheal diameter in response to the test conditions were confirmed by fluoroscopy. We conclude that continuous measurement of volume changes in the cuff reflects corresponding changes in tracheal diameter.

Animals↗
PubMed1995

Increased nitric oxide in exhaled gas as an early marker of lung inflammation in a model of sepsis.

Nitric Oxide (NO) has been implicated in the pathologic vasodilation of sepsis. Because NO can be measured in the exhaled gas of animals and humans, we hypothesized that increases in exhaled NO would occur in a septic model. Using a blinded design, 10 male Sprague-Dawley rats (300 to 400 g) were anesthetized, paralyzed, tracheotomized, and randomized (5/group) to receive an intravenous injection of either lipopolysaccharide (LPS) (Salmonella typhosa, 20 mg/kg) or placebo (equal volume of saline). Thereafter, exhaled gas was collected and measurements of NO concentration were made using chemiluminescence every 20 min for 300 min during ventilation (RR 40 breaths/min, VT 3 ml; PEEP 0, FIO2 0.21). Another group of 10 animals (5 LPS; 5 control) were treated in the same fashion and then killed at 240 min and an arterial blood sample obtained for blood gas and TNF alpha determinations. Pressure volume (PV) curves were constructed and lungs removed, preserved, and submitted for histologic evaluation. LPS-treated rats had lower mean arterial pressures than the control group, p < 0.0001. No significant differences in static lung compliance and PV curves were found in the two groups. TNF alpha levels were greater in the LPS group (1.40 +/- 0.24 ng/ml) versus control group (0.09 +/- 0.04 ng/ml), p < 0.001. By contrast to the control group, exhaled NO concentration rose in all LPS-treated rats at approximately 100 min and at about 160 min reached a plateau that was 6 times greater than control levels (p < 0.0001). There was greater interstitial, airspace, and total lung injury in the LPS group (p = 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Oxidoreductases↗
PubMed1991

Continuous cardiac output determination by thermodeprivation.

A modified thermodilution catheter (KATS catheter) capable of monitoring continuous cardiac output by thermodeprivation and preserving its conventional function was devised. The KATS catheter has a thermistor incorporated closer to the tip of the catheter in addition to the usual thermistor used for conventional thermodilution. This additional thermistor is heated by a constant electric current but is capable of measuring its own temperature. The degree of heat deprivation is detected as the cooling of the thermistor, which is proportionally larger with larger blood velocity. Since blood flow is not the only source of heat deprivation, the actual formula was empirically derived by performing in vitro studies. Cardiac output can be determined by assuming the cross sectional area of the pulmonary artery is stationary. Calibration can be derived from a cardiac output measurement by the usual thermodilution method with the same catheter. The KATS catheter readings correlated significantly with conventional thermodilution values and electromagnetic flowmeter readings in anesthetized dogs. Continuous cardiac output measurement by the KATS catheter appears to be a promising technique.

Journal Article↗
PubMed1982

Oxygenation during high-frequency ventilation compared with conventional mechanical ventilation in two models of lung injury.

Oxygenation and mean lung volume were investigated during high frequency oscillation (HFO) and conventional mechanical ventilation (CMV) in two models of lung disease and related to the lung mechanics of the lesions. Oleic acid (n = 10) or lung lavage (n = 12) pulmonary injury was induced in a series of rabbits. Each animal was alternately ventilated with HFO (15 Hz sinusoidal wave form) and CMV (flow generator I:E, 1:2; f, 30 breaths/min; VT, 10 to 15 ml/kg) at matched mean airway pressure. Pao2 was measured 5 minutes after onset of ventilation. In the lung lavage model Pao2 was significantly greater during HFO than CMV (Pao2 228 +/- 116 torr vs 71 +/- 42 torr) provided that mean airway pressure was greater than the distinct opening pressure characteristic of this lesion. In the oleic acid model oxygenation was again superior during HFO (Pao2 269 +/- 116 torr vs 110 +/- 83 torr), but only if HFO was preceded by a sustained inflation. Plethysmography in a subset of six rabbits from each group revealed that the improvements in oxygenation were associated with significantly higher mean lung volumes during HFO than CMV (58 +/- 30 ml vs 29 +/- 14 ml lung lavage model, 45 +/- 15 ml vs 30.9 +/- 13 ml on the oleic acid model). The importance of a sustained inflation in rapidly optimizing gas exchange during HFO but not CMV was demonstrated. A sustained inflation resulted in immediate and sustained increases in Pao2 (from 134 +/- 102 torr to 274 +/0 124 torr in the oleic acid model; from 115 +/- 105 torr to 291 +/- 143 torr in the lung lavage model) and mean lung volume (41.8 +/- 11 to 53.8 +/- 9.7 ml in the oleic acid model, 30.9 +/- 7.7 ml to 42.8 +/- 5 ml in the lung lavage model). It is suggested that in these two particular models of lung disease, HFO, when combined with a sustained inflation (to provide opening forces), can more fully exploit the pressure volume hysteresis of unstable lung units than CMV, thereby resulting in the larger mean lung volumes and better oxygenation observed during HFO.

Animals↗
PubMed1980

Needle tracheostomy: a laboratory study.

Percutaneous needle tracheostomy and transtracheal ventilation continues to be advocated for the management of upper airway obstruction. Recent studies recommend the use of artificial ventilation. However, as apparatus for this is not always available and because there remains some doubt regarding conditions for successful use of needle tracheostomy during spontaneous respiration, we undertook such a study in dogs. Pressure-flow characteristics of short hollow needles 18-10 SWG were first determined. The smallest of these (14 SWG Bardic Intracath) that would deliver flow sufficient (by calculation) to meet the respiratory requirement of 10-13 kg laboratory dogs was selected for further study. Respiration was possible by spontaneous or artificial methods in the presence of complete tracheal occlusion. Little or no deterioration was noted in an hour of such breathing. Artificial ventilation by machine and by hand could considerably lower PaCO2. We conclude that the technique is possible provided appropriate needles are selected and care is given to their method of use.

Airway Obstruction↗
PubMed1979

The consequences of diaphragmatic muscle fatigue in the newborn infant.

We have previously demonstrated that diaphragmatic muscle fatigue can be diagnosed in infants from spectral frequency analysis of the surface diaphragmatic electromyogram. This requires a digital computer, but the analysis takes several days. Spectral frequency changes, however, can be accurately reflected by band pass filtering and expressing the ratio of high-frequency power to low-frequency power. A fall in this ratio of greater than 20% indicates muscle fatigue. Using a simple analog device to obtain this ratio permits the results to be immediately available; we have used this method to study weaning from mechanical ventilators in ten infants. With a successful weaning step there is no significant change in the ratio, whereas an unsuccessful weaning step invariably leads to a decrease in the ratio of greater than 20%, which precedes CO2 retention and clinical deterioration. These data indicate that diaphragmatic muscle fatigue plays an important role in the infant's response to lung disease. Monitoring of the high/low frequency ratio may be helpful in weaning infants from assisted ventilation.

Computers, Analog↗
PubMed1979

Diaphragmatic muscle tone.

It is generally believed that there is a scarcity of muscle spindles in the diaphragm and that there is no tonic activity at end expiration. This conclusion is based mainly on animal studies and the difficulty in differentiating tonic electromyogram activity from noise. We have, however, found a number of muscle spindles in the newborn human diagphragm, concentrated in the region of the central tendon. We also tried to detect tonic activity by decreasing it (by rapid-eye movement (REM) sleep or anesthesia) or increasing it (with abdominal loading). During REM sleep in five infants and five adults, using subcostal electrodes were observed a marked fall in tonic activity (P less than 0.001) compared to non-REM or quiet sleep. We also observed a reduction in diaphragmatic tonic activity with halothane anesthesia (P less than 0.001). With esophageal electrodes in adult subjects, there was a rise in tonic diaphragmatic activity proportional to the amount of abdomina load (P less than 0.001). We conclude that there are muscle spindles in the human diaphragm and that there is tonic activity at end expiration.

Adult↗
PubMed1978

A respiratory jacket for ventilatory measurements in children.

The properties of an air-filled polyurethane-coated nylon jacket for measuring volume parameters were determined on a model and in 13 subjects. There was a linear relationship between jacket pressure on a logarithmic scale and the lung volume change over an operating pressure range of 0.7-6 cmH2O. The magnitude of pressure change was frequency dependent. The magnitude of a calibration signal was reduced by superimposed tidal breathing. For the jacket tested, the calibration signal during tidal breathing was 87% of the calibration during apnea. With these properties established, a calibration technique was devised and tested on 13 infants. Corrected tidal volumes (VT) obtained with the jacket correlated well with those obtained with a pneumotachograph (r = 0.986). At the operating pressures used the jacket caused no significant change in functional residual capacity (FRC), VT, or frequency. The jacket is a reliable technique for measurement of VT and immediate changes in FRC in awake children.

Child, Preschool↗
PubMed1977

Sodium nitroprusside: factors which attenuate its action. Studies with the isolated gracilis muscle of the dog.

In a laboratory preparation of the isolated, acutely denervated, and separately perfused canine gracilis muscle we have made the following observations: 1. At physiological pH, sodium nitroprusside significantly decreases the vascular resistance; 2. At physiological pH, cyanide significantly attenuates the effect of sodium nitroprusside; 3. In an acidaemic milieu, our data suggest that the effect of sodium nitroprusside may be attenuated. We speculate that patients who manifest resistance to the hypotensive effect of sodium nitroprusside may not normally eliminate the cyanide that is released from the biodegradation of sodium nitroprusside. They accumulate free cyanide which interferes with the action of sodium nitroprusside at the receptor level, leading to administration of more nitroprusside and setting in motion a positive feedback vicious cycle. When one is faced with the problem of an abnormal response to sodium nitroprusside in a fit patient, although many factors may be involved, we suggest that the possibility of rising blood cyanide levels and acidosis be given high priority.

Animals↗