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Biomedical subjects

K Belani

Publications and source records attributed to K Belani.

16 recordsLinked to original sources
PubMed1997

The effect of opioids on thermoregulatory responses in humans and the special antishivering action of meperidine.

In summary, both mu-receptor and combined mu/kappa-receptor opioids impair thermoregulatory control. Alfentanil, a pure mu-receptor agonist slightly increased the thresholds for sweating and markedly decreased the thresholds for vasoconstriction and shivering. However, the vasoconstriction-to-shivering range remained normal during alfentanil administration as it does during general anesthesia. Meperidine, a combined mu- and kappa-receptor agonist, also slightly increased the threshold for sweating and reduced the thresholds for vasoconstriction. However, meperidine reduced the shivering threshold twice as much as the vasoconstriction threshold, thus significantly increasing the vasoconstriction-to-shivering range. Furthermore, shivering during meperidine administration, once triggered, was of low intensity suggesting that the drug also decreased the gain of shivering. The special antishivering action of meperidine appears to result, at least in part, from its kappa-receptor activity.

Alfentanil↗
PubMed1995

Evaluation of the Augustine Guide for difficult tracheal intubation.

Successful tracheal intubation with Augustine Guide (Augustine Medical, Inc., Eden Prairie, MN) in patients with normal airways has recently been described. There are no studies describing Augustine Guide (AG) use in patients with difficult airways. Accordingly, we studied AG intubation in a population of patients with expected difficult airways due to cervical spine pathology, limited mouth opening, obesity, facial trauma or deformity due to previous operation or radiation and in patients with unexpectedly difficult airways. A total of 44 patients were studied. The AG was used as a primary intubating tool in patients with known difficult airways (n = 36) and as a secondary intubating tool in patients with unexpected inability to intubate using conventional direct laryngoscopy (n = 8). Airway difficulty was predicted by history and physical examination. Intubations were performed under general anaesthesia in 40 of the 44 patients studied. In four patients with predictably difficult airways, topical anaesthesia and sedation were used. Backup methods to achieve intubation were available. Thirty-two of the 36 with known or suspected difficult airways were classified as Mallampati Class III or IV. In the remaining eight patients the preoperative examination suggested an easy airway; however, after induction of general anaesthesia, their laryngeal inlet could not be seen using direct laryngoscopy. Using the AG, all were intubated successfully (36/44 at the first attempt, in 8/44 repositioning of the AG to allow successful laryngeal entry of the stylet was necessary). There were no failures or complications secondary to AG use. This study shows that the AG is a useful device for oral tracheal intubation in patients with known or unexpectedly difficult airways.

Adult↗
PubMed1995

Desflurane reduces the gain of thermoregulatory arteriovenous shunt vasoconstriction in humans.

BACKGROUND: Thermoregulatory responses, such as arteriovenous shunt vasoconstriction, provide substantial protection against core hypothermia. A response can be characterized by its threshold (core temperature triggering response), gain (rate at which response intensity increases, once triggered), and maximum response intensity. Reduced gain decreases the efficacy of a thermoregulatory response at a given threshold because response intensity will increase more slowly than usual. The effects of general anesthesia on the gain of arteriovenous shunt vasoconstriction have not been reported. Accordingly, we tested the hypothesis that desflurane decreases the gain of centrally mediated vasoconstriction. METHODS: We studied seven healthy male volunteers. Each was studied twice: (1) desflurane (end-tidal concentration 0.4 minimum alveolar concentration); and (2) control (no anesthesia). Mean skin and fingertip temperatures were controlled at 35.5 degrees C throughout the study. Core temperature was reduced at a rate of 1.5 degrees C/h by central venous infusion of cold fluid. Fingertip arteriovenous shunt flow was measured using venous occlusion volume plethysmography at 1-min intervals. Flow was also evaluated using the perfusion index and laser Doppler flowmetry. Vasoconstriction thresholds were calculated as the core temperatures triggering fingertip flows of 1.0 ml/min (beginning of vasoconstriction) and 0.25 ml/min (intense vasoconstriction). The gain of vasoconstriction was considered to be the slope of the fingertip flow versus core temperature regression within the linear range from 1.0 ml/min to 0.15 ml/min. The minimum observed flow was considered maximum vasoconstriction intensity. Data are presented as means +/- SD; P < 0.01 was considered statistically significant. RESULTS: The vasoconstriction threshold (when defined using a flow of 1.0 ml/min) was reduced from 36.8 +/- 0.3 degrees C to 35.6 +/- 0.3 degrees C by desflurane anesthesia (P < 0.01). Desflurane reduced the gain of vasoconstriction by a factor of three, from 2.4 to 0.8 ml.min-1.degrees C-1 (P < 0.01). Gains, as determined by the perfusion index and laser Doppler flowmetry, were likewise reduced (P < 0.01). The threshold on the control day was only 0.2 +/- 0.1 degrees C less when significant vasoconstriction was defined as a flow of 0.25 ml/min rather than 1.0 ml/min. Because gain was reduced, however, the threshold during desflurane administration was 0.8 +/- 0.2 degrees C less when significant vasoconstriction was defined by a flow of 0.25 ml/min. Minimum flows were comparable and near zero with and without anesthesia. CONCLUSIONS: The threshold reduction (1.2 degrees C/0.4 minimum alveolar concentration) was similar to that observed previously during isoflurane anesthesia. Similarly, it is established already that maximum vasoconstriction intensity is comparable with and without isoflurane anesthesia. However, the data also indicate that even relatively low desflurane concentrations markedly reduce the gain of vasoconstriction. It is likely that reduced gain (i.e., slow onset of vasoconstriction) contributes to core hypothermia in some surgical patients.

Adult↗
PubMed1993

Leg heat content continues to decrease during the core temperature plateau in humans anesthetized with isoflurane.

BACKGROUND: Sufficient hypothermia during anesthesia provokes thermoregulatory responses, but the clinical significance of these responses remains unknown. Nonshivering thermogenesis does not increase metabolic heat production in anesthetized adults. Vasoconstriction reduces cutaneous heat loss, but the initial decrease appears insufficient to cause a thermal steady state (heat production equaling heat loss). Accordingly, the authors tested the hypotheses that: 1) thermoregulatory vasoconstriction prevents further core hypothermia; and 2) the resulting stable core temperature is not a thermal steady state, but, instead, is accompanied for several hours by a continued reduction in body heat content. METHODS: Six healthy volunteers were anesthetized with isoflurane (0.8%) and paralyzed with vecuronium. Core hypothermia was induced by fan cooling, and continued for 3 h after vasoconstriction in the legs was detected. Leg heat content was calculated from six needle thermocouples and skin temperature, by integrating the resulting parabolic regression over volume. RESULTS: Core temperature decreased 1.0 +/- 0.2 degrees C in the 1 h before vasoconstriction, but only 0.4 +/- 0.3 degrees C in the subsequent 3 h. This temperature decrease, evenly distributed throughout the body, would reduce leg heat content 10 kcal. However, measured leg heat content decreased 49 +/- 18 kcal in the 3 h after vasoconstriction. CONCLUSIONS: These data thus indicate that thermoregulatory vasoconstriction produces a clinically important reduction in the rate of core cooling. This core temperature plateau resulted, at least in part, from sequestration of metabolic heat to the core which allowed core temperature to remain nearly constant, despite a continually decreasing body heat content.

Anesthesia, Inhalation↗
PubMed1993

Thermoregulatory responses to hyperthermia during isoflurane anesthesia in humans.

The authors tested the hypotheses that isoflurane anesthesia increases the threshold for sweating but minimally decreases the gain (sensitivity) or maximum intensity of this response and that thermoregulatory responses to hyperthermia are similar in anesthetized men and women. Sweating in response to core hyperthermia was studied in five men and five women during 0, 0.8, and 1.2% end-tidal isoflurane anesthesia. Thigh sweating was quantified by measuring gas flow, relative humidity, and temperature passing over a known surface area. The distal esophageal temperature triggering sweating was considered the sweating threshold, and gain was defined as the core temperature increment required to increase sweating rate from 25 to 75% of maximum observed intensity. The sweating threshold increased linearly with isoflurane concentration from 36.6 +/- 0.1 to 38.1 +/- 0.1 degrees C in the men and from 37.1 +/- 0.3 to 38.3 +/- 0.2 degrees C in the women. The thresholds were significantly higher in women than in men. Gain and maximum sweating intensities were similar at each anesthetic concentration and in men and women. These data indicate that isoflurane anesthesia significantly increases the threshold triggering thermoregulatory sweating but that gain and maximum sweating rate are relatively well preserved.

Anesthesia↗
PubMed1992

Thermoregulatory vasoconstriction during propofol/nitrous oxide anesthesia in humans: threshold and oxyhemoglobin saturation.

To determine the thermoregulatory effects of propofol and nitrous oxide, we measured the threshold for peripheral vasoconstriction in seven volunteers over a total of 13 study days. We also evaluated the effect of vasoconstriction on oxyhemoglobin saturation (SpO2). Anesthesia was induced with an intravenous bolus dose of propofol (2 mg/kg), followed by an infusion of 180 micrograms.kg-1 x min-1 for 15 min, and maintained with 60% nitrous oxide and propofol (80-160 micrograms.kg-1 x min-1). Central and skin surface temperatures and SpO2 (using two different pulse oximeters) were measured continuously; plasma propofol concentrations and arterial PO2 were measured at 15-min intervals. Volunteers were cooled with a circulating water blanket until definitive peripheral vasoconstriction was detected. The tympanic membrane temperature triggering vasoconstriction was considered the thermoregulatory threshold. Vasoconstriction developed on seven study days during propofol/nitrous oxide anesthesia at a central temperature of 33.3 +/- 1.0 degrees C (mean +/- SD) and plasma propofol concentration of 3.9 +/- 1.1 micrograms/mL. The thresholds during anesthesia were significantly lower than those during the control period (36.7 +/- 0.3 degrees C), but the correlation between plasma propofol concentrations and vasoconstriction thresholds was poor. On the remaining six study days, vasoconstriction did not develop despite central temperatures ranging from 32.1 to 32.7 degrees C. Corresponding propofol concentrations were 4.1-10.9 micrograms/mL. These data suggest that anesthesia with propofol, in typical clinical concentrations, and 60% nitrous oxide substantially inhibits thermoregulatory vasoconstriction. Vasoconstriction increased SpO2 by approximately 2% without a significant concomitant change in PO2. The observed increase in SpO2 probably reflects decreased transmission of arterial pulsations to venous blood in the finger.

Adult↗
PubMed1991

Association of exotoxin-producing group A streptococci and severe disease in children.

Clinical features and microbiologic data on all cases of serious (hospitalized) Group A streptococcal infections in children managed at our institution between 1985 and 1988 are presented. All 6 cases were caused by toxin-producing strains. Four of 6 were toxin A-producing strains whereas none of 58 community-acquired (Group A streptococcal) pharyngeal isolates in the same period was a toxin A producer. A review of the literature on the incidence of toxin A-producing strains provides information suggesting a resurgence of such strains in the late 1980s after a relative disappearance of toxin B production in isolates from these patients was also significantly greater than in the isolates acquired from the community in uncomplicated pharyngitis. These findings suggest a role for exotoxin in severe manifestations of Group A streptococcal disease in children.

Adolescent↗
PubMed1989

Lyme disease in children.

Lyme disease is an increasing health risk for children. Pediatricians should become familiar with the different clinical syndromes caused by the Borrelia burgdorferi. Appropriate antibiotic therapy must be initiated and follow-up of these children should be a part of the management as some may develop (tertiary) chronic borreliosis. Lyme disease should be considered in the diagnostic work-up of heart block, childhood arthritis and in undiagnosed peripheral and central nervous system disease. Serologic tests appear to be quite specific and sensitive in children with late stage disease in our experience. Newer diagnostic tests to detect infection during the early stage will optimize the management of Lyme disease and further decrease the incidence of long-term sequelae.

Anti-Bacterial Agents↗
PubMed1988

Resolution of obstructive sleep apnea in Hurler syndrome after bone marrow transplantation.

Hurler syndrome, a lethal inborn error of lysosomal metabolism, results from the systemic accumulation of glycosaminoglycan. The progressive deposition of glycosaminoglycan in tissues of the upper aerodigestive tract has been suspected as the cause of airway obstruction, and many children have required tracheostomy. In a 3-year-old patient with Hurler syndrome, polysomnography confirmed the clinical impression of obstructive sleep apnea. Biopsy of an enlarged tonsil demonstrated that more than half the tissue volume resulted from abnormal lysosomal inclusions in macrophages. Three months after transplantation, repeat testing demonstrated resolution of airway obstruction, and 6 months after transplantation, tonsil biopsy showed complete absence of lysosomal inclusions. Bone marrow transplantation produces effective metabolic correction for Hurler syndrome and may be life-saving for patients with obstructive apnea.

Airway Obstruction↗
PubMed1985

Open- versus closed-chest cardiac compressions in a canine model of pediatric cardiopulmonary resuscitation.

Whether or not the principles of adult resuscitation apply to the pediatric population remains unknown. In order to study this issue, a pediatric animal model was developed using puppies 6-12 weeks of age and 2-8 kg in weight. Hemodynamic status was assessed using standard methods, and measured global cerebral blood flow was assessed using the nitrous oxide (Kety-Schmidt) technique after placement of a catheter in the sagittal sinus. In this initial study, five puppies resuscitated with closed-chest cardiac compression (CCCC) were compared with five receiving open-chest cardiac compression (OCCC). Although mean systolic arterial pressures were equal with both methods during resuscitation (40 versus 49 mm Hg, P = 0.19), OCCC produced a greater cardiac output and a higher cerebral blood flow (5 versus 18 ml/100 g/min, P = 0.008). Only one of five dogs treated with CCCC had a blood flow during resuscitation greater than 15 ml/100 g/min, as compared with four of five receiving OCCC. Finally, three of five dogs in the CCCC group experienced liver lacerations, while none who were resuscitated by OCCC sustained any gross visceral injuries.

Animals↗
PubMed1983

Peripheral postcapillary venous pressure: a new, more sensitive monitor of effective blood volume during hemorrhagic shock and resuscitation.

Peripheral postcapillary venous pressure (PCVP) and mixed venous oxygen saturation (SvO2 or PASO2) have been shown to be sensitive indicators of volume status and appear to reflect the adequacy of peripheral perfusion during controlled bleeding. This study demonstrates that in an open-chest dog model with controlled venous return, PCVP is closely and linearly (r2 = 0.6) correlated with cardiac output (CO). Furthermore, oxygen saturation as measured in the central venous system (CVSO2) and peripheral vein PVSO2) were found to be closely and linearly related to PASO2 (r = 0.72 to 0.99 and 0.91 to 0.98, respectively). Thus PCVP, CVSO2, and PVSO2 represent easily and safely obtainable parameters that closely reflect major physiologic variables. During resuscitation after controlled hemorrhage, the PCVP and PVSO2 accurately reflected the restoration of blood volume and were as good as CO and central saturations. Central venous and pulmonary wedge pressures both poorly reflected the return to full volume repletion (P less than 0.01). Thus, PCVP and PVSO2 seem to be reliable indices of volume status and perfusion and do not require invasive, central monitoring.

Animals↗
PubMed1982

Peripheral postcapillary venous pressure--a new hemodynamic monitoring parameter.

Peripheral postcapillary venous pressure (PCVP) appears to be an indicator of peripheral perfusion (cutaneous blood flow) in the experimental animal. Eighteen male mongrel dogs under balanced anesthesia were subjected to either slow, continuous hemorrhage 0.65 ml/kg/min) or plasma expansion with dextran 40 (0.80 ml/kg/min) over a period of 1 hour. Peripheral PCVP, cental venous pressure arterial pressure, cardiac output (CO), mixed venous oxygen saturation, pulmonary arterial pressure, and pulmonary wedge pressure were monitored on a continuous basis. The only parameter that consistently gave a predictable measure of the degree of induced volume change without requiring pulmonary arterial catheterization was PCVP. PCVP showed a close correlation with CO (r = 0.96).

Animals↗