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Ishihara, Hironori; Shimodate, Yuki; Koh, Hiroaki; Isozaki, Ken-ichi; Tsubo, Toshihito; Matsuki, Akitomo
doi: 10.1007/bf03009314pmid: 8425240
Blood or plasma glucose concentration can be measured accurately and rapidly. However, after a glucose challenge metabolism may modify glucose kinetics, so that glucose has not been used as an indicator for dilution volumetry. To test the hypothesis that the initial distribution volume of glucose (IDVG) reflects cardiac output rather than glucose metabolism in the critically ill, the relationship between IDVG and thermodilution cardiac output was evaluated at 27 points in 13 non-surgical, critically ill patients without congestive heart failure. The IDVG was calculated from incremental plasma glucose concentrations using a one compartment model. Correlations were obtained between the IDVG and cardiac output (r = 0.89, n = 27, P < 0.001), and between the incremental plasma glucose concentrations three minutes after the injection and the IDVG (r = 0.94, n = 27, P < 0.001). No difference was found between the IDVG with or without continuous insulin infusions. The results indicate that the IDVG reflects cardiac output rather than glucose metabolism in patients without congestive heart failure.
doi: 10.1007/bf03009318pmid: 8093860
Three doses of salbutamol 125 μg iv were given, over 3.5 hr, to a 28-yr-old healthy, previously non-asthmatic man during thiopentone-O2/ N2O-isoflurane anaesthesia for treatment and prophylaxis of bronchospasm. Force of contraction of the adductor pollicis was measured before and after the last two injections. Initially, the patient was given pancuronium, 5 mg. Salbutamol, 125 μg iv, was given when T1 blockade was 45%. Blockade increased to 66% over five minutes and returned to 45% after 18 min. Vecuronium was subsequently used to maintain relaxation. At the end of surgery, salbutamol was followed by an increase in T1 blockade, from 66% to 86%, over five minutes which returned to 66% after ten minutes. It is concluded that intravenous salbutamol potentiates the neuromuscular blocking effect of nondepolarizing muscle relaxants.
Verbessem, Daisy; Camu, Frederic; Van de Velde, Anne
doi: 10.1007/bf03009309pmid: 8425242
Continuous gastroesophageal pH monitoring was used to evaluate the effect of ranitidine on gastroesophageal reflux (GOR) in 60 patients scheduled for elective non-gastrointestinal abdominal or gynaecological surgery. The patients were randomly assigned to receive a single dose of ranitidine 50 mg either iv (RANIV group) or im (RANIM group) or a placebo iv (PLAC group) 90 min before surgery. The pH was measured continuously for six hours in the lower oesophagus using a flexible calibrated glass electrode. A pH < 4.0 was chosen as the boundary for defining occurrence of acid GOR. Both ranitidine treatments reduced the total number of acid reflux episodes and the global reflux index (P < 0.05). The duration of the acid reflux episodes (sum of refluxes) and the number of acid reflux episodes longer than five minutes were markedly decreased by ranitidine but the mean duration of the reflux episodes was unaffected. The pH values at induction, intubation, surgical incision and extubation were similar in the PLAC and RANIV groups but more acid than in the RANIM group. The mean pH of reflux episodes was less acid in both ranitidine groups than in the PLAC group (P < 0.05). Also the number of very acid refluxes (pH < 2.5) decreased with ranitidine (P < 0.05). Intramuscular and intravenous administration of ranitidine provide protection against gastroesophageal reflux, with shorter duration of reflux episodes occurring in the intramuscular group. Regardless of the administration of ranitidine, protection against gastroesophageal reflux is incomplete; the frequency of reflux episodes is reduced but not eliminated.
Mishra, Yogendra; Ramzan, Iqbal
doi: 10.1007/bf03009315pmid: 8381053
The hypothesis that the histamine H2 receptor blocker ranitidine potentiates neuromuscular paralysis during anaesthesia was tested in vivo in urethane anaesthetised and mechanically ventilated rats. Succinylcholine was administered as a bolus and constant-rate infusion to maintain 48.5% (±2.5 SEM) tibialis anterior muscle paralysis in 14 rats. Ranitidine 2.5, 5, 10, or 20 mg · kg−1 iv, was then administered into groups of three or five rats. Ranitidine produced an immediate potentiation of neuromuscular paralysis followed by a transient reversal and then a continued steady-state potentiation. Peak potentiation occurred within 20 (±3.3) sec and was maintained in all the rats to steady-state. Peak reversal was evident 70 (±8.1) sec after ranitidine administration. There was an excellent relationship (r2 = 0.98, P < 0.001) between peak potentiation and serum ranitidine concentration with 50% potentiation occurring at 25.8 (±1.1) μg · ml−1. There was a weak relationship (r2 = 0.39, P < 0.05) between peak reversal and serum ranitidine but potentiation at steady-state was not correlated to serum ranitidine concentration (r2 = 0.19, P > 0.05). These results show that ranitidine alters the neuromuscular action of succinylcholine in rats in a similar manner to cimetidine.
Allen, Gregory C.; Byford, Larry J.; Shamji, Farid M.
doi: 10.1007/bf03009317pmid: 8425243
We report a malignant hyperthermia- susceptible patient who required investigation for a large, symptomatic anterior mediastinal mass. Multiple attempts at tissue diagnosis under local anaesthesia were unsuccessful. Following awake fibreoptic tracheal intubation, general anaesthesia was administered using ketamine, midazolam, and nitrous oxide, maintaining spontaneous ventilation. Prophylactic dantrolene was not used, to avoid potential muscle weakness and respiratory compromise. Diagnostic mediastinotomy was performed without incident. We conclude that ketamine anaesthesia is appropriate for patients with anterior mediastinal masses, and is considered safe in malignant hyperthermiasusceptible patients.
Kao, Y. J.; Mian, Tan; Kleinman, Sam; Racz, Gabor B.
doi: 10.1007/bf03009322pmid: 8425246
A case is presented of hyperkalaemia (13.6 mEq · L−1) occurring during cardiopulmonary bypass using warm blood cardioplegia (K+ 40–60 mEq · L−1). Treatment with epinephrine, calcium chloride, sodium bicarbonate, and furosemide reduced K+ to 6.5 mEq · L−1 within 30 min and myocardial performance was enhanced with amrinone and cardiac rhythm was controlled with A-V segmental pacing. It is believed that the hyperkalaemia resulted from a combination of the surgical procedure (mitral valve replacement) and the use of warm cardioplegia. The purpose of this report is to increase the awareness of the possibility of hyperkalaemia with warm cardioplegia and to describe a successful therapeutic regimen.
Fassoulaki, Argyro; Sarantopoulos, Constantine; Papilas, Konstantine
doi: 10.1007/bf03009310pmid: 8425236
The effect of flumazenil (F) on the duration of anaesthesia produced by a single dose of thiopentone (T) and propofol (P) was investigated in a placebo-controlled double-blind trial. Eighty-four patients anaesthetized with N2O in O2 and either thiopentone 7 mg · kg−1 or propofol 3 mg · kg−1 for minor gynaecological procedures were studied. Patients were randomly allocated to pretreatment with either 0.5 mg of flumazenil (F) or 5 ml of normal saline (NS) in one of the following groups: T/NS, T/F, P/NS, or P/F. Anaesthetic requirements were assessed by recording the time between the injection of anaesthetic and the first movement observed during the procedure. The time elapsed from the administration of thiopentone to the first movement was 6.5 ± 1.6 min for the T/NS group and 5.3 ± 2.4 min for the T/F group (P < 0.05). The first movement after propofol administration was observed at 7.0 ± 2.2 min in the P/NS group and at 7.1 ± 4.5 min in the P/F group (NS). These data suggest that pretreatment with 0.5 mg of flumazenil iv reduces the duration of thiopentone but not of propofol anaesthesia.
Toso, Carlos E Reyes; Rodríguez, Ricardo R.; Renauld, Aurora; Sverdlik, Rita C.; Linares, Laura M.
doi: 10.1007/bf03009316pmid: 8425241
The purpose of this study was to determine the effect of thiopentone anaesthesia on glucose metabolism. Blood sugar (BS), serum immunoreactive insulin (IRI) and serum non-esterified fatty acid (NEFA) concentrations were measured during the course of (1) an intravenous glucose tolerance test (IVGTT), and (2) an intravenous insulin test (ITT), in conscious and anaesthetized fasted dogs. The IVGTTs were repeated in dogs under alpha-or beta-adrenergic blockade, induced by phentolamine or propranolol. During the IVGTT, the anaesthetized dogs showed glucose intolerance (blood sugar levels were higher than in the control group) and little serum IRI response to hyperglycaemia was detected. An attenuated initial decrease and a slower rebound of NEFA concentration was observed in anaesthetized animals than in controls. Phentolamine administration (5 mg · kg−1 iv) partly restored the IRI response without affecting the BS levels; propanolol (1 mg · kg−1 iv) had no effect. Anaesthetized dogs showed a moderate resistance to insulin induced hypoglycaemic action and a lack of serum NEFA response during counter-regulation of hypoglycaemia, while in conscious controls an intense rebound was observed. Hyperinsulinaemia after iv insulin administration was longer in anaesthetized dogs than in controls. The insulin distribution space was 78% of body weight and insulin t1/2 in blood group compared with 54% and 16 min, in controls. We conclude that thiopentone provokes disturbances in glucose and serum NEFA metabolisms and abolishes the serum IRI response to hyperglycaemia. These effects are influenced by extrapancreatic factors regulating serum IRI levels and by an alpha-adrenergic mechanism, via the inhibition of insulin secretion.
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