British journal of anaesthesia
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Randomized Controlled Trial Comparative Study Clinical Trial
Non-invasive measurement of cardiac output during induction of anaesthesia and tracheal intubation: thiopentone and propofol compared.
We have investigated the haemodynamic changes in response to induction of anaesthesia and tracheal intubation in patients who received either thiopentone 5 mg kg-1 or propofol 3 mg kg-1 followed by atracurium 0.5 mg kg-1 and fentanyl 1.5 micrograms kg-1. Anaesthesia was maintained with 0.6% enflurane and 50% nitrous oxide in oxygen with assisted ventilation. Cardiac output and heart rate (HR) were monitored continuously with a transthoracic impedence monitor. ⋯ Both variables increased from preinduction values 1 min after tracheal intubation (P less than 0.001). In contrast, both MAP and SVR decreased after induction in the propofol group (P less than 0.001) and did not differ from preinduction values 1 min after tracheal intubation. MAP and SVR were greater in the thiopentone group compared with the propofol group after induction and tracheal intubation (P less than 0.01).
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Randomized Controlled Trial Comparative Study Clinical Trial
Antagonism of intense atracurium-induced neuromuscular block in children.
Antagonism of intense neuromuscular block induced by atracurium 0.5 mg kg-1 was attempted in four groups of six children using one of two doses of neostigmine (0.05 mg kg-1 and 0.1 mg kg-1) or of edrophonium (0.5 mg kg-1 and 1.0 mg kg-1) when the first twitch of the post-tetanic count (PTC1) was 10% of control. For comparison with normal practice, a fifth group received neostigmine 0.05 mg kg-1 when the first twitch of the train-of-four was 10% of control. ⋯ Doubling the doses of the anticholinesterases did not reduce the recovery time and had the effect of increasing variability. We conclude that there is no clinical advantage in attempting to antagonize intense neuromuscular block in children using normal or increased doses of neostigmine or edrophonium.
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We have examined the safety of induced hypotension produced by extradural anaesthesia in patients with medically controlled hypertension. The haemodynamic response to induced hypotension was assessed in 38 non-hypertensive and 31 controlled hypertensive patients. All received extradural anaesthesia to T4 or above which decreased mean arterial pressure to 52 mm Hg and 55 mm Hg in normotensive and hypertensive patients, respectively. ⋯ None developed acute renal failure or stroke. There were three deaths; one of a patient who had hypertension. This suggests that induced hypotension with extradural anaesthesia is a safe technique for patients with medically controlled hypertension undergoing total hip arthroplasty.
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We have studied, in six normal subjects, the effect of nitrous oxide sedation on the ventilatory pattern and oxygen saturation using pulse oximetry (SpO2) after hyperventilation to an end-tidal carbon dioxide partial pressure (PE'CO2) of 3 kPa. This value of PE'CO2 was shown to be less than the apnoeic threshold of all these subjects when their ventilation vs PE'CO2 response curves were plotted. All subjects became apnoeic when told to relax following hyperventilation while breathing 75% nitrous oxide for 90 s. ⋯ It was concluded that subjects who are sedated with nitrous oxide behave similarly to those who are anaesthetized rather than to those who were fully conscious, in that they become apnoeic below the apnoeic threshold point. The reduction in SpO2 after hyperventilation was explained almost entirely by apnoea and may explain abnormalities of respiratory control and hypoxaemia in patients recovering from general anaesthesia or sedation accompanied by hypocapnia. This mechanism may be of importance in obstetric patients after breathing Entonox, when apnoea and hypoxaemia may reduce oxygen delivery to the fetus.