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Apnea spinal

GABAergic presynaptic inhibition of excitatory transmission of primary afferent neurones of the spinal cord resulting in epileptiform convulsions, myosis, and dyspnea with more or less prolonged apnea. [Pg.102]

Cardiovascular effect. [6]-shogaol, administered intravenously to rats at a dose of 0.5 mg/kg, produced a rapid fall in blood pressure, bradycardia, and apnea. There was a marked pressure pressor response in blood pressure that occurred after the rapid fall. A dose of 3.6 pM produced inotropic and chronotropic actions on isolated atria in rats. The effect disappeared by repeated injections or pretreatment of 100 mg/kg administered subcutaneously ° k Intravenous doses of 0.1 to 0.5 pg produced a pressor response in a dose dependent manner. The response was markedly reduced by spinal destruction at the sacral cord level. Norepinephrine (10 pg/kg, intravenously) induced pressor response that was not affected by spinal destruction. In rats in which the spinal cord was destroyed at the thoracic cord level, [6]-shogaol-induced pressor response was reduced by hexamethonium (10 mg/kg, intravenously) and phentolamine (10 mg/ kg, intravenously). When the spinal cord was destroyed at the sacral level, the pressor response was not affected by these blockades. In the hindquarters of rats that were perfused with rat s blood, [6]-shogaol produced two pressor responses on the perfusion pressure. The first was accompanied by a rise in systemic blood pressure, was re-... [Pg.530]

In 10 stable patients maintained on methadone (50-120 mg/day) and nine healthy subjects assessed using polysomnography, the methadone-maintained patients had more abnormalities of sleep architecture, with a higher prevalence of central sleep apnea (23). Methadone depresses respiration, probably by acting on p opioid receptors in the ventral surface of the medulla and possibly on other receptor sites in the lung and spinal cord. All the patients taking methadone also used benzodiazepines and cannabis, which may have influenced the above findings. [Pg.579]

A 68-year-old man developed total spinal anesthesia after the administration of 20 ml of ropivacaine 1% without a prior test dose via an epidural catheter, which was inadvertently placed intrathecally (83). Initial aspiration of both the Touhy needle and the catheter failed to identify the intrathecal position of the catheter. The patient noted weakness in his right leg immediately after the end of the injection. This was followed by weakness in his right arm, asystole, apnea, and loss of consciousness. Ventricular escape beats were noted and sinus rhythm returned after mask ventilation with 100% oxygen and the administration of atropine 1 mg and ephedrine 50 mg. He was able to open his eyes, but remained apneic and was therefore intubated and ventilated. Cardiovascular stabihty was maintained with incremental boluses of ephedrine to a total of 60 mg. He regained consciousness and was successfully extubated 145 minutes later. AH sensory and motor deficits had resolved within 8 hours and no neurological deficit or transient neurological symptoms were detected 5 days later. [Pg.2130]

There is a potential risk that spinal anesthesia will cause apnea in premature infants. However, spinal anesthesia with a sound technique has been used safely in high-risk infants. Tetracaine was used in 142 such cases only two infants had serious adverse effects, one with unexplained but treatable apnea and one in whom too high a block resulted in respiratory arrest (196). [Pg.2134]

Two former preterm infants (postconceptual age 38 weeks) both received spinal anesthetics for inguinal herniorrhaphy (block level T4—6) (197). No other medications were given. Both infants had frequent episodes of perioperative apnea and associated bradycardia. One had a 20-second bout of apnea, with an oxygen saturation of 70% and a heart rate of 80/minute, the other a 30-second bout of apnea, with a saturation of 70% and a heart rate of 60/minute. These episodes persisted for 8 hours into the postoperative period in one of the infants. [Pg.2134]

Inadvertent spinal anesthesia and subsequent nervous system toxicity, for example with transient paralysis or apnea, are the main complications of stellate ganglion block (SEDA-22, 140). It has been suggested that ultrasound guidance when performing the block might improve safety (357). The use of very small test doses and an anterior approach to the stellate ganglion are recommended preventive measures. [Pg.2146]

Tobias JD, Burd RS, Helikson MA. Apnea following spinal anaesthesia in two former pre-term infants. Can J Anaesth 1998 45(10) 985-9. [Pg.2153]

Respiratory The risk of postoperative spells of apnea in preterm infants has promoted the use of spinal anesthesia, because of improved safety. However, high spinal anesthesia has been associated with respiratory failure in a preterm infant [33" ]. The authors concluded that the cephalad spread of spinal anesthesia is less... [Pg.284]


See other pages where Apnea spinal is mentioned: [Pg.710]    [Pg.1788]    [Pg.578]    [Pg.121]   


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