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Advantages And Disadvantages Of Bupivacaine

Decent Essays

LOCAL ANAESTHETICS BUPIVACAINE Figure 10 Bupivacaine is an amide linked local anaesthetic .Bupivacaine has a relatively slow onset of action (approximately 30 min) but a prolonged duration of action. These features are related to its physicochemical characteristics particularly its pKa value and extensive protein binding. Its main advantage compared to lidocaine and prilocaine is its prolonged duration of action, and it is commonly used to produce infiltration and conduction anaesthesia. In addition, it is the standard drug that is used to produce extradural lumbar and thoracic blockade and to produce spinal subarachnoid anaesthesia. The main disadvantage of bupivacaine is its ability to cause significant cardiotoxicity, …show more content…

When bupivacaine (0.25%) is used to produce minor nerve blockade, it has a relatively rapid onset of action (3–6 min), and a long duration of action (2–6 h). Mixtures of bupivacaine with other local anaesthetics (lidocaine, prilocaine) are commonly used to combine for a rapid onset with a prolonged duration of action. Bupivacaine is also frequently used to produce brachial plexus or sciatic nerve blockade. In these conditions, its onset of action is more variable, mainly due to the presence of connective tissue barriers, which restrict access to its site of action. The use of a nerve stimulator may assist the accurate localization of the site of injection. When bupivacaine is used to produce major nerve blockade, it has a relatively slow onset of action (20–25 min), but sensory anaesthesia usually persists for 4–10 hours, and occasionally lasts for 24 hours. Persistent paraesthesia after nerve blockade is probably due to mechanical trauma, rather than to other …show more content…

The management of local anaesthetic toxicity can be challenging, and in the case of cardiac toxicity, prolonged resuscitation efforts may be necessary. Therefore, understanding the circumstances that can lead to systemic toxicity of local anaesthetics and being prepared for treatment is essential to optimize the patient outcome. Systemic toxicity is typically manifested as central nervous system (CNS) toxicity (tinnitus, disorientation, and ultimately, seizures) or cardiovascular toxicity (hypotension, dysrhythmias, and cardiac arrest). The dose capable of causing CNS symptoms is typically lower than the dose and concentration that result in cardiovascular toxicity. This is because the CNS is more susceptible to local anaesthetic toxicity than the cardiovascular system. However, bupivacaine toxicity may not adhere to this sequence, and cardiac toxicity may precede the neurologic symptoms. Although less common, cardiovascular toxicity is more serious and more difficult to treat than CNS

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