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首页> 外文期刊>Toxicological reviews >Pharmacology, pathophysiology and management of calcium channel blocker and beta-blocker toxicity.
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Pharmacology, pathophysiology and management of calcium channel blocker and beta-blocker toxicity.

机译：钙通道阻滞剂和β受体阻滞剂的药理，病理生理和管理。

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Calcium channel blockers (CCB) and beta-blockers (BB) account for approximately 40% of cardiovascular drug exposures reported to the American Association of Poison Centers. However, these drugs represent >65% of deaths from cardiovascular medications. Yet, caring for patients poisoned with these medications can be extremely difficult. Severely poisoned patients may have profound bradycardia and hypotension that is refractory to standard medications used for circulatory support.Calcium plays a pivotal role in cardiovascular function. The flow of calcium across cell membranes is necessary for cardiac automaticity, conduction and contraction, as well as maintenance of vascular tone. Through differing mechanisms, CCB and BB interfere with calcium fluxes across cell membranes. CCB directly block calcium flow through L-type calcium channels found in the heart, vasculature and pancreas, whereas BB decrease calcium flow by modifying the channels via second messenger systems. Interruption of calcium fluxes leads to decreased intracellular calcium producing cardiovascular dysfunction that, in the most severe situations, results in cardiovascular collapse.Although, CCB and BB have different mechanisms of action, their physiological and toxic effects are similar. However, differences exist between these drug classes and between drugs in each class. Diltiazem and especially verapamil tend to produce the most hypotension, bradycardia, conduction disturbances and deaths of the CCB. Nifedipine and other dihydropyridines are generally less lethal and tend to produce sinus tachycardia instead of bradycardia with fewer conduction disturbances.BB have a wider array of properties influencing their toxicity compared with CCB. BB possessing membrane stabilising activity are associated with the largest proportion of fatalities from BB overdose. Sotalol overdoses, in addition to bradycardia and hypotension, can cause torsade de pointes. Although BB and CCB poisoning can present in a similar fashion with hypotension and bradycardia, CCB toxicity is often associated with significant hyperglycaemia and acidosis because of complex metabolic derangements related to these medications.Despite differences, treatment of poisoning is nearly identical for BB and CCB, with some additional considerations given to specific BB. Initial management of critically ill patients consists of supporting airway, breathing and circulation. However, maintenance of adequate circulation in poisoned patients often requires a multitude of simultaneous therapies including intravenous fluids, vasopressors, calcium, glucagon, phosphodiesterase inhibitors, high-dose insulin, a relatively new therapy, and mechanical devices. This article provides a detailed review of the pharmacology, pathophysiology, clinical presentation and treatment strategies for CCB and BB overdoses.
机译：钙通道阻滞剂（CCB）和β阻滞剂（BB）约占美国毒物中心协会报告的心血管药物暴露量的40％。但是，这些药物占心血管药物死亡人数的> 65％。然而，照顾被这些药物中毒的患者可能非常困难。重度中毒的患者可能患有严重的心动过缓和低血压，这对于循环支持的标准药物是难治的。钙在心血管功能中起关键作用。钙穿过细胞膜的流动对于心脏自动，传导和收缩以及维持血管张力是必需的。通过不同的机制，CCB和BB会干扰细胞膜上的钙通量。 CCB直接阻止钙流经心脏，脉管系统和胰腺中的L型钙通道，而BB通过通过第二信使系统修改通道来减少钙流。钙通量的中断导致细胞内钙减少，从而导致心血管功能障碍，在最严重的情况下会导致心血管功能衰竭。尽管CCB和BB具有不同的作用机理，但其生理和毒性作用相似。但是，这些药物类别之间以及每个类别中的药物之间存在差异。地尔硫卓，尤其是维拉帕米，往往会导致低血压，心动过缓，传导障碍和CCB死亡。硝苯地平和其他二氢吡啶类化合物的致死性通常较低，并且倾向于产生窦性心动过速而不是心动过缓，而传导障碍较少。与CCB相比，BB具有更广泛的影响其毒性的特性。具有膜稳定活性的BB与BB过量致死的最大比例有关。除心动过缓和低血压外，过量服用索他洛尔可导致尖尖扭转综合征。尽管BB和CCB中毒的发生方式与低血压和心动过缓相似，但由于与这些药物相关的复杂代谢紊乱​​，CCB毒性通常与显着的高血糖症和酸中毒相关。并针对特定BB进行了一些其他考虑。重症患者的初始管理包括支持气道，呼吸和循环。然而，中毒患者维持足够的血液循环通常需要多种同时疗法，包括静脉输液，升压药，钙，胰高血糖素，磷酸二酯酶抑制剂，大剂量胰岛素，相对较新的疗法和机械装置。本文详细介绍了CCB和BB过量的药理，病理生理，临床表现和治疗策略。

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