![]() Some societies use Oxford Academic personal accounts to provide access to their members. If you do not have a society account or have forgotten your username or password, please contact your society. Do not use an Oxford Academic personal account. When on the society site, please use the credentials provided by that society.If you see ‘Sign in through society site’ in the sign in pane within a journal: Many societies offer single sign-on between the society website and Oxford Academic. Society member access to a journal is achieved in one of the following ways: If you cannot sign in, please contact your librarian. If your institution is not listed or you cannot sign in to your institution’s website, please contact your librarian or administrator.Įnter your library card number to sign in. Following successful sign in, you will be returned to Oxford Academic.When on the institution site, please use the credentials provided by your institution.Select your institution from the list provided, which will take you to your institution's website to sign in. ![]() Click Sign in through your institution.Shibboleth / Open Athens technology is used to provide single sign-on between your institution’s website and Oxford Academic. This authentication occurs automatically, and it is not possible to sign out of an IP authenticated account.Ĭhoose this option to get remote access when outside your institution. Typically, access is provided across an institutional network to a range of IP addresses. If you are a member of an institution with an active account, you may be able to access content in one of the following ways: ![]() Get help with access Institutional accessĪccess to content on Oxford Academic is often provided through institutional subscriptions and purchases. For cases of CCB poisoning where cardiotoxicity is evident, a combination of calcium and epinephrine should be used initially, reserving HDIDK for refractory cases. For cases of β-blocker poisoning where symptomatic bradycardia and hypotension are present, high-dose glucagon is considered the first-line antidote. Poisoning by β-blockers or CCBs usually produces hypotension and bradycardia, which may be refractory to standard resuscitation measures. Health-system pharmacists should be aware that when these drugs are used as antidotes, higher than normal dosing is needed.Ĭonclusion. For cases of CCB poisoning where cardiotoxicity is evident, first-line therapy is a combination of calcium and epinephrine high-dose insulin with supplemental dextrose and potassium therapy (HDIDK) is reserved for refractory cases. ![]() Traditionally, antidotes for CCB overdose have included calcium, glucagon, adrenergic drugs, and amrinone. However, in β-blocker poisoning where symptomatic bradycardia and hypotension are present, high-dose glucagon is considered the first-line antidote. Therapies include β-agonists, glucagon, and phosphodiesterase inhibitors. Poisoning by CCBs is characterized by cardiovascular toxicity with hypotension and conduction disturbances, including sinus bradycardia and varying degrees of atrioventricular block. The common feature of β-blocker toxicity is excessive blockade of the β-receptors resulting in bradycardia and hypotension. In overdose, β-blockers and CCBs have similar presentation and treatment overlaps and are often refractory to standard resuscitation measures. Beta-blockers and CCBs represent the most important classes of cardiovascular drugs. Overdoses with cardiovascular drugs are associated with significant morbidity and mortality. The toxic effects and treatment of β-adrenergic blocker and calcium-channel blocker (CCB) overdose are reviewed.
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