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[每周一问]NO.15-Cardiopulmonary resuscitation (CPR)

Cardiopulmonary resuscitation (CPR) is a skill that has significant impact on asystolic patient survival. We'll discuss some recent changes in the performance of this skill. Today we'll discuss some special challenges in resuscitation.
1.  What should be the response to cocaine toxicity?
2.  What should be the response to tricyclic overdose?
3.  What should the response be to acute opiate overdose?
今天我们讨论关于急救复苏中的一些特殊问题：
1.  可卡因中毒如何处理？
2.  三环类抗抑郁药过量如何处理？
3.  急性阿片剂过量如何处理？

Toxicity, Cocaine

Antidepressant Overdose and Treatment
Management of Opiate Withdrawal

本期参考答案：
1.可卡因中毒如何处理？
药物导致的高血压急症常作用短暂，常不需要有创治疗。可卡因特别被强调与高血压、室性心律失常和冠状动脉综合征相关。治疗其中毒的关键是避免β受体阻滞剂（Ⅲ级）的使用，特别是非选择性阻滞剂如心得安，因为其导致无法对抗的α肾上腺素能兴奋，加重高血压[1]。地西泮（Ⅱa级）除了作用短暂、titrateable（可滴定？）抗高血压药如硝酸盐类（Ⅰ级）应该作为治疗的首选。如果是难治性高血压，可以考虑使用α肾上腺素能阻滞剂（Ⅱb级），此时需注意心动过速和低血压的出现[2]。
2.三环类药物过量如何处理？
三环抗抑郁药（TCA）为钠通道阻滞剂，可导致心室传导的延长（增加PR和QT间期）与最终单一型VT[3]。最常见临床特征是口干、视力模糊、瞳孔散大、窦性心动过速、锥体束征和嗜睡。重度中毒时，可出现昏迷、子痫、呼吸抑制、低血压和心律失常。
对于TCAs中度的治疗主要是支持，然而，很多人推荐进行洗胃[4]。因为这些病人常处于低氧血症和酸中毒，作为一种姑息性治疗可能导致呼吸性碱中毒，直到碳酸氢钠（Ⅱa级）使用。
子痫应该使用安定或氯乙甲噻唑[镇静催眠、抗惊厥药]治疗。低血压应该给于补液，必要时给于拟交感神经药（多巴胺或多巴酚丁胺）。仅在低血压纠正失败情况下的循环衰竭时，使用抗心律失常药，如利多卡因和普鲁卡因酰胺（不确定级），因为其副作用未能充分研究。虽然毒扁豆碱[拟胆碱药]可逆转TCA中毒的大多数体征，但是是通过其严重的毒性作用而起效的，可产生明显副作用。即使如此，毒扁豆碱液应该被保留用于那些有昏迷或顽固性心脏毒性或子痫并发症的患者。最后，药物筛选和TCA血清浓度的定量测定在少数存在严重的、罕见或持续时间长的症状的病人中可能是有用的。
3.急性阿片剂过量如何处理？
如果呼吸功能不全的病人怀疑有阿片剂过量而脉搏存在，应该给于肌肉（IM）、皮下（SC）或静脉注射纳洛酮。IM和SC途径对于静脉吸毒者可减少严重脱瘾性脑综合征的发生率。纳洛酮的初次剂量为0.4-0.8mg静注或0.8mg肌注或SC，并应达到预期的呼吸反射和充分的通气[2]。不推荐达到完全唤醒的程度，因为突然对阿片剂的阻断可增加一些并发症的发生，如肺水肿、室性心律失常以及严重的躁动[5]。

What should be the response to cocaine toxicity?
Drug induced hypertensive emergencies are often short lived, and often aggressive therapy is not needed. Cocaine in particular is noted to be associated with hypertension, ventricular arryhthmias, and acute coronary syndromes. The important key to the treatment of this toxicity is avoiding the use of beta blockers (Class III), especially nonselective agents such as propranolol, as this allows for unopposed alpha adrenergic stimulation and worsening of the hypertension (1). Benzodiazepines (Class IIa) in addition to a short acting, titrateable antihypertensive such as nitrates (Class I) should be the first line of therapy. Should the hypertension be refractory, the use of alpha adrenergic blocking agents (Class IIb) may be considered, keeping in mind that tachycardia and hypotension may result (2).
What should be the response to tricyclic overdose?
Tricyclic antidepressants (TCA) are sodium channel blockers that may result in prolongation of ventricular conduction (increases the PR and QT intervals) and ultimately monomorphic VT (3). The most common clinical features are dry mouth, blurred vision, dilated pupils, sinus tachycardia, pyramidal neurological signs, and drowsiness. In severe poisoning, there may be coma, convulsions, respiratory depression, hypotension, and arrythmias.
Treatment of poisoning due to the TCAs is mainly supportive, however, gastric aspiration and lavage has been recommened by some (4). As these patient are often hypoxemic and acidotic, respiratory alkalosis can be induced as a temporizing measure, until the drug of choice sodium bicarbonate (Class IIa) can be used. Convulsions should be treated with diazepam or chlormethiazole. Hypotension should be treated by fluid replacement and sympathomimetic agents (dopamine or dobutamine) if necessary. Antiarrhythmic drugs, e.g., lidocaine and procainamide (Class indeterminate), should be employed only if there is evidence of circulatory failure which fails to respond to correction of hypotension, as their effects have not been adequately studied. Although physostigmine salicylate can reverse most of the features of TCA poisoning, its effects are short-lived in serious toxicity and it can produce significant side effects. As such, physostigmine should be reserved for those patients who have complications of coma or who have resistant cardiotoxicity or convulsions. Finally, drug screening and quantitative determination of tricyclic antidepressant serum concentrations can be useful in a minority of patients who have severe, unusual or prolonged symptoms.
What should the response be to acute opiate overdose?
If a pulse exists in patients with respiratory insufficiency suspected of an opiate overdose, naloxone should be administered, either intramuscularly, subcutaneously, or intravenously. IM and SC routes may provide less risk of severe withdrawal in patients addicted to IV narcotics. The initial dose of naloxone in 0.4-0.8 mg IV or 0.8 mg IM or SC and should be given to the desired endpoint of adequte airway reflexes and ventilation (2). The goal of complete arousal is not recommended, as the abrupt withdrawal from opiates may increase such complications as pulmonary edema, ventricular arrhythmias, and severe agitation (5).
References:
1.  Ramoska E, Sacchetti AD. Propranolol-induced hypertension in treatment of cocaine intoxication. Ann Emerg Med. 1985;14(11):1112-3.
2.  Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Part 6: advanced cardiovascular life support: 7C: a guide to the International ACLS algorithms. The American Heart Association in collaboration with the International Liaison Committee on Resuscitation. Circulation. 2000;102(8 Suppl)142-57.
3.  Kresse-Hermsdorf M, Muller-Oerlinghausen B. Tricyclic neuroleptic and antidepressant overdose: epidemiological, electrocardiographic, and clinical features--a survey of 92 cases. Pharmacopsychiatry. 1990;23 Suppl 1:17-22.
4.  Crome P. Poisoning due to tricyclic antidepressant overdosage. Clinical presentation and treatment. Med Toxicol. 1986;1(4):261-85.
5.  Brown TC. Tricyclic antidepressant overdosage: experimental studies on the management of circulatory complications. Clin Toxicol. 1976;9(2):255-72.
6.  Evans LE, Swainson CP, Roscoe P, Prescott LF. Treatment of drug overdosage with naloxone, a specific narcotic antagonist. Lancet. 1973;1(7801):452-5.
Site Editor: Stephen B. Corn, M.D. and B. Scott Segal, M.D.
Department of Anesthesia, Harvard Medical School
Founders and Editors-in-Chief: Stephen B. Corn, M.D. and B. Scott Segal, M.D.
Department of Anesthesiology, Perioperative and Pain Medicine, Harvard Medical School